United States
               Environmental Protection
               Agency
              Environmental Criteria and
              A-ssessrrent Office
              Research Triangle Park NC 27711
EPA-600/8-82-02(
December 1982
Final Report
               Research and Development
?/EPA
Air Quality
Criteria for
Oxides of Nitrogen

-------
                                  EPA-600/8-82-026F
                                  December 1982
AIR  QUALITY CRITERIA
               FOR
OXIDES  OF NITROGEN
            FINAL REPORT
  Environmental Criteria and Assessment Office
 Office of Health and Environmental Assessment
     Office of Research and Development
    U.S. Environmental Protection Agency
      Research Triangle Park, IM.C. 27711

-------
                NOTICE

Mention of trade names or commercial products
does not constitute endorsement or recommenda-
tion for use.
                   n

-------
                                  PREFACE

    , This  criteria document  focuses  on  a  review and  assessment  of  the
effects  on  human  health  and  welfare of the  nitrogen  oxides,  nitric oxide
(NO)  and  nitrogen dioxide  (NCL),  and the  related  compounds,  nitrites,
nitrates, nitrogenous acids, and nitrosami'nes.  Although the emphasis is on
presentation of  health  and welfare effects data, other scientific data are
presented in order to provide a better understanding of these pollutants in
the environment.   To this end, separate chapters are included which discuss
the  nitrogen  cycle,  sources and emissions,  atmospheric  chemical  processes
which  transform  emissions  of  nitrogen oxides  into related  airborne  com-
pounds,  transport  and  removal  processes,  measurement methods,  and atmo-
spheric concentrations of nitrogenous pollutants.
     Of  the  oxides of  nitrogen which  occur in the atmosphere, NO-  is  the
compound  of most  concern  for human  health.   Controlled human  exposure
studies  indicate  that  in  some  subjects increases  in  airway  resistance of
the pulmonary  system  are  produced  by short exposure to NOo  concentrations
in the range of 1300 to 3760 ug/m   (0.7 to 2.0 ppm).  Studies  of population
exposure  have  demonstrated increased incidences of  acute  respiratory  ill-
ness in young  children  associated  with combustion products from gas  stoves
of which N02 is a significant component, but the exact effective concentra-
tions and exposure times are difficult to  determine.
     Although  animal  studies  do provide  support for  the  mechanism  of  in-
creased  susceptibility  to some respiratory  pathogens as  a consequence of
NO  exposure,  they cannot provide  quantitative data.    Increases  in  animal

-------
susceptibility due to repeated short-term exposures eventually are as large
as those produced by continuous exposure to the same concentration.
     Many other  effects have  been  shown  to  occur in  animals  at exposure
concentrations comparable  to those causing increases  in  susceptibility to
respiratory  infections.    Usually,  these  have  not  been demonstrated  iYi
humans, but the potential for their occurrence cannot be ignored.
     Air pollution  degrades  the appearance of distant  objects  and  reduces
the range at which they can be distinguished from the background.   Nitrogen
dioxide  does  not  significantly reduce visual range but can be responsible
for a  portion of  the  brownish coloration  observed in polluted  air.   NCL
acts as  a  blue-minus  filter for  transmitted light.  The  strength  of this
filter effect  is   theoretically  determined by the integral  of NOo  concen-
tration along  the  sight path.   An NO* concentration-times-distance  product
of  less than  0.1   ppm-km  NO* is  sufficient to produce a  color shift which
is  distinguishable  in   carefully  controlled  laboratory   tests.   However,
empirical  observations  under a variety of conditions are  needed  to deter-
mine the perceptibility of NOp in ambient air.
     Nitrogen  dioxide   and  particulate  nitrates  may  also   contribute  to
pollutant haze.  The discoloration of the horizon sky due  to N(L absorption
is  determined  by the  relative concentrations of  NO-  and light-scattering
particles.   At a visual range of 100 km, typical  of the rural  great plains
area .of the  United  States, as  little  as  0.003  ppm (6 ug/m ) N02 can color
the horizon noticeably.   At a visual range of 10 km, typical  of urban haze,
at  least  .0.03 ppm (60  pg/m )  N02   would be required  to  produce the same
effect.  Estimates  of  the  possible ro.Te played by particulate nitrates are
currently hampered by the lack of high-quality data on their concentrations
in ambient air.
                                     iv                        .

-------
     Oxides  of  nitrogen  as a class are major precursors to acidic precipi-
tation, which is defined as rainwater or snow having a pH of less than 5.6,
the  minimum  expected  from  atmospheric  carbon  dioxide.    Currently,  the
annual  average  pH of  precipitation in  the  northeastern United  States  is
between 4.0  and 5.0, and average pH values around 4.5 have been reported as
far  south  as northern Florida.   The pH of individual rain events may be as
low  as  2.2 to 3.0.   Data,  based  on computations from chemical analyses of
rain, indicate  that  the  area affected by acidic rainfall has grown signif-
icantly over the  past 20 years.  In the United States, sulfuric and nitric
acids  make  the  primary  contributions  to  the  acidity in  precipitation.
There  is   strong  evidence  that the  role  of  the  nitrate  ion  has  become
increasingly important in recent years.
     A number of direct effects of acidic precipitation on both terrestrial
and.  aquatic  biota have  been  reported.   The effects  include  tissue  damage
and  physiological impairment  in plants,  lethal  effects on fish, and possi-
ble  impacts  on  host-parasite  or  pathogenic processes.  These  effects  may
occur at  specific short  periods  during an  organism's life  cycle,  or  may
develop after repeated exposure.  The ecological consequences of effects on
specific terrestrial  organisms or  on  the quality  of soils  have  not been
well   measured.   The  long-term effects  of acidification  on  aquatic  eco-
systems are widespread, regionally and globally, and can include decimation
of fish populations.   Little is known about the  recovery of ecosystems from
such effects, but liming of soils and Takes has  been successful  in a limited
number of cases.
     Oxides of nitrogen have also been shown to  affect vegetation adversely.
When crops  are exposed to nitrogen dioxide alone in controlled studies,  the

-------
  ambient concentrations producing measurable injury are above those normally
  occurring  in  this country.    Exceptions  to this generality  have been ob-
  served:  the  growth of  Kentucky bluegrass was reduced about  25  percent by
  exposures to 210 |jg/m  (0.11 ppm) N02 for 103.5 hours per week for 20 weeks
  during the  winter months.   A  number of controlled  studies  on  mixtures of
 ' nitrogen  dioxide  with sulfur  dioxide, show effects  greater,  in  some casesy
  much greater, than those effects caused by the individual pollutants alone.
  Some  leaf injury  to  pinto bean, radish, soybean, tomato,  oat  and tobacco
  occurred  after  4-hour  exposure to 280 |jg/m   (0.15 ppm)  N02 in combination
  with 260  [jg/m   (0.1  ppm) S02-   Similar results were  observed in green peas
  and Swiss  chard.   Kentucky bluegrass showed reductions in yield parameters
                                                                      2
  ranging from 30 to 90 percent upon exposure for 20 weeks to 210 (jg/m  (0.11
                                        3
  ppm) N02  in  combination  with 290 (jg/m   (0.11  ppm)  S02 for 103.5 hours per
  week.
       Nitrogen dioxide has been found to cause deleterious effects to a wide
  variety  of textile  dyes and  fabrics,  plastics,  and  rubber.   Significant
  fading of certain dyes on cotton and rayon has been shown after 12 weeks of
                      o
  exposure  to  94 pg/m   (0.05  ppm) N02 at high  humidity  and temperature .(90
  percent,  90°F).  Similar effects were obtained under similar conditions for
                                     2
•  various dyes on nylon,  at 188 ug/m  (0.1 ppm).  Yellowing of several white
  fabrics  has  been  shown  in exposure to  376 ug/m  (0.2  ppm) for 8 hours.
  Nitrates  and  nitrogenous acids have been  implicated  as  possible causative
  and/or accelerating agents in the wet corrosion of metals and deterioration
  of electrical contracts.
                                      VI

-------
                                 ABSTRACT
                    o

     This document  is  an evaluation and assessment  of  scientific informa-
tion relative to determining the health and welfare effects associated with
exposure to  various  concentrations  of  nitrogen oxides in ambient air.   The
document is  not intended  as  a complete,  detailed literature  review.   It
does not  cite every published article relating to oxides-of  nitrogen and
their effects  in the  environment.   The literature  through 1978  has  been
reviewed thoroughly  for  information relative to criteria.  The  major  gaps
in  our   current  knowledge,  relative  to  criteria,  have been  identified.
     Though  the  emphasis  is   on  the  presentation of  data on  health  and
welfare  effects, other scientific  data  are  presented and evaluated in order
to provide a better understanding  of the pollutants in the environment.   To
this end,  separate  chapters  concerning the  properties  and principles  of
formation,  emissions,  analytical  methods of  measurement,  observed ambient
concentrations, the global  cycle,  effects  on vegetation  and microorganisms,
mammalian  metabolism,  effects on  experimental  animals,  and  effects  on
humans  are  included.
                                    vn

-------
                               TABLE OF CONTENTS
                                                                         Page

PREFACE	.  .  .  .  .       iii
ABSTRACT	       vii
LIST OF FIGURES	       xvi
LIST OF TABLES	        xx
LIST OF ABBREVIATIONS, ACRONYMS AND SYMBOLS 	       xxy
CONTRIBUTORS AND REVIEWERS	     xxxrv
SCIENCE ADVISORY BOARD COMMITTEE  	      xlii

1.   SUMMARY  OF EFFECTS OF OXIDES OF NITROGEN AND RELATED COMPOUNDS
     ON HUMAN HEALTH AND WELFARE	       1-1
     1.1  INTRODUCTION	       1-1
     1.2  SOURCES, TRANSFORMATIONS AND AMBIENT LEVELS OF NITROGEN
          OXIDES	i    1-2
     1.3  EFFECTS OF NITROGEN OXIDES ON HUMAN HEALTH  .	       1-3
          1.3.1  Nitrogen Dioxide Respiratory System Effects  .  .  .       1-4
                 1.3.1.1  Controlled Human Exposure Studies ....       1-5
                 1.3.1.2  Human Epidemiology Studies  	       1-12
                 1.3.1.3  Animal Tox.icology Studies	       1-20
-.         1.3.2  N02 Sensory System Effects	       1-21
          1.3.3  Summary of Major Health Effects Conclusions.  .  .  .       1-26
     1.4  WELFARE EFFECTS OF NITROGEN OXIDES  	       1-27
          1.4.1  Nitrogen Oxides, Acidic Deposition Processes,
     .   • •  -      and Effects	       1-28
          1.4.2  Effects of NO  on Ecosystems and Vegetation  .  .  .       1-35
          1.4.3  Effects of Nitrogen Oxides on Materials  .....       1-37
          1.4.4  Effects of Nitrogen on Visibility	       1-39

2.   INTRODUCTION	       2-1

3.   GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NO  AND NO -
     DERIVED POLLUTANTS	x.  .......       3-1
     3.1  INTRODUCTION AND OVERVIEW	       3-1
     3.2  NITROGEN OXIDES	       3-2
          3.2.1  Nitric Oxide (NO)	       3-2
          3.2.2  Nitrogen Dioxide (N0?) 	       3-9
          3.2.3  Nitrous Oxide (N?0) *	       3-9
          3.2.4  Unsymmetrical Nitrogen Trioxide (OONO)  	       3-10
          3.2.5  Symmetrical Nitrogen Trioxide (NO,)  	       3-10
          3.2.6  Dinitrogen Trioxide (Np03) ...   	       3-11
          3.2.7  Dinitrogen Tetroxide (N90d)  	       3-11
     3.3  NITRATES, NITRITES, AND NITROGEN^ACIDS	  .       3-11
     3.4  AMMONIA (NhU)	       3-13
     3.5  N-NITROSO COMPOUNDS 	       3-13
     3.6  SUMMARY	       3-14
          3.6.1  Nitrogen Oxides	       3-15
          3.6.2  Nitrates, Nitrites and Nitrogen Acids   .......       3-15
          3.6.3  N-Nitroso Compounds  	       3-16
     3.7  REFERENCES FOR CHAPTER 3  .  .  .  .	       3-17
                                   v i i i

-------
                                                                         Page

4.   THE NITROGEN CYCLE	        4-1
     4.1  INTRODUCTION	:	        4-1
     4.2  THE NITROGEN CYCLE	        4-1
     4.3  THE GLOBAL CIRCULATION OF NITROGEN	        4-4
          4.3.1  Important Nitrogen Fluxes  	        4-4
                 4.3.1.1  Biological Nitrogen Fixation  	        4-5
                 4.3.1.2  Industrial Nitrogen Fixation  	        4-8
                 4.3.1.3  Nitrogen Fixation by Other Processes  .  .        4-8
                 4.3.1.4  Nitrates, Nitrites and the Nitrogen Cycle       4-8
                 4.3.1.5  Nitrates as Fertilizers  	        4-8
     4.4  AMMONIFICATION AND NITRIFICATION  	        4-9
     4.5  NITRIC OXIDE, NITROGEN DIOXIDE AND THE NITROGEN CYCLE .  .        4-9
     4.6  NITROUS OXIDE AND THE NITROGEN CYCLE  	        4-11
     4.7  ORGANIC NITROGEN AND THE NITROGEN CYCLE  	        4-12
     4.8  AMMONIA AND THE NITROGEN CYCLE	        4-14
     4.9  DENITRIFICATION	        4-14
     4.10 ACIDIC PRECIPITATION  	        4-15
     4.11 SUMMARY	        4-15
     4.12 REFERENCES FOR CHAPTER 4	        4-19

5.   SOURCES AND EMISSIONS	        5-1
     5.1  INTRODUCTION	        5-1
     5.2  ANTHROPOGENIC EMISSIONS OF NO   	        5-1
          5.2.1  Global Sources of NO  x	        5-2
          5.2.2  Sources of NO  in thl United States	      * 5-2
     5.3  EMISSIONS OF AMMONIAX	        5-14
     5.4  AGRICULTURAL USAGE OF NITROGENOUS COMPOUNDS 	        5-16
     5.5  SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS.  .        5-16
          5.5.1  Anthropogenic Sources of N-Nitroso  Compounds .  .  .        5-16
     :     5.5.2  Volatilization from Other Media  	        5-19
          5.5.3  Atmospheric Formation:   N-Nitroso Precursors .  .  .        5-19
          5.5.4  N-Nitrosamines in Food, Water and Tobacco
                 Products	        5-20
     5.6  SUMMARY	        5-21
          5.6.1  Sources and Emissions of NO	        5-21
          5.6.2  Sources and Emissions of Otner  Nitrogenous
                 Compounds	'	        5-22
     5.7  REFERENCES FOR CHAPTER 5	        5-23

6.   ENVIRONMENTAL TRANSPORT AND TRANSFORMATION  	      .6-1
     6.1  CHEMISTRY OF THE OXIDES OF NITROGEN IN THE LOWER
          ATMOSPHERE	        6-1
          6.1.1  Reactions Involving Oxides of Nitrogen ......        6-2
          6.1.2  Laboratory Evidence of the NO~-to-Precursor
                 Relationship	    	        6-12
          6.1.3  NO  Chemistry in Plumes	        6-15
          6.1.4  Computer Simulation of Atmospheric  Chemistry .  .  .        6-16
     6.2  NITRITE AND NITRATE FORMATION	        6-18

-------
     6.3  TRANSPORT AND REMOVAL OF NITROGENOUS SPECIES  	       6-22
          6.3.1  Transport and Diffusion	       6-23
          6.3.2  Removal  Processes  	       6-24
                 6.3.2.1  Dry Deposition of Gases 	       6-26
                 6.3.2.2  Dry Deposition of Particles 	       6-?7
                 6.3.2.3  Wet Deposition  	       6-2
          6.3.3  Source-Receptor Relationships  .	       6-2b
     6.4  MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION 	       6-30
          6.4.1  Non-Photochemical Reaction of Gaseous Amines              li
                 with Oxides of Nitrogen and Nitrous Acid 	       6-30
          6.4.2  Photochemical Reactions of Amines  	       6-32
          6.4.3  Formation of Nitrosamine in Atmospheric
                 Aerosols	       6-37
          6.4.4  Environmental Implications 	  	       6-37.
     6.5  SUMMARY	       6-38
          6.5.1  Chemistry of Oxides of Nitrogen in the Lower
                 Atmosphere	       6-38
          6.5.2  Nitrate and Nitrite Formation  	       6-39
          6.5.3  Transport and Removal  of Nitrogenous Species ...       6-40
          6.5.4  Mechanisms of Atmospheric Nitrosamine Formation  .       6-40
          6.5.5  Source-Receptor Relationships  .	       6-41
     6.6  REFERENCES FOR CHAPTER 6	       ,6-42

7.    SAMPLING AND ANALYSIS FOR AMBIENT  NO  AND
     NO -DERIVED POLLUTANTS	x	       7-1
     7.1  INTRODUCTION	       7-1
     7.2  ANALYTICAL METHODS FOR NO	       7-5
          7.2.1  The Reference Meth6d for N02:
                 Gas-Phase Chemiluminescence  	       7-5
          7.2.2  Other Analytical  Methods for NO?	       7-6
                 7.2.2.1  Griess-Saltzman Method  	       7-6
                          7.2.2.1.1  General description of method.       7-6
                          7.2.2.1.2  Continuous Saltzman procedures       7-7
                          7.2.2.1.3  Manual Saltzman procedure.  .  .       7-8
                 7.2.2.2  Jacobs-Hochheiser Method  	       7-9
                 7.2.2.3  Triethanolamine Method  .  	       7-10
                 1.2.2A  Sodium Arsenite Method	       7-10
                 7.2.2.5  TGS-ANSA Method 	       7-'ll
                 7.2.2.6  Other Methods 	       7-12
                 7.2.2.7  Summary of Accuracy and Precision
                          of N0? Measuring Methods	       7-12
          7.2.3  Analytical Methods for NO	       7-14
          7.2.4  Sampling for'NO	       7-14
          7.2.5  Calibration of NO and  N02 Monitoring
                 Instruments	       7-16
     7.3  ANALYTICAL METHODS AND SAMPLING FOR NITRIC ACID 	       7-18
     7.4  ANALYTICAL METHODS AND SAMPLING FOR NITRATE 	       7-19
          7.4.1  Sampling for Nitrate from Airborne Particulate
                 Matter	       7-19
          7.4.2  Analysis of Nitrate from Airborne Particulate
                 Matter	       7-23

-------
          7.4.3  Nitrate in Water	       7-25
          7.4.4  Nitrate in Soil	«	       7-27
          7.4.5  Nitrate in Plant and Animal Tissue	       7-29
     7.5  SAMPLING AND ANALYTICAL METHODS FOR NITROSAMINES  ....       7-29
          7.5.1  Nitrosamines in Air	       7-29
          7.5.2  Nitrosamines in Water	  .	       7-30
          7.5.3  Nitrosamines in Food	       7-30
     7.6  SUMMARY	'	       7-30
     7.7  REFERENCES FOR CHAPTER 7	       7-32

8.   OBSERVED ATMOSPHERIC CONCENTRATIONS OF NOV AND OTHER
     NITROGENOUS COMPOUNDS	x	      8-1
     8.1  ATMOSPHERIC CONCENTRATIONS OF'WT 	       8-1
          8.1.1  Background Concentrations of NO	       8-2
          8.1.2  Ambient Concentrations of NO	       8-3
                 8.1.2.1  Monitoring for NO  x	       8-3
                 8.1.2.2  Sources of Data .	       8-5
          8.1.3  Historical Measurements of NO  Concentrations  .  .       8-5
          8.1.4  Recent Trends in NO- Concentrations  	       8-14
          8.1.5  Seasonal Variations in N0? Concentrations  ....       8-14
          8.1.6  Recently Observed Atmospheric Concentrations
                 of N02	       8-14
          8.1.7  Spatial and Temporal  Variations of NO^
                 Concentrations as Related to Estimation of
                 Human Exposures	       8-50
                 8.1.7.1  Spatial and Temporal Variations of
                          Local N02 Concentrations	       8-50
                 8.1.7.2  Estimating Human Exposure 	       8-64
     8.2  ATMOSPHERIC CONCENTRATIONS OF NITRATES  	       8-73
     8.3  ATMOSPHERIC CONCENTRATIONS OF N-NITROSO COMPOUNDS ....       8-74
     8.4  SUMMARY	       8-74
          8.4.1  Atmospheric Concentrations of NO,,	       8-74
          8.4.2  Atmospheric Concentrations of Nitrates 	       8-76
          8.4.3  Atmospheric Concentrations of N-Nitroso
                 Compounds	       8-76
     8.5  REFERENCES FOR CHAPTER 8	       8-77

9.   PERTURBATIONS OF THE STRATOSPHERIC OZONE LAYER 	       9-1
     9.1  INTRODUCTION	       9-1
     9.2  DIRECT ROLE OF NITROGEN OXIDES IN THE OZONE
          BALANCE OF THE ATMOSPHERE	       9-2
     9.3  INDIRECT ROLE OF NITROGEN OXIDES IN THE OZONE
          BALANCE OF THE ATMOSPHERE	       9-3
     9.4  OTHER ATMOSPHERIC EFFECTS OF NITROGENOUS COMPOUNDS  ...       9-4
     9.5  SUMMARY	       9-6
     9.6  REFERENCES FOR CHAPTER 9	       9-7

-------
                                                                             Page

10.   EFFECTS OF NITROGEN OXIDES ON VISIBILITY 	  10-1
     10.1 NITROGEN OXIDES AND LIGHT SCATTERING AND ABSORPTION 	  10-1
     10.2 EFFECT OF NITROGEN DIOXIDE ON COLOR	 .	  10-2
          10.2.1  Nitrogen Dioxide and Plumes 	  10-2
          10.2.2  Nitrogen Dioxide and Haze	10-2
     10.3 EFFECT OF PARTICULATE NITRATES ON VISUAL RANGE	  10-4
     10.4 SUMMARY	  10-8
     10.5 REFERENCES FOR CHAPTER 10	,  10-H
                                                                           \
11.   ACIDIC DEPOSITION  	  11-1
     11.1  INTRODUCTION	'	11-1
          11.1.1    Overview of the Problem 	  11-1
          11.1.2    Ecosystem Dynamics  	  11-6
     11.2  CAUSES OF ACIDIC PRECIPITATION   	  11-L
          11.2.1    Emissions of Nitrogen and Sulfur Oxides 	  ll-i;
          11.2.2    Transport of Nitrogen and Sulfur Oxides 	  11-L
          11.2.3    Formation 	  11-2:
                    11.2.3.1  Composition and pH of Precipitation 	  11-21
                    11.2.3.2  Seasonal Variations in Nitrates and Sulfates.  11-2!
                    11.2.3.3  Geographic Extent of Acidic Precipitation .   .  11-3!
          11.2.4    Acidic Deposition 	 .  	  11-3!
     11.3 EFFECTS OF ACIDIC DEPOSITION	11-3!
          11.3.1    Aquatic Ecosystems	11-3'
                    11.3.1.1  Acidification of Lakes and Streams  	  11-3
                    11.3.1.2  Effects on Decomposition  	  11-4
                    11.3.1.3  Effect on Primary Producers and Primary
                              Productivity  	  11-4!
                    11.3.1.4  Effects on Invertebrates	  11-5!
                    11.3.1.5  Effects on Fish	11-5!
                    11.3.1.6  Effects on Vertebrates Other Than Fish  ...  11-6'
          11.3.2    Terrestrial Ecosystems	  11-61
                    11.3.2.1  Effects on Soils	  11-6!
                    11.3.2.2  Effects on Vegetation 	  11-7!
                              11.3.2.2.1  Direct Effects on Vegetation  .   .  11-7'
                    11.3.2.3  Effects on Human Health 	  11-8'
                    11.3.2.4  Effects of Acidic Precipitation on Materials.  11-8'
     11.4 ASSESSMENT OF SENSITIVE AREAS	11-91
          11.4.1    Aquatic Ecosystems	'  11-9!
          11.4.2   'Terrestrial Ecosystems  	  11-91
     11.5 SUMMARY .	  ll-H
     11.6 REFERENCES.	  11-H

12.   EFFECTS OF NITROGEN OXIDES ON NATURAL ECOSYSTEMS,
     VEGETATION AND MICROORGANISMS  	  12-1
     12.1  INTRODUCTION	12-1
     12.2  EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS	  12-2
           12.2.1  Effects of Nitrates	  12-5
                                   XII

-------
           12.2.2  Terrestrial Ecosystems 	   12-6
           12.2.3  Effects of Nitrogen Oxides 	   12-8
                   12.2.3.1  Effects on Terrestrial Plant
                             Communities	  .   12-8
                   12.2.3.2  Effects on Animal Communities  ........   12-9
                   12.2.3.3  Effects of Nitrogen Oxides on
                             Microbial Processes in Nature  	   12-10
           12.2.4  Aquatic Ecosystems Nitrogen and Eutrophication   ....   12-10
                   12.2.4.1  Eutrophication of Lakes  	   12-11
                   12.2.4.2  Eutrophication in Coastal Waters   	   12-14
                   12.2.4.3  Nitrogen Cycling in Eutrophic Lakes  .....   12-15
                   12.2.4.4  Form of Nitrogen Entering Lakes  	  .  .   12-17
           12.2.5  The Value of a Natural  Ecosystem   	   12-18
     12.3  EFFECTS ON NITROGEN OXIDES ON VEGETATION   	  ...   12-20
           12.3.1  Factors Affecting Sensitivity of Vegetation
                   to Oxides of Nitrogen	12-20
           12.3.2  Mode of Action   	12-25
           12.3.3  Visible Symptoms of N0? Injury   	   12-28
           12.3.4  Dose Response  .  .  .	12-29
                    12.3.4.1  Foliar Injury 	   12-29!
                    12.3.4.2  Growth  	   12~34:
           12.3.5  Effects of Gas Mixtures on Plants  	   12-40
                    12.3.5.1  Nitrogen Dioxide and Sulfur Dioxide 	   12-40
                    12.3.5.2  Nitrogen Dioxide With Other Pollutants.  .  .  .   12-44
     12.4  SUMMARY	12-45
           12.4.1  Effects on Ecosystems  	   12-45
           12.4.2  Effects on Vegetation  	   12-46
     12.5  REFERENCES FOR CHAPTER 12	12-47

13.   EFFECTS OF NITROGEN OXIDES ON MATERIALS  	   13-1
     13.1  EFFECTS OF NITROGEN DIOXIDE ON  TEXTILES  	   13-1
           13.1.1  Fading of Dyes by NO   	13-1
                   13.1.1.1  Fading of Dyes on Cellulose  Acetate  	   13-1
                   13.1.1.2  Fading of Dyes on Cotton  and Viscose
                             Rayon (Cellulosics)	13-2
                   13.1.1.3  Fading of Dyes on Nylon	   13-13
                   13.1.1.4  Fading of Dyes on Polyester	   13-13
                   13.1.1.5  Economic  Costs of NO -Induced Dye
                             Fading	   13-15
           13.1.2  Yellowing of White  Fibers by NO	  .   13-15
           13.1.3  Degradation of Textile  Fibers b$ NO  	   13-19
     13.2  EFFECTS OF NITROGEN DIOXIDE ON  PLASTICS ANDX
           ELASTOMERS	13-19
     13.3  CORROSION  OF METALS BY NITROGEN DIOXIDE	   13-20
           13.3.1  Pitting Corrosion  	   13-21
           13.3.2  Stress Corrosion   	   13-21
           13.3.3  Selective Leaching  	   13-21
           13.3.4  Correlation of Corrosion Rate with  Pollution  	   13-21
     13.4  REFERENCES FOR CHAPTER 13	13-26
                                    XTM

-------
14.   STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS  	   14-1
15.
14.1
14.2































14.3
14.4
14.5
14.6
14.7
14.8
INTRODUCTION 	 	
NITROGEN DIOXIDE 	
14.2.1 Respiratory Tract Transport and Absorption . . . .
14.2.2 Mortality 	 	 	
14.2.3 Pulmonary Effects 	
14.2.3.1 Host defense mechanisms 	
14.2.3.1.1 Interaction with
infectious agents 	
14.2.3.1.2 Mucociliary transport . . .
14.2.3.1.3 Alveolar macrophage . . . .
14.2.3.1.4 Immune system 	
14.2.3.2 Lung Biochemistry 	
14.2.3.2.1 Introduction 	
14.2.3.2.2 Lipid and diet effects . . .
14.2.3.2.3 Sulfhydryl compounds and
pyridine nucleotides ....
14.2.3.2.4 Effects on lung amino
acids, proteins, and
enzymes 	
14.2.3.2.5 Potential defense
mechanisms 	
14.2.3.3 Morphology Studies 	
14.2.3.4 Pulmonary Function . . . 	 	
14.2.3.5 Studies of Hyperplasia 	 ...
14.2.3.6 Edemagenesis and Tolerance 	
14.2.4 Extrapulmonary Effects 	
14.2.4.1 Nitrogen Dioxide-induced Changes in
Hematology and Blood Chemistry 	
14.2.4.2 Central Nervous System and
Behavioral Effects 	
14.2.4.3 Biochemical Markers of Organ Effects . .
14.2.4.4 Teratogenesis and Mutagenesis 	
14.2.4.5 Effects of NO,, on Body Weights 	
DIRECT EFFECT OF COMPLEX MIXTURES 	
NITRIC OXIDE 	
NITRIC ACID AND NITRATES 	
N-NITROSO COMPOUNDS 	
SUMMARY 	
REFERENCES FOR CHAPTER 14 	
EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN 	
15.1
15.2




INTRODUCTION 	
CONTROLLED HUMAN EXPOSURE STUDIES 	
15.2.1 Studies of Sensory Effects 	
15.2.1.1 Effects of Nitrogen Dioxide on
Sensory Systems 	
15.2.1.2 Sensory Effects Due to Exposure to
. . . 14-1
.- . . 14-1
. . . 14-1
. . . 14-3
. . . T4-3
. . . 1-3

i 14-3
. . . /• J-t o
. . . '14-18
. . . 14-18
. . . 14-24
. . . 14-28
. . . 14-28
. . . 14-28

. . . 14-38


. . . 14-38

. . . 14-40
. . . 14-41
. . . 14-49
. . . 14-54
. . . 14-57
. . . 14-59

. . . 14-59

. . . 14-63
. . . 14-63
. . . 14-68
. . . 14-71
. . . 14-71
. . . 14-78
. . . , 14-80
. . . 'i 14-82
. . . 14-84
. . . 14- 11C
. . . 15-1
. . . 15-1
. . . 15-3
. . . 15-3

. . . 15-3

                             Combinations of Nitrogen Dioxide and
                             Other Pollutants	   15-6
           15.2.2  Pulmonary Function 	   15-8
                   15.2.2.1  Controlled Studies of the Effect of
                             Nitrogen Dioxide on Pulmonary Function
                             in Healthy Subjects  	   15-8

                                   xiv

-------
                   15.2.2.2  The Effects of Nitrogen Dioxide
                             Exposure on Pulmonary Function in
                             Sensitive Subjects 	  15-17
     15.3  EPIDEMIOLOGICAL STUDIES  	  15-22
           15.3.1  Effects of N0? on Pulmonary Function	:{,.   .  15-22
           15.3.2  Effects of NO^ on Acute Respiratory Illness  	  15-27
                   15.3.2.1  Effects Associated with Ambient
                             Exposures	15-27
                   15.3.2.2  Effects Associated with Indoor
                             Exposures	15-29
                             15.3.2.2.1  Tobacco smoking studies  	  15-29
                             15.3.2.2.2  Community studies of gas
                                         combustion products  	  15-30
           15.3.3  Effects of NCL Pollution on Prevalence of
                   Chronic Respiratory Disease  	  15-38
           15.3.4  Extrapulmonary Effects of Exposure to NCL  	  15-39
     15.4  ACCIDENTAL AND OCCUPATIONAL EXPOSURES	*	15-40
     15.5  EFFECTS OF NO -DERIVED COMPOUNDS	  .  15-41
           15.5.1  Nitrates, Nitrites and Nitric Acid 	  15-42
           15.5.2  Nitrosamines 	  15-44
           15.5.3  Other Compounds  	  15-45
     15.6  SUMMARY AND CONCLUSIONS	15-46
           15.6.1  N02 Effects	15-46
                   15.6.1.1  Pulmonary function effects 	  15-46
                   15.6.1.2  Acute respiratory disease effects  	  15-50
                   15.6.1.3  Chronic respiratory disease effects  .  . .,; .  .  15-53
                   15.6.1.4  Sensory system effects 	  15-56
           15.6.2  Effects of NO -Derived Compounds 	  15-56
     15.7  REFERENCES ...........  	  15-57

GLOSSARY	G-l
                                    xv

-------
                               LIST OF FIGURES

Figure                                                                   Page

 ,1-1.     Average pH  Isopleths as Determined from  Laboratory Analyses
          of Precipitation Samples, Weighted by the  Reported Quantity
          of Precipitation	   1-30
 1-2.     Idealized Conceptual Framework  Illustrating the "Law of
          Tolerance"	'.....   1-3^

4 3-1.     Absorption  Spectrum  of Nitric Oxide  .	   3-5

 4-1.     Simplified  Global  Nitrogen Cycle (Terrestrial Systems)   .  .  .   4-2

 5-1.     Historic NO Emissions by Source Groups  	   5-4
 5-2.     Recent NO   Emissions by Source  Groups 	   5-7
 5-3.     Distribution of 1972 Nationwide NO   Emissions by Degree  of
          Urbanization	   5-8
 5-4.     Total NO  Emissions  by U.S. County	   5-10
 5-5.     Total NO* Emission Density by U.S. County	   5-11
 5-6.     Percent NO   Emissions Contributed by Major Point Sources   .  .   5-12
 5-7.     Trends in U.S. Usage of Nitrogenous Materials Applied as
          Fertilizer	   5-17

 6-1.     Paths of Nitrate Formation in the Atmosphere  	   6-21
 6-2.     Schematic Illustration of Scales of Motion in the Atmosphere.   6-25
 6-3.     Formation and  Decay  of Diethylnitrosamine, in the Dark and in
          Sunlight, from Diethylamine and from Triethylamine  	   6-36

 7-1.     Absolute Error in  N09, AN09, for 10 Seconds in Dark Sampling
          Line	 . .	   7-17

 8-1.     Trend Lines for Nitric Oxide Annual Averages in Five
          CAMP Cities	   8-8
 .8-2.     Trend Lines for Nitrogen Dioxide Annual  Averages in Five
          CAMP Cities	   8-11
 8-3.     Trends in N02  Air  Quality, Los  Angeles Basin, 1965-1974  .  .  .   8-13
 8-4.     Annual Air  Quality Statistics and Three-Year Moving
          Averages at Camden,  New Jersey	   8-,15
 8-5.     Annual Air  Quality Statistics and Three-Year Moving
          Averages at Downtown Los Angeles, California  	   8-16
 8-6.     Annual Air  Quality Statistics and Three-Year Moving
          Averages at Azusa, California 	   8-17
 .8-7.     Annual Air  Quality Statistics and Three-Year Moving
          Averages at Newark,  New Jersey  	   8-18
 8-8.     Annual Air  Quality Statistics and Three-Year Moving
          Averages at Portland, Oregon  	   8-19
 8-9.     Annual Average of  Daily Maximum 1-Hour N0? (4-Year Running
          Mean) in the Los Angeles Basin	   8-20
 8-10.    Seasonal N02 Concentration Patterns  of Three U.S. Urban
          Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations).  8-22
 8-11.    Seasonal NOp Concentration Patterns of Four U.S. Urban
          Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations).  8-23
 8-12.    Distribution of Maximum/Mean N0? Ratios  for 120 Urban
          Locations Averaged Over the Yeafs 1972,  1973, and 1974   .  .  .   8-41

                                    xv i

-------
                                                                          • Page

8-13.    Trends in the Maximum Mean N02 Ratio for Two Groups of Sites. .    8-42
8-14.    Average Diurnal Pattern for tne Month During Which the
         Highest 1-Hour N02 Concentrations were Reported 	    8-44
8-15.    One-Hr Average Concentration Profiles on Day of Peak NCL
         Concentration for Three U.S.  Cities	    8-45
8-16.    One-Hour NO,, Concentrations During Three Days of High
         Pollution in Three U.S. Cities	    8-46
8-17.    Nitric Oxide and Nitrogen Dioxide Concentrations at an Urban
         and a Rural Site in St. Louis, Missouri, on January 27-28,
         1976	    8-47
8-18.    Pollutant Concentrations in Central City St. Louis,
         October 1, 1976	    8-51
8-19.    St. Louis RAMS Station Locations	    8-59
8-20.    Location and Elevation of Clinch River Power Plant
         Monitoring Stations 	  	    8-65
8-21.    Population Exposed to N0« Daily Maximum Hourly Concentration
         Above the California One-Hour Standard at Various Frequencies .    8-69
8-22.    Population Exposed to N02 Hourly Average Concentration Above
         the California One-Hour Standard at Various Frequencies ....    8-71

10-1.    Transmittance of N0? Plumes for Selected Values of the
         Concentration - Distance Product  	    10-3
10-2.    Relative Horizon Brightness for Selected Values of the
         Concentration - Visual Range Product  	    10-5
10-3.    Normalized Light Scattering by Aerosols as a Function of
         Particle Diameter 	 ....    10-7

11-1.    The sulfur cycle	    11-9
11-2.    Law of tolerance	    11-11
11-3.    Historical patterns of fossil  fuel  consumption in the United
         States (adapted from Hubbert (1976)).  .	    11-14
11-4.    Forms of local  coal usage in the United States.   Electric power
         generation is currently the primary user of coal	    11-15
11-5A.    Trends in emissions of sulfur dioxides	    11-16
11-5B.    Trends in emissions of nitrogen oxides (1978) 	  11-16
11-6.    Characterization of U.S.  sulfur oxide emissions density by
         state	    11-17
11-7.    Characterization of U.S.  nitrogen oxide emissions density by
         state	    11-18
11-8.    The transport and deposition of atmospheric pollutants,
         particularly oxides of sulfur and nitrogen, that contribute
         to acidic precipitation	    11-20
11-9.    Trends in mean annual  concentrations of sulfate, ammonium and
         nitrate in precipitation	    11-23
11-10.    Comparison of weighted mean monthly concentrations of sulfate
         in incident precipitation collected in Walker Branch Watershed,
         TN, (WBW) and four MAP35 precipitation chemistry monitoring
         stations in New York,  Pennsylvania, and Virginia	 .    11-26

                                   xvii

-------
 Figure                                                                      Page

 11-11.    Seasonal  variations  in  pH(A)  and  ammonium  and  nitrate  concen-
       .   trations  (B)  in wet-only  precipitation at  Gainesville,  Florida  .   11-28
 11-12.    Seasonal  variation of precipitation pH in  the  New York
          Metropolitan  Area	    11-30
 11-13.    History of  acidic precipitation at various  sites in  and adjacent
          to  the State  of New  York	    11-32
 11-14.    pH  of rain  sample as measured .in  the  laboratory and  used in
          combination with the reported amount  of  precipitation  ......    11-34
tll-15.    Annual mas's transfer rates  of sulfate expressed as a percentage     *
          of  the estimated total  annual flux of the  element to the forest
          floor beneath a representative chestnut  oak stand ........    11-36
 11-16.    Schematic representation  of the hydrogen ion cycle	    11-39
 11-17.    pH  and calcium concentrations in  lakes in  northern and north-
•          western Norway sampled  as part of the regional survey  of 1975  .    11-42
 11-18.    The pH values and sulfur  loads in lake waters  with extremely
          sensitive surroundings	    11-43
 11-19.    Total dissolved Al as a function  of pH level in lakes  in
          acidified areas in Europe and North America	    11-45
 11-20.    pH  levels in  Little  Moose Lake, Adirondack  region of New York
          State, at a depth of 3  meters and at  the lake  outlet.  ......    11-46
 11-21.    Numbers of  phytoplankton  species  in 60 lakes having  different
          pH  values on  the Swedish  West Coast,  August 1976	-..    11-50
 11-22.    Percentage  distribution of  phytoplankton species and their
          biomasses	    11-51
 11-23.    The number  of species of  crustacean zooplankton observed in 57
          lakes during  a synoptic survey of lakes  in  Southern  Norway. .  .    11-56
 11-24.    Frequency distribution  of pH  and  fish population status in
          Adirondack  Mountain  lakes greater than 610  meters evaluation.
          Fish population status  determined by  survey gill netting
          during the  summer of 1975 (Schofield, 1976b)	  ....    11-59
 11-25.    Frequency distribution  of pH  and  fish population status in 40
          Adirondack  lakes greater  than 610 meters elevation,  surveyed
          during the  period 1929-1937 and again in 1975  (Schofield,
          1976b)	    11-60
 11-26.    Norwegian salmon fishery  statistics for  68  unacidified and 7
          acidified rivers	    11-62
 11-27.    Showing the exchangeable  ions of  a soil  with pH+7, the_ soil
          solution  composition, and the replacement  of Na  by  H   from
          acid rain	    11-67
 11-28.    Regions in  North America  with lakes that are sensitive to
          acidification by acid precipitation 	    11-92
.'11-29.    Equivalent  percent composition of major  ions in Adirondack lake
          surface waters (215  lakes)  sampled in June  1975	    11-94
 11-30.    Percent frequency distribution of sulfate  concentrations in
          surface water from lakes  in sensitive regions  (Schofield,
          1979)	    11-95
 11-31.    Soils of  the  Eastern United States sensitive to acid rain-
          fall (McFee,  1980).	    11-97

                                   xv i i i

-------
           Figure                                                                     Page

           12-1.     Schematic Representation of the Nitrogen Cycle Emphasizing
                    Human Activities that Affect the Flux of Nitrogen	   12-3
           12-2.     A Global Nitrogen Cycle	   12-7
           12-3.     Simplified Biological Nitrogen Cycle, Showing Major Molecular
                    Transformations 	   12-16
           12-4.     Schematic Presentation of Environmental Effects of Manipulation
                    of the Nitrogen Cycle	-	   12-38
           12-5.     Areal Loading Rates for Nitrogen Plotted Against Mean Depth
                    of Lakes	   12-39

           14-1.     Regression Lines of Percent Mortality of Mice Versus Length
                    of Continuous Exposure to Various NCL Concentrations Prior
                    to Challenge with Bacteria  ....  7	   14-12
           14-2.     Percent Mortality of Mice Versus the Length of Either
                    Continuous or Intermittent Exposure to 6,600 (jg/m  (3.5
                    ppm) NO- Prior to Challenge with Streptococci ..........   14-13
           14-3.     Percent Mortality of Mice Versus Length of Either Continuous  -
                    or Intermittent Exposure to 2,800 (jg/m  (1.5 ppm) N02
                    Prior to Challenge with Streptococci  	   14-14
           14-4.     Temporal Sequence of Injury and Repair Hypothesized from
                    Short-Term Single Exposure of Less Than 8 Hours	   14-95
           14-5.     Proportionality Between Effect (Cell Death) and
                    Concentration of N02 During a Constant Exposure Period  ....   14-102
           14-6.     Temporal Sequence of Jjijury and Repair Hypothesized from
                    Continuous Exposure to N09 as Observed in Experimental
                    Animals	  /	   14-103
-\

                                                xix

-------
                                  LIST OF TABLES
Table

 1-1.  Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
       in Controlled Studies of Healthy Humans Adults 	
 1-2.  Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
       in Controlled Studies of Sensitive Humans Adults 	
 1-3.  Quantitative Community Health Epidemiological Studies on
       Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
 1-4.;  Effects of Exposure to Nitrogen Dioxide in the Home on
       Lung Function and the Incidence of Acute Respiratory Disease
       in Epidemiology Studies of Homes with Gas Stoves 	
 1-5.  Summary of Studies Demonstrating Health Effects in Animals at
       Low (< 2.0 ppm) N02 Exposure Levels  	
 1-6.  Effects of Exposure to Nitrogen Dioxide on Sensory Receptors
       in Controlled Human Studies  	

 3-1.  Theoretical  Concentrations of Nitrogen Oxides and Nitrogen
       Acids Which  Would be Present at Equilibrium with Molecular
       Nitrogen,  Molecular Oxygen, and Water in Air at 25 C, 1 ATM,
       50 Percent Relative Humdiity  	
 3-2.  Some Physical and Thermodynamic Properties of the Nitrogen
       Oxides	
 3-3. .Theoretical  Equilibrium Concentrations of Nitric Oxide and
       Nitrogen Dioxide in'Air (50 Percent Relative Humidity) at
       Various Temperatures  	
 3-4.  Theoretical  Concentrations of Dinitrogen Trioxide and
       Dinitrogen Tetroxide in Equilibrium with Various Levels of
       Gaseous Nitric Oxide and Nitrogen Dioxide in Air at 25°C.  .  .

 4-1.  Distribution of Nitrogen in Major Compartments  	
 4-2.  Estimates  of Global Nitrogen Fixation in the Biosphere  .  .  .
 4-3.  Estimates  of Global Emissions and Fluxes of Oxides of
       Nitrogen and Related Compounds  	
 4-4.  Estimates  of the Global Flux of Nitrates and Nitrites ....
 4-5.  Estimates  of Global Flux of NO  	
 4-6.  Estimates  of the Global Flux or Nitrous Oxide 	
 4-7.  Estimates  of the Global Flux of Ammonia and Ammonia Compounds.
 4-8.  Estimates  of Global Denitrification 	

 5-1.  Estimated  Annual Global Emissions of Nitrogen Dioxide
       (Anthropogenic) 	
 5-2.  Historic Nationwide NO  Emission Estimates 1940-1970  ....
 5-3.  Recent Nationwide NO  Emission Estimates 1970-1976  	
 5-4.  NO/NO  Ratios in Emissions from Various Source Types  ....
 5-5.  Estimated  Ammonia Emission from Fertilizer Application and
       Industrial Chemical Production in U.S.  (1975) 	
Page


1-6

1-11

1-14


1-17

1-22

1-25
3-3

3-4


3-8


3-12

4-5
4-6

4-7
4-9
4-10
4-13
4-16
4-17
5-2
5-3
5-5
5-13

5-15
                                       xx

-------
Table                                                                      Page

 5-6.  Nitrogenous Compounds Applied as Fertilizer in the U.S.
       1955-1976		       5-18

 6-1.  Reactions of Alkoxyl, Alkylperoxyl and Acylperoxyl
       Radicals with NO and NO,  .	       6-9
 6-2.  Summary of Conclusions from Smog Chamber Experiments   . .  .   .       6-14
 6-3.  Predicted Nitrite and Nitrate Concentrations in Simulation
       of Experiment EC-237 of the Statewide Air Pollution Research
       Center of University of California, Riverside, Using the
       Chemical Mechanism of Falls and Seinfeld  	       6-19
 6-4.  Maximum Concentrations and Yields of the Products of
       Diethylamine and Triethylamine  	       6-38

 7-1.  Performance Specifications for Nitrogen Dioxide Automated
       Methods	       7-3
 7-2.  Consistent Relationship Test Specifications for Nitrogen
       Dioxide	       7-3
 7-3.  Statistical  Analysis of NO, Measuring Method Differences  .   .       7-13
 7-4.  Summary of Reliability of NO,, Analytical Methods in Common
       Use as Obtained by Collaborative Testing  	       7-15
 7-5.  Results of 1977 Formal Audit on In-service Chemiluminescent
       Analyzers in St.  Louis	^.	       7-16
 7-6.  Summary of Nitric Acid Detection Techniques 	       7-20
 7-7.  Comparison of Nitrate Collected on Various Filter Types .  .   .       7-22
 7-8.  Analytical Methods for Nitrate in Water	       7-26
 7-9.  Methods for Determination of Nitrate in Soils 	       7-28

 8-1.  Background NO  Measurements. .	       8-3
 8-2.  Yearly Average and Maximum Concentrations of Nitric Oxide
       at Camp Stations, Measured by the Continuous Saltzman                 ;
       Colorimetric Method 	       8-6
 8-3..  Five-Yr Averages of Nitric Oxide Concentrations at Camp
       Stations, Measured by Continuous Saltzman Colorimetric
       Method	       8-9
 8-4.  Yearly Average and Maximum Concentrations of Nitrogen
       Dioxide at Camp Stations, Measured by the Continuous
       Saltzman Colorimetric Method  	       8-10
 8-5.  Five-Year Averages of Nitrogen Dioxide Concentrations at Camp
       Stations,, Measured by the Continuous Saltzman Colorimetric
       Method	       8-12
 8-6.  Five-Year Changes in Ambient NO,, Concentrations	       8-21
 8-7.  Ratio of Maximum Observed Hourly Nitrogen Dioxide Concen-
       trations to Annual Means During 1975 for Selected Locations  .       8-25
 8-8.  Frequency Distribution of 1975 Hourly NO,, Concentrations at
       Various Sites in U.S.  Urban Areas ...  7	       8-27
                                       xxi

-------
Table                                                                      Page

8-9.    Frequency Distribution of 1976, 1978, and 1980 Hourly Nitrogen
       Dioxide Concentrations at Various U.S.  Sites  	     8-28
8-10.  Frequency Distribution of 1976, 1978, and 1980 24-Hr Average
       NO, Concentrations at Various Sites in U.S.  Urban Areas ....     8-32
8-11.  Distribution by Time of Day of One-hour Maximum NO,,
       Concentrations for One Month in 1975 for Selected Drban                !
       Sites	     8-49
8-12.  Mean and Top Five Nitrogen Dioxide Concentrations Reported
       From 18 Individual RAMS Stations in St.  Louis During 1976 .  .   .     8-52
8-13.  Geographical Variation of Hourly ML Concentrations
       During a Period of High N02 Concentrations	     8-56
8-14.  High Concentrations of Nitrogen Oxides,  St.  Louis,
       Missouri, 1976	     8-60
8-15.  Monthly Trends in Hourly NO and N0« Concentrations,
       Massey Building, Fairfax County, Virginia, 1977 	     8-61
8-16.  Monthly Trends in Hourly NO and NO,, Concentrations,
       Lewinsville Station, Fairfax County, Virginia, 1977 	     8-62
8-17.  Monthly Trends in Hourly NO and N0? Concentrations,
       Seven Corners Station, Fairfax County,  Virginia, 1977 	     8-63
8-18.  Mean NO  Concentrations from Isolated Point Source in
       Complex Terrain (Clinch River Power Plant)	     8-66
8-19.  Ten Highest Hourly Average NO  Concentrations
       Observed at Each Monitoring Site for Isolated Source
       (Clinch River Power Plant)	   .     8-67
8-20.  Regionwide Impact of Weekday-Weekend Phenomena on
       Population Exposure to Nitrogen Dioxide 	     8-70
8-21.  U.S.  Population at Risk to Various 1974 N02 Hourly
       Ambient Concentrations	     8-72

11-1.  Composition of Ecosystems 	     11-7
11-2.  Mean pH Values in the New York Metropolitan Area (1975-1977).   .     11-29
11-3.  Storm Type Classification	     11-29
11-4.  Chemical Composition (Mean ± Standard Deviation) of Acid Lakes
       (pH <5) in Regions Receiving Highly Acidic Precipitation
       (pH <4.5), and of Soft-Water Lakes in Areas Not Subject to
       Highly Acidic Precipitation (pH >4.8) 	  ...     11-41
11-5.  pH levels Identified in Field Surveys as Critical to Long-Term
       Survival of Fish Populations	     11-63
11-6.  Potential Effects of Acid Precipitation on Soils	     11-68
11-7.  Types of Direct, Visible Injury Reported in Response to Acidic
       Wet Disposition	     11-78
11-8.  Thresholds for Visible Injury and Growth Effects Associated
       with Experimental Studies of Wet Deposition of Acidic
       Substances (Alter Jacobson, 1980a,b)	     11-81
11-9.  Lead and Cooper Concentration and pH of Water from Pipes
       Carrying Outflow from Hinckley Basin and Hanns and Steele
       Creek Basin, Near Amsterdam, New York	     11-88
11-10.  Composition of Rain and Hoarfrost at Headingley, Leeds	     11-90
11-11.  The Sensitivity to Acid Precipitation Based, on Buffer
       Capacity Against pH-Change, Retention of H , and Adverse
       Effects on Soils	     11-98
                                      xx ii

-------
Table                                                                      Page

12-1.   Common Trophic State Indicators and Their Responses to
        Eutrophication 	     12-12
12-2.   Water Use Problems Resulting from Eutrophication  	     12-13
12-3.   Nitrate-N Loadings to Lake Wingra	     12-17
12-4.   Relative Sensitivity of Several Plant Species to  Nitrogen
        Dioxide	     12-21
12-5.   Acute Inury to Selected Crops After a 1-hr Exposure to
        Nitrogen Dioxide 	     12-31
12-6.   Percent Leaf Area Injured by Designated Dosage of Nitrogen
        Dioxide	     12-32
12-7.   Projected N0? Exposures for 5 Percent Injury Levels on
        Selected Vegetation  	     12-35
12-8.   Effect of Chronic N02 Exposures on Plant Growth and Yield  .   .     12-36
12-9.   Plant Response to Suffur Dioxide and Nitrogen Dioxide
        Mixtures	     12-42
12-10.  The Effects of NOp and SO,, Singularly and in Combination on the
        Growth of Several Grasses: 	     12-43

13-1.   Fading of Dyes on Cellulose Acetate and Cellulosics
        {Cotton and Rayon)   	     13-3
13-2.   Color Changes on Dyed Fabric—Exposed Without Sunlight
        in. Pollution and Rural  Areas 	     13-5
13-3.   Typical Concentrations of Atmospheric Contaminants in
        Exposure Areas 	     13-7
13-4.   Exposure Sites	     13-9
13-5.   Average Fading of 20 Dye-Fabric Combinations After 12
        Weeks Exposure to Nitrogen Dioxide	     13-11
13-6.   Effect of Nitrogen Dioxide on Fading of Dyes on Nylon
        and .Polyester	     13-14.
13-7.   Estimated Costs of Dye Fading in Textiles	     13-16
13-8.   Yellowing of Whites by Nitrogen Dioxide  	     13-18
13-9.   Corrosion of Metals by Nitrogen Dioxide  	   .     13-24

14-1.   Respiratory Tract Transport and Absorption   	     14-2
14-2.   Mortality from N02 Exposure for 1 to 8 hours   	     14-4
14-3.   Interaction with Infectious Agents 	     14-6
14-4.   The Influence of Concentration and Time on Enhancement
        of Mortality Resulting From Various NO- Concentrations ....     14-11
14-5.   Mucociliary Transport	     14-19
14-6.   Alveolar Macrophages 	     14-21
14-7.   Immunological  Effects  	     14-25
14-8.   Effects of NCL on Lung Biochemistry	     14-29
14-9.   Effect of N0? on Lung Morphology	       14-42
14-10..  Pulmonary Functions  	     14-50
14-11.  Studies of Potential  Hyperplasia 	     14-55
14-12.  Production of Lung Edema by N0?	     14-58
14-13.  Tolerance to N09 Exposures .	     14-60
                       c.
                                       xxm

-------
Table                                                                      Page

14-14.   Nitrogen Dioxide-Induced Changes in Hematology  	       14-61
14-15.   Central  Nervous System and Behavioral  Effects	  .       14-64
14-16.   Biochemical  Markers of Organ Effects  .  .  .  . „	       14-65
14-17.   Studies  of Potential Mutagenesis, Teratogenesis 	       14-69
14-18.   Extrapulmonary Effects of N0?:   Body Weight 	      -14-72
14-19.   Nitric Oxide	       14-79
14-20.   Nitric Acid and Nitrates	       14-81
14-21.   Summary  of Effects in Animals at Concentrations of
        10 ppm or Less	       14-85

15-1.    Effects  of Exposure to Nitrogen Dioxide on Sensory
        Receptors in Controlled Human Studies  	       15-5
15-2.    Effects  of Exposure to Combinations of Pollutants on
        Sensory  Receptors in Controlled Human  Studies 	       15-7
15-3.    Effects  of Exposure to Nitrogen Dioxide on Pulmonary
        Function in Controlled Studies  of Healthy Humans  	       15-9
15-4.    Effects  of Exposure to Nitrogen Dioxide on Pulmonary
        Function in Controlled Studies  of Sensitive Humans  	       15-18
15-5.    Quantitative Community Health Epidemiological  Studies on
        Effects  of Exposure to Nitrogen Dioxide on Pulmonary Function      15-24
15-6.    Effects  of Exposure to Nitrogen Dioxide in the Home on
        the Incidence of Acute Respiratory Disease in Epidemiology
        Studies  Involving Gas Stoves	       15-31
15-7.    Nitrogen Dioxide Levels Reported in Gas and Electric Stove
        Homes	       15-54
                                      xxiv

-------
                    ABBREVIATIONS, ACRONYMS, AND SYMBOLS
 O             O           _TQ
 A             Angstrom (10    meter)

"A" strain     A particular type of influenza virus

AaDOp          Difference between alveolar and arterialized partial
               pressure of oxygen

AAS            Atomic absorption spectroscopy

AATCC          American Association of Textile Chemists and Colorists

Ad             A particular strain of laboratory mouse

AICHE          American Institute of Chemical Engineers

AM             Alveolar macrophage

AMP            Adenosine monophosphate; adenosine 5'  phosphate

ANSA           8-anilino-l-naphthalene-sulfonic acid

APCD           Air Pollution Control District

APHA           American Public Health Association

A/PR/8         A particular strain of influenza virus

A/PR/8/34      A particular strain of influenza virus

AQCR           Air Quality Control  Region

AQSM           Air Quality Simulation Model

ASTM           American Society for Testing  and Materials

atm            One atmosphere, a unit of pressure

ATP            Adenosine triphosphate

avg            Average

BAKI           Potassium iodide solution acidified with boric acid

BHA            Butylated hydroxyanisole

BHT            Butylated hydroxytoluene

BP             Blood pressure


                                    xxv

-------
 scat
C3H
C57BL
C57BL/6
cAMP
GAMP
CD-I
cGMP
°C
14C
CHE
CL;
CLdyn
CLstat
cm
CNS
CO
co2
CoA
C.OH
CPK
CR-1
CRD
CV
C x T
Extinction coefficient due to scatter by aerosols
A particular strain of laboratory mouse
A particular strain of laboratory mouse
A particular strain of laboratory mouse
Cyclic adenosine monophosphate; adenosine 5'-phosphate
Community Air Monitoring Program
A particular strain of laboratory mouse
Cyclic guanosine monophosphate; guanosine 5'-phosphate
Degrees Celsius (Centigrade)
A radioactive form of carbon
Cholinesterase
Lung compliance
Dynamic lung compliance
Static lung compliance
Centimeter
Central nervous system; the brain and spinal  cord
Carbon monoxide
Carbon dioxide
Coenzyme A
Coefficient of haze
Creatine phosphokinase
A particular strain of laboratory mouse
Chronic respiratory disease
Closing volume
Exposure concentration in ppm multiplied by time of
exposure in hours or other time measurement
Day
                                    xxvi

-------
DEN            Diethylnitrosamine (also DENA)
DIFKIN         Diffusion Kinetics Model
DL-Q           Diffusion capacity of the lung for carbon monoxide
DMN            Dimethylnitrosamine
DMA            Deoxyribonucleic acid
D = CT         Dose equals concentration multiplied by time
DPPD           N,N diphenylphenylenediamine
EC             Prefix of International Commission on Enzymes' identification
               numbers
EKG            Electrocardiogram
EPA            U.S. Environmental Protection Agency
°F             Degrees Fahrenheit
FEF:           Forced expiratory flow
FET            First-edge time
FEV            Forced expiratory volume
FEV-, Q         One-second forced expiratory volume
FEVg 7r        0.75-second forced expiratory volume
FRM            Federal Reference Method for air quality measurement
ft             Foot
FT             Fourier transform spectroscopy (also FS)
FVC            Forced vital capacity
g .             Gram
G6P            Glucose-6-phosphate
GC             Guanylate cyclase
GL             Gas chromatography
GC-MS          Gas chromatograph in combination with mass spectrometry
GM             General Motors Corporation
                                   xxvn

-------
GMP            Guanosine 5'-phosphate; guanosine monophosphate



GSH            A tripeptide, glutathione (reduced form)



GSSG           The disulfide (oxidized) form of GSH



H'              Hydrogen (free radical)



 H             Tritium; a radioactive form of hydrogen



ha             Hectare



HbCL           Oxyhemoglobin



HN02           Nitrous acid (also HONO)



HNO,           Nitric acid (also HOMO,)
   •3      .                           £


HO1            Hydroxyl free radical (also OH)



H0«'           Hydroperoxyl free radical



HQ?NO          Pernitrous acid



H02N02         Pernitric acid (also HOON02)



hr             Hour



HR             Heart rate



hv             Planck's constant (h) times the frequency of radiated

               energy (v) = Quanta of energy (E)



H202           Hydrogen peroxide



H?S            Hydrogen sulfide



H2SO.          Sulfuric acid



IARC           International Agency for Research on Cancer



Ig             Immunoglobulins



IgA            Immunoglobulin A fraction



IgG            Immunoglobulin G fraction



IgG-,           Immunoglobulin G-, fraction



IgGp           Immunoglobulin G2 fraction



IgM            Immunoglobulin M fraction







                                   xxviii

-------
in             Inch
IR             Infrared
k              Rate constant or dissociation constants
kg             Kilograms
km             Kilometer
1              Liter (also £)
LC50           Lethal concentration 50%; that concentration which is
               lethal to 50 percent of test subjects
LD50           Lethal dose 50%; dose which is lethal to 50 percent of
               the subjects
LT50           The time required for 50 percent of the test animals
               to die when given a lethal dose
LDH            Lactic acid (lactate) dehydrogenase
LPS            Bacterial lipopolysaccharide
m              Meter
M              Molar
M              Third body (in a reaction)
MAK            'Maximum permissible concentration (in Germany)
max            Maximum
MFR            Maximal  flow rate
|jg/m           Micrograms per cubic meter
mg/m           Milligrams per cubic meter
Mg             Magnesium
ml             Milliliter
mM             Millimoles
MMD            Mass median diameter
MMFR           Mid-maximal  flow rate
mo             Month
                                   xxix

-------
MPC            Maximum permissible concentration (in the U.S.S.R.)
MT             Metric Ton
N              Nitrogen
N              Normal
13
  N            A radioactive form of nitrogen
N-6-MI         N-nitrosoheptamethyleneimine
NA             Not applicable
NAAQS          National Ambient Air Quality Standard
NaCl           Sodium chloride; common table salt
NAD+           Nicotinamide-adenine dinucleotide (+ indicates oxidized
               form)
NADB           National Air Data Bank
NADH           Nicotinamide-adenine dinucleotide (reduced form)
NADPH          Nicotinamide-adenine dinucleotide phosphate (reduced
               form)
NaOH           Sodium hydroxide
NAS            National Academy of Sciences
NASN           National Air Surveillance Network
NDIR           Nondispersive infrared
NEDA           N-(l-Naphthyl)-ethylenediamine dihydrochloride
NEDS           National Emissions Data System
NEIC           National Enforcement Investigations Center
ng             Nanogram
NH»            Ammonium ion or radial
nm             Nanometer
NO             Nitric oxide
NOHb           Nitrosylhemoglobin
                                    xxx

-------
NO             Nitrogen oxides
  /V
N?0            Nitrous oxide
NO,,            Nitrogen dioxide
N203           Dinitrogen trioxide
NpO.           Dinitrogen tetroxide
NSF            National Science Foundation
0              Atomic oxygen
0( D)          Excited atomic oxygen
0              Ozone
OH             Hydroxyl group
0(
32
0( P..)          Ground state^ atomic oxygen
  P            A radioactive form of phosphorus
               Alveolar partial pressure of carbon dioxide
               Arterial partial pressure of carbon dioxide
PAH            p-Ammiohippuric acid
PAN            Peroxyacetyl nitrate
PaOv,           Arterial partial pressure of oxygen
PAO,,           Alveolar partial pressure of oxygen
pH             Log of the reciprocal of the hydrogen ion concentration
PHA            Phytohemagglutinin
P0?            Partial oxygen pressure
ppb            Parts per billion
pphm           Parts per hundred million
ppm            Parts per million
ppt            Parts per trillion
Q              Cardiac output
QRS            A complex of three distinct electrocardiogram waves which
               represent the beginning of ventricular contraction
                                   xxx i

-------
 RAMS            Regional  Air Monitoring System
 RAPS            Regional  Air Pollution Study
 R              Airway resistance
!RBC             Red blood cell;  erythrocyte
 RM             Reference method for air quality measurement
 RNA             Ribonuclei-c acid
 RV             Residual  volume
 SAI             Science Applications,  Inc.
 SD             Standard deviation
 SCOT            Serum glutamic-oxaloacetic  transaminase
 SGPT            Serum glutamic-pyruvic transaminase
 SH-             Sulfhydryl group
 SMSA            Standard Metropolitan  Statistical Area
 SN             Suspended nitrates
 S02             Sulfur dioxide
 SPF             Specific pathogen free
 SR             Specific airway  resistance
   aw
 SRM             Standard reference material
 SS             Suspended sulfates
 STP             Standard temperature and pressure
 TEA             Triethanolamine
                             r                  -i p
 Tg             Terragram; 10 metric  tons  or 10   grams
 TGS-ANSA       A 24-hour method for the detection of analysis of NO-
                in ambient air
 tiC             Total lung capacity
 TPTT            20 percent transport time
 TSP             Total suspended  particulate
                                    xxxi i

-------
USEPA          U.S. Environmental Protection Agency
UV             Ultraviolet radiation
VC             Vital capacity
VE             Ventilatory volume
VEE            Venezuelan equine encephalomyelitis (virus)
V              Maximum expiratory flow rate
 maX
V.-p             Total volume
V/V            Volume per volume
WBC            White blood cells
wk             Week
yr             Year
Zn             Zinc
ug             Microgram
ul             Microliter
urn             Micrometer
>              Greater than
<              Less than
•^              Approximately
                                  xxxm

-------
                         CONTRIBUTORS  AND  REVIEWERS
 Principal  authors:

 Dr.  Charles  E.  Anderson,  Department  of Botany,  North  Carolina  State Univer-
     sity,  Raleigh,  North  Carolina.

 Dr.  Paul  J.  Crutzen,  National  Center for Atmospheric  Research,  Boulder,
     Colorado.

 Dr.  Sandor J.  Freedman,  System Sciences, Inc.,  Chapel  Hill,  North  Carolina.

 Dr.  J.  H.  B.  Garner,  Environmental  Criteria  and Assessment Office,  U.S.
     Environmental  Protection Agency, Research  Triangle Park,  North  Carolina.

 Dr.  Judith A.  Graham,  Health Effects Research  Laboratory,  U.S.  Environmental
     Protection Agency,  Research Triangle Park,  North  Carolina.

 Dr.  Daniel Grosjean,  Statewide Air  Pollution Research Center,  University
     of  California,  Riverside,  California.

 Dr.  Steven M.  Horvath,  Institute of  Environmental  Stress,  University of
     California at  Santa  Barbara, Santa Barbara, California.

 Dr.  Gory  J.  Love,  Consultant,  System Sciences,  Inc.,  Chapel  Hill,  North
     Carolina.

 Dr.  Daniel B.  Menzel,  Department of  Pharmacology,  Duke University,  Durham,
     North Carolina.

iDr.  Joseph Roycroft,  Jr.,  Health Effects Research  Laboratory,  U.S.  Environ-
     mental Protection Agency,  Research Triangle Park,  North Carolina.

 Dr.  Victor S.  Salvin,  University of  North Carolina,  Greensboro, North
     Carolina.

I Dr.  John  H.  Seinfeld,  Department of  Chemical Engineering,  California
     Institute of Technology, Pasadena, California.

 Dr.  John  C.  Trijonis,  Technology Service Corporation,,  Santa Fe, New Mexico.

 Dr.  Warren H.  White,  Technology Service Corporation,  Pasadena,  California.


 Contributing authors  and  reviewers:

 Dr.  Martin Alexander,  Department of  Agronomy,- Cornell  University,  Ithaca,
     New York.

 Dr.  Patrick  L.  Brezonik,  Department  of Environmental  Engineering Sciences,
     University of  Florida, Gainesville, Florida.

                                    xxxiv

-------
Dr. John B. Clements, Environmental Monitoring and Support Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr. T. Timothy Crocker, Department of Community and Environmental Medicine,
    University of California, Irvine, California.

Dr. :Basil Dimitriades, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. George M. Duggan, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Richard Ehrlich, Illinois Institute of Technology Research Institute,
    Chicago, Illinois.

Mr. Robert B. Faoro, Monitoring and Data Analysis Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. C. Eugene Feigley,  Department of Environmental Health, University of
    South Carolina, Columbia, South Carolina.

Dr. Jack Fishman, National Center for Atmospheric Research, Boulder,
    Colorado.

Dr. Robert Frank, Department of Environmental Health, University of Washing-
    ton, Seattle, Washington.

Dr. Elliot Goldstein, Department of Internal Medicine, University of
    California, Davis,  California.
.Dr. Lester D. Grant, Environmental Criteria and Assessment Office, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Mark M. Greenberg, Environmental Criteria and Assessment Office, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr. Jack D. Hackney, Rancho Los Amigos Hospital Campus, University of
    Southern California, Downey, California.

Mr. Albert V. Hardy, System Sciences, Inc., Chapel Hill, North Carolina.

Dr. Steven M. Horvath, Institute of Environmental Stress, University of
    California, Santa Barbara, California.

Dr. Harvey E. Jeffries, Department of Environmental  Sciences and Engineering,
    University of North Carolina, Chapel Hill, North Carolina.

Dr. Evaldo Kothny, California State Department of Health, Berkeley, California.
                                    xxxv

-------
Mr.  William S.  Lanier, Industrial Environmental Research Laboratory, U.S.  ,
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr.  David J.  McKep, Environmental Criteria and Assessment Office, U.S.  Environ-
    mental Protection Agency, Research Triangle Park, North Carolina.

Dr.  Sidney S.  Mirvish, Eppley Institute for Research in Cancer, University
    of Nebraska, Omaha, Nebraska.

Mr.  Larry J.  Purdue, Environmental Monitoring and Support Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr.  Carl M.  Shy, Institute of Environmental Health, University of North
    Carolina,  Chapel Hill, North Carolina.

Mr.  Herschel  H.  Slater, PEDCo Environmental, Inc., Durham, North Carolina.

Mr.  Mark G.  Smith, System Sciences, Inc., Chapel Hill, North Carolina.

Dr.  Edward P.  Stahel, Department of Chemical Engineering, North Carolina
    State University, Raleigh, North Carolina.

Dr.  David T.  Tingey, Corvallis Environmental Research Laboratory, U.S.
    EnvironmentalProtection Agency, Corvallis, Oregon.
Reviewers:

Mr. Gerald G. Akland, Environmental Monitoring and Support Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr. Aubrey P. Altschuller, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Mark R.  Antell, Division of Stationary Source Enforcement, U.S. Environ-
    mental  Protection Agency, Washington, D.C.

Mr. John D.  Bachmann, Strategies and Air Standards Division, Office of Air
    Quality Planning, and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Ronald L. Baron, Health Effects Research  Laboratory, U.S. Environmental
    Protection Agency, Research Triangle Park, North Carolina.

Mr. Norman J. Beloin, Surveillance and Analysis Division, Region I, U.S.
    Environmental Protection Agency, Boston, Massachusetts.

Mr. Michael  A. Berry, Environmental Criteria and Assessment Office, U.S.:.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Frank M.  Black, Environmental Sciences Research Laboratory, U.S.  Environ-
    mental  Protection Agency, Research Triangle Park, North Carolina.
                                   xxxvi

-------
Ms. Frances P. Bradow, Environmental Criteria and Assessment Office, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Dr. Joseph J. Bufalini, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Ronald C. Campbell, Strategies and Air Standards Division, Office of
    Air Quality Planning and Standards, U.S. Environmental Protection
    Agency, Research Triangle Park, North Carolina.
                                                          i
Mr. Angelo P. Capparella, Environmental Criteria and Assessment Office,
    U.S. Environmental Protection Agency, Research Triangle Park,
    North Carolina.

Capt.  Harvey J.  Clewell, III, Civil and Environmental Engineering Develop-
    ment Office, Tyndall Air Force Base, Florida.

Mr. Stanton Coerr, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. David L.  Coffin, Health Effects Research Laboratory, U.S.  Environmental
    Protection Agency, Research Triangle Park, North Carolina.

.Dr. Henry S.  Cole, Monitoring and Data Analysis Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Ellis B.  Cowling, Department of Plant Pathology, North Carolina State
    University,  Raleigh, North Carolina.

Mr. Swep T.  Davis, Deputy Assistant Administrator for Water Planning and
  .  Standards, Office of Water and Waste Management, U.S.  Environmental
    Protection Agency, Washington, D.C.

Dr. Kenneth L. Demerjian, Environmental  Sciences Research Laboratory, U.S.
    Environmental  Protection Agency, Research Triangle Park, North Carolina.

Dr. Marcia C.  Dodge, Environmental Sciences  Research Laboratory, U.S.
    Environmental  Protection Agency, Research Triangle Park, North Carolina.

Dr. Thomas G.  Dzubay, Environmental Sciences Research Laboratory, U.S.
    Environmental  Protection Agency, Research Triangle Park, North Carolina.

Mr. Thomas G.  Ellestad, Environmental Sciences Research Laboratory, U.S.
    Environmental  Protection Agency, Research Triangle Park, North Carolina.

Mr. Douglas Fennel!, Environmental Criteria  and Assessment Office, U.S.
    Environmental  Protection Agency, Research Triangle Park, North Carolina.

Mr. Neil H.  Frank, Monitoring and Data Analysis Division,  Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Gustave Freeman, Stanford Research Institute, Menlo Park,  California.
                                 xxxvi i

-------
Dr.  Donald E.  Gardner, Health Effects Research Laboratory, U.S. Environ-
    mental Protection Agency, Research Triangle Park, N.C.

Dr.  Philip L.  Hanst, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr.  Fred H.  Haynie, Environmental Sciences Research Laboratory, U.S.  Envi-
    ronmental  Protection Agency, Research Triangle Park, North Carolina.

Dr.  Walter W.  Heck, Department of Botany, North Carolina State University,
    Raleigh, North Carolina.

Mr.  George C.  Holzworth, Environmental Sciences Research Laboratory,  U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr.  Allen Hoyt, Environmental Criteria and Assessment Office, U.S.  Envi-
    ronmental  Protection Agency, Research Triangle Park, North Carolina.

Dr.  F.  Gordon Hueter, Health Effects Research Laboratory, U.S.  Environ-
    mental Protection Agency, Research Triangle Park, North Carolina.

Mr.  Michael  H.  Jones, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr.  John H.  Knelson, Health Effects Research Laboratory, U.S. Environmental
    Protection Agency, Research Triangle Park, North Carolina.

Dr.  Kenneth T.  Krost, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Ms.  Pamela A.  Mealer, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Mr.  Thomas R.  McCurdy, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Mr.  Thomas B.  McMullen, Environmental Criteria and Assessment Office, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr.  M.  Rodney Midgett, Environmental Monitoring and Support Laboratory,
    U.S.  Environmental Protection Agency, Research Triangle Park, North
    Carolina.

Mr.  Edwin L. Meyer, Monitoring and Data Analysis Division, Office of Air
    Quality Planning,and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Mr.  William Nelson, Health Effects Research Laboratory, U.S. Environmental
    Protection Agency, Research .Triangle Park, North Carolina.

                                  'xxxviii

-------
Mr. Stephen Nesnow, Health Effects Research Laboratory, U.S. Environmental
    Protection Agency, Research Triangle Park, North Carolina.

Mr. John R. O'Connor, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Mr. Joseph Padgett, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Mr. Dennis J.  Reutter, Environmental Sciences Research Laboratory, U.S.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Harvey M.  Richmond, Strategies and Air Standards Division, Office of
    Air Quality Planning and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Harold G.  Richter, Monitoring and Data Analysis Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Ms. Karen Rourke, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr. Joseph Seitler, Office of Toxic Substances, U.S.  Environmental Protec-
    tion Agency, Washington, D.C.

Mr. Donald H.  Sennett, Monitoring and Data Analysis Division, Office of Air
    Quality Planning and Standards, U.S. Environmental Protection Agency,
    Research Triangle Park, North Carolina,

Mr. Larry L.  Sims, Air Surveillance and Investigation Section, Region X,
    U.S. Environmental Protection Agency, Seattle, Washington.

Mr. James R.  Smith, Health Effects Research Laboratory, U.S.  Environmental
    Protection Agency, Research Triangle Park, North Carolina.

Dr. Carl R. Sova, Air Engineering Branch, Region IV,  U.S.  Environmental
    Protection Agency, Atlanta, Georgia.

Mr. Robert K.  Stevens, Environmental Sciences Research Laboratory, U.S.
    Env.ironmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Orin W. Stopinski, Health Effects Research Laboratory, U.S.  Environ-
    mental  Protection Agency, Research Triangle Park, North Carolina.

Mr. Joseph Suggs, Health Effects Research Laboratory, U.S. Environmental
    Protection Agency, Research Triangle Park, North Carolina.

Mr. Matthew Van Hook, Air, Noise and Radiation Division, U.S. Environmental
    Protection Agency, Washington, D.C.

                                   xxx ix

-------
Dr.  David E.  Weber, Corvallis Environmental Research Laboratory, U.S. Envi-
    ronmental Protection Agency, Corvallis, Oregon.

Mr.  Albert H. Wehe, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S.  Environmental Protection Agency,
    Research Triangle Park, North Carolina.

Dr.  Jerome Weslowski, California State Department of Health, Berkeley, California.

Mr.  Larry Zaragoza, Strategies and Air Standards Division, Office of Air
    Quality Planning and Standards, U.S.  Enviornmental Protection Agency,
    Research Triangle Park, North Carolina.
                                     xl

-------
   J
   f                               •
   • I
Project management, editing, production, and word processing  at  System
Sciences, Inc., Chapel Hill, North Carolina, under contract to the  Environ-
mental Criteria and Assessment Office, U.S. Environmental  Protection  Agency,
Research Triangle Park, North Carolina:

     Dr.  Edgar A. Parsons
     Ms.  Gayla Benignus
     Dr.  Sandor J. Freedman
     Ms.  Doris M. Lange
     Ms.  Elsa M. Lewis-Heise
     Ms.  Jeannine A.  McFarland
     Ms.  Trudy E. Oakes
     Ms.  Diane Robinson
     Ms.  E.  L. Rusten
     Mr.  Mark G. Smith
     Mr.  Robert E. Wenzel

Word processing and other assistance at the Environmental  Criteria  and
Assistance Office, U.S. Environmental Protection Agency,  Research Triangle
Park, North Carolina:   	

     Ms.  Del a Bates "
     Ms.  Diane ChappeTijtS?:
   1  Ms.  Constance Van^OoJsten
     Ms.  Evelynne Rash ^n
     Ms.  Donna Wicker
                                    xli

-------
                   CLEAN AIR SCIENCE ADVISORY COMMITTEE
                        SUBCOMMITTEE ON AIR QUALITY
                      CRITERIA FOR OXIDES OF NITROGEN
CHAIRMAN:
Dr.  Sheldon K.  Friedlander, Vice Chairman of Chemical Engineering, Department
     of Chemical, Nuclear, and Thermal Engineering, School of Engineering and
     Applied Science, University of California, Los Angeles, California  90024

MEMBERS:

Dr.  Mary 0. Amdur, Department of Nutrition and Food Science, Room 16-339,
     Massachusetts Institute of Technology, Cambridge, Massachusetts  02139
Dr.  Domingo M.  Aviado, Allied Chemical, P.O.  Box 1021 R, Morristown, New
     Jersey  07960
Dr.  Judy A. Bean, College of Medicine, Department of Preventive Medicine and
     Environmental Health, University of Iowa, Iowa City, Iowa  52242

Dr.  Robert Dorfman, Department of Economics,  Harvard University, 325 Lattauer,
     Cambridge, Massachusetts  02138

Mr.  Harry H.  Hovey, Jr., New York Department of Environmental Conservation, 50
     Wolf Road, Albany, New York  12233

Dr.  Donald H.  Pack, 1826 Opalocka Drive, McLean, Virginia  22101

STAFF OFFICER:

Dr.  Terry F.  Yosie, Science Advisory Board, U.S. Environmental Protection
     Agency,  Washington, D.C.  20460
                                   xlii

-------
                   1.  SUMMARY OF EFFECTS OF OXIDES OF NITROGEN AND RELATED
                             COMPOUNDS ON HUMAN HEALTH AND WELFARE

1.1  INTRODUCTION
     This  criteria  document critically  evaluates scientific  information  on both  short-  and
long-term  health and welfare  effects of  nitrogen  oxides as  well  as  other nitrogenous com-
pounds,  such  as  nitric  and nitrous  acids,  nitrites,  nitrates, and nitrosamines.  Pursuant to
Sections 108  and 109 of the Clean  Air  Act, as amended in 1977, it is to serve as a basis for
evaluating  the  need to  promulgate  National Ambient  Air  Quality Standards  for  any  or  all  of
these compounds.   The scientific evidence reviewed includes significant new research published
since the first edition of Air Quality Criteria for Nitrogen Oxides in 1971.
     Major questions addressed in this document include the following:
              (1)  What are identifiable health effects associated with exposure to
                   airborne nitrogenous compounds?
              (2)  At what level(s) of exposure do such health effects occur in humans?
              (3)  Are there population subgroups especially susceptible to the effects
                   of exposure to airborne nitrogenous compounds?
              (4)  What are the major welfare effects on visibility, vegetation, and
                   materials associated with airborne nitrogenous compounds?
              (5)  At what concentration levels do effects on visibility, vegetation
                   and materials occur?
              (6)  To what degree do airborne nitrogenous  compounds contribute to
                   large-scale environmental effects such  as acidic precipitation?
              (7)  Are presently available techniques for  measuring atmospheric levels
                   of nitrogenous compounds adequate?

              (8)  What are the major sources of airborne  nitrogenous compounds?

              (9)  What concentrations of nitrogenous compounds of concern occur in
                   ambient air?
     This present chapter summarizes available  data on the effects on human health and welfare
of nitrogen  oxides  (NO ), consisting principally of nitrogen dioxide  (NOp)  and  nitric oxide
(NO), and other nitrogenous compounds which may be derived from NO  through atmospheric  trans-
formations.   Since N02 has  been  most conclusively demonstrated  to  exert deleterious effects,
the  emphasis  here has been  placed  on  the interpretation of  data bearing  on  N02  effects  in
order to estimate ambient  air  concentration levels at which  such effects on human health and
welfare occur.   Information on natural and man-made sources,  atmospheric chemical and physical
transformations,  techniques of sampling  and analysis, and additional  data on ambient concen-
trations are also summarized in the  present chapter.   The  reader is referred  to the subsequent
document chapters for more detailed  information on all of  the above topics.
                                              1-1

-------
1.2  SOURCES, TRANSFORMATIONS AND AMBIENT LEVELS OF NITROGEN OXIDES
     Oxides  of  nitrogen  have their  origin  in a  number  of  natural  and  man-made  processes
(Chapters 4  and 5).   In terms of sources  giving  rise to significant human exposure, however,
the most  important  emissions  occur  as a result of man's burning of fossil fuels such as coal,
oil or  gasoline.   Emissions  from  motor vehicles  (mobile combustion) and  from installations
burning fossil fuels  (stationary combustion) are the two  largest  sources,  constituting about
44 percent  and  51  percent  of the  nationwide NO   emissions,  respectively,  in  1976,   In the
stationary combustion category,  electric utilities were responsible for approximately 56 per-
cent of the  NO   emissions and industrial combustion accounted for another 38 percent.   In the
mobile combustion category,  highway vehicle emissions constituted  about  77 percent, with the
rest attributable to non-highway vehicles.
     In most ambient situations,  NOp is not emitted directly into the atmosphere in significant
amounts (typically  less  than  10  percent of NO  emissions).   It is important to note, however,
that NOp  forms upwards  of 30 to 50  percent of the total  NO  emissions from certain diesel and
jet turbine  engines under  specific load  conditions.   Diesel  emissions  of NOp  may  become  of
concern  in  local  situations  if  there  is  a widespread  increase in the  use of diesel-powered
vehicles.   NO- is formed,  generally,  from the oxidation of the more commonly emitted compound
nitric oxide  (NO).   The chemical pathways  by which  NO  is transformed to NO^are  complex and
involve other atmospheric  constituents  such as hydrocarbons and ozone.   Also,  NOp is not the
final  product of  atmospheric reactions.   It may  decompose  in  the presence of  sunLight  or  it
may undergo  further transformation  into gaseous  nitric acid  (HNO,) and/or nitrate  aerosols,
small   particles  suspended  in ambient  air  (Chapter 6).   For these  and other reasons,  the
relationship between NO   emissions  and resulting ambient N09 concentrations is neither direct
                        A                                    £                                 ,
nor constant.
     Oxides  of  nitrogen and  their  atmospheric transformation products may be  transported  in
ambient air  over  distances  ranging  up to hundreds of kilometers from the emissions source and
over times ranging  up  to several days.  Ultimate  removal  from the air occurs by a variety  of
processes including  uptake  by vegetation,  deposition on surfaces and precipitation by rain  or
snow.   The  times and  distances  involved  in  the' transformation,  transport,  and removal  of
atmospheric nitrogenous  compounds indicate that these pollutants  not  only  exert an  impact  in
proximity  to primary  sources,   but are also  of  concern in  relation  to deleterious  effects
exerted at considerable distances from points of initial  emission or transformation.   The con-
tribution of  nitric  acid to the phenomenon  of  acidic precipitation,  which may occur hundreds
of  kilometers from  a source or sources  of NO ,  is an example  of  such a  non-local  impact
(Chapter 11).
     It  has  been  suggested  that oxides of nitrogen may react in  the atmosphere  with amines
emitted by certain sources to produce nitrosamines.  However, there is little evidence to date
to indicate that this reaction takes place  in ambient situations or that the atmospheric route
for human exposure to this class of  compounds is a cause for concern.
                                              1-2

-------
      In general, adequate methodology  now exists  for sampling and  analysis  of  NCL  concentra-
 tiohs in ambient air (Chapter 7).   Techniques for  routine  determination  of  atmospheric  concen-
trations of nitric  acid and  nitrate aerosols, however,  are currently only  in  the developmental
 stage.
      Various government  agencies  have routinely  monitored  NCL  for some time.   The  following
 summary of recent  ambient levels  of N0~  occurring nationwide  is  given to place  in perspective
 the  concentration  levels associated with  the health  and welfare effects discussed later  in
 this chapter.   Chapter 8 contains a more  thorough  survey of  available  monitoring data.  The
 reader should note  that not  all  persons living or  working  in the  areas mentioned will actually
 experience the  NO-  concentrations  cited.   Moreover,  considering  the  likelihood  that  fixed
 monitoring sites may not  intercept  the maximum N0~  concentration,  there is a possibility that
 the concentrations  reported  underestimate the exposure  experienced  by at least some portion  of
 the population  in the areas  cited.
      Examination of selected nationwide  monitoring  data  for 1975 to 1980  reveals that  during
 at least one of  these  years,  peak 1-hour N0?  concentrations  equalling  or  exceeding  750  ug/m
 (0.4 ppm)  were  experienced  in  Los  Angeles  and several  other California  sites;  Ashland,
 Kentucky;  and Port  Huron, Michigan.   Additional sites  reporting  at  least one peak hourly con-
 centration equalling or exceeding 500  ug/m   (0.27 ppm) include:   Phoenix,  Arizona; St.  Louis,
 Missouri;  New  York  City, New York;  14  additional  California  sites;  Springfield,   Illinois;
 Cincinnati,  Ohio;  and  Saginaw and  Southfield,  Michigan.   Other scattered sites, distributed
 nationwide,  reported  maxima close  to this  value.    Recurrent   NO,  hourly concentrations   in
                    3
 excess  of  250 ug/ m  (0.14 ppm)  were  quite  common  nationwide in 1975 to  1980.
      Annual  arithmetic  means for NO-  concentrations  in 1976 exceeded 100 ug/m  (0.053 ppm)  at
 Anaheim,  El  Cajon,  Riverside, San  Diego,  and Temple City,  California.   Other sites  reporting
 yearly   arithmetic  means  for  1976  equalling  or  exceeding 100  ug/m   (0.053  ppm)  included
 Chicago,  Illinois,  and Southfield, Michigan.   However, virtually none  of  the same monitoring
 sites still  operating in 1980 reported values  above 100 ug/m  in that year (except for one  in
                    2
 San Diego;  114  ug/m ).
 1.3  EFFECTS OF  NITROGEN  OXIDES  ON HUMAN  HEALTH
      As  summarized  above, nitric oxide (NO)  is the  most   prevalent  oxide of  nitrogen directly
 emitted  into the ambient air as  the result of anthropogenic activities  such as fossil fuel
 combustion.   In  addition,  other  compounds,  such as nitrogen  dioxide  (NO-),  gaseous nitric acid
 (HN03),  nitrites and nitrate  aerosols,  have been  clearly established as  being  formed in the
 ambient  air as  the  result of atmospheric chemical reactions  of  NO  and  other nitrogen oxides
 with non-nitrogenous substances.   The formation of nitrosamines in  the ambient air has been
 suggested,  but  not  convincingly  demonstrated.
      Concern  has been expressed about  possible harmful health effects of virtually all of the
 above types of  nitrogen  oxide  compounds.   Despite  such  concern and considerable scientific
 inquiry  on the  subject,  there  now exist relatively  little  hard  data linking specific health
 effects  to the majority of  the  above  nitrogen oxide compounds.   The one notable exception  is
 nitrogen dioxide.
                                               1-3

-------
     The  literature  reviewed in detail  in  Chapter 15 of this document  indicates  that  nitric
oxide (NO) is not of direct concern for human health effects at typical  ambient air concentra-
tion levels recorded over U.S.  cities.   Similarly,  there is presently no evidence that nitrites
at  levels  ordinarily  found in the atmosphere  are  of concern for human  health.   In addition,
although  it  has been  suggested that  atmospheric  nitrates may  be  associated with increased
numbers of asthmatic  attacks,  no data are presently  available  that are sufficient upon which
to base firm conclusions regarding the subject.
     The  lack  of strong  evidence,  or even  conclusive pertinent studies,  associating  health
effects with most nitrogen oxide compounds is in  striking  contrast to  the more  extensive and
convincing data base which links a number of specific health effects to  nitrogen  dioxide (N0~).
     Information on NO^  formation  and  its effects  is, therefore, most heavily emphasized both
in  the  present summary  chapter and elsewhere  in  this  document.   In regard to the  types  of
health  effects  of  NO^  most definitively  characterized to date,  the effects of  NCL  on  the
respiratory system  have  been most extensively delineated and appear  to  be of most concern in
terms  of  both  acute and  long-term  health  implications.   Major attention  is  accorded here  to
the  summary  and interpretation  of key studies and the overall  pattern  of  results  bearing  on
respiratory system effects of NCk.
1.3.1  Nitrogen Dioxide Respiratory System Effects
     Nitrogen dioxide's  effects  on  human and animal  respiratory systems  span a broad  spectrum
both  in  terms   of initial  severity and  ultimate   long-term health  impact.   The  continuum  of '
observed  N02  effects  ranges  from  (1)   death or  irreversible  pulmonary  damage seen  with
accidental high exposures  to NO^ primarily in occupational  settings;  through (2) less severe,
but  significant short-term and  chronic tissue damage, functional impairment, and exacerbation
of  other  disease processes observed  at  lower  exposure  levels;   to  (3)   comparatively  mild
transient effects,  such  as  impaired  olfactory reception,  which commence  at  still lower NO-
levels.
     Acute  high level exposures  to N09  that  have  occurred  accidentally  or  in  occupational
                                                                     3
settings demonstrate that concentrations  in the range of 560,000 ug/m  (300 ppm)  or higher are
                                                                                             3
likely to  result in  rapid death.   Concentrations  in the  range  of 280,000  to  380,000 ug/m
(150-200 ppm)  are  not  likely  to cause  immediate  death, but severe  respiratory  distress  and
death occur after a  period of 2 to 3 weeks.   In such cases,  the cause is  almost always bronchi-
olitis fibrosa  obliterans.  Non-fatal  acute exposures  to  94,000 to 190,000  ug/m   (50  to 100
ppm)  N09  are associated with reversible bronchiolitis,  whereas acute exposures to 47,000  to
            3
140,000 ug/m   (25  to  75 ppm)  are  associated  with bronchitis or bronchial  pneumonia and are
usually but  not always  followed by essentially complete  recovery.  It should  be noted that
exposures to such high  levels  of N0«  only typically occur  in connection with certain occupa-
tional or accidental (e.g.  fires) circumstances,  and are not of concern  in relation to ambient
air exposures of the general public.
     In addition to the  above health  effects  induced  by acute  high level  N02 exposures, how-
ever, a variety of  respiratory  system effects have  been reported  to be associated with expo-
sures  to  lower concentrations  of  NO-.  Extensive  literature characterizing  such  effects has
                                              1-4

-------
 resulted from  three general  approaches:   (1)  controlled  human exposure  studies;  (2)  human
 epidemiological  studies; and  (3) animal toxicology  studies.   The  major types of ^-induced
 respiratory  effects  characterized by  these  different  approaches  include:   (1)  increased airway
 resistance  (Ra.,)  and other  indications  of altered pulmonary  function  as  observed  in controlled
              aW
 clinical  studies;  (2) increased  incidence of  human  respiratory  illnesses,  as determined by cer-
 tain  epidemiological  studies;   and  (3) lung tissue  damage and  increased susceptibility to
 respiratory  infection,  as demonstrated  in animal toxicology  studies.
      Collectively, these studies provide evidence indicating that certain  human health effects
 may  occur as the result of exposures to NOp concentrations approaching or falling within the
 range of recorded ambient air NCL levels.   Key studies providing evidence  for  such effects are
 summarized  and  interpreted  below  in  relation to several critical health issues.  Those issues
 include:   (1) consideration of  lowest  effective single N0~  exposure  level(s)  inducing partic-
 ular  respiratory effects in healthy and  sensitive human  subjects;  (2) assessment of lowest
 effective  exposure  levels  at which repeated  or  intermittent N02 exposures produce effects in
 human populations;  and  (3)   consideration ,of  the relative  significance of  observed effects in
 terms of understanding  the  likely impact of ambient N02 exposures on  human  health.
 1.3.1.1   Controlled  Human Exposure Studies—Controlled  human exposure (clinical) studies have
 generated  extensive  information  on  the lowest  effective  dose  levels  for the  induction of
 respiratory  effects  by  single  short-term  N02 exposures.   Some  studies  have  focussed on such
 effects  in  healthy  adults; other studies  have  assessed  respiratory effects in "sensitive"
 members  of  the  population,   e.g.,  individuals with chronic respiratory problems.  Summarized in
 Table 1--1  are the most  important controlled  human exposure  studies of short-term NO- exposure
 effects  on pulmonary functions in healthy adult  subjects.
      The  studies  summarized in  Table 1-1 indicate  that  increased airway  resistance (R,..) and
> ,                                                                                      3W
 other physiological  changes suggesting impaired pulmonary  function  have  been clearly demon-
 strated  to  occur in healthy adults with single  2-hr NO- exposures ranging  from 3760 to 13,200
    3
 ug/m   (2.5  to  7.0  ppm).    Certain studies  also indicate  that significant effects  occur in
 healthy  subjects with shorter (3-15 min) exposures to the same or possibly  lower  levels of NO-
 administered  either  alone or in  combination with NaCl aerosol.
      More  specifically, in  regard to  the  latter  point,  Suzuki  and  Ishikawa  (1965)  observed
 altered  respiratory  function after exposure  of  healthy subjects to NO,  levels of 1300 to 3760
    3
 ug/m  (0.7  to 2.0 ppm)   for  10 minutes.  Their data however, preclude a clear association of
 observed  effects  with  any  particular concentration in the range of 1300 to 3760 ug/m  (0.7 to
 2.0 ppm) N02  exposure.
      Hackney  et  al.  (1978)   reported  no statistically significant changes  in any of the pulmo-
 nary  functions  tested  with the   exception  of a  marginal  loss  in  forced vital capacity after
 exposure to 1880 ug/m   (1.0  ppm)  NO-  for 2 hours on two successive days  (1.5%  mean decrease, P
 <0.05).   The  authors question the health significance of this small, but statistically signifi-
 cant  change  in  forced  vital capacity in healthy subjects  and  suggest that the changes found
 may be due to random variation.

                                              1-5

-------
                         TABLE  1-1.   EFFECTS  OF  EXPOSURE TO  NITROGEN  DIOXIDE ON
                   PULMONARY  FUNCTION IN  CONTROLLED  STUDIES  OF  HEALTHY  HUMAN ADULTS**
Concentration Pollu-
ug/mj
13,000
ppm tant
7.0 N02
No. of
Healthy
Subjects
Several
Exposure
Time
10-120
min.
Effects
Increased
tolerated
increase

R * in some
30W000 ug/ni
in Raw

subjects. Others
(16 ppm) with no
Reference***
Yokoyama,
1972
9,400    5.0   NO,
                                                                                        1977
11       2 hrs.    Increase in R  * and a decrease in AaDO?*   von Nieding
                  with intermittent light exercise.   No3en-   et al.,
                  hancement of the effect when 200 ug/m
                  (0.1 ppm) 03 and 13,000 u/m  (5.0 ppm)
                  SOp were combined with NO- but recovery
                  time apparently extended.
9,400
9,400
7,500
to
9,400
5,600
11,300

5.0 N02
5.0 N02
4.0 NO,
to ^
5.0
3.0 N02
6.0 N02

16 15 min. Significant decrease in DLrr)*
13 15 min. Significant decrease in PaO?* but end ex-
piratory POp* unchanged witn significant
increase in systolic pressure in the
pulmonary artery.
5 10 min. 40% decrease in lung compliance 30 min.
after exposure and increase in expiratory
and inspiratory flow resistance that
reached maximum 30 min. after exposure.
1 5 min. Increase in R * compared to pre-exposure
values (enhanced by NaCl aerosol).
1 5 min. More subjects were tested at higher
exposures.
von Nieding
et al. , 1973
von Nieding
et al. ,
1970
Abe, 1967
Nakamura,
1964


-------
                                       TABLE 1-1.   (continued)
Concentration   Pollu-
 |jg/ma    ppin    tant
 No.  of
 Healthy  Exposure
Subjects    Time    Effects
Reference
1

4
,880

,700
1.

2.
0

5
N09
2
N09
8

8
2

2
hrs.

hrs.
No increase

Increased R.
in R .
aw
with no further impairn
Beil
Ulmer
nent
and
, 1976

14,000    7.5    N02
 9,400    5.0    N02
                    at higher concentrations.  No change in
                    arterial P02 pressure or PCO- pressure.

  16       2 hrs.    Increased sensitivity to a bronchocon-
                    strictor (acetylcholine) at this concen-
                    tration but not at lower concentrations.

   8      14 hrs.    Increase in R   during first 30 min. that
                    was reduced though second hour followed by
                    greater increases measured at 6, 8 and 14
                    hrs.   Also increased susceptibility to a
                    bronchoconstrictor (acetylcholine).
 1,300    0.7    N0?
  to      to
 3,800    2.0
  10      10 mins.  Increased inspiratory and expiratory flow   Suzuki and
                    resistance of approximately 50% and 10% of  Ishikawa,
                    control values measured 10 rnins. after      1965
                    exposure.
 1,880    1.0    N02
  16       2 hrs.   No statistically significant changes
                    in pulmonary function tests with
                    exception of small changes in FVC.
                    (See page 1-9 and 15-17).)
Hackney et al.
1978
 1,150    0.6    N02
  15       2 hrs.   No physiologically significant changes
                    in cardiovascular, metabolic, or
                    pulmonary functions after 15, 30
                    or 60 mins. of exercise.
Folinsbee
et al., 1978

-------
                                                TABLE  1-1.   (continued)
00


Concentration
ug/mj
1,000

1,000
with
560
1,000
with
560
and
45,000
500

500
with
560

500
with
560
and
45,000
1,880
to
3,760

ppm
0.50

0.50

0.29
0.50

0.29

30.0
0.25

0.25

0.29

0.25

0.29

30.0
1.0
to
2.0


Pollu-
tant
°3
3
°3
J
N02
°3
•J
NO,
L.
CO
°3
o
°3
tj
NO,
L.
°3
O
NO,
L.
CO
NO,
L.


No. of
Healthy Exposure
Subjects Time Effects Reference
4 4 hrs. With each group minimal alterations in pul- Hackney
monary function caused by 0., exposure. et al . ,
Effects were not increased By addition of 1975
NO, or NO, and CO to test atmospheres.
L. L.





1 2 hrs. Little or no change in pulmonary function Hackney
found with 03 alone. Addition of NO, or et al. ,
of NO, and CO did not noticeably increase 1975
the effect. Seven subjects included some
believed to be unusually reactive to
respiratory irritants.





10 2 1/2 hrs Alternating exercise and rest produced Posin et al.,
significant decrease for hemoglobin, 1978
hematocrit, and erythrocyte acetyl-
chol inesterase.

-------
                                       TABLE  1-1.   (continued)
                          No.  of
Concentration   Pollu-     Healthy  Exposure
(jg/m-1
100
with
50
and
300
*R
aw
ppm tant Subjects
0.05 N02 11 2
0.025 0Q
3
0.11 so2
airway resistance
Time Effects
Reference
hrs. No effect on R or AaDO?; exposed sub- von Nieding
jects showed increased sensitivity of et al., 1977
bronchial tree
(acetylchol ine)
to pollutants.

to a bronchoconstrictor
over controls not exposed


    AaD02:   difference between alveolar and arterial  blood partial  pressure of oxygen

    DL_0 :   diffusion capacity of the lung for carbon monoxide

    Pa02 :   arterial  partial  pressure of oxygen

    P0?  :   partial  pressure  of oxygen

    PCO? :   partial  pressure  of carbon dioxide

    **By descending order of  lowest concentration evoking a significant effect.

    ***Reference citations are for studies listed in the bibliography for Chapter 15.

-------
     In a similar  study,  Kerr et al.  (1979)  exposed  10 normal healthy adults and 20 subjects
with asthma  and chronic  bronchitis  to 940  ug/m  (0.5  ppm)  N0?  for  2 hours.   Although  the
authors suggest that  the  changes reported in quasistatic compliance for normal healthy adults
may  be  due  to  chance alone,  there  is uncertainty whether  these changes were  due  to normal
daily  variation or to  N02 exposure.   No  other pulmonary  function tests  showed significant
changes  for  the  healthy   adult  group.  Only one of  the healthy  adult group  reported  mild
symptomatic effects associated with exposure to N0?.   The results of the Kerr study concerning
asthmatics and chronic bronchitics are discussed later.
     Beil and  Ulmer  (1976) and  Folinsbee et  al.  (1978) concluded that  there  were  no physio-
logically significant pulmonary effects at exposure levels of 1880 and 1100 ug/m  (1.0 and 0.6
ppm) NO,,  respectively.   Hackney et al. (1975a,b,c) and von Nieding et al.  (1977)  also  con-
                                                                                             3
eluded  that  there were no  physiologically  significant  effects at NOp  levels  below  560 ug/m
(0.3 ppm)  in the  presence of various  other  air pollutants, with the  exception  of  increased
sensitivity to  a  bronchoconstrictor  (acetylcholine)  observed by von  Nieding  et al.  (1977) at
       3                                          3                               3
94 ug/m  (0.05 ppm) NO,, in the presence of,49 ug/m  (0.025 ppm) ozone and 290 ug/m  (0.11  ppm)
so2.
     The latter von Nieding et al.  (1977)  finding, however,  is difficult to interpret in  view
of:  (1) controversy over the health significance of altered sensitivity to bronchoconstrictors
in  healthy  subjects;  (2)  some  uncertainties due to  methodological  differences  between  his
techniques and  other  investigators';  and  (3) no confirmation of the von Nieding et al. (1977)
findings by other  investigators.   Though  the von Nieding et al.  (1977) findings are interest-
ing, they  cannot  be  accepted at this  time as providing conclusive  evidence  for respiratory
effects occurring at  N02  concentrations substantially below 1880  ug/m  (1.0  ppm) for healthy
adult subjects.
     Several  controlled clinical  studies  have also addressed  the  issue of whether detectable
respiratory effects can be induced by N0~ in sensitive human subjects at exposure levels below
those affecting healthy human adults.  Key clinical studies  of the effects of exposure to N0£
on  pulmonary  function in  potentially  susceptible groups  of the  population  are  presented in
Table 1-2.
     The studies by von  Nieding  et al. (1971;  1973)  show that,  in persons with chronic bron-
                                                  3
chitis,  concentrations  of  7,500 and  9,400  ug/m   (4.0  and  5.0  ppm)  produced  decreases in
arterial  partial  pressure  of oxygen  and  increases  in the  difference between  alveolar  and
                                                                                             2
arterial partial  pressure of  oxygen.   Exposures  to  concentrations of  N0~ above 2,800 ug/m
(1.5 ppm), for  periods  considerably less than  1  hour,  also  produced significant increases in
airway resistance.   Thus,  results for bronchitic individuals and healthy individuals appear to
differ little.
                                                                               2
     In  contrast  to  the above results  for  bronchitics,  exposures to 190  ug/m  (0.1 ppm)  N02
for  1  hour were reported  by Orehek (1976) to increase mean airway resistance (R...) in 3 of 20
                                                                                uW
asthmatics and  to  increase the  sensitivity to a bronchoconstrictor (carbachol) in 13 of 20 of
the  same individuals.   In another study (Kerr et al.,  1979),  however, measurements of pulmonary

                                              1-10

-------
                         TABLE 1-2.  EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON
                    PULMONARY FUNCTION  IN CONTROLLED STUDIES OF SENSITIVE HUMAN ADULTS
Concentration
pg/m3
9,400
3,800
to
9,400
940
to
9,400
940
ppm
5.0
2.0
to
5.0
0.5
to
5.0
0.5
No. of
Subjects
14 chronic
bronchitics
25 chronic
bronchitics
63 chronic
bronchitics
10 healthy
7 chronic
Exposure
Time
60 mins.
10 mins.
30
inhal-
ations
2 hrs.
Effects*
No change in mean PAO?, during or after expo-
sure compared with pre-exposure values, but
PaO? decreased significantly in the first 15
mins. Continued exposure for 60 mins. produced
no enhancement of effect.
Significant decrease in PaO? and increase in
AaDO, at 7,500 pg/m (4.0 ppm) and above; no
significant change at 3,800 pg/m (2.0 ppm).
Significant increase in R above 3,000 pgm/
(1.6~ppm); no significant effect below 2,800
pg/m (1.5 ppm).
1 healthy and 1 bronchitic subject reported
slight nasal discharge. 7 asthmatics reported
Reference
von Nieding
et al , 1973
von Nieding
et al. , 1971
von Nieding
et al. , 1971
Kerr, et al . ,
1979
                bronchitics
                13  asthmatics
                                        slight  discomfort.   Bronchitics  and  asthmatics
                                        showed  no  statistically  significant  changes  in
                                        any  pulmonary  functions  tested when  analyzed
                                        as separate  groups  but showed  small,
                                        statistically  significant  changes  in quasistatic
                                        compliance when  analyzed as  a  single group.
   190
           0.1   20 asthmatics  1 hr.
Significant increase in SR   in 3 of 20
asthmatics.   Effect of bronchoconstriction
due to carbachol enhanced after exposure in
13 of 20 asthmatic subjects.   Neither effect
observed in 7 of 20 subjects.
Orehek, 1976
*PAO? :   alveolar partial  pressure of oxygen
SR
  aw
         airway resistance

         specific airway resistance
                                                   AaDO?:   difference  between  alveolar  and  arterial
                                                           blood partial  pressure of  oxygen
                                                   PaO,
                    arterial partial pressure of oxygen

-------
function were not altered in 13 asthmatics or 7 bronchitics as a result of 2 hours of exposure
to 940  ug/m   (0.5  ppm) N02 when  the  groups  were analyzed separately.  When  the  data for the
two groups were  analyzed together,  small but statistically significant changes in quasistatic
compliance and  functional  residual  capacity were reported.   However, the  authors  state  that
the changes reported may be due to chance alone.   Seven asthmatics and one bronchitic reported
some chest discomfort, dyspnea, headache, and/or slight nasal  discharge.
     It should be  noted  that considerable controversy exists  regarding  interpretation of the
Orehek  (1976)  study and  the health  significance  of the increased response  to  a bronchocon-
strictor observed in the study.  Conclusive statements regarding the possible unique status of
asthmatics therefore, cannot be made at this time.  If the Orehek and Kerr studies are further
corroborated, however, then it is suggested that impairment of lung function in asthmatics may
                                     3
be affected at NO,, levels of 940 ug/m  (0.5 ppm) or below.
     The above controlled human exposure studies provide important data concerning the effects
of single short-term NO^ exposures on healthy young adults and certain groups defined a priori
as "sensitive", i.e., bronchitics and asthmatics.  However, members of other presumed sensitive
populations,  e.g.,  children, the elderly, and individuals with chronic cardiovascular disease,
have  not  been tested  in controlled exposure studies  and  are  not likely to  be  tested in the
future.  Because of constraints on the study of such sensitive polulation groups in controlled
exposure experiments, the question of whether such individuals are at greater risk than healthy
young adults  for experiencing respiratory effects with single  or repeated short-term NO- expo-
sures cannot  be conclusively answered, although existing epidemiological  data suggest that this
may be the case for young children.
     Other critical health effects issues cannot be adequately addressed by controlled clinical
studies.  These  include  the  issues  of:    (1)  assessment of pulmonary  impairments  induced by
repeated short-term peak exposures or continuous low-level exposures to NO,,; (2) assessment of
possible exacerbation  of  other disease processes by such NO,,  exposures;  and (3) evaluation of
morphological or structural  tissue  damage associated with NO^  exposures,  whether of a short-
term,   repeated  or  continuous nature.  Some  information  bearing on the above  issues  has  been
obtained by human epidemiological and animal toxicological studies summarized below.
1.3.1.2   Human  Epidemiological  Studies—Epidemiological  studies  of  the  effects  of  community
air pollution are  complicated because there are usually complex mixtures of pollutants in the
air.   Thus,  the  most that can typically be obtained from such studies is the demonstration of
close  associations  between health  effects and  ambient  concentrations of  a  given  mixture of
pollutants or subfractions  of the mixtures.  Furthermore, the association must remain consis-
tent throughout a  variety  of conditions for  likely  causality  to be ascribed to such observa-
tions and only  if  other  possible confounding or  covarying  factors have been adequately taken
into  account.   Epidemiological studies  of air  pollution  effects are also  often hampered by
difficulty in defining actual exposures of study populations.
                                              1-12

-------
      It  is  important  to  note that  community  epidemic "logical  studies  prior to  1973  on the
effects  of  N02 exposure are of questionable  validity due to the use of the  Jacobs-Hochheiser
technique in measuring atmospheric concentrations of  NCL.*  For this reason,  the contributions
of  those community  studies  to  knowledge  concerning  the  effects  of  NCL are  very limited.
Certain  other  community exposure studies, however, provide better aerometric  data as bases for
attempting  to  quantify  ambient  air  NO- exposure effects  and  are  the  central  focus  of the
present  analysis.
      Community exposure  studies  investigating NCL effects on pulmonary function and providing
quantitative data  on associated  ambient air  levels  of  NCL are  summarized in Table 1-3.  Most
of these studies consistently  tend to indicate that reported daily mean concentrations of peak
levels  of  NCL,  or  NCL  in  combination with  other  pollutants  (all less  than  1.0  ppm NCL)
typically had  no significant effects on  lung function in the exposed study populations.
      An  exception  is the  Kagawa  and Toyama  (1975)  study which  showed some correlations in 20
Japanese schoolchildren, 11  years  of age, between decrements in  maximum expiratory flow rate
(Vm^)  or  specific  airway conductance  and  concentrations of NCL or  other  specific pollutant
   max                                                          £
levels  at  the  time  of testing.  One-hr.  NCL concentrations  during testing ranged  from 40 to
         3
360 ug/m   (0.02 to 0.19 ppm), but the data were such as not to  allow for quantitative estima-
tion  of  specific  NCL levels  that might  have  been  associated with the occurrence of pulmonary
function decrements.   Also in the ambient  situation  the effects observed in this  study were
generally   not  associated  with  NCL  alone,  but  rather  with  various  combinations  of  air
pollutants,  including  SCL,  particulate matter, and  0,.  In addition,  weekly  variations  in
specific airway conductance  and  in V     at  25  percent  FVC were most closely correlated with
                                     msx
outdoor  temperature  levels.    These  results  emphasize  that  the  observed respiratory  effects
resulted from  a complex  interaction  of pollutants  including NCL  and do not allow for clear
attribution of an association of  decreased lung function with any specific  ambient air concen-
tration of  NCL.
      Linn et al.  (1976),  Cohen et  al.  (1972),  Burgess  et al.  (1973), and Speizer  and  Ferris
(1973a,b) found no differences in pulmonary function tests in separate epidemiological  studies
which also  involved complex pollutant mixtures in ambient air.
     Several  of  the above  community  epidemiological   studies   also  evaluated  relationships
between  ambient  air  exposures to  N02  at  levels reported in Table 1-3 and  the  occurence  of
chronic  respiratory  diseases,  but found no  significant associations between  the  ambient NOp
exposures and  the  health  endpoints measured.   A few other community epidemiology studies have
been  published which  report  quantitative  associations  between  ambient  N0? exposures  and
increased acute respiratory disease incidence, but the methods employed  in  those  studies (e.g.
use of  the  Jacobs-Hochheiser  method  for monitoring  NCL levels)  were such so as  to preclude
acceptance of the reported quantitative  findings.
*The Jacobs-Hochheiser technique has been withdrawn by EPA and replaced by a new Federal
 Reference Method (chemiluminescence) and other equivalent methods (Chapter 7).
                                              1-13

-------
TABLE 1-3.   QUANTITATIVE COMMUNITY HEALTH EPIDEMIOLOGICAL STUDIES ON EFFECTS
            OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION


N02
Exposure
Concentrations
Measure
High exposure group:
Annual mean
24-hr concentrations

90th percent! le
Estimated 1-hr
a
maximum

Low exposure group:
Annual mean
24-hr concentrations
90th percentile
Estimated 1-hr
maximum

Mean "annual "b 24-hr
concentrations: high
exposure area

low exposure
area

1-hr mean:
high exposure
area
low exposure area


ug/m

96


188
480
to
960

43

113
205
to
430
103
92


75
36

260
to
560
110
to
170
3 ppm

0.051


0.1
0.26
to
0.51

0.01

0.06
0.12
to
0.23
+ 0.055 +
S09 0.035
2 SO
C.
+ 0.04 +
SO. 0.014
* S02
0.14
to
0.30
0.06
to
0.09

Study
Population Effect Reference

Nonsmokers No differences in several ventil- Cohen et al.,
Los Angeles atory measurements including spi- 1972
(adult) rometry and flow volume curves





Nonsmokers
San Diego (adult)




Pulmonary No difference in various pul- Speizer and
function monary function tests. Ferris,
tests admin- 1973a,b
istered to
128 traffic Burgess et al.,
policemen in 1973
urban Boston
and to 140
patrol officers
in nearby sub-
urban areas.



-------
                                               TABLE 1-3.  (continued)



Measure
Los Angeles:
Median hourly N09
L,
90th percentile NO-
£.
Median hourly 0
90th percentile DX
San Francisco:
Median hourly N09
C-
90th percentile N02
Median hourly 0
90th percentile 0
1-hr concentration
at time of testing
(1:00 p.m. )

N02 Exposure
Concentrations
ug/m3 ppm

130 0.07

250 0.13
0.07
0.15

65 0.035

110 0.06
0.02
0.03
40 0.02
to to
360 0.19


Study
Population

205 office
workers in
Los Angeles



439 office
workers in
San Francisco


20 school
children
11 years of
age


Effect

No differences in most tests.
Smokers in both cities showed
greater changes in pulmonary
function than non-smokers.







During warmer part of the year
(April-October) N02> SO and
TSP* significantly correlated
with V * at 25% and 50% FVC*


Reference

Linn, et
al. , 1976









Kagawa and
Toyama,
1975

                                                          and witn1 specific  airway  con-
                                                          ductance.    Temperature was
                                                          the factor most clearly correlated
                                                          with weekly variations  in specific
                                                          airway conductance with V    at
                                                          25% and 50% FVC.   Significant
                                                          correlation between each  of  four
                                                          pollutants (NO,,, NO,  S0?  and TSP)
                                                          and V    at 25% and 50% FVC; but
                                                          no clear delineation of specific
                                                          pollutant concentrations  at  which
                                                          effects occur.
.Estimated at 5 to 10 times annual  mean 24-hour averages
 Mean "annual" concentrations derived from 1-hour measur
*FFV
 V  0.75'
  max   :
 FVC

 TSP
Forced expiratory volume,  0.75 seconds
Maximum expiratory flow rate

Forced vital capacity

Total suspended particulates
                                       measurements using Saltzman technique

-------
     As for the results of other epidemiological studies, some support for accepting the hypo-
thesis that children  are  at special risk for  NCL-induced  increases  in acute respiratory ill-
nesses is derived  from certain British and United  States  studies  on indoor pollution effects
as summarized in Table 1-4.
     These studies  investigated  possible  decrements in lung  function  and/or  increased respi-
ratory symptom  and  illness  rates among children living  in  homes  using gas stoves for cooking
in comparison  to children  from  homes with  electric ranges.   Such  studies are  pertinent  for
present purposes because high temperature gas combustion is a source  of NO,,.
     Several  studies  substantiate  that higher  N0?  levels accumulate  in homes  using gas stoves
in comparison to NO,, levels found in homes with electric stoves.   Melia et al.  (1978) reported
that average N09 concentrations in 2 homes over a 96-hour test period, during which stoves  were
                                          3                                            3
in use for 8.5  to 10 hours, were 136 ug/m  (0.072  ppm) when gas was  burned and 18 (jg/m  (0.01
ppm) in 2 other homes where electricity was used.   In this study the N02 concentrations were
monitored at 1.2  meters  (4 ft) above floor level and 0.6 and 2.2  meters (2 and 7.5 feet) from
either gas or electric stoves.   Other studies, including Goldstein et al.  (1979) and Spengler
et al.  (1979),  confirm that  the  levels  of NO,, in  gas  stove homes  are higher  than  those in
homes  using  electric stoves,  and  studies  by  Wade  et al.  (1975)  and Mitchell  et  al.  (1974)
also provide  additional  estimates of  indoor N0~ levels  resulting from gas stove  usage.   For
                                                                                       3
example,  Wade  et al.  (1975)  reported recurrent daily levels which  averaged  280  ug/m  (0.15
ppm) in the kitchen for two hours around the time when peak concentrations were generated.   In
addition to variations  in  cooking routine,  it  should be noted that a variety  of factors would
be expected  to  influence short-term  peak  averages  including interior house design,  type  and
adjustment of range burners, and presence or absence of positive ventilation.   An instantaneous
                   0
peak of 1,880 ug/m   (1.0  ppm) was also measured on one occasion.   Long-term average NO, con-
                                                                                   3
centrations,  over observation  periods  of  up to 2 weeks ranged from 103 to 145 ug/m  (0.055 to
0.077 ppm).
     In an initial publication regarding the British studies on health effects  associated with
gas stove usage, Melia et al.  (1977) reported a weak association between increased respiratory
illness in  school  children  and  residence  in  homes using gas stoves  versus  electric stoves,
after  a  number of  demographic and  other  potentially confounding variables  were  taken  into
account.   However,  Melia  et  al.  (1977) failed  to  adjust  for tobacco smoking in  the home in
their  first  analysis.   In  other later publications  (Melia et al.,  1979; Goldstein  et al.,
1979;  Florey et al.,  1979)  corrections were made  for the  number of  smokers in  the home and,
again,  weak  associations  between  gas  cooking  and  respiratory illness in  children  were found
(independent of smoking  and  other  factors)  in urban  areas  but not  in rural  ones.   There
appeared,  however,  to be  an  association in  rural  areas  for girls   under  the age  of eight.
Additionally,  four  cohorts  of  children  followed longitudinally  from 1973 to 1977 initially
                                              1-16

-------
                                  TABLE 1-4.   EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE IN THE HOME ON LUNG FUNCTION AND
                                THE INCIDENCE OF  ACUTE RESPIRATORY DISEASE IN EPIDEMIOLOGY STUDIES OF HOMES WITH GAS STOVES
 i
i—•
•-j
Pollutant3
Studies of Children
NO- plus
otner gas stove
combustion products
NO- plus other gas
stove combustion
products
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
NO;,
Concentration
jjg/m3 ppm

NO- concentration
not measured at
time of study
NO, concentration
not measured in
same homes studied
Kitchens:
9-596 (gas) 0.005-0.317
11-353 (elec) 0.006-0.188
Bedrooms:
7.5-318 (gas) 0.004-0.169
6-70 (elec) 0.003-0.037
(by triethanolamine
diffusion samplers)
95 percentile of 24 hr
avg in activity room
39 - 116 ug/oi (.02 -
.06 ppm) (gas) vs.
17.6 - 95.2 ug/mj
(.01 - .05 ppm)
Study
Population

2554 children from homes
using gas to cook compared
to 3204 children from homes
using electricity. Ages 6-11
4827 children
ages 5-10
808 6- and 7-year-old
chi Idren
8,120 children 6-10 yrs old in
6 different communities with
data collected on lung function
and history of illness before
the age of 2
Effects

Proportion of children with one
or more respiratory symptoms
or disease (bronchitis, day or
night cough, morning cough,
cold going to chest, wheeze,
asthma) increased in homes
with gas stoves vs. electric
stove homes (for girls p -0.10;
boys not sig. ) after controlling
for confounding factors.
Higher incidence of respiratory
symptoms and disease associated
with gas stoves (for boys p -0.02;
girls p -0.15) after controlling
for confounding factors
Higher incidence of respiratory
illness in gas-stove homes
(p -0.10). Prevalence not
related to kitchen N0? levels,
but increased with N0? levels
in bed rooms of children in
gas-stove homes. Lung function
not related to NO., levels in
kitchen or bedroom
Significant association between
history of serious respiratory
illness before age 2 and use of
gas stoves (p <.01) and, also,
between lower FEV, FVC levels
and use of gas stoves (p <.01)
Reference

Melia et
Melia et
Florey et
Companion
Melia et
Goldstein
1979


al. , 1977
al. . 1979
al. , 1979
paper to
al. , 1979;
et al. ,
Speizer et al. . 1980
Spengler et al. . 1979
                                 (electric).  Frequent
                                 peaks - 1100 ug/m  (0.6
                                 ppm),max peak - 1880
                                 ug/m  (1.0 ppmT 24 - hr
                                 by modi fied sodium
                                 arsenite; peaks by
                                 chemiluminescence

-------
                                                            TABLE 1-4 (continued)
oo
Pollutant3
NO. plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
N02
Concentration
ug/mj ppra
Sample of households
24 hr avg: gas (.005 -
. 11 ppm); electric
(0 - .06 ppm); outdoors
(.015 - .05 ppm); -.several
peaks > 1880 ug/aT (1.0
ppm). Monitoring location
not reported. 24-hr avgs
by sodium arsenite; peaks
by chemi luminescence
Sample of same
households as reported
above but no new
monitoring reported
Study
Population
128 children 0-5
346 children 6-10
421 children 11-15
174 children under 12
Effects Reference
No significant difference Mitchell et al . , 1974
in reported respiratory See also Keller et al.,
illness between homes with gas 1979a
and electric stoves in children
from birth to 12 years
No evidence that cooking mode Keller et al., 1979b
is associated with the incidence
of acute respiratory illness
Studies of Adults
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
Preliminary measure-
ments peak hourly
470 - 940 ug/BJ
max 1880 ug/m
(1-0 ppm)
See table above
for monitoring
See table above
for monitoring
See table above
for monitoring
Housewives cooking with
gas stoves, compared to
those cooking with
electric stoves
Housewives cooking with
gas stoves, compared to
those cooking with electric
stoves. 146 households
Members of 441 households
Members of 120 households
(subsample of 441 households
above)
No consistent statistically
significant increases in
respiratory illness associated
with gas stove usage
No evidence that cooking with
gas associated with an increase
in respiratory disease
No significant difference in
reported respiratory illness
among adults in gas vs electric
cooking homes
No significant difference among
adults in acute respiratory
disease incidence in gas vs
electric cooking homes
USEPA, 1976
Keller et al. , 1979a
Mitchell et al. . 1974
See also Kel ler et al . ,
1979a
Keller et al. , 1979b

-------
 showed  greater  risk of having one  or  more respiratory symptoms or diseases in homes with gas
 stoves, but the strength of the association varied greatly over the four year study period and
 was  non-significant  for  some  subgroups.   In  reviewing their  overall results,  the British
 authors expressed concern that other, potentially confounding factors,  such as temperature and
 humidity,  may  have  contributed  to the  apparent relationship  between gas  stove  usage and
 increased  respiratory  illness  in school children.  The  same  investigators found no relation-
 ship between gas stove usage and  lung function levels in subsets of the same children.
     Based  on  initial  results  from a  continuing  prospective  epidemiological  study  in the
 United  States,  Speizer et al.  (1980)  reported that children from  households  with  gas stoves
 had  a  greater history of serious respiratory  illness before age 2.   In this study, adjustment
 of rates of illness before age 2  for parental  smoking, socioeconomic status, and other factors
 led  to  a  clear  association  between  increased respiratory illness  and the presence  of gas-
 cooking  devices.   Also  found  were  small  but statistically  significant  lower levels  of two
 measures of pulmonary  function (corrected for height) in school age children from houses with
 gas  stoves.   Monitoring of  a  subset of  the  homes  with gas  facilities revealed  that NO- was
 present in much  higher concentrations than in the outside air,  as reported by Spengler et al.
 (1979).  Continuous NO, measurements in a residence with gas stoves showed that levels exceed-
            33
 ing 500 |jg/m  and even 1000 ug/m  can occur during cooking, with such high levels lasting from
 minutes to hours.   Kitchen  annual  means  may exceed  100 ug/m  (0.6 ppm)  if  one  extrapolates
 from  other studies,  as noted  by  Spengler   et  al.   (1979).   Further,  short-term  hourly N0?
 kitchen levels during  cooking  were noted as possibly being 5 to 10 times  higher  than measured
 mean values.   This is  in  contrast  to  annual average  NOp  levels  of  about 0.02 ppm (and  no
 marked peaks) in homes with electric stoves.
     These findings were  interpreted as suggesting that repeated peak short-term exposures  to
 NCK may be associated  with  increased incidence of respiratory  illness  in  young  preschool-age
 children and  small  decrements  in lung function in school age children.   Hypothesizing of such
 effects being associated  with  repeated  short-term  peak  NO-  exposures   is  based  on  annual
 average levels of  NO,  not  being  very different  in  the gas stove homes versus electric  stove
 homes studied by Spengler  et al.  (1979)  and  Speizer  et al.  (1980).  However,  more definitive
 documentation of  such respiratory  system effects being  associated with  short-term  NO- peak
 exposures   remains to  be  provided based on further data collected beyond those  included in the
 initial  analyses  discussed  by  Speizer  et al.  (1980) and Spengler et al. (1979)  from  their
 continuing prospective epidemiological  study.   This  includes confirmation of  the  basic  find-
 ings reported,  confirmation  of  the exclusion of  socioeconomic status and other  confounding
 factors as important  contributors to the observed relationships,  and more  detailed monitoring
 of indoor  NO, levels in homes of children in the study populations.
     Further  complicating  interpretation of the  above findings  and determination of  the
 strength and  reliability of the  apparent relationships  suggested  by  them are  other studies
which failed  to  find  any associations between gas stove  usage  and increased  respiratory ill-
 ness or  decrements  in  lung  function.  In  a  series  of three related studies,  Mitchell  et al.

                                              1-19

-------
(1974)  and  Keller et  al.  (1979a,b) report  negative findings with respect  to  an association
between the use of gas stoves in the home and an increased incidence of respiratory disease in
both  adults  and children.   Initially  441 households  in a  middle-class  suburb  in  Ohio  were
studied.  A follow-up study on a subsample of 120 of the original  441 households was also  con-
ducted  to verify  the  methodology used previously to  collect health data.   In addition,  these
investigators studied  a  group  of 146 housewives in a community on Long Island,  N.Y., confirm-
ing the negative  results reported earlier by the  U.S.  EPA (1976).   However, the sample  sizes
for children used  in  these studies were  approximately  a factor of 10 smaller than those  used
in both the  British  and American studies  reporting  an  association  between increased respira-
tory  disease  and  gas  cooking.   Also,  it is not  clear that the  households sampled  in  Ohio
constituted a representative sample of the community studied.
1.3.1.3  Animal Toxicology Studies—In addition  to  epidemiological  studies,  animal toxicology
studies provide valuable information regarding induction of respiratory system effects by  NO-.
Although it  is recognized  that  exposure/effect relationships demonstrated  by  animal  studies
are generally not quantitatively directly extrapolatable as indicators of human  health effects
thresholds, they  are,  nevertheless,  highly instructive regarding  probable mechanisms by which
NOp may affect human  pulmonary function  and  damage the  pulmonary defense  system,  possibly
causing  increased human  susceptibility  to  bacterial   infections.   Rather  than attempt  an
exhaustive  summary  here  of the  animal   toxicology  literature assessed   in  Chapter  14,  the
present section concisely highlights key points  from that literature as they relate to effects
observed in human studies.
     The lowest  concentration  of N09 that has  been  shown to produce  measurable  responses  in
                   3
animals is 376  ug/m   (0.2 ppm).   At this concentration, rats exposed for 3 hours had an  inhi-
bition  of the  lung metabolic conversion  of prostaglandin  E~ (a mediator which  acts on smooth
muscle)  to  its   inactive  15-keto  metabolite  18  hours  after  exposure  ceased.   This  could
possibly lead  to  an  alteration of vascular  or  airway smooth muscle tone  and,  therefore,  may
ultimately contribute  to the mediation  of pulmonary function changes,  e.g.,  increased airway
resistance,  observed  with  human exposure  to  higher   levels  (>1.0 ppm)  of HOy-   Since  the
prostaglandin system  is  intimately involved in the local regulation of blood flow in the  lung,
alterations in prostaglandin metabolism may also have profound effects on the perfusion of the
lung and,  subsequently, on the gas exchange of the affected lung.
     Morphological alterations  in  animal lung  tissue,  ranging  from  very  small  changes  in
collagen to emphysema-like changes have also  been observed following NO, exposure.  Very  small
                                                                                             3
changes occurred in rabbits after 24 or 36 days  of exposure (4 hr/day, 5 days/wk) to 470  ug/m
(0.25 ppm).  The  health  significance of the  small collagen changes at low exposure levels are
unknown, but  it  should  be  noted  that  collagen  metabolism  is disrupted  in man  and  animals
during  fibrosis.   Thus  the  initial  small collagen effects  seen after  low-level  N02 exposure
may be  indicative  of  the initiation of processes  of increasingly greater health significance
as they intensify  at  high NO,, exposure levels.   Emphysema-like changes were found in several
                                              1-20

-------
species, most  often  after chronic exposure, to  high  concentrations (18,800 ug/m  . 10 PP"1)
above ambient air NO,, levels.
     Systemic effects  have  also been observed  after  NO,  exposure.   Female mice receiving 470
    3
ug/m   (0.25  ppm) for  3 hours  exhibited  an increase  in  pentobarbital-induced sleeping time.
Such a  response  implies a potential effect on  some  aspect(s) of liver xenobiotic metabolism.
Hematological effects  have  also been observed  in guinea pigs after 7 days of exposure to both
690 ug/m  (0.36 ppm) and 940 ug/m  (0.5 ppm).   There is no evidence available establishing that
the same NCL exposure concentrations may produce similar systemic effects in human beings, and
the potential significance of such effects for human health is unclear at this time.
     Of more obvious  importance are the results of other extensive animal studies that appear
to  be  consistent with  emerging conclusions from  human epidemiological  studies  on  gas stove
usage  discussed  earlier.   The  latter  studies   appear  to  suggest  that  increased  incidence  of
acute respiratory illness  in humans may occur  as a result of repeated short-term exposures  to
NOp.  Pertinent  animal  studies  summarized in Table 1-5 have demonstrated that repeated short-
term exposures increase susceptibility  to some respiratory pathogens  as  much as does contin-
uous exposure to  the  same concentration of N0? (see Section 14.2.3.1.1).   N0? exposures caus-
ing increased infectivity  in animals have been observed across a wide range, beginning at 940
ug/m   (0.5  ppm)  for  repeated  exposures during a  90-day  period and 3760 ug/m   (2.0  ppm) for
single (3 hr) exposures.  The results are interpreted here as providing evidence supportive  of
tentative conclusions emerging  from  the above   "gas stove"  studies,  i.e., that repeated expo-
sure to daily peak  concentrations of NO- may be  effective  in impairing the health of exposed
young children  by increasing vulnerability  to infectious  respiratory diseases.  The  latter
conclusions from the  gas  stove  studies, however,  still must be viewed with caution until  more
definitive results are  obtained.   From  the mouse studies,  it is also apparent that concentra-
tion of NOp has more importance  than time of exposure in producing increased susceptibility  to
bacterial   infection.   Of interest,  the  lowest NO-  concentrations (0.5 to 1.5  ppm)  found  to
induce  such  effects  in animals with repeated  or intermittent  continuous  exposures,  do  not
greatly exceed to the  upper range of repeated  NO-  peak levels found in gas stove usage homes
hypothesized to be associated with increased respiratory illnesses in children.
1.3.2  NOp Sensory System Effects
     In addition  to  the  effects  of N0?  on  pulmonary functions and  its  possible association
with  increased   acute   respiratory  disease  in  young  children,  NOp  also exerts  discernible
effects on  sensory  receptors (Table 1-6).   This  includes  the detection of N09  as  a noxious
                                                                     3
pungent odor  starting  at concentration  levels as  low as 210  ug/m   (0.11  ppm)  of N02  and
occurring immediately upon  exposure.  Under  some exposure conditions,  however,  impairment  of
odor detection occurs.   For  example, impaired  detection of N02 concentrations of 18,800 ug/m
(10 ppm) or more  has  been reported.   In  general, the former sensory effect,  odor detection,  is
not viewed  as a significant  health effect  of concern  (although it  could be  construed  as
affecting human welfare); and the latter olfactory deficit effect,  impairment of odor detec-
tion,  is  of likely negligible  health  concern  in  view of  its temporary,  reversible nature.

                                             1-21

-------
                   TABLE  1-5.   SUMMARY  OF  STUDIES  DEMONSTRATING  HEALTH  EFFECTS  IN  ANIMALS
                                   AT  LOW  (<2.0  ppm)
                                         N02 EXPOSURE LEVELS
     N02
 Concentrations
 ug/md
ppm
                       Effects
                                    N02 measurement method     Reference
 3,760      2.0
             A single 3-hr exposure caused
             increased mortality following
             challenge with an infectious
             agent in mice.
                                     Chemiluminescence
                       Ehrlich et al.,  1977
 2,800      1.5
             After 1 wk continuous expo-
             sure, mice had a significant-
             ly greater increase in suscep-
             tibility to infectious pulmon-
             ary disease compared to inter-
             mittent exposure.
             After 2 wks, no differences
             between continuous and inter-
             mittent exposure modes occurred.
                                     Saltzman and Chemilu-  Gardner et al., 1979
                                     minescence procedures
 1,880      1.0
(daily 2 hr spike)
   188.      0.1
  (continuous)
             Emphysematous alterations in
             mice after 6 mo exposure.
                                     Saltzmanc
                       Port et al.,  1977
   940
0.5
In mice challenged with bac-
teria, there was increased
mortality following a 90-day
continuous exposure or a 180
day intermittent exposure.
Saltzmanc
Ehrlich and
Henry, 1968

-------
                                                 TABLE  1-5.   (continued)
    N02
Concentrations
ug/m3ppm
                        Effects
                                    N0? measurement method     Reference
 940
 940
 0.5
 0.5
A 7-day intermittent exposure
caused enzymatic alterations
in lungs and blood of guinea
pigs.

Intermittent exposure for 6
hr/day for up to 12 mo caused
morphological changes in lung
alveoli of mice.
Saltzman
Donovan  et al.,  1976
                       Blair et al.,  1969
 940
 0.5
Increased susceptibility to
influenza infection in mice.
Saltzman
Ito, 1971
 750
 0.4
Continuous exposure for one
wk caused increase of protein
in lavage fluid in vitamin C
deficient guinea pigs.
                       Sherwin and Carlson, 1973.
 470
 0.25
Swollen collagen fibers
after an intermittent 24
or 36 day exposure of
rabbits
                       Buell, 1970
 667
  to
  94
0.36
 to
0.05
Hematological effects
observed in guinea pigs
after 7 days of.,exposure to
690 or 940 ug/m  (0.36 or
0.5 ppm).
                       Donovan et al., 1976
                       Menzel et al., 1977
                       Mersch et al., 1973

-------
                                                         TABLE 1-5.   (continued)
             N02
         Concentrations
        (jg/m3
 ppm
                        Effects
                                    N0~ measurement method     Reference
         470
0.25
Increased pentobarbital-
induced sleeping time in
female mice after a 3 hr
exposure.   No effects after
2 or 3 days.
Miller et al.,  1980
          376
0.2
Inhibition of meta-
bolism of prostaglandin
E- in rats to its inactive
15-keto metabolite.
Menzel, 1980
         Saltzman,  1954  (See Chapter  7.)
I
ro

-------
TABLE 1-6.   EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY RECEPTORS IN CONTROLLED HUMAN STUDIES
N02 Concen-
trations
ug/m3
790
410
230
230
200
0
to
51,000
2,260
140
150
to
500


ppm
0.42
0.22
0.12
0.12
0.11
0
to
27
1.2
0.07
0.08
to
0.26


No. of
Subjects
8
13
9
14
28
6
6
4
5


Time
until
effect
Immediate
Immediate
Immediate
Immediate
Immediate
54 minutes
Immediate
5 and 25
minutes
Initial
Repeated
over 3
months
No. of
Subjects
Effects Responding
Perception of odor of N02
Perception of odor of N02
Perception of odor of N0?
Perception of odor of NO-
Perception of odor of NO-
No perception of odor of NO- when
concentration was raised slowly from
0 to 51,000 ug/nT
Perception of odor improved when
relative humidity was increased from
55% to 78%
Impairment of dark adaptation
Increased time for dark adaptation
at 500 ug/nT (0.26 ppm)
Initial effect reversed

8/8
8/13
3/9
most
26/28
0/6
6/6
4/4
Not
Reported


Reference
Henschler et al . ,
1960
Ibid.
Ibid.
Shalamberidze,
Feldman, 1974
Henschler et al . ,
1960
Ibid.

Shalamberidze,
Bondareva, 1963



-------
     NC^ exposures  also exert  effects  on other sensory perception  functions.   Probably most
significant is the NO- effect on dark adaptation.   Two different studies (Shalamberidze,  1976,
and Bondareva,  1973)  report data  indicating  that  impairment of dark adaptation  can  occur  in
human subjects  at NCK  exposure levels as  low as  130 to  150  ug/m  (.07 to  .08  ppm).   It  is
difficult to fully appraise the health significance of such an effect,  but it appears  to  be  of
generally negligible  concern except,  perhaps, for  certain occupational  or public safety  situ-
ations where rapid dark adaptation may be important.
1.3.3  Summary of Major Health Effects Conclusions
     Major conclusions regarding NO -associated health effects of most  importance for  conside-
                                   A
ration  in  decision-making regarding  primary  National Ambient  Air Quality  Standards  for NO
                                                                                             A
compounds can be summarized as follows:
              (1)  At concentrations of 9,400 ug/m   (5.0  ppm) or above,  exposure to
                   N02 for as little as 15 minutes  will  both increase airway resistance
                   in healthy human adults and impair the normal transport of gases
                   between the blood and the lungs.
              (2)  In healthy adult individuals, concentrations of 4,700 ug/m  (2.5
                   ppm) NOp for 2 hours have been reported to increase  airway resistance
                   significantly without altering arterialized oxygen pressure.
                   Single exposures for 15 minutes  to NO, at concentrations of 3,000
                       3
                   ug/m  (1.6 ppm) are also likely  to increase airway resistance in
                   healthy adults and individuals with chronic bronchitis but not to
                   interfere with the transport of  gases  between blood  and lungs.
              (3)  Single exposures for times ranging from 15 minutes to 2 hours to
                   NO- at concentrations of 2,800 ug/m  (1.5 ppm) or below have not
                   been shown to affect respiratory function in healthy  individuals
                   or in those with bronchitis.
              (4)  Whether asthmatic subjects are more sensitive than healthy adults
                   in experiencing NO-'induced pulmonary  function changes remains to
                   be definitively resolved.   The results of one controlled human
                   exposure study suggest that some asthmatics may experience chest
                   discomfort,  dyspnea,  headache, and/or  slight nasal discharge
                   following 2 hr exposures to 0.5  ppm NO- but did not  provide
                   convincing evidence of pulmonary function changes in  asthmatics
                   at that N02  concentration.
              (5)  Certain animal studies  demonstrate various mechanisms of action
                   by which pulmonary function changes of the above type may be
                   induced in humans at relatively  low NO- exposure levels and by
                   which increasing by more serious histopathological changes leading
                   to severe emphysematous effects  are manifested at increasingly
                   higher (generally greater than ambient) NO- exposure  levels.

                                              1-26

-------
              (6)  Prospective studies of the effects of indoor air pollution suggest
                   that, in some instances, an increased incidence of respiratory
                   illness in young children may be associated with the use of gas
                   stoves and possibly with NCL produced by these appliances.   Much
                   caution must be applied, however, in fully accepting or using
                   these study findings for risk assessment purposes until:  they
                   are confirmed by further analyses of data subsequently gathered
                   in the prospective studies; potential confounding factors are
                   more definitively ruled out; and clearer exposure/effect relation-
                   ships are defined via more intensive NO- monitoring in gas  stove
                   homes.
              (7)  No definitive estimates can yet be provided for peak 1-2 hr,  24
                   hr, weekly, or annual average N0? exposure levels that may  be
                   associated with any increased respiratory illness in young  children
                   residing in homes using gas stoves,  although some basis exists
                   for suggesting that repeated exposures to peak levels are most
                   likely to be importantly involved.   Peak 1-2 hr NO- levels  ranging
                   up to 0.5-1.0 ppm have been observed in gas stove homes; longer-term
                   weekly average NO^ levels of 0.05 to 0.07 ppm and annual average
                   levels of 0.01 to 0.06 ppm were also found in such homes.
              (8)  Estimates of repeated short-term peak concentrations of ^
                   possibly associated with increased respiratory illness in homes
                   with gas stoves are not markedly below the general  range of the
                   lowest (0.5 to 1.0 ppm) intermittent exposure concentrations
                   found to cause increased susceptibility to respiratory infections
                   in animal  infectivity model studies.
     Placing the  above  conclusions  in  perspective, it  should  be noted that ambient  air  NO^
monitoring  results  in the  United  States  indicate  that peak  1-hr  N0~ concentrations  rarely
exceed  0.4  to  0.5  ppm.   Such  peaks occurred  during  1975  to  1980 in  only  a  few  scattered
locations in the  United  States,  e.g.,  Los Angeles  and  several  other California sites.   Also,
during that period,  annual  average  N0? concentrations  exceeding 0.05 ppm were only found in a
relatively few  scattered locations,  including population centers such as Chicago and Southern
California.
1.4  WELFARE EFFECTS OF NITROGEN OXIDES
     In  addition to  human  health  effects  associated  with  exposures  to  nitrogen  dioxide
discussed above,  considerable attention  has  been accorded  to  the investigation  of possible
effects  of  NO-  and  other  NO   compounds  on aquatic  and  terrestial  ecosystems,  vegetation,
              t               A
visibility,  climate,  and  man-made materials--effects  which may  impact  negatively  on  public
                                              1-27

-------
welfare  in  the United  States.   Concisely summarized  below are key points  derived  from more
detailed discussions  in  Chapters  10-13 of the relationship  of  NO   compounds to the induction
                                                                 A
of such welfare effects.
1.4.1  Nitrogen Oxides, Acidic Deposition Processes, and Effects
     The occurrence  of  acidic deposition, especially in the form of acidic precipitation, has
become  a  matter of  concern   in many  regions of  the  United States, Canada,  northern Europe,
Taiwan  and  Japan.   Acidic precipitation  in the  Adirondack Mountains  of  New York  State,  in
Maine,  in eastern  Canada,  in southern Norway and  in  southwest  Sweden has  been reported to be
associated with acidification of waters in ponds,  lakes and streams with a  resultant disappear-
ance of  animal  and plant life.   Acidic precipitation (rain and  snow) is also believed to have
the  potential  to:    (1)  leach nutrient elements  from sensitive soils,  (2) cause  direct and
indirect injury to forests,  (3) damage monuments  and buildings  made of stone,  and (4) corrode
metals.
     Chapter 11 of this  document  discusses acidic deposition processes and the effects of wet
deposition  of  sulfur and nitrogen oxides  and  their products on aquatic and  terrestrial  eco-
systems.  Dry  deposition  also plays  an important  role, but contributions by this process have
not  been  well  quantified.   Because  sulfur  and nitrogen  oxides are so closely  linked  in the
formation of  acidic precipitation, no attempt has  been made to limit  the  present  discussion
solely to nitrogen oxides.   A more thorough general review of acidic deposition processes and
associated environmental  problems  will be presented in a future  EPA document.
     Sulfur and nitrogen  oxides are  considered to  be  the  main  precursors  in the formation of
acidic  precipitation.   Emissions  of  such compounds involved in acidification  are  attributed
chiefly to the combustion of fossil fuels such as  coal and oil.   Emissions  may occur at ground
level,  as   from  automobile  exhausts, or from 300 meters  (1000   feet)  or  more in  height.
Emissions from natural  sources are  also  involved;  however, in highly industrialized areas,
emissions from manmade sources markedly  exceed  those  from natural sources.   In the eastern
United  States  the  highest emissions  of  sulfur oxides derive  from  electric  power  generators
burning coal.   However,  emissions  of  nitrogen oxides, mainly from  automotive sources, tend to
predominate in the West.  (Information  regarding 'sources  and  emissions of NO   compounds  is
discussed in Chapter 5 of this document.)
     The fate  of   sulfur  and nitrogen oxides, as well as  other  pollutants emitted  intO'the
atmosphere,  depends on their dispersion,  transport, transformation  and deposition.  Sulfur and
nitrogen oxides or their transformation  products  may be deposited  locally or transported long
distances from the  emission sources  (Altshuller  and  McBean,   1979;  Pack,  1978; Cogbill  and
Likens, 1974).   Residence time in  the atmosphere,  therefore, can be brief if the emissions are
deposited locally  or may extend  to days  or  even  weeks if  long range  transport occurs.   The
chemical form  in   which  emissions  ultimately reach the receptor,   the  biological organism or
material affected,   is  determined  by  complex chemical  transformations  that  take place between
the  emission  sources and the receptor.    Long  range transport  over distances  of hundreds  or
thousands of miles  allows time for many chemical  transformations to occur.

                                              1-28

-------
     Sulfates  and  nitrates are  among  the products of the  chemical  transformations of sulfur
oxides  (especially  SCL)  and  nitrogen  oxides.   Ozone and  other photochemical  oxidants  are
believed  to  be involved in the chemical processes that form sulfates and nitrates.  When sul-
fates and  nitrates  combine with atmospheric water, dissociated  forms  of sulfuric (HLSCL)  and
nitric (HNOj)  acids  result; and when these acids are brought to earth in rain and snow, acidic
precipitation  occurs.   Because of  long range  transport,  acidic  precipitation  in a particular
state or  region  can be the result  of  emissions  from  sources in  states  or  regions many miles
away,  rather than  from local  sources.  To  date,  however, the complex nature  of the chemical
transformation processes  has  not  made  it  possible  to demonstrate a direct cause and effect
relationship between emissions of sulfur and nitrogen oxides and the acidity of precipitation.
(Transport, transformation, and deposition of  nitrogen compounds are discussed  in Chapter 6 of
this document; analogous information on sulfur oxides  is discussed in a separate document,  Air
Quality Criteria for Particulate Matter and Sulfur Oxides, U.S.  EPA, 1981).
     Acidic  precipitation  has been  arbitrarily  defined  as precipitation with a  pH less  than
5.6, because  precipitation formed  in  a  geochemically  clean environment would  have  a  pH of
approximately  5.6 due to the combining of carbon dioxide with moisture in the air to form car-
bonic acid.   Currently  the acidity of precipitation in the northeastern United States usually
ranges from pH 3.9 to 5.0; in other regions of the United States precipitation  episodes with a
pH as low as 3.9 have also been reported in areas with average pH levels  above  5.0 (see Figure
1-D-
     The pH of precipitation can vary from event to event, from season to season and from geo-
graphical  area to  geographical area.   Other  substances  in the atmosphere  besides  sulfur  and
nitrogen oxides can cause the pH to shift by making it more acidic or more basic.   For example,
dust and  debris  swept  up in small  amounts from the ground into the atmosphere  may become  com-
ponents of precipitation.   In  the  West and Midwest soil  particles  tend  to  be  more basic,  but
in  the  eastern  United States  they tend to  be acidic.   Also,  in  coastal  areas  sea  spray
strongly  influences  precipitation  chemistry by contributing calcium, potassium,  chlorine  and
sulfates.   In the final analysis,  the pH of precipitation is a measure of the relative contri-
butions of all of these components  (Whelpdale,  1979).
     It is not presently  clear as  to when  precipitation  in the U.S.  began  to  become markedly
more acidic  than  the   5.6  pH  level  expected  for  a  geochemically  clean  environment.   Some
scientists argue  that it began with the industrial  revolution and the burning of large amounts
of coal and  others  estimate that it began  in  the  United States with the introduction of  tall
stacks  in power plants  in the 1950's.   However, other  scientists disagree completely and argue
that rain  has  always been  acidic.  In other words,  no  definitive answer  to the  question exists
at the present time.   Also,  insufficient data presently exist to characterize  with confidence
long-term temporal  trends  in  changes in the pH  of  precipitation  in the  United States, mainly
due  to the pH of rain  not  having  been  continuously monitored over extended periods  of time.
                                              1-29

-------
 I
CO
o
                                   Chart Ptottlno. Legend
                                                          1.0
                        •  Naltauul Atmo»phw*c OeposMon flagrant (NAOP)
                       D  Department of Energy (DOE)
                        B  EmtranmantdProlectbn Agency (EPA/NOAA/WMOI
                       -e- Uniyenll) ol Cnlllomia
                       -O- CoUIOfnte Imlflule ol Tachnoloay
                        &  WulU-Slnle Abnospheiic Poraef
                        '  Production PoUutlon Study (MAP1S)
                        A  Electric Power Rauweh Intttuls (EPRI)
                       ©  Odi Rtdge Natlonel Laboratory
                       O  CtnHttanJUtnoBfltar* Envfcomnenl Sarvtoi (CAMSAP)
                       ^  UftfYOrsHyolArtrara
                       0  UnhonHyol FtorUa
                           Figure 1-1., Average pH isopleths as determined from laboratory analyses of precipitation
                           sample, weighted by the reported quantity of precipitation.
                          Source:  Wisniewski and  Keitz (1981).

-------
     Although  acidic  precipitation (wet deposition) is usually emphasized, it is not the only
process  by  which acids or acidifying  substances  are  added to bodies of water or to the land.
Dry  deposition also  occurs.   Dry  deposition processes  include  gravitational  sedimentation of
particles,  impaction  of  aerosols and the adsorption and absorption of gases by objects at the
earth's  surface  or  by the soil  or water.   Dew,  fog,  and frost are also involved in the depo-
sition processes but do not strictly fall into the category of wet or dry deposition (Galloway
and  Whelpdale,  1980;  Sehmel,  1980; Hicks and Wesley,  1980).  Dry deposition processes are not
as well  understood  as wet deposition at the present time; however, all of the deposition pro-
cesses  contribute to  the gradual  accumulation  of acidic  or acidifying  substances  in  the
environment.
     The most  visible changes associated with acidic deposition, that is both wet and dry pro-
cesses,  are  those  observed in the  lakes and  streams  of the Adirondack Mountains  in New York
State, in Maine,  in  the Pre-cambrian  Shield areas  of  Canada,  in Scotland, and in the Scandi-
navian  countries.    In these  regions,  the pH  of the  fresh  water  bodies  appears to  have
decreased, causing changes in animal and plant populations.
     The chemistry of  fresh  waters is  determined  primarily  by  the geological structure (soil
system and  bedrock)  of  the  lake or stream catchment  basin,  by the ground cover  and  by land
use.   Near coastal areas (up to 100 miles inland) marine salts also may be important in deter-
mining the chemical composition of the  stream,  river or lake.   Sensitivity of a lake to acidi-
fication depends on the acidity of both wet and dry deposition plus the same factors — the soil
system of the  drainage basin,  the canopy effects  of  the  ground cover and  the  composition of
the waterbed bedrock.   The capability,   however, of a lake  and its  drainage basin to neutralize
incoming acidic  substances is determined  largely by  the  composition of  the  bedrocks  (Wright
and  Gjessing,  1976;  Galloway  and Cowling,  1978;  Hendrey et al. , 1980b).  Soft  water  lakes,
those  most   sensitive  to   additions  of  acidic  substances,  are usually  found  in  areas  with
igneous  bedrock which  contributes few soluble  solids  to the  surface  waters,  whereas  hard
waters contain large  concentrations of alkaline  earths (chiefly bicarbonates  of  calcium  and
sometimes magnesium) derived  from limestones  and calcareous sandstones in the drainage  basin.
Alkalinity is  associated with  the increased capacity  of lakes to  neutralize or buffer the  in-
coming acids.  The extent  to  which acidic  precipitation contributes to the acidification pro-
cess  has  yet to be determined.
     The  survival of  natural  living ecosystems in response to marked environmental  changes or
perturbations  depends  upon the  ability of  constituent organisms of which  they are composed to
cope  with the  perturbations  and  to continue reproduction  of  their  species.   Those species of
organisms most sensitive to  particular environmental  changes are  first removed.   However,  the
capacity  of  an ecosystem  to  maintain  internal stability  is  determined by the  ability  of  all
individual  organisms to adjust  and survive, and other  species  or  components  may subsequently
be impacted  in response to the loss of  the  most susceptible species.
                                              1-31

-------
     The  capacity of  organisms to  withstand injury  from weather  extremes, pesticides,  acidic
deposition  or  polluted air  follows the  principle of  limiting factors  (Billings, 1978;  Odum,
1971; Moran  et al.,  1980; Smith,  1980).   According to  this  principle, for each physical  factor
in the  environment  there  exists  for each organism  a minimum  and  a maximum limit  beyond which
no members  of a particular species can survive.   Either too  much or too  little of a  factor
such as heat,  light,  water, or minerals (even though  they  are necessary for life) can  jeopar-
dize the survival  of  an  individual and in  extreme cases  a  species.  The  range of  tolerance
(see Figure  1-2)  of  an organism may be broad  for one  factor and narrow  for another.   The
tolerance  limit for each  species  is determined  by  its genetic makeup and varies  from  species
to species  for the same  reason.   The  range of  tolerance also varies  depending on the age,
stage  of  growth or  growth  form  of an  organism.   Limiting  factors are,  therefore,  factors
which,  when  scarce  or overabundant,  limit  the growth, reproduction and/or distribution of an
organism.
                ZONE OF
              INTOLERANCE
                          LOWER LIMITS
                          OFTOLtHAJICE
                          ZONE OF
                        PHYSIOLOGICAL
                          STRESS
TOLERANCE RANGE
RANGE OF OPTIMUM
  UP9ER UKITS
  OF TOLERANCE
  ZONE OF
PHYSIOLOGICAL
   STRESS
                                   ZONE OF
                                  INTOLERANCE
                         ORGANISMS
                         INFREQUENT
              ORGANISMS
                ABSENT
                                               GREATEST
                                              ABUNDANCE
                        ORGANISMS
                        INFREQUENT
                                  ORGANISMS
                                    ABSENT
                 LOWO-
  -GRAOiEMT-
            ->HIGH
               Figure 1-2.  idealized conceptual framework illustrating the "law of tolerance," which
               postulates a limited tolerance range for various environmental factors within which
               species can survive (adapted from Smith, 1980).
                                                1-32

-------
     Continued or  severe  perturbation of an ecosystem  can  overcome its resistance or prevent
its  recovery,  with the result that the  original  ecosystem  will  be replaced  by  a new system.
In the Adirondack Mountains of New York State, in eastern Canada, and parts of Scandinavia the
original aquatic ecosystems  have been and are continuing to be replaced by ecosystems differ-
ent  from the original due to  acidification  of the aquatic  habitat.   Forest  ecosystems,  how-
ever,  appear thus   far  to have  been  resistant  to changes due to perturbation  or stress  from
acidifying substances.
     The impact of acidic precipitation on aquatic and terrestrial ecosystems is typically not
the  result  of a single or several  individual  precipitation events, but rather  the  result  of
continued additions  of acids  or acidifying substances  over time.   Wet deposition  of acidic
substances on  freshwater  lakes,  streams, and natural  land  areas  is only part of the problem.
Acidic substances exist in gases, aerosols, and particulate matter transferred into the lakes,
streams, and land  areas  by  dry  deposition  as well.   Therefore, all  the  observed biological
effects should not be attributed to acidic precipitation alone.
     The disappearance of fish populations from freshwater lakes  and streams is usually one  of
the most readily observable signs of lake acidification. Death of fish in acidified waters has
been attributed  to  the modification of a number of physiological  processes by a change in pH.
Two  patterns  related  to  pH change have been observed.   The first involves  a sudden short-term
drop in  pH  and the second, a gradual  decrease in pH with time.   Sudden short-term drops in  pH
may  result from  a  winter thaw or the melting of the snow pack in early spring and the release
of the acidic constituents of the snow into the water.
     Long-term gradual increases in acidity,  particularly below pH 5,  interfere with reproduc-
tion and spawning,  producing  a decrease in population  density and  a  shift in size and age  of
the  population to  one consisting primarily of  larger  and older  fish.   Effects on yield often
are  not  recognizable  until the  population is  close to extinction;  this is particularly  true
for  late-maturing  species  with long lives.   Even relatively small increases (5 to 50 percent)
in mortality of fish eggs and fry can decrease yield and bring about extinction.
     In  some  lakes,  concentrations of  aluminum  may be  as  crucial  or more important  than  pH
levels as factors  causing  a  decline in  fish populations  in acidified lakes.   Mobilization  of
certain aluminum compounds in  the water due  to lowered pH,  upsets the osmoregulatory function
of blood in  fish.   Aluminum  toxicity to aquatic  biota  other than fish has not been assessed.
     Although  the   disappearance  of  and/or  reductions  in  fish  populations   are  usually
emphasized as  significant results  of  lake and  stream acidification, also important  are  the
effects  on  other  aquatic organisms  ranging  from  waterfowl to  bacteria.   Organisms at  all
trophic (feeding)  levels  in  the  food web appear  to be affected.  Species  reduction in number
and diversity may  occur,  biomass (total  mass of  living  organisms in  a given  volume of water)
may be altered and  processes  such as primary  production and  decomposition impaired.
     Significant changes  that  have occurred  in aquatic ecosystems  with  increasing  acidity
include the  following:
                                              1-33

-------
        1.    Fish populations are reduced or eliminated.
        2.    Bacterial  decomposition  is  reduced  and  fungi  may  dominate  saprotrophic
             communities.    Organic  debris  accumulates  rapidly,  tying  up  nutrients,  and
             limiting nutrient mineralization and cycling.
        3.    Species diversity and  total  numbers of species  of  aquatic  plants  and animals
             are reduced.   Acid-tolerant species predominate.
        4.    Phytoplankton productivity may  be  reduced due to changes in  nutrient cycling
             and nutrient limitations.
        5.    Biomass and  total productivity  of  benthic macrophytes and  algae  may increase
             due in part to increased lake transparency.
        6.    Numbers  and  biomass of herbivorous  invertebrates decline.   Tolerant inverte-
             brate  species,  e.g.,  air-breathing insects may  become abundant primarily due
             to reduced fish predation.
        7.    Changes in community structure occur at all  trophic  levels.
     An indirect effect of  acidification potentially of concern  to human health is the possi-
ble contamination of  edible  fish and of water  supplies.   Studies  in  Canada and Sweden reveal
high mercury concentrations  in  fish from acidified regions.   Lead  has  been found in plumbing
systems with acidified  water,  and persons drinking the  water could be  affected  by  the lead.
However, no examples  have yet been documented  of  such human  effects  having actually occurred
in response to  acidic precipitation processes.
     Soils  may become gradually  acidified from  an  influx  of  hydrogen  (H ) ions.   Leaching of
the mobilizable  forms  of  mineral nutrients  may  occur.  The rate  of leaching  is  determined by
the buffering  capacity  of the soil  and  the  amount and composition of precipitation.   Unless
the buffering capacity of the soil  is strong and/or the salt content of precipitation is high,
leaching will  in time result in acidification.    Anion mobility is  also an important factor in
the leaching of soil nutrients.   Cations cannot  leach without  the associated anions also leach-
ing.   The capacity  of  soils  to adsorb and retain anions  increases as the  pH  decreases,  when
hydrated oxides of iron and aluminum are present (Wiklander, 1980).
     Sulfur and nitrogen are essential  for optimal plant growth.   Plants  usually obtain nitro-
gen in  the  form of nitrate  from organic  matter during microbial decomposition.   Wet  and dry
deposition  of atmospheric  nitrates is also a major source.   In soils where sulfur and nitrogen
are limiting nutrients,  such deposition may increase growth of some plant species.  The amounts
of nitrogen  entering the  soil  system from  atmospheric  sources  is dependent on  proximity to
industrial   areas,  the  sea  coast,  and marshlands.   The  prevailing winds  and  the  amount of
precipitation in a given region are also important (Halstead and  Rennie,  1977).
     At present  there are no  documented observations  or  measurements  of  changes in  natural
terrestrial  ecosystems or agricultural  productivity directly attributable to acidic precipita-
tion.    The  information  available  regarding vegetational  effects   concerns  the  results  of a
variety of  controlled research  studies,  mainly  using  some  form of "simulated"  acidic rain,
frequently   dilute  sulfuric acid.   The  simulated  "acid  rains" have deposited  hydrogen (H ),
sulfate (SO,")  and nitrate (N03)  ions on vegetation and have caused necrotic lesions in a wide

                                              1-34

-------
variety  of plants  species  under greenhouse and laboratory conditions.   Such  results must be
interpreted with  caution,  however, because growth and  morphology  of leaves under such condi-
tions are  not necessarily typical  of field conditions.
     Damage to monuments and buildings made of stone, corrosion of metals and deterioration of
paint may  also result from acidic  precipitation.  Because sulfur compounds are a dominant com-
ponent  of  acidic precipitation  and  are  deposited  during dry deposition  as  well,  the effects
resulting  from the  two  processes  cannot be clearly distinguished.   Also, deposition of sulfur
compounds  on stone  surfaces may provide a medium for microbial growth that can result in dete-
rioration.
     Several  aspects of  the acidic  precipitation  problem remain  subject to  debate because
existing data are ambiguous or inadequate.  Important unresolved issues include:  (1) the rate
at  which rainfall  is  becoming  more acidic and/or  the  rate at which  the  problem  is becoming
geographically more widespread;   (2)  the  quantitative  contributions  of various acids  to the
overall  acidity  of  rainfall;  (3) the relative extent  to  which the acidity of  rainfall  in a
region depends on local  emissions of nitrogen  and  sulfur  oxides  versus emissions  transported
from distant  sources;  (4)  the  relative  importance  of  changes in  total mass  emission rates
compared to changes in  the nature of the  emission  patterns (ground level versus tall stacks)
in  contributing to  regional  acidification of precipitation;  (5) the  relative  contribution of
wet and dry deposition to the acidification of lakes and streams;  (6) the geographic distribu-
tion of  natural   sources  of  NO ,  SO   and NH-,  and  the  significance and  seasonal ity of their
                               A    A        0
contributions; (7)  the existence and significance  of anthropogenic, non-combustion sources of
S0x, NO   and  HC1;  (8)  the dry deposition rates for  SO ,  NO  ,  sulfate, nitrate and HC1  over
various  terrains  and seasons of the year;  (9)  the  existence  and reliability of long-term pH
measurements  of  lakes and  headwater streams;  (10)  the acceptability  of current models  for
predicting  long  range  transport  of  SO  and  NO  and for  acid  tolerance  of lakes;  (11)  the
 *.                                      A        A
feasibility of using  liming  or  other corrective procedures to  prevent or reverse  acid damage
and the  costs of  such  procedures; (12)  the effects  of SO  and NOX  and hydrogen  ion deposition
on  ecosystem  dynamics  in both aquatic  and terrestrial  ecosystems; (13)  the effectiveness of
fertilization  resulting  from sulfate and  nitrate  deposition on  soils; (14) the  effects,  if
any, of acidic deposition on agricultural  crops, forests and other  native plants; and (15) the
                                                               x,
effects of  acidic deposition on  soil  microbial  processes and nutrient cycling.   A more compre-
hensive evaluation of scientific  evidence  bearing on these  issues  is being prepared as part of
a forthcoming  EPA document on acidic  deposition.
1.4.2  Effects of NO  on Ecosystems and Vegetation
     Chapter 12 discusses  NO  effects  on  ecosystems and vegetation.   Ecosystems represent the
                             A
natural   order by  which  living  organisms  are  bound  to  each  other and  to  their environment.
They are, therefore, essential  to the existence of  any species on  earth, including  man,  and as
life support systems their value  cannot be fully quantified in economic terms.
                                              1-35

-------
     Ecosystems  are  important  in  the production  of  food, in  the regeneration of  essential
nutrients as well  as  atmospheric components, in the  assimilation  or  breakdown of many pollu-
tants from the  air,  water,  and soil, and  in energy flow.   They also  give  aesthetic  pleasure
and improve the quality of life.
     The nitrogen  cycle,  an  ecosystem function, is essential  for all  life because nitrogen is
necessary in the  formation  of all  living matter.   Man  has influenced the cycling of nitrogen
by injecting fixed nitrogen  into the environment  or  contributing  other nitrogenous  compounds
which perturb the cycle.
     Human activities  have  unquestionably  increased the amounts of nitrates  and related com-
pounds  in some  compartments  of the environment. The  effects  of such  increased concentrations
of nitrogen compounds  may be beneficial  or adverse, or both.   Effects of both kinds  may occur
simultaneously, and  may  be  felt in  media  or in  ecological  compartments quite  removed from
those that initially receive anthropogenic nitrogenous inputs.
     Assessment of the influence of  nitrogen oxides  on ecosystems is  complicated by several
factors.  Nitrogen oxides:   (1) react with  abiotic components of the  natural  environment as
well  as with  individual   organisms;  (2)  react with varying numbers of  dissimilar  populations
within  ecosystems; and  (3)  may  suppress  individual  populations  and thus  affect  ecosystem
functioning.
     One function  of ecosystems is  the  cycling  of nutrients such as  nitrogen.   Any effect,
environmental   or  biological,   which  interferes  with  the  recycling  process  could  have  a
deleterious effect on the total ecosystem.
     At  the  present  time there are  insufficient  data  to determine  the impact  of  nitrogen
oxides  as  well  as  other   nitrogen  compounds  on  terrestrial  plant,   animal  or  microbial
communities.   It  is  possible,  however,  to estimate the approximate magnitude of anthropogenic
nitrogen fluxes to ecosystems,  using  the limited  amount of  monitoring data available or mass
balance calculations.  Such  estimates, and quantitative information  about  the  nitrogen cycle
at specific sites  in  the  system under study, make it possible to reach some conclusions about
the possible ecological significance  of  the added nitrogen.   In addition, where the  data base
is more  extensive,  as  it  is for a  number  of lakes in various  stages of eutrophication, more
quantitative dose-response relationships  can be estimated.
     A  reduction in diversity within a plant community results in a reduction in the  amount of
nutrients present  so that the growth of remaining individuals decreases.
     Pollutants  also  act as  predisposing agents  so  that disease, insect  pests  and abiotic
forces  can more  readily  injure the individual members of ecosystems.   The loss of these indi-
viduals result in  reduction in diversity  and simplification of an ecosystem.
     Sensitivity  of  plants  to  nitrogen  oxides  depends  on  a variety  of  factors  including
species,  time  of  day, light,  stage of  maturity,  type  of  injury examined,  soil  moisture,
nitrogen nutrition and the  presence or absence of other air pollutants such as sulfur dioxide
and ozone.
                                              1-36

-------
     When  exposures  to  N0?  alone are  considered,  the  ambient concentrations  that produce
measurable  injury  are higher than those that normally occur in the United States (Chapter 8).
                                                                          3
Tomato  (Lycopersicon esculentum) plants exposed continuously  to  470  ug/m  (0.25 ppm) for 128
days exhibited  a decreased growth and a yield reduction of 12 percent.  Leaf drop and reduced
yield  occurred  in  orange  trees exposed  to  470 ug/m   (0.25  ppm)  continuously  for  8 months.
Pinto  bean  ( Phaseolus  vulgaris),  endive  (Cicorium endivia) and cotton  (Gossypium  hirsutum)
exhibited  slight leaf spotting after 48  hours  of exposure to 1,880  ug/m   (1.0  ppm).   Other
reports cited no injury in beans (Phaseolus vulgaris), tobacco (Nicotiana tabacum),  or petunia
(Petunia multiflora) with a 2-hour exposure to the same concentration.
     Exceptions  to  this  generality,  however,  have been observed.   For example,  the  growth of
Kentucky  bluegrass  was significantly  reduced (approximately 25 percent) by  exposures  to 210
ug/m   (0.11 ppm)  N09 for 103.5 hours per week for 20 weeks during the winter months.   Similar
exposures to other  grass species generally had no deletrious effect on plant growth.
     Nitrogen  dioxide  concentrations  ranging  from  188  to   1,880 ug/m   (0.1  to  1.0  ppm)
increased chlorophyll  content  in  pea (Pisum sativum) seedlings from 5 to  10  percent.   The
significance  of  the increased  chlorophyll is not  known.   Some species of  lichens exposed to
3,760 ug/m  (2.0 ppm) for 6 hours showed reduced chlorophyll content.
     In contrast to studies cited on the effects of N0~ alone,  a number of studies on mixtures
of N02  and  SO-  showed that the  N0?  injury threshold was  significantly decreased and that the
effects of the two  gases in combination were at least additive and usually more than  additive.
Concentrations at which observable injury occurred were well within  the ambient concentrations
of N09  and  SO,  occurring  in some  areas  of the  U.S.   A combination  of 188 ug/m  (0.1 ppm) N09
             3
and 262 ug/m  (0.1  ppm)  S02 for 4  hours caused moderate  leaf injury  in pinto bean  (Phaseolus
vulgaris), radish (Raphanus sativus), soybean  (Glycine max), tomato  (Lycopersicon esculentum),
oat (Avena  sativa), and  tobacco (Nicotiana tabacum).   Exposure to 282 ug/m  (0.15 ppm)  N09 in
                          3                                                                   3
combination with 262  ug/m  (0.1 ppm) S09 for  4 hours caused more injury.   Neither 3,760 ug/m
                              3
(2.0 ppm)  NO-, nor  1,310  ug/m  (0.5  ppm)  SO, alone  caused injury.   Research  data from grass
                                                          3                            3
species exposed  for 20 weeks to concentrations of 210 ug/m  (0.11 ppm)  N02 and 290 ug/m   (0.11
ppm) SOp  for 103.5 hours per  week showed significant reductions in yield  parameters  ranging
from 30 to  90 percent indicating that concentrations  of  these  two  gases  occurring  simultane-
ously can have major deletrious effects on plant growth.
1.4.3  Effects of Nitrogen Oxides on Materials
     The  damaging   effects  of  atmospheric  oxides  of  nitrogen  have   been  established   for  a
variety of  materials including  dyes,  fibers, plastics,  rubber,  and  metals  as  discussed  in
Chapter 13 of this document.
     Field  exposures  of  cotton, viscose rayon,  cellulose acetate,  and nylon  fabrics  colored
with representative dyes  demonstrate that fading  occurs  for  specific dyes in  air containing
NCL, 03, and  SOp.   These  exposures were carried out  in ambient air  and protected against sun-
light.   Chamber  studies  using  individual  pollutants N02,  0.,,  and  S02  have  shown that some
                                              1-37

-------
individual  dye-fiber combinations  exhibit color  fading  only  in  response to  NO-  exposure,
whereas others are  susceptible  to 03, as  well  as  combinations  of N02 and 03_   S02 introduced
an accelerant effect.   Disperse dyes used for  cellulose  acetate  and rayon include vulnerable
anthraquinone blues and  reds.    The  cellulosic  fibers  cotton  and  viscose rayon,  dyed  with
certain widely used direct dyes, vat dyes, and fiber reactive  dyes, suffer severe  fading on
chamber  exposures   to  940 ug/m  (0.5  ppm)  N02  under high  humidity  (90  percent)  and  high
temperature  (90°F)  conditions.    Significant  fading is observed  on  12  weeks  exposure to  94
ug/m  (0.05 ppm)  N09 under high humidity and temperature conditions (90 percent,  90°F).
                                                                            3
     Acid dyes on nylon fade on exposure to N02 at.levels  as low as 188 ug/m  (0.1 ppm), under
similar conditions.   Dyed  polyester  fabrics  are highly resistant to NOp-induced  fading.  How-
ever, permanent  press  fabrics  of polyester cotton and textured  polyester exhibited unexpected
fading when first marketed.  The fading was in the disperse dye  which migrated  under high  heat
conditions of curing or heat setting to the reactive medium of  resins and other  surface addi-
tives.
     The yellowing of white fabrics is documented for polyurethane segmented fibers (Lycra and
Spandex), rubberized cotton, optically  brightened acetate, and nylon.   Yellowing  is also re-
ported on fabrics which were finished with softeners or anti-static agents.  Nitrogen dioxide
was  demonstrated to be  the pollutant responsible for color change, with 0, and S02 showing no
effect.    Chamber  studies  using NO- concentrations  of  376 ug/m   (0.2 ppm)  for 8 hours  showed
yellowing equivalent to that on garments returned to manufacturers.
     The  tensile  strength of  fabrics may be  adversely affected by  the  hydrolytic  action of
acid  aerosols.   Nitrogen  dioxide  has been demonstrated  to oxidize  the  terminal  amine group
(-NH9) of nylon  to  the degree  that  the  fiber  has less affinity for acid-type  dyes.   Nylon 66
                                                               3
may  suffer chain  scission when exposed to 1,880  to 9,400 ug/m   (1.0 to  5.0 ppm)  NO^.   Field
exposures of  fibers emphasize  the action  of acids  derived from $62, although  N02 may also be
present  in  high  concentrations  in  urban  sites.   Information  on  the contribution  of  N02 to
degradation is incomplete.
     Although a  survey  of the  market for  plastics  predicts the use of 1.78 billion pounds in
1982, there  is very little information on the  effects  of N02 on polyethylene, polypropylene,
polystyrene, polyvinylchloride,  polyacrylonitrile,  polyamides and polyurethanes.  Aging tests
involve sunlight exposure  as  well as exposure  to  ambient air.   Chamber exposure of the above
plastics to  combinations  of  SO,,, N02, and 03 has resulted in deterioration.  Nitrogen dioxide
alone has caused  chain scission in nylon and polyurethane at concentrations of  1,880 and 9,400
ug/m  (1.0 to 5.0 ppm).
     The extensive  data  on corrosion of metals in polluted areas relate the corrosion effects
to the S02  concentrations.   The presence of N02 and its contribution is not evaluated despite
its presence as acid aerosol in appreciable concentrations.
     Ammonium nitrates  were  implicated  as a factor  in  the stress corrosion cracking of wires
made  of  nickel brass alloy used  in  telephone  equipment.   Since nitrate salts  have been shown
                                              1-38

-------
to  be more hygroscopic  than either  chloride  or sulfate salts, the  presence  of nitrates may
lower  the  humidity  requirements  for the formation of an aqueous electrolyte system in the wet
corrosion of metals.
1.4.4  Effects of Nitrogen Oxides on Visibility
     As  discussed  in Chapter 10,  regarding NO  effects on visibility,  ambient  air pollution
                                               A
degrades the  appearance  of distant objects and reduces the range at which they can be distin-
guished  from  the  background.   These effects are manifest not only in visible plumes,  but also
in  large-scale, hazy  air masses.   Haze and plumes can result in the discoloration, deteriora-
tion, and loss of scenic vistas,  particularly in areas of the southwestern United States  where
visibility is  generally  good.   Under extreme conditions reduced visual  range and contrast due
to  haze  and  plumes  may  impede air  traffic.   NO- does not significantly  reduce  visual  range;
however, NOp  can  be responsible  for a portion of the brownish coloration observed in  polluted
air.   It should be  noted that non-nitrate  particulate  matter has  also  been implicated in the
production of a  significant portion  of brownish  coloration.   Under  certain  circumstances,
brown plumes  may be distinguished tens of kilometers downwind of their sources.
     Nitrogen dioxide in the atmosphere acts as a blue-minus  filter for  transmitted light.   It
tends to impart a  brownish color to targets, including the sky viewed through the plume.   The
strength of  this  filter  effect  is  determined  by the  amount of NOp concentration along the
sight path; i.e., theoretically,  similar effects are exerted by a 1 kilometer-wide plume con-
taining  0.1  ppm (190 ug/m )  of  N09 or  a  0.1  kilometer-wide plume containing 1.0 ppm (1,900
    3
ug/m ) of  NOp.   Less than 0.1 ppm-km  NOp  is  sufficient  to produce a color shift  which  is
distinguishable in  carefully controlled, color-matching  tests.   Reports  from one laboratory
using NOp-containing  sighting tubes  indicate a visible color threshold  of 0.06 ppm-km for the
typical  observer.    This  value was  supported by  a  few field observations of NOp  plumes  from
nitric acid manufacturing  plants  under  varying operating conditions.   The  value cited refers
to  the effect of  NOp in the absence  of atmospheric aerosol.   Empirical  observations  under  a
variety of conditions are needed  to determine the perceptibility of NOp  in ambient air.
     Plume coloration due  to NOp  is modified by particulate  matter and  depends on a number  of
factors  such  as  sun  angle,  surrounding scenery,'sky cover,  viewing angle,  human perception
parameters, and  pollutant  loading.   Suspended  particles  generally  scatter  in  the  forward
direction and can thus cause a  haze layer  or a plume to appear bright in forward scatter (sun
in  front of the observer)  and  dark  in  back scatter (sun in   back of  the observer) because  of
the angular variation in scattered airlight.   This effect can  vary  with background,  sky,  and
objects.   Aerosol  optical  effects  alone are capable  of  imparting  a reddish brown color  to  a
haze  layer when viewed  in backward scatter,  NOp would increase the degree of  coloration  in
such a situation.    When  the  sun  is in  front of the observer, however,  light scattered toward
him by  the plume  tends  to washout  the  brownish light transmitted from  beyond.    Under  these
conditions, light  scattering by  particles  diminishes the  plume  coloration  caused   by  NOp.
Estimates of  the magnitude  of  this effect  attributable to particulate  nitrates  are currently
hampered by the lack of  data on particulate  nitrate  concentrations  in ambient air.

                                              1-39

-------
     The discoloration of the horizon sky in an urban, or more extensive regional area, due to
NCk' absorption,  is  determined by the relative concentrations of N0~ and light-scattering par-
ticles, other  environmental  conditions,  and  the physiological  response of  the observer.   A
concentration-visual range product  of 0.3 ppm-km NO,, corresponds  to  color shift which should
be detectable  in  a  polluted  layer viewed against relatively clean sky.   However, this has not
been  tested  in  a variety of circumstances.   At  a visual  range  of 100  km, typical  of the
northern Great Plains area of the U.S., 0.003 ppm (6 ug/m ) NO-, would be expected to color the
                                                                                            3
horizon noticeably.   At  a  visual range of  10  km,  typical  of urban haze,  0.03  ppm (60 ug/m )
NOp would be  required  to produce the same effect.   However, quantitative theoretical  calcula-
tions  of  human perception of NO-,  are  not fully developed  and  experimental  observations are
needed to evaluate the effect.
     Independent of  absorption  of NO-,  wavelength-dependent scattering by small particles can
also produce a noticeable brown coloration in polluted air masses.   A significant contribution
to this phenomenon  by  particulate nitrates is not  expected in most urban areas.  However, an
assessment of  the role  of  nitrate  aerosols  in  the  discoloration and  degradation  of visual
range  must  await the  availability  of  a  sufficient data base on  ambient  particulate nitrate
concentrations.
                                              1-40

-------
                                       2.  INTRODUCTION

     Molecular  nitrogen  (N,,) and oxygen  (02)  are normal  constituents of  the  air we breathe.
Together they  comprise  well  over 90 percent of the earth's atmosphere, and both are essential
to  life.   As  a gas in the atmosphere, 0, is vital to the respiration of all life forms except
the anaerobes.  N? is essentially inert in all but the nitrogen-fixing organisms.  Through the
action of natural or man-made processes, however, the two elements can combine with each other
or  with  other  elements  to form toxic  compounds.   This  air quality criteria document compiles
in  a  single  source document available information about  the  formation and occurrence of such
compounds in the atmosphere, and evidence of their effects on man and the biosphere.
     The  initial  Air Quality  Criteria for  Nitrogen  Oxides  (EPA  Publication  No. AP-84)  was
published  by  the  U.S.   Environmental  Protection  Agency  (USEPA)  in  1971.   The  information
presented provided the  basis for the present annual  air quality standard for nitrogen dioxide
(NOp),  an  arithmetic  average not to exceed  100  ug/m  (0.05 ppm).  At  the time, insufficient
information was  available to  support  promulgation of a  short-term  standard.   However,  since
the annual standard does not preclude short-term peak N0~ concentrations which may be harmful,
the Congress,  in the 1977  amendments to  the Clean  Air  Act,  required  that the  air  quality
criteria document for nitrogen oxides (NO ) be revised.   In addition to the question of short-
                                         J\
term  exposure,  this  document  is  required  to  address  nitric  and  nitrous acids,  nitrates,
nitrites,  nitrosamines  and  other  derivatives of  oxides  of  nitrogen.   N0? is  the  principal
subject of this document, since available evidence indicates it is the nitrogenous compound of
most concern for human  health and welfare.  However, the  health and welfare effects of other
airborne nitrogen compounds including other nitrogen  oxides, nitrogen acids, nitrates,  nitrites,
nitrosamines and other derivative compounds are also  presented.  Also included  are descriptions
of the complex chemical  reactions occurring in po"nuted  atmospheres that link,  to some extent,
the atmospheric concentrations  of  nitrogen oxides with  the presence of photochemical oxidants
such as  ozone.  The  ozone/NO  relationship is discussed  in  greater detail in  the Air Quality
Criteria for Ozone  and Other Photochemical  Oxidants,  EPA-600/8-78-004.
     Nitrogen  oxides  are  produced  when  fossil  fuels are  burned, both  by the  oxidation  of
nitrogen in the  fuel  and by the high-temperature oxidation of atmospheric nitrogen.   Most NO
emissions occur as nitric  oxide (NO).   Available evidence  indicates  that nitric oxide in the
ambient air is  not of direct concern for  human  health  and welfare.  NO  is, however,  further
oxidized in the amosphere  to a variety of other  nitrogenous  compounds.   Of these,  N02 is the
compound of most concern.
     Increases  in  the  U.S.  consumption  of  energy  will   stimulate increasing  combustion  of
fossil fuels which can  result in an increase in  NO  emissions.  Atmospheric concentrations of
                                                   A
NOp and  other  nitrogenous compounds  are,  therefore, likely  to become higher  in  the  future,
especially if NO  emissions control  actions do not keep  pace with energy production.
                A
                                            2-1

-------
     Considerable information has been developed since publication of the original Air Quality
Criteria for Nitrogen Oxides in 1971.   Information reviewed in this document which demonstrates
the  toxicity  of a  number  of nitrogen  compounds  has  been  derived  from  a variety  of  human,
animal, and ecological  studies.   For  example, studies of  both  animals and humans demonstrate
relationships  between exposure  to  NCu and various aspects of pulmonary function, particularly
those  types  of  physiological   or  pathological  changes  that  may  lead  to the  development  of
chronic respiratory disease.  Other studies have been concerned with the effect of NCL exposure
on  susceptibility  to  acute respiratory  disease.   Adverse effects  of nitrogen  compounds  on
plants and inanimate materials have also been reported.
     The  determination  of  the  effects  of  exposure  to  airborne  nitrogen compounds  on  human
health encounters four major difficulties.  The first is that nitrogen compounds comprise only
a portion of  a  complex  of pollutants in  the  ambient air.   Adverse effects found in epidemio-
logical studies may  result  from exposure to individual compounds or a combination of multiple
compounds.   Epidemiologists,   evaluating   community  studies,  have  not  been  able   to  assess
unequivocally  the effects of  exposure to individual  compounds.   Consequently,  it is useful  to
use  the  combined results of  epidemiological  and  animal studies  to  assess  potential  harmful
effects.   Animal studies  reported  in  this document show the effects of exposure to  individual
compounds as  well  as certain effects of  the  compounds in combination.   In  some cases,  these
studies also show,  for individual animal species,  the maximum dose of the pollutant  tolerated,
target organs,  mechanisms of  action,  and lowest effective dose.   In addition,  the studies can
show whether there  is a  consistency of effects across a variety of animal  species.
     The second  problem is  the difficulty  of assessing,  with a high degree of  accuracy,  the
actual day-to-day exposure to NO  of individuals or populations in ambient situations.   Because
                                A
there  are  a  limited  number of monitoring  stations,  air measurement data  are  not  completely
representative of actual human exposure.  This difficulty is compounded by the  mobility of the
population,  the portion  of each day spent inside buildings,  and the variability of atmospheric
concentrations of pollutants over short distances.
     The third problem encountered in  determining  the effects of exposure to nitrogen compounds
is  that  dose/response  data derived  from  animal'studies cannot  readily be  extrapolated  to
humans.  Indications  of probable effects  on  humans  can  be obtained  from  the  animal studies,
and a consistent effect among animal species,  especially when primates are included, increases
confidence that a similar effect may occur in humans.
     The fourth problem is the determination of effective exposure time.   NO  community studies
usually use data on  annual  or daily mean levels  of exposure.  Only  occasionally  are  hourly
values provided.   Based on  animal  studies, however,  it may be  inferred  that  repeated  inter-
mittent exposure to daily  peak values may be  more  significant in  the production  of adverse
health effects  than  is an  equivalent  or even  greater total  dose delivered  by  continuous
exposure to the  observed  long-term averages.   If  this is true, the protection  of human health
                                            2-2

-------
is  achieved  more effectively  by reducing  the  peak concentrations  rather  than  the long-term
means.   The  subject of  effective control  strategies,  however,  is  outside the  scope  of this
document.
      In  response  to  the  1977 Clean Air Act Amendments, this document provides a summarization
of  available  data relevant to the effects on human health and welfare of exposure to nitrogen
oxides  or other  toxic  materials evolving  from nitrogen oxides  in the  atmosphere.   Various
sections  of   the  document  provide  information  on  (1)  the  intensity  and frequency,  in this
country,  of   the  occurrence  of  significant  atmospheric  concentrations of toxic  nitrogenous
compounds  and their  sources, (2) the  results of  animal  studies concerned with  the  effect of
short- or  long-term exposures to these compounds,  (3) the results of controlled human exposure
studies,  (4)  the results  of community exposure  studies,  (5)  the  results of studies  of  the
effects  of atmospheric  nitrogenous compounds  on visibility,  ecologic systems, plants,  and
materials  and  (6)  the  relationship  of these compounds  to large-scale phenomena such as acidic
precipitation and perturbations of the stratospheric ozone layer.
     This  document does  not constitute a detailed literature  review of the subjects covered.
Not  every  published  manuscript  is  cited;  however,  major publications  relevant  to  the  topics
covered are included.
     In reviewing and summarizing the literature,  an attempt has been made to  present alterna-
tive  points  of view where scientific  controversy exists.    In  some  instances,  considerations
bearing on the  quality  of studies have been  included.   The  needs for subsequent studies have
not, for the  most part,  been addressed.
     Chapter   1  summarizes those effects on  human  health and welfare which are  considered of
most  concern,  and through  interpretation of  study  results,  defines, to  the  degree  possible,
the  pollutant  concentration levels  at which adverse effects are discernible.   Other  chapter
summaries  appear  at the  ends of individual  chapters  covering  information  not presented  in
Chapter 1.
     As is appropriate in a criteria document,  the  discussion  is  descriptive of the range of
exposures and the attendant effects.   Information  is presented,  and  the evidence  is  evaluated,
but  no judgments  are made concerning the  maximum  levels  of  exposure that should  be  permitted.
Such judgments would be recommendations concerning air  quality standards and management,  which
are prescriptive in nature, and not  within the purview  of this document.
                                            2-3

-------

-------
                     3.  GENERAL CHEMICAL AND PHYSICAL PROPERTTIES OF N0v
                                  AND NOX-DERIVED POLLUTANTS            x

3.1  INTRODUCTION AND OVERVIEW
     In  this  chapter  some  general  chemical  and  physical  properties of  NO  *  and NO -derived
                                                                           A        A
pollutants are  discussed  by way of introduction to the complex chemical and  physical interac-
tions which may occur in the atmosphere and other media.   The discussion will be significantly
augmented throughout the document as particular topics are discussed in depth.
     There are  eight  oxides of nitrogen (NO  )  that  may  be present in the ambient air:  nitric
oxide  (NO),  nitrogen  dioxide  (NO,,),  nitrous  oxide. (NpO),  unsymmetrical   nitrogen  trioxide
(OONO),  symmetrical  nitrogen  trioxide  (ON(O)O),  dinitrogen  trioxide  (N^j),  dinitrogen
tetroxide (N204), and dinitrogen pentoxide (NpOr).
      Of these, NO and NOp are generally considered the most important in the lower troposphere
because they may  be present in significant concentrations  (Chapter  8).   Their interconverti-
bility  in  photochemical  smog  reactions (Chapter  6)  has  frequently  resulted  in  their  being
grouped  together  under  the designation  NO  ,  although  analytic  techniques can  distinguish
clearly between them  (Chapter  7).   Of the  two, NO,,  is  the more toxic and irritating compound
(Chapter 14 and 15).
     Nitrous oxide  is  ubiquitous  even in the absence of  anthropogenic  sources,  since it is a
product of natural  biologic processes in soil (Chapters  4 and 12).   It is not  known, however,
to be  involved  in any photochemical smog reactions.   Although N?0 is not generally considered
to be  an air  pollutant,  it participates  in  upper atmospheric reactions involving  the  ozone
layer (Chapter 9).
     While OONO, ON(0)0, N^O,,  N-O,, and NpOr  may  play a  role in atmospheric  chemical reactions
leading  to  the  transformation, transport, and  ultimate  removal  of nitrogen compounds  from
ambient air  (Chapter  6),  they are  present  only  in very  low concentrations,  even  in polluted
environments.
     Ammonia (NH.,)  is generated, on  a  global scale, during the  decomposition  of nitrogenous
matter in natural  ecosystems  and it may also be  produced  locally in larger  concentrations by
human  activities  such  as  the  maintenance  of  dense  animal  populations  (Chapter 4).   It  is
discussed briefly  in  this  document  to facilitate  understanding of the nitrogen cycle and also
because some researchers have suggested that NH3 is converted to NO  in the atmosphere.
     Other NO -derived compounds which may be  found in polluted air include nitrites, nitrates,
nitrogen acids,  N-nitroso compounds, and  organic compounds  such as the peroxyacyl  nitrates
*For all practical purposes, N0y is the sum of nitrogen dioxide (N02) and nitric oxide (NO).

                                            3-1

-------
(RC(0)OON02,  where R  represents  any  one  of a  large variety  of  possible  organic  groups)
(Chapter 8).
     The peroxyacyl nitrates,  of which peroxyacetyl  nitrate (CH3C(0)OON02,  or PAN)  is of most
concern  in  terms of atmospheric  concentrations,  have been thoroughly reviewed  in  the  recent
EPA document, Air  Quality  Criteria for Ozone and Other Photochemical Oxidants (1978) and will
be given only the briefest discussion in this chapter and elsewhere in this  document.
     Recent discovery of  N-nitroso compounds in air, water, and  food has led  to concern about
possible human  exposure to  this family of  compounds,  some of  which have been shown  to  be
carcinogenic in animals.  Health concerns also have been expressed about  nitrates,  which occur
as a  component  of particulate matter  in the respirable size range,  suspended  in  ambient air
(Chapter 15).   Some of  this particulate nitrate is produced in atmospheric  reactions (Chapter
6).  Nitrates may also occur in significant concentrations in drinking water supplies but this
occurrence is not believed to be the result of atmospheric production.
     Photochemical models  predict  that up  to one-half of the original nitrogen oxides emitted
may be converted on a  daily basis to nitrates and nitric acid (HNO~).  This  atmospheric  produc-
tion of nitric acid is an important component of acid rain (Chapter 11).
     Table 3-1  summarizes  current  theoretical estimates of the  concentrations  of  the various
nitrogen oxides  and acids  that  would be  present in an equilibrium  state  assuming initially
only molecules of nitrogen and oxygen at 1 atm pressure, 25°C and 50 percent relative humidity.
The low  concentrations  of  many of the oxides and acids preclude- direct measurement of most of
them  in  the  ambient air.   Consequently, most studies leading to  predictions of concentrations
rely on theoretical estimates derived from small-scale laboratory studies.
     In  fact,  the  thermodynamic  equilibrium state  is  not  achieved in polluted,  sunlight-
irradiated  atmospheres.    Rather,  expected  concentrations of  pollutants  are   influenced  by
emissions and  subsequent  reactions  and  tend to  be  much  greater  than  those  at equilibrium.
Table  3-1  lists one  set  of estimated  concentrations of  nitrogen  oxides and  acids expected
under  more  realistic .conditions,  derived  from  computer  simulations of photochemical  smog
reactions which might  occur in more or less typical urban environments.
3.2  NITROGEN OXIDES
     Table 3-2 summarizes some important physical properties of nitrogen  oxides under standard
temperature and  pressure  (STP) conditions  of 25°C and  1  atm,  respectively.   The remainder of
this  section describes  chemical  and physical properties of individual nitrogen oxide species.
3.2.1  Nitric Oxide (NO)
     Nitric oxide is an odorless gas.  It is also colorless since its absorption bands are all
at wavelengths  less than  230  nm, well  below the visible wavelengths  (Figure  3-1).   Nitric
oxide  is only  slightly  soluble in water (0.006  g/100 g of water at 24°C and  1 atm pressure).

                                            3-2

-------
   TABLE 3-1.  THEORETICAL CONCENTRATIONS OF NITROGEN OXIDES AND NITROGEN
    ACIDS WHICH WOULD BE PRESENT AT EQUILIBRIUM WITH MOLECULAR NITROGEN,
   MOLECULAR OXYGEN, AND WATER IN AIR AT 25°C, 1 ATM, 50 PERCENT RELATIVE
                    HUMIDITY (Demerjian et al.,  1974)
      Compound
 Concentrations in Hypothetical  Atmosphere, ppm

                     In Typical  Sunlight-irragi-
At Equilibrium        ated, Smoggy Atmosphere
°2
N2
H20
N02
NO
N03
N2°3
N2°4
N2°5
HONO (cis)
HONO (trans)
HON02
2.06 x 105
7.69 x 105
1.56 x 104
1.91 x 10"4
2.69 x 10"10
3.88 x 10"16
2.96 x 10"20
2.48 x 10"13
3.16 x 10"17
7.02 x 10"9
1.60 x 10"8
1.33 x 10"3
2.06 x 105
7.69 x 105
1.56 x 104
10'1
10'1
io"8-io"9
io"8-io"9
io"7-io"8
io"3-io"5
ID'3
lO'3
io"2-io"3
aTheoretical  estimates made using computer simulations of the chemical
 reactions rates in a synthetic smog mixture.
                                   3-3

-------
               TABLE 3-2.   SOME PHYSICAL AND THERMODYNAMIC PROPERTIES OF THE NITROGEN OXIDES
Molecular Melting Boiling
Weight, Point Point
Oxide g/mol °Ca'b °Ca'b
NO 30.01 -163.6 -151.7
N02 46.01 Liquid, solid
forms largely
as N204
N204 92.02 -11.3 21.2
N20 44.02 -102.4 -89.5
N203 76.02 -102 3.5
(decomposes)
N20B 108.01 30 32.4
(decomposes)
Thermodynamic Functions
(Ideal Gas, 1 atm, 25°C)C
Solubility in Enthalpy of
H20(0 C), Formation,
cm3 (STP)XIOO ga kcal/mol
7.34 21.58
Reacts with H90 7.91
forming HON09 and
HONO
Reacts with H?0 2.17
forming HONO, and
HONO i
130.52 19.61
Reacts with H90 19.80
forming HONO
Reacts with H?0 2.7
forming HON02
Entropy,
cal/mol-deg
50.347
57.34
72.72
52.55
73.91
82.8
uMatheson Gas Data Book (Matheson Company,  1966).
 Handbook of Chemistry and Physics (Chemical  Rubber Company,  1969-1970).
 JANAF Thermochemical  Tables (National  Bureau of Standards,  1971).

-------
    50
 I  40
 z
 UJ
 o  30
HI
O
O
z
 o
 CO
 CD
    20
    10
     1500
                 1700
1900
2100
2300
                           WAVELENGTH, A


Figure 3-1. Absorption spectrum of nitric oxide (McNesby and Okabe,
1964).
                           3-5

-------
It has an uneven number of valence electrons, but, unlike NO-, it does not dimerize in the gas
phase.
     Nitric oxide is a principal byproduct of combustion processes, arising from the oxidation
of  molecular  nitrogen  in the  combustion air  and  of organically  bound nitrogen  present  in
certain fuels such  as  coal  and heavy oil.  The oxidation of nitrogen in combustion air occurs
primarily through a  set  of  reactions known  as  the  extended Zeldovitch mechanism (Zeldoritch,
1946):
               N2 + 0 •* NO + N
               N + 02 -> NO + 0
with the additional  equation (extended mechanism)
               N + OH •* NO + H
The high activation energy of the first reaction above (75 kcal/mol) coupled with its essential
function  of  breaking  the strong  N~  triple bond  make  this  the  rate  limiting step  of the
Zeldovitch mechanism.   Due  to  the  high  activation  energy, this  mechanism  for NO production
proceeds  at a  somewhat slower  rate  than  the reactions of  fuel  constituents  and is extremely
temperature sensitive  (Bowman,  1973).   Moreover, the production of atomic oxygen required for
the  first  step  is also highly  temperature  sensitive.   NO formed via  this mechanism  is often
referred to as "thermal N0x."
     In addition  to the  strong temperature dependence  of  the rate of the  first  step of the
Zeldovich mechanism, the temperature also influences the amount of atomic oxygen (0) available
for  the  reaction.   In the immediate vicinity  of a  flame,  the high  temperatures coupled with
the  kinetics  of the  hydrocarbons  in the fuel  can  drive the  oxygen  concentration  to several
times  its  equilibrium  level.   The local  ratio of fuel to air also has a first order effect on
the concentration of atomic oxygen (Bowman, 1973).
     The  reaction  kinetics  of  thermal  NO  formation  is further complicated  by  the fact that
certain hydrocarbon  radicals  can  be effective in splitting the N2 bond through reactions such
as (Fenimore,  1976):
               CH + N2 -> CHN + N
The  rate  of oxidation  of the fuel (and intermediate hydrocarbon radical fragments) is usually
sufficiently  rapid   that  only  negligible quantities  of the  fuel  radicals   are  available  to
attack  the molecular  nitrogen.  However,  under fuel-rich conditions,  this can  become the
dominant  mode  of breaking  the  N2  bond  and, in  turn,  can be responsible  for significant NO
formation  (Engleman  et al.,  1976).   Such reactions  appear to have a relatively low activation
energy and can  proceed at a rate comparable  to oxidation of  the  fuel.   Because of the early
formation  of  NO by  this  mechanism, relative  to that formed  by the  Zeldovitch mechanism,  NO
thus formed  is often  referred  to  as  "prompt  NO."   The importance of  this  mechanism has not
been quantified for practical systems.
                                            3-6

-------
     In fuels such as coal and residual fuel oil, nitrogen compounds are bound within the fuel
matrix.  Typically, Number 6 residual oil contains 0.2 to 0.8 percent by weight bound nitrogen
and coal typically contains 1 to 2 percent.  If this 1 percent nitrogen were converted quanti-
tatively to NO  , it would account for about 2,000 ppm NO  in the exhaust of a coal-fired unit.
              A                                         A
In practice, only a portion of these nitrogen compounds is converted to NO , with the remainder
being  converted to molecular nitrogen  (N2).   Tests  designed to determine the  percent  of the
NO  emissions due  to  oxidation of bound  nitrogen  (Pershing  and Wendt, 1976) show that upward
of 80  percent  of the  NO  from a coal-fired boiler originate from this source.   Details of the
kinetic  mechanisms  involved  in fuel  nitrogen  oxidation are  uncertain  due  in part  to  the
variability of molecular composition among the many types (and sources) of coal  and heavy oils
and to the complex nature  of the  heterogeneous processes  occurring.   Experimental  evidence
does,  however,  lend some insight into the processes involved.  A number of fuel-bound nitrogen
compounds  have   been  cited  (Axworthy  and  Schuman,  1973;  Martin  et  a!.,  1971;  Turner  and
Siegmund,  1972),  but  the degree  of  conversion to  NO   does  not  seem to be  significantly
affected by  the compound type.   NO  conversions  arising from  fuel  sources seem also  to  be
relatively insensitive to temperature  in diffusion flames.   The most  important parameters  in
determining fuel-bound nitrogen  conversion  appear to be  the  local  conditions  prevailing when
the nitrogen is evolved from the fuel.   Under fuel-rich conditions this nitrogen tends to form
Np, whereas under fuel-lean conditions significant amounts of NO  are formed.
     Nitric  oxide   formation  kinetics  in  typical   furnaces  are   not  fast  enough   to  reach
equilibrium levels  in  the high temperature flame zone,  while the NO destruction mechanisms are
far too slow to allow  the NO,  once  formed, to reach equilibrium at typical  stack temperatures.
This is to say that the NO formation process is kinetically  controlled.
     Nitric oxide  and nitrogen  dioxide  produced in  relatively  large concentrations at high
temperatures  in combustion  processes  would  revert  to  lower concentrations  characteristic
approximately of the  equilibrium values  shown  in Table  3-3  were  it not  for  the  fact  that
combustion  equipment  rapidly converts  a large  fraction  of the  thermal  energy available  to
useful  work.  This  results  in  a rapid cooling  of  the  combustion gases and a "freezing-in"  of
the produced  NO and NO,, near concentrations  characteristic  of the high temperature  phase  of
the process.
     A major  implication of the  fact that N0x  emissions are  defined by the kinetics  of  the
process rather than being an  equilibrium phenomenon is that  NO   emissions can  be  effectively
modified by changes in the details  of the combustion  process.   For clean  fuels  such as natural
gas or Number 2  distillate  oil  with no  bound  nitrogen,  the NO formation  is dominated  by the
Zeldovitch  mechanism.   Thus, combustion  modifications which  reduce  peak flame  temperature,
limit   the  gas  residence  time at peak temperatures and/or reduce the amount of  atomic  oxygen
available at high temperatures will  reduce the NO  emissions.   Examples  of such modifications
                                            3-7

-------
TABLE 3-3.   THEORETICAL EQUILIBRIUM CONCENTRATIONS OF NITRIC OXIDE
    AND NITROGEN DIOXIDE IN AIR (50 PERCENT RELATIVE HUMIDITY)
              AT VARIOUS TEMPERATURES (CALVERT, 1977)
                                 Concentration,  |jg/m  (ppm)
 Temperature, °K (°C)                 NO                N02

                                          -in                -A
    298 (24.85)                  3.29 x 10 |~       3-53 x 10 4
                                (2.63 x 10"iU)     (1.88 x 10 *)

    500 (226.85)                 8.18 x 10"J        7.26 x 10~?
 '                               (6.54 x 10~4)      (3.86 x 10 *)

  1,000 (726.85)                      43                3.38
                                     (34.4)            (1.80)

  1,500 (1,226.85)                 1,620               12.35
                                  (1,296)              (6.57)

  2,000 (1,726.85)                 9,946.25            23.88
                                  (7,957)             (12.70)
                              3-8

-------
are  flue  gas recirculation,  reduced  load,  reduced combustion air  preheat  temperature,  water
injection and reduced  excess  air (Bowen and Hall, 1976a, 1976b,  1976c; Bowen and Hall,  1977a,
1977b, 1977c, 1977d, 1977e).
     In furnaces  fired  with coal or heavy oil, the major portion of the NO   emissions is from
fuel-bound nitrogen conversion.   Thus,  combustion modifications  which reduce the availability
of oxygen when  the  nitrogen compounds are evolved  will  reduce the NO  produced.   Examples of
such  modifications  are  reduction  of  the  amount of excess  air during  firing,  establishing
fuel-rich conditions during the  early stages of combustion (staged combustion),  or new  burner
designs that  tailor the  rate  of mixing  between the fuel  and  air  streams (Bowen and  Hall,
1976a, 1976b, 1976c).
3.2.2  Nitrogen Dioxide (NO,,)
     Nitrogen  dioxide   is   a  reddish-orange-brown  gas   with  a  characteristic  pungent  odor.
Although its boiling point  is  21.1°C, the low  partial  pressure  of N02 in the atmosphere pre-
vents  condensation.  Nitrogen  dioxide  is  corrosive and  highly  oxidizing.   It  has  an  uneven
number  of  valence  electrons  and  forms  the  dimer  Np04 at  higher concentrations and  lower
temperatures, but the  dimer is  not important at ambient concentrations.   In the  atmosphere NO
can be oxidized to N02  by the  thermal  reaction:
               2 NO + 02 •* 2 N02
However, this  reaction is of minor importance  in most  urban  ambient  situations,  since  other
chemical processes  are  faster.   The above reaction is  mainly  responsible for the NO,, present
in combustion exhaust  gases.   About 5 to 10  percent  by volume of the  total  emissions  of N0x
from combustion sources is in  the form of N02, although  substantial variations from one  source
to another  have  been   observed.   Under  more dilute ambient  conditions,  photochemical  smog
reactions involving hydrocarbons convert NO  to N02 (Chapter 6).
     Nitrogen dioxide's principal  involvement in photochemical smog stems from  its absorption
of sunlight and  subsequent  decomposition  (photolysis)  to NO and atomic oxygen  (0).   Nitrogen
dioxide is an efficient absorber of light over a broad  range of  ultraviolet and  visible  wave-
lengths.  Only quanta with wavelengths less  than about 430 nm,  however, have sufficient  energy
to cause photolysis.   It  should also  be noted that photons having wavelengths less than  about
290  nm are  largely absorbed  in the  upper  atmosphere.  The  effective range of  wavelengths
responsible for photolysis of  N02 at ground  level is,  therefore,  290 nm to 430 nm.   Because of
its absorption properties,  N02  produces discoloration and reduces  visibility  in the polluted
lower troposphere.
3.2.3  Nitrous Oxide (NpO)
     Nitrous oxide  is   a  colorless  gas with  a slight  odor  at  high  concentrations.   Nitrous
oxide  in  the atmosphere  arises  as one  product of the reduction of  nitrate by  a ubiquitous

                                            3-9

-------
group  of  bacteria  that  use nitrate  as their  terminal  electron acceptor  in the  absence  of
oxygen (denitrification) (Brezonik,  1972;  Delwiche,  1970; Focht and Verstraete,  1977; Keeney,
1973).
     Although  N20  does  not play  a significant  role  in atmospheric  reactions  in  the  lower
troposphere,  it  participates  in  a  mechanism  for  ozone  decomposition in  the  stratosphere.
     Nitrous  oxide  transported   to   the   stratosphere  undergoes  photolysis  by  absorbing
ultraviolet  (UV)  radiation  at wavelengths  below 300  nm  to produce  N2  and singlet  oxygen
(Johnston and Selwyn, 1975):
                   NpO + hv -» N2 + 0('D)    where hv  is a unit of radiant
                                            energy
     Singlet  oxygen,  which  also  is produced  by ozone photolysis,  reacts  with more nitrous
oxide to produce two sets of products:
               N20 + 0('D) -» N2 + 02
                          and
                           -» NO + NO
     The NO  produced  enters a  catalytic cycle, the net result of which is  the regeneration of
NO  and the destruction of ozone:

               03 + hv -* 02 + 0
               N02 + 0 -> NO + 02
     These  reactions  are of concern because  of the  possibility that  increased  N~0 resulting
from denitrification of excess  fertilizer may lead to a decrease of stratospheric ozone (Cast,
1976; Crutzen, 1976) with consequent potential for adverse human health effects.
3.2.4  Unsymmetrical Nitrogen Trioxide (OONO)
     Unsymmetrical   nitrogen trioxide is thought  to  be  an intermediate in the reaction  of NO
with 02:
               NO + 02  j  0-0-N-O
               0-0-N-O  +  NO •* 2N02
     There  is,  however,  no  direct evidence  for the existence  of  this species.   If it does
exist, it  is, nevertheless, of little  importance  in  the chemistry  of polluted atmospheres,
since the N0/02 reaction accounts for very little of the NO oxidized.
3.2.5  Symmetrical  Nitrogen Trioxide (NO.,)
     Symmetrical  nitrogen trioxide has been identified in laboratory systems containing Nt^/Og,
N09/0, and   N90r as an  important  reactive transient  (Johnston,  1966).  It  is  likely  to  be
  L.           £. O
present in photochemical  smog.   This compound can be formed as follows:

               0 + N02 (+ M) -> N03 (+ M)
               N205 (+ M) -> N03 + N02 (+ M)
                                            3-10

-------
 (where M represents any  third  molecule available to remove  a  fraction of the energy involved
 in the reaction.)
      Symmetrical  nitrogen trioxide is  highly  reactive  towards  both nitric  oxide  and nitrogen
 dioxide.
                N03  + NO -»• 2N02
                NO,  + N09  (+  M)  -» N-0,  (+  M)
                                                                        -6     3       -9
      Its  expected concentration  in polluted air is very  low (about  10   (jg/m  or  10   ppm).
 3.2.6  Dinitrogen Trioxide (N.,0,)_ (Also Known  as Nitrogen  Sesquioxide)
      In the atmosphere,  hLO,  is  in  equilibrium with  NO  and  N02  according to the  following
 equation:
               NO +  NO,  j N,0,
                      t-  *   £• 3                                                             _4
 The equilibrium concentrations  at typical  urban levels of  NO  and  N09 range from  about  10
     3-7            -6    3   • ~9
'ug/m  (~10   ppm) to 10   ug/m   (~10    ppm)  (Table  3-4). N90, is  the  anhydride of  nitrous  acid
                                                           £.  O
 and reacts  with  liquid  water to form the  acid:
                N203  + H20 -»  2HONO
 3.2.7  Dinitrogen Tetroxide  (NpO.)  (Also  Known as Nitrogen Tetroxide)
      Dinitrogen  tetroxide is the dimer of N02 formed by the  association  of  N02  molecules.   It
 also readily dissociates  to  establish the equilibrium:
                2N02  \  N204
 Table 3-4  presents  theoretical  predictions  of concentrations of N,,03  and  N20^  in equilibrium
 with various NO and  N02 concentrations.
 3.3  NITRATES,  NITRITES,  AND NITROGEN ACIDS
      Nitric  acid in the   gaseous  state-  is  colorless  and  photochemically  stable.  The  major
 pathway for atmospheric formation of nitric  acid is  given  by:
          •OH  + N02  -» HN03   where -OH is a hydroxyl free radical
 It is a volatile acid, so that at ambient  concentrations in the atmosphere, the vapor would
 not be  expected to coalesce  into  aerosol  and be  retained unless  the aerosol  contains  reactants
 such as ammonia  (NHL)  to neutralize  the acid,  producing particulate  nitrates  (Chapter  6).
      The nitrate ion  (NOO is the most  oxidized  form of nitrogen.  Since  nitrate is  chemically
 unreactive  in  dilute aqueous solution, nearly all  of the  transformations  involving  nitrate in
 natural waters result from  biochemical pathways.   The  nitrate  salts of  all  common  metals  are
 quite soluble.
      Nitrates  can be reduced to  nitrites  by  microbial action.   Many of  the deleterious effects
 of nitrate  result  from its  conversion  to nitrite.   The nitrite  ion represents an  intermediate
 and relatively unstable   oxidation  state (+3)  for nitrogen.    Both  chemical  and  biological
 processes can  result in its  further reduction  to various products, or  its  oxidation  to nitrate.
 Nitrite salts  are also  quite soluble.
                                             3-11

-------
TABLE 3-4.   THEORETICAL CONCENTRATIONS OF DINITROGEN TRIOXIDE AND
     DINITROGEN TETROXIDE IN EQUILIBRIUM WITH VARIOUS LEVELS
       OF CASEOUS NITRIC OXIDE AND NITROGEN DIOXIDE IN AIR
                       AT 25°C (CALVERT, 1977)
Concentration, ppm

NO              N0
0.05            0.05            1.3 x 10~9      1.7 x 10"8

0.10            0.10            5.2 x 10"9      6.8 x 10~8

0.50            0.50            1.3 x 10"7      1.7 x 10"6

1.00            1.00            5.2 x 10"7      6.8 x 10"6
                             3-12

-------
     The nitrite ion is the Lewis base of the weak acid, nitrous acid (HNCL).  When NO and NO-
are present in the atmosphere, HN02 will be formed as a result of the reaction:
               NO + N02 + H20 -> 2HN02
However, in  sunlight-irradiated  atmospheres,  the dominant pathway  for  nitrous acid formation
is:
               •OH + NO •* HONO
     Atmospheric concentrations of HONO are limited by the reverse reaction:
               HONO + hv •* -OH + NO
     Nitrous acid  is  a  weak reducing agent and is oxidized to nitrate only by strong chemical
oxidants and  by nitrifying  bacteria.   Nitrous acid  reacts  with  amino  acids (the  Van Slyke
reactions) to yield  N«.   The reaction of nitrous acid with secondary amines to form N-nitros-
amines is discussed in Section 3.5.
3.4  AMMONIA (NH3)
     Ammonia is a colorless gas with a pungent odor.   It is extremely soluble in water, forming
the ammonium  (NH^ )  and  hydroxy  (OH )  ions.   In the  atmosphere,  ammonia  has  been reported
(Soderlund and  Svensson,  1976) to  be converted  into  oxides  of nitrogen when it  reacts  with
hydroxyl free  radicals  (-OH).  Burns  and Hardy  (1975) report that ammonia  is  oxidized  into
nitrates and nitrites in the atmosphere,  and in geothermal  wells.   In the stratosphere, ammonia
can be dissociated by irradiation with sunlight at wavelengths below 230 nm (McConnell, 1973).
3.5  N-NITROSO COMPOUNDS
     Organic nitroso  compounds contain a nitroso group (-N=0)  attached to a nitrogen or carbon
atom.    According  to  Magee (1971),  N-nitroso  compounds  generally  can  be  divided  into  two
groups—one group  includes the dialkyl,  alkylaryl,  and diaryl  nitrosamines, and  the other,
alkyl  and aryl  nitrosamides.
     The principal chemical  reaction involved  in  the  formation of N-nitrosamines  is  that  of
the secondary amines  with  nitrous  acid.   Nitrosation  is effected by agents  having the structure
ONX, where X = 0-alkoxyl,  N0?, N03,  halogen,  tetrafluoroborate, hydrogen sulfate  or OhL .   The
equilibrium reaction  of  nitrosonium ion (ON ), nitrous acid and nitrite  ion:
               ON+ +  OH"  *  HN02  J  H+  +  N0~
is  shifted  to  the right  at  pH >  7.   The simplest  form  of  nitrosation  of  amines  involves
electrophilic attack  by  the nitrosonium ion and subsequent  deprotonation.
     Mirvish (1970) studied the  kinetics  of dimethylnitrosamine (DMN)  nitrosation  and pointed
out that the chief nitrosating  agent at pH 1 is dinitrogen trioxide,  the anhydride of nitrous
acid,  which  forms reversibly from  two  HNO-  molecules.   The formation  of  nitrosamines  is
dependent on the pK  of  the amine.
                                            3-13

-------
     Nitroso compounds are characteristically photosensitive and the nitroso group is split by
UV radiation.   Gaseous nitrosamines may be denitrosated by visible light.   The electron absorp-
tion spectra of  several  nitrosamines are given in the literature (Rao and Bhaskar, 1969);  the
characteristic spectra  show a low  intensity  absorption  maximum around 360 nm  and an  intense
band around 235  nm.   Nitrosamines show three  relatively  intense  bands in the infrared region
of  7.1-7.4,  7.6-8.6,  and  9.15-9.55  urn.    Nuclear  magnetic  resonance (NMR),  infrared  (IR),
ultraviolet (UV), and mass spectrometry (MS) spectra have been reviewed by Magee et al.  (1976).
     Atmospheric  reactions involving nitrosamines are discussed in Chapter 6.
3.6  SUMMARY
     There are eight  nitrogen oxides which may  be  present in the ambient  air:   nitric  oxide
(NO), nitrogen dioxide (NO,,), nitrous  oxide  (N20),  unsymmetrical  nitrogen  trioxide  (OONO),
symmetrical nitrogen  trioxide  (O-N(O)-O),  dinitrogen  trioxide (N^OO,  dinitrogen  tetroxide
(NpO,),  and dinitrogen pentoxide  (N?0r).
     Of these, NO and N02 are generally considered the most important in the lower troposphere
because  they  may  be  present  in  significant  concentrations  in polluted  atmospheres.   Their
interconvertibility in  photochemical  smog  reactions  has  frequently  resulted in  their  being
grouped  together under  the  designation  NO , although  analytic  techniques  can  distinguish
                                            A
clearly between them.   Of the two, N02 is the more toxic and irritating compound.
     Nitrous oxide  is  ubiquitous  even in the  absence  of anthropogenic sources since  it  is  a
product of natural  biologic processes in soil.   It  is  not known, however, to  be  involved in
any  photochemical  smog  reactions.    Although  N~0 is  not  generally considered  to be an  air
pollutant,  it  is  a principal  reactant  in upper atmospheric  reactions  involving  the  ozone
layer.
     While OONO,  ON(0)0, N203> N,,04, and N^Or may play a role in atmospheric chemical reactions
leading  to the  transformation,  transport,  and  ultimate  removal  of nitrogen  compounds  from
ambient air, they  are  present only in very low concentrations, even in polluted environments.
     Ammonia (NH3) originates on  a global  scale during the decomposition of nitrogenous matter
in  natural  ecosystems  but  it may  also  be produced  locally  by human  activities  such  as  the
maintenance of dense animal populations.   Some researchers have suggested conversion of NH, to
NO  in the atmosphere.
     Compounds derived  from NO  including nitrites, nitrates,  nitrogen acids,  N-nitroso  com-
pounds,  and organic compounds such as the peroxyacyl nitrates [RC(0)OONOp], where R represents
any  one  of a  large  variety  of  possible  organic groups,  may also be  found  in polluted  air.
     The peroxyacyl nitrates,  of  which peroxyacetyl nitrate  [CH3C(0)OON02] or  PAN is of most
concern  in terms of atmospheric  concentrations,  have been thoroughly  reviewed  in the recent
EPA document,  Air Quality Criteria for Ozone and Other Photochemical Oxidants.

                                            3-14

-------
     Recent discovery of N-nitroso compounds (some of which have been shown to be carcinogenic
in  animals)  in  air,  water, food and tobacco products, has led to concern about possible human
exposure to  this  family of compounds.   Health concerns  also  have been expressed about nitric
acid vapor and other nitrates, occurring as a component of particulate matter in the respirable
size  range,  suspended  in  ambient  air.   Some  of these  nitrates  are produced  in atmospheric
reactions.   Nitrates may also occur in significant concentrations in public and private drink-
ing  water,  but this  occurrence  is not  believed to be the result  of atmospheric production.
     Photochemical models  predict  that up to one-half of the original nitrogen oxides emitted
may be converted on a daily basis to nitrates and nitric acid.   This atmospheric production of
nitric acid is an important component of acidic rain.
3.6.1  Nitrogen Oxides
     Nitric  oxide  (NO)  is  an odorless and  colorless gas.  It  is a major  by-product  of  the
combustion process,  arising both  from  the  oxidation  of molecular  nitrogen  in  the  combustion
air and of nitrogen  compounds bound in the  fuel  molecule.   The amount of NO  formed  from  the
oxidation of  molecular  nitrogen  is dependent upon  such  parameters  as peak flame temperature,
quantity of  combustion  air,  and  gas residence time in  the combustion chamber.   The amount of
NO  arising  from oxidation  of fuel-bound nitrogen  does  not seem  to depend  significantly on
either the type of  nitrogen compound involved or the flame  temperature,  but instead  upon  the
specific air-to-fuel  ratio at various  stages in combustion.
     Nitrogen dioxide (N0~) is produced in minor  quantities in  the combustion process  (5 to 10
percent of  the  total oxides  of  nitrogen).   In  terms of  significant atmospheric  loading in
populated areas, N0?  arises  mainly from the conversion  of NO  to N0? by a variety of  chemical
processes in  the atmosphere.   Nitrogen  dioxide is corrosive and highly oxidizing.   Its reddish-
orange-brown  color arises  from its  absorption of  light over a  broad range  of  visible wavelengths.
Because of its strong absorption  in this range (and  also in the ultraviolet spectrum), NOp  can
cause  visibility  reduction and  affect the  spectral  distribution  of  solar  radiation  in  the
polluted,  lower atmosphere.
3.6.2  Nitrates, Nitrites, and Nitrogen Acids
     Other compounds  derived  from oxides of  nitrogen (NO )  by means of  atmospheric  chemical
processes include  nitrites, nitrates,  nitrogen acids,  organic  compounds  such  as  the  peroxyacyl
nitrates,  and, possibly, the N-nitroso  compounds.
     Nitric acid,  a strong acid and powerful  oxidizing agent,  is colorless and photochemically
stable in the gaseous state.   Its  high volatility  prevents condensation  into droplets  in  the
atmosphere unless  the droplets contain reactants such  as ammonia which  neutralize the acid.
Atmospheric  reactions  such   as  this  may result  in  the  formation  of   particulate  nitrates
suspended in  ambient air.

                                            3-15

-------
3.6.3  N-Nitroso Compounds
     The N-nitroso family comprises a wide variety of compounds all containing a nitroso group
(~N=0)  attached  to a  nitrogen  or carbon  atom.   Their  formation  in the  atmosphere  has  been
postulated to proceed  through  chemical  reaction of amines with NO  and N0v-derivatives in gas
                                                                  A       A
phase  reactions  and/or through  atmospheric  reactions  involving  aerosols.   Nitroso compounds
are characteristically photosensitive and the nitroso group is split by the ultraviolet radia-
tion in sunlight.   Gaseous nitrosamines may also be denitrosated by visible light.
                                            3-16

-------
3.7  REFERENCES

Axworthy,  A.   E. ,  and  M.  Schuman.   Investigation  of  the  mechanism  and  chemistry  of  fuel
     nitrogen  conversion to  nitrogen oxides in combustion.  Jjr.  Proceedings, Coal Combustion
     Seminar,  U.  S.  Environmental  Protection Agency, Research  Triangle Park, North Carolina,
     June  19-20,  1973.  EPA-650/2-73-021,  U.   S.  Environmental  Protection  Agency,  Research
     Triangle  Park, NC, September 1973.  pp. 9-41.

Bowen,  J.  S. ,  and  R.  E.  Hall,  Chairmen.   Proceedings  of  the  Stationary  Source Combustion
     Symposium,  Volume  I—Fundamental  Research,   U.  S.  Environmental  Protection  Agency,
     Atlanta,  Georgia,  September   24-26,   1975.    EPA-600/2-76-152a,  U.   S.  Environmental
     Protection Agency, Research Triangle Park, NC, June 1976a.

Bowen,  J.  S. ,  and  R.  E.  Hall,  Chairmen.   Proceedings  of  the  Stationary  Source Combustion
     Symposium,  Volume  II--Fuels and  Process  Research  and  Development, U.  S.  Environmental
     Protection  Agency,  Atlanta,  Georgia,  September 24-26,  1975.    EPA-600/2-76-152b,  U.  S.
     Environmental Protection Agency, Research Triangle Park, NC, June  1976b.

Bowen,  J.  S. ,  and  R.  E.  Hall,  Chairmen.   Proceedings  of  the  Stationary  Source Combustion
     Symposium, Volume  Ill—Field  Testing  and  Surveys,  U. S. Environmental Protection Agency,
     Atlanta,  Georgia,  September  24-26,  1975.   EPA-600/2-76-152c,  U.S.   Environmental  Pro-
     tection Agency, Research Triangle Park, NC, June 1976c.

Bowen,  J.  S. , and  R.  E.  Hall,  Chairmen.   Proceedings  of the  Second  Stationary  Source Com-
     bustion Symposium, Volume I:  Small Industrial,  Commercial,  and  Residential Systems, U.S.
     Environmental  Protection  Agency,  New  Orleans,   Louisiana,  August  29-September  1,  1977.
     EPA-600/7-77-073a, U.S.  Environmental  Protection Agency, Research Triangle Park, NC, July
     1977a.

Bowen,  J.  S., and  R.  E.  Hall,  Chairmen.   Proceedings  of the  Second  Stationary  Source Com-
     bustion Symposium, Volume  II:   Utility and Large Industrial Boilers,  U. S. Environmental
     Protection  Agency,  New  Orleans,  Louisiana,  August  27-September 1, 1977.   EPA-600/7-77-
     073b,  U.  S.  Environmental  Protection  Agency,  Research  Triangle  Park, NC,  July 1977b.

Bowen,  J.  S., and  R.  E.  Hall,  Chairmen.   Proceedings  of the  Second  Stationary  Source Com-
     bustion Symposium, Volume III:   Stationary Engine,  Industrial Process Combustion Systems,
     and Advanced  Processes,  U.  S.  Environmental  Protection  Agency,  New  Orleans, Louisiana,
     August 27-September 1,  1977.   EPA-600/7-77-073c, U.  S.  Environmental  Protection Agency,
     Research Triangle Park,  NC, July 1977c.

Bowen,  J.  S. , and  R.  E.  Hall,  Chairmen.   Proceedings  of the  Second  Stationary  Source Com-
     bustion  Symposium, Volume  IV:   Fundamental Combustion  Research,  U.S.  Environmental  Pro-
     tection Agency, New Orleans,  Louisiana,  August 27-September 1,^ 1977.   EPA-600/7-77-073d,
     U.  S.  Environmental Protection Agency,  Research  Triangle Park,  NC, July 1977d.

Bowen,  J.  S., and  R.  E.  Hall,  Chairmen.   Proceedings  of the  Second  Stationary  Source Com-
     bustion  Symposium,  Volume  V:   Addendum,  U.   S.  Environmental  Protection  Agency,  New
     Orleans,  Louisiana, August  27-September 1,  1977.   EPA-600/7-77-073e,  U. S. Environmental
     Protection Agency, Research Triangle Park, NC,  July 1977e.

Bowman,  C.  T.   Kinetics of  nitric  acid  formation  in combustion processes.   lr\:   Fourteenth
     Symposium  (International)   on   Combustion,  The  Combustion  Institute,   University  Park,
     Pennsylvania,  August  20-25,  1972.   The  Combustion  Institute,  Pittsburgh,  PA,  1973.
     pp.729-738.


                                             3-17

-------
Brezonik, P.  L.   Nitrogen:   sources  and tranformation in  natural  waters,   I_n:  Nutrients  in
     Natural Waters.   H.   E.  Allen  and J. R. Kramer,  eds. ,  Wiley-Interscience, New York,  NY,
     1972.   pp.  1-50.

Burns,  R.   C. ,  and  R.  W.  F.   Hardy.    Nitrogen  Fixation   in  Bacteria  and  Higher  Plants.
     Springer-Verlag, New York, NY, 1975.

Calvert, J.  G.   Nitrogen oxides—their  properties and  effects on  atmospheric light  trans-
     mission.   In:  Nitrogen Oxides.  National Academy of Sciences, Washington,  DC,  1977.   pp.
     4-19.      ~~

Chemical Rubber Company.   Handbook of Chemistry  and  Physics.  Fiftieth edition.  R. C.  Weast,
     ed.  Cleveland, Ohio, 1969-1970.

Council  for  Agricultural   Science  and Technology.   Effect  of  Increased  Nitrogen Fixation  on
     Stratospheric  Ozone.   CAST  Report  No.  53,  Council  for Agricultural  Science  and  Tech-
     nology, Iowa State University, Ames, IA, January  1976.

Crutzen, P.  J.  Upper  limits on atmospheric ozone  reductions following  increased application
     of fixed nitrogen to the soil. Geophys.  Res. Lett. 3:169-172,  1976.

Delwiche, C. C.   The nitrogen cycle.  Sci. Am. 223:137-146, 1970.

Demerjian,  K. L. ,  J.  A.  Kerr, and  J.  G.  Calvert.  The mechanism of  photochemical smog forma-
     tion.   Adv.  Environ.  Sci. Technol. 4:1-262,  1974.

Engleman, V. S.,  V.  J.  Siminski, and  W.  Bartok.   Mechanism  and Kinetics of the Formation  of
     NO  and Other Combustion Pollutants;   Phase II.  Modified  Combustion.  EPA-600/7-76-009b,
     U. S.  Environmental Protection Agency,  Research Triangle  Park, NC, August  1976.

Fenimore, C.  P.   Formation  of  nitric oxide  in premixed  hydrocarbon  flames.   I_n:   Thirteenth
     Symposium  (International)  on  Combustion,  Combustion  Institute,  Salt  Lake City,  Utah,
     August 23-29, 1970.   Combustion Institute, Pittsburgh, PA,  1971.  pp.  373-380.

Focht,  D.  D. ,  and  W.  Verstraete.   Biochemical ecology  of  nitrification and denitrification.
     Adv. Microb.  Ecol.  1:135-214, 1977.

Johnston, H. S.   Experimental chemical kinetics.  Jji:  Gas Phase Reaction Rate  Theory.   Ronald
     Press,  New York, NY,  1966.   pp. 14-34.

Johnston, H. S,.  and G.  S. Selwyn.  New  cross sections for the  absorption  of near ultraviolet
     radiation by nitrous oxide (N20).  Geophys.  Res.  Lett. 2:549-551, 1975.

Keeney, D.   R.  The nitrogen cycle in sediment water systems.  J.  Environ.  Qual.  2:15-29, 1973.

Magee,  P.  N.   Toxicity of nitrosamines:   their  possible human  health hazards.  Food  Cosmet.
     Toxicol.  9:207-218, 1971.

Magee,  P.  N.,  R.   Montesano,  and R.  Preussman.   N-nitroso  compounds  and  related carcinogens.
     In:  Chemical  Carcinogens.   C.  E.  Searle,  ed.,  ACS  Monograph 173,  American  Chemical
     Society, Washington,  DC, 1976.  pp.  491-625.
                                              3-18

-------
Martin, G.  B. ,  D.  W. Pershing  and  E.  E.  Berkau.   Effects  of Fuel  Additives on  Air  Pollutant
     Emissions  from  Distillate-Oil-Fired  Furnaces.   AP-87,  U.  S.  Environmental Protection
     Agency, Research Triangle  Park, NC, June  1971.

Matheson  Company.   Matheson  Gas  Data Book.   Fourth  Edition.   Matheson  Co. ,  Inc.,   East
     Rutherford, NJ, 1966.  pp. 367-391.

McConnell, J. C.  Atmospheric ammonia.  J. Geophys. Res. 78:7812-7820,  1973.

McNesby, J.  R. ,  and H.  Okabe.  Vacuum  ultraviolet photochemistry.  Adv.  Photochem. 3:157-240,
     1964.

Mirvish,  S.  S.   Kinetics of  dimethylamine nitrosation  in  relation  to  nitrosamine carcino-
     genesis.  J. Natl.  Cancer  Inst. (U.S.) 44:633-639, 1970.

National Bureau  of  Standards.   JANAF Thermochemical  Tables.  Second  edition.  NSRDS-NBS  37,
     U.S.  Department of Commerce, Washington,  DC,  June 1971.

Pershing,   D.  W. , and J.  0.   L.  Wendt.   Pulverized coal  combustion:   the influence of  flame
     temperature  and coal  composition  on  thermal  and fuel NO .   Jji:   Sixteenth  Symposium
     (International) on Combustion, The Combustion  Institute, Cambridge,  Massachusetts, August
     15-20, 1976.  The Combustion Institute, Pittsburgh, PA   1976.  pp. 389-399.

Rao, C. N.  R. ,  and K. R.  Bhaskar.   Spectroscopy of the nitroso  group.   Irj:  The  Chemistry of
     the  Nitro  and  Nitroso   Groups.   Part  1.  H.  Feuer,  ed. ,  Interscience Publishers,  New
     York, NY, 1969.  pp. 137-163.

Soderlund, R., and  B.  H.  Svensson.  The global  nitrogen cycle.  In:   Nitrogen, Phosphorus,  and
     Sulfur - Global Cycles:   SCOPE Report No. 7.   Ecol. Bull. (|?):23-73, 1976.

Turner, D.  W. ,  and  C.  W. Siegmund.   Staged combustion and  flue gas  recycle:   potential  for
     minimizing NO   from  fuel  oil combustion.   Presented  at the American Flame  Research  Com-
     mittee, Flame uays,  Chicago, IL, September  5-7, 1972.

U.S. Environmental  Protection  Agency.   Air Quality Criteria  for  Ozone  and Other  Photochemical
     Oxidants.   EPA-600/8-78-004, U.S.  Environmental  Protection  Agency,  Washington,  DC, April
     1978.

Zeldovich,  J.  The oxidation of nitrogen in combustion and explosions.   Acta  Physicochim.  URSS
     21:577-628, 1946.
                                             3-19

-------

-------
                                    4.  THE NITROGEN CYCLE

4.1  INTRODUCTION
     This chapter  presents a  discussion of  the nitrogen  cycle,  pointing out  the  principal
pathways, sources  and  sinks of nitrogen compounds in the environment on a global scale.   This
discussion is  intended  to provide background and perspective  for  the discussions relating to
nitrogen and  nitrogen  oxides  as presented in the other chapters of this document.  One of the
concerns relating to the effects of nitrogen oxide emissions into the atmosphere is the extent
to which  these emissions  impinge  on  the natural cycling of this  important  nutrient element.
     In  addition  to  the  nitrogen cycle,  this  chapter  discusses estimates  of the  flow of
nitrogen through  the various  biogeochemical  compartments  or  pools in the global  cycling of
nitrogen.
     The impact of man's intervention into the nitrogen cycle is discussed in Chapters 5 and 6
which  describe  the sources and the environmental transport of  nitrogen  oxides.   Atmospheric
concentrations are discussed  in Chapter 8,  the possible effects on the ozone layer in Chapter
9, Chapter 11  is  concerned with acidic precipitation, and perturbations of the nitrogen cycle
as evidenced in escosystem effects are specifically discussed in Chapter 12.
4.2  THE NITROGEN CYCLE
     The major source  of nitrogen is the earth's atmosphere where, in molecular form, it is a
major  constituent  (79  percent).   The flow of nitrogen from the atmosphere and its transforma-
tions  in the biosphere are regulated almost entirely by terrestrial and aquatic microorganisms
(Alexander,  1977;  Bolin and Arrhenius, 1977; Delwiche, 1970, 1977).
     In general  outline,  the  nitrogen cycle  is identical  in  terrestrial,  fresh water,  and
oceanic  habitats;  only  the  microorganisms  which  mediate the  various   transformations  are
different (Alexander,  1977; Chen  et  al., 1972;  Keeney,  1973)  (Figure 4-1).   A  discussion of
the step-by-step  cycling of nitrogen follows.
     1.  Biological  Nitrogen  Fixation - Atmospheric  nitrogen gas  (N^)   is transformed  into
ammonia (NH.,  or NHt)  or nitrates (NO- ) in which  form it enters the food chain.   The transfor-
mation is carried  out  by a wide variety  of  microorganisms.   The microorganisms may be either
symbiotic (living  in the roots  of leguminous plants) or nonsymbiotic (living  independently in
the soil)  and the  process may  be accomplished under aerobic  or  anaerobic conditions.
     2.  Organic  Nitrogen Formation  (assimilation)  -- Fixed  nitrogen  as either  nitrates or
ammonia is  assimilated by  plants  and converted  into organic  molecules such  as  amino acids,
proteins,  nucleic  acids and  vitamins.   Plants  are  eaten by  animals  and plant  proteins  are
converted to  animal  proteins.   In addition, carnivores  consume  other animals  as  a  protein
source.  Nitrogen is bound in plant or animal protein  until  the organisms die,  or  as in the
case of animals,  certain products are excreted.
     3.  Deamination or  Ammonification  -- This is a two-step process,  also termed mineraliza-
tion,  in which the excretion  products of animals and  the proteins in dead plants and animals

                                            4-1

-------
 i
ro
                       (f
                       N2
                   MOLECULAR
                   NITROGEN
                       IN
                   ATMOSPHERE
                               BIOLOGICAL FIXATION  ®
                            "OF MOLECULAR NITROGEN &
  ELECTRICAL
     AND
PHOTOCHEMICAL
   FIXATION
          NITROGEN
           OXIDES:
           NO, IMO2
                                                                  VOLCANIC
                                                                  ERUPTION
                                         WEATHERING
                                          OF ROCKS
                                                              FOREST & GRASSLAND FIRES
                                                                                            STORAGE OF
                                                                                           NITROGENOUS
                                                                                           COMPOUNDS IN
                                                                                         SEDIMENTS. SOILS,
                                                                                         AND SEDIMENTARY
                                                                                              ROCKS
ANIMALS IN GRAZING
    FOOD CHAIN
                                           '::'":"'""'"""""'"" DE ATH 'ft WASTES ?&::;%!
                               AUTOTROPHS
                                                                   DETRITUS FOOD CHAIN
                                                                                             AMINO
                                                                                            NITROGEN
                                                                                                NH2
                                                                                               3 NIJRIFICAT ON
                                                                                               l-j^VAV-l.-.^W:^:":":^:^ xo::::
             NITRITE A—_ AMMONIA A— — i
                                   V— J
                                                               V—     NH3
                               DENITRIFICATION
                                                                                                       DENITRIFICATION
                                          Figure 4-1. The nitrogen cycle. Organic phase shaded.

-------
 are  broken down  through  proteolysis to  amino acids.   The amino  acids  in turn are converted
 into  ammonia  (MM,).   The  ammonia may  be  assimilated by  aquatic or terrestrial  plants and
 microorganisms  may  be bound by clay  particles in the soil, or  it may be converted by micro-
 organisms  to  form nitrates in the  process  termed nitrification.   It may  also escape into the
 atmosphere.
     4.   Nitrification --  Nitrates  are formed  through  the  conversion  by  certain specific
 bacteria  of ammonia  first  to nitrite  (NCL )  and  then to  nitrate  (NCL  ).   Nitrates  may be
 assimilated  by plants, washed  downward through the soil into  groundwater or through surface
 runoff  into  streams,  rivers,  and oceans, and  may be transformed  into atmospheric nitrogen or
 reduced to ammonia.
     The  organic phase  of the  nitrogen  cycle  is  complete at  this  point  where  plants and
 microorganisms  are able  to  assimilate the  nitrates  produced.   Under  certain circumstances
 nitrate reduction  occurs;  microorganisms may  convert nitrates back to ammonia via the nitrate
 step.  These processes are the converse of the previous transformations.
     Nitrogen, as indicated above,  once it is  in the nitrate form  may be lost from the soil in
 several ways.   It may  be  assimilated  by  plants  or microorganisms, or  due  to  its solubility
 enter the soil solution and be carried off into the groundwater, lakes and streams, or through
 the process of denitrification converted into  atmospheric nitrogen (N2).
     5.  Denitrification -- Nitrates, through  bacterial action, are converted into atmospheric
 nitrogen.    Denitrification  is  an  anaerobic  process.   Nitrates  (NO.,  )  are  converted  into
 nitrites (N02 ), to nitrous oxide (N20) and finally into nitrogen  gas (N2) which goes off into
 the  atmosphere.   In  the soil,  nitrites rarely  accumulate  under  acidic conditions, nitrites
 decompose spontaneously to  nitric  oxide (NO), and  under  alpine conditions,   they are biologi-
 cally converted  to  N20 and N? (Alexander,  1977).   It  must  be emphasized that this process is
 anaerobic and  that  conversion of nitrates to  nitrites  is  extremely sensitive to the presence
 of  atmospheric oxygen.   If  atmospheric  oxygen  is  present, the  conversion does  not  occur.
     Denitrification  is the  greatest  biological  leak  in   the otherwise  closed soil  cycle
 (Alexander, 1977;  Chapham,  1973).   Through  denitrification, nitrogen becomes  unavailable to
 most plants and microorganisms and, therefore, also to animals.   Nitrogen gas enters the large
 atmospheric  reservoir wherein  its  residence  time may be  as  great  as  10   years  (Delwiche,
 1970).   Nitrous  oxide has  a much shorter residence time.   It may be converted to nitrogen gas
 in the stratosphere or returned by chemical  or biological  processes to the soil  nitrogen pool.
Were it not for biological  nitrogen fixation, the molecular  nitrogen released through denitri-
 fication would be lost to the organisms on earth.
     Another  pathway  in the  atmospheric  phase  of  the  nitrogen cycle  is   the  oxidation  of
 nitrogen by lightening  to  form  nitrogen oxides.   Nitrogen oxides  in turn may react with water
 to form nitrates (Chapham,  1973).
                                            4-3

-------
4.3  THE GLOBAL CIRCULATION OF NITROGEN
     The transformation and  movement  of nitrogen as explained  in  the  foregoing pages related
to the  biogeochemical  circulation  of nitrogen.   The  circulation  of nitrogen  is  a  long term
process.  Global nitrogen resides in a number of different compartments or pools, the principal
ones  being  primary  rocks,   sedimentary  rocks,  deep-sea  sediments, the atmosphere,  and  the
soil-water pool.  The largest of these pools is the atmosphere composed of 79 percent molecular
nitrogen (Bolin  and Arrhenius,  1977;  Delwiche,  1970,  1977).   The atmosphere  is  not  only an
important reservoir  for  nitrogenous compounds  but also serves  as  a principal conduit through
which emissions  of  gaseous  and particulate  forms  of  the  oxides of nitrogen  (NO )  are trans-
formed  and  conveyed between  terrestrial  and aquatic systems.  Sb'derlund  and Svensson (1976)
have  hypothesized that  a  net flow of NO  prevails from terrestrial to  aquatic systems; losses
of  NO  from  aquatic system to  the  atmosphere  were  considered  insignificant.   Nitrogenous
      A
compounds occurring  in  the  atmosphere can be returned to  terrestrial  or aquatic areas princi-
pally via wet (rainfall) or dry (particulate and gaseous)  deposition (Chapter 6).
     The distribution of nitrogen in the major compartments as estimated by Delwiche (1977) is
listed  in Table  4-1.   Delwiche's figures are at variance  with those of Soderlund and Svensson
(1976)  because  of differences  in compartment description; for  example,  "organic sea" as used
by Delwiche includes an "active" 10 cm layer of the ocean  bottom whereas Sdderland and Svensson
              5                                                                               5
give  5.3 x  10  Tg for dissolved  organic  nitrogen.   "Organic  soil" is  total whereas 3.0 x 10
Tg  cited  by  the other  authors  is to  a depth  of one meter.   In any  case the  figures  are
estimates and subject to change as new data are obtained.
                                                                            Q
     Turnover times  for  the  three largest "pools" of  nitrogen  are:   3 x 10  years for atmos-
pheric  nitrogen, 2,500  years for nitrogen in the seas when nitrates and organic compounds are
counted together  and less  than  one year  for  nitrates and  nitrites in  the  soil  (Whittaker,
1975).  Delwiche  (1970,  1977)  has pointed out that  the transfer rates  can  be  estimated only
within  broad  limits.   The only two quantities of  nitrogen known with any  degree  of accuracy
are the amount  of nitrogen  in the  atmosphere  and the rate of  industrial  fixation (Delwiche,
1970).  The  amount  and  the  length of  time  nitrogen  is  in the atmosphere  indicates  why the
atmosphere is the greatest  source of nitrogen, while  the  short period of time nitrogen is in
the soil emphasizes  why nitrogen is often in short supply  as a nutrient element.
4.3.1   Important Nitrogen Fluxes
     Various  authors  have  estimated  the  global  flow of  nitrogen as  it moves  through  the
nitrogen cycle.  The  estimates  of these authors are presented  in  Tables 4-2 and 4-3 for ease
of comparison.  Most  of the estimates are based on extrapolation of experimentally-determined
small-scale emission factors to  the global  scale, but some are crude estimates, arrived at by
balancing mass  flows to  account for unknown  sources.   Particular reference will  be  made to
those portions of the nitrogen cycle which are most influenced by human activities as it is in
this context that the global flow of nitrogen becomes important.
                                            4-4

-------
                    TABLE 4-1.   DISTRIBUTION OF NITROGEN IN MAJOR COMPARTMENTS
             Compartment                  Tg* N                        Reference

          Atmosphere                    3.9 x 109                Garrels  et  al. ,  1975
          Plants and animals             1.0 x 104                Delwiche, 1970
          Organic,  soil                  1.7 x 105                Delwiche, 1970
          Organic,  sea                  8.9 x 10                 Delwiche, 1970
          Inorganic, soil                1.6 x 10                 Delwiche, 1970
          Inorganic, sea                9.9 x 104                Delwiche, 1970
          Sediments                     2.0 x 108                Garrels  et  al. ,  1975
          Delwiche,  1977
          *Tg = 1012 grams

 4.3.1.1  Biological Nitrogen Fixation—Biological  nitrogen fixation  involves  the  reduction  of
 atmospheric  N, to  ammonia  (NH,),  a form of fixed nitrogen which  can be  incorporated  directly
 into the organic substances essential  for  life.   Nitrogen fixation  is important  in the main-
-tenance  of  soil  fertility  in  terrestrial,  aquatic,  and  agricultural  ecosystems.    It  is
 indirectly   responsible  for the  production of  nitrates.   Fixed  forms of  nitrogen  serve  as
-nutrient sources and, in certain  circumstances  involving  high  concentrations,  are  a source  of
 environmental  pollution.
      It has  been estimated  by  Burns  and Hardy that, on a global  basis,  nitrogen  fixation  in
                                                         12
 terrestrial  ecosystems accounts  for 139 Tg  (1 Tg  = 10  g) of  fixed nitrogen produced  each
 year;  leguminous plants  account for  35 Tg  of this  total  with  the  remainder being  produced  in
 forests  and  grasslands  (Burns  and  Hardy,  1975).   Estimates  of  other  investigators differ
 considerably and are  shown  in Tables  4-2 and 4-3.
      Nitrogen  fixation proceeds  slowly in the  presence  of  high  levels  of ammonia and other
 nitrogen-containing compounds,  such as  chemical fertilizer.  Nitrous  oxide  (N20),  a product  of
 catabolic soil  processes,  has  been shown in laboratory situations  to have the potential for
 altering the rates of nitrogen  fixation through inhibition of nitrogenase  (Hardy  and  Knight,
 1966).
      In natural waters,  the blue-green algae are the  principal  agents of nitrogen fixation.
 Fixation of nitrogen  in  aquatic  regions  of the  world have been  estimated by Soderlund and
                                             4-5

-------
TABLE 4-2.   ESTIMATES OF GLOBAL NITROGEN FIXATION
                   IN THE BIOSPHERE
                       TgN/yr

1
N?- fixation (total) 	
terrestrial (biological)...
land and sea (biological)..
aquatic 	
combustion 	
other industrial 	
lightning (atmospheric) ...

Delwiche
(1970)
92
44
N/A
10
18
12
7.6
Burns and
Hardy
(1975)
245
135
175
40
20
30
10
Sdderlund
and Svensson
(1976)
224-324
139
169-269
30-130
19
36
N/A
Robinson
and Robbins
(1975)
166
118
N/A
N/A
16
N/A
N/A

Liu et al
(1977)
227
180
N/A
37
18
36
9

CAST
(1976)
N/A
140
N/A
0.36-3.6
21
N/A
N/A

-------
TABLE 4-3.   ESTIMATES OF GLOBAL EMISSIONS  AND FLUXES OF
         OXIDES OF NITROGEN AND RELATED COMPOUNDS
                           TgN/yr

Biological N.-fixation
( 1 and and sea) . .
Biological denitrif ication
( land and sea) 	
NO emissions from land
to atmosphere 	
NO emissions from land
and sea 	
NO formed by combustion. . .
NO formed by industrial
processes 	
Atmospheric NH, trans-
formation to NO
NH, emissions to atmosphere
Atmospheric production of
NO bv liahtnina 	
Delwiche
(1970)
54
83
(N2,N20)
NA
NA
NA
30
NA
NA
NA
Burns Soderlund Robinson
and Hardy and Svensson and Bobbins Liu et al.
(1975) (1976) (1975) (1977)
175
190(N )
20(N20)
NA
NA
15
30
30
165(land
and sea)
10
169-269
96-191(N,)
36-149(N20)
40-108
NA
19
36
3-8
113-244
(land)
NA
117
338
(N20)
NA
210(NO)
15
NA
NA
870(1 and
and sea)
NA
240
270
(N2.N20)
NA
NA
NA
40
NA
NA
NA
Sze
and Rice
(1976)
260
260
(N2,N20)
NA
NA
NA
NA
NA
NA
NA
CAST
(1976)
NA
171-200
(N2,N20)
NA
NA
NA
NA
NA
NA
NA
Chameides
et al.
(1977)
NA
NA
NA
NA
NA
NA
NA
NA
30-40

-------
Svensson (1976) to be in the range of 20 to 120 Tg N per year.   The abundance of the blue-green
algae, Oscillatoria  thelbautii,  throughout oceanic areas, has been  reported  to account for a
large percentage of the global nitrogen budget (Carpenter and Price,  1976).
4.3.1.2  Industrial Nitrogen Fixation—The  need  for fertilizers  to be used  in  the growing of
crops has resulted  in  the development of the Haber-Bosch process by which inorganically-based
chemical fertilizers  are produced.   Soderlund and Svensson  (1976)  estimate that industrial
fixation processes accounted  for 36 Tg of  fixed  nitrogen produced in 1970,  nearly 30 percent
of the  amount  estimated  from  natural processes.    These  authors  also estimate that combustion
processes account  for  19 Tg  of NO -derived  N  emitted  into the  atmosphere  in  1970.   These
                                    A
processes release primarily NO.
4.3.1.3  Nitrogen Fixation  by  Other  Processes—Minor  amounts  of  nitrogen can be  fixed  in  the
atmosphere  through   chemical   reactions.   Molecular  nitrogen  can react  with  ozone (0,)  in
stratospheric reactions to produce N?0.
     Lightning  flashes  in the  troposphere can  convert  N? to NO  via  reaction  with monatomic
oxygen.   Junge (1958) concluded from analysis of precipitation data that  lightning can contri-
bute  only 10 to 20  percent of the amounts  of nitrate  found in  rain.  However,  there  are no
direct experimental  determinations of this estimate.  Crutzen and Ehhalt  (1977)  estimated that
from 8 to 40 Tg N are fixed each year by lightning.
4.3.1.4  Nitrates,  Nitrites, and the Nitrogen Cycle—The microbial oxidation  of  NH., to nitrates
(NO.,) and nitrites  (N0?)  is  the sole  natural source of nitrate  in the  biosphere (Focht  and
Verstraete,   1977)  other  than  atmospheric  transformations  of  NO   to nitrates  (Chapter  6).
                                                                  A
Because nitrates are  readily  leached from soil and are susceptible to denitrification,  nitri-
fication can  result in  large  losses of  nitrogen from  ammonium-based fertilizers applied to
soils.
     Nitrates are the  fixed nitrogen forms predominant in stream and river effluents.   In the
atmosphere,  transformation reactions involving NO, NO^,  NH3 and acidic aerosols  yield particu-
late nitrates, such as ammonium nitrate.
     Nitrate  is the  predominant  nitrogenous anion  in  atmospheric precipitation.   Nitrite
content is  generally low  (Georgii,  1963).   The  flux of NO.,-N from wet  deposition into ter-
restrial systems was  estimated by Soderlund and  Svensson  (1976)  to  be in a  range of 13 to 30
Tg NO,-N per year.   Deposition in gaseous form was estimated by these authors to be in a range
of 19 to 50  Tg NO^-N per year and 0.2 to 2.8 Tg NO^-N per year as particulates.   By comparison,
global river  discharge  of nitrate nitrogen  (excluding polar  and  desert  areas)  was calculated
at 8.1 Tg   per year (Soderlund and  Svensson,  1976).   These estimates of nitrates and nitrite
fluxes are summarized in Table 4-4.
4.3.1.5  Nitrates as Fertilizers—Man's greatest intervention into natural cycles has occurred
because of  the shortage of nitrogen  as  an available nutrient element in the soil (Delwiche,
1970).  (It  has  been estimated that the amount  of ammonia nitrogen (NH4~N)  that is converted
                                            4-8

-------
                  TABLE 4-4.   ESTIMATES OF THE GLOBAL FLUX OF NITRATES AND NITRITES
                                               TgN/yr


Atmospheric production from N09.
Atmospheric production from NH., 	
Total deposition (land and sea) 	
Total dry deposition (land and sea)...
Total wet deposition (land and sea)...
Burns
and Hardy
(1975)
20
30
60
N/A
N/A
Sbderlund
and Svensson
(1976)
N/A
N/A
18-51
0.3-2.8
18-46
Robinson
and Robbins
(1975)
95
N/A
95
75
20
 by  microorganisms to nitrate nitrogen  (NO,-N)  is  equivalent to the  net  nitrogen  assimilation
            2
 (0.017  kg/m )  by  plants  each year.)   (Bowen,  1966;  Delwiche,  1977)  To  alleviate this  shortage,
 the  limiting   factor  in  plant  growth, industrial fixation of nitrogen  was developed.   At  the
 present time the  amount  of  nitrogen  fixed  industrially  for the  production  of  fertilizer equals
 the  amount  that was  fixed by all  terrestrial  ecosystems before  the  advent  of  modern  agriculture
 (Delwiche,  1970).  The  world's annual,  output  of  industrially  fixed nitrogen was  30 million
:tons  in 1968  and it  has  been  estimated it will reach  or exceed 100 million  tons by  the year
 2000  (Parr, 1973).    Consumption  of  fertilizer nitrogen  in  the  U.S.A.  will  probably  reach 11
imillion tons  in  1980 (Parr, 1973).   The impact of this  environmental  loading has  not, until
 very  recently, been considered.
 4.4   AMMONIFICATION AND  NITRIFICATION
      Nitrogen  fixation  and  denitrification  processes  in natural  systems result in increased
 concentrations of ammonium  ions (NH.) in the  soil or  in aquatic  systems as a  result  of ammonia
 (NH3) hydration.  These  ions may  be  utilized  by  plants  and bacteria to  produce protein.
      Ammonification  is  an important  process  in  the renewal  of the  limited supply of inorganic
 nitrogen.   Organic compounds, such as amino acids resulting  from decay  processes, are  converted
 into  NH., and ammonium ions.  Volatilization of ammonia  from  soils may increase the atmospheric
 burden  of   NO  as NH, undergoes atmospheric  transformation  (Chameides  et al. , 1977;  National
             A       O
 Research Council, 1978).
 4.5   NITRIC OXIDE, NITROGEN DIOXIDE  AND  THE NITROGEN  CYCLE
      Total  N0y emissions to the atmosphere from  terrestrial  sources were reported by Soderlund
 and  Svensson  (1976)  to  be  in the range of 8 to 25 Tg  N  per  year.  Estimates  of other authors
 regarding NO   emissions  are presented in Tables  4-3 and 4-5.

                                            4-9

-------
TABLE 4-5.   ESTIMATES OF THE GLOBAL FLUX OF NO
                   (NO AND N0?)               >
                      TgN/yr *

Natural emissions from land to
atmosphere 	
Natural emissions from land and sea
to atmosphere 	
Tropospheric production by lightning
Stratospheric production from N?0...
Atmospheric production from NH, 	
Production during combustion. ...
Other industrial production 	
Total land deposition 	
Total aquatic deposition 	
Total wet deposition (as nitrates;
land and sea) 	
Total dry deposition (land and sea).
Burns
and Hardy
(1975)
N/A
N/A
10
5
N/A
15
30
31
18
49
11
Soderlund and
Svensson
(1976)
21-89
N/A
N/A
0.3
3-8
19
36
32-83
11-33
18-46
25-70
Robinson
and Robbins
(1975)
N/A
210
N/A
2
N/A
15
N/A
N/A
N/A
75
151
Crutzen
and Ehhalt
(1977)
N/A
N/A
8-40
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
Chameides
et al.
(1977)
N/A
N/A
30-40
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A

-------
     While  40  to 108  Tg NO -N per  year  have been estimated to  be  released from terrestrial
sources  to  the atmosphere,  the  bulk is reabsorbed and  only  8  to 25 Tg  NO  -N  escapes to the
                                                                           A
troposphere  (Sb'derlund and  Svensson,  1976).    Hill  (1971)  has reported that  NO  and NOp are
absorbed from  the  atmosphere by plants.  Using data  obtained from the experiments of Makarov
(1969) and  those  of Kim (1973), Soderlund  and  Svensson (1976)  estimate that soil contributes
to  the  atmosphere  between 1 to  14  Tg N in the form  of NO and NO-;  losses  from aquatic eco-
systems  to  the atmosphere were considered by these authors to be minor.  The principal source
of gaseous NOX in terrestrial systems is believed to be the chemical  decomposition of nitrates
(Soderlund and Svensson, 1976).
     In  the  stratosphere, NO  and  N02  can  be produced  through  photolysi-s  and transformation
reactions involving  N20  and  03-   Small amounts of  these products (about 0.3 Tg annually) are
expected to reenter the troposphere, mainly as N0? and HNO-.
     Tropospheric ammonia  may be converted to NO,  and indirectly to  NOp,  via reaction with
hydroxyl  free  radicals  (-OH).   Soderlund  and Svensson (1976)  estimate that  this  reaction
accounts for  3 to  8  Tg  NO -N produced annually.   A  higher  estimate (20 to 40  Tg NO -N) was
                           X                                                           X
reported by Chameides and co-workers (1977).
     Tropospheric production of  NO   during  lightning discharges has  been estimated to account
for 8 to 40 Tg NO -N per year (Chameides et al., 1977; Griffing, 1977; Noxon, 1976).
                 X
     The work  of  Chameides et al.   (1977) suggests  that lightning is a  significant  source of
NO , producing about 30 to 40 Tg NO -N per year.  If this estimate is correct,  lightning could
  X                                X
account for as much as 50 percent of the total atmospheric production of NO  on a global basis
                                                                           X
(Chameides  et  al.,  1977), or  a level  comparable to  one  estimate of  the  global  average of
man-made NO  emissions (Crutzen et al., 1978;  Noxon, 1978).
     Direct observations by Noxon (1976) during a lightning storm indicate that ambient concen-
trations of NOp may be enhanced by a factor of 500 over the normal level.   The  enhanced levels
decayed  rapidly  after passage  of  the  storm.   Liu  et al.  (1977) estimated  NO   production by
lightning at 9 Tg N per year.
     Recent studies of the global carbon cycle indicate that burning  of wood and other biomass,
largely in tropical  land-clearing,  may release significant quantities of NO   (National Research
                                                                           A
Council, 1978).
     Atmospheric NO  returns to  earth by two principal mechanisms:   wet deposition (rain) and
dry deposition (gaseous  and  particulate).   Dry deposition has been estimated to be twice that
of wet deposition over the same areas (Soderlund and Svensson, 1976).
     Tropospheric reactions  and transport  considerations  are  discussed  in  more detail  in
Chapter 6.
4.6  NITROUS OXIDE AND THE NITROGEN  CYCLE
     Nitrous oxide  is  released  from denitrification and nitrification  processes  in  soils and
aquatic environments and  is  transformed in  stratospheric chemical reactions.  It is not known
to be involved in  tropospheric  reactions.   After release from  soil  or water,  NpO diffuses to

                                            4-11

-------
the  stratosphere  and may  be  converted to  oxygen,  nitrogen,  and  oxides of  nitrogen (Junge,
1972).  The stratosphere represents the only known atmospheric sink for NpO.
     From  a  review of  the literature, Soderlund  and Svensson (1976) estimated  the  N?0 flux
from  soils to  the atmosphere  in the  range  of  16 to 69 Tg N^O-N per year.   These authors also
estimate that  N^O derived from  denitrification  processes  account  for at least  10  percent of
the  total  amount  of  nitrogen  denitrified.  The authors caution, however, that the data avail-
able  are too  limited  to draw more precise estimates.   CAST (1976)  estimated ^0 production in
soils at 7 Tg N per year.
     Total  annual marine production and release to the atmosphere of N^O was recently estimated
at 4  to  10 Tg-N by Cohen and Gordon (1979).  This estimate was based on new information which
indicates major deficiencies  in  divergent earlier estimates by Hahn (1974)  and Hahn and Junge
(1977), who proposed  a  net source of 16 to 160 Tg-N/yr, and McElroy et al.  (1976),  who argued
that the ocean could be a sink for 40 Tg-N/yr of atmospheric NLO.
     Soderlund and Svensson (1976),  using data obtained by  Junge  (1972),  estimate that 18 Tg
NpO-N per year  is conveyed from the  troposphere  to  the stratosphere and converted to N^, 0.,,
and NOX.   These estimates are summarized in Table 4-6.
     Nitrous oxide is  important  in the regulation of the amount of ozone in the stratosphere.
Crutzen  (1974)  has suggested  that an increase of  1  percent of the emission  rate  of nitrous
oxide may  cause  a 0.2 percent decrease in  stratospheric  ozone, thus increasing the amount of
ultraviolet  radiation  reaching  the  earth.   The potential  effect  of coal-  and  gas-burning
processes (Pierotti and Rasmussen,  1976) and the increased use of fertilizer nitrogen (Bremner
and  Blackner,  1978)  on  increasing N~0 levels  has  been  suggested  to be a cause  of concern
regarding 0.>  destruction.   Pierroti  and  Rasmussen (1976)  report  that  coal-burning  and gas-
burning industrial processes may account for approximately 2 Tg N-O-N produced each year.  Liu
and  co-workers  (1977) suggest that other  land-based  sources of N^O could  include  sewage and
nitrogen waste treatment plants.
     Nitrous oxide has  been  reported  to be released  from  soils during nitrification of added
ammonium- or  urea-based fertilizers  under  aerobic conditions  (Bremner and  Blackmer,  1978).
Urea is rapidly hydrolyzed by a soil enzyme, urease, to form ammonium carbonate.   Of the added
nitrogen, approximately  0.04  percent  was  released as N20.   Nitrous oxide also is discussed in
relation to denitrification in Section 4.9.
4.7  ORGANIC NITROGEN AND THE NITROGEN CYCLE
     Large transfers  of organic nitrogen compounds are found  within  aquatic  and terrestrial
systems  (Soderlund and  Svensson,   1976).   The  nitrogen  flow  between  these  systems  and the
atmosphere is much less than the internal  circulations.
     Man's agricultural  activities have been  reported  to  be a cause  of depletion  of organic
matter  in  soils  (Paul,  1977;  Stanford et al.,  1975).   Soderlund  and Svensson  (1976) have
                                            4-12

-------
TABLE 4-6.   ESTIMATES OF THE GLOBAL FLUX OF NITROUS  OXIDE
                           TgN/yr

Natural emissions from land
to atmosphere 	
Natural emissions from land
and sea to atmosphere 	
Natural emissions from aquatic
areas to atmosphere 	
Produced during atmospheric
reaction of N? with ozone

Burns
and Hardy
(1975)
13
20
7
15

Soderlund
and Svensson
(1976)
16-69
N/A
20-80
N/A

Robinson
and Robbins
(1975)
N/A
342
N/A
N/A

Crutzen
and Ehhalt
(1977)
12-80
N/A
40-90
N/A

CAST
(1976)
7
N/A
N/A
N/A


-------
estimated that 6 to 13 x 10  Tg-N are lost each year on a global basis (an order-of-magnitude-
type estimate for  agricultural  lands only).   Losses due to forest cutting were not taken into
consideration.
     Annual wet deposition  of organic nitrogen has been  estimated  to be in a  range  of 10 to
100 Tg (Sdderlund and Svensson, 1976).  An average organic nitrogen content of 0.1 to 1.0 mg N
per  liter  of terrestrial  precipitation  was used  as  the basis for  the  calculation.   Organic
nitrogen in  river  discharge was estimated at 9.9  Tg  per year (Sbderlund and Svensson, 1976).
4.8  AMMONIA AND THE NITROGEN CYCLE
     There is considerable  uncertainty  as to the sources of atmospheric NhU.  A global source
strength of  113  to 224 Tg-N per year has been estimated (Sb'derlund and Svensson, 1976), based
on  balancing  of estimated  total deposition.   Sources  such as excreta from  wild and  domestic
animals and humans (Denmead et al., 1974; Healey et al., 1970; Luebs et al.,  1973; Stanford et
al., 1975) and  coal  combustion (Burns and Hardy,  1975;  Georgii, 1963; Sb'derlund and Svensson,
1976)  may  account for  a quarter  of  this total.    Other  likely major sources  of NH3 include
decomposition of organic matter other than excreta, forest fires,  and other wild fires, losses
from  manufacture,  handling  and  application  of  ammonia-based  fertilizers  (Sbderlund  and
Svensson,  1976)  volatilization  from oceans  (Bouldin  et al., 1974),  and possibly  from  the
senescing  leaves of  living  plants  (Farquhar et al. , 1979).  Estimation of atmospheric release
from natural  and  agricultural  areas  is  complicated  by the observation that  plant  cover  can
reabsorb  substantial  amounts  of  the  NH., released at  ground  level  in  these  areas  (Denmead
et al., 1976).
     It has been  proposed  that atmospheric NH., may be  converted  to NOX by  reaction  with  -OH
radicals  (McConnell,  1973; McConnell  and McElroy, 1973).   A  recent  estimate of  the annual
magnitude  of  this  source  is  20 to  40  Tg  NOX~N  (Chameides et al.,  1977).   McConnell (1973)
concluded that this reaction and heterogeneous losses  are the dominant tropospheric NH3 removal
mechanisms.  Atmospheric NH3  returns  to terrestrial and aquatic systems via precipitation (as
ammonium salts), by dry deposition  of gaseous NH-,  and  particulate  ammonium compounds (Sbderlund
and Svensson, 1976), and by direct  gaseous uptake by plants (Denmead et al.,  1976).  Estimates
of global flux of ammonia are summarized in Table 4-7.
4.9  DENAZIFICATION
     In contrast to  nitrogen  fixation,  denitrification results in  the release of fixed forms
of  nitrogen,  principally N?0 and N~  with  small  amounts of NO, into  the  atmosphere.   Ammonia
production also  has  been reported  (Payne, 1973;  Stanford et al., 1975).  As  plants  decay,  a
ubiquitous group of  specialized microorganisms (e.g.,  Pseudomonas denitrificans) in soils and
in aquatic systems reduce nitrates  and nitrites to nitrogenous gases.  Without these bacteria,
most of  the  atmospheric nitrogen would be in the oceans or in sediments (Delwiche, 1970).   On
a time  scale  of millions of years, losses of these gases to the atmosphere are believed to be
roughly  balanced  by the  amounts  of  N   fixed by  natural  processes  (Sbderlund  and Svensson,
                                            4-14

-------
1976).   The  ratio  of N2 to N20 produced is an area of current interest because of the role of
HJy in the destruction of stratospheric ozone (Chapter 9).
     Delwiche  (1970)  estimated  that 83 Tg of N^O-N  is  produced annually from terrestrial and
oceanic  sources.  Estimates of other investigators of the extent of global denitrification are
considerably  higher  than those of  Delwiche.  These  estimates, as well as  other  estimates of
the global budget for nitrogenous compounds, are presented in Tables 4-3 and 4-8.   Soil factors
such as  acidity (Focht,  1974; Nommik, 1956), moisture content (Soderlund and Svensson, 1976),
temperature  (Nommik,  1956;  Stanford et al., 1975), and  oxygen content (Cady and Bartholomew,
1960; Nommik,  1956)  determine proportions  of NO, N20 or N~ produced.   Major factors affecting
the extent of denitrification losses in soils  include  availability  of an organic carbon sub-
.strate (Focht,  1974;  National Research Council, 1978),  moisture  content,  presence or absence
of a  cover crop (Burford and Stefanson, 1973),  and  the type of fertilizer applied (Broadbent
and Clark, 1965; Rolston et al. , 1976).
     Conditions  favoring release of  N^O from  nitrates  include  high  soil  acidity  (low pH),
presence  of  Q~, limited  amounts  of easily metabolizable organic  compounds,  low  temperatures
and high  initial concentrations  of  nitrates.   Acidity and  temperature factors which increase
N20 production also tend to  decrease  the  absolute rate of denitrification  (Stanford  et al.,
1975).   Molecular   nitrogen  is  the principal  end product  under  true anaerobic  conditions
(National Research  Council,  1978).   Nommik  (1956)  reported that NO production is  favored in
acidic anaerobic  systems exposed to  large  amounts of nitrite.   However,  such conditions are
not likely to occur  in natural  systems.   Anaerobic conditions are promoted when soil moisture
content  increases,  reducing  the diffusion  of oxygen  through the soil  pore  spaces  (Soderlund
and Svensson,  1976).   The  production of N?0 by  denitrification processes  has been reviewed by
CAST (1976),  Hahn and Junge (1977),  and Crutzen  and Ehhalt (1977).
     Denitrification also occurs in  aquatic ecosystems,  and the limited data available suggest
that oceanic  systems contribute greater  amounts of  N~  and  N?0  to the atmosphere  than ter-
restrial  systems (Soderlund and Svensson,  1976).   Lake sediments are believed to provide ideal
conditions for  denitrifying organisms  (Keeney  et al., 1971;  National  Research Council, 1978).
4.10  ACIDIC  PRECIPITATION
     Increased amounts of  NO   released to  the  atmosphere is of concern due to their contribu-
tion to  the   acidification  of precipitation  (Likens,  1976).   A full discussion pertaining to
acidic precipitation appears in Chapter 11.
4.11  SUMMARY
     Nitrogen  is an  element  necessary for  all  life.   The maintenance of an  adequate  balance
among nitrogen-containing compounds  is  essential  to  the integrity of  all  ecosystems on earth.
Nitrogen   resides in  five  major  reservoirs:   primary  rocks,  sedimentary rocks,  the deep-sea
sediment, the  atmosphere,  and the  soil-water pool.   The web  of pathways and  fluxes  by  which
oxides of nitrogen  and associated nitrogenous compounds  are produced,  transformed, transported,
                                            4-15

-------
             TABLE 4-7.   ESTIMATES OF GLOBAL FLUX OF AMMONIA AND AMMONIUM COMPOUNDS
                                              TgN/yr
                                              Burns
                                            and Hardy
                                             (1975)
              Sdderlund
             and Svensson
                (1976)
                 Robinson
                and Robbins
                  (1975)
    Volatilized from land and sea.
    Volatilized from land	
    Produced from burning of coal.
    Terrestrial wet deposition....
    Wet deposition over oceans....
    Terrestrial dry deposition
      (gaseous)	
    Dry deposition over oceans
      (gaseous)	
    Precipitation as NH. (land
      and sea)	
    Dry deposition as NHt (land
      and sea)	
    Converted to NO  in atmosphere	
165
N/A
  5
N/A
N/A

N/A

N/A

140

N/A
N/A
  N/A
113-244
  4-12
 30-60
  8-25

 57-114

 10-20

 38-85

  3-8
  5-17
860
N/A
N/A
N/A
N/A

679

N/A

150

N/A
 40
and stored  in the  principal  nitrogen reservoirs,  are commonly  referred  to as  the  nitrogen
cycle.
     An  understanding  of  the nitrogen  cycle  is  important in  placing in  perspective  man's
intervention as discussed in other chapters of this document.
     The atmosphere, composed  of  79 percent molecular nitrogen (N,,), is not only an important
reservoir  for nitrogenous  compounds but  also  serves as a  principal  conduit  through  which
emissions of gaseous and particulate forms of the oxides of nitrogen (NO )  are transformed and
conveyed  between  terrestrial  and  aquatic  systems.    Nitrogenous  compounds occurring in  the
atmosphere can be  returned  to terrestrial or  aquatic  areas  principally via wet (rainfall) or
dry (particulate and gaseous) deposition.
     Most estimates  of the global  flows  of  nitrogen compounds are  based  on extrapolation of
experimentally-determined small-scale  emission factors  to  the global  scale;  some are  crude
estimates, arrived at by balancing mass flows to account for unknown sources.  Since published
estimates differ  greatly,  it  is  difficult to assess  with any certainty  the fraction of N0x
                                            4-16

-------
TABLE 4-8.   ESTIMATES OF GLOBAL DENITRIFICATION
                      TgN/yr


Biological denitrification
(total) 	
terrestrial 	
aquatic 	

Delwiche
(1970)
83
43
40
Burns and
Hardy
(1975)
210
140
70
Soderlund
and Svensson
(1976)
132-340
107-161
25-179
Sze and
Rice
(1976)
260
135
125

Liu et al.
(1977)
245
127
118

CAST
(1976)
171-200
71-100
100

-------
emissions globally which  arise  from man's activities.   In terms  of  their contribution to NO
                                                                                             A
concentrations in polluted  urban  airsheds,  however,  it seems clear that natural ,processes are
generally negligible (see Chapter 8).
     The extent to which  the use of industrially fixed nitrogen in agriculture has  influenced
the nitrogen  cycle,  the  role of nitrous  oxide  in  the  nitrogen cycle,  and the significance of
increased amount of ammonia due to human activities are all  matters of  concern.
                                            4-18

-------
4.12  REFERENCES

Alexander, M.   Introduction  to Soil Microbiology.  2nd  Edition.   John Wiley  &  Sons,  Inc.,  New
     York, NY, 1977.

Bolin, B., and  E.  Arrhenius,  Eds.  Nitrogen - an essential  life  factor  and a growing environ-
     mental hazard:  Report from Nobel Symposium No. 38.  Ambio 6:96-105,  1977.

Bouldin,  D.  R. , R.  L.  Johnson, C.  Burda,  and C.-W.  Kao.   Losses of inorganic nitrogen  from
     aquatic systems.  J. Environ. Qual. 3:107-114, 1974.

Bowen, H. J.  M.   Trace Elements in Biochemistry.  Academic  Press,  Inc.,  Ltd., London, England,
     1966.

Bremner, J. M. ,  and A.  M. Blackmer.  Nitrous oxide:  emission from  soils  during nitrification
     of fertilizer nitrogen.    Science (Washington,  D.C.) 199:295-296, 1978.

Broadbent, F. E. ,  and  F.  Clark.  Denitrification.  In:  Soil Nitrogen.  W. V.  Bartholomew  and
     F.  E. Clark,  eds.,  American Society of Agronomy,  Inc., Madison, WI, 1965.   pp.  344-359.

Burford, J. R. ,  and R.  C. Stefanson.  Measurements of gaseous losses of  nitrogen from  soils.
     Soil Biol.  Biochem.  5:133-141, 1973.

Burns, R. C.,  and R. W.  F. Hardy.  Nitrogen Fixation in Bacteria  and  Higher Plants.   Springer-
     Verlag,  New York,  NY, 1975.

Cady, F.  B. ,  and   W.  V.  Bartholomew.   Sequential products of  anaerobic denitrification  in
     Norfolk soil material.   Soil Sci. Soc.  Am. Proc.  24:477-482,  1960.

Carpenter, E.  J. ,  and  C.  C.  Price, IV.  Marine Oscillatoria (Trichodesmium):   explanation  for
     aerobic nitrogen fixation without heterocysts"!Science (Washington,  D.C.) 191:1278-1280,
     1976.

Chameides, W.  L., D. H.  Stedman, R. R. Dickerson, D. W. Rusch, and R. J. Cicerone.  NO   produc-
     tion in lightning.   J.  Atmos.  Sci.  34:143-149, 1977.

Chapham, W. B. ,  Jr.   Natural  Ecosystems.  The  MacMillan Co.,  New York, NY,  1973.  pp.  40-42.

Chen, R.  L. ,  D.  R.  Keeney, and J. A. Konrad.   Nitrification  in sediments of selected  Wisconsin
     lakes.   J.  Environ.  Qual.  1:151-154, 1972.

Cohen, Y. ,  and  L.   I.  Gordon.    Nitrous  oxide  production in the  ocean.   JGR J. Geophys. Res.
     84:347-353, 1979.

Council  for  Agricultural  Science  and Technology.  Effect  of Increased Nitrogen Fixation  on
     Stratospheric  Ozone.  CAST Report No. 53, Council  for Agricultural Science  and Technology,
     Iowa State University,  Ames, IA, January 1976.

Crutzen,  P.  J.   Estimation  of possible variations in total ozone  due  to natural causes  and
     human activities.   Ambio  3:201-210, 1974.

Crutzen,  P.  J.  , and D.   H.  Ehhalt.   Effects  of nitrogen  fertilizers  and combustion in  the
     stratospheric  ozone layer.  Ambio 6:112-117, 1977.
                                             4-19

-------
Crutzen, P. J. ,  I.  S.  A. Isaksen,  and  J.  R. McAfee.  The  impact of the chlorocarbon  industry
     on the ozone layer.   JGR J. Geophys. Res. 83:345-363,  1978.

Delwiche, C.  C.  The nitrogen cycle.  Sci. Am. 223:137-146, 1970.

Delwiche, C.  C.  Energy relations in the global nitrogen cycle.  Ambio 6:106-111,  1977.

Denmead, 0. T. , J.  R. Freney, and J. R.  Simpson.  A closed  ammonia cycle within  a  plant  canopy.
     Soil Biol. Biochem.  8:161-164, 1976.

Denmead, 0.  T. ,  J.  R.  Simpson,  and  J.  R.  Freney.   Ammonia  flux  into  the atmosphere  from  a
     grazed pasture.   Science (Washington, D.C.) 185:609-610,  1974.

Farquhar, G.   D. , R.  Wetselaar,  and P.  M. Firth.  Ammonia volatilization from  senescing  leaves
     of maize.  Science (Washington, D.C.) 203:1257-1258, 1979.

Focht, D.  D.    The  effect of temperature,  pH and aeration  on  the  production of nitrous  oxide
     and gaseous nitrogen—a zero-order kinetic model.  Soil Sci. 118:173-179, 1974.

Focht, D.  D. , and W.  Verstraete.  Biochemical ecology  of  nitrification and  denitrification.
   -Adv. Microb.  Ecol.  1:135-214, 1977.

Garrels, R.  M. ,  F.  T.  Mackenzie,  and  C.  Hunt.  Chemical  Cycles  and  the Global  Environment:
     Assessing Human Influences,  William Kaufman, Inc., Los Angeles, CA, 1975.

Georgii, H.-W.  Oxides of  nitrogen and ammonia  in  the atmosphere.  J. Geophys. Res.  68:3963-
     3970,  1963.                                                                        ~~

Griffing, G.  W.  Ozone and oxides of nitrogen production during  thunderstorms.   JGR  J. Geophy.
     Res. 82:943-950, 1977.

Hahn, J.   The North  Atlantic Ocean as  a  source of atmospheric  N20.  Tellus 26:160-168,  1974.

Hahn, J., and C.  E. Junge.   Atmospheric nitrous oxide:  a critical review.   Z. Naturforsch. A.
     32A:190-214, 1977.

Hardy,  R.  W.  F. ,  and  E.   Knight,  Jr.   Reduction  of N20 by  biological  N?-fixing  systems.
     Biochem.  Biophys.  Res.  Commun. 23:409-414, 1966.

Healy, T.  V.,  H. A.  C.  McKay,  A.  Pilbeam,  and D. Scargill.   Ammonia  and ammonium  sulfate in
     the troposphere over the United Kingdom.  J. Geophys.  Res.  75:2317-2321,  1970.

Hill, A.  C.   Vegetation:  a sink for  atmospheric pollutants.   J.  Air Pollut.  Control  Assoc.
     21:341-346, 1972.

Junge, C.  E.   The  distribution of ammonia  and nitrate in rainwater  over the  United States.
     Trans. Am. Geophys.  Union.  39:241-248,  1958.

Junge, C.  E.    The  cycle  of atmospheric  gases - natural and manmade.  Q. J. R.  Meteorol.  Soc.
     98:711-728, 1972.

Keeney,  D.  R.  The  nitrogen cycle  in  sediment-water  systems.   J. Environ.  Qual.   2:15-29,
     1973.
                                             4-20

-------
Keeney, D. R., R. L. Chen, and D. A. Graetz.   Importance of devitrification  and  nitrate  reduc-
     tion  in sediments to  the  nitrogen  budgets of  lakes.   Nature (London) ^3:66-67,  1971.

Kim, C.  M.  Influence  of vegetation  types on the intensity  of ammonia and nitrogen dioxide
     liberation from soil.  Soil Biol. Biochem.  5:163-166, 1973.

Likens, G. E.  Acid precipitation.  Chem. Eng. News 54:29-43,  1976.

Liu,  S.   C. ,  R.   J.  Cicerone,  T.   M.  Donahue,  and W.  L.  Chameides.   Sources  and sinks  of
     atmospheric  N20  and  the  possible  ozone  reduction  due  to  industrial  fixed nitrogen
     fertilizers.  Tellus 29:251-263, 1977.

Luebs,  R.  E. ,  K.  R.  Davis,  and  A.  E.   Laag.   Enrichment  of the  atmosphere  with nitrogen
     compounds volatilized from  a large diary  area.  J. Environ. Qual.  2:137-141,  1973.

Makarov,  B.  N.    Liberation  of  nitrogen  dioxide from  soil.   Sov.  Soil  Sci.  (Engl. Transl.)
     1:49-53, 1969.

McConnell, J. C.   Atmospheric ammonia.  J.  Geophys. Res. 78:7812-7820,  1973.

McConnell, J. C. , and M. B.  McElroy.  Odd nitrogen  in the atmosphere.   J. Atmos.  Sci. 3_0:1465-
     1480, 1973.

McElroy, M.  B. ,  J.  W.  Elkins, S. C. Wofsy, and Y.  L.  Yung.  Sources and sinks for atmospheric
     N20.   Rev.  Geophys. Space Phys. 14:143-150, 1976.

National  Research  Council.   Nitrates:     An  Environment  Assessment.    National  Academy  of
     Sciences,  Washington, DC, 1978.

Nommik, H.   Investigations  on  denitrification in  soil.  Acta Agric.  Scand. 6:195-228,  1956.

Noxon,   J.  F.   Atmospheric  nitrogen  fixation by  lightning.   Geophys.   Res.  Lett.  3:463-465,
     1976.

Noxon,  J.  F.   Tropospheric N02>  JGR J. Geophys. Res.  83:3051-3057, 1978.

Parr, J.  F.  Chemical  and biochemical considerations  for  maximizing the efficiency of  ferti-
     lizer nitrogen.  J. Environ. Qual. 2:75-84, 1973.

Paul, E.  A.  Nitrogen  cycling in terrestrial  ecosystems.   In:   Environmental Biogeochemistry,
     Volume  I:   Carbon, Nitrogen,  Phosphorus, Sulfur and  Selenium  Cycles,  Proceedings  of the
     2nd  International  Symposium,  Canada  Centre  for  Inland  Waters  and  Others,  Hamilton,
     Ontario, Canada,  April  8-12,  1975.    J.  0.  Nriagu,   ed. , Ann Arbor  Science  Publishers,
     Inc., Ann Arbor, MI,  1977.  pp. 225-243.

Payne,  W.   J.  Reduction of  nitrogenous oxides by microorganisms.   Bacteriol. Rev.  37:409-452,
     1973.

Pierotti,  D., and R. A.  Rasmussen.  Combustion as a source of  nitrous oxide  in the atmosphere.
     Geophys. Res. Lett. 3:265-267,  1976.

Robinson,   E. ,  and  R.   C.  Robbins.    Gaseous   atmospheric  pollutants  from   urban  and natural
     sources.  Jn:  The Changing Global  Environment.   S.  F. Singer, ed., D. Reidel  Publ.  Co.,
     Boston,  MA,  1975.   pp.  111-123.


                                             4-21

-------
Rolston,  D.   E. ,   M.  Fried,  and  D.  A.  Goldhamer.   Denitn'fication measured  directly  from
     nitrogen and nitrous oxide gas fluxes.  Soil Sci. Soc. Am. J.  40:259-266,  1976.

Soderlund, R. , and B.  H.  Svensson.  The global nitrogen  cycle.   In:  Nitrogen,  Phosphorus,  and
     Sulfur-Global Cycles:  SCOPE Report 7.  Ecol.  Bull.  (22):23-73,  1976.

Stanford, G.   Nitrogen in soils.  Plant Food Rev. 1:2-4,  7, 1969.

Stanford, G., J.  0.  Legg, S. Dzienia,  and E.  C.  Simpson, Jr.  Denitn'fication  and associated
     nitrogen transformation in soils.  Soil Sci. 120:147-152,  1975.

Sze, N.  D. ,  and  H. Rice.   Nitrogen cycle factors  contributing to N~0 production  from  ferti-
     lizers.   Geophy.  Res. Lett. 3:343-346, 1976.                    ^

Whittaker, Robert H.  Communities and Ecosystems.   2nd Edition.   MacMillan  Publishing Co.,  New
     York, NY, 1975.
                                              4-22

-------
                                   5.  SOURCES AND EMISSIONS

5.1  INTRODUCTION
     This chapter primarily reviews significant anthropogenic sources of nitrogenous compounds
which directly  affect  human health or which  may  participate in atmospheric chemical pathways
leading to effects on human health and welfare.  Particular emphasis is placed on emissions of
NO  for  two  reasons:   (1) N09  is  a  pollutant of major concern  for  human  health (Chapter 15)
  A                          £
and (2)  atmospheric  transformation products of NO  such as nitric acid (HNO,) and particulate
                                                  A                         O
nitrates are  of concern both for their effects on human health and their role in the acidifi-
cation of precipitation (Chapter 11).   Emissions of nitrates,  nitrites  and nitrogenous acids
are not  discussed because,  except in a  few  special  situations (such as  in  the  vicinity of
nitric acid plants for HN03 or certain agricultural  operations for particulate nitrates),  they
do not result in significant ambient concentrations.   Atmospheric production and ambient  con-
centrations of  these  compounds  are discussed  in Chapters 6 and 8, respectively.   Agricultural
usage of  nitrogenous compounds  is  reviewed because  of recent discussion  of  possible  pertur-
bations of the stratospheric ozone layer by nitrous  oxide (NpO) (Chapter 9), which is produced
in part  from fertilizer  not  utilized by  plants.   Sources  of  N-nitroso  compounds  and their
possible precursors are reviewed as background material for a discussion of atmospheric burdens
of these pollutants actually observed in ambient air (Chapter 8).  Sources  of ammonia are  dis-
cussed because  some  researchers have suggested that it is converted to NO   in the atmosphere.
5.2  ANTHROPOGENIC EMISSIONS OF NOX
     Global  estimates  of natural  emissions of nitrogenous compounds  including  NO   have  been
discussed in  detail  in  Chapter 4.   Since various authors differ greatly in their estimates of
natural  emissions, it  is difficult to assess  with  any certainty the  fraction of  NO  emitted
globally from human activities.
     In highly industrialized or populous localities,  anthropogenic emissions of  NO and/or N02
assume primary  importance.   Mobile  combustion and  fossil-fuel  power  generators  are  the two
largest source categories.  In addition,  industrial  processes and agricultural  operations  pro-
duce minor quantities.   Although certain industrial  processes, such as  nitric acid plants, and
certain agricultural  activities, such as  the application  of fertilizer  or the  operation of
animal  feedlots, may result  in  localized emissions  of  other nitrogenous  compounds, which  have
potential as  NO   sources  through atmospheric  transformation  only  NO and  NOp are,  in general,
considered to be the  primary pollutants;  the other nitrogen oxides are  mainly products  of  atmo-
spheric reactions (Chapter 6).
     In interpreting the  emissions  inventories to be presented throughout  this chapter, it is
important to  note that  NO   emissions  are  generally calculated as though  the compound being
emitted were N0?.  This method of presentation serves the purpose of allowing ready comparison
of different  sources.   Because  of  the  interconvertibility of NO and N0?  in photochemical  smog
reactions,  such  an approach  has some merit and avoids  the difficulty  in interpretation asso-
ciated with different ratios of N0/N02  being emitted  by different sources.   Two points, however,

                                          5-1

-------
should be  noted:   (1)  although NO  is  the  dominant NO  compound emitted  by  most sources, NO,
                                                      A                                      £
fractions  from  sources  do vary somewhat with  source  type and (2) conversion of NO  emissions
                                                                                   A
to N02 takes  place over spatial and temporal scales which vary with the particular local cir-
cumstances of atmospheric  pollutant mix, climatology  and  topography.   For these reasons, NO
emission  inventories  do not  necessarily accurately reflect  the potential  of various sources
for producing ambient N02 concentrations.
5,2.1  Global Sources of NO
     Table 5-1 presents historical estimates of the man-made global production of NO  (Robinson
and  Robbins,  1972,1975).   These  estimates  are based  on  1966 fuel  consumption  figures (U.S.
Bureau of  the Census,  1967)  and emission factors available in 1965 (Mayer, 1965).   From these
data, Robinson and Robbins (1975) estimated global NO  emissions from anthropogenic sources to
           6
be 48 x  10  metric tons per year  (expressed as N02).   These authors also estimated the ratio
of natural emissions of NO  from terrestrial  and  aquatic sources  to those from anthropogenic
                           A
sources  to be about  7  to 1.    An  earlier estimate by  Robinson and  Robbins (1972)  had set the
ratio of  natural  emissions  to anthropogenic emissions at  15  to  I.   The downward revision was
based on a 55 percent lower estimate of the amount of N02 emitted by natural sources.

          TABLE 5-1.   ESTIMATED ANNUAL GLOBAL EMISSIONS OF NITROGEN DIOXIDE (ANTHROPOGENIC)
                           (106 metric tons per year, expressed as N07)

Source
Total combustion and refining
Coal combustion
Petroleum refining
Gasoline combustion
Other oil combustion
Natural gas combustion
Other combustion
Emissions Emissions as N
48.0
24.4
0.6
6.8
12.8
1.9
1.5
14.6
7.4
0.2
2.1
3.9
0.5
0.5
% Total
100
51
1
14
27
4
3

         Source:   Robinson and Robbins, 1975.

     A different  estimate was provided  by  Soderlund and Svensson  (1976),  who  concluded that
the ratio of  NO   emissions from natural  sources to emissions from anthropogenic sources could
range  from  roughly 1:1  to 4 or 5:1.   It  is  clear that there  are  considerable uncertainties
associated with global  estimates  of natural NO  emissions  (Chapter 4).   In particular, esti-
mates of different authors on the magnitude of NO  emissions from soils vary greatly.   Defini-
tive experiments  have yet to be performed.
5.2.2  Sources of N0x in the United States
     Table 5-2 and Figure  5-1  provide  historical  data  on estimated emissions  of  N0x in the
United States for  the  years 1940 through 1970.  A significant upward trend  in  the two major
                                          5-2

-------
                            TABLE 5-2.  HISTORIC NATIONWIDE NOV EMISSION
                               6         ESTIMATES 1940-1970  X
                            (10  metric tons per year, expressed as N0)

Source Category
TRANSPORTATION
Motor vehicles
Aircraft
Railroads
Marine use
Nonhighway use
STATIONARY FUEL COMBUSTION
Electric utilities
Industrial combustion
Commercial
Residential
INDUSTRIAL PROCESS LOSSES
SOLID WASTE DISPOSAL
AGRICULTURAL BURNING
MISCELLANEOUS
Total
1940
2.9
2.7
0
0
0.1
0.2
3.2
0.5
1.8
0.1
0.9
0
0.1
0.2
0.7
7.1
1950
4.7
4.1
0
0.2
0.1
0.3
3.9
1.1
1.8
0.1
0.9
0.1
0.2
0.2
0.4
9.4
1960
7.2
6.6
0
0.1
0.1
0.4
4.7
2.1
1.6
0.2
0.8
0.1
0.2
0.2
0.2
12.7
1970
10.6
8.3
0.3
0.1
0.2
1.8
9.1
4.3
4.1
0.2
0.5
0.2
0.4
0.3
0.1
20.6

         NOTE:   A zero in this table indicates emissions of less than 50,000 metric
                tons/yr.   Some totals do not agree due to rounding off.
         Source:   Cavender et al.,  1973.

source categories,  transportation  and  stationary  fuel combustion,  is  discernible  over  this
30-year period.   Total NO  emissions almost tripled.   Recent emissions estimates, by year, for
1970  through  1976 are presented in  Table  5-3 and.Figure 5-2.   Emissions  from transportation
sources  increased  by about 20  percent  but emissions from  stationary fuel  combustion sources
and total emissions did not exhibit monotonic behavior.
     Minor discrepancies between Tables 5-2 and 5-3  for  the  year 1970  may be due to rounding
errors and/or  to  changes  in estimation  methods used  for  producing the  two tables.  It  is
believed, however, that trends assessment is reliable within each table.   The change in source
category nomenclature is also to be noted.
     Figure 5-3 shows  the  distribution  of NO  emissions by type of Air  Quality Control Region
(AQCR) for  1972.   Large urban  AQCR's,  i.e.  those having a Standard  Metropolitan Statistical
Area  (SMSA) population exceeding 1,000,000,  accounted for more  than  half  (53 percent) of the
NO  emissions.   The  population  in  these same SMSA's  was  only 38.5 percent of the  total  U.S.
  1\
population in 1970 (U.S.  Bureau of  the Census, 1973).

                                          5-3

-------
co
 o
 CO
 CO

 CO
 o
    25
    20
 S. .16
10
                          ALL OTHER SOURCES


                          (INDUSTRIAL, SOLID WASTE)
                                                STATIONARY FUEL


                                                COMBUSTION
                                 TRANSPORTATION SOURCES
             1940
                       1950
1960
                                                        1970
                                 YEAR
     Figure 5-1.  Historic NOX emissions by source groups. (Values

     shown for each year are cumulative over source groups.)



     Source:  Cavender et al. (1973).
                                    5-4

-------
TABLE 5-3.6 RECENT NATIONWIDE N0x EMISSION ESTIMATES
       (10  metric tons/yr, expressed as N09)

Source Category
TRANSPORTATION
Highway vehicles
Nonhighway vehicles
STATIONARY FUEL COMBUSTION
Electric utilities
Industrial
Residential, commercial
and institutional
INDUSTRIAL PROCESSES
Chemicals
Petroleum refining
Metals
Mineral products
Oil and gas production
and marketing
Industrial organic
solvent use
Other processes
1970
8.4
6.3
2.1
10.9
5.1
5.1

0.7
0.6
0.2
0.3
0
0.1

0

0
0
1971
8.9
6.7
2.2
11.2
5.4
5.1

0.7
0.6
0.2
0.3
0
0.1

0

0
0
1972
9.4
7.1
2.3
11.7
5.9
5.1

0.7
0.7
0.3
0.3
0
0.1

0

0
0
1973
9.7
7.3
2.4
12.1
6.3
5.1

0.7
0.7
0.3
0.3
0
0.1

0

0
0
1974
9.6
7.3
2.3
11.9
6.2
5.0

0.7
0.7
0.3
0.3
0
0.1

0

0
0
1975
9.9
7.6
2.3
11.2
6.1
4.5

0.6
0.7
0.3
0.3
0
0.1

0

0
0
1976
10.1
7.8
2.3
11.8
6.6
4.5

0.7
0.6
0.3
0.3
0
0.1

0

0
0
                  (continued)

-------
                                         TABLE 5-3.   (continued)

Source Category
SOLID WASTE DISPOSAL
MISCELLANEOUS
Forest wildfires and
managed burning
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic
solvent use
Totals
1970
0.3
0.2

0.1
0
0.1
0

0
20.4
1971
0.3
0.3

0.2
0
0.1
0

0
21.3
1972
0.2
0.2

0.1
0
0.1
0

0
22.2
1973
0.2
0.2

0.1
0
0.1
0

0
22.9
1974
0.2
0.2

0.1
0
0.1
0

0
22.6
1975
0.2
0.2

0.1
0
0.1
0

0
22.2
1976
0.1
0.3

0.2
0
0.1
0

0
23.0

NOTE:   A zero in this table indicates emissions of less than 50,000 metric tons/yr.



Source:   U.S.  EPA, 1977a.

-------
 I
(O
 o
 GO


 O

 00
 V)
O
z
     25
     20
15
     10
                ALL OTHER SOURCES (INDUSTRIAL, SOLID WASTE)
                      STATIONARY FUEL COMBUSTION
               I
                 I
                        TRANSPORTATION SOURCES
I
             1970   11971
                      1972    1973



                            YEAR
     1974   1975    1976
      Figure 5-2.  Recent I\IOX emissions by source groups. (Values

      shown for each year are cumulative over source groups.)



      Source: Sparks (1976).
                                      5-7

-------
/MEDIUM SIZED
URBAN A OCR'S
24%
SMALL URBAN/*
AQCR'S >^
\10% S
LARGE
URBAN
53%
AQCR Urbanization3
Large Urban
Medium-sized Urban
Small Urban
Rural
Total
Emissions,
106 tons/yr
11.71
5.30
2.36
2.88
22.25
        a. Urbanization is based on largest SMS A population
          in an AQCR:
             Large Urban = SMS A population 1,000,000
             Medium-sized Urban = SMSA population
              250,000-1,000,000
             Small Urban = SMSA population 50,000-250,000
             Rural = AQCR containing no SMSA

        b. Miscellaneous sources accounting for 160,000
          tons/yr are not included.
Figure 5-3.  Distribution of 1972 nationwide NOX emissions by
degree of urbanization (National Research Council, 1975).
                                5-8

-------
     A  clear  picture of the nationwide distribution of NO  emissions can be obtained from the
                                                          A
U.S'. maps reproduced in Figures 5-4 through 5-6.  Figure 5-4 shows total NO  emissions by U.S.
counties  as  compiled in the National Emissions Data System (NEDS) file of February 1978 (U.S.
EPA,  1978).   Regions  of  high  source concentrations are evident  near  populous and industrial
areas.  When the total NO  emissions per unit area (emission density) is plotted (Figure 5-5),
the  nationwide  distribution  tends to be more uniform than when emission totals alone are con-
sidered.  Areas of relatively high emission densities are still evident throughout the eastern
states  and the midwest and on the west coast.  The percent contribution of major point sources
to total NO  emissions is plotted by U.S. county in Figure 5-6.  Comparison of this figure and
           A                 -                                        .,   -
Figure  5-4  reveals that, in general,  major point sources make a  significant  contribution to
total NO  emissions in those areas where NO  emissions are high.  (In this discussion, a major
        A                                  X
point source is defined as one for which the yearly NO  emissions exceed 100 tons.)
     Table 5-4  documents  NO/NO   ratios in emissions from a variety of source types.  Examina-
tion of the  table  reveals that NO  is  the  dominant oxide of nitrogen  emitted  by most sources
with NO-  generally  comprising  less than 10  percent  of  the total  NO  emissions.  It is inter-
esting  to note, however, that NO,, forms upwards of 30 to 50 percent of the total NO  emissions
from certain  diesel  and  jet  turbine engines  under specific  load conditions.   Tail  gas  from
nitric  acid  plants,  if  uncontrolled,  may  contain  about 50 percent N02-   The  variations in
NO/NO   ratios by  source  type  reported in the table are possibly of some, significance in local
situations.   An example might be in the immediate vicinity of a high-volume roadway carrying a
significant number of  diesel-powered vehicles.   Situations of this type may assume increasing
importance in the  future  because  of the increasing  interest  in diesel-powered vehicles which
generally have greater fuel  economy than those with gasoline engines.
     The  national  trends  shown in  Figures 5-1  and  5-2 do not reflect  considerable  local  or
regional  differences  in the relative amounts  of  NO  emitted by the major  source  categories.
For example, motor vehicles  have  been estimated to contribute  approximately 90 percent of the
NO   emissions  in  Sacramento,  California  (California Department of  Public Health,  1966).   In
San  Francisco,  California, they  are  estimated to  contribute  about  56 percent  (California
Department of  Public Health,  1966), while  in  northwestern  Indiana the estimate is  8 percent
(Ozolins and Rehmann,  1968).  Motor vehicle emissions  in Los  Angeles  County,  California,  in-
creased 6-fold  from  1940  to  1970  (County of Los Angeles, 1971), compared to a 3-fold national
increase.
     While industrial process  losses (NO  emissions from noncombustion  industrial sources)  are
minor on  a  national  level, these emissions  can be important  near individual  sources.   Manu-
facturing of nitric acid,  explosives and fertilizers, and petroleum refining are the principal
activities 'in these source categories.
     Aircraft are  not considered a major source of NO  on the national  scale.   Their impact in
                                                     A
the  immediate  vicinity of major  airports  has  been discussed  recently (George  et  al.,  1972;
Jordan  and  Broderick,  1979).   Although  the total  NO   emissions associated with  landing  and
takeoff operations  at a large  airport can be several thousand tons per  year,  most NO  emissions

                                          5-9

-------
                                                                                 ONS  /  YERR
                                                                                  3.000 -
                                                                                 10.000 -
                                                                                 30.000
  <  3.000
   10.000
   30.000
- 100.000
> 100.000
Figure 5-4.  Total NOX emissions by U.S. county(U.S. EPA, 1978).

-------
en
i
                                                                                                                  TONS/SO  MI
                           Figure 5-5. Total NO
                                             x emission density by U S. county (U.S. EPA. t978,.

-------
Ul

I—'
r-o
PERCENT
                      Figure 5-6. Percent NOX emissions contributed by major point sources, by county (over 100 tons/yr)
                      (U.S. EPA, 1978).

-------
     TABLE 5-4.  NO/NO,, RATIOS IN EMISSIONS FROM VARIOUS SOURCE TYPES
 Source Type
                              NO/NO
                  Reference
Uncontrolled tail-gas from nitric
 acid plants

Petroleum refinery heaters--
 using natural gas
Linear ceramic tunnel kiln
Rotary cement kilns
Steel soaking pit—natural gas
Wood/bark boiler
Black liquor recovery boiler
Carbon monoxide boiler
Large 2-cycle internal combustion
 engine—natural gas
Combined cycle gas turbine

Gas turbine electrical generator—
 #2 fuel oil
                                            Gerstle and
                                            Peterson,  1966

                                            Hunter et  al.,
                                            1979
   * 0.50


  0.93-1.00
  0.90-1.00
  0.94-1.00
  0.97-0.99
  0.84-0.97
  0.91-1.00
  0.98-1.00

  0.80-1.00
  0.83-0.99
                            0.55-1.00       Wasser,  1976
                       (no load)-(full  load)
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
 #6 fuel oil
Industrial boi
 refinery gas
Diesel-powered
lers--natural  gas
lers--#2 fuel  oil
lers—PS 300 fuel
lers--#6 fuel  oil
lers—coal
lers--refinery gas
lers--natural  gas and

lers--natural  gas and

 passenger  car--Nissan'
Diesel-powered passenger car--
 Peugeot 204d
Diesel-powered passenger car--
 various Mercedes
Diesel-powered truck and bus--
 various engines

Mobile vehicles internal gasoline
 combustion engine
Aircraft turbines (JT3D, TF30)
  0.90-1.00
  0.95-0.99
   * 0.96
  0.96-1.00
  0.95-1.00
   * 0.95

   * 1.00

   * 1.00

  0.77-0.91
(idle)-(SOmph)
  0.46-0.99
(idle)-(50mph)

  0.88-1.00


  0.73-0.98


  0.99-1.00
Cato et al.
1976
Braddock and
Bradow, 1975
Springer and
Stahman, 1977a
                                            Springer  and
                                            Stahman,  1977b

                                            Wimmer  and
                                            Reynolds, 1962
                                            Campau  and
                                            Neerman,  1966
                            0.13-0.28(idle)dSouza  and
                            0.73-0.92        Daley,  1978
                         (takeoff &  cruise)
Earlier studies (Lozano et al.,  1968;  Chase and Hum,  1970)  did  not report
such high idle concentrations of NO,,.
                                5-13

-------
occur  during  approach,  takeoff and  climb  out,  distributing these emissions up  to  3,000 feet
above ground level and up to 10 miles from the airport.   Even though high NO^/NO  ratios occur
during  idle  of some  aircraft  turbines (Table 5-4),  total  emissions at idle are low.   It is
currently estimated that  high-altitude  emissions from existing and  projected  aircraft fleets
do not represent a significant source of NO  with respect to possible effects on stratospheric
ozone, although substantial uncertainties remain (Broderick, 1978).
     Factors influencing seasonal  variabilities in mobile source NO  emissions include tempera-
ture dependences  of emissions  per vehicle mile  (about  a 35 percent decrease in emissions for
an ambient temperature  increase  from 20 to 90°F) (Ashby et al., 1974), and changes  in vehicle
miles  travelled seasonally  (about  18 percent  higher in summer  than in  winter,  nationwide)
(Federal  Highway   Administration,   1978).   Further  differences exist  between   vehicle  miles
travelled in urban and rural areas and among states in different parts of the country (Federal
Highway Administration, 1978).  Variations in NO  emissions are also expected due to seasonal
variation in power production from fossil fuel generating plants,  which is estimated at 15 per-
cent on a  nationwide  basis (U.S.  Department  of  Energy,  1978).   Production is greatest in the
summer and  least  in  the spring.   Greater variations and different seasonal patterns have been
reported for  different areas of  the country (California Department  of  Public  Health,  1966).
Diurnal variations, notably those associated with motor vehicle traffic, are also important in
their potential impact upon ambient air quality.
     It should  also  be noted that  the  influence of the source categories  considered  in this
section upon ambient concentrations at a given location depends upon factors such as land use,
weather and  climate,  and  topography.   Emission  estimates have  other limitations as  well.
Aside from possible errors in establishing the emissions from each source, the spatial  distri-
bution of  sources  is  usually not well known, since the inventories usually cover large areas.
There  is very  little  temporal  resolution, which  can often  lead to  poor  understanding  of the
expected exposure.   Many  sources  are  intermittent.   Representing   such  a source  by  annual
emission  data,  therefore,   underestimates  the  potential   for short-term exposures.   Also,
meteorological   parameters  exhibit both  seasonal  and diurnal  variability, which can  greatly
affect the impact of particular sources on ambient pollution levels.
5.3  EMISSIONS OF AMMONIA
     On a  global  basis,  abiotic  emissions of ammonia (NH.,) represent only a small fraction of
the  total  emissions  of  NH.,  (National  Research Council,   1978;  Robinson and  Robbins,  1972;
Soderlund  and  Svensson, 1976).   Soderlund and  Svensson (1976) calculated that anthropogenic
                                                                c-            c.
emissions  (from coal  combustion)  accounted  for between 4  x  10  to  12 x  10  metric tons per
year.  A global loss of 7 x 10  metric tons NH3-N per year from inefficiencies in handling and
applying ammonia-based  fertilizers was  reported by the Council  for Agricultural  Science and
Technology  (CAST)  (1976).   A  recent report (National Research Council,  1978)  indicated that
the United States accounts for about 25 percent of the global use of ammonia-based fertilizer.
Another source  (National  Research Council, 1979) has reported estimated NH3 emissions for the
                                          5-14

-------
United  States  at  a much lower level, as shown in Table 5-5.  Discrepancies in these estimates
by  various  authors preclude  any firm  judgements  at this time as  to  NHL emissions resulting
from fertilizer usage.
                 TABLE 5-5.  ESTIMATED AMMONIA EMISSION FROM FERTILIZER APPLICATION
                          AND INDUSTRIAL CHEMICAL PRODUCTION IN U.S.  (1975)

Source of Emission
Ammonia Production
Direct application of
anhydrous ammonia
Ammonium nitrate
Petroleum refineries
Sodium carbonate
(Solvay process)
Di ammonium phosphate
Ammoni ator-granul ators
Urea
Miscellaneous emission from
fertilizer production
Beehive coke ovens
Total
Ammonia Emission
tons/yr
, 19,000
168,000
59,000
32,000
14,000
10,000
10,000
4,000
2,000
1,000
319,000
Rate
tons N/yr
15,600
138,400
48,600
26,400
11,500
8,200
8,200
3,300
1,600 _
800
262,600

         a"Direct application" is the term used in agriculture when a chemical
          fertilizer is applied to the soil without combining or mixing it with
          any other chemical.   Direct application of anhydrous ammonia involves
          transportation of ammonia to a storage area and to nurse tanks,  metering,
          and injection into soil.

         Source:   (National Research Council,  1979).


     In addition to volatilization of NH~ from use of fertilizers, emissions from feedlots may

represent a  significant local  and  regional source  of  ammonia.  A  National Research  Council

report on ammonia  indicated that 50 to 100 percent of the urea-nitrogen in urine generated in

feedlots  may  volatilize as ammonia (National  Research  Council, 1979).   As  urea  is  rapidly

hydrolyzed into NH,  and C00,  atmospheric contributions  of NH,, from feedlot-generated urine of
                                                                                          6
an estimated cattle  population  of  132 million in the United States could  amount to  2 x 10  to

4 x  10  metric tons  NhL-N per year.  This amount  is between one-fourth and  one-half  of the

rate of anthropogenic  emissions  of  nitrogenous compounds (excluding N«0)  to the atmosphere in

the United States  (National Research Council,  1978).

                                          5-15

-------
5.4  AGRICULTURAL USAGE OF NITROGENOUS COMPOUNDS
     Nitrogenous  material  applied  as fertilizer  participates  in  the  nitrogen  cycle via  a
variety of pathways  (Chapters  4 and 12).   Emissions of ammonia from agricultural  sources  have
been discussed  above  in  Section 5.3.   Excess fertilizer may  be of concern also:   (a) by  con-
tributing an  anthropogenically produced  burden  to stratospheric  concentrations  of  N^O  with
consequent potential  for  attenuation  of  the ozone layer (see Chapter 9) and (b) by contribut-
ing, through  run-off  from agricultural  lands, to both nitrate pollution of drinking water and
to changes in  natural  aquatic  ecosystems.  The data presented in Figure 5-7 and Table 5-6 are
intended to  place usage  of  nitrogenous   materials  applied  as fertilizer in the  U.S.  in  his-
torical perspective.   Examination of Table 5-6 reveals that the total  nitrogen applied as  fer-
tilizer has  increased  more  than a factor of  5  from 1955 to  1976.  Applications  of anhydrous
ammonia have increased more than 14-fold  and applications of nitrogen solutions have increased
more than fifty times in the same period.
5.5  SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS
     N-nitroso compounds  may be emitted  to the atmosphere  during their production or use, and
have been postulated  to  occur  by atmospheric formation  or  volatilization  from water or soil.
Additional  routes of  human  exposure to N-nitroso compounds may include drinking  water, foods
and tobacco products.
5.5.1  Anthropogenic Sources of N-Nitroso Compounds
     Possible direct anthropogenic sources of N-nitroso compounds include industrial processes
in which  these compounds  are  intermediate or  final  products, reactants or additives; or in
which they may occur incidentally as impurities.   While over 20 N-nitroso compounds are listed
as  products  in  recent commercial  directories  (Chem Sources,  1975,1977;  Stanford  Research
Institute,  1977), only four of  these were either sold in quantities over 1000 pounds yearly or
resulted in  annual  sales  over  $1,000.  Although the  patent  literature on  N-nitroso compounds
is sizeable,  many are currently synthesized only for research purposes.  The well-known toxic
and  carcinogenic  effects  of some  N-nitroso  compounds and  related regulatory actions  (U.S.
Department of Labor, 1974) have apparently discouraged their general use.
     The two  N-nitroso compounds  produced in greatest quantity, diphenylnitrosamine and dini-
trosopentamethylenetetramine, are used in the rubber industry as a vulcanizing retarder and a
blowing agent,  respectively  (Magee,  1972).   Neither has been found carcinogenic in laboratory
tests on male rats (Boyland et  al.,  1968).
     Several   less  direct  sources of  ambient  N-nitroso compounds have  been  postulated.   Some
samples of cured  meats,  fish and fish meal, soya bean oil  and tobacco have been shown to  con-
tain N-nitroso  concentrations   rarely  exceeding  1.0  ppm  (Fiddler,  1975; Ender et  al.,  1964;
Hedler, 1971; Hedler  et  al.,  1972;  Hoffman et  al.,  1974).   Release of small  quantities of N-
nitroso compounds may  occur  in the processing of such products.  Emissions occurring as a re-
sult of certain combustion processes have also been suspected.  Analysis for emissions of  nitro-
samines (usually only N-nitrosodimethylamine) has been carried out as part of research programs
                                          5-16

-------
 o
ID
 O
 a
 <
 GO
 D
                                            AMMONIUM NITRATE

                                            NITROGEN SOLUTIONS

                                            ANHYDROUS AMMONIA

                                            UREA
     1955
                  1960
1965


 YEAR
1970
1975
 Figure 5-7.   Trends in U.S. usage of nitrogenous material applied
    fertilizer (Gerstle and Peterson, 1966).
as
                                    5-17

-------
CJl
                          TABLE 5-6.   NITROGENOUS  COMPOUNDS  APPLIED AS FERTILIZER IN THE U.S.  1955-1976
                                                 (usage  in  10  tons  of material  )

Material Applied
Total N
Ammonium Nitrate
Anhydrous Ammonia
Aqua Ammonia
Nitrogen Solutions
Urea
Ammonium Sulfate
Sodium Nitrate
1955
1.96
1.12
.34
.23
.11
.07
.52
.62
1960
2.74
1.23
.71
.43
.65
.14
.53
.45
1965
4.64
1.63
1.56
.82
1.92
.43
.77
.30
1970
7.46
2.84
3.47
.70
3.24
.53
.78
.09
1973
8.30
3.28
3.41
.66
3.41
.96
.95
.06
1974
9.16
3.17
4.18
.72
4.05
1.03
.93
.05
1975
8.61
2.81
4.02
.70
4.11
1.15
.82
.08
1976
10.34
2.94
4.91
.68
5.55
1.62
1.04
.06

         aNumbers are rounded to two  decimal  places.
        Source:  Hargett,  1977.
CO

-------
involving automobiles, diesel engines, emission control systems, and fuels and fuel additives.
Tests  by  five  different groups using different techniques all produced negative results (U.S.
EPA, 1977d), although  Fine et al.  (1976a,  1976b,  1976c)  reported the presence of several un-
identified N-nitroso  compounds  in the exhaust of  a  truck diesel  engine and an automobile in-
ternal  combustion  engine.    No  firm explanation of  these different  results  can  be  given at
present.       .                 '
5.5.2  Volatilization from Other Media
     Some N-nitroso  compounds, particularly  those with low molecular weights,  may  reach the
atmosphere through volatilization from soil and water.  These compounds may be present in soil
or water as deposits or effluents from industrial or agricultural  sources, or may be formed d_e
novo from  appropriate precursors in water  or soil.   Nitrosamines have been  found in several
commercial herbicides (Fine and Ross, 1976) which,  upon application,  could be volatilized from
surface water  or  soil.   Volatilization may also occur from N-nitroso compounds formed jm situ.
Formation of N-nitroso  compounds  in soil and water  samples  has been demonstrated under labo-
ratory, conditions  (Ayanaba and Alexander, 1974; Ayanabe  et  al. ,  1973;  Elespuru and Lijinsky,
1973; Tate and Alexander, 1974; Wolfe et al.,  1976).   Most of these experiments involve pesti-
cides  or  pesticide ingredients  and nitrites, nitrates  or nitrous acid,  at  levels  which may
reasonably be  expected to  occur  in some  farming  or feedlot operations.   Direct  evidence is
lacking, however,  for the volatilization of N-nitroso compounds.
5.5.3  Atmospheric Formation:  N-Nitroso Precursors
     Possible  mechanisms   for  atmospheric  formation  of  N-nitroso  compounds  are  reviewed  in
Chapter 6.   In  addition  to the considerations presented  in  Chapter  6,  it has been postulated
that nitrosamines may  be  formed and emitted  from  industrial  processes  using amines to modify
fly-ash resistivity (U.S.  EPA,  1977d;  Cavanaugh et al., 1975).   A study,  however,  reported no
detection of nitrosamines  in emissions from a power plant using such amine additives (Sparks,
1976).
     In  general,   preliminary  considerations  of  the  atmospheric mechanisms  suggested  that
ambient concentrations of  nitrosamines  should be investigated  in  the  vicinity  of  emitters of
two classes  of  airborne precursors:   (1) oxides of  nitrogen,  nitrites,  and/or nitrates and (2)
amines, amides, or other related compounds (U.S.  EPA, 1977d).   Sources  leading to ambient con-
centrations  of the nitrogen  compounds  have been discussed above  in  Section 5.2.   With regard
to  the second  group,  the  only suspected  N-nitroso  precursors for which sources  have  been
extensively   documented  are  the amines.   As  of 1975,  at least  32  companies were  producing
various amines  (Chem  Sources,  1975).   Amines may  be emitted  directly from  these production
facilities,  and also may  be  emitted during subsequent use in many manufacturing processes and
products.   Amines have  been  identified in emissions  from decomposition  of livestock and poul-
try manure,  air sampled over  cattle  feedlots,  and  exhaust  from  rendering of  animal  matter
(Peters  and  Blackwood,  1977;  Shuval  and  Gruenar,  1972; U.S.  EPA,  1977d).   Volatility  and
                                          5-19

-------
water-solubility of  various amines results  in  extensive dispersal  of these  compounds  in the
atmosphere, water and soil (Walker et al., 1976).   Results of investigations of ambient concen-
trations of N-nitroso  compounds  in the vicinity of suspected sources are discussed in Section
8.3.  These investigations  have  failed to detect evidence of atmospheric N-nitroso formation.
5.5.4  N-Nitrosamines in Food,  Water and Tobacco Products
     This  section  reviews briefly  the major non-atmospheric" routes of human  exposure  to N-
nitroso  compounds  in order to place  possible  exposure via the atmospheric  route  in  perspec-
tive.
     A variety  of  raw  and processed foods have been tested for N-nitroso compounds.   A review
of earlier qualitative  studies was published by Sebranek  and  Cassens  (1973).  Scanlan (1975)
has summarized  a  number of the studies reported since 1970.   These  recent studies concentrate
on processed meats  and fish,  in  which  m'trosamines,  nitrosopiperidine  and nitrosopyrrolidine
have been  identified at  levels  usually  considerably  less than 1 ppm.   Raw  and  cooked  bacon
samples were found by several  investigators to contain 1.5 to 139 ppb nitrosopyrrolidine (NPY)
and 1.0  to  30  ppb dimethylnitrosamine (DMN) (Allison et al., 1972;  Crosby et al.,  1972;  Fazio
et al.,  1973;  Fiddler  et al.,  1974; Havery  et  al. ,  1976; Pensabene et  al., 1974;  Sen et al.,
1973a,1974).   Other  meat  products  (including luncheon meat, frankfurters  and other  sausages)
were found to  contain  3 to 105 ppb NPY, 1 to 94 ppb DMN, 2 to 25 ppb diethylnitrosaroine (DEN)
and 50 to  60  ppb nitrosopiperidine (NPi)  (Allison  et  al., 1972;  Fazio  et al., 1972;  Panalaks
et al.,  1973,1974;  Sen,  1972;  Sen et  al.,  1973b;  Wasserman  et al., 1972).  Raw and  processed
fish products  have  shown  1 to 26  ppb  DMN and  1 to 6 ppb NPY (Allison et al., 1972;  Crosby et
al., 1972; Fazio  et  al.,  1971),  with some fish meal samples  containing  as much as 450 ppb DMN
(Sen et al., 1972).   Cheese samples were found to contain up to 4 ppb DMN,  1.5 ppb DEN and 1.0
ppb NPY  (Allison  et  al. ,  1972; Crosby  et  al.,  1972).   Negative results have been obtained in
other tests for nitrosamines on many food samples,  including bacon,  ham  and other pork products,
fats and oils,  cheeses, and total diet samples  (Havery et al.,  1976).
     Contamination of  drinking water  with N-nitroso coumpounds may  occur  through  water-borne
emissions  from  the   industrial sources discussed  in  Section 5.5.1  or by  nitrosation  of pre-
cursors  found  in natural  bodies  of water  or  water  supply  and treatment  systems  (U.S.  EPA,
1977b,1977c,1977d).   N-nitroso  compounds  have  been  found  in  industrial  wastewater, and in
samples  taken  from  water  near industrial  facilities.   Nitrosation   in lake  water  samples has
been demonstrated in the laboratory (Ayanaba and Alexander, 1974).   Analyses of drinking water
have either failed  to  detect  N-nitroso compounds  or  have  shown concentrations in the 0.1 ppb
range (Fine et al.,   1976b,1976c).
     There may  be  significant  exposure to N-nitroso compounds  in use  of cigarettes  and other
tobacco products.  Mainstream smoke of blended unfiltered U.S.  cigarettes was found to contain
the following  N-nitroso  compounds  (amounts in nanograms per cigarette):   nitrosodimethylamine
(84),  nitrosoethylmethylamine  (30),  nitrosonornicotine  (137),  and  nitrosodiethylamine (<5)
(Hoffman et al.,  1975).   N'-nitrosonornicotine  found in a variety of chewing tobacco products
                                          5-20

-------
indicates that  such  unsmoked products may  also  be  sources of exposure to N-nitroso compounds
(Hoffman et al., 1974).
5.6  SUMMARY
5.6.1  Sources  and Emissions of NQ^
                               ,   A
     Oxides of  nitrogen have their origin in a number of natural (Chapter 4) and anthropogenic
processes.  Since  various  authors differ greatly in  their estimates  of natural emissions, it
is  difficult  to assess with any  certainty  the fraction of total  global  NO   emissions origi-
nating from human  activities.   In terms of sources giving rise to significant human exposure,
however, the  most  important emissions occur as a result of man's burning of fossil fuels such
as coal, oil or gasoline.   Mobile combustion and fossil-fuel stationary combustion are the two
largest source  categories, comprising about 44 percent and 51 percent of the nationwide anthro-
pogenic  NO   emissions, respectively,  1976.   In the  stationary  combustion  category,  electric
utilities were  responsible  for  approximately  56 percent  of  the  anthropogenic  NO  emissions,
                                                                                  A
and industrial  combustion accounted for another 38 percent.  In the mobile combustion category,
highway  vehicle  emissions  comprised  about  77  percent,  with  the  rest  attributable  to
non-highway vehicles.   In  addition,   non-combustion  industrial  processes  such  as  petroleum
refining and  manufacture  of nitric acid, explosives and fertilizers may produce quantities of
NO  which, while minor on a national basis,  may be significant near individual sources.
  A
     In most  ambient  situations  nitrogen dioxide (NO,), the  NO   compound of most concern for
human health  and welfare,  is not emitted directly  into  the atmosphere in significant amounts
(typically less than 5 percent of NO  emissions occur as N02).  It arises mainly from the oxi-
dation in  the atmosphere of the  more commonly emitted compound nitric  oxide  (NO).   However,
some minor  source  types,  notably a number of diesel and jet turbine engines do, under certain
load conditions, emit a significant fraction of their NO  emissions as NOp.
     In general, the relationship between the magnitude of NO  emissions and resulting ambient
NOo concentrations  is neither direct nor constant.   The influence of sources upon ambient con-
centrations  at  a given location  depends not only on  details  of the emissions from the source
but also upon  such  factors  as the presence  or  absence of other atmospheric constituents such
as hydrocarbons and ozone,  as well as  land use, weather and climate, and topography.
     Estimates  of  historical  emissions  for the years  1940 through 1970 indicate  that  total
anthropogenic  emissions  of  NO   almost tripled during that period.  More recently,  emissions
from transportation sources increased  by about 20 percent from 1970 to 1976,  but emissions from
stationary combustion  sources  and total  emissions  did not exhibit a monotonic  upward trend.
Examination  of  NO  emissions  inventories by U.S. county reveals  that,  in general,  both  point
                 A
and area sources  contribute  significantly in those places where total  NO  emissions are high.
                                                                         A
There are, however,  considerable  local  or regional differences in the  relative amounts of NO
emitted by  the major source categories.   For  example,  motor vehicles  have been  estimated to
contribute approximately 90  percent  of  the NO  emissions in Sacramento,  California, while the
                                              A
corresponding statistic in northwestern  Indiana is only  8 percent.   Emissions  may also exhibit
                                          5-21

-------
a significant diurnal  and/or seasonal  variability.   The seasonal  variation in power production
from fossil  fuel  generating  plants,  e.g.,  is about 15 percent on a nationwide basis.   Diurnal
variations in traffic  volume usually lead to marked daily emission profiles for mobile sources.
Representing such sources  by  annual  emissions data only may underestimate their potential  for
producing high short-term concentrations.   Meteorological variables also exhibit both seasonal
and diurnal  variability, which  can greatly affect the impact of particular sources on ambient
pollution levels.
5.6.2  Sources and Emissions of Other Nitrogenous Compounds
     Principal anthropogenic sources of ammonia (which some researchers have suggested is con-
verted to NO  in the atmosphere) include coal combustion, inefficiencies in handling and apply-
            A.
ing ammonia-based fertilizers,  and volatilization of the urea-nitrogen in animal urine gener-
ated in  feedlots.   The  last  source has  been estimated to contribute  between  one-fourth  and
one-half  of  all  the  anthropogenically  produced nitrogenous  compounds emitted  yearly  to  the
atmosphere in the United States (N?0 is not included in this estimate).
     The use of nitrogen-based fertilizer (which some researchers have implicated in increased
N?0  emissions  leading  to  possible  depletion  of  the  stratospheric  ozone  layer)  has  risen
markedly  in  the  last  two decades  in the United States.   The total nitrogen applied as ferti-
lizer has  increased by  more  than  a factor  of 5 from 1955 to 1976.  Applications of anhydrous
ammonia have increased more than 14-fold and applications of nitrogen solutions have increased
more than 50  times  during  the  same  period.   However,  recent estimates  of the  effects  of
increased N?0 on  stratospheric  ozone  indicate a much smaller effect than previously suspected
(Chapter 9).
     Possible direct  atmospheric  sources  of N-nitroso compounds (some of which are known car-
cinogens) include industrial  processes  in which these compounds are intermediate or final pro-
ducts,  reactants or additives,  or may  occur  incidentally  as  impurities.   Other than NO ,  the
only proposed N-nitroso  precursors for which sources have been extensively documented are  the
amines.   Amines have  been  identified  in emissions from decomposition of livestock and poultry
manure,  air  sampled over cattle feedlots,  and exhaust from rendering of animal matter.   There
is, however,  little or  no  evidence to date  to  indicate that the  atmospheric  route for human
exposure to nitrosamines is a cause for concern (Chapter 8).
                                          5-22

-------
 5.7  REFERENCES

 Allison,  T.  G., G.  B.  Cox,  and R.  S.  Kirk.   The determination of steam-volatile N-nitrosamines
      in  foodstuffs  by  formation  of  electron-capturing  derivatives from  electrochemically
      derived amines.  Analyst (London) 97:915-920, 1972.

 Ashby,  H. A.,  R.  C.  Stahman, B.  H.  Eccleston  and R.  W. Hum.  Vehicle  emissions—summer to
      winter.    Presented  at   the   Automobile  Engineering  Meeting,  Society  of  Automotive
      Engineers, Toronto,  Canada,  October 21-24,  1974.   SAE technical paper no.  741053.

 Ayanaba,  A.   and M.  Alexander.   Transformation  of  methylamines and  formation  of a hazardous
      product, dimethylnitrosamine, in  samples  of treated sewage and  lake water.   J.  Environ.
      Qual.  3:83-89,  1974.

 Ayanaba,  A. , W. Verstraete,  and  M.  Alexander.   Formation of dimethylnitrosamine,  a carcinogen
      and  mutagen,  in  soils  treated  with nitrogen  compounds.   Soil  Sci.  Soc.  Am.  Proc.  37:
      565-568, 1973.

 Boyland,  E.,  R.  L.  Carter,  J.  W.  Gorrod, and F.  J.  C.  Roe.   Carcinogenic properties of certain
      rubber.additives.   Eur.  J.  Cancer 4:233-239, 1968.

 Braddock, J.  N.,   and  R.  L.   Bradow.   Emissions patterns  of  diesel-powered passenger  cars.
      Presented at the Fuels  and  Lubricants  Meeting, Society of Automotive Engineers,  Houston,
      TX,  June 3-5,  1975.   SAE technical paper no. 750682.

 Broderick, A. J.   Stratospheric effects from aviation.   J.  Aircr.  15:643-653, 1978.

 California  Department of Public Health.   The Oxides of  Nitrogen in Air Pollution.  California
      Department of  Public Health,  Bureau of  Air Sanitation,  Berkeley, CA,  January  1966.

.rCampau, R. M.,  and  J.  C.  Neerman.   Continuous mass  spectrometric determination of  nitric  oxide
      in  automotive  exhaust.    Presented at  the Automotive  Engineering  Congress,  Society of
      Automotive Engineering,   Detroit,  MI,   January  10-14, 1966.   SAE  technical  paper  no.
      660116.

 Cato,  G.  A., L. J.  Muzio,  and D.  E.  Shore.   Field  Testing:   Application of Combustion Modifi-
      cations  to Control  Pollution  Emissions  from Industrial Boilers—Phase II.   EPA-600/2-76-
      086a,  U.S.  Environmental Protection  Agency,  Research Triangle  Park,  NC,  April  1976.

 Cavanaugh, G.,  C.  E.  Burklin,  J.  C.  Dickerson,  H. E.  Lebowitz,  S.  S. Tan,  G.  R.  Smithson, Jr.,
      H.  Nack, and J. H.  Oxley.   Potentially Hazardous  Emissions  from the Extraction  and Pro-
     .cessing   of  Coal   and  Oil.    EPA-650/2-75-038,  U.S.  Environmental  Protection  Agency,
      Research Triangle Park,  NC,  April 1975.

 Cavender, J.  H. , D. S.  Kircher,  and A. J.  Hoffman.   Nationwide Air Pollutant Emission Trends
      1940-1970.   AP-115,  U.S. Environmental  Protection Agency,  Research Triangle Park,  NC,
      January  1973.

 Chase,  J. 0.,  and  R.  W.  Hum.  Measuring gaseous  emissions from an  aircraft turbine  engine.
      Presented  at the  National Air  Transportation Meeting, Society  of Automotive  Engineers,
      New  York,  NY,  April  20-23, 1970.   SAE technical  paper no.  700249.
                                              5-23

-------
Chem Sources - USA.   Directories Publishing Company, Flemington, New Jersey, 1975.

Chem Sources - USA.   Directories Publishing Company, Flemington, New Jersey, 1977.

Council for  Agricultural  Science  and Technology.   Effect  of  Increased  Nitrogen Fixation on
     Stratospheric Ozone.   CAST Report  No.  53, Council  for  Agricultural  Science and Techno-
     logy, Iowa State University, Ames, IA, January 1976.

County of Los Angeles.   Profile of Air Pollution Control. County of Los Angeles, Air Pollution
     Control District,  Los Angeles, CA, 1971.

Crosby, N.  T. ,  J.  K. Foreman,  J.  F.  Palframan, and R.  Sawyer.   Estimation of steam-volatile
     N-nitrosamines  in  foods at the 1 mg/kg level.  Nature (London) 238:342-343, 1972.

Elespuru,   R.  K. , and  W.  Lijinsky.    The. formation  of  carcinogenic  nitroso  compounds from
     nitrite  and  some  types  of  agricultural  chemicals.   Food Cosmet.  Toxicol.  ll.:807-817,
     1973.

Ender,  F. ,  G.  Havre,  A.  Helgebostad,  N.  Koppang,  R.  Madsen,  and  L.   Ceh.   Isolation and
     identification   of  a  hepatotoxic  factor  in  herring meal  produced  from  sodium nitrite
     preserved herring.   Naturwissenschaften 5_1: 637-638, 1964.

Fazio, T.  ,  R.  H.  White,  and J. W.  Howard.  Analysis of nitrite-and/or nitrate-processed meats
     for N-nitrosodimethylamine.  J.  Assoc. Off. Anal.  Chem.  54:1157-1159,  1972.

Fazio, T.  ,  R.  H.  White,  L.   R.  Dusold,  and J. W. Howard.  Nitrosopyrrolidine in cooked bacon.
     J. Assoc. Off.  Anal.  Chem. 56:919-921, 1973.

Fazio, T. ,  J. N. Damico,  J.  W.  Howard,   R.  H. White, and J.  0.  Watts.   Gas chromatographic
     determination and  mass  spectrometric  confirmation  of N-nitrosodimethylamine  in smoke-
     processed marine fish.   J. Agric. Food Chem. 19:250-253, 1971.

Federal Highway Administration.   Traffic Volume  Trends, Tables  5A,  5B,  and  9A.   November-
     December  1978.    Computer  Printout  available from  Highway Statistics  Division,  400 7th
     St.,  SW, Washington, D.C., 20590.

Fiddler,  W.   The  occurrence  and  determination  of  N-nitroso  compounds.  Toxicol.  Appl.
     Pharmacol. 31:352-360,  1975.

Fiddler, W. , J. W. Pensabene, J. C. Fagan, E. J. Thome, E. G.  Piotrowski,  and A. E. Wasserman.
     The  role of  lean  and  adipose   tissue  on the  formation  of  nitrosopyrrol idine  in fried
     bacon.  J. Food Sci.  39:1070-1071, 1974.

Fine,  D.  H.  and D.  Ross.    Paper presented  at the  American  Chemical  Society  Meeting,  San
     Francisco, California,  September  1976.   Cited In:  Rawls, R.  L.   Nitrosamines found in
     commercial pesticides.   Chem.  Eng. News 54:33-34, 1976.

Fine,  D.  H.,  D.  P.  Rounbehler, and N. M.  Belcher.  N-nitroso compounds:   detection in ambient
     air.   Science (Washington, D.C.) 192:1328-1330, 1976a.

Fine,  D.  H. ,  D.  P.  Rounbehler, N. M.  Belcher, and S.  S. Epstein.  N-nitroso compounds  in air
     and water.  Jji:   Environmental N-nitroso Compounds Analysis and Formation, Proceedings of
     a Working Conference, International Agency for Research on Cancer, Tallinn, Estonian SSR,
     October  1-3, 1975.   E.  A. Walker,  P.  Bogovski,   L.  Griciute,  and  W.  Davis,  eds. , IARC
     Scientific  Publications  No.  14,  International  Agency  for Research on  Cancer,  Lyon,
     France, 1976b.   pp.  401-408.
                                             5-24

-------
Fine,  D.  H. ,  D.  P. Rounbehler,  N.  M.  Belcher, and  S.  S.  Epstein.   N-nitroso  compounds  in  the
     environment.   In:   International  Conference  on  Environmental  Sensing  and  Assessment,
     Volume  2,  A  Joint  Conference Comprising  the International  Symposium on  Environmental
     Monitoring  and  the  Third  Joint  Conference  on Sensing  Environmental  Pollutants,  World
    . Health Organization  and Others, Las Vegas,  Nevada,  September 14-19, 1975.   Institute of
     Electrical  &  Electronics Engineers,  Inc., New  York,  NY, 1976c.   session 30-7.

George,  R.  E. , J.  S.   Nevitt, and  J.  A.  Verssen.   Jet  aircraft  operations:  impact on  the  air
     environment.  J.  Air Pollut.  Control Assoc.  22:507-515, 1972.

Gerstle,  R.  W. ,  and   R.  F.  Peterson.   Atmospheric  Emissions  from  Nitric Acid  Manufacturing
     Processes.  Public  Health  Service Pub. No. 999-AP-27, U. S.  Department of  Health,  Educa-
     tion, and Welfare, Cincinnati, OH, 1966.

Hargett,  N.  L.  1976  Fertilizer  Summary  Data.   Bulletin  Y-112,  Tennessee Valley  Authority,
     National  Fertilizer Development Center, Muscle  Shoals, AL,  March,  1977.

Havery,  D.  C., D.  A.   Kline,  E.  M. Miletta, F.  L.  Joe, Jr.,  and  T.  Fazio.   A survey of food
     products  for  volatile  N-nitrosamines.   J.  Assoc.  Off.  Anal.  Chem.  59:540-546,   1976.

Hedler,  L.  A  possible method for  the detection of  nitrosamines in  fats  and oils.   J. Am.  Oil
     Chem. Soc.  48:329A, 1971.

Hedler,  L. ,  H.  Kaunitz,  P.  Marquardt, H.  Fales, and  R.  E. Johnson.   Detection of  N-nitroso
     compounds by  gas  chromatography  (nitrogen detector)  in  soyabean  oil  extract.  _In:   N-
     nitroso Compounds Analysis and  Formation,  Proceedings of  a Working Conference,   Inter-
     national  Agency  for Research on  Cancer,  Heidelberg, Germany,  October 13-15,  1971.   P.
     Bogovski, R.  Preussmann,  E.  A. Walker, and  W.  Davis, eds.,  IARC  Scientific  Publications
     No.  3,  International  Agency  for  Research  on Cancer,  Lyon, France,  1972.   pp.   71-73.

Hoffman, D. , G.  Rathkamp,  and Y.  Y. Lin.   Chemical studies on  tobacco smoke.   XXVI.  On  the
     isolation and identification  of volatile and  non-volatile  N-nitrosamines and  hydrazines
     in  cigarette   smoke.    In:   N-nitroso  Compounds   in  the  Environment,  Proceedings  of  a
     Working Conference,  International  Agency  for  Research on  Cancer, Lyon,  France, October
     17-20, 1973.  P.   Bogovski, E.  A. Walker, and W. Davis, eds.,  IARC  Scientific  Publications
     No.  9,  International  Agency  for  Research  on  Cancer, Lyon,  France, 1975.   pp. 159-165.

Hoffman,  D. ,  S.  S. Hecht, R. M. Ornaf,  and E.  L.  Wynder.   N'-nitrosonornicotine  in tobacco.
     Science (Washington, D.C.) 186:265-267, 1974.

Hunter,  S. C. , W.  A.  Carter, M. W.  McElroy, S.  S.  Cherry, and  H. J. Buening.   Application of
     Combustion  Modifications to  Industrial  Combustion   Equipment.   EPA-600/7-79-015a, U.S.
     Environmental  Protection Agency, Research Triangle Park, NC,  January  1979.

Jordan,  B. C., and A.  J.  Broderick.  Emissions  of oxides of nitrogen  from aircraft.  J.  Air
     Pollut.  Control Assoc.  29:119-124, 1979.

Lozano, E. R., W. W.  Melvin, and S. Hochheiser.  Air pollution emissions  from jet engines.   J.
     Air Pollut.  Control Assoc.  18:392-394,  1968.

Magee,   P.  N.   Possibilities  of hazard from  nitrosamines  in industry.   Ann.  Occup.  Hyg.  15:19-
     22, 1972.
                                             5-25

-------
Mayer, M.   A  Compilation of Air Pollution Emission Factors  for Combustion  Processes,  Gasoline
     Evaporation,  and  Selected  Industrial  Processes.   U.S.  Department of Health,  Education,
     and Welfare, Public Health Service, Cincinnati, OH, May 1965.

National Research  Council.   Air Quality and  Stationary  Source Emission Control.   A Report  by
     the Commission  on  Natural  Resources,  National Academy of  Sciences,  National  Academy  of
     Engineering,  National   Research  Council.   Serial  No.  94-4,  U.S.  Senate,  Committee  on
     Public Works, Washington, DC, March 1975.

National  Research  Council.    Nitrates:   An  Environmental  Assessment.  National  Academy  of
     Sciences, Washington, DC, 1978.

National Research Council.  Ammonia.   University Park Press,  Baltimore, MD,  1979.

Ozolins, G. and  C.  Rehmann.   Air Pollution Emission Inventory of Northwest Indiana.   A  Preli-
     minary Survey.   National Center  for Air  Pollution  Control Publication APTD-68-4,  U.S.
     Department  of  Health,   Education  and Welfare,  Public   Health  Service,  Bureau  of Disease
     Prevention and Environment Control, Durham, NC, April 1968.

Panalaks, T.,  J.  R. lyengar, and N. P. Sen.    Nitrate, nitrite  and dimethylnitrosamine  in cured
     meat products.  J. Assoc. Off. Anal. Chem.  56:621-625,  1973.

Panalaks, T. , J.  R.  lyengar, B. A. Donaldson,  W.  F.  Miles,  and N.  P.  Sen.   Further survey  of
     cured  meat  products  for volatile N-nitrosamines.  J. Assoc. Off.  Anal.  Chem.  57:806-812,
     1974.

Pensabene,  J.  W.  , W.  Fiddler, R. A. Gates, J.  C. Fagan, and  A. E. Wasserman.  Effect of  frying
     and other   cooking  conditions on  nitrosopyrrolidine formation  in bacon.    J.  Food  Sci.
    .39:314-316,  1974.

Peters, J.   A. and T.  R. Blackwood.   Source  Assessment:   Beef Cattle Feedlots.   EPA-600/2-77-
     107, U.S. Environmental Protection Agency,  Research Triangle Park, NC, June  1977.

Robinson,  E. ,  and R.  C.  Robbins.   Emissions, concentrations  and fate  of gaseous  atmospheric
     pollutants.   If}-.   Air  Pollution  Control, Part II.   W.  Strauss,  ed. , Wiley-Interscience,
     New York, NY, 1972.  pp. 1-93.

Robinson,  E. ,  and  R.   C.  Robbins.   Gaseous  atmospheric  pollutants  from urban  and natural
     sources.   J_n:  The  Changing Global Environment.   S. F.  Singer, ed., D.  Reidel  Publ.  Co.,
     Boston, MA,  1975.   pp.  111-123.

Scanlan, R. A.  N-nitrosamines in food.  CRC  Crit.  Rev. Food  Technol. 5:357-402,  1975.

Sebranek, J.  G.  and  R.  G. Cassens.  Nitrosamines:   a review.  J. Milk  Food Technol. 3_6:76-91,
     1973.

Sen,  N.  P.   The  evidence  for the presence  of dimethylnitrosamine  in meat products.    Food
     Cosmet. Toxicol.  10:219-223, 1972.

Sen, N.  P., B.  Donaldson, J.  R.  lyengar,  and T.  Panalaks.   Nitrosopyrrolidine and dimethyl-
     nitrosamine  in bacon.  Nature (London) 241:473-474, 1973a.

Sen, N. P., J. R. lyengar, B. A. Donaldson,  and T.  Panalaks.   Effect of sodium  nitrite concen-
     tration  on  the  formation  of  nitrosopyrrolidine and  dimethylnitrosamine in fried  bacon.
     J. Agric. Food Chem. 22:540-541,  1974.

                                              5-26

-------
Sen, N.  P.,  L.  A.  Schwinghamer,  B.  A.  Donaldson, and W. F. Miles.  N-nitrosodimethylamine  in
     fish meal.   J. Agric. Food Chem. 20:1280-1281, 1972.

Sen, N.  P.,  W.  F.  Miles, B.  Donaldson,  T.  Panalaks, and J.  R.  lyengar.   Formation of  nitro-
     samines in a meat curing mixture.  Nature (London)  245:104-105, 1973b.

Shuval,  H.  I.,  and  N.  Gruener.   Epidemiological and  toxicological  aspects  of  nitrates and
     nitrites in the environment.  Am. J. Public  Health  62:1045-1052, 1972.

Soderlund, R. and  B.  H.  Svensson.  The global nitrogen  cycle.  In:  Nitrogen, Phosphorus, and
     Sulfur-Global  Cycles:  SCOPE  Report No. 7.   Ecol.   Bull. (227:23-73,  1976.

Souza, A. F. , and  P.  S.  Daley.   U.S.  Air Force  Turbine Engine  Emission  Survey.   Volume III.
     Engine  Model   Summaries.    CEEDO-TR-78-34,   U.S.  Air  Force  Systems  Command,  Civil  and
     Environmental  Engineering  Development Office,  Tyndall Air  Force  Base,  FL,  August 1978.

Sparks,  L. E.   Effect  of a Flyash Conditioning Agent on Power Plant Emissions.  EPA-600/7-76-
     027, U.S.  Environmental  Protection  Agency, Research  Triangle  Park, NC,  October 1976.

Springer, K.  J. ,  and R.   C.  Stahman.   Diesel car emissions—emphasis  on  particulate and sul-
     fate.   Presented  at  the International  Automotive  Engineering Congress  and Exposition,
     Society of Automotive  Engineers, Detroit,  MI, February 28-March 4, 1977a.  SAE technical
     paper no.  770254.

Springer, K.  J.,  and  R.  C.   Stahman.   Unregulated  emissions from  diesels  used  in trucks and
     buses.   Presented  at the  International  Automotive Engineering  Congress and Exposition,
     Society Automotive  Engineers, Detroit,  MI,  February  28-March 4, 1977b.   SAE technical
     paper no.  770258.

Stanford  Research  Institute.   1977 Directory of  Chemical Producers—United States of America.
     Stanford Research  Institute, Chemical  Information Services,  Menlo  Park,  CA, 1977.  pp.
     716-717, 824-825,  and 848-849.

Tate,  R.  L.  and M.  Alexander.    Formation  of dimethyl amine and  diethyl amine in  soil  treated
     with pesticides.   Soil Sci. 118:317-321, 1974.

U.S. Bureau of the  Census.  Statistical Abstract  of the  United States:   1967.   U.S. Department
     of Commerce, Washington, DC, 1967.

U.S. Bureau  of  the Census.   City and  County Data Book, 1972.   U.S.  Department  of Commerce,
     Washington, DC,  1973.

U.   S.  Department of  Energy.   Energy  Data  Reports.  DOE/EIA-0049/1, U.S. Department of Energy,
     Washington, DC,  May  1978.

U.   S.  Department  of  Labor.   Occupational  safety  and  health standards:   carcinogens.   Fed.
     Regist.  39:3756-3797, January 29, 1974.

U.   S.  Environmental  Protection Agency.   National  Air  Quality  and Emissions  Trends  Report,
     1976.  EPA-450/1-77-022,  U.S.  Environmental  Protection Agency,  Research Triangle Park,
     NC,  December 1977a.

U.  S. Environmental Protection Agency.  Reconnaissance of Environmental Levels of Nitrosamines
     in  the  Central  United  States.   EPA-330/1-77-001,   U.S.  Environmental Protection Agency,
     Denver,  CO, February 1977b.

                                             5-27

-------
U. S.  Environmental  Protection Agency.  Reconnaisance of Environmental  Levels of  Nitrosamines
     in  the  Southeastern  United   States.   EPA-330/1-77-009,  U.S.  Environmental  Protection
     Agency, Denver, CO, August 1977c.

U. S.  Environmental  Protection Agency.  Scientific  and  Technical  Assessment Report  on  Nitro-
     samines.  EPA-600/6-77-001, U.S.  Environmental  Protection Agency, Research  Triangle Park,
     NC, June 1977d.

U. S. Environmental Protection Agency.  Data extracted from the National  Emissions  Data  System
     (NEDS),  maintained by  the  EPA  National  Air Data  Branch,  Durham,  N.C.,  February  1978.

Walker,  P.,  J.  Gordon,  L.  Thomas,  R.  Ouellette.   Environmental  Assessment  of  Atmospheric
     Nitrosamines.  EPA  Contract  No.  68-02-1495, The MITRE  Corporation, McLean, VA,  February
     1976.

Wasser, J.  H.  Emission characteristics of small gas turbine engines.  In:   Proceedings  of  the
     Stationary  Source  Combustion  Symposium,   Volume  III:   Field Testing  and  Surveys, U.S.
     Environmental  Protection  Agency,  Research Triangle  Park,   NC,  September  24-26,   1975.
     EPA-600/2-76-152c, U.S. Environmental Protection Agency, Research Triangle  Park,  NC, June
     1976.   pp. IV-227-IV-253.

Wasserman,  A. E., W. Fiddler, R. C. Doerr, S. F. Osman,  and C. J.  Dooley.  Dimethylnitrosamine
     in frankfurters.   Food Cosmet. Toxicol. 10:681-684, 1972.

Wimnier,  D.  B. ,  and  L.  A.  McReynolds.   Nitrogen oxides  and  engine  combustion.   SAE  Trans.
     70:733-744,  1962.

Wolfe,  N.  L. , R.  G.  Zepp,  J.  A.   Gordon,  and  R. G.  Fincher.   N-nitrosamine  formation from
     atrazine.  Bull.  Environ. Contam. Toxicol.  15:342-347, 1976.
                                             5-28

-------
                        6.  ENVIRONMENTAL TRANSPORT AND TRANSFORMATION

     This chapter  is  an assessment of the atmospheric behavior of the oxides of nitrogen.   It
is  concerned  with the  processes  and  mechanisms  that govern  the  dispersion and geographical
movement  of  the oxides  of nitrogen  from  their sources, the  chemical  and  physical  transfor-
mations  that  may occur within  the atmosphere or in  removal  processes,  atmospheric  residence
times, and removal mechanisms.
     The  predominant  form of the  oxides  of  nitrogen emitted  to the  atmosphere  from man-made
sources  is nitric  oxide.   In the atmosphere, nitric oxide is converted chemically to a number
of  secondary  products,  including  nitrogen dioxide,  nitrites,  nitrates,  and nitrosamines.   In
addition, nitric oxide emissions contribute chemically to ozone formation.  The chemical trans-
formation of  the oxides  of  nitrogen  to  these  secondary products  occurs  simultaneously with
transport and  removal.   The  object of this chapter  is to provide a brief survey of the trans-
formation and  transport  of nitrogen oxides.   Appropriate references  are  provided  for further
detail.   Section 6.1  is  devoted  to  the  chemistry of  the  oxides of  nitrogen  in  the  lower
atmosphere.    The reactions involving  oxides  of nitrogen are  first summarized  and discussed.
Then,  laboratory evidence on  the  relationship between  NO-  levels and precursors  is  cited.
Chemical  reactions occurring in plumes and computer  simulation of atmosphere chemistry are  dis
cussed.  The  formation  of nitrites and nitrates is  surveyed in Section 6.2.  Section 6.3 dis-
cusses the transport and removal of nitrogenous  species and currently  available  techniques  for
predicting atmospheric  NOp  concentrations when  sources of  NO   are  known  (source-receptor
relations).   Section 6.4 is devoted to the chemistry of nitrosamine formation.
6.1  CHEMISTRY OF THE OXIDES OF NITROGEN IN THE  LOWER ATMOSPHERE
     Solar radiation  triggers a series of reactions in the  atmosphere between gaseous organic
molecules and nitrogen oxides,  producing a wide  variety of secondary pollutants.   The totality
of primary and secondary pollutants involved  in  these photochemical reactions is  known as phot
chemical  smog.  To understand the chemistry of the oxides of nitrogen  in the lower  atmosphere,
it  is  necessary  to  consider the interactions that  take  place between the  oxides  of nitrogen
and  organic  constituents.   Several  reviews  of  atmospheric chemistry  are  available  (Heiklen,
1976; Seinfeld, 1975;  Stern,  1976), as are detailed  discussions of  reaction mechanisms (Baldwi
et  al.,  1977;  Carter  et at. ,  1979; Demerjian et  al.,  1974;  Falls  and Seinfeld,  1978; Whitten
and Hogo, 1977)  and  rate constants (Hampson  and Garvin,  1978).  In this section the  chemistry
of the oxides of nitrogen in the lower atmosphere  is briefly reviewed.   The above-cited refer-
ences should  be consulted for more  detail.
     Most of  the  chemistry that occurs in a  sunlight-irradiated urban atmosphere involves  the
interaction  of a variety of unstable, excited molecules and  molecular  fragments  that  have only
a transitory  existence.   These species  include:  the unexcited and  first  excited electronic
                                                     3                                   1
states of the oxygen atom, triplet-P oxygen atoms  [0( P)], and singlet-D oxygen  atoms [0( D)];
ozone (On);  symmetrical  nitrogen trioxide (NO.,); dinitrogen  pentoxide  (N205); hydroxyl radical
                                             6-1

-------
(HO);  alkylperoxyl  radicals  (RO^);  acylperoxyl  radicals RCfO^;  and other  less  important
species.  In the formulas, R represents a methyl (CH3), ethyl (C^H^), or another, more complex
hydrocarbon  radical.   The paths  by which  these  intermediates are  formed and  destroyed  are
important  keys  in  explaining the  chemical  changes  that occur  in the  polluted  atmosphere.
6.1.1.   Reactions Involving Oxides of Nitrogen
     The major portion of the total oxides of nitrogen emitted by combustion sources is nitric
oxide  (NO).  The  rate  at which NO is converted to nitrogen dioxide (ML) through oxidation by
the oxygen in air:
               2NO + 02 -» 2N02                              (6-1)
is proportional to  the square of the nitric oxide concentration since two molecules of NO are
required for the oxidation; it is, therefore, very sensitive to changes in nitric oxide concen-
tration.  Reaction 6-1 can be important in the vicinity of sources in generating up to 25 per-
cent of total  NO   during the initial  state  of  dilution with air when the concentration of NO
                 A
is still  quite  high.   Reaction  6-1 is much  too slow,  however, to account for any significant
fraction  of  the  nitric  oxide to  nitrogen  dioxide conversion  in the  atmosphere  for typical
ambient levels of nitric oxide.
     Since sunlight triggers  the  phenomenon of photochemical  smog  formation,  it is important
to recognize those  constituents  that will absorb light energy.  In some cases, these constit-
uents  decompose or  become activated for reaction.  A  dominant sunlight absorber in the urban
atmosphere  is  the brown  gas, nitrogen  dioxide.   Light absorption at wavelengths  <430 nm can
cause  the  rupture of  one of  the  nitrogen-oxygen  (N-0) bonds  in  the  nitrogen  dioxide (0-N-O)
molecule and generate  the reactive ground state oxygen atom, the triplet-P oxygen atom, and a
nitric oxide molecule.   The efficiency of this process is wavelength-dependent:
          N02 + sunlight (290-430 nm) -> 0(3P) + NO          (6-2)
The highly  reactive triplet-P oxygen atom formed in air collides frequently with oxygen mole-
cules.   During such encounters ozone may be formed:
          0(3P) + 02 + M -» 03 + M                           (6-3)
M  in  this equation represents  a  nitrogen,  oxygen,  or other third molecule  that  absorbs  the
excess  vibrational  energy released,  thereby stabilizing the ozone produced.   For most concen-
tration conditions common in polluted atmospheres, the very reactive ozone molecules regenerate
nitrogen dioxide by reaction with nitric oxide:
               03 + NO -» N02 + 02                           (6-4)
Alternatively, ozone may  react  with nitrogen dioxide  to  create  a new transient species, sym-
metrical nitrogen trioxide:
               03 + N02 -» N03 + 02                          (6-5)
The  nitrate species forms  dinitrogen pentoxide,  the  reactive anhydride  of  nitric  acid,  by
reaction with nitrogen dioxide:
               N03 +,.N02 -> N205                             (6-6)
                                             6-2

-------
Dinitrogen pentoxide may redissociate to  form symmetrical  nitrogen  trioxide  and  nitrogen  diox-
ide or possibly react with water to form  nitric acid  (HON05):
                        N90, •» NO, + NO,                   *           (6-7)
                   or    * D     J     i
                        N205 + H20 -» 2HON02                           (6-8)

The following reactions may take place between oxygen atoms and N0?  and  NO:


                        N0? + 0(3P) •* NO  + 0-                         (6-9)
                   or           3
                        NO, + DTP) + M -» NO, + M                     (610)
                   or          3
                        NO + 0(JP) + M •*  N02 + M                      (6-11)

         Also, NO and NO, may react to regenerate N0?:

                        N03 + NO -» 2N02                               (6-12)

              Nitrous acid is produced by:

                        NO + N02 + H20 -»  2HONO                        (6-13)

         and may react bimolecularly to regenerate the original reactants:

                        MONO + HONO -»• NO  + N02 + H20                  (6-14)

         The unexcited and first excited  electronic state  of the oxygen  atom are

         produced by ozone photolysis in  sunlight:

                               290-350 nm   -» 0? +0(1D) or 0(3P)      (6-15)
              0, + sunlight                          ,
               6               450-700 nm   •* 02 + 0(JP)              (6-15b)

              The singlet-D oxygen [0( D)] atom is much more reactive than the
                                          •3
         ground state triplet-P oxygen [0( P)] atom.   For  example, it reacts effici-

         ently during collision with a water molecule to form an important transient

         species in the atmosphere, the hydroxyl radical:

                        0(1D) + H20 -» 2HO                             (6-16)

         This radical is also formed through the photodecomposition of nitrous acid

         (HONO):

                   HONO + sunlight (290-400 nm) ^  HO + NO            (6-17)

         The hydroxyl radical can reassociate with nitrogen dioxide to produce nitric

         acid:

                        HO + N02 + M -> HON02 + M                      (6-18)
or form nitrous acid by reacting with nitric oxide:
               HO + NO + M •* HONO + M                       (6-19)


                                             6-3

-------
     A  careful  review of  the net  results  of reactions  6-1 through  6-19  reveals that these
reactions alone cannot explain the rapid conversion of NO to NCL observed in the ambient atmos-
phere.  In fact, if these reactions alone occurred, the original supply of nitrogen dioxide in
our atmosphere would be slightly depleted under irradiation with sunlight, and a small and near
constant  level  of ozone  would be created  in  a  few minutes.  The key  to  the  observed nitric
oxide  to  nitrogen dioxide  conversion lies  in a sequence of  reactions  between  the transient
species present and other reactive molecules such as the hydrocarbons and aldehydes present in
the polluted atmosphere.
     In the presence of hydrocarbons the number of reactions greatly increases.  Thus, the hy-
droxyl  radicals  produced by  reactions 6-16 and  6-17 can react with  a hydrocarbon (paraffin,
olefin, aromatic, or any compound having C-H bonds):
                OH + Hydrocarbon -» R- + H20                 (6-20)
     Reaction  6-20  produces  an  alkyl  radical  (R-)  which  contains  a  free  electron.   This
radical quickly  picks up  an  oxygen  molecule  from the  air  to form  a peroxyl  radical  ROp-:
               R- + 02 8 R02-                                (6-21)
Typically, the next  reaction  in the  series  converts  NO  to  N0? and produces an  oxyl  radical,
RO-:
               R02-  + NO -> RO- + N02                        (6-22)
A hydrogen abstraction by molecular oxygen may then produce a hydroperoxyl radical, H02-.   The
rest of such an RO-  radical typically forms a carbonyl compound, OHC:
               RO- + 02 •* OHC + H02-                        (6-23)
Finally, the hydroperoxyl radical (H0?) can react with a second NO to form N0?  to complete the
cycle:
               H02-  + NO •* OH- + N02                        (6-24)
Although this  description  is  very simplified, these series  of reactions contain the essential
features of NO to N0? oxidation and subsequent ozone formation.
     The initial  source  of radicals is very important; although the rate and yield of oxidant
formation depend on many other factors, the length of the induction period before accumulation
of oxidant depends  strongly on the initial  concentration of radicals.   (The length of the in-
duction period  is important  primarily in constant light intensity  smog  chambers.   Diurnally
varying radiation tends to lessen the importance  considerably.)  In smog chambers and possibly
in the  ambient atmosphere, the  photolysis   of nitrous acid,  reaction 6-17,  may  be  the  most
important initial source of radicals.  Nitrous acid has been detected in smog chambers in con-
centrations sufficient to explain the observed induction time for smog chemistry, but the con-
centrations necessary to  initiate smog chemistry in the  atmosphere  are below  the limits mea-
sured by most modern instruments.
     Another possible  source  of  radicals  in  the  atmosphere  is the  photolysis  of aldehydes:
               RCHO + hv •* HCO + R-                         (6-25)
Aldehydes are emitted from many sources,  including automobiles.  They are also  formed in smog.
                                             6-4

-------
     During the  course of the overall  smog  formation process, the  free  radical pool  is main-
tained  by several  sources,  but the  dominant one  appears  to be  photolysis of the aldehydes
formed  from  the  initial  hydrocarbons.   Since  the reactions of free  radicals  with NO form  a
cyclic  process,  any additional  source  of radicals will add to the pool and  increase the cycle
rate.   Conversely,  any reaction that  removes  free  radicals will slow the  cycle  rate.   For exam
pie, a  primary radical sink and a primary sink for oxides of nitrogen  is  reaction 6-18 to form
nitric  acid.
     The  hydrocarbon classes important  in the chemistry of the polluted troposphere are alkane
olefins,  and aromatics.   In addition, the oxygenated  hydrocarbons, such as aldehydes,  ketones,
esters,  ethers,  and alcohol are  also important.   A  great variety  of  chemical  reactions take
place among these organic species and the free radicals cited above.   The reactions of typical
hydrocarbon species are  now discussed  briefly.  Throughout  the  discussion references to more
extensive coverages are given.
     The  most  important  atmospheric  reaction involving alkanes is  with  the OH radical.   For
n-butane, for example, the reaction is
                    CH.,CH<,CH9CH,+ OH- -»•  CH,CH9CH9CH0-  + H00           (6-26a)
                     J  ^  i  J     and  6  L  *  *     *
                                     ->  CH3CH2CHCH3 +  H20             (6-26b)
The  alkyl  radicals will  rapidly  add  0^ to form the  corresponding  peroxyalkyl  radicals,  e.g.
                    CH3CH2CH2CH2- + 02 + M -»• CH3CH2CH2CH202- + M      (6-27)
(subsequently the third  body  M will  not  be indicated).   A  reaction  of  substantially lesser
importance is with  oxygen atoms,
                                    ,   Qy
                    CH.CH-CH-CH, + OrP) ^OH- + CH-,CH,CH,CH909-      (6-28a)
                     j^^j         and        *
-------
In  each  case the  free  radical product  will  quickly  react  with 02 to  produce  a  peroxyalkyl
radical that is capable of converting NO to NCk.
     Ozone-olefin reactions are a source of free radicals and stable products in air pollution
chemistry.  The initial  attack of Q^ on an olefin produces an unstable intermediate, which may
decompose  by  several pathways  (Niki,  1979;  O'Neal  and Blumstein, 1973).   For  propylene,  for
example, the initial step in the reaction with 03 is believed to be:


                                                    A
                                    A          CH.CH-CH,
                                   0  0     S*   6     d
             CH3CH = CH2 + 03 + CH3CH-CH2            -0              (6-30)
                                          ^^^  .0  \
                                                 CH3CH-CH2
Subsequent  decomposition  of  the  products  leads to  a  variety of  free radicals  and  stable
products (Herron and Huie, 1977; Niki  et al.,  1977).  The mechanisms of ozone-olefin reactions
are still under considerable study,  although most of the potential  paths have been delineated.
     The reaction of olefins  with atomic oxygen plays a  minor role in olefin consumption and
radical and product formation.  Again, for propylene the reaction is:
                                   3
                   CH3CH = CH2 4 0(  P) -> CH3CH2-  + HCO              (6-31a)
                                       or
                                       -» CH-.CO +  CH-                (6-31b)
                                       or  J      J
                                       •» CH3CH2CHO                  (6-31c)
     The mechanism of photooxidation of aromatic  species in the atmosphere is perhaps the area
of greatest uncertainty  in  atmospheric hydrocarbon  chemistry.   The principal reaction of aro-
matics is with the hydroxyl  radical  (Hendry, 1979;  Perry et al., 1977).   For aromatic-OH reac-
tions,  the initial  step  can  be  either  addition  to  or abstraction  from the  aromatic  ring
(Kenley et  al.,  1978).   The free radical addition  products  may then react,  most  likely with
either  02  or N02,  leading  to  the  cresols or  nitrotoluenes,  respectively.  The  abstraction
route  probably  leads to  benzaldehyde.   The mechanism  of aromatic-OH reactions is  yet  to be
clarified.
     Aldehydes,  both aliphatic and aromatic, occur as  primary and secondary pollutants and are
direct precursors  of free  radicals  in the atmosphere (Lloyd,  1979).   Consequently, aldehyde
chemistry represents an important  subject area in  atmospheric  chemistry.   Although aldehydes
are the main oxygenated  hydrocarbons generally considered with respect to their role in atmos-
pheric chemistry,  other classes  of  oxygenated hydrocarbons, such as  ketones,  esters,  ethers
and alcohols,  are present and participate to a somewhat lesser extent.   Major secondary sources
of aldehydes include the reactions of ozone and OH radicals with hydrocarbons, and radical de-
composition products.  In addition,  aromatic aldehydes can be formed as an ultimate consequence
of the reaction of  OH with aromatics, e.g. benzaldehyde.   The aldehydic hydrogen-carbon bond

                                             6-6

-------
in aldehydes is relatively weak (CH bond strength is 86 kcal/mol  ).  Consequently, this hydro-
gen  atom  will  be  susceptible under atmospheric  conditions  to attack by radical species, such
as 0(3P), 0(1D), OH, and H02.  Of these OH is by far the most dominant.  Hydroxyl radicals are
generally  thought  to abstract  a  H-atom  from  aldehydes—chiefly the  aldehydic H-atoms, i.e.
               OH + RCHO -» H90 + RCO                        (6-32)
                                                  6             -3
If one  assumes  an  atmospheric concentration of  10   radicals  cm  ,  the rates of decay of HCHO
and  CH3CHO by reaction with OH are approximately 4.2 percent and 5.8 percent per hour, respec-
tively  (Lloyd, 1979).
     The  photodissociation  of aldehydes  is  an important radical generation  mechanism in the
formation  of photochemical  air  pollution.   The  reactions  that  are  most  significant  can  be
generalized  in terms of a radical  and a molecular route:

                        RCHO + hv •* R + HCO                          (6-33a)
                                 and
                                  •* RH + CO                          (6-33b)
(Reaction 6-33a was  previously  given as reaction 6-25.)  The radical route is the more impor-
tant one from the point of view of atmospheric chemistry.
     As hydrocarbons are  oxidized  in photochemical  smog,  they generally produce formaldehyde,
HCHO,  at  some point.   Considerable attention  has  been given  to  formaldehyde  photolysis  in
recent years.  There appears to be general agreement that the primary paths are:
                        HCHO + hv •* H- + HCO                         (6-34a)
                                 and
                                  •* H2 + CO                          (6-34b)
     Moortgat and  Warneck (1979)  recently  measured the  quantum yield for the photolysis  of
formaldehyde.  Their results imply that the radical  pathway (reaction 6-34a) and the nonradical
pathway (reaction 6-34b) occur at approximately equal rates under typical  atmospheric conditions
     Another primary reaction path  of formaldehyde in photochemical smog is the reaction with
OH-:
                         HCHO + OH-  	   HpO + HCO                        (A)
     In order  to  compare  the  rates of  photolysis  with the  depletion of  formaldehyde  by  OH
reaction,  one can calculate a photolysis rate of approximately 13 percent per hour for a solar
zenith angle of 20° using the value of the photodissociation rate given by Horowitz and Calvert
(1978).
     Formaldehyde  photolysis  represents  an  important  source of  radicals  in  smog  chemistry
through reaction  of  the products  with  02  yielding the  hydroperoxyl  radical, HO,,-.   Thus:
                         H- + 02 + M 	   H02- + M                       (B)
                           HCO-  +  02 	   H02- +  CO                      (C)
     Since reactions B  and C are very  fast  in normal  atmospheres, reactions  6-34a  and 6-34b
are frequently written as:
                         HCHO + hv  202    2 H02- +  CO                       (0)
                     and HCHO + OH-0^     H20 + HOj-  + CO                 (E)
                                             6-7

-------
     A rate constant  for reaction E was recently recommended by the NASA Panel for Data Eval-
uation (National Aeronautics and Space Administration, 1979).
     Acetaldehyde, ChLCHO, also appears to play a significant role in smog chemistry.   In this
case, photolysis proceeds mainly by the radical pathway:  (Calvert and Pitts, 1966).
                         CH3CHO + hv -   CH^ + HCO-                      (F)
     Another primary reaction is the abstraction of hydrogen by the OH radical:
                         CH3CHO + OH- - '   CH3 C(O)- + H20                (G)
     Subsequent reactions of the product radicals of reactions F and G with atmospheric 0? are
very fast so that one may write:
                         CH3CHO + hv  202    CH30^ + HO^ + CO                (H)
                         and CH3CHO +~OTTr~  02     CH3C(0)02« + H20          (I)
     Acetaldehyde chemistry  thus introduces  the  chemistry of alkylperoxy  radicals  (ROp via
the methylperoxy radical, CH,OA; and the chemistry of peroxyacyl  nitrates [RCCOjOpNO,,] via the
formation of peroxyacetyl nitrate (PAN) from the acetylperoxy radical, CH3(CO)Oi (see reactions
6-42 ff below).
     In addition  to  aldehydes,  the ketones, methyethylketone and acetone are known to play a
role in photochemical  smog (Demerjian et al., 1974).
     The interaction with NO and N0? of the organic free radicals produced by hydrocarbon oxi-
dation represents an  extremely important aspect of the chemistry of the oxides of nitrogen in
the polluted atmosphere.   The radicals can be classed according to:

                                                            acyl
                                                            acyl ate
                                                            peroxyacyl
In air  it can  be  assumed that  combination with 02  is  the  sole fate of  alkyl  (R-)  and acyl
(RCO-) radicals and that the reaction is essentially instantaneous.   Consequently, in reactions
with alkyl or acyl  radicals as products, these products are often written as the corresponding
peroxy radicals.  Also,  acylate  radicals will decompose  rapidly  to  give an alkyl radical and
COp.    Therefore,  only  alkoxyl,  peroxyalkyl,  and  peroxyacyl  radicals  need to  be  considered
explicitly in  terms  of  NO  chemistry.   Table 6-1 shows the various reaction combinations that
are important between these radicals and NO and N02-
     The  reactions of OH with N02 and  NO  are reasonably well understood and have been previ-
ously listed as reactions 6-18 and 6-19.  Rate constants for these two reactions are available
(Hampson and Garvin,  1978).
     The  rate  constant  for the reaction of  H02  and  NO has recently been determined by direct
means and  is  substantially larger than previously calculated  indirectly (Howard and Evenson,

                                             6-8
R-
RO-
ROO-




alkyl
alkoxyl
peroxyalkyl




0
RC-
0
n
RCO-
0
RCOO

-------
TABLE 6-1.   REACTIONS OF ALKOXYL, ALKYLPEROXYL AND ACYLPEROXYL RADICALS WITH NO AND NO,

NO N02
Free Radical Reaction Reference
OH OH + NO -> HONO Hampson and
Garvin, 1978
H0~ H09 + NO -> N0? + OH Howard and
* * L Evenson, 1977
RO RO + NO •> RONO Batt et al . ,
(RONO + hv -» RO + NO) 1975
R02 R02 + NO -> N02 + RO
•* RON02
RCO~ RGO, + NO -»• N09 .+ RC09 Cox and Roffey,
j 6 ^ t ig?7
Hendry and
Kenley, 1977
Reaction
OH +
H02
(H02
RO +
(R02
RC03
(RCO
N02 -» HON02
+ NO, -* HONO + 0,
^ ^ H02N02
N02 •* H02 + N02)
NO, -> RON09
^ ^ RCHO'i+ HONO
4- MO -* on Kin
' MUn ~ l\\J n\V\J r\
N02 •* R02 -•- N02)
,NO, -» RCO, + NO,)
-J ^ -J ^
Reference
Tsang et al . ,
1977
Howard, 1977
Graham et al . ,
1977
Wiebe et al . ,
1973

Cox and Roffey,
1977
Hendry and
Kenley, 1977

-------
1977).  The HCL-NO reaction, as noted earlier, is a key reaction in the atmospheric conversion
of NO to N02.
     The  reaction  of H02  and NCL  has  the following  two  possible mechanisms (Howard, 1977).
Reaction 6-35b is not considered to be important in atmospheric chemistry:
                        HO, + NO, -» H09N09                           (6-35a)
                        H02 + N02 -» MONO + 02                        (6-35b)
In  addition,  the peroxynitric  acid  formed in reaction 6-35a  thermally decomposes as follows
(Graham et al. , 1977):
                        H02N02 -> H02 + N02                           (6-36)
At  the  present time  it appears  that,  at the temperatures prevalent  in summer smog episodes
(>20°C), peroxynitric acid does not represent an appreciable sink for NO- because  of the rapid
thermal decomposition reaction 6-36.   At lower temperatures H02N02 will  achieve higher concen-
trations and its importance as a sink for N02 increases.
     The reactions  of RO,  R02 and RCO., with NO and N02 represent key reactions in the conver-
sion of NO to N02 and the formation of organic nitrites and nitrates.
     The main alkoxyl radical reactions with NO and NO- are:
                        RO- + NO -» RONO                              (6-37a)
                                 or
                                 -» RCHO + HNO                        (6-37b)
                                and
                        RO- + N02 -» RON02                            (6-38c)
                                 or
                                  -> RCHO + HONO                      (6-38b)
     The reaction of alkylperoxyl radicals with NO is generally assumed  to proceed by the oxi-
dation of NO to NO- with formation of an alkoxyl radical:
              '          R02- + NO -> N02 + RO-                        (6-22)
Reaction 6-22 is believed to be an important route for the oxidation of  NO to N02  in the atmos-
phere (the alkoxyl  radical  may react further to  produce  H02,  which also converts NO to N02).
     It has been postulated that longer chain peroxyalkyl  radicals (n>4) from alkane photooxi-
dation will add  to  NO to form  an  excited complex that can be stabilized  to produce an alkyl
nitrate (Darnall et al., 1976):
                        R02- + NO + RON02                            (6-39)
     The peroxyalkyl-N02 reaction proceeds principally by
                        R02- + N02 -» R02N02                          (6-40)
The peroxynitrate may thermally decompose according to
                        RO^N02 •* R02- + N02                          (6-41)
Measured rate  constants for  the  R02-N02  reaction  and the R02N02  decomposition are not cur-
rently available.
                                             6-10

-------
     Peroxyacyl  nitrates  have  long  been recognized  as  important components of photochemical
air  pollution  (U.S.  EPA,  1978).   Peroxyacetyl  nitrate  (PAN)  exists  in equilibrium with the
peroxyacyl radical and NO,,:
                           00
                        CH3COO- + N02 + CH3COON02                    (6-42)
         There exists a competition between NO and N02 for the peroxyacyl radical
         through:
                           0              0
                        CH3COO- + NO •* CH-jCO- + N02                  (6-43)
The acetyl radical will rapidly decompose as follows:
                           0
                        CH3CO- •* CH3- + C02                          (6-44)
followed by:
                        CH3- + 02 -» CH302-                           (6-21)
                        CH302- + NO -> CH30- + N02                    (6-22)
                        CH30- + 02 -» HCHO + H02-                     (6-23)
                        HO^ + NO •* OH- + N02                        (6-24)
Thus, PAN chemistry  is  intimately interwoven in  the  NO  to N0? conversion process.  Rate con-
stants for reactions 6-42  and 6-43 have recently been reported by two groups of investigators
(Cox and Roffey, 1977;  Hendry and Kenley, 1977).
     The chemistry of the oxides of nitrogen in a hydrocarbon-containing atmosphere can be sum-
marized as follows:  the  major observed phenomenon  in the system is conversion of  NO to N02
and formation of a variety of nitrogen-containing species, such as nitrites and nitrates.   The
conversion of NO to N02 is accompanied by accumulation of 0.,.   N02 serves as both an initiator
and terminator of  the  chain reactions that result  in conversion of NO  to  N02  and buildup of
0.,.  Termination of the chain reactions leads to nitric acid and organic nitrates.   The nature
of the system can be explained by considering its behavior as a function of the initial concen-
trations of NO  and hydrocarbon in the irradiation of a static system,  as well as the ratio of
two reactants,  i.e, the [HC]/[NO ] ratio.
     At low  [HC]/[NO ]  ratios  (usually ratios of less than  about 1 to 2/1) the rate at which
                    X
NO is converted to NO,,  is influenced by the availability of organic compounds.  Therefore, the
effects of reducing organic compounds are to slow the conversion of NO to N02, thereby lowering
the N02/N0 ratio.  When  this occurs, a larger  proportion of  the NO that  is converted to N02
occurs through the destruction  of ozone.   This then has  to the overall effect of reducing the
rate of ozone  formation.   If the oxidation of  NO by organics is delayed sufficiently so that
the sun has passed its  zenith before significant amounts  of N0« are created, photodissociation
of NO,,  will  be  diminished and less  ozone will  accumulate  on that day.   At moderately high

                                             6-11

-------
[HC]/[NOX] ratios  (usually  greater  than about 5 to  8/1),  the  greater availability of organic
radicals means that  all  of these radicals are  not  consumed as rapidly in  reactions  with NO,
and more  reactions  between  the radicals and NO- are able to occur.   Thus,  the amount of ozone
formed and accumulated  begins  to become limited by  the  availability of NO ,  and becomes less
sensitive to additional  organic precursors.   At very high [HC]/[NO ]  ratios (greater than about
20 to  30/1),  ozone  cannot  accumulate  because  either  the  ozone is consumed  by  reaction with
hydrocarbons or radical-radical termination reactions occur which reduce oxygen atom and, hence,
ultimate ozone concentration.
     Identification of the nitrogen-containing products in  atmospheric reactions has been under
investigation for  a  number  of  years (Gay and  Bufalini,  1971;  Pitts, 1977; Spicer and Miller,
1976).   In general, the most important gaseous nitrogen-containing products in the NO -organic
system are nitric acid and PAN.  As noted,  reactions of NO  and  N0? with free radicals produce,
in addition to nitrous,  nitric, and peroxynitric acids, a variety of  organic nitrogen-contain-
ing species (Table  6-1).   There currently  exist important  areas of uncertainty with regard to
the formation  of nitrogen-containing  products  in  atmospheric  reactions.   The extent  of for-
mation and decomposition of peroxynitrates,  I^NOp,  is unknown, and rate constants for the key
reactions in the series, R0~ +  NO, are yet  to be determined.
6.1.2  Laboratory Evidence of the NO,-to-Precursor  Relationship
     In the  previous section,   the  nature  of chemical  reactions involving  oxides  of nitrogen
and hydrocarbons  in the  atmosphere was discussed.   These reactions  have  traditionally been
studied experimentally  in  laboratory  vessels called smog chambers.   These  chambers character-
istically employ radiation  sources  that closely approximate the UV portion of the solar spec-
trum as observed at  the earth's surface and clean,  chemically  inert  interior surfaces.   It is
believed that the chemical processes that take place in smog chambers are  similar to those that
take place in the atmosphere.
     The  presence  of surfaces   in a smog chamber may,  however,  be a source  of  difficulty in
interpreting chamber results because  of possible surface-catalyzed reactions  or absorption of
species on the walls.   In addition, most chamber experiments have been conducted by initially
injecting fixed amounts of reactants rather than simulating the continuous  time-varying injec-
tion and  dilution  of reactants that  characterize  the ambient  situation.   Nevertheless,  the
behavior  of  irradiated  mixtures of oxides of  nitrogen and hydrocarbons in smog  chambers  has
served as the foundation for our understanding of atmospheric chemical mechanisms.
     Considerable effort  has been devoted  to the development  of  chemical  reaction mechanisms
that are  capable of  describing the processes observed in smog  chambers (Baldwin et al., 1977;
Carter et al., 1979; Demerjian  et al., 1974;  Falls  and Seinfeld,  1978; Whitten and Hogo, 1977).
Smog chambers have been used extensively to determine how concentrations of NO  and other photo-
                                                                              A
chemical products respond to changes in the initial  composition of nitrogen oxides and organics.
A previous Criteria  Document (U.S.  EPA, 1978) discusses smog  chamber evidence concerning the
relationship between'ozone/oxidant  and the  photochemical precursors.   This section focuses on
how NO- concentrations respond  to changes in the input levels of organics  and nitrogen oxides.

                                             6-12

-------
     Several  researchers  have used  smog chambers  to  investigate the  dependence of nitrogen
dioxide concentrations on the levels of precursor inputs:
    • The University of North Carolina (UNC) study, using an 11,000 cubic-foot (311 m ) outdoor
     Teflon chamber, a simulated urban hydrocarbon mix, and twelve-hour irradiations (Jeffries
     et al., 1975)
    • The Bureau  of Mines study, using a 100 cubic-foot (2.8 m ) aluminum-glass chamber, auto-
     exhaust hydrocarbons, and six-hour irradiations (Dimitriades, 1972,1977)
    • The General  Motors  study,  using a 300 cubic-foot (8.5 m ) stainless steel-glass chamber,
     a simulated Los Angeles hydrocarbon mix, and six-hour irradiations (Huess, 1975)
                                                                                      o
    • The University of California at Riverside  study,  using a 225  cubic-foot  (6.4 m ) glass
     chamber, a simulated Los Angeles hydrocarbon mix,  and six-hour irradiations (Pitts et al.,
     1976)
    • The Health,  Education  and  Welfare (HEW) study, using  a 335 cubic-foot (9.5 m ) chamber,
     auto-exhaust  hydrocarbons, and  up  to ten-hour irradiation time  (Korth  et al., 1964) and
                                                  3
    • The HEW  study, using a 335 cubic-foot (9.5 m ) chamber, toluene and m-xylene, and 6-hour
     irradiations  (Altshuller et al., 1970).
     Trijonis (1978,1980) has recently reviewed the results of these studies, as summarized in
Table 6-2.   As  indicated  in Table 6-2,  the various chamber studies basically agree concerning
the dependence of maximum N0? and average N0? on NO  input.   With other factors held constant,
maximum NCL and average NO,, tend to be proportional to  initial NO .   The minor deviations away
from proportionality that  sometimes  occur tend to be in the direction of a slightly less than
proportional  relationship,   i.e.,  a  50  percent  reduction  in  NO   input sometimes  produces
slightly less than a 50 percent  reduction in N0?.
     There   is  less agreement among  the  chamber  studies concerning the  dependence  of  NO, on
initial  hydrocarbon concentrations.   With respect  to  maximum NOp,  the Bureau  of Mines study
indicates  essentially no dependence on hydrocarbons.   However, three other studies suggest that
hydrocarbon reductions decrease maximum NOp  concentrations.   The UNC,  General  Motors,  and UC
Riverside  studies  indicate  that  50 percent hydrocarbon control tends  to  decrease maximal N0~
by 10-20 percent, 25 percent, and 10-15 percent,  respectively.
     With  respect  to average N0?,  the Bureau of Mines  study indicates that hydrocarbon reduc-
tions would tend to increase N0? dosage.  This result is consistent with the theoretical argu-
ment of Stephens  (1973), who hypothesized that hydrocarbon  reduction  would  increase  average
NOp because these  reductions would delay and suppress  the chemical  reactions that consume N02
after it reaches  a peak.   However, the General Motors  chamber  study, the UC Riverside study,
and the  two HEW studies indicate that hydrocarbons produce no consistent effect on average NOp
concentrations.   The UNC experiments  imply that a 50 percent reduction in hydrocarbons produces
about a 20  percent decrease in  average NOp.   There is  some question about the UNC conclusion,
however,  because the UNC chamber runs were of a 10-hour duration and the NOp levels at the end
of the experiments were greater  when  hydrocarbons were  reduced.   The extra NOp remaining after
                                             6-13

-------
                        TABLE 6-2.  SUMMARY OF CONCLUSIONS FROM SMOG CHAMBER EXPERIMENTS

CHAMBER STUDY
University of North
Carolina (Jeffries
et al. , 1975)
MAXIMAL N
Dependence
on NOV
.A
Proportional
or slightly
less than
proportional
Dependence
on HC
50% HC reduc-
tion reduces
maximal NO,
by 10% to 20%
AVERAGE N(
Dependence
on NOX
Proportional
or slightly
less than
proportional
Dependence
on HC
Uncertain, 50% HC
reduction may de-
crease average
N02 by 20% or may
increase average
en
i
Bureau of Mines
(Dimitriades,
1972,1977)

General Motors
(Huess, 1975)
      UC Riverside
      (Pitts et al.,
      1976)
      HEW, Auto Exhaust
      (Korth et al.,
      1964)

      HEW, Toluene
      (Altshuller et
      al., 1970)
                               Proportional
                               Slightly less
                               than propor-
                               tional
Proportional
                   No effect
50% HC reduc-
tion reduces
maximal NO,
by 25%    <•


50% HC control
reduces maximal
NO. by 10% to
                                                  I1V7 ry

                                                  15%
Proportional
Proportional
to slightly
less than
proportional


Proportional
                                        Proportional
                                        Proportional
50% HC reduction
increases average
N02 by 10% to 30%

No effect
                      No effect
                     No consistent
                     effect
                     No effect

-------
the 10-hour period could cause an increase in 24-hour average NOp, even though average NO, was
reduced during the first 10 hours.
     Considering the  results  of  all the chamber studies, Trijonis suggested a consensus based
on  existing  chamber results which  would  appear to be as  follows:   fifty percent hydrocarbon
reduction  would  have little effect on  average  NOp concentrations (a change  of  + 10 percent)
but would yield moderate decreases  in maximal NOp  (a reduction of about 10 to 20 percent).   It
should  be noted  that  these  conclusions  are  meant  to  apply  to one  basic type  of ambient
situation—the situation of well-mixed urban air.
     Some  additional  support  for these conclusions was provided recently by studies of actual
ambient data on NO  and hydrocarbon levels from a  number of cities in the U.S.  Using empirical
modelling  and  historical  trend  analysis,  Trijonis (1978,1980) concluded that the ambient data
were  generally consistent  with   the  consensus  of chamber  results.    The  exact form  of  the
NOp/precursor  relationship, however,  was  found to vary somewhat from one location to another,
presumably depending  on local  hydrocarbon/NO  ratios, on  the  details  of the hydrocarbon mix,
                                             A
and on specific meteorological conditions.
     Reference is made also to another body of data due to Pitts et al.  (1977) (collected for a
different  purpose) which  also  contains potential  information on  the  relationship between NO
and its precursors.   However,  the data have not  been analyzed to date  for  its  pertinence to
the NO  precursor question.
6.1.3  NOX Chemistry in Plumes
     The  atmospheric  chemistry involving  oxides of nitrogen in plumes  from major fuel burning
installations  is  essentially  that described  earlier.   However,  the  relatively  high concen-
trations of NO and NO^ in such plumes compared with those in the ambient urban atmosphere leads
to certain chemical  phenomena particularly characteristic of plumes.   For e^dinpl?, within or a
few exit  diameters  downwind  of  a  source  such as  the stack  of a power  plant or the exhaust
system of a motor vfijn'cte, the relatively high NO concentrations which  may be present can pro-
duce NO.- in significant amounts through reaction 6-1 given sufficient Op.  As another example,
ambient ozone  may  be  quickly  scavenged  in  the plume by  the large quantities  of  NO through
reaction 6-4.  Because  the  rate  of the NO-0., reaction is fast relative to that of dilution of
the plume, the rate  of conversion of  NO  to  NO- is controlled by the rate at which ambient 0,^
is entrained into the  plume by turbulent mixing (Hegg et al.,  1977;  Kewley,  1978; Shu et al.,
1978;  White, 1977).   There  is  some nitric acid produced  in power plant plumes during the day-
light hours through  the oxidation of nitric oxide (reaction 6-1) and  the subsequent photodisso-
ciation of NO-  (reaction  6-2),  then followed  by the  combination  of  N02  with NO^  and  H^O
(reactions 6-10  and  6-8).  The  generation of  nitrous acid is also probable  since  the stack
gases will contain NO,  NOp, and  HpO (reaction 6-13).   Since nitrous  acid will photodissociate
to give hydroxyl radicals  (reaction 6-17), more nitric acid can be produced by reaction 6-18.
Thus,  although the  free radical  concentration is expected to b* low in  power plant plumes,  some
NO  will  be converted to nitric acid.   In addition, after sufficiently  long travel times during
                                             6-15

-------
which  ambient  hydrocarbons  have  been mixed with the plume  constituents, the  usual  free  radical
reactions described  earlier occur, possibly  leading to 0,  production.
     There  are several  studies  in which  measurements  have been made  of  the concentrations  of
pollutants  in  power plant  plumes  (Davis  et  al.,  1974; Hegg et  al.,  1977; White  et al.,  1976).
The  most difficult current  problem  is  predicting the  rate at  which NO is converted  to  NOp  in
such a plume.
6.1.4   Computer  Simulation  of  Atmospheric Chemistry
     A key  problem underlying the development and evaluation of kinetic  mechanisms for  atmos-
pheric chemistry is determining the sensitivity  of the concentration  predictions  to  those.un-
certain aspects  of the reaction scheme.   Such a determination can  serve as a  valuable  guide
for  future  experimental  studies and for  identifying those parameters  that,  when varied  within
accepted bounds, will be most  influential on the  predictions of the  mechanism.
     Although  the  qualitative aspects of the chemistry  of the polluted  troposphere  appear  to
be reasonably  well  understood, there are  many important details that still need  to be investi-
gated  before a complete quantitative understanding of the  photochemical smog system is possible.
Several  groups (Baldwin  et  al., 1977;  Carter et  al.,  1979; Demerjian et al., 1974;  Falls and
Seinfeld, 1978;  Whitten  and Hogo, 1977)  have formulated chemical  reaction mechanisms for pol-
luted  tropospheric  chemistry.  Some of these are  based on  specific surrogate hydrocarbon chem-
istries; in others,  attempts have  been made  to simulate the complex  ambient  atmospheric  system
by  representing  the  general features of the hydrocarbon  chemistry.   All   mechanisms contain
.aspects  of  uncertainty,  whether in unknown  rate  constants, in  the importance of competing re-
action paths,  or  in the manner of  representing the reaction  of  a  generalized species.  The
measure  of  the accuracy of  a mechanism  is usually based on the  extent  of  agreement between pre-
dicted concentration  profiles  and  those generated experimentally in  smog  chambers.
     With the  recent elucidation  of the  chemistry  of  the reactions of OH and HOp with  NO and
NO-,  the inorganic  portion of  the  photochemical smog mechanism  is  now,  by and  large, well
understood.  Uncertainties  remaining include
         • photolysis  rates
         • alkane-OH product distributions
         • olefin-OH  and olefin-0,  product distributions
         • aromatic  chemistry
         • alkoxyl  radical reactions
         • ROX/NOX  reactions
     A major  uncertainty in the predictions lies in the specification of values of the  photo-
lysis  rate  constants.  For  analyzing smog chamber data, photolysis  rate  constants relative  to
the  reported  value for NO- are  frequently   used.   Photolysis rate constants as  a  function  of
wavelength  can be  calculated from:
                    co
               K, = 2 a.(A)<|>.(\)I(\) d\                     (6-45)
                 J      J     J
                                              6-16

-------
               K-    = photolysis rate constant for species j
                J
               a- (A) = absorption cross section of species j
where
                   .  = quantum yield for the photolysis of species j
               I (A.)  = actinic irradiance
Data applicable to some atmospheric systems have been compiled by Schere and Demerjian (1977).
For  species  such as  NO-,  MONO,  and  (k, extensive  experimental  determinations of absorption
cross  sections  are thought to  be fairly reliable.   However, since  cross  section and quantum
yield data for formaldehyde, higher aldehydes, and alkyl nitrites are much less well character-
ized, many photolysis  rate constants  are subject to a  large uncertainty.   Of course, even if
absorption cross  sections and  quantum yields  could be determined  accurately  for all photo-
sensitive species,  uncertainties  in atmospheric photolysis  rate  constants  would still exist,
as  meteorological  conditions,  clouds,  dust,  and aerosols cause  unknown variances in actinic
irradiance.
     Whereas rate constants  in  the inorganic portion of  the mechanism are known  fairly well,
many more uncertainties, both in  reaction rate constants and products, are associated with the
organic  reaction  steps.    Still to  be  determined are product distributions  and reaction rate
constants for  the  initial  steps  of the  reactions  of OH and  hydrocarbon species,  the largest
uncertainties  lying in  the routes  of  the various  radical  species produced.   For  example,
although rate constants for alkane-OH reactions are well established, the ratio of internal to
external abstraction for  all  alkanes  is not  known.   Addition to Op to form peroxyalkyl (RC^)
radicals can be  considered as  the sole fate of the alkyl  radicals first produced  in alkane-OH
reactions, but  after  the  formation of alkoxyl  radicals through the conversion  of NO  to NOp,
the  reaction  mechanism  becomes  uncertain.    Alkoxyl  radicals  can  decompose,  react  with  Op,
isqmerize, or react with NO or NOp, with the importance and rate of each reaction path depend-
ing on the nature of the alkoxyl group.  Even for the most studied of the alkane-OH reactions,
the relative rates between decomposition, isomerization, and reaction with  Op,  NO, and NOp for
alkoxyl  radicals have not been measured,  but must be estimated (Baldwin et al . , 1977).
     Less well  understood  than  alkane  reaction mechanisms  are olefin oxidation processes,
primarily by OH.   Olefin-OH reactions  may proceed by addition or abstraction.   For smaller ole-
fins, the addition  path predominates.   However,  the abstraction fraction  increases  with  the
size of  the  olefin.   Along the addition path  for  terminally bonded olefins,  there  is uncer-
tainty  as  to  the  ratio of  internal  to external  addition.   Similar  to  alkyl  radicals,  the
hydroxy-alkyl  radicals formed in the initial OH addition to olefins are thought to immediately
add  Op  to form  hydroxy- peroxyalkyl radicals  and  thereafter react  with NO  to give  NOg  and
hydroxy-alkoxyl species.   The fate  of  the hydroxy-alkoxyl  radicals is subject to speculation,
although the  analogous alkoxyl  reaction  paths of decomposition,  isomerization,  and  reaction
with NO, NO- and Op are most likely possibilities.
     The inherent uncertainty of the decomposition,  reaction with Op, and isomerization of the
alkoxyl  and  hydroxy-alkoxyl radicals class  can be represented by the generalized reaction step:
               RO -» aH02 + (l-cr)R02 +  pHCHO  + yRCHO         (6-46)
                                             6-17

-------
From the earlier  discussions  of alkoxyl radical  behavior,  RO always gives rise to either H02
or R02  in  any of the decomposition, isomerization, or Op reaction pathways.  Hence, the stoi-
chiometric coefficients  representing  the fraction of HOp and ROp found in the lumped RO reac-
tion should sum to one.   Since the RO lumped species represents a large class of different-sized
radicals and  because  splits  between reaction paths for  even  specific radicals are unknown, a
can have a value in the range 0 to 1.   Many RO reaction routes produce aldehydes.   Thus, 0 < 0
< 1 and 0 < Y £ 1-  Since the composition of the RO radical pool is continually changing during
the course of a photooxidation, the actual  values of a, p, and y are functions of time.   Thus,
the selection of constant values of these coefficients introduces uncertainty.
     A comprehensive sensitivity/uncertainty analysis of photochemical smog mechanisms has been
carried out by Falls et al.  (1979).  In this study the effects of rate constant and mechanistic un<
tainties on predicted concentrations are illustrated.
6.2  NITRITE AND NITRATE FORMATION
     The oxides of nitrogen are converted eventually to nitrites and nitrates by the reactions
given  in  Section 6.1.   In particular,  the  following  gaseous nitrites and  nitrates  have been
identified:
          MONO           nitrous acid
          HON02          nitric acid
          HOpNOp         peroxynitric acid
          RONO           alkyl nitrite
          RON02          alkyl nitrate
                    0
                    ii
                   RCOON02        peroxyacylnitrate (PAN)
          ROpNOp         peroxyalkyl nitrate

In addition  to these gaseous  species,  particulate  nitrites and nitrates may be  formed.   The
object of  this  section  is to present estimates  of  the importance of the various  nitrites and
nitrates.   In most  cases,  estimates are necessary'because ambient measurements of the concen-
tration level of all but a very few of the species are lacking.
     Typical   ambient  concentration levels  of  the gaseous  nitrogen-containing species  listed
above can  be  estimated  from  simulations of smog chamber experiments using chemical mechanisms
representing the hydrocarbon-NO  chemistry.   Table 6-3 lists calculated, concentrations of MONO,
HON02, H02N02,  RONO,  RON02,  RC.(0)OON02, and R02N02 for smog chamber experiment EC-237 carried
out at the Statewide Air Pollution Research Center of the University of California, Riverside,
using the  chemical  mechanism  of Falls and  Seinfeld (1978).   The conditions of the experiment
are given  in the  footnote  of Table  6-3.   The  simulated and predicted  concentrations  of the
major measured species,  such as NO, NO, 0,.,  PAN, and hydrocarbons, agreed well.
                                             6-18

-------
            TABLE 6-3.  PREDICTED NITRITE AND NITRATE CONCENTRATIONS IN SIMULATION OF
               EXPERIMENT EC-237 OF THE STATEWIDE AIR POLLUTION RESEARCH CENTER OF
                         UNIVERSITY OF CALIFORNIA, RIVERSIDE, USING THE
                         CHEMICAL MECHANISM OF FALLS AND SEINFELD (1978)


HONO
HON02
H02N02
RONO
RON02
0
RCOON02
on MO
i\U rtliU f\

60 min.
0.0061
0.067
0.00083
0.0030
0.0041
0.025
0.034
Concentration
180 min.
0.00040
0.22
0.0019
0.00054
0.0070
0.089
0.075
, ppm
300 min.
0.00036
0.29
0.0025
0.000080
0.0072
0.13
0.098

Conditions of the experiment: T = 3Q3°K, k, = 0.3
[NO] = 0.377, [H«0] = 2.4 x 10*. [C0]^= 0.96
[Alkanes] = 1.488, [Non-ethylene Olefins] =
[Aromatic?] = 0.177, [HONO] (assumed}-^ 8.1
ppm). Dilution rate = 2.93 8 10 min .
min , [NO,] = 0.106,
, [Aldehydes]0 = 0.0012,
0.15, [C2HJ° = 0.875,
(All concentrations in
     The concentrations of  HONO,  H02N02, and RONO are predicted to be small  relative to those
of NO and N0?.   Each of these species has decomposition reactions,
               HONO + hv -» OH- + NO                         (6-17)
               H02N02 •+ H02- + N02                          (6-36)
               RONO + hv -> RO- + NO                         (6-47)
that, at the temperatures  and solar intensities prevalent in the experiment  and in the summer
atmosphere, are fast enough to insure that the concentrations of each of the  three species are
low.   At lower  solar  intensities  than those  in  the  experiment,  HONO and RONO can be expected
to reach higher  concentrations,  and at lower temperatures,  such as those in  the stratosphere,
H02N02 may accumulate.
     Under daytime conditions the reactions that govern the  concentration of  HONO are 6-17 and
6-19.   At  night,  however,   the  only apparent  destruction  route  for  HONO  is  reaction  6-14.
Depending  on the  relative  importance of reactions 6-19,  6-13,  and 6-14, HONO  may  reach sub-
stantial concentrations  under nighttime conditions.   A lower limit on  the  nighttime concen-
tration  of HONO can be estimated  from  the equilibrium HONO concentration based  on reactions
6-13 and 6-14.
                                             6-19

-------
                                  K13[NO][N02][H20]
                       [MONO] =      ;   k^                          (6-48)

At [NO] =  [NO,]  =0.1 ppm,  [H,0]  = 2.4 x 104 ppm (50 percent relative humidity), the equili-
                                                                  -?
brium MONO concentration calculated from equation 6-48 is 1.9 x 10   ppm.
     Like MONO,  H02N02  and RONO,  PAN undergoes  both  formation  and decomposition steps (reac-
tions 6-42a,b).  Unlike  these  former species, however,  the  balance  between the formation and
decomposition reactions is such that PAN may achieve appreciable concentration levels relative
to those  of  NO and NO,,.   Because  the  decomposition reaction for  PAN  is  strongly temperature
dependent, the steady state  PAN  concentration  is highly dependent  on the  temperature.   As
temperature increases the  role  of PAN  as an N02 sink decreases markedly;  at low temperatures,
on the other  hand,  steady state PAN concentrations can reach rather substantial  levels.
     Little is  known  about the existence and  importance of peroxynitrates other than HO^NO-,
and PAN.  It was presumed in the mechanism  on which the results  of  Table  6-3  are based that
R02N02  thermally decomposes  at a  rate  between those for HO?NO? and PAN.  Assessment of the
importance of  R02N02  as  a sink for NO   will  depend on measurement of  the  rates of reactions
6-40 and 6-41.
     In contrast to the  other  species  of Table 6-3, nitric  acid and alkyl nitrates apparently
do not undergo  appreciable decomposition reactions.  Thus, these two species potentially  serve
as important  atmospheric sinks  for N02.   Both nitric acid and alkyl nitrates may remain in the
gas phase or react  with other atmospheric constituents,  such as ammonia,  to produce low  vapor
pressure  species that  have  a  tendency  to  condense on  existing particles  or  homogeneously
nude ate to  form particles.
     Figure 6-1 depicts the potential  paths by which particulate nitrate species may be formed
from NO and N0?.   Path  1  involves  the  formation of gaseous nitric acid  by reactions 6-8 and
6-18.    Nitric  acid  concentrations  resulting  from these  two reactions  for  the  simulated smog
chamber experiment  have been  given in Table 6-3.   Comparisons of the individual  rates of  reac-
tions 6-8 and  6-18  indicate  that  reaction 6-18  is the predominant route for gas-phase nitric
acid formation  under  typical daytime  conditions.  Nitric  acid vapor, once  formed,  may then
react with  NH,, a  ubiquitous  atmospheric  constituent  with  both natural and  anthropogenic
sources, to produce ammonium  nitrate,  NH.NO, (path 2), which at standard temperature and  pres-
sure, exists  as a solid.   Alternatively, the nitric acid vapor may tie absorbed directly into a
particle (path 3),  although  thermodynamic and kinetic considerations  favor reaction with NH^
to form NH.N03  as the path of conversion of gaseous nitric acid to nitrate in particulate form
(Brandner et al.,  1962;  Morris  and Niki, 1971;  Stelson et al., 1979).  Path  4 involves the
direct  absorption  of  NO  and  N02   into  an atmospheric particle,  a route  that   is  likely for
certain aqueous particles, particularly when accompanied by  the absorption of ammonia (path 5)
(Orel and Seinfeld,  1977).  Path 6 depicts the formation of  organic nitrates through reactions
                                             6-20

-------
|OH,,HO2, H2OJ
  Figure 6-1.  Paths of nitrate formation in the atmosphere
  (Orel and Seinfeld, 1977).
                           6-21

-------
such as  6-38a,  followed by absorption of these nitrates into particles.   At present little is
known about the existence or importance of mechanisms such as that depicted by path 6.
     There have been  a number of measurements of  nitric  acid and particulate nitrate concen-
trations in ambient air, and several of these are summarized in Chapter 8.   Many of the measure-
ments have identified the particulate nitrate as  NH.NO,, suggesting that the aerosol may consist
                     +
of solid NH^NOg or NH4 and N0"3 in solution in approximate stoichiometric balance.   It is diffi-
cult to estimate the relative importance of the paths in Figure 6-1 for several reasons.  First,
the rate of  reaction  of nitric acid and ammonia  is not well known, although the forward reac-
tion is probably rapid and, in fact, can be presumed to be in equilibrium with the dissociation
of solid ammonium nitrate (Brandner et al., 1962; Morris and Niki, 1971;  Stelson et al .  , 1979).

               NH3(g), + HON02(g) JNH4N0                    (6-49)
Second, the rate of absorption of NO and NO- into existing particles depends on the composition
and size of  each  particle and cannot generally  be  predicted a priori.  In  either case it is
apparent that  the presence  pf  NH3  is  required, either to  form  NH.NO, or  to  neutralize  the
acidity of a liquid droplet in which NO and N0? dissolve.
     The current state of understanding of atmospheric inorganic nitrate formation can be sum-
marized as follows.   The  principal  gas-phase nitrate forming  reaction is  reaction 6-18.   The
nitric acid  vapor  formed  in reaction 6-18 probably  reacts  rapidly with ammonia to form small
particles of solid ammonium nitrate such that the equilibrium of reaction 6-49 is established.
In competition  with  the  nitric  acid/ammonium nitrate  path is the path consisting  of direct
absorption of NO  and  N0~  into aqueous droplets.   The relative rates of these two paths cannot
be determined  in  general.   Although measurements of particulate  organic  nitrate levels  have
been reported (Grosjean and Friedlander, 1980),  the mechanisms of formation of organic aerosol
nitrates have not  been fully identified.
6.3  TRANSPORT AND REMOVAL OF NITROGENOUS SPECIES
     The general behavior of nitrogenous species  in the atmosphere can be described as follows.
Nitric oxide emissions are converted partially to nitrogen dioxide within the urban atmosphere
as a result of gas-phase reactions.   Simultaneously,  NO,, is converted to nitric acid vapor  and
NO and NO- may  also  be absorbed  into existing particles.   The mixture of  gases and particles
is transported  downwind of  the  source region, accompanied by continuous conversion of more of
the NO  gases to particulate nitrates.   Also occurring simultaneously is surface absorption of
NO and NO- as well  as of particles containing nitrate.   Eventually, rainout and washout serve
to remove more of  the remaining gases and particles.
     The object of studying the  transport and removal  processes  of nitrogenous species is to
develop the capability to predict the atmospheric residence time of nitrogenous species as  they
are transported downwind  from  a  source-rich area.   Several  recent studies have been reported
in which  measurements (usually airborne) have been  carried out downwind  of  large urban  com-
plexes in order to obtain material balances on gaseous and particulate pollutants (Breeding et

                                             6-22

-------
al., 1976; Stampfer and Anderson, 1975).  A goal of these studies is to determine the relative
roles of transport, removal and conversion of gaseous to particulate pollutants on the overall
pollutant material balance downwind of a major urban source.  On the basis of the previous dis-
cussion in this  section it is possible to make rough estimates of the relative roles of these
processes in determining the ultimate fate of nitrogenous species.
     In the  quantitative  analysis of urban plume data, it is necessary to have a mathematical
model capable  of describing the behavior of both gaseous and particulate pollutants and their
interrelations.  Such a model would, in principle, include both gaseous and particulate phases
with detailed treatments of gas-phase and particulate-phase chemistry, as well as size distri-
butions of the particles.
     There currently  exist a  number  of mathematical  models capable  of  relating  emissions  of
primary gaseous species to airborne concentration levels of both primary and secondary gaseous
pollutants.   The models include details of atmospheric chemistry and meteorology and have been
exercised in a  variety  of situations.  Models  that  relate  emissions  of primary and secondary
gaseous and  particulate pollutants,  including  description of particle  size  distribution and
chemical composition, are  currently under development and  not yet  available  for general use.
In view of this,  a "first-order" model that contains all the major mechanisms influencing the
airborne concentrations of gaseous and particulate pollutants can be formulated, one that does
not  include  details  of atmospheric  chemistry  and particle size distribution,  but  treats the
competing processes of advection, turbulent diffusion, conversion of gaseous species to partic-
ulate material,  settling,  deposition,  washout  and rainout.  Such a  "first-order"  model is  in
essence a material balance,  designed to provide  estimates  of  the  fraction of pollutants that
still remains  airborne  at  a certain distance downwind of the source and the fraction that has
been removed  by deposition  and  gas-to-particle  conversion.   A  model  of  this type  has been
developed by  Peterson  and Seinfeld (1977)  and  applied to the prediction  of  airborne concen-
trations of  gaseous  and particulate  pollutants  in  the  case in which gases  are  converted  to
secondary particulate matter.  Although the model of  Peterson and  Seinfeld is a quantitative
framework within which  to  evaluate each of these effects, at this  time only qualitative esti-
mates for nitrogen-containing species are possible because of lack  of knowledge of the relevant
rates and coefficients  for such  a model.   The  execution of experimental measurements in urban
plumes  and correlation with physical and chemical rate data to predict fractions of nitrogenous
species that  are removed  by  various paths  has yet  to  be performed.  See Section  6.3.3 for
further discussion.
     In this section the  general  nature of the  transport and removal of nitrogeneous species
is briefly discussed.
6.3.1  Transport and  Diffusion
     Some atmospheric processes  play  an important role in the dispersion of air pollutants  on
large spatial scales,  and  others  are important  on small spatial  scales.   The interactions amonc
these processes, and  their overlapping influences on eventual pollutant distributions, are very
                                             6-23

-------
complex.  A classical example, shown in Figure 6-2, is the effect of atmospheric turbulence of
different scales on pollutant transport and dispersion.
     The  spatial  and temporal scales  of  interest to the  long-range  transport of nitrogenous
and other pollutant  species  are  on the order  of several  hundred kilometers and several days.
As shown in Figure 6-2, the atmospheric motions  important on these scales range from mesoscale
convection to synoptic-scale cyclonic waves.
     Changes of wind  speed and direction in the lowest layer of the atmosphere are the result
of many  competing  physical processes.   The interaction between  the  synoptic-scale air motion
and the  surface boundary  layer usually produces complex flow patterns.  These patterns change
hourly,  daily and  seasonally.   They also vary  spatially,  especially  where terrain is nonuni-
form and  the  heating  or cooling of the surface  is inhomogeneous.  Vertical air motions result
from divergence in synoptic  and mesoscale  wind  flow.   They are also  produced  by viscous  and
frictional forces  in  the  boundary layer and can be  particularly large and highly variable in
regions  of complex terrain.   Although  vertical velocities generated by these processes have a
magnitude of  only 1-10 centimeters  per second,  which  is  1-2  orders of  magnitude  less  than
generally observed horizontal  wind speeds  near  the surface,  they  have significant effects on
the net  transport  and dispersion of air pollutants.  Accurate  estimates of the vertical  com-
ponents of the wind vectors are extremely difficult to obtain on a routine basis, particularly
in the first few hundred meters of the surface.  Further,  they vary drastically with horizontal
wind speed  and  the  radiation balance of  the  surface.   While vertical  diffusion is  dominant
generally in  the   first 10 to 30  km away  from the source,  lateral  (or  horizontal)  diffusion
becomes important   in pollutant transport over large distances.  Vertical  diffusion in the  tro-
posphere  is  limited  to about 10  km  in  mid-latitudes while  the  lateral  transport eventually
varies through 360 degrees.
6.3.2  Removal Processes
     The  atmospheric  residence times  of nitrogenous  species (lifetimes) are  of  the  order of
days to  weeks,  while  their inter-specie lifetimes (chemical  transformation)  might only be as
short as fractions of a second.
     Atmospheric residence times are governed by the efficiency with which species are removed
from  the atmosphere.   The  removal  (or  cleansing)  efficiency  depends  considerably  on  the
specific  physical  and chemical  nature of  the  species.   For  example, NO, N02,  and  HN03  are
removed  within  clouds and/or by  rain  with  different  efficiencies due to  the  different solu-
bility and vapor pressure characteristics of the three gases.
     There are two types of removal processes that occur in the atmosphere:
         • dry deposition
         • precipitations scavenging (wet deposition)
Mathematical models capable  of describing  the behavior of both gaseous and particulate pollu-
tants must  include removal terms, particularly  for the important nitrogenous species, such as
nitric acid and nitrate aerosol.
                                             6-24

-------
•o
o
(J
CO
M
o:
HI
o
cc
i
o





106
1 week —

105
IJ — .. •
day

104
IU
1 hr-
103


*5
102
1 min-

10

1





DOMAIN OF INTEREST
TO REGIONAL
AIR QUALITY STUDIES
Vp«
CUMULONIMBUS CON- ^&":'
VECTION (LAND-SEA [i^
BREEZES AND MOUN- v •'•:'•
TAIN-VALLEY WINDS) X.- 	 -*•£
r ^. '•:•: :•
8 ^ :+£

I !
j CUMULUS |
j CONVEC- I
a TION I ^
j -^

(^ Ol
ATMOSPHERIC 0 ''$& ""
- TURBULENCE S ^^-^
( V I x- ^>VX
^^^"v^^"
I Sx ^ I S

I-- 	 5
9 S
! PLANETARY j
8 WAVES S
! (EXTRA- 5
a 	 1 TROPICAL S
IcVCLOMld ^CLONES, I
.-.-4WAVES ' ANT|-
•™-:-:-f(HURRI j CYCLONES)
:•:•: x^CANES) 5 5
X'l '•''£''• '' '•' ''• g J
•:wr;'J«?>«o- *tfj£* •* ,< ^^
:i|i: •:!$•: '• : :| ^x ^
•••'••**'*"' '-j^-g /
- •J,{$?>
^
^
S

' J


CIRCUMFERENCE
OF EARTH
I I ill
10m     100m     1km
                                         10km
                 100km    1000km  10.000km 100,000km
            MICROSCALE
          METEOROLOGICAL
               STUDY
CONVENTIONAL URBAN
   AIRSHED STUDY
                                                REGIONAL
                                             AIRSHED STUDY
                         CHARACTERISTIC LATERAL LENGTH SCALE
            Figure 6-2. Schematic illustration of scales of motion in the atmosphere.
                                              6-25

-------
6.3.2.1  Dry Deposition of Gases—Gaseous nitrogeneous species are removed from the atmosphere
by surface absorption, so-called deposition.  The rate at which an airborne species of concen-
tration c.j (micrograms per cubic meter) is removed across a horizontal surface of unit area at
an elevation z   is  often expressed as c.^. where v^  is  the  so-called "deposition velocity,"
which depends on the value of z .
     Vegetation has been  shown  capable of removing significant amounts of N0~ and NO from the
atmosphere.  Tingey (1968) showed that alfalfa and oats absorbed NO, from the air in excess of
         ~12
100  x  10    moles  per square meter per  second  when exposed to an  atmosphere  containing 460
ug/m  NOp (or 1 x 10   moles per cubic meter).   More recent work by Rogers et al.  (1977), using
a continuous reactor  technique,  indicated that the  N0«  uptake  in  both corn (Zea mays 1.) and
soybean  (Glycine  max.  L.)  could  be well  represented  by a chemical  kinetic  model  having two
reactants, the pollutant  and  the  leaf surface.  The second order rate constant for N02 uptake
was  independent  of  NO^   concentrations  and  leaf surface area,  but directly  dependent upon
inverse  total  diffusion  resistance.   Tingey  (1968)  extrapolated  his  data to  estimate the
removal of NO, from the Salt Lake Valley in Utah.   On an annual  basis, removal of NO, from the
                                                      3
valley with  an ambient NO, concentration of 9.6  ug/m   (0.005 ppm), which  is  about  3-4 times
                          £                                   c
greater than background  NO, levels, would total  about  3  x 10  kg NO,.   This  may be compared
                                                                            9
with an estimated total global anthropogenic annual N02 emissions of 53 x 10  kg (Robinson and
Robbins, 1970).
     Hill (1971)  found in his experiments on the uptake rate of gases by an alfalfa canopy that
NO was absorbed with a deposition velocity of 0.1 cm/sec and NO, was absorbed at a velocity of
                                                                                3
2 cm/sec  when  present in  the air of the chamber  at a concentration of  96  ug/m   (0.05 ppm).
Using  ambient  NO,, concentrations found  in  those  areas of Southern California  from  August to
October of  1968,  and  assuming  a continuous alfalfa cover,  Hill  estimated  that  NO,  could be .
                               2
removed at a rate of 0.1 gram/m /day.
     Nitrogen oxides (especially N?0) have long been known to be produced by biological action
in soils.  Recently,  however,  Abeles  et al. (1971) found that soils could absorb N02 from the
atmosphere as well.   They found that when  air  containing NO, was passed over  soil  in a test
                                                                                             3
chamber, the concentration  of NO, in the air  was reduced from an  initial  value  of  190 x 10
    3                      33
ug/m  (100 ppm) to 5.7 x 10  ug/m  (3.0 ppm) over a 24-hour period.   When soil was autoclaved,
                                                                           3     3
the total  NO, present over the same time period  was reduced from 186 x 10  ug/m  (97 ppm) to
             4      -
only 25 x  10  pg/m  (13 ppm).  This result would point to a biological sink for NOp in soils.
Ghiorse and Alexander (1976),  however,  report finding essentially no difference in N02 removal
by soil  from air  in a closed system when their soil (Lima loam) was either nonsterile, auto-
claved or y-irradiated.  The authors point out that autoclaving may drastically alter the phy-
sical and chemical properties of soil  and thus introduce artifacts in such studies.  They con-
clude that the role of microorganisms in the  fate of N0~ in soils is not so much in sorption
but in conversion of nitrite (resulting from such sorption) into nitrate.
     Nitric  oxide  may be absorbed by  soils, but  is then oxidized  almost immediately to NOp.
Mortland  (1965)  has noted that transition  metal  ions  in the soil promote  NO absorption.  If

                                             6-26

-------
the  soil  is  saturated with  alkaline  earth  cations  though,  absorption  of  NO  is  halted.
Sundareson  et  al.  (1967) found that  alkaline-earth  zeolites  readily absorb NO and release it
as NO  and  HMO, when heated.  To date, the role of organic matter in the absorption of nitroge
     X         
-------
     The  capture  of gases  and  particles  by falling raindrops  is  called  washout.   Typically,
the duration of washout is relatively short compared with that of rainout.  However, pollutant
concentrations at  the  cloud level  are frequently much  lower  than those near the ground where
washout occurs.  Thus, rainout and washout can be of similar importance.  The uptake of NO  by
                                                 1                                         A
rain  depends  on physical  parameters such  as  rainfall   intensities  and  raindrop  size  distri
butions, and on the chemical composition of the raindrops.   Models of washout generally reduce
to  two  limiting cases,  mass-transfer-limited  and chemical-reaction  limited.   In  the former,
the rate controlling step for absorption is the diffusion of the gases to the falling drop; in
the latter, chemical equilibrium in the drop controls the quantity absorbed.   The study of Dana
et al. (1975) suggests that for SCL under typical atmospheric conditions washout is often mass-
transfer-limited.   Similar studies for washout of NO  have yet to be performed.
6.3.3  Source-Receptor Relationships
     The previous sections of this chapter have addressed the scientific basis for our current
understanding of the atmospheric chemical  processes describing the transformation of NO, which
is the dominant N0x compound emitted by most sources,  into the more toxic N02>  and its subse-
quent further  transformation, transport  and removal.   This section  addresses the  question of
predicting the N02 concentration experienced by a receptor, such as a human being,  due to given
emissions of NO  (see Chapter 5).   Methodology for estimating human exposure using ambient con
centration data derived from fixed monitoring sites is  discussed in Chapter 8.
     Until very  recently,  the  problem  of  predicting N0?  concentrations  has received  little
attention in the  literature.   However,  relationships among ambient nitrogen oxides, hydrocar-
bons  (HC) and  ozone/oxidant (0  )  have been considered  in connection with the question of pre-
dicting ambient ozone  concentrations  (U.S.  EPA,  1978).   Some of the methodology applicable to
the ozone problem  has  potential  usefulness in the case  of NO  source-receptor  relationships.
                                                              A
In this regard  two very recent reviews are  available (Cole  and Summerhays,  1979;  Anderson et
al.,  1978).   In addition,  a critical review of  atmospheric modeling has  also  been published
(Turner,  1979).
     Relationships between emissions and 0 /NO -related  air quality have been pursued following
three distinct approaches  that  differ mainly in  degree  of empiricism.  In order of decreasing
empiricism, these approaches are as follows:
              (1)   Empirical Approach.  This approach entails statistically or
                   nonstatistically associating ambient  air quality data either  with
                   ambient concentrations of precursors  or with precursor emission
                   rates.   These associations are clearly not cause-effect in nature,
                   and their intended use is not  to predict absolute air quality;
                   rather,  it is to estimate changes in  air quality resulting from
                   changes in emission rates.
              (2)   Mechanistic Models of 0 /HC/NO .   This approach entails deriving
                   cause-effect relationships between oxidant and precursors through
                   laboratory testing and chemical mechanistic simulations.  As  in
                   the preceding case, this approach is  intended to predict only
                   changes in air quality resulting from changes in emission rates.
                                             6-28

-------
              (3)  Air Quality Simulation Model (AQSM) Approach.  This approach
                   entails deriving the requisite air quality-emission relationships
                   through mathematical representation of the transport, dispersion,
                   transformation, and deposition processes.  Its intended use is to
                   predict absolute levels of air quality from given emission rates
                   and meteorological data.
     The air  quality-emissions  relationships or "models" developed  to  date  through all these
approaches are  applicable  only  to the urban problem, or to situations in which the geographi-
cal  dimension of the  source-receptor relationship  is  comparable to that of  the  urban area.
Techniques for  estimating  short-term N02 concentrations arising from point sources alone have
been discussed by Cole and Summerhays (1979).
     Since the first two approaches predict only changes in air quality resulting from changes
in emission rates rather than absolute levels of air quality, their utility lies mostly in the
technical  area  of air quality management.   The  third  approach is most pertinent  to  the dis-
cussion in this section.
     If predictions  from AQSM models could be made  reliably and with a reasonable effort, it
would be possible, e.g.,  to:
                  • Determine the impact of different source types and/or individual
                   sources upon absolute air quality.
                  • Augment ambient monitoring data with calculated data at points
                   intermediate to the limited number of monitoring sites practically
                   available.   Such new data would be useful in a number of appli-
                   cations including the location of "hot spots" and the estimation
                   of human exposure to NCL concentrations.
     Assessment of the specific  impacts  on air quality of the various source types in the NOp
problem requires  consideration  of  such  parameters  as local pollutant  sources  and/or concen-
trations, meteorology, and topography,  all  of which vary  from  area to area.   Development and
validation of AQSM  models  applicable to the  N02  problem,  currently underway at U.S.  EPA and
elsewhere,  have reached a stage where it is now becoming possible to evaluate their usefulness
and accuracy.  At the  present time, however, the literature contains  little documentation of
specific applications of  AQSMs.   For this reason,  a  meaningful  discussion of source impacts on
air quality could not be  included in this document.
     In general, the utility of model types  for the  above purposes depends not only on the com-
pleteness with which they  describe the chemical  and physical processes characterizing the NO^
problem, but also on the  type of situation to be modelled.   For example, prediction of N02 con-
centrations very  close to  a  highway in the  absence  of all  other NO   sources  except  lines of
mobile vehicles might, for  practical  purposes,  be made  using  a model  which did not take into
account the  free  radical  chemistry described previously since  these  reactions would probably
not have time to occur.   On the other hand,  prediction of N0? concentrations on an  urban scale
resulting from a combination of point and area sources would probably require consideration of
the complex chemistry reviewed in this chapter.
                                             6-29

-------
     In summary, it may be stated that the prospects for estimating NOp concentrations at local
receptor points are quite promising but it is not possible to estimate reliably their accuracy
or usefulness based on currently reported applications.
6.4  MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION
     This section is limited to a discussion of specific reactions possibly leading to the for-
mation of nitrosamines and related compounds in the atmosphere.
     Three mechanisms will be discussed in this section:
        • Non-photochemical  reactions of  gaseous  amines with oxides  of  nitrogen and nitrous
          acid
        • Photochemical reactions of amines with oxides of nitrogen in the gas phase
        • Heterogenous nitrosamine formation processes in atmospheric aerosols
The first two  processes  have been the object  of  recent experimental studies, including simu-
lation experiments  in  environmental  chambers,  and will be examined in some detail.  The third
process involving aerosol particles is purely speculative at this time and will be briefly dis-
cussed in terms of the corresponding evidence in the bulk (liquid) phase.
6.4.1    Non-Photochemical Reaction of Gaseous Amines with Oxides of Nitrogen and Nitrous Acid
     Bretschneider  and Matz  (1973,1976)   reported  the  fast formation of diethylnitrosamine
(DENA) when reacting  50-100  ppm of  diethylamine  and  nitrogen  dioxide.   DENA  formed  within
seconds and was reportedly stable for weeks in the dark in the glass reaction vessel.   Dimethyl-
nitrosamine was  formed in the same way from  dimethylamine and N02.   The  authors also  report
that nitrosamine formation can be catalyzed by S02.
     A fast reaction between diethylamine and N02 was also reported by Gehlert and Rolle (1977),
who achieved in a few minutes a 90 percent conversion to diethylnitrosamine at 25°C.   They pro-
posed the following rate equation:
               -d(N09)/dt - k (dimethylamine) (NO,)2        (6-51)
                                      82-21
with a  rate constant  k^-,  = 6.5 x  10  S,   Mol    s  .   Initial  reactant  concentrations  ranged
            -6             5       -I
from 4  x 10    to  6 x  10   Mol  £  .   The other major product  of the reaction  was  the amine
nitrate (aerosol),  corresponding to the overall equation:
          2 N02 + 2(C2H5)2NH -» (C2H5)2NNO + (C2H5)2NH2N03   (6-52)
     Neurath and  co-workers  (1965,1976)  investigated  the effect of adding  several  amines  on
the thermal  oxidation of nitric oxide to nitrogen dioxide in the presence of 10 percent oxygen.
Addition of secondary  amines  (dimethyl,  diethyl,  methyl -n-butyl, and pyrrolidine) doubled the
rate of NO oxidation, presumably due to nitrosamine formation:
               NO + N02 -> N203                              (6-53)
               N203 + 2 R2NH -> 2 R2NNO + H20                (6-54)
where R = alkyl  group.   Addition of  tertiary  amines  (trimethyl,  diethyl-methyl, and N-methyl
pyrrolidine) also  increased  the NO oxidation  rate,  thus indicating that  tertiary amine also
reacted with  the oxides  of  nitrogen  under these conditions.  The  reactions  of  dimethylamine
                                             6-30

-------
and d i ethyl ami ne with  NO in the presence  of  10 percent oxygen were also followed by directly
measuring the (decreasing) amine concentration.  No reaction was observed between diethylamine
and NO in nitrogen.
     Dushumin and  Sopach (1976)  also report a  rapid  reaction  between dimethylamine, N^O^ (in
equilibrium  with  NOp)  and  ozone  to  form dimethylnitrosamine with  a 50  percent conversion
achieved in  less  than  10 minutes.   Since other reaction products included formaldehyde (HCHO)
and dimethylnitramine [(CHO-NNO^], it is suspected that photochemical reactions took place as
well, as is discussed in the next sub-section (6.4.2).  Field measurements were performed near
a chemical  complex, and dimethylnitrosamine was found in the frost near the complex as well as
in the air up to 30 kilometers from the complex.
     In complete contrast  with  the above studies, low yields of nitrosamines were obtained by
Hanst et al.  (1977),  Grosjean et al. (1978), and Pitts et al.  (1978) in experiments involving
dark reactions of ppm levels of alkylamines and nitrogen oxides in humid air.
     Hanst et  al.  (1977), using long  path infrared spectroscopy, followed  the  reaction  of 1
ppm dimethyl amine  with  0.5 ppm HOMO (in equilibrium  with  2 ppm NO,  2  ppm  N0~ and 13,000 ppm
water vapor)  in  air  in a  9  x  0.3  m diameter cylindrical glass cell.   Dimethylnitrosamine was
formed in yields of 10 to 30 percent, and the rate of amine disappearance was ~4 percent min  .
     Grosjean et al.  (1978)  and  Pitts et  al.  (1978)  also  report low yields of nitrosamine in
the dark  reaction of ~0.5 ppm amine  with 0.8 ppm NO  and  0.16  ppm NO, in  air  at 30 percent
                         3
relative humidity in 50 m  Teflon chambers.  Nitrosamine yields were 2.8 percent from diethyla-
mine and ^1 percent from dimethylamine.  The tertiary amine triethylamine also yielded diethyl-
nitrosamine  (0.8  percent yield),  while trimethylamine  yielded traces  of dimethylnitrosamine.
For all four  amines  the nitrosamines were the  only  gas phase products found after 2 hours of
reaction in the dark.   Light-scattering aerosols were also formed.
     Assuming a bimolecular reaction between the amine and nitrous acid, and using the nitrous
acid equilibrium constant  of Chan  et al.  (1976),  Hanst et al.  (1977) estimated an amine dis-
appearance  rate of 0.8 ppm min  .   This would constitute an upper limit for nitrosamine forma-
tion since (a) the nitrosamine  yield is not necessarily 100 percent of the reacted amine, (b)
some of the amine may be lost on  the walls  of the reaction  vessel  rather than by chemical  reac-
tion,  and  (c)  nitrous  acid  formation may  be  controlled  by  heterogeneous  rather  than homo-
geneous processes.
     With respect  to  the  latter,  Cox and  Derwent (1976)  reported  decomposition of  150 ppm
HONO at a  rate  of  10 to 15  ppm  hr  ,  i.e.,  "*•  200  times  slower  than the rate predicted using
the data of  Chan,  et  al.  More recently,  Kaiser  and  Wu (1977) reinvestigated the kinetics of
formation and decomposition of nitrous acid:
               NO + N02 + H20 -» 2 HONO                      (6-55)
               2 HONO •* NO + N02  +  H20                      (6-56)
                                             6-31

-------
They found  the  reactions to be heterogeneous  under  all  surface conditions tested.  They also
estimated upper limits for the homogeneous rate constants:
               kx < 4.4 x 10"40 cm6 molecule"2 s"1
               k2 < 1 x 10"20 cm3 molecule"1 s"1
which are more than 100 times slower than those of Chan et al. (1976).  Thus, homogeneous (gas
phase) formation  of  nitrous acid seems too  slow  to  account for HONO formation in the studies
of Hanst  at al.  (1977) and Grosjean et  al.  (1978),  and heterogeneous formation (being itself
very slow) may account for the low nitrosamine yields reported by these authors.  Pitts et al.
(1978) also  note  that the observed formation  of  nitrosamines from tertiary amines, for which
no gas phase mechanism could be proposed, may be entirely heterogeneous.   Such processes for
the  formation of  nitrosamines from  tertiary amines  have been well  documented  in  the  bulk
(liquid) phase (Ohshima and Kawabata,  1978; Smith and Loeppky, 1967).
     Finally, it  should  be  noted that the accepted mechanism for the liquid phase nitrosation
of secondary amines  involves  N203 (Mirvish,  1975; Ridd, 1961; Scanlan, 1975) according to the
reactions:
               2 HONO j N203 + H20                          (6-57)
               N203 + R2NH -» R2NNO + HONO                   (6-58)
and that the corresponding rate of nitrosation, r = k (amine) (HONO)  , may apply to the studies
of Hanst  and of  Pitts and Grosjean in which HONO formation seems to be controlled by hetero-
geneous processes.  The  mechanisms  of  Gehlert and Rolle  (1977)  and Neurath et al. (1976) for
the gas phase  reaction also involve N,,03   (or NO and NO-).  Furthermore,  Hanst et al. (1977)
reported that the  amine  disappearance  rate in a mixture containing 1 ppm dimethylamine, 4 ppm
NO, and 1 ppm N02 in dry nitrogen  (i.e.,  under conditions notjconducive  to the formation of
nitrous acid)  was comparable to that  measured in the amine-HONO-NO  -water  mixture  in air (1
            -1                    -1
percent min   and 4  percent  min  ,  respectively).   Thus,  the  conflicting evidence currently
available does not permit firm conclusions regarding the rates, yields and mechanisms of nitro-
samine formation from amines and oxides of nitrogen in the dark.
6.4.2  Photochemical  Reactions of Amines
     In the  smog chamber experiments described in the previous section (Grosjean et al., 1978;
Pitts  et  al. ,  1978), amine-NO -air  mixtures  were  also  exposed  to sunlight for  -\-2 hours.
Diethyl-and triethylamine reacted rapidly to  form ozone, peroxyacetylnitrate (PAN) and acetal-
dehyde  as   the  major  gas  phase products,  as  well  as  light scattering  aerosols consisting
essentially of the amine nitrates.   Several other products were formed in the gas phase includ-
ing diethylnitramine  [(CjHrJ-NNO^]  and several ethyl substituted  amides.   These  products and
the corresponding yields are listed in Table  6-4.
     Irradiation of dimethylamine and  trimethylamine under the same conditions yielded ozone,
formaldehyde, dimethylnitramine [(CH-O^NNO-J  and  several  methyl substituted amides in the gas
phase  as  well as aerosol products  (Pitts  et al., 1978).   Reaction products of dimethylamine
that  have  also  been  identified  by other  investigators  include formaldehyde  (Dushumin and
                                             6-32

-------
                                 TABLE  6-4.   MAXIMUM CONCENTRATIONS AND YIELDS OF THE PRODUCTS OF
                            DIETHYLAMINE  AND  TRIETHYLAMINE (GROSJEAN ET AL.,  1978; PITTS ET AL. , 1978)
cr>
i
co
CO





Product
GAS PHASE
Ozone
Acetaldehyde
PAN
GAS PHASE (by GC-MS)
Dark
Diethyl ni trosami ne
Sunl ight
Die.thylni trosami nec
Diethyl ni trami ne
Diethyl formamide
Diethylacetamide
Ethylacetamide
Unidentified, MW=87d
Diacetamide
From (C0H5)0NH
Molar
Maximum Conversion
Concentration Yield,
Formula ug/m3 ppb %

03 290
CH^CHO 300 30b
h
CH3CO-OON02 41 4


(C2H5)2NNO 59 14 2.8

(C?Hr)?NNO (destroyed)
(C2H5)2NN02 780 162 32
(C2H5)2NCHO 29 7.0 1.4
(C2H5) NCOCH 3.6 0.8 0.2
C2H5NHCOCH3 42 12 2.4
--
(CH3CO)2NH


Maximum
From


Concentration
ug/m3






17

38
177
178
15
48
41
trace
ppb

260
700
72


4.1

9.1
37
43
3.2
13
12

(C0H ) N
Mol ar
Conversion
Yield,
%a


47b
5b


0.8

1.8
7.4
8.6
0.6
2.6
2.4

                                                            (continued)

-------
                                             TABLE 6-4.  (continued)
Product
AEROSOL PHASE6
Sunlight
b . (maximum value)
sea L
TSP
Acetamide
Di ethyl hydroxyl ami ne
Nitrates
Fv^rvm t C 9 R ' 9

Maximum
Concentration
Formula ug/m ppb
4 x 10'V1
60
CH3CONH2 3
(C9H,-),NOH
L. -J L.
NO^ 42
NH From
Molar
Conversion Maximum
Yield, Concentration
% ug/m ppb
46 x 10'V1
370
0.2 8.7
7.6
158
(C0H,)0N
Molar
Conversion
Yield,
%d
0.7
0.4

 Initial amine concentrations =0.5 ppm (calculated from amount injected).
 Taking into account the number of ethyl  groups in DEA and TEA.
GNot corrected for artifact formation (maximum ~ 10% of the observed concentration).
 Assuming same mass spectrometer response as diethylacetamide.
"Based on volumes sampled:
27.9 m3 (DEA) and 30.8 m3 (TEA).

-------
Sopach, 1976; Hanst et al., 1977), dimethylnitramine (Dushumin and Sopach, 1976; Tuazon et al.,
1978),  and  the  amine  nitrate aerosol  (Dushumin and Sopach,  1976;  Gehlert  and Rolle, 1977).
     In the experiments conducted with  secondary amines (diethyl and dimethyl), the nitrosamine
formed  in the dark was progressively destroyed in sunlight, as was reported before for dimethyl-
nitrosamine  (Bretschneider and Matz,  1973,1976; Hanst  et al., 1977)  and diethylnitrosamine
(Bretschneider  and Matz,  1973,1976).   In  contrast,  the  concentration  of diethylnitrosamine
formed  in the dark from the tertiary amine, triethylamine, increased upon  irradiation for ^ 60
minutes, reaching  a  level  about 3 times  its  average concentration in the dark prior to being
destroyed upon further exposure to sunlight (Figure 6-3).
     The mechanism proposed by the authors (Grosjean et al., 1978; Pitts et al., 1978) involves
hydroxyl radical (OH) abstraction on a  secondary C-H bond  to produce an alkyl radical, as shown
here for triethylamine:
               (C2H5)3N + OH -» (C2H5)2NCHCH3        ,        (6-59)
followed by the well-known sequence R + 0  ^ RO  , RO  + NO •* NO  + RO (Demerjian et al., 1974.
The  alkoxy  radical RO  then decomposes to  give two  of the  major  products,  acetaldehyde and
di ethylacetami de:
                        0
               (C-H,.)., NCHCH, -» CH,CHO  (C.HjJl            (6-60)
                 c b 1.      J     a       e. b i
                              -> (C H ^ NPHO + f*H            ffi-fi"l^
     Further reactions of  acetaldehyde  lead to  PAN, another  major  product.   The diethylamino
radical, (C2Hr)2N,  reacts  with  NO  and N02  to  form  diethylnitrosamine  and diethylnitramine,
respectively:
               (C2H5)2N  NO •* (C2H5)2NNO                    (6-62)
               (C2H5)2N  N02 -»• (C2H5)2NN02                  (6-63)
It  is   assumed,  by analogy  with  the   simplest  dialkylamino  radical,  NH2,  that  reaction  of
(C2Hc)2N with oxygen is very slow [this has received confirmation very recently in the case of
NH2 (Lesclaux and Demissy,  1978)].
     A recent study by Calvert et al.  (1978) of the photolysis of dimethylnitrosamine has shown
that the dimethylamine radical,  (CH.,)0N,  can react with  NO  almost  10  times faster than with
                                 7
02 and  with N02  approximately 10  times  faster  than  with 0?.  Nitrous acid and CH3N=CH2 were
also identified  as major products.   These results  suggest that dimethylamine radicals formed
in a NO-N02-polluted atmosphere have a good chance of forming nitrosamines and nitramines even
though the concentrations of NO and N02 are very small  when compared to the amount of molecular
oxygen present.
     In the  case of the secondary  amine, diethylamine, the  larger  nitramine  yield indicates
that the diethylamine radical  is also produced by other reactions, including OH abstraction on
the N-H bond:
               (C2H5)2NH +  OH -> (C2H5)2N + H20              (6-64)
     Rate constants  for  the OH-amine  reaction  have been  measured recently  (Atkinson  et al.  ,
1977,1978)  and are consistent  with  both  N-H  and  C-H  abstraction.   Alkylamines  react  quite

                                             6-35

-------
5
<
CO
O.
LU
E
                             TIME, hours
                   DARK
SUNLIGHT
 Figure 6-3. Formation and decay of diethylnitrosamine, in the dark
 and in sunlight, from  diethylnitrosamine (open squares)  and from
 triethylamine (open circles)(Pitts et al, 1978).
                              6-36

-------
rapidly with OH,  with atmospheric half-lives of 2-3 hours at typical OH concentrations in the
lower troposphere (Atkinson et al.,  1978).
     The  efficient  formation and accumulation  of  nitramines (reaction 6-63)  is  due  to their
stability in sunlight (Grosjean  et  al., 1978; Pitts et al., 1978).   In contrast,  nitrosamines
photodecompose readily:
                                   hv
                             R2NNO -» R2N + NO                        (6-65)
and  their concentration  in  sunlight  is dicated  by  the competing  reactions 6-62 and 6-65.
Results shown  in  Figure  6-3 for triethylamine indicate that photochemical formation (reaction
6-62) may prevail  upon photodecomposition during daytime under certain conditions, in contra-
diction with the generally accepted idea that any nitrosamine present at night in  the  atmosphere
should  be  rapidly destroyed  after  sunrise  (U.S.  EPA,  1977; Hanst  et  al.,  1977).   Processes
other than photodecomposition, such as direct oxidation of nitrosamines to nitramines  by ozone
or other oxidizing species, have not been investigated.
6.4.3  Formation of Nitrosamine in Atmospheric Aerosols
     Heterogeneous formation  in  acid aerosols  has  been  suggested (U.S. EPA,  1976) as  a  pos-
sible mechanism for  nitrosamine  production  in the  atmosphere.   The absorption of  basic amines
by acidic aerosol  droplets  (containing  sulfuric acid and/or ammonium  bisulfate),  followed by
reaction  with  nitrite, nitrous acid, or  other  species,  could  theoretically  lead  to  the  for-
mation  of nitrosamines.    The acid  media would favor  nitrosamine  formation  (Mirvish,  1975;
Ridd, 1961;  Scanlan, 1975)  and  would prevent rapid photodecomposition during daylight hours
since the  absorption of  nitrosamines  is greatly  attenuated in acid solutions (Chow  et  al.,
1972).
     This hypothetical mechanism, which is  intuitively plausible, warrants  several comments.
First,   basic  species, such  as  ammonia,  which  are present  in  ambient air  at higher  concen-
trations  than  amines, may compete  effectively for  absorption  in  acidic  aerosol droplets.
Second,  nitrosamines  photolyze readily in aqueous solutions  (Chow et  al. ,  1972; Polo and Chow,
1976) and atmospheric  aerosols  seldom achieve the   high acidity  (pH  ^ 1)  necessary to prevent
photodecomposition.    It  should  be pointed  out,  however,  that  acidic aerosols  are  not neces-
sarily required, since several  studies  have shown  that nitrosation proceeds quite effectively
at neutral and/or alkaline pH by  free radical processes (Challis and  Kyrtopoulos,  1977) or due
to catalysis by carbonyl  compounds  or metal  ions (Keefer, 1976;  Keefer and  Roller,  1973).
Finally, irrespective  of  the  aerosol  acidity, reactions  of  nitrosamine with oxidizing species
in aqueous aerosol  droplets may lead to the  formation  of,  for example,  nitramines.
6.4.4  Environmental  Implications
     Of the  three  mechanisms discussed  above,  nitrosation  in  atmospheric  aerosols is  purely
speculative at  this time.   The two other processes  involve photochemical and non-photochemical
reactions of amines  with  oxides  of nitrogen and  related species and may be  relevant  to the
formation of nitrosamines in the  atmosphere.
                                             6-37

-------
     Nighttime production of nitrosamines:  Conflicting results are presented in the literature
concerning nitrosamine formation rates and yields from secondary and tertiary amines.   Several
investigators  report  low yields (a  few  percent),  essentially controlled by  the  slow  rate of
nitrous  acid  formation   through  heterogeneous  processes,  while  others  report  high  yields
achieved within minutes.
     Nitrosamines have been shown to form from secondary (Grosjean et al., 1978; Hanst et al.,
1977; Pitts et al., 1978) and tertiary amines (Grosjean et al., 1978; Pitts et al.  , 1978) under
simulated atmospheric conditions.   Primary amines have not been investigated but should receive
some attention  since  they have been shown  to  produce nitrosamines,  albeit  in  low yields,  in
the liquid phase (Wartheson et al.,  1975).
     If one  accepts  the  low yields  of Hanst et  al.  (1977), Grosjean et al.  (1978), and Pitts
et al.  (1978), nighttime concentrations of nitrosamines in typical  urban atmospheric conditions
should be quite low.   However, caution should be exercised when extrapolating these laboratory
and smog chamber data to the ambient atmosphere.
     Photochemical reactions of amines:   Secondary and  tertiary  amines  react readily with the
hydroxyl   radical  to  form  aldehydes,  PAN,  ozone,  nitramines, several  amides,  and the  amine
nitrate aerosol.   Nitrosamines are  also formed  but photodecompose  rapidly.   Little  is  known
about ambient levels of amines, but  they are presumably low (£ 10 ppb),  and daytime nitrosamine
levels should be quite low due to their rapid photodecomposition.   However, photochemical for-
mation of diethylnitrosamine from the tertiary amine, triethylamine,  has been shown to prevail
over photodecomposition for ~ 1 hour in full sunlight (maximum yield ^ 2 percent).
     Products  other  than  nitrosamines,   i.e.,  nitramines  and amides,   may   represent  health
hazards and may warrant further investigation.   In industrial environments where, for example,
50-500 ppb of amine might be released into polluted urban air, nitramines (10-30 percent yield,
or 5 to  150  ppb)  and amides  (5-15  percent,  or 0.5 to 75 ppb) may form  in sunlight. Dimethyl-
nitramine (Druckery et al., 1961;  Goodall and Kennedy, 1976) and acetamide (Jackson and Dessau,
1961; Weisburger  et  al. ,  1969) are  carcinogenic, while  dimethylformamide  has been identified
in urban  air (Pellizzari,  1977) and has  been  shown  to undergo nitrosation  (Lijinsky  et al.,
1972; Walker  et al.,  1976).   Another amide,  N,N-'dimethyl-acetamide,  has been identified in
diesel  crankcase emissions (Hare and Montalvo,  1977).
6.5  SUMMARY
6.5.1  Chemistry of Oxides of Nitrogen in the Lower Atmosphere
     Nitrogen oxides undergo many reactions in the lower atmosphere.   Triggered by solar radi-
ation,  photochemical  reactions involving nitrogen oxides and other compounds, principally gase-
ous organic  molecules, result in  formation of reactive  species  capable of initiating a large
number of  subsequent  reactions.   In particular,  although anthropogenic  emissions of N0x occur
principally  as  NO, atmospheric reactions  may  produce the more toxic and  irritating  compound
NO,  which is of direct concern to human health.
                                             6-38

-------
     The  reactive species, which include a variety of unstable, excited molecules and molecular
 fragments  having only  transitory  existence  and/or occurring  only in extremely  low concen-
 trations,  are  the  principal  agents through which chemical changes  occur in the polluted urban
 atmosphere.  Many of the reaction sequences involving these unstable or short-lived intermedi-
 ates  are  complex in  nature,  leading inevitably to  short-term  variations  in nitrogen dioxide
 concentrations,  depending upon a variety of factors  such as radiant energy input, temperature,
 and the presence or absence of a variety of hydrocarbons.  The dependence of NO- concentrations
 on  hydrocarbons  results in a coupling between the chemistry of the oxides of nitrogen and the
 photochemical  oxidants, causing  atmospheric  concentrations  of  either  type of  pollutant to
 depend, to some extent,  on  atmospheric  concentrations  of the other.   There  is considerable
 current  research on  the  precise relationships  among ambient  concentrations  of NO   and  the
                                                                                    A
 photochemical oxidants.
     Most  of  the current  knowledge both of  atmospheric  chemical  pathways and of the end pro-
 ducts  of  these  reactions  rests on  controlled  experiments  conducted in small-scale laboratory
 smog chambers.   It  is believed that  the  chemical  processes  that take place in these chambers
 are similar to those that take place  in the atmosphere.   It is important to note, however,  that
 our current  understanding  of nitrogen chemistry is  not complete and that reaction details and
rate constants  may  be subject to change or new reactions of substantial importance may remain
 to be  discovered.
     A number of smog chamber studies using simulated urban atmospheres have been conducted in
 order  to  define the relationship between  levels  of NO  and  hydrocarbon  inputs  and resulting
 NCL concentrations.   The results show that, with other factors held constant, both average and
 maximum N0~ concentrations tend to  be proportional to initial  NO  inputs.   While some disagree-
1         L-                                                     A
 ment is reported from different chamber studies on the precise effect of hydrocarbon reduction
 on  NO- concentrations,  a  consensus would seem  to be as  follows:   Fifty  percent hydrocarbon
 reduction  would  have  little  effect on average  N0~ concentrations  (a change of  + 10 percent)
 but would yield moderate decreases  in maximal NO, (a reduction of about 10 to 20 percent).   It
 should  be noted  that  these  conclusions  are  meant  to apply  to  one  basic type  of ambient
 situation—the situation of well-mixed urban air.
 6.5.2  Nitrate and Nitrite Formation
     In experimental simulations of a daily cycle of polluted atmospheres, peroxyacetyl nitrate
 (PAN), known to  be  very toxic to plants,  may  be  the conversion  product  of  up  to one-half of
 the oxides of  nitrogen.   PAN,  however, is not the final product of these gas-phase reactions,
 since  it  may  decompose.   The most  likely  final gaseous  product is nitric acid,  a strong acid
 and a powerful oxidizing agent.   Photochemical  models of diurnal atmospheric reactions predict
 that up to one-half of the original  oxides of nitrogen is converted to nitric acid and nitrates.
 It  is  believed  that  nitrates  are  formed  when  nitric acid vapor reacts  rapidly  with ambient
 ammonia  to  form small  solid  particles  of  ammonium  nitrate.   Another possible  mechanism
 resulting  in aerosol  formation  consists  of the direct absorption of NO  into aqueous droplets
                                                                       X
                                             6-39

-------
in  the  presence of ambient ammonia.   The  relative importance of these  two  mechanisms is not
presently known.
     Nitric acid produced in the atmosphere is an  important component of acidic rain.  Particu-
late nitrates  may  be of concern as a component of respirable participate matter.   Both nitric
acid and participate nitrates are of concern for adverse effects on human health.
6.5.3  Transport and Removal of Nitrogenous Species
     Over travel distances  measured in hundreds of  kilometers,  more  than half the total mass
of  most  pollutants, including  nitrogenous species,  may  be removed from the  atmosphere by a
variety of  processes.   These  processes are usually  grouped  into the  two generic classes, dry
and wet deposition.  Gaseous nitrogenous species may be removed by surface absorption (dry depo-
sition).  Vegetation and  soil  are capable of  removing  significant  amounts  of NO and N0? from
the atmosphere by this mechanism.  Dry deposition  of particulate nitrogenous species may occur
through  sedimentation,  Brownian diffusion,  and  impaction.   The  rate  or  removal   by  these
mechanisms  is  strongly dependent on wind  speed  and  the detailed properties of the deposition
surface.  Rainout and washout are two wet deposition mechanisms by which nitrogenous gases and
particulates may be removed from the atmosphere.  Rainout  refers  to  removal processes taking
place within a cloud; washout refers to removal of aerosols and gases below the cloud layer by
precipitation.   The  uptake  of  NO  by rain depends upon such parameters as rainfall intensity,
raindrop size,  and  the chemical  composition of the droplets.   To date, the detailed processes
of NO  removal have not been thoroughly studied.
     A
6.5.4  Mechanisms of Atmospheric Nitrosamine Formation
     Three mechanisms possibly leading to the atmospheric formation of nitrosamines and related
compounds are as follows:
        • Non-photochemical  reactions of  gaseous  amines with oxides  of  nitrogen and nitrous
          acid
        • Photochemical reactions of amines with oxides of nitrogen in the gas phase
        • Heterogeneous nitrosamine formation processes in atmospheric aerosols.
The first two  processes  have  been the object  of recent experimental  studies, including simu-
lation experiments  in  environmental  chambers.   The third process  involving  aerosol  particles
is purely speculative at this  time.
     Conflicting results are presented in the literature concerning nitrosamine formation rates
and yields from secondary and tertiary amines.   Several investigators report low yields (a few
percent) essentially  controlled by  the  slow  rate of  nitrous acid  formation  through hetero-
geneous processes,  while others report high yields achieved within minutes.
     Nitrosamines have been shown  to form from  secondary  and tertiary amines under simulated
atmospheric conditions.   Primary  amines  have not  been  investiaged.   If one accepts the lowest
yields reported, nighttime concentrations of nitrosamines under typical urban conditions would
not be  significant.  However,  caution should be exercised when extrapolating these laboratory
and smog chamber data  to the ambient  atmosphere,  especially  in view of the lack of consensus
on formation rates.

                                             6-40

-------
     In sunlight-irradiated atmospheres,  secondary  and tertiary amines react readily with the
hydroxyl radical to  form  aldehydes,  PAN, ozone, nitramines, several  amides, and amine nitrate
aerosol.   Nitrosamines  are  also formed  but  photodecompose rapidly.   Little  is  known  about
ambient levels  of  amines,  but  they are  presumably low  (< 10 ppb),  and  daytime  nitrosamine
levels should be quite low due to their rapid photodecomposition.   However, photochemical  for-
mation of diethylnitrosamine from the tertiary amine,  triethylamine,  has been shown to prevail
over photodecomposition for ~ 1 hour in full sunlight (maximum yield  ^ 2 percent).
     Products  other  than  nitrosamines,   i.e.,  nitramines  and  amides,  may represent  health
hazards and  may warrant  further investigation.  Near certain  industrial  environments  where,
for example, 50-500  ppb  of amine might be released into polluted urban air, nitramines  (10-30
percent yield  or 5  to 150 ppb)  and  amides  (5-15 percent, or 0.5  to  75 ppb) may form in  sun-
light.
6.5.5  Source-Receptor Relationships
     The question  of predicting  the N02 concentration  experienced  by a  receptor,  such  as  a
human being, due to  given  emissions of  NO   has received little  attention  in  the literature
until very recently.   Relationships  among ambient NO , hydrocarbons,  and ozone which make use
of the  complex  chemistry  described  above have been considered in connection with the question
of predicting ambient ozone concentrations.   Some of the methodology  (which includes a variety
of air quality  simulation models) applicable to the ozone problem has  potential  application to
the case of NO   source-receptor relationships.   However,  neither development nor validation of
these models  for the N02  problem has reached a stage where it is possible to evaluate with any
certainty  either their usefulness  or  accuracy.  For  this  reason, no  general  statements can
prudently be made at this time concerning the  specific  impacts on air quality of  various NOX
source types.  Such  considerations  must  await documentation of adequate modelling  procedures.
                                             6-41

-------
6.6  REFERENCES

Abeles,  F.  B. ,  L.  E.  Craker,  L.  E.  Forrence,  and G.  R.  Leather.   Fate of air  pollutants:
     removal of ethylene,  sulfur dioxide, and nitrogen dioxide  by  soil.   Science  (Washington,
     D.C.) 173:914-916, 1971.

Altshuller,  A.  P., S.  L.  Kopczynski,  W.  A.  Lonneman,  F.  D.  Sutterfield,  and D.  L.  Wilson.
     Photochemical  reactivities of  aromatic hydrocarbon-nitrogen  oxide  and related  systems.
     Environ. Sci. Technol. 4:44-49, 1970.

Anderson,  G.  E. ,   P.  M.  Roth,  and  T.   W.  Tesche.   Modeling  and Prediction of Nitrogen  Oxide
     Concentrations  and  Their  Distribution.   Prepared  by  Systems  Applications,  Inc.,  for
     American Petroleum Institute, 2101 L Street, N.W., Washington, D.C.  20037.  EF78-32R,  May
     1978.

Atkinson,  R. ,  R.   A.  Perry,  and J.   N.   Pitts,  Jr.   Rate constants  for  the reaction of the  OH
     radical with  CH3SH  and CH3NH2  over  the temperature  range 299-426°K.  J. Chem.  Phys.  66:
     1578-1581,  1977.

Atkinson,  R. ,  R.   A.  Perry and J.  N.  Pitts,  Jr.   Rate constants for  the reactions of the  OH
     radical with  (CH3)2NH,  (CH3)3N  and  C2H5NH2  over  the temperature  range  298-426°K.   J.
     Chem. Phys.  68:1850-1853,  1978.

Baldwin,  A.  C.,  J. R.  Barker,  D.  M.   Golden,  and D.  G.  Hendry.   Photochemical  smog.   Rate
     parameter estimates and computer  simulations.   J. Phys. Chem.  81:2483-2492, 1977.

Batt,  L. , R. D.  McCulloch,  and R.  T.  Milne.   Thermochemical  and kinetic  studies of  alkyl
     nitrates (RONO) - D(RO-NO), the reactions between RO and NO, and the decomposition of  RO.
     lr\:   Proceedings of  the  Symposium  on  Chemical  Kinetics  Data  for  the Upper and  Lower
     Atmosphere,   Stanford  Research  Institute,  Warrenton,  Virginia,  September  15-18,  1974.
     Int. J.  Chem. Kinet. Symp.  (1):441-461, 1975.

Brandner,  J.  D. ,  N.  M.  Junk,  J.  W.   Lawrence,  and J.  Robins.   Vapor  pressure  of  ammonium
     nitrate.  J.  Chem.  Eng. Data 7:227-228, 1962.

Breeding, R.  J. ,  H. B. Klonis,  J. P. Lodge,  Jr., J. B. Pate, D.  C.  Sheesly, T. R.  Englert,  and
     D.  R.  Sears.  Measurements  of  atmospheric  pollutants  in  the St.  Louis  area.  Atmos.
     Environ. 10:181-194, 1976.

Bretschneider,  K.  ,  and  J.  Matz.  Nitrosamines (NA)  in the atmospheric air  and  in the air  at
     the workplace.  Arch. Geschwulstforsch., 42:36-41, 1973.

Bretschneider,  K. ,  and J.  Matz.  Occurrence  and  analysis of  nitrosamines  in  air.   Ir\:   En-
     vironmental   N-nitroso  Compounds  Analysis .and Formation,  Proceedings of  a  Working  Con-
     ference, International Agency for Research on Cancer, Tallinn, Estonian  SSR,  October 1-3,
     1975.  E.  A.  Walker, P. Bogovski,  L. Griciute, and W. Davis, eds. ,  IARC  Scientific Publi-
     cations No.  14,  International  Agency  for  Research  on  Cancer,  Lyon, France,  1976.   pp.
     395-399.

Calvert, J. G.  and J.  N. Pitts,  Jr.  Photochemistry.  John Wiley  and Sons,  Inc., New York,  NY,
     1966.  p.  371.
                                             6-42

-------
Calvert,  J.  G. ,  Fu-Su,  C.  R.  Lindley, W. M.  Uselman,  and J. H.  Shaw.   The use of  long  path
     FT-IR  spectroscopy  in  kinetic  studies  of  reactive molecules  of atmospheric  interest.
     Paper #26,  presented at the Miami  Beach  ACS Annual meeting,  Physical  Chemistry Section,
     September 10-15, 1978.

Carter, W.  P.  L. ,  A. C.  Lloyd,  J.  L. Sprung, and J. N.  Pitts,  Jr.   Computer  modeling of  smog
     chamber data:   progress in validation  of a  detailed mechanism  for  the photooxidation of
     propene and n-butane  in photochemical smog.  Int. J.  Chem.  Kinet.  11:45-101,  1979.

Challis,  B.  C., and S.  A.  Kyrtopoulos.  Rapid  formation of  carcinogenic  N-nitrosamines  in
     aqueous alkaline solutions.  Br.  J.  Cancer 35:693-696, 1977.

Chamberlain, A.  C.    Radioactive aerosols  and vapours.  Contemp.  Phys.  8:561-581,  1967.

Chan, W.  H. ,  R.  J.   Nordstrom, J. G.  Calvert,  and J. H.  Shaw.  Kinetic study of  HONO  formation
     and  decay  reactions  in gaseous  mixtures of HONO,  NO,  NO,,  HLO, and N9.   Environ.  Sci.
     Technol. 10:674-682,  1976.                                ^   ^         ^

Chow, Y.  L., M.  P.  Lau,  R. A. Perry,  and  J.  N. S. Tarn.   Photoreactions of  nitroso compounds in
     solution.   XX.  Photoreduction,  photoelimination and photoaddition of nitrosamines.   Can.
     J. Chem. 50:1044-1050,  1972.

Cole, H.  S., and J.   E. Summerhays.  A  review of techniques available  for  estimating short-term
     N02  concentrations.   J. Air Pollut.  Control Assoc.  29:812-817, 1979.

Cox, R. A. ,  and  R.   G. Derwent.  The  ultra-violet absorption  spectrum of  gaseous  nitrous acid.
     J. Photochem.  6:23-34,  1976.

Cox, R. A., and M.  J. Roffey.  Thermal decomposition of  peroxyacetylnitrate  in the presence of
     nitric oxide.    Environ. Sci. Technol. 11:900-906, 1977.

Dana, M. T. , J.  M.  Hales,  and M. A. Wolf.  Rain scavenging of S0~  and sulfate  from power plant
     plumes.   JGR J.  Geophys. Res. 80:4119-4129, 1975.           *

Darnall,  K. R. ,  W.  P. L. Carter, A. M. Winer,  A.  C.  Lloyd, and J.  N.  Pitts,  Jr.   Importance of
     R02  + NO  in alkyl  nitrate  formation from C4-C6 alkane photooxidations  under  simulated
     atmospheric conditions.  J. Phys. Chem.  80:1948-1950, 1976.

Davis,  D.  D., G.  Smith, and  K.  Klauber.   Trace gas analysis of power  plant plumes via aircraft
     measurement:  03,  NO ,  and SOp chemistry.  Science  (Washington,  D.C.)  186:733-736, 1974.

Demerjian, J. , J. A. Kerr, and J. G.  Calvert.  The mechanism of photochemical smog formation.
     Adv.  Environ.  Sci.  Technol. 4:1-262,  1974.

Dimitriades, B.   Effects of hydrocarbons  and  nitrogen oxides on photochemical smog formation.
     Environ.  Sci.  Technol. 6:253-260, 1972.

Dimitriades,  B.   Oxidant control  strategies.  Part I.   Urban oxidant control  strategy derived
     from existing smog chamber data.  Environ. Sci. Technol. 11:80-88, 1977.

Druckrey,   H. ,  R.  Preussmann, D.  Schmahl, and M.  Muller.  The  chemical constitution  and  car-
     cinogenic effects of  the nitrosamines.  Naturwissenchaften  48:134-135,  1961.
                                             6-43

-------
Dushumin,  K.  K.,  and E.  D.  Sopach.   The  role of  reactions  of  dimethyl ami ne  with  nitrogen
     tetraoxide and ozone in atmospheric pollution.  Gig. Sanit. (7):14-18, 1976.

Falls, A.  H. ,  and  J.  H.  Seinfeld.   Continued development of  a  kinetic  mechanism for photo-
     chemical  smog.  Environ. Set. Technol. 12:1398-1406, 1978.

Falls, A.  H. ,  G.   J.  McRae,  and J.  H.  Seinfeld.   Sensitivity  and  uncertainty  of  reaction
     mechanisms for photochemical air  pollution.   Int.  J.  Chem.   Kinet.  11:1137-1162, 1979.

Gay,  B.  W. ,  Jr.,  and J.  J.  Bufalini.   Nitric  acid and  the  nitrogen balance  of irradiated
     hydrocarbons  in  the presence  of oxides of nitrogen.   Environ.  Sci.  Technol. 5:422-425,
     1971.

Gehlert,  P., and W.  Rolle.   Formation of  diethylnitrosamine  by reaction  of diethylamine with
     nitrogen  dioxide in the gas phase.   Experientia 3_3:579-581, 1977.

Ghiorse,  W.  C., and M. Alexander.  Effect of microorganisms on  the  sorption and  fate of sulfur.
     dioxide and nitrogen dioxide in soil.  J. Environ. Qua!. 5_:227-230, 1976.

Goodall,  G. M. ,  and T.  H.  Kennedy.  Carcinogenicity of dimethylnitramine  in  NZR rats  and NZO
     mice.   Cancer Lett. 1:295-298, 1976.

Graham, R.  A.,  A.  M.  Winer, and J. N. Pitts, Jr.  Temperature  dependence  of the uni-molecular
     decomposition  of pernitric  acid and its atmospheric implications.  Chem. Phys. Lett. 51:
     215-220,  1977.

Grosjean, D.  T., and S.  K. Friedlander.   Formation of organic aerosols from cyclic olefins and
     diolefins.  In:   The Character and Origins  of Smog Aerosols:   A  Digest of Results From
     the California Aerosol  Characterization Experiment (ACHEX).   Adv. Environ. Sci.  technol.
     9:435-473, 1980.                                       |

Grosjean, D. T., K.  Van Cauwenberghe, J.  Schmid,  and J.  N. Pitts, Jr.  Formation of  nitrosa-
     mines  and  nitramines  by photooxidation of amines under simulated atmospheric conditions.
     I_n:   Proceedings,  4th  Joint Conference on  Sensing  of  Environmental  Pollutants,  American
     Chemical   Society  and  Others,  New  Orleans,  Louisiana,  November  6-11,  1977.    American
     Chemical  Society, Washington, DC, 1978.  pp. 196-199.

Hampson,  R.  F. , Jr., and D. Garvin, Eds.  Reaction. Rate and Photochemical  Data for Atmospheric
     Chemistry--1977.    National  Bureau  of Standards  Special  Publication  513, U.S. Department
     of Commerce,  National Bureau of Standards, Washington, DC, May 1978.

Hanst, P. L. ,  J.  W. Spence, and  M.  Miller.   Atmospheric chemistry of N-nitroso diethylamine.
     Environ.  Sci.  Technol. 11:403-405, 1977.

Hare, C.  T. ,  and  D. A.  Montalvo.  Diesel Crankcase Emissions Characterization.  EPA-460/3-77-
     016, U.S.  Environmental Protection Agency, Ann Arbor, MI,  September 1977.

Hegg, D. , P.  V. Hobbs, L. F. Radke, and H.  Harrison.  Ozone and nitrogen oxides  in power plant
     plumes.   J_n:   International Conference  on Photochemical  Oxidant  Pollution and  Its Con-
     trol,  Proceedings:   Volume  I,  U.S.  Environmental  Protection  Agency  and Others,  Raleigh,
     North   Carolina,  September  12-17,   1976.   B.   Dimitriades, ed. ,  EPA-600/3-77-001a,  U.S.
     Environmental   Protection  Agency,  Research Triangle Park,  NC,  January 1977.  pp.  173-183.

Heicklen, J.   Atmospheric Chemistry.  Academic Press, Inc., New York, NY,  1976.
                                             6-44

-------
Hendry, D.  G.   Reactions of aromatic compounds in the atmosphere,   In:   Chemical  Kinetic  Data
     Needs  for  Modeling  the Lower Troposphere, Proceedings  of a Workshop,  National  Bureau  of
     Standards  and  Others,  Reston, Virginia, May  15-17,  1978.   J.  T.  Herron,  R.  E.  Huie, and
     J. A.  Hodgeson,  eds. ,  NBS Special Publication 557, U.S. Department  of  Commerce,  National
     Bureau of  Standards, Washington, DC, August 1979.  pp. 85-96.

Hendry, D. G.,  and R. A.  Kenley.   Generation of peroxy radicals  from  peroxy  nitrates  (RO?NO?).
     Decomposition of peroxyacyl nitrates.  J. Am. Chem. Soc. 99:3198-3199,  1977.

Herron, J.  T. ,  and  R.  E.  Huie.   Stopped-flow studies  of the  mechanism of ozone-alkene re-
     actions in the gas phase.  Ethylene.  J. Am.  Chem. Soc. 99:5430-5435, 1977.

Heuss, J.  M.   Smog Chamber Simulation of the Los Angeles Atmosphere.   General  Motors  Research
     Publication GMR-1082, General Motors Corp., Warren, MI, 1975.

Hill,  A.  C.  Vegetation:  a  sink  for atmospheric pollutants.   J.  Air Pollut.  Control  Assoc.
     21:341-346, 1971.

Horowitz, A.,  and J. G.  Calvert.   The quantum efficiency of the  primary processes  in  formalde-
     hyde  photolysis at  313° A and  25 degrees  C.   Int.  J.  Chem.  Kinet.  10:713-732, 1978.

Howard, C.  J.   Kinetics  of the reaction  of  H02  with N02-  J. Chem.  Phys. 67:5258-5262, 1977.

Howard, C.  J.,  and  K.  M.  Evenson.   Kinetics of  the reaction of H09 with NO.   Geophys.  Res.
     Lett. 4:437-440, 1977.                                           *

Jackson,   B. , and  F.  I.  Dessau.  Liver tumors in rats fed acetamide.   Lab. Invest.  10:909-923,
     1961.

Jeffries,   H. ,  D.  Fox, and  R.  Kamens.   Outdoor Smog Chamber  Studies:   Effect of  Hydrocarbon
     Reduction  on  Nitrogen Dioxide.  EPA-650/3-75-011,  U.S.  Environmental Protection  Agency,
     Research Triangle Park, NC, June 1975.

Kaiser, E.  W. ,  and  C.  H.  Wu.  A  kinetic  study  of the gas  phase  formation and decomposition
     reactions  of nitrous acid.  J. Phys. Chem.  81:1701-1706, 1977.

Keefer, L.  K.   Promotion  of  N-nitrosation reactions by  metal  complexes.  In:   Environmental
     N-nitroso  Compounds Analysis  and Formation,  Proceedings of a  Working Conference,  Inter-
     national  Agency  for  Research  on Cancer, Tallinn, Estonian  SSR,  October 1-3,  1975.  E.  A.
     Walker, P.  Bogovski,  L.   Griciute,  and  W.  Davis, eds.,  IARC  Scientific Publications No.
     14,  International Agency for  Research on Cancer, Lyon, France, 1976.  pp.  153-159.

Keefer, L.  K.,  and  P.  P. Roller.   N-nitrosation  by  nitrite ion  in  neutral  and basic  medium.
     Science (Washington, D.C.) 181:1245-1246, 1973.

Kenley, R.  A.,  J.  E.  Davenport,  and D.  G.   Hendry.   Hydroxyl  radical reactions  in  the gas
     phase.  Products and  pathways for the  reaction  of  OH with toluene.   J.  Phys. Chem.  82:
     1095-1096,  1978.

Kewley, D. J.   Atmospheric dispersion of a chemically reacting plume.   Atmos. Environ.  12:1895-
     1900, 1978.

Korth, M.   W., A.  H.  Rose, and  R.  C.  Stahman.   Effects of  hydrocarbons to oxides  of  nitrogen
     ratio  on  irradiated auto  exhaust.   Part 1.   J.  Air  Pollut.  Control Assoc.   14:168-175,
     1964.


                                             6-45

-------
Lesclaux,  R.,  and M.  Demissy.   On  the  reaction of NH9  radical  with oxygen.   Nouv. J.  Chim.
     1:443-444, 1978.                                  *

Lijinsky, W.,  L.  Keefer,  E.  Conrad, and R. van  de Bogart.  Nitrosation  of  tertiary  amines  and
     some biologic implications.  J. Natl. Cancer Inst. (U.S.) 49:1239-1249, 1972.

Liu, M.-K. ,  D. R.  Durran,  and M.  J.  Meldgrin.   The  Development  of a Regional Air  Pollution
     Model and Its  Application to the Northern  Great  Plains.  EPA-908/1-77-001, U.S. Environ-
     mental Protection Agency, Denver, CO, July  1977.

Lloyd,   A.  C.   Tropospheric  chemistry of" aldehydes.   In:   Chemical Kinetic  Data  Needs  for
     Modeling  the  Lower  Troposphere, Proceedings of a Workshop,  National  Bureau  of  Standards
     and  Others,  Reston, Virginia,  May 15-17,  1978.   J.  T.  Herron, R.  E.  Huie,  and J.   A.
     Hodgeson, eds., NBS Special Publication 557, U.S. Department  of Commerce,  National  Bureau
     of Standards, Washington, DC, August 1979.  pp. 27-48.

Mirvish, S. S.  Formation of N-nitroso compounds:  chemistry, kinetics and  i_n vivo occurrence.
     Toxicol. Appl. Pharmacol. 31:325-351, 1975.

Moortgat,  G.   K. ,  and P.  Warneck.   CO and  H2 quantum  yields  in  the  photodecomposition  of
     Formaldehyde in air.  J. Chem.  Phys. 70:3639-3651, 1979.

Morris, E. D. ,  and H.  Niki.  Mass  spectrometric study of  the reactions  of nitric acid with 0
     atoms and H atoms.  J.  Phys.  Chem. 75:3193-3194,  1971.

Mortland, M.   M.   Nitric  oxide absorption by  clay  minerals.  Soil Sci.  Soc. Am. Proc.  29:514-
     519, 1965.

National  Aeronautics  and Space Administration.   Update  of rate  constant tables,   jji:    Upper
     Atmospheric  Programs Bulletin No. 79-4.  National Aeronautics  and Space  Administration,
     Washington, DC, April 1979.  pp. 9-10.

Neurath, G.  B. , M.  Diinger,  and F. G. Pein.  Interaction  of nitrogen oxides, oxygen  and amines
     in  gaseous mixtures.   In:    Environmental  N-nitroso  Compounds  Analysis  and  Formation,
     Proceedings  of  a Working  Conference,   International  Agency  for  Research  on  Cancer,
     Tallinn, Estonian SSR,  October  1-3, 1975.   E.  A.  Walker, P. Bogovski,  L. Griciute,  and W.
     Davis,  eds.,  IARC Scientific  Publications No.  14,  International  Agency  for Research  on
     Cancer,  Lyon, France, 1976.  pp. 215-225.

Neurath, G.  B. , B.  Pirmann, H. Luttich,  and  H.  Wichern.    N-nitroso binding in tobacco smoke.
     Beitr. Tabakforsch.  3:251-252,  1965.

Niki,  H.   An  evaluation  of chemical  kinetic  data needs  for modeling the lower  troposphere:
     reactions  of  olefins with hydroxyl  radical and  with  ozone.  J_n:   Chemical   Kinetic Data
     Needs for  Modeling  the Lower Troposphere,  Proceedings of a Workshop, National  Bureau of
     Standards  and Others,  Reston,  Virginia,  May 15-17,  1978.   J.  T. Herron,  R.  E.  Huie,  and
     J. A. Hodgeson, eds., NBS Special Publication 557, U.  S. Department  of Commerce, National
     Bureau of Standards, Washington, DC, August 1979.  pp. 7-24.

Niki,  H. ,  P.   D.  Maker,  C.  M.  Savage,  and L.  P. Breitenbach.   Fourier transform IR spectro-
     scopic observation of  propylene ozonide  in the gas  phase reaction  of  ozone-cis-2-butene-
     formaldehyde.  Chem.  Phys. Lett. 46:327-330, 1977.
                                             6-46

-------
Ohshima, H. ,  and  T.  Kawabata.  Mechanism of n-nitrosodimethylamine  formation  from  trimethyla-
     mine  and  trimethylaminoxide.   In:
     ceedings  of  a Working  Conference,
     New Hampshire, August 22-24, 1977.
     and W. Davis, eds., IARC Scientific
     on Cancer, Lyon, France, 1978.  pp.
                             Environmental  Aspects of  N-nitroso Compounds,  Pro-
                           International Agency  for  Research on Cancer,  Durham,
                           E. A. Walker, M. Castegnaro,  L.  Griciute,  R.  E.  Lyle,
                           Publications No. 19,  International  gency  for  Research
                           143-153.
O'Neal, H.  E.
     J. Chem.
,  and C. Blumstein.  A new mechanism  for gas phase  ozone-olefin  reactions.
Kinet.  5:397-413, 1973.
Int.
Orel,  A.  E. ,  and J.  H.  Seinfeld.   Nitrate formation  in  atmospheric aerosols.  Environ.  Sci.
     Technol.  11:1000-1007, 1977.

Pellizzari, E.  D.   The Measurement of Carcinogenic Vapors  in Ambient Atmospheres.   EPA-600/7-
     77-055,   U.S.   Environmental  Protection  Agency,   Research  Triangle Park,  NC,  June  1977.

Perry,  R.  A. ,  R.  Atkinson,  and J.  N.   Pitts,  Jr.   Kinetics  and mechanism  of the gas  phase
     reaction of OH radicals  with  aromatic hydrocarbons  over  the temperature  range 296-473K.
     J. Phys.  Chem.  81:296-304, 1977.

Peterson, T.   W. ,  and J.  H. Seinfeld.  Mathematical  model for  transport,  interconversion,  and
     removal   of  gaseous  and  particulate  air  pollutants--application to  the  urban  plume.
     Atmos. Environ. 11:1171-1184 1977.

Pitts,  J.  N. , Jr.   Mechanism  of Photochemical.Reactions in Urban  Air.   Volume I:  Chemistry
     Studies.    EPA-600/3-77-014a,   U.S.   Environmental Protection  Agency,  Research  Triangle
     Park, NC, February 1977.

Pitts,  J.  N. ,  Jr.,  K.  R. Darnell,  A. M.  Winer, and J.  M.  McAfee.  Mechanisms  of Photochemical
     Reactions  in Urban  Air.   Volume II:  Chamber Studies.   EPA-600/3-77-014b, U.  S.  Environ-
     mental Protection Agency, Research Triangle Park,  NC, February 1977.

Pitts,  J.  N. , Jr.,  D.  Grosjean,  K. Van  Cauwenberghe, J. P.  Schmid, and  D.  R. Fitz.    Photo-
     oxidation  of  aliphatic   amines  under  simulated  atmospheric  conditions:   formation of
     nitrosamines,  nitramines,  amides  and photochemical  oxidant.   Environ.  Sci.  Technol.  12:
     946-953,  1978.

Pitts,  J. N.  Jr.,  A.  M.  Winer,  K.  R.  Darnell,  G.  J.  Doyle, and J. M. McAfee.  Chemical  Conse-
     quences  of Air Quality Standards and of Control  Implementation Programs:   Roles of  Hydro-
     carbons,  Oxides  of  Nitrogen,   and Aged  Smog in the  Production  of  Photochemical  Oxidant.
     Final Report.   California Air  Resources Board Contract  No. 4-214,  University  of  Cali-
     fornia,  Statewide Air Pollution Research Center,  Riverside, CA, May 1976.

Polo, J., and Y. L.  Chow.  Efficient degradation of nitrosamines by photolysis.  In:   Environ-
     mental N-nitroso  Compounds  Analysis and Formation,  Proceedings  of a  Working  Conference,
     International   Agency  for Research  on  Cancer,  Tallinn, Estonian SSR,  October 1-3,  1975.
     E. A. Walker,  P. Bogovski,  and L.  Griciute,  eds., IARC  Scientific  Publication  No.  14,
     International  Agency for Research on Cancer, Lyon, France, 1976.  pp.  473-486.

Ridd, J. H.   Nitrosation, diazotisation and deamination.   Q. Rev. Chem.  Soc. 15:418-441,  1961.

Robinson, E. , and R.  C.  Robbins.   Gaseous nitrogen compound pollutants from urban  and natural
     sources.   J.  Air Pollut.  Control Assoc.  20:303-306,  1970.
                                             6-47

-------
Rogers, H. H. ,  H.  E.  Jeffries, E.  P.  Stahel,  W. W.  Heck.  L.  A.  Ripperton,  and A.  M. Wither-
     spoon..   Measuring  air pollutant  uptake  by plants:  a  direct  kinetic technique.  J.  Air
     Pollut.  Control Assoc. 27:1192-1197, 1977,

Scanlan,  R.  A.   N-nitrosamines  in foods.   CRC Crit.  Rev.  Food  Technol.   5:357-402,   1975.

Schere, K. L. ,  and K.  L. Demerjian.  Calculation of  Selected Photolytic  Rate Constants Over  a
     Diurnal   Range.   A  Computer  Algorithm.   EPA-600/4-77-015,  U.S.  Environmental  Protection
     Agency,  Research Triangle Park, NC, March 1977.

Seinfeld,   J.   H.    Air  Pollution:   Physical  and  Chemical  Fundamentals.   McGraw-Hill   Book
     Company, New York, 1975.

Shu, W.  R. ,  R.  C.  Lamb, and J.  H.  Seinfeld.   A model  of  second-order chemical  reactions in
     turbulent  fluid -  Part II.   Application to atmospheric plumes.  Atmos.  Environ. 12:1695-
     1704, 1978.

Smith,   P.  A.  S. ,  and R.  N. Loeppky.   Nitrosative  cleavage  of  tertiary amines.   J.  Am.   Chem.
     Soc.  89:1147-1157, 1967.'

Spicer, C. W. ,  and D.  F. Miller.   Nitrogen  balance in  smog chamber  studies.  J.  Air Pollut.
     Control  Assoc. 26:45-50,  1976.

Stampfer,  J.  F., Jr., and J. A.  Anderson.  Locating the  St.  Louis urban plume at 80  and 120 km
     and some of its characteristics. Atmos.  Environ. 9:301-313, 1975.

Stelson, A. W. ,  S.  K.  Friedlander,  and  J.  H.  Seinfeld.  Note  on the equilibrium relationship
     between  gaseous  nitric  acid  and  ammonia  and  particulate  ammonium  nitrate.   Atmos.
     Environ.   13:369-371, 1979.

Stephens,  E.   R.   Photochemical  formation of oxidants.   In:   Proceedings of  the Conference on
     Health  Effects  of  Air  Pollutants,  National  Academy  of  Sciences—National  Research
     Council, Washington,  D.C.,  October 3-5,  1973.   Serial  No.  93-15,  U.S.  Senate,  Committee
     on Public Works, Washington, DC, November.1973.  pp. 465-487.

Stern,   A.  C. ,  Ed.   Air Pollution.   3rd Edition.   Volume III.    Measuring, Monitoring,  and
     Surveillance of Air Pollution.  Academic Press,  Inc., New  York, NY,  1976.

Sundareson, B.  B. , C.   I.  Harding,  F.  P.  May,  and E.  R.  Hendrickson.  Adsorption of nitrogen
     oxides from waste gas.  Environ. Sci. Technol. 1:151-156,  1967.

Tingey, D. T.   Foliar  Absorption of Nitrogen Dioxide.   M. A. Thesis, University of  Utah,  Salt
     Lake City, UT, June 1968.

Trijonis,  J.   Empirical Relationships Between Atmospheric Nitrogen  Dioxide  and Its Precursors.
     EPA-600/3-78-018,   U.S.   Environmental  Protection   Agency,  Research  Triangle  Park,  NC,
     February 1978.

Trijonis,  J.    Dependence of ambient N02 on precursor control.  In:  Implications of the  Clean
     Air  Act  Amendments  of 1977 and  of Energy  Considerations  for Air Pollutions Control.
     AIChE Symp. Ser.  76(196):240-248, 1980.
                                             6-48

-------
Tsang,  W. ,  D.  Garvin, and  R.  L.  Brown.  NBS  Chemical  Kinetics Data Survey—The  Formation  of
     Nitric Acid from Hydroxyl and  Nitrogen  Dioxide,  1977.

Tuazon,  E.  C. ,  A.  M. Winer,  R.  A.  Graham, J.  P.  Schmid,  and  J.  N.  Pitts,  Jr.   Fourier trans-
     form  infrared detection  of  nitramines  in irradiated amine-NO   systems.   Environ.  Sci.
     Technol. 12:954-958, 1978.                                     x

Turner,  D.  B.   Atmospheric dispersion modeling:  a  critical  review.   J.  Air  Pollut.  Control
     Assoc. 29:502-519, 1979.

U.  S.  Environmental  Protection Agency.   Assessment of  Scientific Information  on Nitrosamines,
     Report of  an  ad hoc Study Group  of  the  USEPA Science Advisory  Board  Executive  Committee,
     August 1976.   pp. 24-25.

U.  S.  Environmental  Protection Agency.   Scientific and Technical Assessment  Report  on Nitro-
     samines.  EPA-600/6-77-001, U.S.  Environmental Protection Agency,  Research Triangle Park,
     NC, June 1977.

U.  S. Environmental Protection Agency.  Air Quality Criteria for  Ozone  and  Other Photochemical
     Oxidants.   EPA-600/8-78-004,  U.S. Environmental  Protection  Agency, Washington,  DC, April
     1978.

Walker,  P.,  J.  Gordon,  L.  Thomas, and R. Oullette.   Environmental  Assessment  of Atmospheric
     Nitrosamines.   EPA  Contract  No.   68-02-1495,  The Mitre Corporation, McLean, VA,  February
     1976.

Wartheson,  J.  J. ,  R.  A.  Scanlan,  D.  P.  Bills, and  L.  M.  Libbey.   Formation  of  heterocyclic
     n-nitrosamines  from  reaction  of  nitrite  and selected primary  diamines and amino acids.
     J. Agric.  Food Chem. 23:898-902,  1975.

Weibe,  H. A.,  A.  Villa,  T.   M. Hellman, and J.  Heicklen.   Photolysis of methyl  nitrite in the
     presence of nitric  oxide, nitrogen  dioxide and oxygen.   J.  Am. Chem.  Soc.  95:7-13, 1973.

Weisburger, J.  H. , R.  S.   Yamamoto,  R.  M. Glass,  and  H.  H.  Frankel.  Prevention by  arginine
     glutamate of  the carcinogenicity of acetamide  in rats.   Toxicol.  Appl.  Pharmacol. 14:
     163-175, 1969.

White, W. H.  NO -03 photochemistry in power plant plumes:  comparison  of theory with  observa-
     tion.  Environ.  Sci.  Technol.  11:995-1000,  1977.

White, W. H. ,  J.  A.  Anderson, D.  L.  Blumenthal, R.  B.  Husar,  N.  V. Gillani,  J. D.  Husar, and
     W.  E.  Wilson,  Jr.   Formation and  transport of   secondary  air   pollutants:   ozone and
     aerosols  in  the St.  Louis  urban plume.   Science  (Washington,  D.C.) 194:187-189,  1976.

Whitten, G.  Z. , and H. Hogo.  Mathematical Modeling of  Simulated  Photochemical  Smog.   EPA-600/
     3-77-011,  U.S. Environmental Protection Agency, Research  Triangle  Park, NC, January 1977.
                                             6-49

-------
             7.  SAMPLING AND ANALYSIS FOR AMBIENT N0v AND NO -DERIVED POLLUTANTS
    i                                                 "       "

7.1  INTRODUCTION
     This chapter  summarizes  a variety of methods used for measuring oxides of nitrogen (NO )
                                                                                            A
and other pollutants which may be derived from NO  through atmospheric transformations (Chapter
                                                 s\
6).   Emphasis  is placed upon  describing  methodology currently available or  in   general   use
for routine monitoring of ambient pollutant concentrations.
     An  appreciation of  some of  the  errors  involved  in present  monitoring  techniques  is
important in  evaluating the  quality of  ambient  pollution data.  Three types  of  errors  are
discussed in this section:   interferences, systematic errors and random errors.
     The measurement of individual pollutants in ambient air is complicated by the presence of
other  airborne  chemicals  which  may  produce  responses in  the measuring  apparatus  generally
indistinguishable  from  those produced   by  the  pollutant being  monitored.   These  spurious
responses are  known as "interferences."  Extensive tests are conducted by the U.S. Environmenta
Protection Agency  (U.S.  EPA)  and/or other laboratories on potential  interferences in proposed
measurement  techniques  before  they  are  considered  suitable  for  routine monitoring.   This
chapter describes reported interferences for the methods listed.   It should be noted, however,
that  not all  potential  interferences have  equal  significance.   Their  magnitude  will,  in
general, depend  on the ambient  concentrations  of the interfering species,  the  inherent sen-
sitivity of  a given  procedure to spurious responses,  and,  in some cases, on details  of  the
measuring apparatus  which  may  vary  from  instrument  to  instrument.   An  analytic  technique
sensitive to  interference  may still be useful  if the interfering species  occurs only  in  low
concentrations in ambient air or may otherwise be accounted for.
     In  addition to  errors  introduced by  interferences,  a given  analytic technique  may  be
subject  to  systematic over-  or  underestimation of the pollutant  concentration  which  affects
the accuracy  with  which these concentrations are known.   Such errors are  known as  "biases."
The assessment of the magnitude of such biases for a given analytical  method generally requires
extensive testing  by a  number of  laboratories  sampling  the  same pollutant  concentration  in
ambient air (collaborative testing).
     Random errors  introduced by  unknown factors such as variability in  detailed  procedures
used by different operators or sensitivity of the method to small uncontrollable  variations in
operational  parameters  are generally  known collectively  as  an imprecision in the method.   A
measure of this  type  of error often  used  is  the  standard deviation of a set of  measurements.
Once the standard  deviation  is known, it may be expected  on statistical  grounds  that about 95
percent  of  measurements made  on the  same  ambient air sample  will  yield  values for  the  N0~
concentration which differ from the average by at most + 2 standard deviations.   The  precision
of a method is also often assessed in collaborative testing procedures.   The results  of testing
for these two error types are described in this  chapter where  available.
                                            7-1

-------
     A critical  analysis  of techniques for measuring  nitrogen  oxides  in ambient air has been
repbrted  very  recently by  Saltzman (1980).   In  addition,  a  historical  review of  USEPA N02
monitoring methodology requirements has been given by Purdue and Mauser (1980).
     In considering  the  analytic techniques described below  it  must  be noted that the state-
of-the-art  of  measurement  technology  is  constantly  changing.   For  this  reason,  techniques
currently in use or recommended for use may be replaced by better methods at some future time,
techniques which are  presently in the  development stage  may  become routine in the future, or
entirely new techniques may be developed.
     Since the publication  in 1971 of the original document Air Quality Criteria for Nitrogen
Oxides, there  have  been  significant changes in the  technology  associated with measurement of
ambient concentrations of  both NO and  N02-  In addition,  concern about the potential adverse
human  health  implications of  ambient concentrations  of  other NO -derived  compounds  such as
suspended nitrates,  nitric-acid, and  N-nitroso compounds  has led both  to  development  of new
analytic  techniques, and  to a  reexamination  of  existing  methodology for  their measurement.
     With regard to the measurement of N02, the original  Federal Reference Method,  the Jacobs-
Hochheiser technique,  was  discovered  to have unresolvable technical  difficulties.   The USEPA
published the  following  brief summary of these difficulties  on  June  8, 1973 when  it withdrew
the method (U.S.  EPA, 1973):

                   ". . .  EPA's analysis indicates that the reference  method
                   is deficient in two aspects.   First, the method over-
                   estimates nitrogen dioxide concentrations at low levels
                   and underestimates them at high levels because the  col-
                   lection efficiency of the absorbing reagent is dependent
                   upon nitrogen dioxide concentration being measured.
                   Second, the method is subject to positive interference
                   by nitric oxide.   Since the variable collection effici-
                   ency problem cannot be resolved, this  method can no
                   longer serve as the reference method."

     After extensive testing, the USEPA promulgated,  on December 1, 1976, the chemiluminescence
measurement principle  and associated  calibration .procedures  (U.S. EPA, 1976b) upon  which a
number of chemiluminescent  analytical  instruments are based,   These  analyzers,  once approved
by  the  U.S.  EPA (1975)  are referred  to  as Reference Methods.   For purpose of  simplicity in
the descriptions to  follow,  however,  the term Reference  Method  is meant to apply  both to the
measurement  principle and   to  the  instruments  based thereupon.  The  required  performance
specifications  which acceptable  continuous  chemiluminescence  analyzers must meet are shown in
Table 7-1.
     Equivalent  methods   are methods  based  on  measurement  principles  different  from  the
reference  method.    Two   kinds  of  equivalent methods   are  possible—manual  and  automated
(continuous monitoring analyzers).  Candidate automated methods may be designated as equivalent
methods if  they  meet  the  performance  specifications  listed  in  Table  7-1  and  demonstrate a

                                            7-2

-------
                  TABLE 7-1.  PERFORMANCE SPECIFICATIONS FOR NITROGEN DIOXIDE
                              AUTOMATED METHODS (U.S. EPA, 1976b)

Performance Parameter
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

Range
Noise
Lower detectable limit
Interference equivalent
Each interferant
Total interferant
Zero drift, 12 and 24 hr
Span drift, 24 hr
20 percent of upper range limit
80 percent of upper range limit
Lag time
Rise time
Fall time
Precision
20 percent of upper range limit
80 percent of upper range limit
Units
ppm
ppm
ppm
ppm
ppm
ppm
%
%
minutes
minutes
minutes

ppm
ppm
Nitrogen
Dioxide
0-0.5
0.005
0.01
+0.02
"0.04
+0.02
+20.0
+5.0
20.0
15.0
15.0

0.02
0.03

consistent  relationship  to  the  reference  method  during  side-by-side  ambient  monitoring.
Candidate  manual  methods  need only  demonstrate  a  consistent  relationship to  the  reference
method  to  be  designated as  equivalent  methods.   Table  7-2 shows  the test  specifications
which must be met to demonstrate a consistent relationship with the reference method.

                    TABLE 7-2.   CONSISTENT RELATIONSHIP TEST SPECIFICATIONS
                                FOR NITROGEN DIOXIDE (U.S. EPA, 1976b)
                    Concentration Range,         Maximum Discrepancy
                         ppm HO 2                 Specification, ppm

                    Low 0.02 to 0.08                     0.02
                    Medium 0.10 to 0.20                  0.02
                    High 0.25 to 0.35                    0.03
                                            7-3

-------
     In addition  to  the Reference Method, several  other  methods,  notably those designated in
SAROAD (see  Chapter  8)  as the instrumental  colorimetric  Griess-Saltzman  method,  the Lyshkow-
modified Griess-Saltzman  method,  the triethanolamine method, the  sodium  arsenite  method,  and
the  TGS-ANSA method have  also been  extensively  tested and are currently  in   widespread  use
and/or have been extensively tested, and are  available for routine measurement of ambient N0?
concentrations.  .Both  the sodium  arsenite  method and the TGS-ANSA method  were designated as
equivalent methods as of December 14, 1977.   This means data obtained by these two methods are
accepted by  EPA  as equivalent to chemiluminescence data (Reference Method) for the purpose of
establishing  attainment  status  with  respect  to  the National  Ambient Air Quality  Standard
(NAAQS)  for NO .  The  manual Griess-Saltzman  method,  although not  usually used  in  ambient
monitoring,  is discussed  because  a number of studies pertinent to an assessment of the health
effects have used this method in laboratory situations (Chapters 14 and 15).
     Although adequate chemical techniques exist for the determination of the nitrate fraction
of suspended particulate  matter  in ambient air,  a  number  of very recent reports have pointed
to significant  nitrate  artifact  formation  on  the  glass  fiber filters in  widespread  use  for
collecting the particulate matter.  At this time, therefore, most of the existing data base on
urban  ambient  nitrate concentrations  must  be  considered  to be of doubtful  validity.   Since
consistent  relationship  to   the  reference  method  during  side-by-side  ambient  monitoring.
Candidate  manual  methods  need only  demonstrate  a  consistent  relationship to the  reference
method to  be designated as equivalent methods.   Table 7-2 shows the test specifications which
must   be   met  to   demonstrate   a   consistent   relationship   with   the   reference   method.
positive artifact  formation  has  been shown to  be associated with conversion  of  ambient  NCL
and/or nitric  acid  (HNCO to nitrates and since  sulfuric  acid aerosol has been implicated in
removal of nitrate, data from certain background sites may be validated in special  cases where
it can  be  shown  that  the concentrations  of these  species  were  sufficiently  low  during  the
monitoring period of interest.
     Recent  discovery of  N-nitroso  compounds in food, water, and ambient air has  prompted the
development  of  a variety of  new  instrumental  techniques  in the last  few  years.   Measurement
technology  is  still  developing and insufficient time  has elapsed for careful  evaluation of
existing techniques.   In particular,  some  difficulties have  been reported to be  associated
with artifact formation under certain sampling conditions.
     Development of  long-pathlength  infrared  absorption techniques has recently made possible
the observation of nitric acid in ambient air.   However, the technique is presently too elabo-
rate  for   routine  monitoring  applications.   Other  techniques  for  quantitative  analysis  of
nitric acid vapor have been reported but have not yet been carefully evaluated.
     The sections  in this chapter  describing briefly the analysis of nitrate  in  media other
than air (e.g.,  water,  soil, and plant  and  animal  tissue) are included for two reasons:   (1)
the basic methodology is similar to that used for analyzing aqueous extracts of nitrate partic-
ulate matter drawn from the ambient air and (2).it is believed appropriate to make some

                                            7-4

-------
estimate of  human  exposure from different media  with  a view towards placing exposure via the
atmospheric  route  in  perspective.   Similar considerations prompted  the  inclusion of material
on techniques for measuring N-nitroso compounds in food and water.
7.2  ANALYTICAL METHODS FOR NO
                              X
     Many methods  have  been used to measure NO  concentrations in air.   Some of these methods
directly  measure  the  species  of  interest;  others  require  that  the  species be  oxidized  or
reduced,  or  separated  from  interferences  before  the  measurement  is  made.    Of particular
importance in this regard is the new Reference Method, the continuous chemiluminescence method.
The  method  is specific  for NO  but  may easily  be  modified for  measurement of  N0?  by first
quantitatively reducing the NO,, to NO.  The regulatory specifications relating to  the Reference
Method (RM) are prescribed in Title 40 of the Code of Federal Regulations, Part 50, Appendix F.
7.2.1  The Reference Method for NO,,:   Gas-Phase Chemi luminescence
     Atmospheric concentrations  are  measured  indirectly by first reducing  the  N02 quantita-
tively to NO,  then reacting the resultant NO  with  03 and measuring the  light  intensity from
the reaction.
     The use of the gas-phase chemiluminescent reaction of NO and 0, for quantitative measure-
ment of NO was reported initially by Fontijn et al.  (1970) and some improvements were described
by Stedman et al.  (1972).   The sample air stream is mixed with air containing a high 0, concen-
tration (approximately 1 percent).   The reaction of NO and 0, forms excited N09 molecules, the
                                                            •J                 L.
number of which  is proportional to  the  NO concentration.   Some  of  the  excited  N02 molecules
emit electromagnetic  radiation with  wavelengths  between 600  and 2000 nm, with  a maximum  at
1200 nm  (Clough and  Thrush,  1967).   The  reaction  chamber  is held  at reduced  pressures  to
decrease the  collisional  deactivation,  and  the  emitted  radiation is measured  with  a photo-
multiplier tube and associated electronics.   To reduce  interferences of  the chemiluminescent
reactions of ozone with  other species, optical filters can be employed (Stevens and Hodgeson,
1973).   Typical commercial  chemiluminescence  instruments can detect concentrations  as  low  as
9.5 ug/m3 (0.005 ppm)  (Katz, 1976).
     Since the detection  of  N02 by the  RM is  directly dependent on the analyzer's capability
to reduce N02  to  NO,  it is  important  that the conversion be essentially  quantitative  over a
wide range of N02 concentrations.
     Catalytic reduction of N09 to NO is commonly employed in chemiluminescence NO-NO  instru-
                              L.                                                      X
ments.   These  instruments measure NO  alone  by  passing the sample directly  to  the detector.
The total  concentration of NO and N02 (NO ) is measured by drawing the sample through a cataly-
tic reduction unit prior to entering the detector.  NO- concentrations are obtained by subtrac-
tion.
     Winer et al.  (1974)  studied the reactions of  various  nitrogen  compounds over carbon and
molybdenum converters.  It  was found that not  only  N02 but peroxyacetyl  nitrate  (PAN)  and a
                                            7-5

-------
wide variety of  organic  nitrogen compounds were reduced to NO quantitatively; nitroethane and
nitric acid were partially reduced.   Joshi and Bufalini (1978) report non-quantitative positive
inferences from  halocarbons  in  commercial instruments using  a  heated  carbon converter.   They
also  speculate  that  instruments using  high  temperature  stainless  steel  converters may  be
subject to interferences  from chlorinated hydrocarbons.   The authors suggest replacing heated
carbon  converters  with  FeSO. converters;  however,  this  technique  has not  been  thoroughly
evaluated.  There  is  also evidence  that converters operating at high temperatures may oxidize
ammonia (NH3) to NO  (U.S. EPA,  1973).    This  can  be of importance in measuring NO- exposures
in animal studies, where  elevated levels of NHg may be  present as a  result of biologic pro-
cesses.   It  is  not  expected to  be of  importance  in ambient  situations using  EPA  approved
analyzers.
     While care  must  be   exercised  in  the  use of  chemiluminescence  instruments  because  of
potential interferences,  in most ambient situations  NO  plus NO^ are present  in  much higher
concentrations than interfering species.
     Results  of the USEPA's collaborative quality assurance testing of the method (Constant et
al.,  1975a)  showed  that, for one-hour  instrumental  averaging  times  for N09  concentrations
                            3
ranging from 50  to 300 |jg/m  (0.027 to  0.16  ppm),  the method has an average negative bias of
five percent with  a  standard deviation of about 14 percent for equivalent samples measured by
different laboratories.
     One  collaborator  had very  large  biases,  and  another collaborator  had unstable biases.
EPA concluded that for most collaborators (8 out of 10),  however, the bias is small and well-
balanced.   The method is satisfactory for averaging times  of one hour or more.
7.2.2  Other  Analytical Methods for NO,
7.2.2.1  Griess-Saltzman Method
7.2.2.1.1  General  description of method.  This chemical  method for collection and analysis of
N02 was originally proposed  by  Ilosvay  (Threadwell  and Hall,  1935).   Many variations of this
method exist, including both manual  and automated versions.
     The  principle of the  reaction  is  thought  to be the formation of  nitrous acid by the
reaction of NO- with  water.  This in turn is reacted with  an aromatic amine to form a diazonium
salt.    In  a  further  step,  addition of  an  organic coupling agent forms  a  deeply-colored azo
dye.   The amount of NO- collected is related to the light  absorbance of the solution.
     Many variations  of the Griess-Ilosvay reaction have been explored; the variation developed
by Saltzman  (1954) is  one of the most widely  used.   A manual version of this method has been
designated as  a  Tentative  Method by the  Intersociety Committee  on  Methods for  Ambient Air
Sampling and Analysis  (1977c),   and was adopted as  a standard method by the American Society
for Testing and Materials  (ASTM,  1974a).   It has been shown that many different reagent formu-
lations are  possible so  long as they  all  contain  a diazotizer,  a coupler, a  buffer,  and a
surfactant (Kothny and Mueller,  1966).
                                            7-6

-------
     If an  extended  sampling time is required  in  the manual  version, the azo  dye  may suffer
bleaching by  SCL.   Saltzman (1954) recommended addition of acetone to prevent this.  In addi-
tion, if the sample is collected in an evacuated bottle or syringe, a long waiting period such
as might  occur  in a manual  procedure may  cause some NO to be  oxidized  to N02 (ASTM, 1974a).
     Since  the  conversion  of  NC^ to azo  dye  is  not quantitative, a factor  is  introduced to
represent the  conversion efficiency  under a  given  set of experimental  conditions.   This is
often  termed  the  "stoichiometric  factor."  If the  experimental  conditions  are the  same as
Saltzman1s  original  formulation  (1954) or  his modified  version  (1960) the  stoichiometric
factor  has  been   reported   to be  0.72 (Saltzman,  1954,  1960; Saltzman  and  Wartburg,  1965;
Shaw, 1967).  Scaringelli et al. (1970) obtained a value of 0.764.    However,  recent, unpubli-
shed work by two California groups, the California Air Resources Board (CARB)  and the Califor-
nia Department of Health Services' Air and Industrial Hygiene Laboratory (AIHL), has shown that
measurements performed by  the  manual  Saltzman technique are sensitive to the  exact concentra-
tion of the coupling compound NEDA used in the reagent (Horrocks et al.,  1981).   Careful  evalu-
ation  showed  that values  obtained using  either  the original  Saltzman  reagent  (1954)  (0.5
percent sulfanilic acid,  14 percent  acetic  acid,  and  .002  percent  NEDA)  or  the modified
Saltzman reagent  (1960)  (0.5 percent  sulfanilic acid, 5 percent acetic  acid,  and .005 percent
NEDA) are biased  approximately  13 percent  too high.   The stoichiometric factor is less sensi-
tive to variations  in  the concentrations of acetic and sulfanilic  acids and is independent of
relative  humidity,  temperature  of  the  absorbing  agent, and  nitrogen dioxide  concentration.
7.2.2.1.2   Continuous Saltzman Procedures.   In  this  procedure,  N0? in ambient air is continu-
ously absorbed in a solution of diazotizing-coupling reagents  to form an azo-dye which absorbs
light,   with  a  maximum  absorbance  at approximately  540  nm.    The  transmittance,  which  is  a
function  of  the N02 concentration, is  measured continuously  in a colorimeter  and  the output
read on a  recorder or a digital  voltmeter.
     The continuous Saltzman procedure  currently  used in ambient  air monitoring has recently
been evaluated  by  Margeson  and  Fuerst (1975).   The results show that static calibration  (with
solutions  prepared to  contain  known quantities of  the nitrite ion) is not uniformly reliable,
due  to  variable  collection efficiency  of the absorption  system.   Dynamic calibration  pro-
cedures by means of a reliable  NOp permeation device, such as  the National Bureau of Standards
Standard Reference Material  1629,  are recommended  since collection efficiency  errors and the
use of stoichiometric factors are  eliminated by virtue of the  fact  that  errors,  if they exist,
cancel  out.   Ozone  has been reported  to be  a negative interferent in the  continuous version
of the  method (Baumgardner et  al., 1975).
     Recently however, Adema (1979)  could not confirm  the interference  in one experimental
arrangement of  a  modified  manual  method.    Two specific variants of the   continuous  method
have been  used  widely  for ambient air monitoring.    Although  both  are continuous colorimetric
techniques suitable  for  averaging  times of one hour or more,  they  differ in the  use of two
distinct absorbing solutions, in which azo  dyes are formed.   The first,  sometimes known as the

                                            7-7

-------
instrumental colorimetric Griess-Saltzman  method,  uses a modification of  the  originally pro-
posed reagent  for  manual  analysis (Saltzman, 1954) and  contains  0.5 percent sulfanilic acid,
5.0 percent acetic acid, and 0.005 percent NEDA (Saltzman, 1960).  Interferences by three alkyl
nitrites, ethyl,  n-butyl,  and  isoamyl  have been  reported in  a  manual  procedure  using this
solution  (Thomas  et al., 1956).   The  second method,   sometimes known  as  the Lyshkow-modified
Griess-Saltzman method, uses  an absorbing solution consisting  of  0.15 percent sulfanilamide,
1.5 percent tartaric acid, 0.005 percent N-(l-naphthyl)-ethylenediamine dihydrochloride (NEDA),
and 0.005 percent  2-naphthol-3, 6-disulfonic acid disodium salt.   Both variants are useful in
the range of  ambient  concentrations from 19 to 9,400 pg/m  (0.01 to 5.0 ppm).   Results of the
                                                               •3
USEPA's quality assurance testing over the range 90 to 370 ug/m  (0.05 to 0.2 ppm) indicate an
average bias of  six percent with a 13 percent standard deviation among different laboratories
testing equivalent  samples  (Constant  et al., 1975b).   Estimates of bias for different labora-
tories, however,  varied considerably.
     EPA  concluded that  the overall  average  results are reasonably  accurate but  that  the
method may  produce  extremely inaccurate readings in an unpredictable fashion.   About half the
collaborators did  achieve fairly stable results for the  experiment,  leading EPA to offer the
subjective  judgment  that  although  the  method  is  difficult to use, it will  produce reliable
results in some hands.
7.2.2.1.3  Manual Saltzman Procedure.    In  this  method, N0? in ambient air is drawn at a known
rate through an absorbing solution (Saltzman, 1954) in a fritted-glass bubbler for a specified
time period,  producing an azo-dye.  The  absorbance of the solution  is  subsequently measured
manually  with  a  spectrophotometer.   The  NO,,  concentrations  present in  ambient air  may be
related to the absorbance of the azo-dye solution by calibration with other solutions contain-
ing known quantities of the  nitrite ion.
     The  manual  Saltzman  procedure is  described  in this section because  a  number  of studies
bearing on the effects of NO^ on human health have reported using this procedure (see Chapters
14 and 15).   When fritted bubblers are employed, the method has been reported to have a usable
range of 10 to 9,400 (jg/m  (0.005 to 5.0 ppm).   A precision of 1 percent of the mean concentra-
tion  is  obtainable  (Intersociety Committee for  Ambient Air  Sampling and  Analysis,  1977c).
     ASTM has  evaluated the precision  and  accuracy of the measurement  in ambient  situations
(1974b).   A  fritted bubbler, cleaned  with  dichromate  solution,  was  used  exclusively  in  the
evaluation.   The  nominal flow rate for sampling was 0.4 liter/minute.   Ten feet of TFE fluoro-
carbon tubing having a nominal   inside  diameter of 8 mm was used as a sample probe prior to the
fritted  bubbler.   The  technique used  to  evaluate the  accuracy  of the  method was  to  spike
ambient air, containing t\0y> with additional, accurately known, concentrations of NOp and then
to attempt  to  measure  the spiking concentrations.   The :NO- used for spiking was obtained from
a  permeation  tube.   Results  showed  an overall positive  bias  of 18 percent  in  measuring  the
                                            7-8

-------
spike  concentrations.   It-should,  however, be noted  that  the bias varied significantly among
the  seven  laboratories  participating in the study and was, moreover, dependent on N0~ concen-
tration.
     It  should  be  noted that this evaluation technique subjects the method to possible inter-
ferences  from other pollutants  in ambient air.   As such,  it may be  taken  to, represent the
accuracy of  results,  in the same  N09  concentration  range,  expected in health-related studies
                                                                                  3
which  use  ambient air.   Maximum  ambient  N0?  concentrations were about  250  pg/m  during the
test and maximum total N00 (ambient plus spike) concentrations used in the test were about 400
    3
ug/m .    Extrapolation  of the test results to  situations where high N0?  levels were measured
without dilution must be viewed as speculative.
     In  the  case of studies which are  carefully  controlled with regard  to  the occurrence of
pollutants  other than  N02,   it  may  be expected  that  the  accuracy of  the method  would be
significantly improved, although a similar interlaboratory test under interference-free condi-
tions  is lacking in the literature.
     As discussed in Section 7.2.2.1.1, recent measurements have resulted in a redetermination
of the stoichiometric factor for the Saltzman technique.   These results have possible important
implications  for the  numerical  values of  effects  levels  reported  both  in animal (Chapter 14)
and  human  (Chapter 15) studies.   They strongly suggest  that results  obtained  by  the manual
Saltzman technique  and referred  to Saltzman1s original  stoichiometric  factor  are,  in fact,
about 14 percent too high, i.e., effects probably occurred at lower levels than those reported.
7.2.2.2  Jacobs-Hochheiser Method—The Jacobs-Hochheiser technique  was  formerly the  Federal
Reference  Method,  but  is currently  unacceptable for  air pollution  work for  reasons  cited
above.   This  technique  is  discussed here mainly because  the method was  frequently employed in
past years in obtaining data for use in epidemiological  studies.
     The method  was  developed by  Jacobs and Hochheiser  (1958) to  avoid  the  bleaching  of the
azo dye  by  SO^  that  occurs in the Griess-Saltzman method.   Nitrogen dioxide is absorbed in a
solution of sodium hydroxide (NaOH) with butanol  added as a surfactant to improve gas transfer
when using a  fritted  bubbler.   After sampling, any sulfite from absorbed SOp is oxidized with
hydrogen peroxide.   The nitrite  in solution, is not affected.   The  solution may then be stored
for 48  hours  or  more  before analysis.   To quantitate the nitrite in solution, the solution is
first  acidified  with  phosphoric acid.   A diazotizer and  a coupling agent are  then  added to
produce an azo dye.   Solution absorbance is then measured spectrophotometrically.   The original
method  was designed for  intermittent 40-minute sampling but  was later  modified for composite
sampling over 24 hours.   This method, modified  again, was employed  by the National Air Sampling
Network (NASN) (Morgan  et  al.,  1967a,  1967b) and  was adopted as the Federal  Reference Method
in 1971 (U.S. EPA,  1971).
     The National  Academy of  Sciences document, on  nitrogen oxides  (Kothny,  1977) cites  an
extensive list of references  documenting that the  sampling efficiency of the Jacobs-Hochheiser
method  is affected by  sampling  flow rate, porosity  of bubbler frits,  liquid level,  sampling-

                                            7-9

-------
 container  material,  incoming pollutant concentration,  and  contaminants present  in  the  sample.
Sampling efficiencies,  in  the work  reviewed,  ranged  from  15 to  78  percent when 0.1N NaOH  alone
 was  used as  an  absorbant.   In addition  to  the varying  efficiency with which  NO-  is  removed  from
 the  gas sample,  the measurement  also  is affected  by  the stoichiometric factor.   This  factor is
 also variable and may be  affected  by the presence  of  hydrogen donors (Christie et al.,  1970;
 Huygen  and Steerman,  1971; Morgan  et al.,  1967a,  1967b;  Nash,  1970).  A composite  of 11  sites
 sampled in the  NASN network gave an average  stoichiometric  factor  of 62 + 7  percent (Morgan et
 al.,  1967a).  The  range  of measurable concentrations is related to the percent transmission of
 azo  dye  solutions measurable with  a  spectrophotometer.   With 50 ml of absorbing reagent  and a
 sample  flow  rate of 200 ml/min  for 24  hours,  the  range of  the method is 20  to 740  ug/m  (0.01
 to  0.4  ppm)  NO, (Katz,  1976).   Katz  (1976) reported  relative  standard deviations  of 14.4  and
                                                          3
 21.5 percent at  NO,,  concentrations  of  140 and 200 ug/m  (0.07  and  0.11 ppm),  respectively.
      Because the sampling efficiency and  stoichiometric  factor are significantly  affected  by
 the  details  of  the method employed,  by N0?  concentration,  and by constituents  of the sample
 other than NO^, the use of many modifications of the  Jacobs-Hochheiser method  in  air  quality
 and  epidemiological  studies  has led to  data  of  questionable  quality, or  even questionable
 relative comparability.
 7.2.2.3   Triethanolamine Method—The  method  described by  Levaggi  et  al.   (1973)  utilizes  an
 absorbing  solution  of  triethanolamine   and  n-butanol  surfactant.    After collection,  the
 analysis  for nitrite  is performed with  Griess-Saltzman  reagent  to  produce the  azo  dye  for
 spectrophotometric  measurements.   Sampling  efficiencies  up to  95 to  99  percent have been
 reported (Intersociety Committee for  Ambient  Air  Sampling and Analysis, 1977c; Levaggi  et al . ,
 1973).  The  U.S. EPA has  recently  reported  (Ellis and Margeson, 1974) a laboratory evaluation
 of  the  method  for each of three  absorbing  solutions (0.1N TEA  with  n-butanol added at  the
 concentration  levels  3  ml/1,  0.5  ml/1  and  0.0  ml/1).   The results  indicate   the collection
 efficiency to  be  constant,  at  approximately  80 percent  for  the first two  solutions  (78.8
                                                                 3
 percent for  the last solution),  over the  range of 30  to  700 ug/m   (0.01 to  0.37 ppm) if  glass
 frits are  used.   If restricted  orifices,  which are  less  fragile and cheaper than glass frits,
 are  used,  the collection  efficiency  falls  to about  50 percent.   For this reason,  the  U.S. EPA
 did  not subject the method to  collaborative testing  so  that no  reliable  measure  of accuracy
 and  precision is  presently available.   No  interference  is expected  from  S02,  03,  or  NO  at
 ambient levels  and the  sample solutions are  stable  for three weeks after sampling.   The  accu-
 racy is considered to be  comparable  to that of  the Griess-Saltzman method  (Katz,  1976) with
 bias errors   less  than  two  percent at  a  stoichiometric  factor of 0.764  (Scaringelli et al.,
 1970).  This method is presently considered  to  be  a  24-hour method.
 7.2.2.4   Sodium-Arsenite Method—The  use  of  an alkaline  solution  of sodium  arsenite
 to absorb N02 was described  by  Christie  et al.  (1970) and  Merryman  et al.  (1973).  Christie
                                             7-10

-------
et al.  reported  a  collection efficiency of 95 percent using an orifice bubbler.  The U.S. EPA
recently has evaluated the sodium-arsenite procedure (Beard and Margeson, 1974) and has desig-
nated  it an  equivalent method as of December 14, 1977.  The method is presently considered to
be a  24-hour  method.   The results showed that the procedure has a constant collection effici-
                                                                                             3
ency  for NO^  of  82 percent  over  the  recommended useful  concentration range,  20  to  750 ug/m
(0.01  to  0.4 ppm).   Results of  the  USEPA's collaborative  quality  assurance  testing  of the
method  indicate a negative bias of three percent with an interlaboratory standard deviation of
11  ug/m   independent  of  concentration  (Constant  et  al.  ,  1974b).    EPA  concluded  that the
measurement errors were essentially uniform for all collaborators, although some dependence on
N02 level  was noted.   Eight of ten collaborators exhibited a uniform percent bias over all N02
levels  tested.
     Following absorption,  any sulfite  is oxidized with  peroxide and  the solution  is  then
acidified with phosphoric  acid.   The  azo dye is formed by addition of sulfanilamide and N-(l-
naphthyl) ethylenediamine dihydrochloride.   According to Katz (1976),  NO in the air sample can
produce a  positive  interference  by increasing the  N0? response  in the sample by 5 to 15 per-
cent  of the NOp  actually  present.  Carbon  dioxide,  in excess of typical  ambient concentra-
tions,  can  lead  to  a negative interference and the method response is affected by sample flow
rates  in  excess  of  300  ml/min.   The samples  are  stable for six weeks.   Recently,  the USEPA
also has conducted an  evaluation  of potential NO  and  C0«  interferences (Beard et al., 1975).
Results show  that,  in  the range 50 to  310 |jg/m3 (0.04 to 0.25 ppm)  NO and 360,000 to 900,000
    3
ug/m   (200 to 500  ppm) C09,  the  average effect  of these interferents is  to  increase the in-
                               3                              3
dicated N02 response by 10 ug/m  over the range 50 to 250 ug/m  N0? (0.03 to 0.13 ppm).
7.2.2.5  TGS-ANSA Method—A  24-hour manual  method for  the  detection and  analysis  of  N02 in
ambient air,  the TGS-ANSA method was first  reported  by  Mulik  et al.  (1974).   It  has  been
designated an equivalent  method  to the RM as  of December  17, 1977.    Ambient  air is bubbled,
via a  restricted  orifice,  through a solution containing triethanolamine, o-methoxyphenol, and
sodium  metabisulfite.   The  NO^ gas  in the  ambient sample is converted to nitrite  ion (NOp)
which is then analyzed by diazotization and coupling using sulfanilamide and the ammonium salt
of 8-anilino-l-naphthalene-sulfonic  acid  (ANSA).  • The  absorbance is read  at 550  nm.   The
function of  the  triethanolamine   is  to provide a basic collecting  medium (Levaggi  et  al.,
1973).  The  addition of o-methoxyphenol raises  the collection efficiency  to  93  percent  when
using  a restricted  orifice  (Nash,  1970).   The sodium metabisulfite  inhibits  free-radical
formation and, hence, the formation of quinones from the o-methoxyphenol  as the solution ages.
     The collection  efficiency  for NO-  is  constant at concentrations  between  20 and 700 ug/m
(0.01  and  0.37 ppm),  which is the range of  the  method with 50 ml of absorbing reagent and  a
sampling rate of 200 cm /min for 24 hours.   No interferences were reported at  an NO, concentra-
                 3
tion of 100  ug/m  (0.05 ppm) for the "following pollutants  at the levels shown in parentheses:
                                            7-11

-------
ammonia  (205  ug/m3 or  0.29  ppm); CO  (154,000  |jg/m3  or 134 ppm); formaldehyde  (750  ug/m3 or
0.61 ppm); NO  (734 ug/m3 or 0.59 ppm),  phenol  (150 |jg/m3 or 0.04 ppm);  0, (400 |jg/m3 or 0.2
                       3
ppm); and 502 ^3^ ^m  or ®'^ PP"1)'   ^he absorbing reagent is stable for three weeks before
sampling  and  the  collected samples  are stable  for  three weeks  after sampling  (Fuerst  and
Margeson, 1974; Mulik et al., 1974).
     Results  of  U.S.  EPA's  collaborative  quality assurance testing (Constant et  al.,  1974a)
indicate a lower  detectable  limit < 15 ug/m  (0.008 ppm), an average bias of 9.5 ug/m  (0.005
ppm) over the range of 50-300 ug/m  (0.03 to 0.16 ppm), and an interlaboratory standard devia-
                3
tion of 8.8 ug/m  (0.005 ppm).   EPA concluded that the errors were essentially uniform for all
collaborators.   The biases shown were nearly independent of the  NO, level.
7.2.2.6  Other Methods—In addition  to the standard wet chemical  methods for NO^ measurement,
many  other  techniques  have been  explored.   Molecular correlation  spectrometry  compares  a
molecular absorption band  of a sample or plume  with  the corresponding absorption  band of N02
stored in the  spectrometer (Williams and Kolitz, 1968).   Spectrometers  processing the second
derivative of  sample  transmissivity  with respect to wavelength have  been  employed to measure
N02 as well  as  NO (Hager and Anderson, 1970).   Infrared lasers  and infrared spectrometry have
been applied  by Hanst (1970), Hinkley and Kelley (1971) and Kreuzer and Patel (1971).
7.2.2.7   Summary of Accuracy and Precision of NO,,  Measuring Methods—Purdue  et  al.   (1975)
reported an extensive  comparison  of both intra- and intermethod accuracy and precision of the
chemiluminescent, sodium arsenite, TGS-ANSA and continuous colorimetric (Lyshkow  modification)
procedures for NO^ measurement.  The study was conducted under carefully controlled laboratory
conditions using skilled technicians.  Ambient air spiked with N02 was sampled by two  identical
instruments for  each  method tested.    In the  case  of  manual methods four  samples  were  taken.
The N09  spikes were  varied randomly from day to day  over a 20-day sampling schedule.   Spikes
                           3
ranging  from 0 to 800 ug/m  were used.  The  sampling period was  of 22 hours duration.   Table
7-3 gives  the  results  of  a statistical  analysis  of the  intra-  and  intermethod differences.
     Examination  of the  table  reveals  that the  average  difference  between any of  the methods
was never greater than 7.5 ug/m  N09.  The worst case of intramethod differences  occurred with
                                                                             3
the continuous colorimetric  method  where there was a  small  bias  of 7.5 ug/m  NOp  between the
data  from  the  two  analyzers.   The  correlation  coefficients  for  the  intermethod  comparisons
were greater than 0.985  in all cases.    In another  phase of the study, no intermethod differ-
ences  could  be attributed  to  concentrations of nitric oxide, carbon dioxide,  ozone,  total
sulfur, or total  suspended particulate matter in the ambient air samples.  Significant  negative
interference  in the  continuous colorimetric  method was  found at  N09 concentrations of 75 and
        3                                                               3
100 ug/m  in  the presence of ozone at concentrations of 353 and  667 ug/m .   At an ozone concen-
tration of 100 pg/m , no interference was detected.   At NO concentrations as high as 302 pg/m
no  interference was  found  in the sodium arsenite procedure,  although  NO has been  cited  as  a
positive interferent in the method.
                                            7-12

-------
TABLE 7-3.
                STATISTICAL ANALYSIS OF  N02  MEASURING  METHOD  DIFFERENCE'

Sampling Spiked Ambient
Comparison
Intramethod
Chemil/Chemil
Color/Color
ARS/ARS (A)
ARS/ARS (B)
TGS/TGS (A)
TGS/TGS (B)
ARS (AVARS (B)
RGS (A)/TGS (B)
Intermethod
Chemil/Color
Chemil/ARS
Chemil/TGS
Color/ARS
Color/TGS
ARS/TGS
Pairs

22
20
22
22
20
22
22
20

20
22
20
20
18
20
Meanb
(|jg/niJ)

1.
7.
0.
0.
-0.
0.
-2.
0.

3.
-1.
5.
-3.
3.
7.

3
5
6
2
9
2
6
6

8
9
6
8
8
5
Air
95%,
Standard C.I.
Dev. Lower Upper

5.
7.
5.
5.
3.
9.
5.
7.

7.
9.
9.
11.
11.
7.

6
5
6
6
8
4
6
6

5
4
4
3
3
5

-1.
3.
-1.
-1.
-1.
-3.
-5.
-3.

0.
-5.
+0.
-9.
-1.
+3.

1
8
9
9
9
8
6
8

0
6
9
4
9
8

3.
11.
+3.
1.
0.
+3.
+0.
+3.

+7.
+1.
9.
1.
9.
11.

3
3
8
9
8
8
1
8

5
9
4
5
4
3


Corr.
Coeff.

0.
0.
0.
0.
0.
0.
0.
0.

0.
0.
0.
0.
0.
0.

999
995
997
996
999
992
997
996

994
991
990
989
985
994

Extracted from  Purdue   et  al.  (1975).
  Signed difference.
 cStandard deviation.
  95 percent confidence  interval  of  mean  difference.
 Correlation coefficient between paired  values  in  calculating mean
  difference.
                                   7-13

-------
     A summary  of  available  reliability estimates derived  from  collaborative testing studies
is  given  in  Table  7-4  for  four  ambient  air monitoring  procedures:   Chemiluminescence,
Griess-Saltzman  (continuous  colorimetric  using  dynamic  calibration),  TGS-ANSA,  and  sodium
arsenite.  Measures  of  accuracy  (bias) and precision (standard deviation) listed in the table
are derived from collaborative testing experiments conducted recently by EPA (Constant et al.,
1974a, 1974b,  1975a,  1975b,).   In this type  of  testing,  a number of collaborators,  following
analytical procedures  according  to  specified guidelines,  sample the  same  ambient  air spiked
with known N0~ concentrations.   The collaborators are generally skilled in ambient air monitor-
ing so that  the results reported may  reasonably be  taken to represent  an  upper limit on the
accuracy  and precision obtainable  in routine monitoring.   The  reader  should  note  that  the
values for accuracy and precision presented  in  the  table  represent averages of data reported
by  all  collaborators over  the entire  concentration ranges tested.   Since  the  accuracy  and
precision obtained  may  depend  upon the NOp concentrations  sampled  and,  moreover, in the case
of the Griess-Saltzmann procedure,  upon the  individual collaborator  performing the  test,  the
reader is referred  to the original reports for  a detailed statistical discussion of the test
results.
     Recently, a formal audit  was performed on continuous chemiluminescent analyzers (Monitor
Labs 8440) in  service in  the St.  Louis  Regional Air Pollution Study (Smith and Strong, 1977)
(see Chapter  8).    Table  7-5 summarizes the  results of  the  audit.   Three  audit  levels were
used:   0, 150  and  355 |jg/m  NO-.   "Acceptable"  limits for the difference between measured NC^
values and known  audit  NO,  concentrations were  established for the purposes  of the study at
                        3
+19, +30,  and +71  (jg/m  respectively.  At  the   0 audit  level   all  23 analyzers were  within
limits;  at an  audit level of 150 fjg/m  , three analyzers  were  found to "very narrowly" exceed
                               o
specified  limits;   at  355 pg/m   one  different   analyzer  "very narrowly"  exceeded  specified
limits.  Statistics  for the  entire network showed average differences of less than 10 percent
at both  the  150 and 355 ug/m  audit NO- concentrations.   Standard deviations were equal to or
less than 10  percent for both non-zero audit levels.
7.2.3  Analytical  Methods  for NO
     Numerous methods, other than the chemiluminescence procedure (discussed in Section 7.2.1),
can be  used  for direct measurement  of  NO;   however,  none  are widely used  presently for  air
quality monitoring.   These methods  include:   ferrous sulfate (FeSo,)  absorption and spectro-
photometric measurement of the resulting colored complexion,  (Norwitz, 1966), and ultraviolet
(Sweeney et al., 1964) and infrared (Lord et al., 1974) spectroscopy.   The spectroscopic tech-
niques require  long pathlengths when  used to measure concentrations  in  typical ambient air.
Mass spectrometry  and gas chromatography  also may  be employed, but  these  methods  are rather
elaborate and expensive.
7.2.4  Sampling for N0x
     Sampling  technique is   a  particularly important consideration for  the  measurement of NO
and NO-.   Nitric  oxide and  NOp  in the  atmosphere during  the  day  are involved in  very rapid

                                            7-14

-------
                    TABLE 7-4.   SUMMARY OF RELIABILITY OF NO  ANALYTICAL METHODS IN COMMON USE AS OBIA1NED BY COLLABORATIVE TESIING
                                (CONSTANT ET AL.,  1974a,  19?4b, 1975a, 1975b)
 I
I—>
en

Range of NO.
Concentrations
Used in Test
Method (ug/m3)
Chemi luminescence 80-300
(Reference Method)



Sodium Arsenite 50-300
(Equivalent Method)




TGS-ANSA 50-300
(Equivalent Method)


Griess-Sal tzman 90-370
(Continuous Colorimetric
with dynamic calibration;
both variants cited in
7.2.2.T)



Bias
(Average
for all
Tests)
-8 ug/m
or
-5%


6. 2 ug/m
or
•v3%



9.5 ug/m3
or
•v. -5%

16.1 ug/n3b
or
•v 6%




Standard Practical
Deviation Lower
(Average Detection
for all Limi t
Tests) (pg/m1) Comments (Reference)
14% <22 One collaborator had very large biases,
and another had unstable biases. For most
collaborators (8 out of 10), however, the
bias was small and well balanced. (Constant
et al. , 1975a)
11 ug/m < 9 Measurement errors were essentially uniform
for all collaborators, although some depen-
dence on NO, level was noted. 8 of 10 col-
laborators exhibited a uniform percent bias
over all NO, levels tested. (Constant et. al.,
1974b)
11.6 (jg/m <15 Errors were essentially uniform for all col-
laborators. The biases shown were nearly
independent of NO, level for range tested.
(Constant et al. , 1974a)
32.7 |jg/m <19 Although overall results are reasonably accu-
rate, method may produce quite inaccurate
readings in an unpredictable fashion. About
half of the collaborators did achieve fairly
stable results. Subjectively, then, the
method will produce reliable results in some
hands. (Constant et al., 1975b)

                   Depends  in  detail  upon NO, concentration.
Depends significantly on laboratory performing test.

-------
                     TABLE 7-5.  RESULTS OF 1977 FORMAL AUDIT ON IN-SERVICE
                                 CHEMILUMINESCENT ANALYZERS IN ST.  LOUIS
                                 (SMITH AND STRONG, 1977)

Number
Audited
23


Number
Found
Opera-
tional
23


Audit
Level
(pg/m3)
0
150
355
"Acceptable"
Limits for
Difference
(ug/m3)
+19
+30
+71
Number
Outside
Limits
0
3
1
Average
Difference
for Network
(ug/m3)
+2
-11
-28
Standard
Deviation
for Network
(|jg/m3)
6
15
26

reactions which keep 03 in a photostat!onary state.   The rate of photolysis of N02 (forming NO
and 0  and thus  0,)  is nearly  equal  to  the  reaction of the  NO  and 0-, to form  N0?.   When a
sample is drawn  into  a dark sampling line, photolysis ceases while NO continues to react with
0, to  form  NOp.   Thus,  long residence  times  in sampling  lines  must be  avoided  to  obtain a
representative  sample.   Sampling technique requirements  for a given error in  tolerance were
discussed by  Butcher  and Ruff  (1971).   For example,  Figure 7-1,  adapted  from  these  authors,
shows the absolute  error  in N02 introduced in  10 seconds in a dark  sampling line due to the
presence of 0,  and/or NO  in the line in varying concentrations.   In general,  due to the reac-
tive properties  of NO ,  only  glass  or  Teflon  materials should  be  used  in  sampling trains.
     If NO and N02 are to be measured separately by  a method specific for N02, it is necessary
to remove N02 from the  sample, then oxidize  NO to  N02 and  measure the N02  concentration.
Several selective absorbers for N02 have been  employed, but  some of the N02 is converted to NO
in all  the  absorbers  tested.   Absorbents include Griess-Saltzman  reagent (Huygen,  1970) and
granules impregnated with triethanolamine (Intersociety Committee  for Ambient  Air Sampling and
Analysis, 1977c;  Levaggi  et al. , 1972).   The triethanolamine  is  reported to be  the  best ab-
sorbent, with only two to four percent of the  incoming N0? converted to NO.
     When NO  is  to  be measured by a method specific to N02, either with or without removal of
N0~ from  the  sample,  it  is  necessary to oxidize NO  to  NQ2 in the gas phase.   The  most fre-
quently used oxidizer is chromic oxide on a fire brick granule support (Intersociety Committee
for Ambient  Air Sampling and Analysis, 1977c;  Levaggi  et al., 1974).  This material gives over
99 percent oxidation  when the  relative humidity in the  sample is  between 20 and 80  percent.
The chromic  oxide also removes  S0~.
     Considerations relating  to the  reduction  of N02  to NO  have  been discussed  in Section
7.2.1.
7.2.5  Calibration of NO and N00 Monitoring Instruments
     Calibration of monitoring  instruments or  methods may be accomplished either by measuring
a gas of known concentration or by comparing measurements of a stable source with measurements
of the same  source made by a primary  reference  method.
                                            7-16

-------
a.
a.
OC
I-
Z
LU
O

O
o
 n
O
    0.01 =
   0.005 -
   0.002 -

   0.001
      0.001
                    0.01           0.10

                 NO CONCENTRATION, ppm
                                                 1.0
Figure 7-1. Absolute error in INIO2 and  ANOoforlO
seconds in dark sampling line (Butcher and Run, 1971).
                          7-17

-------
     Standard gas  sources  are  the principal means by which NO and NCL measurement instruments
are calibrated.   The preparation  of standard mixtures  of NO in nitrogen was  studied  by the
National Bureau of Standards (Hughes, 1975).  The initial accuracy with which standards may be
prepared, based  on either  pressure  or mass  measurements, is  quite good.   The  stability of
mixtures at concentrations above about 50 ppm is satisfactory with only 0 to 1 percent average
change  in  concentrations over  a  seven-month  period.   Other sources which  have been employed
occasionally  include  permeation   of  compressed  NO  through  membranes  to  produce  dilute  NO
streams  (Hughes,   1975),    electrolytic  generation  (Hersch and  Deuringer,   1963),  catalytic
reduction of  a known  concentration  of NO,, (Breitenbach and Shelef, 1973),  Qr Dno^0ivsl-s Of
known N02 concentrations and rapid dilution (Guicherit, 1972).
     The permeation  tube is the only direct  source  of dilute N0? mixtures  in  widespread use
(O'Keefe and Ortman,  1966;  Scaringelli  et  al., 1970; Shy, 1970; Shy et al. , 1970).  It may be
calibrated  by  weighing  or by  rarely  used micromanometric  measurements.   The  other  common
procedure used to calibrate NO, measurement instruments is gas-phase titration.   Stable sources
of known concentrations  of both NO and 0,  are required.   A dilute stream of NO is measured by
NO methods.   The 0., is added to the stream  at a constant rate.  The decrease in NO by reaction
with the added  ozone is equal  to the N02 formed.  Thus,  a known NO,, concentration is created.
The U.S. EPA  (1976a)  recommends the combined use of permeation tubes and gas-phase titration,
using one technique to check the other.
7.3  ANALYTICAL METHODS AND SAMPLING FOR NITRIC ACID
     Monitoring for  ambient  nitric acid is complicated both by the low concentrations present
and by  the  fact that nitric acid  in  the  atmosphere  is in the gaseous state.  Collection of a
representative  sample without  artifact  formation presents  some technical  difficulties.   In
general, also,  sampling  of nitric acid from ambient  air is made difficult by its tendency to
adhere  to  the  walls  of the sampling  lines.   It  may be necessary to heat  sampling lines to
prevent condensation of water,  which would  result in removal of HNO,.
     A  microcoulometric  method designed  to measure  nitric  acid was developed  by Miller and
Spicer  (1975;  Spicer and Miller,  1976).   A Mast microcoulomb detection  cell was adapted for
sensing acid gases in samples pretreated with ethylene to remove ozone.
     Readings  from samples  introduced  directly  into the  cell  indicate total  acid content.
Another sample  of  the test mixture is passed through loosely-packed nylon fiber which removes
the nitric  acid.   The  cell  reading of  this  sample  is  representative  of  total  acid content
except nitric acid.  Thus, nitric acid concentrations are obtained by subtraction.
     The sensitivity  of  this  method at a signal-to-noise ratio of two to one is approximately
2 ppb.   No detectable interferences have been reported from S02, NO,,, PAN, H,,S041 and formalde-
hyde  (CH20).    It  should,  however,  be  noted  that Spicer  et  al.  (1978a)  report significant
artifact nitrate  formation  on  nylon filters under conditions  of very high N07 concentrations
            3
(56,400 ug/m ;  30 ppm) and high humidity.    Although concentrations of this magnitude would not
                                            7-18

-------
be expected to occur in ambient situations, the possible implications of these reported inter-
ferences  for  measurements obtained  by  the microcoulometric method have yet  to  be evaluated.
     Using  air  streams passing  through a cellulose filter  impregnated  with  sodium chloride,
Okita  et  al.  (1976)  report  collection  efficiencies  for nitric  acid ranging from  93 to 100
percent.  Interferences from N09 were reported over a range of N09 concentrations up to 15,000
    3                                                    3
ug/m   (8.0  ppm).   The  equivalent of about  1 ug NO,,-N/m  of  artifact  gaseous  nitrate corre-
                    3
sponded to  188  ug/m  (0.1 ppm) N09  being  passed through the filter at relative humidities of
                                                                                             3
55 to  72  percent.   Ozone did  not  enhance  artifact  formation at a concentra tion of 980 ug/m
(0.73 ppm)  in the presence of 1,372 ug/m  (0.73 ppm) NCL.  Interferences from PAN and n-propyl
nitrate were  cited  as  negligible or very  small.   Nitrate formation from  N02  increased with
increasing  relative humidity.
     Recently, Tuazon  et al.  (1978)  have  reported  measurements of nitric  acid  under ambient
conditions  with a  detection  limit of 2 ppb.   The system achieves this sensitivity by means of
a folded-path optical  system which results in pathlengths  of  up to 2  km  in  the sample cell.
Fringes produced in a high-resolution infrared Michelson interferometer, coupled to the sample
cell,  are  scanned optically.  The resultant  variations  in  signal are  related to  the Fourier
transform of  the  spectrum which  is  recovered  automatically by  appropriate  data  processing.
     A  summary  of  the current status of methods to measure atmospheric nitric  acid  has been
published very  recently (Stevens  and McClenny,  1979).   Table 7-6 summarizes  the techniques
considered.
     Methodology  for  measuring   nitric  acid  is  still   in  the  development  stage.   Studies
conducted to  date  are  not sufficient to assess  with  any degree of confidence the suitability
of the methods described in this section for routine ambient monitoring.
7.4  ANALYTICAL METHODS AND SAMPLING FOR NITRATE
     Nitrate  analyses  have  been  performed  routinely  for many  years and  a  large  number  of
chemical methods have been reported.   Since analytical  methods  for inorganic nitrate generally
proceed by aqueous extraction, the final chemical quantitative  determination of ion concentra-
tions is similar for samples  drawn from air,  water,  and soil.
7.4.1  Sampling for Nitrate From Airborne Particulate Matter
     Particulate nitrate  as  a  fraction  of total  suspended  particulates has been  sampled  in
this country  largely by  standardized sampling techniques using  high  volume (HIVOL) samplers.
USEPA  minimum  specifications  for  the  HIVOL  are  well documented  (U.S.  EPA,  1971).    A
continuous  24-hour  sample of  ambient air, typically  at flow  rates  of approximately  1  to  2
standard cubic meters per minute,  is  drawn through a glass fiber filter  which  traps the partic-
ulate matter.   The upper size limit of particulate matter collected depends on the  geometry of
the sampler housing but is generally above about 30  urn in aerodynamic  diameter,  well  above the
respirable  size  range.   The  sampler  thus  collects  all  of the  respirable material  and some
                                            7-19

-------
                                                TABLE 7-6.   SUMMARY OF NITRIC ACID DETECTION TECHNIQUES"
              Technique
Procedure
  Minimum
 Detectable
Level  (ppbv)
Interferences
   Tested
For, To Date
Reference
              Cheroiluminescence
Simple modification of chemilumin-
escence procedure used for NO
    5.0        NO, NO., PAN, organic
               nitrates
                       Joseph and Spicer, 1978
              Chemiluminescence     Adaptation of sensitive chemilumin-
                                    escence NO  monitor described by

                                    Ritter et al.,  1978
                                        0.3        NO, N02, PAN, organic
                                                   nitrates
                                        Kelly and Stedman, 1979

                                        Likens, 1976
 i
r\3
O
              Fourier Transform
              Spectrometer
Long path infrared spectrometry
    5.0        Most gaseous species in  Tuazon et al.,
               normal ambient air       1979, 1978
Microcoulometry
Coloriraetry
Sample conditioning with ethylene to 5.0
remove ozone interference; differ-
ence method using direct reading
and reading after nylon trap which
removes HN03
Reduction to NH. of fixed organic <0.1
nitrogen collected on nylon filter,
followed by indophenol ammonia
test. Teflon prefilter.
0 NO SO., H2SO,,
nth, HCHO, PAN/HCOOH,
HN02
Nht, particulate
nitrate
Miller and
Spicer et
Lazrus et
1968, 1979
Spicer, 1975
al. , 1978a, 1978b
al.,
              Colorimetry
Collection of HNO, on NaCl impreg-
nated filters, followed by extrac-
tion and hydrazine reduction-
diazotization analysis of nitrate
    0.1        N0?, particulate
               nitrate
                       Okita et al., 1976
                       Forrest et al.,  1979
              Electron Capture
              Gas Chromatography
Collection of HNO^ on nylon or cot-
ton, extraction, Conversion to

nitrobenzene analysis by gas
Chromatography
    0.1        NOp, particulate
               nitrate
                       Hare et al.,  1979

                       Tesch and Sievers, 1979

                       Ross et al.,  1975
              Adapted from Stevens and McClenny, 1979

-------
fraction of the non-respirable material suspended in ambient air.  In typical nitrate monitor-
ing,  a  portion of the HIVOL  filter  is subjected to aqueous extraction  and the water-soluble
nitrate analyzed as described below in Section 7.4.2.
     Recent  reports  point to  serious difficulties associated  with the  routine  use  of glass
fiber filters.  In a study of nitrate  in auto exhaust,  Pierson et al. (1974) report that glass
fiber filters collected about twice the amount of nitrate when compared to quartz fiber filters.
Nitrate also  was  found on glass fiber filters which were inserted downstream of either quartz
or  glass  fiber  primary  filters,  providing  additional  evidence  of artifact  formation  from
gaseous  constituents.   Spicer  (1976) reported  that glass  fiber filters  completely  removed
gaseous nitric  acid  when  in low concentration in gas streams,  while Teflon and quartz filters
showed no corresponding effect.   O'Brien et al.  (1974)  describe very unusual results of parti-
cle  size  distribution determinations  of  photochemical   aerosol  collected  in  the  Los  Angeles
basin using a cascade impactor where all  particle size  fractions were collected on glass fiber
filters.  The  authors  speculated  that conversion of gaseous nitrate precursors on the filter
masked the true nitrate size distribution.
     Okita et  al.  (1976)  report that  untreated glass fiber  filters  collect nitric acid vapor
with a  highly  variable collection efficiency (0-56 percent), suggesting erratic nitrate arti-
fact formation in urban atmospheres containing nitric acid.
     In  an  intensive  laboratory   investigation  of  interferences  in  atmospheric  particulate
nitrate sampling,  Spicer,  Schumacher  and  co-workers (1978a) concluded  that all  five  types of
glass filters  investigated  exhibited  serious  artifact  formation due to  collection of gaseous
nitric  acid  and,  to  some extent, NOp as  nitrate.   Cellulose  acetate and  nylon  filters  were
also reported to exhibit severe interferences from nitric acid.   Negligible interferences  were
reported for polycarbonate  and  Teflon filters.   Interferences on  quartz  fiber filters varied
with the filter  type,  with ADL Microquartz showing the  least effect at  N09 concentrations of
        3
592 ug/m  (0.315 ppm).  When  a  variety of quartz filter types  were tested, the greatest quan-
tity of artifact  nitrate  was  formed on the Gelman AE filter.  Artifact nitrate formed on  this
filter was  calculated to  be  less than  2  ug/m   (0.001  ppm) during a  standard  24-hour HIVOL
measurement.   The estimate was derived from drawing air  samples of about 1 m  containing 4,512
    0
ug/m  (2.4 ppm) NO, through the filters.   The relative  humidity was 30 + 10 percent.
     Most recently,  Spicer  and  Schumacher  (1977) reported the'  results  of a comparison  of
nitrate  concentrations  in  samples collected on  various filter  types  in  Upland,  California
during October and November,  1976 (Table  7-7).   During  the  experiment,  meteorological condi-
tions varied  from  warm,  hazy  weather to  hot,  dry,  very  clean desert wind conditions.   Nitrate
analyses were performed by  ion  exchange  chromatography.   All filter types used had comparable
particle collection efficiencies according to the manufacturer's specifications.   The  ratio of
nitrate collected on  Glass 1 to that collected simultaneously with identical HIVOL samplers on
Quartz 2 ranged from  4.8 to 36.6 and averaged 18.9.   The ratio  of nitrate collected on Glass 2
to Quartz 2  ranged from 2.8 to 49  and averaged 10.9.

                                            7-21

-------
                                 TABLE 7-7.   COMPARISON OF  NITRATE COLLECTED ON VARIOUS TILTERd TYPES
                                             (SPICER AND SCHUMACHER,  1977;  SPICER ET AL.,  1978a)
ro
ro
DaLe
Oct. 15
Oct. 18
Oct. 19
Oct. 20
Oct. 21
Oct. 22
Oct. 25
Filter
Quartz 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 2
Quartz 2
NO"
ug/m
1.6
1.6
14.1
0.39
17.0
1.2
28.7
2.3
18.8
0.82
11.2
0.49
38.4
0.78
Date Filter
Oct. 26 Quartz 1
Quartz 2
Oct. 27 Glass 2
Quartz 2
Oct. 28 Glass 1
Quartz 2
Oct. 29 Quartz 1
Quartz 2
Nov. 1 Quartz 2
Quartz 2
New. 2 Glass 2
Quartz 2
Nov. 3 Quartz 1
Quartz 2
NO" 3
(jg/m Date
1.3 Nov. 4
2.1
3.9 Nov. 5
0.52
9.1 Nov. 9
1.9
1.8 Nov. 10
2.9
1.7 Nov. 11
1.7
9.1 Nov. 12
1.6
0.68 Nov. 15
1.1
Fi Her
Glass 2
Quartz 2
Glass 2
Quartz 2
Glass 2
Quartz 2
Quartz 1
Quartz 2
Quartz 2
Quartz 2
Glass 2
Quartz 2
Glass 2
Quartz 2
NO'
l>g/m
3.0
1. 1
6.1
0.98
18.4
3.1
1.9
2.3
2.0
1.9
6.0
1.3
14.3
3.0

Glass 1 - "EPA Type" Gelman AA.
Glass 2 - Gelman A.
Quartz 1 - High purity quartz filter developed by Arthur D.  Little under contract to EPA.
Quartz 2 - Pal If lex QAST.

-------
     Recently, Marker  et  al.  (1977) have reported laboratory observations of loss of particu-
late  nitrate  from collecting  filters  through  chemical  reaction with  sulfuric  acid aerosol,
formed  from  the photochemical  oxidation  of SO-.    Most recently, Appel  and coworkers (1979,
1980) have conducted  several  studies bearing on  both  positive  artifact formation and loss of
nitrate  from  a variety  of filter  media.   They concluded  that gaseous HNO,  is  the principal
source  of  artifact nitrate  formation,  NCL  collection  only became  substantial  at  high ozone
levels.   Ambient  particulate nitrate values (at  San Jose  and  Los Alamitos,  California)  dif-
fered by up  to a factor of 2.4 depending upon filter medium and sampling rate,  in contrast to
the much larger sampling errors reported by Spicer and Schumacher (1977).   Fluoropore (Teflon)
filters  in low volume  samplers were subject  to  small  error although, under laboratory condi-
tions,  passage of  NhU- and HNO^-free air through the filter could result in the loss of up to
50 percent of the particulate nitrate.   This is consistent  with the relatively high vapor  pres-
sure of ammonium nitrate (see page 6-49).   They also reported that at low HMO, levels nitrate,
on  glass  fiber filters,  indicated  (within  about  3 percent) total nitrate,  i.e.,  particulate
nitrate  plus  HNO->  rather than  particulate  nitrate  alone.   They concluded that  the  degree of
error associated with  glass  fiber filter media could  be expected to vary with  location,  time
of year and day,  paralleling changes in nitric acid levels.
     These results  point to  the  conclusion  that  most  of  the  existing data  on  urban ambient
nitrate  concentrations  must be considered  to  be  of doubtful   validity.   It  is,  furthermore,
doubtful that any of these data can be corrected even if mechanisms for artifact formation are
clarified in  the future  since nitric acid,  which presently appears to play a significant  role
in positive artifact formation, is not routinely monitored.
     It  is,  however,  possible that data from  certain    monitoring sites may be  validated in
special   cases  where  it can be  shown that  the species responsible for  the  artifact processes
were all sufficiently low during the monitoring period of interest.
7.4.2  Analysis of  Nitrate from Airborne Particulate Matter
     Although most of the nitrate  analysis methods described in this  section found application
originally in  analyzing  nitrate  in samples of  natural  waters,  they  have also  been  used to
analyze  nitrate  in  aqueous  extracts  of  particulate matter  (Hermance et  al.,  1971)  and  in
solutions  obtained  through  absorption  of  nitrogen  oxides   contained   in  streams  of   air
(Kieselbach,  1944b; Kothny, 1974).
     The oldest  procedures  for  analyzing   nitrate  used  brucine ^-^^O^)  (Intersociety
Committee for  Ambient  Air  Sampling  and Analysis,  1977a, Jenkins  and Medsker,  1964;  Lunge and
Lwoff,  1894;  Robinson et al.,  1959)  or  phenoldisulfonic acid (ASTM,  1968;  Beatty  et  al., 1943;
Eastoe and  Pollard, 1950;  Intersociety  Committee for Ambient Air Sampling and Analysis, 1977d;
Taras,  1950).  Newer procedures  extensively  used to analyze nitrate in atmospheric particulate
matter extracts involve the  nitration  of xylenols [(CH3)2C6H3OH] and separation  of  the nitro-
derivative  by  extraction  or  distillation  (Andrews,  1964;   Buckett  et al. ,  1955; Hartley and
Asai, 1960;  Holler  and Huch,  1949; Intersociety Committee for Ambient Air Sampling and Analysis,

                                            7-23

-------
1977b; Swain, 1957;  Yagoda  and Goldman, 1943).   Recent comparison  of a 2,4-xylenol  procedure
(Intersociety Committee  for  Ambient Air  Sampling  and  Analysis,  1977b)  with  the  automated
copper-cadmium reduction and  diazotization  method  (Technicon,  1978) in samples collected near
high  density  vehicular traffic,  demonstrated  a negative  interference in the former  up  to  a
factor of 3 (Appel  et al.,  1977).
     Nitration of  chromotropic  acid [C,0H4(OH)2(SCLH)2]  (West  and  Ramachandran,  1966)  and
coumarin  (CgHgCL)  analogs   (Laby  and Morton, 1966;  Skujins,  1964)  also  have been  reported.
Small amounts of nitrate can  be assayed by  the  quenching  of  the fluorescence after nitration
of fluorescein (C^nH-jpOc) (Axelrod  et al.,  1970).    Nitrate analysis  can  also be accomplished
through reduction with Devarda alloy to ammonia  (NhL) (Kieselbach, 1944a;  Richardson, 1938) or
reduction of nitrate to nitrite by zinc (Chow and Johnstone,  1962),  cadmium (Morris and Riley,
1963;  Strickland  and  Parsons, 1972;  Wood  et  al.,  1967)  or  hydrazine (NH-NH-)  (Mullin  and
Riley, 1955).  Automation instituted by the NASN  improved the  hydrazine  reduction process by
curtailing  the  unwanted effects  resulting  from  its  sensitivity  to  motion  (Morgan  et  al.,
1967b).    The  addition of antimony  sulfate  [Sb^SO^),] eliminates  the  chloride  interferences
found in  most nitration  methods (West and Ramachandran,  1966).   One brucine procedure circum-
vents the  effect of  chlorides by adding an  excess  of sodium  chloride before nitration (Inter-
society Committee for Ambient Air Sampling and Analysis,  1977a).
     Nitrate analysis by ion-selective electrodes has been  used but  has several  disadvantages:
potential drifts caused  by  agitation speed, necessity of  frequent  re-standardization,  inter-
ferences  caused  by  nonspecificity  of electrodes  which  respond  to  other ions in  the aqueous
extracts, and non-stoichiometric absorption  of the  gases  in the collecting reagent (DiMartini,
1970; Driscoll et al., 1972; Gordievski  et al.,  1972).   In  atmospheric analysis,  the electrode
procedure has no advantage  over direct UV  determination of either  nitrite formed in an alka-
line  absorbent (Altshuller  and Wartburg,  1960)  or  nitrate  (Cawse, 1967) obtained after oxida-
tion  and  absorption  of  nitrogen  oxides in  alkaline permanganate (Kieselbach, 1944b;  Kothny,
1974).   Microscopic  techniques also  allow  analysis  of individual  nitrate  particles  (Bigg et
al., 1974).
     Small et al (1975)  report an application of  'ion  exchange  chromatography to the measure-
ment of a wide variety of cations and anions including the  nitrate and nitrite ion.  The novel
feature of the method  is  the  use of  a  second  ion  exchange "stripper" column  (after a conven-
tional separating column) which effectively  eliminates or neutralizes the eluting ions.  Since
only  the  species of  interest  in  a  background of deionized water leaves  the  stripper column,
concentration determinations  may  be  made  by a simple  and  sensitive conductometric technique.
Mulik et  al  (1976)  report  the application  of  this  technique to  measurement  of  water-soluble
nitrate  on  HIVOL filters.   The  separator column,  containing  a  strong  basic  resin,  separates
anions  in a background  of  carbonate eluant. The  stripper column,  containing  a  strong acid
resin, converts the  sample  ion and the carbonate  eluant to  nitric  and carbonic  acid, respec-
tively.    Since  carbonic acid  has  low conductivity,  the nitrate   ion  alone is  effectively
measured  in  a conductivity  detector.   Under the  experimental conditions,  sensitivity of 0.1
                                            7-24

-------
pg/m£  was  reported.   The  related standard  deviation was  1  percent  (95  percent confidence
level)  for ten  replicate  injections  at  the  5 ug/ml level.  At  this  concentration level, no
interferences  were found  from  fluoride,  chloride,  nitrite,  sulfite, sulfate,  silicate, or
carbonate.  Positive interferences were found for bromide and phosphate but the authors suggest
techniques  for eliminating these.
     In  other  recent  work,  Glover and Hoffsommer  (1974)  and Ross et al (1975) report a tech-
nique  for  assay  of  aqueous nitrate  and  nitrite  extractions  by conversion  to nitrobenzene.
Both techniques  involve the  nitration  of benzene  in the  presence  of sulfuric  acid  to  form
nitrobenzene, a  relatively stable compound, followed by gas chromatographic analysis.   Careful
calibration is  required  in  both procedures,  since  a  significant fraction of the nitrobenzene
formed may  be lost to the acid layer.   Ross et al.  recommend a calibration procedure whereby a
standard  is subject to the same reaction procedures as the unknown, while Glover and Hoffsommer
use internal calibration with added nitrotoluene.  The lower detection limits reported by  Ross
                               -12
et al.  are in  the range of  10   g  nitrobenzene  in a 1 u£ sample.  Conversion efficiences for
KN03,  KN02  and  HN03  were reported as 90.3 +  7.9,  100.4 + 4.2 and 99.9 + 5.2 percent,  respec-
tively.  Glover and Hoffsommer report, similar recovery rates for KN03 and KN02.
     Several methods  in  current use for analysis  of  nitrate in water and soil  are applicable
also  to  analysis  of  nitrate  derived from ambient air  samples  (Sections 7.4.3  and  7.4.4).
7.4.3  Nitrate in Water
     Current methodology for determination of nitrate in water is summarized in Table  7-8.   No
single method  is  satisfactory  over the broad range of concentrations and water matrices to be
found  in  environmental  samples.   Since  nitrate species are  highly  labile,  a variety  of tech-
niques have been  used  to preserve them during storage, including refrigeration, freezing,  and
addition  of sulfuric  acid  and of  mercuric  chloride.  Simple  refrigeration is  adequate  for
periods  up  to  a  day;  freezing is effective for  longer preservation (Brezonik and Lee, 1966).
Mercuric  chloride  is  effective,  especially when coupled with  refrigeration  or freezing,  but
the mercuric  ion slowly degrades  columns used  in various reduction methods (Table  7-8)  and
also is toxic (Howe and Holley, 1969;  U.S.  EPA, 1974).
     The  strong  absorption  of  the  nitrate ion in  the range 210-220 nm allows direct  spectro-
photometric measurement  (Altshuller  and  Wartburg, 1960;  Bastian et  al.,  1957;  Mertens  and
Massart, 1973).   Iron and nitrite are significant interferants.   Absorbance of nitrate is also
influenced  by  changes  in acidity.   At 210 nm,  a  variation of 20 percent  in perchloric acid
concentration causes  an  error of  approximately  5  parts per thousand  in  nitrate  measurement.
One author's report indicates that the spectrophotometric method is three times  more sensitive
than the brucine method (Noll,  1945).
     Nitrate ion  selective  electrodes  have also been used for measurement of nitrate  in water
(Keeney  et  al. ,  1970;  Langmuir and Jacobson,  1970).  The method, however, is not currently in
widespread use.
                                            7-25

-------
             TABLE 7-8.   ANALYTICAL METHODS FOR NITRATE IN WATER
Method
                           Range
                           (mg/£
                     nitrate-nitrogen)
Interferences
Reference
 1.  UV absorbance

 2.  Ion selective
    electrode
                          0.1-10
                          0.2 - 1400

Nitration and Oxidation Reactions

 3.  Phenoldisulfonic
    acid
 4.  Brucine

 5.  Chromotropic


 6.  Automated
    fluorimetric
    with substituted
    benzophenone

 7.  Szechrome

Reduction Methods

 8.  Zinc
 9.  Amalgamated
    cadmium
10.  Copperized
    cadmium
                          0.1 - 2.0

                          0.1 - 5.0


                          0.05- 4.0




                          0.05- 1.0



                          0.02- 1.0



                         <0.01- 1.0



                         <0.01- 1.0
11.  Hydrazine-copper     <0.01- 1.0
Organic matter

Chloride, ionic
strength
                                        Chloride
Many, but all
readily removed
APHA, 1976


APHA, 1976




APHA, 1976

APHA, 1976

APHA, 1976
Organic color,       Afghan and
chloride, sulfide,   Ryan, 1975
but readily removed
Unknown
Sensitivity
varies with age
of column

Sensitivity
varies with age
of column

Sensitivity
varies with age
of column
                                        Reduction is pH
                                        sensitive
12.  Devarda's alloy
                            2 ->200
Szekely, 1975
O'Brien and
Fiore, 1962
APHA, 1976
Technicon, 1978
U.S.  EPA, 1974
APHA, 1976
Strickland and
Parsons, 1972

Kamphake,
1976

APHA, 1976
                                   7-26

-------
     Wet  chemical  methods for  nitrate  analysis  are colorimetric and  fall  generally into two
major reaction categories:  (1) nitration reactions which involve the substitution of a hydro-
gen in an aromatic compound by the NCL moiety, and (2) reduction of nitrate to nitrite.
     Nitration  and oxidation  reactions  generally  require  a  strong  acid  medium as well  as
heating.   Since  it is  desirable  that  only  one  extraction  be  used for all  forms  of mineral
nitrogen, methods  of  analysis  not subject to chloride interference are preferred because many
air samples may contain chloride derived from suspended sea salts.   Some nitration methods are
subject  to  serious chloride  interferences.   While chloride  interferences  can  be  eliminated
from the brucine method (Intersociety Committee for Ambient Air Sampling and Analysis, 1977a),
experience  has  shown  that results  obtained  using  this method  are difficult  to  reproduce.
Interferences  from nitrite and  chlorine can  be  eliminated in  the chromotropic  acid  method
(APHA, 1976).
     Procedures which involve reduction of nitrate to nitrite are widely used because there is
a  simple,  sensitive  and well-tested  analytical  procedure  for  determination of  the nitrite
(NCO ion (Section 7.2.1).  Although nitrate is readily reduced by a variety of agents includ-
ing hydrazine,  metallic  zinc  or  cadmium, difficulties  with quantitative  recovery  have been
reported  (Henriksen,  1965; Mullin  and Riley, 1955;  Nydahl, 1976;  O'Brien and  Fiore,  1962;
Strickland and Parsons,  1972;  Technicon,  1978; U.S.  EPA,  1974).   Techniques  presently recom-
mended to avoid these difficulties have been documented by the  American Public Health Associa-
tion (Stainton, 1974).   Columns  using copperized cadmium (Strickland  and  Parsons,  1972; U.S.
EPA, 1974)  or amalgamated cadmium  granules  (National  Research  Council, 1978)  or copperized
cadmium  wire (Bremner  1965)  give  stoichiometric or  near  stoichiometric  reductions.   These
methods  are  widely used  and  are regarded  as accurate,  sensitive  and  acceptable  procedures
(APHA,  1976;  National  Research Council, 1978; U.S.  EPA, 1974).   Nitrate can  be reduced quanti-
tatively to ammonia by Devarda's alloy and subsequently analyzed  by titration or colorimetric-
ally.
7.4.4  Nitrate in  Soil
     As in the case of certain techniques for measurement of nitrate in water, some techniques
used in analysis  for nitrate  in soil  can be adapted for atmospheric  work.
     Nitrate levels in  soil  samples  can change rapidly through nitrification, denitrification
and flushing of nitrate.   Biocides  have been used to  prevent  microbial activity but they are
often ineffective  (Bremner, 1965).   Cold storage (Allen and Grimshaw,  1962)  and rapid  air or
oven drying  have  also  been  used.   Most extraction  methods  employ a  salt solution such  as
CaSO,,  KpSO, or KC1  (Bremner,  1965).   Methods of removing turbidity include flocculation with
aluminum hydroxide  (Cawse, 1967)  or calcium  salts as  well  as  the  use  of activated  charcoal,
ion exchange resins or  hydrogen peroxide, but the  last  three  techniques may cause changes in
nitrate content (Bremner,  1965).  Ultraviolet methods used in  analysis of atmospheric nitrate
samples  require similar  flocculation  techniques  to  remove turbidity,   color  and  other  inter-
ferences.
     Analytical  methods are summarized in Table 7-9.
                                            7-27

-------
                                TABLE  7-9.  METHODS  FOR DETERMINATION OF  NITRATE  IN SOILS
              Method
                        Range,  mg/£c
       Interferences
References
ro
CD
          1.  Ion electrode
          2.  Phenoldisulfonic
             acid

          3.  Brucine
          4.  Reduction of NO,
             by Cd Griess-  i
             Illosvay method
                           2 -1400
                         0.1 - 2
                         0.1 - 2
                         0.02-0.1
5.  Reduction to NH3 by     1 -1000
   Devarda alloy, steam
   distillation of NH,

6.  UV absorbance
Chloride, bromide, nitrite, iodide,  Carlson and
sulfide, ionic strength              Keeney, 1971

Chloride, organic matter, nitrite    Bremner, 1965
None
Bremner, 1965; Bremner
and Keeney, 1965,
APHA, 1976

Bremner, 1965; Bremner
and Keeney, 1965
APHA, 1976
                                                    Labile  amide,  phosphate,  nitrite     Bremner,  1965
                                                                                        Cawse,  1967
          Range on soil  basis  varies  widely  depending  on  soil:solution  ratio  of  extractant.

-------
7.4.5  Nitrate in Plant and Animal Tissue
     Methods analogous to those described above have been applied to measurement of nitrate in
plant  and  animal tissue.   Nitrate  ion concentrations have been  measured  in tobacco extracts
using a spectrophotometric procedure (Barkemeyer, 1966).   Wegner (1972) has described a proce-
dure for determining  both nitrate and nitrite  in  biological  fluids.   Fudge and Truman (1973)
described the analysis of nitrate and nitrite in meat products.  Methods of analysis for plant
tissue have been recently described by Carlson and Keeney (1971).
 7.5  SAMPLING AND ANALYTICAL METHODS FOR NITROSAMINES
     The sampling and analytical techniques for nitrosamines depend on the medium in which the
nitrosamine to be sampled and analyzed is found.
     Since  it  is of  some importance  to  place human  exposure via the  atmospheric  medium in
perspective  with regard  to other media  such as  food and potable  water,  the  discussion of
analytical   techniques in  this section  includes  methodology  appropriate  to the  three  most
important media:   air, food and water.
7.5.1  Nitrosamines in Air
     Because of  the  low  nitrosamine  concentrations in air, sample concentration  methods  are
necessary.   One  suitable  concentration procedure is the adsorption of nitrosamines on a solid
substance.  Bretschneider  and  Matz  (1976)  report using chemically pure active carbon.   Another
effective  technique  is the  use of chemically  bonded stationary  phases (Pellizzari  et  al.,
1975).   In  this  method,  nitrosamines  are collected by passing air through a cartridge packed
with a solidsorbent.   Samples  are desorbed by flash heating the cartridge contents into a gas
chromatographic column.   The  chromatograph  may then be interfaced  to  a mass spectrometer for
component  identification   and   measurement.   The  sorbents  Tenax  and   Chromosorb  have  been
evaluated at sampling  rates  up to 9 £/min.   Results  showed that they maintained efficiencies
of > 90 percent.   Carbowax 600 and 400, and oxypropionitrile,  coated or chemically bonded to  a
support,  were also highly efficient (>  90 percent).
     EPA's  National  Enforcement Investigations Center (U.S.  EPA,  1977a,  1977b) reports the use
of a basic  collecting medium (IN  KOH)  shielded by foil to preclude irradiation by light.   The
KOH solutions are subsequently  extracted  with dichloromethane.  Before  evaporative concentra-
tion,  2,2,4 ' trimethylpentate was  added  as a  keeper.   It is   important  in  using  either solid
sorbents  or  liquid KOH  traps, that the  procedure be  carefully checked  to ensure  that  the
measurement is  free  of artifacts.
     Fine et al.  (1974)  have developed a  method   for detecting N-nitroso compounds based on
catalytic cleavage of the N-NO bond and the subsequent infrared detection of chemiluminescence.
The technique,  called  thermal  energy  analysis (TEA),  is  coupled  with  gas chromatography and,
sometimes,  with high-pressure liquid chromatography (Fine  and Rounbehler, 1975).   The technique
is highly  sensitive  with a detection  limit of  about  1  ng/m£.   The  TEA detector operates by
splitting the nitrosyl radical  off  N-nitroso compounds coming from a  chromatographic column.
                                            7-29

-------
The  nitrosyl  radical  is then  reacted with  ozone, yielding  excited nitrogen dioxide  which
subsequently decays to the ground state by emission of near-infrared radiation.   The intensity
of this radiation is proportional to the number of nitrosyl  radicals present.   Artifact forma-
tion has not been reported to be a significant problem in the method (Pellizzari,  1977).    TEA
responses  have   also  been  reported for  some  compounds  containing  the 0-nitroso,  0-nitro,
C-nitroso, and N-nitroso  groups  and two recent papers  describe  approaches  for distinguishing
N-nitroso responses (Hansen et al.,  1979;  Krull et al.,  1979).
7.5.2  Nitrosamines in Water
     The usual precautions  employed in the collection  of samples  for organic analysis should
be followed when sampling water for nitrosamine analysis.   Stabilization to pH 8 may be needed
and  samples  should be protected from  light and kept cold because  of  the  photosensitivity of
nitrosamines.
     Several analytical  procedures  for the determination of N-nitroso compounds in water have
been reported.   Fine et  al  (1975)  reported two  concentration and  extraction procedures—one
based  on  a liquid-liquid  extraction,  and the  other based  on  the adsorption  of  the organic
fraction and  its  subsequent extraction with chloroform.  Gas chromatography and high-pressure
liquid, chromatography,   each  combined  with  detection  by TEA,  have  been  used  by  Fine  and
co-workers  (1975)  to measure  part  per trillion  concentrations  of volatile  and  non-volatile
non-ionic nitroso compounds, respectively, in water supplies.
     Older techniques for  the  detection and estimation of N-nitrosamines in water are polaro-
graphy  (Walters,  1971)  and colorimetry (Mohler and Mayrhofer, 1968), but  neither  method has
the  sensitivity  required  for  environmental samples.  Furthermore,  the colorimetric method has
exacting experimental conditions and cannot be used for complicated mixtures.
7.5.3  Nitrosamines in Food
     Determination of nitrosamines  in  foodstuffs  is made difficult by the complexity of food,
many components  of  which contain nitrogen and react chemically in a manner similar to nitros-
amines.  Many methods  have  been used to detect nitrosamines in  food, including polarography,
UV absorption, thin  layer chromatography,  and gas chromatography,  but these methods generally
have been  plagued  with  contamination and  artifact problems.   Gas chromatography-mass spectro-
metry  (GC-MS) is  presently  the most acceptable procedure for  the  measurement of nitrosamines
in food.   Wassermann  (1972) and Eisenbrand (1975)  have  published  surveys  of analytical  tech-
niques used in the isolation and detection of nitrosamines.
     GC-MS  also  appears  to be  the most  acceptable method for  analysis  of  nitrosamines  in
tobacco smoke, but  nitrogen-specific GC detectors  have also been  used (Spincer and Westcott,
1976).
7.6  SUMMARY
     Since the publication  in  1971  of the original document Air Quality Criteria for Nitrogen
Oxides, there have  been significant changes in the technology associated  with measurement of
ambient concentrations of NO  and NO -derived pollutants.
                            A       X

                                            7-30

-------
     With regard to the measurement of NCL, the original Reference Method, the Jacobs-Hochheiser
technique, was discovered to have unresolvable technical difficulties and was withdrawn by the
U.S. Environmental  Protection  Agency on June 8,  1973.   Since that time, adequate methodology
has been validated for measuring both NO and NO- in concentrations encountered in ambient air.
Accurate  techniques utilizing  standardized  gas  sources,  permeation  tubes,  or  a  gas-phase
titration have commonly been used for calibration.  The chemiluminescence technique is specific
for NO.  Nitrogen dioxide concentrations can be determined also with appropriate modifications
of  this  method.   Such  a modification was adopted on December 1, 1976,  as the Reference Method
for NO- measurements.   As of December 14, 1977, the sodium-arsenite procedure and the TGS-ANSA
method were  designated  equivalent  methods, suitable for 24-hour instrumental averaging times.
The chemiluminescence method must be used with care when modified for measurement of N0~ since
a number of  compounds  which may be  present  in  the atmosphere may  interfere  with  the instru-
ment's accuracy.   Variations of the Griess-Saltzman method are specific for N0?.   Under certain
circumstances, ozone can be a significant negative interferent in the method.   Dynamic calibra-
tion  of  the  Griess-Saltzman methods  in  current use  is  considered  necessary  for  reliable
measurement.
     Although adequate chemical  techniques exist-for the determination  of the nitrate fraction
of  suspended  particulate  matter in ambient air,  a  number of very recent reports have pointed
to  significant  positive nitrate artifact  formation  on the glass  fiber  filters  in widespread
use for collecting the particulate.   In addition,  negative artifacts result from the volatili-
zation of the ammonium nitrate.   At this time, therefore, almost the entire urban data base on
ambient nitrate concentrations must be considered to be of doubtful validity.
     Recent discovery of N-nitroso compounds in food, water, tobacco products, and ambient air
has  prompted the  development  of a  variety of  new  instrumental  techniques  in  the  last  few
years.    Measurement technology  is   still  developing  and  insufficient  time has  elapsed  for
careful evaluation of existing techniques, particularly in the area of  sampling.
     Development of long  pathlength  infrared absorption techniques has recently made possible
the observation  of nitric  acid in ambient air,  but  the procedure is  expensive and  does  not
currently lend itself to routine atmospheric measurement.  Other analytical  methods are avail-
able for routine monitoring but have yet to be carefully evaluated.
                                            7-31

-------
7.7  REFERENCES

Adema, E.  H.   Ozone interference in the determination of nitrogen dioxide by a modified manual
     Saltzman method.   Anal.  Chem.  51:1002-1005, 1979.

Afghan, B. K. ,  and J.  F.  Ryan.  Substituted benzophenone as a  fluorometric  reagent in auto-
     mated determination of nitrate.   Anal. Chem. 47:2347-2353, 1975.

Allen,  S.  E. ,  and H.  M.  Grimshaw.   Effect  of  low-temperature  storage  on  the extractable
     nutrient ions in soils.   J. Sci.  Food Agric. 13:525-529, 1962.

Altshuller,  A.  P.,  and A.  F.  Wartburg.   Ultraviolet  determination  of nitrogen  dioxide as
     nitrite  ion.   Anal.  Chem.  32:174-177, 1960.

American Public Health  Association.   Standard Methods for the Examination  of Water and Waste-
     water.   14th  Edition.   American  Public Health  Association,  Washington, DC,  1976.   pp.
     418-433.

American Society for Testing  and Materials, Committee D-22 on Methods of Atmospheric Sampling
     and  Analysis.   Standard  method   of  test  for oxides of  nitrogen  in  gaseous  combustion
     products,  (phenol  disulfonic  acid  procedure) ASTM Designation:    D  1608-60 (Reapproved
     1967).   Iji:   The  1968 Book of ASTM  Standards with Related  Material.   Part 23.   Water;
     Atmospheric Analysis.  American   Society  for Testing and  Materials,  Philadelphia, 1968.
     pp. 461-465.

American  Society  for Testing  and  Materials,  D-22  Committee on Sampling and Analysis  of At-
     mospheres.   Standard  method  of  test  for nitrogen  dioxide  content  of  the  atmosphere
     (Griess-Saltzman reaction)  ASTM   Designation:   D1607-69.   I_n:  1974 Annual  Book of ASTM
     Standards,  Part 26.   Gaseous  fuels;  Coal  and Coke;  Atmospheric Analyses.   American
     Society   for   Testing  and Materials,  Philadelphia, Pennsylvania,  1974a.    pp.  317-322.

American  Society  for Testing  and  Materials.   Interlaboratory  Cooperative Study of the Pre-
     cision  and Accuracy  of  the Measurement  of Nitrogen Dioxide Content in  the  Atmosphere
     Using ASTM Method D1607.   ASTM Data Series  Publication DS55, American  Society for Testing
     and Materials, Philadelphia, PA,  1974b.

Andrews,  D.  W. W.   A  sensitive method  for determining  nitrate  in water with 2,6-xylenol.
     Analyst  (London) 89:730-734, 1964.

Appel,  B.  R.  ,  E.  M.  Hoffer,  E.  L.  Kothny, and  S. M. Wall.   Interference  in 2,4-xylenol pro-
     cedure  for nitrate determination  in atmospheric aerosols.   Environ.  Sci.  Technol.  11:
     189-190, 1977.

Appel,  B.  R.  ,  S.  M.  Wall,  Y.   Tokiwa,  and M. Haik.   Interference effects in  sampling particu-
     late nitrate in ambient air.  Atmos.  Environ. 13:319-325, 1979.

Appel,  B.  R. ,  S.  M.  Wall,  Y.  Tokiwa, and M.  Haik.   Simultaneous nitric acid, particulate
     nitrate   and  acidity  measurements in ambient air.   Atmos.   Environ.   14:549-554, 1980.

Axelrod,  H.   D. ,  J.  E.   Bonelli,  and   J.  P.  Lodge, Jr.   Fluorimetric determination  of trace
     nitrates.  Anal.  Chim. Acta 51:21-24, 1970.

Barkemeyer,  V.  H.   The  determination  of  nitrate  in   tobacco  by UV-spectrometry.   Beitr.
     Tabakforsch.  3:455-459,  1966.
                                             7-32

-------
Bastian,  R. ,  R.  Weberling,  and  F.  Pal ill a.   Ultraviolet spectrophotometric determination  of
     nitrate.   Application to  analysis  of alkaline  earth carbonates.   Anal.  Chem.  29:1795-
     1797, 1957.                                                                       ~

Baumgardner, R. E., T. A.  Clark,  J. A.  Hodgeson and  R.  K. Stevens.   Determination  of an ozone
     interference  in  the continuous Saltzman  nitrogen dioxide procedure.   Anal.  Chem.  £7:515-
     521, 1975.

Beard,  M.  E. ,  and J.  H.  Margeson.   An  Evaluation of Arsenite  Procedure for Determination  of
     Nitrogen Dioxide  in Ambient  Air.  EPA-650/4-74-048,  U.S. Environmental  Protection Agency,
     Research Triangle Park, NC,  November  1974.

Beard,  M.  E. ,  J.  C.  Suggs, and J.  H. Margeson.  Evaluation of Effects  of NO, C02 and Sampling
     Flow Rate on Arsenite Procedure for Measurement  of  N02 in Ambient  Air.   EPA-650/4-75-019,
     U.S. Environmental  Protection  Agency, Research Triangle  Park, NC,  April  1975.

Beatty,  R.  L. ,  L.  B.  Berger,  and H.  H.  Schrenk.   Determination  of  the Oxides of  Nitrogen  by
     the  Phenoldisulfonic  Acid Method.   Report of Investigations 3687,  U.S.  Department of the
     Interior, Bureau of Mines, Pittsburgh, PA, February  1943.

Bigg,  E.  K. ,  A.  Ono,  and J.  A.  Williams.   Chemical tests  for  individual  submicron  aerosol
     particles.  Atmos.  Environ.  8:1-13, 1974.

Breitenbach, L. P.,  and  M. Shelef.  Development  of  method for the analysis  of N02  and NH3  by
     NO-measuring instruments.   J.  Air Pollut. Control Assoc. £3:128-131, 1973.

Bremner,  J.   M.    Inorganic  forms  of   nitrogen.    I_n:    Methods  of  Soil  Analysis.   Part  2:
     Chemical  and Microbiological   Properties.   C.   A.   Black,  ed. ,   Agronomy  Series  No.   9,
     American Society of Agronomy,  Inc., Madison, WI, 1965.   pp.  1179-1237.

Bremner, J. M. , and  D.  R. Keeney.   Steam  distillation methods for determination of  ammonium,
     nitrate and nitrite.  Anal.  Chim.  Acta 32:485-495,  1965.

Bretschneider, K., and J. Matz.   Occurrence and analysis  of nitrosamines  in  air.  In:   Environ-
     mental N-Nitroso  Compounds  Analysis and  Formation,  Proceedings  of a Working  Conference,
     International Agency  for  Research  on Cancer, Tallinn,  Estonian SSR,  October 1-3,  1975.
     E. A. Walker, P.  Bogovski,   L. Griciute,  and W.  Davis, eds., IARC  Scientific Publications
     No.  14,  International Agency  for  Research on Cancer, Lyon,  France,  1976.   pp.  395-399.

Brezonik, P.  L., and  G. F. Lee.   Preservation  of water samples for inorganic  nitrogen  analysis
     with mercuric chloride.    Inter. J.   Air Water Pollut. 10:549-553, 1966.

Buckett, J. , W. D. Duffield,   and R. F.  Milton.   The determination of  nitrate  and nitrite  in
     soil.  Analyst (London)  80:141-145, 1955.

Butcher,  S.  S. ,  and  R.  E. Ruff.   Effect  of  inlet residence time  on analysis  of  atmospheric
     nitrogen oxides  and ozone.   Anal.  Chem.  43:1890-1892, 1971.

Carlson,  R.  M. ,  and  D.  R. Keeney.   Specific  ion  electrodes:   techniques  and  uses  in  soil,
     plant, and water analysis.  Jji:  Instrumental Methods for the Analysis  of Soils  and  Plant
     Tissue.   L.  M. Walsh, ed., Soil Science Society  of America, Inc.,  Madison, WI,  1971.  pp.
     39-65.
                                             7-33

-------
Cawse, P. A.   The determination of nitrate in soil solutions by ultraviolet spectrophotometry.
     Analyst (London) 92:311-315, 1967.

Chow, T. J. ,  and M.  S.  Johnstone.   Determination of nitrate in  sea  water.   Anal.  Chim. Acta
     27:441-446, 1962.

Christie, A.  A.,  R.  G.  Lidzey, and  D.  W.  F.  Radford.  Field methods for the determination of
     nitrogen dioxide in air.  Analyst (London) 95:519-524, 1970.

Clough,   P.  N. ,  and  B.  A.  Thrush.  Mechanism of chemiluminescent  reaction between nitric oxide
     and ozone.   Trans.  Faraday Soc.  63:915-925,  1967.

Constant, P.  C. , Jr.,  M.  C.  Sharp,  and G.  W.   Scheil.   Collaborative  Test of  the TGS-ANSA
     Method  for  Measurement  of  Nitrogen  Dioxide  in Ambient  Air.    EPA-650/4-74-046,  U.S.
     Environmental Protection Agency, Research Triangle Park, NC, September 1974a.

Constant, P.  C. , Jr.,  M.  C.  Sharp,  and  G.  W.  Scheil.  Collaborative Testing  of Methods for
     Measurements of  N02  in  Ambient Air.  Volume  I—Report of  Testing.   EPA-650/4-74-019a,
     U.S. Environmental  Protection Agency, Research Triangle Park, NC, June 1974b.

Constant, P.  C. , Jr.,  M.  C.  Sharp,  and  G.  W.  Scheil.  Collaborative Test  of  the Chemi lumi-
     nescent Method  for Measurement  of N02 in Ambient Air.   EPA-650/4-75-013,  U.S.  Environ-
     mental  Protection Agency, Research Triangle  Park, NC, February 1975a.

Constant, P.  C. , Jr.,  M.  C.  Sharp,  and  G.  W.  Scheil.  Collaborative Test  of  the Continuous
     Colorimetric Method for Measurement of Nitrogen Dioxide in Ambient Air.   EPA-650/4-75-011,
     U.S. Environmental  Protection Agency, Research Triangle Park, NC, February 1975b.

DiMartini,  R.   Determination  of  nitrogen dioxide and nitric oxide  in  the  parts per million
     range  in flowing gaseous mixtures by means of the nitrate-specific-ion electrode.  Anal.
     Chem.  42:1102-1105, 1970.

Driscoll, J.  N. ,  A.  W.  Berger, J. H. Becker, J. T.  Funkhouser, and J. R. Valentine.  Determi-
     nation of oxides of  nitrogen in combustion  effluents  with  a nitrate ion selective elec-
     trode.   J.  Air Pollut.  Control  Assoc. 22:119-122, 1972.

Eastoe,   J.   E. ,  and A.   G. Pollard.   A modified phenoldisulphonic acid  method for determining
     nitrates in soil  extracts etc.   J. Sci. Food Agric. 1:266-269,  1950.

Eisenbrand,   G.   Recent  developments  in  trace  analysis  of  volatile nitrosamines:   a brief
     review.   |ri: N-nitroso  Compounds in the Environment,  Proceedings of a Working Conference,
     International Agency  for  Research  on  Cancer,   Lyon,  France,  October  17-20,  1973.   P.
     Bogovski,  E.  A.  Walker,  and W.  Davis,  eds.,  IARC Scientific Publication  No.  9, Inter-
     national Agency for Research on Cancer, Lyon, France, 1975.   pp.  6-11.

Ellis, E. C. , and  J.  H. Margeson.   Evaluation  of Triethanolamine Procedure for Determination
     of   Nitrogen Dioxide  in  Ambient  Air.    EPA-650/4-74-031,  U.S.  Environmental  Protection
     Agency,  Research Triangle Park,  NC, July 1974.

Fine, D.  H. ,  and D.  P.  Rounbehler.  Trace analysis of volatile N-nitroso compounds by combined
     gas chromatography and  thermal  energy analysis.   J. Chromatogr. 109:271-279, 1975.

Fine, D. H. , F.  Rufeh, and  D.  Lieb.   Group analysis of  volatile  and  non-volatile N-nitroso
     compounds.   Nature (London) 247:309-310, 1974.
                                             7-34

-------
Fine,  D.  H. ,  D.  P.  Rounbehler, F. Huffman, A.  W.  Garrison, N. C.  Wolfe,  and S.  S.  Epstein.
     Analysis  of volatile  N-nitroso  compounds  in  drinking water  at the  part  per  trillion
     level.  Bull. Environ. Contam. Toxicol. 14:404-410, 1975.

Fontijn,  A.,  A.   J.  Sabadell,   and  R.  J.  Ronco.   Homogeneous chemiluminescent measurement of
     nitric oxide with ozone.   Implications for continuous selective monitoring of gaseous air
     pollutants.   Anal. Chem. 42:575-579,  1970.

Forrest,  J. ,  R.  L.  Tanner, D.   Spandau,  T.  D'Ottavio, and L. Newman.  Determination of atmos-
     pheric  HN03  with Nad-impregnated filters  at high  volume flow  rates.   In:   Current
     Methods  to   Measure  Atmospheric  Nitric  Acid  and  Nitrate  Artifacts,  Presentations  at a
     Workshop, U.S.  Environmental  Protection Agency, Southern  Pines,  North Carolina, October
     3-4,  1978.   R.  K.  Stevens, ed. ,  EPA-600/2-79-051,  U.S.  Environmental  Protection Agency,
     Research Triangle Park, NC, March 1979.  pp. 51-61.

Fudge, R., and R. W.  Truman.  The nitrate and nitrite contents of meat products -- a survey by
     Public Analysts'  Laboratories in  South  Wales  and the  southwest of England.   J. Assoc.
     Public Anal. 11:19-27, 1973.

Fuerst,  R. G. , and  J.  H.  Margeson.  An  Evaluation of TGS-ANSA Procedure for Determination of
     Nitrogen Dioxide in Ambient Air.   EPA-650/4-74-047, U.S. Environmental Protection Agency,
     Research Triangle Park, NC, November 1974.

Glover, D. J., and J. C.  Hoffsommer.  Gas chromatographic analysis of nitrate and nitrite ions
     in microgram quantities by conversion to nitrobenzene.   J. Chromatogr. 94:334-337, 1974.

Gordievskii,  A.  V.,  A.  Y.  Syrchenkov,  V. V. Sergievskii, and N. I. Savvin.  Nitrate-selective
     membrane electrodes.   Elektrokhimiya 8:520-521, 1972.

Guicherit, R.   Indirect determination  of nitrogen  oxides  by  a  chemiluminescence  technique.
     Atmos. Environ.  6:807-814, 1972.

Hager, R.  N. , Jr. ,  and R.  C. Anderson.   Theory  of the derivative spectrometer.  J.  Opt.  Soc.
     Am.  60:1444-1449, 1970.

Hansen, T. J. , M.  C.  Archer, and  S. R.  Tannenbaum.   Characterization of pyrolysis conditions
     and  interference  by other  compounds in the chemiluminescence detection of nitrosamines.
     Anal. Chem.  51:1526-1528,  1979.

Hanst, P. L.   Infrared spectroscopy and  infrared lasers in air pollution research and monitor-
     ing.  Appl.  Spectrosc.  24:161-174, 1970.

Hare, R.   J. ,  M.  T,  Wininger, and W. D.  Ross.   Selective collection and measurement of gaseous
     HMOs in ambient air.   In:   Current Methods to Measure Atmospheric Nitric Acid and Nitrate
     Artifacts,   Presentations  at a Workshop,  U.S.  Environmental  Protection Agency, Southern
     Pines, North  Carolina, October 3-4,  1978.    R.  K. Stevens,  ed. ,  EPA-600/2-79-051,  U.S.
     Environmental .Protection  Agency,  Research  Triangle  Park, NC,  March 1979.   pp.  63-65.

Harker, A. B, , L.  W.  Richards, and W.  E. Clark.   The effect of atmospheric S02 photochemistry
     upon observed nitrate  concentrations in aerosols.  Atmos. Environ. 11:87-91, 1977.

Hartley,  A. M. ,  and  R.  I.  Asai.   Suggested method for nitrate determination with 2,6-xylenol
     reagent.   J. Am. Water Works Assoc.  52:255-258, 1960.
                                             7-35

-------
Henriksen, A.   An automatic  method for  determining  nitrate and  nitrite  in  fresh and saline
     waters.   Analyst (London) 90:83-88, 1965.

Hermance, H.  W. ,  C.  A.  Russell, E. J.  Bauer, T.  F. Egan, and H. V. Wadlow.  Relation of air-
     borne nitrate  to telephone  equipment damage.    Environ.  Sci. Technol.  5:781-785,  1971.

Hersch, P.,  and  R.  Deuringer.   Trace addition  of  nitric oxide and nitrogen dioxide to air by
     electrolysis.  J. Air Pollut.  Control Assoc.  13:538-541, 1963.

Hinkley,  E.  D. ,   and  P.  L.   Kelley.   Detection of  air pollutants  with  tunable diode lasers.
     Science  (Washington, D.C.) 171:635-639,  1971.

Holler, A. C.,  and R. V.  Huch.  Colon'metric  determination of nitrates and nitric acid esters.
     Isometric xylenols as reagents.  Anal. Chem.  21:1385-1389, 1949.

Horrocks, J.  A.,  M.  Imada,  and J.  G.  Wendt.  Determination of the  Saltzman Factor with gravi-
     metrically  certified  permeation  devices.   Draft,  California Air  Resources  Board  and
     California Department of Health Services, El  Monte and Berkeley,  CA, March 1981.

Howe,  L.  H. ,  III, and C. W.  Holley.   Comparisons  of mercuric (II) chloride and sulfuric acid
     as preservatives  for  nitrogen forms  in  water samples.  Environ.  Sci. Technol. 3:478-481,
     1969.

Hughes, E. E.   Development  of standard  reference materials  for  air quality measurement.   ISA
     Trans.  14:281-291, 1975.

Huygen,  I. R.  C.   Reaction of  nitrogen dioxide  with Griess type  reagents.   Anal.  Chem.  42:
     407-409, 1970.

Huygen, C. ,  and P. H. Steerman.  The determination of nitrogen dioxide in air after absorption
     in a modified alkaline solution.   Atmos. Environ. 5:887-889, 1971.

Intersociety  Committee  for Ambient  Air Sampling  and Analysis.   Tentative  method of analysis
     for  nitrate in  atmospheric  particulate matter (brucine method).   _In:    Methods  of  Air
     Sampling and Analysis.   2nd Edition.  M.  Katz,  ed. ,  American Public Health Association,
     Washington, DC, 1977a.   pp. 521-523.

Intersociety  Committee  for Ambient  Air Sampling  and Analysis.   Tentative  method of analysis
     for total  nitrogen oxides as  nitrate  (phenoldisulfonic acid method).  Jji:  Methods of Air
     Sampling and Analysis.   2nd Edition.  M.  Katz,  ed. ,  American Public Health Association,
     Washington, DC, 1977b.   pp. 534-438.

Intersociety  Committee for  Ambient Air  Sampling and Analysis.  Recommended method of analysis
     for  nitrogen dioxide  content  of the  atmosphere (Griess-Saltzman Reaction).  I_n:  Methods
     of Air  Sampling and Analysis.  2nd  Edition.    M.  Katz,  ed. , American Public Health Asso-
     ciation, Washington, DC, 1977c.  pp.  527-534.

Intersociety  Committee  for Ambient  Air Sampling  and Analysis.   Tentative  method of analysis
     for nitrate  in atmospheric particulate matter, (2,4-xylenol method (1)).    In:  Methods of
     Air  Sampling and Analysis.   2nd Edition.  M.  Katz,  ed.,  American Public  Health Associa-
     tion, Washington, DC, 1977d.  pp. 518-520.

Jacobs, M. B. ,  and S. Hochheiser.  Continuous sampling and ultramicrodetermination of nitrogen
     dioxide  in air.  Anal.  Chem.  30:426-428, 1958.
                                             7-36

-------
Jenkins,  D. ,   and  L.  L.  Medsker.   Brucine  method for  determination  of nitrate  in  ocean,
     estuarine, and fresh water.  Anal. Chem. 36:610-612, 1964.

Joseph,  D.  W. ,  and  C.  W.   Spicer.   Chemiluminescence  method for  atmospheric monitoring  of
     nitric acid and nitrogen oxides.  Anal.  Chem.  50:1400-1403, 1978.

Joshi, S. B.,  and  J.  J. Bufalini!   Halocarbon  interferences in chemiluminescent  measurements
     of NO .   Environ. Sci.  Techno!. 12:597-599,  1978.

Kamphake, L.   J. ,  S.  A.  Hannah, and  J.  M.  Cohen.   Automated analysis  for  nitrate  by  hydrazine
     reduction.  Water Res.  1:205-216, 1976.

Katz,  M.   Nitrogen  compounds  and  oxidants.   In:   Air  Pollution.   Volume  III.   Measuring,
     Monitoring, and  Surveillance  of Air Pollution.   A.  C.  Stern, ed. , Academic  Press,  Inc.,
     New York, NY, 1976.  pp. 259-305.

Keeney,  D.  R. ,  B.   H.  Byrnes, and  J.  J.  Genson.   Determination  of  nitrate  in  waters with
     nitrate-selective ion electrode.  Analyst (London) 95:383-386, 1970.

Kelly, T. J..,  and D. H.  Stedman.  Chemi luminescence measurements of HN03 in air.   I_n:  Current
     Methods   to Measure  Atmospheric Nitric  Acid  and  Nitrate  Artifacts,  Presentations at  a
     Workshop, U. S.  Environmental  Protection Agency, Southern Pines,  North Carolina, October
     3-4, 1978.  R.  K.  Stevens, ed. , EPA-600/2-79-051,  U.S.  Environmental Protection Agency,
     Research  Triangle Park, NC, March 1979.  pp. 37-43.

Kieselbach,  R.  Microdetermination  of nitrates  by  the  Devarda  method.  Ind.  Eng. Chem.  Anal.
     Ed.  16:764-766, 1944a.

Kieselbach,  R.   Microdetermination of nitric oxide in gases.   Ind.  Eng.  Chem. Anal. Ed.  16:
     766-771,  1944b.

Kothny, E.  L.   The Direct Determination of Nitrogen Oxides.   Air and  Industrial Hygiene  Labor-
     atory Method No.  48, 1974.  State of California Department of Health, 1974.

Kothny,  E.  L.  Analytical methodology for  the  determination of nitrogen  oxides  in  air.   I_n:
     Nitrogen  Oxides.   National Academy of Sciences, Washington, DC,  1977.  pp. 31-55.

Kothny,  E.  L. ,  and  P.  K.   Mueller.   Sub-minute .continuous  nitrogen  dioxide  analysis.   Iji:
     Proceedings of the  1st  International  Clean  Air Congress,  Part I,  International  Union  of
     Air  Pollution  Prevention  Associations, London,  England,  October 4-7,  1966.    National
     Society  for Clean Air,  London, England, 1966.  pp. 182-184.

Kreuzer,  L. G. ,  and C.  K. N.  Patel.   Nitric oxide air  pollution:   detection  by  optoacoustic
     spectroscopy.   Science  (Washington, D.C.) 173:45-47, 1971.

Krull, I. S. ,  E. U.  Goff, G.  G. Hoffman, and D.  H.  Fine.  Confirmatory  methods  for the thermal
     energy determination of  N-nitroso  compounds at trace  levels.   Anal.  Chem. 51:1706-1709,
     1979.                                                                        ~

Laby, R.  H. , and T.  C. Morton.  Estimation of nitrates by nitration of  7-hydroxy-4, 8-dimethyl
     coumarin.  Nature (London) 210:298-299, 1966.

Langmuir, D. ,   and  R.  L.  Jacobson.    Specific-ion electrode determination of  nitrate in some
     freshwater and sewage effluents.  Environ.  Sci. Technol. 4:834-838, 1970.
                                             7-37

-------
Lazrus, A.  L. ,  B..  W.  Gandrud, and J. P. Greenberg.  Indophenol ammonia test  in measurement of
     HN03 and N03.   In:   Current Methods to Measure Atmospheric Nitric Acid  and Nitrate Arti-
     facts,   Presentations  at  a Workshop,  U.  S,  Environmental  Protection  Agency,   Southern
     Pines,   North  Carolina,  October  3-4,  1978.   R.  K.  Stevens,  ed. ,  EPA-600/2-79-051, U.S.
     Environmental  Protection  Agency,  Research  Triangle Park,  NC,  March  1979.   pp. 45-50.

Lazrus, A.  L. ,  E.  Lorange,  and J.  P.  Lodge,  Jr.    New  automated microanalyses for total inor-
     ganic  fixed  nitrogen and  for sulfate  ion in water.  In:  Trace  Inorganics  in Water, A
     Symposium  at  the 153rd  Meeting,  American Chemical  Society,  Miami  Beach, Florida, April
     10-13,   1967.   R.  F.  Gould,  ed. ,  Advances   in  Chemistry  Series  73,  American  Chemical
     Society, Washington, DC, 1968.  pp. 164-171.

Levaggi,  D.  A.,  W. Siu, and M. Feldstein.  A new method for measuring average 24-hour  nitrogen
     dioxide concentrations  in  the atmosphere.  J. Air Pollut. Control Assoc. 23:30-33, 1973.

Levaggi,   D.  A., W.  Siu,  M.   Feldstein,  and E. L.  Kothny.   Quantitative  separation of nitric
     oxide  from nitrogen  dioxide at atmospheric concentration  ranges.  Environ. Sci.  Technol.
     6:250-252,  1972.

Levaggi,   D.  A.,  E.   L.  Kothny, T.  Belsky,  E.  R. deVera,  and P.  K.  Mueller.   Quantitative
     analysis of  nitric  oxide  in presence  of  nitrogen  dioxide at atmospheric concentrations.
     Environ. Sci. Technol.  8:348-350, 1974.

Likens, G. E.  Acid precipitation.   Chem. Eng.  News 54:29-44, 1976.

Lord, H.   C. ,  W.  D.  Egan, F.   L.  Johnson, and  L. C. Mclntosh.   Measurement of exhaust  emission
     in piston  and  diesel  engines by dispersive  spectrum.   J.  Air Pollut. Control Assoc. 24:
     136-139, 1974.

Lunge, G. ,  and  A.  Lwoff.   Identification and  determination  of very small amounts of  nitrogen
     dioxide.  Z.  Angew.  Chem.  12:345-350, 1894.

Margeson,  J. H. ,  and  R.  G.  Fuerst.    Evaluation of  a Continuous  Colorimetric  Method  for
     Measurement  of   Nitrogen  Dioxide in Ambient Air.    EPA-650/4-75-022,  U.S.  Environmental
     Protection Agency, Research Triangle Park, NC, April 1975.

Merryman, E. L.  , C.  W. Spicer, and A. Levy.   Evaluation of arsenite-modified  Jacobs-Hochheiser
     procedure.   Environ. Sci. Technol. 7:1056-1059, 1973.

Mertens,  J.  , and D.  L. Massart.  The determination  of nitrate in mineral waters by potentiome-
     try and UV spectrophotometry.   Bull.  Soc. Chim. Belg. 82:179-190, 1973.

Miller, D.  F. ,  and  C. W. Spicer.  Measurement  of  nitric  acid in smog.  J. Air Pollut.  Control
     Assoc.  25:940-942, 1975.

Mohler,  K.,  and 0.  L.  Mayrhofer.    Evidence  and  determination of nitrosamines  in food.   Z.
     Lebensm. Unter.  Forsch.  135:313-318, 1968.

Morgan, G.  B. ,  C.  Golden,  and E.  C.  Tabor.   New  and improved  procedures for gas sampling and
     analysis in The National Air Sampling Network.  J. Air Pollut. Control Assoc. 17:300-304,
     1967a.
                                             7-38

-------
Morgan, G.  B. ,  E.  C.  Tabor, C.  Golden,  and H. Clements.  Automated laboratory procedures for
     the  analysis  of  air  pollutants.   In:   Automation  in  Analytical  Chemistry,  Technicon
     Instruments Corporation  Symposium, White  Plains, New  York,  October  19,  1966.   Mediad,
     Inc., White Plains, NY, 1967b.  pp. 534-541.

Morris, A.  W. ,  and J.  P. Riley.  The determination of nitrate in sea water.  Anal. Chim. Acta
     29:272-279, 1963.

Mulik, J. ,  R.  Puckett,  D.  Williams, and E.  Sawicki.   Ion chromatographic  analysis of sulfate
     and nitrate in ambient aerosols.  Anal. Lett. 9:653-663, 1976.

Mulik, J. ,  R.  Fuerst,  M. Guyer,  J.  Meeker, and E. Sawicki.   Development and optimization of
     twenty-four hour  manual  methods  for  the collection  and  colorimetric  analysis of  atmos-
     pheric N02- Int.  J. Environ. Anal. Chem. 3:333-348, 1974.

Mullin, J.  B. ,  and J.   P.  Riley.   The spectrophotometric  determination  of  nitrate in natural
     waters,  with  particular  reference to sea  water.    Anal.  Chim.   Acta 12:464-480,  1955.

Nash,  T.   An efficient  absorbing reagent  for nitrogen dioxide.   Atmos. Environ. 4:661-665,
     1970.

National   Research   Council.   Nitrates:   An  Environmental Assessment.   National  Academy  of
     Sciences, Washington, DC,  1978.

Noll,  C.  A.  Determination of  nitrate  in  boiler water by Brucine  Reagent.   Ind. Eng.  Chem.
     17:426-428, 1945.

Norwitz,  G.  A  colorimetric method for determination of oxides of nitrogen.  Analyst (London)
     91:553-558, 1966.

Nydahl, F.   On the optimum conditions  for the reduction of nitrate  to nitrite by cadmium.
     Talanta 23:349-357, 1976.

O'Brien,  J. E. , and J.  Fiore.   Robot chemist determines nitrates in sewage  and wastes.  Wastes
     Eng.  33:128-132,  1962.

O'Brien,   R.  J. , J. R.   Holmes,  R. J. Reynolds, J.  W.  Remoy, and A. H.  Bockian.   Analysis of
     photochemical  aerosols in  Los Angeles Basin according to particle size.  Presented  at the
     67th  Annual  meeting,.  Air  Pollution  Control  Association,  Denver,  CO,  June  9-13,  1974.
     Paper no.  74-155.

O'Keefe,  A.  E. ,  and G.  C.  Ortman.  Primary standards for  trace gas analysis.  Anal. Chem. 38:
     760-763, 1966.

Okita, T. ,  S.  Morimoto, M.  Izawa,  and S.  Konno.    Measurement  of gaseous and particulate
     nitrates in the atmosphere.  Atmos. Environ.  10:1085-1089, 1976.

Pellizzari,  E.  D.    The  Measurement  of  Carcinogenic Vapors   in   Ambient   Atmospheres.
     EPA-600/7-77-055,  U.S. Environmental  Protection  Agency,  Research Triangle Park, NC, June
     1977.

Pellizzari, E.  D. , J.  E.  Bunch,  B.  H.  Carpenter,  and E.  Sawicki.   Collection and analysis of
     trace  organic  vapor pollutants  in ambient  atmospheres.   Technique for evaluating con-
     centration of  vapors by sorbent media.   Environ.  Sci.  Technol. 9:552-555, 1975.
                                             7-39

-------
Pierson, W.  R. ,   J.  W.  Butler, and  D.  A.  Trayser.   Nitrate  and  nitric  acid  emission from
     catalyst-equipped automotive systems.   Environ. Lett. 7:267-272, 1974.

Purdue, L.  J. , and  T.  R.  Hauser.  Review of U.S. Environmental Protection Agency N02 monitor-
     ing methodology  requirements.   In:   Nitrogen Oxides  and  Their  Effects  on  Health,  A
     Symposium from  a  Joint Conference,  American  Chemical  Society and  Checmial  Society  of
     Japan, Honolulu,  Hawaii,  April  4-5, 1979.  S.  D.  Lee, ed., Ann Arbor Science Publishers,
     Inc.,  Ann Arbor, MI,  1980.   pp.  51-76.

Purdue, L.   J., G. G.  Akland,  and  E.  C.  Tabor.   Comparison  of  Methods  for Determination of
     Nitrogen Dioxide in Ambient Air.   EPA-650/4-75-023, U.S.   Environmental Protection Agency,
     Research Triangle Park, NC, June 1975.

Richardson,  H.  L.   The nitrogen  cycle  in grassland  soils;  with  special  reference  to the
     Rothamsted Park grass  experiment.   J.  Agric. Sci.  28:73-121, 1938.

Robinson,  J. B. D. ,  M.  D.  V. Allen,  and P. Gacoka.   The determination of  soil nitrates with a
    .brucine reagent.  Analyst (London) 84:635-640,  1959.

Ross,   W.  D. ,  G.  W.  Butler, T. G.  Duffy, W.  R.   Rehg,  M.  T. Wininger,  and R.  E.  Sievers.
     Analysis  for  aqueous   nitrates  and  nitrites and  gaseous  oxides of  nitrogen by electron
     capture gas  chromatography.  J.  Chromatogr. H2:719-727,   1975.

Saltzman,  B.  E.  Colorimetric microdetermination of nitrogen dioxide in the atmosphere.  Anal.
     Chem.  26:1949-1955, 1954.

Saltzman,  B. E.   Modified  nitrogen dioxide reagent for  recording air analyzers.  Anal. Chem.
     32:135-136,  1960.

Saltzman,   B.  E.   Critique  of  measurement  techniques  for  ambient  nitrogen   oxides.   I_n:
     Nitrogen  Oxides  and   Their Effects  on  Health,  A  Symposium   from  a  Joint Conference,
     American  Chemical  Society  and  Chemical  Society  of Japan,  Honolulu,  Hawaii,  April 4-5,
     1979.    S. D.  Lee, ed. ,  Ann Arbor  Science Publishers,  Inc.,  Ann Arbor,  MI,  1980.  pp.
     31-50.

Saltzman,   B.  E.,  and  A.  F.  Wartburg,  Jr.  Precision  flow dilution system for standard low
     concentrations of nitrogen dioxide.   Anal. Chem.  37:1261-1264, 1965.

Scaringelli,   F.  P.,  E.  Rosenberg,  and  K.  A.  Rehme.    Comparison  of permeation  devices and
     nitrite ion  as  standards  of  colorimetric  determination of nitrogen dioxide.   Environ.
     Sci.  Technol. 4:924-929, 1970.

Schumacher,  P. M.,   and C.  W.  Spicer.   Interferences  in  sampling  of particulate atmospheric
     nitrate.  Paper presented  at the  172nd  annual   American Chemical  Society meeting, San
     Francisco, August 1976.

Shaw,  J. T.  The  measurement of nitrogen  dioxide  in  the air.  Atmos. Environ.  1:81-85, 1967.

Shy, C. M.   The Chattanooga Study.   J.  Air Pollut.  Control Assoc. 20:832-833, 1970.

Shy, C. M.  ,  J. P.  Creason, M. E. Pearlman, F.  E. McClain, F.   B. Benson, and  M.  M. Young.  The
     Chattanooga  school children study:  effects of community exposure to nitrogen dioxide.  I.
     Methods,  description  of  pollutant  exposure and results  of ventilatory  function testing.
     J. Air Pollution Control Assoc.  20:539-545, 1970.
                                             7-40

-------
Skujins, J.  J.   Spectrophotometric determination of nitrate with 4-methylumbel 1iferone.  Anal.
     Chem.  36:240-241, 1964.

Small, H. , T.  S.  Stevens,  and W.  C.  Bauman.   Novel  ion exchange chromatographic method using
     conductimetfic detection.  Anal. Chem. 47:1801-1809, 1975.

Smith,  F.  and  R.  Strong.   Independent  Performance Audits on  RAMS  Station Sensors—Audit #4.
     Interim  Report.    EPA  Contract No.  68-02-2407,  Research  Triangle  Institute,  Research
     Triangle Park, NC, May 1977.

Spicer, C.  W.  The Fate of Nitrogen Oxides in the Atmosphere.  EPA-600/3-76-030, U.S. Environ-
     mental  Protection Agency, Research Triangle Park, NC, March 1976.

Spicer, C.  W. , and D.  F.  Miller.  Nitrogen  balance  in smog chamber  studies.   J.  Air Pollut.
     Control  Assoc. 26:45-50,  1976.

Spicer,  C.   W. ,  and  P.  M.  Schumacher.    Interferences  in  sampling  atmospheric  particulate
     nitrate.  Atmos.  Environ. 11:873-876, 1977.

Spicer, C. W. ,  G.  F.  Ward,  and B.  W. Gay,  Jr.  A further  evaluation of  microcoulometry for
     atmospheric  nitric acid monitoring.   Anal.  Lett.  All:85-95, 1978b.

Spicer, C.  W.,  P.  M. Schumacher, J. A. Kouyoumjian, and D.  W. Joseph.  Sampling and Analytical
     Methodology  for Atmospheric Particulate Nitrates.   Final Report.  EPA-600/2-78-067, U. S.
     Environmental Protection  Agency, Research Triangle Park, NC, April 1978a.

Spincer, D. ,  and  D.  T.  Westcott.  Formation  of nitrosodimethylamine in smoke from cigarettes
     manufactured  from  different  tobacco  types.    In:   Environmental   N-nitroso  Compounds
     Analysis and  Formation,  Proceedings  of a Working  Conference,  International  Agency for
     Research on  Cancer, Tallinn, Estonian SSR,  October 1-3,  1975.   E. A. Walker, P. Bogovski,
     L. Griciute,  and  W.  Davis,  eds.,   IARC  Scientific  Publications No.  14,  International
     Agency for Research on Cancer, Lyon, France, 1976.  pp.  133-139.

Stainton,  M.  P.   Simple  efficient reduction  column for  use  in the automated determination of
     nitrate  in water.   Anal.  Chem. 46:1616, 1974.

Stedman, D.   H.  ,  E.  E.  Daby,  F.   Stuhl, and H. Niki.   Analysis  of  ozone and nitric oxide by a
     chemiluminescent method  in  laboratory and  atmospheric studies of photochemical smog.  J.
     Air Pollut.  Control Assoc.  22:260-263, 1972.

Stevens, R.  K. , and J.  A.  Hodgeson.  Applications of chemiluminescent reactions to the measure-
     ment of  air  pollutants.   Anal. Chem. 45:443A-449A, 1973.

Stevens, R.  K.  and W.  A.  McClenny.   Introduction.   In:   Current Methods to Measure Atmospheric
     Nitric   Acid  and  Nitrate  Artifacts,  Presentations  at a  Workshop,   U.S.  Environmental
     Protection Agency,  Southern  Pines,   North  Carolina, October  3-4, 1978.   R.  K.  Stevens,
     ed:,  EPA-600/2-79-051, U.S.  Environmental  Protection Agency,  Research Triangle Park, NC,
     March 1979.   pp.  1-7.
                                             7-41

-------
Strickland, J.  D.  H. ,  and T.  R.  Parsons.   A Practical  Handbook  of Seawater Analysis,  Second
     Edition.    Bulletin  167,  Fisheries  Research Board,  Ottawa,  Ontario,  Canada,  1972.  pp.
     71-76.

Swain,  J.  S.    Determination  of  nitrates  in boiler  water by 1:3 xylen-4-ol   (2:4-xylenol).
     Chem.  Ind. (London): 479-480, April 20, 1957.

Sweeney, M. P. ,  D.  J.  Swartz, G.  A. Rost, R. MacPhee, and J. Chao.  Continuous  measurement of
     oxides of nitrogen  in  auto  exhaust.   J.  Air  Pollut.  Control Assoc.  14:249-254,  1964.

Szekely,  E.    Szechrome  analytical  reagents.   Research  Department  Authority,  Ben-Gurion
     University, Negev,  Israel, 1975.

Taras,  M.  J.    Phenoldisulfonic  acid  method  of determining  nitrate  in water.   Photometric
     study.  Anal.  Chem.  22:1020-1022, 1950.

Technicon  Industrial Systems.   Technicon Auto Analyzer  II.   Nitrate and Nitrite in Water and
     Waste Water (Range:   0.04-2.0 mg N/I).  Industrial  Method No.  100-70W/B, Technicon  Instru-
     ments Corp., Tarrytown, NY, January 1978.

Tesch,  J. ,  and R.   Sievers.   Selective  collection and measurement  of  particulate  nitrate and
     gaseous HN03 in ambient air.   I_n:  Current Methods  to Measure  Atmospheric Nitric  Acid and
     Nitrate  Artifacts,   Presentations  at a  Workshop,  U.S.  Environmental  Protection Agency,
     Southern Pines, North Carolina, October 3-4, 1978.   R. K. Stevens, ed., EPA-600/2-79-051,
     U.S. Environmental  Protection Agency, Research Triangle Park,  NC, March 1979.  pp.  67-77.

Thomas,  M.  D. , J.   A.  MacLeod, R.  C.  Robbins,  R.  C. Goettelman,  R.  W.  Eldridge, and  L. H.
     Rogers.    Automatic  apparatus for  determination of  nitric oxide  and nitrogen dioxide in
     the atmosphere.  Anal. Chem.  28:1810-1816, 1956.

Treadwell, F.   P.,  and  W. T. Hall.   Analytical  chemistry.  I_n:   Quantitative Analysis,  Volume
     II, 8th ed.  John Wiley and Sons, Inc., New York, 1935.  p. 318.

Tuazon,  E. C. ,  A.  M.  Winer, R. A.  Graham, and J. N. Pitts, Jr.  Measurements of ambient HN03
     in  the  California  south  coast air  basin  by kilometer  pathlength  Fourier transform in-
     frared spectrometry.  I_n:   Current Methods to Measure Atmospheric Nitric Acid  and Nitrate
     Artifacts,  Presentations  at  a  Workshop,  U.S.   Environmental  Protection Agency,  Southern
     Pines, North  Carolina, October  3-4,  1978.  R.  K.   Stevens,  ed. , EPA-600/2-79-051,  U.S.
     Environmental   Protection  Agency,  Research  Triangle Park,  NC,  March 1979.   pp.   9-26.

Tuazon,  E. C. ,  R.  A.  Graham, A. M.  Winer, R. R. Easton,  J. N. Pitts, Jr.,  and P. L. Hanst.   A
     kilometer pathlength  Fourier-transform  infrared system for the study  of trace pollutants
     in ambient and synthetic atmospheres.  Atmos. Environ. 12:865-875, 1978.

U.S.   Environmental  Protection  Agency.    National  primary  and  secondary  ambient air quality
     standards.  Fed.  Regist. 36:8186-8201, April 30, 1971.

U.S.  Environmental  Protection Agency.  Tentative method  for continuous measurement  of  nitrogen
     dioxide (chemiluminescent).  Fed. Regist. 38:15177-15180, June 8, 1973.

U.S.   Environmental  Protection  Agency.   Methods  for Chemical  Analysis  of  Water and Wastes.
     EPA-625/16-74-003.  Office of Technology Transfer,  Washington, D.C.,  1974.
                                             7-42

-------
U.S. Environmental Protection Agency.  Ambient air monitoring  reference  and  equivalent  methods.
     Fed. Regist. 40:7042-7070, February 18, 1975.

U.  S.  Environmental  Protection  Agency.   Ambient  air  monitoring  references  and  equivalent
     methods.  Code of Federal Regulations, Title 40,  Part  50,  1976a.

U.S. Environmental  Protection Agency.   Nitrogen dioxide measurement principle  and  calibration
     procedure.  Fed. Regist. 4J:52686-52695, December 1, 1976b.

U. S. Environmental Protection Agency.  Reconnaissance of Environmental  Levels  of Nitrosamines
     in  the  Central United  States.   EPA-330/1-77-001,  U.S.  Environmental  Protection  Agency,
     Denver, CO, February 1977a.

U. S. Environmental Protection Agency.  Reconnaissance of Environmental  Levels  of Nitrosamines
     in  the  Southeastern United  States.   EPA-330/1-77-009,  U.S.  Environmental   Protection
     Agency, Denver, CO, August 1977b.

Walters,   C.  L.  The  detection and  estimation  of trace  amounts of  N-nitrosamines in a  food
     matrix.    Lab.  Pract. 20:574-578, 1971.

Wasserman, A.  E.  A  survey  of  analytical  procedures for  nitrosamines.   Jjr.  N-Nitroso  Com-
     pounds Analysis and Formation,  Proceedings of a  Working  Conference,  International Agency
     for  Research  on  Cancer,  Heidelberg, Germany,   October  13-15,   1971.   P.  Bogovski,  R.
     Preussmann, E.  A.  Walker,  and W. Davis, eds. ,  IARC Scientific Publication No. 3, Inter-
     national Agency for Research on Cancer, Lyon, France,  1972.  pp.  10-15.

Wegner, T. N.   Simple  and sensitive procedure for determining  nitrate and nitrite  in mixtures
     in biological fluids.  J. Dairy Sci. 55:642-644,  1972.

West, P.   W. ,  and T.  P.  Ramachandran.  Spectrophotometric determination of nitrate  using chro-
     motropic acid.  Anal. Chim. Acta 35:317-324, 1966.

Williams, D.  T., and B.  L. Kolitz.  Molecular correlation spectrometry.  Appl.  Opt.  7:607-616,
     1968.

Winer,  A.  M. ,  J.  W.  Peters,  J.  P.  Smith,  and  J.  N.  Pitts,  Jr.   Response of  commercial
     chemiluminescent N0-N02  analyzers  to  other nitrogen-containing compounds.  Environ.  Sci.
     Technol.  8:1118-1121, 1974.

Wood, E.  D. ,  F. A.  J. Armstrong, and F.  A.  Richards.    Determination of nitrate  in sea water  by
     cadmium-copper reduction to nitrite.  J.  Mar. Biol.  Assoc. U.  K.  47:23-31, 1967.

Yagoda, H., and F.  H. Goldman.  Analysis of atmospheric contaminants containing nitrate group-
     ings.  J. Ind. Hyg.  Toxicol. 25:440-444, 1943.
                                             7-43

-------
                        8.  OBSERVED ATMOSPHERIC CONCENTRATIONS OF NO
                                AND OTHER NITROGENOUS COMPOUNDS      x

8.1  ATMOSPHERIC CONCENTRATIONS OF NOV
                                     A
     In  this  section,  selected  examples of  ambient concentrations of  NO  are  presented  in
                                                                           A
order  to  place possible  human exposure  in  nationwide perspective.  N02  is  given particular
emphasis since it is the oxide of nitrogen of most concern to human health.  The data presentei
are  not  intended   to  be  a  compendium  of  ambient  monitoring  activities.   They  have  been
summarized to give a representative picture of N0? concentrations in the United States and,  in
particular, to  provide  a  rational  basis for  deciding  whether or  not existing  ambient  N02
levels are a  cause  for concern when viewed  in  the context of the  health  and welfare effects
reviewed elsewhere in this document.
     The relationship,  nationwide, between  short-term peaks and annual  average concentrations
is reviewed to  estimate the variability in peak-to-mean ratios of NOp concentrations.  If the
variability is  small,  then  a rational  basis for  protecting  human  health and welfare might be
derived from  either  considerations of  the lowest  peak concentrations  or of the lowest annual
means  considered tolerable.   If  the  variability  is  large,  then  this fact would  point  to  the
necessity  of  considering  separately the  effects  of peak  and long-term  NO,,  concentrations.
     The question of whether or not any "typical"  diurnal  .pattern of N02 concentrations exists
nationwide is  discussed.  This question has bearing on the problem of estimating human exposure
to  ambient NOp  concentrations.    Other  considerations  bearing on  human  exposure   are  also
illustrated with recent  data  on  the  temporal and  spatial  variability of N02 concentrations  in
a single airshed.   Data are also presented to illustrate  certain general types of atmospheric
mechanisms potentially  leading to  high short-term N02 concentrations.   An example is given  of
late morning NOp peaks which typify photochemical  pollution processes such as occur frequently
in the Los Angeles  area and elsewhere.   Also illustrated is another,  less familiar, mechanism,
ozone titration, in  which  NO  is  rapidly  oxidized  to  N02  by ambient ozone.  This mechanism  is
of interest because  of its potential  for producing high NOp concentrations both in urban areas
and  in  plumes from  point sources.   Peak  concentrations  so produced generally  occur  later  in
the day than  those produced by photochemical  processes.
     Where examples  of atmospheric mechanisms leading to high N02 concentrations are  described.
the  examples  are  to  be  viewed as illustrative only.  Detailed  evaluations of  the relative
importance of  different mechanisms as well as the  relative impacts  of various source  types  and
appropriate ameliorative  actions  are  outside  the scope  of  this document and are  best  con-
sidered in the State Implementation Plans on a case-by-case,  area-by-area basis.
     It is  important to  note  that although a  careful  attempt has  been made  to  include  only
high quality  monitoring data  in  this  chapter, the  data  cited have not  usually  been derived
from monitoring activities  subject to  a formal  quality assurance program.   Identification  of
the analytic  procedures  used  to  obtain the data  cited  in this section  is generally  available

                                            8-1

-------
in the tables  accompanying  the text.   Reference is made  to Chapter 7 of  this  document  for a
discussion of  the reliability  of  these procedures.   In  the absence  of a  formal  program  of
audit for  the  wide  variety  of laboratories  conducting ambient monitoring, the  estimates  of
reliability  given  in  Chapter  7  are best  considered as  upper  bounds.    Specifically,  the
California Air  Resources  Board's  (CARB)  Air Monitoring Technical  Advisory  Committee  (AMTAC)
composed of the  CARB,  the Air Industrial  Hygiene Laboratory,  EPA Region IX,  and the local  air
pollution  control  districts,  have reported  NO ,   NO,  and  N09 concentrations  to  be on  the
                                                J\             £
average biased   about  14   percent higher than  the true value.   The bias  was independently
determined by three  agencies  participating in AMTAC and applies to any analyzer calibrated  by
the manual Saltzman  procedure.   This  affects virtually all California  sites.   A joint report
is being prepared by the Air Industrial Hygiene Laboratory Section of the Department of Health
Services and  the CARB regarding factors  affecting the Saltzman reagent.  The  formulation  of
the  reagent  used  in the  calibration procedure  contained 0.5  percent  sulfanilic acid,  5.0
percent acetic  acid, and 0.005 percent NEDA  (see  Chapter  7).   The bias  reported  applies  to
both static and dynamic calibration procedures.   All the California data cited  in this  chapter
are to be considered subject to biases of the reported magnitude.
8.1.1  Background Concentrations of NO
     Data on background concentrations of nitrogen  oxides  are extremely limited.  Robinson  and
Robbins (1972)  summarized measurements of NO and  N02  concentrations  from  various  locations,
such  as  Panama,  the mid-Pacific,  Florida,  Hawaii,  Ireland, North  Carolina, Pike's  Peak,  and
Antarctica.  From  these  data, they estimated  that  the mean background NO and  N0~  concentra-
tions for  land areas  between 65°N and  65°S are  3.8  ug/m3 (0.002 ppm) and 7.5  |jg/m3 (0.004
ppm), respectively.  The  measurements cited  for North  Carolina  and Pike's  Peak indicate that
background concentrations of  NO and N0? combined can  range from 0.001 to 0.005 ppm in remote
areas of the United States (Robinson and Robbins, 1972).
     More  recent measurements  using  modern  methods  have  yielded  results  pointing to  lower
values.    Noxon  (1975)  reports lower tropospheric N09 concentrations  at  a  remote  site  in
                                        3
Colorado  mountains   of  up to  0.20 ug/m   (0.0001  ppm) measured  by  ground-based  absorption
spectroscopy.   In  a more extensive study, Noxon (1978) reports detailed  background  measure-
ments at the Colorado  site  and at  a number of other widely dispersed locations using methodo-
logy with  a  sensitivity  of  0.03 ug/m  (0.015 ppb)  at sea  level.  The author concludes  that in
the truly  unpolluted troposphere the  column abundance of  N09 is less than 5 x  10   molecules/
  2
cm .   Assuming an  effective  length for the NO, column of  about  2 km (Chameides, 1975;  Crutzen
                                                                                             3
et al., 1978),  this  implies  a ground level  N0? background  concentration of less than 0.3 ug/m
(0.15 ppb).  If  the length  of the  column is 0.5 km (Ritter et al., 1979), background NO, con-
                         3
centrations of  0.94 ug/m   (0.5 ppb)  would  be  implied.  In addition, Noxon reports  that  the
ground level  N0~ concentration produced  at  distances  greater  than 50  km  from urban  centers
seldom exceeds  that for  truly unpolluted air  by  more than  a  factor of  2.   Measurements  by
                                            8-2

-------
Ritter  et  al.  (1979) using chemiluminescence analyzers at a site in Michigan showed NO  long-
   .                                                                                    A
term  average  concentrations  in presumably clean air  coming  from Canada to be in the range of
0.56  to 0.94 |jg/m  (0.3 to 0.5 ppb).  Measurements made at the Colorado site led Ritter et al.
to conclude  that  tropospheric NO  is confined  to  the lower 0.5 km of the troposphere.   Table
8-1,  taken directly  from Ritter et al., summarizes background NO  measurements.

                 TABLE 8-1.  BACKGROUND N0x MEASUREMENTS (RITTER ET AL., 1979)

Author
Junge (1956)
Lodge and Pate (1966)
Breeding et al . (1973)
Moore (1974)
Drummond (1976)
Cox (1977)
Galbally (1977)
Ritter et al. (1979)
Location
Florida
Panama
Central U.S.
Boulder, CO
Wyoming
Ireland
S. Australia
Rural MI
Fritz Peak, CO
Date
1956
1966
1973
1974
1976
1977
1977
1977
1977
NO Concentration
Observed, ppb
1.0-2.0
0.5
1.0-3.0
0.1-0.3
0.1-0.4
0.2-2.0
0.1-0.5
0.3-0.5
0.2 and up

8.1.2  Ambient Concentrations of NO
8.1.2.1  Monitoring for NO --Data from stationary monitoring sites may be used to estimate the
exposure experienced  by nearby receptors.  The  air  arriving at a fixed  observation  point at
any time has a unique history.   The aspects of this history which determine the ambient concen-
trations and relative amounts of nitrogen oxides are the sources encountered along the trajec-
tory and  a variety  of  meteorological variables.   Atmospheric reactions,  such  as  those that
oxidize NO to N0?, are functions of the concentrations of pollutants  emitted to the atmosphere,
temperature, sunlight, and  time.   Other  meteorological factors, such  as  wind speed,  vertical
temperature structure, and the region's topography, affect the dispersion and dilution of both
the directly emitted pollutants and the products of atmospheric reactions.
     Given the complex  nature  of the processes which  give  rise to potential human exposures,
one practical means of estimating these exposures is by monitoring atmospheric concentrations.
Air monitoring data  relevant to assessing ambient levels of NO  or NO -derived pollutants are
collected to meet a variety of specific objectives including:
                                            8-3

-------
               •  Determination of current air quality and trend analysis
               •  Determination of the state of attainment of National
                 Ambient Air Quality Standards
               •  Preparation of environmental impact statements
               •  Development of effective control  strategies and
                 evaluation of their effectiveness
               •  Development and validation of mathematical  models
                 which relate the strength of source emissions to
                 predicted concentrations for a variety of meteorological
                 and topographic conditions
               •  Research, such as studies of the  effects of ambient air
                 pollution on human health and welfare.

     In general,  each  specific  objective requires special  consideration as  to  site location,
frequency and  techniques of sampling, and  the  total  amount of  data  collected.   For example,
several years of N0?  data from a number of strategically located sites distributed nationwide
might  be  required  for  national  pollutant  trends  analysis.   A greater number  of  sites,  also
collecting data  on a  regular  basis  throughout the year, might be necessary  for determining
compliance with the National Ambient Air Quality Standards.   In contrast,  only a few carefully
chosen days  of detailed  measurements of various  pollutant concentrations and  emissions,  and
meteorological  parameters  as well,  might suffice for validation of  mathematical  air quality
models.  The ambient air quality data reported in  this chapter are mainly related to the first
of the above objectives.
     Once an air monitoring station's location is chosen, additional  practical  considerations
arise  relating to  the  actual placement of  probes  for sampling ambient air.  Building surfaces
and other obstacles may possibly scavenge N0~ from ambient air.   For this  reason, probes must
be located a certain  minimum distance away  from  such obstacles.   It is important, also, that
the  oxides  of nitrogen  in  the parcel  of air sampled  have  had  sufficient time  to undergo
atmospheric chemical reactions  (such as  conversion of NO emissions  to NO-)  characteristic of
the polluted atmosphere.   For  this  reason,  and  to avoid  sampling  air dominated  by any one
source,  probes  must  also  be  located  some minimum  distance from  primary   sources.   Siting
considerations  have  been reviewed  in more  detail  by Ludwig  and  Shelar (1978);  and EPA has
proposed  guidelines  for air  quality  surveillance  and data reporting which  include  more
detailed  discussion  of  considerations   noted  briefly  in  this  section  (U.S.  Environmental
Protection Agency,  1978).
                                            8-4

-------
8.1.2.2  Sources of Data—The  emphasis  in monitoring NO  has  been  primarily on NCk, since it
is  the  only nitrogen  oxide for which  a  National  Ambient Air Quality  Standard  has  been set.
The  most complete  collection  of  monitoring  data  for  the  United States  is  EPA's National
Aerometric  Data  Bank  (NADB),  which receives data  from  a variety of Federal, state,  and local
air monitoring programs.  The analytical methods with sufficient temporal resolution  to assess
short-term  exposures are continuous versions of the Griess-Saltzman method (e.g., the Lyshkow-
modified  Griess-Saltzman)   and  chemiluminescence.    These  data  are reported as  1-hr  average
concentrations  and  are archived  in  SAROAD  (Storage  and  Retrieval  of  Aerometric Data)  a
computer-assisted  storage   and  retrieval  system  of  EPA's  NADB.   Other  data, using  24-hr
instrumental averaging,  are also available in SAROAD.  Most of these data were obtained using
the sodium  arsenite  method.   Most frequently, these data are not collected every day but on a
regular schedule yielding 24-hr measurements, typically once every 6 days.
     Another important  source  of data in recent years,  albeit only from the greater  St.  Louis
area, is the  intensive  monitoring activity carried  out  as  part of the Regional Air  Pollution
Study (RAPS).   Nitrogen dioxide  data from this  study  are  routinely  available on  an  hourly
basis (minute-by-minute  data  are also available) as  obtained  with  chemiluminescence monitors
at 25 Regional  Air  Monitoring Sites  (RAMS).   These  data are archived in  a  special  RAPS data
base maintained at EPA's Research Triangle Park Environmental Research Center.
8.1.3  Historical Measurements of NO  Concentrations
     In  past  years,  the EPA  Continuous  Air  Monitoring Program (CAMP)  provided  the data  set
covering  the  longest  period   of time  on both  NO  and  N02  concentrations available in this
country.   Caution  is  necessary  in  using these  data because  collection and  reporting  proce-
dures were  not  subject  to  detailed quality  assurance checks and more than  one  operation  and
maintenance procedure may  have been  used over the years  at a given site.   However,  the data
base presented here does not  include  data taken by the Jacobs-Hochheiser method, because this
method has  been  withdrawn  by  EPA (Chapter 7).   The data collected provide a useful  historical
perspective on trends of NO  concentrations.   Table  8-2 presents  12 years of measurements of
                            A
nitrogen oxide (NO)  at  6 CAMP stations for  the  time period 1962-1973.   The annual  average NO
concentrations  are  plotted  in  Figure  8-1.   Trends  in  concentrations  during  1962-1973 were
generally upward for all sites monitored.   When the annual  means are grouped by 5-year periods,
1962-1966 and  1967-1971 (Table 8-3),  both   the  second  highest value  and the  annual  means
averaged over all CAMP cities  showed an increase of about 15 percent from the earlier to later
time  period.   Similar,   though  more  geographically  variable,  results  obtained  for nitrogen
dioxide  (N02) concentrations  at  most  CAMP sites (Table  8-4, 8-5; Figure 8-2).   St.  Louis data
showed a marked decrease, however,  in  both annual  average concentrations and average  of  second
highest  value between the two  5-year periods  (Table 8-5).   Upward trends in annual  average  N02
concentrations were observed  in  3  of  the 5 CAMP  cities  over the 9-year period, 1963 to 1971.
Figure 8-3  is a  graphical  presentation of changes in N02 air quality in the Los Angeles basin
between  the years 1965  and 1974.  The average increase in annual means for 11 stations  in  the
basin was about  20  percent, but individual  area results varied widely,  as seen in Figure 8-3.
                                           8-5

-------
                                TABLE 8-2.   YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITRIC OXIDE AT CAMP STATIONS,
                                               MEASURED BY THE CONTINUOUS SALTZMAN COLORIMETRIC METHOD (U.S.  EPA.  1975a)
00

Concentration,
Denver
Year
1962
1963
1964
1965
1966
1967
1968
1969
Mean
--
--
--
37
(30)
49
(39)
49
(39)
49
(39)
49
(39)
Max
--
--
--
652
(522)
627
(502)
590
(472)
738
(590)
677
(542)
Washington
Mean
37
(30)
49
(39)
49
(39)
37
(30)
49
(39)
62
(50)
49
(39)
49
(39)
Max
788
(630)
1,060
(848)
1.070
(856)
751
(600)
1,240
(1,000)
1,390
(1,112)
837
(670)
959
(767)
, pg/m3 (ppb), 25°C
Chicago
Mean
123
(98)
123
(98)
123
(98)
123
(98)
123
(98)
98
(78)
86
(")
135
(108)
Max
739
(704)
615
(492)
1,105
(884)
750
(600)
775
(620)
763
(610)
739
(591)
1,920
(1,536)
St. Louis
Mean
--
--
49
(39)
37
(30)
37
(30)
49
(39)
37
(30)
37
(30)
Max
--
--
923
(738)
443
(354)
688
(550)
393
(314)
492
(394)
873
(698)
Cincinnati
Mean
37
(30)
37
(30)
49
(39)
37
(30)
49
(39)
37
(30)
74
(60)
49
(39)
Max
702
(562)
615
(492)
787
(630)
750
(600)
1,230
(984)
1,685
(1,348)
1,242
(994)
861
(689)
Phi ladelphia
Mean Max
25 431
(20) (345)
62 1.845
(50) (1,476)
62 1,400
(50) (1,120)
62 1,083
(50) (866)
74 2.290
(60) (1.832)
74 1,820
(60) (1,456)
62 1,735
(50) (1,388)
49 1,083
(39) (866)
                                                                          (continued)

-------
TABLE 8-2.  (continued)

Concentration, ug/m (ppb).
Denver
Year Mean
1970 62
(50)
1971 62
(50)
1972 74
(60)
1973 74
(60)
-j 	 , 	
Max
750
(600)
677
(542)
788
(630)
652
(522)
Washington
Mean
62
(50)
49
(39)
86
(69)
123
(98)
Max
1,430
(1,144)
775
(620)
825
(660)
640
(512)
Chicago
Mean
172
(137)
135
(108)
160
(128)
221
(177)
Max
2,240
(1.792)
824
(659)
787
(630)
775
(620)
25°C

St. Louis
Mean
62
(50)
62
(50)
62
(50)
74
(60)
Max
689
(551)
615
(492)
714
(571)
750
(600)


Cincinnati
Mean
49
(39)
62
(50)
49
(39)
49
(39)
Max
960
(768)
750
(600)
763
(610)
689
(551)


Phi lade) phi a
Mean
74
(60)
49
(39)
62
(50)
--
Max
1.672
(1,338)
935
(748)
800
(640)
--

-------
                                                 &MICA6O C8MP'
<€


1
                                              9EWVER CAMP
                                                      S
•800

" so
        J	I
                                             PHILADELPHIA CAW
                                             t    a   e    !
                                                          T
                                                 ST. S.OUIS CAM?
            °S2  "O  '©«  °®5  *S6  °®y  °®8  'S3  TO  71

                                  YEAR
      Figure 8-1.  Trend lines for nitric oxide annual averages in five
      CAMP cities. —D— :data satisfying NADB minimum sampling
      criteria; —o— : invalid average (based on incomplete data).
      *!Mote change in ordinate scale for these data (U.S. EPA,  1973).
                               8-8

-------
           TABLE  8-3.   FIVE-YEAR AVERAGES OF NITRIC OXIDE  CONCENTRATIONS AT CAMP STATIONS,
                       MEASURED BY  CONTINUOUS  SALTZMAN COLORIMETRIC METHOD (U.S. EPA, (1973)
Station
                  Average-Concentration,
                           (ppb),  25°C
                                                   Average  of  Annual
                                                  2nd Highest  Value
                                                          (ppb),  25°C
 1962-1966
1967-1971
Change, %
1962-1966
1967-1971
Change, %
  Chicago

  Cincinnati

  Denver         44.9 (35.9)

  Philadelphia   55.2 (44.2)

  St.  Louis      39.8 (31.8)

CAMP average      61.2 (49.0)
122.6 (98.1)   125.4 (100.3)      + 2

 43.8 (35.0)    53.6 (42.9)       +22

                54.4 (43.52)      +21

                65.4 (52.3)       +18

                47.6 (38.1)       +19

                69.3 (55.4)       +13
                              731 (584.8)

                              782 (625.6)

                              633 (506.4)
                                 969 (775.2)

                               1,067 (853.6)

                                 620 (496.0)
                            1,331 (1,064.8)   1,395 (1,116.0)

                              541 (287.8)       578 (462.4)

                              804 (643.2)       926 (740.8)
                                    +32

                                    +36

                                    - 2

                                    + 5

                                    + 7

                                    +15

-------
TABLE 8-4.   YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITROGEN DIOXIDE AT CAMP STATIONS.
            MEASURED BY THE CONINUOUS SALTZMAN COLORIMETRIC METHOD (U.S.  EPA,  1975a)
Concentration, pg/m , at 25°C
Denver




00
i
i — •
o






Year
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
Mean
—
—
--
75
56
75
75
56
75
75
75
94
Max
--
--
--
507
602
583
488
620
639
676
583
846
Washington
Mean
56
56
75
56
75
75
94
75
94
75
113
--
Max
545
394
413
770
319
376
432
432
545
413
1,202
--
Chicago
Mean
75
75
94
75
113
94
94
94
113
113
94
132
Max
394
376
865
319
564
470
319
358
395
1,090
413
676
St. Louis
Mean
--
—
56
56
56
38
38
56
56
56
94
56
Max
-
--
394
226
357
282
319
714
244
244
376
508
Cincinnati
Mean
56
56
56
56
75
56
56
56
75
56
75
75
Max
470
377
620
301
432
432
1,036
394
433
301
319
207
Philadelphia
Mean
38
75
75
75
75
75
75
75
94
75
75
--
Max
226
584
471
358
413
413
358
245
377
770
545
--

-------
to
LU
cc
LU
 CM
O
200

100
  0
100
 50
  0
100
 50
  0
100
 50
  0
100
 50
                                                 CHICAGO CAMP
                                                 I    I     I
                                                     i     r
                          CINCINNATI CAMP
                            I    I     I
                                       n
                                           •CD-
                                                  DENVER CAMP
                       PHILADELPHIA CAMP
               I    I    I     I    I     I
n   o   n
 I    I     I
                                   T    I
                                   u   u
                                           n
                                                 ST. LOUIS CAMP
                                                 I    I     I
            '62  '63  '64   '65  '66   '67  '68  '69  '70  '71   '72
                                 YEAR

 Figure 8-2.  Trend  lines for nitrogen dioxide annual averages in five
 CAMP cities. -D—  : data satisfying IMADB minimum sampling cri-
 teria;-O- :  invalid average  (based on incomplete data).  *Mote change
 in ordinate scale for these data (U.S. EPA, 1973).
                                8-11

-------
                                            TABLE 8-5.  FIVE-YEAR AVERAGES OF NITROGEN DIOXIDE CONCENTRATIONS AT CAMP STATIONS,

                                                        MEASURED BY THE CONTINUOUS SALTZMAN COLORIHETRIC METHOD (U.S. EPA. 1973)
CO
I
Average, Concentration ,
pg/ni (ppb), 25°C
Station
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
CAMP average
1962-1966
86.1 (45.8)
62.0 (33.0)
66.0 (35.1)
67.7 (36.0)
58.5 (31.1)
68.1 (36.2)
1967-1971
101.2 (53.8)
60.0 (31.9)
67.9 (36.1)
77.6 (41.3)
54.2 (28.8)
72.2 (38.4)
Change, %
+18
- 3
+ 3
+15
- 7
+ 6
Average of Annual
2nd Highest Value.
ug/m (ppb), 25 C
1962-1966
444 (236.2)
391 (208.0)
498 (264.9)
361 (192.0)
320 (170.2)
403 (214.4)
1967-1971
499 (265.4)
367 (195.2)
493 (262.2)
414 (220.2)
267 (142.0)
408 (217.0)
Change, %
+12
- 6
- 1
+15
-16
+ 1

-------
                                    +3%
                                         0%<    +50%
   ™    .            _
+ 1 7%   .y J" ~— •- r-J
lk                         \
                           1
                                           '<
                                   +7%J +36% '-.
                                               "
                                               >
 AVERAGE N02 CONCENTRATION CHANGE (11 STATIONS): +20%
Figure 8-3.  Trends in IMO2 air quality, Los Angeles Basin, 1965-1974
(Trijonis et al., 1976).
                           8-13

-------
8.1.4  Recent Trends in NO., Concentrations
     Examination of  data  on trends in NCL  concentrations  during more recent years presents a
variable  picture  at  selected   sites  across  the  nation  (Figures 8-4  through  8-9).   Since
measured  concentrations,  particularly those  dealing with short-term  peak  excursions,  may be
expected  to  depend upon specific site considerations  as  well  as varying meteorological para-
meters, the  only data  presented are those from the same site over the years plotted.   Consis-
tent downward  trends are  observed at Camden, New Jersey, for all statistics presented (Figure
8-4).  A  generally downward trend for peak  one-hour  levels  is also discernible  at a site in
downtown  Los Angeles (Figure 8-5), accompanied by a relatively level pattern for other statis-
tics  plotted;  and  in   Azusa,  California  (Figure  8-6),  similar  generally  level  trends  are
apparent  for all statistics plotted for 1971-1980.   Nitrogen dioxide air quality seems to have
steadily  improved  in  Newark,  New Jersey  (Figure  8-7) from  1971 to  1977,  the  last year of
available N02  data at  the Newark site plotted.  No clearcut trend is discernible in Portland,
Oregon  (Figure  8-8),  although  an  unusually  high  one-hour  peak  level  was recorded in  1979
during a  day on which  several other  air  pollutants  (such as CO)  were  also  markedly  elevated
over  usual  levels.  Figure  8-9  shows trends  in  a 4-year running  average  of  annual  averages
(during  1970-1975)  of  daily maximum  1-hr N02 concentrations  in  the  Los  Angeles basin.   A
marked decrease  in  both  the highest annual average  and  in  the mean of 5  sites  is apparent,
although  the lowest annual average increased over the same period.  By comparison (Table 8-6),
N02  concentrations  spanning the  years  1969 to  1974 generally increased for  nearby  sites in
rapid growth areas of Orange County, California, whereas other California sites listed in TabTe
8-6 generally experienced declines in N0~ levels.
8.1.5  Seasonal Variations in NO,, Concentrations
     In  this  section, a  few  examples  of  seasonal   variations  in  N02  concentrations  are
presented which  demonstrate  that no single nationwide pattern exists for the monthly averages
of daily  maximum 1-hr  data.   The month-to-month variations  in  average N02 concentrations may
be  the combined  result of  high  photochemical  activity  in  the summer months,  time-varying
emissions of NO  (with high emissions of  NO  during the winter  in  some areas),  time-varying
emissions of hydrocarbons,  and  area-specific  meteorological conditions throughout  the year.
     The  data  presented are,  for the most part, averaged  over several years of monitoring, a
procedure which  may be expected to yield  representative patterns for  the  regions reported.
Examination of Figures  8-10 and 8-11 reveals that Chicago, Illinois, experiences a marked peak
in  N02 concentrations  during the  summer  months  while  concentrations in  Denver,  Colorado,
appear to peak in  the  winter.    In contrast  to the above patterns, certain  sites in  southern
California (Los Angeles, Azusa, and Pomona) do not exhibit a marked seasonality.  (The pattern
for  Lennox,  as published  in Trijonis,  1978,  was  discovered to be a duplicate of  the  Denver
pattern and is corrected here).
8.1.6  Recently Observed Atmospheric Concentrations of NO.,
     In  this  section,   representative examples of observed concentrations  of N02 in  recent
years are presented.   In summary, the data cited illustrate the following points:
                                            8-14

-------
 1100
 1000  —
      ANNUAL STATISTICS
	J-YEAR MOVING AVERAGES
— X — INCOMPLETE DATA
                     MAXIMUM ONE-HOUR OBSERVATION
                           99th PERCENTILE
                           90lh PERCENTILE
                          ARITHMETIC MEAN
                       COLORIMETRIC - GRIESS  SALTZMAN
     •68     '69     70     71     72     73      74     75     76      77     78     79     "80
Figure 8-4. Annual air quality and 3-year moving averages at Camden, New Jersey. [Data adapted from Trijomi
[1978], augmented with data from SAROAD.j
                                                   8-15

-------
  I

  en

  O
  P
  4
  cc

  2
  HI
  0

  O
  U
  LU
  O
  X
  g
  o

  in
  o
  o
  cc

  z
                                                                ANNUAL STATISTICS

                                                          	3-YEAR MOVING AVERAGES
                                                 MAXIMUM ONE-HOUR OBSERVATIONS
                               COLORIM£TRIC - LYSHKOW [14-; POSITIVE BIAS,
O
111

z
p

o
u
in
5


g
         '63   '64  '65  '66  '67   '68  '69   70  71   72  73   74  75   76   77  78  79  '80



                                              YEAR



Figure 8-5. Annual air qualtiy statistics and 3-year moving averages at downtown Los Angeles.

California. [Data adapted  from Trijonis [1978], augmented with data from SAROAD.j
                                              8-16

-------
 5
 z
 o
 u
 z
 o
 o
 LLJ
 o
 X
 O
 LU
 O
 O
 cc
900



800



700



600



500



400



300



200

   I

100
O
  MAXIMUM ONE-HOUR OBSERVATIONS
 \	,*.:•


	 x

  99lh PERCENTILE
                                                       ANNUAL STATISTICS

                                                   • • • • 3-YEAR MOVING AVERAGES '

                                                   -X- INCOMPLETE DATA
            90th PERCENTILE
                                      COLORIMETRIC - LYSHKOW [14°= POSITIVE BIAS
        63  '64  '65  '66  '67  '68  '69  70   '71  '72  73   74  75  76   77  78  79   '80
Figure 8-6. Annual air quality statistics and 3-year moving averages at Azusa, California. [Data
adapted from Trijonis  [1978], augmented with data from SAROAD.]
                                             8-17

-------
    700
    600 -r
z
o
p

tr

Z
LU
u
z
o
u
LU
D
x
UJ
O
O
a


1
                                                                       ANNUAL STATISTICS

                                                                 	3-YEAR MOVING AVERAGES

                                                                 — X — INCOMPLETE DATA
                               MAXIMUM ONE-HOUR OBSERVATION   I
                                                              V
99th PEHCENTILE
90lh PERCENTILE
                                      ARITHMETIC MEAN
                              COLOHIMETRIC - GRIESS  SALTZMAN
                                                                                       79    '80
  Figure 8-7. Annual air quality statistics and 3-year moving averages at Newark, New Jersey. [Data
  adapted from Trijonis [1978], augmented with data from SAROAD.]
                                                8-18

-------
I
"tt
Z
g
LU
u
Z
o
o
LU
o
X
O
5
z
UJ
o
o
                                                       ANNUAL STATISTICS

                                                > •  • • •  3-YEAR MOVING AVERAGES

                                                — X —  INCOMPLETE DATA
                   MAXIMUM ONE-HOUR OBSERVATIONS
                         99th PERCENTILE
                         90th PERCENTILE
                      COLORIMETRIC  LYSHKOW


                                  I        I
CHEMILUMINESCENCE


              I
       70
               71
  Figure 8-8.  Annual air quality statistics and 3-year moving averages at Portland, Oregon. [Data
  adapted from Trijonis [1978], augmented with data from SAROAD.]
                                                 8-19

-------
   340
   320
   300
   280
O  260
Z  240
O
u
 rvi
O

   220
   200
   180
                                  HIGHEST AVERAGE
                            BASINWIDE MEAN (5 SITES)
                                  LOWEST AVERAGE
             1970
1971
                               1972


                               YEAR
1973
                            1974
                  1975
Figure 8-9.  Annual average of daily maximum 1-hour IM02 (4-year

running mean) in the Los Angeles Basin (U.S. EPA, 1976a).
                             8-20

-------
      TABLE 8-6.  FIVE-YEAR CHANGES IN AMBIENT N02 CONCENTRATIONS'

NET PERCENTAGE CHANGE IN NO, CONCEN
TRATIONS FROM 1969 TO 1974
STATIONS
LOS ANGELES BASIN SITES
Orange County: Anaheim
(rapid growth) La Habra
Average for Orange County
Los .Angeles County: Azusa
(slow growth) Lennox
Los Angeles
L.A. (Westwood)
L.A. (Reseda)
Average for Los Angeles County
OTHER CALIFORNIA SITES
Oakland
Pittsburg
Redwood City
Sal inas
San Rafael
Santa Cruz
Stockton
Average for Other California Sites
NEW JERSEY SITES
Bayonne
Camden
Newark
Average for .New Jersey Sites
OTHER SITES
Chicago, IL
Portland, OR
Annual
Mean

+ 9%
+99%
+54%
+17%
- 7%
- 5%
+ 8%
- 4%
+ 3%

- 7%
- 8%
-24%
- 1%
+ 5%
+15%
- 3%
- 3%

-27%
- 9%
+ 2%
-14%

+32%
-.7%
90th
Percenti le

+ 5%
+60%
+33%
+ 7%
-11%
- 2%
+113
-10%
- 1%

- 9%
- 4%
-25%
- 1%
0%
-24%
-44%
-15%

-18%
- 7%
0%
- 8%

+51%
+44%
Yearly
Maximum

+13%
+72%
+43%
+ 6%
+ 1%
-28%
+32%
-13%
- 1%

-14%
-12%
- 9%
+27%
0%
-27%
-21%
- 8%

-36%
-52%
0%
-24%

+94%
- 3%

Adapted from Trijonis (1978).
                                  8-21

-------
      10
D.
a


2

O
DC

H

Z
LU

U


O

O
I


I

z'
g



cc
t-

u
U

O
O
 a
 a



O
z
HI
O


O
O
       15
       10
       15
       10
              HOUSTON/MAE 1975-1976


              I     I     I	I
                                       I
                                  6    7



                                  MONTH
                             I     I
              DENVER 1967-1973
                                                 I	I
                                  6    7



                                  MONTH
                                 T
              CHICAGO 1969 1973



              III     I
                                  67




                                  MONTH
                                                        NO-
                                                     10    11
                                                      10    11    12
                                                 9   10    11    12
                                                                12
 Figure 8-10.   Seasonal  NC>2 concentration patterns  of  three  U.S.

 urban  sites  (monthly averages of daily maximum 1-hr  concentra-


 tions). Adapted from Trijonis (1978).
                                   8-22

-------
CO

ro
OJ
             25
I    20
CL
a

z"

9.    15
        z
        LU
        u
        z
        o
        u
     10
        E

        I

        o
        u

        o
        u
                    AZUSA 1969-1974
                                   567



                                       MONTH
                                         8     9    10   11   12
     20
     15
             10
                    POMONA 1969-1974
               1    2   3    4     5    6    7    8     9    10   11   12


                                       MONTH
                                                                            Q.
                                                                            a
                                                                    z
                                                                    iu
                                                                    U

                                                                    O
                                                                    u
                                                                                20
                                                                                 15
                                                                                 10
                                                                     a
                                                                     a i

                                                                     Z
                                                                     o
                                                                    z
                                                                    UJ
                                                                    y
                                                                    z
                                                                    o
                                                                    o
                                                                                LOS ANGELES 1969-1974


                                                                                I     I     I     I     I
                                                                                2345678



                                                                                                    MONTH
15
10
                                                                                LENNOX 1969-1974 (SEE TEXT)
                                          9    10    11    12
                                                                                                                                  NO-
                                                                                       1    I     I     I     I     I     I     I     I      I
                                                                           1    2    3    4    5    6    7    8    9    10    11   12


                                                                                                    MONTH
         Figure 8-11.   Seasonal NO2 concentration patterns  of  four U.S. urban sites (monthly averages of daily  maximum  1-hr concentrations).

         Adapted from Trijonis (1978).

-------
        •  Annual average concentrations of NOp are not a reliable index of short-term (3-hr or
          less) human exposure.
        •  Although  a distinct recurrent diurnal  pattern  is  discernible in some  areas  of  the
          country, in many areas peak diurnal values occur at almost any time of day.
        •  Nitrogen dioxide levels of concern on a short-term basis may occur not only in urban
          areas, but also in certain small  cities and suburban areas.
     Reference  is made  to Tables 8-7, 8-8,  and  8-9 for the identification of analytic proce-
dures used to obtain data on ambient NCL concentrations cited in this  section.
     Examination  of  Tables 8-7  and 8-8 for 1975,  and Table 8-9 for  1976-1980,  reveals  that
during at least one of these years,  peak  1-hr N09 concentrations equalling or  exceeding  750
    3
ug/m  (0.4 ppm) were experienced in:  Los Angeles and several other California sites;  Ashland,
Kentucky;  and  Port  Huron,  Michigan.  Additional  sites reporting at least one peak hourly con-
centration equalling or  exceeding  500 pg/m  (0.27  ppm) during  those  years include:   Phoenix,
Arizona;   St.   Louis,  Missouri;  New  York  City,  New  York;  14  additional  California  sites;
Springfield,   Illinois;   Cincinnati,  Ohio;  and   Saginaw  and  Southfield,   Michigan.    Other
scattered  sites,  distributed  nationwide,  reported maxima close to this  value,  including some
approaching  500 (jg/m   in  1980.   As shown in Tables 8-7 to 8-9 recurrent NO, hourly concentra-
                            3
tions in excess of  250  pg/m  (0.14 ppm) were  quite common nationwide in both 1975 and subse-
quent years, but  very  few exceeded 750 pg/m  (0.4  ppm).   Table 8-10 presents data  for 24-hr
average N02  concentrations at  various  sites in  1976  to  1980.   It is  important  to  note  that
only  data  from  monitoring stations  meeting  EPA National  Air Data  Branch (NADB)  sampling
criteria*  were chosen  for listing in this  section.   The  number  of stations meeting these
criteria varies from year to  year, so that  many of the areas reported in Tables 8-9 and 8-10
are  not  identical with those  listed  in  Tables 8-7 and 8-8  for 1975.   The data  for  the  wide
range of  areas represented  in  these  four  tables do  show, however, that occasional  peak  NO^
concentrations of possible concern for human health (see Chapter 15)  occurred in the nation in
the mid-1970s.   More recently available data for  1976-1980 from the SAROAD system suggest that
basically  the  same  patterns  of occasional  peak N0~ levels approaching or exceeding 0.4 to 0.5
ppm still  occur from time to time in scattered areas of the United States.
 * NADB sampling criteria are as follows:
1)  For continuous observations with sampling intervals of less than 24 hours:
    a)  Data representing  quarterly periods must reflect a minimum of 75 percent of the total
        number of possible observations for the applicable quarter.
    b)  Data  representing annual  periods  must reflect  a  minimum of 75 percent  of  the total
        number of possible observations for the applicable year.
2)  For noncontinuous observations with sampling intervals of 24 hours or greater:
    a)  Data  representing quarterly periods  must  reflect a minimum  of  five  observations  for
        the applicable quarter.   Should  there be no measurements  in  1 of the 3 months of  the
        quarter, each remaining  month  must have no  less  than  2  observations  reported for  the
        applicable period.
    b)  Data representing  annual  periods must reflect four  quarters  of observation that have
        satisfied the quarterly criteria.
                                            8-24

-------
                        TABLE 8-7.   RATIO OF  MAXIMUM  OBSERVED  HOURLY  NITROGEN  DIOXIDE
            CONCENTRATIONS TO ANNUAL MEANS  DURING  1975  FOR  SELECTED LOCATIONS  (U.S.  EPA,  1977a)*
               State
00

ro
             Kentucky
                                                                               3
                                                                           [jg/m
                                                   Maximum  hourly  concentration -  yearly arithmetic mean
Location
 Method Au
Paducah
Louisville
Ashland
714/66 =10.8

895/85 =10.5
Method Bl
California












Colorado
Georgia
Illinois



Anaheim
Azusa
Costa Mesa
Los Angeles

Lynwood
San Bernadino
Napa
San Francisco
Barstow
Fontana
Chula Vista
Visalia
Denver3
Atlanta
Chicago3


East St. Louis
940/101= 9.3
696/112= 6.2
658/58 =11.3
1053/126= 8.4
1128/129= 8.7
602/97 =6.2
470/76 =6.2
188/49 =3.8
432/62 =7.0
432/39 =11.1
-
-
-
-
-
.
-
-
-
_
-
-
-
-
-
-
'
-
-
489/78 =6.3
451/64 =7.1
226/48 =4.7
555/96 =5.8
489/76 =6.4
395/104= 3.8
395/109= 3.6
244/41 =6.0
293/65 =4.5
                                                                                    348/84 4.1
                                                  (continued)

-------
                                              TABLE 8-7.   (continued)

State
Ma i ne
Maryland
Michigan
Oregon
Texas
Location
Bangor
Essex
Grand Rapids
Detroit
Portland
Dallas
ug/m
Maximum hourly concentration -
Method Ab
270/49 =5.5
-
279/67 =4.2
207/50 =4.1
-
yearly arithmetic mean
Method BC
-
282/53 =5.3
338/58 =5.8
-
432/32 =13.5

CD
I
ro
en
 More than one station reporting.

 Method A:   Instrumental Colorimetric-Lyshkow (MOD) method, a variation of
 the continuous Greiss-Saltzman Method.

 Method B:   Instrumental Chemiluminescence Method.          ..
*For comparison purposes, pote that:  1.0 ppm N0_ = 1880 ug/m ; 0.5 ppm ~ 940
 ug/m ; 0.1 ppm = 188 ug/m ;  0.05 ppm = 94 ug/m ;  and 0.01 ppm =? 18.8 ug/m .

-------
    TABLE 8-8.  FREQUENCY DISTRIBUTION OF 1975 HOURLY NO, CONCENTRATIONS
           AT VARIOUS SITES IN U.S. URBAN AREAS (U.S. EPR, 1977a)*
                                Concentrations (ug/m )          Maximum
                                equalled or exceeded by         observed
                             stated percent of observations   concentration
Location
Arizona
Phoenix
Cal ifornia
Los Angeles
Redlandsj:
Redlands
Riverside,
Riverside
San Diego,
San Diego
Colorado
Denver,
Denver
Kentucky
Ashland3
Michigan,
Detroit
Missouri
St. Louis3
New Jersey
Newark,
Newark
New York .
n
New York City
Ohio b
Cincinnati
Pennsylvania ,
Philadelphia
Texas ,
Dallas0
W

271

526
282
226
301
395
226
395

282
265

297
150

338

273
226


226

282

301

132
5%

188

301
169
150
226
282
150
282

188
177

209
113

244

169
169


169

150

226

94
10%

152

226
132
132
188
226
113
226

150
149

173
94

207

150
132


132

103

207

75
50%

69

94
56
56
94
113
38
113

94
90

68
56

75

81
75


56

47

113

19
(ug/m3)

660

1053
545
357
564
658
508
865

432
483

895
338

658

494
376


526

395

451

432

 Obtained by Instrumental  Colorimetric-Lyshkow (Mod) method,  a variation
 of the Griess-Saltzman method.

 Obtained by Chemiluminescence Method.

 Obtained by Instrumental  Colorimetric-Griess-Saltzman method.
*For comparison purposes,  note tbat:  1.0 ppm NOp = 1880 ug/m  ;  0.5 ppm
 = 940 ug/m ; 0.1 ppm = 188 ug/m ;  0.05 ppm = 94 ug/m ;  and 0.01 ppm
 = 18.8 ug/in .
                                   8-27

-------
TABLE 8-9.   FREQUENCY DISTRIBUTION OF 1976, 1978. AND 1980 HOURLY NITROGEN
   DIOXIDE CONCENTRATIONS AT VARIOUS U.S.  SITES (U.S. EPA. 1976c, 1979, 1981)*
Location SAROAD Site ID Method
Arizona
Phoenix 030600002G01


Tucson 030860002G01
CD
1
ro
00 California
Anaheim 050230001101


Chino 051300001101


Costa Mesa 051740002101


El Cajon 055300002101


Fontana 052680001101


Fremont 052780001101


La Habra 053620001101



Instrumental
Chemi luminescence

Instrumental
Chemi 1 umi nescence



Griess-Sal tzman
(Lyshkow)

Instrumental
Chemi luminescence

Griess-Saltzman3
(Lyshkow)

Instrumental
Chemi luminescence

Instrumental
Chemi luminescence

Griess-Sal tzman
(Lyshkow)

Griess-Sal tzman
(Lyshkow)

Year

1976
1978
1980
1976
1978
1980


1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Concentrations equalled or
exceeded by stated percent
of observations (ug/m )
1% 10% SOX

226
150
91
132
150
301


395
338
226
414
226
-
301
263
263
320
301
244
244
-
207
301
207
~
320
-
-

150
75
38
94
100
150


188
150
132
132
150
-
132
113
113
188
169
169
132
-
132
150
113
""
169
-
"

56
38
5
56
56
56


94
75
56
19
94
-
19
38
38
94
94
94
56
-
56
56
56
- "
75
-
"
Maximum
observed
concentration
(pg/m )

451
226
132
451
432
414


865
564
470
602
301
-
639
564
583
545
508
338
564
-
470
526
320

526
-

2nd Highest Yearly
observed arithmetic
concentration mean.
(pg/m ) (ug/m )

432
207
132
357
301
414


752
545
395
583
282
-
639
545
526
489
432
282
508
-
432
526
282

508
-


60
44h
17b
51b
61°
69


103
90b
7l"
54b
94
-
53b
53b
50
108
1Mb
95°
63
K
73°
80
66

91
~


-------
                                                          TABLE 8-9.  (continued)
00
 I
ro
to
Concentrations equalled or
exceeded by stated percent
of observations (ug/m )
Location
California (cont. )
Oakland


Oceanside


Redlands


Riverside


San Diego


San Diego


San Jose


San Jose


SAROAD Site ID Method

055300004F01 Instrumental
Chemi luminescence

055320003101 Instrumental
Chemi luminescence

056200001101 Instrumental
Chemi 1 umi nescence

056400005F01 Instrumental
Chemi 1 umi nescence

056800006101 Instrumental
Chemi luminescence

056800004101 Instrumental
Chemi luminescence

056980004A05 Instrumental
Chemi luminescence

056980004101 Griess-Sal tzmana
(Lyshkow)

Year

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1%

301
-
-
263
244
207
169
-
-
338
301
282
244
226
226
357
376
320
301
-
-
320
244
207
10%

150
-
-
113
113
75
75
-
-
207
169
150
113
132
113
188
207
207
169
-
-
169
13Z
132
50%

56
-
-
38
56
38
38
-
-
94
94
75
56
56
38
94
94
94
66
-
-
75
75
75
Maximum
observed
concentration
(ug/mJ)

545
-
-
620
602
357
470
-
-
564
564
414
451
432
357
585
940
470
479
-
-
526
414
301
2nd highest
observed
concentration
(ug/mj)

489
-
-
620
545
338
451
-
-
526
489
395
451
395
357
564
846
451
461
-
-
507
414
282
Yearly
arithmetic
mean.

77
-
-
57b
58b
40b
47
-
-
113b
101b
90
63b
7"b
55P
105
112b
114°
86
-
~
86
78.
D
79

-------
                                                              TABLE 8-9. (continued)
CD
 i
to
O

Concentrations equalled 01
exceeded by stated percent
of observations (ug/m )
Location
Georgia
Atlanta


Illinois
Chicago


Chicago


Springfield


Kentucky
Ashland


Michigan
Port Huron


Saginaw


Southfield


SAROAD Site ID Method

110200001F01 Instrumental
Chemi luminescence


141122001P10 Instrumental
Chemi luminescence

141122002A05 Instrumental
Chemi luminescence

147280003F01 Instrumental
Chemi 1 umi nescence


180080008F01 Griess-Saltzman3
(Lyshkow)


234340003F01 Griess-Saltzman3
(Lyshkow)

234760002F01 Griess-Saltzman3
(Lyshkow)

234880002F01 Griess-Saltzman*


Year

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
1%

160
160
160

273
-
-
263
-
-
90
113
-

209
141
-

222
188
-
291
312
120
363
292
-
10%

103
113
104

179
-
-
169
-
-
55
70
-

113
75
-

121
145
-
154
169
89
181
163
-
50%

66
66
56

113
-r
-
94
-
-
19
36
-

55
34
-

65
71
-
76
86
45
83
102
-
• Maximum
: observed
concentration
(ug/m )

244
348
301

461
-
-
461
-
-
519
239
-

572
306
-

832
450
-
643
649
189
645
365
-
2nd highest
observed
concentration
(ug/mj)

216
292
273

442
-
-
442
-
-
293
205
-

464
275
-

815
438
-
622
629
180
585
361
-
Yearly
arithmetic
mean,
(ug/ni )

67b
72b
61b

116
-
-
108
-
-
"b
40b
-

63h
41b
-

73h
79b
~
86b
94b
48°
100
106
-

-------
                                                  TABLE 8-9. (continued)
Concentrations equalled or
exceeded by stated percent
of observations (uq/m )
Location
New Jersey
Newark


Ohio
Q-, Cincinnati
i
CJ
t->
Pennsylvania
Philadelphia


Utah
Salt Lake City


Salt Lake City


SAROAD Site ID Method

313480002A05 Instrumental
Chemi 1 umi nescence


361220019A05 Instrumental
Chemi luminescence


397140023H01 Grei ss-Saltzmana
(Lyshkow)


460920001F01 Instrumental
Chemi luminescence

460920001A05 Instrumental
Chemi 1 umi nescence

Year

1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1%

226
-
167

147
150
103

188
-
-

244
188
207
226
-

10%

122
-
117

94
98
70

113
-
-

132
113
113
132
-

50*

75
-
66

56
47
38

75
-
-

75
56
56
75
-

• Maximum
. observed
concentration
(ug/mj)

338
-
196

677
254
150

451
-
-

470
263
357
470
-

2nd highest
observed
concentration
(ug/ni )

320
-
192

508
235
145

451
-
-

451
263
357
432
-

Yearly
arithmetic
mean,
(ug/m )

80
h
70

60
55
41

74
-
-

8°b
65b
61D
75
-

 Data  obtained using dynamic  calibration  procedures.

 Data  not satisfying NADB  minimum  sampling  criteria.

*For comparison ourposes.  note  that:   1.0 ppm  NO   ~  1880  ug/m ;  0.5  ppm ? ppm940 ug/m  0.1  ppm ~  188  ug/m ;  0.05 ppm ~ 94 ug/m ;  and 0.01
 ppm = 18.8 ug/m .

-------
TABLE 8-10. FREQUENCY DISTRIBUTION OF 1976, 1978, AND 1980 24-HOUR AVERAGE NO, CONCENTRATIONS AT VARIOUS SITES
IN U.S. URBAN AREAS (ALL DATA OBTAINED BY SODIUM ARSENITE METHOD) (U.S. EPA, 1976c. 1979, 1981)a
Concentrations
Second or exceeded by

Location
Alabama
Birmingham


Alaska
Fairbanks


Arizona
Tucson


Arkansas
oo Little Rock
i
CO
PO
California
Fresno


Long Beach


San Bernadino


Colorado
Denver



Site Code

010380003P01
II
II

020160001P01
ii
11

030860001F01
11
11

041440003F01
11
11

052800002F01
II
II
054100001F01
"
11
056680001F01
"
11

060580001P01
11
"

Year

1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
Maximum
fug/nO

127
" -
-

110
-
-

127
-
-

105
93
79

147
-
-
339
-
-
156
-
-

163
-
-
highest
(ug/m )

117
-
-

103
-
-

96
-
-

100
72
76

133
-
-
285
-
-
154
-
-

140
-
-
(ug/m ) equalled
stated percent
of observations
10%

107
-
-

85
-
-

69
-
-

65
58
53

118
-
-
215
-
-
124
-
. -

102
-
-
50%

66
-
-

59
-
-

45
-
-

32
28
27

49
-
-
101
-
-
78
-
-

46
-
-
Annual
arithmetic
mean..
(ug/m )

69
-
-

59
-
-

47
-
-

37
31
30

58
-
-
119
-
-
85
-
-

55
-
-

-------
                                                    TABLE 8-10.  (continued)
CD
co
to
Location
Connecticut
Bridgeport


Greenwich


Florida
Jacksonvi 1 le








Orlando


Georgia
Atlanta











Hacon


Site Code

070060123F01
"
11
070330008F01
070060004F01
070330004F01

101960033H01
11
"
101960002P01
"
11
101960032H01
II
11
103280004F01
11
11

110200038G02

II
110200001P01
II
II
110200039G01
11
11
110200041G01
11
n
113440008F01
113440007F02
113440007F02
Year

1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
I960
Maximum

143
134
207
101
93
123

138
-
-
100
-
-
93
50
-
91
71
74

133
60
106
123
73
-
120
99
98
100
74
-
109
84
92
C
Second
highest
(ug/m )

139
130
196
80
80
101

91
-
-
89
-
-
81
47
-
76
57
72

81
52
73
95
69
-
115
88
93
92
60
-
85
58
86
Concentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10*

123
108
114
54
65
82

90
-
-
79
-
-
67
47
-
50
47
64

72
52
64
94
69
-
92
88
72
83
60
-
71
53
58
50%

66
62
69
33
38
47

55
-
-
59
-
-
50
34
-
32
34
40

48
44
42
56
44
-
64
54
42
45
32
-
36
30
32
Annii.i 1
arithmetic
mean
(ug/ni )

70
66
78
36
39
52

59
-
-
58
-
-
53.
33b
-
32h
34b
41

52.
41b
41
61.
45b
-
59h
59b
39
51h
33b
-
40
33b
36

-------
TABLE 8-10.  (continued)

Location
Idaho
Boise City


11 1 inois
Chicago





Peoria


Indiana
Indianapolis




CD
i
cx> Iowa
Bellevue


Kentucky
Ashland





Paducah


Site Code

130220007F01
II
"

141220002P01
n
"
141220001P01
n
"
146080001P01
11
"

152040025H01
11
11
152040015H01
n
n

280180002F01
II
II

180080003F01
11
11
180080008F01
"
"
183180020F01
11
n
Year

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/mj)

96
-
-

172
-
-
117
-
-
94
-
-

308
-
-
128
-
92

126
-
-

94
173
92
93
84
-
90
-
-
C
Second
highest
(ug/m )

83
-
-

140
-
-
113
-
-
72
-
-

132
-
,-
122
-
90

97
-
-

93
123
87
89
79
-
82
-
-
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10*

66
-
-

130
-
-
99
-
-
68
-
-

86
-
-
89
-
90

87
-
-

79
72
65
76
76
-
71
-
-
50%

47
-
-

91
-
-
70
-
'
52
-
-

50
-
-
53
-
51

41
-
-

46
30
42
43
38
-
40
-
-
Annual
arithmetic
mean..
(ugV)

50
-
-

91
-
-
73
-
^
51
-
-

56
-
-
54
-
55b

46
-
-

48
35b
41
47
41
-
44
-
-

-------
                                                   TABLE 8-10. (continued)
CO
Location
Louisiana
Baton Rouge


Maine
Bangor


Maryland
Baltimore





Silver Spring


Michigan
Detroit








Minnesota
St. Paul


Site Code

190280002F01
11
11

200100001F01
11
"
S
210120018F01
11
"
210120007H01
11
11
2U480005G01
"
"

231180001P01
11
H
231180018F01
H
ii
2311B0016F01
11
"

243300031P01
11
11
rear

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
Maximum

102
89
119

126
80
-

137
-
-
90
103
-
98
-
-

138
-
-
123
-
-
99
-
-

91
126
103
C
Second
highest
(ug/m )

88
88
93

103
70
-

134
-
-
88
94
-
82
-
-

122
-
-
115
-
-
86
-
-

83
113
86
loncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%

75
68
71

80
61
-

95
-
-
80
93
-
66
-
-

91
-
-
105
-
-
67
-
-

71
86
68
50*

48
47
52

50
42
-

60
-
-
57
60
-
38
-
-

62
-
-
62
-
•
45
-
-

52
56
49
Annual
arithmetic
mean.

51
49
54

51b
46b
-

63
-
-
57.
62b
-
39
-
-

66
-
-
68
-
-
48
-
-

54
58
47

-------
                                                       TABLE 8-10.  (continued)
00
i
to
01
Location
Missouri
Kansas City


St. Louis





Nebraska
Lincoln


New Hampshire
Nashua


North Carolina
Beloont


Charlotte


Wins ton- Sal em


Site Code

171800012P01
11
11
264280072P01
11
11
264280001P01
"
"

281560004G01
11
281560012G01

300480005F01
11
"

340300001F02
11
340300003F02
340700001G01
-'"vv
11
344460002G02
11
11
Year

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/m )

147
-
-
136
-
-
Ill
-
-

112
120
86

151
-
-

107
-
84
84
112
154
80
95
148
C
Second
highest
(ug/m-5)

147
-
-
127
-
-
105
-
-

91
59
86

116
-
-

103
-
57
80
103
132
68
91
94
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%

69
-
• -
109
-
-
94
-
-

70
21
69

76
-
-

96
-
57
67
88
91
65
76
55
50*

49
-
-
71
-
-
64
-
-

45
11
48

46
-
-

67
-
28
46
54
54
43
39
24
Annual
arithmetic
mean,
(ug/mj)

50
-
-
73
"
-
59
-
-

46
14
47

54
-
-

73
h
31°
48
57
58
45
43
33

-------
                                                   TABLE 8-10.  (continued)
oo
OJ
Location
Ohio
Akron





Campbell


Cincinnati




Cleveland




Moraine


Toledo


Oklahoma
Tulsa


Oregon
Portland


Site Code

360060006H01
11
11
360060004H01
II
11
360960001101
11
11
361220018H01
"
361220019P01
"
H
361300033H01
H
11
361300012H01
11
"
364550001G01
ii
"
366600007H01
II
"
373000112F01
11
11

381460001P01
" •
ii
Year

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
19SO
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
Maximum
(ug/m )

96
139
93
100
135
86
128
110
103
158
105
-
121
-
-
193
259
136
189
222
132
126
-
-
117
162
102
193
-
-

102
-
-
C
Second
highest
(ug/m )

91
109
93
91
126
83
125
100
90
139
100
-
98
-
-
181
247
126
175
207
121
91
-
-
115
116
101
157
-
-

98
-
-
oncentrat ions (ug/m ) equalled
or exceeded by stated percent
of observations
10*

70
87
75
82
82
76
92
79
84
106
105
-
89
-
-
127
197
112
127
135
115
84
-
-
80
92
90
119
-
-

90
-
-
50%

45
52
53
48
47
52
60
51
45
61
95
-
61
-
-
83
92
71
87
92
79
52
-
-
53
58
59
68
-
-

53
-
-
Annua 1
ari thmetic
mean3
(ug/m )

46
57
54
53
53
52
63
54
51
70.
93b
-
62
-
-
88.
109b
68
87
99
78
53
-
-
56
64
59
74
-
-

57
-
-

-------
                                                     TABLE 8-10.  (continued)
CD

Co
00
Location
South Carolina
Mount Pleasant


Spartanburg


Tennessee
Chattanooga


Eastridge


Knoxville


Nashville


Texas
Austin





Dallas








Site Code

42170000 1F01
ii
"
422040001F01
11
"

440380025G01
"
ii
44C900001G01
"
"
441740005G01
"
•i
442540002G01
••
11

450220004F01
"
"
450220012F01
"
11
451310023H01
11
11
451310002F01
"
11
451310002H01
11
"
Year

1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
I960
1976
1978
1980
1976
1978
1980
Maximum
(ug/mj)

118
43
63
121
105
119

94
-
-
124
-
-
119
-
-
145
125
156

117
94
75
93
106
-
91
231
-
97
238
265
108
. 133
-
(
Second
highest
(ug/ni )

74
34
40
90
99
45

92
-
-
95
-
-
114
-
-
115
124
140

71
86
70
79
77
-
88
190
-
96
165
202
105
131
-
loncentrdtions (ug/m ) equalled
or exceeded by stated percent
of observations
10%

37
29
32
74
83
43

74
-
"
64
-
-
101
-
-
97
106
113

47
86
55
58
57
-
77
112
-
83
127
183
eo
104
-
50%

16
14
9
38
28
3

48
-
-
46
-
-
70
-
-
64
56
54

27
44
32
20
17
-
50
54
-
52
74
84
57
62
-
Annual
arithmetic
mean,
(pg/m )

20
16..
15b
42
33..
18b

51
-
-
47
-
-
70
-
-
69
65n
60b

30.
46b
35
24
22
-
51
63
-
52
77.
98b
57
63
-

-------
                                                         TABLE  8-10.  (continued)
CD
 i
to
10
Location
Fort Worth





Houston


Utah
Salt Lake City


Washington
Seattle


Wisconsin
Hi Iwaukee


Site Code
451880021H02
"
11
451880022H02
11
11
452560009H01
"
it

460920001POX
11
11

491840001P01
"
11

512200045F01
"

Year
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
Maximum
(ug/m )
153
94
-
138
91
-
162
170
128

364
-
-

119
139
-

148
133
81
C
Second
highest
(ug/ni )
143
94
-
124
66
-
137
116
101

182
-
-

114
113
-

115
125
76
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%
102
94
-
95
91
-
127
102
99

120
-
-

91
113
-

88
95
76
50%
74
65
-
63
61
-
56
66
30

57
-
-

66
90
-

62
65
54
Annual
arithmetic
mean.,
(ug/m )
71.
74b
-
61b
59b
-
64
Mb
46

70
-
-

66h
93b
-

60
67b
57b
               aFor comparison purposes,  note  that:  1.0  ppm N0?  =  1880  ug/m3;  0.5  ppm
                = 94 ug/n> :  and 0.01  ppro  =  18.8 ug/m .


                Data do not  satisfy NAOB  minimum sampling criteria.
940 ug/m3; 0.1 ppm = 188 ug/m3; 0.05 ppm

-------
     Since the  National  Ambient Air Quality Standard for N02 is stated in terms of the annual
arithmetic mean, much attention has focused on long-term averages.   One question which arises,
then, is whether observed annual averages are an adequate index of the frequency and levels of
short-term exposures.  The data in Table 8-7, taken from SAROAD, show the ratios of the maximum
hourly N02 concentrations to the annual means ov various cities for 1975.   These ratios ranged
from about  3.6 in  Chicago,  Illinois,  to  13.5 in  Dallas,  Texas.   Thus,  it may  be  seen that
these ratios,  between  the highest 1-hr  NCL  value  during 1975 and the  annual  arithmetic mean
for  1975,  were quite  different in various  parts  of the nation.  To  further  illustrate this
point,   Figure  8-12  shows  the  distribution  of maximum-to-mean  NCL  ratios  averaged  over  the
years 1972, 1973,  and 1974 for 120 urban sites (Trijonis, 1978).  Over 70 percent of the sites
have maximum-to-mean ratios  in  the range of  5  to  8;  about 8 percent of the sites have ratios
exceeding 10.   Figure 8-13 shows long-term trends in the maximum-to-mean NOp ratios for groups
of sites  in New Jersey and  in  the  Los Angeles basin (Trijonis, 1978).   (No Jacobs-Hochheiser
data were used.)   It  is  important  to  note  that  although the  averaging procedure  might  be
expected  to smooth  out fluctuations in  the  data,  there  is,  nevertheless, no consistent value
over the  years for  the  ratio  in  either area.  Looking back  on  Figures 8-4  to 8-8,  marked
variations in peak to mean ratios over many years at the same or different sites are apparent.
It may  be concluded,  therefore, that  the annual mean  is not a  good  indicator  of the highest
short-term exposure level in the geographic areas considered.
     Table 8-8  shows the frequency distribution of 1-hr N0~  measurements at various sites in
1975 (U.S.  EPA, 1977a).   It may  be  seen here  that  there was  great variability across  the
nation  for all  the  percentile values presented.  Also,  it is obvious that the median value is
not  always  indicative  of  the potential  for short-term  exposure.  For  instance,  Los Angeles,
Riverside, and San Diego, California,  had high median values of 94 (0.05 ppm),  113 (0.06 ppm),
             3
and  113  ug/m   (0.06  ppm)  respectively.   St.  Louis, Missouri,  on the  other  hand,  had  the
moderate  median  value  of  75 ug/m  (0.040  ppm),  but  exceeded  more than half  the California
sites reported  for  the one-percentile level.  It may  also  be seen from  this table  that some
small cities  may  experience  peak  concentrations of  NOp even  higher  than  those  observed in
center-city locations  in  major  metropolitan areas.'   Ashland, Kentucky, reported  a maximum of
895  ug/m   (0.48 ppm), which exceeded  the  maximum reported in  most major  metropolitan areas
across   the  country.   A  similar conclusion may be  drawn from Table 8-9,  in that Port Huron,
Michigan, reported a peak value of 832 ug/m  (0.44  ppm),  which is exceeded in the listing only
by Anaheim, California.
     Two  major factors  that affect  NOp concentrations, mobile  source emissions and  photo-
chemical oxidation,  have fairly consistent diurnal  patterns in most urban  areas.  These usually
contribute, to  the  observed diurnal  variation  in  NO   concentrations.   Such  a  variation  is
typified  by a  rapid increase in N0~  in  the  morning as  the result  of  NO  emissions and photo-
chemical conversion to N0~.  This is followed by a  decrease of NO^ in the  midmorning hours due
to advection  and  increasing vertical  dispersion and  also loss of NO^  in various atmospheric

                                            8-40

-------
s
o

I
u.
O
15
B
c
                    468

                       MAXIMUM/MEAN RATIO
  Figure 8-12. Distribution of maximum/mean IM02 ratios for 120
  urban locations averaged over the years 1972, 1973, and 1974
  (adapted from Trijonis, 1978).
                                       8-41

-------
cc
 (M
o
z
<
UJ
5
O

5
i
x
 I
I     I     I     I
          I     I
     T
I
V
I
T
I
              b

           I	I
                l
'64   '65   '66   '67  '68  '69  '70  '71    '72   '73   '74

                     YEAR
           '64   '65  '66  '67  '68   '69  '70   '71   '72   '73   74

                                YEAR


     Figure 8-13. Trends in the maximum mean NOo ratio for two
     groups of sites:  (a) average of five locations within the Los
     Angeles  Basin (Anaheim, La Habra,  Azusa, Pomona, San Ber-
     nadino); (b) average of two New Jersey sites (Bayonne and
     Newark).

     Source:  Adapted from Trijonis (1978).
                                 8-42

-------
transformation  reactions.   Peaks  in the NOp concentration are often observed corresponding to
emissions  occurring during  the  late  afternoon  rush hour.   In  some areas,  small  lunchtime
maxima  occur.   At  many sites  evening peaks  occur.   Ground-level  NO  concentrations  usually
build up slowly during the night.
     To illustrate variations of NOp, concentration data from the month of the highest observed
1-hr  NOp  concentration in three cities  are  presented in Figure 8-14  (U.S.  EPA,  1975b).   The
monthly average 1-hr  measurements  were computed  separately  for each hour  of  the  day.   This
gives  the  composite diurnal  pattern as  shown in Figure  8-14 for the  month  containing  that
year's  highest  reported short-term  (1-hr) concentration.   The  data  from  Los  Angeles during
January 1975,  and Denver  during  April  1975,  followed the "typical"  urban pattern described
above,  although the  average NOp levels  in  Los Angeles were considerably higher.   The pattern
for Chicago  during  June 1975, was quite different.  The extremely broad peak with the maximum
between 2:00 and  3:00  p.m.  was the  result of  individual  daily maxima which did  not occur at
the same time  of  day during  the month  of June.  This is one illustration of the fact that no
standard diurnal pattern exists nationwide.
     To further illustrate  the  diurnal trends  in  the  same three cities, data from the day of
the highest  1-hr  N02 concentration  in  1975  are plotted (U.S.  EPA, 1975b)  (Figure  8-15).   In
all three  cities  the  diurnal patterns  are  similar to  the average patterns.   The extremely
sharp,  high  peak  in  the Los Angeles data exemplifies the combined effects of poor atmospheric
dispersion,  high  emissions,  and photochemical  activity which are quite common in this region.
     In Figure  8-16, 1-hr  average NOp concentration data  are  plotted versus time for periods
of 3  days  during  which high NOp levels were observed (U.S. EPA,  1975b).   The Los Angeles  data
showed a diurnal profile typical for the area on the afternoon on January 15, during which the
NOp concentration  climbed  steadily  after  a  small  morning peak.   This  situation  was probably
the result of  low wind speeds and  a strong  elevated inversion restricting both advection and
dilution.   The  data for  Ashland,   Kentucky,  show the  same basic diurnal  trend  seen  in  Los
Angeles on the  first two  days and much  lower  levels on the third day.   The data from McLean,
Virginia,   at much lower  overall  concentration  values,  had quite  a  different pattern.   The
major increase in N0? concentration did not take place until 5:00 or 6:00 p.m.
     Figure  8-17  shows  the  NOp  and  NO concentration profiles  obtained from a center-city
station in St.  Louis,  Missouri,  and the NOp concentration from  a rural  site,  45 km north of
the center-city location (U.S. EPA, 1976b).  The center-city site showed a rapid buildup of NO
during the morning with a slower rise in the NO, concentration.   The rural site, at this time,
reported NO- concentrations  at or  near  the  instrumental limits  of detection.    During  the
morning and early afternoon, the winds experienced at both sites  were  light and from the north-
west.   Between 1:00 and 2:00 p.m.  the wind direction at the center-city site shifted and began
coming  from  the south  and  south-east over the  next  several  hours.   A similar  change occurred
between 5:00 and  6:00  p.m.  at the rural  site.   After the shift in direction,  the  wind speed
increased  somewhat at the rural  site, and more  gradually increased in  the downtown area.   Since

                                            8-43

-------
OO
                                                                                                             LOS ANGELES. JANUARY 1975
                                                                                                             DENVER. APRIL 1975
                                                                                                             CHICAGO JUNE 1975
               24
       Figure 8-14.  Average diurnal pattern for the month during which the highest 1-hoiir NO2 concentrations were reported (U.S. EPA. 1975b).

-------
CD
I
                                                                                                    LOS ANGELES, CALIFORNIA. JANUARY 17. 1975

                                                                                                    DENVER. COLORADO. APRIL 5. 1975

                                                                                                    CHICAGO. ILLINOIS. June 21, 1975
              Figure 815. One hour average concentration profiles on day of peak NC>2 concentration for three U.S. cities (U.S. EPA, 1975b).

-------
                                                                                                               ASHLAND. KENTUCKY, NOVEMBER 1920. 1975

                                                                                                               LOS ANGELES. CALIFORNIA. JANUARY 15 17. 1975

                                                                                                               MclEAN. VIRGINIA. AUGUST 27 ?9. 1975
-p.
en
                           MIDNIGHT
                                                  NOON
                                                                     MIDNIGHT
                                                                                            NOON


                                                                                         TIMEOFDAV
                                                                                                               MIDNIGHT
                                                                                                                                      NOON
                                 Figure 816. One-hour NC>2 concentrations during three day! of high pollution in three U.S. citiel (U.S. EPA. 1975b).

-------
   0.10
  (188.0)
NO2 AT RAMS STATION 5 (CENTER CITVI
NO2 AT RAMS STATION 22 (45 km NORTH OF CENTER CITV)
                                                   12
                                                                  15

                                                              TIME, hours
                                                                                18
                                                                                               21
0.22
(271)

0.20
(246)
Figure 8-17.  Nitric oxide and nitrogen dioxide concentrations at an urban and a rural site in St. Louis, Missouri, on January 27-28, 1976
(U.S. EPA, 1976b).

-------
other monitoring sites  in  and around St. Louis did  not show a consistent,  concomitant varia-
tion of N02  concentrations,  the most likely explanation  for  the  data presented is dispersion
or plume  impaction  from a  variety of industrial  sources,  located roughly to the south of the
sites reported herein.
     The above discussion indicates that short-term excursions of N02 concentrations to levels
well above  the average  can  occur at night  and are not  necessarily  associated directly with
traffic emission and photochemical  oxidation,  even though the levels shown  in Figure 8-17 are
considerably  lower  than those  associated  with the  morning peaks  shown  in Figures  8-15 and
8-16.  To further  illustrate  this phenomenon,  the monthly  maximum  concentrations  observed at
each hour of  the   day  are  listed  for  selected   individual  months from six  geographically-
dispersed urban locations in Table 8-11  (U.S.  EPA, 1975b).
     The  data from  Newark,   New  Jersey,  show  peak  concentrations   in  the  late hours  before
midnight,  and only  a   mild  diurnal  variation  for  the rest of  the day.   Portland,  Oregon,
experienced   consistently  elevated  maxima   for   all   hours  between  2:00  and  11:00  p.m.
Los  Angeles,  California,   as  expected  from  the  previous   data,  experienced  the  highest
short-term  NO-  levels   in  the  mid-morning  hours  and  a marked diurnal  pattern.   Chicago,
Illinois,  exhibited only a  mild diurnal  pattern in monthly maximum concentration for the month
illustrated.    In Denver, Colorado, elevated  N02   levels  are  apparent from 9:00 a.m.  to 7:00
p.m.  In  El  Paso,  Texas, both morning and early  evening elevations in N02  concentrations are
apparent.   It  also  can  ,be  seen that, for all  hours  on at least one day during the month, N02
concentrations exceeded the monthly mean.
     To summarize,   the  above  data indicate that  very  high  N02 concentrations, of  a few hours
duration,  can  occur in  urban areas associated with the Los Angeles-type diurnal  pattern of
photochemical air pollution.   In  some  cities,  the diurnal  N02  peak can be  lower but may last
longer.    In  other  areas,  relatively  high concentrations  may occur  almost  any time  of day.
Some qualitative  insight  into possible causes  for the  different  diurnal   patterns  observed
may  be gleaned  from examination of Figure 8-18.   This  figure presents data from  RAPS  on NO,
N02, and  0,  concentrations  for part of one day in St.  Louis, Missouri.  It  is presented for
illustrative purposes only.
     On the  day in  question, October 1, 1976, the  winds were sufficiently calm  so  that the
pollutant profiles  and  patterns  were  the result of  local  processes rather  than pollutant
transport.   In  the early  morning hours before sunrise,  Figure 8-18  shows  a  significant and
constant  NO- concentration,  presumably carried  over  from the  previous day.  During  these
hours,  the 0, concentration is quite low, near the instrumental detection limits.  Nitric oxide
concentrations are  high, most probably the result  of continuous emissions during the night and
early morning hours.  There is no discernible N02  formation.  After  sunrise,  the N02 concentra-
tion increased  sharply as a  result  of  photochemical reactions.  Photochemical  generation of
N02  is followed  by  a concomitant rapid  increase  in  03 concentrations, which depresses the NO
concentrations until the later afternoon hours when decreasing radiant  energy and increasing

                                            8-48

-------
TABLE 8-11.   DISTRIBUTION BY TIME OF DAY OF ONE-HOUR MAXIMUM N0? CONCENTRATIONS'
        FOR ONE MONTH IN 1975 FOR SELECTED URBAN SITES (U.S. EPA, 1976b)
(pg/m3)


12 am
1 am
2 am
3 am
4 am
5 am
6 am
7 am
8 am
9 am
10 am
11 am
12 am
1 pm
2 pm
3 pm
4 pm
5 pm
6 pm
7 pm
8 pm
9 pm
10 pm
11 pm
Monthly
average
of all
hours
Newark
New Jersey
(July)
160
160
160
160
140
140
160
180
200
210
230
200
200
180
200
200
200
230
200
160
180
230
350
330
96



Los Angeles
Cal ifornia
(September)
320
280
240
210
240
240
260
430
850
1100
660
260
240
230
190
170
170
230
240
260
260
280
300
300
130



Denver
Colorado
(November)
__.b
130
130
110
160
190
230
240
170
300
300
320
330
250
210
300
230
250
240
300
270
220
180
140
98



Portland
Oregon
(May)
110
94
94
94
94
75
75
94
110
110
110
130
110
110
170
170
150
150
150
150
150
150
150
130
51



Chicago
111 inois
(September)
180
160
160
150
150
160
220
260
210
220
, 240
300
340
260
260
260
250
230
210
210
200
200
180
200
110



El Paso
Texas
(October)
94
75
75
75
75
170
75
150
150
150
130
110
56
94
94
75
170
150
230
210
170
130
110
110
51




 Data presented to two significant figures only.
"'NO data available.
                                   8-49

-------
NO emissions overwhelm  the ozone generating mechanism.  From about 4:00 to 6:00 p.m. there is
still  sufficient  ozone  present  to  oxidize  NO  to  N02 rapidly in  a  simple  titration reaction
apparently  not involving  hydrocarbons.    This  ozone  scavenging mechanism  would seem  to be
identical to that observed in plumes from power plants (Section 6.1.3).   Significant quantities
of NO  are oxidized leading to  high  nighttime  N02  concentrations.   It may  be  postulated that
this  mechanism is  operative  also in  other localities exhibiting  elevated N0?  levels  after
photochemical  activity,  including  N02 photodissociation,  decreases in  the  evening.   Rapid
reaction  of  NO and 03 leading to increased NO,, concentrations has also  been observed across a
high-traffic-volume freeway in Los Angeles (Fankhauser, 1977).
     Although  the  data  presented  in  Figure 8-18  were carefully chosen as  an unusually good
example  of  ozone  scavenging,  Table  8-12  shows  that  elevated N02 levels in the  late  evening
hours  are a fairly  common phenomenon in  the  Greater St.  Louis area.  Fifty-three  of  the 89
high N02  values reported  in Table 8-12 occurred between  the hours of 7:00 p.m.  and 6:00 a.m.
     Variations in the values for peak concentrations and annual  means from station to  station
for  the  densely-monitored  St.  Louis area  documented  in  Table 8-12 are also an  indication of
the  possible  importance  of local  sources  and  small-scale meteorological  and  topographical
features  in determining ambient pollutant concentrations.
8.1.7  Spatial  and Temporal Variations of N00 Concentrations as Related  to
       Estimation of Human Exposure
     Currently, if a single monitoring station in an Air Quality Control  Region (AQCR)  reports
ambient  concentrations  in  excess  of  that  safe for  human  health and welfare,  this fact is
considered  cause  for concern.   While  this  assumption appears reasonable if human  health  and •
welfare  are  to be  protected,  particularly if the monitoring station has  been located in urban
or  other  population  centers  specifically  to  monitor  population  exposure  (SAROAD  purpose
designation  01,  population-oriented), it  may  be  of  interest for  some  purposes  to consider
methods for estimating human exposures in more detail.  Some considerations involved in  making
such exposure estimates  are discussed in this section.
8.1.7.1  Spatial and temporal  variations of local NO,, concentrations—Table 8-13 gives  the  N02
hourly concentrations measured at all  25  RAMS  sites in St.  Louis during  a  period of high
pollution for  this  area  from  7 a.m.  on October 1,  1976 to 2 a.m.  on the  following day.   It is
presented as one illustration of the geographic and temporal variability  of maximum N0?  concen-
trations which may  be experienced in a single  airshed.   It should be noted that few areas in
this country are as densely monitored as St. Louis  was during 1975-76.
     Sources of NO   in  the St. Louis  area  include mobile  vehicles,  other area sources,  and a
wide variety of industrial  point sources.   The data presented are not necessarily to be taken
as typical  of  urban areas  since the  impact  of  a number of  factors  including  source emission
strengths, their diurnal  emission patterns, meteorological  factors, topography  and the  presence
of other photochemical pollutants and their precursors may vary from area to area.   In  general,
a meaningful  survey of the  phenomenology  or  possible causes of the variability  of high  N02
concentrations on  a nationwide basis is lacking in  the literature.
                                            8-50

-------
CD


cn
    a   0.20

    Z~
    o


    <
    en
    i-
    z
    ui
    U
    Z
    o
    o
    2   o.io
                                                                                                        3


                                                                                                       NO
              NO FORMATION


              OF NO,
. PHOTOCHEMICAL FORMATION OF NO-
OZONE SCAVENGING


FORMATION OF NO,
             NIGHTTIME NO2 CARRYOVER


            L—L	
                                               \



                                              /
                               AFTERNOON NO., CARRYOVER
                          SUNRISE
                                                  10           12           14
                                                           TIME OF DAY (CST)
                                                                                        16
                                                                                                    18
                                                                           20
     Figure 8-18.  Pollutant concentrations in Central City St. Louis, October 1, 1976, average of RAMS sites 101, 102, 106, and 107. Illustra

     tion of photochemical and ozone scavenging formation of NO2 (U.S. EPA, 1976b).

-------
                     TABLE 8-12.   MEAN AND TOP FIVE HOURLY NITROGEN DIOXIDE CONCENTRATIONS REPORTED FROM
                           18 INDIVIDUAL RAMS STATIONS IN ST. LOUIS DURING 1976 (U.S. EPA, 1976b)
00
(J1

Site Number
101
(Center-city)



104




105




107




108




Date of
Measurement
Nov.
Nov.
Nov.
Nov.
Nov.
May
Oct.
May
Oct.
Oct.


Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Aug.
Oct.
Sept
Aug.
July
Aug.
Oct.
19
19
19
19
19
1
1
1
1
2


1
1
1
1
1
1
2
25
2
. 1
30
26
30
2
Time of
Measurement
10
9
8
7
11
7
6
8
5
6
_ _. f ^
	 1"
7
10
8
9
6
7
7
9
8
7
8
11
9
8
pm
pm
pm
pm
pm
am
pm
am
pm
pm
irst value
pm
pm
pm
pm
pm
pm
pm .
am
am
am
am
am
am
am
Cone
ug/m
481
454
443
434
411
293
291
287
284
284
inval
350
337
334
332
358
353
271
266
263
636
566
321
312
291
Distance from
§ntration Arithmetic Mean Site 101

0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
idate
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
ppm ug/m"' ppm
2556 53 0.0282
2415
2358
2310
2187
1559 48 0.0253
1549
1526
1512
1509

!U
1864 44 0.0235
1795
1776
1768
1907 57 0.0305
1880
1441
1413
1400
3383 33 0.0174
3010
1707
1659
1548
(km)
0




<4





<4



<4




<20




                                                         (continued)

-------
                                                    TABLE  8-12.  (continued)
CO
in
u>

Date of
Site Number Measurement
109 Apr. 30
Oct. 1
Oct. 1
Oct. 1
Apr. 7
114 Oct. 2
Oct. 2
Oct. 2
Oct. 1
Oct. 2
115 Dec. 4
Oct. 2
May 10
Sept. 22
July 6
116 May 7
May 7
Oct. 2
Oct. 1
Oct. 1
102 Oct. 1
Oct. 2
Oct. 2
Oct. 1
Oct. 1
Time of
Measurement
8 am
6 pm
7 pm
8 pm
12 am
8 am
12 am
3 am
9 pm
9 am
10 am
8 am
10 am
9 am
11 pm
11 pm
10 pm
7 pm
8 pm
7 pm
7 pm
8 am
9 am
6 pm
8 pm
Concgr
ug/m
289
216
197
186
173
305
281
276
275
273
286
170
152
145
128
457
326
228
206
206
374
365
363
354
331
itration Arithmetic Mean
ppm ug/m ppm
0.1537 26 0.0138
0.1147
0.1049
0.0991
0.0922
0.1524 32 0.0172
0.1495
0.1466
0.1462
0.1452
0.1520 22 0.0116
0.0903
0.0809
0.0771
0.0682
0.2430 23 0.0120
0.1734
0.1214
0.1098
0.1094
0.1990 62 0.0329
0.1940
0.1929
0.1882
0.1762
Distance from
Site 101
(km)
<20




<20




<20




<20




<10




                                                          (continued)

-------
                                                  TABLE  8-12.  (continued)
00
in

Site Number
106




110




111




112




117




Date of
Measurement
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Feb. 24
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Aug. 23
Oct. 1
Oct. 1
May 19
May 19
May 19
May 19
May 19
Time of
Measurement
10 pm
9 pm
11 pm
7 pm
8 pm
7 am
7 pm
6 pm
10 pm
11 pm
8 pm
7 pm
9 pm
6 pm
10 pm
11 pm
10 pm
8 am
7 pm
9 pm
2 am
6 am
4 am
3 am
5 am
Concei
ug/m
460
446
442
408
405
405
263
257
201
200
419
406
399
387
368
318
317
315
308
308
676
566
544
461
360
ntration Arithmetic Mean
ppm ug/m ppm
0.2449 56 0.0298
0.2375
0.2352
0.2169
0.2156
0.2155 34 0.0182
0.1398
0.1366
0.1069
0.1067
0.2230 45 0.0241
0.2161
0.2121
0.2060
0.1956
0.1689 52 0.0275
'0.1686
0.1677
0.1637
0.1636
0.3594 21 0.0110
0.3008
0.2891
0.2450
0.1914
Distance from
Site 101
(km)
<10




<10




<10




<10




<20




                                                              (continued)

-------
                                                   TABLE  8-12.  (continued)
oo
I
en
en

Date of
Site Number Measurement
118 Sept. 17
Sept. 15
Nov. 6
Nov. 6
Nov. 6
119 Feb. 3
Feb. 3
Feb. 3
Feb. 3
Feb. 3
120 Oct. 11
Sept. 3
Oct. 11
Oct. 11
Aug. 23
Time of
Measurement
8 am
10 am
9 pm
8 pm
7 pm
11 pm
10 pm
8 pm
9 pm
7 pm
6 pm
7 am
8 am
7 pm
8 am
Concer
|jg/m
149
136
134
132
127
360
343
336
336
316
360
296
258
248
236
itration Arithmetic Mean
ppm pg/m ppm
0.0791 21 0.0111
0.0722
0.0715
0.0705
0.0677
0.1917 35 0.0184
0.1825
0.1787
0.1786
0.1681
0.1916 37 0.0198
0.1430
0.1372
0.1322
0.1254
Distance from
Site 101
(km)
<20




y20




<20






-------
               Table 8-13.  GEOGRAPHICAL VARIATION OF HOURLY NO. CONCENTRATIONS DURING A PERIOD Of HIGH NO., CONCENTRATIONS (U.S. EPA, 1976b)

                                                         [St. Couis, October 1 and 2. 1976 (ppm)]
CD
en
cr>
RAMS
Stat
101
102
103
104
105
106
Hour of Day
ion 789
0.07 0.12 0.12 0.18
0 07 0 12 0.17 0 11
0.05 0.10 0.15 0 12

0.05 0.07 0.12 0.14
0.07 0.11 0.10 0.08
10 11 12
0.14 0.08 0.09
0 12 0 10 0 08
0 10 0.07 0 06

0.07 0.04 0.05
0.08 0.06 0.06

13
0.09
0 06
0 04
0.07
0.07
0.05

14
0.10
0 05
0 02
0.07
0.10
0.06

15
0.06
0 07
0.03
0.08
0.06
0.10

16
0.12
0 13
0.06
0.15
0.08
0.11

17
0.19
0 19
0 15
0.15
0.17
0.17

18
0.20
0 20
0.16
0.15
0.19
0.22

19
0.19
0 18
0.13
0.15
0.18
0.22

20
0 17
0.14
0.13
0.18
0.24

21
0.18
A
0.15
0.13
0.18
0.24

22
0.16
0.13
0.13
0.11
0.13
0.24

23
0.17
ft
0.12
0.09
0.11
0.20
24 1 2
A «
* *
0.09 0.08
0.08 0.07
0.08 0.08
0.17 0.15
* n 1 *»
            108   0.06  0.10  0.09  0.08  0.05  0.05  0.02  0.03  0.02  0.02  0.04  0.10  0.04  0.09  0.11  0.12  0.11  0.11  0.09  0.10


            109   *     *     *     *     0.02  0.01  0.02  0.03  0.02  0.02  0.04  0.11  0.10  0.10  0.08  0.08  0.07  0.05  0.04  0.04



            110   0.03  0.04  0.08  0.07  0.04  0.01  0.02  0.04  0.06  0.05  0.08  0.14  0.14  0.10  0.10  0.11  0.11  0.09  0.07  0.07



            111   0.05  0.07  0.08  0.06  0.04  0.04  0.03  0.03  0.04  0.06  0.11  0.21  0.22  0.22  0.21  0.20  0.17  0.13  0.12  0.08


            112   0.05  0.06  0.05  0.06  0.08  0.05  0.04  0.02  0.03  0.06  0.16  0.15  0.16  0.16  0.16  0.17  0.17  0.15  0.15  0.13


            113**************     0.21  0.20  0.21  0.21  0.18  0.17




                                                            (continued)

-------
                                                            TABLE 8-13.  (continued)
                                                                    Hour of Day
          RAMS	
          Station        7      8     9     10    11    12    13    14    15    16    17    18    19    20    21    22    23    24     1


          114   *      *      *      *     0.04  0.03  0.03  0.03  0.01  0.01  0-04  0.07  0.07  0.09  0.15  0.13  0.13  0.15  0.14  0.14

          115   0.04   0.07   0.07   0.05  0.03  0.02  0.02  0.03  0.03  0.03  0.04  0.05  0.05  0.03  0.03  0.03  0.06  0.05  0.04  0.03

          116   0.04   0.06   0.04   0.03  0.02  0.01  0.01  0.01  0.02  0.02  0.03  0.05  0.11  0.11  0.10  0.07  0.05  0.04  0.04  0.05

          117   0.03   0.02   0.02   0.01  0.01  0.01  0.00  0.01  0.02  0.02  0.02  0.02  0.02  0.04  0.07  0.07  0.06  0.04  0.07  0.05

          118   0.02   0.02   0.02   0.02  0.01  0.01  0.01  0.02  0.02  0.03  0.04  0.03  0.03  0.03  0.05  0.06  0.04  0.03  0.06  0.05
CD
^        119   0.04   0.04   0.04   0.03  0.03  0.02  0.02  0.02  0.02  0.03  0.04  0.07  0.10  0.12  0.11  0.10  0.10  0.10  0.09  0.07
--si
          ^20   *      *      *      *     *    *     *     0 01  *     *     *     *     *     *     *     *     *     *     *     *

          121   0.05   0.04   0.02   0.01  0.03  0.02  0.01  0.00  0.00  0.01  0.01  0.02  0.08  0.14  0.16  0.13  0.12  0.17  0.14  0.09

          122   0.00   0.00   0.00   0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.01  0.01  0.01  0.01  0.01  0.02  *     *     *

          123   0.00   *      *      0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.00  ********

          124   0.03   0.02   0.01   0.01  0.01  0.01  0.00  0.00  0.02  0.03  0.04  0.03  0.02  0.01  0.01  0.01  0.01  0.02  0.02  0.01

          125   0.01   0.01   0.01   0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.00  0.01  0.00  0.00  0.00  0.00  0.00  0.01  0.01  0.01



          *Data missing.

-------
     Figure 8-19  shows the  locations  of the  25 RAMS  sites.   The concentric  circles  locate
these stations within distances of 4, 10, 20 and 40 km of "center-city" Station 101.   Compari-
son of Table  8-14  and Figure 8-19 reveals that with a 4 km radius the peak hourly N0~ concen-
trations  varied from  0.15  to. 0.20 ppm; within  a 10 km radius values  ranged from 0.15 to 0.24
ppm; within a 20 km radius  a four-fold variation from 0.06 to 0.24 was experienced; and within
a 40 km  radius  values ranging from  0.01  to  0.24 ppm were reported.   The  major peak occurred
after  sundown  at  almost  all  sites,  presumably due  to  the ozone  titration mechanism.   A
subsidiary photochemical peak is discernible in the late morning at central sites.   Significant
N02 carry-over  is  evident  at the start of the period reported.   Both  the duration and time of
occurrence  of peak  hourly values is  variable  from  station  to  station  as indicated  by  the
underlined portions in Table 8-13.
     Another  way  of viewing  the  extent  of  the variability  of NO  concentrations in  the St.
Louis area is presented in  Table 8-14.   This table is intended to illustrate the occurrence of
high NO- concentrations  shown  by monitoring throughout an airshed  even though the events may
not take place  at  the same times and may not be associated with the same air mass.  The sites
represented in  the  tables  are located in a  center-city location subject to nearby automobile
and truck  traffic  (101);  in an outlying  city  location  within a few kilometers of an electric
power plant and a  number of heavy industrial sites (104); and in a high-density single family
residential community (111).  It can  be seen from these tables that both the highest  NO hourly
readings  and  the  corresponding  NO/NO-  ratios  are  quite  different for Station 111  than for
Stations   101  and  104.   Some evidence  of spatial  smoothing  in  both  the  highest and  second
highest hourly NO^ concentrations by  month is apparent in the data.
     A somewhat  different   scenario  is  presented by  the  same  type  of data  (Fairfax  County;
Keyes et  al.) (Tables  8-15 through  8-17)  from three monitoring stations  in  Fairfax  County,
Virginia,  near Washington,  D.C.   These stations are  located  in  an  urban complex dominated by
area sources  (70  percent of N0x  emissions  from area sources).    Locations  for the monitoring
stations  cited  in  the  table include  an office complex,  a high-volume  transportation  intersec-
tion, and  a  suburban  commercial  center.   The  maximum separation  between stations is approxi-
mately 15 km.
     The  data reported  show a considerable variation in the ratio of  the highest hourly NO to
the corresponding  hourly N02,  suggesting a considerable  variation  in  local  NO area  emissions
or  in  monitor  siting.   Nevertheless,  it is  important to  note  that  the  highest hourly  N02
concentrations reported by  month are  quite similar at all  stations.   Presently, an insufficient
number of  analyses  have been conducted on a nationwide basis to determine whether or not this
observation is typical of area-source-dominated urban airsheds.
     In  a  final scenario,   very  recent ground level  NO   measurements from a  large isolated
source in complex terrain are presented (Pickering et al., 1980).   (Individual  N02 values were
not reported.)  Measurements of this  type are extremely rare in the literature.  Exhaust gases
from the  712 MW  Clinch River power plant,  burning low sulfur coal,   are  emitted  through two

                                            8-58

-------
00
 I
(Jl
                                                                       CRYSTAL CITY
                                        NOTE: Site* are aligned in approximate concentric circles of 4, 10. 20. and 40 km. respectively; adapted from Nelson (1979).




                                                                       Figure 8-19.  St. Louis RAMS station locations.

-------
TABLE 8-14.  HIGH CONCENTRATIONS OF NITROGEN OXIDES,
     ST.  LOUIS, MISSOURI, 1976 (U.S. EPA, 1976b)

Month
RAMS STATION 101
January
February
March
April
May
June
RAMS STATION 104
January
February
March
April
May
June
RAMS STATION 111
January
February
March
April
May
June
Highest-NO
(Mg/m >

329
475
260
500
179
303

362
474
303
406
276
228

644
617
456
434
267
226
Corresponding

126
59
147
199
*
190

111
103
99
91
*
99

76
*
134
128
*
152
Highest3N02

162
146
147
247
175
225

111
194
121
293
155
151

109
124
136
182
143
181
2nd Highest
N02 (ug/m )

152
140
140
207
163
211

96
173
120
293
152
126

101
116
134
180
130 "
176
                    8-60

-------
         TABLE 8-15.  MONTHLY TRENDS IN HOURLY NO AND NO- CONCENTRATIONS,
     MASSEY BUILDING STATION, FAIRFAX COUNTY, VIRGINIA, I977a  (KEYES  ET AL.)

Month
January
February
March
April
May
June
July
August
September
October
November
December
Highest NO
(ug/nT)
655
650
350
230
40
80
20
70
125
420
680
645
Corresponding
N02 (jjg/m )
140
105
105
120
20
85
65

95
75
43
120
Highest.,
N02 (|jg/m )
160
190
140
160
180
170
85
95
115
225
115
120
2nd Highest
N02 (ug/m )
150
170
130

130
160
75
75
105
130
105
115

                            3
Annual Average NO,,:   40 ug/m


Second Highest N02:   190 ug/m


Peak/mean =4.8


 Data from Fairfax County (Va.) Air Pollution Control Agency.
                                   8-61

-------
         TABLE 8-16.   MONTHLY TRENDS IN HOURLY NO AND NO, CONCENTRATIONS,
       LEWINSVILLE STATION, FAIRFAX COUNTY, VIRGINIA, 1977  (KEYES ET AL.)

Month
January
February
March
April
May
June
July
August
September
October
November
December
Highesjj NO
680
630

615
380
290
290
650
515
580
700
680
Corresponding
65
65

95
120
180
75
10
75
40
45
75
Highest3
130
290

190
290
225
170
280
280
160
140
130
2nd Highest
125
225

180
255
205
140
265
235
150
130
120

Annual Average NO,:   56 ug/m

Second Highest NO-:   280 ^g/m

Peak/mean =5.0

aData from Fairfax County (Va.) Air Pollution Control Agency.
                                   8-62

-------
        TABLE 8-17.  MONTHLY TRENDS IN HOURLY NO AND N0? CONCENTRATIONS,
      SEVEN CORNERS STATION, FAIRFAX COUNTY, VIRGINIA, 1977a (KEYES ET AL.)

Month
January
February
March
April
May
June
July
August
September
October
Highes| NO
630
620
540
665
240
170
185
320
505
420
Corresponding
N02 (M9/m )
10
50
0
0
40
20
55
105
105
85
Highest.
N02 (ug/m )
150
205
120
265
190
140
170
235
205
160
2nd Highest
N02 (ug/nv )
120
145
110
195
170
130
150
150
170
150

Annual Average NO-:    46

Second Highest N02:   235

Peak/mean =5.1

aData from Fairfax County (Va.) Air Pollution Control Agency.
                                   8-63

-------
stacks, 42 m  apart,  each 138 m high.   The  surrounding terrain has ridges exceeding 1.5 times
stack height within 3 to 5 km of the plant in all quadrants of the compass.   Figure 8-20 shows
the location and elevation of the monitoring sites.   Table 8-18 gives the mean of one-hour NO
                                                                                             A
concentrations  over  an  extended  monitoring period  from  November 20,  1976 to  September  30,
1977.    It  is  important  to  note that the average  values  reported are  subject  to  large error
since many readings were near the detection  limit of the analytical instruments.  The data do,
however, indicate  the  magnitude of the average values.  Much greater confidence can be placed
in  the  individual  10  highest  NO   readings  recorded at each site (Table 8-19).   Perhaps  the
most significant point  to  note for this discussion are the extremely high peak to mean ratios
for NO  observed at  all  sites   (compare Tables  8-18  and 8-19).   Although detailed analysis of
the frequency distribution of high NO  concentrations has  yet to be made, it seems appropriate
to  state that the  probability  is small  for  detecting the  maximum impact of a plume with fixed
monitoring stations.   This observation may be expected to  hold true also in regions subject to
a variety of point  and area sources.  In terms of estimating human exposure due to large point
sources,  therefore,  fixed  monitoring  sites  may be  expected  to  provide  data mainly  on  the
long-term average impact of such sources.
8.1.7.2   Estimating  human exposure—The  examples  of  local  variability  of  significant  NO-
concentrations just presented  have some bearing on  the question  of  estimating human exposure
to  this pollutant.    Such an estimation might  include  a study of the spatial variation of N0?
concentrations  for time  periods  during  which  human health  and/or welfare  are  or may  be
adversely affected and  might take into account the mobility of the population at risk.   In an
area like Fairfax  County,  it  is possible that  the  relatively small  spatial variation in high
NO- concentrations  which  is  evident from the  data presented  in Table 8-14 might enable esti-
mates of exposure to high NO- concentrations to be made from data gathered at a single monitor-
ing station.   In an area like St.  Louis, more detailed monitoring might be required due to the
greater variation  in ambient levels  across  this  urban area.   In  addition,  the  occurrence of
high NOp concentrations during  the late evening hours when most of the population is presumably
indoors would point to the desirability of considering relationships  between indoor and outdoor
pollutant concentrations.   These  are only  a few examples of the  methodological  difficulties
associated with detailed estimates of actual human exposure.
     Few attempts  to perform  such exposure estimates  have been  reported  in  the  literature.
Recently,  an exposure  model  has been reported  for the Los Angeles area (Horie et al.,  1977).
The main thrust  of this work was  to  estimate  population  exposure to NO- concentrations  as  a
percentage of time the  population was potentially exposed to NO, concentrations exceeding the
                                                            T
California Ambient Air Quality Standard  (CAAQS) (470  ug/m  or 0.25 ppm for  1-hr averages).
Presentation of  this model  is  in no  sense  intended  to reflect on consideration of a National
Ambient  Air  Quality  Standard but  is  included  only to  illustrate   an  existing  exposure
methodology.
                                            8-64

-------
CD
                                                                                   15 KM

                                                                   10 KM   NASH'SFORD
                                                    5 KM

                                        CARBO    ^J-
                                        ^   CLEVELAN
                               Figure 8-20.  Location and elevation of Clinch River Power Plant monitoring stations (Pickering et al., 1980).

-------
       TABLE 8-18.   MEAN NOV CONCENTRATIONS FOR ISOLATED POINT SOURCE

IN COMPLEX TERRAIN (CLINCH RIVER POWER PLANT) (ppb) (PICKERING et al., 1980)
 Station                    NO              N09                NO
                              A.               £



 Tower                      29              15                 15



 Munsey                      75                  1



 Hockey                      53                  2



 Lambert                     -



 Johnson                     -



 Castle                     25              11                 13



 Kents                      11               7                  3



 Nashs                      15               9                  6
                                 8-66

-------
                        TABLE 8-19.  TEN HIGHEST HOURLY AVERAGE  NOV  CONCENTRATIONS  OBSERVED  AT  EACH
                  MONITORING SITE  FOR  ISOLATED  SOURCE  (CLINCH  RIVER  POWER  PLANT)  (PICKERING  ET  AL., 1980)
i
CTl




Rank
1
2
3
4
5
6
7
8
9
10



Rank
1
2
3
4
5
6
7
8
9
10

NO
Cone.
(ppb)
619
549
482
467
457
448
430
420
414
397

NO
Cone?
(ppb)
834
601
553
262
235
229
228
226
211
207
Tower


Date
1/28/77
12/30/76
3/15/77
12/30/76
7/7/77
1/26/77
1/28/77
12/23/76
12/30/76
12/23/76
Nashs


Date
8/10/77
Will
8/10/77
2/10/77
7/8/77
2/10/77
7/12/77
2/11/77
Will
5/6/77



Hour
10
14
11
20
8
20
13
10
16
9



Hour
16
12
15
12
10
11
10
12
13
10

NO
Cone.
(ppb)
568
399
329
255
219
205
170
164
146
130

NO
Con?.
(ppb)
816
589
464
435
410
394
375
365
350
290
Hockey


Date
6/30/77
7/5/77
8/15/77
6/30/77
7/6/77
7/2/77
4/20/77
3/21/77
5/14/77
7/20/77
Castle


Date
2/15/77
2/8/77
2/8/77
2/11/77
2/11/77
2/11/77
2/8/77
2/11/77
2/10/77
2/11/77



Hour
5
3
9
4
8
6
4
11
10
3



Hour
15
11
10
9
10
11
12
12
10
8

NO
Cone.
(ppb)
353
103
101
92
89
83
80
79
79
78

NO
Con?.
(ppb)
419
408
297
280
276
252
206
186
173
170
Kents


Date
8/13/77
2/19/77
8/8/77
12/14/76
11/24/76
12/14/76
8/8/77
8/6/77
12/19/76
1/13/77
Munsey


Date
3/9/77
3/9/77
7/6/77
7/6/77
3/9/77
3/9/77
6/16/77
3/21/77
3/9/77
7/2/77



Hour
22
4
7
11
24
12
3
15
6
17



Hour
9
8
9
8
7
10
8
11
11
6

-------
     In the model, NOp data for 1973 from 26 monitoring stations were combined with population
data from  Regional  Statistical  Areas (RSAs) developed by  the Southern California Association
of Governments  and  employment data, computed for each RSA from 1970 Census data.   A number of
receptor points were assigned to each RSA according to the size of the population and the land
area.   The number of people associated with  each  receptor point was  then  computed.   For the
non-working population,  exposure estimates were made by  assuming this  sub-population  to be
stationary.  In the  case of workers, the population  was  stratified by the residence location
and by the working location.  Air quality data in the latter case was classified into two time
categories:  (1) non-working time and (2) working time (weekdays 7 am to 6 pm).   Additionally,
weekday-weekend differences in exposure were assessed from data on weekday-weekend differences
in air quality.
     Using  the  static population  assumption,  the distribution  of the  population  exposed at
various frequencies  of standard violations (population-at-risk  distribution) were  determined
for  both   N02   hourly  average concentrations  and NCk  daily  maximum  hourly  concentrations.
Figure 8-21 shows  the distributions of the population exposed at various percentages of days
exceeded during three  time periods; all the time,  weekdays and weekends.  It can be seen that
the entire  population  was  exposed for a smaller percentage of days during weekends  than  week-
days.  An  average  person in the Los Angeles  AQCR  was exposed to NO-  air pollution above the
CAAQS  4.4  percent of  the  days  during weekdays, and  only  2.1 percent of the days  during the
weekends (Table 8-20).
     The distribution  of the  population exposed at various  percentages  of  hours exceeded is
shown  in  Figure 8-22.   Again, the  entire population  was  exposed for  a  smaller  percentage of
hours  above  the CAAQS  during weekends than  weekdays.   Therefore,  it can be  concluded that
people in  the Los Angeles AQCR were less frequently exposed to a concentration above the  CAAQS
during weekends  than weekdays because  of the  markedly  better N0? air  quality  over weekends.
     The  regionwide  impacts of  weekday-weekend  phenomena on  population exposure  to  NO- are
summarized  in  Table  8-20.   The  regional  averages of  daily  risk  frequency  and hourly risk
frequency  were, respectively,  3.7 percent of the days and 0.46 percent of the hours.  In  other
words, an  average person in the Los Angeles  Basin was exposed in 1973 to a concentration  above
the CAAQS  14 days per year or 40 hours per year.   The regional averages of daily risk frequency
are 4.4 percent of  the days during weekdays and 2.1  percent of the days during  weekends.  The
regional averages of  hourly risk frequency are  0.57  percent of the hours during weekdays and
0.18 percent of  the  hours  during weekends.   Therefore,  it can be said that in 1973  an average
person  in the  Los  Angeles Basin  received  a  less  frequent exposure  above the  CAAQS during
weekends than weekdays by 2.3 percent of the days or  by 0.39 percent of the hours.
     Table 8-20 also  presents the regional  averages  of risk frequency, which were computed by
considering  diurnal   population  movement   between   residence  and   workplace  (values  in
parentheses).    The  refined estimates  of  regional  average  risk frequency are close to  but  a
                                            8-68

-------
                I  I  I  I I  I  II  I  I  I  I  1  I  I  I  I  I  I  I  I  I  I  j  I   !_
u
z
LU

o
LLJ
CC
U.
Q
01
	 ALL TIME

	 WEEKDAY

	 WEEKEND
Z
LU
cc
o
5
O
LLJ

O
a.
X
UJ
Z
O
D
a
O
a
u.
O

O
P
O
<
cc
u.
    0.01
         I  I  I  I  I  I  I  I  I I  I \  I  I  I  \ I  I  I \  I  I  I
                            5                    10

                PERCENT OF DAYS ABOVE THE CALIFORNIA STANDARD


        Figure 8-21.  Population exposed to IMC>2 daily maximum hourly

        concentration above the California one-hour standard at various

        frequencies (Horie et al., 1977).
                               15
                                        8-69

-------
 TABLE 8-20.   REGIONWIDE IMPACT OF WEEKDAY-WEEKEND PHENOMENA ON POPULATION
            EXPOSURE TO NITROGEN DIOXIDE:   DAYS AND HOURS EXCEEDING
         THE  CALIFORNIA AMBIENT AIR QUALITY STANDARD (FAIRFAX COUNTY)

Time Period
All time
Weekday
Weekend
Weekday /Weekend
Difference
Percent of Days Exceeded3
3.7 (3.8)
4.4 (4.5)
2.1 (2.1)
+2.3 (+2.4)
Percent of Hours Exceeded
0.46 (0.50)
0.57 (0.63)
0.18 (0.18)
+0.39 (+0.45)

Percentages in parentheses computed based on the mobile population assumption.
                                  8-70

-------
o

UJ

o
O
u
<
I

Z
Ul
CC
O


Q
UJ
1/7
O
o.
X
UJ

z
o
CL
o
Q.
LL
O
z
o
\-
o
<
cc
0.1
   0.01
               I  I  I  I   I  I  I  I  I  I    I  I  I  I  I  I  !  I  I  II  I  I  I  L_
                                         ALL TIME

                        \          	 WEEKDAY

                         \
                                   	 WEEKEND
         Mill I  I  I I  I  I  I  I  \\  I  I  h^  I  I  I  IM  I  I  I  I
                          0.5                   1                   1.5

             PERCENT OF HOURS ABOVE THE CALIFORNIA STANDARD
     Figure 8-22. Population exposed to NO? hourly average concentration
     above the California one-hour standard (470 ^g/m^; 0.25 ppm) at vari-
     ous frequencies.


     Source:  Horie et al., 1977.
                                      8-71

-------
little greater than those based on the static population assumption.   According to the refined
estimates, an  average person in  the  Los  Angeles Basin received less  frequent exposure above
the CAAQS during  weekends  than  weekdays by 2.4  percent  of the days or by 0.45 percent of the
hours.
     A  rough  nationwide  estimate of  the  population  at  risk to various  levels of  NCL  air
pollution can  be  obtained from a data  base recently described (Freedman et  al. ,  1978).   The
data  base includes  data  on monitoring for all counties in the contiguous United States (taken
directly  from  1974  SAROAD  file)  along  with 1970  Census data.   For  the  purposes  of  this
analysis, the assumption  is  made  that the  entire  county  population  is potentially at risk to
the second highest  one-hour  N02 concentration reported in the county, provided that the moni-
toring site reporting  was  located specifically to monitor population exposure (SAROAD purpose
code  01).   In  1974,  121  U.S.   counties having  total  population of 65,009,289  persons  had at
least one  monitor reporting such hourly  NO,,  data.   Of  these counties 112  were  selected as
having data which warranted inclusion in this analysis.   The results of the  population-at-risk
computation is  presented in Table  8-21.   Fifty-seven percent of the U.S.  population in counties
reporting one-hour  N09 data in 1974 were  potentially  at risk  to  one-hour  NO, concentrations
                       3
which exceeded 250 ug/m  at least  twice during the year;  29 percent to one-hour N00 concentra-
                             3
tions which exceeded  500  ug/m   at least twice during the year; and 14 percent to one-hour N09
                                        3
concentrations  which  exceeded   750 ug/m  at  least  twice  during the year.  The  population at
risk  comprised at  least  41,  21, and 10 million people  for the corresponding N02 concentration
levels.   More  sophisticated  and/or more  recent  exposure  estimates on a nationwide  level  are
lacking in the  literature.

                             TABLE 8-21.  U.S. POPULATION AT RISK TO
                          VARIOUS  1974 N02 HOURLY AMBIENT CONCENTRATIONS3

County
Count
68
24
6
1974 Second Highest % Monitored
1-hour N02 3 Total 1970 Population Population Potentially
Concentration (ug/m ) Potentially at Risk at Risk
250
500
750
41,837,864 57
21,341,617 29
10,106,698 14

          Computed from data in Freedman et al.  (1978).
                                            8-72

-------
8.2  ATMOSPHERIC CONCENTRATIONS OF NITRATES
     Although extensive monitoring has been carried out for nitrates suspended in ambient air,
recent  reports  (Section  7.4.1)  document  serious and  apparently  unresolvable  difficulties
associated  with nitrate  artifact  formation  on  the  filter  media  routinely used  to collect
samples.   At present,  therefore, it  seems  most  prudent  to  report  data  only for  those few
recent  measurements  which were collected  using  Teflon  filters not believed  to  be  subject to
the positive artifact formation reported.
     It  should be  noted,  however,  that Marker et  al.  (1977)  report  that  nitrate  could be
removed from  glass  fiber filters when aerosols containing sulfate passed through the filters.
Since  the  same mechanism  may operate when  Teflon filters are used, the  data  reported below
must be considered as preliminary.
     A 24-hr sample from Philadelphia, Pennsylvania, on February 24, 1977, indicated an ambient
nitrate concentration of 0.18 M9/m   in "the fine particle fraction (<2.4(j) of a sample collected
by  a  dichotomous  sampler  using  Teflon filters  (Dzubay  and  Stevens,  1975;  Stevens  et  al.,
1978b).  Data from Glendora, California, obtained with a dichotomous sampler during 10 days in
early  March,  1978,  show  nitrate concentration  ranging  from 0.17  to 0.47 |jg/m   in the  fine
fraction with  a mean of 0.28 ug/m   (Stevens  et al. ,  1978a).   Concentrations  from  the coarse
fraction (particles with  aerodynamic diameter between 2.4 u and 16 u) range from 0.06 to 0.83
ug/m   with  a mean  of 0.22  ug/m  .   Measurements  at  a  number  of  sites near  freeways  in Los
                                                                  o
Angeles gave  fine  fraction nitrate  concentrations up to  2.0  ug/m  and similar readings up to
2.1 ug/m  at nearby background sites (Dzubay et al., 1979).  Nitrate did not increase signifi-
cantly  in  the  roadway  (Trijonis, 1978).  Other data from  California  obtained  using  quartz
filters are summarized in Table 7-7  and in Spicer et al.  (1978).
     Few measurements of  ambient nitric  acid  vapor concentrations  have been  carried  out.
Sampling from aircraft  in  non-urban areas at altitudes  ranging from 0.2 to 8 km was conducted
by Huebert and  Lazrus (1978) during August and September of 1977.   Those areas not influenced
by urban plumes evidenced  concentrations ranging  from 0.05  to 0.75 ug/m   (0.02  to  0.3 ppb),
with most values below 0.4 ug/m  (0.15 ppb).
     Miller and Spicer (1974), using a modified microcoulometric method, report up to 25 ug/m
(10 ppb)  HN03  in  Los Angeles,  California.   In  a  more  extensive report,  Spicer  (1977) cites
measurements in St.  Louis,  Missouri,  for 26 days during  July and August  1973,  yielding maximum
                                              3                                          3
23-hr  average  HNOj  concentrations of  30 ug/m  (12 ppb)  and  a 1-hr maximum  of 200  ug/m   (80
ppb).    In  West  Corvina, California, 29  sampling  days during August and  September  1973,  gave
                                   3                                        3
23-hr average values  up  to 65 ug/m  (26 ppb)  and  a 1-hr maximum of 78  ug/m  (31  ppb).   Hanst
et al.  (1975),  in  failing to detect HNO-, in  Pasadena,  California,  set an upper limit of 25
    3
ug/m   (10  ppb) on  its concentration  in this  area.   Recently, Tuazon  et al.  (1978)  report
observing up  to 15 ug/m   (6 ppb)  in  Riverside,  California,  during approximately  one  day of
monitoring in October 1976.
                                            8-73

-------
     The data  available are not sufficient  to  place human exposure to  suspended  nitrates or
nitric acid vapor  in  nationwide perspective.  Furthermore, extreme  caution  must be exercised
in  interpreting  any health  studies  making  use  of ambient nitrate  data  derived using filter
media that are subject to artifact formation.
8.3  ATMOSPHERIC CONCENTRATIONS OF N-NITROSO COMPOUNDS
     Although  ambient  atmospheric  data on  N-nitroso compounds are sparse when  viewed from a
nationwide  perspective,  a   number  of  measurements  from  scattered locations,  mostly  near
suspected  sources,  have been  reported.  Some of  these  data are presented in  this  section in
order to indicate  the  possible magnitude of the  existing atmospheric  burden of this class of
compounds.
     Fine  (1976a,b) first reported  dimethylnitrosamine  (DMN)  in ambient  air in 1975.   Levels
                      3                                             3
ranged up to 0.95 ug/m  in Baltimore,  Maryland,  and up to 0.051 ug/m  in Belle, West Virginia.
Later, Fine (1976) reported concentrations up to 15 ug/m  near the same site  in Baltimore and,
independently, Pellizzari  (1977) reported  values  up to  32 ug/m  from the  same area  using a
different  analytical method.   Fine  (1976) reported a level of 0.8 ug/m  for  a 3-minute sample
taken  in  New  York City,  New  York.   Fine  (1976a,b)  failed  to  detect DMN  in  Philadelphia,
Pennsylvania;   Waltham,  Massachusetts;  and  at a site near  Wilmington,  Delaware.   Sampling by
EPA's National Enforcement  Investigations Center (NEIC) (U.S.  EPA, 1977b) showed little indi-
cation of  N-nitroso compounds  in the vicinity of suspected sources at 32 locations in Kansas,
Missouri, Illinois, Indiana, Iowa,  and Nebraska  when contamination problems were resolved.   No
evidence was   found  by NEIC  to substantiate secondary production  in  the vicinity of  amine
sources.    In  other monitoring by NEIC  (U.S.  EPA,  1977c) near  suspected  sources  in Mclntosh,
Alabama;  Charlotte and  Salisbury,  North Carolina; and Chattanooga, Tennessee, only one sample
near the Alabama  site  showed evidence of N-nitroso  compounds  (0.040 ug/m  DMN) in the atmos-
phere.   Fine  (1976)  reported  monitoring  for atmospheric  DMN  at  several  sites in  New York,
New Jersey, and Massachusetts under a variety of meteorological conditions.  DMN was not found
in  any  of  25  samples  taken throughout northern New Jersey; nor  in any of  15  samples in  the
Boston, Massachusetts,  area.   Only  one of 18 samples in New York City showed a measurable  DMN
concentration  (0.016  ug/m ).   Since a cryogenic  trap was used in the  sampling  procedure  for
this measurement, the possibility of artifact formation  cannot be ruled out.
     In  summary,  these measurements point  to the  conclusion  that  the  atmospheric  route  for
N-nitroso compounds is not a significant pathway for possible  human exposure.  In addition, no
evidence has been found to date for the nitrosation of amines  in ambient air.
8.4  SUMMARY
8.4.1  Atmospheric Concentrations of NO,,
     Examination of both  historical  data and for  the years 1975 to 1980  allows  some  general
conclusions to be drawn about the nationwide experience  with respect to ambient NOp concentra-
tions.  In summary, the data cited illustrate the following points.
                                            8-74

-------
        • Annual average concentrations of NCL are not reliable index of short-term (3 hour or
          less) human exposure, and vice versa.
        • Although  a distinct recurrent diurnal  pattern  is discernible in  some  areas  of the
          country,  in  many areas  peak diurnal values  may occur  at almost any  time  of day.
        • Just as there is no standard diurnal pattern nationwide for peak N0? concentrations,
          there  is  also no  standard nationwide pattern for the  month-by-month  variations in
          monthly averages of  daily maximum 1-hr concentrations.   Peak monthly averages occur
          at different times of year in different locations.
        • The  direction  and  magnitude of recent  trends in N02 concentrations also tend to be
          area-specific.
        • The  oxidation  of NO to NCk  by ozone scavenging  (chemical reaction with ambient 0,,
          which  is  generated photochemically  during  daylight  hours) may at some  times  be an
          important mechanism in some areas of the country for producing high NO^ levels after
          photochemical activity has ceased.   In other areas photochemical  reactions involving
          ambient hydrocarbons may be the dominant mechanism.
     The  following  summary of recent  ambient  levels  of NCL occurring nationwide  is  given to
provide perspective on the concentration levels associated with the health  and welfare effects
discussed elsewhere in this document.
     Examination of  selected  nationwide  monitoring  data for 1975  to 1980  reveals that during
at  least  one of  these years, peak  1-hr  NO^ concentrations equalling or exceeding  750 ug/m
(0.4  ppm)  were   experienced  in  Los  Angeles  and  several  other  California sites;  Ashland,
Kentucky; and  Port  Huron,  Michigan.   Additional sites reporting at least one peak hourly con-
centration equalling or  exceeding  500 ug/m  (0.27 ppm)  include:   Phoenix,  Arizona; St.  Louis,
Missouri; New  York  City,  New York;  14 additional  California sites; Springfield,  Illinois;
Cincinnati,  Ohio; and  Saginaw  and  Southfield, Michigan.   Other sites, distributed nationwide,
reported  maxima  close  to  this  value.   Recurrent NO, hourly concentrations in excess  of 250
    3
ug/m  (0.14 ppm) were quite common nationwide in 1975 to 1980.
     The  data  also  show  that Long  Beach,  California;  Indianapolis,  Indiana;  and  Salt  Lake
City, Utah,  all experienced at least one day when the 24-hr average N09 concentration exceeded
        3
300 ug/m   (0.16  ppm)  during  1975 to  1980.   In addition,  San Bernadino, California;  Denver,
Colorado; Chicago,  Illinois;  Nashua,  New  Hampshire;  Cincinnati  and Cleveland,   Ohio;  Tulsa,
Oklahoma; and  Fort  Worth  and  Houston, Texas,  all  reported at  least one 24-hr  period where
average N00 concentrations exceeded 150 ug/m  (0.08  ppm).
                                                                              3
     Annual  arithmetic means  for  N02 concentrations in  1976 exceeded 100 ug/m  (0.053 ppm) at
Anaheim,  El Cajon,  Riverside,  San  Diego,  and Temple  City,  California.   Other sites reporting
                                                                3
yearly arithmetic means for 1976 equalling  or exceeding  100 ug/m  (0.053  ppm) included Chicago,
Illinois, and  Southfield,  Michigan.   However,  by 1980  virtually none of the still  operating
monitoring  sites  reported  annual  average  levels over 100  ug/m   (except one  in  San  Diego;
114 ug/m3).

                                            8-75

-------
8.4.2  Atmospheric Concentrations of Nitrates
     Few high quality data exist on concentrations of nitrates suspended in ambient air.   Very
recent data,  taken by sampling  techniques  not subject to positive artifact  formation,  range
              3                                           3
from 0.18 ug/m  in Philadelphia, Pennsylvania,  to 2.1 ug/m  at sites in Los Angeles.   The data
available are not sufficient to place human exposure in nationwide perspective.
8.4.3  Atmospheric Concentrations of N-Nitroso  Compounds
     N-nitroso compounds  have  recently  been observed in ambient air,  mostly at locations near
known or  suspected sources.   The  data reported  to date  are  indicators only  of  atmospheric
burdens  at a  few  special  locations.   No evidence  has  been reported to substantiate secondary
production in the vicinity of amine sources.
     Observed concentrations of  dimethylnitrosamine (DMN) ranged up to  32  pg/m  at a site in
Baltimore, Maryland,  near a known emission source.   An extensive monitoring  survey  by  EPA's
National   Enforcement  Investigation  Center showed  no  indication  of  N-nitrosamines in  the
vicinity of 32 suspected  sources throughout the Midwest.   Similar monitoring at four sites in
the Southeast yielded  a  trace  of DMN in only  one sample from one site.   Similar results were
obtained  in  sampling by  other researchers  in  the  greater New York-New Jersey  area  and near
Boston,  Massachusetts.   Considering the small and infrequently observed atmospheric burdens of
nitrosamines reported,  in conjunction with  the  potential human exposure from certain foodstuffs
and tobacco,  the  atmospheric  route  for human  exposure does  not,  at  this time, seem to  be  a
significant one.
                                            8-76

-------
8.5  REFERENCES

Breeding, R. J. ,  J.  P.  Lodge, Jr., J.  B.  Pate, D. C. Sheesley, H. B. Klonis, B. Fogle, J. A.
     Anderson,  T.  R.  Englert, P.  L. Haagenson, R. B. McBeth, A. L. Morris, R. Pogue, and A. F.
     Wartburg.   Background trace gas concentrations in the central United States.  J. Geophys.
     Res. 78:7057-7064, 1973.

Chameides, W.  L.  Tropospheric  odd nitrogen  and the atmospheric  water vapor  cycle.   JGR J.
     Geophys. Res. 80:4989-4996, 1975.

Cox, R.  A.   Some  measurements of  ground  level  NO,  N0g and 0, concentrations at an unpolluted
     maritime site.   Tellus 29:356-362, 1977.         ^      d

Crutzen, P.   J.  ,  I.  S.  A.  Isaksen,  and J.  R. McAfee.   The impact of the chlorocarbon industry
     on the  ozone layer.   JGR J.  Geophys.  Res. 83:345-363, 1978.

Drummond, J. W.   Atmospheric Measurements of Nitric  Oxide  Using  a Chemiluminescent Detector.
     Ph.D.  thesis, University of Wyoming,  Laramie, WY, 1976.

Dzubay,  T.  G. , and  R.  K.  Stevens.  Ambient air analysis with dichotomous  sampler and x-ray
     fluorescence spectrometer.   Environmental" Science and Technology 9:663-668, 1975.

Dzubay, T. G. ,  R.  K.  Stevens, and  L.  W.  Richards.    Composition of aerosols over Los Angeles
     freeways.   Atmos.  Environ.  13:653-659,  1979.

Fairfax County.   Hourly monitoring data available from Air Pollution Control Division, Health
     Department, 4080 Chain Bridge Road, Fairfax, Virginia  22030.

Fankhauser,   R.   K.  Nitric  oxide,  nitrogen dioxide, ozone  interrelationships across the free-
     way.  In:   Symposium for Discussion of  the  Los Angeles Catalyst Study, U.S. Environmental
     Protection   Agency,   Research  Triangle   Park,   North   Carolina,   April   12-13,  1977.
     EPA-600/4-77-036,  U.S.  Environmental  Protection  Agency,  Research Triangle Park, NC, June
     1977.   pp. 343-357.

Fine,  D.  H.    Final  Report  of  Monitoring  for  N-nitroso  Compounds  in the  States  of  West
     Virginia.,   New York,  New Jersey,  and Massachusetts.   EPA  Contract  No.  68-02-2363.   U.S.
     Environmental Protection Agency,  Research Triangle Park,  North  Carolina,  November 1976.

Fine, D. H.  , D.  P.  Rounbehler,  N.  M.  Belcher,  and S. S.  Epstein.  N-/iitroso compounds in the
     environment.    In:   International  Conference  on Environmental  Sensing and  Assessment,
     Volume   2,  A  Joint  Conference  Comprising  the  International Symposium  on Environmental
     Monitoring and Third  Joint  Conference  on Sensing Environmental  Pollutants,  World Health
     Organization  and   Others,   Las  Vegas,  Nevada,  September  14-19,   1975.   Institute  of
     Electrical & Electronics Engineers, Inc., New York,  NY,  1976a.  session 30-7.

Fine, D. H.  , D.  P.  Rounbehler,  N.  M.  Belcher,  and S. S.  Epstein.  N-nitroso compounds in air
     and water.  In:   Environmental N-nitroso Compounds Analysis and Formation,  Proceedings of
     a Working  CorfFerence,  International Agency for Research on Cancer, Tallinn, Estonian SSR,
     October 1-3,  1975.    E.  A.  Walker,  P.  Bogovski,  L-.  Griciute,  and  W.  Davis,  ed. ,  IARC
     Scientific  Publications No.   14,  International  Agency  for Research  on   Cancer,  Lyon,
     France,  1976b.   pp.  401-408.
                                             8-77

-------
Freedman,  S.  J. ,  E.  Lewis-Heise,  J.  D. Wilson,  and A.  V. Hardy,  Jr.   Population at Risk  to
     Various Air Pollution Exposures:   Data Base  "POPATRISK."  EPA-600/1-78-051,  U.S.  Environ-
     mental Protection Agency, Research Triangle  Park, NC, June 1978.

Galbally, I. E.  Measurement of nitrogen oxides in the background atmosphere.  J_n:  Air  Pollu-
     tion  Measurement  Techniques,  Parts I  and  II,  Report and Lectures  of the World  Meteoro-
     logical Organization Air Pollution Measurement Techniques Conference, Gothenburg, Sweden,
     October  11-15,  1976.   WMO No.  460,  Special  Environmental Report  No.  10, World  Meteoro-
     logical Organization, Geneva, Switzerland, 1977.  pp. 179-185.

Hanst, P.  L. ,  E.  W.  Wilson, R. K.  Patterson,  8.  W. Gay,  Jr., L.  W. Chaney, and  C. S. Burton.
     A Spectroscopic  Study of California Smog.   EPA-650/4-75-006,  U.S.  Environmental Protec-
     tion Agency,  Research Triangle Park, NC, February 1975.

Marker, A.  B. ,  L.  W.  Richards, and W. E. Clark.  The effect of atmospheric S02 photochemistry
     upon observed nitrate concentrations in aerosols.  Atmos. Environ. 11:87-91,  1977.

Horie, Y. ,  A.  S.  Chaplin,  and E.  D.  Helfenbein.  Population Exposure to Oxidants  and  Nitrogen
     Dioxide  in  Los Angeles.   Volume II:    Weekday/Weekend  and  Population  Mobility  Effects.
     EPA-450/3-77-004b,  U.S.   Environmental  Protection  Agency,   Research  Triangle  Park,  NC,
     January 1977.

Huebert,  B. J. , and  A.  L.  Lazrus.  Global  tropospheric  measurements of nitric acid vapor and
     particulate matter.  Geophys.  Res. Lett. 5:577-580, 1978.

Junge, C. E.  Recent investigations in air chemistry.  Tellus 8:127-139, 1956.

Keyes, D.   L. ,  B.  Kumar,  R.   D.  Coleman,  and R.  0.  Reid.   The  material presented on the
     Washington, D.C.  area is  largely due  to  Energy and Environmental  Analysis, Inc., 1111
     North 19th Street, Arlington, Virginia  22209.

Lodge, J.  P. , Jr. ,  and J. B.  Pate.   Atmospheric gases and  particulates  in Panama.   Science
     (Washington,  D.C.) 153:3734,  408-410,  1966.

Ludwig, F.  L. ,  and  E.  Shelar.   Site Selection for the Monitoring of Photochemical Air Pollut-
     ants.  EPA-450/3-78-013,  U.S.  Environmental  Protection  Agency,  Research Triangle Park,
     NC,  April 1978.

Miller, D.  F. ,  and  C.  W.  Spicer.   A continuous analyzer for detecting nitric  acid.  Presented
     at  the 67th  Annual  Meeting,  Air  Pollution  Control  Association,  Denver, CO, June 9-13,
     1974.  paper no. 74-17.

Moore, H.   Isotopic measurement  of  atmospheric  nitrogen  compounds.  Tellus 26:169-174, 1974.

Nelson, E.  Regional  Air  Pollution Study.   High  Volume  Filter Measurements of Suspended Par-
     ticulate  Matter.   EPA-600/4-79-003,   U.S.  Environmental   Protection  Agency,   Research
     Triangle Park,  NC, January 1979.

Noxon,  J.  F.   Nitrogen dioxide in the  stratosphere and  troposphere measured by  ground-based
     absorption spectroscopy.   Science (Washington, D.C.)  189:547-549, 1975.

Noxon, J. F.  Tropospheric N02-  JGR J. Geophys.  Res. 83:3051-3057, 1978.

Pellizzari, E.  D.   The Measurement of Carcinogenic Vapors in Ambient Atmospheres.  EPA-600/7-
     77-055,  U.S.  Environmental  Protection Agency,  Research Triangle  Park, NC,  June 1977.


                                             8-78

-------
 Pickering, K.  E. ,  R.  H.  Woodward, and R.  C.  Koch.   Power Plant Stack Plumes in Complex Terrain:
      Data Analysis  and  Characterization  of  Plume Behavior.   EPA-600/7-80-008,  U.S.  Environ-
      mental  Protection Agency, Research Triangle Park, NC, January 1980.

 Ritter, R.  A.,  D. H.  Stedman, and T. J.  Kelly.   Ground level measurements  of  nitric oxide,
      nitrogen dioxide and ozone in rural  air.   In:   Nitrogenous Air Pollutants, Proceedings of
      .a  Symposium,  175th  National  Meeting,  American  Chemical  Society,  Anaheim,  California,
      March 12-17,  1978.   D.  Grosjean,  ed.,  Ann Arbor Science Publishers, Inc., Ann Arbor, MI,
      1979.  pp.  325-343.

 Robinson,  E. , and R.  C.  Robbins.   Emissions, concentrations,  and fate of gaseous atmospheric
      pollutants,   jjr.  Air  Pollution  Control.   Part II. W.  Strauss,  ed. , Wiley-Interscience,
      New York,  NY, 1972.   pp.  1-93.
 Spicer,  C.  W.   The fate of nitrogen oxides in the atmosphere.
      7:163-261, 1977.
Adv.  Environmental Sci. Technol,
 Spicer,  C.  W.,  P.  M.  Schumacher,  J.  A.  Kouyoumjian, and D.  W.  Joseph.   Sampling and Analytical
      Methodology for Atmospheric  Particulate Nitrates.   Final  Report.   EPA-600/ 2-78-067, U.S.
      Environmental  Protection Agency, Research Triangle Park,  NC, April 1978.

 Stevens,  R.  K. ,  T. G.  Dzubay,  G. Russwurm,  and  D.  Rickel.   Sampling and  analysis  of atmos-
      pheric sulfates and  related  species.   In:   Sulfur in the  Atmosphere,  Proceedings of the
      International   Symposium,  United  Nations  Environmental  Program  and  Others,  Dubrovnik,
      Yugoslavia,  September 7-14,  1977.   Atmos. Environ. 12:55-68, 1978b.

 Stevens,  R. K.  , T.  G.  Dzubay,  D.  T. Mage,  R.  Burton,  G.  Russwurm, and E. Tew.  Comparison of
      nitrates  and   sulfates  collected  by  Hi-yol  and dichotomous  samplers.   Presented  to
      American Chemical  Society,  Division of Environmental  Chemistry,  Miami,  Florida,  September
      1978a.

.Trijonis,   J.    Empirical   Relationships   Between  Atmospheric   Nitrogen   Dioxide   and  Its
      Precursors.    EPA-600/3-78-018,  U.S.  Environmental  Protection Agency,   Research  Triangle
      Park,  NC,  February 1978.

 Trijonis,  J. ,  et  al.   The  Relationship of  Ambient  N02  to  Hydrocarbon  and  NO   Emissions.
      Draft  report  from Technology Service  Corporation to EPA  under Contract No.  68-02-2299.
      U.S.   Environmental   Protection  Agency,  Office  of  Research and Development,  Research
      Triangle Park, NC.

 Tuazon,  E.  C. ,  R.  A.  Graham,  A.  M.  Winer,  R.  R. Easton, J.  N.  Pitts,  Jr., and P.  L.  Hanst.  A
      kilometer  pathlength Fourier-transform infrared  system  for the  study of trace pollutants
      in  ambient and synthetic atmospheres.   Atmos.  Environ.  12:865-875, 1978.

 U.  S. Environmental Protection Agency.   Air quality and emissions trends.   I_n:  The National
      Air  Monitoring  Program:  Air Quality  and Emissions  Trends—Annual Report.   Volume  1.
      EPA-450/l-73-001a,   U.S.  Environmental  Protection Agency,  Research Triangle Park,  NC,
      August 1973.   pp.  4-1-4-41.

 U.  S. Environmental Protection Agency.   National Aerometric Data Bank,  1975a.

 U.  S. Environmental Agency.  SAROAD.   Data reported were abstracted  from the 1975 SAROAD raw
      data file  maintained at  the  National  Air  Data Branch,  Durham, NC,  1975b.
                                              8-79

-------
U.   S.  Environmental  Protection Agency.   National  Air  Quality  and Emissions  Trends Report,
     1975.   EPA-450/1-76-002,  U.S.  Environmental  Protection Agency,  Research  Triangle Park,
     NC,  November 1976a.

U.  S.  Environmental Protection Agency.  RAPS.  Data reported are abstracted from the 1976 data
     file  for  the Regional  Air  Pollution  Study  program maintained  at  the Environmental
     Research Center,  Research Triangle Park, NC, 1976b.

U.  S.   Environmental Protection  Agency.   SAROAD.  Data  reported  were abstracted from the 1976
     SAROAD raw data  file maintained  at the  National Air Data  Branch, Durham,  NC,  1976c.

U.   S.  Environmental  Protection Agency.   Air Quality Data  - 1975  Annual  Statistics Including
     Summaries  with Reference to Standards.  EPA-450/2-77-002,  U.S.  Environmental Protection
     Agency, Research  Triangle Park, NC, May 1977a.

U.  S.  Environmental Protection Agency.  Reconnaissance of Environmental Levels of Nitrosamines
     in the Central  United States.   EPA-330/1-77-001,  U.S. Environmental  Protection Agency,
     Denver, CO, February 1977b.

U.  S.  Environmental Protection Agency.  Reconnaissance of Environmental Levels of Nitrosamines
     in  the  Southeastern  United  States.   EPA-330/1-77-009,   U.S.  Environmental  Protection
     Agency, Denver, CO, August 1977c.

U.S. Environmental  Protection Agency.   Air Quality  Data  - 1978  Annual  Statistics including
     Summaries  with Reference to Standards.  EPA-450/4-79-037,  U.S.  Environmental Protection
     Agency, Research  Triangle Park, NC, November 1979.

U.S. Environmental  Protection Agency.   Air Quality  Data  - 1980  Annual  Statistics Including
     Summaries  with Reference to Standards.  EPA-450/4-81-027,  U.S.  Environmental Protection
     Agency, Research  Triangle Park, NC, August 1981.
                                             8-80

-------
                      9.  PERTURBATIONS OF THE STRATOSPHERIC OZONE LAYER

9.1  INTRODUCTION
     Since the  beginning  of this decade it has been increasingly clear that a number of man's
activities can  lead  to  reductions in stratospheric  ozone,  which protects life at the earth's
surface from  potentially  harmful  ultraviolet radiation.  Initially  attention  was  directed to
the pollution of  the stratosphere by direct  injections  of  water vapor and oxides of nitrogen
(NO and N02)  from high-flying aircraft (Crutzen, 1971; Johnston, 1971).  It had been proposed
by Crutzen (1970)  that  NO  (NO + N02) could catalyze the destruction of ozone and control its
stratospheric abundance by the set of photochemical reactions:
                        03  + hv -» 0 + 02                                      (9-1)
                                       (wavelengths shorter than 1140 nm)
                        0   + N02 •* NO  + 02                                   (9-2)
                        NO  + 03  •* N02 + 02                                   (9-3)
                            2 03  -> 3 02                                       net
     The main  sdurce of  NO  in  the  stratosphere  is probably the oxidation  of  nitrous oxide
(N20)  via  the  reactions  (Crutzen,  1971; Nicolet  and Vergison, 1971;  McElroy and McConnell,
1971):
                   0,    + hv  -» 0(ln.) + 0,                                    (9-4)
                    J                     £
                                            (wavelengths shorter than 310 nm)
                        O^D) + N20 •* 2 NO                                     (9-5)
Because of  its relatively  low solubility and  low  reactivity in water, nitrous  oxide  is  not
removed in clouds  and  through precipitation in the troposphere.  In contrast, direct transport
of NO  and N0«  into  the stratosphere  from the  earth's  surface is strongly  prohibited  by  wet
removal of  N0? and  especially its oxidation product HNO,,  which is formed  by  the reaction:
                        OH + NO, (+M)  -» HNO, (+M)                              (9-6)
                                                                          1
     The  hydroxyl  radical  (OH)  is  primarily formed  by the  attack  of 0( D)  on  water  vapor,
following reaction 9-4, above:
                        O^D) + H20 -»  2 OH                                     (9-7)
     This radical, and  therefore  also ozone, plays an  extremely  important  role in the  photo-
chemistry of the atmosphere.   In the troposphere (0-10 km in middle and high latitudes,  or  0-lf
km in  the tropics)  it  attacks a host  of gases which otherwise would be inert, such as CO,  H2,
hydrocarbons and  chlorinated hydrocarbons.   This ensures  that only a small  portion  (~10% or
less) of  the ground  level  emissions of such  gases  can  reach the stratosphere.   As a result,
photochemical   activity  in  the  stratosphere  is   strongly  limited  and ozone  is  protected from
                                             9-1

-------
otherwise larger  destruction.   Nitrous  oxide, however, is nearly inert to attack by all known
tropospheric gases, including OH (Biermann et al., 1976).
9.2  DIRECT ROLE OF NITROGEN OXIDES IN THE OZONE BALANCE OF THE ATMOSPHERE
     The oxides of nitrogen, NOX, play a remarkable catalytic role in the ozone balance of the
atmosphere.   Above about  24 km, the net effect  of N0x additions to the stratosphere is ozone
destruction by  the set  of reactions already discussed (reactions 9-1,  9-2,  9-3).   At lower
altitudes the  opposite  is true.   The  essential  reason  for  this  is  the  following  set  of
reactions.

                        R02 + NO -» RO + N02                                    (9-8)
                        N02 + hv •* NO + 0                                      (9-9)
                        0   + 02 + M  + 03 + M                                 (9-10)
                        R02 + 02 •* RO + 03                                     net

     This is the  same  set of reactions which is at the core of ozone production under photo-
chemical smog conditions, when reactions 9-8 through 9-10 are preceded by reactions of the type
                        R + 02 +. M -> R02 + M                                   (9-11)
with the net result:   R + 2 0^  •»  RO + 0,.  The radical R can here stand for such radicals as
CHoCO and  H.   In the  non-urban  troposphere,  ozone production may, however,  still  take place
from  the oxidation of hydrocarbons emitted  by  vegetation  and  of carbon monoxide,  provided
sufficient  NO   is present.   In the  case of  carbon monoxide the  sequence  of reactions starts
with
                        CO + OH (+M) -» H + C02 (+M)                            (9-12)
followed by reaction 9-11 (with R = H) and reactions 9-8 through 9-10, leading  to   the   net
result:   CO + 2 02 -» C02 + 0^.   Because it is conceivable that both carbon monoxide and nitric
oxide concentrations have been increasing due to human activities, there is a discrete possibi-
lity of worldwide ozone increases,  especially in the Northern Hemisphere's troposphere (Fishman
and Crutzen, 1978).
     It  should  be added  that  the  origin  of  tropospheric ozone  is currently  not well known.
Traditional  thinking  in the meteorological  community explained the presence  of  ozone in the
troposphere by its formation in the stratosphere (Chapman, 1930) via the reaction

                        02 + hv       -» 2 0   (\ < 240 nm)                      (9-13)
                        0  + 02 + M -> 03 + M    (x2)                           (9-14)

                               3 02 -» 2 03                                     net

and its downward transport into the troposphere in the vicinity of frontal zones or tropopause
breaks (Danielsen and Mohnen, 1977).  The tropospheric ozone production taking place near urban

                                             9-2

-------
centers was  thought  to be only of  minor global  importance.   However, it seems now that ozone
production can  also  take place in the "clean" troposphere as long as NOV volume mixing ratios
                       -11
are not too small (> 10   ), because of  the fast rate of reaction 9-8.
     In the  Tower  stratosphere (~1O24  km) the  chain  of reactions 9-8 through 9-10 (with R =
H) tends to counteract the effect of the reactions
                        OH  + 03 •* H02 + 02                                    (9-15)
                        H02 + 03 -» OH +  2 02                                   (9-16)
                            2 03 -» 3 02                                        net
         by deferring it into the sequence
                        OH  + 03 •* H02 + 02
                        H02 + NO •* OH +  N02
                        N02 + hv •* NO + 0
                        no net chemical effect
     Additions of NO to the lower stratosphere, therefore, tend to increase local ozone concen-
trations  by  causing smaller  ozone  losses.   The importance of the  ozone-producing  aspects of
NO  catalysis  below about 24 km is  dramatically  emphasized  by the recent discovery of Howard
and Evenson  (1977),  who  found reaction 9-8  to  be  at least an order  of  magnitude faster than
previously determined  through indirect  measurements of the rate constant.   This finding has
resulted  in  substantial  downward revisions of estimated  total ozone  column reductions due to
stratospheric NO  additions from high-flying aircraft.  As a result of the peculiar photochem-
ical action  of  N0x, we notice also a decrease in altitude of the center of gravity of strato-
spheric ozone  by  transfer of mass from above 24 km to below 24 km.   As NO  is produced by the
oxidation  of NJ)  via  reactions 9-4  and 9-5,  the  same  conclusions  are valid  regarding the
possible  effects  of  a  future  rise  in  the  atmospheric  content of  nitrous  oxide.   Such an
increase may be caused by man's intervention  in  the nitrogen  cycle through an increasing use
of nitrogen fertilizer and other agricultural activities.
9.3  INDIRECT ROLE OF NITROUS OXIDE IN THE OZONE BALANCE OF THE ATMOSPHERE
     In addition to the direct effects to the stratospheric ozone layer caused by the catalytic
cycle involving the nitrogen  oxides,  the existence  of  NO  also  has an important influence on
the impact  of  catalytic  ozone  destruction  initiated  by  other  atmospheric  constituents.  In
particular, catalytic destruction of stratospheric ozone via reactive chlorine species proceeds
as follows:
                        03 + hv •* 0 + 02                                       (9-17)
                        0 + CIO -»• Cl + 02                                      (9-18)
                        03 + Cl  -» CIO + 02                                     (9-19)
                           2 03 •* 3 02                                         net
                                             9-3

-------
The  initial  release of Cl (and  subsequent  formation  of CIO) to the  stratosphere  occurs  when
degradation  of  chlorinated compounds such as chlorofluoromethanes  (e.g.,  fluorocarbon-11 and
fluorocarbon-12), methyl  chloroform,  and methyl  chloride takes place  by  either direct photo-
lysis  or  attack by  reactive species which  prevail  in the  stratosphere  (Molina  and Rowland,
1974).  However, the  ozone-destroying frequencies of these  catalytic  cycles  are  not additive
since  the  presence  of both reactive  chlorine and  reactive  nitrogen compounds may result  in a
short-circuit of either  catalytic  cycle.   For  example, the formation of  chlorine  nitrate  in
the stratosphere through the reaction
               CIO + N02 + M -> C10N02 + M                             (9-20)
removes both reactive chlorine and nitrogen from the atmosphere which would have otherwise been
able  to take part  in catalytic ozone-destroying cycles.  As a result, the inclusion of C10NCL
in stratospheric models of ozone depletion predictions lowered the depletion estimates by  about
a factor of two  (Crutzen et al., 1978).
      Lastly,  it  should be pointed  out  that  new  measurements of reaction  rates which involve
only  reactive nitrogen species can likewise influence other catalytic cycles of ozone destruc-
tion.  A  good example  of such an  occurrence is  the  recently reported rate  constant for the
reaction
               H02 + NO -> OH + N02                                    (9-8)
by Howard and Evenson (1977), which was shown to proceed much faster than  had been
         previously believed (Hampson and Garvin,  1975).  An increase in  this rate constant
                       OH
         increases the ^ ratio in the model  calculations.   Because more  OH is calculated

by the numerical models,  smaller concentrations of HC1  are computed to exist.   Since  HC1  is
one  of the primary reservoirs  of  reactive  chlorine species, the  increased  OH concentrations
which  have  been  brought about by the reaction of  NO  with HO,,, result in  the release of  more
chlorine atoms into the atmospheric system via
               HC1  + OH -» H20 + Cl                                     (9-21)
Thus,  it is  important to  point out  that  the  nitrogen cycle in the  stratosphere  has a direct
bearing on the catalyzing power of other stratospheric cycles involving the ozone  layer.   This
interaction may  be  interfering or enhancing depending on  which  region  of the ozone layer  is
being examined or at which altitudes certain reactions dominate the overall chemistry.
9.4  OTHER ATMOSPHERIC EFFECTS OF NITROGENOUS COMPOUNDS
     The environmental  effects  of  ozone changes  in the  stratosphere  are,  however,  not solely
related to  the   function  of  ozone  as  a shield against the penetration  of  solar ultraviolet
radiation to ground  level.   Ozone  is also an important gas for the heat  budget  of the atmo-
sphere.  An effective lowering of the center of  gravity of the ozone layer, which  would be the
result  of  NO    additions  to the  stratosphere,   may  have  significant climatic  implications
(Ramanathan, 1974), as it may cause a warming of the lower stratosphere and the earth's surface
                                             9-4

-------
by  the  increased absorption  of  ultraviolet solar radiation and enhanced  trapping  of thermal
9.6 urn radiation emitted from the warm surface of the earth.
     The significance of nitrous oxide is also not restricted to its importance as a source of
stratospheric NO  via  reactions  9-4 and 9-5.  Because of its absorption bands at about 7.8 urn
                A
and 17.0 |jm, nitrous oxide (N20) likewise contributes significantly to the atmospheric "green-
house" effect by  trapping  outgoing terrestrial radiation.   It  has,  therefore,  been estimated
that a doubling of the atmospheric NpO content could cause an increase in surface temperatures
by  as much  as  0.7°K (Wang et al.,  1976).   Several  recent studies  have been designed to esti-
mate the possible extent of future atmospheric NpO  build-up due to increased use of nitrogen
fertilizer  (Council  for  Agricultural  Science and Technology, 1976; Crutzen, 1976; Crutzen and
Ehhalt,  1977; Liu et al.,  1976; McElroy, 1974; McElroy  et  al., 1977; Rice and Sze, 1976; Sze
and Rice, 1976).  It is  difficult, however, to estimate the doubling time with any certainty.
Three important  but poorly  understood factors determining  the release of NpO  from soil and
water to the atmosphere are the following:
     I.    The release  of N/,0  in  the  denitrification process.   This  microbiological process,
          which is currently  considered  to  be the main source of atmospheric  NpO, takes place
          in anaerobic  microenvironments,  and  involves  the reduction  of nitrate  to NpO and
          molecular  nitrogen  (Np).   It  is  this  process which presumably balances nitrogen
          fixation,   i.e., the conversion  of Np to fixed nitrogen.   A growing  amount of obser-
          vational evidence is  now accumulating,  which indicates that the yield of NpO versus
          Np in agricultural  and  water environments is  less than  20 percent  (Delwiche, 1977;
          Rolston,  1977).   It  remains,  however,  important  to  gather  additional  information
          from field studies to improve the  data base for this important environmental factor.
     2.    The pathway of fertilizer  nitrogen in the environment.   This  involves knowledge of
          such factors as the  actual  amount of denitrification  in  agricultural  fields, leach-
          ing of  nitrate to  groundwater,  volatilization of  ammonia and its transport and con-
          versions in the atmosphere,  the  cycling and decomposition  of  animal  manures in the
          environment,   and  the  extent  of   transfer  of  agricultural  fixed  nitrogen to  the
          natural  ecosystems,  which  may be  expected  to  have much  longer  turnover  times than
          those  systems which are  directly  affected by agriculture.  Studies  of these matters
          have been  conducted by  Liu  et al.  (1976),  McElroy  et al. (1977),  and  Crutzen and
          Ehhalt (1977).
     3.    The role of the oceans in the worldwide  NpO budget. While initial studies indicated
          a   large source of NpO in the  oceans (National Research  Council, 1978),  recent in-
          vestigations  point  towards  a much smaller role of oceans in the global  NpO budget
          (Hahn,  1974;  Weiss,  1977).
     The scientific  problems  connected with possible future increases in atmospheric NpO con-
centrations  are being  investigated by  several  research groups and  the issue has been reviewed
in  a  recently  published report  by an  ad  hoc  committee of the  National Research Council,
(1978).   The issue  is  further complicated by  the fact  that the nitrogen cycle  is  coupled to

                                             9-5

-------
other cycles, such as those of carbon and phosphorus (Simpson et al., 1977).   It is, therefore,
fair to say  that  many years of active research are needed to assess reliably this potentially
important global environmental issue.
9.5  SUMMARY
     Stratospheric ozone  protects  life  at the earth's surface from potentially harmful ultra-
violet radiation from the sun.  The main source of NO  in the stratosphere is the oxidation of
                                                     A
nitrous oxide  (N~0).   Nitrous oxide  is  ubiquitous,  even in the absence  of  human activities,
since  it  is  a  product of  natural  biologic  processes in soil, but  significant  quantities may
also arise from the  denitrification of the  increased  quantities  of fixed nitrogen, which are
introduced into the nitrogen cycle by the growing use of nitrogen fertilizers.   Recent reports
indicate  that  somewhat less  than  20 percent  of the "excess" nitrogen  eventually  escapes as
N20, with  most of the  rest returned to the atmosphere  as  Np.   Since N~0 is not  believed to
take part  in any  atmospheric chemical reactions below  the  stratosphere,  all the N-O produced
terrestrially is available for stratospheric reactions.   The concern expressed by some authors
in the recent  past,  that  N20 arising from  excess  fertilizer might decrease  the total strato-
spheric ozone by  as  much  as 20 percent  for a  100 percent increase in total  N20, has recently
been reevaluated  in  the  light of new information  on rate constants for certain stratospheric
chemical   reaction pathways.   These  new  considerations  point  to  the  likelihood  of  a  much
smaller dependence of total stratospheric ozone on N?0 abundance.
     Ozone is also an important gas for the heat budget of the atmosphere.   An  effective low-
ering of  the "center of gravity" of  the  ozone layer,  which would  be  the result of NO  addi-
tions to the stratosphere, may have significant climatic implications.   Nitrous  oxide likewise
contributes to  the atmospheric "greenhouse"  effect by trapping outgoing terrestrial  radiation.
One author recently  estimated that a doubling of the atmospheric burden of N~0  could'increase
surface temperatures  by as much as 0.7°C.  It is difficult, however, to estimate the doubling
time with  any  certainty.   Since global  estimates of the end effects of excess fertilizer rest
on a number  of  poorly known parameters,  and  since the issues are  further complicated by the
fact that  the  nitrogen  cycle is coupled to  other cycles, such as the carbon  cycle,  no defini-
tive conclusions can prudently be drawn.
                                             9-6

-------
9.6  REFERENCES

Biermann, H.  W. ,  C.  Zetzch, and  F.  Stuhl.   Rate constant for  the  reaction of OH with  N«0  at
     298k.  Ber. Bunsenges. Phys. Chem. 80:909-911, 1976.                                 ^

Chapman,  S.   A theory  of upper  atmospheric ozone.  Mem. R.  Meteorol.  Soc. 3:103-125,  1930.

Cohen, Y. , and L.  I. Gordon.  Nitrous oxide  production  in the ocean.  JGR J. Geophys.  Res. 84:
     347-353, 1979.

Council  for  Agricultural  Science and Technology.   Effect  of  Increased Nitrogen Fixation  on
     Atmospheric Ozone.   CAST  Report No.  53, Council for Agricultural Science  and Technology,
     Iowa State University, Ames, IA, January 1976.

Crutzen,  P.  J.  The influence of  nitrogen oxides on the atmospheric ozone content.   Q. J. Roy.
     Met. Soc. 96:320-325, 1970.

Crutzen,  P.  J.   Ozone  production rates in  an  oxygen-hydrogen-nitrogen  oxide  atmosphere.   J.
     Geophys. Res.  76:7311-7328,  1971.

Crutzen,  P.   J.   Upper limits on  atmospheric ozone  reductions following  increased applications
     of fixed nitrogen to the soil.  Geophys. Res.  Letter 3:169-172, 1976.

Crutzen,  P.   J. ,  and  D.  H.  Ehhalt.   Effects  of nitrogen  fertilizers  and  combustion on the
     stratospheric ozone layers.  Ambio 6:112-117,  1977.

Crutzen,  P.   J. ,  I.  S.  A. , Isaksen, and J. R. McAfee.  The impact of the chlorocarbon  industry
     on the  ozone layer.  JGR J.  Geophys.  Res. 83:345-363, 1978.

Danielsen, E. F.,  and V. A. Mohnen.  Project dustorm report:   ozone transport,  j_n situ measure-
     ments and  meteorological  anlyses of tropopause folding.   JGR  J.  Geophys. Res. 82:  5867-
     5877, 1977.

Delwiche, C.  C.   Nitrous oxide and denitrification.  In:  Denitrification  Seminar,  The  Ferti-
     lizer Institute, San  Francisco,  California, October 25-27,  1977.   The Fertilizer  Insti-
     tute, Washington, DC, 1977.  8 pp.

Fishman,  J.  ,  and  P.  J.  Crutzen.  The  origin of  ozone in  the troposphere.   Nature  (London)
     274:855-858,  1978.

Hahn,  J.   The  North  Atlantic  Ocean  as a  source  of atmospheric NpO.   Tellus 26:160,   1974.

Hampson,  R.   F. , Jr.,  and D. Garvin,  Eds.   Chemical Kinetics and Photochemical  Data  for  Model-
     ing Atmospheric Chemistry.    NBS Technical Note 866, U.S. Department of  Commerce,  National
     Bureau  of Standards, Washington, DC,  June 1975.

Howard, C.  J. ,  and K.  M.  Evenson.  Kinetics of the  reaction of H0? with  NO.   Geophys. Res.
     Letters 4:437-440,  1977.

Johnston, H.  S.  Reduction of stratospheric ozone by nitrogen oxide catalysts  from  supersonic
     transport exhaust.   Science  (Washington, D.C.) 173:517-522, 1971.
                                             9-7

-------
Liu,  S.  C. ,  R.  J.  Cicernone,  T.  M.  Donahue, and W.  L.  Chameides.   Limitation  of  fertilizer
     induced ozone reduction by the long  lifetime of  the  reservoir of  fixed  nitrogen.   Geophys.
     Res. Letter 3:157-160, 1976.

McElroy, M.  B.   Statement of Michael B. McElroy.  In:   Fluorocarbons--Impact on Health and the
     Environment:   Hearings"  before  the  Subcommvttee   on   Public  Health   and  Environment,
     Committee on Interstate and Foreign  Commerce.  Serial No.  93-110,  U.S.  Congress,  House of
     Representatives, Washington, DC, December 11-12,  1974.   pp.  336-346.

McElroy, M.  B. ,  and J.  C.  McConnell.   Nitrous oxide:  a natural  source of  stratospheric  NO.
     J. Atmos.  Sci.  28:1095-1098, 1971.

McElroy, M.  B. ,  S.  C.  Wofsy, and  Y. 1.  Yung.  The nitrogen  cycle:   perturbations  due  to man
     and their  impact  on atmospheric N90  and 07.   Phil.  Trans.  R. Soc.  London B:   Biol.  Sci.
     277:159-181, 1977.                L        6

Molina,  M.  J.,  and F.  S.  Rowland.   Stratospheric  sink  for chlorofluoromethanes:    chlorine
     atom-catalysed destruction of ozone.  Nature (London) 249:810-812,  1974.

National  Research  Council.   Nitrates:    An  Environmental   Assessment.  National  Academy  of
     Science, Washington, DC, 1978.

Nicolet, M. ,  and E.  Vergison.   Nitrous  oxide  in the stratosphere.   Aeron. Acta A(90):l-16,
     1971.

Ramanathan,  V.    A  simplified stratospheric radiative  transfer  model: theoretical  estimates of
     the thermal  structure  of the basic  and  perturbed stratosphere.   Paper  given at  AIAA/AMS
     2nd Int.  Conf.  Environmental  Impact  Aerospace Operations  in High Atmosphere,  San  Diego,
     July 8-10, 1974.

Rice, H., and N. D.  Sze.  The Analysis of  Fertilizer  Impacts  on the Ozone Layer—Final  Report.
     Document  P-2123,  Environmental  Research and Technology, Inc.,  Washington,  DC, September
     1976.

Rolston, D.  E.   Field-measured  flux of nitrous oxide  from soil.   I_n:  Denitrification  Seminar,
     The Fertilizer Institute,  San Francisco, California, October 25-27,  1977.   The  Fertilizer
     Institute, Washington, DC,  1977.  6  pp.

Simpson, H.   J.,  W.  S.  Broecker, R.  M.  Garrels,  S.'  P. Gessel,  H. D. Holland, W.  T.  Holser, C.
     Junge,  I.   R.  Kaplan,  M.  B. McElroy,  W.  Michaelis,  K.  Mopper, M.  Schidlowski,  W.  Seiler,
     J.  H.  Steele,  S.  C. Wofsy, and R. F. Wollast.   Man  and  the  global  nitrogen  cycle:   group
     report.    I_n:  Global  Chemical  Cycles and Their  Alterations  by Man, Report  of  the  Dahlem
     Workshop,   Dahlem   Konferenzen,  Berlin,  Germany,  November  15-19,  1976.   W.  Stumm,  ed. ,
     Dahlem Konferenzen, Berlin, Germany,  1977.  pp. 253-274.

Sze, N.  D.,  and H.  Rice.   Nitrogen  cycle factors contributing to  N?0 production from  ferti-
     lizers.   Geophys.  Res. Letter 3:343-346, 1976.

Wang,  W.  C., Y.  L.  Yung,  A.  A.  Lacis,  T.  Mo,  and J. E. Hansen.   Greenhouse  effects  due to
     man-made  perturbations of trace  gases.   Science (Washington, D.C.)  194:685-690,  1976.

Weiss,  R. F.   Nitrous  oxide in the atmosphere and the sea.   Jji:  Denitrification Seminar,  The
     Fertilizer  Institute,  San Francisco, California,  October 25-27,  1977.   The  Fertilizer
     Institute, Washington, DC,  1977.  3  pp.
                                             9-8

-------
                         10.  EFFECTS OF NITROGEN OXIDES ON VISIBILITY

     Air pollution  degrades  the appearance of distant  objects  and  reduces the range at which
they can be distinguished from the background.  These effects are manifested not only in visi-
ble plumes, but  also in large-scale, hazy  air masses  (Husar et al.  , 1976).   Haze  and plumes
can result  in  the deterioration and loss  of  scenic  vistas,  particularly in areas such as the
southwestern  U.S.  where  visibility is  generally good.   Under  extreme  conditions,  reduced
visual range  and  contrast  due to haze and  plumes  may impede air traffic.   NO^ can be respon-
sible  for  a portion  of the  brownish  coloration often  observed  in polluted  air (Hodkinson,
1966;  Husar and  White,  1976).  However,  it should also be noted that non-nitrate particulate
matter has  been  implicated  in the production of a significant fraction of brownish coloration
(Husar and  White,  1976).   In addition,  where nitrates  occur as fine particles, they may con-
tribute  to  the reduction of  visual  range  (White and Roberts, 1977; Trijonis  et  al.,  1978b).
(See Chapter  6 for a discussion of  atmospheric  processes  resulting  in ambient burdens of NOp
and particulate nitrate.)
10.1  NITROGEN OXIDES AND LIGHT SCATTERING AND ABSORPTION
     Deterioration  in visibility  is  due  to the  absorption and  scattering  of light by gaseous
molecules and suspended solid or liquid particles (Middleton, 1952).   Absorbed light is trans-
formed into other  forms of  energy,  such as heat,  while scattered light is re-radiated in all
directions with  no  change  in wavelength.   The importance of  each process is determined by the
absorption  and scattering  coefficients, b  and b .    These  coefficients  specify the  rate at
                                           3      5
which a beam of light is attenuated in passing through the atmosphere:
               dl /I  =  -b dx,  and  dl/I  =  -bdx,
                 da            So
where  I  is  the intensity of  the beam, and dl  and dl   are the changes  in  I due to absorption
                                              a        s
and scattering over the incremental distance dx.   The sum of  the absorption and scattering co-
efficients is  the total  extinction coefficient,  b = b  + b..
                                                     a    s
     The absorption  and scattering  coefficients  of particulate matter and  the different gases
are additive.   It is, therefore, meaningful to speak  of the impact of an individual  species on
visibility.   The effects of gases  and particulate matter can be distinguished as  follows (the
subscripts g and p denote the respective  contributions  from gases and particulates):
                    b  =  ba  + bs
                       =  b     +b    +   b    +   b
                           ag      ap      sg       sp
In polluted atmospheres, the  term  bao  is dominated,  at visible wavelengths, by the contribu-
                                    ag
tion from NO,,, which absorbs  strongly in the  blue region of  the spectrum.   The scattering due
to trace gases  is  negligible, so that b    can be  regarded as the constant  background due to
Rayleigh scattering by clean air.   Absorption  and scattering  by particles depend on their size
and  composition  (National   Air Pollution  Control  Administration,  1969).    Nitrate  compounds
may  constitute a  significant fraction  in  the  optically  important  particle size  range,  but
current  information  on  ambient  nitrate  concentrations  is  insufficient  to  make any conclusive
assessment.
                                             10-1

-------
10.2  EFFECT OF NITROGEN DIOXIDE ON COLOR
     Under typical ambient conditions, light scattering dominates total  extinction,
 which  is  related to reduction of  contrast and  visual  range.  The most  significant  optical
effect  of   N02,  however,  involves  discoloration.   The absorption coefficient for  N0?  can  be
used to calculate the visual impact of N02 in the atmosphere (Dixon,  1940).
10.2.1  Nitrogen Dioxide and Plumes
     Under certain circumstances,  brown  plumes  may be distinguished tens  of kilometers down-
wind  of their sources.    Nitrogen  dioxide  in a  plume  acts  as a blue-minus  filter  for  trans-
mitted  light.   It tends  to impart  a brownish  color  to targets,  including the sky,  viewed
through the plume.   The  strength  of this filter  effect  is  determined  by the  integral  of  N02
concentration along the  sight path; e.g., theoretically similar effects  would be  produced by a
1 kilometer-wide plume containing  0.1 ppm  (190 ng/m ) NO,  or a 0.1 kilometer-wide  plume con-
                           q                             t-
taining 1.0 ppm (1,900 [jg/m ) N02.
     Figure 10-1  shows  the  calculated  transmittance  of particle-free  N02 plumes for  several
values  of  the  concentration-distance  product.   Less than 0.1 ppm-km N02 is sufficient  to pro-
duce  a  color  shift  which  is   distinguishable  in carefully-controlled, color-matching  tests
(MacAdam,  1942).   Reports  from  one laboratory using NO^-containing  sighting tubes  indicate a
visible color  threshold  of 0.06 ppm-km for the  typical observer.   This  value was supported  by
a few  field  observations  of  N0~  plumes  from nitric  acid manufacturing plants  under  varying
operating  conditions  (Hardison, 1970).    The  value cited refers  to  the effect of  N0?  in  the
absence  of atmospheric  aerosol.   Empirical  observations  under a  variety  of conditions  are
needed to determine the  perceptibility of N02 in ambient air.
     Discoloration of plumes and haze layers by  N02 is  modified by particulate matter and also
depends  on a   number  of  factors such  as sun angle,  surrounding scenery, sky cover,  viewing
angle, human perception  parameters, and pollutant loading.   The relative importance  of  aerosol
or N02  in  determining the color and appearance  of  a  plume  or haze layer can be  addressed,  in
part, in  terms of the relative extinction  as a function of  wavelength.   Suspended particles
generally  scatter much more in  the forward direction  than  in any other direction.   This fact
means a  plume  or  haze layer can appear  bright  in forward  scatter (sun  in  front  of  the  obser-
ver) and dark  in  back scatter   (sun in back of  the observer) because of the  angular variation
in scattered air  light.   This  effect can vary with background sky and  objects.   Aerosol  opti-
cal  effects alone are capable  of  imparting a reddish  brown  color to a  haze  layer when  viewed
in  backward   scatter.   N02  would  increase  the degree  of  coloration  in  such  a  situation
(Ahlquist  and  Charlson,  1969;  Charlson  et al.,  1978).   When the sun is  in  front  of  the  obser-
ver,  however,  light  scattered  toward  him  by particles  in  the  plume  tends  to  wash out  the
brownish light  transmitted from beyond.   Under these conditions, particle  scattering  dimin-
ishes the  plume  coloration.  Specific  circumstances  of brown layers  must  be observed on a
case-by-case basis.
10.2.2  Nitrogen Dioxide and Haze
     A  common  feature of  pollutant haze is its  brown  color.   The discoloration of the  horizon
sky  due to N02  absorption is  determined by the  relative  concentrations of N02  and  light-
                                             10-2

-------
u
z
<
a:
      4000



        BLUE
5000              6000



    WAVELENGTH, 2,
7000



RED
    Figure 10-1. Transmittance exp(-b|\JC)2x) °' ^"^2 P'umes f°r

    selected values of the concentration-distance product (Adapted

    from Hodkinson, 1966.)
                                   10-3

-------
scattering particles.   In  a uniform atmosphere, the effect  of  NO- at any given wavelength is
described by the following relationship (Robinson, 1968):


              Bhorizon/Bhorizon"N02^ = °> =     ~      = " +      ^'*
where Bhorizon and Bhorizon^N02-' = °^ are the bri9ntness of the horizon sky, with and without
N02.
     The ratio bNCL/b  is more easily related to experience when expressed in terms of concen-
tration, [NOp], and visual range, VR.  As discussed in Section 10.3, visual range under certain
simplifying assumptions  is  inversely  proportional  to extinction, which is typically dominated
by  scattering.  Samuels  et  al.  (1973) compared  human  observations with instrumental measure-
ments  and  found  indications  that VR  and  b  are  related by  the  formula,  VR  = (3  +  l)/b .
Since,  in  addition,  b^ is proportional to  [NO-],  it follows that the ratio bN02/b  is pro-
portional to the product [NO,,] VR.  Figure 10-2 shows, for several  values of this product, the
calculated alteration  contributed by  N02 to horizon brightness which is in turn a function of
aerosol  scattering.   It  should  be noted that this calculation neglects the wavelength depend-
ence  of the scattering,  which  can be  substantial  in relatively  clean air  and mitigates the
discoloring effects of NO-.
     The interpretation  of  Figure 10-2  is  similar  to that of Figure  10-1.   A  concentration-
visual  range product  of  0.3 ppm-km N0~  corresponds  to  a color shift which should be detect-
able  in a  polluted  layer  viewed against  relatively clean  sky.   At  a  visual range  of 100
kilometers, typical of the rural northern great plains area of the United States, 0.003 ppm (6
    3
ug/m ) NO, might suffice to color the horizon noticeably.  At a visual range of 10 kilometers,
                                         3
typical  of  urban  haze,  0.03 ppm  (60 ug/m )  NOp  might be required to produce the same effect.
However, quantitative theoretical calculations of human perception of NO^ are not fully devel-
oped and experimental observations are needed to evaluate the actual effect.
     Independent of  absorption  by NO^,  wavelength-dependent scattering by small particles can
also  produce  a noticeable  brown  coloration  in  polluted air masses  (Husar  and White,  1976).
Unlike  the coloration  due to  absorption, which is independent of sun angle,  the brown colora-
tion contributed by scattering is most intense when the sun is in back of the observer.
10.3  EFFECT OF PARTICULATE NITRATES ON VISUAL RANGE
     The visual range  in a  uniform atmosphere is inversely proportional to the extinction co-
efficient.   For  a "standard" observer,  the Koschmeider  formula expressing  this relationship
is:
               VR = 3.9/b
where b  is  the extinction coefficient.   Taking account of the response as a function of wave-
length  of  the  light-adapted eye of a "standard  observer"  and of the wavelength dependence of
                                             10-4

-------
     1.0
     0.9
     o.e
     0.7
e
•    0.6
o"

1   O.S
 I
 5
 I...
B
     0.3
     0.2
     0.'
       4000

        BLUE
6000               6000

    WAVELENGTH.A
 7000

RED
     Figure 10-2.  Relative horizon brightness, bs/(bs + b^o-?'. for
     selected values of the concentration-visual product, assuriiing
     bj = 3/{visual range).  (Adapted from Hodkinson, 196G.)
                                10-5

-------
Rayleigh scattering,  it  is  possible to compute a  mean  extinction coefficient in a pure atmo-
sphere  containing  no aerosols  and no  light  absorbing gases  under standard  temperature  and
                      o
pressure conditions (0 C, 1.013 bars).   The value of b   so obtained (Penndorf, 1957) is about
        4-1                                         S9  .
0.12 (10 m)  ,  corresponding to a visual range of about 320 km.
     Recently,  Malm (1979) has examined critically the concept of visual  range as a measure of
visibility.  The  simple  Koschmeider formula,  which generally works reasonably  well  in urban
areas  (Horvath  and Noll, 1969), is shown  to  depend upon a number  of  simplifying assumptions
such as:  a homogeneous atmosphere, a flat earth,  a horizontal viewing  aspect, a black target,
and a  sky  radiance which is the same  at  the  object as at  the  viewing point.  Depending upon
particular circumstances, these assumptions may have a marked effect upon the relation between
the visual range calculated from the Koschmeider formula and the real  visual range defined as
the distance from  a  target  at which a  given  (threshold)  contrast is achieved.   Malm suggests
that visibility may be better characterized by apparent target contrast or by color changes of
selected vistas rather than  by visual  range.
     A definitive  assessment  of  the contribution made by nitrate aerosols to total extinction
(and therefore  to  degradation  of visibility)  is not  possible  because  sufficient high-quality
data  are  not available  for particulate nitrates.   However,  to  the extent  that  particulate
nitrates are secondary aerosols  formed in the 0.1  to  1 micron size range (Lee and Patterson,
1969), it  would be expected,  on theoretical  grounds, that  they would  be efficient scatterers
of light.   As  shown  in  Figure 10-3, light scattering per unit mass  of  aerosol exhibits a pro-
nounced resonance at a particle size of 0.5 microns, which is  approximately equal to the wave-
length of the center of the  spectrum of visible light.
     Theoretical calculations based on  the Mie theory of light scattering from aerosols indi-
cate that  particles  found  in  the 0.1 to 1 micron  size range (such  as  in secondary aerosols)
should exhibit  extinction coefficients  per unit mass on  the  order  of  0.06 + 0.03,  where  the
units are (104m)"1/(Mg/m3) (Latimer et  al.  , 1978a,  1978b,  1978c; Ursenback et al., 1978; White
and Roberts,  1977).  Similar calculations  indicate that particles occurring in the coarse size
range  above  2  microns,  such  as  dust  or  sea spray  (Bradway and  Record,  1978;  Whitby  and
Sverdrup 1980), should exhibit  much lower extinction coefficients per  unit mass, on the order
of 0.006  + 0.003  where the units  are  (104m)~V(ug/m3)  (Latimer et  al.,  1978a,  1978b,  1978c;
Ursenback  et al.,  1978;  White and  Roberts, 1977).   These results are confirmed by empirical
studies (Cass,   1976;  Trijonis  et al.,  1978a,1978b; Waggoner  et al., 1976; White and Roberts,
1977), which typically  find  extinction  coefficients per  unit  mass of  sulfates (a prevalent
secondary  aerosol)  to be 0.04  to  0.10 (10 m)   /((jg/m  ).   For the  remainder of  TSP (mostly
coarse particles),  the extinction coefficient  per unit mass is 0.004 to 0.01 (10 m)  /(ug/m ).
     Because nitrate aerosols  tend to be  hygroscopic,   light-scattering per  unit mass  of
nitrate can rise significantly  with increasing relative  humidity (Covert,  1974; Hidy et al.,
1974).   As relative  humidity increases,  the mass  of  water  attached  to  nitrate particles
increases and corresponding  shifts  in the  particle size distribution occur.  These effects  are
                                             10-6

-------
I    o.io
(-
z

KPT 008
w  E
Z _- 0.06
2?
<  — 0.04
in
t-
I
U    0.02
                                     I   I    T
I    I     I   I
        ,
        0.030,050.070.10   0.2  0.3   0.50.7  1.0    2.0 3.0  5.07.010.0


                        PARTICLE DIAMETER, microns


 Figure 10-3. Normalized light scattering by aerosols as a function of

particle diameter.  Computed for unit density spherical particles of

refractive index  1.5 (White and Roberts,  1977).
                            10-7

-------
especially  pronounced  at  relative  humidities  above  70%;  at  very high  relative  humidities
(90-100%),  rather  small  shifts  in  relative  humidity  may produce  pronounced changes  in  the
amounts of light-scattering from a fixed amount of nitrate aerosol.
     Even though nitrate aerosols  are suspected of occurring in the optically critical  0.1 to
1  micron  size   range,  and  even  though  light-scattering by  nitrates  may  be  significantly
augmented by relative humidity effects, the actual contributions of nitrate to haze levels  may
not be  significant  because ambient nitrate levels may be very low (see data in Chapter 8).   A
complete characterization  of  the role nitrates play in visibility degradation must wait until
high-quality data bases on nitrates are generated.
10.4  SUMMARY
     Air pollution  degrades  the  appearance of distant objects  and  reduces the range at which
they can be distinguished from the background.  These effects are manifest not only in visible
plumes, but also in large-scale, hazy air masses.  Haze and  plumes can result in the deterio-
ration  and  loss of  scenic vistas,  particularly  in areas of  the  southwestern  United  States
where  visibility  is generally good.   Under  extreme conditions reduced visual range  and con-
trast due to haze and plumes may impede air traffic.  NO- can be responsible for  a  portion of
the  brownish  coloration  observed  in  polluted air.   However,  it  should  be noted that non-
nitrate particulate matter has also been implicated in the production of a significant portion
of brownish coloration.  Under  certain circumstances,  brown plumes  may  be distinguished tens
of kilometers downwind of their sources.
     Nitrogen dioxide  in a plume acts as a blue-minus filter for transmitted light.   It tends
to  impart  a  brownish  color  to  targets,  including the  sky viewed  through the plume.   The
strength of  this filter effect  is  determined  by the amount  of NO^  concentration  along  the
sight path; i.e.,  theoretically  similar effects would be produced by a 1 kilometer-wide plume
containing 0.1  ppm  (190  ug/m)  of NO, or a 0.1 kilometer-wide plume containing 1.0 ppm (1,900
    3
ug/m )  of  NOp.   Based on  laboratory  tests  plus  very limited supporting  observations  in  the
field, the visible  threshold  for coloration produced by NO-  in the atmosphere might be  a con-
centration-distance product  of  about  0.06  ppm-km.  Empirical  observations under  a  variety  of
conditions are needed to  determine the perceptibility of N0?  in ambient air.
     Plume coloration due to N0? is modified by particulate matter,  and depends on a number of
factors such  as sun angle,  surrounding scenery,  sky  cover, viewing  angle,  human  perception
parameters, and pollutant  loading.    Suspended  particles generally scatter  in the  forward
direction, and can  thus cause a haze layer or a plume to appear bright in forward scatter (sun
in front of the observer)  and dark  in  back  scatter (sun in back of the observer) because of
the angular variation  in scattered air  light.  This  effect  can vary with  background  sky  and
objects.  Aerosol  optical  effects alone are  capable of  imparting a reddish  brown color to a
haze  layer when viewed in backward  scatter.   N0? would  increase the degree  of  coloration  in
such a  situation.   When  the sun is  in  front  of the observer,  however, light scattered  toward
him by  particles in the  plume tends  to  wash  out  the brownish light  transmitted from beyond.
                                             10-8

-------
Under these conditions, particle scattering diminishes the plume coloration.  Estimates of the
magnitude  of  this effect attributable  to  particulate nitrates are currently  hampered by the
lack of data on particulate nitrate concentrations in ambient air.
     Nitrogen  dioxide  and particulate  nitrates  may  also  contribute  to  pollutant  haze.   The
discoloration of  the  horizon  sky due to NCL  absorption  is determined by the relative concen-
trations of NCL  and  light-scattering particles.   A concentration-visual  range  product of 0.3
ppm-km N0? corresponds  to a color shift which should be detectable in a polluted layer viewed
against a  relatively  clean  sky.   At a visual  range of 100 km, typical of the rural  U.S.  great
                          3
plains, 0.003  ppm (6  (j/m )  N09 might  suffice to color the horizon  noticeably.  At  a visual
                                                          3
range of 10  km,  typical of urban  haze,  0.03  ppm (60 ug/m ) NOp might  be required  to produce
the  same  effect.   For  the reason  cited above,  no reasonable  estimate  of particulate nitrate
contribution to this  phenomenon  can currently be made.   Similarly, an  assessment of the role
of nitrate aerosols in the degradation of visual  range must await the  availability of a suffi-
cient data base on ambient particulate nitrate concentrations.
                                             10-9

-------
10.5  REFERENCES

Ahlquist, N. C. ,  and R.  J. Charlson.  Measurement of the wavelength dependence of atmospheric
     extinction due to scatter.  Atmos. Environ. 3:551-564, 1969.

Bradway,  R.  M.,  and  F.  A.  Record.   National  Assessment  of the  Urban  Particulate Problem.
     Volume II.   Particle Characterization.  EPA-450/3-76-025,  U.S.  Environmental Protection
     Agency, Research Triangle Park, NC, July 1978.

Cass, G.  R.  The  Relationship between Sulfate Air Quality and Visibility at Los Angeles.  EQL
     Memorandum No. 18, California Institute of Technology, Pasadena, CA, August 1976.

Charlson, R. J. ,  A.  P.  Waggoner, and J. F. Thielke.  Visibility protection for Class I Areas:
     The  Technical  Basis.   CEQ517714498,  Council  of  Environmental Quality,  Washington, DC,
     August 1978.

Covert,  D.  S.   A Study  of  the Relationship of Chemical  Composition  and Humidity  to  Light
     Scattering by Aerosols.  Ph.D.  Thesis, University of Washington, Seattle, WA, 1974.

Dixon,  J.  K.   Absorption  coefficient  of  nitrogen dioxide in the  visible  spectrum.   J.  Chem.
     Phys. 8:157-160, 1940.

Hardison, L. C.  Techniques for controlling  the oxides of nitrogen.   J.  Air Pollut.  Control
     Assoc.  20:377-382, 1970.

Hidy, G.  M. , B.  Appel, R. J. Charlson, W. E.  Clark, D. Covert, S.  K. Friedlander, R. Giaugue,
     S.  Heisler,  W.  W.  Ho,  J. J.  Huntzicker,  T.  Novakov,  L. W.  Richards,  R.  Ragaini, T. B.
     Smith,  G.   Sverdrup,  S.  Twiss,  A. Waggoner,  H.  H.  Wang,  J. J.  Wesolowski,  K.  T.  Whitby,
     and W.  White.  Characterization of Aerosols in California (ACHEX).  Final Report.  Volume
     IV.  Analysis and  Interpretation of Data.   ARB-R-358-74-37, State  of  California, Air
     Resources  Board, Sacramento, CA, September 1974.

Hodkinson,  J.   R.    Calculations of  colour  and visibility  in  urban atmospheres  polluted by
     gaseous N02-   Air Water Pollut. 10:137-144, 1966.

Horvath,  H. ,  and  K.   E.  Noll.  The  relationship  between atmospheric light  scattering co-
     efficient  and visibility.  Atmos. Environ.  3:543-552 1969.

Husar,  R. B. ,  N.  V.  Gillani,  J. D.  Husar, and  D. E. Patterson.  A study of long range trans-
     port from  visibility observations,  trajectory analysis, and local air pollution monitor-
     ing  data.   _In:   Air Pollution:   Proceedings of the Seventh International Technical  Meet-
     ing  on  Air  Pollution Modeling and Its Application,  North  Atlantic Treaty Organization,
     Airlie House, Virginia,  September 7-10,  1976.  N.51, North Atlantic Treaty Organization,
     Committee   on the  Challenges   to  Modern Society, Berlin,  Germany, 1976.   pp.  469-486.

Husar,  R.  B. ,   and W.  H.  White.   On the  color  of the  Los Angeles  smog.   Atmos.  Environ. 10:
     199-204, 1976.

Latimer,  D.  A., R.  W. Bergstrom, S. R. Hayes, M.-K. Liu, J.  H.  Seinfeld, G. Z. Whitten,  M. A.
     Wojcik, and  M.  J.  Hillyer.   The Development of Mathematical Models for the Prediction of
     Anthropogenic Visibility Impairment.  Volume  I.   EPA-450/3-78-110a,  U.S.  Environmental
     Protection Agency, Washington, DC, September 1978a.
                                             10-10

-------
Latimer, D.  A.,  R.  W.  Bergstrom, S. R. Hayes, M.-K.  Liu, J. H. Seinfeld, G. Z. Whitten, M. A.
     Wojcik, and  M.  J.  Hillyer.  The Development of  Mathematical Models  for the  Prediction of
     Anthropogenic  Visibility  Impairment.   Volume  II:   Appendices.   EPA-450/3-78-110b,  U.S.
     Environmental Protection Agency, Washington, DC,  September 1978b.

Latimer, D.  A.,  R.  W.  Bergstrom, S. R. Hayes, M.-K.  Liu, J. H. Seinfeld, G. Z. Whitten, M. A.
     Wojcik, and  M.  J.  Hillyer.  The Development of  Mathematical Models  for the  Prediction of
     Anthropogenic  Visibility Impairment.   Volume  III:   Case  Studies for Selected Scenarios.
     EPA-450/3-78-110c,  U.S.   Environmental  Protection  Agency,   Washington,   DC,  September,
     1978c.

Lee,  R.  E. ,  and  R.  K.  Patterson.   Size  determination  of atmospheric  phosphate,  nitrate,
     chloride,  and  ammonium  particulate  in several  urban  areas.   Atmos. Environ. 3:249-255,
     1969.

MacAdam, D.  L.   Visual  sensitivities to color  differences  in daylight.  J. Opt. Soc. Am. 32:
     247-273, 1942.

Malm,  W.   Considerations  in the measurement  of visibility.   J.  Air  Pollut.  Control   Assoc.
     29:1042-1052, 1979.

Middleton,  W.  E.  K.   Vision Through the  Atmosphere.   University  of Toronto Press,  Toronto,
     Ontario, Canada, 1952.

National Air Pollution  Control  Administration.   Air  Quality Criteria for Particulate Matter.
     AP-49,  U.S.   Department   of  Health,  Education,  and  Welfare,  Public   Health  Service,
     Washington, DC, January 1969.

Penndorf,  R. B.   Tables of the  refractive  index for standard air and  the Rayleigh scattering
     coefficient  for  the  spectral  region  between  0.2 and  20.0  mm  and  their application to
     atmospheric optics.  J. Optical Soc.  Amer.  47:176,  1957.

Robinson,  E.   Effect  on  the   physical properties  of  the  atmosphere.   I.n:   Air Pollution.
     Second  Edition.   Volume I:  Air Pollution  and  Its Effects.   A.  C.  Stern, ed. ,  Academic
     Press, Inc., New York, NY, 1968.  pp.  349-400.

Samuels, J. J. , S. Twiss, and E. W.  Wong.   Visibility, Light Scattering and Mass  Concentration
     of  Particulate  Matter.   Report of  the California Tri-City  Aerosol   Sampling  Project.
     State  of California, Air Resources Board, Sacramento, CA, July  1973.

Trijonis, J.  C., K.  Yuan, and R. B.  Husar.   Visibility in the Northeast:  Long-term Visibility
     Trends  and  Visibility/Pollutant  Relationships.   EPA-600/3-78-075,  U.S.   Environmental
     Protection Agency, Research Triangle Park,  NC,  August 1978a.

Trijonis, J.  C. , K.  Yuan, and R. B.  Husar.   Visibility in the Southwest—an Exploration  of the
     Historical  Data  Base.  EPA-600/3-78-039, U.S.   Environmental  Protection Agency,  Research
     Triangle Park, NC, April 1978b.

Ursenbach,  W. 0., A.  C.  Hill, and W. H.  Edwards.  Visibility models  for the arid  and  semi-arid
     western United  States.   Presented at  the Seventy-First  Annual  Meeting,  Air   Pollution
     Control  Association, Houston, TX, June 25-30, 1978.

Waggoner,  A.  P.,  A. J.  Vanderpol,   R.  J.  Charlson,  S.  Larsen,  L.  Granat, and  C.   Tragardh.
     Sulfate-light scattering ratio as an index of the role of sulphur  in tropospheric optics.
     Nature (London) 261:120-122, 1976.


                                             10-11

-------
Whitby, K. T. ,  and G.  M. Sverdrup.  California aerosols:  their physical and chemical  charac-
     teristics.   In:   The Character and  Origins  of Smog Aerosols:   A  Digest of Results  From
     the California Aerosol  Characterization Experiment (ACHEX).  Adv. Environ. Sci. Technol.
     9:477-525, 1980.

White, W.  H.,  and P. T. Roberts.  On the nature and origins of visibility-reducing aerosols  in
     the Los Angeles Air Basin.  Atmos. Environ. 11:803-812, 1977.
                                             10-12

-------
                                    11.   ACIDIC DEPOSITION

11.1  INTRODUCTION
     The  occurrence  of  acidic precipitation  in  many  regions of  the  United  Sates,  Canada,
northern Europe, Taiwan and Japan has become a major environmental concern.   Acidic precipita-
tion in the  Adirondack Mountains  of New York State, in the eastern Precambrian Shield area of
Canada, in southern  Norway and in southwest Sweden has been associated with the acidification
of waters in ponds, lakes and streams with a resultant disappearance of animal  and plant life.
Acidic precipitation (rain and snow), also is believed to have the potential for leaching ele-
ments  from  sensitive soils,  causing direct  and  indirect  injury to forests.   It  also  has  the
potential  for  damaging monuments  and  buildings made  of  stone, for corroding  metals  and  for
deteriorating paint.
     The  story  of acidic  precipitation  is an ever-changing one.   New  information concerning
the  phenomenon  is  forthcoming nearly  every  day.   The  sections  that  follow emphasize  the
effects of  wet deposition of  sulfur and  nitrogen oxides  and  their products  on  aquatic  and
terrestrial   ecosystems.   Dry deposition  also  plays an  important role,  but contributions  by
this process  have not  been  quantified.    Because  sulfur  and  nitrogen  oxides   are  so  closely
linked in the  formation of acidic precipitation,  no attempt  has  been  made to  limit  the dis-
cussion which follows to the  main topic of this document,  nitrogen oxides.
     Chapter 12 emphasizes the  effects  of the dry deposition of nitrogen oxides on vegetation
and ecosystems.   The  sources  and  emissions of nitrogen oxides  are discussed in Chapter 5  and
those  of  sulfur  oxides  in  Air Quality  Criteria  for Particulate  Matter and  Sulfur  Oxides.
Chapter 6 discusses  the transformation  and transport of nitrogen oxides.   Ambient air concen-
trations are discussed in Chapter 8, and the nitrogen cycle in Chapter  4.
11.1.1  Overview of the Problem
     The generally held  hypothesis  is  that sulfur  and  nitrogen compounds are  largely respon-
sible  for the  acidity of  precipitation.   The  emissions  of the sulfur  and  nitrogen compounds
involved in  acidification are attributed chiefly to the combustion of fossil fuels.  Emissions
may occur at ground level, as from automobile exhausts,  or from stacks  of 1000  feet or more in
height.  Emissions from  natural  sources  are also  involved; however, in highly industrialized
areas,  emissions from man-made sources  well exceed those from natural  sources.   In the eastern
United States the  highest emissions of sulfur oxides are  from electric  power generators using
coal, while  in  the West,  emissions of nitrogen  oxides,"chiefly from automotive sources, pre-
dominate.
     The  fate  of   sulfur  and  nitrogen  oxides,  as  well as  other pollutants emitted  into  the
atmosphere,  depends on their  dispersion,  transport, transformation and  deposition.   Sulfur  and
nitrogen  oxides  may  be  deposited  locally  or  transported long  distances  from  the  emission
sources.   Therefore,  residence time in  the atmosphere  will  be brief  if  the emissions  are
deposited  locally  or may  extend  to days  or even  weeks  if long range  transport  occurs.   The

-------
chemical form  in which emissions ultimately  reach  the receptor is determined  by  the  complex
chemical transformations that  take  place between the emission sources and the receptor.   Long
range  transport  over  distances of  hundreds  or even  thousands  of miles  allows  time for  a
greater number of chemical  transformations to occur.
     Sulfates and  nitrates are among  the products  of the chemical transformations  of sulfur
and  nitrogen  oxides.   Ozone and other  photochemical  oxidants are believed to  be  involved  in
the  chemical  processes that form them.   When sulfates and nitrates  combine  with  atmospheric
water, dissociated forms of  sulfuric (HLSO.) and nitric (HNO.) acids  result.  When  these  acids
are  brought  to  earth  in  rain  and  snow,  acidic  precipitation occurs.  Because of  long  range
transport,  acidic precipitation in a particular state or region can be the result  of emissions
from sources in  states or  regions many miles  away,  rather than from local  sources.   To  date,
however, the complex  nature  of the  chemical transformation processes  has not made  it possible
to demonstrate a direct cause and effect relationship between emissions of sulfur  and nitrogen
oxides and the acidity of precipitation.
     Acidic precipitation  is arbitrarily  defined as  precipitation with  a pH  less  than  5.6.
This value has been selected because precipitation formed in a geochemically clean  environment
would have a pH  of approximately 5.6 due  to  the combining of carbon  dioxide  in  the air  with
water  to  form  carbonic acid.   Acidity of  solutions  is determined  by the  concentration  of
hydrogen ions (H  ) present and is expressed  in  terms  of pH  units—the negative logarithm  of
the  concentration  of   hydrogen  ions.   The  pH  scale ranges from  0 to  14,  with a value  of  7
representing a neutral  solution.  Solutions with values less  than  7  are acidic, while values
greater than 7 are basic.   Because  pH is a logarithmic scale, a change of one unit represents
a tenfold change in acidity,  hence pH 3 is ten times as acidic as  pH 4.   Currently  the  acidity
of precipitation  in  the northeastern  United  States  normally ranges  from  pH 3.0 to  5.0;  in
other regions of  the  United  States  precipitation episodes with a  pH  as low as 3.0  have  been
reported.   For  comparison, the pH of  some familiar substances are:  cow's milk,  6.6;  tomato
juice, 4.3; cola (soft drink) 2.8,  and lemon juice,  2.3.
     The pH  of  precipitation  can  vary from  event  to  event,  from season to season and  from
geographical  area  to   geographical  area.   Substances  in  the  atmosphere  can  cause the pH  to
shift by making  it more acidic or more basic.   Dust and debris swept  up in  small amounts  from
the  ground  into  the   atmosphere  may  become  components  of   precipitation.    In the West  and
Midwest soil  particles tend to be more basic,  but in the eastern United States they tend  to  be
acidic.   Gaseous ammonia from  decaying organic matter makes  precipitation  more acidic,  so  in
areas  where  there   are   large  stockyards  or  other  sources  of  organic  matter,   acidic
precipitation would be more likely to occur.
     In the  eastern  United  States  sulfur  oxide  emissions  are greater than  nitrogen  oxides,
therefore,  sulfates are greater contributors  to the  formation  of acids in  precipitation  in
                                           11-2

-------
this region.  The ratio between the two emissions, however, has been decreasing.   Sulfate con-
centrations are greater in summer than in winter in the eastern United States.  In California,
however,  around some  of  the  larger  cities,  nitrates  contribute more  to  the  formation  of
acidity  in  rainfall.   In  coastal  areas sea  spray  strongly influences percipitation chemistry
by contributing  calcium,  potassium,  chlorine and  sulfates.   In  the  final  analysis, the pH of
precipitation is a measure of the relative contributions of all of these components.
     The  impact  of  acidic precipitation on lakes, streams, ponds, forests, fields and manmade
objects,  therefore,  is not the result  of  a  single,  or even  of  several  precipitation events,
but the  result  of  continued additions of  acids  or acidifying substances over time.  When did
precipitation  become  acidic?    Some   scientists   state  that  it  began  with the  industrial
revolution  and  the  burning of  large amounts of coal; others say it began in the United States
with the  introduction  of  tall  stacks in power plants in the 1950's;  other scientists disagree
completely and state that rain  has always been acidic.  In other words, no definitive answer to
the question  exists  at the present time,  nor  is  there data to  indicate with any accuracy pH
trends  in precipitation.   The pH of  rain  has  not been continuously monitored  in  the United
States for any period of time,  so no data exist.   In Scandinavia, on  the other hand, the pH of
rain has been monitored for many years, therefore a determination of  the time of origin can be
made.
     Though acidic  precipitation (wet  deposition)  is  usually emphasized,  it  is  not  the only
process by  which acids or acidifying substances are added to bodies  of water or to the land.
Dry deposition  also  occurs.  During  wet  deposition  substances such  as  sulfur  and  nitrogen
oxides  are  scavenged  by  precipitation  (rain and  snow)  and  deposited  on the surface of the
earth.    Dry deposition processes  include gravitational sedimentation of  particles, impaction
of aerosols and  the  sorption and absorption of  gases  by  objects at  the earth's  surface or by
the soil  or water.   Gases, particles and solid and liquid aerosols can be removed by both wet
and dry  deposition.  Dew,  fog and frost are  also  involved in the  deposition  processes but  do
not strictly  fall  into the category of wet  or  dry deposition.  Dry  deposition  processes are
not as well understood as wet  deposition at the  present  time, however,  all  of the  deposition
processes contribute  to the gradual  accumulation' of  acidic or acidifying  substances in the
environment.   In any   event,  percipitation  at  the   present  time  is  acidic  and has  been
associated  with  changes  in ponds,  lakes and  streams that are  considered  by  humans  to  be
detrimental  to their welfare.
     The  most  visible  changes  associated  with acidic  deposition, that is  both wet  and dry
processes, are those observed in the lakes and streams  of  the Adirondack Mountains in New York
State,  the  Pre-cambrian Shield areas of Canada  and  in the Scandinavian countries.   In these
regions the pH  of the  fresh water bodies  has  decreased,  causing changes in  animal  and plant
populations.  The most readily  observable has been the  decrease in fish  populations.
     The chemistry of  fresh  waters  is determined  primarily  by  the geological structure (soil
system and  bedrock)  of the  lake  or stream catchment  basin,  by  the  ground cover and  by land
                                           11-3

-------
use.   Near coastal  areas  (up to 100 miles)  marine  salts  also may be important in determining
the chemical  composition of the stream, river or lake.
     Sensitivity of a lake to acidification depends  on the acidity of both wet and dry deposi-
tion plus the  same  factors—the soil system of the  drainage  basin, the canopy effects of the
ground cover and the composition of the waterbed bedrock—that determine the chemical  composi-
tion of  fresh  water  bodies.   The capability,  however,  of a lake and its  drainage  basin  to
neutralize incoming  acidic substances  is  determined largely  by  the composition  of  the  bed-
rocks.
     Soft water  lakes,  those  most sensitive to  additions of acidic substances,  are usually
found  in  areas  with igneous  bedrock  which contributes  few solids  to  the  surface  waters,
whereas hard waters  contain  large concentrations  of alkaline  earths  (chiefly bicarbonates  of
calcium and  sometimes  magnesium) derived  from  limestones and calcareous  sandstones  in  the
drainage basin.  Alkalinity  is associated  with the  increased  capacity  of lakes to neutralize
or buffer  the  incoming acids.   The extent  to  which acidic precipitation  contributes  to  the
acidification process has  yet to be determined.
     The disappearance of  fish populations  from freshwater lakes  and streams is usually one  of
the most readily observable signs of lake acidification.  Death of  fish in  acidified waters has
been attributed  to  the  modification of a number of  physiological  processes  by a change in pH.
Two patterns of  pH  change have been observed.   The  first involves a sudden  short-term drop  in
pH and the second,  a gradual decrease  in  pH with time.   Sudden  short-term  drops  in  pH often
result from  a  winter thaw or the  melting  of the  snow pack in early spring  and the release  of
the acidic  constituents of  the snow into  the water.  Fish may  be killed at  pH  levels above
those normally causing death.
     A  gradual  decrease  in  pH,  particularly  below 5,  can  interfere  with  reproduction  and
spawning of  fish  until  elimination of the  population occurs.   In  some lakes, aluminum mobili-
zation in  fresh waters at a pH below 5 has resulted in  fish mortality and  appears  to be  as
important as pH.
     Although  the  disappearance of  and/or reductions  in fish populations  are usually empha-
sized as  significant results  of  lake  and  stream acidification,  changes  of  equal  or greater
importance are the  effects  on other  aquatic  organisms  ranging  from waterfowl  to  bacteria.
Organisms at all  tropic (feeding) levels in the  food web  appear  to be affected.   Species re-
duction in  number and  diversity  may occur, biomass (total  number of living  organisms  in a
given volume of  water)  may be altered and  processes such as primary production and decomposi-
tion impaired.
     Primary production and  decomposition  are the bases  of the  two major  food webs  (grazing
and detrital) within an ecosystem by which  energy  is passed along  from one organism to another
through a  series of  steps of eating and  being eaten.   Green plants, through  the  process  of
photosynthesis, are  the primary energy producers  in the grazing  web,  while bacteria  initiate
the detrital food web by  feeding on dead  organic matter.   Disruption of either  of these  two
food webs results in a decrease in the supply of minerals and nutrients, interferes with their

                                           11-4

-------
 cycling  and also reduces energy flow  within the affected ecosystems.  Acidification of lakes
 and  streams  affects both these processes when alteration  of the species composition and struc-
 ture of  the pondweed and algae  plant  communities occurs due to a slowing down in the rate of
 microbial decomposition.
      At  present there  are  no documented  observations or measurements  of changes in natural
 terrestrial  ecosystems  that can be directly attributed to acidic precipitation.  The informa-
 tion available is  an  accumulation of  the results  of a wide  variety of controlled research
 approaches  largely  in  the laboratory,  using in most  instances some form of "simulated" acidic
 rain,  frequently dilute  sulfuric  acid.  The  simulated  "acid rains"  have deposited hydrogen
 (H+),  sulfate  (SO^")  and nitrate  (NO^) ions on vegetation and have caused nicrotic lesions in
 a  wide variety  of  plants species  under  greenhouse  and  laboratory  conditions.   Such results
 must be  interpreted with caution, however,  because  the  growth and morphology of leaves under
 greenhouse conditions are often  not typical  of field  conditions.  Based on laboratory studies,
 the  sensitivity  of  plants to acidic deposition seems  to be associated with the wettability of
 leaf surfaces.  The shorter  the time  of  contact, the lower the resulting  dose  and the less
 likelihood of  injury.
      Soils  may become  gradually acidified from an  influx of hydrogen (H ) ions.   Leaching of
 the  mobilizable forms  of mineral  nutrients  may  occur. The rate of  leaching  is determined by
 the  buffering  capacity of the  soil  and the amount  and  composition  of precipitation.   Unless
 the  buffering capacity of the soil is  strong and/or the salt content of precipitation is high,
 leaching will  in time  result in acidification.   At  present  there are no studies showing this
 process has  occurred because of  acidic precipitation.
      Damage  to  monuments  and buildings made of stone, and corrosion of metals can result from
:acidic precipitation.   Because  sulfur compounds are  a dominant  component of acidic precipi -
 tation and  are deposited during dry deposition  also, the effects resulting from the two pro-
 cesses  cannot  be distinguished.   In  addition,  the   deposition of  sulfur compounds  on  stone
 surfaces provides a medium for microbial growth that  can result in deterioration.
      Human  health effects  due to the  acidification  of lakes  and rivers have been postulated.
 Fish  in  acidified water may contain toxic metals  mobilized  due to the  acidity of the water.
 Drinking water  may  contain toxic metals or  leach  lead from the pipes bringing water into the
 homes. Humans  eating contaminated  fish or drinking  contaminated water  could  become  ill.   No
 instances of these effects having occurred have been  documented.
      Several aspects  of  the acidic  precipitation problem  remain  subject to  debate  because
 existing data  are ambiguous  or  inadequate.  Important issues  include:   (1)  the rate at which
 rainfall is  becoming more acidic and the rate at which the problem is becoming geographically
 more  widespread;  (2) the  quantitative contributions of  various acids to  the  overall  acidity
 of  rainfall; (3) the  relative  extent  to  which the  acidity of rainfall  in a region depends
 on  local  emissions  of  nitrogen  and  sulfur  oxides versus emissions  transported  from distant
                                           11-5

-------
sources;  (4)  the  relative  importance  of changes  in total mass  emission rates  compared  to
changes in the  nature  of the emission patterns (ground level versus tall stacks) in contribu-
ting to regional  acidification  of precipitation; and (5) the relative contribution of wet and
dry deposition to the acidification of lakes and streams.
11.1.2  Ecosystem Dynamics
     The  emission  of sulfur  and  nitrogen oxides  into the  atmosphere,  their transformation,
transport and deposition,  either  as acidic precipitation or in dry form, as well  as  the re-
sponses of aquatic  and  terrestrial  ecosystems to acidic  deposition are all  natural phenomena
that have been  in  existence as long as humans can remember.  Environmental problems arise be-
cause  the natural  systems  are  being overloaded  by  emissions  from the  combustion  of fossil
fuels from anthropogenic sources.
     Life on the  planet  Earth depends on the movement of energy and minerals through the bio-
sphere, that  thin layer  of life surrounding  the earth.  The  living  systems  (forest, grass-
lands,  cultivated  fields,  lakes,  rivers,  estuaries  and  oceans) within  the  biosphere obtain
energy  from the  sun,  nutrients  from the earth's crust, the lithosphere, gases from the atmos-
phere and water  from  the hydrosphere.   All of  the  living systems are interdependent.   Energy
and nutrients move  from  one to another.  The  living  systems together with their physical en-
vironment, the  lithosphere,  hydrosphere  and atmosphere, make  up  the  ecosystem that  is the
planet Earth (Billings,  1978; Boughey, 1971; Odum, 1971; Smith,  1980).
     Ecosystems  are  basically energy processing  systems "whose  components  have  evolved to-
gether  over  a long period of time.  The boundaries  of the system are  determined  by  the en-
vironment, that  is, by  what forms of life can be sustained by the environmental conditions  of
a  particular  region.   Plant  and  animal populations  within the system  represent  the  objects
through which the system functions" (Smith, 1980).
     Ecosystems  are  composed  of  biotic  (living)  and  abiotic  (non-living)  components.   The
biotic component consists of:  (a) producers, green plants that capture the energy of the sun;
(b) consumers  that utilize  the  food stored  by the  producers  for their  energy;  and  (c) the
decomposers who  break down dead organic matter and convert it into inorganic compounds again.
(See Table 11-1).   The  abiotic  components are  the  soil  matrix, sediment, particulate matter,
dissolved organic matter and nutrients in aquatic systems, and dead or inactive organic matter
in terrestrial systems (See Table 11-1) (Billings, 1978; Boughey, 1971; Smith, 1980).
     Ecosystems  are  open  systems.  They  both  receive from  and  contribute to  the  environment
that  surrounds  them.   The  environment  contributes gases,  nutrients,  and energy.   Ecosystems
utilize these substances  and,  in  turn,  make their  own contributions  to the environment.  En-
ergy  flows  through the  system  unidirectionally while water, gases and  nutrients  are  usually
recycled and fed back into the system.   The functioning of ecosystems is greatly influenced by
the extent to which  the gases and nutrients are fed back into the system.  When materials are
not returned  to an ecosystem through  recycling,  they must be obtained  in  another way.   The
organismal populations are the structural elements of the ecosystem through which energy flows
and nutrients are cycled (Smith, 1980; Billings, 1978; Odum, 1971).

                                           11-6

-------
                   TABLE 11-1.   COMPOSITION OF ECOSYSTEMS*
     Component
     Description
Biotic (biological):
 Individuals

 Producers
 Consumers
 Decomposers

 Populations

 Communities

Abiotic (physical):
 Energy
 Water
 Atmosphere
 Fire
 Topography
 Geological
  strata
Plants, animals (man), and microorganisms.
 These are either producers, consumers, or
 decomposers.
Green plants.
Herbivores, carnivores.
Macroorganisms (mites, earthworms, millipedes,
 and slugs) and microorganisms (bacteria
 and fungi).
Groups of interbreeding organisms of the same
 kind, producers, consumers or decomposers,
 occupying a particular habitat.
Interacting populations linked together by
 their responses to a common environment.
Radiation, light, temperature, and heat flow.
Liquid, ice, etc.
Gases and wind.
Combustion.
Surface features.
Soil, a complex system.   Nutrients.   (Minerals)
''Adapted from:   Billings (1978)
                                      11-7

-------
     Energy from the sun is the driving force in ecosystems.   If the sun's energy were cut off
all ecosystems  would cease  to  function.   The  energy  of  the sun is captured  by  green plants
through the  process of photosynthesis  and  stored  in  plant  tissues.   This stored  energy is
passed along through  ecosystems  by a series of feeding  steps,  known as food chains, in which
organisms eat  and  are eaten.  Energy flows  through  ecosystems  in two major food  chains,  the
grazing food chain  and  the detrital food chain.  The amount of energy that passes through the
two food  chains  varies  from community to  community.   The detrital  food chain  is  dominant in
most  terrestrial  and shallow-water  ecosystems.  The  grazing food chain  may  be  dominant in
deep-water aquatic  ecosystems  (Smith,  1980).   The fundamental processes involved in these two
food  chains  are  photosynthesis,   the  capture  of energy  from  the sun  by green  plants,  and
decomposition,   the  final   dissipation of  energy and  the  reduction  of  organic  matter  into
inorganic nutrients.
     In addition  to the  flow  of  energy,  the  existence  of the living world depends upon the
circulation of nutrients  through  the ecosystems.  Both energy  and  nutrients move through the
ecosystem as organic  matter.   It  is not possible to separate one from the other.   Both influ-
ence the  abundance  of organisms,  the metabolic rate at which they live and the complexity and
structure of  the ecosystem  (Smith,  1980).  Nutrients,  unlike  energy, after  moving from the
living to the nonliving return to the living components of the ecosystem in a perpetual cycle.
It is through  the  cycling of nutrients that plants  and  animals obtain the minerals necessary
for their existence.
     The gaseous and  sedimentary  cycles  are the two basic types of nutrient or biogeochemical
cycles.    The  gaseous cycles involve  carbon,  oxygen and nitrogen.  Water,  also,  is sometimes
considered as belonging to the gaseous cycle.  In the gaseous cycles,  the main nutrient reser-
voirs  are the  atmosphere  and  the  ocean.  In the sedimentary  cycle,  to which  phosphorus
belongs,  the  soil   and  rocks of  the earth's crust  are the reservoir.   The  sulfur  cycle  is  a
combination of the two cycles because it has reservoirs in both the atmosphere and the earth's
crust.
     Nitrogen,  sulfur and  water  cycles  are  involved in acidic  deposition.   Nitrogen, through
the agency of  plants  (chiefly  legumes and blue green algae), moves from the atmosphere to the
soil and  back  (see  Figure 4-1, Chapter 4).  Human  intrusion into the nitrogen cycles include
the addition of  nitrogen  oxides  to the atmosphere and nitrates to aquatic ecosystems.  Sulfur
enters  the  atmosphere  from volcanic  eruptions, from the surface of  the ocean,  from  gases
released  in  the decomposition processes and from the  combustion of fossil  fuels  (see Figure
11-1).  Both the  nitrogen and  sulfur cycles have been overloaded by the combustion of fossil
fuels by  man.   For  these  cycles  to function, an ecosystem must possess a number of structured
relationships among its components.  By  changing the  amounts  of nitrogen  and  sulfur moving
through  the  cycles,  humans  have   perturbed  or upset  the  structured  relationships  that  have
existed  for  thousands  of  years  and  altered the  movement  of the  elements  through  the
ecosystems.   The pathways  the  elements  take through the system depend upon the interaction of
the populations  and their  relationships  to each other  in  terms of eating and  being eaten.

                                           11-8

-------
                                                                        Photochemical
                                                                         Oxidation
                                        Direct Utilization
                                       of Atmospheric SO?
                                           by Plants
  Animals in the
Grazing Food Chain
   Inorganic
    Sulfate  V
     SO4
            A	
Weathering
 of Rocks
                                        Death & Wastes
                                          O  <>
Detritus Food Chain
— Oxi
^
Bacterial . Sulfh
cation Heduction( Su
ydryl
fur
toH2S N R-SH
1 — - s
-fc-


\
jlfideX^ oxidation
L_\



^ 1
I 	
1
1
V
Er
                                                                                   Forest &
                                                                                  Grassland
                                                                                    Fires
                                                                                                SO,
                                               Spontaneous
                                                Oxidation
                                                    in
                                               Atmosphere
                                                                             Volcanic
                                                                                        -H7S
    Sulfur Compounds in
   Sediments, Fuels, Soils,
   and Sedimentary Rocks
                                                                                 Combustion
                                                                                     of
                                                                              Sulfur-Containing
                                                                                    Fuels
             Figure 11-1. The sulfur cycle (organic phase bounded by dashed line).

             Source:  Chapham (1973).
                                             11-9

-------
     Change is one  of  the basic characteristics of our environment.   Weather changes from day
to day, temperatures rise and fall, rains come and go, soils erode, volcanoes erupt, and winds
blow across  the  land.    These  are natural phenomena.  Significant environmental  changes also
result when  human  beings clear forests,  build  cities and factories, and dam  rivers.   All  of
these  environmental  changes influence  the organisms  that  live in  the ecosystems  where  the
changes are occurring (Moran et al., 1980).
     Existing studies indicate that changes occurring within ecosystems, in response to pollu-
tion or other  disturbances,  follow definite patterns  that  are  similar even in different eco-
systems.   It is, therefore,  possible to predict the basic biotic responses of an ecosystem to
disturbances such  as  caused by  environmental  stress (Garrett,  1967;  Odum,  1965;  Woodwell,
1962,  1970).   These responses to  disturbance  are  (1) removal  of sensitive  organisms  at the
species and subspecies  level  due  to differential kill;  (2)  reduction in the number of plants
and  animals  (standing  crop);   (3)  inhibition  of  growth  or reduction  in  productivity;  (4)
disruption of food  chains; (5) return to a previous state of development; and (6) modification
in the rates of nutrient cycling.
     Ecosystems  can respond to  environmental  changes   or  perturbations  only  through  the
response of the populations of organisms of which they are composed (Smith,  1980).   Species of
organisms sensitive  to  environmental  changes  are removed.  Therefore, the capacity of an eco-
system to maintain  internal  stability is determined by the ability of individual organisms to
adjust their physiology  or behavior.   The success with  which an organism copes with environ-
mental  changes  is  determined by  its  ability  to produce   reproducing  offspring.  The size and
success of  a population  depends  upon  the  collective ability  of  organisms to  reproduce and
maintain their numbers  in a particular environment.   Those organisms that adjust best contri-
bute most to future  generations because they have the greatest  number of progeny in the popu-
lation (Billings, 1978; Odum, 1971; Smith, 1980; Woodwell, 1962, 1970).
     The capacity of organisms  to withstand injury  from  weather  extremes,  pesticides,  acidic
deposition or polluted air follows the principle of limiting factors  (Billings, 1978; Moran et
al., 1980; Odum, 1971;  Smith 1980).  According to this principle,  for each physical factor in
the environment  there  exists for  each organism  a minimum and a maximum limit beyond which no
members of a particular species can survive.    Either too much  or too little of a factor such
as  heat,  light,  water, or minerals  (even  though they are necessary  for  life)  can jeopardize
the survival of  an  individual  and  in extreme  cases  a species (Billings, 1978; Boughey, 1971;
Moran et al.,  1980;  Odum, 1971; Smith,  1980).   The range of tolerance (see Figure 11-2) of an
organism may  be  broad  for one factor  and  narrow  for another.   The  tolerance  limit for each
species is determined  by its genetic makeup and  varies  from species to species for the same
reason.  The range  of  tolerance also varies depending on the age, stage of  growth  or  growth
form of  an organism.   Limiting factors  are,  therefore, factors which, when  scarce or over-
abundant, limit  the  growth,  reproduction and/or distribution of an  organism (Billings, 1978;
Boughey,  1971; Moran et al., 1980; Odum, 1971; Smith, 1980).  The increasing acidity of water
in lakes and streams is such a factor.

                                           11-10

-------
  ZONE OF
INTOLERANCE
               IOWER LIMITS
               OF TOLERANCt
               ZONE OF
            PHYSIOLOGICAL
               STRESS
TOLERANCE RANGE
RANGE OF OPTIMUM
   UWEH LIMITS
   OFTOLER«»C[
   ZONE OF
PHYSIOLOGICAL
   STRESS
                                           ZONE OF
                                         INTOLERANCE
              ORGANISMS
             INFREQUENT
ORGANISMS
  ABSENT
                                        GREATEST
                                       ABUNDANCE
                             ORGANISMS
                             INFREQUENT
                                          ORGANISMS
                                           ABSENT
   LOW«-
   -GRADIENT-
               ->HIGH
                            Figure 11-2.  Law of tolerance.
                            Source:   Adapted from Smith  (1980).
                                          11-11

-------
     Organisms can exist only within their range of tolerance.   Some populations of organisms,
annual plants,  insects, and  mice,  for  example,  respond rapidly.   They increase  in  numbers
under favorable conditions  and  decline  rapidly when conditions  are  unfavorable.   Populations
of  other  organisms,  such  as trees  and wolves,  fluctuate  less  in  response to  favorable  or
unfavorable conditions.   Ecosystems that  contain both types  of populations are more stable
bacause they  are  able to absorb changes and  still  persist  because the  structure of  the  eco-
system permits it to persist even though populations within  it fluctuate widely  in response to
environmental   changes  (Moiling,  1973;   Smith,  1980).  Other  ecosystems are  resistant;  their
structure enables  them to  resist  changes.  Typically,  most resistant  ecosystems  have  large
living components,  trees  for example,  and store nutrients and energy in the standing biomass.
Such resistant systems,  such as forests, once  highly  disturbed  are  very slow in returning to
their original state (Smith, 1980).
     Aquatic ecosystems which lack  components in which energy and nutrients may be stored for
long  periods  of  time usually are not  very resistant to environmental  changes  (Smith, 1980).
For example, an influx of pollutants such as effluents  from  sewage disrupts the  system because
more nutrients enter  the  system than it can handle.  However,  since the nutrients are not re-
tained or recycled  within  the system it returns  to its  original state  in  a relatively  short
time after the perturbation is removed.
     No barriers  exist between  the various environmental  factors  or  between  an organism or
biotic community  and  its  environment.   Because an  ecosystem  is  a complex of interacting com-
ponents,  if one  factor  is  changed,  almost all  will  change  eventually.   "The ecosystem reacts
as a whole.   It  is  practically   impossible to  wall  off a single  factor  or  organism in nature
and control it at will  without  affecting the rest of the ecosystem.   Any change no matter how
small is reflected  in some way  throughout the ecosystem:   no 'walls'  have yet been discovered
that prevent these interactions  from taking place" (Billings, 1978).
     Continued or severe  perturbation  of an ecosystem can  overcome  its resistance or prevent
its recovery with the result that the original ecosystem will be replaced by a new system.  In
the Adirondack Mountains of  New York  State,  in  eastern Canada and parts  of Scandinavia the
original  aquatic  ecosystems have been  and are  continuing  to be replaced  by ecosystems  dif-
ferent from the  original   due  to  acidification  of the  aquatic habitat.   Forest  ecosystems
appear to   be more   resistant  because,  thus  far,  changes  due  to  stress from  acidifying
substances have not  been  detected.   The sections that follow  discuss  the response of aquatic
and  terrestrial  ecosystems  to   stressing  or  perturbation  by  acidic  deposition.   Sulfur and
nitrogen  oxide emissions,  their  transformation,  transport   and  deposition  in  acidic  form is
elucidated in the context of the ecosystem processes that were discussed above.
11.2  CAUSES OF ACIDIC PRECIPITATION
11.2.1  Emissions of Nitrogen and Sulfur Oxides
     The  generally held hypothesis is that nitrogen and sulfur compounds are largely responsi-
ble for  the acidity  of precipitation  (Bolin  et  al.,  1972; Likens and  Borman,  1974;  Likens,

                                           11-12

-------
1976;  Smith,  1872).  The  emissions  of  the nitrogen  and  sulfur  compounds  involved in  the
acidification are attributed  chiefly to the combustion of  fossil  fuels.   Natural sources can
also  be  involved;  however,   in  highly  industrialized  areas  emissions from  manmade sources
usually exceed those from natural sources (see Chapter 5).
     Since 1900  there  has been a nearly  exponential  increase in the consumption  of  gas,  and
oil in the United  States (see Figure  11-3).   Although  the total consumption  of  coal  has  not
increased greatly since  about 1925,  the consumption of oil and gas has continued to rise pre-
cipitously,  thus overshadowing  coal  as  the dominant  fuel  source during  the past  50  years
(Hubbert, 1976).  Within this overall  increase  in fossil-fuel use, however,  there  have been
shifts in the pattern  of consumption.   Whereas a considerable proportion of coal was used for
transportation and heating, oil and gas have since taken over these functions, and now coal  is
predominantly devoted  to electric power  generation (Figure  11-4).   In  fact,  electric  power
generation is the primary factor accounting for an absolute increase in coal consumption over
the past two  decades.   (The  decline in coal use  in the 1930s was  due to the general  economic
depression,  and the  decline in the 1950s was due to the availability of relatively inexpensive
oil  and  gas.)    Approximately  550  MM  tons   (Robinson,  1978)  were  used  annually  during
1918-1928 compared  to  672 MM tons during  1979  (Hamilton, 1980).   There was,  however,  a sea-
sonal shift in  the  pattern of coal  consumption.   Summer  coal  consumption has increased since
I960, while winter  consumption  has  decreased due  to  increased summer usage  by the  electric
utilities.
     These changes  in  the pattern of fuel use  have been accompanied by changes in the pattern
of pollutant emissions.  Figure 11-5A and 11-5B illustrate the rise since 1940 in emissions  of
sulfur and  nitrogen oxides,   the  primary  gaseous  pollutants resulting  from  the  combustion  of
fossil fuels.   Although  there has been a net increase in both categories, the more consistent
rise  has been  in emissions of nitrogen oxides.   Almost all (93 percent) emissions  of sulfur
oxides in the United  States  arise  from stationary point  sources,  principally industrial  and
power plant  stacks.   Nitrogen oxide pollutants,  on  the  other hand, originate  about equally
from  transportation  (mobile)  sources  and  from  stationary sources, which include  not only
industrial  and  power  plants, but  residential and institutional   heating  equipment  as well
(Office of Air  Quality Planning and Standards, 1978).   (see Tables 5-2 and  5-3,  Chapter  5.)
     The geographic  distributions of sources of the gaseous precursors of acidic precipitation
are depicted in  Figures  11-6  and 11-7.  Clearly,  the dominant sources of sulfur oxides in the
United States are in  the eastern half of the country,  particularly the  northeastern quadrant.
Major nitrogen  oxide  sources  also show a  tendency  to  be concentrated  somewhat  in the north-
eastern quadrant of  the country.
     Chapter 5,   Section  5.2.2 should be consulted  for  a  more detailed account of the sources
and emissions  of nitrogen oxides.
11.2.2  Transport of Nitrogen and Sulfur Oxides
     Among the factors  influencing  the formation as well  as the location where acidic deposi-
tion occurs  is  the  long-range transport of nitrogen and sulfur oxides.   Neither the gases nor

                                           11-13

-------
                                                         2050
Figure 11-3. Historical patterns of fossil fuel consumption in the
United States (adapted from Hubbert, 1976).
                           11-14

-------

z
o
I-
o.
5
D

O
o

o
CJ
>
_l
DC
LU
800


700


600


500


400


300


200


100


  0
                         I      I
                                                   I     I
                   TOTAL
                                         - OTHER  _


                                         -OVENCOKE




                                          ELECTRIC

                                          UTILITIES
RES. &COMM.
    HEATING

 RAILROADS
  1900   10    20    30    40   50
                             YEAR
                              60
                                             70   80   90  2000
Figure 11-4. Forms of coal usage in the United States. Electric
  power generation is currently the primary user of coal. (Data
  from U.S. Bureau of Mines, Minerals Yearbooks 1933-1974)
                          11-15

-------
V)
in
t/i

i
IU
in

O
UJ

 x

O
    35
    30
    20
    15
2   io
      1940
    35




    30
4A
c
O

.S   25
*-




S   20
    15
    10
     0

     1940
                        TRANSPORTATION
1950
 1960


YEAR
1970
1980
               T
TOTAL
         TRANSPORTATION



               I	I
1950
 1960


YEAR
1970
                                                           1980
   Figure 11-5a. Trends in emissions of sulfur dioxides.


   Figure 11-5b. Trends in emissions of nitrogen oxides.


   Source:  Office of Air Quality Planning and Standards

   (1978).
                                11-16

-------
         KEY
EMISSION  DENSITY, tons/mi"2

D«

    5~10
20-50


>50
r?l 10-20
                Figure 11-6. Characterization of U.S. SOX emissions density by state (U.S. Dept. of Energy, 1981).
                (Roman numerals indicate EPA Regions.)

-------
oo
         EMISSION  DENSITY, tons/mi'
                             20-50

                             >30
                          Figure 11-7. Characterization of U.S. NOX emissions density by state (U.S. Dept. of Energy, 1981).
                          (Roman numerals indicate EPA Regions.)

-------
their transformation products always remain near the sources from which they have been emitted.
They may be  transported  for long distances downwind (Altshuller and McBean, 1979; CogbilT and
Likens, 1974; Pack et: al. ,  1978).
     The geographic  picture of  the problem of  acidic precipitation in North  America  can be
better understood in  the  light of some information on prevailing wind patterns.  Winds  trans-
port the  precursors of acidic precipitation from  their  points of origin  to  areas  where the
acidified rain and  snow  eventually fall.   Prevailing  winds  in  the eastern United States tend
to be from the west and southwest.  Atmospheric pollutants, therefore, are carried in a  gener-
ally northeasterly  direction.   Thus,  pollution  originating in  the Ohio  River  valley  can be
carried toward the  New England states.  Seasonal meteorological patterns,  however, can  modify
the direction of  windflow,  particularly in the summer.  The Maritime Tropical  air masses from
the Gulf of Mexico that occur in late summer have the greatest potential for the formation and
transport  of high  concentrations  of  sulfate  into the  northeastern  United States  and  into
eastern Canada (Altshuller and McBean,  1969).
     Cogbill  and  Likens (1974)  associated acidic rainfall in central  New  York during 1972-73
with high altitude  air masses transported into the region from the Midwest.  They stated that
the NO  and  S02  that is involved in acidic rain formation may be transported distances  of 300
to 1500 km.   Reports  by  Miller et  al., (1978)  Wolff et  al.  , (1979)  and Galvin et al.  (1978)
all support  the  concept  that the trajectories of  the  air masses which come from the Midwest
carry sulfur and nitrogen compounds which  acidify precipitation in New York State.
     A significant though disputed factor  in this transport picture is the  height at which the
pollutants are emitted.  Industrial  and power plant smokestacks emit their effluents into the
atmosphere at  higher elevations than  do  motor  vehicles or most space  heating  equipment.   In
fact, there  has  been  a trend since the 1960s toward building higher stacks as  a means of dis-
persing pollutants  and thereby reducing  pollutant concentrations in  the vicinity  of  power
plants, smelters,  and similar  sources (Grennard and  Ross,  1974).  The result  has  been that
sulfur and nitrogen  oxides  are carried by prevailing  winds  for long distances and allowed to
diffuse  over  greater  areas  through  the  atmosphere (See Figure  11-8.).   Concomitantly,
long-range transport  allows greater time  for chemical reactions  to convert  these  pollutant
gases  into particulate forms  which are more  easily  removed by  wet processes  (Eliassen and
Saltbones,  1975;  Prahm et   al.,  1976; Smith  and  Jeffrey,  1975).   Chapter 6  discusses  the
chemical  transformations and wet  and  dry deposition  as  well   as  transport and  diffusion of
nitrogen oxides  in  the atmosphere.  Sulfates  and  nitrates combine with atmospheric  water to
form dissociated  forms of  nitric  (HN03)  and  sulfuric (H2S04) acids.   These  acids  are  con-
sidered to be the main components of acidic precipitation.
     The mechanisms  of these  chemical  reactions are  quite  complex  and  depend  on a host of
variables  ranging  from physical  properties  of the  pollutants  to weather  conditions and the
presence of  catalytic  or interacting agents (Fisher,  1978).   Although  these processes  of at-
mospheric  chemistry are not well  understood,  it does  appear that  the long-range transport of
                                           11-19

-------
      PREVAILING WINDS
ro
o
                                                          DRY DEPOSITION
                                                    (ATMOSPHERIC CHEMICAL REACTIONS


                                                          iAND TRANSFORMATIONS^
                          Figure 11-8.  The transport and deposition of atmospheric pollutants, particularly oxides of sulfur and

                          nitrogen, that contribute to acidic precipitation.



                          Source: Modified from U.S. EPA (1979).

-------
 sulfur  compounds  can cover 1000 to  2000  km  over three  to  five days  (Pack  et  al. ,  1978).  Thus,
 the  impact of sulfur pollutants  in the  form of acidic precipitation  may be far removed from
 their  points of  origin.   It  is  not yet clear whether the  atmospheric transport of  nitrogen
 oxide  pollutants  is comparable to  that  of  sulfur compounds, (Pack,  1978)  but  in  the northeast
 nitrates  are currently thought to  contribute 15 to 30 percent of the  acidity  of  polluted pre-
 cipitation.   This figure  has  increased  over  the  past few years and  is  expected to  increase
 still  further in  the future  (National  Research Council, 1978).
 11.2.3  Formation
     Precipitation  is that portion  of  the global water cycle by which  water  vapor from the at-
 mosphere  is converted  to  rain or  snow  and  then  is deposited on  the earth  surfaces (Smith,
 1980).  Water  moves into the  atmosphere by evaporation and transpiration  (water  vapor lost by
 vegetation).   Once  it  reaches the  atmosphere,  the water vapor  is cooled,  then condenses on
 solid  particles and soon reaches  equilibrium with atmospheric gases.   One  of the  gases is car-
 bon  dioxide.  As  carbon dioxode dissolves in water, carbonic acid (hLCO,)  is formed.  Carbonic
 acid is a weak acid and in  distilled water only dissociates slightly, yielding  hydrogen ions
 and  bicarbonate  ions  (HC03 ).   When  in  equilibrium with  normal atmospheric  concentrations and
 pressures  of carbon dioxide,  the pH of  rain and snow  is  approximately (Likens et al., 1979).
     The  pH of  precipitation  may vary and  become  more basic or more  acidic depending on sub-
 stances in the  atmosphere.   Dust and  debris may be swept from the  ground  in small amounts and
 into the  atmosphere  where  it can become  a component of  rain.   Soil particles are usually
                                                                                2+
 slightly  basic in distilled water and  release positive ions, such as calcium (Ca  ), magnesium
   2+                +                   +
 (Mg  ), potassium (K ), and  sodium  (Na )  into  solution.  Bicarbonate usually is  the corre-
 sponding  negative ion.   Decaying organic matter adds  gaseous  ammonia  to  the  atmosphere.  Am-
 monia  gas  in rain or snow forms ammonium ions (NH.  ) and  tends to increase the pH.  In coastal
iareas  sea  spray  plays  a strong  role in the chemistry of  precipitation.   The important ions
 entering  into precipitation—sodium,  magnesium,  calcium, potassium,  and the anions chloride
   _                  o-
 (Cl  )  and sulfate (S04  )--are also those  most  abundant  in ocean water  (Likens, 1976; Likens
 et al., 1979).
     Gases,  in  addition to  C02,  which enter precipitation, are  sulfur dioxide ($02) and the
 nitrogen  oxides  (NO ).   Some  sulfur gases  originate  from natural  sources,  e.g.  volcanoes and
 swamps.   Others  originate  from industrial  emissions.  In the wet atmosphere,  both SOp and hLS
 can  be oxidized  to sulfuric acid.   Nitrogen oxides in the atmosphere are converted to nitric
 acid (Likens,  1976;  Likens et al. ,  1979).   Strong  acids  dissociate  completely  in dilute aque-
 ous  solutions  and lower the pH to  less  than 5.6.  Acidic precipitation has  been  considered by
 many scientists to be rain or  snow  with  a pH below  5.6. (Galloway and  Cowling, 1978; Likens et
 al., 1979;  Wood,  1975).
     Additional acidic  or  potentially acidifying substances present in both wet  and dry depo-
 sition  are sulfur trioxide (S0,~),  sulfate S0.~),  nitric oxide (NO),  nitrogen dioxide (NO,),
                             -                 *
 nitrite (NOp ),  nitrate (NO, ),  ammonium (NH. ), chlorine  (Cl  )  hydrochloric acid (HC1), and
 Brdnsted  acids [e.g., dissolved iron (Fe) and ammonium (NH^ )] (Whelpdale, 1979).

                                            11-21

-------
     The amounts of the various substances in the atmosphere originating from seawater,  desert
sands, volcanic islands, or  vegetated  land influence the chemistry  of  natural  precipitation.
In regions  with calcareous  soils,  calcium and  bicarbonate may enter  precipitation as  dust,
subsequently increasing the pH of rain  or snow to 6.0 or above (Likens et al.,  1979).
11.2.3.1  Composition and pH of Precipitation—Sulfur  and  nitrogen compounds are  chiefly  re-
sponsible for the acidity of precipitation.   Continuous measurement of pH in  rain by Likens  et
al.,   (1972)  for  the  Hubbard Brook  Experimental  Forest in Hew Hampshire from 1964 to  1971
indicated the precipitation was acid with an annual  weighted average pH  range of 4.03 to 4.19.
(A weighted average takes  into account the amount  of  rain  as well as its composition.)  Cog-
bill   and  Likens (1974) using precipitation  from  the Ithaca area,  and  Hubbard  Brook reported
that  their analysis of  precipitation which consistently had a pH of less than 4.4 showed that
65 percent of  the  acidity  was due to  H-SO,,  30  percent to HMO,,  and  less  than 5 percent was
due to HC1.   Hendry  (1977)  found that  sulfate contributed  69 percent, nitrate 23 percent,  and
chloride  8  percent  of the  free  acidity  in  rainfall  at Gainesville,  Florida, during  1976.
     In 1976,  Likens  (1976)  reported  that the  continued  monitoring of  precipitation  at  the
Hubbard Brook  Forest  through 1974 indicated the  mean annual pH for the  years 1964-1974  ranged
from   4.03 to  4.21.   No statistically  significant trend  was noted; however,  pH  values  of  2.1
and 3.0 were observed for individual  storms at various locations.   The increased deposition  of
hydrogen ion was  due  to an increase in nitric acid  in the  precipitation (rain and snow) fall-
ing there.  This  change in the composition of acidic  precipitation suggests that the  sources
of nitrogen oxide emissions increased while those for sulfur oxides remained  constant.
     The acidity of precipitation is a reflection of the free hydrogen  ions  in  precipitation.
The contribution of sulfate  and nitrate anions has  changed with  time,  and analysis indicates
that  the  nitrate  anion  makes up an ever-increasing  fraction of the total negative ion  equiva-
lents.  Following the reasoning of Granat (1972),  Likens et  al. (1976) found  [assuming  2H  per
  2-                           +           2-
SO.  ion  as  in H?SO.  or one H  ion per SO.  as in (NH.-..SO.] that the contribution of  sulfate
to acidity declined from 83 to 66 percent of the  total  acidity between 1964 to 1974 at  Hubbard
Brook, and the contribution of nitrate  increased  from 15 to  30 percent of the total during the
same  period.   Furthermore,  increased annual  input' of H  was closely correlated with increased
input of nitrate,  but there was little  correlation between  H  input and sulfate  input.
     Data for  nitrate,  ammonium,  and sulfate in  rain  at Ithaca and Geneva,  New York,  consti-
tute  the  longest  record of precipitation chemistry  in the  United States (Likens, 1972).   Data
are available from 1915 to the present, but long  gaps exist  in the  measurements, especially at
the Geneva  site.   Figures  11-9 (A)  to  (C)  show  that marked changes in  composition have  oc-
curred at Ithaca:  a gradual decline in  ammonium,  an  increase in nitrate beginning around 1945,
and a marked decrease in sulfate starting between 1945 and 1950.  Early data  for Ithaca  showed
higher concentrations of sulfate in winter than in summer,  presumably because of greater local
burning of coal  in  winter.   Data for 1971 showed the reverse trend, however, with nearly half
the annual  sulfate  input occurring during the months  of June  to  August.  Likens  (1972) con-
cluded that, despite deficiencies in the historical  data and questions

                                           11-22

-------
Z
01


UJ
K
<

t-
i
                I
                        I   I   I   I   I   I   I
              1920   1930  1940  1950   1960


                           YEAR
                                           1970
          0.7

          0.6


          0.5


          0.4


          0.3


          0.2


          0.1

           0
J	I
                  I   I   I   I
I   I   I
              1920  1930  1940  1950  1960  1970


                           YEAR
                                                     4
                                                     Z
                                      —
                                      =

                                      Z
                                              1920  1930  1940  1950  1960   1970


                                                          YEAR
0.6

0.5


0.4


0.3


0.2


0.1

 0
I
J	I
                                                                      J	I
                                                 1968   1970  1972  1974


                                                       YEAR
        SOURCE: (A), (B), and (C) modified from Likens (1972); (D) modified from Likens (1976).


 Figure  11-9.  Trends in mean annual concentrations of sulfate, ammonia, and nitrate in precipitation.
(A), (B), and (C) present long-term data for Ithaca, New York;  (D) presents data for eight years averaged
over eight sites in New York and one in Pennsylvania. One point in (A), for 1946-47, is believed to be an
anomaly (see Likens, 1972, for discussion).
                                              11-23

-------
concerning their  reliability,  the  trends  are  real  and can  be  explained by  changes  in fuel
consumption patterns,  i.e.,  natural  gas began to replace  coal  for home heating near the time
of  the  shifts in  precipitation  chemistry.   On  the basis of United  States  Geological  Survey
data for  nine  stations,  Likens (1976)  reported  a sharp increase in nitrate concentrations in
New York state during the past decade [Figure 11-9 (D)].
     Galvin and Cline (1978) sampled the snow in a wilderness area of northern New York State.
Analysis  of  the  samples  by ion chromatography  indicated that only  nitrate  and  sulfate were
present in appreciable quantities with the concentration of nitrate being larger than sulfate.
The absence of chloride in the samples suggests that the source of the nitrate and sulfate was
inland.
     Data for eastern North America indicate a roughly three-fold increase in nitrate in rain-
fall since  1955,  whereas  sulfate  in rain  has  roughly doubled in this  period.   According to
Nisbet  (1975),  sulfate/nitrate  ratios   in  rainfall  averaged about  4  in the  eastern  United
States  in 1955-1956,  but the average ratio had fallen to about 3 in 1972-1973.  Nisbet calcu-
lated that the fraction of H  deposition attributable to nitrate rose from 19 percent in 1955-
1956 to 24 percent in 1972-1973, while the deposition attributable to H2S04 decreased from 80
to 73 percent.
                                          2-      +
     Lindberg et al.  (1979) noted  that SO,  and  H   were by  far the  dominant constituents of
precipitation at the  Walker Branch Watershed,  Tennessee.  Comparison with  the annual  average
concentration of major  elements  in rain at the Walker Branch Watershed on an equivalent basis
indicated that H  constitutes approximately 50 percent of the cationic strength and trace ele-
ments account  for  only  0.2 percent.  Sulfate constituted approximately 65 percent of the ani-
onic strength  and  on  an equivalent basis was  3.5 times more concentrated than NO,,  the next
most  abundant anion.    The incident  precipitation  for  the 2-year  (1976-1977) period  was
described as  "a dilute  mineral acid solution", primarily H-SO,,  at a pH approximating 4.2 and
containing relatively minor  amounts of  various trace salts  (Lindberg et  al., 1979).   In
Florida, Hendry (1977)  and Hendry  and  Brezonik  (1980)  found that  sulfate contributed 69 per-
cent,  nitrate 23  percent,  and  chloride  8  percent  of  the  free  acidity  in   rainfall  at
Gainesville,  Florida,  during 1976.
                                        2-
     Based on most reports, sulfate (SO, ) appears  to be the predominant anion in acidic pre-
cipitation in  the  Eastern  United  States.   In  the west  in California,  however,  nitrate (NO,)
seems to  predominate.    Liljestrand  and Morgan  (1978) reported that  their analyses  of  acidic
rainfall collected from  February 1976 to September  1977 in the Pasedena, CA, area showed that
the  volume-weighted  mean pH was 4.0, with  nitric  acid being 32 percent more  important as  a
source of acidity  than  sulfuric  acid.  The  major cations  present  were H , NH.,  K ,  Ca   and
  2+                                 -    -       2-
Mg   while  the major  anions  were  Cl ,  NO,  and  SO.  .   McColl and Bush  (1978)  also  noted the
strong influence of nitrate on rain  in the  Berkeley,  CA,  region.   However,  they note that in
                                                             2-
bulk precipitation (wet  plus  dry fall-out) that sulfate (SO. )  constituted  50 percent of the
total anions.
                                           11-24

-------
     Nearly all  of  the nitrate in rainfall  is  formed in the atmosphere  from  NO  .   Little is
derived  from wind  erosion  of nitrate salts in soils.   Similarly, nearly all of the sulfate in
rainfall  is  formed in the atmosphere  from S02 (National Research Council,  1978).   Thus,  all
atmospherically  derived  nitrate  and  sulfate contribute to the acidification of precipitation,
since H  is associated stoichiometrically with the formation of each.   A second stoichiometric
process  that  affects  the  acidity of rain  is  the reaction  of nitric and  sulfuric  acids  with
ammonia  or other alkaline  substances (e.g., dust particles) in the atmosphere to form neutral
nitrate  and sulfate aerosols.   To the extent  that  such  neutralization  occurs, the acidity of
precipitation will be  reduced  (National  Research Council, 1978).  However,  since much of the
ammonium ion reaching  soil  is  converted to  nitrate,  these  neutral  salts still have an acidi-
fying effect on the soil.
11.2.3.2   Seasonal  Variations  in Nitrates  and  Sulfates—Seasonal  fluctuations  in composition
as well as pH of rainfall have been reported by many workers.  In addition, the composition of
rainfall and pH  fluctuates  from event to  event,  from locality to locality, and from storm to
storm.
                  2-       +
     In  general  SO.   and H  concentrations in precipitation  in  the  eastern United States are
higher  in the  summer  than  in the winter.   Wolff  et al.  (1979)  found this  to be true for the
New York Metropolitan  Area.   Hornbeck et al. (1977) and Miller et al.  (1978) both stated  that
a summer maximum for  sulfate was associated with an increase in hydrogen ion concentration in
upstate  New York,  the  Hubbard  Brook Experimental Forest  in  New Hampshire, and in portions of
Pennsylvania.   Pack (1978) using data (1977) from the four  original  MAP3S (Multistate Atmos-
pheric  Power  Production  Pollution  Study)  precipitation   chemistry  networks,  plotted   the
weighted monthly sulfate ion  concentrations  (Figure 11-10).  Maximum  sulfate concentrations
occurred  from  June through  August.   Lindberg  et al. (1979)  studying  wetfall deposition  of
                                                                         2-      +
sulfate  in the Walker  Branch Watershed,  also noted summer maxima for  SO.   and H .   Using the
same MAP3S  data  as did  Pack,  they  plotted weighted  mean  concentrations of  sulfate  in  rain
collected  from   November  1976  through  November  1977.   The  concentrations  at Walker  Branch
Watershed, Tennessee,  are lower than all  of the stations  except remote Whiteface Mountain,  New
York.    The  regional  nature  of  the wet  deposition  of sulfate  is apparent.   Reasons  for  the
existence of the  high  summer maxima of sulfate for the eastern United States are discussed in
some detail  in  Chapter 5, Section 5.3.4.
     Seasonal  variations of  nitrogen  compounds and of pH in  precipitation have been reported
by  several  workers,  but no  simple  trends  are  apparent  (see U.S.  Environmental  Protection
Agency  Air Quality  Criteria for  Particulate Matter  and Sulfur Oxides, 1981).   Hoeft  et  al.
(1972)  found relatively  constant  levels  of nitrate  in  rain and snow collected  in Wisconsin
throughout the year, but deposition  of ammonia and organic  nitrogen  was lowest in winter and
highest  in  spring,  perhaps  because  of the  thawing  of  frozen  animal  wastes.   Haines  (1976)
reported large  random  variations, but relatively small seasonal variations, for nitrogen forms
in wet-only precipitation at Sapelo  Island, Georgia;  nitrogen concentrations were lowest  dur-
ing the  rainy  months   of July  and  September.   The  highest nitrogen loadings  occurred  during

                                           11-25

-------
Figure 11-10. Comparison of weighted mean monthly concentrations of sulfate
in incident precipitation collected in Walker Branch Watershed, Tenn.  (WBW)
and four MAP3S precipitation chemistry monitoring stations in New York,
Pennsylvania, and Virginia (Lindberg et al., 1979).
                                11-26

-------
July  and  were  associated with the lowest  range  in pH, 4.2-4.8.  Hendry (1977) and Hendry and
Brezonik  (1980)  found  relatively smooth seasonal trends in ammonia and nitrate concentrations
in both wet-only and bulk collections (wet- and dryfall) at Gainesville, Florida, with lowest
concentrations in winter (Figure 11-11).   In addition, the pH of the bulk precipitation showed
no seasonal trend.  Wet-only collections,  however, showed the lowest pH value (4.0) during the
spring and  summer.   This historical  record suggests there has been an increase in the concen-
tration of  inorganic nitrogen in Florida over the past 20 years.
      Scavenging  by  rainfall  produces large changes  in atmospheric  contaminant concentrations
during a  given rainfall  event.   The decline  in  constituent  levels  is usually rapid, at least
in  localized  convective  showers,  and  low,  steady-state  concentrations are  usually reached
within the  first half hour of a rain event.
      Major  ions   [chloride  (Cl  ) and  sulfate (SO.")],  inorganic  forms  of  nitrogen  [nitrate
(N03  )  and ammonium  (NH.  )],  total  phosphorus  and  pH  were  measured  in rain  collected  in
5-minute  segments  within three  individual rainstorms.   Initially,  rapid decreases  were  ob-
served for  nitrate  and  ammonium and total  phosphorus.   There was also a decrease  in pH  from
4.65  to   4.4.   Steady  state  concentrations  were  reached  in  10 minutes.   Two  other  storms
sampled in  the  same manner  showed  similar but less  defined patterns (Hendrey  and Brezonik,
1980).
     Wolff  et  al.  (1979) examined  spatial meteorological and seasonal factors associated with
the pH  of precipitation in the  New  York Metropolitan Area.   Seventy-two  events  were studied
rom 1975  through 1977.   There  was  some  site-to-site variability among the  eight  sites  they
studied in  the Manhattan area (Table 11-2).  They  also  noted that the pH varied according to
storm type  (Table  11-3).   Storms with a continental origin have a lower  pH than storms  origi-
nating over the  ocean.   The  storms with  trajectories from  the  south and  southwest had  the
lowest pH's, while  those from the north and  east  had the highest pH's  (Wolff  et al.,  1979).
     The  mean  pH of precipitation falling  on the  New York Metropolitan Area  during  a  2-year
(1975 to  1977) study was 4.28;  however, a pronounced seasonal  variation was observed (Figure
11-12).   The minimum pH at all  sites except Manhattan occurred during July to September,  while
the maximum occurred during October to December,   the minimum pH in  Manhattan, however,  occur-
red January to March and then gradually increased through the year.   The  lowest pH of 4.12  for
the New York  Metropolitan area  occurred  during the summer  months  (Wolff et  al.,  1979).   In
general,   the pH  of  rain  is usually  lower  in  the summer than in  the  winter  and is associated
with the high summertime sulfate concentrations.   In addition, the lowest pH's were associated
with  cold  fronts  and air mass type  precipitation  events.  These  events  occur more frequently
during the  summer months.   The  lower pH's  also occurred on westerly or  southwesterly  winds
(Wolff et  al., 1979).
     Seasonal   variations  in  pH  measured  at  several  sites  in  New  York  State 70  km  (45  mi.)
apart demonstrated a significant difference between seasons  (Winter had  an average pH of 4.2;
summer,  3.9.)  but no significant  difference between  sites.   In New  Hampshire,  however,  six
                                           11-27

-------
     4.80
     4.60
1.   4.40
     4.20
     0.40
                                                        I    I
            J	I
                                               I	I
                                               MAM
O
     0.30
cc £
u
O
u
     0.20
0.10
            JASONDJFMAM.J

            	1976	*4+	1977
                                  MONTH


  Figure 11-11. Seasonal variations in pH (A) and ammonium and
  nitrate concentrations (B) in wet-only precipitation at Gainesville,
  Florida.  Values are monthly volume-weighted averages of levels
  in rain from individual storms  (Hendry, 1977).
                           11-28

-------
        TABLE 11-2.   MEAN pH VALUES IN THE NEW YORK METROPOLITAN
                             AREA (1975-1977)
       Site            Mean pH        SD    No.  obsd         Range
Caldwell, N.J.
Piscataway, N.J.
Cranford, N.J.
Bronx, N.Y.
Manhattan, N.Y.
High Point, N.J.
Queens, N.Y.
Port Chester, N.Y.
All sites
4.32
4.25
4.34
4.31
4.29
4.25
4.63
4.60
4.28
0.26
0.36
0.34
0.37
0.25
0.30
0.35
0.19
0.32
50
64
48
57
39
25
20
21
72
3.35-5.60
3.57-5.50
3.44-5.95
3.42-5.75
3.80-5.50
3.74-4.90
3.98-5.28
4.00-5.10
3.50-5.16

From Wolff et al.  (1979).
                    TABLE 11-3.   STORM TYPE CLASSIFICATION


Type
Description of dominant storm
system
No.
obsd
Mean
pH

1

2

3
4
5
6
7
8
Closed low-pressure system which formed
over continental N. Amer.
Closed low-pressure system which formed in
Gulf of Mexico or over Atlantic Ocean
Closed low which passed to W or N of N.Y.C.
Closed low which passed to S or E of N.Y.C.
Cold front in absence of closed low
Air mass thunderstorm
Hurricane Belle
Unclassified
22

21

26
17
16
5
1
6
4.35

4.43

4.39
4.39
4.17
3.91
5.16
4.31

From Wolff et al.  (1979).
                                    11-29

-------
      4.3
      4.3
      4.4
 a    4.3
      4.2
      4.0    JFM      AMJ     JAS      ONO

          MONTHS OF THE  YEAR (ISTi through 1977)
Figure 11-12.  Seasonal variation of precipitation pH in the
New York Metropolitan Area (Wolff et al, 1979).
                      11-30

-------
summer storms sampled  at  4 sites less than 3 km (2 mi.) apart showed a significant difference
(3.8 to 4.2) indicating considerable variation in pH may occur in the same storm.
     Stensland (1978,  1980)  compared  the precipitation chemistry for  1954  and 1977 at a site
in central  Illinois.   The pH for the 1954  samples  had not been measured, but were calculated
and compared with those measured in 1977.  The corrected pH for 1954 was 6.05; the pH for 1977
was 4.1.   The more  basic pH in 1954, according  to the author, could  have  resulted  from low
levels of  acidic ions  (e.g.  sulfate or  nitrate) or  from high amounts  of basic  ions  (e.g.
calcium and magnesium).  Stensland suggests that the higher pH in 1954 was due to calcium (Ca  )
and magnesium (Mg  ) ions  from the soil.
11.2.3.3  Geographic Extent  of Acidic Precipitation—Acidic  precipitation has  been a reality
in New  York State  for an undetermined  period  of time.   Data collected  by  the United States
Geological Survey (Harr and Coffey, 1975) over a ten-year period are presented in Figure 11-13.
These curves  represent  the pH of precipitation at eight different locations in New York State
and one location  in  Pennsylvania.   Each of  these  locations  represents an area within a given
watershed.   The  pH of precipitation has  remained nearly at the same general  average during the
entire ten-year period; therefore,  since data for  the  years  prior  to 1965  are lacking, it is
difficult to  determine  when  the  pH in precipitation first began to decrease (Harr and Coffey,
1975).
     That precipitation is acidic  in  parts of the  country other than the northeastern United
States is apparent (see Figure 11-14).   Average pH values around 4.5 have been reported as far
south as  northern Florida (Hendry  and  Brezonik,  1980; Likens,  1976),  from  Illinois  (Irving,
1978),  the  Denver area of Colorado (Lewis  and Grant,  1980)  the San  Francisco  Bay  area  of
California  (McColl  and Bush, 1978;  Williams, 1978),  Pasadena, California  (Liljestrand  and
Morgan,  1978),  the  Puget  Sound  area of  Washington (Larsen  et  al.,  1975),  and  from eastern
Canada (Dillon et al.,  1978; Glass et al.,  1979).   Data from the San  Francisco  Bay  area in-
dicate that precipitation  has be come more  acidic  in  that region since 1957-1958 (McColl  and
Bush,  1978).  The pH  decreased from 5.9 during 1957-1958  to  4.0 in 1974, and seems to be re-
lated to an increase in the NCs  concentration (McColl  and Bush, 1978).  Another report, using
data from the California  Air Resources  Board (CARB) (Williams, 1978), states that acidic pre-
cipitation  has  been reported  from  such widespread  areas  as Pasadena, Palo  Alto,  Davis,  and
Lake Tahoe.
     Studies in the Great Smoky  Mountain National  Park  (Herrmann  and Baron, 1980) indicate a
downward trend in pH has occurred there  over the past twenty years.   Over a  period of 20 years,
there has been a drop in pH from a range of 5.3-5.6 to  4.3 in 1979.
     The absence  of a  precipitation  monitoring  network  throughout  the  United States  in  the
past makes  determination  of  trends  in pH extremely  difficult  and  controversial.   This short-
coming has been  rectified  recently through the establishment of the National  Atmospheric Depo-
sition  Program  funded  by State,  Federal   and  private  agencies and  headquartered  at  North
Carolina  State  University,  Raleigh,  N.C.    Under  the  program, monitoring  stations  collect
                                           11-31

-------
7.0

6.0


S.O

40


3.0

0.0*


7.0

6.0


S.O


4.0

3.0

o.o'i


6.0


S.O

4.0


3.0

o.o"




6.0


S.O

4:0

0.0*
                                                    ALBANY. NEW YORK
                                             ALLEGHENY STATE PARK. NEW YORK
                                                  ATHENS. PENNSYLVANIA
                                                    CANTON, NEW YORK
              1965
                         1366
                                    1967
                                               196B
                                                          1969
                                                          YEAR
                                                                      1970
                                                                                1971
                                                                                           1972
                                                                                                       1973
Figure 11-13.  History of acidic precipitation at various sites in and adjacent
(Harr and Coffey,  1975).
                                                                               to State of New York
                                                   11-32

-------
   7.0


   6.0


   50


   40

   0.0*




   7.0


   60


*  SO


   4.0

   0.0*
                                          HINCKLEY.NEWVORK
                                          MAYS POINT, NEW YORK
70


6.0


5,0


4.0
                                           MINEOLA. NEW YORK
6.0


5,0


4 0

00
                                          ROCK HILL. NEW YORK
                                           UPTON, NEW YORK
5.0 I	
       1965
                                                                                 1972
                                                                                            1973
   Figure 11-13 (cont'd).  History of acidic precipitation at various sites in and adjacent to State
   of New York (Harr and Coffey, 1975).
                                           11-33

-------
        Ched Plotting Legend
                                • I
NattoMl Almmptoric Depo«lnoo PIDO/MII (NADP)
OctMrlmenl ol Energy (DOE)
Envfronmenlti Prolwlkm Aoawy (EPA/NOAA/WHO)
      V of CtlHomt*
      Intiilut* ol Technology
      io Almotptwrtc Power
Production Poirutton Sludy (14AP3S)
Etocirtc Po«w RM«VC*I Imlllut* (EPHI»
O*fe Rtdg* NiiKmtl Laboratory
                  oiifimil S*rvtca (CANSAP)
  Figure  11-14.  pH of rain samples as measured in the laboratory and used in combination with the
  reported amount of precipitation.
Source:  Wisniewski and Keitz (1981).

-------
precipitation  samples,  determine their pH  and  then send the samples  to  a Central Analytical
Laboratory in Illinois to be analyzed.  This long-term network plans to have 75 to 100 collec-
tion sites throughout the United States; 74 are already operational.
11.2.4  Acidic Deposition
     The previous  sections  of  this chapter have discussed the formation, composition and geo-
graphic distribution  of  acidic  precipitation.   Usually when  the  effects  of acidic deposition
are discussed, emphasis  is  placed on the effects  resulting  from the scavenging of sulfur and
nitrogen compounds  by precipitation.   Dry  deposition of gaseous and  particulate  and aerosol
forms  of  these compounds also  occurs  and  is  beginning to receive more  emphasis  in research
(Chamberlain, 1980; Galloway and Wheledale, 1980;  Schlesinger and  Hasey,  1980;  Schmel,  1980;
Stensland,   1980).   Gaseous  compounds  reach the  surface  of  the  earth by  turbulent transfer
while  particulate  sulfates  and  nitrates reach the earth's surface by gravitational sedimenta-
tion,  turbulent transfer  and  impaction (Galloway and Whelpdale,  1980; Hicks and Wesely,  1980;
Schmel, 1980).  A  comparison  of the relative significance of wet and dry deposition is diffi-
cult.    Dry  deposition,  however,  is  always  removing pollutants  from the  atmosphere,  while
removal by wet deposition is  intermittent  (Schmel,  1980).  Marenco and Fontan (1976) suggest
that  dry  deposition  is  more  important  than wet  in  removing  air  pollutants  from  manmade
sources.
     Lindberg et al.  (1979)  have calculated the annual mass transfer rates of sulfates to the
forest  floor  in Tennessee (Figure 11-15).   Their calculations for SO.  suggest wet deposition
by incident precipitation to be 27 percent compared with a total  dry deposition of 13 percent.
The dry deposition  and  foliar  absorption of S(L,  a very  important component, is missing from
this calculation.    The wet  and  dry deposition percentages are only an indication of the  rela-
tive magnitude of  the two processes.   The percentages do, however,  point out that the effects
of  acidic  deposition  usually  attributed  to precipitation  scavenging  alone are  probably  a
result of both wet  and  dry  deposition.   At the present time the  accuracy with which dry  depo-
sition can be measured is still  under question.
     The studies  of McColl  and  Bush  (1978),  Hendry and Brezonik (1980),  and Schlesinger and
Hasey  (1980)  also  point  out that  both  wet  and  dry deposition are  important when  considering
                +     2-         -
the effects of H  ,  SO. ,  and NO, ions on aquatic and terrestrial  receptors.
     The effects  of the dry  deposition of SCL and particulate  matter on vegetation and terres-
trial  ecosystems  is discussed in Chapter 8.   The processes of  wet and dry deposition of sulfur
oxides  are discussed  in  Chapter 6 of Air Quality Criteria for Particulate  Matter and Sulfur
Oxides.  The  nitrogen cycle  is  discussed in Chapter 4, transformation and transport of nitro-
gen oxides  in Chapter 6 and  the  effects of nitrogen oxides on  vegetation in Chapter 12 of this
document.
11.3  EFFECTS OF  ACIDIC  DEPOSITION
     Acidic precipitation has  been  implicated  in the degradation  of  aquatic ecosystems,  the
disintegration of stone  buildings  and monuments and  as a potential source of harm to forests
and other  terrestrial  ecosystems.  The sections that follow discuss  these effects.

                                           11-35

-------
                   IN CLOUD
                 PRECIPITATION
                  SCAVENGING
                     25%
                                           TOTAL DRY
                                           DEPOSITION
                 BELOW CLOUD
                 PRECIPITATION
                  SCAVENGING
           M
          i  '• •
        4 V 'ill
TO LEAFY
 CANOPY
                  TO GROUND
               (DORMANT PERIOD)
                      2%,
    i   i 'u  ,i
  I  ',"1 i  i a" Ml'i •
INCIDENT PRECIPITATION
                                                               TO BRANCHES
                                                             (DORMANT PERIOD
                                                                    1%
                                                  WASH-OFF 0
                                                 DRY DEPOSITION
                                   EXTERNAL
                                     FLUX
                                100%
Figure 11-15. Annual mass transfer rates of sulfate expressed as a percentage of the estimated
total annual flux of the element to the forest floor beneath a representative chestnut oak stand
(Lindbergetal., 1979).
                                   11-36

-------
11.3.1  Aquatic Ecosystems
     Acidification  of  surface waters  is  a major  problem in regions  of  southern Scandinavia
(Aimer  et  al. ,  1974;  Gjessing et  al., 1976;  Oden,  1968),  Scotland  (Wright  et  al. ,  1980a),
eastern  Canada (Beamish  and  Harvey,  1972;  Dillon  et  al., 1978),  and  the  eastern  United
States  -  in the  Adirondack Region of  New York  State  (Pfeiffer and  Festa,  1980;  Schofield,
1976a,b,c,d),  in  Maine  (Davis  et al. ,  1978),  and  in northern  Florida  (Crisman et al. ,  1980).
Damage  to  fisheries  is  the most obvious affect of acidification on freshwater lite.   The d.is-
appearance of fish  populations from acidified freshwater lakes  and streams was first  noted in
southern Norway in  the  1920's.  In 1959,  Dannevig (1959)  proposed  that acidic deposition was
the probable cause  for  acidification  and  thus far the  loss  of fish populations (Leivestad et
al.,  1976).   Subsequent studies  have  verified this  postulate.   Declines  in  fish populations
have  been  related to acidification of surface waters in  southern  Norway (Jensen and  Snekvik,
1972; Wright and  Snekvik,  1978), southwestern Sweden (Aimer et al.,  1974) southwestern Scot-
land  (Wright et al., 1980a), the Adirondack Region of New York State (Schofield, 1976a,b,c,d),
and the LaCloche  Mountain  Region in southern Ontario (Beamish  and  Harvey, 1972).  Acidifica-
tion  may also have  serious repercussions  on  other aquatic  biota  inhabiting  these  systems.
Changes  in the acidity  and chemistry of freshwater affect the communities of organisms  living
there.  Pertinent details of these effects are described in the  following sections.
11.3.1.1   Acidification of  Lakes and Streams—Precipitation  enters  lakes  directly as rain or
snow  or indirectly as runoff  of  seepage  water from the surrounding watershed.   The  relative
magnitude of the  influents  from these two sources is dependent  on  the  surface area and  volume
of  the  lake,  and  the  size of the watershed and  its soil  volume  and type.   In  general,  the
watershed plays a dominant role in determining the composition of water entering the  lake.   As
a result, the  water will be strongly influenced by processes  in  the edaphic environment  of the
watershed,  such  as weathering,  ion exchange,  uptake and release  of  ions by  plants,  carbon
dioxide production by vegetation, microbial  respiration, and  reduction  and oxidation  reactions
of  sulfur  and  nitrogen  compounds (Seip, 1980).  Precipitation  as  a direct source of  water to
the lake plays a  relatively greater role when lake  areas  are large in comparison to  the size
of the watershed.
     Acidification  of  surface  waters  results  when  the  sources of hydrogen  ion exceed  the
ability of an ecosystem  to neutralize the  hydrogen  ion.   In general,  the soils  and  crust of
the earth  are composed  principally of basic materials with  large  capacities to buffer  acids.
However, areas where bedrock  is particularly  resistant  to weathering  and soils  are  thin  and
poorly  developed  have much  less neutralizing  ability.   This inability  to neutralize  hydrogen
ion does  not  arise  from  a limited  soil  or mineral  buffering  capacity.  Instead low  cation
exchange capacity and  slow  mineral  dissolution rates in relation to  the relatively short re-
tention time of water  within  the soil system may  result  in  incomplete neutralization of soil
waters  and acidification of surface waters (Driscoll, 1980).   Characteristics  of regions sen-
sitive to surface  water acidification  are  discussed in more detail  in  Section 11.4.1.
                                           11-37

-------
     Sources of hydrogen ion to the edaphic-aquatic system include,  besides acidic deposition,
mechanisms for internal  generation  of hydrogen ion - oxidation reactions (e.g.,  pyrite oxida-
tion, nutrification), cation  uptake  by vegetation (e.g., uptake of  NH.   or Ca  ), or genera-
tion of organic  acids  from incomplete organic litter decomposition  (Figure 11-16).  The rela-
tive importance  of  the  hydrogen ion content  in  acidic  deposition  to the overall  hydrogen ion
budget of an ecosystem has been discussed by many researchers (Rosenquist, 1976;  SNSF Project,
1977).
     The consensus  is that changes  in internal hydrogen ion generation related to land use or
other changes  (e.g., Drablos  and Sevaldrud, 1980) can  not  consistently  account for the wide-
spread  acidification of  surface waters  occurring  in  .southern  Scandinavia,  the  Adirondack
Region  of  New York, the LaCloche Mountain  Area of Ontario, and elsewhere.   Driscoll  (1980)
developed a hydrogen ion budget for the Hubbard  Brook  Area in New  Hampshire.   Based on these
calculations,  atmospheric hydrogen ion sources represent 48 percent  of the total  Hubbard Brook
ecosystem hydrogen ion sources.
     As noted  above, freshwater ecosystem  sensitive to inputs of acids are generally in areas
of poor soil  development and  underlain by highly siliceous types of bedrock resistant to dis-
solution through weathering (Likens  et al,  1979).   As  a  result,  surface waters  in such areas
typically contain  very   low concentrations  of ions  derived from weathering.  The waters  are
diluted .with  low levels  of dissolved salts  and inorganic carbon, and low in acid neutralizing
capacity.   The  chemical  composition  of  acid  lakes  is  summarized  in Table 11-4  for  lakes in
southern Norway  (Gjessing  et  al., 1976), the  west coast (Hornstrbm et al. , 1973),  and west-
central  regions   of Sweden  (Grahn,  1977),  the   LaCloche  Mountains  of   southeastern  Ontario
(Beamish,  1976), and the vicinity of Sudbury, Ontario (Scheider et  al.,  1975), as well  as for
lakes  not  yet affected  by acidification but  in regions of similar geological  substrata in
west-central  Norway  (Gjessing et al. , 1976)  and the experimental lakes  area  of  northwestern
Ontario (Armstrong  and  Schindler,  1971).   Basic  cation concentrations (Ca, Mg, Na, K) are low
(e.g.,  calcium levels of 18-450 ueq/liter or 0.4  - 9 mg/liter) relative to world-wide averages
[15  mg/liter  calcium  (Livingstone,  1963)].   Bicarbonate  is  the  predominant anion in  most
freshwaters (Stumm  and  Morgan, 1970).  However,  in  acid lakes in regions  affected  by  acidic
deposition, sulfate replaces  bicarbonate  as  the dominant  anion (Beamish, 1976; Wright  and
Gjessing,  1976).   With a decreasing pH level in acid lakes,  the importance of the hydrogen ion
to the total cation content increases.
     Surveys to determine the  extent of effects of acidic deposition on the chemistry of lakes
have been conducted  in  Norway (Wright and  Snekvik,  1978;  Wright and Henriksen,  1978),  Sweden
(Aimer  et  al., 1974; Dickson,  1975),  Scotland (Wright  et al. ,  1980a),  the LaCloche Mountain
area of Ontario  (Beamish  and  Harvey,  1972),  the  Muskoka-Haliburton  Area of  south-central
Ontario (Dillon et al.,  1978), and the Adirondack Region of New York State (Schofield, 1976b),
Maine  (Davis  et  al. , 1978),  and Pennsylvania (Arnold  et al. ,  1980).   In  regions of similar
geological substrata  not receiving  acidic  deposition,  lake  pH levels  average  5.6-6.7 (Arm-
strong  and  Schindler,  1971).   Of  155  lakes  systematically surveyed  in southern  Norway in

                                           11-38

-------
     ALLOCHTHONOUS SOURCES OF HYDROGEN ION
            PRECIPITATION,
            DRY DEPOSITION,
         X   DRAINAGE WATER
     p- ECOSYSTEM BOUNDARY
HYDROGEN ION
   SOURCES

OXIDATION RXN
CATION UPTAKE
    PYRITE
  OXIDATION
 NH+ UPTAKE
                             HYDROGEN ION
                                SINKS

                            REDUCTION RXN
                             ANION UPTAKE
                                OXIDE
                             WEATHERING
            STREAM EXPORTS
              H+,HC03~, OH-LIGANDS,
              ORGANIC ANIONS
Figure 11-16. Schematic representation of the hydrogen ion
cycle (Driscoll, 1980).
                       11-39

-------
October 1974, over  70  percent had pH levels  below  6.0,  56 percent below 5.5,  and  24 percent
below  5.0  (Wright and  Henriksen,  1978).   Of  700 lakes  in  the SjJrlandet  Region of  southern
Norway surveyed in 1974 to 1975 (May-November), 65 percent had pH levels below 5.0 (Wright and
Snekvik, 1978).    On the  west coast of Sweden, of 321 lakes  investigated during 1968-1970,  93
percent had  a pH  level  5.5 or lower.   Fifty-three  percent had pH levels between 4.0 and 4.5
(Dickson,  1975).  In the  LaCloche Mountain Region of Ontario, 47 percent of 150 lakes sampled
in  1971  had pH  levels  less  than  5.5,  and  22 percent had  pH levels below  4.5  (Beamish and
Harvey, 1972).  In  the  Adirondacks,  52 percent of  the  high  elevation (> 610 m)  lakes  had pH
values below  5.0  (Schofield,  1976b).   In each of these studies, the  pH level  of an  individual
lake could  be related  to, in most cases,  the  intensity of the acidic deposition and  the geo-
logic environment of the watershed.   Atmospheric contributions of sea salts  are  also important
in coastal  regions.
     Several methods have  been  developed  to assess the degree  of  acidification in  a  lake and
relate it to  inputs  of hydrogen ion or sulfate.  Henriksen (1979)  utilized  alkalinity-calcium
and pH-calcium relationships in lakes to estimate the degree  of acidification experienced by a
surface water.   This  technique  is  based  on  the  premise  that  when  carbonic acid  weathering
occurs one  equivalent  of  alkalinity  (acid neutralizing capacity)  is  released  to the aquatic
environment for every  equivalent of basic cation (Ca,  Mg, K, or Na) dissolved.  On the other
hand,  if mineral  acid  weathering is occurring, for  example  as  a result of  acidic deposition,
one equivalent of hydrogen ion is comsumed for every equivalent of  cation solubilized.   There-
fore,  for  a given  basic  cation  level,  there  is less  aqueous acid  neutralizing capacity  in
lakes  in  systems  experiencing  strong  acid weathering  than   in  systems  experiencing  carbonic
acid weathering.  When  comparing alkalinity plots from two watersheds, one experiencing strong
acid contributions  and the  other undergoing largely carbonic  acid weathering  (assuming both
watersheds   have  similar edaphic  environments), the difference in alkalinity between  the two
plots for a given calcium level  (the dominant basic  cation) should  be indicative of  the amount
of  strong acid  the  watershed receives  and  the degree of acidification of  the  surface  water.
For waters  with pH  levels below 5.6, alkalinity is  approximately equal to the negative of the
hydrogen  ion concentration.   Therefore,  pH  level  can  be   substituted  for  alkalinity,  and
pH-calcium   plots  developed (Figure 11-17).  Data of  this type for Norway  indicate that sig-
nificant acidification  of lakes  has  occurred  in areas receiving precipitation  with volume-
weighted average  concentrations  of  H  above 20-25 |jeq/liter  (pH 4.7-4.6) and sulfate concen-
trations above 1 mg/liter (20 ueq/liter) (Henriksen, 1979).
     Henriksen (1979) also utilized the concentration of excess sulfate in lake  water  (sulfate
in excess of that of marine origin) to estimate acidification.  This  suggests  that bicarbonate
anions lost  in  acidified  lakes  have been  replaced  by an  equivalent  amount  of sulfate.   Aimer
et  al.  (1978) plot pH  levels in  Swedish lakes  as  a function of excess sulfur  load (excess
sulfur in lake water multiplied by the yearly runoff) (Figure 11-18).   Based on  this relation-
ship,  they  estimate that  the most sensitive lakes  in Sweden may resist  a  load of  only about
                                           11-40

-------
                            TABLE  11-4.  CHEMICAL COMPOSITION (MEAN ± STANDARD DEVIATION) OF ACID LAKES (pH •*>) 1N REGIONS RECEIVING HIGHLY
                            ACIDIC PRECIPIIAFION (pH <4.b), AND OF SOFT-WATER LAKES IN AREAS NOT SUBJECT TO HI GHLV ACIDIC PRECIPITATION
                                                                             (pH >4.8)
Region
I. LAKES IN ACID AREAS

Southernmost
Norway

Sweden
West-centra 1
Sweden
North America
La Cloche Mtns,
Ontario

Sudbury ,
Ontario
11. LAKES IN UNAFFECTED
Scandinav ia
West-central
Norway
North America
Exper i mental
Lakes Area,
Ontario
No. of
lakes


Measured: 26
Less s w*:

Less s w*:
Measured: 6
Less s w*:

Measured: 4
Less s w*:

Measured: 4
Less s w*:
AREAS

Measured: 23
Less s w*;

Measured: 40
Less s w*.

Speci fie
tomJuclancetl H (pH)


27*10 18*11 (4.76)
18

«*»
47+23 22+15 (4.66)
22

38+8 20+9 (4.7)
20

120+40 36+5 (4.5)
36


13+3 6±2 (5.2)
6

19 0.2-2 (5.6-6.7)
0.2-2


Na


70+40
9

-50
165+120
20

26+4
9

100±30
50


50+20
9

40
4


K


5+3
4

13
15+8
12

10±3
10

40+10
40


3±1
3

10
10


Ca


56+35
50

-
75+10
70

150+25
150

450±180
450


ia+9
16

80
80


Mg


41+16
25


80+40
50

75±B
65

310+120
300


16+5
7

75
65

~ M-q/1
HCOn


11+26
11
0
0
-
"
0
0

8+2
8


13+8
13

60
60



HCl


71+ 45
0
440
0
170+90
0
22+6
0

50+20*
0


46*21
0

40
0



SO,, N03


100*33 4+2
92 4
200 8
155 8
200+70 19+4
180 19
290+40
290

800+290
800


33+8 5+2
30 5

60 r( ncf!


fiji-i'. inq
el al. . 19/6

el al. , 19/6
Grdhn, 19//

Beamish,


Armstrong,
1971


Gjessing
el al. . 1976

Armstrong,
1971



 "Less s w = Concentrations after subtracting the seauater  contribution  according  to  the procedure explained by
   Wri(|ht and Cjessing (1976).
"Dala (or 112 lakes
 IMeasured after past liming of the lakes
t^iS/cm al 20T

-------
 a
     7.0
     7.5
                                             [Cal
Figure 11-17. pH and calcium concentrations in lakes in northern and northwestern Norway
sampled as part of the regional survey of 1975, in lakes in northwestern Norway sampled in
1977  (o)  and in  lakes  in southernmost  and southeastern Norway sampled  in 1974 («).
Southern Norway receives highly acid precipitation (pH 4.2-4.5} and a large number of lakes
have lost their fish populations due to high acidity. Inset shows areas in which  these lakes
are located. Areas south of isoline receive precipitation more acid than pH 4.6 (Henriksen, 1979).

                                       ! 11-42

-------
  I
  a
                                                                         CURVE 2
        0123

                               EXCESS S IN LAKE WATER. g/m2/vear

Figure 11-18, The pH value and sulfur loads in lake waters with extremely sensitive surroundings
(curve 1) and  with slightly less sensitive surroundings (curve  2). (Load  = concentration  of
"excess" sulfur multiplied by the yearly runoff.) (Aimer et al., 1978).
                                         11-43

-------
       2                                               ?
0.3 g/m   of  sulfur in lake water  each  year.   At 1 g/m   of  sulfur,  the pH level  of  the  lake
will probably decrease below 5.0.
     Elevated metal concentrations  (e.g.,  aluminum,  zinc, manganese, and/or  iron)  in surface
waters are often  associated  with  acidification (Beamish,  1976; Hutchinson et al.,  1978;  Scho-
field and  Trojnar, 1980; Wright  and Gjessing,  1976).   Mobility  of all  these  metals  is  in-
creased at  low  pH values (Stumm and  Morgan,  1970).   For example, an inverse correlation  be-
tween aluminum  concentration and  pH  level has  been  identified  for lakes in  the Adirondack
Region of New York State,  southern Norway, the  west  coast of Sweden,  and Scotland (Wright et
al.  , 1980b). (Figure  11-19).   Aluminum  appears to be the primary element mobilized by strong
acid inputs in precipitation and dry deposition (Cronan,  1978).
     Aluminum is   the  third most  abundant element by  weight  in  the  earth's  crust  (Foster,
1971).  In general, aluminum is extremely insoluble and  retained within  the edaphic environ-
ment.   However,  with  increased hydrogen  ion  inputs  (via acidic  deposition or  other sources)
into  the  edaphic  environment,  aluminum  is  rapidly mobilized.   Cronan and  Schofield  (1979)
suggest that input of strong acids may inhibit  the  historical trend of aluminum accumulation
in  the B  soil  horizon.   Consequently, aluminum  tends to  be  transported through the soil  pro-
file and  into streams and  lakes.   Evidence from  field  data  (Schofield  and Trojnar, 1980)  and
laboratory experiments (Driscoll et  al.,  1979; Muniz and  Leivestad, 1980)  suggest that these
elevated aluminum  levels may be toxic to  fish.   Concentration of aluminum may  be  as  or  more
important than pH  levels as a factor leading to declining fish populations in acidified lakes.
Aluminum toxicity to aquatic biota other than fish has not been assessed.
     Surface water  chemistry,  particularly in streams and rivers, may  be  highly variable  with
time.   Since many  of  the neutralization reactions in soils  are kinetically slow,  the quality
of the leachate from the edaphic system into the aquatic system varies  with the retention  time
of  water  in the  soil  (Johnson et  al.,  1969).   The  longer  the contact period  of water  with
lower soil strata,  the  greater the neutralization of acid contribution  from precipitation  and
dry deposition.   Therefore, during periods of heavy rainfall  or snowmelt,  and rapid water  dis-
charge, pH levels in receiving waters may be relatively depressed.
     Many of the  regions  currently affected by acidification experience freezing temperatures
during the winter  and accumulation of a snowpack.  In  the Adirondack  Region of New  York  ap-
proximately 55 percent of the annual precipitation occurs during the winter months  (Schofield,
1976b).   Much  of  the  acid  load deposited in  winter  accumulates in the snowpack,  and  may be
released during a relatively short time period during snowmelt in the spring.   In addition, on
melting,  50  to  80  percent  of the  pollutant  load (including  hydrogen ion and sulfate)  may be
released  in  the first  30  percent of the  meltwater  (Johannessen and Henriksen, 1978).  As  a
result, melting of the  snowpack and ice cover  can  result in  a  large influx  of acidic pollu-
tants into lakes  and  streams (Figure 11-20) (Gjessing et al., 1976; Hultberg, 1977; Schofield
and Trojnar, 1980).  The rapid flux of this meltwater through the edaphic  environment, and its
interaction  with  only upper soil  horizons,  limits  neutralization of the acid  content.  As  a
result, surface waters  only  moderately  acidic during most of the year may experience extreme

                                           11-44

-------
1000


~oi
=1 100
<
10
t
- I
\
SOUTH NORWAY 1974
^^~
ft
^~ • ft* •
— •* • *•« • •
«_«_ 9 ft
1
154 LAKES 	
•
ft •
•
.' *f "•*
•
9

I
1000


en
5 100
10
— | | _
SCOTLAND
	 72 LAKES 	
	 *.'."•• 	
"': ' • " '• '.
V
9
1 1 '
1567845678
pH
1000




1 100
<
10
4
_ [
1 — "
WEST COAST SWEDEN
ft *

— ft
0
• ' 7
«
1
37 LAKES 	

—
^^^
1
5671
1000




5 100
10
t i
PH
' .- ' '
	 " ° ADIRONDACKS USA 	
134 LAKES
~~ %'*r{:;'*'. * •
• ..^.v
^^ *A*' • • " • ~~~
' " ..** . * • *
. • * •'•'' '
• ft • •
« •
• •
I .
15678
pH pH
Figure 11-19.  Total dissolved  Al as a function  of pH level in lakes in acidified areas in Europe and
North America (Wright et al., 1980b).
                                             11-45

-------
 a
                                             F

                                          1976/77
M
Figure 11-20. pH levels in Little Moose Lake, Adirondack region of New York State, at a depth of 3
meters and at the lake outlet (adapted from Schofield and Trojnar, 1980).
                                                     11-46

-------
drops  in  pH level  during  the spring  thaw.   Basic  cation concentrations (Ca, Mg,  Na,  K)  may
also  be  lower  during this time period (Johannessen  et al.,  1980).  Similar  but  usually less
drastic pH drops in surface waters (particularly streams) may occur during extended periods of
heavy  rainfall  (Driscoll,  1980).   These  short  term  changes  in water chemistry may have sig-
nificant impacts on aquatic biota.
11.3.1.2   Effects  on  Decomposition—The  processing  of dead organic matter  (detritus)  plays a
central role  in the  energetics  of  lake  and stream  ecosystems  (Wetzel, 1975).   The  organic
matter may have been generated either  internally (autochthonous) via photosynthesis within  the
aquatic ecosystem or produced outside the lake or stream (allochthonous) and later exported to
the aquatic system.   Detritus  is  an important food source for bacteria, fungi, some protozoa,
and other  animals.   These  organisms through the utilization  of  detritus release  energy, min-
erals  and  other compounds  stored in  the  organic  matter back into the environment.   Initial
processing of coarse particulate detritus is often  accomplished by benthic invertebrate fauna.
Among  other  things, the particles  are physically  broken down into smaller  units,  increasing
their  surface area.   Biochemical  transformations of particulate and dissolved organic  matter
occur  via  microbial metabolism and  are  fundamental  to the  dynamics of  nutrient  cycling  and
energy flux within the aquatic ecosystem.
     In general, the growth and reproduction of microorganisms is greatly affected by hydrogen
ion concentration  (Rheinheimer,  1971).  Many bacteria  can grow  only  within the range  pH  4-9
and the optimum  for most aquatic  bacteria  is between  pH 6.5 and  8.5.   There  are  more acidi-
philic fungi than  bacteria;  consequently in acid waters and  sediments  the proportion of fungi
in the microflora  is  greater than in waters or sediments with neutral  or slightly alkaline pH
levels.  Most aquatic fungi require free oxygen for growth (Rheinheimer, 1971).
     Numerous studies have  indicated that acidification of surface waters  results  in  a shift
in microbial species and a reduction in microbial activity and decomposition rates.   It should
be noted,  however,  that microorganisms in general are highly  adaptive.   Given sufficient time,
a given species  may adapt  to acid conditions or an acid-tolerant species may invade and colo-
nize  acidified  surface  waters.   Therefore,  some caution is necessary  in  interpreting  short-
term experiments on  the  effects  of acidification 'on microbial  activity and decomposition.   On
the other  hand,  increased  accumulations  of dead organic  matter  (as  a  result of decreased  de-
composition rates)  are commonly noted in acidic lakes and streams.
     Abnormal  accumulations of coarse  organic matter have been observed on the bottoms  of  six
Swedish lakes.   The pH levels in these lakes in July 1973 were approximately 4.4 to 5.4.  Over
the last three  to  four  decades,  pH levels appear to have decreased 1.4 to 1.7 pH  units  (Grahn
et al.,  1974).   In  both  Sweden  and Canada,  acidified lakes have been  treated with  alkaline
substances  to  raise  pH  levels.   One  result of this  treatment has been an  acceleration  of
organic decomposition processes and elimination of  excess accumulations of detritus (Andersson
et al.,  1975;   Scheider  et  al. ,  1975).   Litterbags  containing coarse  particulate  detrital
matter have  been  used  to  monitor  decomposition rates  in acidified  lakes  and streams.   In
general,  the rates  of weight loss  were reduced in acidic waters when compared with more

                                           11-47

-------
neutral waters  (Leivestad et al. ,  1976;  Traaen,  1980;  Peterson, 1980).  Traaen  (1980)  found
that after 12 months  of incubation dried birch leaves or aspen sticks showed a weight loss of
50-80 percent in waters with pH levels 6 to 7 as compared to only a 30-50 percent weight loss
in waters with  pH  4 to 5.   Petersen  (1980)  likewise found reduced weight  loss  of leaf packs
incubated in an acidic  stream when compared to  leaf packs in either a stream not affected by
acidification or  a stream  neutralized with  addition  of  lime.   Petersen,  however,  found  no
evidence of differences  in  microbial  respiration between  the  streams.   The acidic stream did
show a  reduction  in  the  invertebrate functional  group that  specializes in  processing  large
particles (shredders).   Gahnstrb'm et  al.  (1980) found  no significant  differences  in oxygen
consumption by  sediments  from  acidified  and non-acidified lakes.  Rates of  glucose decompo-
sition were  also  studied  in lake  sediment-water  systems  adapted  to pH values  from  3  to 9.
Glucose transformation  increased  at pH levels above 6.   Lime treatment of acidic Lake Hb'gsjb'n
in  Sweden also  increased rates of  glucose  processing.   However in a  humic  lake,  the maximum
rate of glucose transformation  occurred  at the i_n  situ value pH 5 (Gahnstrom  et al., 1980).
     Laboratory and  field experiments involving decomposition  rates  have  fairly consistently
found decreasing microbial  activity with increasing acidity.   Traaen (1980) found that litter
decomposition at pH level 5.2 was  only  50  percent of that at pH 7.0 and at pH  3.5,  only 30
percent that at pH  7.0.   In addition, increasing  acidity  (pH 7.0 to 3.5) led to a shift from
bacterial to  fungal dominance.   Incubations  of profundal  lake  sediments  at pH  4,  5,  and 6
indicated a significant reduction in community respiration with increasing acidity, as well as
a possible inhibition  of  nitrification and a lowering of sediment redox potentials.   Bick and
Drews  (1973)  studied the decomposition  of  peptone in the  laboratory.   With  decreasing  pH,
total bacterial cell  counts and numbers  of species of ciliated protozoans decreased, decompo-
sition and nitrification were reduced and oxidation of ammonia ceased below pH 5.   At pH 4 and
lower, the number of fungi increased.
     Disruption of the detrital trophic structure and the resultant interference with nutrient
and energy cycling within the aquatic ecosystem may be one of the major consequences of acidi-
fication.  Investigations into the effects of acidification on decomposition have, apparently,
produced somewhat inconsistent results.  However, many of these apparent inconsistencies arise
only from  a  lack  of  complete  understanding  of the mechanisms relating acidity  and rates of
decomposition.   It  is  fairly clear that  in acidic lakes and streams unusually large accumula-
tions of detritus  occur,  and these accumulations are  related, directly or indirectly, to the
low pH level.   The processing of organic  matter has been reduced.   In addition, this accumula-
tion of  organic debris  plus the development  of  extensive mats  of filamentous  algae on lake
bottoms  (discussed  in  Section  11.3.1.3)  may effectively seal  off  the mineral  sediments from
interactions  with the  overlying water.  As a result, regeneration of nutrient supplies to the
water column is  reduced both by reduced  processing and mineralization of dead organic matter
and by  limiting  sediment-water interactions.   Primary productivity within  the  aquatic system
may be substantially reduced as a result of this process (Section 11.3.1.3).  These ideas have
                                           11-48

-------
been formulated  into  the hypothesis of "self-accelerating  oligotrophication"  by Grahn et al.
(1974).
11.3.1.3   Effect on Primary Producers and Primary Productivity—Organisms  obtain their  food
(energy)  directly  or indirectly  from  solar energy.   Sunlight, carbon  dioxide,  and  water are
used by primary producers (phytoplankton, other algae, mosses, and macrophytes) in the process
of photosynthesis to form sugars which are used by" the plants or stored as starch.  The stored
energy may  be  used by the plants  or  pass through the food  chain  or web.   Energy in any food
chain  or  web  passes through several trophic  levels.   Each  link in the food chain is termed a
trophic  level.   The major  trophic levels are the primary  producers,  herbivores, carnivores,
and  the  decomposers.   Energy  in  an ecosystem  moves primarily along two  main pathways:   the
grazing  food  chain  (primary  producers-herbivores-carnivores)  and  the  detrital food  chain
(Billings,  1978;  Odum,  1971;  Smith,  1980).   Interactions between these two  food chains  are,
however, extensive.  Green plants convert solar energy to organic matter and, as such, are the
base for  both  food chains.   The grazing  food  chain  involves primarily living organic matter;
the detrital food chain, dead organic matter.  Any changes as a result of acidification in the
green plants and primary production within the aquatic ecosystem may therefore have a profound
effect on all  other organisms  in the  aquatic  food  web.   As noted in Section 11.3.1.2, a por-
tion of  the detrital  food chain is supported by dead organic matter imported into the aquatic
system from external sources.
     Extensive  surveys  of acidic  lakes  in  Norway  and Sweden (Aimer et  al. ,  1978;  Leivestad
et al.,  1976)  have  observed  changes  in  species  composition  and  reduced  diversity  of
phytoplankton correlated with decreasing lake pH level (Figure 11-21).   Generally at normal  pH
values of 6 to 8,  lakes in  the west  coast region of  Sweden  contain 30 to 80 species of phy-
toplankton  per 100-ml  sample in  mid-August.   Lakes with pH below 5 were  found  to  have  only
about a  dozen  species.   In  some very acid  lakes  (pH<4),  only three species  were noted.   The
greatest  changes  in species composition  occurred in the  pH interval 5-6.   The  most striking
change was the disappearance of many diatoms and blue-green algae.   The families Chlorophyceae
(green  algae)  and  Chrysophyceae   (golden-brown  algae) also had  greatly reduced numbers  of
species  in  acidic  lakes (Figure  11-22).   Dinofla'gellates constituted the bulk  of  the phyto-
plankton  biomass  in  the most  acidic  lakes (Aimer  et  al.,  1978).   Similar phenomena  were
observed in a regional survey of 55 lakes in southern Norway (Leivestad et al., 1976) and in a
study  of  nine lakes  in  Ontario (Stokes,  1980).   Changes in species composition and reduced
diversity have also been noted in  communities  of attached algae  (periphyton)  (Aimer et  al.,
1978; Leivestad et  al. ,  1976).   Mougeotia, a green  algae, often proliferates on substrates  in
acidic streams and lakes.
     Shifts in the types and numbers of species present may or may not affect the total levels
of primary  productivity  and  algal  biomass in acidic  lakes.   Species favored by acidic condi-
tions may  or may  not  have   comparable  photosynthetic efficiencies or  desirability  as  a  prey
item  for herbivores.   On  the  other hand,  decreased availability of  nutrients   in  acidic
water  as  a  result of reduced  rates  of decomposition (Section 11.3.1.2) may  decrease primary

                                           11-49

-------
    80


    70


M   60
UJ
O
a   50
00
u.
    40
00
                      I     I     I     I     I     I      I
                                                           I     I     I     I     I     I     I
                                                            PHYTOPLANKTON SPECIES IN 60 LAKES
                                                            ON THE SWEDISH WEST COAST
                                                            AUGUST 1976
    30
z

    20


    10

     0
      pH   4.1   4.3  4.5  4.7   4.9   5.1   5.3  5.5   5,7   5.9   6.1   6.3  6.5   6.7   6.9   7.1

 NUMBER   11043243312103310020350541231011
OF LAKES

     Figure 11-21. Numbers of phytoplankton species in 60 lakes having different pH values on the Swedish
     West Coast, August 1976 (adapted from Aimer et al., 1978).
                                                11-50

-------
           pH 4.60-5.45
     pH 6.25-7.70
                                  BIOMASS
                                  SPECIES
                       DIATOMEAE
                     \ CHLOROPHYCEAE
                    ^t
                       CHRYSOPHYCEAE
CYANOPHYCEAE


PYRROPHYTA


SEPTEMBER 1972
Figure 11-22.  Percentage distribution of phytoplankton species and their biomasses.
September 1972, west coast of Sweden.    Biomass = living weight per unit area
(adapted from Aimer et al., 1978).
                                     11-51

-------
productivity regardless  of  algal  species  involved.   In field surveys and  experiments,  rela-
tionships between pH  level  and  total  algal  biomass and/or productivity were not as  consistent
as the relationship between  pH and species diversity.
     Kwiatkowski  and  Roff  (1976)  identified  a significant linear  relationship  of  decreasing
chlorophyll  a  concentrations (indicative  of  algal biomass)  with declining  pH  level  in  six
lakes near Sudbury,  Ontario, with a pH range of 4.05 to 7.15.   In addition,  primary  productiv-
ity was  reduced .in  the  two  most acid  lakes (pH 4-4.6).   Stokes (1980) also  reports  a decrease
in total phytoplankton  biomass  with decreasing pH  level  for  nine lakes  in  the same region of
Ontario.   Crisman   et  al.   (1980)  reported a  linear  decrease  in  functional  chlorophyll  a
measurements with declining  pH  for 11 lakes in northern Florida, pH range 4.5 to 6.9.  On  the
other hand, Aimer et  al.  (1978) note  that in  58 nutrient-poor lakes in the  Swedish  west  coast
region,  the largest mean phytoplankton biomass occurred in the most acid  lakes (pH <4.5).   Van
and Stokes  (1978) concluded that they have no evidence that the  phytoplankton biomass  in Car-
lyle Lake,  with  a  summer pH level about 5.1,  is below that observed in circumneutral lakes in
the same region.   In a continuing whole-lake acidification project (Schindler et al., 1980),  a
lowering of the  epilimnion  pH  level  from 6.7-7.0  in  1976  to 5.7-5.9 in 1978  resulted  in no
significant change  in the chlorophyll  concentration or primary  production.    Both j_n situ  and
experimental acidification  have resulted in large increases in periphyton populations (Hall et
al., 1980;  Hendrey, 1976;   Muller,  1980).   Hendrey  (1976)  and  Muller (1980)  observed carbon,
uptake by periphyton  incubated  ui vitro.   They found  that,  although the total rate of photo-
synthesis increased with decreasing pH level  due  to  the  larger  biomass  at  the  lower pH,  the
photosynthesis per unit  biomass decreased with pH.
     From the above discussion  it is  obvious that  not  only is there no  clear correlation  be-
tween pH level  and algal  biomass  or  productivity, but  the  effects of  acidification appear
inconsistent between  systems.   Again,  these apparent inconsistencies probably  reflect a lack
of knowledge about  exact mechanisms relating  acidification and  lake metabolism,  and also  the
complexity  of these mechanisms  and interactions.   Changes  in  the  algal  community biomass  and
productivity probably reflect the  balance  between a number  of  potentially  opposing factors;
those that  tend  to  decrease productivity and biomass  versus  those that  tend to increase pro-
ductivity and/or biomass when acidity  increases.  Factors working to decrease productivity  and
biomass  with declining  pH  levels may  include:  (1)  a  shift in pH level below that optimal  for
algal growth,  (2) decreased  nutrient availability as a result of  decreased decomposition  rates
and  a  sealing-off  of the  mineral  sediments  from  the lake water; and (3)  decreased nutrient
availability as  a  result of changes   in  aquatic  chemistry with acidification.   For example,
despite  the fact that the optional pH  range for growth of label 1 aria flocculosa is between  5.0
to  5.3  (Cholonsky,  1968) or  higher (Kallqvist  et  al. , 1975), this  species  dominated  experi-
mentally acidified  stream communities  at pH level  4  in three out of five replicates (Hendrey
et al.,  1980a).  As noted  in Section  11.3.1.1, aluminum concentrations increase with decreas-
ing pH  level  in  acidified  lakes and streams.    Aluminum is also  a very effective precipitator
of phosphorus, particularly in  the pH range 5  to  6 (Dickson, 1978;  Stumm  and Morgan, 1970).

                                           11-52

-------
In  oligotrophic  lakes, phosphorus  is most  commonly  the  limiting  nutrient for  primary  pro-
ductivity (Schindler,  1975;  Wetzel,  1975).   Therefore, chemical interactions between aluminum
and phosphorus may result in a decreasing availability of phosphorus with decreasing pH level,
and, as a result, decreased primary production.
     Factors working to  increase  productivity and/or biomass with  acidification  of a lake or
stream may  include:    (1)  decreased  loss of  algal  biomass to  herbivores;  (2)  increased  lake
transparency; and  (3)  increased  nutrient  availability resulting from  nutrient  enrichment of
precipitation.    Decreased  population of  invertebrates  (as  discussed  in Section  7.3.1.4),
particularly herbivorous  invertebrates,  may  decrease  grazing pressure  on  algae  and result in
unusual  accumulations  of  biomass.   Hendrey  (1976)   and  Hall  et  al.  (1980)   include  this
mechanism as one hypothesis to explain their observation of increased biomass of periphyton at
pH level  4 despite a decreased production rate per unit biomass.
     Increases in  lake transparency  over time have been correlated with lake acidification in
Sweden (Aimer  et al.,  1978) and the  Adirondack Region  of New York  (Schofield,  1976c).   In
addition, after  the  second year of experimental  lake  acidification (pH 6.7-7.0 to 5.7-5.9) in
northwestern Ontario  (Schindler et  al.,  1980),  lake  transparency  increased by  1-2 m.   These
increases in  transparency  have not  been correlated with  decreases  in  phytoplankton biomass.
Two mechanisms have  been  proposed.   Aluminum acts as  a  very  efficient precipitator for humic
substances.   Dickson  (1978) found that  humic substances  are readily  precipitated  in  the pH
range 4.0 to 5.0.   Dickson (1978) and Aimer  et  al.  (1978) suggest that increases in aluminum
levels with  lake  acidification  (Section  11.3.1.1) have resulted in increased precipitation of
humics from  the  water  column and therefore increased  lake transparency.   Aimer et al.  (1978)
provide data for  one  lake on the  west coast of Sweden.   The pH level declined  from above  6 to
about 4.5 between 1940  and 1975.  The secchi  disc reading increased from about  3m to about 10m
over the  same  period.   Organic matter in the water  (as estimated by KMnO.  demand) decreased
from 24 to  8 mg/liter  from 1958 to 1973.   Schindler et al. (1980)  on the other hand, found no
change in levels  of  dissolved organic carbon with acidification.   Instead,  changes in hydro-
lysis of  organic  matter  with declining pH level  may  affect the light absorbancy characteris-
tics of the  molecules.   Levels  of particulate organic carbon, and  changes with pH level,  were
not reported by Schindler et al. (1980).                                              >
     Acidification of  precipitation  (and  dry  deposition) has  been  accompanied  by increases in
levels of sulfate  and  nitrate.   Both of these are  nutrients  required by plants.   However, as
noted above, the  primary  nutrient limiting primary productivity in most oligotrophic lakes is
phosphorus.   Aimer et  al.  (1978)  report  that atmospheric  deposition  rates of  phosphorus  have
also  increased  in  recent  years.    The world-wide  extent  of  the  correlation between  acidic
deposition and  increased  atmospheric  phosphorus  loading,  however,  is not known.   It is  expect-
ed that changes in atmospheric phosphorus loading would be much more localized  than changes in
acidic deposition.  It is possible  that  in some  areas  increased  atmospheric loading of phos-
phorus has occurred  in recent years  coincidently with increased acidic deposition.   Increased
phosphorus nutrient loading into lakes may then  increase primary production rates.

                                           11-53

-------
     The effect  of acidification on  primary productivity  and algal biomass of  a particular
stream  or  lake  system depends  upon  the  balance  of  the above  forces.   Differences  in  the
importance of these factors between  systems may account for inconsistencies in the response of
different  aquatic  systems  to acidic  deposition.   Acidification does,  however,  result in  a
definite change  in the nutrient  and energy flux  of  the aquatic system, and this  change  may
eventually limit.the total system biomass and productivity.
     Acidification of lakes has also been correlated with changes in the macrophyte community.
Documentation for these changes comes mainly from lakes in Sweden.   Grahn (1977) reported that
in five  to six  lakes  studies in the last  three  to five decades  the  macrophyte communities
dominated  by  Lobelia and  Isoetes  have  regressed,  whereas  communities  dominated by Sphagnum
mosses have expanded.   Acidity levels in these  lakes  apparently  have increased approximately
1.3 to  1.7 pH  units  since the  1930-40's.   In  acid  lakes where conditions  are  suitable  the
Sphagnum peat moss  may  cover  more than  50  percent of the bottom above the 4-m depth, and  may
also grow  at  much  lower depths (Aimer et al.,  1978).   The Sphagnum invasion may start at lake
pH levels  just  below  6 (Aimer et al., 1978).   Similar growths of Sphagnum occur in Norwegian
lakes (Galloway,  1978).    Increases in Sphagnum  as a benthic macrophyte  have  been documented
from one lake in the Adirondack Region of New York (Hendrey and Vertucci, 1980).
     Under acid conditions the Sphagnum moss appears to simply outgrow flowering plant aquatic
macrophytes.    In  laboratory  tests,  the growth  and  productivity  of  the rooted  macrophyte
Lobelia was reduced  by  75 percent at  a  pH  of  4, compared with the control (pH 4.3-5.5).   The
period  of  flowering was  delayed  by  ten  days at the  low pH (Laake, 1976).  At  low pH levels
(pH<5),  essentially  all  the  available inorganic  carbon  is  in the form  of carbon  dioxide or
carbonic acid  (Stumm and  Morgan,  1970).   As  a  result,  conditions may  be  more favorable  for
Sphagnum, an acidophile that is not  able to utilize the carbonate ion.
     Besides  the  shift in  macrophyte species,  the  invasion  of Sphagnum  into  acid lakes  may
have  four  other  impacts   on  the aquatic  ecosystem.   Sphagnum has  a very high  ion-exchange
capacity, withdrawing basic cations  such as Ca   from solution and releasing H  (Aimer et al.,
1978; Anschutz  and Gessner, 1954).   As  a  result,  the presence of  Sphagnum may intensify  the
acidification of the  system and decrease the  availability  of  basic cations from other biota.
Second,  dense  growths of  Sphagnum  form a  biotype that  is an  unsuitable  substratum for many
benthic  invertebrates  (Grahn,  1977).   Growths  of  Sphagnum  in acidic  lakes are  also  often
associated  with  felts  of white  mosses  (benthic  filamentous algae)  and  accumulations  of
non-decomposed organic matter.   In  combination,  these organisms and organic matter may form a
very effective seal.  Interactions between the water column and the mineral sediments, and the
potential  for recycling  of nutrients from the sediments  back into the  water body,  may be
reduced (Grahn, 1977;  Grahn et al., 1974).  These soft bottoms may also be colonized by other
macrophytes.    In  Sweden,  Aimer  et  al.   (1978)  report  that  growths of  Juncus,  Sparaganium,
Utricularia,   Nuphar,  and/or  Nymphaea,  in  addition  to Sphagnum, may  be extensive  in acidic
lakes.  Thus  primary production  by  macrophytes in  lakes with  suitable bottoms  may  be very
                                           11-54

-------
large.   Increased  lake transparency  may also  increase  benthic macrophyte  and algal  primary
productivity.
11.3.1.4  Effects on Invertebrates--In  regional  surveys  conducted in southern Norway (Hendrey
and Wright, 1976), the west coast of Sweden (Aimer et al., 1978), the LaCloche Mountain Region
of Canada (Sprules, 1975), and near Sudbury, Ontario (Roff and Kwiatkowski, 1977),  numbers of
species  of zooplankton were  strongly  correlated  with  pH  level  (Figure  11-23).   Changes  in
community structure were  most noticeable at pH levels below 5.  Certain species (e.g., of the
genera Bosmina, Cyclops,  Diaptomus,  and rotiferans, of the  genera  Polyarthra,  Keratella, and
Kellicottia) apparently have  a high tolerance of acidic conditions and were commonly found in
the pH interval 4.4  to 7.9.   Others, such as cladocerans of the Daphnia genus,  apparently are
more sensitive and were only rarely found at pH <6 (Aimer et al., 1978).
     Similar studies of the  relationship between pH level and biomass or productivity of zoo-
plankton are not  available.   Proposed mechanisms for interactions  between lake acidification
and zooplankton populations are therefore largely hypothetical.
     The  species,  population size,  and productivity  of  zooplankton  are  affected both  by
changes  in  the quality and  quantity of  the  food supply and  shifts  in predator populations.
Changes  in  zooplankton  species and production in response to changes in fish populations have
been clearly demonstrated  (Brooks  and Dodson, ,1965; Dodson, 1974; Walters and Vincent, 1973).
Elimination  of fish  predators often  results  in  dominance of  the zooplankton  community  by
large-bodied species.   Absence  of  invertebrate predators (e.g., large-bodied carnivorous zoo-
plankton) as a  result  of  fish predation or other  reasons  often results  in  the  prevalence  of
small-bodied species (Lynch,  1979). .  Surveys  of acidic  lake waters often have shown the domi-
nance of small-bodied  herbivores  in the zooplankton community  (Hendrey et al. , 1980a).   Fish
also  often  are absent at  these  pH levels (Section 11.3.1.5).   Different zooplankton  species
may  have different physiological  tolerances  to  depressed  pH  levels  (e.g., Potts  and  Frye,
1979).   Food  supplies,  feeding habits,  and grazing  of  zooplankton may  also be  altered with
acidification  as  a consequence of changes  in phytoplankton  species  composition  and/or de-
creases  in  biomass  or productivity of  phytoplankton.   Zooplankton also  rely on  bacteria and
detrital  organic matter for  part  of their food supply.   Thus  an inhibition of  the microbiota
or  a  reduction  in  microbial  decomposition  (Section  11.3.1.2)  may also  affect  zooplankton
populations. "These alternate  mechanisms  postulate for  changes  in  community structure and/or
production of/zooplankton  communities probably play an important role in zooplankton responses
to acidification.
     Synoptic and intensive  studies  of  lakes  and streams have  also demonstrated that  numbers
of species of benthic  invertebrates are  reduced along a  gradient of decreasing pH level  (Aimer
et  al.,  1978;  Conroy  et  al. , 1976;  Leivestad  et al. ,  1976;  Roff  and  Kwiatkowski,  1977;
Sutcliffe and  Carrick,  1973).    In 1500 freshwater localities in Norway studied from 1953-73,
snails were generally present only in lakes with  pH  levels above 6 (0kland, 1980).  Likewise
Gammarus   Lacustris,  a  freshwater  shrimp  and  an  important element  in  the  diet of  fish  in
Scandinavia, was not  found at pH levels  below 6.0 (0kland,  1980).  Experimental  investigations

                                           11-55

-------
 C/J
 LLJ
 0.
 "   -,
 LL   3
 O
 cc
 Ul
 00

 D
 Z   _
          4.0-4.49     4.5-4.99     5.0-5.49     5.5-5.99    6.0-6.49
            2        '  9          16          7          11
>6.5   pH INTERVAL

 12    NUMBER OF LAKES
Figure 11-23.  The number  of species of crustacean zooplankton observed in 57 lakes during a
synoptic survey of lakes in southern Norway (Leivestad et al., 1976).
                                               11-56

-------
have  shown that  adults  of  this  species cannot  tolerate two  days  of exposure  to pH  5.0
(Leivestad et al., 1976).   Eggs were reared at six different pH levels (4.0 to 6.8).   At a pH
of  4.5  a  majority  of the embryos  died within  24 hours.  Thus  the short-term acidification
which often  occurs during the spring  melt  of snow  could eliminate  this  species  from  small
lakes (Leivestad et  al. , 1976).   Fiance (1977) concluded that ephemeropterans (mayflies) were
particularly  sensitive   to  low pH  levels  and their  populations were  reduced  in  headwater
streams of the  Hubbard  Brook watershed in New Hampshire.  In laboratory studies, Bell (1971),
Bell and  Nebecker  (1969), and Raddum (1978) measured the tolerance of some stream macroinver-
tebrates to low pH levels.  Tolerance seems to be in the order caddisflies > stoneflies > may-
flies (Hendrey et al., 1980a).
                                                                               2         2
     Leivestad  et  al. (1976)  reported  on decreased  standing crops  (numbers/m   and  g/m )  of
benthic invertebrates in two  lakes with pH  levels  near 4.5 as compared to five lakes with pH
near 6.0.  Chironamids  were  the dominant group  in  all  lakes.   No fish were found in the acid
lakes.   Lack  of predation by fish should  favor  increases in  benthic biomass, the opposite of
that observed.  Hendrey  et al.  (1980a), on the other hand, from data from eight Ontario  lakes
(pH 4.3 - < 5.7) reported no  reduction in abundance of benthos related to pH level.
     Air-breathing aquatic insects  (e.g.,  backswimmers, water boatmen, water striders) appear
very tolerant of  acidic  environments.   Population densities are often greater in acidic  lakes
and  in  the most  acid lakes   than  in  circumneutral  lakes.  Abundance  of  these  large  inverte-
brates may be related to reduced fish predation (Hendrey et al. ,  1980a).
     Hall   et  al.  (1980)  experimentally  acidified a stream  to  pH  4 and monitored reactions of
macroinvertebrate  populations.  Initially following acidification  there was a 13-fold increase
in  downstream drift  of  insect  larvae.   Organisms  in  the  collector and  scraper  functional
groups were affected  more than predators.  Benthic samples from  the acidified zone of Norris
Brook contained 75 percent fewer individuals than those for reference areas.  There was also a
37 percent reduction  in  insect emergence; members of  the collector  group were most affected.
Insects seem  to be  particularly sensitive at emergence (Bell, 1971).  Many species of aquatic
insects  emerge  early in  the  spring  through  cracks   in  the  ice   and  snow  cover.   These
early-emerging insects are therefore  exposed in m'any cases to the extremely acidic conditions
associated with snowmelt (Hagen and Langeland, 1973).
     Low  pH  also  appeared to  prevent  permanent  colonization by  a  number of  invertebrate
species, primarily  herbivores,  in acidified  reaches  of River Dudden, England  (Sutcliffe  and
Carrick, 1973).   Ephemeroptera, trichoptera,  Ancylus  (Gastropoda) and Gammarus  were absent in
these reaches.
     Damage to  invertebrate   communities  may  influence other components  of the food  chain.
Observations   that  herbivorous  invertebrates  are  especially reduced in  acidic  streams,  as
reported in Norris Brook and  River Dudden, support the hypothesis  (Hall et al.,  1980;  Hendrey,
1976) that changes  in  invertebrate  populations may  be responsible  for  increased  periphytic
                                           11-57

-------
algal  accumulations  in  acidic streams  and benthic  regions  of acidic lakes (Hendrey et  al.,
196iOa).   Benthic  invertebrates  also  assist with  the essential  function  of processing  dead
organic matter.   Petersen (1980)  noted that decomposition of  coarse particulate  organic  matter
in leaf packs was  lower  in an acidic  stream than in two  streams with circumneutral  pH  levels.
The invertebrate community  also  showed  a reduction  in the invertebrate  functional  group  that
specializes in  processing  large particles  (shredders).   In  unstressed aquatic ecosystems,  a
continuous   emergence  of  different  insect  species  is  available to  predators  from spring  to
autumn.   In acid-stressed  lakes  or streams, the variety  and  numbers of prey may  be  reduced.
Periods may be  expected to  occur  in which the amount  of prey  available  to  fish (or other
predators)  is  diminished.
11.3.1.5  Effects on Fish—Acidification of  surface  waters  has had its most obvious,  and  per-
haps the most  severe,  impact on fish populations.   Increasing acidity has  resulted not  just  in
changes in  species  composition  or  decreases in biomass but in many cases  in total  elimination
of populations  of  fish from a given  lake  or  stream.   Extensive depletion of fish  stocks has
occurred in large regions of Norway,  Sweden, and parts of eastern North America.   Both  commer-
cial and sport  fisheries  have been affected in these  areas.   However, precise  assessments  of
losses—in   terms  of  population  extinctions,  reductions  in  yields,  or  economic and  social
impacts—either have not been attempted or are still in  the  process of evaluation.  Potential
damage to fish  populations  inhabiting other acid-sensitive aquatic ecosystems  in  New  England,
the Appalachians,  and  parts  of  southeastern,  north  central,  and  northwestern United  States
have not yet been assessed (Galloway,  1978).
     Declines  in fish populations  have  been related to acidification of surface waters  in the
Adirondack  Region of New  York State (Schofield, 1976a),  southern  Norway  (Jensen  and  Snekvik,
1972;  Wright and Snekvik,  1978),  southwestern Sweden (Aimer  et al., 1974),  the  LaCloche Moun-
tain Region in  southern  Ontario  (Beamish and Harvey, 1972),  and southwestern Scotland  (Wright
et al., 1980a).  Schofield  (1976a,  1976d)  estimated that  in  1975  fish populations in  75  per-
cent of Adirondack  lakes  at high elevation (<610 m) had  been adversely affected by acidifica-
tion.   Fifty-one percent  of the lakes  had pH values less  than 5, and 90 percent  of these lakes
were devoid of  fish life  (Figure 11-24).   Comparable  data for the period 1929 to  1937 indi-
cated that  during that time only about 4 percent of these lakes had pH values below 5  and  were
devoid of fish  (Figure 11-25).   Therefore, entire fish  communities  consisting  of brook trout
( Salvelinus  fontinalis),   lake   trout  (Salvelinus namaycush),  white  sucker  ( Catostomus
commersoni), brown  bullhead  (Icaturus nebulosus) and several  cyprinid species were apparently
eliminated  over a period  of 40 years.   This decrease in fish  populations was associated  with a
decline in  lake pH level.   A survey of more than 2000 lakes in southern Norway,  begun  in 1971,
found that  about one third of these  lakes had lost  their  fish  population  (primarily brown
trout, Sal mo  trutta L.)  since the 1940's  (Wright  and Snekvik,  1978).  Fish  population  status
was inversely related to  lake pH level  (Leivestad  et  al., 1976).   Declines in  salmon  popula-
tions  in southern  Norwegian rivers were reported  as early as the  1920's.   Catch  of  Atlantic
                                           11-58

-------
     20
 e/5
 O
 cc
 m   10
NO FISH PRESENT


FISH PRESENT
                                             PH

Figure 11-24. Frequency distribution of pH and fish population status in Adirondack Mountain
 lakes greater than 610 meters elevation. Fish population status determined by survey gill netting
 during the summer of 1975.

 Source: Schofield (1976a).
                                                11-59

-------
      20
      10
   o
   CC
   UJ
   m
   2
   D
   Z
      10
                                        1975

                               NO FISH PRESENT


                               FISH PRESENT
1930s
             i-n
                             6

                             PH
Figure 11-25.  Frequency distribution of pH and fish pop-
ulation status in 40 Adirondack lakes greater than 610 meters
elevation, surveyed during the period 1929-1937 and  again in
1975.

Source:  Schofield (1976a).
                           11-60

-------
salmon  (Sal mo salar,  L.)  in  nine  acidified southern Norwegian rivers  is  now virtually zero
(Figure 11-26).   In  northern and western  rivers  not  affected by  acidification,  no distinct
downward trend in catch has occurred (Jensen and Snekvik, 1972; Leivestad et al. ,  1976; Wright
et al., 1976).   Similar  changes have been observed in Sweden (Aimer et al., 1974) where it is
estimated that 10,000  lakes  have been acidified to a pH less than 6.0 and 5,000 below a pH of
5.0  (Dickson,  1975).   Populations   of  lake  trout,  lake herring  (Coregonus  artedii),  white
suckers, and  other  species  disappeared rapidly during the 1960's from a group of  remote lakes
in the LaCloche Mountain Region of Ontario (Beamish et al.,  1975).
     It is difficult  to  determine at what pH level fish species disappear from lakes.   Disap-
pearance of the  fish  is  usually not due to massive fish kills, but is the result  of a gradual
depletion of  the  population  following reproductive failures (Leivestad  et  al. ,  1976).   Field
surveys in Scandinav.ia and eastern North America (Aimer et al., 1974;  Schofield,  1976a, 1976b,
1976c; Wright  and Snekvik,  1978)  suggest that  many species  do  not  occur  in lakes  with  pH
values below 5.0.
    c-jp                     •
 ,«.,;'However,   large  spatial  and  temporal  functions  in  pH, and  the  possibility   for  "refuge
areas" from acidic  conditions  during critical periods make  it extremely difficult to general-
ize about effects of acidification on fish populations based on grab samples or annual  mean pH
levels.  The  pH  levels  identified in the literature as critical for reproduction  of a species
or correlated  with  the  absence of   a  species in  lake  surveys are summarized in  Table  11-5.
Values range from pH 4.4 to over 6.0, and are highly species dependent.
     Recent field and  laboratory  studies (Baker and Schofield,  1980;  Dickson,  1978; Driscoll
et al.,  1979; Muniz  and  Leivestad, 1980;  Schofield and Trojnar,  1980) .have  indicated that
aluminum levels in  acidic  surface waters (Section 11.3.1.1, Figure 11-19) may be  highly toxic
to fish  (and  perhaps other biota).    Schofield  and"Trojnar  (1980)  analyzed  survival  of  brook
trout  stocked  into  53  Adirondack lakes as a  function  of 12 water quality parameters.   Levels
of pH, calcium, magnesium,  and  aluminum were significantly different between the two groups of
lakes, with and without trout survival.   However, after accounting for the effects of aluminum
concentrations on differences  between  the  two groups of  lakes,  differences  in calcium,  magne-
sium,  and  pH  levels  were  no   longer  significant.   Aluminum,  therefore,  appears to be  the
primary chemical  factor controlling  survival  of trout in  these  lakes.   Likewise, in laboratory
experiments with  natural Adirondack waters  and synthetic acidified aluminum solutions, levels
of aluminum,  and  not the  pH level  per ^e_, determined survival and growth of  fry of brook trout
and white suckers  (Baker  and  Schofield,  1980).   In addition, speciation of aluminum had a sub-
stantial  effect on  aluminum  toxicity.   Complexation of aluminum with  organic chelates elimin-
ated  aluminum  toxicity to  fry (Baker  and  Schofield, 1980;  Driscoll  et al.,  1979).    As  a
result, waters high  in organic carbon,  e.g., acidic bog  lakes,  may be less  toxic  to fish than
surface waters at similar pH  levels  but with lower levels of dissolved organic carbon.
                                           11-61

-------
  STAVANGER
                            RIVER TOVDAL
                                                              RIVER OALALVEN
                                                                                  '«.
        300
        250
    v>

    O 1 200
        150
              I      I     1
            1900
1920
1940
1960
1980
     v>
         30
         20
         10
            1900
                                              i      I      r
                                               7 ACID RIVERS
1920
1940
                                                   1960
                                       1980
Figure 11-26. Norwegian salmon fishery statistics for 68 unacidified and 7 acidified

rivers (adapted from Aimer et al., 1978).
                                 11-62

-------
                       TABLE 11-5.   pH LEVELS IDENTIFIED IN FIELD SURVEYS AS
                        CRITICAL TO LONG-TERM SURVIVAL OF FISH POPULATIONS

Family
Salmom'dae

Species
Brook trout (Salvelinus
fontinalis)
Lake trout (Salvelinus
namaycush)
Critical pH
5.0
5.1
5.2-5.5
Reference
Schofield, 1976c
Schofield, 1976c
Beamish, 1976
                  Brown trout (Salmo trutta)
                  Arctic char (Salvel inus alpinus)
5.0
     5.2
Aimer et al.,  1978
Aimer et al.,  1978
Percidae
Catostomidae
Ictaluridae
Cyprinidae
Centrarchidae
Esocidae

Perch (Perca fluviatilis)
Yellow perch (Perca flayescens)
Walleye (Stigostedion vitreum)
White sucker (Catostomus
commersoni)
Brown bullhead (Icaturus
nebulosus)
Minnow (Phoxinus phoxinus)
Roach (Rutilus Rutilus)
Lake chub (Couesius plumbeus)
Creekchub (Semotilus atromaculatus)
Commonshi ner (Notfopis cornutas)
Goldenshiner (Notemigonus
crysoleucas)
Smallmouth bass (Micropterus
dolomieui)
Rock bass (Ambloplites rupestris)
Pike (Esox lucius)

4.4-4.9
4.5-4.7
5.5-6.0+
4.7-5.2
5.1
4.7-5.2
5.0
5.5
5.5
4.5-4.7
5.0
5.5
4.9
5.5-6.0+
4.7-5.2
4.4-4.9
Aimer et al . , 1978
Beamish, 1976
Beamish, 1976
Beamish, 1976
Schofield, 1976c
Beamish, 1976
Schofield, 1976c
Aimer et al. , 1978
Aimer et al . , 1978
Beamish, 1976
Schofield, 1976c
Schofield, 1976c
Schofield, 1976c
Beamish, 1976
Beamish, 1976
Aimer et al. , 1978

     Inorganic  aluminum  levels,  and not  low pH  levels,  may therefore  be  a primary  factor
leading to declining  fish  populations  in acidified lakes  and  streams.   However,  many labora-
tory or  i_n situ  field  experiments  have been conducted  on  the effects of pH on  fish without
taking into account aluminum  or other  metal  concentrations  in  naturally  acidic  waters.   As a
result, many  of the conclusions based  on  these  experiments regarding pH  levels  critical  for
fish survival  are suspect.   Therefore these experiments will not be reviewed  here.
     Sensitivity of fish  and other  biota  to low pH  levels  has  also been shown to  depend  on
aqueous calcium  levels  (Bua  and Snekvik, 1972;  Trojnar, 1977;  Wright and Snekvik,  1978).   In
southern Norway,  the  mean  calcium level in  lakes  studied  was approximately  1.1  mg/liter,  as
compared to about  3 mg/liter  in the LaCloche Mountain  Region  (Table 11-4) or 2.1 mg/liter  in
                                           11-63

-------
the  Adirondack  Region  (Schofield,  1976b).   In  Norwegian  lakes,  Wright and  Snekvik  (1978)
identified pH and calcium levels as the two most important chemical  parameters related to fish
status.
     Decreased recruitment of young  fish has been cited  as  the primary factor leading to the
gradual  extinction of fish populations (Leivestad et al. ,  1976; Rosseland et al. ,  1980;  Wright
and  Snekvik,  1978).    Field observations  (Aimer et  al.,  1974;   Beamish,  1974;  Jensen  and
Snekvik,  1972;  Schofield,  1976a)  indicate  changes  in  population  structure over time  with
acidification.   Declining fish  populations  consist primarily of older  and  larger  fish with a
decrease in total population density.   Recruitment failure may result from inhibition  of adult
fish spawning  and/or increased  mortality  of eggs  and  larvae.   Effects  on  spawning  and  de-
creased egg  deposition  may  be  associated  with  disrupted  spawning  behavior  and/or effects  of
acidification on reproductive physiology in maturing adults (Lockhart and Lutz, 1977).    Field
observations by  Beamish et  al.,  (1975) related  reproductive failure in white suckers  to  an
inability of  females to  release  their  eggs.   On the  other hand,  Amundsen  and Lunder  (1974)
observed total mortality  of  naturally spawned trout eggs  in  an acid brook  a  few weeks  after
spawning.   A summary  of Norwegian  studies  (Leivestad et al.,  1976)  concluded that  egg and fry
mortality is the  main cause  of fish reproduction failure.  Spawning periods and occurrence  of
early life  history stages for  many  fish  species coincide with  periods of  extreme  acidity,
particularly during and immediately after snowmelt in the  spring.
     In  some lakes,  fish population decreases  are associated  with  a  lack  of  older  fish
(Rosseland et  al. , 1980).   In  Lake  Tveitvatn  on the  Tovdal  River  in  southern Norway,  brown
trout mortality  apparently  occurs primarily after  the first spawning.  Since 1976,  no fish
past spawning  age have  been found and  population density has decreased steadily  (Rosseland
et al.,  1980).    Fish  kills  of adult salmon in rivers in southern  Norway have been  recorded  as
early as 1911 (Leivestad et al., 1976).
     When evaluating  the  potential  effects of acidification on fish, or other biotic, popula-
tions,   it is very important  to keep  in  mind the highly diversified nature of aquatic systems
spatially, seasonally,  and  year-to-year.  As a  result  of this diversity,  it  is necessary  to
evaluate each system  independently  in assessing the reaction  of  the population to  acidifica-
tion.   Survival  of a fish population may depend more on the availability of refuge  areas from
acid conditions  during  spring  melt  or of  one tributary predominantly  fed by baseflow  and
supplying an adequate area for spawning than on  mean annual  pH, calcium, or inorganic  aluminum
levels.
11.3.1.6   Effects on Vertebrates Other Than  Fish—Certain species  of amphibians  may be  the
vertebrate animals,  other than  fish,  most immediately and directly affected by acidic deposi-
tion (Rough  and  Wilson,  1977).   Their vulnerability is due  to their reproductive  habits.   In
temperate regions, most  species of frogs and toads,  and approximately half of the  terrestrial
salamanders, lay  eggs in ponds.  Many  of  these species breed  in temporary  pools formed each
year by accumulation of rain and melted snow.  Approximately 50 percent of the species of toads
                                           11-64

-------
 and frogs in the United States regularly breed in ephemeral pools; about one-third of the sal-
 amander  species  that have aquatic  eggs  and larvae and terrestrial  adults  breed in temporary
 pools.   Most  of  these pools  are small and collect drainage from a limited area.  As a result,
 the acidity of  the eater in these pools is strongly influenced by the pH of the precipitation
 that  fills  them.  Ephemeral  pools  are  usually more acidic than  adjacent  permanent bodies of
 water.   Rough  and Wilson  (1977)  report that  in 1975,  in the vicinity of  Ithaca,  N.Y. ,  the
 average  pH of  12 temporary ponds was 4.5 (range 3.5 to 7.0), while the average pH of six per-
 manent ponds was 6.1 (range 5.5 to 7.0).   Amphibian eggs and larvae in temporary pools are ex-
 posed to these acidic conditions.
     Rough and Wilson  (1977)  and Rough (1976) studied the effect of pH level on embryonic de-
 velopment of  two common  species of salamanders:   the spotted salamander (Ambystoma maculatum)
 and the  Jefferson  salamander  (A.  jeffersonianum).   In  laboratory experiments,  embryos of the
 spotted  salamander tolerated  pH levels from 6 to 10 but had greatest hatching success at pH 7
 to 9.  The Jefferson salamander tolerated pH levels 4 to 8 and was most successful at 5 to 6.
 Mortality of  embryos rose abruptly beyond the  tolerance  limits.   In a four-year  study  of a
 large  breeding   pond  (pH 5.0-6.5)  938 adult  spotted  salamanders produced  486 metamorphosed
 juveniles (0.52 juveniles/adult), while 686 adult Jefferson salamanders produced 2157 juvenile
 (3.14  juveniles/adult).   Based on  these findings,  Rough  and Wilson  (1977)  predict that  con-
 tinued acidic  deposition may  result  in substantial  shift in  salamander  and  other amphibian
 populations.
     Gosner and Black (1957)  report that only acid-tolerant species of amphibians can breed in
 the acid (pH  3.6 to 5.2)  sphagnoceous bogs  in the New Jersey Pine Barrens.
     Frog populations in  Tranevatten,  a lake near Gothenberg, Sweden, acidified by acidic pre-
 cipitation,  have also been  investigated (Hagstrom,  1977;  Hendrey,  1978).   The lake  has  pH
 levels ranging from 4.0 to 4.5.  All fish have disappeared, and frogs belonging to the species
 Rana temporaria  and  Bufo  bufo are being elimated.   At the time of the study (1977) only adult
 frogs eight to ten years old were found.  Many egg masses of Rana temporaria were observed in
 1974,  but few were  found in  1977,  and the  few larvae (tadpoles) observed  at  that time died.
     Frogs and  salamanders  are  important  predators on invertebrates, such  as  mosquitoes  and
 other pest species, in pools,  puddles, and  lakes.  They also are themselves important prey for
 higher tropic  levels  in an ecosystem.   In many habitats salamanders are the most abundant ver-
 tebrates.  In a  New  Hampshire  forest,  for  example,  salamanders were found to exceed birds  and
mammals in both numbers and biomass (Hanken et al.,  1980).
     The elimination of  fish  and  vegetation from lakes by  acidification  may have an indirect
effect on a variety of vertebrates:   species of fish-eating birds (e.g.,  the bald eagle, loon,
and osprey),   fish-eating mammals  (e.g., mink and  otter),  and  dabbling  ducks which  feed on
aquatic vegetation.  In  fact,  any animal that depends on  aquatic organisms (plant or animal)
 for a portion  of its  food may be affected.
                                           11-65

-------
     Increasing acidity in  freshwater  habitats  results in shifts in species,  populations,  and
communities.   Virtually all  trophic levels are affected.
11.3.2  Terrestrial  Ecosystems
     Determining the effects  of  acidic precipitation on terrestrial ecosystems is not an easy
task.    In  aquatic  ecosystems  it  has  been  possible  to measure  changes in pH that  occur  in
acidified waters and  then observe the  response  of.organisms living in aquatic  ecosystems  to
the shifts  in pH.   In  the  case  of  terrestrial  ecosystems the  situation  is  more complicated
since no component  of  terrestrial  ecosystems appears  to be as sensitive to  acidic precipitation
as organisms  living in  poorly buffered aquatic ecosystems.   Nonetheless,  soils and vegetation
may be  affected,  directly  or indirectly,  by acidic precipitation, albeit  in,  complex  ways.
11.3.2.1  Effects on Soils—Acidity  is  a  critical  factor in the  behavior  of  natural  or agri-
cultural soils.   Soil  acidity influences  the  availability  of  plant nutrients  and  various
microbiological processes which are  necessary for the functioning  of  terrestrial  ecosystems,
therefore,  there  is  concern  that  acidic  precipitation  over time  could  have  an  acidifying
effect on soils through  the addition of  hydrogen  ions.   As  water containing  hydrogen cations
(usually from weak  acids) moves  through the  soil, some  of  the hydrogen ions  replace  adsorbed
exchangeable cations,  such as  Ca  , Mg  ,  K ,  and Na   (see Figure 11-27).   The removed cations
are then carried deep  into  the soil  profile or into  the ground water.   In  native soils hydro-
gen ions are derived from the  following sources:  (Wiklander,  1979)
     1.    nutrient  uptake by plants—the roots adsorb cation
                                +
          nutrients  and desorb H ;
     2.    C02 produced by plant roots and  micro-organisms;
     3.    oxidation  of NH4+  and S, FeS2> and H2$ to HN03 and H2S04;
     4.    very acid  litter in  coniferous forests, the main acidifying
          source for the A and B horizons;
     5.    atmospheric  deposition of H-SO,  and some HNO,,  N0x, HC1 and
          NH4+ (after  nitrification to HN03).

In addition to  the  acidifying factors listed above,  the use of ammonium fertilizers on culti-
vated lands  increases  the  hydrogen  cations in the water solution.  Ammonium  fertilizers  are
oxidized by  bacteria  to  form nitrate  (NO^ )  and  hydrogen  ions (H )  (Donahue et  al.,  1977).
Increased  leaching  causes  soils  to become  lower in  basic  Ca  ,  Mg   , Na  ,  and  K   cations
(Donahue et al., 1977).   Sensitivity to leaching is  according to the following sequence:   Na
» K+ >  Mg2+ > Ca2+  (Wiklander, 1979).
     Norton (1977)   cited  the  potential effects of acidic deposition on soils that are listed
in Table 11-6.  Of  those listed,  only the increased  mobility of cations and  their accelerated
loss has been  observed  in field experiments.   Overrein (1972) observed an  increase in calcium
leaching under  simulated acid rain  conditions  and increased loss by  leaching of  Ca   ,  Mg  ,
                                           11-66

-------
  SOIL PARTICLES
                        ACID RAIN
SOIL SOLUTION
~
-
WEATHERING— ».
-
•*•
*
+


Ca24
K*
Na*— T
NH;
SO2"
H3por


Ca24
Mg24
"H* K4
Na*
NOJ
so,2-
fc
V J
CAN BE LEACHE
Figure 11-27. Showing the exchangeable ions
of a soil with pH   7, the soil solution com-
position, and the replacement of Na+ by H+
from acid rain (Wiklander, 1979).
                   11-67

-------
         TABLE 11-6.   POTENTIAL EFFECTS OF ACID PRECIPITATION ON SOILS

               Effect                                      Comment

        Increased mobility of                 Mobility changes are essentially
          most elements                         in the order:  monovalent,
                                                divalent, trivalent cations.
        Increased loss of                     Under certain circumstances may
          existing clay minerals                be compensated for by production
                                                of clay minerals which do not
                                                have essential (stoichiometric)
                                                alkalies or alkali earths.
        A change in cation                    Depending on conditions, this
          exchange capacity                     may be an increase or a decrease.
        A general propor-                     In initially impoverished or
          tionate increase in                   unbuffered soil, the removal
          the removal of all                     may be significant on a time
          cations from the soil                 scale of 10 to 100 years.
        An increased flux in
          nutrients through the
          ecosystem below the
          root zone

Source:   Norton (1977).

and Al    were observed  by  Cronan (1980)  when  he treated New  Hampshire  soils  with  simulated
acid rain at a pH 4.4.
     Wiklander (1979)  notes  that  in  humid areas leaching leads to a gradual  decrease of plant
nutrients in  available  and mobilizable forms.   The rate of nutrient decrease is determined by
the buffering  capacity of the soil  and  the  amount and composition  of  precipitation  (pH  and
salt  content).  Leaching  sooner or  later  leads  to  soil  acidification   unless the  buffering
capacity of the  soil  is strong and/or the  salt concentration of precipitation is high.   Soil
acidification  influences  the  amount of  exchangeable  nutrients  and  is  also  likely  to affect
various  biological processes  in the soil.
                                                      2~
     Acidic precipitation increases the amounts of S04   and N03  entering the soils.   Nitrate
is easily  leached from  soil;  however, because it  is usually deficient   in the soil  for both
plants  and  soil  microorganisms,  it  is rapidly  taken up  and retained  within  the  soil-plant
system  (Abrahamsen  et al.,  1976; Abrahamsen  and  Dollard,  1979; Gjessing et  al. , 1976).   The
fate of  sulfate is determined by its  mobility.   Retention of sulfate in soils appears to depend
on the  amount  of  hydrous oxides of iron and aluminum present.  The amounts of these  compounds
present  varies with  the soil  type.   Insignificant amounts of the hydrated oxides  of  iron (Fe)
and aluminum  (Al)  are found  in organic soils; therefore, sulfate retention is low (Abrahamsen
and Dollard,  1979).   The presence of  hydrated  oxides of iron and  aluminum,  however,  is only
                                           11-68

-------
one of the factors associated with the capability of a soil to retain sulfur.  The capacity of
soils to  adsorb  and retain anions increases  as  the pH decreases and with the salt concentra-
tion.  Polyvalent  anions of  soluble  salts added experimentally  to  soils increases adsorption
and decreases leaching of salt cations.  The effectiveness of the anions studied in preventing
leaching was in the following order:   Cl~ ~ N03" < S042 < H2P04" (Wiklander, 1980).  Additions
of  sulfuric  acid  to a  soil  will have  no effect  on  cation  leaching  unless the  sulfate  is
mobile,  as  cations  cannot  leach without  associated anions  (Johnson  et al.,  1980;  Johnson,
1980; Johnson and Cole, 1980).
     Leaching of  soil  nutrients  is efficiently  inhibited  by  vegetation growing on it.   Plant
roots take up  the nutrients frequently  in  larger  amounts  than required by the plants.   Large
amounts of these  nutrients  will  later be deposited on the soil surface as litter or as leach-
ate from the vegetation canopy (Abrahamsen and Dollard, 1979).
     In lysimeter  experiments  in Norway, plots with vegetation cover were used.   One plot had
a dense  layer  of  the grass, Deschampsia flexuosa (L.) Trin.  and the other a less dense cover.
The soil  retained  50 percent of the  SO.    added to it.   The  greatest  amount was  retained in
the lysimeters covered  with grass; the relative retention increased with increasing additions
of sulfate (Abrahamsen  and  Dollard,  1979).   Leaching  of  cations  from  the soil was reduced by
                         2-                          2+       2+
the retention of  the SO,   ; however, leaching of Ca   and Mg   increased significantly as the
acidity of the simulated  rain increased. In the most acid treatment leaching of Al was highly
significant.   The  behavior  of K , NO., ,  and  NH.  was  different in  the  two  lysimeter series.
These ions were  retained  in the grass-covered lysimeters  whereas  there was a net leaching of
K  and  NO,   in the  other  series.   Statistically significant effects were  obtained  only  when
the pH of the simulated rain was 3.0 or lower (Abrahamsen and Dollard,  1979).
     The Scandinavian  lysimeter  experiments  appear to demonstrate that the  relative  rate  of
adsorption  of  sulphate  increases  as  the  amounts  applied  are  increased.   In  the  control
lysimeters the output/input  ratio  was approximately one.   These1 results are in agreement  with
results of watershed  studies  which frequently appear to  demonstrate that,  on an annual  basis,
sulfate outflow is  equal  to or greater  than  the amounts  being added (Abrahamsen and Dollard,
1979; Gjessing et  al. ,  1976).   Increased outflow'may  be  attributed to dry deposition and the
weathering of sulfur-bearing rocks.  The increased deposition of sulfate via acidic precipita-
tion  appears  to  have  increased the  leaching of  sulfate  from the  soil.   Together with  the
retention of hydrogen  ions  in the soil  this  results  in  an increased leaching of the nutrient
cations K+,  Ca +,  Mg +,  Mn  (Abrahamsen  and  Dollard, 1979).   Shriner  and  Henderson,  (1978)
however,  in their  study  of  sulfur distribution  and  cycling  in the Walker Branch Watershed in
eastern Tennessee noted the additions of sulfate sulfur by precipitation were greater than the
amount lost in stream  flow.   Analysis of the  biomass  and  soil concentrations of sulfur indi-
cated that sulfur was being retained in the mineral soil  horizon.   It is suggested  that leach-
ing from  organic  soil  horizons  may be  the mechanism by  which sulfur  is  transferred  to  the
mineral  horizon.   Indirect evidence suggests that vegetation scavenging of atmospheric sulfate
                                           11-69

-------
plays an important role by adding to the amounts of sulfur entering the forest system over wet
and dry deposition.
     Studies of the  nutrient  cycling of sulfur in a number of forest ecosystems indicate that
some  ecosystems  accumulate  (Heinricks  and  Mayer,  1977;  Johnson et  al.,  1980;  Shriner  and
Henderson,  1978)  while other ecosystems  maintain a balance between the additions and losses of
sulfur or show a  net loss (Cole and  Johnson,  1977).   Sulfur accumulation appears to be asso-
ciated with sulfate  adsorption  in  subsoil  horizons.   Sulfate adsorption is strongly dependent
on pH.   Little adsorption occurs above pH 6-7  (Harward and Reisenaur, 1966).   The  amount of
sulfate in a soil  is a function of  a soil's adsorption properties and the  amount of sulfate
that has been added  to the soil, integrated  over time.   Soil properties may favor the adsorp-
tion of sulfate;  however,  the net annual  accumulation of sulfate at any specific time will be
influenced  by the degree of soil saturation (Johnson et al., 1980).
     McFee  et al.  (1977)  calculated that 1000 cm  of rainfall  at pH 4.0 could reduce the base
saturation  of the upper 6 cm of a midwestern  United States forest soil by  15 percent and lower
the pH of the A-l horizon (the  surface  layer  in most agricultural soils)  by  0.5 units if no
countering   forces  are operating  in the soil.   They note,  however,  that  many counteracting
forces could  reduce  the  final  effect of  acidic precipitation,  including the  release  of  new
cations to  exchange sites by weathering  and nutrient recycling by vegetation.
     Lowered soil  pH also influences the  availability  and toxicity of metals  to plants.   In
general, potentially  toxic  metals  become  more  available  as  pH  decreases.    Ulrich  (1975)
reported that aluminum  released by acidified soils could be phytotoxic if acid rain continued
for a  long  period.  The degree of  ion leaching  increased with decreases in pH, but the amount
of cations  leached was  far less than the  amount of acid added  (Malmer,  1976).   Baker et al.
(1977) found that sulfur dioxide in precipitation increased the extractable acidity and alumi-
num, and decreased the  exchangeable bases, especially calcium and magnesium.   Although dilute
sulfuric acid  in  sandy  podsolic  soils caused  a  significantly decreased  pH  of  the  leached
material, the  amount of  acid applied  (not  more than  twice the yearly  airborne supply over
southern Scandinavia)  did not  acidify  soil  as  much as did nitrate  fertilizer  (Tamm  et al.,
1977).  Highly acidic  rainfall,  frequently with a pH less than 3.0, in combination with heavy
metal particulate fallout from smelters, has  caused soils to become toxic  to seedling survival
and  establishment  according to  observations by  Hutchinson and Whitby  (1977).   Very low soil
pH's  are associated  with  mobility of toxic  aluminum compounds in the soils.   High acidity,
high sulfur, and  heavy metals in the rainfall have caused fundamental  changes in the structure
of soil organic matter.   The sulfate and  heavy  metals  were borne by air  from the smelters in
the Sudbury area  of  Ontario and brought to earth by dry and wet deposition.   Among the metals
                                           11-70

-------
deposited in rainfall and dustfall were nickel, copper, cobalt, iron, zinc, and lead.  Most of
these  metals  are retained  in the upper  layers  of  soil,  except in  very  acid  or  sandy soils.
     The  accumulation of  metals  is  mainly  an  exchange  phenomenon.   Organic components  of
litter,  humus,  and  soil  may  bind  heavy  metals as stable complexes  (Tyler,  1972).   The heavy
metals  when  bound may  interfere with litter decay  and nutrient cycling, and in this manner
interfere with  ecosystem functioning  (Tyler, 1972).   Acidic  precipitation,  by  altering  the
equilibria of  the metal complexes through  mobilization,  may have a negative  effect upon  the
residence time of the heavy metals in soil and litter (Tyler, 1972, 1977).
     Biological  processes  in  the soil  necessary for  plant growth can  be  affected  by  soil
acidification.    Nitrogen fixation,  decomposition  of  organic  material,   and  mineralization,
especially of  nitrogen,  phosphorus  and  sulfur,  might be  affected (Abrahamsen  and Dollard,
1979; Alexander,  1980;  Malmer,  1976;  Tamm et al. , 1977).   Nearly all of the  nitrogen, most of
the phosphorus and  sulfur  as well as other nutrient elements in the soil  are bound in organic
combination.  In this form,  the elements are largely or entirely unavailable for utilization by
higher  plants  (Alexander,  1980).   It is principally  through  the activity of  heterotrophic
microorganisms that  nitrogen, phosphorus,  and sulfur  are  made available to  the autotrophic
higher plants.   Thus, the microbial processes that -lead to the conversion of  the organic forms
of these elements to the inorganic state are crucial for maintaining plant life in natural  or
agricultural   ecosystems.   The   key  role  of  these  degradative processes is  the  fact  that
nitrogen is  limiting for food production  in much of the world and governs primary  productivity
in many terrestrial  habitats (Alexander,  1980).
     Many,  and  probably most,   microbial  transformations  in  soil  may  be  brought  about  by
several species.   Therefore,  the reduction or elimination of one population is  not necessarily
detrimental  since a  second  population,  not affected  by the  stress,  may fill the  partially or
totally vacated niche.  For example,  the  conversion of organic nitrogen compounds  to inorganic
forms  is  characteristically  catalyzed by a  number  of species, often quite  dissimilar,  and a
physical or  chemical perturbation affecting one of  the  species may not seriously  alter  the
rate of the  conversion.   On the other hand,  there are a few processes that are  in  fact carried
out, so  far  as  it  is now  known,  by only  a single  species, and elimination  of  that species
could have serious  consequences.  Examples  of this  are  the nitrification  process,  in which
ammonium is  converted  to  nitrate,  and  the  nodulation of  leguminous  plants, for  which  the
bacteria are  reasonably specific according to the leguminous host (Alexander, 1980).
     The nitrification process  is  one  of the best indicators of pH stress because the respon-
sible organisms,  presumably largely autotrophic bacteria,  are sensitive both  in culture and in
nature  to increasing acidity  (Dancer  et al., 1973).   Although nitrification will  sometimes
occur at pH  values  below 5.0,  characteristically the  rate  decreases with increasing acidity
and often is  undetectable much below  pH 4.5.   Limited data suggest  that the process of sulfate
reduction to  sulfide in soil  is markedly inhibited  below  a pH of 6.0 (Connell  and Patrick,
                                           11-71

-------
1968)  and studies of the presumably responsible organisms in culture attest to the inhibition
linked with the acid conditions (Alexander, 1980).
     Blue-green algae have  been  found to be absent  from  acid soils even though there is both
adequate moisture and exposure  to sunlight.   Studies by Wodzinski et al. (1977) attest to the
sensitivity of these  organisms  to acidity.   Inhibition of the  rates of both CO- fixation and
nitrogen fixation was noted.
     Studies concerned with the acidification of soil by nitrogen fertilizers or sulfur amend-
ments, as well  as comparisons of the microbial  populations in soils with dissimilar pH values,
attest to the  sensitivity  of bacteria to  increasing  hydrogen ion concentrations.   Character-
istically,  the numbers  of  these organisms  decline,  and  not  only is  the total  bacterial
community reduced in numbers, but individual  physiological groups are also reduced (Alexander,
1980).  The  actinomycetes   (taxonomically  considered to be bacteria) also  are  generally less
abundant as the pH decreases, while the relative abundance of fungi increases,  possibly due to
a lack of  competition  from other heterotrophs (Dancer et al., 1973).  The pH of soil  not only
influences the microbial community  at large but also those specialized populations that colo-
nize the root surfaces (Alexander, 1980).
     It is difficult  to  make generalizations concerning  the  effects of soil acidification on
microorganisms.   Many  microbial  processes that are important  for  plant growth  are  clearly
suppressed as the pH declines; however, the inhibition noted in one soil at a given pH may not
be noted  at  the  same pH in  another  soil  (Alexander, 1980).   The capacity of some microorgan-
isms to become acclimated  to changes  in pH  suggests the  need to  study  this phenomenon using
environments that  have  been maintained at different pH values  for  some  time.   Typically the
studies have  been done  with soils maintained  only  for short periods  at  the  greater  acidity
(Alexander, 1980).   The consequences  of  increased acidity in the  subterranean ecosystem are
totally unclear.
     Adding nitrate and  other forms of nitrogen from the atmosphere to ecosystems is  an inte-
gral function of the terrestrial  nitrogen cycle.  Higher plants and microorganisms can assimi-
late the inorganic forms rapidly.   The contribution of inorganic nitrogen in wet precipitation
(rain plus snow)  is usually equivalent to only a few percent of the total nitrogen assimilated
annually by plants in terrestrial  ecosystems; however, total  nitrogen contributions, including
organic nitrogen, in  bulk  precipitation  (rainfall  plus dry fallout) can be significant, espe-
cially in unfertilized natural systems.
     Atmospheric  contributions  of  nitrate can  range from  less than  0.1  kg   N/ha/yr  in the
Northwest (Fredericksen, 1972) to 4.9 kg N/ha/yr  in  the  eastern United States (Henderson and
Harris, 1975;  Likens  et  al. , 1970).   Inorganic nitrogen  (ammonia-N  plus nitrate-N) additions
in wet precipitation  ranged from  less than 0.5  kg/ha/yr  to  more than 3.5 kg/ha/yr in Junge's
study (1958) of  rainfall over the United States.  On the other hand, total nitrogen  loads in
bulk precipitation range from less  than 5 kg/ha/yr in desert regions of the West to more than
                                           11-72

-------
30  kg/ha/yr  near  barnyards  in  the  Midwest.   Total  contributions  of  nitrogen  from  the
atmosphere  commonly range  from  about  10  to 20  kg  N/ha/yr  for  most  of the  United  States
(National Research Council, 1978).
     In  comparison,  rates  of annual  uptake by plants  range from 11 to 125 kg N/ha/yr in eco-
systems  selected  from  several  bioclimatic zones (National Research Council, 1978).  Since the
lowest  additions  are generally  associated with  desert areas where rates  of  uptake  by  plants
are low,  and  the  highest additions usually occur  in moist areas where plant  uptake is high,
the contributions  of ammonia and nitrate from rainfall  to terrestrial ecosystems are equiva-
lent to about 1 to 10 percent of annual plant uptake.  The typical additions of total nitrogen
in bulk  precipitation,  on  the other hand, represent from about 8 to 25 percent of the  annual
plant  requirements  in eastern  deciduous  and western  coniferous  forest  ecosystems.   Although
these comparisons suggest that plant growth in terrestrial ecosystems depends to a significant
extent on atmospheric  deposition,  it  is not  yet possible to estimate the importance of these
contributions by comparing them with the biological fixation and mineralization of nitrogen in
the soil.  In nutrient-impoverished ecosystems,  such  as  badly eroded abandoned  croplands or
soils subjected to  prolonged leaching  by acidic precipitation, nitrogen additions from  atmos-
pheric depositions are certainly important to biological productivity.  In largely unperturbed
forests,  recycled  nitrogen from  the  soil  organic  pool   is  the  chief source  of  nitrogen  for
plants, but nitrogen to support increased production must come either from biological fixation
or from atmospheric contributions.  It seems possible, therefore, that man-generated contribu-
tions could play  a significant ecological  role in  a relatively large portion of the forested
areas near industrialized regions (National  Research Council, 1978).
     Sulfur,  like  nitrogen,  is essential for  optimal plant  growth.   Plants  usually  obtain
sulfur from the soil in the form of sulfate.   The amount of mineral  sulfur in soils is usually
low and  its  release  from organic matter during microbial  decomposition  is a major source for
plants (Donahue et  al. ,  1977).   Another major source  is  the wet and dry deposition of  atmos-
pheric sulfur (Brady, 1974; Donahue et al.,  1977;  Jones, 1975).
     In agricultural soils  crop residues,  manure,  irrigation  water,  and  fertilizers and soil
amendments  are  important sources of sulfur.  The' amounts of  sulfur entering  the  soil  system
from atmospheric  sources is  dependent  on proximity  to industrial  areas,  the  sea coast,  and
marshlands.   The prevailing  winds  and  the amount of  precipitation  in a given region are also
important  (Halsteand  and   Rennie,  1977).    Near  fossil-fueled  power  plants  and  industrial
installations the amount of sulfur in  precipitation may be as much as 150 pounds per acre (168
kg/ha) or more (Jones,  1975).  By contrast,  in rural areas, based on the equal  distribution of
sulfur oxide emissions over the coterminous   states, the  amount  of  sulfur in precipitation is
generally well below the  average 15 pounds per acre (17 kg/ha).   Approximately 5 to 7  pounds
per acre  (7 to  8  kg/ha)  per year  were  reported  for Oregon  in  1966 (Jones, 1975).  Shinn and
Lynn (1979)  have  estimated  that in the  northeastern United States,  the  area where precipi-
tation is most  acidic,  approximately  5 x  10  tons  of  sulfate per  year  is  removed by rain
                                           11-73

-------
(Brady, 1974).   Hoeft et al.  (1972) estimated the overall average sulfur as sulfate deposition
at 26 pounds of sulfur/acre per year (30 kg S/ha per year).   Estimates for rural areas were 14
pounds of sulfur  per  acre per year (16 kg/ha/yr).   Approximately 40 to 50 percent of the sul-
fur  additions  occurred from  November to  February.   Tabatabai  and  Laflen (1976)  found  that
SO.-S  deposition  in Iowa  was  greatest in  fall  and winter when precipitation  was  low.   They
also estimated that  the  additions  of sulfur by  precipitation  were the same for Ames, Iowa in
1976 as  were reported for 1923, approximately  15  Ibs/acre.   The  average  annual  additions of
sulfur by  precipitation  were  similar to that  reported for rural  Wisconsin by  Hoeft et al.
(1972)
     Experimental  data have shown that even though  plants are supplied with adequate soil  sul-
fate they can absorb 25 to 35 percent of their sulfur from the  atmosphere (Brady,  1974).   Par-
ticularly if the soil sulfur is low and atmosphere  sulfur high, most of the sulfur required by
the plant can  come  from  the atmosphere (Brady,  1974).   Atmospheric sulfur would be of benefit
chiefly to plants growing on lands  with a low sulfur content (Brezonik, 1976).
     Tree species vary  in their ability to  utilize  sulfur.  Nitrogen and sulfur are'biochem-
ically associated in plant proteins, therefore,  a close relationship exists between the two in
plants.  Apparently, nitrogen is only taken up at the rate at which sulfur is available.   Pro-
tein formation is,  therefore,  limited by the amount of sulfur available (Turner and Lambert,
1980).    Conifers  accumulate  as sulfate any  sulfur  beyond the  amount  required  to  balance the
available nitrogen.   Protein  formation  proceeds at the  rate at  which nitrogen becomes avail-
able.  Trees  are  not  injured  when sulfur  is applied  as sulfate rather than  SQy  (Turner and
Lambert,  1980).
   .  When  discussing  the  effects   of  acidic precipitation,  or  the  effects  of  sulfates or
nitrates on  soils,  a distinction  should be made between managed  and  unmanaged soils.   There
appears  to  be  general  agreement that managed  agricultural  soils are  less  susceptible  to the
influences of  acidic precipitation than are unmanaged  forest  or rangeland soils.   On managed
soils more than adequate amounts of lime are used to counteract the acidifying effects of fer-
tilizers in agricultural  soils.  Ammonium fertilizers,  usually  as ammonium sulfate [(NH.USO.]
or ammonium  nitrate,  (NH.NO,)  are  oxidized by bacteria to form sulfate (SO.  ) and/or nitrate
(NO.,)  and  hydrogen  ions  (H  )  (Brady,  1974; Donahue et al., 1977).   The  release  of hydrogen
ions into the  soil  causes the soil to become acidified.  Hydrogen ions are also released into
the soil when  plants  take up mineral nutrients.  Hence, substances (notably various complexes
of ammonium  and sulfate  ions), although of  neutral  pH,  or  nearly so, are acidifying in their
effects when they are taken up by plants or animals.   Thus,  the concept of "acidifying precip-
itation"  must be added to the concept of "acid precipitation."
     The acidifying effects  of fertilization or acidic  precipitation  is  countered in managed
soils  through  the use  of  lime.  Liming tends to raise  the pH and thereby eliminate most major
problems associated with  acidic  soils (Donahue et al.,  1977;  Likens et al., 1977).   Costs of
liming all  natural  soils  would  be prohibitive  as  well as  extremely  difficult to  carry  out.
                                           11-74

-------
     Precipitation   may   add  many  chemicals  to   terrestrial,   aquatic,   and  agricultural
ecosystems.   In  addition to  sulfur and  nitrogen,  phosphorus and  potassium are biologically
most  important  because they  often are  in  limited  supply  in the  soil  (Likens  et  al.  1977).
Other  chemicals  of  varying  biological  importance and varying concentration  found  in precipi
tation  over  North  America are  the following:   chlorine,  sodium, calcium,  magnesium,  iron,
nickel, copper, zinc, cadmium, lead, manganese, (Beamish, 1976; Brezonik, 1976; Hutchinson and
Whitby, 1977) mercury,  (Brezonik,  1976) and cobalt  (Hutchinson  and Whitby, 1977).   Rain over
Britain and  the  Netherlands,  according to Gorham,  (1976)  contained the following elements in
addition  to  those reported  for  North American precipitation:   aluminum,  arsenic,  beryllium,
cerium, chromium,  cesium, antimony,  scandium, selenium, thorium,  and  vanadium.  Again  it is
obvious that many of these  elements  will  be  found  in precipitation  in highly industrialized
areas  and  will  not be of biological  importance  until  they enter an  ecosystem  where  they may
come  into  contact with some  form  of  life,  as in the  case  of heavy metals  in  the  waters and
soils  near Sudbury,  Ontario.  Of  chemical  elements found  in precipitation,  magnesium,  iron,
copper, zinc, arid  manganese  are  essential in  small amounts for the growth of plants;  however,
at  high  concentrations these  elements,  as  well  as the  other heavy metals, can be  toxic to
plants  and  animals.   Furthermore, the  acidity  of  precipitation  can  affect  the  solubility,
mobility,   and toxicity  of these  elements to the  foliage or roots of plants and to  animals or
microorganisms that may ingest or decompose these plants.
     Wiklander (1979)  has pointed  out  that based  on  the  ion exchange theory,  ion  exchange
experiments,  and  the leaching of  soil  samples,  the following conclusions  can  be drawn  about
the acidifying effect on soils through the atmospheric deposition of mineral acids.
     1.   At  a soil  pH  >  6.0 acids are  fully  neutralized by decomposition of CaGO, and  other
          unstable minerals and by cation exchange.
     2.   At  soil  pH F  5.5 the efficiency of  the proton to decompose minerals and  to replace
                         2+    2+   +         +
          exchangeable Ca  ,  Mg  ,  K  ,  and  Na  decreases with the soil  pH.   Consequently, the
          acidifying effect of mineral  acids on soils decreases, but the effect on  the runoff
          water increases in the  very acid soils.
                     2+     2+   +          +
     3.   Salts of CA   ,  Mg   , K , and NH.   in the precipitation counteract the absorption of
          protons and, in  that way, the decrease of the base saturation.  A proportion of the
          acids percolate through the soil and acidify the runoff.
     The  sensitivity of  various  soils  to  acidic  precipitation depends  on the soil  buffer
capacity and  on  the  soil  pH.   Noncalcareous sandy soils with pH J 5 are the most sensitive to
acidification; however,  acidic soils would be most likely to release aluminum.
     Very  acid  soils are  less  sensitive to further acidification  because they are  already
adjusted by  soil  formation to acidity and  are therefore more stable.   In  these  soils  easily
weatherable minerals have  disappeared,  base  saturation  is  low,  and the pH of the soil may be
less  than  that  of precipitation.   The  low  nutrient level  is a  crucial factor which  limits
                                           11-75

-------
productivity in these  soils.   Even a slight decrease  in  nutrient status by leaching may have
a detrimental effect on  plant yield (Wiklander, 1979).   Fertilization  appears to be the only
preventive measure.
     In properly  managed cultivated soils,  acidic precipitation  should cause  only  a slight
increase  in  the  lime  requirement, with  the cost  compensated  for by  the supply  of  sulfur,
nitrogen,  magnesium, potassium, and calcium made available to plants (Wiklander, 1979).
11.3.2.2  Effects on Vegetation—The atmosphere, as well as the soil,  is a source of nutrients
for plants.  Chemical  elements reach the plant surface via  wet and dry deposition.  Nitrates
and sulfates  are  not  the  only components  of  precipitation  falling  onto the  plant surface.
Other chemical  elements (cadmium,  lead,  zinc, manganese),  at least partially soluble in water,
are deposited on  the  surface of vegetation  and may be assimilated by it, usually through the
leaves.  An average raindrop deposited on trees in a typical  forest washes over three tiers of
foliage before it  reaches  the soil.  The effects  of acidic precipitation may be beneficial or
deleterious  depending  on  its  chemical  composition,  the species  of  plant  on  which  it  is
deposited, and  the physiological  condition  and maturity  of the plant  (Galloway and Cowling,
1978).   Substances  accumulated on  the  leaf  surfaces strongly  influence the  chemical composi-
tion of precipitation not only at the leaf surface, but also when it reaches the forest floor.
The  chemistry   of  precipitation  reaching the  forest  floor is  considerably  different  from
that collected  above the  forest  canopy or  a  ground  level  where the canopy  has no influence
(Lindberg  et  al. ,  1979).   Except  for the  hydrogen ion  (H  )  the mean  concentrations of all
elements  (lead,   manganese,   zinc  and  cadmium) studied  in  the Walker  Branch Watershed  in
Tennessee  found by  Lindberg  et al. (1979) to be present in greater amounts in the throughfall
than 'in  incident  rain.  The presence of  trace elements was  more variable  than  that of the
sulfate and hydrogen  ions.   Throughfall  with a pH   4.5 appeared to be a more dilute solution
of  sulfuric  acid  than rain  not influenced  by  the forest canopy.   The  solution was  found to
contain a relatively higher concentration of  alkaline earth salts of  sulfate  and nitrate as
well as a somewhat higher concentration of trace elements  (Lindberg et al., 1979).
     Lee  and  Weber (1980)  studied the effects of sulfuric  acid  rain  on two model  hardwood
forests.  The experiment, conducted under controlled field conditions, consisted of the appli-
cation of simulated sulfuric acid rain (pH values  of 3.0,  3.5, and 4.0), and a control  rain of
pH  5.6  to the  two model  forest ecosystems for a duration  of 3 and 1/2 years.   Rainfall appli-
cations  approximated  the  annual   amounts  of  areas  in  which  sugar  maple  and red  alder
communities normally occur.
     In evaluating the results of the study,  the authors conclude that a well  developed forest
canopy  and litter  layer can  increase the  pH   and  concentration of  bases  (i.e.,  calcium and
magnesium) in  rainwater.   Such conditions  would   tend to decrease the  acidification  rate of
forest  soils  by acid  rain.   However,  as  bases are continually leached  from the  soil column
these  cations  could eventually be lost  from  the ecosystem and unavailable  to influence the
                                           11-76

-------
acidification reactions.  Changes in the ionic and pH balance of forest systems may impact the
productivity of  forests through acidity-induced changes in  the  nutrient  cycling process, de-
composition, reproduction, tree growth, and the-structure of forest systems.
     The additions  of  hydrogen, sulfate and nitrate  ions  to soil  and plant systems have both
positive and negative  effects.   It has generally been assumed that the free hydrogen ion con-
centration in acidic precipitation is the component that is most likely to cause direct, harm-
ful  effects  on  vegetation  (Jacobson,  1980a).   Experimental studies  support  this assumption;
however, to  date,  there are no confirmed  reports  of  exposure  to ambient acidic precipitation
causing foliar  symptoms on  field grown vegetation in the continental  United States (Jacobson,
1980a) and Canada (Linzon, personal communication, 1980).
11.3.2.2.1   Direct effects  on vegetation.    Hydrogen   ion  concentrations  equivalent to  that
measured in  more acidic  rain events  (<  pH 3.0)  have been observed  experimentally to cause
tissue injury  in the form of necrotic lesions to a wide variety of plant species under green-
house and laboratory conditions. This visible injury has been reported as occurring between pH
3.0 and 3.6 (Shriner, 1980).  The various types of direct effects which have been reported are
shown  in  Table  11-7.   Such effects must  be interpreted with caution because  the  growth and
morphology of  leaves on plants grown  in greenhouses  frequently  are atypical  of field condi  -
tions (Shriner, 1980).
     Small  necrotic lesions, the most common form of direct injury, appear to be the result of
the  collection  and retention  of  water on  plant surfaces  and  the subsequent  evaporation of
these  water  droplets  once  a   lesion  occurs.   The  depression   formed  by the  lesion  further
enhances the  collection of water.   A  large percentage  of the   leaf area  may  exhibit  lesions
after repeated  exposures  to simulated  acid rain at pH concentrations  of 3.1,  2.7, 2.5 and 2.3
(Evans et al.,  1977a,  1977b).   In leaves  injured  by  simulated  acidic rain, collapse and dis-
tortion of  epidermal  cells on the upper surface is  frequently  followed  by injury  to the
palisade cells  and ultimately both leaf surfaces are affected (Evans et al. , 1977b).   Evans et
al.  (1978) using six clones of Populus spp. hybrids  found that leaves that had  just  reached
full expansion were  more  sensitive to simulated acid  rain  at pH 3.4, 3.1, 2.9,  and 2.7 than
were unexpended  or  those  which were fully expanded.   On two of  the clones, gall formation due
to  abnormal  cell proliferation and  enlargement occurred.   Other effects  attributed to simu-
lated acid  rain include  the  modification  of  the  leaf surface, e.g.   epicuticular  waxes, and
alteration of physiological  processes such as carbon fixation and allocation.
     Lee  et  al.  (1980)  studied  the  effects  of simulated  acidic  precipitation   on  crops.
Depending  on the crop  studied, they reported  positive,  negative or no effects on  crop yield
when exposed to sulfuric acid  rain  at pH values of  3.0,  3.5 and 4.0 when compared to crops
exposed to  a control  rain  of  pH  5.6.   The yield  of tomatoes, green  peppers, strawberries,
alfalfa,  orchard grass  and timothy were  stimulated.   Yields  of  radishes, carrots,  mustard
greens and broccoli  were inhibited.   Potatoes were ambiguously  affected except at pH 3.0 where
                                           11-77

-------
                  TABLE 11-7.   TYPES OF DIRECT, VISIBLE INJURY REPORTED IN RESPONSE TO ACIDIC WET  DISPOSITION
I
~--J
00
Injury Type
Pitting, curl
shortening, death
1-mm necrotic lesions,
premature abscission



Cuticular erosion

Chlorosis

(A) small , shallow
circular depressions:
slight chlorosis

(B) larger lesions,
chlorosis always present
palisade collapse

(C) 1-mm necrotic lesions
general distortion
(D) 2-mm bifacial necrosis
due to coalescence of
smaller lesions, total
tissue collapse.
Wrinkled leaves, excessive
adventitious budding, pre-
Species pH Range
Yellow birch 2.3-4.7

Kidney bean, 3.2
soybean,
loblolly pine,
E. white pine,
willow oak
Willow oak 3.2

Sunflower, 2.3-5.7
bean
Sunflower, 2. 7
bean


Sunflower, 2.7
bean


Sunflower, 2.7
bean
Sunflower, 2.7
bean


Bean 1.5-3.0

Reference Remarks
Wood and Bormann (1974)

Shriner et al . (1974)




Shriner (1978a)
Lang, et al . (1978)
Evans et al .
(1977b)
Evans et al. More frequent near
(1977b) veins. (A) - (D)
represent sequential
stages of lesion
Evans et al. development, through
(1977b) time, up to 72 h (one
6-min rain event daily
for 3 d)
Evans et al .
(1977b)
Evans et al .
(1977b)


Ferenbaugh
(1976)
         mature abscission

-------
                                                TABLE  11-7  (Continued).

Injury Type
Incipient bronzed spot

Bifacial necrotic pitting


Necrotic lesions,
premature abscission



Marginal and tip necrosis


Galls, hypertrophy,
hyperplasia
Dead leaf cells
Species
Bean

Bean


E. white pine,
scotch pine,
spinach,
sunflower,
bean
Bean, poplar,
soybean, ash
birch, corn,
wheat
Hybrid poplar

Soybean
pH Range
2.0-3.0

2.0-3.0


2.6-3.4




Submicron
H2S04
aerosol

2.7-3.4

3.1
Reference
Hindawi et al .
(1980)
Hindawi et al .
(1980)

Jacobsen and
van Leuken
(1977)


Lang et al .
(1978)

Evans et al.
(1978)
Irving (1979)
Remarks
After first few hours

After 24 h (reported
pool ing of drops =
more injury)
Injury associated with
droplet location
within 24-48 h.









Shriner (1980).

-------
their yield as well as that of beets was inhibited.   Visible injury of tomatoes could possibly
have  decreased  their market value.   In  sweet corn, stem and  leaf  production  was stimulated,
but no  statistically  significant effects on yield  were  observed for 15 other crops.  Results
suggest that  the  possibility  of yield's being affected by acid rain depends on the portion of
the plant  being utilized as well  as  the species.   Plants were  regularly  examined for foliar
injury associated with acid rain.  Of the 35 cultivars examined, the foliage of 31 was injured
at pH 3.0;  28 at pH 3.5; and 5 at pH 4.0.   Foliar injury was not generally related to effects
on yield.   However,  foliar injury  of  swiss  chard,  mustard  greens,  and spinach  was severe
enough to  adversely  affect  marketability.   These results are from a single growing season and
therefore considered to be preliminary.
     Studies  indicate  that  wet  deposition  of acidic or  acidifying  substances  may result in a
range of  direct or  indirect  effects on vegetation.   Environmental  conditions  before, during
and after  a precipitation event affect  the  responses  of vegetation.  Nutrient  status of the
soil,  plant nutrient requirements,  plant sensitivity and growth stage and the total loading or
                                  +     -
deposition of critical ions e.g. H , N03  and SO^  all  play a role in determining vegetational
response to acidic precipitation.
     Wettability of leaves appears  to be an important factor in the response of plants to acid
deposition.   This  has  been  demonstrated in the work of Evans et al.  (1977b), Jacobson and Van
Leuken (1977), and Shriner (1978a), who variously report a threshold of between pH 3.1 and 3.5
for development  of foliar lesions  on  beans.   The  cultivars of Phaseolus  vulgaris  L.  used in
the above  studies are  all  relatively  non-waxy  and therefore  fairly easily wettable.   Waxy
leaves apparently  minimize  the contact  time  for the acid solutions, thus  accounting for the
<400X  increase   in H   ion  concentration  required to   induce  visible  injury.   Table  11-8
summarizes the  thresholds,  including range,  species sensitivity, concentration,  and time, for
visible injury  associated with  experimental  studies of wet deposition  of acidic substances.
     Leaching of  chemical elements  from exposed plant surfaces is  an  important  effect rain,
fog,   mist,  and  dew  have  on vegetation.   Substances  leached  include  a great  diversity of
materials.   All of  the essential  minerals, amino acids,  carbohydrate  growth regulators, free
sugars,  pectic  substances,  organic acids,  vitamins, alkaloids, and alleopathic substances are
among the  materials which have  been detected  in plant leachates (Tukey, 1970).   Many factors
influence the quantity  and  quality of the substances leached from foliage.  They include fac-
tors  associated directly with the plant as well as those associated with the environment.  Not
only  are there  differences  among species with respect to leaching,  but individual differences
also  exist among  individual  leaves of the same crop and even the same plant, depending on the
physiological age  of  the  leaf.   Young,  actively  growing tissues  are  relatively  immune to
leaching  of   mineral  nutrients  and  carbohydrates,  while mature  tissue  which is  approaching
                                           11-80

-------
                TABLE  11-8.   THRESHOLDS  FOR VISIBLE  INJURY AND GROWTH  EFFECTS  ASSOCIATED WITH  EXPERIMENTAL
                         STUDIES OF WET  DEPOSITION OF ACIDIC  SUBSTANCES  (AFTER JACOBSON, 1980a, b)
00

Effect
Foliar lesions, decrease
in growth
Foliar aberrations,
decrease in growth
Foliar lesions
Foliar lesions
Foliar lesions
Foliar lesions
Foliar symptons, no
reduced growth
Increased growth,
i ncreased/decreased
nutrient content
Reduced growth
Reduced yield
Reduced growth
Reduced yield
Species
Yel low birch
Bean
Bean, sunflower
Bean
Hybrid poplar
Sunflower
Soybean
Lettuce
Pinto bean
Pinto bean
Soybean
Soybean
Threshold
pH 3.1
pH 2.5
pH 3.1
pH 3.2
pH 3.4
pH 3.4
pH 3.0
pH 3.0, 3.2
pH 3.1
pH 2.7
pH 3.1
pH 2.5
Reference
Wood and
Bormann (1974)
Ferenbaugh
(1976)
Evans et al .
(1977b)
Shriner (1978a)
Evans et al .
(1978)
Jocobson and
Van Leuken (1977)
Jacobson (1980b)
Jacobson (1980b)
X
Jacobson (1980b)



Remarks
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse (varied
with S04~ & N03")
greenhouse




-------
                                           TABLE  11-8  (Continued).

Effect
Increased yield
Foliar symptoms
Reduced growth
Reduced yield
Reduced quality
No foliar symptoms, or
effects on growth
No foliar symptoms, but
a) decreased growth, yield
b) increased yield
No effect on growth, yield
Reduced quality
Species
Soybean
Tomato
Tomato
Tomato
Tomato
Soybean
Soybean
Soybean
Soybean
Tomato
Tomato
Threshold Reference Remarks
pH 3.1
pH 3.0 Jacobson (1980b) greenhouse
pH 3.0
pH 3.0
pH 3.0
pH 3.1 Irving (1979) field
pH 2.8 Jacobsen (1980b) field, low ozone
pH 2.8 field, high ozone
pH 2.8 field, low ozone
pH 3.0 Jacobson (1980b) field
pH 3.0 field

 Highest pH to elicit a negative response,  or lowest pH to elicit a positive response



Shriner (1980).

-------
senescence  is  very susceptible.   The stage of plant  development,  temperature,  and rainwater
falling on  foliage  and running down plant stems or tree bark influences leaching.  Rainwater,
which  naturally has  a  pH  of  about 5.6,  washing over  vegetation  may become  enriched  with
substances leached from the tissues (Nihlgard, 1970).
     Leaching  of  organic and inorganic materials  from vegetation to the soil is  part  of the
normal  functioning  of terrestrial  ecosystems.   The nutrient  flow from one  component  of the
ecosystem  to  another  is  an important  phase  of nutrient cycling  (Comerford  and White,  1977;
Eaton  et  al. ,   1973).    Plant  leachates  have  an  effect upon soil  texture,  aeration,  permea-
bility,  and exchange  capacity.   Leachates, by influencing the  number  and behavior of  soil
microorganisms, affect soil-forming  processes,  soil fertility,  and susceptibility or immunity
of plants to soil  pests and plant-chemical interactions (Tukey,  1970).
     It  has  been demonstrated  under experimental  conditions that  precipitation of increased
acidity can increase  the leaching of various cations  and organic carbon from the tree  canopy
(Abrahamsen et  al., 1976; Wood and Bormann, 1975).  Foliar  losses of potassium, magnesium, and
calcium from bean plants and maple seedlings were  found to  increase as the acidity of an arti-
ficial  mist was increased.  Below a pH  of 3.0 tissue damage  occurred;  however, significant
increases  in leaching  were  measured at pH  3.3  and 4.0 with no observable tissue damage (Wood
and  Bormann,   1975).   Hindawi   et  al.  (1980)  also  noted  that as the  acidity  of  acid  mist
increased  so   did   the   foliar  leaching  of  nitrogen, calcium,  phosphorous, and  magnesium.
Potassium  concentrations were  not  affected,  while the  concentration  of sulfur  increased.
Abrahamsen  and Dollard  (1979),   in  experiments  using Norway  spruce (Picea  abies  L.  Karst),
observed that  despite  increased leaching under the most acid treatment, there was no evidence
of change  in   the  foliar cation content.   Wood and Bormann (1977),  using  Eastern  white  pine
(Pinus  strobus  L.),  also noted no significant changes  in calcium, magnesium or potassium con-
tent of needles.   Tukey (1970) states  that increased  leaching of nutrients  from foliage can
accelerate nutrient uptake by plants.  No injury will  occur to the plants as long as roots can
absorb  nutrients to  replace those being leached;  however,  injury could occur if nutrients are
in short supply.  To  date,  the effects,  if  any,  of the increased leaching of substances from
vegetation by acidic precipitation remain unclear.
     Some experimental evidence suggests  that acidic  solutions  affect the chlorophyll  content
of leaves  and   the  rate  of  photosynthesis.   Sheridan   and Rosenstreter  (1973)  reported  marked
reduction of photosynthesis  in  a  moss exposed to  increasing  H   ion concentrations.   Sheridan
and Rosenstreter (1973),  Ferenbaugh (1976), and Hindawi et al.  (1980) reported reduced chloro-
phyll  content  as  a  result  of  tissue exposure  to  acid solutions.  In the  case  of Ferenbaugh
(1976), however, the significant reductions in chlorophyll  in the leaves of Phaseolus vulgaris
at pH  2.0  were associated with large areas  of  necrosis.   A significant aspect  of  this  study
was the loss of capacity by the plant  to produce carbohydrates.   The rate of  respiration in
these plants showed only a slight  but significant  increase while the rate of photosynthesis at
                                           11-83

-------
pH 2.0  increased  nearly  fourfold as determined by oxygen evolution. Ferenbaugh concluded that
due to  a reduction  in  biomass  accumulation  and sugar and  starch  concentrations,  photophos-
phorylation  in  the treated  plants  was  in  some  way being uncoupled by  the  acidic  solutions.
     Irving (1979) reported a higher chlorophyll  content and an increase in the rate of photo-
synthesis in  field-grown soybeans  exposed  to simulated  rain at pH 3.1.  She  attributed  the
increases to  improved nutrition  due  to the  sulfur and nitrogen components  of  the simulated
acid rain overcoming any negative effects.
     Vegetation is commonly exposed to gaseous phytotoxicants such as ozone and sulfur dioxide
at the same time as acidic precipitation.  Little information is available upon which to eval-
uate the  potential for  determining the effects  of the interaction of  wet-and  dry-deposited
pollutants on vegetation.  Preliminary studies by Shriner (1978b), Irving (1979), and Jacobson
et al.  (1980) suggest that  interactions may  occur.   Irving (1979) found  that  simulated acid
precipitation at  pH  of  3.1 tended to limit the decrease in photosynthesis observed when field
-grown soybeans were  exposed 17 times during the growing  season to 0.19 ppm of SO,,.   Shriner
(1978b), however,  reported  no  significant  interaction between multiple  exposure  to simulated
rain at  p  4.0 and four  S02  exposures  (3 ppm peak for  1  hr.)  upon the  growth of  bush beans.
Shriner (1978b) also exposed plants to 0.15 ppm ozone (4 3-hour exposures) in between 4 weekly
exposures to  rainfall of pH 4.0, and observed a  significant growth reduction at the  time of
harvest.   Jacobson et al. (1980),  using open-top exposure chambers with field-grown soybeans,
compared growth and yield between three pH  levels of simulated rain (pH 2.8,  3.4, and 4.0)  and
two levels  of ozone  (<0.03  and  <0.12  ppm).   Results demonstrated that  ozone  depressed both
growth  and  yield  of  soybeans with  all  three rain  treatments,   but that the depression  was
greatest with the  most  acidic rain.  Ozone concentrations equal  to or  greater than those used
in the studies are common in most areas of  the northeastern United States where acidic deposi-
tion is a problem (Jacobson et al. , 1980); therefore,  the potential  for ozone-acidic deposi-
tion interaction is great.
     Shriner (1978a) studied the effect of  acidic precipitation on host-parasite interactions.
Simulated acid rain with a pH of 3.2 inhibited the  development of bean rust  and production of
telia (a stage  in the rust  life  cycle)  by  the  oak-leaf rust fungus Cronartium fusiforme.   It
also inhibited reproduction  of  root-knot nematodes  and inhibited or stimulated development of
halo blight  of  bean  seedlings  depending on  the time  in  the disease cycle  during which  the
simulated acid rain was  applied.   The effects which  inhibited disease development could result
in a net  benefit  to plant health.  Shriner (1977, 1980) also observed  that root nodulation by
Rhizobium on  common  beans  and soybeans was inhibited by the simulated  acid rain, suggesting a
potential for reduced nitrogen fixation by  legumes so effected.
     Plants such  as  mosses  and lichens are particularly sensitive to changes in  precipitation
chemistry because many of their nutrient requirements are obtained directly through  precipita-
tion.   These plant forms are typically absent from regions with high chronic  SO^  air pollution
                                           11-84

-------
and  acidic  precipitation  (Denison et  al. ,  1977;  Sheridan  and Rosenstreter,  1973).   Gorham
(1976) and  Giddings and Galloway  (1976)  have written reviews  concerning  this  problem.   Most
investigations on  the  effects  of  air  pollution  on epiphytes  have dealt  with  gaseous pollu-
tants.   Very  few   studies  have  considered  acidic  precipitation.   Denison  et al.  (1977),
however,  did  observe that  the nitrogen-fixing ability of the epiphytic lichen Lobaria oregana
was  reduced when treated  with simulated rainfall with  a pH of 4.0 and below.  Investigations
concerning the effects  of acidic precipitation on epiphytic microbial  populations are very few
(Abrahamsen and Dollard,  1979).
     Limited  fertilization  could occur  in  the bracken  fern  Pteridium  aquilinum  under condi-
tions of acidic precipitation (pH and sulfate concentrations) that prevail  in the northeastern
United States.  Evans and Bozzone (1977), using buffered solutions to  simulate acidic precipi-
tation,  observed   that  flagellar  movement  of  sperm was  reduced at  pH  levels below  5.8.
Fertilization  was  reduced after exposure to pH's below 4.2.   Sporophyte  production  was  also
reduced by  50  percent  at pH  levels below 4.2 when  compared  to 5.8.   Addition  of sulfate (86
mM)  decreased  fertilization  at  least 50 percent at all pH values observed.  In another study,
Evans and Bozzone  (1978)  observed  that both  sperm  motility  and fertilization in gametopnytes
of Pteridium  aquilinum were  reduced  when anions  of  sulfate,  nitrate,  and chloride  were added
to buffered solutions.
     Sulfur and nitrogen  in precipitation have been shown to play an important role  in vegeta-
tional response to  acidic deposition.   Jacobson et al. (1980) investigated the impact of simu-
lated acidic  rain  on the  growth of  lettuce  at acidities of pH 5.7 and 3.2.   At pH  3.2,  solu-
tions were  compared with  N03:S04 mass ratios of 20:1, 2:1, and 1:7.5.   The high nitrate at pH
3.2  showed  no difference  from the treatments  controls  at pH 5.7  for  those  growth  parameters
(root dry  weight,  apical  leaf dry weight)  that responded to treatment; however, the results
were  significantly less   than those  from  the low  nitrogen,  high sulfur,  treatment.   These
observations  suggest that sulfur  was  possibly a  limiting factor  in  the nutrition  of  these
plants, with the result that the plant response to sulfur overwhelmed  the hydrogen ion effect.
Other  studies  also have  cited the  beneficial  effects of  simulated acidic  precipitation.
Irving and  Miller  (1978)  observed  that an  acidic simulant had  a positive effect on producti-
vity of field-grown  soybeans  as  reflected by seed weight.   Increased  growth was attributed to
a fertilizing  effect from  sulfur and nitrogen delaying senescence.  Irving and Miller (1978),
in the same  study,  also  exposed soybeans to  S0~  and acidic precipitation.  No visible injury
was apparent in any of  the plots; however,  a histological study revealed significant increases
in the number  of dead  mesophyll  cells in all plots  when compared to the control.   The propor-
tion  of  dead mesophyll cells of plants exposed  to  acid rain and S02  combined was  more  than
additive when  compared to  the effects of each taken singly.   Wood and Bormann (1977) reported
an increase in needle length and the  weight  of seedlings of Eastern white pine with  increasing
acidity of  simulated  precipitation where  sulfuric   and  nitric  acid were  used  to acidify the
                                           11-85

-------
mist.  Increased growth  was  attributed to increased N(L  application.   Abrahamson and Dollard
(1979) also presented data suggesting positive growth responses in forest tree species result-
ing  from nitrogen  and  sulfur in simulated rain.   Simulated  acidic precipitation was observed
to increase the growth of Scots pine saplings in experiments conducted in Norway.  Saplings in
plots watered with  acid  rain of pH  3.0,  2.5,  and 2.0 grew more  than  the control plots.   The
application of  acid rain  increased the  nitrogen  and  sulfur content of  the  needles.   As  the
acidity of the artificial rain was adjusted using sulfuric acid only, the increased growth  was
probably due  to  increased  nitrogen  mineralization and  uptake.   Turner and  Lambert  (1980)
reported evidence  indicating  a positive growth response  in  Monterey pine from the deposition
of sulfur in ambient precipitation in Australia.
     Acidifying forest soils  that  are  already acid  by  acidic  precipitation  or air pollutants
is a  slow  process.   Growth effects probably could  not  be detected for a long time.   To iden-
tify the possible  effects  of acidification on poor pine forests, Tamm et al.  (1977)  conducted
experiments using 50 kg and 100 kg of sulfur per hectare as dilute sulfuric acid (0.4 percent)
applied annually with and without NPK (nitrogen, phosphorous, potassium) fertilizer.   Nitrogen
was  found  to  be the limiting  factor  at both experimental sites.   Acidification  produced no
observable influence on  tree  growth.   Lysimeter and soil  incubation experiments conducted at
the  same time  as  the experiments described above suggest that even moderate  additions of  sul-
furic acid or sulfur to soil  affect soil biological processes,  particularly nitrogen  turnover.
The  soil incubation  studies  indicated  that additions of sulfuric acid increased the  amount of
mineral nitrogen but lowered the amount of nitrate.
     Soil  fertility  may  increase as a  result  of acidic precipitation  as  nitrate  and sulfate
ions,  common  components  of  chemical  fertilizers,  are  deposited; however, the  advantages of
such additions are  possibly  short-lived as depletion of  nutrient cations through accelerated
leaching could eventually  retard  growth (Wood, 1975).   Laboratory  investigations  by Overrein
(1972) have  demonstrated that  leaching of potassium,  magnesium, and  calcium,  all  important
plant nutrients, is  accelerated by increased acidity of rain.   Field studies  in Sweden corre-
late decreases in soil  pH with increased additions of acid (Oden et al., 1972).
     Major uncertainty in estimating effects of acid rain on forest productivity is the capac-
ity  of forest  soils to buffer  against  leaching by hydrogen ions.   Forest canopies  have  been
found to filter  90  percent of the  hydrogen  ions  from  rain (pH 4.0)  falling  on the  landscape
during the growing  season  (Eaton et al.,  1973).   As a result, solutions  reaching the  forest
floor  are  less  acidic  (pH  5.0).    Mayer and  Ulrich  (1977),  however,  point out that  their
studies suggest that for  most elements  the addition by precipitation (wetfall  plus dryfall) to
the  soil  beneath the  tree  canopy  is  considerably  larger  than  that by  precipitation  to  the
canopy surface  as  measured  by rain gauges  on  a  non-forested area.   The leaching  of  meta-
bolites,  mainly  from leaf  surfaces, and  the washing out from leaves,  branches,  and stems of
airborne particles  and  atmospheric aerosols  intercepted by  trees  from the  atmosphere,  are
suggested as the reason for the mineral increase.
                                           11-86

-------
     Forest  ecosystems  are complicated  biological  organizations.  Acidic  precipitation will
cause some  components within  the ecosystem to respond  even  though it is not possible at pre-
sent to  evaluate  the  changes  that occur.  The impact of the changes on the ecosystem can only
be determined with certainty after the passage of a long period of time.
11.3.2.3  Effects on Human Health—One effect  of  acidification that is potentially of concern
to human health is the possible contamination by toxic metals of edible fish and of water sup-
plies.    Studies  in  Sweden  (Landner and  Larsson,  1972;  Turk  and  Peters,  1977),  Canada
(Tomlinson, 1979;  Brouzes et al., 1977),  and the United States (Tomlinson, 1979) have revealed
high mercury  concentrations in fish from acidified regions.   Methylation of mercury to mono-
methyl   mercury occurs  at low pH  while  dimethyl  mercury  forms  at  higher pH  (Fagestrom  and
Jerneldv,  1972).   Monomethyl  mercury  in the water  passing  through the  gills  of  fish reacts
with thiol  groups  in  the  hemoglobin of  the blood  and  is  then  transferred to  the  muscle.
Methyl  mercury is  eliminated very slowly from fish; therefore, it accumulates with  age.
     Tomlinson  (1979)  reports  that  in  the Bell  River area  of  Canada  precipitation  is  the
source  of  mercury.   Both  methyl  mercury and  inorganic mercury were  found  in  precipitation.
The source of mercury in snow and rain was not known at the time of the study.
     Zinc,  manganese,   and aluminum  concentrations  also  increase as  the  acidity of  lakes
increases  (Schofield,   1976b).   The  ingestion  of fish  contaminated by these metals is  a
distinct possibility.
     Another  human health aspect  is  the  possibility that,  as  drinking-water  reservoirs
acidify, owing to  acidic  precipitation,  the increased concentrations  of  metals  may exceed  the
public-health  limits.   The  increased metal  concentrations  in drinking  water  are  caused  by
increased watershed weathering and,  more important, increased leaching  of  metals  from house-
hold plumbing.  Indeed,  in  New York State,  water from the  Hinckley Reservoir has acidified to
such an  extent  that  "lead concentrations in water  in contact with household plumbing systems
exceed  the  maximum  levels for  human use  recommended by  the New York State  Department  of
Health" (Turk and  Peters, 1977).   The lead and copper concentrations in pipes which have stood
over night (U) and those in which the water was used (F) are depicted  in  Table 11-9.
11.3.2.4   Effects  of Acidic Precipitation on  Materials—Acidic precipitation can   damage  the
abiotic as well as  the  biotic components of an ecosystem.   Of particular concern in this sec-
tion are the deteriorative effects of acidic precipitation  on materials and cultural artifacts
of manmade  ecosystems.   At present  in  most  areas,  the dominant  factor in  the formation  of
acidic   precipitation  is  sulfur,  usually  as  sulfur dioxide  (Cowling  and   Dochinger,  1978;
Likens,  1976).  Because  of  this  fact, it is difficult to  isolate the  effect of  acidic precipi
tation  from changes induced by sulfur pollution in general.   (The effects of sulfur oxides on
materials are discussed  in  Chapter  10.)   High acidity promotes corrosion because the hydrogen
ions act as  a sink for  the electrons liberated during the  critical corrosion process (Nriagu,
1978).   Precipitation as  rain  affects corrosion by forming a layer of moisture  on  the surface
                                           11-87

-------
                    TABLE 11-9.   LEAD AND COPPER CONCENTRATION AND pH OF WATER
                     FROM PIPES CARRYING OUTFLOW FROM HINCKLEY BASIN AND HANNS
                         AND STEELE CREEK BASIN, NEAR AMSTERDAM,  NEW YORK

Collection site
and date
Hinckley Dam
Nov. 21, 1974
Nov. 21, 1974
Nov. 7, 1974
Nov. 7, 1974
Oct. 1, 1974
Oct. 1, 1974
Aug. 15, 1974
Aug. 15, 1974
Amsterdam
Jan. 6, 1975
Jan. 6, 1975
Pipe -,
condition

U
F
U
F
U
F
U
F

U
F
Copper
(ug/1)

600
20
460
37
570
30
760
40

2900
80
Lead
(ug/1)

66
2
40
6
52
5
88
2

240
3
PH

—
7.4
6.3
6.3
6.8
7.1
6.3
6.3

4.5
5.0

          U, unflushed, (water stands in pipes all  night);  F,  flushed
          From Turk and Peters (1977).
                                         +                  2"
of the material and by adding hydrogen (H ) and sulfate (S02  ) ions as corrosion stimulators.
Rain  also  washes  out  the  sulfates  deposited  during  dry  deposition and thus serves  a  useful
function by removing the sulfate and stopping corrosion (Kucera,  1976).   Rain plays a critical
role  in the  corrosive  process because in  areas where  dry  deposition predominates the washing
effect  is  greatest,  while  in areas where  the dry and  wet  deposition processes  are roughly
equal,  the  corrosive  effect is greater (Kucera, 1976).   The corrosion effect, particularly of
certain metals, in  areas  where the pH of precipitation is  very low may be greatly enhanced by
that  precipitation  (Kucera, 1976).  In  a  Swedish  study the  sulfur  content  of  precipitation,
                  2
expressed as meq/m  per year, was found to correlate closely with the corrosion  rate of  steel.
The metals most likely to be corroded by precipitation with a low pH are those whose corrosion
resistance may be  ascribed  to a protective layer  of basic  carbonates, sulfates, or oxides, as
used  on zinc  or  copper.   The decrease in  pH  of rainwater  to 4.0  or lower may  accelerate the
dissolution of the protective coatings (Kucera, 1976).
     Materials reported  to  be  affected  by acidic  precipitation,  in addition  to  steel,  are:
copper  materials,  linseed  oil,  alkyd  paints  on  wood, antirust  paints on  steel,  limestone,
sandstone,  concrete,  and both cement-lime  and lime  plaster  (Cowling and  Dochinger,  1978).
                                           11-88

-------
     Stone is one of the oldest building materials used by man and has traditionally been con-
sidered one  of  the  most durable because  structures  such  as the pyramids, which have survived
since  antiquity,  are  made of stone.  What  is  usually forgotten is that  the  structures  built
with stone that was not durable have long since disappeared (Sereda, 1977).
     Atmospheric sulphur  compounds  (mainly  sulfur dioxide, with subsidiary amounts  of sulfur
trioxide and ammonium  sulfate)  react with the carbonates  in  limestone and dolomites, calcar-
eous sandstone  and  mortars  to form calcium  sulfate  (gypsum).   The results of these reactions
are blistering,  scaling,  and loss  of surface  cohesion, which  in turn induces similar effects
in neighboring materials not in themselves susceptible to  direct attack (Sereda, 1977).
     Sulfates have  been  implicated  by Winkler (1966) as  very  important in the disintegration
of stone.   The surface flaking on the Egyptian granite obelisk (Cleopatra's Needle) in Central
Park,  New  York  is  cited as an example.  The  deterioration occurred within  two years of  its
erection in 1880.
     A  classic  example of  the  effects of  the changing chemical climate on  the  stability  of
stone is the deterioration of the Madonna at Herten Castle, near Recklinghausen, Westphalia  in
Germany.  The sculpture  of  porous  Baumberg sandstone was  erected  in  1702.   Pictures taken  of
the Madonna  in  1908 shows slight to moderate damage during the first 206 years.  The features
of the  Madonna--eyes,  nose,  mouth  and hair--are  readily discernable.   In pictures  taken  in
1969 after 267 years,  no features are visible (Cowling and Dochinger,  1978).
     It is not certain in what form sulfur is absorbed into stone,  as  a gas (SCO  forming sul-
furous  or sulfuric  acid  or  whether it  is deposited  in  rain.   Rain and hoarfrost  both contain
sulfur  compounds.   Schaffer (1932)  compared  the  sulfate  ion  in  both  rain  and  hoarfrost  at
Heachingley,  Leeds,  England  in 1932 (Table 11-10) and showed that the  content  of hoarfrost was
approximately 7  times  greater  than  rain.   Wet stone surfaces  unquestionably increase the con-
densation  or  absorption  of  sulfates.   Stonework kept dry and shielded  from  rain,  condensing
dew,  or hoarfrost will  be damaged  less by SCL pollution than  stone surfaces which are exposed
(Sereda, 1977).
     Acid  rain  may  leach ions from stonework  just as acidic  runoff and  ground water leaches
ions  from soils  or  bedrock;  however, at the present  time it  is not possible  to attribute the
deleterious  effects  of atmospheric  sulfur pollution to specific compounds.
     Microbial   action  can also contribute  to  the deterioration of stone surfaces.   Tiano  et
al.  (1975) isolated  large numbers  (250 to 20,000 cells  per gram) of sulfate-reducing bacteria
from  the stones  of  two historical  buildings of Florence,  Italy.   The  majority of  the bacteria
belonged  to  the  genus Thiobacillus.   This genus of  chemosynthetic  aerobic  microorganisms
oxidizes sulfide, elemental   sulfur,  and thiosulphate to sulfate to obtain  energy (Andersson,
1975).   Limestone  buildings and particularly  mortar used  in  the  construction of brick and
stone buildings  are  particularly susceptible to when Thiobacillus can  convert  reduced forms  of
sulfur  to sulfuric  acid.   Sulfate  in acidic  precipitation as  well as other  sulfur  compounds
                                           11-89

-------
           TABLE 11-10.   COMPOSITION OF RAIN AND HOARFROST AT HEADINGLEY,  LEEDS
                                 Average rain                     Hoarfrost
                               parts per million              parts per million
Suspended matter
Tar
Ash
Acidity
Sulphur as SO,
Sulphur as SO-
Total sulphur
Chlorine
Nitrogen as NH^
Nitrogen as N-Oc
Nitrogen as albuminoid
115
15
28
1.9
22
5.7
27.7
7.3
1.98
0.196
0.434
4620
158
67
102.9
148
41.0
189.0
94.6
8.57
0.0
1.618

       Schaffer (1932).

deposited  in  dry  deposition could  permit the  formation of  sulfur compounds utilizable  by
microorganisms.   (For more  information  concerning  the effects of  sulfur  oxides  on materials,
please consult Chapter 10).
11.4  ASSESSMENT OF SENSITIVE AREAS
11.4.1  Aquatic Ecosystems
     Why do some lakes  become acidified by acidic precipitation  and others not?   What deter-
mines susceptibility?  Are terrestrial  ecosystems likely to be susceptible;  if so,  which ones?
     The sensitivity of  lakes  to  acidification is  determined by:   (1) the acidity  of both wet
deposition (precipitation)  and dry  deposition,  (2)  the  hydrology of the  lake, (3)  the  soil
system, geology, and  canopy effects, (4) the surface water.   Given acidic  precipitation, the
soil system and associated canopy  effects are  most  important.   The hydrology of lakes includes
the sources, amounts, and pathways of  water entering and leaving a lake.   The capability of a
lake and its drainage basin to neutralize acidic contributions as well  as the mineral content
of its  surface  water  is largely governed by  the composition  of the bedrock of the watershed.
The chemical weathering  of  the watershed strongly  influences the salinity (ionic  composition)
                                           11-90

-------
and  the  alkalinity  (hardness  and  softness)  of the  surface  water of  a lake  (Wetzel,  1975;
Wright and Gjessing, 1976; Wright and Henriksen, 1978).   The cation exchange capacity and wea-
thering rate of the watershed and the alkalinity of the surface water determine the ability of
the system to neutralize the acidity of precipitation.
     Lakes vulnerable to  acidic  precipitation have been shown to have watersheds whose geolo-
gical  composition  is  highly resistant  to  chemical   weathering  (Galloway and  Cowling,  1978;
Wright and  Gjessing,  1976; Wright  and  Henriksen,  1978).   In addition,  the watersheds  of the
vulnerable lakes usually  have  thin, poor soils and are poorly vegetated.  The cation exchange
capacity of such soils is low and, therefore, its buffering capacity is low (Schofield,  1979b;
Wright and Henriksen,  1978).
     Wright and  Henriksen  (1978)  point out  that  the  chemistry of Norwegian  lakes  could  be
accounted for primarily on the basis of bedrock geology.  They examined 155 lakes and observed
that 59 of  them  lay in granite or felsic gneiss basins.  Water in these lakes was low in most
major  ions  and  had low electrical  conductivity.   [The  fewer  the minerals in water  the lower
its  conductivity  (Wetzel, 1975).]  The  waters  in  the lakes surveyed were "among the softest
waters  in  the  world"  (Wright and  Henriksen,  1978).   Sedimentary  rocks  generally  weather
readily,  whereas igneous rocks are highly resistant.   The Adirondacks,  as pointed out by Scho-
field  (1979a),  have granite bedrock  with much  of the  area  covered with  a  mantle  of  mixed
-gneisses.   Shallow soils  predominate  in the area.   Thus, areas are susceptible to acidifica-
tion.
     Limestone terrains, on the other hand,  are capable of buffering intense concentrations  of
acids.   Glacially derived sediment has been  found to be more important than bedrock in assimi-
lating acidic precipitation  in  the Canadian Shield area  (Kramer,  1976).   Generally, however,
bedrock geology  is the  best  predictor of  the  sensitivity of  aquatic ecosystems  to  acidic
precipitation (Hendrey et al.,  1980b).
     Areas with  aquatic  ecosystems that  have  the  potential  for  being sensitive  to  acidic
precipitation are  shown  in  Figure 11-28.  In  Figure  11-27, the  shaded areas  on the  map indi-
cate that the bedrock  is  composed of igneous  or metamorphic  rock while in the unshaded areas
it  is  of  calcareous or  sedimentary rock.   Metamorphic and igneous bedrock  weathers slowly;
therefore,  lakes in areas with  this type of bedrock would be  expected to be  dilute and of low
alkalinity [<0.5 meq  HCOj/liter  (Galloway  and Cowling, 1978)].   Galloway and  Cowling  (1978)
verified   this  hypothesis by  compiling alkalinity  data.   The  lakes  having  low  alkalinity
existed in regions  having igneous and metamorphic  rock (Galloway and Cowling, 1978).   Hendrey
et  al.  (1980b)  have  developed  new bedrock geology maps  of the  eastern  United States  for
predicting areas which  might be  impacted by  acidic  precipitation.   The new  maps  permit  much
greater  resolution for  detecting  sensitivity  than  has been  previously available  for the
region.                                     '
     Henriksen (1979)  has developed a  lake acidification "indicator model"  using pH-calcium
and calcium-alkalinity relationships as  an  indicator for determining decreased  surface  water
                                           11-91

-------
Figure 11-28. Regions in North America with lakes that are sensitive to acidification by acid
precipitation (Galloway and Cowling, 1978).
                                    11-92

-------
acidification.  The  indicator  is  based on the observation  that in pristine lake environments
(e.g., Northwest  Norway  or the Experimental Lakes Area  in  Northwest Ontario, Canada) calcium
is  accompanied  by a proportional amount  of  bicarbonate because carbonic acid  is  the primary
chemical  weathering agent.   The pH-calcium relationship found for such regions is thus defined
as the reference level  for unacidified lakes.  Acidified lakes (e.g., Southeast Norway and the
Adirondack region) will exhibit lower pH or lower alkalinity than the reference lakes, at com-
parable calcium levels, due to the replacement of bicarbonate by strong acid anions.
     Schofield  (1979b) has illustrated the use of Henriksen's model with data from Norway,  the
Adirondacks,  and  the Experimental  Lakes Area of Ontario, Canada.  In the acidified lakes sul-
fate replaces bicarbonate  as  the  major anion present (Figures 11-29 and 11-30) and is derived
primarily from precipitation.   Since the bicarbonate lost in acidified lakes has been replaced
by an  equivalent  amount  of sulfate, the concentration of excess sulfate serves as  an index  of
the amount  of acidification  that  has taken place.   Henriksen (1979) compared estimated acidi-
fication in Norwegian  lakes  to the pH and sulfate concentrations in the prevailing precipita-
tion and concluded  that  significant lake acidification had occurred in areas receiving preci-
pitation with an  annual  average  (volume weighted) pH  below 4.6 to 4.7 and sulfate concentra-
tions  above 1 mg/1.  This  approximate threshold of precipitation acidity may be applicable  to
sensitive lake districts in  other regions as well.   For reference,  the estimated  annual bulk
deposition sulfate for  the  acidified lake districts in the Adirondacks and southern Norway are
approximately 30  to 60  kg SO./ha,  as compared with only 5 to  10 kg SO./ha  in  the  reference
areas  of northern  Norway and  the Experimental  Lakes Area in Ontario.   A comparison of lake  pH
with regional  sulfate loading levels in Sweden suggests that critical  loading levels  for sensi-
tive lakes  are  in the  range  of 15  to  20 kg SO./ha/yr.  The amount of precipitation  must also
be considered since it  affects total sulfate additions.
     The  report  by Hendrey  et al.  (1980b) compared pre-1970 data with post-1975 data.   A marked
decline in both  alkalinity  and pH of sensitive waters of North Carolina and New Hampshire were
tested.  In the former,  pH and alkalinity have  decreased  in 80 percent of the streams and  in
the latter  pH has  decreased  90 percent since 1949.   These areas are predicted to be  sensitive
by the geological  map  on  the basis  of  their  earlier alkalinity values.   Detailed  county  by
county maps  of  other  states  in  the  eastern United  States suggest the  sensitivity  of these
regions to acidic  precipitation.
     Though bedrock geology generally  is a good predictor of the susceptibility of an area  to
acidification due  to acidic precipitation, other factors also have an influence.   Florida, for
example,  is underlaid  by highly  calcareous and phosphate rock,  suggesting  that acidification
of  lakes  and  streams  is  highly  unlikely.   Many  of the  soils,  however,  (particularly  in
northern  Florida)  are  very mature,  have  been  highly  leached of calcium carbonate, and,  as  a
result, some  lakes in  which groundwater  infilow  is  minimal  have become  acidified  (Hendry and
Brezonik,  1980).   Conversely,  there  are  areas in Maine with granitic bedrock where lakes have
                                           11-93

-------
o
Z
LU


O
                               40           60


                           EQUIVALENT PERCENT
eo
    Figure 11-29. Equivalent percent composition of major ions in Adirondack lake
    surface waters (215 lakes) sampled in June 1975.


    Source: Schofield (1979b).
                                    11-94

-------
   30
   10
                                               NW  Norway
                                                         (58)
   to
CJ   0

-------
not become acidified, despite receiving precipitation with an average pH of approximately 4.3,
because the  drainage basins contain lime-bearing  till  and marine clay (Davis et  al.,  1978).
Small amounts of  limestone  in  a drainage basin  exert  a strong influence on water quality  in
terrain which would otherwise  be  vulnerable to  acidification.   Soils in Maine in  the  areas
where the  pH of  lakes  has decreased  due to acidic  precipitation are immature,  coarse,  and
shallow and  are  derived largely from granitic material  and commonly have a low capacity  for
assimilating hydrogen ions  from leachate and surface runoff in lake watersheds (Davis et al.,
1978).   The occurrence of limestone outcroppings  in the Adirondack Mountains  of New York state
are highly correlated with lake pH levels.  The  occurrence of limestone apparently  counteracts
any effects  of acidic  precipitation.   Consequently, when predicting vulnerability  of a parti-
cular region to  acidification,  a careful classification of rock mixtures should be  made.   Rock
formations should be  classified according to their potential buffering capacity,  and the type
of soil overlying the  formations should be  noted.   Local  variations  in bedrock and soils  are
very important in explaining variations in acidification between lakes within an area.
11.4.2  Terrestrial  Ecosystems
     Predicting  the sensitivity of terrestrial ecosystems to acidic precipitation  is much more
difficult  than  for  aquatic  ecosystems.   With aquatic  ecosystems it  is  possible  to compare
affected ecosystems  with  unaffected  ones and note where the changes have  occurred.  With ter-
restrial ecosystems, comparisons  are  difficult  to make because the effects of  acidic precipi-
tation  have  been difficult  to  detect.    Therefore,  predictions regarding the  sensitivity  of
terrestrial ecosystems  must, as much as possible, use the data which link the  two  ecosystems,
i.e., data on bedrock  geology.   Since, in most  regions  of the world, bedrock is  not exposed
but  is  covered  with  soil,  it   is  the  sensitivity  of  different types  of soil which must  be
assessed.   Therefore, the first step is to define "sensitivity" as it is used here  in relation
to soils and acidic precipitation.   Sensitivity  of soils to acidification  alone,  though it  may
be the  most  important  long-term effect, is too  narrow a concept.   Soils influence  the quality
of waters in associated streams and lakes and may be changed in ways other than simple pH-base
saturation relationships, e.g.,  microbiological  populations of the surface layers,  accelerated
loss of aluminum by  leaching.   Therefore,  criteria  need to  be  used that would  relate soil
"sensitivity" to any  important  change  brought about in the local  ecosystem by  acid precipita-
tion (McFee,  1980).
     All soils are  not  equally  susceptible to acidification.   Sensitivity to  leaching and to
loss of buffering capacity  varies  according to the  type  of parent material  from which a soil
is derived.  Buffering  capacity is greatest in soils  derived  from sedimentary rocks, especi-
ally those containing carbonates,  and  least in  soils derived from hard crystalline rocks such
as granites and  quartzites (Gorham, 1958).  Soil  buffering capacity varies widely  in different
regions of  the  country  (Figure 11-31).   Unfortunately,  many  of  the areas now receiving  the
most acidic  precipitation also  are  those with  relatively low natural buffering  capacities.
                                           11-96

-------
                                                 REGIONS WITH SIGNIFICANT
                                                 AREAS OF SOILS THAT ARE

                                                      NON SENSITIVE
                                                      SLIGHTLY SENSITIVE
                                                      SENSITIVE

                                                 WITHIN THE EASTERN U.S.
Figure 11-31. Soils of the eastern United States sensitive to acid rainfall (McFee, 1980).
                                     11-97

-------
     The buffering capacity of soil  depends on mineralogy,  texture,  structure,  organic matter,
pH, base saturation,  salt  content,  and soil  permeability.   Above a  pH of 5.5 virtually all  of
the H   ions,  irrespective  of  source, are  retained  by ion exchange  and  chemical  weathering.
Below pH 5.5,  the retention of the H  ion decreases with the soil pH in a manner determined  by
the composition  of the  soil  (Donahue et al., 1977).   With  a successive drop  in  the  soil  pH
below 5.0,  an increasing  proportion  of hydrogen  ions (H  ) and deposited  sulfuric  acid  will
pass through  the soil  and acidify runoff water  (Donahue  et al., 1977).   The  sensitivity  of
different soils based on pH, texture,  and calcite  content is summarized in Table 11-11.

           TABLE 11-11.   THE  SENSITIVITY  TO  ACID PRECIPITATION  BASED  ON:   BUFFER
        CAPACITY AGAINST pH-CHANGE, RETENTION  OF  H ,  AND ADVERSE EFFECTS  ON SOILS

Noncalcareous

Buffering
H retention
Adverse
effects
Calcareous
soils
Very high
Maximal
None
clays
pH > 6
High
Great
Moderate
sandy soils
pH > 6
Low
Great
Considerable
Cultivated
soils
pH > 5
High
Great
None -
slight
Acid
soils
pH < 5
Moderate
Slight
Slight

     Reference:   Wiklander (1979).

     Soils are the most  stable component of a terrestrial  ecosystem.   Any changes which occur
in  this  component would  probably  have  far-reaching  effects.   McFee  (1980)  has  listed  four
parameters which are  of importance  in estimating the sensitivity of soils to acidic precipita-
tion.   They are:
     1.    The total  buffering or  cation exchange capacity which  is  provided
          primarily by clay and soil  organic matter.
     2.    The base saturation of that exchange capacity which  can be estimated
          from the pH of the soil.
     3.    The management  system  imposed on  the soil;  is it  cultivated  and
          amended with fertilizers or  lime  or renewed by flooding or by other
          additions?
     4.    The presence or absence of  carbonates in the soil profile.
     In order  that the  factors  listed  above  could be  used in broad  scale mapping  of soils,
McFee evaluated them  for wide applicability  and ready  availability.  In natural  soils the most
serious effects would be caused by  changes in pH by leaching of soil minerals.  Susceptibility
of soils  to  changes  in either of  these  categories  is most closely associated with the cation
exchange capacity  (CEC).   Soil  with  a low CEC and a circumneutral  pH is likely to have the pH
rapidly reduced by an  influx of acid.   Soils  with  a  high CEC, however, are strongly buffered
against pH changes or changes in the  composition of the leachate.   Acidic soils with a pH near
that of acidic precipitation will  not rapidly change  pH due to acidic precipitation, but will

                                           11-98

-------
probably  release  Al    ions into  the  leachate  (McFee,  1980).   Soils having  a low CEC  are
usually  low  in plant  nutrients;  therefore, significant  changes  in  their  productivity  could
occur with only a slight loss of nutrients (McFee,  1980).
     Even though CEC or buffering capacity does not completely define soil  sensitivity to pos-
sible  influents  of acid,  for  the reasons  given above it  was the  primary  criterion  used  by
McFee  for  the regional  mapping  of soil  sensitivity to  acidic  precipitation  in  the  eastern
United States.  Further, though  it  is frequently stated  in much  of the literature that  soils
with  low CEC or  sandy soils having  low  organic matter are likely to be most  susceptible  to
effects  of  acidic  precipitation,  the  "low CEC"  values   are not  quantified?   To develop  a
working  set  of  classes,  it was necessary to make  certain assumptions and  "worst case"  calcu-
lations.   Since soils  in general  are rather resistant  to change  due to additions of  acid,  a
fairly high  addition  of  acid was assumed and  the  question  asked, "What is  the  maximum effect
that  it  can   have  on  soil,  and  how   high would  the CEC  have to be  to resist  that  effect?"
(McFee, 1980)
     To  determine  sensitivity  of  a  soil, McFee arbitrarily chose a span  of 25  years.   It was
hypothesized  that  a significant  effect  could occur  if  the  maximum  influx  of acid (100  cm  of
precipitation at pH 3.7  per annum)  during that  period  equaled 10 to 25 percent of the cation
exchange capacity  in  the top 25 cm of  soil.   Soils  are considered  slightly  sensitive  if  the
top 25 cm of soil  has an average CEC of 6.2 to 15.4 meq/100 g (assuming a  bulk  density of  1.3
g/cc).   If the  same  influx of acid exceeds  25  percent of  the  CEC  in the top 25  cm,  i.e., when
the CEC is less than 6.2 meq/100 g,  the  soils are considered sensitive.
     Based on the  above  concepts,  the soils of the eastern United States  including effects  of
cultivation   were  mapped  (Figure  11-30)  by McFee.  The  areas containing  most of the  soils
potentially   sensitive  to  acidic  precipitation are  in  the upper  Coastal  Plain  and  Piedmont
regions of the southeast, along the Appalachian Highlands, through the east  central  and north-
eastern areas, and in  the Adirondack Mountains  of New York (McFee, 1980).   The present limited
state  of knowledge  regarding the  effects  of acidic  precipitation on  soils   makes  a more
definitive judgment of the location   of  areas  with  the  most sensitive soils  difficult at  the
present time.
     The capacity of  soils to  absorb and retain anions also  important in  determining whether
soils will become  acidified  was  not  discussed  by McFee  (1980).  The capacity for anion absor-
ption  is great  in soils  rich in  hydrated oxides  of  aluminum  (Al)  and  iron   (Fe).  Reduced
leaching of  salt cations is of great  significance not only in  helping to prevent soil  acidifi-
cation but in geochemical  circulation of nutrients,  fertilization in agriculture and  prevent-
ing water  pollution (Johnson  et  al.,  1980;  Johnson,   1980;  Wiklander,  1980).    (See  Section
11.3.2.1)  This  parameter,  as  well  as those  listed  by McFee  (1980)  should  be  used  in
determining  the sensitivity of soils  to  acidification by both  wet  and dry  deposition.
                                           11-99

-------
11.5  SUMMARY
     Occurrence of acidic  precipitation  (rain and snow) in many regions of the United States,
Canada, and  Scandanavia  has  been implicated  in the  disappearance  or reduction of fish, other
animals,  and plant  life  in  ponds,  lakes,  and  streams.   In addition,  acidic  precipitation
possesses the potential  for  impoverishing sensitive soils, degrading  natural  areas,  injuring
forests, and damaging monuments and buildings made of stone.
     Sulfur  and nitrogen  oxides,  emitted through the combustion of fossil fuels are the chief
contributors to the  acidification  of precipitation.   The  fate  of  sulfur and nitrogen oxides,
as well as  other  pollutants  emitted into the atmosphere,  depends  on their dispersion, trans-
port, transformation and  deposition.   Emissions from automobiles occur at ground level, those
from electric power  generators  from smoke stacks 1000  feet  or more in height.   Transport and
transformation of  the  sulfur  and  nitrogen  oxides  are  in part associated with  the  height at
which they  are emitted.   The greater the height,  the greater the likelihood of a longer resi-
dence time  in the atmosphere  and  a  greater opportunity  for chemical  transformation  of the
oxides to sulfates,  nitrates  or other compounds.   Ozone  and  other photochemical oxidants are
believed  to  be  involved  in  the chemical  transformations.   Because of  long  range  transport,
acidic  precipitation in  a particular state or  region  can  be the  result of  emissions  from
sources in  states  or regions hundreds of miles away rather  than local  sources.  To  date the
complex nature of the chemical transformation  processes  has  not made the demonstration  of a
direct cause  and  effect  relationship between emissions of sulfur  and  nitrogen oxides and the
acidity of precipitation possible.
     Natural emissions of  sulfur  and nitrogen compounds are  also involved in the formation of
acidic  precipitation;   however,  in  industrialized   regions  anthropogenic  emissions  exceed
natural emissions.
     Precipitation is  conventionally  defined  as  being acidic  if  its  pH  is  less than  5.6.
Currently the acidity of  precipitation   in  the northeastern United  States,  the region  most
severely  impacted, ranges  from  pH  3.0 to 5.0.  Precipitation episodes with a pH as  low as 3.0
have been reported for  other regions of  the United  States.   The pH of precipitation can vary
from event  to event, from season to  season  and from geographical  area  to geographical area.
     The  impact  of  acidic precipitation on  aquatic  and terristrial  ecosystems is  not the
result of a  single  or  several  precipitation  events,  but  the  result of continued additions of
acids or  acidifying  substances  over time.  Wet deposition of acidic substances on  freshwater
lakes, streams,, and  natural  land areas is only part of the  problem.  Acidic substances exist
in gases, aerosols, and particulate matter transferred into the lakes,  streams,  and  land areas
by dry deposition.   Therefore  all  the observed biological effects  should not be attributed to
acidic precipitation alone.
     Sensitivity  of a lake to acidification depends on the acidity  of both wet and dry deposi-
tion, the soil system  of the drainage basin,  canopy effects  of ground cover and the composi-
tion of the watershed bedrock.
                                           11-100

-------
     Ecosystems  can  respond  to  environmental  changes  or  perturbations  only  through  the
response of  the populations  of  organisms of  which they are composed.   Species  of organisms
sensitive to  environmental  changes are  removed.   Therefore,  the capacity of  an  ecosystem to
maintain internal  stability is determined  by the  ability  of  individual organisms  to adjust
their physiology  or behavior.  The  success with  which an organism  copes with environmental
changes is determined  by  its  ability to yield reproducing offspring.   The size and success of
a population  depends  upon  the collective ability of organisms to reproduce and maintain their
numbers  in  a  particular  environment.   Those  organisms that adjust  best contribute  most  to
future generations because they have the greatest number of  progeny in the population.
     The capacity of  organisms  to withstand injury from  weather  extremes,  pesticides, acidic
deposition or polluted  air  follows  the principle of limiting  factors.   According  to  this
principle,  for each  physical  factor  in the  environment  there  exists  for  each  organism  a
minimum  and  a  maximum limit  beyond  which  no members  of  a  particular species  can  survive.
Either too much or too little  of a factor such as heat, light, water,  or minerals  (even though
they are necessary for life) can jeopardize  the survival of  an individual  and in extreme cases
a species.   When  one  limiting factor is removed another takes its place.   The range of toler-
ance of an organism may be broad  for one factor, narrow for another.   The tolerance limit for
each species  is  determined  by its genetic makeup  and  varies  from species to  species  for the
same reason.   The range of tolerance also  varies depending on  the  age, stage  of  growth or
growth form  of an organism.  Limiting  factors  are, therefore,  factors which,  when  scarce or
overabundant,  limit  the  growth,  reproduction  and/or  distribution  of  an  organism.   The
increasing acidity  of water  in  lakes and streams  appears  to be such  a  factor.   Significant
changes  that  have  occurred   in   aquatic  ecosystems   with  increasing acidity  include  the
following:

        1.    Fish populations  are  reduced or eliminated.
        2.    Bacterial decomposition  is  reduced  and fungi  may  dominate saprotrophic  communi-
             ties.   Organic  debris  accumulates  rapidly,  tying  up  nutrients,  and  limiting
             nutrient  mineralization and cycling. .
        3.    Species diversity and total  numbers of species of  aquatic plants and animals are
             reduced.   Acid-tolerant species  dominate.
        4.    Phytoplankton  productivity may be  reduced due  to changes in nutrient cycling and
             nutrient  limitations.
        5.    Biomass and total productivity  of benthic macrophytes and algae  may  increase due
             partially to increased lake transparency.
        6.    Numbers and biomass  of  herbivorous  invertebrates decline.   Tolerant  invertebrate
             species,  e.g., air-breathing bugs  (water-boatmen,  back-swimmers, water striders)
             may become abundant primarily due to reduced  fish predation.
        7.    Changes in community  structure  occur at all trophic levels.
                                           11-101

-------
     Studies indicate that  pH  concentrations  between 6.0 and 5.0 inhibit reproduction of many
species of  aquatic  organisms.   Fish populations become  seriously  affected  at a pH lower than
5.0.
     Disappearance of fish  from  lakes  and streams follows  two  general  patterns.   One results
from sudden short-term  shifts  in pH,  the other  arises  from a long-term decrease in the pH of
the water.  A  major injection  of acids and other soluble substances occurs  when polluted snow
melts during warm periods in winter or early spring.   Fish kills are a dramatic consequence of
such episodic injections.
     Long-term  increases  in acidity  interfere  with reproduction  and  spawning,  producing  a
decrease in population density  and a shift in  size and age of the population to one consisting
primarily of  larger and  older  fish.   Effects  on  yield often are not  recognizable  until  the
population  is  close to extinction; this  is  particularly true for  late-maturing  species  with
long lives.  Even  relatively small  increases  (5 to  50  percent)  in mortality of fish eggs and
fry can decrease yield and bring about extinction.
     Aluminum  is  mobilized  at  low  pH values.   Concentrations  of  aluminum  may be  as  or  more
important than pH  levels  as factors leading to declining fish populations in acidified lakes.
Certain aluminum compounds in the water upset  the osmoregulatory function of the blood in fish.
Aluminum toxicity to aquatic biota other than  fish has not been assessed.
     An indirect  effect of acidification potentially  of concern to human  health  is possible
heavy metal contamination of edible fish and  of water supplies.   Studies in Canada and Sweden
reveal  high mercury  concentrations  in  fish from acidified regions.   Lead and copper have  been
found  in  plumbing systems with  acidified water,  and persons drinking the  water  could suffer
from lead or copper poisoning.
     Acidic precipitation may  indirectly  influence terrestrial  plant productivity by altering
the  supply  and  availability  of  soil  nutrients.   Adidification  increases  leaching  of  plant
nutrients (such as  calcium,  magnesium,  potassium,  iron, and manganese)  and  increases the  rate
of.  weathering  of  most  minerals.   It  also  makes   phosphorous  less  available  to  plants.
Acidification also  decreases the rate  of many soil microbiological  processes such as nitrogen
fixation by Rhizobium bacteria  on legumes and by  the  free-living  Azotobacter, mineralization
of nitrogen from  forest litter,  nitrification of  ammonium  compounds, and overall  decay rates
of forest floor litter.
     At present  there are  no  documented observations  or measurements of  changes  in natural
terrestrial  ecosystems that  can be directly attributed to acidic precipitation.  This does not
necessarily  indicate  that  none   are  occurring.    The  information  available  on  vegetational
effects is  an  accumulation  of  the results of  a wide  variety of controlled research approaches
largely  in  the  laboratory, using  in  most instances  some  form  of  "simulated" acidic  rain,
frequently  dilute  sulfuric  acid.   The  simulated  "acid  rains"  have deposited hydrogen (H ),
sulfate (SO* ) and nitrate (NO,) ions  on vegetation and have caused necrotic lesions in a wide
                                           11-102

-------
variety of  plants  species under  greenhouse  and  laboratory conditions.   Such  results  must  be
interpreted with caution,  however, because  the  growth  and morphology of  leaves  under green-
house  conditions  are  often  atypical  of  field conditions.   Based on   laboratory  studies,
sensitivity of  plants  to acidic  depositions seems  to  be associated with the  wettability  of
leaf surfaces.  The  shorter  the  time of contact, the  lower  the resulting dose,  and  the  less
likelihood of injury.
     Erosion of monuments and  buildings made of  stone and corrosion of  metals can result  from
acidic precipitation.  Because sulfur  compounds  are a dominant component  of  acidic precipita-
tion  and   are  deposited  during  dry  deposition also,  the  effects  resulting  from  the  two
processes  cannot be  distinguished.   In addition, the deposition of  sulfur compounds  on stone
surfaces provides  a  medium for microbial growth that can result in  deterioration.
                                           11-103

-------
11.6  REFERENCES

Abrahamsen, G. ,  and G.  J.  Dollard.   Effects  of acid precipitation  on  forest vegetation and
     soil.   ^n:   Ecological  Effects  of  Acid  Precipitation,  Report  of  a  Workshop,  Electric
     Power  Research  Institute, Gatehouse-of-Fleet,  Galloway,  Scotland,  September 4-7, 1978.
     M.  J.   Wood,  ed. ,  EPRI  SOA77-403, Electric  Power  Research Institute, Palo Alto, CA, July
     1979.   Section 4.2.  17pp.

Abrahamsen, G. ,  R.  Horntvedt,  and B.  Tveite.   Impacts  of  acid precipitation  on coniferous
     forest ecosystems.   I_n:   First  International  Symposium on  Acid  Precipitation  and the
     Forest Ecosystem,  U.S.  Department of Agriculture and Others,  Columbus,  Ohio, May 12-15,
     1975.   Water Air Soil Pollut. 8:57-73, 1977.

Abrahamsen, G. ,  K.  Bjor,  R.  Horntvedt, and B.  Tveite.   Effects of acid precipitation on coni-
     ferous forest.   In:  Impact  of Acid Precipitation on Forest and Freshwater Ecosystems in
     Norway:  Summary Report on the Research Results from the Phase I (1972-1975) of the SNSF-
     Project.   F.  H.  Braekke,  ed. ,  Research  Report FR  6/76, SNSF  Project,  Oslo-As,  Norway,
     March 1976.   pp 37-63.

Alexander,   M.   Effects of  acidity on  microorganisms  and microbial  processes  in  soil.   J_n:
     Effects of  Acid  Precipitation on Terrestrial Ecosystems, North Atlantic Treaty Organiza-
     tion,   Toronto,  Ontario, Canada,  May  21-27,  1978.   T.  C. Hutchinson  and  M.  Havas, eds.  ,
     Plenum Press, New York, NY, 1980.  pp. 363-374.

Aimer,  B. , W.  Dickson,  C.  Ekstrb'm,  and  E.  Hbrnstrom.    Sulfur  pollution  and  the  aquatic
     ecosystem.  In:  Sulfur  in the Environment, Part II:  Ecological Impacts.  J. 0.  Nriagu,
     ed.,  John Wiley & Sons, Inc., New York, NY, 1978.   pp.  271-311.

Aimer, B. ,  W.  Dickson,  C.  Ekstrbm, E. Hornstrom,  and  U.  Miller.  Effects of acidification on
     Swedish lakes.   Ambio 3:30-36, 1974.

Altshuller, A. P., and G.  A. McBean.  The LRTAP Problem in North America:  a Preliminary Over-
     view.   United  States-Canada   Research  Consultation  Group on  the  Long-Range transport of
     Air Pollutants, Research Triangle Park, NC, and Downsview, Ontario, Canada, 1979.

Amundsen,  T. ,  and K. Lunder.  Report on fishery-biological surveys in Tjagevatn and Sonstevatn
     in Grandsherod, Notodden  in  Telemark.  Fiskerikonsulenten  i  Ost-Norge,  Direktoratet for
     vitt  og ferskvannsfisk, Oslo, 1974.   13 pp.

Andersson,   I.,  0.  Grahn,  H.  Hultberg,  and   L.  Landner.   Jamforande  undersokning  av olika
     tekniker  for  aterstallande   av   fdrsurade  sjoar.   [Research  for  developing  different
     techniques for removing acid from lakes.]  STU Report 73-3651.  Stockholm:  Institute for
     Water and Air Research, 1975.  Cited in:   Galloway, 1978.  pp. 63-75.

Anschiitz,   J. ,  and F. Gessner.   Der loneraustausch  bei torfmoosen  (Sphagnum).   [Ion exchange
     near   peat  moss (Sphagnum).]   Flora  141:178-236, 1954.   Cited in:   Aimer  et al., 1978.

Armstrong,   F.   A.  J. ,  and D. W. Schindler.  Preliminary chemical  characterization of waters in
     the experimental  lakes  area,  Northwestern Ontario.  J.  Fish. Res. Board Can. 28: 171-187,
     1971.                                                                         ~~

Arnold,  D.  E. , R.  W.  Light,  and  V.   J.  Dymond.   Probable  Effects  of Acid  Precipitation on
     Pennsylvania Waters.   EPA  600/3-80-012,  U.S.  Environmental  Protection Agency, Corvallis,
     OR, January 1980.
                                          11-104

-------
Baker, J.  P., and C. L. Schofield.  Aluminum toxicity to fish as related to acid precipitation
     and Adirondack surface water quality.  TJI:  Ecological Impact of Acid Precipitation, Pro-
     ceedings of an  International Conference,  SNSF  Project,  Sartfefjord,  Norway,  March 11-14,
     1980.   0.  Drablrfs  and A.  Tollan, eds., SNSF Project, Oslo-As, Norway, October 1980.  pp.
     292-293.

Baker, J.  P.,  D.  Hocking, and M.  Nyborg.   Acidity of open  and  intercepted precipitation in
     forests  and  effects   on  forest  soils  in  Alberta,  Canada.   In:   First International
     Symposium  on  Acid  Precipitation  and the Forest Ecosystem, U.S. "Department of Agriculture
     and Others,  Columbus, Ohio,  May 12-15,  1975.   Water Air Soil  Pollut.  7:449-460, 1977.

Beamish,  R.  J.   Growth and survival of  white  suckers  (Catostomus commersoni)  in an acidified
     lake.   J. Fish Res. Board Can. 31:49-54, 1974.

Beamish,  R.  J.   Acidification of  lakes  in  Canada by acid  precipitation and the resulting
     effects  on fishes.   J_n:   First  International  Symposium on  Acid Precipitation  and the
     Forest Ecosystem,  U.S.  Department of Agriculture and Others,  Columbus,  Ohio,  May 12-15,
     1975.   Water Air Soil  Pollut. 6:501-514, 1976.

Beamish,  R. J., and H.  H.  Harvey.   Acidification of the La Cloche Mountain Lakes, Ontario, and
     resulting fish mortalities.   J. Fish. Res. Board Can.  29:1131-1143, 1972.

Beamish,  R.  J. ,  W.  L.  Lockhart,  J. C. Van Loon, and H. H.  Harvey.   Long-term acidification of
     a lake and resulting effects on fishes.  Ambio 4:98-102, 1975.

Bell, H.  L.   Effect of low pH on the survival and  emergence  of  aquatic  insects.   Water Res.
     5:313-319, 1971.

Bell, H.  L. ,  and A.  V. Nebecker.   Preliminary  studies on the tolerance of aquatic insects to
     low pH.  J. Kansas Entomological  Soc. 42:230-236, 1969.

Bick, H. ,  and E.  F.  Drews.  Autopurification  and  ciliated  protozoa  in  an  acid environment
     (model study).  Hydrobiologia 42:393-402,  1973.

Billings,  W. D.   Plants and the Ecosystem.  3rd Edition.   Wadsworth Publishing Company, Inc.,
     Belmont, CA, 1978.  pp. 1-62.

Bolin, B. ,   L.  Granat,  L.  Ingelstam, M. Johannesson, E. Mattsson,  S. Oden, H. Rodhe, and C. 0.
     Tamm.   Air Pollution Across  National Boundaries:  The Impact on the Environment of Sulfur
     in Air  and  Precipitation.   Sweden's Case Study for  the  United Nations Conference on the
     Human  Environment.  P.A.  Norstedt and Sons, Stockholm, Sweden, 1972.

Boughey,  A.  S.   Fundamental  Ecology.   Intext Educational  Publishers,  Scraton,  PA,  1971.  pp.
     11-50.

Brady, N.   C.   The  Nature  and Property of Soils.   8th Edition.  McMillan Publishing Co., Inc.,
     New York, NY,  1974.  pp.  462-472.

Braekke,  F.  H. ,  Ed.    Impact  of  Acid  Precipitation on Forest  and Freshwater Ecosystems in
     Norway:  Summary Report on the Research Results frog) the Phase I (1972-1975) of the SNSF-
     Project.  Research Report 6/76, SNSF Project, Oslo-As, Norway, March 1976.

Brezonik,  P.  L.  Nutrients and other biologically active substances in atmospheric precipita-
     tion.    In:   Atmospheric  Contribution  to  the  Chemistry  of  Lake  Waters,  First Specialty
     Conference  of  the International   Association  for Great  Lakes Research,  Longford Mills,
     Ontario, Canada,  September   28 - October  1,  1975.  J. Great  Lakes Res.  2(suppl.  1):166-
     186,  1976.
                                          11-105

-------
Brock, T.  D.   Lower  pH limit  for the existence of blue-green  algae:   evolutionary and eco-
     logical implications.   Science (Washington, D.C.) 179:480-483, 1973.

Brooks, J.  L. ,  and S.  I. Dodson.   Predation,  body size and composition of plankton.  Science
     150:28-35, 1965.

Brosset,  C.  Air-borne acid.  Ambio 2:2-9, 1973.

Brouzes,   R.  J.  P., R.  A.  N.  McLean,  and G.  H.  Tomlinson.   Mercury -  the  Link Between pH of
     Natural Waters  and the  Mercury  Content  of Fish.   Paper  presented at  a meeting of the
     Panel on Mercury  of the Coordinating Committee  for  Scientific and Technical Assessments
     of  Environmental  Pollutants,  National  Academy  of  Sciences,  National  Research Council,
     Washington, DC, May 3, 1977.  Montreal, Quebec:  Domtar Research Center,  1977.

Bua, B. ,  and  E.  Snekvik.  Hatching experiments  with  roe  of salmonid fish 1966-1971.  Effects
     of  acidity  and salt content  of  hatchery water.   Vann 7:86-93,  1972.   Cited i_n:  Wright
     and Snekvik, 1978.

Chamberlain, A.  C.   Dry deposition of  sulfur dioxide.   J_n:   Atmospheric Sulfur Deposition:
     Environmental Impact and Health Effects,  Proceedings of the Second Life  Sciences Symposium,
     Oak Ridge National Laboratory and Others, Gatlinburg, Tennessee, October  14-18,  1979.  D.
     S. Shriner, C. R.  Richmond, and S. E. Lindberg, eds., Ann Arbor Science  Publishers, Inc.,
     Ann Arbor, MI, 1980.  pp. 185-197.

Chapham,  W. B. , Jr.  Natural Ecosystems.  The  Macmillan Co., New York, NY, 1973.

Cholonky,  B.  J.   Die  Okologie  der diatomeen  in Binnengewasser.   [The  ecology of diatoms in
     inland waters.]  Cramer, Weinheim, 1968.  Cited i_n:   Hendrey et al., 1980b.

Cogbill,  C. V.   The history and character of acid precipitation in  eastern North America.  Iji:
     First  International  Symposium on   Acid  Precipitation  and the  Forest  Ecosystem,  U.S.
     Department  of  Agriculture  and Others,  Columbus,  Ohio, May 12-15,  1975.   Water Air Soil
     Pollut.  6:407-413, 1976.

Cogbill,  C. V.   The effect of acid precipitation on tree growth in  eastern North America.  _In:
     First International Symposium on Acid Precipitation and the Forest Ecosystem, U.S. Depart-
     ment of Agriculture and Others,  Columbus, Ohio, May 12-15, 1975.  Water  Air Soil Pollut.
     8:89-93, 1977.

Cogbill,   C.  V.,  and   G.  E.   Likens.   Acid  precipitation  in  the northeastern United States.
     Water Resour. Res. 10:1133-1137,  1974.

Cole, D.  W. ,  and D.  W. Johnson.  Atmospheric  sulfate additions and cation leaching in a Doug-
     las  fir ecosystem.  Water Resour.  Res.  13:313-317, 1977.

Comerford, N. B. ,  and  E.  H. , White.   Nutrient content  of throughfall  in  paper birch and red
     pine stands in northern Minnesota.  Can.  J. For.  Res.  7:556-561, 1977.

Connell,  W. E., and W.  H. Patrick, Jr.   Sulfate reduction in soil:  effects of redox  potential
     and pH.   Science (Washington, D.C.) 159:86-87, 1968.

Conroy, N. , K.  Hawley,  W.  Keller, and  C.  Lafrance.   Influences of the atmosphere on lakes in
     the  Sudbury  area.   In:   Atmospheric Contribution to  the  Chemistry of Lake Waters, First
     Specialty Conference of  the International Association for Great Lakes Research, Langford
     Mills,  Ontario,   Canada,   September  28  -  October  1,  1975.   J.  Great  Lakes  Res.
     2(suppl.l):146-165, 1976.
                                          11-106

-------
Cowling,  E.  B. ,  and L. S. Dochinger.  The  changing  chemistry  of  precipitation and its effects
     on vegetation and materials,   I_n:   Control  and  Dispersion of Air  Pollutants:   Emphasis on
     N0v  and Particulte Emissions.  AICHE Symp.  Ser.  74(175):134-142,  1978.
       A                                              ^^™

Crisman,  T.  L. ,   R.  L.  Schulze,  P. L.  Brezonik,  and S.  A.  Bloom.   Acid precipitation:   the
     biotic  response in  Florida  lakes.   J_n:   Ecological  Impact  of Acid Precipitation,  Pro-
     ceedings of  an  International  Conference,  SNSF  Project,  Sarjdefjord, Norway,  March  11-14,
     1980.  D. Drablefs and A. Tollan,  eds.,  SNSF Project,  Oslos-As,  Norway,  October 1980.   pp.
     296-298.

Cronan,  C.  S.    Solution chemistry   of a  New Hampshire subalpine  ecosystem:   biochemical
     patterns and processes.   Ph.D.  Thesis,  Dartmouth  College,   Hanover,  NH,  1978.   248  pp.

Cronan, C. S.  Consequences  of  sulfuric  acid inputs  to a forest soil.   I_n:   Atmospheric Sulfur
     Deposition:    Environmental  Impact  and  Health  Effects,  Proceedings of  the  Second  Life
     Sciences  Symposium,  Oak  Ridge  National  Laboratory  and  Others,  Gatlinburg,  Tennessee,
     October 14-18,  1979.   D.  S.  Shriner,  C.  R. Richmond, and S.  E. Lindberg,  eds.,  Ann Arbor
     Science Publishers,  Inc., Ann  Arbor, MI,  1980.   pp. 335-343.

Cronan,  C.  S. ,   and C.  L.   Schofield.   Aluminum  leeching response  to  acid  precipitation:
     effects  on   high-elevation  watersheds  in the  Northeast.   Science  (Washington,  D.C.)
     204:304-306, 1979.

Dancer, W.  S. ,  L.  A.  Peterson,  and  G.  Chesters.   Ammonification  and  nitrification of N as
     influenced by  soil   pH  and previous N treatments.    Soil Sci.  Soc.  Am.   Proc.  37:67-69,
     1973.

Dannevig,  G.  Influence  of  precipitation on the acidity of water courses and on  fish stocks.
     Jeger  og  Fisker.  3:116-118,  1959.   Cited  in:   Leivestad et al.,  1976;  Wright  et al.,
     1976; Wright and Snekvik, 1978.

Davis,   R.  B. ,  M.  0.  Smith,  J.  H.  Baily,  and S. A.  Norton.   Acidification  of  Maine  (U.S.A.)
     lakes  by  acidic precipitation.   Verh. Int. Ver. Theor.  Angew Limnol.  20:532-537,  1978.

Denison, R., B.  Caldwell, B.  Bormann,  L.  Eldred, C.  Swanberg,  and  S. Anderson.   The effects of
     acid  rain  on  nitrogen  fixation  in western  Washington   coniferous  forests.   I_n:   First
     International Symposium on  Acid  Precipitation  and  the  Forest Ecosystem,  U.S.  Department
     of  Agriculture  and  Others,  Columbus, Ohio,   May 12-15,  1975.   Water  Air Soil  Pollut.
     8:21-34, 1977.

Dickson,  W.   The acidification  of Swedish lakes..   Fish.  Board  Swed.  Inst.   Freshwater Res.
     Drottningholm Rep. (54):8-20,  1975.

Dickson,  W.   Some  effects   of  the acidification  of Swedish  lakes.   Verh.   Int.  Ver.  Theor.
     Angew. Limnol.  20:851-856,  1978.

Dillon, P.  J.,  D. S.  Jefferies, W.  Snyder,  R. Reid, N.  D.   Van, D.  Evans,  J. Moss, and  W.
     A. Scheider.    Acidic  precipitation   in   south-central   Ontario:    recent observations.
     J. Fish.  Res. Board Can. 35:809-815, 1978.

Dodson,  S.  I.   Zooplankton  competition and  predation:   an  experimental  test  of the  size-
     efficiency hypothesis.   Ecology 5_5:605-613, 1974.

Donahue, R. L.,  R. W. Miller, and J. C.  Shickluna.    Soils:  An Introduction  to  Soils  and Plant
     Growth.  4th  Edition.   Prentice-Hall,  Inc.,  Englewood Cliffs,  NJ,  1977.  pp.  244-248.
                                          11-107

-------
Drablds, D. ,  and I.  Sevaldrud.  Lake acidification, fish damage, and utilization of outfields.1
     A comparative survey  of six highland areas, southeastern Norway.  In:  Ecological Impact
     of  Acid  Precipitation,  Proceedings  of  an  International  Conference,  SNSF  Project,
     Sande£jprd, Norway,  March 11-14,  1980.   D.  Drablrfs  and A.  Tollan,  eds.,  SNSF Project,
     Oslo-As, Norway, October 1980.   pp. 354-355.

Driscoll, C.  T.  Chemical  characterization of some dilute  acidified lakes and streams in the
     Adirondack region of New York state.  Ph.D.  Thesis, Cornell University, Ithaca, New York,
     1980.   309 pp.

Driscoll, C.  T. ,  Jr.,  J.  P.  Baker,   J.  J.  Bisogni,  Jr.,  and  C.  L.  Schofield.   Effect of
     aluminum speciation  on  fish in dilute  acidified  waters.   Nature  (London) 284:161-163,
     1979.

Dvorak, A.  J. ,  B.  G.  Lewis,  P. C.  Chee, J.  D.  Jastrow, J.  C. Prioleau, E. H. Dettmann, F. C.
     Kornegay, L.  G.  Soholt, R. F.  Freeman, III,  D. L. Mabes, W. S. Vinikour, R.  M. Goldstein,
     P. A.  Merry,  E.  W.  Walbridge,  R. R. Hinchman, and E. D.  Pentecost.   Impacts of Coal-Fired
     Power  Plants  on Fish,  Wildlife,  and Their Habitats.   FWS/OBS-78/28,  U.S.  Department of
     the Interior,  Fish and Wildlife Service, Ann Arbbor, MI, March 1978.   pp. 64-70.

Eaton, J. S., G. E.  Likens, and F.  H. Bormann.  Throughfall  and Stemflow Chemistry in a North-
     ern Hardwood Forest.   J. Ecol.   61:495-508,  1973.

Eliassen, A., and J.  Saltbones.  Decay and transformation rates of S02 as estimated from emis-
     sion data,  trajectories and measured air concentrations.  Atmos Environ. 9:425-429, 1975.

European Inland Fisheries  Advisory  Committee.  Water quality criteria for European freshwater
     fish -  extreme pH values and inland fisheries.  Water Res.  3:593-611, 1969.

Evans, L. S. , and  D.  M.  Bozzone.   Effect  of buffered solutions and sulfate on vegetative and
     sexual  development in gametophytes of Pteridium aquilinum.   Am. J.  Bot. 64:897-902, 1977.

Evans, L. S. , and  D.  M.  Bozzone.   Effect  of buffered solutions and various anions on vegeta-
     tive  and  sexual  development   in  gametophytes  of  Pteridium aquilinum.   Can.   J.  Bot.
     56:779-785, 1978.

Evans,  L.  S. ,  and T.  M.   Curry.   Differential   responses of plant  foilage  to simulated acid
     rain.   Am.  J.  Bot.  66:953-962,  1979.

Evans,  L.  S. ,  N.   F.  Gmur,  and F.  Da  Costa.   Leaf surface  and  histological  perturbations of
     leaves of Phaseolus vulgari's and Helianthus annuus after exposure to simulated acid rain.
     Am. J.  Bot. 64:903-913, 1977b.

Evans, L. S. , N.  F.  Gmur, and F.  Da Costa.  Foliar response of six clones of hybrid poplar to
     simulated acid rain.   Phytopathology 68:847-856, 1978.

Evans, L. S., N. F.  Gmur,  and J. J.  Kelsch.  Perturbations of upper leaf surface structures by
     simulated acid rain.   Environ.  Exp. Bot. 17:145-149, 1977a.

Fagestrom,  T. ,  and A.  Jernelov.  Some  aspects of  the quantitative ecology of mercury.  Water
     Res. 6:1193-1202, 1972.

Ferenbaugh,  R.  W.   Effects of simulated acid rain on Phaseolus vulgari's L. (Fabaceae).  Am. J.
     Bot. 63:283-288, 1976.

Fiance,  S.  B.   Distribution  and  biology of mayflies  and  stoneflies  of Hubbard  Brook,  New
     Hampshire,  MS.   Thesis, Cornell University,  Ithaca, NY, 1977.
                                          11-108

-------
Fisher,  B.  E.  A.   Long-range  transport  and deposition of  sulfur  oxides.   In:   Sulfur  in  the
     Environment.    Part I:   The Atmospheric  Cycle.   J.  0.  Nriagu, ed. ,  John Wiley &  Sons,
     Inc., New York, NY, 1978.   pp. 243-295.

Foster, R. J.  Geology.  Charles E. Merrill  Publishing Co., Columbus, OH,  1971.

Fredriksen,  R.  L.   Nutrient  budget of  a Douglas-fir forest  on  an experimental watershed  in
     western Oregon.   Iji:   Research on Coniferous  Forest  Ecosystems:   First Year  Progress  in
     the Coniferous Forest Biome, US/IBP,  Proceedings of a  Symposium, Forty-Fifth Annual  Meet-
     ing, Northwest Scientific Association, Bellingham, Washington, March  23-24, 1972.   J.  F.
     Franklin, L.   J.  Dempster, and R. H.  Waring, eds., U.S. Department  of  Agriculture,  Forest
     Service, Portland, OR, 1972.  pp. 115-131.

Gahnstrom, G., G.  Andersson, and S. Fleischer.  Decomposition  and  exchange  processes  in  acidi-
     fied  lake  sediment.   In:  Ecological  Impact of  Acid Precipitation,  Proceedings  of  an
     International  Conference,  SNSF   Project, Sandefiord,  Norway,  March  11-14,   1980.   D.
     Drablds and A. Tollan,  eds.,  SNSF  Project,  Oslo-As,  Norway, October  1980.  pp.  306-307.

Galloway,  J.  N.    Effects  of  sulfur  oxides  on  aquatic  ecosystems.   I_n:   Sulfur Oxides.
     National Academy of Sciences, Washington, DC,  1978.  pp.  63-79.

Galloway, J. N. ,  and  E. B. Cowling.   The effects of precipitation  on aquatic  and  terrestrial
     ecosystems:   a proposed precipitation network.  J. Air Pollut.  Control  Assoc.  28:229-235,
     1978.

Galloway, J. N., and D. M.  Whelpdale.   An  atmospheric sulfur budget  for  eastern North America.
     Atmos.  Environ. 14:409-417, 1980.

Galvin,  P.  J. ,  and J.  A.  Cline.  Measurement of anions  in the  snow  cover of  the Adirondack
     Mountains.   Atmos. Environ. 12:1163-1167, 1978.

Galvin, P.  J. ,  P.  J.  Samson,  P. E. Coffey, and  D. Romano.   Transport  of  sulfate  to New York
     State.   Environ.  Sci.  Technol. 12:580-584, 1978.

Garrett,  A.    Compositional   changes   of   ecosystem  during  chronic  gamma  irradiation.    hi:
     Proceedings  of  the  Second  National  Symposium  on  Radioecology,  U.S.   Atomic  Energy
     Commission and Others,  Ann Arbor,  Michigan,  May 15-17,  1967.   D. J.  Nelson and  F.  C.
     Evans,  eds.,  CONF-670503, U.S.  Atomic  Energy Commission,  Oak Ridge, TN, March 1969.   pp.
     99-109.

Giddings,  J. ,  and  J.  N.   Galloway.    The effects  of  acid  precipitation  on aquatic  and
     terrestrial   ecosystems.    In:    Literature   Reviews  on  Acid  Precipitation.   Cornell
     University,  Centers for  Environmental Quality Management  and Water Resources and  Marine
     Sciences, Ithaca, NY,  March 1976.  40 pp.

Gjessing,  E.  T. ,  A.  Henriksen,   M.  Johannessen,  and   R.   F.  Wright.    Effects   of acid
     precipitation on  freshwater chemistry.    J.n:    Impact of  Acid Precipitation on Forest  and
     Freshwater Ecosystems in  Norway:   Summary Report on the Research Results from  the Phase I
     (1972-1975) ofo the  SNSF-Project.   F.  H.  Braekke,  ed. ,  Research  Report  FR  6/76, SNSF
     Project, Oslo-As, Norway, March 1976.   pp. 65-85.

Glass,  N. R. , G.  E.  Glass, and  P.  J.  Rennie.   Effects of  acid precipitation.   Environ. Sci.
     Technol. 13:1350-1355, 1979.

Gorham,  E.   On  the acidity and  salinity  of rain.  Geochim.  Cosmochim.  Acta 7:231-239,  1955.
                                          11-109

-------
Gorham,  E.    The  influence  and  importance  of  daily weather  conditions  in  the  supply of
     chloride, sulfate and other ions to fresh waters  from atmospheric precipitation.   Philos.
     Trans.  R. Soc. London Ser. B. 241:147-178, 1958.

Gorham,  E.   Acid  precipitation  and its influence  upon  aquatic  ecosystems—an overview.   I_n:
     First  International  Symposium  on Acid  Precipitation  and  the  Forest  Ecosystem,  U.S.
     Department  of Agriculture and  Others,  Columbus,  Ohio, May  12-15,  1975.   Water Air  Soil
     Poll lit. 6:457-481, 1976.

Gosner, K.  L., and I.  H. Black.  The effects of acidity on the development and hatching  of New
     Jersey frogs.  Ecology 38:256-262, 1957.

Grahn, 0.   Macrophyte  succession  in Swedish lakes  caused by deposition of  airborne acid  sub-
     stances.    In:   First  International  Symposium   on  Acid  Precipitation  and  the   Forest
     Ecosystem,  U.S.  Department of  Agriculture  and Others, Columbus, Ohio, May 12-15, 1975.
     Water Air Soil Pollut. 7:295-305,  1977.

Grahn, 0. ,  H. Hultberg,  and  L.  Landner.   Oligotrophication--a  self-accelerating  process in
     lakes subjected to excessive supply of acid substances.  Ambio 3:93-94, 1974.

Granat,  L.    On   the  relation  between  pH  and   the  chemical  composition  in   atmospheric
     precipitation.  Tellus 24:550-560, 1972.

Grennard, A., and F.   Ross.   Progress  report on  sulfur dioxide.  Combustion  45:4-9, 1974.

Hagen, A., and A.  Langeland.    Polluted  snow in southern Norway and the effect of the meltwater
     on freshwater and aquatic organisms.  Environ. Pollut. 5:45-57, 1973.

Hagstrom, T.   Grodornas  fb'rsvinnande i an fdrsurad sjo.   [Disappearance of  frogs from  an  acid
     lake.]  Sveriges Natur 11/77:367-369, 1977.   Cited in:  Hendrey, 1978.

Haines, E.  B.   Nitrogen content and acidity of rain on the Georgia coast.  Water Resour. Bull.
     12:1223-1231, 1976.

Hall,  R.  J. ,  G.  E. Likens, S.  B.  Fiance,  and G.  R. Hendrey.  Experimental  acidification  of  a
     stream  in  the  Hubbard  Brook  Experimental   Forest,  New Hampshire.   Ecology  61:976-989,
     1980.

Halstead, R.  L. ,  and  P.  J. Rennie.   Effects  of  sulphur on soils in Canada.  j_n:   Sulphur and
     its  Inorganic Derivatives in the Canadian Environment.  NRCC No. 15015, National Research
     Council  of   Canada,  NRC  Assoicate Committee  on  Scientific  Criteria  for  Environmental
     Quality,  Ottawa,  Canada,  1977.   pp. 181-219.  '

Hamilton, W.  C.   Personal  communication to Dr. J. H.  B.  Garner, U.S. Environmental Protection
     Agency, Research Triangle Park, NC, January 31, 1980.

Hanken, I. , J.  F.  Lynch, and  D. B.  Wake.   Salamander invasion of the tropies.  Natural Hist.
     89:47-53, 1980.

Harr, T.  E.  , and P. E.  Coffey.   Acid Precipitation  in  New York State.  Technical Paper  No.  43,
     New  York  State Department of Environmental  Conservation, Albany, NY, July 1975.   pp.  21-
     29.

Harward,  M.  E. ,  and  H.  H.  Reisenaur.   Movement and reactions of inorganic  soil sulfur.   Soil
     Sci. 101:326-335,  1966.

Heinrichs,  H. ,  and R.   Mayer.   Distribution and  cycling of  major and  trace  elements   in  two
     central forest ecosystems.  J.  Environ.  Qual. 6:402-407, 1977.


                                          11-110

-------
Henderson, G. S. , and W. F. Harris.  An ecosystem approach to characterization of the nitrogen
     cycle in a deciduous forest watershed.  I_n:  Forest Soils and Forest  Land Management, Pro-
     ceedings of  the 4th  North American  Forest Soils Conference,  Laval  University, Quebec,
     Ontario,  Canada,  August  1973.   B.  Bernier  and C.  H.  Winget,  eds. ,  Les  Presses de
     1'Universite Laval, Quebec, Ontariao, Canada, 1975.  pp. 179-193.

Hendrey, G. R.  Effects of pH on the Growth of Periphytic Algae in Artificial Stream Channels.
     Report IR 25/76, SNSF Project, Oslo-As, Norway, October 1976.

Hendrey, G.  R.   Aquatics  Task Force on  Environmental  Assessment of the Atikokan Power Plant:
     Effects  on Aquatic Organisms.   BNL 50932, U.S. Department of Energy, Brookhaven National
     Laboratory, Upton, NY, November 1978.

Hendrey, G.  R., and  F.  A. Vertucci.   Benthic  plant  communities in  acidic Lake Colden, New
     York:    sphagnum  and  the  algal  mat.   _Iri:   Ecological Impact of Acid Precipitation,  Pro-
     ceedings of an  International  Conference,  SNSF  Project, .Sartfef jord,  Norway, March 11-14,
     1980.   D.  Drablds  and A.  Tollan, eds., SNSF Project, Oslo-As,  Norway, October 1980.  pp.
     314-315.

Hendrey, G.  R. ,  and R.  F. Wright.   Acid precipitation in Norway:   effects  on  aquatic fauna.
     Ijr.  Atmospheric Contribution to the Chemistry of Lake Waters,  First  Specialty Conference
     of  the   International  Association  for  Great  Lakes  Research,  Longford Mills,  Ontario,
     Canada,   September  28  -  October 1, 1975.   J.  Great Lakes Res.  2(suppl. 1):192-207, 1976.

Hendrey, G. R.,  N.  D.  Yan, and K. J. Baumgartner.  Responses of freshwater plants and inverte-
     brates  to  acidification.    Presented  at the EPA/OECD International  Symposium for Inland
     Waters and Lake Restoration, Portland, ME, September 8-12, 1980a.

Hendrey, G.  R. , J.  N.  Galloway, S. A.  Norton,  C. L. Schofield, P. W.  Shaffer and D. A. Burns.
     Geological  and Hydrochemical  Sensitivity  of the Eastern United States to Acid Precipita-
     tion.    EPA-600/3-80-024,  U.S.  Environmental   Protection  Agency, Corvallis,  OR,  January
     1980b.

Hendry,  C.  D.,  Jr.   The  Chemistry  of  Precipitation in North-Central Florida.   M.S.  Thesis,
     University of Florida, Department of Environmental Engineering  Sciences, Gainesville, FL,
     1977.

Hendry, C.  D. ,  Jr.,  and P.  L. Brezonik.   Chemistry of precipitation  at Gainesville, Florida.
     Environ. Sci.  Techno!.  14:843-849, 1980.

Henriksen,  A.   A  simple  approach  for identifying and  measuring  acidification  of freshwater.
     Nature (London) 278:542-545, 1979.

Herrmann,  R. ,  and  J. Baron.   Aluminum  mobilization in acid  stream  environments,  Great Smoky
     Mountains National Park,  U.S.A.   Jjv.   Ecological   Impact of  Acid Precipitation, Proceed-
     ings of an International  Conference, SNSF  Project, Sandefjord,  Norway, March 11-14, 1980.
     D.  Drabltls and  A.  Tollan,  eds.,  SNSF  Project, Oslo-As,  Norway,  October  1980.   pp.
     218-219.
                                          11-111

-------
Hicks, B.  B. ,  and  M.  L. Wesely.   Turbulent transfer processes  to  a surface and  interaction
     with  vegetation,   In:   Atmospheric  Sulfur Deposition:   Environmental  Impact and Health
     Effects, Proceedings of the Second Life Sciences Symposium,  Oak  Ridge National Laboratory
     and Others, Gatlinburg,  Tennessee,  October 14-18,  1979.   D.  S.  Shriner, C.  R. Richmond,
     and S.  E.  Lindberg, eds.,  Ann Arbor  Science  Publishers,  Inc.,  Ann Arbor, MI, 1980.  pp.
     199-207.

Hindawi,  I.  J. ,  J. A.  Rea,  and W. L. Griffis.   Response of bush bean  exposed  to acid mist.
     Am.  J. Bot.  67:168-172, 1980.

Hoeft, R.  G. ,  D.  R.  Keeney, and L. M. Walsh.  Nitrogen and sulfur in precipitation and sulfur
     dioxide in the atmosphere in Wisconsin.  J. Environ. Qual. 1:203-208, 1972.

Holling,  C.  C.   Resilience and  stability  of ecological  systems.   Annu.  Rev.  Ecol.  Syst.
     4:1-23, 1973.

Hornbeck, J. W.,  G. E.  Likens, and J.  S.  Eaton.  Seasonal patterns in acidity of precipitation
     and their implications  for forest stream ecosystems.  lr\:   First International Symposium
     on  Acid  Precipitation  and  the   Forest Ecosystem,  U.S.   Department  of  Agriculture  and
     Others, Columbus,  Ohio, May 12-15, 1975.  Water Air Soil Pollut. 7:355-365, 1977.

Hprnstrbm,   E. , C.  Ekstrom,  U.  Miller, W.  Dickson.   Effects of the  Acidification  on  Lakes in
     the Swedish  West  Coast Region.   Statens  Naturvardsverk,  Slona,  Sweden,  Publikationer
     1973:  7.  Cited ir\:   Wright and Gjessing, 1976.

Hubbert,  M.  K.   Outlook for fuel  reserves.   In:   McGraw-Hill  Encyclopedia  of  Energy.   D. N.
     Lapedes, ed.,  McGraw-Hill  Inc., New York, NY, 1976.  pp 11-23.

Hultberg,  H.   Thermally stratified  acid water  in  late  winter—a key  factor  inducing self-
     accelerating processes which  increase acidification,  In:   First International Symposium
     on  Acid  Precipitation  and  the   Forest Ecosystem,  U.S.   Department  of  Agriculture  and
     Others, Columbus,  Ohio, May 12-15, 1975.  Water Air Soil Pollut. 7:279-294, 1977.

Hutchinson, T. C. ,  and  L.  M.  Whitby.   The  effects  of acid rainfall  and heavy metal  particu-
     lates   on  a boreal  forest  ecosystem  near  the Sudbury  smelting region of  Canada.   In:
     First   International Symposium  on  Acid  Precipitation  and   the  Forest  Ecosystem,   U.S.
     Department of  Agriculture  and Others,  Columbus,  Ohio, May  12-15,  1975.  Water  Air  Soil
     Pollut. 7:421-438,  1977.

Hutchinson, T. C. ,  W.  Gizym,  M. Havas, and V. Zoberns.  Effects  of long-term lignite burns on
     Arctic  ecosystems  at  the  Smoking Hills, N.W-T.   Jji:  Trace Substances in Environmental
     Health-XII,  D.  D.  Hemphill,  ed. ,  University  of Missouri,  Columbia,  Missouri,  1978.
     pp.  317-332.

Irving,  P.   M.   Rainfall activity  at  Argonne.   I_n:  Radiological  and  Environmental  Research
     Division Annual Report:   Ecology, January through December 1978.  ANL-78-65 (Pt.  3),  U.S.
     Department of  Energy,  Argonne National  Laboratory, Argonne,  IL,  1978.  pp. 21-23.

Irving, P.   M.  Response  of  Field-Grown Soybeans  to Acid  Precipitation Alone and  in Combina-
     tion  with  Sulfur  Dioxide.   PhD.  Thesis,  University of Wisconsin,  Milwaukee, WI, 1979.

Irving, P.   M. , and J.  E. Miller.   The effects of acid precipitation alone and in combination
     with  sulfur  dioxide  on  field-grown  soybeans.    Jji:    Radiological   and  Environmental
     Research Division Annual  Report:   Ecology, January through December 1978.  ANL-78-65  (Pt.
     3),  U.S.  Department  of  Energy,  Argonne  National   Laboratory,  Argonne, IL,  1978.   pp.
     17-20.
                                          11-112

-------
Jacbbson,  J.  S.   Experimental  studies  on  the  phytotoxicity  of  acidic  precipitation:   the
     United States  experience.   In:   Effects of  Acid Precipitation on Terrestrial  Ecosystems,
     North Atlantic Treaty OrganTzation,  Toronto, Ontario,  Canada,  May  21-27,  1978.   T.  C.
     Hutchinson and M. Havas, eds. , Plenum Press,  New York, NY, 1980a.  pp.  151-160.

Jacobson,  J.   S.    The  influence  of  rainfall   composition  on  the  yield  and  quality  of
     agricultural   crops.   jji:   Ecological  Impact of  Acid Precipitation,  Proceedings  of  an
     International Conference, SNSF Project, iandefjord, Norway, March 11-14,  1980.  D.  Drabl«(s
     and A. Tollan, eds., SNSF Project, Oslo-As,  Norway, October 1980b.  pp. 41-46.

Jacobson,  J.  S. ,  and  P.  Van Leuken.   Effects  of  acidic precipitation  on vegetation.   In:
     Proceedings  of the Fourth  International  Clean Air Congress,  International  Union  of  Air
     Pollution Prevention Associations,  Tokyo,  Japan, May  16-20, 1977.  S.  Kasuga, N. Suzuki,
     T. Yamada, G.  Kimura,  K. Inagaki, and K. Onoe, eds.,  The Japanese Union  of  Air Pollution
     Prevention Associations, Tokyo, Japan, 1977.  pp. 124-127.

Jacobson, J.  S. , J. Troiano,  L. J. Colavito, L.  I. Heller,  and D. C. McCune.   Polluted rain  and
     plant growth.  Jji:  Polluted Rain, Twelfth International Rochester Conference  on Environ-
     mental Toxicity,  University of  Rochester,  Rochester, New York, May  21-23,  1979.   T.  Y.
     Toribara, M.  W. Miller,  and P. E. Morrow, eds., Environmental Science  Research Volume  17,
     Plenum Press, New York,  NY, 1980.  pp. 291-305.

Jensen, K. W. ,  and E.  Snekvik.  Low pH levels wipe out salmon and trout populations in  south-
     ernmost Norway.  Ambio 1:223-225, 1972.

Johannessen,   M. ,  and  A.  Henriksen.   Chemistry  of snow meltwater:   changes  in  concentration
     during melting.  Water Resour. Res.  14:615-619, 1978.

Johannessen,   M. ,  A.  Skartvedt,  and  R.  F.  Wright.  Streamwater  chemistry before, during  and
     after  snowmelt.    I_n:    Ecological   Impact   of  Acid  Precipitation,   Proceedings   of  an
     International  Conference,  SNSF   Project,  Sandefj,ord,  Norway,  March  11-14,  1980.    D.
     Drablrfs and  A.  Tollan,  eds., SNSF Project,  Oslo-As,  Norway,  October  1980.   pp. 224-225.

Johnson, N. M. , G.  E.  Likens, F. H.  Bormann, D. W. Fisher, and R. S. Pierce.  A  working model
-,:    for the variation in stream water chemistry at the Hubbard Brook Experimental  Forest,  New
     Hampshire.   Water Resources Res.  5:  1353-1363, 1969.

Johnson, D. W.   Site susceptibility to  leaching  by H2S04  in acid  rainfall.   I_n:  Effects  of
     Acid  Precipitation  on  Terrestrial  Ecosystems,  North  Atlantic  Treaty   Organization,
     Toronto,  Ontario,  Canada,  May 21-27,  1978.   T.  C.  Hutchinson and M.  Havas,  eds.,  Plenum
     Press, New York, NY, 1980.  pp.  525-535.

Johnson, D. W.,  and D.  W. Cole.  Anion mobility in sols:  Relevance to nutrient transport  from
     forest ecosystems.  Environ. International  3:79-90, 1980.

Johnson, D. W. , J.  W.  Hornbeck, J. M. Kelly,  W.   T. Swank, and D. E. Todd.  Regional patterns
     of soil  sulfate  accumulation:   relevance to  ecosystem sulfur  budgets.   In:    Atmospheric
     Sulfur Deposition:   Environmental Impact  and Health  Effects,  Proceedings  of the  Second
     Life Sciences Symposium, Oak Ridge National Laboratory and Others, Gatlinburg, Tennessee,
     October  14-18,  1979.   D.  Shriner,  C. R.  Richmond,  and S.  E.  Lindberg,  eds., Ann Arbor
     Science Publishers, Inc., Ann Arbor, MI, 1980.  pp. 507-520.

Jones.  M.  B.   Sulfur in agricultural  lands.  J_n:   Sulfur in the Environment.   Revised Edition.
     Missouri  Botanical Garden, St. Louis,  Mo.,  July 1975.  pp. 146-158.

Junge,   C.  E.   The  distribution  of ammonia  and nitrate in rainwater  over the United States.
     Trans. Am.  Geophys. Union 39:241-248,  1958.
                                          11-113

-------
Kallqvist, T.,  R.  Romstad, and J. Kotai.   Preliminary study of pH-effects on algal communities
     in experimental channels.  SNSF-Project IR 7/75, 1975.  Cited HI:  Hendrey et al., 1980a.

Kramer, J. R.  Geochemical  and lithological factors  in  acid precipitation,  ^n:  Proceedings
     of the First International Symposium on Acid Precipitation and the Forest Ecosystem, U.S.
     Department of  Agriculture  and  Others,  Columbus, Ohio,  May  12-15,  1975.  L. S.  Doch.inger
     and T. A.  Seliga, eds., NEFES/77-1,  U.S. Department of Agriculture, Forest Service, Upper
     Darby, PA, August 1976.   pp. 611-618.

Kucera, V.  Effects  of  sulfur dioxide and  acid  precipitation  on metals and anti-rust painted
     steel.  Ambio 5:243-248, 1976.

Kwiatkowski,  R. E. ,  and  J.  C. Roff.  Effects of acidity on the phytoplankton and primary pro-
     ductivity  of selected northern Ontario lakes.  Can.  J. Bot.  54:2546-2561, 1976.

Laake,  M.   Effekter  av  lav pH  pa  produksjon,  nedbryting og stoffkretsl^p  i  littoralsonen.
     [Effects  of  low pH  on the  production,  breaking down of harmful  substances  in a coastal
     region.]  Research  Project IR  29/76,  1432  Aas-NLH,  Norway:   SNSF-Project, Secretariat,
     1976.  Cited in:  Galloway, 1978.

Landner,  L. , and  P.  0.   Larsson.  Biological  Effects of Mercury Fall-Out  Into  Lakes from the
     Atmosphere,  IUL Report B115.  Stockholm:  Institute for Water and Air  Research,  1972.  18
     pp.   (in  Swedish, translated  by H.  Altosaar,  Domtar  Research Centre, December  23, 1975)

Lang, D.  S. , S.  V.  Krupa, and  D.  S.  Shriner.   Injury to  vegetation  incited by sulfuric acid
     aerosols  and  acidic rain.  Presented  at  the 71st Annual Meeting,  Air Pollution Control
     Association, Houston, TX, June 25-30, 1978.   Paper No. 78-7.3.

Larson, T. V.,  R.  J. Charlson, E. J. Knudson, G.  D.  Christian, and H.  Harrison.   The  influence
     of a  sulfur dioxide point source on the rain  chemistry  of a single  storm  in the Puget
     Sound region.   Water Air Soil  Pollut. 4:319-328, 1975.

Lee,  J.  J. ,  and  D.  E.  Weber.   Effects of  Sulfuric Acid  Rain on  Two Model Hardwood Forests:
     Throughfall,  Litter Leachate,  and  Soil  Solution.    EPA-600/3-80-014,  U.S.  Environmental
     Protection Agency,  Corvallis,  OR, January 1980.

Lee,  J.  J. ,  G. E.  Neely,  and S. C.  Perrigan.   Sulfuric  Acid Rain Effects on  Crop Yield and
     Foliar Injury.   EPA-600/3-80-016,  U.S. Environmental  Protection  Agency,  Corvallis, OR,
     January  1980.

Leivestad, H. , G.  Hendrey,  I.  P.   Muniz,  and E.  Snekvik.  Effects  of  acid precipitation on
     freshwater organisms.   In:   Impact  of Acid Precipitation on  Forest  and Freshwater Eco-
     systems  in Norway:   Summary Report  on the  Research  Results  from the  Phase I (1972-19^5)
     of the SNSF-Project.  F. H. Braekke, ed., Research Report FR 6/76, SNSF Project, Oslo-As,
     Norway,  March 1976.   pp. 87-111.

Lewis, W.  M., Jr., and M. C.  Grant.   Acid precipitation in the western United States.  Science
     (Washington, D.C.)  207:176-177, 1980.

Likens, G. E.  The  Chemistry of Precipitation in  the Centra.!  Finger Lakes Region.   Technical
     Report 50,  Cornell  University,  Water  Resources and  Marine  Science  Center,  Ithaca, NY,
     October  1972.

Likens, G. E.   Acid precipitation.   Chem.  Eng.  News 54:29-44, 1976.

Likens, G.  E.  ,  and  F.  H.  Bormann.   Acid  rain:   a serious regional  environmental problem.
     Science  (Washington, D.C.) 184:1176-1179, 1974.

Likens, G. E. , F.  H.  Bormann,  and N. M.  Johnson.   Acid  rain.   Environment 14:33-40, 1972.

                                          11-114

-------
Likens, G.  E. ,  J.  S.  Eaton, and  J.  N.  Galloway.  Precipitation  as  a source of  nutrients  for
     terrestrial and aquatic ecosystems.  Jji:  Precipitation Scavenging  (1974), Proceedings of
     a  Symposium,  Illinois  State Water Survey and Others, Champaign,  Illinois, October 14-18,
     1974.   ERDA  Symposium  Series  41,  Energy  Research and  Development  Administration,  Oak
     Ridge, TN, June 1977.  pp. 552-570.

Likens,  G.  E. ,  R.  F.   Wright,  J.  N.  Galloway,  and  T.  J.  Butler.   Acid rain.   Sci.   Am.
     241:43-51, 1979.

Likens, G.  E. ,  F.  H.  Bormann,  J.  S.  Eaton,  R.  S.  Pierce, and  N.  M.  Johnson.   Hydrogen  ion
     input  to  the Hubbard  Brook Experimental  Forest, New Hampshire,  during the  last decade.
     In:   First  International  Symposium on Acid  Precipitation  and the Forest Ecosystem, U.S.
     Department  of Agriculture  and  Others,  Columbus, Ohio, May  12-15,  1975.   Water Air Soil
     Pollut. 6:435-445, 1976.

Likens, G.  E. ,  F.  H.  Bormann, N. M. Johnson, D.  W. Fisher, and R. S.  Pierce.  Effects of cut-
     ting  and  herbicide treatment   on  nutrient  budgets  in  the Hubbard  Brook  Watershed -
     ecosystem.  Ecol.  Monogr.  40:23-47, 1970.

Liljestrand, H. M., and J. J. Morgan.  Chemical composition of acid precipitation  in Pasadena,
     Calif.  Environ.  Sci. Technol. 12:1271-1273, 1978.

Lindberg,   S. E. ,  R.  C.  Harriss, R.  R.  Turner,  D. S.   Shriner, and D. D. Huff.  Mechanisms  and
     Rates  of  Atmospheric Deposition  of  Selected Trace Elements and  Sulfate  to a Deciduous
     Forest  Watershed.   ORNL/TM  6674,  Environmental  Sciences Division Pub. No.  1299,  U.S.
     Department of Energy, Oak Ridge National Laboratory, Oak Ridge, TN, June 1979.

Linzon, S.  N.    Statement  made to  workshop  reviewers,  Research  Triangle  Park,  NC, November
     1980.

Livingstone,  D.  A.  Chemical  composition of  rivers   and  lakes.   In:   Data of Geochemistry.
     Sixth  Edition.   G.  M.   Fleischer,  ed. ,  Geological  Survey  Professional  Paper 440-G,  U.S.
     Government Printing Office, Washington,  DC,  1963.

Lockhart,   W.  L. ,  and A.  Lutz.   Preliminary  biochemical observations  of fishes  inhabiting an
     acidified lake in Ontario, Canada.   I_n:   First International  Symposium  on Acid  Precipita-
     tion and the Forest Ecosystem, U.S. Department of Agriculture and Others, Columbus, Ohio,
  •   May 12-15, 1975.   Water Air Soil Pollut. 7:317-332, 1977.

Lynch,   H.    Predation,  competition  and zooplankton community structure: an experimental study.
     Limnol. Oceanogr.  24:253-272, 1979.

Malmer, N.  Acid precipitation:  chemical  changes in the soil.  Ambio 5:231-234, 1976.

Marenco, A., and J.  Fontan.   Influence of dry deposition on the  residence time of particulate
     pollutants  in the   troposphere.   lr\:   Atmosphere-Surface  Exchange  of  Particulate  and
     Gaseous Pollutants (1974), Proceedings of a Symposium, Battelle Pacific Northwest Labora-
     tories and  Others,  Richland,  Washington,  September 4-6, 1974.  ERDA Symposium  Series  38,
     Energy Reasearch and Development Administration,   Oak Ridge,  TN, January 1976.   pp. 54-61.

Mayer,   R.  ,  and  B.  Ulrich.   Acidity of  precipitation  as  influenced by the filtering of atmos-
     pheric  sulphur  and  nitrogen  compounds—its role in  the  element balance and  effect on
     soil.  In:  First International Symposium on Acid Precipitation and the Forest  Ecosystem,
     U.S.   Department  of  Agriculture  and  Others,  Columbus, Ohio,  May  12-15, 1975.   Water Air
     Soil  Pollut. 7:409-416, 1977.
                                          11-115

-------
McColl, J. G. ,  and D.  S. Bush.   Precipitation  and throughfall chemistry  in the San Francisco
     Bay Area.  J. Environ.  Qua! 7:352-357, 1978.

McFee, W. W.   Sensitivity of Soil Regions To Long Term Acid Precipitation.  EPA-600/3-80-013,
     U.S. Environmental Protection Agency, Corvallis, OR, January 1980.

McFee, W.  W. , J.  M.  Kelly,  and R. H.  Beck.   Acid precipitation effects  on  soil  pH and base
     saturation of  exchange  sites.   In:  First  International  Symposium on Acid Precipitation
     and the  Forest  Ecosystem,  U.S.  "Department  of Agriculture and Others, Columbus, Ohio, May
     12-15, 1975.   Water Air Soil Pollut. 7:401-408, 1977.

Miller, J. M.,  J.  N.  Galloway, G. E.  Likens.   Origin of air masses producing acid precipita-
     tion at  Ithaca,  New York,  a preliminary  report.    Geophys.  Res.  Lett.  5:757-760, 1978.

Moran, J. M. ,  M.  D.  Morgan, and J. H. Wiersma.   Introduction to Environmental Science.  W. H.
     Freeman and Co., San Francisco,  CA, 1980.    pp. 7-75.

Miiller,  P.   Effects of artificial acidification on the  growth of  periphyton.   Can.  J. Fish.
     Aquat.  Sci. 37:355-363, 1980.

Muniz, I. P., and H. Leivestad.  Toxic effects of aluminum on the brown trout, Salmo trutta L.
     In:   Ecological Impact of Acid Precipitation, Proceedings of an International Conference,
     SNSF Project, iandefjord, Norway, March 11-14, 1980.  D. Drablrfs and  A. Tollan, eds., SNS.F
     Project, Oslo-As, Norway, October 1980.  pp. 320-321.

National   Research  Council.    Nitrates:   An  Environmental  Assessment.   National  Academy  of
     Sciences, Washington, DC, 1978.   pp. 275-317, 370-434.

Nieboer,   E. ,  D.  H.  S.  Richardson, K.  J.  Puckett and F. D.  Tomassini.   The phytotoxicity of
     sulfur  dioxide in  relation  to  measureable responses in  lichens.    lr\:   Effects  of  Air
     Pollutants on  Plants,  Society  for Experimental Biology,  Liverpool,  England,  April  10,
     1975.   T.  A.  Mansfield, ed. ,  Cambridge  University  Press,  London,  England,  1976.   pp.
     61-85.
     o
Nihlgard, B.   Precipitation,  its chemical composition and effect on soil  water in a beech and
     a spruce forest in south Sweden.  Oikos 21:208-217,  1970.

Nisbet,  I.    Sulfates  and  acidity  in  precipitation:   their relationship  to  emissions  and
     regional  transport  of  sulfur oxides.   In:   Air Quality and  Stationary Source Emission
     Control.  A  report  by  the Commission on^Jatural Resources, National  Academy of Sciences,
     National Academy of Engineering, National Research Council.   Serial No. 94-4, U.S. Senate
     Committee on Public Works, Washington, DC,  March 1975.  pp.  276-312.

Norton,  S.  A.   Changes  in  chemical processes  in soils  caused  by acid  precipitation.   In:
     First  International Symposium   on Acid  .Precipitation  and the  Forest  Ecosystem,  UTS".
     Department of  Agriculture and  Others,  Columbus, Ohio, May 12-15,  1975.   Water Air Soil
     Pollut.   7:389-400, 1977.

Nriagu,  J.  0.  Deteriorative  effects of  sulfur pollution on materials.   In:   Sulfur in the
     Environment.   Part  II:   Ecological Impacts.  J. 0.  Nriagu, ed. , John WTley & Sons, Inc.,
     New York, NY, 1978.  pp. 1-59.

Oden,  S.   The  Acidification  of  Air and  Precipitation  and  Its  Consequences on  the  Natural
     Environment.    Ecology   Committee   Bulletin  No.  1,  State  National  Science  Research
     Committee, Stockholm, Sweden, May 1968.
                                          11-116

-------
Oden,  S.   Acid  precipitation:   A world concern.  In:  Proceedings of the Conference on Emerg-
     ing Environmental Problems, Acid Precipitation, May 19-20, 1975, The Institute on Man and
     Science, Rensselaerville,  N.Y.   U.S. Environmental Protection  Agency,  Region II.   Water
     Resources  and  Marine Sciences  Center,  Cornell  Univeristy  and Center  for Environmental
     Quality  Management,  Cornell  University,  EPA-902/9-75-001,  November  1975.    pp.  5-44.

Oden,  S. ,  R.  Anderson,  and  M.  Barting.   The  long-term changes in  the  chemistry  of soils in
     Scandanavia due  to  acid precipitation.   Iji:    Supporting  Studies  to Air Pollution Across
     National Boundaries,  Sweden's  Case Study for the United Nations, Conference on the Human
     Environment.   B.  Bolin,   ed.,  Royal  Ministries  of  Foreign  Affairs  and  Agriculture,
     Stockholm,  Sweden, 1972.  p.  20.

Odum,  E.  P.   Summary.   I_n:   Ecological  Effects  of Nuclear War,  Proceedings  of a Symposium,
     Ecological  Society of America, Amherst, Massachusetts, August 1963.  G.  M. Woodwell, ed. ,
     BNL 917(C-43), Brookhaven National Laboratory, Upton, NY, August 1965.   pp. 69-72.

Odum,  E. P.   Fundamentals of Ecology.   Third Edition.   W.  B.  Saunders Co.,  Philadelphia, PA,
     1971.   p. 5, 8-139.

Office of  Air Quality Planning  and Standards.   National Air Quality, Monitoring and Emissions
     Trends Report,  1977.   EPA-450/2-78-052, U.S.  Environmental  Protection  Agency, Research
     Triangle Park, NC, December 1978.

0kland,  J.   Distribution and  ecology  of  the  freshwater  snails  (Gastropoda)  of  Norway.
     Malacologia 9:143-151, 1969.

0kland, J.  , and  K.  A. 0kland.   pH level  and  food organisms for fish:   studies of 1,000 lakes
     in Norway.   In:  Ecological Impact of Acid Precipitation, Proceedings of an International
     Conference, SNSF Project,  Sandefjord,  Norway,  March  11-14,   1980.   D.   Drableis  and  A.
     Tollan,  eds.,  SNSF Project, Oslo-As, Norway,  October 1980.  pp.  326-327.

0kland, K. A.  On  the distribution and  ecology  of Gammarus lacustris G. 0.  Sars  in Norway,
     with notes  on  its morphology and biology.   Nytt Mag. Zool. 17:111-152,  1969.

0kland, K. A.  Mussels and  crustaceans:   studies of 1,000  lakes  in Norway.   In:   Ecological
     Impact of Acid  Precipitation,  Proceedings  of an International  Conference, SNSF Project,
     Sandefjord, Norway,  March  11-14,  1980.   D.  Drablrfs  and A.  Tollan, eds., SNSF Project,
     Oslo-As,  Norway, October 1980.   pp. 324-325.

Overrein,   L.  N.   Sulphur pollution  patterns  observed;  leaching of  calcium   in  forest  soil
     determined.   Ambio 1:145-147,  1972.

Pack, D. H. ,  G.  J.  Ferber, J.   L. Heffter,  K.  Telegadas, J. K.  Angell,  W.  H.  Hoecker,  and L.
     Machta.   Meterology  of  long-range  transport.  In:   Sulfur in the Atmosphere,  Proceedings
     of  the   International  Symposium,  United   Nations  Environmental  Program  and  Others,
     Dubrovnik,  Yugoslavia, September 7-14, 1977.   Atmos. Environ.  12:425-444,  1978.

Pack, D. W.   Sulfate  behavior  in eastern  U.S.  precipitation.   Geophys.  Res.  Lett.  5:673-674,
     1978.

Peterson,  R.   C.   Dynamics of coarse particulate organic material processing in diversified pH
     regimes.   Presented  at  the Internat.  Conf.  The Ecological  Impact of Acid Precipitation,
     March  11-14, 1980,

Pfeiffer,  M. , and  P.  Festa.   Acidity status of lakes in the Adirondack region of New York in
     relation to fish resources.   Publication  FW-P168,  New York State, Department of Environ-
     mental Conservation, Albany,  NY, August 1980.
                                          11-117

-------
Potts, D. T. W. ,  and C.  Frye.   The effect of pH and salt content on sodium balance in Daphnia
     magna and Acantholeberis curvirostris (Crustacea; Cladocera).  J. Comp. Physitil.  Series B
     129:289-294,  1979.

Rough, F.  H.   Acid  precipitation  and embryonic  mortality of  spotted salamanders, Ambystoma
     maculatum.   Science (Washington, D.C.) 192:68-70, 1976.

Rough, F.  H. ,  and  R.  E.  Wilson.   Acid  precipitation  and reproductive  success  of Ambystoma
     salamanders.    Iji:   First  International  Symposium on  Acid  Precipitation  and  the Forest
     Ecosystem,  U.S.  Department  of  Agriculture and Others, Columbus,  Ohio,  May  12-15, 1975.
     Water Air Soil Pollut.  7:307-316, 1977.

Prahm, L. P.,  U.  Torp, and R. M.  Stern.  Deposition and transformation rates of sulphur oxides
     during atmospheric transport over the Atlantic.  Tell us 28:355-372, 1976.

Raddum, G.  Invertebrates:   quality  and  quantity as  fish  food.   In:   Limnological Aspects of
     Acid Precipitation,  Proceedings of the International Workshop, U.S. Environmental Protec-
     tion Agency and  Others,  Sagamore, New York, September 25-28,  1978.   G. R. Hendrey, ed.,
     BNL51074,  U.S.  Department of  Energy,  Brookhaven  National  Laboratory, Upton,  NY,  1978.
     pp.  17-24.

Rheinheimer, G.   Aquatic Microbiology.  John Wiley & Sons, New York, 1971.

Robinson, E. ,  R.  B.  Husar,  and J.  N. Galloway.  Sulfur oxides in the atmosphere.   In:  Sulfur
     Oxides.  National Academy of Sciences, Washington, DC, 1978.  pp. 18-62.

Roff,  J.  R. ,   and  R.  E.  Kwiatkowski.   Zooplankton  and  zoobenthos  communities  of  selected
     northern  Ontario lakes  of different acidities.   Can. J. Zool. 55:899-911, 1977.

Rosenqvist, I.  T.   A contributor towards analysis of buffer properties of geological materials
     against strong  acids in precipitation water, report written for the Council  for Research
     in Natural  Sciences,  Norwegian General Research Council, 1976.

Rosseland,  B.   0.,   I.  Sevaldrud,  D.   Svalastog,  and I.  P.  Muniz.   Studies  on freshwater fish
     populations -  effects  of  acidification on reproduction, population structure, growth and
     food selection.  Jji:   Ecological  Impact of Acid  Precipitation,  Proceedings  of an Inter-
     national  Conference,  SNSF Project, S§ndefjord,  Norway, March 11-14, 1980.  D. Drabltfs and
     A. Tollan,  eds., SNSF Project, Oslo-As, Norway, October 1980.  pp. 336-337.

Schaffer, R. J.   The Weathering  of Natural Building Stones.  Spec. Ref. No. 18, London, HMSO,
     1932.  Cited jn:  Sereda,  1977.

Scheider,  W. ,  J.   Adamski,  and  M.   Paylor.   Reclamation  of  Acidified  Lakes Near  Sudbury,
     Ontario.   Ontario  Ministry  of  the  Environment,  Rexdale,   Ontario,  Canada,  June  1975.
                                                                                    c
Schindler, D.  W.   Whole  lake eutrophication experiments with phosphorus, nitrogen and carbon.
     Verh. Internat. Verein. Limnol.  19:577-582, 1975.

Schindler, D.  W. ,  R.  Wagemann, R.  B.  Cook,  T.  Ruszczynski, and J. Prokopowich.  Experimental
     acidification  of  Lake  223,  experimental  lakes area:  background data and the first three
     years of  acidification.  Can.  J. Fish. Aquat. Sci. 37:342-354, 1980.

Schlesinger, W.  H. ,  and  M.  M.  Hasey.  The nutrient content of precipitation, dry fallout, and
     intercepted  aerosols   in  the   chaparral  of   southern  California.    Am.   Midi.   Nat.
     103:114-122,  1980.
                                          11-118

-------
Schofield, C. L.  Acid precipitation:  effects on fish.  Ambio. 5:228-230, 1976a.

Schofield, C.  L.   Dynamics and Management of Adirondack Fish Populations.   I.  Natural Waters
     with Lethal  Conditions  for Fish.   I-a.  Acidification of Adirondack Lakes by Atmospheric
     Precipitation:  Extent  and Magnitude of the Problem.  Final Report.  Project No. F-28-R,
     State of New York, Department of Environmental Conservation, Albany, NY, 1976b.

Schofield, C.  L.   Dynamics and Management of Adirondack Fish Populations.   I.  Natural Waters
     with Lethal  conditions  for Fish.   I-b.  Acidification of Adirondack Lakes by Atmospheric
     Precipitation:  Long  Term  and Seasonal Trends.  Project No. F-28-R-4,  State of New York,
     Department of Environmental Conservation, Albany, NY, 1976c.

Schofield, C. L.  Lake acidification in the Adirondack Mountains of New York:  causes and con-
     sequences.   I_n:   Proceedings  of the First  International  Symposium  on Acid Precipitation
     and the  Forest  Ecosystem,  U.S.  Department of Agriculture and Others, Columbus, Ohio, May
     12-15,   1975.   L.  S.  Dochinger  and  T.  A.   Seliga,  eds.,  NEFES/77-1,  U.S.  Department of
     Agriculture Forest Service, Upper Darby, PA, August 1976d.  p. 477.

Schofield, C. L.  The acid precipitation phenomenon and its impact in the Adirondack Mountains
     of New York State.  _In:   Scientific Papers from the Public Meeting on Acid Precipitation,
     New York  State  Assembly Committee on Environmental Conservation and Others, Lake Placid,
     New York,  May  4-5,  1978.   H.  H. Izard and J. S.  Jacobson, eds., New York State Assembly,
     Science and Technology Staff,  Albany, NY, March 1979a.  p. 86-91.

Schofield, C.  L.   Effects of  acid  rain  on lakes.   Presented at the  Session on  Acid  Rain,
     National  Convention of the  American Society  of Civil Engineers,  Boston, MA,  April  2,
     1979b.

Schofield, C. L., and J.  R. Trojnar.   Aluminum toxicity to brook trout (Salvelinus fontinalis)
     in acidified waters.  In:   Polluted Rain, Twelfth  International  Rochester Conference on
     Environmental Toxicity,  University of  Rochester,  Rochester, New York, May 21-23,  1979.
     T. Y.  Toribara, M.   W.  Miller,  and  P.  E.  Morrow,  eds.,  Environmental Science Research
     Volume  17, Plenum Press, New York, NY, 1980.  pp. 341-366.

Sehmel, G.  A.  Particle  and gas  dry  deposition:  a  review.   Atmos. Environ.   14:983-1011,
     1980.

Seip,  H.  M.   Acidification  of  freshwater-sources and mechanisms.   In:   Ecological  Impact of
     Acid Precipitation,  Proceedings  of an International Conference,"3NSF Project, Sandefjogd,
     Norway,   March  11-14, 1980.   D.  Drablds  and  A.  Tollan, eds.,  SNSF  Project,  Oslo-As,
     Norway,  October 1980.  pp.  358-366.

Sereda, P.  J.  Effects of sulphur on  building materials.   In:   Sulphur and its Organic Deriva-
     tives in the  Canadian Environment.   NRC No. 15015,  National  Research  Council of Canada,
     NRC Associate Committee  on Scientific Criteria For Environmental Quality, Ottawa, Canada,
     1977.   pp.  359-426.

Sheridan,  R.   P.,  and R.  Rosenstreter.   The effect  of hydrogen ion concentration in simulated
     rain on the moss Tortula rural is (Hedw) Sm.   Bryologist 76:168-173,  1973.

Shinn,   J.  H. ,  and  S.  Lynn.   Do  man-made  sources  affect the  sulfur cycle  of northeastern
     states?   Environ.  Sci. Technol.  13:1062-1067, 1979.

Shriner, D.  S.  Effects of simulated  rain acidified with sulfuric acid on host-parasite inter-
     actions.   In:   First International  Symposium  on Acid Precipitation and the  Forest Eco-
     system,   U.S.  Department  of  Agriculture  and  Others,  Columbus,  Ohio,   May  12-15,  1975.
     Water Air Soil  Pollut. 8:9-14, 1977.
                                          11-119

-------
Shriner,  D.  S.   Effects  of  simulated  acidic  rain  on  host-parasite  interactions  in plant
     diseases.   Phytopathology 68:213-218, 1978a.

Shriner,  D.  S.   Interactions  between acidic  precipitation and SO,  or  0,:   Effects on plant
     response.   Phytopathol.  News, 12:153, 1978b.

Shriner,  D.  S.   Terrestrial  vegetation -  air  pollutant interactions:  nongaseous pollutants,
     wet  deposition.   Presented  at  the International Conference  on  Air Pollutants and Their
     Effects on Terrestrial Ecosystems, Banff, Alberta, Canada, May 10-17, 1980.

Shriner,  D.  S. ,  and G.  S. Henderson.   Sulfur distribution and cycling  in a deciduous forest
     watershed.   J. Environ.  Qual. 7:392-397, 1978.

Shriner, D. S., M.  DeCot, and E.  B. Cowling.  Simulated acid rain  caused direct  injury to vege-
     tation.  Proc. Am.  Phytopath. Soc. 1:112, 1974.

Smith,  F.  B. ,  and  G.  H. Jeffrey.  Airborne  transport of sulfur dioxide  from the UK.   Atmos.
     Environ. 9:643-659, 1975.

Smith, R. A.  Air and Rain:  The  Beginnings of Chemical Climatology.   Longmans,  Green, London,
     1872.  600 pp.

Smith,  R.  L.   Ecology and Field  Biology.   3rd Edition.   Harper and  Row,  New York, NY, 1980.
     pp. 11-199.

SNSF Project.  Acid  precipitation and some alternative sources as the cause  of  the acidifying
     water  courses.    Norway's   Agrarian   Science  Research Board,  Norway's  Technical  Nature
     Science Research Board,  Dept. of Environmental Protection, ed. ,  A. Tollan,  1977.

Sprules, G. W.   Midsummer crustacean zooplankton communities in acid-stressed lakes.  J. Fish.
     Res. Board Can.  32:389-395,  1975.

Stensland, G. J.   A  comparison of precipitation  chemistry  data at a central Illinois site  in
     1954  and  in 1977.   Presented at 71st Annual  Meeting,  Air Pollution  Control Association,
     Houston, TX, June 25-26, 1978.  Paper No. 78-48.7.

Stensland,  G.  J.   Precipitation  chemistry  trends  in the northeastern  United States.   lr\:
     Polluted  Rain,   Twelfth  International  Rochester Conference  on  Environmental  Toxicity,
     University of  Rochester, Rochester,  New York,  May  21-23, 1979.   T.  Y.  Toribara,  M.   W.
     Miller, and P.  E.  Morrow,  eds. , Environmental  Science Research Volume  17,  Plenum Press,
     New York,  NY,  1980.  pp.  87-108.

Stokes,  P.   Phytoplankton  of  acidic  lakes  in  Killarney  Ontario:   community  structure related
     to  water  chemistry  abstracts  of  voluntary  contributions.    In:    Proc.   International
     Conference  OQ, the  Ecological  Impact of  Acid  Precipitation,  "March  1980, SNSF-project
     report, Oslo-As, Norway, 1980.

Stumm,  W. , and  J.  J.  Morgan.    Aquatic   Chemistry,  Wiley-Interscience,  New York,  NY,  1970.

Sutcliffe, D. W., and T. R. Carrick.   Studies on mountain streams  in  the English lake district
     I.  pH,  calcium,  and  the  distribution of invertebrates in the River Duddon.  Freshwater
     Biol. 3:437-462, 1973.

Tabatabai, M. A.,  and J. M.  Laflen.   Nitrogen and sulfur  content  and pH  of precipitation  in
     Iowa.  J.  Environ. Qual.  5:108-112, 1976.
                                          11-120

-------
Tamm, C.  0.,  G.  Wiklander, and B. Popovic.  Effects of applications of  sulphuric  acid to  poor
     pine  forests.   In:    First  International  Symposium on  Acid  Precipitation and the  Forest
     Ecosystem,  U.S.  Department  of  Agriculture and Others,  Columbus,  Ohio,  May  12-15, 1975.
     Water Air Soil Pollut. 8:75-87, 1977.

Tiano,  P.,  R.  Bianchi,  G.  Gargani, and S. Vannuci.  Research on the presence  of sulphur-cycle
     bacteria  in  the  stone of some historical  buildings  in Florence.    Plant  Soil 43:211-217,
     1975.

Tomlinson,  G.  H.   Acidic  precipitation  and  mercury in Canadian  lakes  and fish.   |n:   Scien-
     tific  Papers from  the  Public  Meeting  on Acid  Precipitation,  New  York State Assembly
     Committee on Environmental Conservation and Others, Lake Placid, New  York, May 4-5, 1978.
     H.   H.  Izard and  J.   S.  Jacobson,  eds. ,  New York  State Assembly,  Science and Technology
     Staff, Albany, NY, March 1979.  pp. 104-118.

Traaen,  T.  S.   Effects  of acidity on decomposition of organic matter in aquatic environments.
     I_n:  Ecological  Impact of Acid Precipitation, Proceedings of an International Conference,
     SNSF  Project,  Sandfcfjord, Norway,  March  11-14,  1980.   D.  Drablds  and  A.  Tollan, eds.,
     SNSF Project, Oslo-As, Norway, October 1980.  pp.  340-341.

Trojnar,  J.  R.   Egg  and larval survival  of  white suckers (Catostomus  commersoni) at low pH.
     J.  Fish. Res. Board Can.  34:262-266, 1977.

Tukey,  H.  B. ,  Jr.   The leaching of substances from plants.  Annu. Rev.  Plant  Physiol. 21:305-
     324, 1970.

Turk, J. T., and N.  E.  Peters.  Acid-Rain Weathering of a Metasedimentary  Rock Basin, Herkimer
     County, New  York.   Open  File Report 77-538,  U.S.  Department of the  Interior, Geological
     Survey, Washington, DC, July 1977.

Turk, J. T. , and N.  E.  Peters.  Acid-rain Weathering of a metasedimentary  rock basin, Herkimer
     County, New  York.   J_n:   Scientific Papers from the Public Meeting on Acid Precipitation,
     New York  State Assembly  Committee  on Environmental Conservation and Others,  Lake Placid,
     New York, May 4-5,  1978.   H. H.  Izard and J. S. Oacobson, eds., New York State Assembly,
     Science and Technology Staff, Albany, NY,  March 1979.   pp. 136-145.

Turner,  J.,  and  M. J.  Lambert.  Sulfur nutrition of forests.  I_n:  Atmospheric Sulfur Deposi-
     tion:  Environmental  Impact  and  Health  Effects, Proceedings of  the Second Life Sciences
     Symposium, Oak Ridge  National  Laboratory  and Others, Gatlinburg,  Tennessee,  October 14-
     18,  1979.   D.  S.   Shriner,  C. R.  Richmond,  and S.  E.  Lindberg, eds. ,  Ann Arbor Science
  .   Publishers,  Inc.,  Ann Arbor,  MI,  1980.   pp. 321-333.

Tyler, G.   Heavy metals pollute nature,  may reduce productivity, Ambio 1:52-59, 1972.

Tyler, G.   Leaching rates  of  heavy metal ions  in forest  soil.  Water Air Soil Pollut.   9:137-
     148, 1977.

U.S.  Bureau  of Mines.    Minerals  Yearbook 1952.   Volume   II.  Area  Reports:   Domestic.   U.S.
     Department of the Interior,  Washington,  DC, 1954.   p. 117.

U.S.  Bureau  of Mines.    Minerals  Yearbook 1974.   Volume   II.  Area  Reports:   Domestic.   U.S.
     Department of the Interior,  Washington,  DC, 1976.   p. 392.

U.S.  Department of Commerce.   Climatic  Atlas of the United  States.   National Climatic Center,
     Asheville, NC,  June 1968.
                                          11-121

-------
U.S.  Department of  Energy.   Acid  Rain Information  Book.   Final  Report.   DOE/EP-0018,  U.S.
     Department of Energy, Washington, DC, May 1981.  pp. 2-12--2-13.

U.S.  Environmental  Protection  Agency.   The Acid  Precipitation  Problem.   [Pamphlet].   U.S.
     Environmental  Protection  Agency,  Environmental   Research   Laboratory,  Corvallis,  OR,
     October 1979.

U.S. Environmental  Protection  Agency.   Air  Quality Criteria for  Participate Matter  and Sulfur
     Oxides.  Draft Final.   U.S.  Environmental  Protection Agency,  Research Triangle Park, NC,
     1981.

Ulrich,  B.   Environmental influences  on the nutrient  cycle of  a  beech  forest on  acid soil.
     Forstwiss.  Centralbl. 94:280-287, 1975.

Walters,  C. J. ,  and R.  E. Vincent.   Potential  productivity of an  alpine  lake as  indicated by
     removal and reintroduction of fish.  Trans. Amer. Fish Soc.  102:675-697, 1973.

Wetzel,  R.  G.    Limnology,  p.  287-621,  W.  B.  Saunders  Co., Philadelphia,  PA,  1975.   743 pp.

Whelpdale, 0.  M.  Acidic deposition,   hi:  Ecological Effects of  Acid Precipitation,  Report of
     a  Workshop,  Electric Power  Research Institute, Gatehouse-of-Fleet,  Galloway,  Scotland,
     September 4-7, 1978.   M. J. Wood, ed.,  EPRI SOA77-403, Electric Power Research  Institute,
     Palo Alto, CA, July 1979.   Section 4.1.  22 pp.

Wiklander,  L.   Leaching  and  acidification of soils.  I_n:  Ecological Effects of Acid Precipi-
     tation,  Report of  a Workshop,   Electric  Power Research  Institute,  Gatehouse-of-Fleet,
     Galloway, Scotland, September 4-7, 1978.  M. J. Wood, ed., EPRI SOA77-403, Electric Power
     Research Institute, Palo Alto, CA, July 1979.  Section 4.3.   24 pp.

Wiklander,  L.   Interaction  between  cations and  anions  influencing adsorption  and  leaching.
     J_n:   Effects  of  Acid  Precipitation  on Terrestrial  Ecosystems,  North  Atlantic  Treaty
     Organization, Toronto,  Ontario,  Canada, May 21-27, 1978.   T.  C. Hutchinson and M.  Havas,
     eds., Plenum Press, New York, NY, 1980.  pp.•239-254.

Williams, W. T.   Acid  rain:   the California context.  Citizens Better  Environ.:   6-8,  10, May
     1978.

Winkler,  E. M.   Important agents of weathering for building and  monumental stone.   Eng. Geol.
     (Amsterdam) 1:381-400, 1966.

Wisniewski, J. ,  and E.  L.  Keitz.   Acid  rain deposition  patterns in  the continental  United
     States.  Submitted to Bull. Am. Meteorol. Soc., 1981.

Wodzinski,  R.  S. ,  D.   P.  Labeda,  and M.  Alexander.    Toxicity   of  SO,,  and  NO  :   selective
     inhibition  of  blue-green  algae by bisulfite and nitrite.   J.  Air  Pollut. Control.  Assoc.
     27:891-893, 1977.

Wolff,  G.  T. ,  P. J.  Lioy,  H.  Golub,  and J.  S.  Hawkins.  Acid precipitation  in   the New  York
     Metropolitan  Area:    its   relationship  to  meteorological  factors.   Env.  Sci.  Technol.
     13:209-212, 1979.
                                                                                v

Wood,  T.   Acid  Precipitation.   In:    Sulfur  in  the Environment.   Revised Edition.   Missouri
     Botanical Garden,  St. Louis,~~MO,  July 1975.  pp. 39-50.

Wood, T., and F. H.  Bormann.   The effects of an artificial acid mist upon  the growth of Betula
     alleghaniensis  Britt. Environ. Pollut. 7:259-267,  1974.
                                          11-122

-------
Wright,  R.  F. ,  N.  Conroy,  W.  T.  Dickson,  R.  Harriman, A.  Henriksen,  and  C.  L.  Schofield.
     Acidified  lake districts  of  the world:   a  comparison of  water chemistry  of lakes  in
     southern Norway,  southern  Sweden, southwestern Scotland, the Adirondack Mountains  of  New
     York, and  southeastern  Ontario.   I_n:    Ecological  Impact  of  Acid Precipitation, Proceed-
     ings of an International Conference, SNSF Project,  Sajidefjord, Norway, March  11-14,  1980.
     D.  Drableis and A.  Tollan,  eds. ,  SNSF  Project,  Oslo-As, Norway,  October 1980b.  pp. 377-
     379.

Wright,  R. F., T.  Dale, E. T. Gjessing, G.  R. Hendrey, A. Henriksen, M. Johannessen, and  I.  P.
     Muniz.    Impact of  acid precipitation  on  freshwater  ecosystems  in  Norway.   _£n:    First
     International  Symposium  on Acid  Precipitation and  the  Forest  Ecosystem, U.S.  Department
     of  Agriculture and  Others,  Columbus,  Ohio,  May  12-15,  1975.   Water  Air  Soil  Pollut.
     6:483-499,  1976.

Van, N.  D.,  and P.  Stokes.  Phytoplankton of an  acidic lake, and  its responses to  experimental
     alterations of pH.  Environ. Conserv.  5:93-100, 1978.
                                          11-123

-------

-------
     12.   EFFECTS OF  NITROGEN  OXIDES  ON  NATURAL  ECOSYSTEMS,  VEGETATION  AND MICROORGANISMS

12.1  INTRODUCTION
     Ecosystems are  complex  self-sustaining natural  systems and are composed of living organ-
isms and the several nonliving components of the environment within which the organisms exist.
Within  an  ecosystem are included all of  the interactions that bind the  living and nonliving
components together  into a stable system, i.e., the interactions between organisms or communi-
ties of organisms,  the  relationships between  organisms and the physical  environment  and the
interactions of the  various  aspects of the  nonliving  environment  (Boughey, 1971; Odum, 1971;
Smith,  1974; Whittaker,  1975).   After centuries of relatively stable annual climatic and geo-
chemical conditions, they may become self-perpetuating (Boughey, 1971,  Odum, 1971; Smith, 1974;
Whittaker, 1975).
     Evaluating the  contribution of functioning natural ecosystems to  human welfare is a very
complex task and involves weighing both economic and human social  values;  however, it is clear
that this  natural  order by which living organisms are bound to each other and to their envir-
onment  is  essential  to the existence of  any species  on earth, including  man  (Boughey,  1971;
Odum, 1971; Smith,  1974;  Whittaker, 1975).   As life  support  systems,  the value of ecosystems
cannot be quantified in economic terms.
     This  chapter  discusses  the  effects  in general  of nitrogen oxides on  natural  ecosystems
and, more specifically, their effects on certain species of plants  and  microorganisms.
12.2  EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS
     Climatic,  physiochemical,  or biological  changes,  regardless  of their  source  of  nature,
will  affect  the  functioning of an  ecosystem.   Some ecosystems  are  durable  and  relatively
stable when subjected  to  a given environmental change; others  become  unstable given the same
change.
     It  is  difficult to assess  the  complex cause and effect relationships  of any  pollutant,
even when it is studied using only a single organism.   When attempting  to  assess such relation-
ships within populations, communities and ecosystems,  the problems  become  even greater.   Addi-
tional  complications in  determining the effects of a  single  pollutant  on natural  communities
are created by the presence  of multiple contaminants  that  may  promote  synergistic  or  antago-
nistic effects.
     The response  of ecosystems to environmental changes or perturbations  is determined by the
response of their  constituent  organisms.   The factors which determine  the  response of organ-
isms and changes which  may occur within ecosystems  are discussed  in Section 11.1.2   Ecosystem
Dynamics in Chapter 11.
     Terrestrial,   marine,  and freshwater ecosystems  are functionally important  to  the  inte-
grity of the biosphere.   They are important:   (1) in  the  production of food;  (2) the  mainte-
nance of  forests;  (3)  as global  support  systems  for  the regeneration of  essential  nutrients
and atomspheric components;  (4)  for their  aesthetic  value in  maintaining  natural  vegetative
communties; and (5) in  the assimilation  or destruction of many pollutants  from the air,  water,
and soil.
                                           12-1

-------
     Of the many  functions  occurring within ecosystems, the  flow  of energy and nutrients are
among the most important.   Energy flows through an ecosystem in only one direction while nutri-
ents are recirculated (Boughey, 1971; Odum, 1971; Smith, 1974; Whittaker, 1975).
     Nitrogen, one of the nutrients recirculated by ecosystems, is  an element essential to all
life.   It  is  necessary  in the formation of  the  cells of which all living matter is composed.
The  production of  virtually  all  food depends directly or indirectly on biologically available
nitrogen.   The most  abundant source of nitrogen is the atmosphere  of which molecular nitrogen
composes 78 percent (Smith,  1974, Whittaker, 1975).  However,  most  organisms are unable to use
molecular nitrogen,  therefore,  it  must be converted  into  another  chemical  form.  Nitrogen is
made available to organisms  through the conversion or fixation of molecular nitrogen into bio-
logically available compounds.  These transformations of nitrogen are regulated almost entire-
ly  by  terrestrial  and aquatic microorganisms  through a complicated series  of  reactions that
are  collectively  termed  the  "nitrogen  cycle."   These transformations  are more  accurately
described as  a "nitrogen  web" because the  image  of  a simple   loop of  compounds through which
nitrogen successively passes bears little resemblance to reality.
     The nitrogen cycle or  web has been greatly modified by man,  both locally and on a global
scale,   through agricultural  activity,  industrial  production,  fuel  burning and waste disposal.
     The nitrogen cycle  in  the biosphere and the modifications caused by man's activities are
discussed in Chapter 4.
     In terrestrial  and  aquatic  systems,  the major  nonbiological  processes  of the nitrogen
cycle involve phase transformations rather than chemical reactions.   These transport processes
include volatilization of ammonia  and other gaseous  forms  of  nitrogen;  sedimentation of par-
ticulate forms of organic nitrogen;  and  sorption  (e.g.,  of ammonium  ions  by  clays).   Under-
standing of the  biospheric  nitrogen cycle and  of  the factors that control  the cycle depends
primarily on an understanding of biological principles, especially  those of microbial ecology.
     The biological  transformations shown  in  Figure  4-1  (Chapter 4) involve  only  six major
processes (Figure 12-1).   These processes are discussed here in outline only.  For details see
Chapter 4.
     These  processes are:
1.    Assimilation of  inorganic forms of nitrogen (primarily ammonia or nitrates) by plants and
microorganisms to  form  organic  nitrogen,  e.g., amino  acids,  proteins,  purines, pyrimidines,
and  nucleic acids.   In  this  report the term  ammonia  is used  for gaseous NH, and collectively
for  NH.+ plus NH3,  when  there,  is  no need  or  intention to distinguish  between these forms.
Ammonium (ion) is used specifically to indicate the cationic form NH.+.
2.   Heterotrophic conversion of organic nitrogen from one organisms (food and prey) to another
organism (consumer  or  predator).   Nitrogen  is bound  in  plant or  animal  protein  until  the
organisms die or  as the  case of animals certain products are excreted.
3.    Ammonification,  the  decomposition  of  organic nitrogen to ammonia.   (The  ammonia may be
assimilated by aquatic or terrestrial plants and microorganisms, may be bound by clay particles
                                           12-2

-------
                                                  (4)
                                                 (1,5)
                                                         NO,
  (2)
Figure 12-1.  Simplified biological nitrogen cycle, showing major
molecular transformations. Numbers in parentheses correspond
to numbered processes discussed in text: (1) assimilation;
(2) heterotrophic conversion; (3) ammonification; (4) nitrifica-
tion; (5) denitrification; (6) nitrogen fixation (National
Research Council, 1978).
                       12-3

-------
in the  soil,  or  it may be converted  by  microorganisms to form nitrates in the process termed
nitrification.  It may also escape into the air.).
4.  Nitrification, the  oxidation  of ammonium to nitrite and nitrate through microbial  action.
Nitrates may  be  assimilated by plants,  washed  downward through the soil  into  groundwater or
through surface runoff  into  streams,  rivers and oceans or may be transformed into atmospheric
nitrogen or reduced to ammonia.
5.  Denitrification,  implies the gaseous loss of nitrogen, usually as molecular nitrogen (N~),
nitrous oxide (N20) or nitric oxide (NO), to the atmosphere as a result of microbial  reduction
of  nitrate.   Nitrate  is   reduced  to  nitrous oxide  (N^O) and  molecular nitrogen (N2)  under
anaerobic conditions.   Nitrates (N03 ) are converted into nitrites (NO- ), to nitrous oxide (a
gas) (N20) and finally into nitrogen gas (N^) which goes off into the atmosphere.   In the soil,
nitrites rarely accumulate  under  acidic  conditions but are decomposed  spontaneously  to nitric
oxide  (NO),  and  under alkaline  conditions  they  are  biologically converted  to N~0  and  N2
(Alexander, 1977a;  Brock,  1970).    It must  be  emphasized that this process  is  anaerobic  and
that conversion of nitrates  to  nitrites is extremely sensitive to the  presence of atmospheric
oxygen.   If  atmospheric  oxygen is  present, the  conversion does  not occur.  Some  evidence
exists  for the nonbiological  chemical production of nitrogen gas or nitrogen oxides  (Delwiche
and                                        Bryan,                                        1976).
6.   Biological Nitrogen Fixation   is  the  transformation  of  atmospheric  nitrogen  gas  into
ammonia, nitrates and  other  nitrogen-containing compounds.  The transformation is carried  out
by a  variety  of  microorganisms.   The microorganisms  may be either symbiotic  (living  in  the
roots of leguminous plants) or nonsymbiotic (living independently in the soil) and the process
may be accomplished under aerobic  or anaerobic conditions.
     The predominant agents of assimilation in water are autotrophic algae and on land, higher
plants.   In   soils,  bacteria  are   important  agents  of assimilation  of inorganic  nitrogen.
Heterotrophic conversions  (e.g., of organic nitrogen in  plants  to  animal protein) are highly
complicated processes involving numerous steps,  but are not treated in  any detail  here.
     Ammom'fication  and  nitrification   together  constitute  the  process  of  mineralization.
Bacteria and fungi are the principal agents of ammonification in soils; autolysis of  cells  and
excretion  of  ammonia  by   zooplankton  and  fish are  important  processes in  aquatic  systems.
Ammonification is  important in renewing the limited supply of  inorganic  nitrogen for futher
assimilation  and  growth by  plants.   Nitrification is mediated  primarily  by  aerobic bacteria
that obtain their  energy  by oxidizing ammonia to nitrite and nitrate.   Nitrification converts
ammonia, which  is volatile  but readily  absorbable,  into nitrate,  a  nonvolatile but  easily
leached form.
     On an ecosystem scale, denitrification is considered sink since the products (N2 and N20)
are readily  lost  to  the  atmosphere  and most organisms cannot use  nitrogen  in  these  gaseous
forms.   Denitrification is  carried out by a  ubiquitous  group  of bacteria that use nitrate as
their terminal electron acceptor in the absence of oxygen.
                                           12-4

-------
      Nitrogen fixation is  important  as a souce of available nitrogen for plant growth in both
 natural and  managed agricultural ecosystems.  On  a  global  scale and over millions  of years,
 nitrogen  fixation  balances  the  losses  by denitrification;  on time  scales  of  decades  to
 thousands  of years,  the  two  processes may be out of phase without significantly affecting the
 nitrogen content of the global  atmosphere.
      Nitrogen fixation is  only  an indirect source of  nitrate  in the biosphere, but this pro-
 cess is important  in  global  nitrogen balances, and in the current controversy over the deple-
 tion of stratospheric ozone by  N?0.   (See Chapter 9).
      Numerous texts,  monographs,  and papers  review the  nitrogen  cycle, (Alexander,  1977a;
 Bartholomew and Clark, 1965; Brezonik,  1972, Brock,  1970; Delwiche,  1970; Delwiche and Bryan,
 1976;  Delwiche,  1977, Hutchinson,  1944;  Hutchinson,  1954; Hutchinson,  1957; Keeney,  1973;
 Sb'derlund  and Svensson, 1976) and other reviews cover specific  aspects of the cycle in detail.
 This discussion  emphasizes the  processes of the nitrogen  cycle  that  are  important  to an under-
 standing of the accumulation of nitrate and its transformation in the biosphere.   Because the
 literature dealing  with  nitrate and  the nitrogen  cycle  is  so  extensive, no  attempt  has  been
 made to provide  exhaustive documentation here.
      As indicated above,  of  the many functions occurring within  ecosystems,  the  recycling of
 nutrients  is  one of the most  important.   The nitrogen cycle is  one example of the  cycling of a
 cycling process  could be  detrimental  to the lives of plants and animals.
 12.2.1  Effects  of Nitrates
      Ecological  effects   of  increased  nitrates  can  be   beneficial  or  detrimental  or  both.
 Effects of both kinds  may occur simultaneously, may cause  effects  in media  or in  ecological
 compartments  quite  removed from those  that initially  receive  the manmade nitrogenous  injec-
.tions.   In some natural  ecosystems,  such as lakes  and  estuaries,  the addition of  nitrogen can
"contribute to eutrophic  conditions that  are considered  undesirable.  Nitrate  as  nitric  acid
 contributes to  the  acidity of   rainfall  (Chapter 11)  and some  nitrates and  related  compounds
 are toxic  to  plants, animals  and microorganisms.
      In most  nonagricultural  terrestrial  ecosystems,  the  major  processes  that provide nitrogen
 for plant  growth  are  mineralization  (ammonification  and  nitrification)  of soil  organic nitro-
 gen  and  biological   fixation  of  atmospheric  nitrogen.   When  fluxes of  nitrogen enter  such
 systems as a result of human activities, the  added  inputs  in  many  cases represent a signifi-
 cant fraction of  total nitrogen inputs.   On the basis  of such  mass-balance considerations,  it
 seems  likely  that  such  fluxes  are important  nutrient sources  that could support  increased
 biotic  productivity  (National Research Council, 1978).
      Except in  ecosystems  that  receive  fertilizer or  nitrogenous wastes, the  most  important
 manmade contributions  are  likely to  be  from atmospheric  pathways, total  (inorganic  plus
 organic) nitrogen  loadings  in   wet and dry  precipitation may  be equivalent to from 8  to  25
 percent of  the  nitrogen used  by  plants  in  different natural  ecosystems.   Even in  heavily
 managed ecosystems,  annual  atmospheric fluxes may be  substantial;  for instance,  the calculated
                                            12-5

-------
total  nitrogen  contribution from  precipitation  and from gaseous deposition  over  the  Florida
peninsula exceed by  a  factor of two the amount of nitrogen applied as fertilizer to the agri-
cultural land area within the region (National Research Council, 1978).
     Predicting the  effects  of  nitrates and other anthropogenic nitrogen compounds on  natural
ecosystems involves  much  greater  uncertainties than does prediction  of  the yield response of
an  agricultural  crop.   First,  it  is  far  more difficult  to  determine  accurately  the actual
anthropogenic nitrogen  contributions to most ecosystems;  this is especially  true  for terre-
strial systems,  where the major influxes are from atmospheric deposition.  Second,  far  less is
known  of  the responses  of  nonagricultural plant  communities to increased  supplies of fixed
nitrogen than is  known  for  cultivated crops.   It is possible, however,  to estimate the appro-
ximate magnitude of  anthropogenic  nitrogen fluxes to  ecosystems, using  the limited amount of
monitoring data available or mass-balance calculations (see Appendix  A of the National  Academy
of  Sciences:  Nitrates;  an Environmental Assessment) (National  Research  Council,  1978).   Such
estimates, and  quantitative  information  about the  nitrogen  cycle  at  specific  sites   in  the
system under study,  make  it possible to reach some  conclusions about the possible ecological
significance  of the added nitrogen.  In addition, where the data base is more extensive, as it
is  for  a  number  of lakes in various stages of eutrophication, more  quantitative  dose-response
relationships can be estimated.
     Living organisms are exposed  to nitrates and related compounds  through air, water, soil,
and food webs.   The rate of exposure depends on proximity to sources  and on a great many envi-
ronmental   transport  and  transformation processes  (illustrated  in  Figure  12-2).   Biological
productivity  can  be  increased  deliberately  by  fertilization, as in agricultural crops,  or
accidentally  through run off to terrestrial or lake systems.
12.2.2  Terrestrial Ecosystems
     Additions  of  nitrate and  other forms  of nitrogen from the atmosphere to ecosystems is an
integral  function  of the terrestrial  nitrogen cycle.   Higher plants  and  microorganisms  can
assimilate the inorganic  forms  rapidly.   The contribution of inorganic nitrogen  in wet preci-
pitation (rain plus  snow) is usually equivalent to  only  a few percent  of  the total  nitrogen
assimilated annually by plants in terrestrial  ecosystems;  however total  nitrogen  contributions,
including organic  nitrogen,  in  bulk precipitation (rainfall  plus dry fallout) can be  signifi-
cant, especially in unfertilized natural systems.
     In absolute terms,  atmospheric  contributions  of nitrate  can range  from less  than 0.1 kg
N/ha-yr in the  Northwest (e.g., Fredericksen, 1972)  to  4.9  kg N/ha-yr  in  the eastern United
States (Henderson  and Harris,  1975;  Likens et al., 1970).   Inorganic nitrogen (ammonia-N plus
nitrate-N) loadings  in  wet  precipitation ranged  from  less than 0.5  kg/ha-yr to  more  than 3.5
kg/ha-yr in Junge's (1958) study of rainfall over the United States.   On the other hand, total
nitrogen loads in  bulk  precipitation range from  less than 5 kg/ha-yr in desert regions of the
West to more than  30 kg/ha-yr near barnyards in  the Midwest.   Total  contributions  of  nitrogen
from  the  atmosphere  commonly  range  from  about  10 to 20  kg  N/ha-yr  for most  of  the United
States (National  Research Council,  1978).

                                           12-6

-------
AIR
                         NO
                                       PANS. NO"
                                       AEROSOLS
        COMBUSTION
                                                                   . N2O.
                                                                                              OZONE
                                                                                              DEPLETION
                                                                                                        INCREASED.
                                                                                                        UV
                                                                                                                         CLIMATE
                                                                                                                         MODIFICATION
      FERTILIZER
      NOj, NH4+
LAND
            RUNOFF
               NO,
                                       VOLATILIZATION
                                       NH,
                     ^ [ INCREASED
                          PRODUCTIVITY
FOOD
PRODUCTION
                                                      DENITRIFICATION
                         NO,
                                          -NH.
1
NO-
1 3
WASTE
DISPOSAL
1

                           T
                       .UPTAKE BY
                        VEGETATION
                                                                                          VEGETATION,
                                                                                          LITTER BUFFERING
                                                                                           JSOIL
                                                                                           BUFFERING
                                                                                                                     TOXICITY
                                                                      SOIL
                                                                NO3  BUFFERING
                                                       NITRIFICATION
                                                               NO,
                                                       ACCUMULATION
                                                       IN SOIL AND
                                                       GHOUNDWATER
                                              NH,
                                                                                      ACID
                                                                                      SOIL
                                                                                  (SOIL
                                                                                  (BUFFERING
                                                                          NO-
                                                                          LEACHING
                                                                                          H+ LEACHING
                                                                                                                     I
                                                                                                                BIOLOGICAL
                                                                                                                EFFECTS
                                                                                                                T
WATER
                       •NO,
                                                     -B*
                                                            INCREASING
                                                            N:P
                                                            IMBALANCE
                                                                                        LOWpH.
                                                                                        TOXICITY
                                                                                 BIOLOGICAL
                                                                                 EFFECTS
 Figure 12-2. Schematic presentation of environmental effects of manipulation of the nitrogen cycle. Human-caused perturbations are shown
 at left, culminating in ecological and climatic effects, at right. Processes that buffer against the effects are indicated with the symbol(  [X] )
 on the arrows representing the appropriate pathways (National Research Council, 1978);

-------
     In  comparison,  rates  of  annual  uptake by  plants range  from  11 to  125 kg  N/ha-yr  in
selected ecosystems  from  several  bioclimatic zones (National  Research  Council,  1978).   Since
the  lowest  additions are  generally associated with  desert areas,  where  rates  of  uptake  by
plants are  low,  and  the highest additions  usually  occur in moist areas where plant uptake is
high,  the  contributions of  ammonia and  nitrate  from  rainfall to terrestrial  ecosystems are
equivalent to about 1 to 10 percent of annual plant uptake.  The typical fluxes (additions)  of
total  nitrogen  in  bulk  precipitation,  on the other hand, represent from about 8 to 25 percent
of  the  annual  plant needs  in  eastern  deciduous  and  western coniferous  forest ecosystems.
Although these  comparisons suggest that  plant  growth in terrestrial ecosystems  depends  to .a
significant extent on atmospheric  loadings, it is not yet possible to estimate the importance
of  these contributions  when  compared  to biological  nitrogen  fixation and  mineralization  of
nitrogen in  the soil.    In nutrient-impoverished ecosystems,  such as  badly  eroded abandoned
croplands or  soils  subjected  to prolonged  leaching by  acid precipitation,  nitrogen additions
from atmospheric fluxes  are  certainly  important to biological  productivity.   Such sites,  how-
ever,  are  relatively limited  in  extent.    In  largely unperturbed forests,  recycled nitrogen
from the soil organic  pool  is the chief source  of nitrogen for plants,  but  new nitrogen  to
support  increased  production must  come  either from  biological  fixation or  from atmospheric
influxes.  It seems  possible,  therefore,  that man generated contributions  could play a signi-
ficant ecological role  in a relatively large portion of the forested  areas  near industrialized
regions.
12.2.3  Effects  of Nitrogen Oxides
12.2.3.1  Terrestrial Plant Communities—Studies  of plant  communities  suggest that individual
species  differ appreciably  in  their sensitivity to chemical stress,  and that such differences
are reflected in the changes occurring within plant communities.   A common  alteration in a com-
munity under  stress  is  the  elimination  of  the more  sensitive populations and  an increasing
abundance of species that tolerate or are favored by the stress (Woodwell,  1970).   The response
of plant populations or  species to an environmental perturbation will  depend upon life cycles
of the plants,  microhabitats  in which they are growing, and their genetic  constitution (geno-
type).    Abundant evidence  exists   to  show  that  in  plant communities undergoing structural
changes  that reduce  environmental  or  biological  variability  new  species  become  dominant
(Botkin,  1976;  Daniel,  1963;  Jordan,  1969,;  Keever,  1953; McCormick,  1963;  McCormick,  1969;
Miller, 1973; Miller and Yoshiyama, 1973;  Smith, 1974; Treshow, 1968; Woodwell, 1962; Woodwell,
1963;  Woodwell,  1970).   Furthermore, the specific  pollutant to which  a community is exposed
for prolonged periods of  time will govern the capacity of the  community to  recover.   In turn,
an alteration in the community composition,  size of the community,  or its  rate of energy fixa-
tion will  influence  the animal populations  in  the  vicinity and microorganisms  in the  under-
lying soil.   These changes, in their turn, will  modify the behavioral patterns or alter compe-
tion among  the prevalent organisms.
     Investigations of  the influence of nitrogen oxides on economically important plant species
have revealed differential  susceptibility of plant species, differential effects due to diurnal
conditions  and age, and  difficulties in predicting synergistic  effects  when  a plant population
                                           12-8

-------
is exposed  to  more than one pollutant  simultaneously.   Little  information is known about the
specific  effect of  nitrogen  oxides on  plants  in natural  communities.   Evidence  of  visible
injury to plant communities  has seldom been demonstrated.   In fact, visible injury may repre-
sent only a fraction of the actual harm done to terrestrial communities.   Evidence exists, how-
ever, that  the  vigor and survival rate of plants have been affected deleteriously by air pol-
lution (Hepting, 1964).   Many  instances of injury to higher plants that have been ascribed to
pathogens or unknown factors may, in fact, reflect a toxicity associated with nitrogen oxides.
Nevertheless,  since  plants respond  simultaneously  to many environmental factors,  it  is  fre-
quently difficult  to  determine  which of the potential  environmental  stresses are responsible
for damage  to  the  major species or to the community composition.   Thus,  it is likely that the
response  to modest  nitrogen oxide  stresses  would  not be recognized  because the  vigor and
visual  appearance  of  plants would  be  influenced  by  temperature, soil  type and  moisture,
drainage, interspecific  competition, and  other  factors.   Only severe injury  could  likely be
ascribed to a particular pollutional episode (Hepting, 1964).
     The agent  of  stress  may have ecological  importance inasmuch  as  the species  tolerance to
such environmental factors  as  moisture, temperature, and  light, its  capacity to  compete, and
its ability to withstand attack  by  parasitic  organisms,  may be affected  as  well.   Moreover,
physiological  aspects  of  plant development, including  growth,  photosynthetic  and respiratory
rate, and flowering  may  be influenced by the  pollutant.  These alterations in the environment
and in the plant community will  influence energy flow through the  ecosystem, its productivity,
and the succession of indigenous species.
     Studies have  been  conducted on the effect of air pollutants  on ecosystems and plant com-
munities (Parmeter and Cobb, 1972;  Wenger et  al.,  1971).   It  is the  general conclusion of
these investigations that further research on  the influence of nitrogen oxides on  plant commu-
nities  is  required.   The  available information  clearly  is  too small  to  warrant  meaningful
generalizations at this time;  however,  there  is  information  detailing the  effects on indivi-
dual  plant species.  These effects are discussed in  Section 12.3.
12.2.3.2  Effects  on Animal Communities—Surprisingly  little  attention has been  given  to the
effect of nitrogen oxides  on animal populations  or  communities.   Although  laboratory studies
of a few  individual  species  have been  carried out,  it  is  difficult to extrapolate from these
laboratory tests on  animals  maintained  under  careful conditions, to populations in the field.
The interaction  of the various  stresses  in  nature  and the  uncertainty of  cause  and effect
relationships make any conclusions  from  laboratory studies  quite tenuous.   Because  species
differ enormously  in their  susceptibility to air  pollutants,  extrapolation  from  laboratory
tests on one species  to potential effects on another is  fraught with problems.
     One of the few studies conducted on animal  populations is that of McArn et al.  (1974) who
reported that granule-rich microphages appeared in the lung tissues of English sparrows nesting
in urban areas with high pollution levels.   The microphages were not reported to be present in
the  lungs   of  sparrows  inhabiting windswept,  unpolluted   areas.   In this study,  potential
chronic effects could not be determined owing  to the relatively short life-span of these birds.

                                           12-9

-------
     Beyond this limited  amount  of knowledge, the literature concerning the effects of nitro-
gen oxides on  natural  animal  populations or  communities  is  extremely sparse.   No conclusions
can be drawn about  whether ambient levels of nitrogen oxides in the atmosphere have an effect
on the composition or functioning of animal  communities or populations.
12.2.3.3    Effects  of  Nitrogen  Oxides  on Microbial  Processes  in Nature—Microorganisms    are
essential for the functioning of key processes in terrestrial,  marine, and freshwater communi-
ties.    They  are  the chief  agents  for  decomposing  organic materials  in soils  and  waters.
Microfloras are the  major agents for destruction of synthetic  chemicals introduced into soils
and waters.  Marine  algae are essential  for  the  generation  of the oxygen required to sustain
life in all higher animals.  In soil, the bacteria, fungi, and  actinomycetes convert compounds
of nitrogen,  sulfur,  and  phosphorus to the  inorganic state,  thereby providing plants with the
required inorganic nutrients.   Biologic nitrogen fixation and nitrification are affected sole-
ly  by  these microscopic   organisms,  which  also  maintain soil structure  and  form  the  humus
important  to abundant plant growth.  In  addition,  many of the pathogens  that  are constantly
discharged into soils and  waterways are eliminated by microbial actions.
     Since microorganisms  are  critical  to the balance of ecosystems,  any disturbance in their
activities could have serious  consequences  on a local, regional,  or global scale.   The poten-
tial impact on  microorganisms by substances  as widespread and pervasive as the nitrogen oxides
must therefore be assessed.   Surprisingly,  this subject  has been  neglected to date.   The few
data are based  on NO  concentrations in excess of those found in the atmosphere.
     Therefore, the  knowledge  concerning  the potential impact  of  nitrogen oxides on microbial
processes in  soils and waters is  sparse.  Although ambient concentrations probably do not sig-
nificantly affect biologic processes in natural ecosystems, it  is  not possible to support this
view with experimental data (Alexander,  1977b).
12.2.4  Aquatic Ecosystems, Nitrogen and Eutrophication
     The overenrichment of  surface  waters,  usually lakes, with nutrients  is  termed eutrophi-
cation.   This  process results in  an array of water quality changes  that are generally regarded
as  undersirable.   Phosphorus  and nitrogen  are  the most  important nutrients that stimulate
eutrophication, and  in  most  lakes phosphorus  is considered  the more  critical  of the two.   In
coastal   and estuarine ecosystems,  however,  nitrogen  is more often the  limiting nutrient and
nitrogen  inputs  may  control  eutrophication.   Furthermore,  in many  already-eutrophic  lakes,
biotic productivity  is  controlled by nitrogen, because the N/P ratios of pollutants from many
cultural   sources  (e.g.,  domestic  sewage) are far  below the ratios  needed for  plant  growth.
The role of nitrogen in cultural  eutrophication therefore appears  to be important,  although it
is complex and  poorly quantified  relative to the role of phosphorus.
     The sources of manmade nitrogen reaching surface waters  include sewage, industrial  wastes,
animal  manures, surface runoff and sub-surface transport of  nutrients from urban and agricul-
tural  lands,  and atmospheric  fluxes.   It has been estimated  (National Research Council,  1978)
                                           12-10

-------
that more than 90 percent of the nitrogen entering surface waters comes from nonpoint sources,
and that  more  than  80 percent of that portion is from agricultural  lands (including livestock
feedlots).  Because nitrogen forms in aquatic systems are readily interconvertible, all  nitro-
gen inputs, rather than nitrate per se, must be considered.
     The  average  atmospheric input  of 10 to  20 kg  N/ha-yr  that is typical for  most  of the
United States  is  also a sufficient nutrient  loading  to  support a moderate increase in  biotic
productivity in some lakes, especially shallow, oligotrophic lakes that may be nitrogen-limited.
Atmospheric nitrogen fluxes may contribute to slight eutrophication  in such cases;  however, it
is unlikely that these inputs alone would induce serious  water quality problems.
12.2.4.1  Eutrophication of  Lakes—Cultural or  man-induced  eutrophication  has been one  of the
most  intensively  studied water quality problems  in  the  past ten to  fifteen  years.   Although
many lakes become naturally more productive and nutrient-rich as they fill  in and age,  natural
eutrophication is a slow process, and its effects are unlikely to be perceived within a  single
human  lifetime.   However,  addition  of excessive amounts of nutrients  from  sewage effluents,
agricultural  runoff,  urban  runoff and  other  anthropogenic  sources  can  greatly  modify  the
characteristics of lake in a matter of a few years;  the literature is replete with  examples of
this phenomenon.
     The  over-enrichment  or eutrophication  of  surface waters,  usually  lakes, with nutrients
results in an array of water quality changes that are generally considered  undesirable.   These
changes most commonly  include  the proliferation or  "blooms" of algae and aquatic macrophytes,
the depletion  of  dissolved  oxygen in bottom water,   a decrease in water clarity,  the loss of
cold water  fisheries,  shortened food  chains,  and takeover  by rough  fish.   Table  12-1  summa-
rizes  changes  in  common  trophic state indicators that occur  when lakes become eutrophic,  and
Table 12-2 lists some common water use problems that may  result from eutrophication.
     Eutrophication  is  usually  considered undesirable.   This  somewhat  narrow viewpoint,  how-
ever,  ignores  the fact that nutrient-rich waters are more  productive not only  of algae,  but
also of  fish.   Lakes  are  not  now a  significant  source  of  protein  in the United  States,  but
lake fish  may be an  important food  resource  in a  food-hungry world.   Many  sports  fishermen
prefer moderately eutrophic  lakes,  unless they are   seeking coldwater fish,  which  cannot sur-
vive in  such  lakes  because  of oxygen depletion  in  the  cold bottom  waters.  A  conflict  thus
exists between the desires of some fishermen and the preferences of  swimmers and  other recrea-
tional  users of  lakes,  who generally favor the  clearest  and  most oligotrophic situation.   On
the other  hand,  continued  nutrient  enrichment eventually  is  undesirable to sport fishermen
also,  since  game fish disappear,  rough  fish predominate, and excessive aquatic weed  growths
may hinder or prevent boating in highly eutrophic lakes.
     For  some  functions  of  some  oligotrophic lakes,  where  nitrogen  may  be  the  limiting
nutrient, the  contribution from  runoff or  atmosphere fluxes may be  essential to  maintaining
biological productivity.  The point  at which the effects on  productivity  of nitrate input to
                                           12-11

-------
                TABLE 12-1.  COMMON TROPHIC STATE INDICATORS
                   AND THEIR RESPONSES TO EUTROPHICATION  .
Physical Indicators                             ,

Transparency (D)
     (Secchi disc reading)

Chemical Indicators

Nutrient concentrations (I)
     (e.g., annual average and spring maximum)
Conductivity (I)
Dissolved solids (I)
Hypolimnetic oxygen (D)
     (generally goes to zero except in very deep eutrophic lakes)
Epilimnetic oxygen supersaturation (I)
                     2
Biological Indicators

Algal bloom frequency (I)
Algal species diversity (D)
Chlorophyll a (I)
Proportion of blue green algae in plankton (I)
Primary production (I)
Littoral vegetation (I)
Zooplankton (I)
Fish (I)
Bottom fauna (I)
Bottom fauna diversity (D)


 (I) after parameter signifies that value increases with eutrophication;
. (D) signifies that value decreases with eutrophication.
2
 Biological parameters have important qualitative changes, i.e., species
 changes as well as quantitative (biomass) changes as eutrophication proceeds.

SOURCE:   (Brezonick, 1969).
                                12-12

-------
       TABLE 12-2.  WATER USE PROBLEMS RESULTING FROM EUTROPHICATION



Water Treatment Problems

     Increased color and turbidity in raw water

     Increased taste and odor (necessitating the use of activated carbon)

     Increased chlorine demand

     Shortened filter runs

Recreational Problems

     Loss of desirable fish and increase in rough fish

     Increased costs in boat and dock maintenance resulting from fouling

     Boat access problems from aquatic vegetation

     Economic losses to owners of resorts and fish camps as fewer people
       swim, fish and boat in lakes with algal  blooms

     Public health problems--swimmers' diseases (mainly eye, ear, nose and
       throat infections)

     General loss in lake's aesthetic appeal

Agricultural Problems

     Transmissibility of water in canals impaired by extensive macrophyte
       growths

     Toxicity of algal  blooms to cattle and wildlife

     Increases in water loss in arid regions caused by evapotranspiration
       from floating vegetation



SOURCE:   (Brezonick, 1969).
                                12-13

-------
aquatic ecosystems cease to be beneficial is influenced by a number of factors.   Some of these
are discussed below.
     Because phosphorus  and nitrogen are  the  nutrients  that limit production  in  most lakes,
these  two  nutrients  are  most  important in  stimulating  eutrophication  (Vollenweider,  1968).
Oligotrophic lakes (low  in nutrients) are commonly thought  to  be phosphorus-limited (Deevey,
1972;  Hutchinson, 1973),  because  of the relative paucity of phosphorus in the bioshphere com-
pared  to  nitrogen,  and because the  phosphorus  in minerals and soils  is  relatively immobile,
whereas nitrogen  compounds  are  quite mobile.   Lake Tahoe (California, Nevada) is a well-known
example of  a nitrogen-limited  oligotrophic lake.   In highly eutrophic  lakes  nitrogen is fre-
quently the  limiting  nutrient,  most often because domestic  sewage, the chief nutrient source
for many  eutrophic  lakes,  is imbalanced with  respect to nitrogen and  phosphorus.   The total
N/P ration (by weight) in sewage is about 3:1 to 4:1,  largely because  of the widespread use of
phosphate detergents.  By  comparison,  the  annual  N/P ratio  of  healthy plants is about 7:1 to
8:1 (by weight).
     Miller et  al. (1974)  conducted algal  nutrient bioassays on waters from 49 lakes through-
out the United States and found that phosphorus limited growth in 35 lakes;  nitrogen was limit-
ing in  eight lakes;  and  some other nutrient was limiting in six.   The incidence of phosphorus
noted in National Eutrophication Survey data on Florida lakes (National Research Council, 1978).
12.2.4.2  Eutrophication  in Coastal Waters—Studies of  estuarine waters  at  several  locations
along  the  east coast  of  United States  have  indicated  that  low concentrations  of dissolved
nitrogen limit  primary production  (Goldman et  al.,  1973;  Goldman, 1976; Ryther  and Dunstan,
1971; Thayer, 1971).
     Additions  of nitrate  to  such  estuarine systems stimulate primary production and can pro-
duce changes in  the  dominant  species of plants,  leading  to cultural  eutorphication and ulti-
mately to deterioration of water quality.   However,  the significance of nitrogen as a limiting
nutrient varies  in different  estuaries  and even on a  spatial  and temporal basis within a sin-
gle estuarine  system  [e.g., Thayer (1971), Estabrook (1973),  Goldman  (1976)].   Furthermore,
not  all  estuaries are  nitrogen-limited;  Myers (1977)  found that  phosphate  was  the  primary
limiting nutrient  in near-shore waters  off the  Gulf of Mexico  near  Appalachicola,  Florida.
The high  degree of  heterogeneity  in the  role  of  nitrogen  as  a  control  of productivity  in
coastal  areas  makes   it  difficult  to establish  quantitative  relationships  between  nitrate
loading and water quality.
     The reasons  that nitrogen is  more important  as a limiting  nutrient  in  marine  coastal
waters than in  fresh  waters are uncertain.   A higher rate of phosphorus exchange between sedi-
ment and water  in saline  waters is one possibility.   It  has also been suggested that denitri-
fication of  the nitrate  that  diffuses into  anoxic  sediments limits  the amount  of available
nitrogen in estuarine areas, but this hypothesis needs further study.
     A number of  symposia  have  treated the causes and consequences of eutrophication in con-
siderable detail  (Allen  and Kramer,  1971;  Likens,  1971;  Middlebrooks et al.,  1973;  National
                                           12-14

-------
Research  Council,  1969).   The  problem  of  cultural  eutrophication clearly  is not  solely  a
nitrogen-related phenomenon,  nor is  nitrate the only or  often  even the main form of nitrogen
input.  Our  focus  in this section is on current efforts to quantify the relationships between
nutrient  loading and trophic states, and on evidence for the extent to which nitrate contri-
butes to eutrophication problems.
     Sawyer  (1974) was  the  first to determine  critical nutrient  levels associated with water
quality degradation  in lakes.  He concluded from a study of 17 lakes in southeastern Wisconsin
that  lakes with  spring  maximum concentrations of more than 300 mg/1 of inorganic nitrogen and
more  than  10 to  15 mg/1 of  orthophosphate-P  could  be expected to have algal  nuisances in the
summer.    These  numbers  have been widely quoted and  used  as water  quality  guidelines  in many
areas of  the United  States,  in  spite of the  narrow data  base from which they were developed.
     Vollenweider (1968,  in  a classic  study,  developed the concept of nutrient loading rates
and presented graphs of critical areas  nutrient loading  (grams  of nitrogen or phosphorus per
square meter of lake surface  per year)  versus  mean depth, as management  guidelines.   Figure
12-3 presents Vollenweiger1s loading graph  for nitrogen.   Vollenweider  (1968)  presented a semi-
theoretical mass balance nutrient model  as  the basis for his loading graphs.
     Simple nutrient input-output models have provided insights  into the dynamics of nutrients
in  lakes,  and they  offer  a  rational basis  for the development of  critical  nutrient  loading
rates and  lake  management guidelines (e.g., Dillon  and  Rigler,  1975).  Such models  to date,
however,  have been oriented  primarily  toward phosphorus,   under the assumption  that it is the
key limiting  nutrient  in  lakes.   Further studies are needed  to  develop more  accurate loading
guidelines for  nitrogen and to  obtain quantitative  data  to apply  the  input-output  models  to
nitrogen-limited systems.
12.2.4.3   Nitrogen  Cycling in Eutrophic  Lakes—Eutrophication  leads not only to increased rates
of  nitrogen  cycling  in  lakes; it also provides  conditions  for  some reactions in the nitrogen
cycle that  normally  do not  occur in oligotrophic  lakes.   For example, nitrogen  fixation  by
blue-green algae is essentially limited  to  eutrophic lakes (Home,  1977; Stewart et al., 1971).
Although  blue-green algae are cosmopolitan,  they are seldom the  dominant phylum in  oligotrophic
lakes, and nitrogen-fixing species (e.g., Anabaena  spp., Aphanizomenon  flos-aquae)  are rare  in
non-eutrophic lakes.   This fact  is  ironic  in view  of the  well-known inhibition of  fixation  by
high concentrations  of  inorganic nitrogen.   However,  fixation in  eutrophic lakes is generally
associated with  nitrogen depauperate periods,  such  as late summer in temperate surface waters.
Maximum bloom development by nitrogen-fixing  blue-green  algae requires an  adequate supply  of
phosphorus, and dissolved phosphorus is  usually growth-limiting in  oligotrophic waters.   For
example,  Vanderhoef  et  al.  (1974)  studied  nitrogen fixation  in Green  Bay  (Lake Michigan) and
found that the nonfixing blue-green  Microcystis  predominated in  areas where all  nutrients were
high.   Nitrogen-fixing Aphanizomenon increased with  declining  combined  nitrogen concentrations
and showed increased  efficiency of fixation as inorganic  nitrogen  levels decreased.   The stand-
ing crop  of this species decreased with  decreasing  phosphate concentrations.  Finally,  diatoms
                                           12-15

-------
   10.0
    5.0
2 .

5


3
z
LU
O
O
CC
UJ
cc
    2.0
    1.0
    0.5
    0.2
             EUTROPHIC LAKES
                                     OLIGOTROPHIC LAKES
                               I
                                         I
                              10        20


                           MEAN DEPTH, meters
                                                      50
100
  Figure 12-3. Areal loading rates for nitrogen plotted against mean
  depth of lakes (Volienweider, 1968).
                        12-16

-------
predominated in the northern reaches of the bay (40 km from the Fox River, the major tributary
and source of nutrients for the bay).
     The  importance  of nitrogen  fixation  in  the nitrogen budgets of  lakes  is controversial.
Most  reports  indicate  relatively  low  contributions  (<15  percent)  in  lakes where  fixation
occurs  at  all,  but  a  few where  fixation  supplies  up to 50  percent of the  annual  nitrogen
input have been  reported.   Even in the typical case where fixation makes only a small  contri-
bution to the total loading,  however,  the process is still significant in maintaining nuisance
blue-green algal  blooms in lake surface waters.
     Denitrification occurs  in the anoxic  hypolimnia of stratified eutrophic lakes,  and  can
represent a significant term  in lacustrine nitrogen  balances  (see  National  Research Council,
1978).  Denitrification also  occurs in the anoxic sediments  of lakes.   The  sources of  nitrate
for  sediment  denitrification  may  be  upward  seepage of  groundwater,  downward diffusion  of
nitrate  from  the  lake water  column,   or  nitrification  in  the  oxygenated  surface layer  of
sediment.   Sediment denitrification can occur in oligotrophic lakes,  since their sediments  are
also anoxic.   However, Chen  et al.  (1972)  reported much higher rates in  sediments  from a hard
water eutrophic lake than  in those from a soft water oligotrophic lake.
12.2.4.4  Form of Nitrogen Entering Lakes—It  is  difficult to  generalize about the percentage
of the  total  nitrogen  loading to lakes that  is  contributed  as nitrate.   Nutrient  budgets  are
generally presented  by source (streams,  rainfall,  sewage  effluents,  etc.)  rather  than  by
nitrogen form.   Lake Wingra,  Wisconsin  (National  Research Council, 1978)  represents one of  the
few cases where  nitrogen  loading rates have  been  broken down  according to form.   Table 12-3
indicates that 47  percent of  the  total nitrogen loading to  Lake  Wingra was in  the  form  of
nitrate.

                        TABLE 12-3.   NITRATE-N LOADINGS TO LAKE WINGRA
Source
Precipitation on
lake surface
Dry fallout
Spring flow
Urban runoff
Average
TOTAL
Kilograms
N03~-N/yr
440
480
4,140
600
_ _ _
5,660
Percent
N as NO
40
22
96
13
" ~
47
Total
3~'N






     SOURCt:   (National  Research Council,  1978).

                                           12-17

-------
     Inorganic  nitrogen forms  in  lake water  are  so readily  interconvertible that  there  is
probably little to be gained from detailed analysis of this topic.   Measured concentrations  of
ammonia and  nitrate  in  rainfall are roughly comparable, although large short-term, local, and
regional variations  occur  (National  Research Council, 1978).  Rainfall  in  industrialized and
urbanized  regions  has  exhibited  increasing  nitrate  levels  over  the  past  several  decades
(Likens, 1972).   Urban  runoff  and sewage effluents vary widely in their nitrogen composition,
making generalizations  tenuous.   Kluesener  and Lee (Kluesener, 1972;  Kluesener and Lee, 1974)
summarized average  nitrogen  component  concentrations from several urban  runoff  studies.   The
grand means  of the  data  they  collected  are:   NH,-N,  0.44  mg/liter; NO, -N,  0.51 mg/liter;
organic nitrogen,  2.0 mg/liter.
     In summary, the contribution of nitrate to eutrophication is uncertain,  because of a lack
of data dealing with nitrate per se, and due to the ease with which various forms of nitrogen
are interconverted.  Nitrogen  contributions  from human activities can promote increased bio-
logical  productivity in aquatic systems,  but the role of nitrogen in  eutrophication is under-
stood  much  less   quantitatively  than  the   role  of  phosphorus.   The  effects that  nitrogen
additions  may  have  on  productivity,  phytoplankton sucession,  and  'other  processes  within
aquatic ecosystems are certain to be influenced by other variables,  such as light and tempera-
ture;  however, there  is  little quantitative information available  regarding the  raltionships
among these factors.
12.2.5  The Value  of a Natural  Ecosystem
     Ecosystems are  usually evaluated  by modern man  solely on the  basis  of their economic
value to him,  i.e.,  dollars and cents  value to  man.   This economic value,  in turn, is depen-
dent on the extent to which man can manipulate  the ecosystem for his own purpose.   This single-
purpose point  of  view makes it difficult to explain  the many benefits of a natural ecosystem
to  man's  welfare   in  terms of  the  conventional  cost-benefit  analysis.   Natural   forests  are
among the most efficient in the fixation of solar energy.   Most agriculture,  by comparison,  is
inefficient in total energy fixed;  however,  in transforming solar energy into food for man  it
may be highly efficient, so agriculture is emphasized (Woodwell,  1978).
     Many functions  of  natural  ecosystems and  their benefits  to  man  are unknown  to the deci-
sion  makers.   Gosselink  et al.  (1974)  have,  however,  placed  a  value on  a tidal  marsh  by
assigning monetary  values  to  the  multiple  contributions  to man's  welfare  such  as fish nur-
series,  food  suppliers, and waste-treatment  fucntions of the  marsh.   They  estimate the total
social values to range from $50,000 to $80,000  per acre.
     Using four different  categories,  Gosselink  et al.   (1974) developed  a  step-wise means  of
assessing the  true  value  of natural tidal marshes to society as a whole.   The value was based
on commercial  usage, social  usage and the monetary value of natural  ("undeveloped") estuarine
environments.
     The categories  or  levels  of marshlands to which monetary values were assigned are:  (1)
commercial  and recreational  use,  e.g., shell fish production and sport fishing;  (2) potential
for development,  e.g.,  aquaculture, draining  for  industrial  use;  (3) waste  assimilation  or

                                           12-18

-------
treatment,  e.g.,  tertiary sewage  treatment,  and (4) total life  support  values,  e.g.,  global
cycling of  nitrogen  and sulfur, as protective  "breakwaters."   The round-figure values calcu-
lated in terms of (a) annual return and (b) an income-capitalized value were:  (1) a.  $100; b.
$2,000; (2)  a.  $1,000;  b.  $20,000; (3) a.  $2,500;  b.  $50,000; and (4) a. $4,100; b.  $82,000.
     The foregoing estimates  for category (1) were  based  on  identifiable 1974 commercial and
recreational uses for which monetary values could be determined rather well.   For category (2)
the  income-capitalization  approach was  used to  estimate the  values  for development potential
and  for  aquaculture.   The  estimates  for  tertiary  sewage  treatment (3)  and  life  support (4)
represent estimates of  what  man would have to  pay  for this useful work that is now performed
by an acre of estuary were it not available to do this work.
     Shortcomings exist  in  evaluating  the environment solely  in  terms  of direct uses or pro-
ducts.   "Such  cost-accounting  ignores the extremely valuable  life-support  work  that natural
areas carry on without any development or direct use by man.  It is this 'free work of nature'
that is grossly, undervalued, simply because it has always been taken for granted or assumed to
be unlimited  in  capacity"  (Gosselink  et al. , 1974).   Development by man of  a  salt  marsh may
adversely affect  its  functioning  in  tertiary  sewage  treatment or as  a  life support system,
therefore, it is important to evaluate it before deciding what kind of development, if any, is
in the  long-term best  interest of both  the  environment  and  the economy (Gosselink et al.,
1974).
     Westman (1977) also  evaluated the  benefits of natural ecosystems by estimating the mone-
tary costs  associated  with the  loss of the  free services  (absorption  or air pollution,  pro-
vided  by  the ecosystems.  Westman estimated that  the oxidant  damage  to the  San Bernardino
National  Forest  could  result  in a cost of $27 million  per year  (1973 dollars)  for  sediment
removal alone due to erosion as long as  the forest remained in the early stages of succession.
     Estimates of the  cost  in currency  of the values of  items and qualities  such as clean air
and  water,  untamed  wildlife,  and  wilderness,  once  regarded  as priceless,  are an  attempt to
rationalize the activities of civilization (Westman, 1977).  When estimating  the monetary cost
in currency  of  the  values  lost through the damaging of  ecosystems,  the assumption is usually
made that the decision  makers will  choose  the alternative which is most socially beneficial as
indicated by costs compared  to benefits.   As Westman  (1977)  points  out,  the assumption "that
decisions that maximize benefits cost  ratios simultaneously optimize social  equity and utility"
are based on certain inherent corollaries.   These are:
               "(1)  The human species  has  the exclusive right  to use and manipulate
               nature for its own purposes.  (2) Monetary units are socially  acceptable
               as means to equate the  value of natural  resources destroyed and those
               developed.   (3) The value  of services lost during the interval before
               the replacement or substitution of the usurped  resource has occurred
               is included in the cost of  the damaged resource.   (4) The amount of
     ,          compensation in monetary  units  accurately  reflects the full value of
               the loss to each loser  in  the transaction.   (5) The value of  the item
               to future generations has  been judged and  included in an accurate way
               in the total value.   (6)   The benefits of  development accrue  to the
                                           12-19

-------
               same sectors of society, and in the same proportions, as the
               sectors on whom the costs are levied, or acceptable compensation
               has been transferred.  Each of these assumptions, and others not
               listed, can and have been challenged" (Westman, 1977).

In  the  case of  (4)  above, for  example,  the  losses incurred when  the  development  of natural
ecosystems  are  involved,  include species  other  than  man.   These losses are  seldom,  if ever,
compensated.  The  public  at  large also is usually not consulted to determine whether the dol-
lar  compensation  is  adequate  and acceptable.    Frequently,  there  is  no  direct compensation.
Corollary  (5)  can never  be  fulfilled  because  it is  impossible  to determine  accurately the
value to future generations.
     It  should  be remembered  that ecosystems are  life support  systems  and  therefore  their
worth, in the final analysis,  cannot be valued in dollars and cents.
12.3  EFFECTS OF NITROGEN OXIDES ON VEGETATION
     Of the various nitrogen oxides (NO ) in the ambient air (Chapter 8) only nitric oxide (NO)
and  nitrogen dioxide  (NO,,)  are considered important phytotoxicants.  The direct effect of NO
on  vegetation  are  usually associated  with and confined to  areas near  specific  industrial
sources.    For  example,  vegetation injury  from exposure  to NO- has been observed  near nitric
acid  factories  and arsenals,  but there are no  published reports on vegetation  injury in the
field due to NO or other oxides of nitrogen.
     The direct  effects of NO   on vegetation are  reviewed  in this chapter  with  emphasis  on
studies relating NO  effects  to known exposure  concentrations and durations.   Since most avail-
                   A
able  data  pertained  to  NOp,  this pollutant receives  the most attention.   Also, when  NO- was
experimentally combined with other pollutants  such as S02,  injury occurred at much  lower doses
than had been found in earlier studies with NOp alone.   This  suggests that, in certain circum-
stances NOp  in  conjuction with  other  gases  in  the ambient air may  behave synergistically.
     The contribution of NO  to the increased  acidity of precipitation and its effects on eco-
systems is discussed in Chapter 11.
12.2.1  Factors  Affecting Sensitivity of Vegetation to Oxides of Nitrogen
     A notable feature  of  the response of vegetation  to  NOp stress is the  varied  degrees  of
NOp-induced injury.   This  variation  ranges from overt leaf  chlorosis and necrosis  to alter-
ations of  leaf  metabolism.  These  differing responses can be explained by  the physiological
processes affecting NOp  uptake  into the leaf,  pollutant toxicity at target sites and cellular
repair capacity.   Since  plants   develop  as a  consequence of  environmental-genotypic inter-
actions,  each plant possesses  a unique set o structural and functional  properties which change
continuously in  response  to  genetic  and environmental  stimuli.   These  interactions  between
environmental  and  genetic  factors underlie and explain the  dissimilar  plant responses to N0?
exposures.
     Information on relative  sensitivity (differential  response) to NOp is summarized in Table
12-4.  The three  classes  -  susceptible, intermediate, and tolerant -  are approximate because
                                           12-20

-------
                             TABLE 12-4.  RELATIVE SENSITIVITY OF SEVERAL PLANT SPECIES TO NITROGEN DIOXIDE (HECK AND TINGEY, 1979;
                            MACLEAN, 1977; TAYLOR AND MACLEAN, 1970; TAYLOR ET AL., 1975, U.S. ENVIRONMENTAL PROTECTION AGENCY, 1971)
            Plant Type
     Susceptible
     Intermediate
                                        Tolerant
        Coniferous Trees
I
N)
        Field Crops & Grasses
        Fruit Trees
                                     Larix decidua Mill.
                                       (European Larch)
                                     Larix leptolepis Gord.
                                       (Japanese larch)
Avena sativa L.  (Oats)
cv.  Clintland 64
cv.  329-80
cv.  Pendek
Bromus inermis,  L.
  (Bromegrass)
cv.  Sac Smooth
Hordeum distichon L.
  (Barleyl
Medicago sativa, L.  (Alfalfa)
Nicotians glutinosa L. (Tobacco)
Nicotiana tobacum L.  (Tobacco)
Scorzonera hispanica L.
  (Viper1s grass)
T._ incarnatum L. (Crimson or
  Italian Clover)
Trifolum pratense L.  (Red clover)
Triticum vulgare. Vill.  (Wheat)
cv.  Wells
Vicia sativa L.  (Spring vetch)

Hal us sj>. (Showy apple)
Abies alba Mill. (White Fir)

Abies homolepis Sieb. & Zucc.
   (Nikko or Japanese fir)
Abies pectinata DC (Common
   Silver Fir)
Chamaecyparis Lawsoniana [Murr. ]
   Parl (Lawson's cypress)
Picea glauca [Moench] Voss
   fwhite Spruce)
Picea pungens glauca. Regel
 (Colorado Blue Spruce)

Gossypium hirsutum,  L. (Cotton)
cv. Acala 4-42
cv. Paymaster
Nicotiana tabcacum,  L. (Tobacco)
cv7White Gold
cv. Bel-B
cv. Bel W3
Poa annua, L. (Annual bluegrass)
Secale cereale  L. (Rye)
Triticum aestivum L.  (Wheat)
Zea Mays L. (Sweet Corn)
                                                                        Citrus sg. (Orange, grapefruit,
                                                                           tangelo)
                                                                        Pinus Hugo Turra (Knee pine or
                                                                           dwarf mountain pine)
                                                                        Pinus nigra Arnold (Austrian pine)
                                                                        Taxus baccata L.  (English yew)
Nicotiana tabacum, L.  (Tobacco)
cv.  Burley 21
Poa pratensis L.  (Kentucky bluegrass)
Sorghum sp.fSorghum)
cv.  Martin
Zea Hays L.  (Corn)
cv.  Pioneer 509-W
cv.  Golden Cross
                                     Hosta plantaginea (Lam.) Aschers
                                        (Fragrant plantian lily)

-------
                                                              TABLE  12-4  (continued)
             Plant Type
     Susceptible
                                                                              Intermediate
                                                                                                                 Tolerant
                                      Mains sylvestris  Hill.
                                        fApple)
                                      Pyrus communis  L.  (Wild Pear)
        Garden Crops
        Ornamental Shrubs
           and Flowers
 I
hJ
r-o
  	    (Leek)
  ium qraveolens L.  (Celery)

Brassica oleracea botrytis. L.
  rBroccoli) cv. Calabrese
Caucus carota L. (Carrot)
Lactuca sativa. L.  (Lettuce)
Petroselinum hortense Nym.
  (Parsley)
Phaseolus vulgaris,  L.  (Bean)
cv.  Pinto
Pi sum sativum L. (Pea)
Raphaims sativus L.  (Radish)
cv.  Cherry Belle
Rheum rhaponticum L.  (Rhubarb)
Sinapis alba (White  mustard)
Antirrhinum majus L.
  (Giant Snapdragon)
Begonia multiflora (Tuberous-
  rooted begonia)
Begonia rex, Putz.  (Begonia)
  cv.  Thousand Wonders White
Bougainvillea spectabilis
  Willd. (Bougainvillea)
Callistcphus chinensis ! L.1
  Nees (China aster)
Chrysanthemum sg. (Chrysan-
  santhemum)
  cv.  Oreyon
Hibiscus Rosa-sinensis L.
  (Chinese^ hibiscus)
Impatiens sultani, Hook.
  (Sultana) cv.  White Imp
                                   Citrus sinensis (L.) Osbeck
                                       fNavel Orange)
Apium graveolens rapaceum
   (Celery)
Cichorium Endivia, L. (Endive)
  Ruffee
Fragaria chiloensis
  grandiflora (Pine  strawberry)
Lycopersicon esculentum, Mill
  (Tomato)
cv.  Roma
Phaseolus uulgaris humi1 is
  Alef.  (Bush bean)
Solanum tuberosurc L.  (Potato)
Dahlia variabilis Willd.
  (DahlTal
Fuchsia hybrida Voss (Fuchsia)
Gardenia jasminpides Ellis
  (Cape Jasmine)
Gardenia radicans Thunb.
  (GardenTal
Ixora coccinea L. (Ixora)
Ligustrum licidum Ait.
  (Ligustrum)
Petunia X hybrida Hort.
  Volm.-Andr. (Coiranon
  Garden Petunia)
Pi ttosporum tobi ra Ait.
  (Japanese pittosporum)
Rhododendron catawbiense Michx.
  (Catawaba rhododendron)
Allium cepa L.  (Onion)
Asparagus officinal is L.  (Asparagus)
Brassica oaulorapa Pasq.  (Kohlrabi)
Brassica oleracea acephala DC (Kale)
Brassica oleracea capitata L.
   (Cabbagu)
Brassica oleiacea capitiata rubra L.
   (Red cahbaye)
Cucumis salivus, L. (Cucumber)
cv. Long HarkeLeer
PhaseoI in vulgjris, L. (Bush Bean)
Carissa carandas L. (Cariisa)
Codiaeum varieq.jlum Blume (Croton)
Chrysanthemum le^canthemum L. (Daisy)
Convallari majajis L.  (Lily-of-the-valley)
Erica carnea L.  (Spring heath)
Gladiolus communis L.  (Gladiolus)
Erica ^£. (HeatTT)
Hosta s£. (PUntain lily)
Juniperus coi.ferta Parl. (Shore juniper)
Rhodudendron 6j>. (Alaska)

-------
                                                             TABLE 1Z-4 (continued)
            Plant Type
     Susceptible
                                                                             Intermediate
                                                                                                                Tolerant
       Trees & Shrubs
K>
I
       Weeds
Lathyrus odoratus L. (Sweet pea)
Lupinus augustifolius L. (Lupine)
Nerium oleander L. (Oleander)
Pyracantha coccinea Roem.
  (Fire thorn1)
Rhododendron canescens  (Michx.)
  Sweet (Hoary Azalea)
Rosa sjg. (Rose)
Vinca minor L. (Periwinkle)
  cv. Bright Eyes

Betula pendula Roth. (European
  white birch)
Helaleuca leucadendra (L.) L.
  (Brittlewood)
Brassica sp. (Mustard)
Helianthus annuus L.
                                       (Common Sunflower)
Acer platanoides L. (Norway
  maplei
Acer palmatum Thunb.
                                                                          (Japanese maple)
                                                                        Tilia grandiflora (Summer)
                                                                        Ti lia cordata Mill.  (Small-
                                                                          leaved European linden)
Halva parviflora L.
  (Cheeseweed)
Stellaria media [L.] Cyrill
  (Chickweed)
Taraxacum officinale Weuer
  (Dandelion)
Carpiniii. betulus L.  (European horrih**Mn)
Fagus by Ivatica L.  (Beech)
Fagus byl v/atica atropurpurea Kirchr>
  (Purp IK- leaved beech)
Ginyko bi loba L.  (Gingko)
Quercus r^bur L.  (English oak)
Robinia pbgudoacacia L. (Black looj"5'-)
Sambucus nigra L.  (European elder)
             Huds.  (Scotch elm)
Ulmus monuna With.  (Mountain ela)

Amaranthus retroflexus L.  (Pigweed;
Cheii'jpodium album L.  (Lamb1 s-quart<»*rs)
Chenopodiug] sp.  (Neetle-leaved goo'>*^ oot)

-------
they are  based on subjective criteria  obtained  from several sources.  Most  of  the classifi-
cations  are  developed  from  experimental  fumigations  conducted  at various  locations,  at
different  times  of  the year,  under  different environmental  conditions  using  different  N02
exposure concentrations.  Methods  for  assessing  injury, such as percentage of leaves injured,
amount of  leaf surface affected,  defoliation, etc.  also varied.  Therefore, a  plant  species
considered tolerant by  one  investigator may be considered  susceptible by another.   Also,  the
interaction between genetic and environmental  factors that control  plant  sensitivity is such,
that given  different  sets  of environmental parameters  or other variables,  the  relative  N0_
sensitivity of species or cultivars within species can change.
     A given  plant  and  its individual  leaves, will  vary in sensitivity  to NCL,  depending on
the  stage  of  development.   In  tobacco  (Nicotiana  sj>.) the  oldest  leaves became  chlorotic,
middle age  leaves  became  chlorotic  with necrotic  lesions, and injury to the younger leaves
was limited to necrosis  (Van Haut and Stratmann,  1967).   In Ixora (Ixora  coccinea) (Maclean et
al., 1968) mustard (Brassica,  ^p_.), (Benedict and Breen, 1955) and tobacco (Nicotiana glutinosa)
(Benedict and  Breen,  1955) the older  leaves were  more sensitive.    In other species  such as
chickweed  (Stellaria  media),  dandelion  (Taraxacum  officinale),   and   pigweed  (Amaranthus
retroflexus)  the  middle age  leaves  were more sensitive.   However,  in sunflower (Helianthus
annuus) middle age  and  older  leaves respond similarly  (Benedict and Breen,  1955).   In citrus
(Citrus s£.) necrosis was most severe on the youngest leaves (Maclean et  al.,  1968).  Emerging
or  elongating  needles of  conifers were more  susceptible  than  mature  needles  (Van Haut  and
Stratmann, 1967).
     Only a few studies  have reported the influence of edaphic factors on  plant  sensitivity to
NC^.   Increasing  soil moisture  increased  sensitivity  in  several  weed and vegetable  species
(Benedict and Breen, 1955; Kato  et al.,  1974a).
     Because of a possible  relationship between  atmospheric NCL  and nitrogen metabolism,  the
influence of soil  nitrogen on the plant response  to NCL has been studied.   Rogers et al.  (1979)
was  unable  to show differences in NCL  uptake  in  corn (Zea mays)  or  soybean   (Glycine  max)
plants that were grown in soil with varying levels of nitrogen.   In  contrast,  Srivastava et al.
(1975c) reported that N02 uptake in bean (Phaseolus vulgaris) decreased with increasing levels
of soil nitrogen.   They  also reported that NCL-induced foliar injury decreased with increasing
levels of soil  nitrogen.   Similar results were found  in studies of other vegetables (Kato et
al., 1974a;  Kato  et  al. ,  1974b).  Zahn  (1975)  reported  that  increasing the  available  soil
nitrogen  reduced  NCL-induced  foliar injury.  However,  Troiano and Leone (1974)  found  that
tobacco (Nicotiana  glutinosa) grown on a low level  of soil nitrogen was  more  resistant  than
when grown on a higher level of  soil nitrogen.   Kato et al. (1974a,  1974b) reported that plants
grown  on  NH.-N source were more  sensitive  to  NCL-induced  injury and contained  higher levels
of  foliar  nitrite  after NCL  exposure  than  plants  grown on a  NO,-N  source.    Kidney  beans
(Phaseolus vulgaris) and sunflower (Helianthus  annuus) were grown on either ammonium, nitrate,
nitrite or minus nitrogen sources.  The plants  that received either  nitrate or nitrite  through
                                            12-24

-------
the  nutrient  solution contained  less  nitrite  in  the foliage following a  3-hour exposure to
7.52  mg/m3  (4 ppm)  N02  than plants  grown on  minus  nitrogen or  ammonium (Yoneyama  et  al.,
1979).   Similarly,  tomato  (Lycopersicon  esculentum) and  sunflower (Helianthus  annuus)  were
grown at three  levels of nitrogen nutrition  ranging  from  26 to 260 ppm N  (Matsumaru  et al. ,
1979).   The  plants  were  exposed  to  0.56 mg/m3  (0.3  ppm)  NOp for 2 weeks.   Plant  growth was
depressed between 0  and  approximately 21% with no clear trend between the  nitrogen concentra-
tion in the growth media and growth reductions.
     Nitrogen nutrition  can  influence  the effects of NO on  tomatoes (Anderson and Mansfield,
1979).  The plants were  grown on either  low, medium,  or high levels of soil  nitrogen  and ex-
posed to a  concentration range  0 to 0.98 mg/m3 (0.8 ppm)  NO for  50 days.   At a low level of
soil  nitrogen,  plant growth increased with increasing  levels of NO.  At the  medium level  of
soil nitrogen, the 0.49  and 0.08 mg/m3 (0.4  and 0.8 ppm)  levels  of NO  significantly  reduced
growth.   At the high level of soil nitrogen, all levels of  NO reduced plant growth compared to
the controls.
     Several researchers have studied the effect of light and time of day on plant sensitivity
to NOp.   Zahn (1975)  noted that  alfalfa (Medicago sativa) exposed to N02 during the night were
injured more extensively than plants  exposed during the day.   These findings were supported by
Czech and  Nothdurft  (1952)  who  discovered  that the  toxic  dose for  1-hour  exposures of sugar
beets (Beta vulgaris) was 10 times greater in the day time, 188 mg/m3 (100  ppm) than at night,
18.8 mg/m3  (10  ppm).   Van Haut  and Stratmann (1967)  found leaf injury in  oats (Avena  sativa)
was greater at  night,  but they  also reported that  once injury was initiated, the development
of necrotic lesions  was  more rapid on warm sunny days.   Kato et al.  (1974a,b) determined that
vegetable plants  were severely  injured  from N0«  exposures  in the  dark and  contained higher
foliar levels of  nitrite than plants exposed in  the  light.   Taylor (1968) reported that bean
(Phaseolus  vulgaris)  plants were  injured by 5.6 mg/m3  (3 ppm)  NOp in the darkness and  that
this dose caused  as  much damage as 11.3  mg/m3  (6 ppm) N0_ in the light.   Zeevaart (1076) ex-
posed 9 plant species to N02 in  both  light and dark.   Eight species exhibited more damage when
exposed in the  dark.   Injury was associated with an increase in nitrite and a decrease in ex-
pressed cell  sap  pH;  fumigation of the plants  with  NH, +  N0~ reduced  injury.   However,  with
                                                       o     c.
tobacco (Nicotiana glutinosa) light  was  required for injury  to develop and there was no asso-
ciation between injury and  either nitrite or cell  sap  pH.   In studies with several vegetable
plants,  Inden (1975)  showed  that  plants  were most  sensitive  when  exposed  to N02 in the dark.
Also  leaves  treated  with the photosynthetic  inhibitor  DCMU  were very sensitive  to N02 expo-
sures in the light.   Plant susceptibility also varies at different times during the day.  In  a
series of 2-hr exposures  beginning at 0800-1000  hours and ending at 2000-2200 hours, injury to
rye (Secale cereale)  plants  was  greatest  at mid-day (Van Haut and Stratmann, 1967).
12.3.2  Mode of Action
     Since  NO-'induced perturbations occur  at cellular sites within mesophyll tissue,  N02 up-
take into the  leaf  is requred.   Absorption is governed by  factors regulating gaseous exchange
                                            12-25

-------
between the atmosphere and the leaf (Nobel, 1974).   The N0? diffuses from the boundary layer--
bulk air  interface  and  terminates with extraction onto  mesophyll  cell  surfaces.   The driving
force  for NCL  uptake is a  concentration gradient  and  net movement  along this  gradient  is
impeded  by  several   leaf  resistances:   boundary layer,  stomatal  and mesophyll  (residual)
resistance.
     Rodgers et.al.  (1979)  suggested that N02 uptake  in corn  (Zea mays) and soybean (Glycine
max) was  directly  related  to stomatal resistance  in  the NO- concentration range of 0 to 1.09
mg/m3 (0.58 ppm).   Also, NO- uptake increased with light intensity through the action of light
on stomatal  resistance.   In  studies with beans (Phaseolus vulgaris) and higher NOo concentra-
tions over the  range of 0 to 13.16  mg/m3 (7 ppm), NOo uptake  was controlled more by internal
leaf  factors  (mesophyll  resistance)  than  stomatal  resistance  (Srivastava  et   al.,  1975a,
1975b); N02  uptake  was  also  reported to increase with concentration and decline with increas-
ing exposure time.   The N0? uptake rate in the dark was approximately one-half the rate in the
light.   Sunflower  (Helianthus annuus)  leaves absorbed approximately 14 percent as much NO- in
the  dark  as  in the  light (Yoneyama  et al.  ,  1979).   Even  though  NO-  uptake  in  the  dark is
lower,  N02 exposures in the dark cause greater injury (see 12.2.1).
     Nitrogen dioxide  reacts in  water to produce  nitrate,  NO, , and  nitrite  N09  in dilute
                                                               •J                  £.
solutions.  Similar  reactions would be expected  when NO-  dissolves  in  the aqueous layer sur-
rounding  leaf  mesophyll  cells.    Plants  contain  the  enzymes,  nitrate  reductase  that  reduces
nitrate to nitrite,  and nitrite reductase that  reduces  nitrite to ammonia which  can  then  be
metabolized  into  organic nitrogen  compounds.  The  nitrate reductase is induced  in  plants  by
the presence of its  substrate,  nitrate.   Zeevaart (1974) grew  plants with ammonia as the sole
nitrogen  source and showed  that  f^  exposures induced nitrate reductase  activity and enzyme
activity  increased  with NO- concentration and duration  of exposure.   Yoneyama et al.  (1979)
showed  that  exposure  to 7.52  mg/m3  (4  ppm) NO-  for  6  hours  increased  nitrite  reductase
activity from 2- to 3-fold.
     Faller (1972) grew sunflowers (Helianthus annuus) on a nitrogen free media and exposed the
plants to N02  for  three weeks at NO- concentrations  ranging from 0 to 6 mg/m3 (3.2 ppm).   The
control plants  showed severe signs of nitrogen deficiency and restricted growth.   However,  the
sypmtoms of  nitrogen  deficiency  decreased and plant growth increased as the NO- concentration
increased up to 29  percent  more than the control  levels.   Also the nitrogen  content  of  the
plants was  significantly increased by the exposure.   Results  of this  study  show  that plants
can  use  atmospheric sources  of  nitrogen  (i.e.,   NO-) as their sole  nitrogen  source.   Tomato
(Lycopersicon esculentum), sunflower  (He!ianthus  annuus),  and  corn (Zea mays) derived approx-
imately 16,  22  and 14% of their nitrogen, respectively,  from NO- when the plants were exposed
to 0.56  mg/m3  (0.3  ppm)  for 2  weeks  (Matsumaru et  al., 1979).   The absorption  rate  of NO,,,
based on  plant  dry weight,  showed little change  with soil  nutrition and ranged around approx-
imately 0.8 mg/g  dry weight/day  for tomato and sunflower to 0.3 mg/g dry weight/day for corn.
     Zeevaart (1976) grew peas (Pisum sativum) with ammonia as  the only nitrogen source.  When
exposed to NO-, nitrate and nitrite accumulated in the leaves.   At the beginning of the
                                            12-26

-------
exposures the  nitrate  to nitrite ratio was near 1, but with time, nitrite accumulated in the
leaves while nitrate did not, suggesting that nitrate was converted to another compound.   This
finding appears  to  be  related to the  induction  of nitrate reductase (Zeevaart, 1976).  Expo-
sures also  increased the soluble amino (NHj) groups in several plants and the protein content
increased by  10-20 percent.  Troiano  and  Leone (1977) reported  that  N02 exposures increased
the organic nitrogen content of tomato plants (Lycopersicon esculentum).
     Matsushima  (1972)  found  that exposure to 75.2 mg/m3 (40 ppm) N09 for 16 hours stimulated
                                    14
amino acid  synthesis (indicated  by   C labeling)  although  there  was little change in organic
acid  synthesis.   Using  very  high concentrations  of    NOo (0.01-5  percent  by  volume) Durmi-
shidze and  Nutzsubidze  (1976)  showed that 10 species of decidious trees, 5 species of grasses
and 5 species  of coniferous trees readily assimilated isotopically-labeled   N02 and incorpo-
rated it  into amino acids.   Spinach  (Spinacia  oleracea) was  exposed  to 7.52  mg/m3  (4  ppm)
  N02 for 2.5 hours to  determine the metabolic fate of the nitrogen from the N0? (Yoneyama and
Sasakawa, 1979).   Isotopically  labeled nitrogen was  incorporated  into  both amino acids  and
amides  in  a   pattern  suggesting  that the  nitrogen  was assimilated  through   the  glutamine
sythethase/glutamate synthase pathway.  Rogers  et al.  (1979) reported that the  plants accumu-
lated isotopically  labeled  nitrogen proportional  to  the ambient  NOp concentration  over  at
range of 0.19 to 0.75 mg/m3 (0.1 to 0.4 ppm).   Following a 3-hour exposure to 0.60 mg/m3  (0.32
ppm)  N02,  over  97%  of  the absorbed    N02 was  incorporated into  reduced nitrogen compounds.
However, the majority of this  nitrogen remained  in  foliage, with only 3-5% being exported to
the roots.
     When plants  are exposed to  high  levels  of NOp  the injured leaves  frequently exhibit a
waxy  or  water-soaked appearance  prior to necrosis.   This suggests that  cell  membranes  were
disrupted, possibly beyond  repair.   Berge  (1963) suggested that  N0« may cause  cellular  plas-
molysis  implying  damage to cellular  membranes.   He  also noted  a  decline  in  starch grains.
     Felmeister and colleagues (1970) discussed the propensity  of NO- to attach  to lipid  mono-
layers,  especially  those monolayers  containing  unsaturated lipids.   These  lipids  have  been
proposed  to  be components  of  biological   membranes.   The work of Estefan et al.  (1970)  sug-
gested that the  products of NO* action on lipid m'onolayers included both transient and stable
free  radicals.   Because  of the  high  concentrations  used  in their  experiments, it is  not
apparent that a similar response would occur at ambient concentrations.
     Well burn  et  al.  (1972) studied  the   effects  of  NOg  exposures  on the  ultrastructure of
chloroplasts i_n  vivo.   Broad  bean (Vicia  faba) plants were exposed for 1 hour to 1.9, 3.8, or
5.6 mg/m3 (1.0,  2.0, or 3.0 ppm).  The leaves were harvested  immediately after exposure  and
prepared  for  electron  microscopy.  Examination  of  the chloroplasts showed  that  N0?  caused a
swelling of the  thylakoids  associated with the stroma.  These  swellings  appeared to be rever-
sible since  thylakoid  swelling  was not observed in chloroplasts of leaves  exposed to unpol-
luted air immediately following  NO 2 fumigation.
     Kandler and Ullrich  (1964)  demonstrated  that there  was a reduced amount of carotene and
chlorophyll  in leaves after actue NO^ exposure.   Some species of lichens  exposed to 3.76  mg/m3
                                            12-27

-------
(2.0 ppm) N02  for  6 hours had reduced chlorophyll content; a dose of 7.52 mg/m3 (4.0 ppm) N02
for 6  hours reduced chlorophyll content  even  further (Nash, 1976)..  In  contrast,  Taylor and
Eaton  (1966)  found  that chlorophyll  content  increased following  chronic exposures to  NO-.
Similarly,  Horsman  and Wellburn (1975)  found that 0.188  to 1.88 mg/m3  (0.1 to  1.0  ppm) N02
applied to  pea  (Pisum  sativum)  seedlings increased their chlorophyll content 5 to 10 percent.
They also noted  the deeper green color and  downward  curving of the leaves observed by  Taylor
and Eaton (1966).
     hi vivo experiments  performed  by Hill  and Bennett (1970) showed that both NO and NO- in-
hibited apparent photosynthesis  of  oat (Avena sativa) and alfalfa (Medicago sativa) plants at
concentrations  below those  that  cause foliar lesions.  The threshold dose for this inhibition
was 0.74 mg/m3  (0.6 ppm) for NO and 1.13 mg/m3 (0.6 ppm) for N02 in 90 minute fumigations, but
the inhibition occurred  faster  for NO than N09.   The NO -induced inhibition of photosynthesis
                                              C.         A
was not  permanent.   The  rate  of recovery  for a given NOinduced inhibition  level  was  faster
than for NO,,.   Recovery from NO-inhibited photosynthesis was generally complete within 1 hour.
Full recovery from  NO,,-induced  inhibition of more than 25 percent required more than 4  hours.
However,  complete  recovery of non-foliar  injured plants was noted  consistently  within  1 day
following fumigation.   In fumigations  introducing both NO and N02  (1:1) simultaneously, the
degree  of  inhibition of  apparent  photosynthesis was the  same  as the sum of that  induced by
each pollutant  when introduced separately.
     Capron and  Mansfield  (1976)   found  a  reduction in  the photosynthetic  rate  of  tomato
(Lycopersicon  esculentum) plants exposed  to 0.47 mg/m3  (0.25 ppm)  N02,  0.31 mg/m3 (0.25 ppm)
NO or higher concentrations over a  20-hour period.  The effect of the two gases in combination
was an  additive  inhibition  of photosynthesis.   Srivastava  et al.  (1975a) studied the effects
of N02  on the  gas  exchange of the  primary leaves of bean (Phaseolus vulgaris).   Apparent pho-
tosynthesis and  dark respiration were  both  inhibited by N02 concentrations  between  1.88 and
13.5 mg/m3  (1  and  7 ppm).  The degree  of  inhibition  increased with increasing N0? concentra-
tion and exposure time.   In exposures to N02, transpiration rate was effected less than  photo-
synthesis or respiration.   Hence,  it was proposed  that  the principal effects  of  N02 on leaf
gas exchange occurred  in the  leaf  mesophyll cells  and  not on the stomata  (Hill  and Bennett,
1970;  Srivastava et al., 1975a).
12.3.3  Visible Symptoms of NO, Injury
     No one visual  symptom  or set  of  symptoms  reliably  indicates plant exposure to N02>   The
diagnosis of injury resulting  from N02 is often  difficult (Applied Science Associates, Inc.,
1976;  Taylor and Maclean,  1970).   The injury pattern may vary within a species, cultivar, age
of leaf, season of year, and/or pollutant dose.
     Acute  foliar  marking produced  by high concentrations of nitrogen  dioxide exposures are
characterized  by water-soaked  lesions which appear first  on  the  upper  leaf surface, followed
by rapid  tissue  collapse.   With time these lesions extend through the leaf and produce  small,
irregular necrotic patches.   Necrotic areas are usually white to tan or brown and resemble S0?-
induced symptoms.  Lesions occur between the veins of all sensitive plants, and may be
                                            12-28

-------
located anywhere on a leaf surface, but they are most prominent at the apex along the margins.
In monocots,  acute  N0«  exposures most often  result  in  yellow to ivory to white necrosis that
begins at  or  just  below the tips  of  the  leaf blades.  Necrotic margins  and  striped necrotic
lesions between the veins also occur.   In most grains and grasses,  injury from acute exposures
affects the entire width of the leaf blade.
     In conifers,  acute N0? injury usually  begins  at the needle tips  and  progresses towards
the base.    The  boundary between healthy and  injured  tissues  is sharply delineated by a brown
or red-brown  band.   Young emerging needles show N0_ injury at the tips, whereas older needles
may develop necrosis in  the  central   or  basal  portions of the  needles.   Injured  needles  may
drop prematurely.
     Chlorosis  is one symptom  of chronic NC^ exposure but is nonspecific and can be a symptom
of injury  caused by other pollutants.  For many chronic exposures,  chlorosis precedes the  ap-
pearance of chronic lesions.   Cereal,  grains, and corn leaves often develop longitudinal chlo-
rotic bands before necrosis develops.   In monocots,  chlorosis may occur as transition zones be-
tween healthy tissue and the necrotic  tips.   In some broad leaf plants, chlorosis from chronic
N02 exposures begins with many small yellow-green areas  on the leaf surface which may merge as
exposure continues.   In some  species,  chlorosis may be  concentrated  near the  leaf margins.
12.3.4  Dose Response
     Exposures  to most  pollutants,  including NO ,  are usually classified arbitrarily as acute
or chronic.   In experimental  fumigations,  acute exposures are  of  short duration at high pol-
lutant concentrations.   Chronic  exposures  are for longer periods (usually intermittent, occa-
sionally continuous) at  low concentrations.   The ranges  of concentrations and durations of  ex-
posure (doses)  for  acute  and  chronic  exposures  have  not  been defined.  Most botanic investi-
gators would designate  NO^ exposures of 3 to 5 mg/m3 (1.6 to 2.66 ppm) or greater for up to 48
hours as  acute  and  those  for  longer  periods at lower concentrations as  chronic.   However,
these definitions do not  apply in the field  near sources of NO  emissions.   There,  an acute
exposure is  any single exposure  causing plant  injury.   The  term  "chronic"   is applied to a
series of  exposures  that  result in injury where no  single  exposure has  an effect  by itself.
12.3.4.1  Foliar Injury-Thomas (1952) observed that leaves  of plants growing near  nitric acid
factories  often  had brown and  black spots near the leaf  margins.  This was an early indication
that oxides of  nitrogen may  be phototoxic.   Haagen-Smit (1951) was  one of the first to recog-
nize the importance of  N02 in  causing  photochemical  smog effects on  vegetation.  He found that
N02 added  to  experimental fumigation  mixtures  caused plant  injury  similar to that  caused by
ozone, but  he provided  no information on the direct effects on plants.  Subsequently, Haagen-
Smit et al.  (1952) tested N0~  at 0.75 mg/m3 (0.4  ppm)  on  5 species  but observed  no injury.
Middleton   (1958),  Middleton et  al.  (1958) and Thomas (1961)  all  recognized that N02 appeared
in photochemically  polluted  atmospheres  as  a by-product of  combustion, but they  postulated
that levels were and would continue to be too low to cause vegetation injury.
     Korth et al.   (1964)  found that beans (Phaselous vulgaris), tobacco  (Nicotiana tobacum),
and petunia  (Petunia multiflora)  were  not injured by  1.88  mg/m3  (1.0 ppm)  N02 for  2 hours.
                                            12-29

-------
Middleton et al.  (1958)  suggested that 5.64-7.52 mg/m3  (3-4  ppm) for 8 hours was a threshold
concentration  that  could  cause  visible  injury  on  pinto  bean  (Phaseolus  vulgaris)  leaves.
     Czech and Nothdurft (1952) fumigated agricultural  and horticultural crops with N02 in the
laboratory and  in small  greenhouses.   Rape (Brassica napus),  wheat  (Triticum  satuvim),  oats
(Avena sativa), peas (Pisum sp_.),  potatoes (Solanum tuberosum), and beans (Phaseolus vulgaris)
showed little or.no injury from 56.4 mg/m3 (30 ppm) NCL for 1 hour.  Alfalfa (Medicago sativa),
sugar beets  (Beta  vulgaris),  winter rye (Secale cereale), and lettuce (Lactuca sativa) showed
some  effects.   Fujiwara  (1973)  reported  that  37.6-94  mg/m3  (20-50 ppm)  NO   for 30 to  60
minutes injured most plants studied.
     Heck (1964)  fumigated cotton (Gossypium hirsutum),  pinto  beans  (Phaseolus  vulgaris) and
endive (Cicorium  endivia) under  controlled conditions with  1.88 mg/m3 (1.0 ppm)  N02  for  48
hours and observed  slight but definite spotting  of  leaves.   There was  no  injury produced  at
1.88 mg/m3 (1.0 ppm) N02 for 12 hours.   In another study, the same species were fumigated  with
0.94, 3.76  and 6.58 mg/m3  (0.5,  2.0,  and 3.5 ppm) N02  for  21  hours.  At  exposures  of  6.58
mg/m3  (3.5  ppm)  N02  mild  necrotic spots  appeared  on cotton  (Gossypium hirsutum)  and  bean
(Phaseolus vulgaris) leaves and the endive leaves (Cicorium endivia) were completely necrotic.
     Taylor and Cardiff  (unpublished  data,  cited in Taylor et al.,  1975) exposed field crops
to N02 in sunlight  chambers.   They found that  several  field  crops exposed to 18.88 mg/m3 (10
ppm) N02 for 90 minutes suffered little or  no  injury;  but in tomato, a 90-rninute exposure  to
28.20 mg/m3  (15 ppm)  increased the extent  of  injury  by  90 percent.   They  concluded  that the
injury threshold  for several  field crops would be 18.80 to 28.20 mg/m3 (10 to 15 ppm) N02 for
90 minutes.
     Maclean et  al.  (1968) exposed 14  ornamental  and  6 citrus  species  to  N02  concentrations
ranging from 18.8  to 470 mg/m3 (10 to  250  ppm) for 0.2 to 8 hours.   Necrosis occurred in the
citrus species  when the  leaves were exposed  to 376 mg/m3 (200  ppm)  for 4 to 8  hours  or 470
mg/m3 (250 ppm) for 1  hour.   Nonspecific marginal and intercostal necrosis developed within 1
hour after exposure.  Young citrus leaves wilted and abscised at some lower doses.
     Heck and Tingey (1979)  conducted  a series of  short  term fumigations which exposed field
and vegetable crops to  various N02 concentrations.  In  one  experiment 10 field and vegetable
species were exposed to  15.04, 30.08,  or 60.16 mg/m3 (8, 16,  or 32 ppm) N02 for 1 hour (Table
12-5).  At 60.16  mg/m3  (32 ppm) levels of NO,,, all species showed visual injury.   However,  at
15.04 mg/m3  (8  ppm)  N02 exposure, only brome  grass  (Bromus  inermis) and tomato (Lycopersicon
esculentum)   exhibited  foliar  injury.    In  a second  experiment, 22 crop species  were  given 9
different time  and  concentrations treatments.   Exposure durations varied  from  0.5 to 7 hours
and N02 concentrations  ranged from 3.76 to 37.6  mg/m3  (2-20  ppm) (Table 12-6).   An important
conclusion from  these  experiments  was  that the  extent  of  injury was  greatest  when  the N02
levels were  high, even  for  short  time periods.  . For  example, cotton  exposed  28.2 mg/m3 (15
ppm) for 1-hour had an  injury rate of  27  percent for the three  most sensitive leaves.  When
cotton was  exposed to  18.8  mg/m3 (10 ppm) N02  for  2-hours  the  comparable  injury  rate was 2
percent.   Therefore dose is not always a good predictor of injury.
                                            12-30

-------
               TABLE 12-5.  ACUTE INJURY TO SELECTED CROPS AFTER A
           1-HOUR EXPOSURE TO NITROGEN DIOXIDE (HECK AND TINGEY, 1979)
Plants .
(Common, Cultivar, Scientific)
Tomato, Roma
(Lycopersicon esculentum)
Wheat, Wellsc
(Triticum durum)
Soybean, Scott
(Glycine max)
Tobacco, Bel W,5
(Nicotiana tabacum)
Bromegrass, Sac Smooth
(Bromus inermis)
Swiss Chard, Fordhook Giant0
(Beta vulgaris cicla)
Tobacco, White Goldb
(Nicotiana tabacum)
Cotton, Acala 4-42c
(Gossypium hirsutum)
Beet, Perfected Detroit0
(Beta vulgaris)
Orchard Grass, Potomac0
(Dactylis glomerata)
Tobacco, Bel W3°

8 ppm
1

0

0

0

2

0

0

0

0

0

0
Injury Index
16 ppm
48

47

26

23

17

11

1

0

0

1

0

32 ppm
100

90

100

97

97

62

70

54

36

18

5
aPlants were exposed in Cincinnati,  Ohio.

 Plants were exposed in August with  light  intensity at 2200 ft-c,
     temperature 28°C,  humidity 75 percent.

    its were exposed in January with light
     temperature 21°C,  humidity 70 percent.
°Plants were exposed in January with light intensity at 1400 ft-c,
 Scientific name is  given only when plant is  first listed.
                                   12-31

-------
              TABLE 12-6.   PERCENT LEAF AREA INJURED BY DESIGNATED DOSAGE OF NITROGEN DIOXIDE  (HECK AND  TINGEY,  1979)
K>

U>
Plants
(Common, Cultivar, Scientific)
Oats, Clintland 64
(Avena sativa)
Radish, Cherry Belle
(Raphanus sativus)
Bromegrass, Sac Smooth
Begonia- Thousand Wonders*
White , (Begonia Rex)
Chrysanthemum, Oregon *
(Chrysanthemum sp.)
Sultana, White Imp *
(Impatiens sultani)
Oats, 329-80b
(Avena sativa)
Cotton, Paymaster
(Gossypium hirsutum)
Wheat, Wells
Cotton, Acala 4-42
Periwinkle, Bright Eyes *
(Vinca minor)
Dosage (ppm x hr) 2. 5
(ppm) 5
(hr) 0.5
0

0

0
0
1

0

2

0

3
0
0

4
4
1
0

0

0
1
1

0

2

0

2
0
0

6
3
2
0

0

0
0
1

0

1

6

1
0
0

10
20
0.5
80

95

69
26
34

51

32

50

31
28
13

14
7
2
2

0

0
0
0

0

1

0

3
0
0

15
15
1
84

90

50
35
41

26

18

27

34
28
20

20
5
4
0

1

1
4
4

0

9

2

3
0
1

20
10
2
39

31

26
49
25

24

14

2

2
1
23

35
5
7
21

2

0
5
1

0

14

1

1
I
I

         Oats, Pendekc
           (Avena sativa)
0    39

-------
                                                          TABLE 12-6 (continued)
I
OJ
u>
Plants
(Common, Cultivar, Scientific)
Broccoli, Calabreese
(Brassica oleracea botrytis)
Tobacco, Bel B
(Nicotiana tabacum)
Tobacco, White Gold
Tobacco, Bel VL
Tobacco, Burley 21
(Nicotiana tabacum)
Corn, Pioneer 509-W
(Zea mays)
Corn, Golden Cross
(Zea mays)
Azalea, Alaska * .
(Rhododendron, sp.)
Sorghum, Martin
(Sorghum, sp. )
Cucumber, Long Marketer
(Cucumis sativus)

Dosage (ppm x hr) 2.5
(ppm) 5
(hr) 0.5
0

0

0
0
0

1

0

0

0

0

4
4
1
0

0

0
0
0

0

0

0

0

0

6
3
2
0

3

I
6
0

0

0

0

0

0

10
20
0.5
19

18

18
15
8

1

0

0

0

0

14
7
2
0

0

0
0
0

0

0

0

0

0

15
15
1
21

17

6
2
0

1

0

1

0

0

20
5
4
0

0

0
0
0

0

0

0

0

0

20
10
2
0

0

0
0
0

0

0

0

0

0

35
5
7
0

0

0
0
0

0

2

0

0

0

         Plants were exposed in Cincinnati, Ohio.  Each value is the average of 4 replicate plants
         except as noted.   Plants are listed in general order of sensitivity.


         Injury estimates based on the average of the three most sensitive leaves except for plants
         indicated (*) when the estimate was based on the total leaves per plant.

-------
     Heck and Tingey  (1979)  summarized the foliar injury  data  from their acute NCL exposures
using the following model:
                    C = AQ + A1I + A2/T
                    C = Concentration ppm
           A ,  A-,, Ap = constants (partial regression coefficients specific
                         for pollutant, plant species and environmental  conditions.
                    I = percent injury
                    T = Time hours

The model recognizes the separate influence of time and concentration and permits the develop-
ment of  three-dimensional  injury response surfaces.   The  model  was used to estimate  the  N02
exposure durations  and  concentrations  necessary to produce injury  on  susceptible,  intermedi-
ate, and tolerant plants at the threshold injury level (Table 12-7).
12.3.4.2  Growth—Czech and  Nothdruft  (1952) using 1-hour exposures to 1,880 mg/m4  (1000 ppm)
N02  reported  that the  fresh weight of  sugar beet (Beta vulgaris) roots were  one-third less
than that of the  control  plants.  Zahn  (1975)  summarized  the  results of chronic exposures of
10  plant  species  to  2-4  mg/m3 (1.06-2.12 ppm) N02  for  213 to 1900 hours  (Table 12-8).   The
effects ranged from  a 37  percent yield  reduction  in  endive to no effect in roses.   Exposures
to 1.13 mg/m3 (0.6 ppm) N02 for 30 days reduced the growth of buckwheat (Fagopyrum esculentum)
and  eggplant  (Solanum melongana)  (Fujiwara,  1973).    The  same  concentration for 51 days  in-
creased the yield  of rice (Oryza sativa).  Stratmann (personal  communication,  cited in Taylor
et  al.,  (1975)  showed  that  bush bean  (Phaseolus  vulgaris) growth was  slowed  by exposure to
1.88 mg/m3  (1.0 ppm)  N02  for 14  days.   He  suggested that a likely threshold  dose  for injury
would be 0.752 mg/m3 (0.4 ppm) N02 over a prolonged time period.
     Taylor and Eaton  (1966) found reduced fresh and dry weights of unifoliar leaves of pinto
bean (Phaseolus vulgaris)  plants exposed to N02 at  0.62 mg/m3  (0.33 ppm) for 10 and 19 days.
Also, leaves from  tomato  plants (Lycopersicon esculentum)  exposed  for  10 and 22 days to 0.21
to  1.17  mg/m3 (0.11 to 0.62 ppm) were usually significantly smaller than corresponding leaves
from non-fumigated  plants.   One  of  the  most  comprehensive reports on the effects  of N02 on
growth and yield is that of Spierings (1971).  Continuous exposures of tomato plants (Lycoper-
sicon esculentum) to  0.47  mg/m3 (0.25 ppm) during the entire growth period (128 days) reduced
growth of leaves,  petioles  and stems.   The  crop matured slightly earlier and there were sub-
stantial decreases  in  fresh  weight yield (22 percent), average fruit weight (12 percent),  and
the number of fruit (11 percent).  After exposures to 0.94 mg/m3 (0.5 ppm) for 10 days or 0.47
mg/m3 (0.25 ppm) for 29 days, fumigated tomato plants were taller than the controls, but stems
were smaller in diameter,  leaves were not as  large,  and the fresh weights of the plants were
less.

                                            12-34

-------
                             TABLE  12-7.   PROJECTED  N09  EXPOSURES  THAT MAY INDUCE 5 PERCENT
                            FOLIAR  INJURY  LEVELS  ON SELECTED  VEGETATION (HECK AND TINGEY, 1979)
Concentrations Producing Injury
Time (hr)

0.5
1.0
2.0
4.0
8.0
Susceptible
ppm
6-10
4-8
3-7
2-6
2-5
m3/m3
11.28-18.80
7.52-15.04
5.64-13.16
3.76-11.28
3.76- 9.40
Intermediate
ppm
9-17
7-14
6-12
5-10
4-9
m3/m3
16.92-31.96
13.16-26.32
11.18-22.56
9.40-18.80
7.52-16.92
Tolerant
ppm
> 16
> 13
> 11.
> 9
> 8
m3/m3
> 30.08
> 24.44
> 20.68
> 16.92
> 15.04
UJ
Ln
      Plant type.

-------
  TABLE 12-8.   EFFECT OF CHRONIC N02 EXPOSURES ON PLANT BROWTH AND YIELD (ZAHN,  1975)
Plant Type
                        Concentration
  Duration
of Exposure
  (hours)
Effect
Wheat
Bush Bean
    334
    639
No effect on grain yield,
but the straw yield was
reduced 12%.

Yield reduced 27%;
Some chlorosis
Endive
Carrot
Radish
Currant
Roses
European Larch
Spruce
2
4
4
2
4
2
2-3
620
357
278
213
357
537
1900
Yield reduced 37%
Yield reduced 30%;
Some chlorosis
Yield reduced 13%
Yield reduced 12%
No injury
No injury
7% decrease in linear
growth. Growth was de-
creased 17% in the year
following the exposure.
 Necrosis did not occur on any plants.
                                         12-36

-------
     Thompson et al.  (1970) exposed navel orange trees to N0? continuously for 290 days.   When
compared  to  trees exposed  to  filtered  air,  those fumigated with  N02  concentrations ranging
from  0.12 to  0.47 mg/m3  (0.06 and  0.25 ppm)  showed a  significant  increase in  fruit  drop
throughout the exposure  period  and a significant reduction both in number and weight of fruit
at  harvest.   At  Upland,  California,  ambient and  twice ambient  levels  of^ NO^ were  added to
carbon filtered  air  supplied  to navel oranges  (Citrus  sinensis)  with  no effects  on leaf drop
or yield (Thompson et al. , 1971).   Recent studies suggested that 0.47 mg/m3 (0.25  ppm) or less
of  N0_  supplied  continuously  for  8  months  will increase  leaf drop and  reduce  the  yield of
navel oranges (Citrus sinensis) Taylor et al., 1975).
     To determine  the  effects  of  NO on the growth of tomatoes (Lycopersicon esculentum),  four
different tomato cultivars  were exposed to 0.49 mg/m3  (0.4 ppm)  NO for 35 days (Anderson and
Mansfield, 1979).   In two cultivars, total  weight,  shoot weight and leaf areas  was  reduced,
however,   in  the  other cultivars,  NO stimulated plant growth.  Exposure of another tomato cul-
tivar to  0.75  mg/m3  (0.4 ppm) NO  for 19 days reduced leaf  area,  leaf  weight and stem weight
(Capron and  Mansfield,  1977).   In  the same  study,  0.19  mg/m3 (0.1 ppm) N02  had  no effect on
plant growth and  the  mixture  of 0.19 mg/m3  (0.1 ppm) N02 and 0.49 mg/m3 (0.4 ppm) NO reduced
growth to  the  same  extent  as the NO alone  (Capron and Mansfield, 1977).  Tomatoes  grown at
three levels  of  soil  nitrogen  and were exposed to a concentration range of 0 to  0.98  mg/m3
(0.8 ppm) NO.  At  harvest (50 days), total  weight,  shoot weight, and  leaf area were measured
(Anderson and Mansfield,  1979).  At  a low level  of  soil  nitrogen, NO  stimulated  plant growth
as  reflected in  all  growth  parameters.   At  a medium  level  of soil nitrogen,  plant growth was
decreased at a concentration  of 0.49 mg/m3 (0.4 ppm)  NO.   At the high  level  of soil nitrogen,
all levels of NO  depressed plant growth.
     Because of  the  inter-relationship between  concentration  and time,  there is no  single
threshold dose for an effect.   Maclean  (1975) summarized the literature to illustrate the re-
lationship between NO,,  concentration and  duration  of  exposure  (dose) for various  effects
(Figure 12-4).   Three  threshold curves  are shown in Figure 12-5.   These are  approximate  esti-
mates, as  reported in  the  literature,   based on various  responses of many plant  species,  to
acute and chronic  N02  doses.   The  threshold curve  for  N02 doses that result in  the  death of
plants is short because it is  based on limited information.   N0? doses  approaching this thresh-
old  result in  complete defoliation of some  species but  are not  lethal.   The  threshold  curve
for  leaf  injury  is based  on  observations at many  NOp  doses.   The shift  in  leaf  injury  from
necrosis   to  chlorosis for  N02  doses along  this curve generally occurred between  10  and 100
hours.   Because no measurable effects have been reported for NOo doses  below  the  lower curve,
it can be considered  as the threshold for metabolic and growth effects.   N02  doses in  the  area
between this  curve and the threshold  curve for leaf injury are those that do  not injure leaves
but often result  in  growth  suppression  or effects on  photosynthesis or other  plant processes.
     These thresholds  (Figure 12-5),  assuming that they are  reasonable  estimates  for vegeta-
tion in general,  can  serve as  points  of  reference to evaluate air quality standards for N02 in
                                            12-37

-------
    1000
     100
                      O'
ID
•o
IT

V)
O
Q.
X
           o'     o'
10
     1.0
                               Fo
                  _l	
                   1.0                10

                         NO-, ppm
                                             H
                                             o
                                               o1
                                            c.O
                                                            100
Figure 12-4. Summary of effects of NC>2 on vegetation. The points
describe a dosage line above which injury was detected (Jordan, 1969).
individual points were taken from the following references: (A) Mid-
dleton et al., 1958; (B) Hill et al.r 1974; (C) Czech and Northdurft,
1952;  (D) H. Strattman (in Taylor et al., 1975); (E) Heck, 1964;
(F) Taylor and Eaton, 1966; (G) Thompson et al., 1970;  and (H)
Matsushima, 1971.
                                l?-38

-------
 Q.
 a

z"
u
z
o
o
                              DAYS



          ,0.01       0.1       1.0       10        100
    1000
100
      10
     1.0
     0.1
                     DEATH
      METABOLI
             II
                              THRESHOLD FOR

                              FOLIAR LESIONS
  0.1       1.0        10       100       1000



             DURATION OF EXPOSURE, hours
                                                         1000
                                                     100
                                                         10
                                                         1.0
                                                      10,000
"o>


z"
o
o
z
o
o
 CNI
O
 Figure 12-5.  Threshold curves for the death of plants, foliar lesions,

 and metabolic or growth effects as related to the nitrogen dioxide

 concentration and the duration of exposure (MacLean, 1975).
                              12-39

-------
the atmosphere in the  absence  of other gases and  they  can be viewed with respect to N02  con-
centrations that  occur in the atmosphere.
12.3.5  Effects of Gas Mixtures on Plants
     Mixtures of dissimilar  pollutants  often  occur in nature.   A typical  combination includes
NOp with sulfur  dioxide  (SOp)  and/or ozone (03).   Reinert  et al.  (1975)  reviewed information
on these types of  pollutant  combinations.   Earlier the  assumption was made that NO  at normal
atmospheric concentrations was  important only on the basis of its participation in the photo-
chemical oxidant reactions.  However,  based on  studies  in which plants were exposed to combi-
nations of pollutants  including NOp  it now appears that ambient concentrations of NQ2 in  con-
junction with  other  pollutants may  have  a direct  effect  on plants.  The results  of these
studies are described.
12.3.5.1   Nitrogen Dioxide and  Sulfur Dioxide—To  determine the impact of  ambient air pollu-
tion on vegetation,  NCL and SOp have  been  evaluated for  their combined effects.
     Tingey et al.  (1971) found that  neither 3.76 mg/m3  (2.0 ppm) NOp nor  1.31 .mg/m3 (0.5  ppm)
SOp alone  caused  foliar  injury.  However,  a  mixture  of  0.188 mg/m3 (0.10  ppm)  NOp  and 0.262
mg/m3  (0.10  ppm)  SOp  administered for 4 hours  caused foliar injury to pinto  bean (Phaseolus
vulgaris),  radish (Raphanus sativus), soybean (Glycine max), tomato (Lycopersicon esculentum),
oat (Avena sativa) and tobacco (Nicotiana  tabacum).  Exposure to 0.282 mg/m3 (0.15 ppm) NOp"in
combination with 0.262 mg/m3  (0.1 ppm) SOp for  4-hours  caused greater foliar injury.  Traces
of foliar  injury were  observed at 0.094 mg/m3  (0.05  ppm) NOp and 0.131 mg/m3 (0.05 ppm)  SOp.
     Matsushima  (1971)  observed more leaf  injury  on  several  plant species from  a mixture  of
NOp and SOp  than  that caused by  each pollutant  alone.   He also tested different sequences  of
exposure.   When NOp exposure  preceded  SOp, the  degree of injury was similar to that resulting
from individual exposures to either gas.   But when SOp exposure was followed by NOp the degree
of leaf  injury increase  as  would be  typical of  simultaneous  exposures  to  both pollutants.
Fujiwara et  al.  (1973)  found greater-than-additive effects when peas (Pisum sativum) were ex-
posed to 0.188 mg/m3  (0.1 ppm) N02 in  combination with  0.262 mg/m3 (0.1 ppm)  S02-  When 0.376
mg/m3 NOp  and  0.524 mg/m3 SOp  (0.2 ppm of each  gas) were used, the effect was only additive.
     When  a  large number of  desert species were exposed  to either SOp or combinations of SOp
and NOp (ratio approximately  4:1) injury  from SOp and mixtures of SOp + NOp was similar (Hill
et al.,  1974).   N02  decreased the foliar  injury  threshold of  S02  on tomatoes (Lycopersicon
esculentum),  geranium  (Pelargonium S£.), and  petunia (Petunia s^.) (de Cormis and Luttringer,
1976).   Exposure to 0.79 mg/m3 (0.3  ppm)   S02 caused  no foliar injury but the same concentra-
tion of S02  in conjunction with 0.94 mg/m3 (0.5 ppm) N02 caused  foliar  injury.   Injury  from
the gas mixture increased with increasing  humidity.
     Observations in  the vicinity of an arsenal  emitting low concentrations  of  both N02 and
SOp found  foliar  injury  on several conifer species which was attributed to the interaction  of
the 2 gases (Skelly et al., 1972).  The maximum  observed 1-hour concentration of NO  was 0.585

                                            12-40

-------
  ppm and 2-hour maximum  for  SQp was 0.670 ppm.   Effects on growth rate of two tree species was
  correlated with  production  activities at  the  arsenal  over a 30-year period  suggesting  that
  mixtures of NOp and SOp  may  reduce plant  growth (Stone and Skelly, 1974).
       Bennett et  al.  (1975)  studied  the  effects of  NOp and SOp mixtures on  radish  (Raphanus
  sativus),  swiss chard (Beta vulgaris). oats (Avena sativa) and  peas  (Pisum sativum).   Treat-
  ments consisted of 1- and 3-hour fumigations with the  pollutants separately and with  SOp and
  N02 (1:1) mixtures in concentrations  ranging from  0.33-2.62 mg/m3 S02 and 0.23-1.88  mg/m3 N02
  (0.125 to 1.0  ppm).  No visible injury occurred on experimental  plants treated with  NO- alone
  or from exposures  to S02  concentrations  of  less than  or equal  to 1.31 mg/m3  (0.5 ppm).   The
  minimum exposure doses which caused visible injury  to radish leaves were  1-hour exposures  to a
  mixture of 0.94 mg/m3  N02 and  1.31 mg/m3  S02 (0.5 ppm of each  gas) or  to  1.95 mg/m3 (0.75  ppm)
  SOp alone.  The  data indicated that S0?  and NOp in  combination  may enhance the phytotoxicity
  of these pollutants, but relatively high  doses  were required to  cause  injury.
       Reinert et  al.  (1975)  summarized the  effects  of gas mixtures  on  foliar  injuries  to a
  number of crops  (Table  12-9).   The data indicate  that ambient  concentrations of NOp  and SO,,
  may interact to injure vegetation.
       A  study  was  conducted to determine  the  effects  of  low concentrations  of N02  and  S02
  singly and in  combination on  the growth  of  four grass  species  (Ashenden,  1979a; Ashenden and
  Mansfield, 1978;  Ashenden and Williams,  1980).  Plants  were  grown and exposed  in four  small
  greenhouses  which received either charcoal  filtered air, 0.21  mg/m3 (0.11  ppm)  N02, 0.29 mg/m3
  (0.11 ppm) SOp or  a mixture of both gases  at  these'same concentrations.   The  plants were ex-
  posed for  103.5  hours   per  week,  which  resulted in  weekly mean concentrations  of 0.13 mg/m3
..; (0.068 ppm)  N02 and 0.18 mg/m3 (0.068  ppm)  S02.   The  plants were  harvested, monthly and  various
•growth parameters  were  measured.   The  results of  the experiments  are  summarized  in Table
,.. 12-10.   Nitrogen  dioxide significantly reduced  growth parameters  of orchard  grass and Kentucky
  bluegrass, but had no effect  or slightly stimulatory effect on  the growth of Italian ryegrass
  and timothy.   However, growth  parameters  of all  the species were  reduced  by  S02-   The combina-
  tion of N02  and S02 significantly reduced the growth  parameters  of all  species  tested and  many
  of the effects  were determined to be synergistic.   These data  were collected during the winter
  when the plants were in  a period of slow  growth which may have increased  the pollutant's toxi-
  city.   However, the data clearly show  that  intermittent exposures to ambient concentrations of
  NOp and SOp singly and  in combination can  significantly depress  yield parameters of  important
  forage grasses.
       Alfalfa (Medicago sativa) exhibited  a  greater-than-additive  response,  i.e.,  a greater in-
  hibition of apparent photosynthesis (COp uptake) when NOp and SOp were applied together for 2
  hours at 0.47 mg/m3 (0.25 ppm) and 0.655  mg/m3  (0.25  ppm) S02  (White et al., 1974).   A  mixture
  of 0.282 mg/m3 (0.15 ppm) N02 and 0.393  mg/m3  (0.15  ppm) S02 for 2-hours  decreased apparent
  photosynthesis  7 percent more  than when  the total  of the two  gases was applied independently.
  At higher concentrations, 0.5  ppm  of each  gas, the effects were  not greater-than-additive.
                                              12-41

-------
                                          TABLE 12-9.   PLANT RESPONSE TO SULFUR DIOXIDE AND NITROGEN DIOXIDE MIXTURES
                                       (TINGEY ET AL.,  1971; MATSUSHIMA, 1971; BENNETT ET AL.,  1975; HILL ET AL., 1974)
 i
j>
NJ
Plant Species
Avena sativa L.
Beta vulgaris var. cicla L.
Lathyrus odoratus L.
Raphanus sativus L.
A. sativa
R. sativus
Phaseolus vulgaris L.
R sativus
Nicotiana tabacum L.
Orzopsis hymendoides (R&S) Ricker
Populus tremuloides Michx.
Sphaeralcea munroana Spach.
P. vulgaris
Lycopersicon esculentum Mill.
Cucumis sativus L.
A. sativa
Capsicum frutescens L.
P. vulgaris Pinto
A. sativa
R. sativus
Glycine max (L. ) Merr.
N. tabacum
L. esculentum
Exposure
Chamber '
CE
CE
CE
CE
CE
CE
CE
CE
GH
F
F
F





GH
GH
GH
GH
GH
GH
S0,/N0,
(fom)
0.75/0.75
0.75/0.75
0.75/0.75
0.75/0.75
0.15-0.25/0.1-0.2
0.15-0.25/0.1-0.2
0.15-0.25/0.1-0.2
0.5/0.5
0.1/0.1
0.5-0.7/0.15-0.21
0.5-0.7/0.15-0.21
0.5-0.7/0.15-0.21
1.5/15
2.3/13
2.3/12
2.4/13
2.4/15
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
Exposure
duration
(hours)
1 or 3
1 or 3 .
1 or 3
1 or 3
4
4
4
1 or 3
4
2
2
2
1.17
1 -
0.67
1
1
4
4
4
4
4
4
Plant
Response
(% injury)
0-5
0-5
0-5
5-8
0
0
0
0-5
0-10
16
1
31
70-75
35-85
50-100
40-75
10-58
0-24
0-27
0-27
0-35
0-18
0-17
Mixture.
Response '
-t-
+
+
+
*
*
*
+
+
0
0
0
+
+
+
-
+
+
+
+
+
+
+
Plant
Age
(weeks)
4-5
1-5
4-5
4-5
2-3
2-3
2-3
4-5
7-8
A
A
A
3-4
3-5
3-4
3-4
5-6
3-4
3-4
3-4
3-4
7-8
5-6
         aCE, Control environment; GH, greenhouse; F, field.


          +, Greater than additive; 0, additive; -, less than additive.


         c* Not defined.

-------
       TABLE 12-10.   THE EFFECTS OF NO- AND  S02 -SINGULARLY AND IN COMBINATION ON  THE GROWTH OF  SEVERAL GRASSES1
                 (Ashenden, 1979a;  Ashenden and Mansfield,  1978; Ashenden and Williams, 1980)
to
I

Response
Leaf Area



Number of Tillers



Dry Weight
green leaves


Dry Weight
dead leaves
and stubble

Dry Weight
roots


2
Species
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Pollutant3
N02
21
17
1+
30+
1
9
17
6
7
29*
10
14+
46*
27*
5
12
11
47*
35+
1+
so2
5
28*
22
11
10
27*
23*
33*
28*
39*
28*
25*
52*
37*
3+
47*
37*
54*
7+
58*
N02 + S02
72*
84*
43*
82*
32*
61*
32*
55*
83*
88*
65*
84*
67*
57*
28*
64*
85*
91*
58*
92*
Effect Synergistic
yes
yes
yes
yes
yes
yes


yes

yes
yes




yes

yes

        Data are expressed  as  percent reductions from the control  and are derived from references 127a  and  127b.
        The exposures were  for 20 weeks (140 days).   Plants were exposed for 103.5 hr/week.   The concentrations
        of NO- and SO- during  exposure were 0.11 ppm which resulted in a weekly average concentration of  0.068
        ppm.
       f\
        The scientific names are:  Orchard grass, Dactyl is glomerata; Kentucky bludgrass, Poa pratensis;  Italian
        ryegrass, Lolium multiforum; Timothy, Phleum pratense.

        Numbers followed by +  indicate increase above the control  and *  indicates significant reductions  of the
        5% significance level  or greater.

-------
Exposures of alfalfa (Medicago sativa) to 0.62 mg/m3 (0.33 ppm) N02 and 2.62 mg/m3 (1 ppm)  S02
at an ambient C0? concentration for 1 to 3 hours reduced the photosynthetic rate approximately
50 percent  (Hou et al., 1977).  When the ambient carbon dioxide  concentration  was  increased
645 ppm, the  inhibitory  effect of N02 and  S02  on photosynthesis was only 50 percent as large
as at  ambient  C02  levels.    In  studies  with pea (Pisum sativum)  Bull  and Mansfield  (1974)
reported that  over  the  concentration range of  0-0.47  mg/m3 (0.25 ppm) NOp  and  0-0.655 mg/m3
(0.025 ppm) S02,  photosynthesis  was  inhibited.   The duration  of  exposure was  not given.   The
effect of  the two  gases  was  additive  in inhibiting  of  photosynthesis.   In  bean  (Phaseolus
vulgaris) when 0.188 mg/m3  (0.10 ppm) N02 and 0.262 mg/m3 (0.10 ppm) S02  were  applied indivi-
dually the  pollutants stimulated short-term increases in transpiration, but the combination of
N02 and S02 decreased the transpiration rate (Ashenden, 1979b).
     Horsman and Wellburn (1975) studied the effects of NO,, and S0? mixtures on several  enzyme
systems in peas  (Pisum  sativum).   Peroxidase activity was  enhanced  somewhat by S02 alone  but
not by N02>   However, 0.188 mg/m3 (0.1 ppm) N02 plus 0.524 mg/m3 (0.2 ppm) S02 for 6 days  in-
creased the  activity by 24 percent.  A  100  percent increase occurred when 0.188  mg/m3  (0.1
ppm)  N0? plus 5.24 mg/m3 (2.0 ppm) S0? was used for 6 days.   The effect was much greater-than-
additive.   The increase  in peroxidase activity was considered a typical stress  response  of  the
plant.   Similar  studies  have  shown  that  glutamate dehydrogenase activity is  stimulated as  a
greaterh-than-additive response by mixtures of N02 and S02 (Wellburn et al.,  1976).
12.3.5.2  Nitrogen Dioxide with Other PoUutants—Matsushima (1971) reported that combinations.
of N02  and 0, were  less injurious  to pepper (Capsicum furtesceans)  and  tomato  (Lycopersicon
esculentum) than similar concentrations of either gas alone.  Loblolly pine and American syca-
more  (Platanus  occidental is) were exposed to either 0.10 mg/m3 (0.05 ppm)  ozone  and/or  0.19
mg/m3  (0.10  ppm) N02 for 6  hours  per day for  25  days  and effects on injury  and  growth  were
determined.   At  this concentration N02 had  no  deletrious effects on  plant  growth  or injury.
The  combination  of  0.,  plus  N0? yielded the  same results  as the  effects of  ozone  alone.
Reinert and Gray (1977)  obtained different results using different pollutant combinations with
radish (Raphanus sativus),  pepper (Capsicum protescerus) and tomato (Lycopersicon esculentum).
They found that  N02>  S02 or 0, were less injurious when used individually than when in  combi-
nations of  N02 + S02,  NO^  +  03,  or S02 + 03-   de Cormis and Luttringer  (1976)  found  that  a
mixture of  0.31 mg/m3  (0.12 ppm) S02>  0.56 mg/m3  N02  (0.3  ppm)  and 0.2 mg/m3  (0.1 ppm) 03
caused extensive leaf necrosis in tomato (Lycopersicon esculentum) within  2 hours.
     It  is  clear from  these limited  data  that levels of  N02 generally  considered  below  the
injury threshold  may interact with  other common air pollutants to  induce  vegetation injury.
Extensive  research  is  needed  to verify  this  phenomenon under field  conditions.   It appears
that concentrations  of  N02  between  0.188 mg/m3  (0.1 ppm)  to 0.47 mg/m3  (0.25 ppm)  can cause
direct effects on vegetation in combination with certain other pollutants.
                                            12-44

-------
12.4  SUMMARY
12.4.1  Effects on Ecosystems
     Ecosystems represent  the  natural  order by which living organisms are bound to each other
and to  their  environment.   They are, therefore, essential  to  the existence of any species on
earth, including man, and as life support systems their value cannot be quantified in economic
terms.
     Ecosystems  are  important  in  the production  of food,  in  the regeneration  of  essential
nutrients as  well  as atmospheric components, in the  assimilation or  breakdown of many pollu-
tants from  the  air,  water, and  soil, and  in energy flow.   They  also  give  aesthetic  pleasure
and improve the quality of life.
     The nitrogen  cycle,  an  ecocystem function, is essential for all  life because nitrogen is
necessary in  the  formation of all  living matter.   Man  has influenced the cycling of nitrogen
by injecting  fixed nitrogen  into the environment  or  contributing other nitrogenous  compounds
which perturb the cycle.
     Human  activities have  unquestionably  increased the amounts  of nitrates  and  related com-
pounds in some  compartments  of the environment.  The effects of such  increased concentrations
of nitrogen compounds may  be beneficial  or adverse, or both.  Effects of both kinds  may occur
simultaneously, and  may  be  felt in media  or  in  ecological  compartments quite  removed from
those that initially  receive anthropogenic nitrogenous inputs.
     Assessment of the  influence of  nitrogen  oxides on ecosystems is  complicated by  several
factors.   Nitrogen oxides:   (1) react with  abiotic components of the  natural  environment as
well   as  with  individual  organisms;  (2)  react with varying  numbers of  dissimilar populations
within ecosystems; and (3) may suppress  individual  populations  and thus affect ecosystem func-
tioning.
     One function of  ecosystems is  the cycling of nutrients such as nitrogen.   Any effect,  en-
vironmental  or  biological, which interferes  with the recycling  process  could have a  deleter-
ious  effect on the total  ecosystem.
     At  the present  time  there  are insufficient  data  to  determine  the impact of  nitrogen
oxides as well  as  other  nitrogen compounds on terrestrial  plant, animal or microbial  communi-
ties.    It   is   possible,  however,   to estimate the  approximate  magnitude   of  anthropogenic
nitrogen fluxes to ecosystems,  using the limited amount of  monitoring data available  or mass
balance calculations.  Such  estimates, and  quantitative information about the  nitrogen cycle
at specific sites  in the  system under study, make  it possible  to reach some conclusions about
the possible ecological significance  of  the added  nitrogen.   In addition, where the  data base
is more extensive, as  it  is for a number  of lakes in various  stages  of eutrophication, more
quantitative dose-response relationships  can be estimated.
     A reduction in diversity within a plant community results  in a reduction in the  amount of
nutrients present so  that  growth of remaining individuals decreases.

                                            12-45

-------
     Pollutants act  as  predisposing agents  so  that disease, insect pests and  abiotic  forces
can more readily  injure  the  individual  members of  ecosystems.   The  loss of  these individuals
results in  reduction in  diversity and simplification of an ecosystem.
12.4.2  Effects on Vegetation
     Sensitivity of plants to  N02 varies with species, time of day,  light,  stage of maturity,
type of injury assayed,  soil  moisture,  and nitrogen nutrition.
     When  exposures  to  N02  alone  are  considered,  the  ambient concentrations  that  produce
measurable  injury are higher  than those that normally occur in the United States (Chapter 8).
Tomato (Lycopersicon esculentum)  plants  exposed continuously to 0.47 mg/m3  (0.25 ppm)  for 128
days were  reduced in growth  and suffered  a decreased yield  of 12  percent.   Leaf drop  and
reduced yield  occurred  in naval  oranges exposed  to 0.47  mg/m3 (0.25 ppm) continuously  for  8
months.  Pinto  beans  (Phaseolus  vulgaris),  endive  (Cicorium  endivia)  and  cotton  (Gossypium
hirsutum) exhibited slight leaf  spotting after 48  hours  of exposure to 1.88 mg/m3  (1.0 ppm).
Reduced growth in bush beans  (Phaseolus vulgaris)  was reported after  a 14-day exposure  to 1.88
mg/m3  (1.0 ppm).  Other  reports  cited no injury in beans  (Phaseolus  vulgaris),  tobacco (Nico-
tiana tabacum), or petunia (Petunia multiflora) after a 2-hour exposure of the same  concentra-
tion.
     Exceptions to this  generality,  however, have been observed.  For  example,  the growth of
Kentucky bluegrass was  significantly reduced (approximately 25 percent)  by  exposures  to 0.21
mg/m3  (0.11 ppm)  N02  for 103.5 hours per week for 20 weeks during the winter months.   Similar
exposures to other grass species generally had no  deletrious effect on plant  growth.
     Nitrogen dioxide concentrations ranging  from 0.188  to  1.88 mg/m3 (0.1 to  1.0 ppm)  in-
creased chlorophyll content  in pea  (Pisum sativum)  seedlings  from 5 to 10  percent.   The sig-
nificance of the increased chlorophyll  is unknown.  Some species of lichens,  a plant sometimes
used as an  indicator  of the  presence of phytotoxic gases, exposed to 3.96 mg/m3 (2.0 ppm) for
6 hours showed a reduced chlorophyll content.
     In contrast to the  studies cited on the effects of N02 alone, a  number of studies  on mix-
tures  of NO,, with  S02  showed that  the  N02 injury  threshold was  significantly  decreased and
that the effects  of  the two  gases  in  combination were at least additive and usually greater-
than-additive.   Concentrations  at   which  observable  injury  occurred  were  well within  the
ambient concentrations of  N02  and SO- occurring  in  some  areas of the United States.   Neither
3.96 mg/m3 (2.0  ppm)  N0? nor  1.21 mg/m3  (0.5  ppm) S02 alone caused  foliar  injury.   Research
data from  grass  species  exposed for 20 weeks  to  concentrations of 0.21 mg/m3  (0.11 ppm)  NO-
and 0.29 mg/m3  (0.11  ppm) S02 for 103.5 hours per week showed significant reductions in yield
parameters  ranging  from 30  to 90 percent  indicating that concentrations of these  two gases
occurring simultaneously can  have major deletrious effects on plant growth.
                                            12-46

-------
12.5  REFERENCES

Alexander, M.  Introduction to Soil Microbiology.  2nd  Edition.  John Wiley &  Sons,  Inc.,  New
     York, NY, 1977a.  pp. 225-330.

Alexander,  M.   Effects  of  nitrogen  oxides  on  natural  ecosystems.   I_n:   Nitrogen  Oxides.
     National Academy of Sciences, Washington, DC, 1977b.  pp.  150-158.

Allen, H. E., and J. R. Kramer, eds.  Nutrients  in Natural Waters.   New York:  John  Wiley  and
     Sons, 1971.

Anderson, L. S.,  and T. A. Mansfield.   The effects of nitric oxide pollution on  the  growth of
     tomato.  Environ.  Pollut. 20:113-121, 1979.

Applied  Science Associates  Incorporated.   Diagnosing Vegetation  Injury  Caused by Air  Pollu-
     tion.   U.S.   Environmental  Protection  Agency,   Office  of  Air  Quality  Planning   and
     Standards,  Research Triangle Park, NC, 1976.  pp.  3-22 - 3-32.

Ashenden, T. W.   The effects of long-term exposures to  S02 and  N02 pollution on  the  growth of
     Dactyl is glomerata L. and Poa pratensis L.   Environ. Pollut. 18:249-258,  1979a.

Ashenden, T. W.   Effects  of S02 and  N02  pollution on  transpiration in Phaseolus  vulgaris L.
     Environ. Pollut. 18:45-50, 1979b.

Ashenden, T. W. ,  and T.  A. Mansfield.  Extreme  pollution sensitivity of grasses when  S02  and
     N02 are present in the atmosphere together.  Nature (London) 273:142-144, 1978.

Ashenden, T.  W. ,  and  I.  A.  D.  Williams.   Growth reductions on  Lolium  multiflorum Lam.   and
     Phleum  pratense  L.  as  a  result  of S02  and N02  pollution.   Environ.   Pollut.  Ser. A
     21:131-139,  1980.

Bartholomew, W.  V.,  and F. E. Clark,  eds.  Soil  Nitrogen.  Agronomy, Vol. 10.   Madison, Wis.
     American Society of Agronomy, Inc. , 1965

Benedict, H.  M. ,  and  W.  H.  Breen.   The use  of weeds  as  a means  of evaluating vegetation
     damage  caused  by  air  pollution.   I_n:   Proceedings of the  Third  National Air  Pollution
    .Symposium,  Stanford  Research  Institute  and Others, Pasadena,  California,  April  18-20,
     1955.  National Air Pollution Symposium, Los Angeles, CA,  1955.  pp. 177-190.

Bennett, J.   H. , A.  C.  Hill, A. Soleimani,  and W. H. Edwards.  Acute effects  of combinations
     of  sulphur  dioxide and  nitrogen dioxide on plants.   Environ.  Pollut.  9:127-132, 1975.

Berge, H.  Phototoxische Immissionen.   Parey Verlag, Berlin.  1963.

Botkin,  0.  B.   The  role  of  species  interactions in  the response  of  a  forest ecosystem to
     environmental perturbation.   In:   Systems Analysis and Simulation in Ecology.  Vol.  IV.
     B. Patten,  ed.   Academic Press, Inc., New York, 1976.  p. 147-171.

Boughey, A.  S.   Fundamental Ecology.  Intext Educational Publishers, Scranton, PA, 1971.   pp.
     11-50.

Brezonick, P. L.   Nitrogen  fixation in some anoxic  lacustrine  environments.   Science  (Wash-
     ington, D.C.).  164:1277-1279, 1969.
                                            12-47

-------
Brezonik, P.  L.   Nitrogen:  sources and transformations in natural waters.   In:   Nutrients  in
     Natural  Waters.   H.  E.  Allen and J. R. Kramer, eds., John Wiley & Sons,  Inc., New York,
     NY, 1972.   pp.  1-50.

Brock,  T.  D.   Biology  of Microorganisms.   Prentice-Hall,  Englewood Cliffs,  NJ  1970.   pp.
     470-471,  485-487.

Bull, J. N. , and  T.  A.  Mansfield.   Photosynthesis  in leaves exposed to  S09 and  N09.  Nature
     (London)  250:443-444, 1974.                                            *       *•

Capron,   T.  M. ,  and T.  A.  Mansfield.    Inhibition  of net  photosynthesis  in  tomato in air
     polluted  with NO and N02-  J. Experimental Botany 27:1181-1186, 1976.

Capron,   T. M. ,  and  T.  A. Mansfield.   Inhibition of  growth in  tomato  by air polluted with
     nitrogen  oxides.  Journal Experimental Botany 28:112-116, 1977.

Chen, R.  L. ,  D.  R.  Keeney,   D.  A.  Graetz,  and A.   J.  Holding.    Dentrification  and  nitrate
     reduction  in Wisconsin lake sediments.  J. Environ. Qual. 1:158-162.   1972.

Czech,  M. , and  W.  Nothdurft.   Investigations  of  the damage to field and  horticultural crops
     by  chlorine,  nitrous  and  sulfur  dioxide  gases.    Landwirtsch.  Forsch.   4:1-36, 1952.

Daniel,   C. P.   Study of  succession  in  fields  irradiated with fast  neutron and  gamma radia-
     tion.    I_n:    Radioecology.   V.  Schultz  and  A.  W.   Klement,  eds.    Proceedings First
     National  Symposium  on Radioecology, Colorado State  University,  Fort  Collins, Colorado,
     September 10-15, 1961.   Reinhold Publ. Corp., New York,  1963.  p. 277-282.

de  Cormis,  L. ,  and  M.   Luttringer.    Effets sur les  vegetaux des pollutants de  1'atmosphere
     lorsqui'ils agissent  simultanement  ou successivement.    Pollut. Atmos.  18:119-128, 1976.

Deevey,   E. S. ,  Jr.   Biogeochemistry of lakes:   major substances.  Pages  14-20, Nutrients and
     Eutrophication.   American  Society  of  Limnology and  Oceanography  Special  Symposia  I,
     edited by G.  E. Likens.    Lawrence, Kans.:   Allen Press.  1972.

Delwiche, C.  C.   The nitrogen  cycle.  Sci.  Am.  223:137-147, 1970.

Delwiche,  C.  C.   Energy  relations  in  the global  nitrogen cycle.  Ambio 6:106-111, 1977.

Delwiche, C.  C., and Bryan, B. A.  Denitrification.   Ann. Rev. Microbiol.   30:241-262.  1976.

Dillon,   P. J. ,  and  F.  H.  Rigler.   A  simple method  for predicting the capacity of a  lake for
     development  based  on  lake  trophic  status.   J.  Fish.  Res.  Bd.  Canada.   32:1519-1531,
     1975.

Durmishidze,  S. V. ,  and N. N.  Nutsubidze.   Absorption and conversion of nitrogen dioxide  by
     higher plants.   Dokl. Biochem.   227:104-107, 1976.

Estabrook, R.   Phytoplankton ecology and  hyrrography of  Apalachicola  Bay.   M. S.   Thesis,
     Florida State University, Tallahassee.  1973.

Estefan, R. M. , E. M. Gause,  and J.  R. Rowlands.  Electron  spin  resonance and  optical  studies
     of  the interaction  between  NO, and unsaturated  lipid components.  Environ. Res.  3:62-78,
     1970.                         *
                                            12-48

-------
Faller, N. Schwefeldioxid, Schewfelwasserstoff, nitrose Case und Ammoniakals  ausschliessliche
     S-bzw.  N-Quellen  der  hgheren Pflanzen.  Z. Pflrnahr. Dung. Bodenk.   131:120-130,  1972.

Felmeister, A.,  M.  Amarat,  and N. D.  Weiner.   Interactions of gaseous air pollutants within
     egglecithin  and  phosphatidyl ethanolamine monomolecular  films.   Atmos.  Environ. 4:311,
     1970.

Fredricksen, R.  L.   Nutrient budget of a  Douglas-fir forest on an experimental watershed in
     western Oregon.   Pages  115-131,  Research on Coniferous  Forest Ecosystems--A Symposium,
     edited by  J.  F.  Franklin, L. J.  Demster, and R. H.  Waring.   Portland,  Oreg.:   Pacific
     Northwest Forest and Range Experiment Station.    1972.

Fujiwara, T.  Effects of nitrogen oxides on plants.    Kogai To Taisaku 9:253-257, 1973.

Fujiwara,  T. ,  T. Umezaea, and  H.  Ishikawa.   Effects of  mixed  air  pollutants on  vegetation.
     I.  Sulfur   dioxide,  nitrogen dioxide and  ozone interact  to  injure pea  and  spinach.
     Central Institute of Electric Power,  Rept. 72007, 1973.  12 p.

Goldman,  J.  C.    Identification of nitrogen  as  a  growth-limiting  factor in  wastewaters and
     coastal marine  waters  through  continuous culture algal  assays.   Water  Res.  10:97-104.
     1976.                                                                         ~~

Goldman, J. C.,  K. R.  Tenose, and H.  I. Stanley.   Inorganic nitrogen removal  from wastewater:
     effect on  phytoplankton growth  in coastal   marine  waters.   Science  (Washington,   D.C.)
     180:955-956, 1973.

Gosselink, J.  G., E.  P.  Odum, and R.  M. Pope.  The Value  of the Tidal Marsh.  Publication No.
     LSU-SG-74-03, Louisiana State University, Center for Wetland Resources,  Baton Rouge, LA,
     May 1974.

Haagen-Smit, A.  J.  What is  smog?   Calif.   Inst. Tech., Res. Bull. 15, 1951.

Haagen-Smit, A.  J. ,  E.  F.  Darley,  M. Zaithlin, H.  Hull, and  W.  Noble.   Investigation of
     injury to plants from  air pollution  in  the  Los  Angeles  area.   Plant  Physiol. 27:18-34.
     1952.

Heck,  W.  W.   Plant  injury  induced by  photochemical  reaction  products  of  propylene-nitrogen
     dioxide mixtures.   J.  Air Pollut.  Control Assoc.  14:255-261, 1964.

Heck, W.  W. , and D.  T.  Tingey.   Nitrogen dioxide:  Time-Concentration Model  to Predict  Acute
     Foliar Injury.   EPA-600/3-79-057, U.S.   Environmental  Protection  Agency, Corvallis, OR,
     May 1979.

Henderson, G.  S. ,  and  W.  F.  Harris.   An  ecosystem  approach to characterization  of the ni-
     trogen  cycle   in  a   deciduous   forest   watershed.     Forest    Soils   and   Forest
     Land  Management,  Proceedings  of  the  4th  North   American   Forest  Soils  Conference,
     Laval University,  Quebec,  Ontario, Canada,  August  1973.   B.  Bernier  and  C.  H.  Winget,
     eds. , Les  Presses  de 1'Universite Laval, Quebec, Ontario, Canada,  1975.   pp.   179-193.
                                            12-49

-------
Hepting, G.  H.   Damage to forests from air pollution.  J. For.  62:630-634, 1964.

Hill, A.  C. ,  and J. H.  Bennett.   Inhibition of apparent photosynthesis  by nitrogen oxides.
     Atmos.  Environ. 4:341-348, 1970.

Hill, A. C. ,  S.  Hill, C.  Lamb, and T.  W.  Barrett.  Sensitivity of native desert vegetation to
     S02 and N02 combined.   J. Air Pollut.  Control Assoc. 24:153-157, 1974.

Home, A. J.  Nitrogen  fixation—A review of  this  phenomenon as a polluting process.  Prog.
     Water Technol.  8:359-372, 1977.

Horsman,  D.  C. ,  and  A.  R.  Wellburn.   Synergistic  effect  of SO  and  N0~  polluted  air upon
     enzyme activity in pea seedlings.  Environ. Pollut. 8:123-133, 1975.

Hou,  L-Y, A. C.  Hil.l,  and A.   Soleimani.   Influence of CO,  on  the  effects of S0? and  N0? on
     alfalfa.   Environ.  Pollut. 12:7-16, 1977.            ^                      ^           .

Hutchinson, G.  E.   Nitrogen  in the biogeochemistry  of the atmosphere.   Amer. Scient. !32:178-
     195.  1944.

Hutchinson, G.  E.   The  biochemistry of the terrestrial atmosphere.  Pages  371-433, The Solar
     System:   II,  The Earth  as  a Planet,  edited by G. P.  Kuiper.   Chicago:   University of
     Chicago Press.   1954.

Hutchinson, G.  E.  A Treatise on Limnology, Vol. 1.  New York:  Wiley.   1957.

Hutchinson, G.   E.    Eutrophication:   the  scientific  background  of a  contemporary practical
     problem.   Amer. J.  Sci.  61:269-279.   1973.

Inden, T.  Reduction of nitrogen dioxide gas injury  on vegetables by light  and its mechanism.
     Nogyo oyobi  (Agr.  Hort.)  50:788-790, 1975.

Jordan,   C. F.   Recovery  of a tropical rain forest after gamma irradiation.  I_n:   Proceedings
     of  the  Second  National   Symposium  on Radioecology, U.S.  Atomic  Energy  Commission and
     Others,  Ann Arbor, Michigan,  May 15-17,  1967.   D.  J. Nelson and  F. C.  Evans,  eds. ,
     CONF-670503, U.S.  Atomic Energy Commission, Oak Ridge,  TN, 1969.  pp.  88-98.

Junge,  C.  E.   The distribution of ammonia and nitrate in  rainwater over the  United States.
     Trans. Amer. Geophys.  Union 39:241-248, 1958.

Kandler,  U. ,   and  H.  Ullrich.   Detection  of  NO, damage  to  leaves.   Naturwissenschaften
     51:518,  1964.                                 *

Kato, T. , S.  Tachibana and T.   Inden.   Studies on the Injuries of Crops by Harmful Gases under
     Covering:    Part 1, Injuries of Vegetables by Gaseous Nitrogen Dioxide  and the Conditions
     Affecting   the  Crop  Susceptibility.    Seibutsu Kenkyo  Chosetsu  (Environmental  Control
     Biology) 12:87-92.   1974a.

Kato, T. , S.  Tachibana and T.   Inden.   Studies on the Injuries of Crops by Harmful Gases Under
     Covering:    Part 2,  On  the  Mechanism  of  Crop  Injury  Due to  Gaseous Nitrogen  Dioxide.
     Siebutsu Kenkyo Chosetsu  (Environ. Control Biology) 12:103-107, 1974b.

Keeney,  D. R.   The  nitrogen cycle in the  sediment-water systems.  J. Environ. Qual.  1:15-29,
     1973.


                                            12-50

-------
Keever,  C.    Present  composition  of some  stands  of  the  former oak-chestnut  forest  in  the
     southern Blue Ridge Mountains.   Ecology  34:44-54,  1953.

Kluesener,  J.  W.  Nutrient  Transport  and  Transformation in  Lake  Wingra, Wisconsin.   Ph.D.
     Thesis,  Program  in Water  Chemistry,  University  of  Wisconsin, Madison.   1972.

Kluesener,  J. W. ,  and G.   F.  Lee,   Nutrient loading from  a  separate  strom sewer  in  Madison,
     Wisconsin.   J. Water  Pollut.  Control Fed. 46:920-936.   1974.

Korth,  M.   W. ,  A.  H.  Rose,  Jr. ,  and  R. C.  Stahman.    Effects  of hydrocarbon  to oxides  of
     nitrogen  ratios  on  irradiated  auto exhaust.   Part  1.   J.  Air  Pollut.  Control  Assoc.
     14:168-175, 1964.  .

Kress,  L.  W.  , and J. M.  Skelly.  The  interaction  of  03,  S02 and  N02  and its  effect  on  the
     growth of  two  forest tree  species.  Pages 128-152  in the Cottrell  Centennial  Symposium,
     Air  Pollution  and  its  Impact  on Agriculture.   California  State College,  Stanislaus,
     Turlock, CA, 1977.

Likens,  G.  E. ,  ed.   Nutrients and  Eutrophication.    Special  Symposia,  Volume I,  American
     Society of Limnology  and  Oceanography.    Lawrence,  Kans.:  Allen Press.  1971.

Likens. G.  E.   The  Chemistry  of Precipitation in the Central Finger Lakes  Region.  Technical
     Report  50,  Cornell  University,  Water  Resources and  Marine  Science Center,  Ithaca,  NY,
     1972.

Likens, G.  E. ,  F.  H.  Bormann,  N.  M.  Johnson, D.  W.  Fisher, and  R.  S.  Pierce.   Effects  of
     cutting  and  herbicide  treatment on nutrient budgets  in  the Hubbard  Brook Watershed -
     ecosystem.   Ecol. Monogr.  40:23-47,  1970.

MacLean,  D.  C.   Nitrogen  oxides  in the role of phytotoxic  air  pollutants.  Staub Reinhalt.
     Luft 35:205-210,  1975.

MacLean,  D.  C.   Effect of  nitrogen  oxides on vegetation.   I_n:   Nitrogen Oxides.   National
     Academy of Sciences,  Washington, DC, 1977.  pp. 197-214.

MacLean, D. C. ,  D.  C.  McCune,  L.  H.  Weinstein,  R.  H.   Mandl  and  G. N. Woodruff.   Effects  of
     acute  hydrogen fluoride and nitrogen  dioxide exposures  on  citrus and ornamental  plants
     of central  Florida.   Environ. Sci.  Technol.  2:444-449, 1968.

Matsumaru,  T. , T. Yoneyama,  T. Totsuka,  and  K.  Shiratori.   Absorption of  atmospheric  N02  by
     plants and  soils.  (I)  Quantitative estimation of  absorbed N02 in plants by  15N method.
     Soil. ci. Plant Nutr.  25:255-265,  1979.

Matsushima, J.  On  composite harm to plants by sulfurous acid gas  and  oxidant.  Sangyo Kogai
     7:218-224,  1971.

Matsushima, J.   Influence  of S02 and N02 on  assimilation of amino acids,  organic  acids,  and
     saccaroids   in  Citrus natsudaidai   seedlings.   Mie Daigaku  Nogakubu  Gakujutsu  Hokoku
     44:131-139, 1972.

McArn,  G.' E. , M.  L.  Boardman,  R.  Munn, and S.  R.  Wellings.  Relationships of pulmonary par-
     ticulates in English  sparrows to  gross air pollution.  J. Wildl.   Dis. 10:335-340,  1974.
                                            12-51

-------
McCormick, J.  F.   Changes in a  herbaceous  plant  community during a three-year period  follow
     up  exposure to  ionizing  radiation  gradients.   lr\:    Radioecology.   Proceedings  First
     National  Symposium  on  Radioecology  Colorado State  University,  Fort Collins, Colorado,
     September  10-15,  1961.   V.  Schultz  and  A.  W.   Klement,  Jr.,  eds.   Reinhold  Publishing
     Corp., New York, 1963.  pp. 271-276.

McCormick, J.  F.   Effects of ionizing  radiation  on a pine  forest.   I_n:   Proceedings of  the
     Second National Symposium on Radioecology, U.S. Atomic Energy Commission and Others,  Ann
     Arbor, Michigan, May 15-17, 1967.  D. J. Nelson and F. C. Evans, eds., CONF-670503, U.S.
     Atomic Energy Commission, Oak Ridge, TN, March 1969.  pp. 78-87.

Middlebrooks,  E.  J. ,  D.  H.   Falkenberg, and  T.  E. Maloney, eds.  Modeling the Eutrophication
     Process:   Proceedings  of  a  Symposium.   Logan,  Utah:    Utah  State  University.    1973.

Middleton, J.  T.  Clean  air essential  for good citrus.  West.  Fruit  Grower.   1:6-9,  1958.

Middleton, J.   T. ,  E.   F.  Darley,  and R.  F.  Brewer.   Damage  to  vegetation  from polluted
     atmospheres.  J. Air Pollut. Control Assoc.   8:9-15, 1958.

Miller,  P. R.   Oxidant-induced  community change  in  a mixed conifer forest.  Li:   Air  Pollu-
     tion  Damage to Vegetation.   A  symposium sponsored by  the  Division  of Agricultural  and
     Food Chemistry; 161st meeting of the American Chemical Society, Los Angeles, California,
     March 31-April  1,  1971.  J. A.  Naegale, ed.   Advances in Chemistry Series 122, American
     Chemical Society, Washington, D.C., 1973.  p. 101-117.

Miller,  P.  R. ,  and  R.  M.  Yoshiyama.   Self-ventilated chambers  of  identification  of oxidant
     damage to vegetation at remote sites.  Environ. Sci. Technol. 7:66-68, 1973.

Miller,  W.  E. ,  T.  E.  Maloney,   and  J.  C.  Greene.   Algal productivity in  49  lake waters  as
     determined by algal assays.  Water Res. 8:667-679, 1974.

Myers,  V.  B.   Nutrient  limitation  of phytoplankton  productivity  in north  Florida coastal
     systems:   technical  considerations,  spatial  patterns,  and  wind-mixing  effects.   Ph.D.
     thesis,   Dpeartment  of  Oceanography,  Florida State  University, Tallahassee, Florida.
     1977.

Nash,  T.  H.    III.    Sensitivity of  lichens to  nitrogen dioxide  fumigations.   Bryologist.
     79(1):103-106, 1976.

National  Research  Council.   Eutrophication:   Causes, Consequences, Correctives.  Proceedings
     of  a  Symposium.   Environmental  Studies Borad, National Academy of Sciences and National
     Academy of Engineering.   National Academy of Sciences, Washington, DC, 1969.

National  Research Council.   Nitrates:    An Environmental  Assessment.    National  Academy  of
     Sciences, Washington, DC, 1978.

Nobel,  P.S.   Introduction to Biophysical  Plant  Physiology.   W.H.   Freeman  and Company,  San
     Francisco.  1974.

Odum,  E.  P.   Summary.   In:   Ecological  Effects  of Nuclear War,  Proceedings  of a  Symposium,
     Ecological  Society  of  America,  Amherst,  Massachusetts,  August 1963.  G.  M.  Woodwell,
     ed. , BNL 917 (C-43), Brookhaven National Laboratory, Upton,  NY, August 1965.   pp.  69-72.

Odum,  E.  P.   Fundamentals of Ecology.  Third  Edition,  W.  B.  Saunders Co., Philadelphia,  PA,
     1971.  p.  5, 8-23.

                                            12-52

-------
Parmeter,  J.  R. ,  Jr. ,  and F.  W.  Cobb, Jr.   Long-term  impingment of aerobiology  systems  on
     plant  production  systems.   I_n:    Ecological   Systems  Approaches  to  Aerobiology.   I.
     Identification of Component Elements and  Their  Functional  Relationships.   Proceedings  of
     a Workshop Conference,  Kansas State University,  Manhattan,  Kansas, January,  6-8,  1972.
     W. S. Benninghoff and R. L. Edmonds, eds., US/IBP Aerobiology Handbook  No.  2,  University
     of Michigan, Ann Arbor, MI, 1972.

Reinert,  R.  A.,  and T.  N. Gray.   Growth of radish, tomato, and  pepper  follow-up exposure  to
     N02, S02, and 03 singly or in combination.  Hort  Sci. 12:402,  1977.

Reinert,  R.  A.,  A.  S.  Heagle, and  W.  W.   Heck.   Plant  responses to pollutant  combinations.
     In:   Responses of  Plants to Air  Pollution.  J.  B.  Mudd  and T.  T.  Kozlowski,  eds.,
     Academic Press, Inc., New York, NY, 1975.  pp.  159-177.

Rogers, H. H. , J.  C.  Campbell, and R. J. Volk.  Nitrogen-15 dioxide  uptake  and  incorporation
     by Phaseolus vulgaris (L.).   Science (Washington, D.C.) 206:333-335, 1979.

Rogers, H.  H.,  H.  E.  Jeffries, and  A. M.  Witherspoon.  Measuring  air pollutant uptake  by
     plants:   nitrogen dioxide.  J. Environ. Qual. 8:551-557, 1979.

Ryther, J.  H. ,  and  W.  M. Dunstan.   Nitrogen, phosphorus and  eutrophication in the  coastal
     marine environment.   Science  (Washington, D.C.) 171:1008-1013,  1971.

Sawyer, C. N.  Fertilization of lakes by agricultural  and urban drainage.  J.  New Engl.  Water
     Works Assoc.  61:109-127, 1947.

Sinclair, W.  A.   Polluted air:  potent new  selective force in forests.   J. For.  67:  305-309,
     1969.

Skelly,  J.  M. ,  L.  D.  Moore,  and L.   L.  Stone.   Symptom  expression of eastern  white  pine
     located near a source of oxides of nitrogen and sulfur dioxide.  Plant  Dis. Rep.  56:3-6,
     1972.

Smith,   R.  L.   Ecology  and  Field Biology.   2nd  ed.   New York,  Harper and  Row.   1974,  p.
     18-258.

Smith,  W.  H.   Air  pollution-effects  on the  structure  and function  of the temperate  forest
     ecosystem.   Environ.  Pollut.  6:111-129, 1974.

Soderlund, R. , and B. H.  Svensson.   The global nitrogen  cycle.   In:   Nitrogen, Phosphorus,
     and Sulfur — Global  Cycles:   SCOPE Report No.  7.    Ecol.  Bull .~122):23-73,  1976.

Spierings, F.  H.  F.  G.   Influence of  fumigations  with N09  on  growth and  yield  of  tomato
     plants.   Neth.  J.  Plant Pathol.   77:194-200, 1971.     *

Srivastava, H.  S., P.  A.  Jolliffe,  and V. C. Runeckles.  Inhibition of a gas  exchange  in bean
     leaves by N02_   Can.  J.  Botany.   53:466-474, 1975a.

Srivastava, H. S. ,  P. A.  Jolliffe, and V.  C.   Runeckles.  The effects of environmental  condi-
     tions on  the inhibition  of  leaf  gas  exchange by  NO,.   Can.  J.  Botany.  53: 475-482,
     1975b.                                                 L

Srivastava, H. S. ,  P. A.  Jolliffe and  V.  C.  Runeckles.   The  influence of  nitrogen  supply
     during growth  on the inhibition  of gas  exchange and visible  damage  to leaves by  N0?.
     Environ.  Pollut.  9:35-47, 1975c.                                                        i

                                            12-53

-------
Stewart, W.  D.  P.,  T.  Mague, G.  P.  Fitzgerald,  and R.  H.  Burris.   Nitrogenase activity  in
     Wisconsin lakes  of  differing degrees of eutrophication.  New Phytol.   70:497-509,  1971.

Stone, L.  L., and J. M.  Skelly.  The growth of two forest tree species adjacent  to a periodic
     source of air pollution.  Phytopathology 54:773-778, 1974.

Taylor, 0.  C.   Effects of oxidant air pollutants.   J. Occup. Med 10:485-492, 1968.

Taylor, 0.  C. ,  and  F.  M.  Eaton.   Suppression of  plant growth  by  nitrogen dioxide.    Plant
     Physiol.  41:132-135, 1966.

Taylor,  0.   C. ,   and  D.  C.  Maclean.    Nitrogen  oxides  and  the  peroxyacyl  nitrates.    In:
     Recognition  of  Air  Pollution Injury to Vegetation:   A Pictorial Atlas.  J. S. Jacobson
     and A.  C.   Hill, eds.,  Air  Pollution Control  Association,  Pittsburgh, PA,  1970.   p.
     E1-E14.

Taylor, 0.  C. ,  C.  R.  Thompson,  D. T.  Tingey,  and R. A.  Reinert.   Oxides of nitrogen.    J,n:
     Responses of Plants to Air  Pollution.  J.  B.  Mudd  and T.  T.  Kozlowski, eds., Academic
     Press, Inc., New York, NY, 1975.   pp. 121-139.

Thayer, G.  W.   Phytoplankton  production  and  the  distribution of  nutrients  in a shallow  un-
     stratified  estuarine  system  near Beaufort,  N.C.    Chesapeake  Sci.  12:240-253,   1971.

Thomas, M.  D.   Gas damage to plants.  Annu. Rev. Plant Physiol.  2:293-322,  1952.

Thomas, M.  D.   Effects  of air pollution  on  plants.   I_n:   Air Pollution.  W.H.O. Monog. Ser.
     46:233-278,  1961.

Thompson,  C.  R. ,  G.  Kats,  and  E. G.  Hensel.   Effects  of ambient  levels  of  N0?  on  navel
     oranges.   Environ.  Sci. Technol.  5:1017-1019, 1971.

Thompson, C. R. ,  E.  G.  Hensel, G. Kats, and 0.  C.  Taylor.  Effects of continuous exposure  of
     navel  oranges to NOp.  Atmos. Environ. 4:349-355, 1970.

Tingey, D.  T. ,  R.  A.  Reinert,  J.  A.   Dunning,  and W.  W.  Heck.   Vegetation injury from  the
     interaction  of N02 and S02-   Phytopathology 61:1506-1511, 1971.

Treshow, M.  The  impact of air pollutants on plant population.  Phytopathology   58:1108-1113,
     1968.

Troiano, J. J. ,  and I.  A. Leone.  Nitrogen nutrition as  it affects total  nitrogen content  of
     Nicotiana  glutinosa  plants  following  nitrogen  dioxide  fumigation.   Phytopathology
     64:587, 1974.

Troiano, J.  J.,   and  I.  A.  Leone.   Changes in  growth  rate  and nitrogen content  of tomato
     plants after exposure to N0~.  Phytopathology 67:1130-1133, 1977.

U.S. Environmental Protection Agency.   Air Quality Criteria for Nitrogen  Oxides.  AP-84, U.S.
     Environmental Protection Agency,  Washington, DC, January  1971.

Vanderhoef, L.  N.,  C.  Y.  Huang,  R.  Musil, and  J.  Williams.   Nitrogen  fixation (acetylene
     reduction)  by phytoplankton in Green Bay, Lake Michigan,  in relation to nutrient concen-
     trations.   Limnol.  Oceanogr. 19:119-125, 1974..
                                            12-54

-------
Van  Haut,  H. ,  and  H.   Stratmann.   Experimental  investigations  of  the  effects of  nitrogen
     dioxide  on plants.   Schriftenr.  LIB  Landesanst.  Immissions Bodennutzungsschutz  Landes
     Nordrhein Westfalen £7):50-70,  1967.

Vollenweider,  R.  A.   Scientific Fundamentals of the  Eutrophication  Lakes  and  Flowing Waters,
     with Particular Reference  to  Phosphorus  and Nitrogen  as  Factors  in  Eutrophication.   OECD
     Technical  Report  DAS/CSI/68.27.    Paris:    Organization  for  Economic  Cooperation  and
     Development.  1968.

Wellburn, A.  R. ,  0.  Majernik,  and  A.  M.  Wellburn.   Effects  of S02 and  N02  polluted  air upon
     the  ultrastructure  of chloroplasts.   Environ.  Pollut.  3:37-49, 1972.

Wellburn, A.  R. ,  T.  M.   Capron, H.-S.  Chan, and  D.  C. Horsman.  Biochemical  effects of  atmos-
     pheric  pollutants   on  plants.   Jn:   Effects of Air  Pollutants on  Plants, Society  for
     Experimental  Biology,  Liverpool,  England,  April  10,  1975.   T.   A.   Mansfield,  ed.,
     Cambridge University  Press, London,  England,  1976.  pp.  105-114.

Wenger,  K.  F. ,  C.  E.  Ostrom, P.  R.  Larson, and  T.  D.  Rudolph.  Potential effects of  global
     atmospheric  conditions on  forest ecosystems,  pp.  192-202.    In W.   H.  Matthews,   F.  E.
     Smith,  and  E.  D.  Goldberg,   Eds.   Man's Impact on  Terrestrial  and  Oceanic Ecosystems.
     Cambridge:  The MIT Press, 1971.

Westman,  W.  E.   How much  are nature's services  worth?   Science  (Washington,  D.C.)   197:960-
     964, 1977.

White,  K.   L. ,  A.   C.  Hill  and J.  H. Bennett.   Synergistic  inhibition  of apparent  photo-
     synthesis  rate  of alfalfa  by  combinations  of  sulfur dioxide and  nitrogen  dioxide.
     Environ. Sci. Technol. 8:574-576, 1974.

Whittaker,  R.  H.   Communities  and Ecosystems.   2nd Edition.  Macmillan  Publishing  Co.,  Inc.,
     New York, NY, 1975.  pp. 1-2, 60-190,  236-302.

Woodwell,   G.  M.    Effects  of   ionizing  radiation  on   terrestrial   ecosystems.   Science
     (Washington, D.C.) 138:572-577, 1962.

Woodwell, G. M.  The ecological effects of  radiation.  Sci. Am.  208:40-49, 1963.

Woodwell, G. M.  Effects of pollution  on  the  structure and  physiology of ecosystems.  Science
     (Washington, D.C.) 168:429-433, 1970.

Woodwell, G.  M.   Eco-forum:   Paradigms Lost.  Bulletin  of  the  Ecological  Soc.  of Am. 59:136-
     140, 1978.

Yoneyama, T. , and H.  Sasakawa.   Transformation of  atmospheric N0? absorbed in  spinach leaves.
     Plant Cell Physiol. 20:263-266, 1979.

Yoneyama, T. ,  H.  Sasakawa,  S.  Ishizuka,  and T.  Totsuka.   Absorption  of  atmospheric  N02  by
     plants and  soils.   (II)   Nitrite accumulation, nitrite reductase  activity and diurnal
     change of N02 absorption in leaves.  Soil Sci. Plant Nutr.  25:267-275,  1979.

Zahn, R.  Gassing experiments with N0? in small  greenhouses.  Staub Reinhalt.  Luft  3_5:194-196,
     1975.
                                            12-55

-------
Zeevaart, A. J.   Induction of nitrate reductase  by  N(L.   Acta Bot. Neerl. 23:345-346, 1974.

Zeevaart, A.  J.   Some  effects  of  fumigating  plants for  short periods  with  NO-.  Environ.
     Pollut. 11:97-108, 1976.
                                            12-56

-------
                         13.  EFFECTS OF NITROGEN OXIDES ON MATERIALS

     The  damaging effects  of  atmospheric nitrogen  oxides  (NO ) have  been  established for a
variety of  materials,  including dyes, fibers, plastics, rubber and metals.  Other atmospheric
components  which  can  damage   materials  include  particulates,  sulfur  dioxide  and  oxidants
(ozone).
     These effects occur through chemical changes which result in lowered material performance
or  service.   This  causes  consumer disappointment  and economic losses,  both to  the  product
manufacturer,  and to  the  nation  at large.   The most  injurious  nitrogen oxide  is  nitrogen
dioxide (NOp).   This chapter presents an evaluation  of the effects of oxides  of nitrogen on
textile dyes, man-made and  natural fibers, plastics, elastomers and metals.
     It should  be pointed  out that some  exposure  situations  described in this chapter, which
lead to an  economic loss (mostly  involving  textiles),  characteristically take place indoors.
Although  indoor  and outdoor  pollutant  concentrations  are  not  always  directly related  or
proportional,  it is reasonable  to expect that  much of the  pollution  in indoor environments
comes  from  ambient  air.   Indoor sources such as gas appliances in  homes or combustion-powered
fork lifts in warehouses may also contribute to indoor pollutant levels.
13.1   EFFECTS OF NITROGEN OXIDES ON TEXTILES
     The types of damage to textiles attributed to NO  action include:
          Fading  of  dyes on  cellulose  acetate (also  known as acetate and  cellulose  acetate
          rayon), cotton, viscose rayon (Upham and Salvin,  1975),  and nylon.
          Color changes on permanent press garments containing polyesters.
          Yellowing of white fabrics.
13.1.1  Fading of Dyes by Nitrogen Oxides
13.1.1.1   Fading of  Dyes on Cellulose Acetate—The  NO   fading  of  acetate,  dyed blue,  or  in
                                                      X
shades  in  which blue is a  component,  results in pronounced  reddening.   Rowe  and Chamberlain
(1937) demonstrated  that the  causative  factors were nitrogen oxides in combustion gases.  The
blue dyes  which were and are still  in widespread use are derivatives of anthraquinone.
     Blue  dyes,  such  as  Disperse Blue 3, a  dye commonly used to test for  the presence  of NO ,
contain amino groups which are susceptible to nitrosation and oxidation by NO .   The  fading of
Disperse Blue 3  as  a result of  NO  action  is caused by the formation of  a nitrosamine at the
vulnerable  alkylamine  site(s),  or the  production  of  a phenolic  group  (-OH)  at the  amine
site(s), through  oxidation  (Couper,  1951).   Both of these  reaction  products  have a red color,
which  is seen when certain fabric-dye combinations are exposed to NO^.
     Salvin  et  al.   (1952)  found  that  cellulose  acetate.is an excellent  absorber  of NO^.
Absorption characteristics  of fibers also are believed to play an  important role in dye-fading
mechanisms.    Polyester  and  polyacrylic  fibers  have  low  NO^  absorption rates  while  nylon,
cotton, viscose rayon and wool  have intermediate rates.   While cellulose acetate and  cellulose
triacetate have  high  NO-  absorption rates,  the NO- is released upon heating.   Nylon  and wool,

                                           13-1

-------
materials  which  contain  reactive amino  groups,   hold  the  NO-  in  chemical  combination  and
release it upon  hydrolysis.   The oxides of nitrogen are retained by cotton and  viscose rayon,
fabrics collectively referred to as cellulosics.
     Both blue and  red  dyes  having the anthraquinone structure are susceptible  to NO  action.
                                                                                     A
These dyes include Disperse Blue 7, Disperse Blue  3, Disperse Red 11 and Disperse Red 55.   The
fading of these dyes is  recognized and noted in shade books published by dye suppliers.
     Asquith and Campbell  (1963)  have noted that  fading  also  occurs with certain yellow dyes
of the diphenylamine class.
     Dye  fading  associated with  NO- exposure of  cellulose acetate  and cellulosics  is  sum-
marized in Table  13-1.   Testing methods predictive  of  dye  fading  have been summarized in the
literature (American  Association of  Textile  Chemists  and  Colorists,  1972; Hemphill  et  al.,
1976;  Salvin,  1974a; Seibert,  1940).   Selected  anthraquinone-b and  blue  dyes  exhibit  high
resistance to fading by  NO  (Salvin and Walker, 1959; Seymour and Salvin, 1949).
     Chemical changes such  as those  cited  in  consumer  complaints  of dye fading  on  cellulose
acetate,  cotton  and rayon,  can  take place within three  months  at  NO-  concentrations  of 380
    3
ug/m  (0.2 ppm)  (Hemphill,  et al., 1976).    Also,  the additional acid introduced by  SO-,  fre-
quently present in significant concentrations  in  ambient air, appears to accelerate the fading
by NO- even though SO-,  by itself, produces no change.   (See Table  13-1.)
13.1.1.2  Fading of Dyes on Cotton and Viscose Rayon (Cellulosicsj—Although  the  effects  of
NO  on  dyed  acetate are well documented, the  effects on  dyes  used  for  the  cellulosic  fibers
  X
have  received  much less attention.   Anomalous cases of fading were reported by  McLendon and
Richardson (1965)  in  their  study of color changes  of dyed cotton placed in gas-heated clothes
dryers.    Additional  effects  reported by  other  investigators  are  summarized  in  Table  13-1.
     The  American  Association  of Textile  Chemists and  Colorists   (AATCC) conducted  service
exposure trials  to  determine  whether air contaminants could be one of the variables  in light-
fastness  tests  (Salvin,  1964; Schmitt, 1960). Urban  and  rural  sites were chosen  in  areas  of
high  and  low  atmospheric  contaminant  concentrations:   Phoenix,   Arizona  (low),  Sarasota,
Florida (low), Los  Angeles,  California (high), and Chicago, Illinois (high).   Sulfur dioxide,
oxides of  nitrogen  and  0, were monitored in  each  exposure  area.  A wide range  of fibers*was
dyed with  a  range  of dyes in common  use  on the  fibers  (Table  13-2).  The fabric samples were
exposed to ambient  air  for  30 and 120  days  in covered  cabinets which  excluded  the  action of
light.  Fading was  demonstrated  on a range of fabrics,  including  cotton and rayon,  for which
the cause  could  be NO , 03 or SO-.  The dyes  applicable to cellulosics which exhibited appre-
ciable  color  change represented  four major classes:  direct,  vat,  sulfur  and  fiber-reactive
dyes.
     Table 13-3  presents  typical  atmospheric  pollutant  concentrations in Los Angeles, Chicago
and the  rural  exposure  sites.  Chicago's high SO-  concentration was principally due to burn-
ing of  coal;  ozone concentrations were low.   The  concentrations of NO  are high  in  both Los
                                           13-2

-------
                            TABLE 13-1.   FADING OF DYES ON CELLULOSE ACETATE AND CELLULOSICS
                                                   (COTTON AND RAYON)
OJ
I

Concentration
of Pollutant
Dyed Fiber
Acetate
Acetate
Acetate
Acetate
Cotton-Rayon
Acetate-
Cotton, Rayon



Exposure Pollutant
Gas heated N02
rooms
Chamber N02
Pittsburgh- N09-0.
Urban, ^ J
Ames-Rural
Chamber N02
Clothes dryer N0~
Los Angeles3 NO-
+ °3
*so2
Chicago3 , N02
°3
+ so2
MQ/m
3,760
3,760
N/A
3,760
1,128-
3,760
489
412
131
414
10
655
ppm
2.0
2.0

2.0
0.6-
2.0
0.26
0.21
0.05
0.22
0.005
0.25
Time Effect
N/A Fading
16 hr Fading
6 mo Fading
16 hr Fading
1 hr Fading
cycle
30 to Fading
120
days


Reference
Rowe and
Chamberlain, 1937
Seibert, 1940
Salvin and
Walker, 1955
Salvin,
et al., 1952
McLendon and
Richardson, 1965
Salvin, 1964



                                                         (continued)

-------
                                             TABLE 13-1 (continued)
co

Dyed Fiber
Cotton-Rayon
Cotton- Rayon

Range of
Fibers
Range of
Fibers
Range of
Fibers
Acetate-
Cotton, Rayon
Acetate-
Cotton, Rayon
Exposure
Chamber
Chamber

Field-Urban,
Rural
Chamber
Chamber
Chamber
Survey
Pollutant
S02-N0£
S02-N02
and 03
S02-N02+03
N02
N02 + Xenon
arc radiation
N02
NO
cn^ H C
bU2, l-l-ji
Concentration
of Pollutant
/ 3
|jg/m ppm
3,760 2.0
N/A

N/A
94 to 0.05 to
940 0.5
940 0.5
94 to 0.05 to
940 0.5
Service
Complaints
Time
16 hr
54 hr

24 mo
12 wk
20 to
80 hr
N/A
N/A
Effect
Fading
Fading

Fading
Fading
Fading
Fading
Fading
Reference
Salvin,
Ajax et

Beloin,
Beloin,
Hemphil
et al. ,
Upham
et al. ,
1969
al. , 1967

1972
1973
1
1976
1976
Upham and
Salvin, 1975

        Concentrations also shown in Table 13-3

-------
         TABLE 13-2.   COLOR CHANGES ON DYED FABRIC-EXPOSED WITHOUT
                      SUNLIGHT IN POLLUTION AND RURAL AREAS

      International Grey Scale;3 5 = no change; Y = yellow; W = weaker;
                   G = greener; R = redder; and B = bluer

Code Index No.
ACETATE
Disperse Red 35
Disperse Blue 27
Oxides of nitrogen
fading control
Disperse Blue 3
Ozone control--grey
dyed with:
Disperse Blue 27
Disperse Red 35
Phoenix

4.5Y
3.0W


3.5
3.0



Los Angeles

4.0Y
2.0W


1.5R
1.5



Chicago

4.5Y
2.5W


2. OR
3.5



Sarasota

4.5Y
2.0W


3.5
2.5



Disperse Yellow 37
Disperse Blue 27
Disperse Red 60
WOOL
Acid Black 26A
Acid Red 89
Acid Violet 1
Acid Blue 92
Acid Red 18
COTTON
Direct Dyes
Direct Red 1
Congo Red B
Direct Red 10
Direct Blue 76
Direct Blue 71
Direct Blue 86
Vats
Vat Yellow 2
Vat Blue 29
Vat Blue 6
Vat Red 10
4.5
4.5
5.0

5.0
5.0
4.5
4.5
5.0


4.0
4.0
4.5
4.0
4.0
4.0

5.0
3G
4.0
5.0
5.0
4.0
5.0

4.5
3.5
4.0
4.0
4.0


1.5
2.5
3.5
2 grey
2.5R
1G

4.0
3G
3.5R
4.5
.4.0
3.5
4.0

3.5
3.5
3.0
2.5
3.5


1.5
2.5
3B
1R
2R
1G

3G
2.5G
3.0
3.5
4.0
4.5
4.5

4.5
2.5Y
4.0
4.0
4.5


3.0
2Y
4.0
4.0
3R
2.5G

5.0
1.5G
4R
5.0
                                 (continued)
SOURCE:   Salvin,  1964.
                                    13-5

-------
                          TABLE 13-2 (continued)

Code Index No.
Fiber Reactives
Reactive Yellow 4
Reactive Red 11
Reactive Blue 9
Reactive Yellow 16
Reactive Yellow 13
Reactive Red 23
Reactive Red 21
Reactive Blue 19
Reactive Blue 21
Reactive Yellow 12
Reactive Red 19
Reactive Red 20
Reactive Blue 17
COTTON
Sulfur Dyes
Sulfur Yellow 2
Sulfur Brown 37
Sulfur Green 2
Sulfur Blue 8
Sulfur Black 1
NYLON
Acid Red 85
Acid Orange 49
Disperse Blue 3
Disperse Red 55
Disperse Red 1
Alizarine Light Blue C
ORLON
Basic Yellow 11
Basic Red 14
Basic Blue 21
Disperse Yellow 3
Disperse Red 59
Disperse Blue 3
Phoenix

5.0
5.0
4.5
5.0
5.0
5.0
5.0
4.5
4G
5.0
5.0
5.0
4.5


3.5R
5.0
3B
4.0
4.5

5.0
5.0
5.0
5.0
5.0
5.0

5.0
5.0
4.5
4.0
5.0
5.0
Los Angeles

5.0
5.0
4R
, 5.0
.5.0
5.0
5.0
3.0
1.5G
4.5
5.0
4.0
3.0


3R
4.5
2. OB
3.5G
4.5

4.5
4.5
4.0
4.5
4.5
4.5

4.0
5.0
4.5
5.0
5.0
5.0
Chicago

4.5
4.5
3. OR
4.0
4.0
4.5
4.0
1R
1.5G
3.5
3.5B
4.0
1 grey


2. OR
4.5
2. OB
3G
4.5

3.0
3.0
3.5
4.0
3.0
3.5

4.0
4.5
• 4.0
4.5
4.5
4.0
Sarasota

4.5
5.0
4.5
5.0
5.0
5.0
5.0
4.0
3G
4.5
4.5
4.5
4.0


2.5R
4.0
2B
4.0
4.5

5.0
4.5
3.0W
3.5
4.5
4.5

4.5
4.5
5.0
4.5
4.5
4.5

The International Grey Scale is a numerical method of showing the degree
of shade change.   It is geometric rather than arithmetic.   Essentially,
a shade change of 4 shows a change which is slight and is  not too easily
recognized.   A shade change of 3 is appreciable and is easily recognized.
A shade change of 2 is severe.   A shade change of 1 is disastrous.   These
numbers are indicative of the shade change with 4 being passable and 3.5
a matter of judgement.
                                   13-6

-------
          TABLE 13-3.   TYPICAL  CONCENTRATIONS3 OF ATMOSPHERIC CONTAMINANTS IN EXPOSURE AREAS


Oxides of Nitrogen
Sulfur Dioxide
Carbon Monoxide
Ozone
Aldehydes
(Phoenixu-raSarasota) Los An9eles
(ppm) (jjg/m ) (ppm) (|jg/m )
0.01 0.26
0.03 80 0.05 130
23.00 26,000
0.06-0.11 120-220 0.21 410
0.3
Chicago
(ppm) (pg/m )
0.22
0.25 650
16.00 18,000
0.005 10


Concentrations shown are average concentrations measured over a two-month period, relative humidity
 data not available.

SOURCE:   Salvin, 1964.

-------
Angeles and Chicago,  and  are of similar magnitude.   These differences in pollutant concentra-
tions  correlate  with the  fact  that the  Disperse Blue 3, which  characteristically  reacts  to
NO ,   showed  pronounced  reddening changes in  both Los  Angeles and Chicago while  being  almost
unchanged (in the International  Grey Scale ratings) in  the rural  exposure areas of Phoenix and
Sarasota  (Table  13-2).    It should  be  noted that humidity  differences are  present  between
Phoenix, which is  dry,  and coastal  Florida, which is humid.   Humidity was not measured  in Los
Angeles and Chicago.
     In a  laboratory experiment (Salvin, 1969)  designed to produce  changes  similar  to those
shown on service exposure, the AATCC NO  test with Disperse Blue  3 was not used.   Instead, the
German  Fastness  Commission test was used,  which  has shown changes in dyes  on cellulose.   In
this   method,  discussed  by  Rabe and Dietrich  (1956) oxides  of nitrogen are  generated  by the
addition of phosphoric  acid to  a dilute  sodium  nitrite  solution.   The dyed  fabric is exposed
to the  nitrogen  oxides  in a closed system  under  high  humidity conditions,  in contrast  to the
AATCC test procedure, in  which  the  nitrogen oxides are generated by combustion of natural gas
or butane under  conditions of  low humidity.  The  dyed  fabrics which showed  fading changes  in
the service exposures in  Los Angeles  and Chicago showed similar  changes  upon laboratory expo-
sure   under  the  high humidity  conditions  of the German  Fastness Commission test  procedure
(Salvin, 1969).
     The effect of NO  on fiber reactive dyes has been  reported by Imperial  Chemical  Industries
                     X
in its  shade  card  of Procion Dyes.   The  vulnerability  of certain reactive dyes  on  cotton  to
N0x also has  been  reported by Hertig  (1968) in his critical  study of the International  Stand-
ards   Organization  test  procedure (Rabe and Dietrich,  1956)  for  color fastness to  NO .   This
method employs high humidity conditions.
     The effects of  air pollutants  were examined by the  U.S.  Environmental  Protection  Agency
(USEPA)  in  laboratory  trials   (Ajax  et  al.,  1967) using the  same  dye-fabric  combinations
employed in  the  AATCC  (Salvin,  1964)  study  (Table  13-2).  The  dye-fabric  combinations  were
exposed  to  air  to which  diluted  auto  exhaust  and S0?  were added  over  a  54-hour  period.
Neither the  auto exhaust  nor  S0? produced significant fading.    However, irradiation  of the
auto   exhaust,  which  contains both  hydrocarbons  and oxides  of nitrogen, gave products which
                                                                                   3
caused  significant fading.   The addition of  SO-  at  a  concentration of  2,620  pg/m   (1.0  ppm)
produced additional  fading.  The  synergistic effect of SO- is suggested as  being responsible
for the observed results.
     Beloin (1972) carried out  a  USEPA  field  exposure  study of  the  fading  of  67 dye-fabric
combinations  (using  56  dyes)  representative of the AATCC  service exposure  described in Table
13-2.   The exposures  were carried  out in eleven nationwide urban and rural  sites for consecu-
tive  three-month periods over a period of two years.
     The  exposure  sites  are listed in  Table 13-4.    Rural  areas were  selected  to  serve  as
controls with the same climatic conditions as the urban areas  but with low levels of pollution.
Phoenix, Arizona  and Sarasota,  Florida  were chosen as low pollution areas  with extremes  in

                                           13-8

-------
                 TABLE 13-4.   EXPOSURE SITES

City
Washington, DC
Poolesville, MD
Tacoma, WA
Purdy, WA
Los Angeles, CA
Santa Paula, CA
Chicago, IL
Argonne, IL
Phoenix, AZ
Sarasota, FL
Cincinnati, OH
Location
Municipal Building
Poolesville High School
Franklin Gault School
PHS Shellfish Laboratory
LA County Air Pollution Control
District Building
Federal Post Office
Central Office Building
Argonne National Laboratory
Desert Sunshine Exposure Tests
Sun Test Unlimited
Taft High School
Type
Urban
Rural
Urban
Rural
Urban
Rural
Urban
Rural
Suburban
Rural
Urban
Average
Fade, NBS
Units3
5.0
4.3
4.3
2.9
5.7
4.0
7.2
4.0
2.7
3.1
4.8

 On the NBS scale, a change of three units is noticeable; three to six
 units are considered appreciable; changes above six units are
 classified as severe.

SOURCE:   Beloin,  1972.
                                    13-9

-------
relative humidity and  high  temperatures.   The exposures were  carried  out in louvered covered
cabinets to avoid exposure to light.   The dye production sales for 28 of the 56 different dyes
tested totalled  over  30  million dollars (U.S. Tariff  Commision,  1967).   Of the 67 dye-fabric
combinations, 25 were cellulosics.
     The sites were monitored for CL, N02 and SO^.   The gas fading control (Disperse Blue 3 on
cellulose  acetate)  showed high  correlation  with NO   concentration.   Fadings on  the  0, test
                                                    A.                                   *J
ribbon were demonstrated in the rural areas as well  as the urban sites.
     It can  be  concluded from the data that  appreciable  fading takes place in the absence of
light.   Of the 67 dye-fabric combinations tested, 64 percent showed appreciable fading.   Urban
sites produce significantly  higher  fading  than corresponding rural sites.  In the presence of
high temperature and  high humidity,  air pollution increases fading rate.   Fading changes were
severe in those fabrics dyed with direct and reactive dyes.
     The  data did  not  isolate  the action  of SOp,  03,  or N02,  but a  statistical  analysis
identified N02 as a significant variable (at 99 percent level) causing fading in some samples.
Chicago samples  incurred highest average fading.   However, Chicago had high concentrations of
S02, as well as N02-
     Beloin  (1973) also  conducted  laboratory studies designed to determine the effects of the
individual air pollutants on dyed fabrics.   Exposure was made of 20 dyed fabrics chosen on the
basis of  their  appreciable change in the  field  study noted above.  Cotton  and  viscose rayon
were 9 of  the 20 dyed fabrics (Table 13-5) used in the trials.  Reactive dyes and one type of
vat dye were used.   The pollutants were SO,,  NO,  N0~, and 0,.  Two concentration levels were
used for nitrogen dioxide:  940 and 94 ug/m  (0.5 ppm and 0.05 ppm).   Temperature and humidity
were  varied:   32°C  and  13°C,  and 90  and 50 percent relative humidity,  respectively.   The
fabrics were exposed for 12 weeks.
     Under  the  higher humidity/temperature  conditions,  N02 at  a concentration  of  940 ug/m
(0.5 ppm),  caused  severe changes on 8  of  the 9  samples.   Significant fading also occurred at
                                                   3
high humidity with an  NO- concentration of 94 |jg/m  (0.05 ppm) (Beloin, 1973).   Color changes
were reported as Hunter Color Units, which  approximate the NBS units.
     The  AATCC  Committee on  Color Fastness  to  Light carried  out light-fastness tests with
added contaminants using Xenon  arc irradiation (Hemphill  et al., 1976).  The objective was to
establish a  relationship between light-fastness  tests made in natural daylight in Florida and
Xenon arc  exposure  in  the laboratory Weatherometer.   The contaminants included separate addi-
tions of 940 |jg/m3 (0.5 ppm) N02, 294 ug/m3 (0.15 ppm) 03 and 786 |jg/m  (0.3 ppm) S02.   In one
trial, all  three contaminants were  added  to  the exposure cycle  under  Xenon arc irradiation.
Of the 29  dyed  fabric combinations exposed,  14  were  cellulosic (cotton or rayon).  The addi-
tion  of  NOp  alone caused  increased  fading  compared  to the  control  in  over half  of dyed
cellulosic fabrics examined.
     Upham  and  co-workers (1976)  carried  out a  chamber   study  of the effect  of atmospheric
pollutants on selected drapery  fabrics.  Fabrics were exposed to 0.05 and 0.5 ppm each of S02

                                           13-10

-------
                TABLE  13-5.  AVERAGE  FADING OF  20  DYE-FADRIC  COMBINATIONS3  AFTER  12  WEEKS  EXPOSURE  TO  NITROGEN  DIOXIDE
                                                  Hunter  Color  Units
94 pg/m3 NO,
Material
Cotton
Rayon
Wool
Cotton
Acrylic
Cotton
Nylon
Wool
Acrylic
Cotton
Wool
Dye
Direct
Direct
Acid
Reactive
Basic
Azoicc
Acid
Acid
Basic
Sulfur
Acid
Color Index No.
Red 1
Red 1
Red 151
Red 2
Red 14
Red
Orange 45
Yellow 65
Yellow 11
Green 2
Violet 1
Low Temp.
Average
12.78eC
7.2
3.4
T
T
T
T
5.6
T
T
T
T
High Temp.
Average
32.22°C
8.0
T
T
T
T
T
17.0
T
T
3.3
T
Low
Humidity
Average
(50% RH)
7.4
T
T
T
T
T
10.1
T
T
T
T
High
Humidity
Average
(90% RH)
7.8
T
T
T
T
T
9.5
T
T
T
T
Low Temp.
Average
12.78 C
18.0
13.4
T
10.4
T
T
21.5
T
T
6.5
T
940 pg/m
High Temp.
Average
32.22°C
20.4
16.3
T
6.9
T
T
27.9
T
T
6.6
T
3 NO,
Low
Humidity
Average
(50% RH)
16.1
12.6
T
9.7
T
T
24.3
T
T
6.1
T

High
Humidity
Average
(90% RH)
22.3
17.0
T
7.6
T
T
25.1
T
T
7.1
4.1
SOURCE:   Be loin,  1973.
                                                                 (continued)

-------
                                                                  TABLE 13-5.   (continued)
CO
I

ro

94 pg/m3 NO,


Material
Cotton
Cellulose
Acetate
Nylon
Cellulose
Acetate
Polyester
Cotton
Cotton
Cotton
Acetate



Dye
Direct
Disperse

Disperse
Disperse

Disperse
Reactive
Reactive
Vat
— 
-------
(131 and  1310  MS/™3),  03 (98 and 980 ug/m3), and N02 (94 and 940 ug/m3) under Xenon arc irra-
diation,  at  various humidities.  The  effect  of N09 was pronounced, especially  on  a vat-dyed
                                                                    3
drapery fabric.   The  most  noticeable color changes were at 940 ug/m  (0.5 ppm) and 90 percent
relative humidity.
     In summary,  the  investigations  by Beloin both  in  the  field study (Beloin,  1972) and the
chamber study (Beloin, 1973) show that, at concentrations of N0? present in urban atmospheres,
representative dyes for  cotton  and rayon will  suffer  serious  fading.   NCk resistant dyes are
available; however, limitations of brightness of shade and difficulty of application introduce
production problems and the  need for  greater  quality  control  resulting,  generally,  in  in-
creased costs.  The AATCC  work confirms the  vulnerability  to  NO,, of several  dyes widely used
on cellulosic fibers,  especially certain blue dyes.
13.1.1.3  Fading of Dyes on Nylon—The  fading of  dyed nylon in  polluted  atmospheres  has been
noted in exposure trials carried out by the AATCC (Salvin, 1964) and by the U.S.  Environmental
Protection Agency  (Beloin,  1972).   However,  consumer  complaints have  been few  and  have been
blamed on  light-produced color  changes in garments, draperies, or in home furnishings for the
nylon fiber normally used in these products.   The standard AATCC test procedure for N0?, which
demonstrated  the vulnerability of the disperse dyes used on acetate, showed little change when
the  same  dyes  were used  on  nylon  (Table 13-6).    The  problem  of  fading on  nylon  became of
considerable  interest  as nylon found use in carpets.  The quality of nylon for this end use is
estimated at  over 500  million pounds, distributed between Nylon 66 and  Nylon 6.
     Field exposures of a range of dyes on nylon,  in areas of high air  pollution  (N02, S02 and
03), resulted  in  unexpected failures of these dyes (Beloin, 1972; Salvin, 1964). In contrast,
the  same  dyes  on  polyester showed no  changes (Table  13-6).   The fading of disperse blue dyes
on nylon  carpets  was  shown to be due  to  03  in  the presence of high humidity (Salvin, 1974b).
Acid dyes, which  are  more  resistant to On, were  substituted as a remedial  measure.   However,
the  remedy presented  additional  problems.   The  vulnerability of acid dyes on  nylon to NO^ was
the  basis  of a  bulletin  issued by Imperial  Chemical Industries (1973)  on a range of acid dyes
marketed  as  Nylomines.   The fading  effect of NOp,  derived from  combustion gases,  was  deter-
mined at  65  and  at 95 percent  relative humidity  on three cycles of exposure  in their tests.
Certain violet  and blue dyes  are rated  as  exhibiting significant change.  The dye  manufac-
turers point out  the  importance of dye selection in carpets and in home furnishings which are
likely to  be exposed  for  long periods  in  air contaminated  with NOo from gas  burner  fumes.
     Acid dyes on  nylon  were included in  the range of dyes exposed to  visible light radiation
and  NO, by Hemphill in the AATCC study (Hemphill  et al. , 1976).  Under  high  humidity  condi-
                                                3
tions and  at an  N02  concentration  of  940  ug/m   (0.5  ppm),  for 30 to 100 hours,  fading  was
found to  be  greater for  certain dyes  in  those  exposures where Xenon arc  irradiation and  N02
were  present  than  in  the  control   exposure with  Xenon  arc  irradiation and  NO^-free  air
(Table 13-6).
13.1.1.4  Fading of Dyes  on Polyester—Polyester  dyed  with  disperse  dyes  did  not show N02~
induced  fading  changes  in AATCC  field  exposures  in  urban atmospheres  of  Chicago and  Los
Angeles (Table 13-6)  (Salvin,  1964).   The same fabrics  in  various  urban sites (Beloin, 1972)
                                           13-13

-------
                             TABLE 13-6.   EFFECT OF NITROGEN DIOXIDE ON FADING OF DYES ON NYLON AND POLYESTER
I
I—I
-p>

Dyed Fibers
Nylon
Polyester
Nylon
Polyester
Nylon
Polyester
Nylon
Nylon
Polyester
Permanent
Press
Polyester
Textured
Double Knit
Concentration
of Pqllutant
Exposure Pollutant
Chicago NO,,
Los Angeles
Chicago NOp
Los Angeles
Urban Sites N02
Urban Sites N02
Chamber N02
High Humidity
Chamber NOp
High Humidity
Chamber N02
High Humidity
Chamber N02
High Humidity
Xenon Arc
Chamber N0?

Chamber N02

ug/m"
188
282
376
282
376
376
188 to
1,880
188 to
1,880
376
940
940

940

ppm
0.1
0.15
0.2
0.15
0.2
0.2
0.1
to 1
0.1
to 1
0.2
0.5
0.5

0.5

Time
30 to 120 days
30 to 120 days
30 to 120 days
30 to 120 days
3 to 24 months
3 to 24 months
12 weeks
12 weeks
48 hours
30 to 120 hours
16 hours

16 hours

Effect
Fading
Unchanged
Fading
Unchanged
Fading
Unchanged
Fading
More
fading than
without N02
Fading

Fading

Reference
Salvin, 1964
Salvin, 1964
Beloin, 1972
Beloin, 1972
Beloin, 1973
Beloin, 1973
Imperial Chemical
Industries, 1973
Hemphill et al . , 1976
Salvin, 1966

Urbanik, 1974


-------
also  showed  no  changes;  high or low  humidity  had no effect.  However, a large number of com-
plaints regarding fading of permanent press garments (65 percent polyester--35 percent cotton)
were  recorded in 1965, when this product first was marketed.
      Investigation  of the anomalous  fading of  polyester  dyes in  permanent  press  fabrics by
Salvin  (1966)  indicated  that fading did not take  place  on dye contained within the polyester
fiber matrix.   Fading was  found to take place  on the surface of the fiber as a result of dye
migration from  the  fiber subsurface to the modified urea-formaldehyde resin used on the blend
to stabilize the cotton.   When exposed to NCL or 03, the components of the resin finish absorb
the contaminants and  fading  occurs.  The measures  which  can be used to eliminate the problem
are (a)  selection  of  dyes  with lower  rate of  migration,  (b) substitution  of  the magnesium
chloride  catalyst  with  zinc  nitrate  and,   (c)  reduction in  quantity  of  non-ionic  surfactant
which acts as  an  acceptor for the  dye  and  an  absorber for  either  NO^ or :03.  Urbanik (1974)
suggests  changes in  the  magnesium  chloride catalyst formulation,  used in the resin finish, in
order to  suppress dye migration.
     The  introduction, in 1966,  of double-knit garments made from textured polyester also was
accompanied  by  cases of  fading  of the garments  attributed to either NCL or  On.   The fading
attributed to  N0~  was noted in those  dyes  of  level  dyeing properties.  Dye  migrates in the
final  heat-setting step to lubricant oils or residual  surfactant on the surface of the fabric,
where fading takes place.
13.1.1.5  Economic Costs  of N0x -induced Dye Fading—Barrett  and  Waddell  (1973),  in a  1973
status report to the U.S. Environmental  Protection Agency,  reported'preliminary estimates that
annual economic costs of  NO -induced dye fading in textiles amounted to $122.1 million.  These
estimates were based on figures reported by Upham and Salvin (1975).
     The economic costs to the nation as a  result of 0, damage to textiles is approximately 70
percent of the costs attributed to  NO  damage.   These costs of NO  and 0, action are tabulated
in Table 13-7.
     The  basis  for  the  estimates  included not only the  reduced wear  life of textiles  of
moderate  fastness to  NO   but also  the costs of research and quality control.   The major share
                       A
of the costs  is the extra expense  involved  in  using  dyes of higher NO  resistance and in the
use of  inhibitors.   Additional  costs  also are  incurred  in dye application  and  in increased
labor expenditures.
     The  factors relating to higher costs  in the  textile  industry as a result of  N0x action
are discussed  in  Chapter 8,  "The   Effects  of  Nitrogen Oxides on Materials,"  in  the National
Academy of Sciences report on nitrogen oxides (Salvin et al., 1977).
13.1.2  Yellowing of White Fabrics  by NO,
     The survey of the effects of air pollutants on textiles (Upham and Salvin, 1975) reported
a number  of  instances in which white fabrics yellowed.   This discoloration occurred in areas
protected from  light.   Causes of yellowing  were not established, except  for  the observation
that contact with ambient air currents seemed to be a causative factor.

                                           13-15

-------
            TABLE 13-7.   ESTIMATED COSTS OF DYE FADING IN TEXTILES

Pollutant
NO Fading on
Fading on
Fading on
Yel lowing
Subtotal
OT Fading on
Fading on
Fading on
Subtotal
Effect $
acetate and triacetate
viscose rayon
cotton
of white acetate-nylon-Spandex

acetate and triacetate
nylon carpets
permanent-press garments

million3
73
22
22
6
122
25
42
17
84

Total

206

aAll  costs rounded to nearest million, therefore some totals do not agree.



SOURCE:   Barrett and Waddell, 1973.
                                    13-16

-------
     Using  18  fabric  samples which  were the  subjects  of manufacturers'  complaints,  Salvin
 (1974c)  investigated the effects of specific air pollutants or combinations and the effects of
 humidity and  temperature.  The products tested  include polyurethane segmented fiber, rubberized
 cotton,  optically-brightened acetate,  nylon,   nylon  treated  with permanent  antistatics,  and
 resin-treated cotton containing softeners (Table 13-8).
     Nitrogen  dioxide was  established as  the pollutant  responsible  for yellowing  of white
 fabrics  in  the  complaint  fabrics  tested.   Yellowing was not demonstrated  when  fabrics were
 exposed  to 0,,  S0~, or hydrogen sulfide (HUS).
     The standard AATCC test procedure (conducted in  low humidity) for effects of N02 does not
 always  result  in the  yellowing  effect observed  on  service  exposure  in  areas  shielded from
 light.   This is  especially  true  of  cotton  and  nylon  fabrics.   Whereas the  standard  test
 procedure  for NO   showed  change  on  cellulose   acetate fabrics,  high  humidity test procedures
                 A
 demonstrated yellowing in nylon.
     Although fibers  without additives do  not show yellowing following  exposure  to  NO^,  the
 polyurethane-segmented fibers (e.g.,  Lycra  and Spandex) are exceptions.   These fibers contain
 urethane  groups  which react  directly with N0~  to  form  yellow-colored nitroso  compounds.
 Yellowing  of Spandex  and  Lycra fibers  occurred in  the  standard AATCC  test for  NO-  fading
 (Salvin,  1974c).  In  the  tests  carried  out,   less  yellowing was  shown  on certain  samples
 submitted which contained inhibitors.
     Garments containing rubberized cotton  did show yellowing on exposure to N02 in the AATCC
 standard  test  procedure.    With  increase  in   temperature  of the  test,  yellowing was  more
 pronounced in those areas  of the garment where rubber is present (Burr and Lannefeld,  1974).
     The antioxidant in rubber employed against ozone action is diphenyl  ethylene diamine.   On
 storage, this  product vaporizes  from the rubber  to the  surface of the  cotton  fabric.   This
 material already  is well  known  as the inhibitor used on cellulose acetates to suppress  fading
 of dyes by N02-   It forms a yellow nitroso compound.
     Optical   brighteners,  compounds  widely  used  to  improve the  whiteness of  fabrics,  are  of
 various  structures  and are  specific  to  particular fibers.   They function by transforming  UV
 radiation  to visible  light  in  the  purple-blue  range.   Brighteners may  react  with NO^  and
 result in yellow-colored compounds.
     The American Association of  Textile  Chemists and Colorists  (1957)  has  conducted a study
 of the yellowing  of a range of softeners.   In the range  of fabrics examined for yellowing  of
 the  softeners,  variable degrees  of  yellowing  were  demonstrated upon  exposure  to NOp.   The
yellowing was especially noted  on  those softeners of a cationic nature.   Softeners have been
 synthesized which are  resistant  to  yellowing by oxides of nitrogen (Dexter Chemical Company).
     The unexpected yellowing of  nylon  treated  with an  antistatic  agent has been  reported
 (Salvin, 1974c).  The  treated nylon  showed no  yellowing on exposure in the standard N02 AATCC
 test method.   Under high humidity and  with an increase in  temperature during testing,  however,
yellowing similar to that obtained in  service testing was  observed.

                                           13-17

-------
                                     TABLE 13-8.  YELLOWING OF WHITES BY NITROGEN DIOXIDE
00

Fiber
Survey
Rubberized
Cotton

Rubberized
Cotton
Spandex
Acetate
Optical
brightener
Nylon
Optical
brightener
Nylon
Anti-stat
finish
Cotton
Cationic
softener
Exposure Pollutant
Service N/A
Complaints
Chamber N0?

Chamber N02
Chamber N02
Chamber N02
Chamber N02
High Humidity
Chamber N02
High Humidity
Chamber N02

Concentration
of Pollutant
ug/m ppm Time Effect
N/A Yellowing
376 0.2 16 hr Yellowing

376 0.2 16 hr Yellowing of
anti-oxidant
376 0.2 8 hr Action on
fiber
376 0.2 8 hr Yellowing
376 0.2 16 hr Yellowing
376 0.2 16 hr Yellowing
376 0.2 16 hr Yellowing

Reference
Upham and
Salvin, 1975
Burr and
Lannefeld,
1974
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c


-------
13.1.3  Degradation of Textile Fibers by Nitrogen Oxides
     Cotton and nylon are the two fibers whose strength is reduced by the hydrolytic action of
acid aerosols.   This  problem assumes economic importance  because  industrial  fabrics comprise
the end use for 18 percent of all fibers, many of which are used in the production of cordage,
belts, tarpaulins and awnings.  These products are exposed to air pollutants over long periods
of time.  Premature losses of strength are costly and create safety hazards.
     A chamber  study  of the combined action  of  N02  and light on cotton  did  demonstrate that
N02 contributed  to  strength loss (Morris, 1966).  Cotton  yarns  were exposed to sunlight.  In
one cabinet, air was filtered through carbon to remove oxides of nitrogen.  The second cabinet
contained  fibers  exposed  to sunlight  and  air  containing  monitored  levels  of 03  and NO-.
Exposure was carried  out for a total of  72  days.   Since the test area (Berkeley, California)
was  low  in SO^,  this  service exposure  would emphasize the effects  of  nitrogen oxides.  The
degradation (strength  loss)  of  the cotton fiber was greater in the presence of the unfiltered
ambient air.   The results  of this study  show that  the combined effects of  sunlight  and NO
                                                                                             A
gave increased  deterioration  over  sunlight alone.   The contributions of Oo and other oxidants
was not determined.
     It is  not  possible to isolate the effects  of  nitrogen oxides from that of sulfur oxides
in field studies  which have shown strength  loss in  cotton (Brysson et al.,  1967;  Brysson  et
a!., 1968;  Morris,  1966;  Travnicek,  1966).  The effect  of N0,> on fiber degradation of cotton
requires further investigation.
     Inconclusive results  were  shown by  Zeronian  et al.  (1971)  in a study of  the  effect  of
N02, combined  with  Xenon  arc  radiation,  on  a  range of man-made fibers,  including  acrylics,
nylons and  polyester.   These  workers  exposed modacrylic-acrylic, nylon,  and  polyester  fibers
to the combined action of Xenon arc radiation and air containing 376 pg/m  (0.2 ppm)  N02 at  30
percent relative  humidity  at  48°C,  and  at 43 percent  relative humidity at 43 C.  The fabrics
were exposed for 108 hours to Xenon arc  irradiation in a Weatherometer and intermittently were
sprayed with water.  The  same series of fabrics was  subjected to identical weathering condi-
tions but without N02.   Modacrylic (Dynel),  acrylic  (Orion),  and polyester showed only slight
differences in degradation  in exposures  with and without N0~.   These materials are considered
resistant  to the action of acids.   The results for  nylon were  not conclusive,  although signif-
icantly greater degradation  (loss  of  tensile strength, increased viscosity)  at  48°C occurred
in the presence of NO^, under irradiation.   Further experimentation  would be suggested to test
N0~ effects in the absence of irradiation and under higher humidity  conditions.
13.2  EFFECTS  OF NITROGEN DIOXIDE ON PLASTICS AND ELASTOMERS
     The maintenance of  strength of  plastics and elastomers upon exposure  of these  materials
to light,  air  and atmospheric contaminants  is a  matter of importance.
     A 1977 survey (Chemical and  Engineering  News,  1977) predicts a  market for these  materials
in 1982 of  1.78 billion pounds.   Under the  generic  term of plastics  are included polyethylene,
propylene,  polystyrene, polyvinyl  chloride, polyacrylonitrile  and polyamides.

                                           13-19

-------
     Aging is the  term  used to denote deterioration of chemical and physical  properties which
can' occur upon weathering.   This degradation has been blamed on the known effects of sunlight.
The comparative resistance  to  sunlight can be shown upon exposure in the laboratory to carbon
or Xenon  arc irradiation.   The  substitution  of plastics for metals,  particularly  in automo-
biles, where  long  periods  of outside  exposure  are involved, brings this problem  into focus.
The effects of air pollutants,  such as N02, have been assessed in laboratory trials.
     The  polymers  which represent the  structures  in  plastics,  as  well  as  textiles,  were
subjected by Jellinek et al. (1969) to the action of SCL, N0?, and ozone obtained by action of
UV radiation on the  oxygen-containing mixture.   These  combinations of  SCL,  NCL,  and  ozone
represent  the  components of smog.   The polymers  include polyethylene,  polypropylene,  poly-
styrene, polyvinyl  chloride, polyacrylonitrile,  butyl rubber and nylon.   All polymers suffered
deterioration in strength.   The  elastomer, butyl rubber, was more  susceptible  to SCL and NCL
than  other polymers.   However,  the effect of CL  on the rubber was more pronounced than that of
the S02 or the N02-
     Jellinek (1970)  examined  the  reaction of linear polymers,  including nylon  and polypropy-
lene,  to  N02  at concentrations of 1,880 to 9,400  (jg/m3  (1.0 to  5.0  ppm).   Nylon  66 suffered
chain scission.  (Chain  scission results in polymers having lower molecular weights and lower
strength.)   Polypropylene  tended to  crosslink.   Chain  scission  of polymers caused by small
concentrations of S02 and N02 took place in the  presence  of air and UV radiation.
     The action of NCL  and  0^  on polyurethane  also  was  investigated by Jellinek (1974).   The
tensile strength  of   linear polyurethane was  reduced  by N02 alone  and also by N02 pl.us 0^.
Chain scission resulting in lower molecular weights and formation of nitro-  and  nitroso-groups
along the polymer backbone  occurred upon exposure to NO,,.
13.3   CORROSION OF METALS BY NITROGEN DIOXIDE
     The corrosion of metals by air pollutants is due to  the presence of acids or salts on the
metal  which  enter  into  electrochemical reactions.   Numerous  small  electrochemical  cells  form
on the  ferrous  metal surfaces  which are  in  contact with  the contaminated air.   Localized
anodes and cathodes form and the electrical conductivity  is increased where  the  surface of the
metal  is wet; the moisture  contains increasing quantities of acid aerosols or anions therefrom.
     The normal rusting  process  is the formation of  an  iron-oxide  which acts as a protective
film.   However, the  presence of an acid aerosol  such  as sulfuric acid,  as derived  from  S02,
can break  down  this  protective oxide  layer, exposing  new surfaces  to electrolytic corrosion.
     An analysis of  the  contributing effects  of air pollutants was offered  in the examination
of the  contributions  of N02  to  corrosion  in  the  review  by  the  National  Research Council
(Salvin et al., 1977).
     The forms of metal  corrosion include new  corrosion (uniform and general attack), galvanic
corrosion, crevice  corrosion,  pitting,  selective  leaching,  and  stress corrosion.   A liquid
film   or  the  presence of a  hydrated salt plays  a  role  in most of these  corrosion  types.   In
attempting to  assess the contribution of nitric  acid aerosols derived  from N02  and nitrate

                                           13-20

-------
salts, the  various  mechanisms of corrosion must be understood to attenuate the problem and to
predict the effect of a variable change.
     Thus  the mechanisms  of  galvanic,  pitting,  crevice,  and  selective  leaching  corrosion
require the presence  of an electrolyte or  solvent.   Hydrated salt solutions can serve as the
electrolyte in galvanic corrosion.
     The general approach taken by investigators to the effects of air pollutants on corrosion
has been  to establish the extent of the damage with the goal  of obtaining data which could be
used  in economic  analyses of corrosion due to air pollutants.  Waddell (1974)in his estimates
of  the economic  damages  of  air  pollution includes  a section on  costs of  metal  corrosion.
Using  data  supplied  by  the Rustoleum Corporation, Barrett  and Waddell (1973) estimated costs
at $7.5 billion in 1958.
     Material  damage  due  to  air pollutants emphasizes S02 as  the major causative agent in the
corrosion of metals (Fink et al., 1971; Gillette, 1975).  Fink and co-workers (1971) estimated
corrosion damage of metals caused by air pollution at approximately $1.5 billion.
     When consideration is given  to the mechanisms of corrosion which are due to electrolytic
action rather  than oxidation,  the  importance of  NCL in the  corrosion  process  emerges.   The
presence of nitrates on surfaces, to give both the requisite hygroscopic film and the electro-
lyte  for  galvanic corrosion,  becomes  important.   The potential of nitrates  in  upsetting the
homogeneity of the protective oxide film becomes a factor.
     Haynie et  al.  (1976)  investigated the  separate  or  combined effects of 502,  NO-  and 0,
under  controlled  conditions  of pollutant,  humidity  and  temperature.   The  materials  tested
included:   weathering steel,  galvanized steel, aluminum alloys, paints, drapery fabrics, vinyl
house  siding,  marble, and white sidewall  tire rubber.  Sulfur dioxide  and  relative humidity
appeared  the  most  important  factors  for  producing  corrosion.   A  similar conclusion  was
reported by Yocum and  Grappore  (1976)in a  review of the effect of  air  pollutants  emanating
from power plants.
     The premature failure of nickel brass springs in telephone equipment primarily in the Los
Angeles area has  been investigated  by Hermance and co-workers (1971).  Although most failures
occurred in California,  springs did  show occasional  failure in other parts of  the country.
This  report reviewed  the  earlier findings that  the  springs had a fogged appearance  and  were
covered with  a  hygroscopic  dust  rich  in  nitrates.   The  failure was  attributed  to  stress
corrosion.   A  survey  of  nitrate  accumulation  was  made in  California  and  other  locations.
Nitrate deposition correlated with  relay failure.
     Previous  laboratory studies by Hermance (1966) and McKinney and Hermance (1967) confirmed
that  hygroscopic  nitrates such as  zinc or  ammonium cause stress  corrosion cracking  of the
anodic nickel   brass  wires.    Salts  of other  anions  under  the  same  conditions did  not cause
                                                                                          2
cracking at the nitrate concentration levels found  in  Los  Angeles.   Up to  about 15 ng/cm  of
surface area,  an  applied  positive  potential  was necessary.  Cracking  was found to be low when
the relative humidity was  less than 50 percent.

                                           13-21

-------
     A field study (Hermance et al., 1971) was made of the incidence of breakage as related to
the' nitrate  accumulation.   The nitrate accumulations were measured in New York City,  Bayonne,
New Jersey,  Philadelphia,  Baltimore,  and Washington, D.C.   Although the  accumulations  were
high,  breakage in these areas was lower than anticipated.
     The important finding illustrated in this work is that the nitrates salts are more hygro-
scopic than  the  chloride and  sulfate  salts.   As  such,  they may lower  the  threshold  humidity
requirements  for  the formation  of  an aqueous  medium,  which can serve as  the  electrolyte or
solvent for wet corrosion.
     Hermance (1966) also  reported  on the failure of other telephone equipment, which did not
involve nickel brass alloys,  that took place in Los Angeles, New York, Detroit and Cleveland.
The nickel  base of palladium-capped contacts of cross box switches  corroded in the presence of
nitrates,  forming bright greenish corrosion products which gradually crept over the palladium
                                                                             o
cap of the contacts.   The heavy nitrate deposits were greater than  15.5 ug/cm .   Stress corro-
sion occurred in the absence of anodic electrical  current.
     The function of NCL  in changing the defect  structure  of many oxides, thereby increasing
or decreasing  the rate  of oxidation of  metals and  alloys,  was suggested  by  Lazareva  et al.
(1973) in  the study of the oxidation of tungsten alloys.
     A field study of the effect of air pollutants on electrical contact materials was carried
out by  Chiaranzelli  and Joba  (1966), in which the  formation  of  corrosion  films  in various
areas   of  pollution  was correlated  with  the  concentration  of pollutants  present.   Nitrogen
dioxide,  SCL, H~S and  dust were monitored.   This  study did not isolate the specific contribu-
tion of NO-2 to the problem of electrical  contacts  although it did point out that areas of high
humidity showed greater corrosion.
     It is  in the study of catastrophic  failure  of materials exposed to  air  pollutants  that
investigators seek to  establish  the specific causative agent.   The long-term exposures by the
ASTM of various  metals  in different  locations sought  to establish which  metal  or alloy was
most resistant.   The case of  the telephone  equipment failure as investigated  by Hermance et
al.  (1971)  did show that  nitrates were  a contributory  factor,  although  no  relation  to the
concentration of NCL in the air was established.
     Gerhard and Haynie  (1974) examined  the cases of catastrophic  failure of metals  in which
structures  failed  unexpectedly,   leading  to  loss  of  life  as well  as well  as  collapse  of the
metal  structure.   Their conclusion was that air pollutants were a probable contribution to the
corrosion  that  was  the  cause  of failure.   However,  there is no finding  that  determined the
relationship between levels of particular pollutants and the occurrence of the failure.
     Nitrogenous compounds, however, were implicated in a situation in which steel cables on a
bridge in Portsmouth,  Ohio failed after 12 years  of service.  The  cause of failure was traced
to river  water contaminated with ammonium  nitrate that had concentrated  at natural  crevices
(Romans,  1965).  Nitrogen dioxide was not considered a factor.
                                           13-22

-------
     A  review  of  the voluminous literature on corrosion has produced no further references to
investigations  of NCL action,  in  the  absence  of SOp.   The above  studies  are summarized in
Table 13-9.
13.4  SUMMARY
     The  damaging effects  of  atmospheric  oxides  of nitrogen  have been  established  for a
variety of  materials  including dyes, fibers, plastics, rubber and metals.   Field exposures of
cotton, viscose rayon,  cellulose acetate, and nylon  fabrics  colored with  representative dyes
demonstrate  that  fading occurs  for  specific  dyes  in  air containing NOp, 03,  and  SO-.   These
exposures  were carried out  in  ambient  air  and protected  against  sunlight.   Chamber studies
using  individual   pollutants  NOp,   CU,  and  SOp  have  shown that  some individual  dye-fiber
combinations exhibit color fading only in response to N0? exposure,  whereas others are suscep-
tible  to  0,,  as  well  as combinations  of NCL  and  0,.  S0?  introduced  an  accelerant effect.
Disperse dyes  used  for cellulose acetate and rayon include vulnerable anthraquinone blues and
reds.   The  cellulosic fibers  cotton  and viscose  rayon,  dyed with certain widely  used  direct
dyes,  vat  dyes,  and  fiber  reactive  dyes,  suffer severe  fading on chamber  exposures  to 940
ug/m   (0.5  ppm) NO,  under high  humidity  (90  percent) and high temperature (90°F) conditions.
                                                                  3
Significant  fading  is observed  on  12 weeks  exposure to  94 (jg/m   (0.05 ppm)  N02  under high
humidity and temperature conditions (90 percent, 90°F).
     Acid dyes on nylon fade on  exposure to NO,, at levels as low as  188 ug/m  (0.1 ppm), under
similar  conditions.    Dyed   polyester fabrics  are highly resistant  to NOp-induced  fading.
However,  permanent .press  fabrics  of  polyester  cotton  and   textured  polyester  exhibited
unexpected  fading when first  marketed.   The fading  was  in  the disperse  dye  which migrated
under  high  heat  conditions  of  curing or  heat  setting  to the  reactive medium  of  resins and
other surface additives.
     The yellowing of white fabrics is documented for polyurethane segmented fibers (Lycra and
Spandex),   rubberized  cotton,  optically brightened  acetate, and  nylon.   Yellowing is  also
reported  on  fabrics  which  were finished  with  softeners or  anti-static  agents.   Nitrogen
dioxide was  demonstrated  to  be the  pollutant  responsible for  color change, with  03 and SO,,
showing no  effect.   Chamber  studies using N0?  concentrations   of 376  ug/m  (0.2  ppm)  for 8
hours showed yellowing equivalent to that on garments  returned to manufacturers.
     The tensile  strength of  fabrics may be  adversely  affected by the hydrolytic action of
acid aerosols.  Nitrogen  dioxide  has been demonstrated  to oxidize the terminal  amine group
(-NH2) of  nylon to  the degree that  the  fiber has  less affinity for acid-type dyes.  Nylon 66
may suffer  chain  scission  when exposed to 1,880  to  9,400 ug/m  (1.0 to 5.0  ppm)  NO,,.   Field
exposures  of fibers  emphasize the  action of  acids derived from S02, although NOg may also be
present in  high  concentrations  in  urban sites.   Information on the  contribution  of  NO,, to
degradation is incomplete.
                                           13-23

-------
                             TABLE 13-9.   CORROSION OF METALS BY NITROGEN  DIOXIDE





co
i
tSi
•fa.


Metal
Mechanics of
Nickel Brass
Nickel Brass
Nickel
Tungsten
Electronic
contacts
Metal parts

Exposure
Corrosion - Function
Los Angeles
Los Angeles
Los Angeles
New York
Chamber
Field
Field

Pollutant
of Nitrates
Nitrates
Nitrates
Nitrates
N02
K02-S02-H2S
N02-S02-03

Effect

Strength
Loss
Strength
Loss
Corrosion
Change oxide
surface
Corrosion
film
Failure

Reference
Salvin et al. , 1977



Hermance et al . , 1971
McKinney and
Hermance, 1967
Hermance, 1966


Lazareva et al . , 1973
Chiaranzelli and
Joba, 1966
Gerhard and Haynie,

1974
Economic Costs of Corrosion
Fink et al.,  1971

-------
     Although a survey  of  the market for plastics  predicts  the use of 1.78 billion pounds in
1982,  there  is  essentially no  information  on  the effects of NO^  on  polyethylene,  polypropy-
lene, polystyrene, polyvinyl chloride, polyacrylonitrile, polyamides and polyurethanes.   Aging
tests  involve sunlight  exposure as well as exposure  to  ambient air.   Chamber exposure of the
above  plastics  to combinations of SO^,  NO^,  and 0, has  resulted  in  deterioration.   Nitrogen
dioxide alone has  caused  chain scission in nylon  and  polyurethane at concentrations of 1,880
and 9,400 |jg/m3' (1.0 to 5.0 ppm).
     The extensive data on  corrosion of metals in polluted areas relate the corrosion effects
to the  502 concentrati°ns-   The presence of NO^ and its  contribution is not evaluated despite
its presence as  acid aerosol in appreciable concentrations.
     Ammonium nitrates were  implicated  as  a factor in the  stress  corrosion cracking of wires
made of nickel  brass  alloy used in  telephone  equipment.   Since nitrate salts have  been shown
to be  more  hygroscopic than  either  chloride  or  sulfate salts, the presence of  nitrates  may
lower the humidity  requirements for  the formation of  an  aqueous electrolyte system  in the wet
corrosion of metals.
                                           13-25

-------
13.5  REFERENCES

Ajax, R.  L. ,  C.  J.  Cohlee, and  J.  B.  Upham.   The effects  of  air pollution on the fading of
     dyed fabrics.   J.  Air Pollut. Control Assoc. 17:220-224, 1967.

American Association of  Textile  Chemists and Colorists.  Cationic softeners—their secondary
     effects on  textile  fabrics.   Intersectional contest paper.  Philadelphia, Pennsylvania.
     Amer. Dyestuff Reporter 46:41, 1957.

American Association of  Textile  Chemists and Colorists.  AATCC Technical Manual.  Volume 48.
     Research Triangle Park, North Carolina. 1972, 370 pp.

Asquith, R.  S. ,  and  B.  Campbell.  Relation between  chemical  structure and fastness to light
     and gas fumes of nitrophenylamine dyes.  J.  Soc. Dyers Colour. 79:678-686, 1963.

Barrett,  L.  B. ,  and  t.  E. Waddell.   Cost of  Air Pollution Damage:  A Status Report.  AP-85,
     U.S. Environmental  Protection Agency, Research Triangle Park, NC, February 1973.

Beloin,   N.  J.   A field study-fading  of dyed fabrics by air  pollution.   Text.  Chem.  Color.
     4:43-48, 1972.

Beloin,   N.  J.   A chamber study-fading  of  dyed fabrics  exposed to  air pollutants.   Text.
     Chem. Color. 5:128-133, 1973.

Brysson, R.  J. ,  B.  J.  Trask, and  A.  S.  Cooper,  Jr.   The durability of cotton textiles:  the
     effects of exposure in contaminated  atmospheres.  Am. Dyest. Rep. £7:15-20, 1968.

Brysson, R.  J. ,  B.  J.  Trask, J.  B. Upham, and S. G.  Booras.  The effects of air pollution on
     exposed cotton fabrics.  J.  Air Pollut. Control  Assoc. 17:294-298, 1967.

Burr, F.  K. , and T.  E.   Lannefeld.   Yellowing  of white fabrics by  gas  fume  fading.   Asian
     Textile J.  2:27, 1974.

Chemical and  Engineering  News.   Reinforced plastics continue  heady  growth.   Chem. Eng. News
     55:22, November 7,  1977.

Chiaranzelli,  R.  V., and E. L.  Joba.   The  effect  of  air pollution on electrical  contact
     materials:   a field study.   J. Air  Pollut. Control Assoc.  16:123-127, 1966.

Couper,   M.   Fading  of   a  dye on cellulose  acetate  by light  and  by  gas fumes:   1,4-bis
     (methylamino)-anthraquinone.  Text.  Res.  J.  21:720-725, 1951.

Dexter  Chemical  Company.   Dextrol  softeners  resistant  to oxides  of  nitrogen.   Technical
     bulletin.

Fink, F. W. ,  F.  H.  Buttner, and  W.  K. Boyd.   Technical-Economic Evaluation of Air-Pollution
     Corrosion Costs on  Metals  in the U.S.  APTD 0654, U.S. Environmental Protection Agency,
     Research Triangle Park, NC,  February 1971.

Gerhard,  J. ,  and F.  H.  Haynie.    Air Pollution  Effects  on Catastrophic  Failure  of Metals.
     EPA-650/3-74-009,  U.S.   Environmental  Protection  Agency,  Research  Triangle  Park,  NC,
     November 1974.

Gillette, D.  G.   Sulfur  dioxide  and material  damage.  J. Air Pollut. Control Assoc. 25:1238-
     1243, 1975.


                                            13-26

-------
Haynie, F.  H. ,  J.  W.  Spence, and  J.  B.  Upham.  Effect of Gaseous  Pollutants  on  Materials—a
     Chamber  Study.    EPA-600/3-76-015,   U.S.  Environmental  Protection  Agency,   Research
     Triangle Park, NC, February 1976.

Hemphill, J.  E. ,  J.  E.  Norton, 0.  S.  Ofjord,  and R.  L.  Stone.   Color fastness  to  light  and
     atmospheric contaminants.  Text. Chem. Color. 8:25-27, 1976.

Hermance,  H.  W.   Combatting the  effects  of  smog  on wire-sprung relays.   Bell  Lab. Rec:
     48-52, 1966.

Hermance,  H.  W. ,  C.  A.  Russell,  E.  J.  Bauer,  T.  F.  Egan,  and H.  V.  Wadlow.   Relation of
     air-borne  nitrate  to  telephone  equipment  damage.   Environ.   Sci.  Technol. 5:781-785,
     1971.

Hertig, J.   Testing  nitric  oxide  fastness-experience  and  recommendations.   Textilveredlung
     3:180-190, 1968.

Imperial  Chemical  Industries.   Nylomine  Dyes:   Effect  of  Burnt  Gas Fumes.   ICI   Bulletin
     D1322, Imperial Chemical Industries Ltd,  Manchester, England,  1973.

Jellinek, H. H.  G.  Chain scission of polymers by small concentrations (1 to 5 ppm)  of  sulfur
     dioxide and  nitrogen  dioxide, respectively, in the presence of air and near ultraviolet
     radiation.   J.  Air Pollut.  Control Assoc.  20:672-674, 1970.

Jellinek, H. H. G.   Degradation of polymers at  low temperatures by N02, 03,  and near-ultra-
     violet light radiation.  Cold Regions Res.  Eng.  Lab.,  Hanover, New Hampshire.   USN  TIS
     AD 782950/OGA,  1974.   31 pp.

Jellinek, H. H. G. ,  F.  Flajsman,  and  F.  J.  Kryman.   Reaction  of S09  and N09 with  polymers.
     J. Appl.  Polym.  Sci.  13:107-116, 1969.                          *        L

Lazareva, I. Y. ,  D.  A.  Prokoshkin, E. V.  Vasil'eva,  and S. A. Skotnikov.  Reactional  diffu-
     sion during  oxidation  of tungsten alloys in an  atmosphere with a high concentration of
     nitrogen.   Prot.  Coat.  Met. (Engl. Transl.) 5:57-60, 1973.

McKinney, N. ,  and H.  W. Hermance.   Stress corrosion cracking  rates  of  a nickel-brass alloy
     under applied potential.   In:   Stress Corrosion Testing, A Symposium, 69th Annual Meet-
     ing, American  Society forTesting  and  Materials,  Atlantic City, New  Jersey,  June .26  -
     July 1, 1966.  ASTM  Special  Technical Publication No.  425, American Society for Testing
     and Materials,  Philadelphia, PA, December 1967.   pp.  274-291.

McLendon, V.,  and F.  Richardson.  Oxides of nitrogen as a factor in color changes of  used  and
     laundered cotton articles.   Am. Dyest. Rep.  54:15-21, 1965.

Morris,  M.  A.   Effect of  weathering  on cotton  fabrics.    Bull.   Calif.  Agric. Exp. Stn.
     (823):l-29, 1966.

Rabe, P.,  and  R.  Dietrich.   A comparison of methods for testing the fastness to gas  fading of
     dyes on acetate.   Am.  Dyest.  Rep. 45:737-740, 1956.

Romans, H.  B.   Stress  Corrosion  Test.'  Environments  and Test  Periods  Report of  ASTM Task
     Group B.   January 1965.   p. 58.
                                            13-27

-------
Rowe, F. M.,  and  K.  A.  J. Chamberlain.   The  "fading" of dyeings on cellulose acetate rayon.
     The  action  of  "burnt  gas  fumes"  (oxides  of  nitrogen,  etc.   in  the  atmosphere)  on
     cellulose acetate rayon dyes.   J.  Soc. Dyers Colour. 52:268-278,  1937.

Salvin, V.  S.   Relation  of atmospheric contaminants  and ozone to lightfastness.  Am. Dyest.
     Rep.  53:33-41, 1964.

Salvin, V.  S.   The effect of dry heat  on disperse dyes.  Am.  Dyest.  Rep.  55:490-501, 1966.

Salvin, V.  S.   Testing atmospheric fading of dyed cotton and rayon.  Am. Dyest.  Rep.  5:28-29,
     1969.

Salvin,  V.   S.    Color  fastness  to  atmospheric  contaminants.   Textile  Chem.   and Color.
     6(7):164-166, 1974a.

Salvin, V.  S.   Color  fastness to atmospheric  contaminants—ozone.   Textile Chem. and Color.
     6:41-45,  1974b.

Salvin, V.  S.   Yellowing  of white  fabrics  due to air  pollutants.   Collected papers of the
     American Association  of Textile Chemists and Colorists.   National Technical  Conference,
     New Orleans,  1974c.   pp. 40-51.

Salvin, V.  S.,  and  R.  A. Walker.   Service  fading of disperse dyestuffs  by chemical agents
     other than the oxides of nitrogen.   Text. Res. J. 25:571-582, 1955.

Salvin, V.  S. ,  and R.  A.  Walker.  Relation  of dye structure  to properties of disperse dyes.
     Am. Dyest.  Rep.  48:35-43, 1959.

Salvin, V.  S. ,  N.  Bornstein, and C.  T.  Bowman.   Effects of N02 on materials.   In:   Nitrogen
     Oxides.  National  Academy of Sciences, Washington,  DC, 1977.  pp.  159-196.

Salvin, V.  S.,  W.  D.  Paist, and W.  J.  Myles.  Advances in theoretical and practical  studies
     of gas fading.  Am.  Dyest.  Rep.  41:297-302, 1952.

Schmitt, C. H.  A.   Lightfastness of dyestuffs on textiles.  A.  Getting best  results  through
     optimum dyeing methods.  B.   Accurate evaluation through proper light test  procedures.
     Am. Dyest.  Rep.  49:974-980, 1960.

Seibert,  C.  A.    Atmospheric (gas)  fading  of colored  cellulose  acetate.   Am.  Dyest.  Rep.
     29:366-374, 1940.

Seymour, G. W. , and  V.  S. Salvin.   Process  of Reacting a Nitro-Hydroxy-Anthraquinone with  a
     Primary Amine and a  Product Thereof.  Patent  No.  2,480,269,  U.S. Patent Office, August
     30, 1949.

Travnic'ek,  Z.   Effects   of  air pollution on  textiles, especially   synthetic  fibers.   In:
     Proceedings of the  1st  International Clean Air  Congress,  Part I,  International  Union of
     Air Pollution Prevention Associations,  London,  England,  October 4-7, 1966.    National
     Society for Clean Air,  London, England, 1966.  pp.  224-226.

Upham,  J.   B.,  and V.  S. Salvin.   Effects  of  Air  Pollutants  on Textile  Fibers and Dyes.
     EPA-650/3-74-008,  U.S.   Environmental  Protection  Agency,  Research  Triangle  Park,  NC,
     February, 1975.
                                            13-28

-------
Upham, J.  B. ,  F.  H.  Haynie,  and  J.  W.  Spence.   Fading of  selected  drapery fabrics by air
     pollutants.   J. Air Pollut. Control Assoc.  26:790-792,  1976.

Urbanik,  A.  Reduction  in  blooming of disperse dyes on durable press  fabrics.  Textile Chem.
     and Color. 6:78-80, 1974.

U.S.  Tariff Commission.  U.S.  production of dyes and synthetic chemicals.  Washington, D.C.,
     1967.
                                                                                    •i
Waddell,  T. E.   The Economic Damages of Air Pollution.  EPA-600/5-74-012, U.S. Environmental
     Protection Agency, Washington, DC, May 1974.

Yocum, J.  E. ,  and N.  Grappone.  Effects of Power Plant Emissions on Materials.  EPRI EC-139,
     Electric  Power Research Institute, Palo Alto, CA, July 1976.

Zeronian,  S.  H. , K.  W.  Alger,  and  S.  T.  Omaye.   Reaction  of  fabrics  made  from synthetic
     fibers to  air contaminated with nitrogen  oxide,  ozone, or  sulfur dioxide.   J_ri:   Pro-
     ceedings   of the  Second  International  Clean Air  Congress,  International Union  of Air
     Pollution Prevention Associations, Washington, D.C., December 6-11,  1970.  H. M. Englund
     and W. T.  Beery,  eds. ,  Academic Press, Inc., New York, NY, 1971.  'pp. 468-476.
                                            13-29

-------

-------
                 14.  STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS

14.1  INTRODUCTION
     The  toxicity  of  the oxides of nitrogen has been studied in a number of species including
man.   Previous reviews  of the  literature  have appeared  in  criteria and  related documents.
Government-sponsored  reviews  include  the  1971  criteria  document  on oxides   of  nitrogen
(U.S.  Environmental  Protection  Agency,  1971),  the  National  Academy  of  Sciences  monograph
(Crocker  et al. ,   1977),  the North  Atlantic Treaty  Organization  document (Committee  on the
Challenges  of  Modern Society,  1973)  and  the USEPA document concerning  short-term effects of
N02  (U.S.  Environmental  Protection Agency,  1978).   A World  Health  Organization monograph has
been recently  published  (World  Health Organization, 1977), as have two excellent  interpretive
reviews by  Coffin  and Stokinger (1977) and by Morrow (1975).   The reader is referred to these
publications for a  general background on the toxicity of the oxides of nitrogen (NO ).
     Most  of the  data presented in  this  chapter  relate to nitrogen  dioxide  (N0~) because it
appears to be  the most toxic oxide of nitrogen and most widely distributed in a manner affect-
ing  human health.   The  data presented are  confined  to animal  studies as  they  may  relate to
human health.
     The  focus of  this  chapter is to present  information  relating  to effects on  animals as a
result of exposures to  nitrogen oxides and  other  nitrogen-containing compounds at concentra-
tions below 9,400  (jg/m   (5  ppm).    Data  derived  from  exposures  to  higher  concentrations of
these compounds have  been presented in concise form.   Except  for a few instances, these data
are presented  in the tables only.
14.2  NITROGEN DIOXIDE
14.2.1  Respiratory Tract Transport and Absorption
     Nitrogen  dioxide   is   soluble   and   can  be  absorbed  in  the  mucous  lining  of  the
nasopharyngeal  cavity where it   converts  to  nitrous  and nitric  acid.   However,  few  data
examining respiratory tract  uptake and  transformation have been published.   (See Table 14-1.)
Yokoyama  (1968)  used isolated  upper airways of  the  dog  and  rabbit to  measure  N02 removal,
which amounted to  42.1  percent  of the incoming NO;, concentration.   Dalhamn and Sjbholm (1963)
measured  the concentration of  N0~  in a stream  of  water-saturated  air before and after it had
been passed  through the  nose and  out a tracheal  cannula inserted in an  anesthetized  rabbit.
Considerable variation occurred  between animals,  but about 50 percent of the incoming NOp was
removed on a single passage through the nasopharyngeal cavity.
     Goldstein et al.  (1977b) exposed monkeys for 9 minutes to 560 to 1,710 pg/m   (0.3 to 0.91
              -] o
ppm) NO- plus   NOp.  During quiet respiration,  50 to 60 percent of the inspired pollutant was
retained  by  the  animal;  radioactivity  was  distributed throughout the  lungs.   Once  absorbed,
NCL or chemical intermediates  derived from NO, remained within the lung for prolonged periods
                      -IT                       f-
following exposure.     N-radioactivity  was  detectable  in extrapulmonary sites  as well.   The
authors postulated that N02 reacted with water in  the nasopharynx and lungs to form nitric and
nitrous acids which then react with pulmonary and  extrapulmonary tissues.

                                             14-1

-------
TABLE 14-1.   RESPIRATORY TRACT TRANSPORT AND ABSORPTION

N02
Concentration Duration
ug/m3
Not
Reported
560 to
1,710
188,000
ppm (min)
Not Not
Reported Reported
0.3 to 9
0.91
100 < 45
Species Effect
Dog and Removal of 42.1% by isolated upper airways.
rabbit Concentration and flow rates not given.
13
Monkey Concurrent exposure to N0? demonstrated that
N0? was evenly distributed fn the lungs and
absorbed into the blood.
Rabbit Absorption of approximately 50% N0? in the
nasopharyngeal cavity.
Reference
Yokoyama, 1968
Goldstein et
al. , 1977b
Dalhamn and
Sjohblm, 1963

i—1
-p*
ro







-------
     Observed  effects  of exposure  to  much higher concentrations of  N0~  include cessation of
cilia beating  (Dalhamn  and  Sjoholm, 1963) and  detection  of nitrates and nitrites in urine of
         ^
animals (Svorcova and Kaut,  1971).
14.2.2  Mortality
     In a  survey  of the acute toxicity  of NO,  to mice, rats, guinea pigs, rabbits, and dogs,
                                                               3
Mine et al.  (1970)  found that concentrations below 94,000 |jg/m  (50 ppm) rarely produced mor-
tality at  exposures  up  to 8 hours.  The effects  varied from species to  species.   (See Table
14-2.)   Dogs  and  rabbits  appear to  be  relatively  resistant  to  acute toxicity.   In rats,
factors associated  with  increased mortality at high concentrations of NOp include cold stress
and adrenalectomy.
     Dietary  supplementation  of Vitamin E (45  to 100 mg d, 1-crtocopherol) has  been  shown to
protect against mortality and  increase mean survival of  animals exposed, for long periods of
                                                              •3
time, to  high concentrations  of NO-  (37,600  to  62,000  ug/m ;  20 to  33 ppm)  (Fletcher  and
Tappel,  1973;  Menzel  et al., 1972).   The  influence  of  dietary  components on  NO-  toxicity is
discussed more fully in Section 14.2.3.2.1.
14.2.3  Pulmonary Effects
14.2.3.1   Host Defense  Mechanisms—In  the  past,  environmental  toxicologists have been  con-
cerned  with  measurement  and  description  of  effects  of  single  toxic  agents  such  as  S0~
(Fairchild et  al.,  1972), N02  (Coffin et al.,  1976;  Ehrlich,  1963;  Purvis and Ehrlich,  1963),
and 0,  (Coffin and Gardner, 1972)  on  host defense mechanisms.   Accumulation of considerable
information  indicates  a pathophysiological interrelationship between exposure to  atmospheric
pollutants and enhanced respiratory susceptibility to bacterial .and viral  infections.
     Due to  practical difficulties  associated  with the  study  of the effects  of air pollutants
on the susceptibility of the human respiratory system to microbial infection,  animal  exposures
have been undertaken and several  models used.
     Normally,  the  lungs are  protected  from viral  and bacterial  infection  by the  combined
activities of the mucociliary,  phagocytic (alveolar macrophage),  and immune systems.   The muco-
ciliary  system,  which  extends from the  nares  to the terminal  bronchioles,   removes  50 to 90
percent  of  deposited particles  within  hours after' they  enter the lung (Cooper  et  al. , 1977;
Murphy,  1964).   It  is  important  to emphasize that  the discontinuous  nature of the  mucous
blanket  precludes  complete  cleansing of  microbes  and particles  from  the   bronchial  tree.
Surviving  microbes and  residual  particles  are  phagocytized,  killed,  and/or  removed  by  macro-
phages that  are attracted to  the foreign bodies by chemotactic factors.   Microorganisms,  upon
entrance  to  the  lung,  also stimulate the formation of  various humoral defense  mechanisms.
Interference, by N0?) with any  of the interdependent  steps in  this complex sequence of humoral
and phagocytic reactions or  with  components of  the mucociliary transport system increases  host
susceptibility to infection.
14.2.3.1.1  Interaction  with infectious agents.   Extensive studies using the  infectivity model
to examine the effect of  NO  on susceptibility to airborne infection are reviewed by Ehrlich
                                             14-3

-------
                         TABLE 14-2.   MORTALITY  FROM N02  EXPOSURE  FOR  1 TO  8 HOURS

N02
Concentration
ug/mj
94,000
to
141,000
141,000
141,000
141,000
141,000
141,000
173,000
ppm
50
to
75
75
75
75
75
75
92
Duration
(hr)
4 or 8
1 to 8
1 to 8
1 to 8
1 to 8
1 to 8
< 8
Species
Rat
Rat
Guinea pig
Rabbit
Dog
Mouse
Mouse
Effect
Increased mortality with cold stress,
adrenal ectomy, and exercise.
No increase with heat or prior N0?
Estimated LT50* 3.7 hr
Estimated LT50 4.0 hr
Estimated LT50 2.7 hr
Estimated LT50 >8 hr
Estimated LT50 2.3 hr
Genetic effects on mortality of inbred
mouse strains. LT50 for CF1, 3.33 hr;
C57BL/6, 6.53 hr
Reference
Hine et al . ,
Hi ne et al . ,
Hine et al . ,
Hine et al . ,
Hine et al . ,
Hine et al . ,
Goldstein et
1973a

1970
1970
1970
1970
1970
1970
al.,

*LT50 = Time at which 50% of the animals would die during continuous exposure to the indicated concentration.

-------
(1975), Coffin  et  al.  (1976) and Gardner  and  Graham (1976).   (See Table 14-3.)  The infecti-
vity model  system  has  been employed successfully with  hamsters  (Ehrlich, 1966), mice (Coffin
and  Gardner,  1972; Coffin  et al.,  1976;  Ehrlich,  1963;  Fairchild et  al.,  1972;  Purvis and
Ehrlich, 1963),  and  squirrel  monkeys (Henry et al., 1970).  Animals are randomly selected for
exposure  to either  a  test substance  in  air  (in  this  case NOp) or  filtered air.   After
exposure,  control  and  exposed animals are placed in  another chamber and exposed  for a brief
period  (approximately  15  minutes)  to  aerosols of  a  specific   infectious  agent,  such  as
Streptoccoccus  pyogenes  (S.  pyogenes),  Klebsiella  pneumoniae (K^_  pneumom'ae),  Diploccoccus
pneumoniae (th_ pneumoniae), influenza A^/Taiwan virus, or A/PR/8 influenza virus.  The animals
are then returned to clean air for a 15-day holding  period and the mortality rates in the NO,,-
exposed and  control  groups are compared.  The mortality of the control  group is usually 15 to
20 percent.  Death is due to pneumonia and its consequences (Gardner and Graham, 1976).
     In a  series  of  investigations,  the relationships  of  concentration  and time to suscepti-
bility  to  respiratory  infection  and to subsequent  mortality in  infections  with  S.  pyogenes
were examined  (Gardner  et al.,  1977b;  Gardner et al.,  1977a, Coffin et al., 1977).   The con-
                                                          0
centrations of  NCL were varied from 1,880 to  26,320  ug/m  (1 to 14 ppm), and the duration of
exposure ranged  from  0.5 to 7 hours so  that  the product of concentration and time equalled a
value of 7.  Exposure to high concentrations of N02  for brief periods of time resulted in more
severe  infections  and  in  greater  mortality  than did prolonged exposures to lower  concentra-
tions of NO,,.   This  indicated that susceptibility to infection was influenced more by concen-
tration of NOp than by duration of exposure.   (See Table 14-4.)
     As depicted in Figure 14-1,  Gardner et al. (Gardner et al.,  1977b),  using the same model,
examined the effect of  varying durations of continuous exposure  on the mortality of mice ex-
posed to  6 constant concentrations  of  NO,  (940 (jg/m  to 52,670  ug/m ; 0.5 to 28  ppm).   S.
                                                              3
pyogenes was  used  for   all  concentrations,  except  940  ug/m  (0.5  ppm),   in  which case  K.
pneumom'ae was  used.   A  linear  dose-response (p <  0.05)  indicated that mortality  increases
with increasing  length  of exposure to  a given concentration of NOp.  Mortality also increased
with increasing concentration  of  NO,,.   When C x T was held constant, the relationship between
concentration and time  produced  significantly  different mortality responses.  At a constant C
                                                                              o
x  T  of  approximately   21  (ppm x  hour),  a  14-hour  exposure at  2,800  ug/m  (1.5  ppm)  N09
                                                                                3
increased mortality by  12.5 percent  whereas a 1.5-hour exposure  at 27,300  ug/m  (14 ppm) NO^
enhanced mortality  by  58.5 percent.  These  studies  confirmed  the previous conclusion  that
concentration is more important  than time  in  determining  the degree of injury induced by NO,,
in this model.   According to Larsen  et  al. (1979),  N02 modeling studies have  shown  that the
concentration (c) of N02 expected to cause a  certain mortality level (z) as a function of the
hours of exposure (t)  can be expressed  as c =  9.55 (2.42)zt  '  .
     Gardner et al.  (1979) also compared the effect  of continuous versus intermittent exposure
to NOp  followed  by  bacterial challenge with S. pyogenes (Figures  14-2,  14-3).   Mice  were
exposed either  continuously or  intermittently (7 hours/day,  7  days/week)   to  2,800  ug/m  or
6,600 pg/m3  (1-5  or  3.5  ppm) N02>   Figure 14-2  illustrates the  results  of  continuous  and

                                             14-5

-------
                                          TABLE 14-3.   INTERACTION WITH INFECTIOUS AGENTS

N02
Concentration
ug/m3
560
to
940

940
940
to
1,880
18,800
ppm
0.3
to
0.5

0.5
0.5
to
1
10
Exposure Species
Continuous, Mouse
3 mo
Continued
3 mo more
Intermit- Mouse
ent 6 or 18
hr/day, to 12 mo
Continuous,
90 days
Continuous Mouse,
39 days female
2 hr/day,
1, 3, 5
days
Infective
Agent Effect Reference
A/PR/8 virus High incidence of adenomatous Motomiya et al.,
proliferation of peripheral 1973
and bronchial epithelial cells.
NOp alone & virus alone caused
less severe alterations.
No enhancement of effect of N0?
and virus.
K. pneumoniae Increased mortality after Ehrlich and
6 mo intermittent exposure Henry, 1968
or after 3, 6, 9, or 12 mo
continuous exposure. Following
12 mo exposure, increased
mortality was significant only
in continuously exposed mice.
A/PR/8 virus Significantly increased suscep- Ito, 1971
tibility to infection.

 1,880      1     17 hr             Mouse      S.  aureus
                                               after N0£

 4,320     2.3
12,400     6.6
2820 to    1.5 to  (See Figure 14-1) Mouse      S.  pyogenes
52,670     28
Bactericidal activity unchanged.
6% decrease in bactericidal
activity (p<0.05).

35% decrease in bactericidal
activity (p<0.01).

Increased mortality with in-
creased time and concentration.
Goldstein et al.,
1973b
Gardner et al.,
1979

-------
TABLE 14-3.   (continued)

N02
Concentration
ug/ms ppm
1,880 1
5,600 3

2,820 1.5






6,600 3.5






8,100 4.5



2,800 1.5
(8,100 4.5)
spike


Exposure Species
3 hr Mouse


Continuous Mouse
or inter-
mittent
7 hr/day,
7 days/wk


Continuous
or inter-
mittent
7 hr/day,
7 days/wk,
to 15 days

1, 3. 5 or Mouse
7 hrs


Cont. 62 hrs. Mouse
then spike for
1, 3.5 or 7 hr. ,
then cont. 18
hrs.
Infective
Agent Effect Reference
S. pyogenes Exercise on continuously moving 11 ling et al . ,
wheels during exposure increased 1980
mortality at 5,600 ug/m (3 ppm)
N02.
S. pyogenes After 1 wk, mortality with con- Gardner et al.,
tinuous exposure greater (p < 1979
0.05) than that for intermit-
tent. After 2 wk, no signif-
icant difference between con-
tinuous and intermittent expo-
sure.
Increased mortality with in-
creased duration of exposure.
No significant difference
between continuous and intermit-
tent exposure. With data adjusted
for total difference in C X T,
mortality essentially the same.
S. pyogenes Mortality proportional to dura- Gardner et al.,
tion when bacterial challenge (1982)
was immediately, but not 18
hrs post exposure
S. pyogenes Mortality increased with 3.5 Gardner et al. ,
and 7 hr. single spike when (1982)
bacterial challenge was
immediately or 18 hrs post
exposure

-------
                                                      TABLE 14-3.  (continued)
I
oo

N02
Concentration
ug/mj ppm
2,800 1.5
(8,100 4.5)
continuous:
100 0.05+
100 0.05 03
with spikes 2x per
200 0.1+
200 03 0.1 03
continuous:
940 0.5
100 0, 0.05 07
Exposure Species
Cont. for 14 d Mouse
spike 2x1 hr/d
5 days/wk x 2 wk
Cont. Mouse
day:
15 days
(spikes-1 hr,
twice/day, 5
days/wk)
Mouse
Infective
Agent Effect
S. pyogenes 1 wk or 2 wk needed for in-
creased mortality depending
on time of infection (See
text for details)
S. pyogenes No effect
S. pyogenes Increased mortality with N00
alone; no effect 0, alone;
Reference
Gardner et al. ,
(1982)
Gardner et al . ,
(1982)
Gardner et al. ,
(1982)
    with spikes 2 x per day:
     1,880     1.0+
                                                                          synergistic effect  0., +  N09
     200 0,
0.1 0-
        continuous:
     2,300     1.2+
       200     0.1 0-
    with spikes 2 x per day:
     4,700     2.5
            Cont.  15 days
            (spikes-1 hr,
            twice/day, 5
            days/wk)
       600 03  0.3 03
     2,800
1.5
Cont.
                    Mouse
Mouse
             >. pyogenes    Increased mortality with NO,
                           alone and 0., alone; additiv^
                           effect of 03 + N02
S.  pyogenes    Elevated temp. (32° C) in-
               creased mortality
                                                Gardner et al.,
                                                (1982)
Gardner et al.,
(1982)

-------
TABLE 14-3.   (continued)

N02
Concentration
ug/m-1
3,570
7,140
13,160
17,200
27,800
3,760
4,700
47,000
9,400
18,800
28,200
6,580
65,830
ppm Exposure
1.9 4 hr
3.8
7
9.2
14.8
2 3 hr
2.5 2 hr
25
5
10
15
3.5 2 hr
35 2 hr
Infective
Species Agent
Mouse Infected with
S. aureus
prior to NO-
exposure



Mouse S. pyogenes
Mouse Challenge
with K.
pneumoniae
before and
after ex-
posure

Mouse K. pneumoniae
challenge
Hamster after
Effect Reference
Physical removal of bacteria Goldstein et al . ,
unchanged at 3,570 and 7,140 1973b
ug/mj (1.9 and 3.8 ppm).
7% lower bactericidal activity
(p<0.05).
14% lower bactericidal activity
50% lower bactericidal activity
Increased mortality (p<0.05) Ehrlich et al.,
1977
No effect og mortality. At Purvis and
47,000 ug/m (25 ppm) effect Ehrlich, 1963
when bacterial challenge was
up to 72 hrs. but not later,
after N02 exposure ceased.
Significant increase in
mortality on K. pneumoniae
challenge 1 and 6 hr post NO-.
When K. pneumoniae challenge
27 hr post WO, effect only at
28,200 ug/m fl5 ppm).
NO, toxic to all species and in- Ehrlich, 1975
creased mortality. Each species
had decreased resistance to NO.

-------
                                              TABLE  14-3.   (continued)

N02
Concentration
|jg/m3
94,050
9,400
ppm Exposure
50 2 hr
5 Continuous,
2 mo
Species
Squirrel
monkey
Squirrel
monkey
Infective
Agent Effect

K. pneumonias One-third died after infection.
and A/PR/8
Reference

Henry et al . ,
1970
19,000      10    Continuous
                  1 mo
 9,400       5    2 mo
19,000      10    1 mo
            virus

                          Death within 2-3 days after in-
                          fection.   Increased susceptibil-
                          ity to infection.   Decreased lung
                          clearance of viable bacteria.

Squirrel    K.  pneumoniae Mortality 2/7.   Bacteria present
monkey                    in lung of survivors upon
                          autopsy.

                          Mortality 1/4.   Bacteria present
                          in lungs of survivors at
                          autopsy.
Henry et al.,
1969
94,000      50    2 hr
                          Mortality 3/3.

-------
        TABLE 14-4.   THE INFLUENCE OF CONCENTRATION AND TIME ON EHNANCEMENT
             OF MORTALITY RESULTING FROM VARIOUS N02 CONCENTRATIONS3

Concentration x time
Concentration
pg/rn3
2,820
6,580
13,160
26,320
52,640
ppm
1.5
3.5
7
14
28

Time
(hrs)
4.7
2.0
1.0
.5
.25
7
%
Mortality
6.4
18.7
30.2
21.7
55.5

Time
(hrs)
9.3
4.0
2.0
1.0
.5
14
%
Mortal ity
10.2
27.0
41.8
44.9
67.2

Time
(hrs)
14.00
6.00
3.00
1.50
.75
21
%
Mortality
12.5
31.9
48.6
58.5
74.0

aThese are predicted values obtained from Figure  1 of Gardner et al.,  1979.
                                      14-11

-------
o
2
01
DC
Q

>
QC
O
o
U

CM
O
U
cc
90


80


70


60


50


40


30

20


10


  0


-10
                                                  1     1     II      II       II      I       II       III
                15  253035

                minutes
                            1

                          •-W-
                                 2357      14    24    48

                                               hours
96
 1416   30     23       6  9  12

days	e»~f-«a	months     "H
                                                             TIME
       Figure 14-1. Regression lines of percent mortality of mice versus length of continuous exposure to various NC>2 concentrations prior to
       challenge with hacterin (Gardner et al., 1977h).

-------
   a:
   O
OJ 01
   O
   a:
       90
       80
       70
       60
       50
       40
       30
       20
       10
—a

  cr
D
                            O
                            n
                           o

                           a
                                                              O CONTINUOUS
                                                              D INTERMITTENT
                                                                                                                      o—
                                                       CONTINUOUS NO2 EXPOSUHEXA
                                                       INTERMITTENT NC»2 EXPOSURE
                                                                    ffV
          0 7
                                                     127
                                                             151
                                                                      175
                                                                              199
                                                                                      223
                                                                                               247
                                                                                                       271
                                                                                                      295
                                                                                                                      343
                                                                   TIME, hours
    Figure 14-2.  Percent mortality of mice versus the length of either continuous or intermittent exposure to 6,600 ug/m^ (3.5 ppmj IMO2 pnor
    to challenge with streptococci (Gardner et al., 1977b; Gardner et al.r 1977a;  Coffin et al., 1977).

-------
O
CE
o
(J
 I
 fM
O
UJ
tr
UJ
    30
    20
t   10
_J
<

tr
O
o
oc
      0 7
                                             O* CONTINUOUS
                                                                                      O




                                                                                      D
                                             D   INTERMITTENT
             D
                    D
                           a
                                                                                         'CONTINUOUS AND INTERMITTENT
                                                                                          TREATMENT MEANS ARE SIGNIFICANTLY
                                                                                          DIFFERENT ATp<0.05
                                                   CONTINUOUS N07 EXPOSURE
                                                 '/ INTERMITTENT NOzEXPOSURE
                         79
                                            151
                                                                                      319
                                                               TIME, hours
                                                                                                                                487
 Figure 14 3.  Percent mortality of mice versus length  of either continuous or intermittent exposure to 2.800

challenge with streptococci (Gardner etal., 1977b; Gardner et al.. 1977a; Coffin et al., 1977).
                                                                                                             (1.5 ppm) NO2 prior to

-------
 intermittent  exposure to  6,600  ug/m  (3.5 ppm)  NO^  for periods up to  15  days.   There was a
 significant increase  in mortality for each of the experimental groups with  increasing duration
 of  exposure.   When the  data were  adjusted  for  the  difference in  C  x  T,  the mortality was
 essentially the  same  for the continuous  and  intermittent groups.   The continuous exposure of
                   3
 mice  to  2,800 ug/m  (1.5 ppm) N0~  increased mortality after 24 hours of exposure.  During the
 first week of exposure, the mortality was significantly  higher in mice exposed continuously to
 NOp than in those exposed intermittently.  By the 14th day of exposure, the difference between
 intermittent and continuous exposure became indistinguishable (Figure 14-3).
     Mice  were  exposed continuously or  intermittently  (6 or 18 hours/day)  to  940 ug/m  (0.5
 ppm)  NOp for up  to 12  months  (Ehrlich and Henry, 1968).   Neither  exposure regimen affected
 murine  resistance  to  K^_  pneumoniae  infection  during   the  first  month.    Those  exposed con-
 tinuously  exhibited decreased  resistance to the  infectious  agent  as demonstrated by enhanced
 (p  <  0.05) mortality  at 3, 6, 9,  and  12 months.   In another  experiment,  an enhancement (p <
 0.1)  did not  occur at 3 months  but was observed after  6 months of exposure.  After 6 months,
 mice  exposed  intermittently  (6  or  18 hours/day) to N0?  showed significant  (p < 0.1) increases
 in  mortality  over  that of controls (18%).  After 12 months exposure to NCL, mice in the three
 experimental  groups showed a reduced capacity  to clear viable bacteria  from  the lung.   This
 was first  observed  after 6 months  in the continuously  exposed mice and after 9 months in the
 two intermittently  exposed  groups.   These changes, however, were not statistically tested for
 significance.   Only the continuously exposed  animals  showed  increased mortality  (23%)  over
 controls following  12  months  exposure.   Therefore, while  it  is  not possible to directly com-
 pare  the results  of studies using  S^_ pyogenes  to those using K^ pneumoniae, the data suggest
 that  as  the concentration  of  N0?  is decreased,  a  longer exposure time  is  necessary  for the
 intermittent  exposure  regimen  to produce a  level  of  effect equivalent to  that  of continuous
 exposure.
     Gardner et al.  (1982)  investigated further the effects of  intermittent exposures on the
 response of  mice  to airborne infections.  The  objective of these studies  was  to investigate
 the toxicity  of spikes of NOp  exposure superimposed on a lower continuous NO^ exposure.   Such
 a regimen approximates the pattern of exposure which man receives in urban environments.   Mice
were exposed to spikes of 8,100 ug/m  (4.5 ppm) for 1,  3.5 or 7 hrs and exposed to S.  pyogenes
either immediately  or 18 hrs afterwards.  Mortality  was proportional  to the duration  of the
 spike when  mice  were  exposed  immediately,  but  mice  recovered  from the exposure  by  18 hrs.
When these same spikes were superimposed on a  continuous  background of 2,800 ug/m  (1.5 ppm)
 for 62  hrs preceding  and 18 hours  following  the spike, mortality was  significantly  enhanced
 (p < 0.05)  only by a spike of 3.5 or 7  hrs when the infectious  agent was administered 18 hours
after the  spike.   Possible  explanations for these differences  in the presence or absence of a
background  exposure are that mice  continuously exposed are not capable of  recovery  or that
alveolar macrophages  or polymorphonuclear  leukocytes  recruited  to the site of  infection are
 impaired by  the  continuous exposure  to  NOp-   The  effect of multiple spikes was  examined  by
                                             14-15

-------
exposing mice  for  2  weeks to two  daily  spikes  (morning and afternoon) of 1 hr of 8,100 ug/m
(4.5 ppm)  superimposed  to a continuous background of  2,800 ug/m  (1.5 ppm).   Spikes were not
superimposed on  the  continuous background  during  weekends.  Mice were exposed  to  the infec-
tious agent  either immediately  before or after the  morning spike.   When the infectious agent
was given before the  morning spike, the increase in mortality did not approach closely that of
a  continuous  exposure to  2800  |jg/m   (1.5  ppm).   However,  in mice exposed after  the morning
spike, by  2  weeks  of exposure,  the  increased mortality over controls approached that equiva-
                                         2
lent to continuous exposure to 2,800 ug/m  (1.5  ppm).
     In this same study, Gardner et al. (1982) also examined the effects of exposure to spikes
of 03 and NO,,,  and heat stress.   At the lowest concentration of 0, and NOp examined, 100 ug/m
(0.05 ppm) with  spikes  of 200 ug/m  (0.1 ppm),  no differences in mortality were observed com-
pared to clean air controls.   When mice were exposed to intermediate (0.5 ppm NOp with 1.0 ppm
spikes  and 0.05 ppm  03  with 0.1  ppm  spikes)  or  high (1.2 ppm N0~  with 2.5 ppm  spikes  and
0.1 ppm 0, with  0.3  ppm  spikes) doses, mortality was increased synergistically;  e.g., mortal-
ity was greater than  the arithmetic sum of the mortality due to the single gas exposure.   When
mice were  stressed by  elevated temperature (32°C),  7 daily,  but  not 4  daily,  exposures to
2,800 ug/m  (1.5 ppm) enhanced mortality and decreased survival times.
     Another stress,   exercise,  was also evaluated with the  infectivity  model  (Illing et al. ,
1980).   Mice running  on an activity wheel during exposure were more susceptible to 5,600 ug/m
(3.0 ppm) than those  resting.
     Gardner et  al.  (1982)  concluded that while a  simple  log-log  relationship exists for the
mortality associated with  a  given exposure-time product with mice continuously exposed to NCL
                                                                                         $
or given  intermittent regular  exposures,  no such  relationship exists  for mice continuously
exposed';to a constant  concentration of NO- upon which are superimposed spikes of greater con-
centration.  The  relationship  is  highly  complex depending  in part upon  the  duration  of the
spike and the time since the last exposure of the spike.
     Mice, hamsters,  and monkeys were exposed to NOp for 2 hours followed by a challenge of K.
pneumoniae (Ehrlich,  1975).   Nitrogen dioxide  enhanced the mortality due to  the  pathogen in
all species tested.   Differing results among species were found.   This could be due to differ-
ing sensitivity  to either the pathogen or  N09,  or  a combination of both.  All three squirrel
                                3
monkeys -exposed  to 94,050 ug/m  (50 ppm)  NO,  died  from the pneumonia (Henry et  al.,  1969).
                                                   T
Lower concentrations  tested  (9,400  to 65,830 ug/m  ;  5  to  35 ppm) had no effect  in monkeys.
The hamster  model,  which exhibited  enhanced  mortality due to N09  at  concentrations > 65,830
    o                                           3
ug/m  (35  ppm)  but not at 9,400 to  47,000  ug/m  (5 to 25 ppm), had intermediate sensitivity.
The mouse  model  was   sensitive  to  NOp  exposure as evidenced  by enhanced mortality following
exposure to  6,580  ug/m3  (3.5 ppm) but not  to 2,820 to 4,700 ug/m3 (1.5 to 2.5 ppm) N02 for 2
hours (Ehrlich,  1975).   No  effect on mortality was  observed in mice exposed for  2 hours to
           o
4,700 ug/m   (2.5 ppm) (Purvis  and  Ehrlich,  1963).   However,  when S.  pyogenes was  the infec-
tious agent,  a 3-hour exposure to 3,760 ug/m  (2 ppm)  NO., caused an increase  (p  < 0.05) in
mortality (Ehrlich et al., 1977).

                                             14-16

-------
     The  persistence  of  the  N02 effect  was  investigated by  Purvis and  Ehrlich  (1963) who
exposed mice  for 2 hours to  NOp  before or after an aerosol challenge with K. pneumoniae.  At
9,400,  18,800,  28,200, and 47,000 (jg/m3  (5,  10,  15,  and 25 ppm) N02> there was a  significant
enhancement  of mortality  in  mice challenged  with  bacteria 1  and 6  hours  after  the N0? ex-
posure.  When  bacterial  challenge was  delayed  for  27  hours,  there was  an  effect  only in the
                            3                                  3
group exposed to 28,200 |jg/m   (15 ppm).   Exposure to 4,700 ug/m  (2.5 ppm) caused no effect at
any of the bacterial challenge times tested.  Exposure of 47,000 ug/m  (25 ppm) N0? for 2 hours
with  subsequent K.  pneumoniae challenge  6 and  14 days later did  not affect mortality.   When
the experimental  regimen  was  reversed  and  mice were  exposed  for 2 hours to  47,000 ug/m  (25
ppm)  NO,,,  mortality was  significantly increased 1,  6,  27,  48 and  72  hours  after bacterial
challenge.   Dose response  studies  in  which  mice were challenged  1  hour after a  2  hour NO,
                                3
exposure showed  that 6,580 ug/m  (3.5  ppm)  had a significant effect; exposure concentrations
of 2,820 and 4,700 (jg/m3 (1.5 and 2.5 ppm) did not.
     Environmental stress  has been  shown  to enhance the  toxic  effect of NO,.   Mice placed on
                                                                  3
continuously moving  exercise  wheels  during exposure to 5,600 ug/m  (3 ppm) N00, but not 1,880
    3
ug/m  (1 ppm),  for 3  hours showed enhanced mortality  over nonexercised N0? exposed mice (p <
0.06) using  the  infectivity model (Illing et al., 1980).   The presence of other environmental
factors,  ozone  (0,)  (Ehrlich et al.,  1977, Gardner  et  al.,  1982)  or tobacco smoke (Henry
et al., 1971),  also  augments  the deleterious effect of NO,, on host resistance to experimental
infection (see Section 14.3).
                                                                         3                3
     Squirrel monkeys  exposed continuously to N02 levels of  18,800 ug/m  and 9,400 ug/m  (10
ppm and 5  ppm)  in air for  1  and  2  months, respectively,  showed increased susceptibility to a
challenge with  K.  pneumoniae or  influenza A/PR/8 virus  and reduced  lung clearance of viable
bacteria (Henry et al., 1970).  All  six animals exposed to 18,800 ug/m  (10 ppm) died within 2
to 3 days of infection with the influenza virus.  At 9,400 ug/m  (5 ppm), one of three monkeys
died.   Susceptibility  to  viral  infection also was enhanced when  the  N09 exposure  occurred 24
                                                           3
hours after  infectious challenge.   Exposure to 94,000 ug/m   (50  ppm) N02 for 2 hours was not
fatal, whereas  the  same  exposure  followed by challenge with  K.  pneumoniae was fatal  to three
out of three monkeys  (Henry et al., 1969).   After  challenge  with K.  pneumoniae,  two of seven
                               3
monkeys exposed  to 9,400  ug/m  (5  ppm)  for  2  months  died and  the rest had  bacteria in the
lungs on autopsy.  After an exposure to 18,800 ug/m  (10  ppm)  for 1 month,  one of four monkeys
died,  and the  pathogen was present  in  the lungs of the remainder of the animals at autopsy 19
to 51 days post-exposure.
     Mice exposed continuously  for  3 months to 560 to 940 ug/m  (0-3  to 0.5 ppm)  NO,, followed
by  challenge with  A/PR/8  influenza  virus  demonstrate  significant  pulmonary  pathological
responses.   Motomiya et al.  (1973)  reported a greater incidence  of adenomatous proliferation
of  bronchial  epithelial  cells following  combined .exposures;  viral   exposures  or N0~  alone
caused less severe alterations  than  the combination of N02 plus  virus.   Continuous N02 expo-
sure for an  additional 3  months did not  enhance  further  the  effect of  N02  or the subsequent
virus  challenge.

                                             14-17

-------
     Ito (1971)  challenged  mice with influenza A/PR/8 virus  after continuous exposure to 940
to 1,880 ug/m3  (0.5 to 1 ppm)  N00  for  39 days and to 18,800 (jg/m3 (10 ppm) NO,  for  2 hours
                                                                             3
daily for  1,  3,  and 5 days.  Acute  and intermittent  exposure to 18,800 ug/m  (10 ppm) NO, as
                                                  3
well  as continuous  exposure to  940 to  1,880  ug/m  (0.5  to 1 ppm) N02 increased the suscepti-
bility of mice to influenza virus as demonstrated by increased mortality.
     The enhancement in mortality following exposure to NO^ and a pathogenic organism could be
due  to  several  factors.    One  could be  a decreased  ability of  the  lung to  kill  bacteria.
Studies by Goldstein  et  al. (1973b, 1974) illustrated this concept in a series of experiments
which show decreased  bactericidal  activity following exposure to  various  pollutants.   In the
first experiments,  mice  breathed aerosols of Staphylococcus  aureus  (S.  aureus) labelled with
                         32
radioactive  phosphorus (   P) and  were then  exposed  to  N02  for  4  hours  (Goldstein  et  al.,
1973b).   Physical  removal  of the bacteria was  not  affected by any of  the N02  concentrations
used up to 27,800 ug/m3 (14.8  ppm).  Concentrations  of  13,200,  17,200, and  27,800  ug/m3 (7,
9.2,  and 14.8  ppm)  N09 lowered bactericidal  activity  by  7, 14,  and 50 percent, respectively,
                                                                                   3
when compared  to controls  (p <  0.05).   Lower concentrations  (3,570 and 7,140  ug/m  ;  1.9 and
3.8 ppm) had no significant effect.   In another experiment, mice  breathed NO,, for 17 hours and
then were  exposed  to  an  aerosol of S.  aureus.  Four hours later  the animals were examined for
the  amount of  bacteria present  in their  lungs.   No difference in the  inhalation  of bacteria
was  found  with  N0?  exposure.   Concentrations of  4,320 and 12,400 ug/m  (2.3 and 6.6 ppm) NO,,
decreased  pulmonary bactericidal activity by 6 and 35 percent, respectively, compared to con-
trol  values  (p  <  0.05).   Exposure to  1,880 ug/m   (1  ppm)   NO,,  had no  significant  effect.
Goldstein  et al.  hypothesized  that the decreased bactericidal activity  was  due to defects in
alveolar  macrophage  function.   The  detailed  effects of  N02 exposure  on  the  function  of
alveolar macrophages are presented  in Section 14.2.3.1.3.
14.2.3.1.2   Mucociliary  transport.   Mucociliary  transport   is  the  principal   mechanism  for
removal  of inspired and aspirated particles from the tracheobronchial  tree.  Concentrations of
N0«  greater  than  9,400 ug/m  (5 ppm) decrease  rates  of  ciliary  beating as  measured J_n vitro
(Kita and Omichi, 1974) and of mucociliary transport j_n vivo (Giordano and  Morrow,  1972).   The
effect of  lower concentrations  of N09  on mucociliary function is unknown.   (See  Table 14-5)
                                                                         3
     Schiff  (1977)  exposed  hamster  tracheal  ring cultures  to  3,760  ug/m  (2 ppm)  N02 for 1.5
hours/day,  5  days/week,  for  1,  2, and  3 weeks.    Tracheal  cultures infected  with  influenza
virus immediately  after  the  initiation of the  NO,, exposure  were not  different from control
infected cultures.   However,  explants  infected  after 1  or  2 weeks  of N02 exposure showed
decreased  ciliary  activity and  morphological  changes compared  to controls  held  in filtered
air.    After  14  days  exposure  to  N0?  non-infected  cultures showed  a decrease  in  ciliary
activity and morphological  changes.   After 4 weeks exposure of the uninfected cultures, there
was  a 63 percent decrease  in ciliary activity.   In addition, tracheal  organ cultures exposed
to N02 exhibited a more rapid production of virus than explants held in filtered air.
14.2.3.1.3   Alveolar  macrophage.   Exposures  of  animals  to  N02  concentrations ranging  from
13,160 to 112,800 ug/m  (7 to 60 ppm) cause a variety of structural and physiological

                                             14-18

-------
                                            TABLE 14-5.  MUCOCILIARY TRANSPORT

N02
Concentration
|jg/m3 ppm Exposure Species
11,280 6 7 days/wk, Rat, female
6 wk



Effect
Increase in TPTT and FET3: decrease in muco-
ciliary velocity, p<0.02. Functional
impairment reversed within 1 wk.


Reference
Giordano and
Morrow, 1972


      TPTT = Twenty percent transport time.
      FET  = First-edge time.
-pa.
I

-------
abnormalities in alveolar  macrophages.   (See Table 14-6.)  Alveolar macrophages (AM) isolated
from  animals exposed  to  these  concentrations  of  NO,,  show diminished  phagocytic  activity,
(Gardner et  al., 1969)  appearance of intracellular dense  bodies,  (Katz  and Laskin,  1976) in-
creased congregation  of AM  on  epithelial cells,  (Sherwin et al., 1968)  enhanced wheat germ
lipase-induced binding  of  autologous  and heterologous red blood cells  to AM,  (Hadley et al.,
1977) increased J_n  vitro penetration of AM by virus,  (Williams et  al.,  1972) reduced j_n vitro
production  of interferon,  (Valand et  al.,  1970) and  increased  mitochondrial  and  decreased
cytoplasmic  NAD+/NADH ratios.   (Mintz,  1972;  Simons et  al., 1974)  An increased  number  of
polymorphonuclear leukocytes was observed in lung lavages of animals exposed to high  levels  of
N02 (Gardner et al., 1969).  (Table 14-6.)
     Aranyi  et  al.  (1976)  used  scanning electron microscopy  (SEM)  to  study the  effect  of
exposure to  Ntk  on  the anatomic  integrity  of mouse alveolar macrophages  which  were lavaged
from the lung.  No  changes in the AM surface  were  observed after  continuous exposure of mice
for 4,  12,  and 24  weeks to  940 ug/m   (0.5 ppm) without peaks or  188  ug/m3 (0.1 ppm) N09 with
                             3
3-hour  peaks at  1,880   ug/m  (1  ppm)  for 5  days/week.   Macrophages  from  mice  continuously
                      3                                    3
exposed to  3,760 ug/m  (2 ppm) without  peaks  or 940  ug/m  (0.5 ppm)  N09 with  1-hour peaks  of
          3
3,760 |jg/m  (2 ppm) N0~ for 5 days/week, showed distinctive morphological alterations after  21
weeks total  exposure.    Loss  of  surface  processes,  appearance  of  fenestrae,  bleb  formation,
denuded surface areas, as well  as, occasionally, complete deterioration  of the  cells  were seen.
Structural  changes  were  still  observed  at the  same N09  concentrations  after continuous expo-
                               3                                    3
sure to a  baseline  of 940 ug/m   (0.5 ppm)  with peaks of 3,760 ug/m  (2 ppm) NOg for 28 or  33
weeks.   These  observations appear to correlate  well  with a reduction in  i_n vitro  phagocytic
activity and increased susceptibility to infection.
     Acton and Myrvik  (1972) administered an intratracheal injection  of parainfluenza-3 virus
to rabbits prior to 3-hour exposures to 9,400, 28,200,  47,000,  or  94,000 ug/m   (5,  15,  25,  or
50 ppm)  N02.   Alveolar macrophages harvested  from  exposed,  as well as  control  animals,  were
challenged with rabbitpox virus.   Macrophages from control animals  infected with influenza had
increased resistance (75 percent)  to pox virus.  However,  there was partial loss of  resistance
                                             o
48 hours  following exposures to  28,200  ug/m   (15  ppm)  NO,.   No  decrease  in  resistance was
                         3
observed with  9,400 ug/m   (5  ppm) NO,.   Phagocytic  capabilities  were  adversely affected  in
                                                           o
macrophages from animals  exposed  to 28,200 to  94,000 ug/m  (15  to 50 ppm) N09.   At  a concen-
                       3
tration of 94,000  ug/m   (50 ppm), NO,, stimulated oxygen uptake and hexose monophosphate shunt
activity in the AM.
     Nitrogen dioxide-induced  alteration of receptor  sites of the alveolar  macrophages has
been studied  by  Goldstein  et  al.  (Goldstein  et al. ,  1977a; Goldstein,  1979).   It  was found
                                                                   3
that j_n  vitro exposure  of rat  alveolar macrophages to 4,512  ug/m  (2.4 ppm) N0« for  1 hour
resulted  in  a 64   percent increase  in agglutination  by concanavalin  A (Goldstein et  al.,
                                                                        3
1977a).   Alveolar macrophages collected  from rats exposed to 22,748 ug/m  (12.1 ppm)  N02 for 2
hours displayed a  40  percent increased  agglutinability to concanavalin  A.  Following exposure
of alveolar  macrophages to  6,768 ug/m   (3.6  ppm)  NOp  for 1 hour, incubation  of macrophages

                                             14-20

-------
                                      TABLE 14-6.  ALVEOLAR MACROPHAGES

N02
Concentration
ug/m3 ppm
940 0.5
188 0.1
[with 3
hr peaks
of 13880
ug/m
(1 ppm)]
3,760 2
940 0.5
[with 1
hr peaks
of 33760
(jg/m
(2 ppm)]
Exposure Species
Continuous exposure Mouse
for 4, 12, 24 wks
Exposure for 4, 12,
24 wks , 5 days/wk
Continuous exposure Mouse
for 21, 28, 33 wks
Continuous exposure
for 21, 28, 33 wks,
5 days/wk
Effect Reference
Alveolar macrophage (AM) surface Aranyi et al.,
unchanged. 1976

Distinct morphological altera- Aranyi et al.,
tions after 21 wk total exposure. 1976
Loss of surface processes, appear-
ance of fenestrae, bleb formation,
denuded surface areas, and complete
deterioration of cells were noted.
 6,768    3.6   1 hr
Rat
22,748   12.1   2 hr
Incubation of macrophages with
3H-concanavalin A revealed no
significant alterations in
binding.   At this concentration,
agglutination was enhanced 47%.

40 percent increase in con-
canavalin A agglutination of
macrophages.
Goldstein  et al.  ,
1977a

-------
                                           TABLE 14-6.   (continued)

N02
Concentration
ug/m3
9,400
28,200
ppm Exposure Species
5 3 hr exposure Rabbit
after infection
15 with parainf luenza-3
virus. Challenge
with rabbit pox virus.
Effect Reference
Control AM had increased Acton and Myrvik,
resistance (75%) to pox virus. 1972
Partial loss of resistance,
following 28,200 ug/m (15 ppm)
47,000
94,000
18,800
25
50
i — »
i
ro
no


13,200
15,000
to
112,800
18,800
47,000
7
8
to
60
10
25
24 hr
3 hr
24 hr

10
                                        Rabbit

                                        Rabbit



                                        Rat
7 wk
continuous
Guinea pig
                                         Decreased phagocytic capabilities
                                         at all  concentrations except
                                         9,400 ug/m  (5 ppm).

                                         Reduction in resistance,
                                         decreased phagocytic
                                         capabilities,  stimulation
                                         of 0? uptake plus hexose-
                                         monophospate shunt activity.

                                         Increased rosette formation in AM  Hadley et al. ,
                                         treated with wheat germ lipase.     1977
                                         Increased number of poly-
                                         morpho-nuclear leukocytes in
                                         lavage fluid persisted for more
                                         than 72 hr.
                                                                                 Gardner et al.
                                                                                 1969
                                              Phagocytic activity was unchanged. Katz and Laskin,
                                              n       ^  u     4-  •               1976
                                              Depressed phagocytosis was
                                              seen on 3rd day of culture.
                                              Macrophages apparently recovered
                                              by 7th day of culture.
63% increase in epithelial cells
positive for macrophage congrega-
tion.   Presence of 7 or more AM
on a single epithelial cell-2.5
times  more frequent.
Sherwin et al.,
1968

-------
                                           TABLE  14-6.   (continued)

N02
Concentration
|jg/m3
19,000
43,300
ppm
10
23
Exposure
3 hr
1 hr
Species
Rabbit
Rabbit
Effect
50% inhibition of phagocytic
activity.
Increased mi tochondrial and
Reference
Gardner et al . ,
1969
Mintz, 1972
47,000
47,000
25   3 hr
25
                      Rabbit
3 hr
Rabbit
decreased cytoplasmic NAD /NADH
were observed.

No development of resistance with
NO-, exposure immediately after
infection with parainfluenza-3
virus or up to 24 hr before viral
inoculation.  Increased lung ab-
sorption of virus.  No effect
on viral potency.

Viral uptake not affected
when infected with para-
inf luenza-3 virus after N0_
exposure.  No inhibition of
viral RNA synthesis.  Twice
as many virus attached and
penetrated exposed AM.
                                                    Valand et al.
                                                    1970
Wi11iams et al. ,
1972

-------
     3                                                                    3
with  H-concanavalin A  revealed no significant alterations in binding of  H-concanavalin A to
the macrophages.   At this concentration of NO,, agglutination was enhanced 47 percent.
                                                                3
     Green and  Schneider (1978)  exposed  baboons to 3,760  ug/m  (2 ppm) NOp for  8  hr/day,  5
days/wk  for  6 months  and  examined the  response of their  alveolar macrophages  to  migration
inhibition factor  (MIF).  MIF  is a substance produced by lymphocytes which inhibits  migration
of macrophages and  thus influences their protective functions.   Two of three of the antigen-
sensitized,  NOp-exposed animals did  not  respond to  MIF.   Macrophages  from  3 of the  4 NOp-
exposed baboons had diminished responsiveness to MIF.
     Voisin  et  al.  (1976;  1977)  exposed guinea pig  macrophages,  i_n  vitro,  to  188,  1,880,
3,760,  and 9,400  ug/m   (0.1,  1, 2, and 5 ppm) NO, for 30 minutes.  The surviving cells showed
                                                               3
decreased bactericidal  activity,  especially  at the  9,400 ug/m   (5 ppm) level,  as well  as re-
                                                                                   3
duction  in ATP content  and  changes in morphology.  Following  exposure to 188 ug/m  (0.1 ppm)
NO,, the  alveolar  macrophage  membranes appeared to  be spread out and to emit cytoplasmic pro-
                                                                                          3
jections.  These  projections were  much more evident upon exposure to 1,880 and 3,760 ug/m  (1
                               3
and 2 ppm) NOp.   At 3,760 ug/m   (2 ppm)  NO,,, the nucleus  became  hard to identify due to its
washed-out appearance.
     Vassallo et  al.  (1973)  found that  jjj vitro exposure  to  N0? for 15 to 20  minutes could
damage the AM.   Phagocytosis  and bactericidal capability were  adversely affected by NOp con-
centrations  at 15  mM  (690  ppm)  (p <  0.05).   Both 5 and 10 mM (230 and 460 ppm)  NOp  increased
  CO, production  from    C-l-   and    C-6-glucose and  from    C-1-pyruvate (p  <  0.05)  in  the
                                                                                        14
resting  AM,  with  similar  results  occurring  in phagocytizing  cells,  except  for the    C-6-
glucose  substrate.  Nitrogen dioxide  diminished the conversion  of formate  to  COp by approxi-
mately 50  percent.   A  concentration  of 0.5  mM  (23 ppm) also prevented  the inhibition of AM
catalase activity caused by  a  subsequent addition of  aminotriazale, whereas NOp  alone did not
inhibit its activity.
14.2.3.1.4   Immune system.   The  effects  of exposures  of animals to NOp on a few  parameters of
the  immune response  have been investigated by  a small  number of  workers  (Antweiller  et al.,
1975; Balchum et  al. ,  1965;  Ehrlich and  Fenters, 1973;  Ehrlich et al., 1975;  Fenters et al.,
1971; Fenters et  al.,  1973;  Kosmider et al., 1973b;  Matsumura, 1970a).  (See Table 14-7.)  It
should be  emphasized  that  local  responses within  the  lung are critical in regard  to anti-
microbial defense and  that  these responses are, for the most part, unstudied.   Ehrlich et al.
                                                                       3                     3
(1975)  exposed  male SPF Swiss  albino mice continuously to 3,760 ug/m   (2 ppm)  or  940 ug/m
(0.5 ppm)  N02 with  daily 1-hour peaks of  3,760  ug/m   (2 ppm)  for 5 days/ week  for  3 months.
After exposure,  all mice were vaccinated with influenza Ap/Taiwan/1/64.  Mean serum neutraliz-
ing antibody  titer  was  four-fold lower with N02 exposure (p < 0.05) than with controls.  Con-
trol mice  breathing filtered  air also showed  a  depressed  serum neutralizing antibody titer 2
weeks after  vaccination (p  <  0.05).   However,  4 to  8 weeks after  vaccination  there  were no
differences  between  controls  and treated.   The hemagglutination  inhibition titer was  not
affected.  Non-vaccinated  mice  exposed   to  either  NO,  regimen  had decreased  serum  IgA  and
                                                           3
increased  serum  IgG-^  (p <  0.05).  Mice breathing 940  ug/m  (0.5 ppm) N02 with peaks of 3,760

                                             14-24

-------
                                                                TABLE 14-7.  IMMUNOLOGICAL EFFECTS
-F=.
I
ro
en
Pollu- Pollutant Concentration
tant ug/m^
N02 3.760
940 with
daily 1 hr
3,760
N02 1,880
N02 1,880
N02 9,400
N02 9,400
9,400
28,200
N02 10,000
NO, 37,600
* 75,200
131,700
ppm
2
0.5 with
daily 1 hr
2
1
1
5
5
5
15
5.3
20
40
70
Exposure Species
24 hr/day, 5 days/wk. Mouse,
3 mo followed by vacci- male
nation with influenza
A2/Tai wan/1/64 virus
Continuous, 493 days; Monkey
challenge 5 times with
monkey adapted influenza
A/PR/8/34 virus during
exposure
6 mo followed by intra- Guinea pig
nasal challenge with
D. pneumoniae
Continuous, to 169 days; Monkey
challenge with mouse
adapted influenza
A/PR/8/34 virus 24 hr
prior to exposure
4 hr/day, 5. days/wk Guinea pig
7.5 hr/day, 5 days/wk
Continuous, 33 days Guinea pig
Gas 30 min, then aerosol Guinea pig
of egg albumin or bovine
serum albumin for 45 min,
Effects
4-fold decrease in serum neutralizing antibody
titer. Hemaggluti nation inhibition titers
unchanged. Before viral challenge, decreased
serum IgA and increased serum IgG... Increased
IgM and IgG. (p < 0.05). Serum IgA unchanged,
IgM increased (p < 0.05) after virus.
Hemaggluti nation inhibition titers unchanged.
Increased mean serum neutralizing antibody
titers after 493 days exposure. Titers
increased 7-fold 21 days post virus. Titers
increased 11-fold 41 days post virus.
Increased respiratory infection. Decreased
hemolytic activity of complement. Decreased
all immunoelectrophoretic fractions. In-
creased mortality following D. pneumoniae.
Hemaggluti nation inhibition titers or amnestic
response unchanged. Initial depression in serum
neutralization titers with return to normal by
133 days.
Lung tissue serum antibodies increased
with intensity and duration of exposure.
No effect on antibody production.
Reference
Ehrlich et al. ,
1975
Fenters et al. ,
1973
Kosmider et al. ,
1973b
Fenters et al. ,
1971
Balchum et al. ,
1965
Antweiler, 1975
Anaphylactic attacks in 50% exposed animals by Matsumura, 1970a
5th aerosol administration at highest concentra-
tion. No effect at lower levels. Hemagglutination
                                          repeated 5-7 times on
                                          different days
tests unchanged.  Less antigen needed in active
cutaneous anaphylaxis test at highest levels
(p < 0.05).

-------
                                                                     TABLE  14-7.   (continued)
     Pollu-    Pollutant  Concentration
      tant       jjg/m3            ppm           Exposure              Species                          Effects                            Reference
 i
INi
CTi
      N07       56,400              30      Exposure  30  min  then      Guinea pig                 Mortality increased at NO.              Matsumura et al.,
               75,200              40      nebulized acetylcholine.                              >  94,000 ug/m  (50 ppm).                 1972
               84,600              45
               94,000              50

      NO.       75,000              40      Sensitized to  egg and     Guinea pig                 Mortality:   20%                         Matsumura, 1970b
              150,000              80      bovine  serum albumin by                                          37%
                                         intraperitoneal  injection;
                                         3  days  later exposure for
                                         30 min  to pollutants then
                                         antigen 30 min later.

-------
(jg/m   (2  ppm)  also had increases  in  IgM and IgG2 (p <  0.05).   A different response was seen
after  the mice received the virus.  Serum IgA increased  (p < 0.05) only when mice were held in
filtered air, vaccinated and exposed to  940 or 3,760 pg/m  (0.5 or 2 ppm) NO-.   Immunoglobulin
M  (IgM)  concentrations  were elevated in all  N09-exposed groups.   A significant increase (p <
                                                                                             •>
0.05)  took  place  in only the following  groups:   (a) continuous exposure to 940 or 3,760 ug/m
                                                            3                                3
(0.5 or 2 ppm), (b) continuous exposure  to 940 or 3,760 ug/m  (0.5 or 2 ppm) or to 3,760 ug/m
(2  ppm),  pre-vaccination and  clean air afterwards,  and.(c) 3 months  filtered  air  and 3,760
ug/m   (2 ppm)  N0?  post-vaccination.   Similar results were observed for IgG? and IgG-, determi-
nations.
     The immune system of monkeys exposed to N02 was studied in an additional series of experi-
ments  (Ehrlich and Renters,  1973; Renters et al., 1971;  Fenters et al., 1973).   Renters et al.
(1971) injected mouse-adapted influenza A/PR/8/34 intratracheally 24 hours prior to continuous
                       3
exposure to  9,400  ug/m   (5  ppm)  N02.   Hemagglutination  inhibition  titers to influenza titers
were not  changed.   Initially  serum neutralization titers were depressed by N0~.   By 133 days,
the effect had disappeared.   The amnestic response was not affected.
     Fenters  et  al.  (1973) described  the  effects  of  continuous  exposures  of  1,880  ug/m
(1 ppm) N02  for 493 days on monkeys challenged five times via intratracheal injection to live
monkey-adapted influenza virus A/PR/8/34 during N02 exposure.  Again,  hemagglutination inhibi-
tion titers were not significantly affected by N0~ exposures.  However, the mean serum neutra-
lizing  antibody  titers  were  significantly  higher in animals  exposed to  N02  for  493  days.
Twenty-one days post-vaccination,  animal  titers  were increased 7-fold  over controls.   Forty-
one days post-challenge, N02~treated animals exhibited an 11-fold enhancement.   Even after 266
days  of  N0?  exposure,  titers  were  higher  when  compared  to  controls.   Again,  the  authors
hypothesized that  NO,, enhanced  the ability of the monkey-adapted virus to become established
and multiply.
     Antweiler et  al.   (1975)  did  not   find  any  alteration in  guinea pig  specific  antibody
titers when compared to controls, even after 33  days  of  exposure to  10,000 ug/m  (5.3 ppm) NO,,.
     On the  basis  of experiments in which  the  continuous  exposure  of guinea  pigs  to  1,880
ug/m   (1 ppm)  NQ?  for  6 months  resulted in  an  increased incidence  of infection, particularly
within the  lung, Kosmider and  colleagues postulated an  adverse  effect of NO,,  on immune func-
tion (Kosmider et  al. ,  1973b).   These investigators  also claimed that NOp causes decreases  in
complement concentrations when measured by  a hemolysis assay; reductions in all  immunoglobulin
fractions when  tested  by immunoelectrophoresis;  and increased  mortality in mice  exposed  to
1,880  ug/m   (1 ppm) of N02 when  infected  intranasally  with  D.  pneumoniae.  Because  of the
importance of these observations, they require confirmation.
     Balchum et al.  (1965)  exposed guinea  pigs  to 9,400  ug/m   (5 ppm) N02 for 4 hours/day,  5
days/week and to 9,400  ug/m3  (5 ppm) N02 or to  28,200 ug/m3 (15 ppm)  N0? for 7-1/2 hours/day,
5  days/week.   There  was a noticeable increase in  the  titer of serum  antibodies  against  Tung
                                               3                        3
tissue in all guinea pigs exposed to 9,400  ug/m   (5 ppm)  or 28,200 pg/m  (15 ppm) N02 as early
as 160 hours after  N0?  inhalation.  The  antibody  titers  increased with the intensity and dura-
tion of exposure  to NO,,.
                                             14-27

-------
14.2.3.2  Lung biochemistry
14.2.3.2.1   Introduction.   Nitrogen  dioxide-related studies of  lung biochemistry  have been
directed  to  either  an  investigation  of  the mechanism  of toxic  action  of NO^  or  to  the
detection of  indicators of  early  damage by  NCL  exposure.   Two theories of  action  of NCL on
biological systems have evolved as a result of these studies.  The dominant theory is that N02
initiates lipid peroxidation,  which  subsequently causes cell injury or death and the symptoms
associated with NO^  inhalation.   The second  theory  is  that N0~ oxidizes low molecular weight
reducing  substances  and proteins.   This  oxidation  results  in  a metabolic dysfunction which
evidences itself  as  the toxic symptom.   Nitrogen dioxide may,  in fact, act by both means and,
as a consequence,  may affect the intermediary metabolism of animals and thus, their growth and
maturation.   Several potential  biochemical  mechanisms related to detoxification  of  N02 or to
responses to  NCL  intoxication have been proposed.   The effects of NCL  exposure  on  lung bio-
chemistry will be discussed in this context.  (See Table 14-8.)
14.2.3.2.2  Lipid and  diet effects.   The dietary background of animals affects their response
to all types of toxicants.   For the most part, diet effects concerning NCL have been neglected
and are  unreported  in  the  literature.  A significant body of evidence has evolved, however, to
support  the  idea  that  lipids  and  vitamin  E  are  the most  important dietary  components in
determining the response of animals to NCL exposure.   Roehm et al.  (1971) studied the j_n vitro
oxidation of  unsaturated  fatty  acids  by CL  and  NCL.   A common mechanism  of action was sug-
gested for  these  two  oxidizing air pollutants.  Both  NO, and CL  initiated  the  oxidation of
                                                          £      O
unsaturated fatty acids  through free radicals.   Typically, an induction period was noted with
either anhydrous thin films or aqueous emulsions of linolenic acid exposed to 2,800 ug/m  (1.5
ppm) NCL.  The addition of free radical  scavenging agents such as vitamin E, butylated hydroxy-
toluene  (BHT),  or butylated  hydroxyanisol  (BHA) delayed the onset of oxidation i_n vitro.  The
rate  of  oxidation of linolenic acid in  thin  films  was proportional  to  concentrations of NCL
                               3
ranging from 940 to 10,200 pg/m  (0.5 to 5.4 ppm).  Thin-layer chromatography of the oxidation
products of linolenic  acid showed a conversion to polar  nitrogen-containing compounds and to
peroxides.  A  proposed  mechanism  of formation  of  these  products  follows  (Menzel,  1976):
                                                  00-
                   C=C   +  N00  -» -C-C-NO,
                    00•                   OOH
                   -C -C-NO,  +  RH •*   -C -C-NO,
                    i   i    2             i   i    i
                   R-  +  02 .->  ROO-  -»  ROOH
Nitrohydroperoxides  and  fatty  acid  hydroperoxides  are  produced  from  the  oxidation  of
unsaturated fatty acids by N0?.  Phenolic antioxidants prevent the autoxidation of unsaturated
                                             14-28

-------
                                     TABLE 14-8.   EFFECTS OF
                                            N02  ON  LUNG  BIOCHEMISTRY
ro
10
              N02
         Concentration
|jg/m3
94
940
94
or 940+
equal
amount
ammonia
376
3,760
35,720
ppm
0.05
0.5
0.05 or
0.5+
equal
amount
ammonia
0.2
2
19
Exposure
8 hr/day,
122 days
3 hr
Species
Guinea
Pig
Rat
Effect
No effect on total weight of phosphol ipid.
Significant alterations (p <0.05) in
individual phospholipid classes.
3
At 376 ug/m (0.2 ppm) inhibition of
conversion of prostaglandin E« (PGEO
to its metabolite (15-keto PGE0) 18
Reference
Trzeciak et al . ,
1977
Menzel ,
1980
          750
        1,880
        5,640
        9,400
        9,400
                                   hr post exposure.   No effect on uptake
                                   or efflux of PGE?.

                                   At 3,760 and 35,720 ug/m3 (2 and 19 ppm),
                                   no effect on uptake of PGE?.   Efflux
                                   altered 18 hr post-exposure.   Conversion
                                                    of PGE2 to 15-keto PGE2
                                                    60 hr post-exposure.
                                                           inhibited 18 and
0.4
1.0
3.0 or
5.0
5.0
72 hr
Guinea Pig
3 hr
Guinea Pig
No effect at 750 ug/m .   Increase in lung
lavage protein and lipid content in
vitamin C depleted but not normal
at 1,880 ug/m .   (See Edema Section
4.2.3.6)

Increased lung lavage protein and lipid
content in vitamin C depleted guinea pigs
after 18 hr post exposure.  (See Edema
Section 4.2.3.6)
Selgrade et al.,
1981
Selgrade et al.,
1981

-------
                                                        TABLE 14-8.   (continued)
CO
O

N02
Concentration
pg/m3 ppm
750 0.4
750 0.4
750 0.4
Exposure
72 hr or
1 wk
Continuous,
1 wk
4 hr/day,
7 days
Species
Guinea Pig
Guinea
pig
Guinea
pig
Effect
No mortality or effect on lung lavage
fluid composition. (See Edema Section
4.2.3.6)
Increase in lung protein content of guinea
pigs with an unquantified vitamin C defi-
ciency, most likely due to plasma leakage
(see edema section 4.2.3.6). Some may
result from cell death.
Increase in acid phosphatase (EC 3.1.3.2).
Reference
Sel grade et al . ,
1981
Sherwin and
Carlson,
1973
Sherwin et al . ,
1974
750 to    0.4 to Continuous
940       0.5      1.5 yr

1,790 to  0.95 to
1,880     I
          940    0.5
                   8 hr/day,
                    7 days
                          8 hr/day,
                            4 mo
Mouse       Growth reduced; vitamin E (30 or 300 mg/kg
            diet) improved growth.
Guinea      Increase in serum LDH, CPK, SCOT, SGPT,
  pig       plasma cholinesterase, lung and plasma
            lysozyme.   Decrease in RBC GSH peroxidase.
            Lung GSH peroxidase and acid phosphatase
            unchanged.

            Decrease in plasma cholinesterase,
            plasma and lung lysozyme, and RBC
            GSH peroxidase.  Lung GSH peroxidase
            unchanged.   Increase in lung acid
            phosphatase.
Csallany,
1975
 Menzel et al.,
 1977

-------
                                                       TABLE 14-8.   (continued)
-P.
i
OJ

N02
Concentration
|jg/m3
940
1,880
ppm Exposure
0.5 Continuous,
1 17 mo
Species
Mouse
Effect
Decreased body weight with vitamin E
deficient, vitamin E supplemented (30 and
Reference
Csallany and
Ayaz, 1978a
         940
1,880

  940
1,880
        3,760
         0.5
                0.5
                1
Continuous,
   17 mo
 Continuous,
 17 mo
 Mouse
Mouse
1,880
1,880
4,330
11,560
1
1
2.3
6.2
Continuous,
2 wk
Continuous,
4 days
Rabbit
Rat
                 Continuous     Guinea
                   1 to 3 wk     pig
300 ppm) and DPPD supplemented (30 ppm).
No change in tissue weight with exception
of increased kidney weight in 1 ppm exposed
animals with vitamin E deficient diet.
Slightly decreased survival rate.

No change in blood and lung GSH-peroxidase
activity.

Suppression of GSH-peroxidase activity.

No increase in lipofuscin or glutathione
peroxidase.  Vitamin E (30 or 300 mg/kg)
prevented lipofuscin accumulation
(EC 1.11.19).

Decrease in lecithin synthesis after 1 wk;
Less marked depression after 2 wk.

Activities of GSH reductase (EC 1.6.4.2)
and glucose-6-phosphate dehydrogenase
(EC 1.1.1.49) increased at 11,560
ug/m  (6.2 ppm) level proportional to
duration of exposure.  Plasma lysozyme
(EC 3.2.1.16) and GSH peroxidase
(EC 1.11.1.9) not affected.  No effects
at 1,880 or 4,330 ug/nr (1 or 2.3 ppm).

Increase in number of lactic acid dehydroge-
nase (EC 1.1.2.3) positive cells with time
exposure.  Suggest Type I  (LDH negative)
cells decrease as Type II  (LDH positive)
cells increase.
Ayaz and
Csallany, 1978
Ayaz and
Csallany,
1977
                                                                                                Seto et al.,
                                                                                                1975

                                                                                                Chow et al.,
                                                                                                1974
                                                                         Sherwin et al.,
                                                                         1972

-------
                                                        TABLE 14-8.   (continued)
              N02
         Concentration
         (jg/m3
ppm
Exposure
Species
                                                     Effect
Reference
CO
ro
         5,450    2.9    Continuous,
                         5 days/wk,
                            9 mo
                      Rat
         5,640    3


        18,800   10
        18,800   10
        28,200   15
       Continuous,     Rat
         17 days

        Continuous
           4 wk
5,640
5,600
13,200
3
3
7
4 hr/day,
4 days
7 days
4 days
Squirrel
monkey
Rat

         4 days
         4 days
                         Increase in lung wet weight (12.7%)  and
                         decrease in total lipid (8.7%).   Decrease
                         in saturated fatty acid content  of lung
                         lavage fluid and tissue.   Increase  in
                         surface tension of lung lavage fluid.

                         Decrease in linoleic and linolenic acid
                         of lavage fluid.

                         Decrease in unsaturated fatty acids  in
                         lavage and lung tissue.   Vitamin E (as
                         d,1-a-tocopheryl  acetate 100 mg/kg diet)
                         reduced NO- effect.

                         Thickening of collagen fibrils.
                         No effects on parameters tested.

                         Increase in lung weight, G-6-PD,
                         glutathione reductase,  glutathione
                         peroxidase.

                         Increase in lung weight, G-6-PD,
                         6-P-gluconate dehydrogenase,
                         glutathione reductase.

                         Increase in lung weight, DMA
                         content, G-6-PD, 6-P-gluconate dehydro-
                         genase, glutathione reductase, disulfide
                         reductase, glutathione  peroxidase,
                         succinate oxidase,  cytochrome oxidase;
                         no effect on lung protein.
                                                         Arner and
                                                         Rhoades,  1973
                                                         Menzel  et al.,
                                                         1972
                                                                                                 Bils,  1976
                                                                                                 Mustafa et al.,
                                                                                                 1979a,  b

-------
                                                      TABLE  14-8.   (continued)
to
OJ
             N02
        Concentration
(jg/nr*
9,400
9,400
9,400
ppm
5
5
5
Exposure
14 to 72 hr
12 hr
0.33, 1, 2
Species
Mouse
Rat
Rat
Effect
Increase in lung protein (14 to 58 hr) by
radio-label .
Incorporation of 14Oproline into
insoluble collagen increased (58%).
Increase in glucose utilization and lactate
Reference
Csallany, 1975
Hackner et al . ,
1976
Ospital et al . ,
 9,400    5
37,600   20
94,000   50

11,000    6
       15.000
       18,800   10
                       and 4 days
                          3 hr
                         4 hr/day,
                           30 days
                  Continuous
                    14 days
                                            production.   Lesser increase in pyruvate     1976
                                            production.
Rabbit
Mouse
Mouse
Benzo(a)pyrene hydroxylase (EC 1.14.12.3)
activity or tracheal mucosa not affected.
Increase in GSH reductase (EC 1.6.4.2) and
glucose-6-phosphate dehydrogenase
(EC 1.1.1.49) activities.

Increase in lung protein.
Palmer et al'. ,
1972
Csallany,
1975
Csallany,
1975
                     5 hr       Hamster
                 once a week   (Vitamin
                   4 to 8 wk    A defi-
                                cient)
            Lipid droplets in alveolar walls.  Alveolar  Kim, 1977; 1978
            necrosis and thickening of epithelial base-
            ment membrane with calcium deposits on inner
            and outer surfaces.   Presence of virus par-
            ticles within epithelial plasma membrane.
            Reduced DNA uptake.   Decrease in basal cell
            growth.  No reversion of Type II from Type I
            cell.  No LDH isoenzyme III in terminal airway.
            Following 8 weeks of exposure, hypertrophy and
            hyperplasia of bronchiolar-epithelial cells,
            diffuse loss of cilia, membrane damage, and
            mitochondrial damage.

-------
                                                TABLE 14-8.   (continued)
      N02
 Concentration
 ug/m3
          ppm
 Exposure     Species
                                                               Effect
                                                          Reference
28,000     15
53,000     28
                    7 days
              Mouse
56,400     30     Continuous    Hamster
                  to 30 days
56,400     30     Continuous    Hamster
                  to 50 days
56,400     30     22 hr/day,     Hamster
                     3 wk
62,040
75,200
           33
           40
Continuous
to 23 days
  5 hr
Rat
Rat
            Increase in GSH levels,  GSH reductase,
            glucose-6-phosphate dehydrogenase,  and  GSH
            peroxidase.

            Increase in lung proteolytic activity and
            in serum antiprotease at 2 days.
            Declined to normal values at 50 days.
                                             Csallany,  1975
                                                                                         Kleinerman and
                                                                                         Rynbrandt,
                                                                                         1976
                                            Increase in lung proteolytic activity at     Rynbrandt and
                                            2 and 5 days,  but the optimum pH was acidic  Kleinerman,
                                            (3.0).   Not active at physiological  pH of    1977
                                            7.2.   Attributed to cathepsins,
                                            C,  D,  and E.
                                                                            A,  B,,  B,
Loss of body weight; increase dry lung
weight; decrease in total lung collagen
within 4 days and total lung elastin with-
in 10 days.   Collagen levels return to
normal by day 14 of exposure.  3 wk fol-
lowing exposure, lung elastin levels had
returned to normal.

High level of dietary antioxidants in-
creased the time until 50% mortality
occurred (LT50).  LT50 of vitamin E
depleted rats was 11.1 days versus 170
days for vitamin E supplemented rats.

                           14
Increased incorporation of   C-palmitic
acid in lung lecithin.  Accumulation of
disaturated lecithin by 6 hr post-NO?
with maximum accumulation by 48 hr.
                                                                                         Kleinerman and Ip,
                                                                                         1979
Menzel et al.,  1972
Blank et al.
1978

-------
                                                        TABLE  14-8.   (continued)
     N02
Concentration
    5~   ppm
                            Exposure
                     Species
                                          Effect
                                                          Reference
         75,200
        132,000
40
70
2 hr
Rat
                                           Benzo(a)pyrene hydroxylase (EC 1.14.12.3),
                                           phenol-0-methyl transferase (EC 2.1.1.25)
                                           and catechol-0-methyl transferase
                                           (EC 2.1.1.6) not affected.
Law et al.
1975
co
ui

-------
fatty  acids  by  N02  by  reacting  with  both  fatty  acid  hydroperoxyl  free  radicals  and
nitrohydroperoxyl  free  radicals  generated by  addition  of N02  to unsaturated  fatty  acids:

                   00-                   OOH
                  -C -C-NO,  +  AOH  -»  -C -C-NO,  +  AO-
                   i   i    £              i   i    £

                  ROD-  +  AOH  -»•  ROOH  +  AO-
where AOH represents a phenolic antioxidant.
     Rats evidenced  increased  mortality  (Fletcher and Tappel, 1973; Menzel  et al. ,  1972) and
decreased content of unsaturated fatty acids in lung lavage fluid (Menzel et al., 1972;  Thomas
et al., 1968) when exposed to N02 concentrations ranging from 18,800 to 62,000 ug/m  (10 to 33
ppm).   The effect was greater in animals fed diets depleted in vitamin  E.
     The effect  of  N09  exposure on the metabolism of vasoactive compounds by the rat lung was
                                                                      ,                      T
studied by Menzel  (1980).   Rats were exposed  for  3  hours to 376 ug/m   (0.2 ppm), 3,760 ug/m
                         3                                                             3
(2 ppm), and  35,720  ug/m  (19 ppm) NO, and their lungs were excised and perfused with  H-Pro-
                 3
sta glandin E9  ( H-PGE9),  a natural product of  the  lung that acts on  smooth muscles, up to 6
                                                                                 3
days at various times.  N09 exposure did not affect the unidirectional  uptake of  H-PGE,, at 0
                                        3
or 18 hr post-exposure,  while efflux of  H-PGE, and its metabolites from the lung were altered
                                               3
18 hours post exposure to 3,760 and 35,720 ug/m  (2 and 19 ppm) N02-  Eighteen hours  following
376, 3,760, and  35,720  ug/m3 (0.2, 2, and 19 ppm) N02, the conversion  of the perfused PGE2 to
its 15-keto  metabolite  was inhibited by 37,  41,  and 62  percent,  respectively.   Recovery was
                                           3
not complete until  60 hr following 376 ug/m  (0.2 ppm) NO, exposure, and 90 hr following 3,760
    3                                                                               3
ug/m  (2 ppm) exposure.   Recovery had not occurred in animals exposed to 35,720 ug/m   (19 ppm)
HOy for a  period of 160 hours post exposure.   No edema was observed following exposure  to any
of the three levels of pollutant.
     Arner and Rhoades  (1973)  exposed rats to 5,450  ug/m  (2.9  ppm) N02 for  24 hours/day,  5
days/week,  for 9 months.   The lung wet weight  increased by 12.7 percent compared to that of
their control counterparts.   The  increase  (p < 0.05)  in lung wet weight was  the  same  as the
increase in lung water content.  The lipid content of the lung was depressed (p < 0.05)  by 8.7
percent.   An  analysis of  the  lungs  showed  that a  decrease  occurred   in  the  total  saturated
fatty  acid  content.   Unfortunately,  values  for unsaturated fatty  acids  of  biological  impor-
tance, such  as   the  essential  fatty  acid  arachidonic acid,  were not   reported.   The surface
tension of extracts  of  the lung increased, and the authors suggest that the increased surface
tension corresponded to a decrease in the lung surfactant concentration.
                                                             3                   3
     Trzeciak et al.  (1977)  exposed guinea pigs to  940  ug/m  (0.5 ppm), 94 ug/m  (0.05 ppm),
or these same  N02  concentrations  plus an equal amount of ammonia, for  8 hours/day for a total
of  122 days.   Lung  phospholipids were  analyzed,  and  no difference was  found in  the  total
weight of  phospholipid  of exposed  versus  control  lungs.  Significant  alterations (p <  0.05)
were  found  in  the  individual  phospholipid  classes.    Decreases  were  noted  in phosphatidyl
ethanolamine,  sphingomyelin,  phosphatidyl  serine,   phosphatidyl  glycerol-3-phosphate,  and

                                             14-36

-------
phosphatidic acid.   Increases  were noted in the  lysophosphatidyl  ethanolamine  content,  while
the phosphatidyl choline (lecithin) content remained constant or was slightly depressed.   Such
changes could be indicative of change in cell type or cell function.
                                                                                             3
     Lecithin synthesis  appeared  to be depressed in the lungs of rabbits exposed to 1,880 |jm
(1 ppm) NO 2 for 2 weeks (Seto et al.,  1975).  The most marked effect was observed after 1 week
of exposure and appeared to decline after the second week of exposure.
                                                                                 •3
     Csallany (1975)  exposed  mice continuously for 1.5 years  to  750 to 940 ug/m  (0.4 to 0.5
ppm) or 1,790  to  1,880 ug/m   (0.95 to  1  ppm)  NO- and  fed  the animals  a basal  diet which was
either deficient  in  or  supplemented  with vitamin E at  30  or 300 mg/kg of  diet.   The author
indicated that  N0?  reduced the growth rate in all four diet groups, but the vitamin E-supple-
mented groups were improved over the non-supplemented groups.   High levels  of vitamin E in the
diet failed to provide greater improvement in growth rate over that of normal amounts of vita-
min  E  in  the  diet.   In other studies from this group, (Ayaz  and Csallany,  1977;  Ayaz and
Csallany,  1978;  Csallany and Ayaz, 1978a)  female weanling  mice were exposed to  940  or  1,880
ug/m  (0.5  or  1 ppm) NOp  continuously  for  17  months.   Animals were divided into three groups
receiving the basal  diet with either a normal  supplement of vitamin E (30  mg/kg) or 300 mg/kg
and  a  third group  supplemented  with  the  synthetic  antioxidant N,N'-diphenylphenylenediamine
(DPPD) at 30  mg/kg.   After 17 months  of  exposure,  the presence of  lipofuscin  pigment in the
liver, lungs, spleen,  heart,  brain, kidney, and uterus was  determined.   While no effect could
be  ascribed  to  NOp  exposure,  vitamin  E supplementation decreased  the  concentration  of  lipo-
fuscin pigment  in  the liver,  but not  in  other  tissues.   Lipofuscin pigment is  proposed to be
an end product of lipid oxidation accumulated in tissues.
     Exposure of  vitamin  A  deficient  hamsters to 18,800 ug/m  (10 ppm) NOp,  5  hours once a
week for 4  to  8 weeks caused  lung  damage  as compared to NO^-exposed,  non-vitamin A deficient
hamsters (Table 14-8) (Kim, 1977; 1978).
     A recent  series of experiments have  investigated the  effect of vitamin C deficiency on
NOp toxicity (Selgrade  et  al., 1981).   Normal  or vitamin C depleted guinea pigs were exposed
to  752,  1880,  5460,  or  9400 ug  (0.4,  1.0, 3.0,  or 5.0  ppm)  N02/m3 for 72  hrs  and  the lung
lavage protein  and  lipid  content determined.   No  effect was observed  in  guinea pigs having
normal vitamin  C  blood  contents,  but depleted guinea  pigs,  having an average of  25% of the
normal blood vitamin C  content,  had 2-5 times  the control lavage fluid and lipid content with
                                                                     3
the exception of  those  guinea pigs exposed to  752 ug (0.4 ppm) N09/m .   Exposure of normal or
                                                    3
vitamin C  depleted guinea pigs exposed  to  752 ug/m   (0.4  ppm)  for as  long as 1  week had no
effect on  the  composition of  the lavage fluid.   At 9400 ug  (5 ppm) N02/m   for  72  hrs  these
changes in lavage fluid composition were correlated with mortality (50%) and alveolar edema as
observed by conventional  light microscopic  histopathology in  vitamin C  depleted  guinea pigs.
When vitamin C depleted guinea pigs were exposed to 9400 ug  (5 ppm) N02/m  for 3 hrs,  increas-
ed  protein  and  lipid contents were not  observed  until 15 hrs after exposure.   These results
conflict with those of Sherwin and Carlson who  found increased protein content of lavage fluid
                                             14-37

-------
from  guinea  pigs exposed  to  752 ug/m  (0.4 ppm) for  1  week.   Differences may be  due  to the
reproducibility of exposure, methods of monitoring NCL during exposure, protein measurement in
the lavage fluid and differences in the degree of vitamin C deficiency.
14.2.3.2.3  Sulfhydryl compounds and pyridine nucleotides.  Oxidation  of  sulfhydryl compounds
and pyridine  nucleotides  in  the lung  is  well-established for  0,  exposures, (Evans  et al.,
1974) but little evidence has been reported for N09.
                                                                            3
      In experiments  involving  exposure of mice to very  high  (>143,000 ug/m , 76 ppm) concen-
trations  of  NOp,  several   investigators  reported that  a  wide variety  of sulfur-containing
compounds reduced  the toxicity  of NO,, (Fairchild et al., 1959; Fairchild  and  Graham,  1963).
For example when  mice were first exposed to benzenethiol (14 ppm)  for 24 to 72 hours prior to
4 hours of NOp  exposure only 1/20 died,  whereas  10/20 of the NO^-exposed mice not pretreated
with  benzenethiol died.   Inferences  drawn from the  protective  effect  of  these compounds sug-
gest  that  sulfhydryl compounds  within the  lung were being oxidized to  disulfides  (Fairchild
et al., 1959).   Included  among  the compounds observed to  exert a  protective effect are:  (1)
hydrogen sulfide  (2)  benzenethiol,  (3) d.crnapthylurea,  (4) phenylthiourea,  and  (5) a number
of thyroid-blocking agents.
                                                                  2
     Ospital  et  al.   (1976)  reported  that exposure  to 9,400 pg/m   (5 ppm)  NOp  for 8  hours
altered the glucose  metabolism  of slices made from the lungs of exposed rats.   Glucose utili-
zation  and   lactate   production  were  increased  by  28  and  43  percent,  respectively,  while
                                                                       o
pyruvate production  rose  by 6 percent.  Exposure of  rats to 9,400  (jg/m  (5 ppm)  NOp for 1, 2,
and 4 days produced similar alterations, but individual values were not reported.   Neither in-
creased hexose  monophosphate shunt nor  citric  acid  (Krebs) cycle activity  could  account for
the  increased  glucose  utilization.   The authors concluded that  NOp  exposure  increased the
activity  of  the  glycolytic pathway and  suggested  that  this  increase may  be  related  to an
increased biosynthesis due to injury.
14.2.3.2.4  Effects on lung amino acids, proteins, and enzymes.   Concentrations of  NO,  >9,400
    3
ug/m  (5 ppm) produce lung edema with concommitant infiltration of serum protein and enzymes.
Alterations   in  the  cell  types  of  the lung  also occur  (see  Section  14.2.3.3).    Thus,  some
reports of changes in lung enzymes and proteins may reflect either  edema or altered cell  popu-
lations rather than direct effects of N09 on lung enzymes.
                                                                3
     Sherwin  et  al.   (1972)  exposed  guinea pigs  to  3,760 ^ig/m  (2 ppm)  NOp for  1, 2,  or 3
weeks.  They examined lung sections histochemically for lactic acid dehydrogenase (LDH).   With
this  technique,  LDH  is  primarily an indicator of Type II pneumocytes rather than Type I.  The
number of Type  II  pneumocytes per alveolus was  determined.   In control  lung sections,  a mean
of  1.9  Type  II  cells per  alveolus  was found  with  a range  of 1.5  to 3.4 Type  II cells per
alveolus in upper  lobes  of the  lung.  A  range  of 1.6 to 3.1 Type  II pneumocytes per alveolus
was found in  the lower lobes.   Exposure to N0? increased the LDH content of the lower lobes of
the lung by  increasing  the number of Type II cells per alveolus (p < 0.05).  The increase was
progressive over the  1-,  2-,  and 3-week exposure period.  The authors  then contended that the
                                             14-38

-------
increase  in  lung  LDH  content was  due  to the  replacement of  Type  I pneumocytes  by Type II
pneumocytes as shown in morphological studies (see Section 14.2.3.3).
     Several  other biochemical  indicators of  lung damage have been  studied.   Sherwin et al.
(1974)  exposed  guinea  pigs with an  unquantified  vitamin  C deficiency to  750  ug/m  (0.4 ppm)
N0~  for  4  hours/day for 7 days and found an increase in acid phosphatase activity (p < 0.05).
An increased aldolase activity was reported by Kosmider et al. (1975) in the blood, liver, and
brain  of NO^-exposed guinea  pigs,  but was  statistically significant only  in liver samples.
Values for the lung and exposure levels were not reported.
     The effect of N02 on the important enzyme benzpyrene hydroxylase was studied by Palmer et
al.  (1972).   Since lung cancer  in  man  is predominantly of bronchial  rather than parenchymal
origin, benzpyrene hydroxylase activity of the tracheobronchial region of the lung was studied
in rabbits which had been exposed to 9,400, 37,600, or 94,000 ug/m3 (5, 20, or 50 ppm) N02 for
3 hours.  No effect was observed on the benzpyrene hydroxylase activities in NO, exposure, but
                                    3
On exposure of  1,400  to 19,600 ug/m  (0.75  to  10 ppm) markedly decreased benzpyrene hydroxy-
lase  activity in  a dose-related  manner.   Law  et al.  (1975)  studied  the  effect of  NO-  on
benzpyrene hydroxylase,  microsomal  0-methyl  transferase,  catechol  0-methyl  transferase, and
supernatant catechol 0-methyl  transferase activities  of the  lungs of rats.   While benzpyrene
hydroxylase activity ,of  the  lung could be induced by treatment with the carcinogen, 3-methyl-
cholanthrene,   exposure  to  75,200 or 132,000  ug/m   (40  or  70 ppm)  NO^  for  2 hours  had  no
effect.  Thus,  the studies of Palmer et  al.  and  Law et  al.  agree that N0~ has  no  effect on
benzpyrene hydroxylase activity of the lung.   The 0-methyl transferase activity studied by Law
et al.  relates  to  the  ability of the lung to metabolize the  important catecholamine hormones.
This metabolism does not appear to be affected by N09 treatment.
                                                                       3
     Menzel et  al.  (1977) exposed  guinea  pigs 8 hr/day to  940  ug/m  (0.5  ppm) NO-  for  4
months.  After an  initial  exposure  of 7  days,  serum  LDH,  total  creatine phosphokinase (CPK),
glutamic-oxalacetic  transaminase   (SCOT),   and   glutamic-pyruvic   transaminase  (SGPT)  were
elevated.  Lung  GSH peroxidase  and  acid phosphatase  were not affected.  In  contrast to the
findings of Chow et al., (1974) lung lysozyme levels were elevated  as were plasma levels.   The
release  of  isomeric  forms  of CPK was characteristic  of generalized  damage  to  the lung.   The
elevation in  total  CPK  was statistically significant (p  < 0.05) while the elevations in LDH,
SCOT,  and  SGPT were  not  significant because  of  the large  variance  in the  exposed groups.
     A major  concern  has  been  the  effect of NO-  exposure on the  structural  proteins  of the
lung, since elastic recoil  is lost  following exposure.   Bils  (1976) reported a thickening of
the collagen  fibrils in  squirrel  monkeys exposed  to  5,640 ug/m   (3  ppm)  N02  for  4  hours/day
for 4  days.   Kosmider  et  al.  (1973a) reported that  the urinary hydroxyprol ine and acid muco-
polysaccharide contents of guinea pigs  exposed  to 1,880 ug/m   (1  ppm) NO-  for  6  months  were
increased (p < 0.05).   Presumably these  increases represented degradation of collagen.  Hacker
et al.  (1976) measured the  incorporation of   C-proline into soluble and insoluble  collagen
fractions in the lungs  of rats exposed to 9,400  ug/m  (5 ppm)  N0?  for 12 hours.  Incorporation
                                             14-39

-------
   14
of   C-proline  into  insoluble collagen was 58 percent greater in the NCL-exposed animals than
in air-exposed  control  groups,  supporting the biochemical evidence for greater collagen turn-
over in NCL-exposed animals.
     Enzymes observed to  have increased activity following exposure to high concentrations of
N0~  included aldolase  (i_n vitro) (Ramazzotto and Rappaport,  1971)  and serum antiprotease (J_n
vivo) (Kleinerman and Rynbrandt, 1976).  Plasma lysozyme activity was reported to be unaffect-
ed (KI vivo) (Chow et al.  , 1974).
14.2.3.2.5   Potential  defense mechanisms.    Menzel   (1970;  1976)  proposed  that  antioxidants
might protect the  lung  from damage by  N0~  by inhibiting lipid peroxidation.  Data related to
this  hypothesis have  been  reported.   (Ayaz  and  Csallany,  1977;  Ayaz  and  Csallany,  1978;
Csallany, 1975;  Fletcher and Tappel,  1973; Menzel  et al., 1972; Thomas et al., 1968)  Chow and
Tappel  (1972)  proposed an  enzymatic  mechanism for  the protection of the  lung  against lipid
peroxidation damage by ozone.  They proposed the following scheme:

         p-oxidation
               t
               ROM   k  4     GSH      .         NADP          Glucose-6-P04
                                            GSH Reductase    G-6-P Dehydrogenase
         RH   ^ ROOH '   v      GSSG     >-'  X    NADPH    '  \   6-Phosphogluconate
                          where R is an aliphatic organic radical
Chow et  al.  (1974)  exposed  rats to  1,880,  4,330, or  11,560  ug/m3 (1, 2.3, or  6.2  ppm)  N02
continuously for  4 days to determine  the  effect on the glutathione peroxidase  system.   They
determined the  activity  of  GSH reductase,  glucose-6-phosphate dehydrogenase, and GSH peroxi-
dase in the soluble fraction of exposed rat lungs.   Linear regression analysis of the correla-
tion between  the N0? concentration and enzymatic  activity  was  found  to have  a significant
positive correlation coefficient  of 0.63 (p < 0.001)  for  GSH  reductase and  0.84 (p  <  0.003)
for glucose-6-phosphate  dehydrogenase.   No correlation was  found  between the  GSH peroxidase
activity and the  NO, exposure concentration.   The activities  of GSH reductase  and glucose-6-
                                                                                   3
phosphate dehydrogenase  were significantly increased during exposure to 11,560 ug/m  (6.2 ppm)
N02.
     Ayaz and Csallany  (1978)  exposed female  mice continuously for 17  months to 940 and 1,880
ug/m  (0.5 and 1 ppm) N0? and fed the animals  a basal  diet which was either deficient in vita-
min E  or supplemented  with  30 or  300 mg/kg  of diet.   Blood,  lung,  and liver  tissues were
assayed  for  glutathione peroxidase  activity.   Exposure to  940  ug/m   (0.5  ppm)  N09  did  not
                                                           3
alter  blood  or  lung GSH  peroxidase;  however,  1,880  ug/m  (1  ppm) NO-  exposure suppressed
enzyme activity.  A  combination  of  vitamin E  deficiency and  1,880 ug/m  (1  ppm) N02 exposure
resulted in the  lowest  GSH  peroxidase in blood and lung.   Liver GSH-peroxidase  was unaffected
by either vitamin deficiency or NOp exposure.

                                             14-40

-------
     Donovan  et al.  (1976) and Menzel  et al.  (1977) exposed guinea  pigs  continuously to 940
|jg/m   (0.5  ppm) NO^ for 4 months.   After an initial short-term exposure  of  7 days or at the
completion  of a  long-term  exposure at  4 months, animals  were killed, and  the  lung  and red
blood  cell  (RBC)  GSH peroxidase levels were determined.  Short-term exposure to NOp depressed
RBC  GSH peroxidase  but  did not  affect lung levels.  Long-term exposure,  on the other hand,
affected neither  lung  nor RBC GSH  peroxidase.   These  studies  confirm the results in rats and
indicate a distinct  difference in the effect of N0? and 03 on the lung.
     Since  protection  against NO,,  occurs  with  vitamin  E,  lipid  peroxidation  most  likely
occurs,  but  the  GSH peroxidase  defense  system  does not  appear to be  induced.  Chow et al.
(1974)  concluded:   "Since  exposure  of  rats  to NO-  has  insignificant  effect  on lung  GSH
peroxidase activity, but had significantly increased the activities of GSH reductase and G-6-P
dehydrogenase,  it appears  that this oxidant attacks mainly glutathione and NADPH  while 03 not
only initiates  lipid peroxidation but also directly attacks these reducing substances."
     Selgrade et  al.  (1981)  expanded the studies of Sherwin and Carlson (1972) on the  effects
of vitamin  C  deficiency on NO^ toxicity.  These studies were aimed at measuring the infiltra-
tion of plasma proteins  into  the  airways as  an index of NOp-induced damage.  The  degree  of
vitamin C deficiency produced  by  Selgrade et al. was  mild,  being  on the average  a  sufficient
reduction  in  vitamin C  intake to produce a 25%  decrease  of the vitamin  C blood levels.   At
                                                         0
high  levels   of  NO- exposure,  9400  ug  (5.0 ppm)  NO-Xm  for  72  hrs,  50%  of the  vitamin  C
depleted guinea pigs died, while none of the normally supplemented  animals was affected.   When
exposed  to  greater  than 752  ug/m   (0.4 ppm),  lavage  fluid  protein  and lipid content  was
increased.   Unlike  the  studies of Sherwin and Carlson (1973),  Selgrade et al. found no effect
            0
at 752 ug/m  (0.4  ppm)  for up  to  1 week.   The vitamin  C  status  of the guinea pigs  in the
Sherwin  and  Carlson study  is  not  documented  in sufficient detail  to  judge if  this   is  the
reason for the discrepancy in the two studies,  but taken together these investigations  support
a role for dietary vitamin C as well as  vitamin E in influencing the susceptibility  of  animals
to NO-.  Since vitamin C is readily oxidized and reduced, it could  serve to detoxify oxidative
products formed by NOp or to maintain the intracellular redox potential.
14.2.3.3  Morphology Studies—Nitrogen  dioxide produces  morphological  alterations starting in
the terminal  airways and adjacent alveoli.   (See Table 14-9.)   A comprehensive summary review
has been prepared by Coffin and Stokinger (1977).
     The events  leading  to  emphysema  from  NO,,  exposure  of  the rat  have been  described  by
Freeman  and  co-workers.   (Cabral-Anderson  et  al.,   1977;-  Evans et  al., 1972; 1973a;  1973b;
1974;  1975; 1976;  1977;  Freeman  et  al.  ,  1966; 1968c;  1972;  Stephens et al.,  1971;  1972)  The
                                                                                    q
earliest alterations resulting from  exposures  to concentrations above  22,600 ug/m  (12 ppm)
were seen within 24 hours of continuous  exposure.  These alterations included  increased macro-
phage  aggregation,   desquamation  of the  Type  I  pneumocytes and ciliated  bronchiolar  cells,
and accumulation  of fibrin  in the  small  airways.   The cuboidal  Type  II  pneumocytes  slowly
differentiate into the  squamous  Type I  cells as  replacements  and  alter the appearance of the
                                             14-41

-------
                                                     TABLE  14-9.   EFFECT OF  NC>2  ON LUNG MORPHOLOGY
-t»




ro

N02
Concentration
|jg/m3
188 +
daily 2-hr
spike of
1,880
470

553
940



940
940
1,880
940
to
1,500
1,030 to
3,000
ppm Exposure Species
0.1 + Continuous, Various
daily 6 mo species
spike
of 1
0.25 4 hr/day, Rabbit
5 days/wk,
24 or 36
days
0.34 6 hrs/day, Mice
5 days/wk
6 wk
0.5 Continuous, Mouse
12 mo



0.5 6, 18, or Mouse
24 hr/day,
to 12 mo
0.5 4 hr Rat
1 1 hr
0.5 Continuous, Mouse
to 1 mo
0.8
0.55 Continuous, Mouse
to 1.6 5 wk
Effect
Emphysematous alterations.
Isolated swollen collagen fibers.

Hyperplasia and hypertrophy of alveolar
type II cells. Decrease in body weight,
spleen weight, and area of splenic lymphoid
nodules.
At 10 days:
Clara cell damage
Loss and shortening of cilia
Alveolar edema in interstitial space
and epithelium
At 35 to 40 days:
Bronchial hyperplasia
At 6 mo:
Fibrosi s
At 12 mo:
Bronchial hyperplasia
Alveolar damage. Interstitial pneumonia
may have confused interpretation.
Degranulation of mast cells. Response
seemed reversible.
Damage to tracheal mucosa and cilia.

Damaged cilia, increase in mucus secretion
by nonciliated cells.
Reference
Port et al. ,
1977
Buell, 1970

Sherwin et al . ,
Kuraitis et al .
Hattori , 1973
Hattori and
Takemura, 1974



Blair et al . ,
1969
Thomas et al . ,
Nakajima et al.
1972
Nakajima et al.
1969
Miyoshi , 1973




1979
, 1979





1967
>
1


-------
                                                 TABLE 14-9.   (continued)
-Pi



OJ

N02
Concentration
ug/m3
1,500




1,880


1,880 to
2,820
3,760



32,000


3,760

3,760

3,800


3,760


32,000

ppm Exposure
0.8 Continuous,
to 33 mo



1 Continuous,
493 days

1 to Continuous,
1.5 1 mo
2 Continuous,
43 days


17


2 Continuous,
3 wk
2 Continuous,
3 wk
2 , Continuous ,
14 mo

2 Continuous,
to 360 days

17 Continuous,
7 days
Species
Rat




Monkey


Mouse

Rat






Guinea
pig
Guinea
pig
Monkey
(Macaca
speciosa)
Rat




Effect
Normal growth. Decreased respiratory rate
(-20%). Tachypnea exaggerated with exposure.
Normal gross and microscopic appearance.
Suggestive evidence of changes in terminal
bronchioles.
Virus-challenged animals had slight emphysema,
thickened bronchial and bronchiolar epithelium
NO, exposure alone produced no effect.
Same morphology as others. Recovery for 1 to
3 mo showed lymphocyte infiltration up to 3 mo
No changes in terminal bronchi. Cilia lost
and altered by 72 hr. Greater cilia loss and
focal hyperplasia by 7 days. Regeneration of
cilia by 14 days. Substantial recovery by 21
Earlier and greater injury of same type
and sequence as at lower level with loss
of Type I cells.
Increased number of LDH positive cells/
alveolus (presumably Type II cells)
Type II cell hypertrophy.

Hypertrophic bronchiolar epithelium, particu-
larly in the area of respiratory bronchiole.
NaCl aerosol had no added effect.
3
At 3,760 ug/m (2 ppm), cell division of Type
II cells peripheral to terminal brochiolar-
alveolar junction seen.
Cell division seen at 24 hr, peak at 2 days,
decreased to preexposure by 5 days.
Reference
Freeman et al . , 1966




Renters et al. , 1973


Chen et al . ,
1972
Stephens et al . ,
1972

days.



Sherwin et al . ,
1972
Sherwin et al . ,
1973
Furiosi et al . ,
1973

Evans et al . ,
1972; 1978a




-------
                                       TABLE 14-9.   (continued)
\
N02
Concentration
ug/m3
32,000
5,640

9,400
18,800
18,800
28,200
ppm Exposure Species
17 Continuous,
1 day
3 4 hr/day, Squirrel
4 days with monkey
intermittent
exercise
5 Continuous, Monkey
10 90 days
10 Continuous, Rat
90 days
15 Continuous,
75 days
Effect Reference
Type II cell proliferation.
Thickening of alveolar wall and basal lamina. Bils, 1976
Interstitial collagen.

Infiltration of macrophages, lymphocytes, and Busey et al.,
occasionally polymorphonuclear leukocytes. 1974
Hyperplasia of bronchiolar epithelium and Type
II cells.
Decrease in length and weight of neonates Freeman et al.,
exposed, delivered and reared in NO,,. 1974b
Delayed lung development in progeny exposed
in utero and raised in N00. 75 days required
18,800
10
Continuous,   Guinea
   6 wk       pig
18,800 to  10 to
47,000       25
          6 mo
19,100 to  10.2 to   12 mo
21,500      11.4
              Dog


              Cat
to make up deficit.

Type II cell hypertrophy, 1 to 6 wk exposure
with increased lamellar bodies within Type II
cells.

Emphysema and death.
                                 Intraluminal  mucus.   Increase in goblet cells.
                                 Thickening of epithelium.   Fly ash (9,950 to
                                 10,200 ug/m ) had no effect.
Yuen and Sherwin,
1971
Riddick et al.,
1968

Kleinerman et al. ,
1976

-------
                                          TABLE 14-9.   (continued)
        N02
   Concentration
              ppm   Exposure	Species
                                                Effect
                                                                           Reference
 28,000
14
48 hrs
 28,000 to   15 to
 32,000       17
 28,200       15
       24 hr

       48 hr
 28,200       15    4 days/wk,
                   5 wk, total
                    31.5 hr

                    5 days/wk,
                    18 wk,
                   total 93.5
                     hr
 28,000       15   Continuous,
                   1,4,10,16
                    and 20 wk

•^28,000       15    Subacute


 28,200       15      24 hr
Rat
            Rat

            Rat

            Rat
                   Rat




                   Rat


                   Hamster
Neonate-20 days of age:   loss of cilia;
flat luminal surface of epithelium.  No
nodules.   No significant injury of Type I
cells.   Weanling-30 to 35 days of age:
tissue nodules (size increases with exposure),
Type I cell injury.  40 days:  hypertrophy
and stratification of nonciliated cells
in terminal bronchioles; polyploid exten-
sions of epithelium in terminal airways.

Division of Clara cells replaced damaged
ciliated cells.
Increased cell division, especially Type II
cells.
No effect on blood methemoglobin.
                        In lung increased atelectasis and alveolar
                        thickening.  In liver increased granular changes,
                        karyolysis and karyorhexis.  Suppressed by
                        Vitamin E supplementation.  No effect on
                        tissue lipofuscin pigment by N0~ exposure or
                        dietary Vitamin E.  Lung lipid extract distri-
                        bution not affected by N0~ exposure.

                        Hyperplasia of terminal bronchiolar and
                        alveolar epithelium reversible on discontinu-
                        ation of exposure; alterations of interstitial
                        structural features of alveoli not reversible.
                        Newborn rats up to age 3 wk relatively resis-
                        tent to exposure compared to mature rats.
                        3H-thymidine (Tdr) 24 hr post-NO-, 1 and 24 hr
                        post TdR, label in smallest ciliated airways,
                        less in trachea.   Increase in lung parenchyma
                        distant from airways.  Deep parenchyma 8% Type
                        II cells of which 11% labelled 24 hr post-NO?.
                        25% AM labelled.   No change in AM population?
Stephens et al.,
1978
                                                              Evans et al.,
                                                              1976
                                                              Evans et al.,
                                                              1974
                                                              Csallany and Ayaz,
                                                              1978a
                                                              Freeman et al.
                                                              1969
                                                              Lunan et al., 1977


                                                              Hackett, 1978

-------
TABLE 14-9.   (continued)

N02
Concentration
ug/m3
28,200
to
32,000
28,200
to
32,000

28,000
to
31,960
32,000

69,000

150,000












ppm Exposure Species
15 48 hr Rat
to
17
15 Continuous, Rat
to lifetime
17

15 12 and 24 hr Rat
to
17
17 Continuous, Rat
90 days
37.2 4 hr Dog

80 3 hr Cat












Effect
Alveolar macrophage division seen with DMA
synthesis.

Bronchial epithelium hypertrophic and meta-
plastic. Increased mucus. Connective tissue
damage. Fibrosis at junction of respiratory
bronchiole and alveoli. Emphysema.
Loss of cytoplasmic projections of nonciliated
(Clara) cells and exfoliation of ciliated cells.

Collagen damage. Large fibers and thickened
basement membrane.
Interstitial edema.
Some alveolar desquamation.
12 and 24 hr post-NCL, degeneration of Clara
cells, loss of cilia distal portion of terminal
bronchioles. Clara cell hyperplasia evident
48 to 168 hr post-NO?. Loss of pneumonocytes
resulted in substantial centroacinar denudation
of basal lamina in lungs 12 and 24 hr post-NO™.
Serous and serofibrinous edema, neutrophilic
emigration and extravasation of erythrocytes
evident 24-hr post-NO? exposure. Peri-
bronchiolar congestion and edema. 50% proximal
alveolar spaces filled with serous edema fluid.
Increased number of AM and hyperplasia of type
II pneumocytes.
Reference
Evans et al. ,
1973a

Freeman et al . ,
1968c; 1972

Stephens et al. , 1971
Evans et al . ,
1978b

Stephens et al . ,
1971
Guidotti and
Liebow, 1977
Langloss et al . ,
1977












-------
parenchyma  into  a  "gland-like"  tissue in the region of the ducts.  Incorporation of  H-thymi-
dine  by Type  II  cells was  observed  within 12  hours  after  initial  exposure, the  number of
labeled  cells  becoming maximal  in about  48 hours and decreasing to  pre-exposure  levels by 6
days,  despite  persistent  exposure  (Evans  et  al.,  1975).  This  pattern of  incorporation of
3                                                                            3
 H-thymidine,  indicative  of cell  replication,  was documented  at 3,760 ug/m   (2  ppm)  N0~ as
                        3
well  as at  32,000  ug/m  (17 ppm)  (Evans  et  al.,  1972).  On continued exposure,  there is a
change  in  the  normally irregular contour formed by the ciliated and nonciliated cuboidal cell
layer  of the terminal  airways  due to  a  loss of the bud-like cytoplasmic projections  of non-
ciliated (Clara)  cells and  the exfoliation of  ciliated cells (Evans et al. ,  1978b).   Later,
aberrations  in ciliogenesis  occur and cilia often  appear within  vacuoles  surrounded by cyto-
plasm.
     Renters et  al.  (1973)  exposed  monkeys to  1880  (jg/m  (1  ppm)  N0~ continuously  for 493
days.   Four  monkeys  were  challenged  with influenza A/PR/8/34  virus one day before and 41, 83,
146, and 266 days  after initiation of NOp  exposure.   Monkeys exposed to N02 and virus devel-
oped  moderate  emphysema with thickened  bronchial and bronchiolar epithelium.   No  effect was
observed in monkeys exposed to N0~ alone or controls.
     Age is  a  factor in determining the response of the lungs to NOj.  Newborn rats up to the
age  of about 3 weeks  are  relatively  resistant to high subacute  concentrations (about 28,000
ug/m ;  15  ppm) compared to more mature animals.   (Lunan  et al.,  1977)  On  the contrary, old
rats about 2 years of age or more have a 24-hour delay in renewing injured  or desquamated Type
I  pneumocytes,  relative to  younger  animals, and  also  have a lower  threshold  for  death from
pulmonary edema induced by N02 (Evans et al., 1977).
     Sherwin and co-workers  (Kuraitis  et  al. ,  1979; Sherwin et  al.,  1979)  exposed mice to 553
    0
ug/m   (0.34  ppm) NOj  6 hours/day,  5  days/week for 6 weeks.   Lactate  dehydrogenase positive
type II cells  were  quantitated  and shown to be hyperplastic and  hypertrophied.   Body weights,
spleen weights, and area of splenic lymphoid nodules were decreased following exposure to N02-
     Buell  (1970) reported  the  isolation  of swollen,  damaged, insoluble collagen  fibers from
the lungs of rabbits exposed to  470 ug/m  (0.25 ppm) for 4 hours/day,  5 days/week for 24 or 36
days.  Modifications of collagenous  tissue  are evident early  and late and  may be reflected in
the increased excretion of collagen degradation products in the  urine.
     While   hyperplasia  of the  terminal  bronchiolar and alveolar epithelium  is reversible on
                                           2
discontinuation of exposure  to  28,000 ug/m  (15 ppm)  N02, the interstitial  structural  altera-
tions  of  alveoli are  not (Freeman et  al., 1969a).   Bronchiolar epithelial  alterations are
observed during  lifetime  exposure  to  3,760 ug/m  (2 ppm)  (Freeman  et al.,  1968a,c).   Similar
changes in  rats without enlargement of lungs have been seen after a lifetime exposure to 1,500
ug/m  (0.8  ppm) NO- (Freeman et  al.,  1968c).
                                                                                             3
     Embryonic  and  adult  hamster tracheal  cells  were  exposed  as   cultures  to 1,880  ug/m
(1 ppm) NO- for 6 hours (Samuelsen et al., 1978).   Cells so treated lost their ability to grow
                                                                                       3
and form colonies.   Hamster  lung  fibroblasts (V-79),  when exposed J_n  vitro  to 216 ug/m  (0.12
ppm) NO- for periods up to 6 hours,  also  failed to divide and  form colonies.

                                             14-47

-------
     Blair et al.  (1969)  did microscopic studies of  the  temporal  alterations of lung morpho-
logy in mice exposed to 940 ug/m  (0.5 ppm) NO-, for 6, 18, and 24 hours per day.   Exposed mice
were found to have expanded alveoli after 3  to  12  months of exposure.   However, interstitial
pneumonia may have confused the interpretation.   Continuous exposures of mice to 940 to 1,500
ug/m  (0.5 to 0.8  ppm) for 1 month  induced  proliferation of epithelial cells of  the mucuous
membranes, degeneration and loss of mucous membranes,  edema in alveolar epithelial  cells, loss
of cilia, and an influx of monocytes.  (Hattori,  1973; Hattori and Takemura,  1974;  Nakajima et
al., 1972;  Nakajima et al.,  1969)  Mice exposed continuously  for 5 weeks to 1,030  to 3,000
ug/m  (0.55  to  1.6  ppm)  NOp exhibited  damaged  cilia  and  an increase in mucus  secretion by
nonciliated cells.
     Furiosi  et  al.  (1973)  investigated  the  influence  of a 14-month  continuous  exposure to
3,800 ug/m3  (2  ppm) N02  and 330  ug/m3  (0.1  ppm)  NaCl  (0.1  to 10.3 urn), alone  and in com-
bination,  on monkeys   (Macaca  speciosa).   Rats were  exposed  simultaneously  but  received
approximately 1,880  ug/m    (1 ppm)  NO,, due  to differences  in  the .exposure  cages.   The NaCl
exposure alone caused no effects.   In monkeys, the NOp exposure resulted in hypertrophy of the
bronchiolar  epithelium,  particularly  in  the area  of  the  respiratory  bronchiole  which  is
confluent  with  the  alveolar duct.   Morphological  changes  were  observed also  in  the more
proximal  bronchiolar  epithelium.   When NaCl  was  combined with  N02, NaCl  appeared  to have no
influence.  Neither were alveolar epithelial  changes noted.   In rats, the results were similar
to an earlier study with  equivocal findings, (Freeman et al., 1966) in which the animals were
exposed to about 1,500 pg/m  (0.8 ppm) N0? for over 2  years.   In the latter study,  (Freeman et
al.  1966)  it was  reported that  rats exposed  continuously up to 33 months exhibited an essen-
tially  normal  gross and  microscopic appearance  with suggestive  evidence  of changes  in  the
terminal bronchioles.
     Recovery from exposure to NO, has been reported (Chen et al.,  1972; Evans et al., 1978b).
                                                         o
In mice  sacrificed after  exposure to 1,880 to 2,820 ug/m  (1 to 1.5 ppm) N02 for 30 days,  the
morphological changes  were  similar to those described above (Chen et al., 1972).   Lymphocytes
infiltrated around the bronchioles during the ensuing  1- to 3-month period in clean air.  This
was not  observed  in mice  sacrificed either  during  or immediately after N02 exposure, leading
the authors to speculate that this might have been an  autoimmune response.
     Bils  (1976)  observed  connective  tissue changes  in  squirrel  monkeys  that  respired 5,640
    q
ug/m   (3 ppm)  N02 for 4  hours/day for  4  days  with  intermittent exercise  during exposure.
Thickening of the alveolar wall  between the air and capillary spaces, in the basal  lamina,  and
in the  interstitial  areas  was seen.  Numerous fenestrations  were  found in the alveolar walls
in the centroacinar area.
     Coffin and Stokinger  (1977)  suggest that fenestrations are related to the pores of Kohn.
Since the frequency of such  pores  differs  among species, attenuation  of  alveolar septae  and
distention of  their  pores  may  be  recognized,  depending on the  species.   Reduction  in  .the
elasticity of  connective  tissue,  regardless  of species,  combined with  the  loss of  Type  I
cells, could result in enlargement of the pores.   They contend that the process may be largely

                                             14-48

-------
irreversible once the pores are enlarged.  Thus, the mechanisms resulting in their appearance,
although fenestration may  not be prominent in all species, may be a hallmark of pathogenesis.
     Port  et  al.  (1977)  investigated the  effects  of NO, on several  species  using  light and
                                                     3
scanning electron  microscopy.  Exposure to 188  ug/m  (0.1 ppm) was continuous  for  6 months.
Upon this  regimen  were  superimposed daily  2-hour peaks  of 1,880 ug/m  (1 ppm) l^.   Although
bronchioles and alveolar  ducts were not found to be remarkable, occasional foci of distended
alveoli  were  seen under  the  pleura.   Large  variations   in  pore size  (up  to 5-fold)  and in
number  (up  to  10  per alveolus) were  seen.  Alveolar pores were thought to be involved in the
development of emphysema induced by NO- in some species but not in others.
                              3                                     3
     In  exposures to  940  ug/m  (0.5 ppm)  for  4  hours or 1,880 ug/m  (1 ppm) for 1 hour,  rats
sustained  reversible  lung-tissue  change (Thomas  et  al.,  1967).   In  tissues from animals  sac-
rificed  immediately  after exposure,  the mast  cells were ruptured and  disoriented  and showed
loss of  cytoplasmic  granules.   The occurrence was  primarily  in  the  pleura, bronchi,  and  sur-
rounding tissues,  but  most markedly  in the mediastinum.   This response  seemed  reversible,
since animals  sacrificed  24 to 27 hours after exposure  appeared to have only a few  ruptured
mast cells.  The  investigators considered  the release of granular material  from the lung  mast
cells  in response  to N0~ inhalation  to  signify  the potential onset of an  acute inflammatory
reaction.
14.2.3.4   Pulmonary  Function—Exposures  of animals  to 9,400  ug/m  (5  ppm) NO^  or  lower  have
been reported to have produced a variety of effects  on pulmonary function.   (See Table 14-10.)
Elevated respiratory  rates  throughout  the  life-span of  rats were observed  after  the animals
                           2
were exposed to 1,500  ug/m   (0.8 ppm) NOp  for periods up to 2.75 years (Freeman et al., 1966;
Haydon et al.,  1965).
     Rats  exposed  to 5,400 ug/m   (2.9 ppm) N02  for 24  hours/day,  5 days/week, for  9 months
exhibited a 13  percent  (p  < 0.05) decrease in  lung compliance and lowered  lung volumes  when
compared to  controls (Arner  and  Rhoades,   1973).   Freeman et al., (1968c)  however,  observed
that resistance to airflow and dynamic compliance were not affected when rats were  exposed for
                     o
2 years to  3,800 ug/m  (2 ppm) N0?.   Tachypnea (rapid breathing) was  observed.
     Rats  and  cats  exhibited a  tendency   toward' increased  respiratory  rates  and  decreased
arterial 0~ partial  pressure  when exposed  to 940 to 38,000  ug/m  (0.5 to  20  ppm)  NO^ (Zorn,
1975b).   Oxygen uptake  in the blood was impaired and remained so several  hours after  exposure
was terminated  (Zorn, 1975a).
     Murphy et al. (1964) exposed guinea pigs to various  concentrations  of NO, between 9,780
               ,                                  ,                           f.
and 24,440 ug/m   (5.2  and  13  ppm).   At  9,780  ug/m   (5.2 ppm), there were  no  significant in-
creases in  respiratory rate  until  after 3 hours of exposure.   When guinea  pigs exposed to  this
concentration for  4 hours  were returned to  clean  air, recovery occurred within approximately 1
hour.    At  higher  concentrations,  respiratory  rates  increased  earlier.    Tidal  volume  also
decreased during the  4-hour  exposure to 9,780  ug/m  (5.2  ppm).   The net effect was  to  maintain
minute  ventilation  at  a  nearly  constant  level.   No  significant alterations in  respiratory
                                                                           2
function in rabbits  were  observed when animals were  exposed  to  9,400  |_g/m   (5 ppm)  NO^ for 6
hours/day over  a period of 18  months  (Wagner  et  al. , 1965).
                                             14-49

-------
TABLE 14-10.  PULMONARY FUNCTIONS
Pollutant
N02
N02

NO,
N02
NO,
N02
NO,
NO,
N02
Concentration
ug/m3 ppm Exposure
940 to 0.5 to Continuous
38,000 20
1,500 0.8 Continuous,
to 2.75 yr

1,880 1 16.5 mo. NO
alone or with
subsequent in-
fluenza virus
A/PR/8/34
challenge.
3,800 2 2 yr
3,800 2 10 yr
16,900 9 5 yr
5,400 2.9 Continuous,
5 days/wk,
9 mo
9,400 5 6 hr/day,
18 mo
9,400 5 7.5 hr/day,
5 days/wk,
5. 5 mo
Species
Rat. cat
Rat

Squirrel
monkey
Rat
Monkey
(Macaca
speciosa).
Pregnant and
offspring
Rat
Rabbit
Guinea pig
Effect
Increased respiratory rates.
Decreased arterial oxygen pressure.
Impaired 02 uptake in blood.
Increased respiratory rates.

Little change In tidal volume, minute
volume, and respiratory rate.
Resistance or dynamic compliance
unchanged. Tachypnea.
No change in mean respiratory rate
or functional residual capacity of
juveniles.
Decreased (13%, p < 0.05) lung com-
pliance and lowered lung volume.
Respiratory function unchanged.
No increase in total resistance to
airflow.
Reference
Zorn. 1975a;
1975b
Freeman et al . ,
1966
Haydon et al. ,
1956
Fenters et al. , 1973
Freeman et al . ,
1968c
Freeman and Juhos,
1976
Arner and Rhoades,
1973
Wagner et al . ,
1965
Balchum et al . ,
1965

-------
TABLE 14-10.   (continued)
Pollutant
NO,
£




NO,
£.








NO,
c

NO,
so|
NO- +
so2
NO,
£
NO, .
Concentration
; ug/m*
9,400
18,800




9,400




18,800




9,780


10,000
10,000
10,000 +
10,000
15,000 to
22,600
ppm
5
10




5




10




5.2


5.3
3.8
5.3 +
3.8
8 to
12
Exposure
Continuous,
90 days




Continuous,
2 mo.
K. pneu-
moniae
challenge
Continuous,
1 mo.
K. pneu-
momae
challenge
4 hr


6 days/wk,
6 mo


continuous,
12 wk
Species
Cynomologus
monkey




Squirrel
monkey








Guinea pig


Guinea pig



Rabbit

Effect
Unchanged with heat stress.
Impaired distribution of ventilation of
the lungs; increased respiratory rates;
decreased tidal volume; addition of heat
stress decreased dynamic compliance of
lungs.
Gradual reduction in tidal volume.
Increased respiratory rate. Minor
changes in minute respiratory volume.
After challenge, minute volumes decreased
and remained depressed.
Elevation in minute respiratory volume
due to increased tidal volume and respira-
tory rate by 2 wk and throughout exposure.
3 days after challenge, marked reduction
in minute volume.
Increased respiratory rate, return to
normal levels in clean air. Decreased
tidal volume.
Respiratory frequency, flow rate, or
minute volume unchanged in all regimens.


Increased nonelastic resistance and
functional residual capacity.
Reference
Coate and Badger,
1974




Henry et al . . 1970









Murphy et al. ,
1964

Antweiler and
Brockhaus, 1976


Davidson et al. ,
1967
         Static lung compliance unchanged.

-------
                                                                     TABLE  14-10.   (continued)
 I
Ul
N3
N02
Concentration
Pollutant ug/m3 ppm
NO, 18,«00 10
. 28.200 15
65,800 35
94.000 50
94.000 50
Exposure
2 hr, K/
pneumoniae
challenge

2 hr, chal
with K. pneu-
moniae after
24~hr
Species Effect Reference
Squirrel Decreased tidal volume, increased respira- Henry et aV. , 1969
monkey, male tory rate 2 to 4 hr post exposure.
and female No enhancement by K. pneumoniae.
No mortality. Less drastic effects
on respiratory function.
Tidal and minute volume decreased by 4 hr.
Mortality: 2/3 within 5 to 72 hr.
Increased respiratory rate.
Tidal volume decreased.
Respiratory rate increased.
Death within 72 hr.
                        94.000        50
                                                 2 hr
            NO,         19,200 to
              *         21,400
10.2 to  Continuous.
11.4        12 mo
Cat
fly ash     10,000 to
            10,200
elutriated  2.100 to
dust of     1,600
fly ash

NO,         28,200        15
                                               Continuous,
                                                 lifetime
                        Rat
 Respiratory rate increased 2-fold.
 Decreased tidal  volumes.
 Minute volumes constant.
 Respiratory rates high for 72 hr,
 •return to normal by 7 days.

 Increased total  airway resistance and
 upstream resistance.
 Decrease in static lung compliance.
•Internal surface area unchanged.
 No effect due to fly ash.
               Increased tidal volumes 50 to 350%.
               Minor increased resistance and de-
               creased compliance 15 to 20 wk.
               Increased emphysema.
                                                            Kleinerman et al. ,
                                                            1976
                                              Freeman et al.
                                              1972

-------
                                                                 TABLE 14-10.  (continued)
N02
Concentration
Pollutant ug/m3
N02 38,400
ppm Exposure Species
20.4 20 to 22 Hamster
hr/day,
7 days/wk,
12 to 14 mo
Effect Reference
Increased total pulmonary resistance Kleinerraan, 1977
during passive ventilation and maximal
airflow with concurrent decreased flow
values. Return to normal within 3 mo.
Static lung compliance unchanged.
Decreased surface area.
          N02          56,000        30
 i
Ul
15 min       Rabbit
          NO-          56,400  to      30  to     7  to  10  days.  Hamster
                      65,800          35       followed by
                                               papain
Redistribution of lung perfusion resulting
in reduced storage activity in peripheral
zones of lung.

NO, + papain increased lung volumes.
Nof + papain increased pulmonary
resistance (p < 0.05).  Pulmonary
resistance unchanged by papain.
von Nieding et al.
1973
                                                                         Niewoehner and
                                                                         Kleinerman, 1973

-------
     Henry et al.  (1970)  exposed male squirrel monkeys continuously to 18,800 and 9,400 ug/m
(10 and  5  ppm)  NO^ for 1 and  2  months,  respectively.   Elevation in minute respiratory volume
due  to  increased  tidal  volume  and  respiratory rate  was  apparent by  2 weeks  and  persisted
                                   q
throughout exposure to  18,800  ug/m  (10 ppm) NOp.   At the end of the exposure period,  monkeys
were challenged  with  K.  pneumoniae;  3 days  later minute volume was  markedly  reduced.   Only
minor  changes in minute respiratory volumes were  noted  in monkeys exposed to  9,400 ug/m  (5
ppm) NOp for  2  months.   The tidal volumes  displayed  a gradual reduction during the  2  months,
while  at the same  time  respiratory rates  increased.   After  challenge  with  bacteria,  minute
volumes decreased and remained depressed.
     Renters et  al.  (1973)  found that monkeys  exposed  to  1,880  ug/m  (1 ppm)  N02 for 16.5
months showed little change  in tidal  volume, minute volume, and respiration rate.  Subsequent
challenge with influenza virus A/PR/8/34 produced no subsequent alterations either.
     Environmental  factors,  such as heat  stress,  in  combination with NO,  exposure  have been
                                                                                          3
examined.  (Coate and Badger, 1974)  Monkeys continuously exposed to 9,400 and 18,800 ug/m  (5
and 10 ppm)  NO^  for 90 days were  stressed  at  a temperature of 31°C versus 24°C for  controls.
At  the  higher concentration, N02  impaired  the distribution of ventilation of  the  lungs,  in-
creased  respiratory rates,  and decreased  tidal volumes.    The  addition  of heat stress  did not
further  impair  distribution of  ventilation,  but  it  did  decrease  dynamic compliance   of  the
                                                                                             3
lungs;  N02 alone did not.   No synergistic  effect was seen at N02 concentrations of 9,400 ug/m
(5 ppm) with heat.
     Freeman and  Juhos (1976) exposed pregnant monkeys  to N0? continuously  and raised their
offspring  in  similar  environments.   Adult  and juvenile  monkeys were  exposed to  3,800  and
16,900 ug/m  (2  and 9  ppm)  NO,  for 10  and  5 years, respectively.   No changes due to exposure
                              *-                                                    &•
could  be seen  in  mean  respiratory  rate or  functional  residual  capacity in  the  juveniles.
14.2.3.5  Studies of Hyperp1asia--Chronic  N02 exposure produces a transient hyperplasia of the
Type II  cells of the  lung.   This  hyperplasia  has  stimulated inquiries into the potential for
neoplasia or tumor formation due to NO^.   (See Table 14-11.)
     The studies  by Ide  and  Otsu (1973) revealed evidence of some tumor  production  in mice
exposed  to 9,400  to 18,800  ug/m3 (5 to 10  ppm) N02 for  2 hours/day,  5 days/week for 50 weeks
after receiving  injections of 0.25 mg 4-nitroquinoline-l-oxide (a lung-tumor-specific carcino-
gen), but N02 did not enhance the tumor production  (i.e., N02 had no synergistic or inhibitory
properties with  a known carcinogen).   No tumors were  observed in mice  exposed  to N0?  alone.
These  data  are  of  questionable  value  for predicting potential interactions  with the  broader
classes of carcinogens.
     Rejthar  and Rejthar  (1975)  exposed  rats to  9,400 ug/m  (5  ppm)  N02  continuously  for
periods of 3, 5,  7, 9,  and 11 weeks.   The  rats  were then  killed.   Following a 3-week  exposure,
the bronchioles  contained uniform cuboidal one-layer epithelium composed of nonciliated cells.
The cells  showed  vacuolization,  and  hyperplastic foci  appeared in the bronchiolar epithelium.
The foci were 2-  to 4-layer pyramidal  formations.   By 5  weeks, extensive hyperplasia composed
of three to four layers of epithelial  cells was apparent.  Centers of cuboidal metaplasia were

                                             14-54                °

-------
                                                           TABLE  14-11.   STUDIES  OF  POTENTIAL HYPERPLAS1A
 i
en
en
Pollutant
Concentration
Pollutant
NO.


CO
Synthetic
Smog
N02
CO
03
so2
N02


N02

ug/mj
940 to
1.500
+
58.000


1,500
5,750
760
5,700
2.360


9,400

ppm
0.5 to
0.6
+
50


0.8
b
0.38
2.2
1.26


5

Exposure
Continuous ,
30 days


23 to 24
hr/day ,
8 to 12 mo



12 hr/day.
3 mo

Continuous,
to 11 wk
Species Effect
House Increased hyperplasia terminal bronchioles
to alveolus. No difference from N02 alone.
CO (115,000 ug/m3, 100 ppm) alone for 30 days
failed to induce hyperplasia.
House By 20 days exposure, increased thickened
bronchial membranes.
By 60'days, very thick membranes appear to
have villus-like hyperplastic folds.
4 months post-exposure, hyperplasia
regressed towards normal.
Rat, prior No effect on fertility.
to breeding Decrease in litter size and neonatal weight.
No teratogenic effects.
Rat Appearance of hyperplastic foci in the
shape of 2 to 4 layer pyramids by 3 wk.
Reference
Nakajima et al . ,
1972


Loosl i et al . ,
1972




Shalamberidze
and
Tsereteli. 1971
Rejthar and
Rejthar, 1975
                                                                             Decreased ciliated cells.
                                                                             Extensive hyperplasia (3 to 4 layers  of
                                                                             epithelium),  cuboidal metaplasia in ad-
                                                                             jacent alveoli  by 5 wk.
                                                                             Hyperplasia in  all bronchioles,
                                                                             decreased bronchiolar lumina, polymorphous
                                                                             epithelium extensive by 7 wk.  Terminal
                                                                             bronchiolar epithelium contained only
                                                                             2 or 3 irregular layers, increased number of
                                                                             ciliated cells  by 9 wk.   By 11 wk return to
                                                                             1 layer epithelium.   Lu"9s at indefinite state
                                                                             of repair from  week 7 on.

-------
                                                                   TABLE 14-11.  (continued).
en
O-i

Pollutant
Concentration
Pollutant pg/mj
NO, 9,400 to
* 18,800

NO, 18,800
C.

NO, 18,800
c.


Auto Exhaust
CO 58,000


N0x
A

C02 (0.07 and
0.37%)
Aldehydes


ppm
5 to
10

10


10




50


(0.2
and
23)


(0.1
and
2.0)
Exposure Species
2 hr/day, Mouse
5 day/wk,
50 wk
2 hr/day, Mouse
5 day/wk,
50 wk
Continuous from Rat
pregnancy to
3 mo after
delivery

6 hr/day, Rat
5 days/wk,
2.5 mo to
2 yr







Effect Reference
Mice given 4-nitroquinoline-l-oxide and Ide and Otsu,
NO,; NO, had no effect on tumor production. 1973
L. £.
Mice given 4-nitroquinoline-l-oxide Otsu and Ide,
(carcinogenic agent) + NOp decreased 1975
incidence of lung tumors.
Decreased litter size and increased mor- Freeman et al.,
tality of neonates up to 15 days post 1974
delivery.
No teratogenic effects noted.

Auto exhaust had no biological effects when Stupfel et al.,
NO was 0.2 ppm. 1973
Exposure to NO (23 ppm) increased number of
spontaneous tumors, cutaneous abscesses,
and bilateral renal sclerosis.
No tumors or abscesses in lungs.






-------
found in adjacent alveoli.  By 7 weeks, hyperplasia was apparent in all bronchioles, thus, nar-
rowing  the bronchiolar  lumina.    Polymorphous  epithelium was  extensive  with  a  few ciliated
cells in  hyperplastic areas.   After 9 weeks, terminal bronchiolar epithelium generally showed
two  or  three  irregular layers.   The number  of  ciliated cells  increased, but cilia were often
located atypically  in intercellular spaces.   A return to a single layer of epithelium without
cilia was  observed  after 11 weeks.  Seven weeks  after exposure to NO,,, the lungs appeared to
be in a state of repair moving towards reversal of the lesions.
     Nakajima et  al.   (1972) exposed  mice to 940 to  1,500  ug/m3 (0.5 to 0.8 ppm)  N02  for 30
days.   Examination  revealed hyperplasia  from the terminal bronchiole  to  the  alveolus.   Mice
exposed to  the  same concentrations of N0? with CO (58,000 ug/m  ; 50 ppm) for 30 days revealed
the  same  hyperplastic  foci  in the  terminal bronchioles.  At exposure concentrations  up  to
115,000 ug/m  (100 ppm) for 30 days, CO by itself failed to induce hyperplasia in mice.
     Stupfel  et  al.   (1973)  exposed rats to automotive exhaust 6 hours/day, 5 days/week  for
periods of  2.5  months to 2 years.  The  exhaust contained 58,000 ug/m  (50  ppm)  CO,  two dif-
ferent  concentrations of  NO  (0.2  and  23   ppm),  C09 (0.07  and 0.37 percent),  along  with
                             A                         C.
aldehydes  (0.1  and 2  ppm).   No  effects  were  observed at  0.2 ppm NO .  At 23 ppm  NO  ,  more
                                                                      A               A
spontaneous tumors  and cutaneous  abscesses  as well  as bilateral renal  sclerosis  were  seen.
14.2.3.6   Edemagenesis and To1erance--Sherwin  and  Carlson  (1973)  reported  an  increase  of
protein in  the  lavage  fluid  from lungs  of  guinea  pigs with  an unquantified vitamin C  defi-
ciency  exposed  continuously to  750 ug/m  (0.4 ppm)  NO-  for  1 week (p <  0.001).   (See  Table
14-12.)   Proteins  were identified  and  measured by disc  electrophoresis.  No  remarkable  dif-
ferences were noted  in the composition of the filtered proteins obtained by pulmonary lavage.
                    3                              3
Mice  injected with   H-rabbit  albumin  accumulated  H  in  their  lungs  following 14  day,  con-
tinuous exposure  to  7,500  to  13,000 ug/m   (4 to  7  ppm) NO-.  (Sherwin  and  Richters,  1971)
Using injected horseradish peroxidase as a marker, this group of researchers  recently reported
increased retention of  protein  in pulmonary air  spaces after  exposure to 940 ug/m   (0.5  ppm)
NO-  for 5  days/week  for  3 weeks  (Sherwin   et  al.,  1977).   Greater  retention  of  horseradish
peroxidase occurred after 6 weeks of exposure.
     Selgrade et   al.   (1981)  reexamined  this  problem  focusing  on  the  role of  vitamin  C
deficiency  in  promoting  of  NO^-induced  edema.    (See  "Section  14.2.3.2.2  Lipid  and  Diet
Effects"  for  a  detailed  description  of  the concentrations,   times and effects.)   They  found
that  vitamin  C  depletion enhanced  both edema formation,  as  measured  by protein and  lipid
content of  the lavage fluid,  and  increased mortality at  9400 ug/m   (5.0  ppm).   There  are
differences in the  two studies,  however.   Selgrade et  al.  found no  effect of exposure  to  752
ug/m  (0.4 ppm)  for up to 1 week whereas Sherwin and Carlson (1973) did.   Selgrade  et al.  also
found a new protein  in the lavage fluid  not found  in serum and found that the  lipid content,
while  increased,  did  not reflect  that  of  the  serum.   Sherwin  and  Carlson  used disc  gel
electrophoresis  to measure protein  content  while Selgrade et al. used the microchemical  Lowry
method.   The qualitative  difference  in  identification of  proteins may also have resulted from
the  use  of gel  scanning  by Selgrade  et al. and the improvements in  gel resolution  brought

                                             14-57

-------
                                               TABLE  14-12.   PRODUCTION OF LUNG EDEMA BY NO,
en
oo

Pollutant
Concentration
ug/m3 ppm.
750 0.4
940 0.5
7,500 to 4 to
13,000 7
56,400 30
Duration
Continuous ,
1 wk
5 days/wk,
3 or 6 wk
Continuous ,
14 days
Continuous ,
to 30 days
Species Effects
Guinea pig Increased proteins in lung
lavage fluid of exposed animals with
an unquantified vitamin C deficiency
detected by disc gel electrophoresis.
Mouse Horseradish peroxidase used as a
marker for proteins showed greater
sequestering in exposed mice at 3 wk
than 6 wk. Suggests edema.
Mouse H rabbit albumin infiltration
indicates lung edema.
Hamster Lung wet weight elevated at 1
and 30 days.
Reference
Sherwin and
Carlson, 1973
Sherwin et al . ,
1977
Sherwin and
Richters, 1971
Kleinerman and
Rynbrandt, 1976

-------
about  in  recent developments  in this  field.   The major difference may  lie,  however,  in the
degree  of  vitamin C  depletion of the  guinea  pigs in the two studies.   Those  of Sherwin and
Carlson  are  not  documented with  blood vitamin C levels.   Selgrade  et  al.  found  only mild
depletion was  necessary.   Consequently, future studies will be  needed to clarify this point.
Taken together, these two studies and those reported above suggest that NCL damage to the lung
can be modified by the dietary intake and that lavage fluid composition is a sensitive measure
of damage to the lung.
     The development  of tolerance  to  lethal  concentrations  of N02 has  been  correlated with
lethal edema  production.   Wagner et al. (1965) examined  the  question  of tolerance along with
several other characteristics.   They found that tolerance could be evoked by prior exposure to
low  or  high  concentrations  of N00,  in young  and  old animals.  (See  Table  14-13)   Mice were
                                                3                                            3
made  tolerant to an  LC50  dose  of  113,000 (jg/m   (60 ppm) by prior  exposure  to 9,400 (jg/m
(5 ppm)  N02  for  7 weeks  (hours/day  not  specified).  Tolerance  disappeared  after  3  months
following removal from the N02 exposure.  Rats also were made tolerant.
14.2.4.  Extrapulmonary Effects
14.2.4.1     Nitrogen  Dioxide-induced Changes  in Hematology  and Blood Chemistry-Exposure   of
experimental  animals  and  humans  to NO,, alone or in combination with other pollutants produces
an array of hematological  perturbations (see Table 14-14) with a biological significance which
is not easily interpretable (see Chapter 15 for human studies).
                                                                 3
     Shalamberidze (1969)  exposed rats continuously  to  100  |jg/m  (0.05 ppm) N02 for 90 days
with no change in blood hemoglobin or erythrocyte   levels.
     A 7-day  exposure  to  940 ug/m   (0.5 ppm)  N02  resulted  tn a depression  in  GSH peroxidase
levels of RBC  in  guinea pigs  (p  <  0.001)  which  was not  observed  after  exposure for 4 months
(Donovan et al., 1976; Menzel et al., 1977).
     Kosmider et al.  (1975) exposed guinea pigs for 8 hours/day for 120 days to 940 ug/m  (0.5
ppm)  N02 with 1,000  ug/m3  (0.39 ppm) S02 or  940  ug/m3  (0.5  ppm)  N02 with  1,000 ug/m3 (0.39
ppm)  SO- and 70 ug/m  (0.1 ppm) ammonia.   Animals  exposed  to N02 and S02, with and without
ammonia, displayed an increase in white blood cells (WBC) and a decrease in RBC and hemoglobin.
Following exposure, a differential count of white  cells revealed a decrease in  neutrophils and
eosinophils and an increase in lymphocytes.
     Mersch et al. (1973)  exposed guinea pigs to  680 ug/m   (0.36  ppm) N02 continuously for 1
week.  Following exposure,  RBC D-2,3-diphosphoglycerate was  significantly increased (p < 0.05),
a measure which could reflect tissue deoxygenation.
     Studies reported by Nakajima and Kusumoto (1970) showed that addition of 58,000 ug/m  (50
ppm)  CO  to  940 to 1,500  ug/m   (0.5  to  0.8  ppm) N02 did  not change  the  carboxyhemoglobin
concentration in the  blood of mice exposed 24 hours/day for 1 to 1.5 months to  CO alone.  They
also exposed  mice  to  1,500 ug/m  (0.8 ppm) N02 for 5 days and found that methemoglobin levels
were not affected (Nakajima and Kusumoto,  1968).
     Mitina (1962)  exposed rabbits to 2,400 to 5,640 ug/m3 (1.3 to  3 ppm) N02 and/or 5,240 ug/nT
(2 ppm) S02 2 hours/day for 15 and 17 weeks.   Exposure to N02 alone produced a  significant rise

                                             14-59

-------
                                          TABLE  14-13.
                                  TOLERANCE TO N02 EXPOSURES

N02
Concentration
ug/m3
9,400
9,400 +
47,000
ppm Duration
5 7 wk
5 + 13 mo
25 + 6 wk
Species Effects Reference
Mouse Challenge with LC50 dose (113,000 ug/m3 Wagner et al.,
(60 ppm) NO- for 5 hr, 24 hr post-exposure) 1965
caused 28% less mortality than in naive mice.
Rat Challenge with NO- (132,000 ug/m3 (70 ppm)
for 5 hr, 3 days post-exposure) caused 0%
         47,000
en
o
25
         18,800       10
         47,000       25
7 wk
         5 hr/day,
         5 days/wk,
         5 hr/day,
         1 day/wk,
         3 wk

         6 hr/day,
          2 days
           mortality compared to 67% in pre-exposed
           controls.

Mouse      Challenge with NO- (132,000 ug/m3 (70 ppm)
           for 5 hr,  3 days post-exposure) caused no
           mortality 24 hr post-challenge compared to
           29% in naive mice.  Tolerance disappeared
           in 1 mo.

Hamster    Tolerance developed to normally lethal 5 hr   Creasia, 1978
           18,800 ug/m  (10 ppm) NO  exposure.   Protec-
           tion against further cytological injury but
           not against the cytotoxic effects of >18,800
           ug/m  (10 ppm) as measured by increased DMA
           synthesis.
                                                    3
           Tolerance to normally lethal 131,600 ug/m
           (70 ppm)  N0_.   Protection against further
           cytological injury.

Rat        Increased tolerance to 141,050 ug/m  (75      Crapo et al.,
           ppm) NO..   Increased G-6-PD, catalase, 4l£    1978
           increase  cytochrome oxidase.  No effect
           on superoxide dismutase.

-------
TABLE 14-14.   NITROGEN DIOXIDE-INDUCED CHANGES IN HEHATOLOGY
Pollutant
Concentration
Pollutant
NO,
NO,
N02

NO
S°2
NO
$
CO
NO,
2

ug/m3^
100
680
940

940 +
1.000
940 +
1,021 +
70
940 to
1,500 +
58,000
1.500
1,880

ppm
0.05
0.36
0.5

0.5 +
0.39
0.5 +
0.39 *
0.1
0.5 to
0.8 +
50
0.8
1

Exposure
Continuous,
90 days
Continuous,
7 days
8 hr/day,
7 days
8 hr/day,
4 mo
8 hr/day,
120 days
Continuous,
1 to 1.5 mo
Continuous ,
5 days
Continuous,
493 days
fol lowed by
influenza
A/PR/8/34
virus
Species Effects
Rat No effect on blood henioglobin or
erythrocytes.
Guinea pig Increased red blood cell D-2,3-diphos-
phoglycerate.
Guinea pig Decrease in RBC GSH peroxidase
(p < 0.001).
No change in RBC GSH peroxidase.
Guinea pig Same effects in both exposures.
Increased WBC and lymphocytes. Decreased
RBC, hemoglobin, neutrophils and
eosinophils.
Mouse Addition of CO to N02 failed to affect
carboxyhemoglobin.
Mouse No effect on metnemoglobin.
Squirrel No effect on hematocrit, hemoglobin, or
monkey clinical biochemical parameters.
Following viral challenge increased
leukocyte count.

Reference
Shalamberidze,
1969
Mersch et al. .
1973
Donovan et al. ,
1976
Henzel et al. ,
1977
Kosmider et al.
1975
Nakajima and
Kusumoto, 1970
Nakajima and
Kusumoto 1968
Renters et al. ,
1973


-------
                                                             TABLE 14-14.  (continued)
 I
CT1

Pollutant
Concentration
Pollutant
NO
NO.
NO
N02
NO,
C

so2
£-
NO,
S02
NO,
NaCl






N0?

NO,
L.

NO.



NO,
£
ug/mj
940
1,880
1,840 +
2,450
2,400 to
5,640

5,240

2,400 +
5,000
3,760 +
330






9,400
18,800
45,100


48,900



73,000 to
310,000
ppm
0.8
1
1.5 +
1.3
1.3 to
3

1.9

1.3 +
1.9
2 +
0.14






5
10
24


26



39 to 5
164
Exposure
16 hr/day,
7 days/wk,
4 yr

2 hr/day,
15 & 17 wk

2 hr/day,
15 wk
2 hr/day,
15 wk
Continuous,
14 mo






Continuous,
90 days
4 hr


191 days



to 60 min

Species
Dog



Rabbit






Monkey,
rat






Cynomolgus
monkey, male
Rabbit


Dog



Dog

Effects
No effects on hematocrit viscosity,
carboxyhemoglobin, or methemoglobin.


Increased leukocytes followed by
decreased phagocytic activity.
Decreased RBC.
Decreased phagocytic activity leukocyte.
No effect on RBC.
No effect on RBC.

Monkey: with or without NaCl, hypertrophy
of respiratory bronchiolar epithelium.
Rat: with or without NaCl, polycythemia
with reduced mean corpuscular volume and
normal mean corpuscular hemoglobin concen-
tration. Neutrophil /lymphocyte ratio
tendency to shift upwards in both animal
species tested.
No effect on hematological parameters.
-
Increased nitrite & nitrate in blood.
Thought to react with hemoglobin producing
methemoglobin.
Increased WBC disappeared following cessa-
tion of NOp. Decreased hematocrit and
hemoglobinf increased mean corpuscular
volume and mean corpuscular hemoglobin.
No effect on hematocrit or platelet counts.

Reference
Bloch et al. ,
1973


Mitina, 1962






Furiosi et al. ,
1973






Coate and Badger,
1974
Svorcova and
Kaut, 1971

Lewi s et a 1 . ,
1973


Carson et al . ,
1962

-------
 in  leukocytes followed by a decrease in their phagocytic activity.  Exposure to N02 alone also
 reduced the number of RBC, while a mixture of NO, and SO, or SO, alone had no effect.
                                                £.£-£.                     n
     Fenters et  al.  (1973)  showed that exposing  male  squirrel  monkeys to 1,880 ug/m  (1 ppm)
 N02  continuously  for 493 days had no significant effect on hematocrit, hemoglobin, total pro-
 tein,  globulins,  chloride,  sodium,  calcium,  potassium, glucose, blood urea, nitrogen, glutam-
 icpyruvic transaminase,  lactate dehydrogenase, and lactate dehydrogenase isoenzymes.  Challenge
 with influenza A/PR/8/34 increased leukocytes in l^-exposed animals above levels in similarly
 challenged controls.
     Coate and  Badger  (1974)  exposed monkeys to 9,400 and 18,800 ug/m  (5 and 10 ppm) N0? for
 90  days with no direct effect on hematological parameters.   In another study, monkeys and rats
                         3                                3
 were exposed to  330  ug/m  (0.14 ppm) NaCl  and  3,760 ug/m  (2 ppm) N02 for 14 months (Furiosi
 et  al.,  1973).   Exposure to N02 with or  without  NaCl  produced polycythemia with reduced mean
 corpuscular  volume  and  approximately  normal mean  corpuscular hemoglobin  concentration.   In
 monkeys and rats exposed to NO, with and without NaCl,  the ratio of neutrophils to lymphocytes
 was greater.
     Bloch et al. (1973) conducted several hematological studies on dogs exposed 16 hours/day,
 7 days/week, for  4 years to 940 pg/m3  (0.76 ppm) NO,  1,880 (jg/m3 (1 ppm) NO,, or 1,840 ug/m3
                             3
 (1.5 ppm) NO plus 2,450 ug/m  (1.3 ppm) N0?.  No changes in hematocrit, viscosity, carboxyhe-
 moglobin, or methemoglobin were found.
 14.2.4.2  Central Nervous System and Behavioral Effects—Information regarding  the  effects  of
 NO-  on the  central  nervous  system  or  on animal  behavior  is  limited to a  few studies,  (see
 Table  14-15), most of which have uncertain relationships to humans.
                                                  3
    .. Tusl et al.  (1973) exposed rats to 9,400 ug/m  (5  ppm) NO- for 8 weeks.   The influence of
 N09  on swimming  of  rats  was  measured.   By  the 5th  and 6th  weeks  of exposure,  swimming
                                                                    3
 performance had decreased 25 percent.  In rats exposed  to 1,880 (jg/m  (1 ppm) N02, performance
was maintained  with a slight tendency toward deterioration.
     Yakimchuk  and Chelikanov  (1972) reported that  rats  exposed  to 600 ug/m   (0.32  ppm)  N02
 for 3 months  developed a delay in their conditioned reflexes to sound and light. Shalamberidze
 (1969) exposed rats  to  100  ug/m  (0.05 ppm)  NO-  for 3 months  with no demonstrated effects  on
 the central  nervous system.
                                           o
     Exposure of  guinea  pigs  to 1,000  ug/m   (0.53 ppm)  N02 8  hours/day for 180 days affected
brain enzyme  levels (Drozdz  et al.,  1975).   Decreases were seen in brain malate dehydrogenase,
alanine aminotransferase, sorbitol  dehydrogenase,  lactate dehydrogenase, adenosine triphospha-
tase,  and 5'-nucleotidase.  Increases were  seen in 1,6-diphosphofructose aldolase,  isocitrate
dehydrogenase,  a-hydroxybutyrate  dehydrogenase,  phosphocreatine  kinase, and  cholinesterase.
14.2.4.3  Biochemical Markers of Organ Effects—A major  goal  has  been the detection  of  early
enzymatic markers  of  NO-  effects.    Studies of  enzyme  levels  in  different  animal  species
indicate that the earliest enzymatic changes  of  nitrogen dioxide effects occur in guinea pigs.
(See Table 14-16)  Several  such  marker enzymes  have  been determined  in blood.   Release  of
                                             14-63

-------
                                                     TABLE  14-15.  CENTRAL NERVOUS SYSTEM AND  BEHAVIORAL  EFFECTS
I
CD
Pollutant
Concentration
Pollutant
NO

NO






NO
2
NO






NO


NO


Auto Exhaust
CO
NO
CO* (0.07
and 0.37%
Aldehydes
ug/m3
100

1,000






600

1,880

9,400

37,600
6.580

14,000


75,000
37,600
15,040

58,000




ppm . Exposure
0.05 Continuous,
3 mo
0.53 8 hr/day,
180 days





0. 32 Conti nuous ,
3 mo
1 20 m in/day.
to 6 mo
5

20
3.5 6 hr/day.
8 wk
7.7 6 hr


40 5 hr
20 1 day
8 19 days

50 6 hr/day,
(0.2 and 23) 5 days/wk,
2.5 mo to
2 yr
(0.1 and 2.0)
Species Effect
Rat No effect un CMS.

Guinea pig Decreased malate, sorbilol, laclate
dehydrogenase; alanine aminotrans ferase ;
AlPase and 5' -nucleotidase. Increased
1 , 6- diphospho fructose aldolase;
isocitraLe, and alpha-hydroxybutyrate
dehydrogenase, phosphocreatine kinase
and chol inesterase.
Rat Decreased conditioned reflexes to sound
and 1 i ght .
Rat More or less constant swimming performance
only slight tendency to deterioration.
Swimming performance decreased 25% by 5th and
6th wk of exposure
Swimming velocity declined from 1st mo.
Decreased swimming performance.

Mouse, male Decreased voluntary running activity.
Return to normal within 24 hr post
exposure.
Rat 20% decrease swimming endurance.
10% decrease swimming endurance.
5% decrease swimming endurance.

Rat, male Decreased sound avoidance reflexes,
learning rate lowered.



Reference
Sha 1 amltpr i 
-------
TABLE 14-16.   BIOCHEMICAL MARKERS OF ORGAN EFFECTS
N02
Concentration
ug/m3
470
to 9.400
940

940
1.000
1.880
2.000
ppm
0.25
to 5
0.5

0.5
(NO ;
mainly*N02)
1
1.05
Exposure
3 hr
8 hr/day,
7 days
8 hr/day,
4 mo.
Continuous,
7-14 days
8 hr/day,
180 days
Continuous,
6 mo
8 hr/day,
180 days
Species Effect
Mouse Increase in pentobarbital-induced sleep time
in female mice only. Repeated daily exposures
caused no effect.
Guinea pig Serum lactic dehydrogenase, total
creatinine phosphokinase, SCOT, and SGPT.
cholinesterase and lysozyrae elevated.
Lysozyme and cholinesterase depressed.
Guinea pig Albumin and globulins found in urine.
Guinea pig Nitrates and nitrites excreted in urine.
Serum cholesterol slightly elevated; total
lipids depressed. Urinary Mg increased while
liver and brain Mg decreased. Hepatic edema
reported.
Guinea pig Protein synthesis inhibited. Body weight, total
serum proteins, and immunoglobul ins decreased.
Guinea pig Plasma changes:
Decreased albumin, seromucoid, cholinesterase,
Reference
Miller et al. , 1980
Menzel et al . ,
1977

Shervin and
Layfield, 1974
Kosmider, 1975
Kosmider et al . ,
1973a
Drozdz et al. ,
1976
                alanin, and aspartate transminases.
                Increased alpha, and beta2 immunoglobulIns.
                Intracellular edema of liver.
                Hepatic changes similar to plasma.

-------
                                                   TABLE  14-16.   (continued)

N02
Concentration
ug/m3 ppm
11,660 6.2
Exposure
Continuous ,
4 days
Species
Rat
Effect
No effect on serum lysozyme.
Reference
Chow et al . ,
1974
     47,000  to   25  to      2  hr
    179,000      95
     56,400
30
                        Rat
Continuous,   Hamster
30 days
                           Plasma corticosterone increased proportional to   Tusl et al.,
                           No,, concentration from 47 to 179 mg/m ;  at 85     1975
                           mg7m  x 5 hr/day levels returned to normal in
                           19 days; at 56 mg/m  x 5 hr/day levels returned
                           to normal in 5 days.
Serum antiprotease levels increased
Kleinerman and
Rynbrandt, 1976
Rynbrandt and
Kleinerman, 1977
I
en
en

-------
lysozyme  into  the blood  from pulmonary  damage  was cited  above (Chow  et  al.,  1974; Donovan
et al, 1976; Menzel et al., 1977).  The CPK isoenzyme patterns seen in N0--exposed guinea pigs
are  difficult  to  differentiate from CPK patterns caused by myocardial damage and are not par-
ticularly useful  (Donovan  et al., 1976).   Plasma cholinesterase (CHE) was significantly (p <
                                                   2
0.001) elevated after  a 7-day exposure to 940 ug/m  (0.5 ppm) N0? but fell on long-term expo-
sure  (4  months)•(p  <  0.001).   CHE  levels are indicators of  hepatic  and myocardial  disease,
being elevated  in hemochromatosis,  and usually depressed during active hepatocellular disease
(MacQueen and  Plant,  1973;  Moore et al.,  1957).   Increased  CHE is seen with cardiac surgery,
but  values  are  depressed  consistently with myocardial  infarction  (MacQueen and Plant, 1973).
Aside  from  metastatic  carcinoma from  the  liver  to  the lung,  pulmonary  disease  including
pneumonia has  not been previously  associated with  changes  in  CHE levels.   Most  likely,  the
alterations  in  SCOT, SGPT,  and  LDH  reported  in the  guinea  pig studies are  related to NO^-
induced  hepatic damage.   (Donovan  et al.,  1976)   The  persistent  alteration in  CHE,  albeit
lower activity, after 4 months exposure to 940 ug/m  (0.5 ppm) N0? suggests an hepatic lesion.
     Another study indicating hepatic damage (Drozdz et  al. ,  1976)  revealed decreased plasma
levels  of  albumin,  seromucoid,   alanine  and  aspartate transaminases  when guinea pigs  were
exposed to 2,000 ug/m  (1.05 ppm) NO,, for 8 hours/day for 180 days.   In agreement with Donovan
et al.  (1976), Drozdz  et  al. (1976)  reported decreased plasma cholinesterase  levels.   This
group also  found  increased serum levels of a,- and p^-immunoglobins.   Electron micrographs of
the  liver  suggested  intracellular  edema.   Kosmider (1975)  reported  decreased  serum choles-
terol, total lipids,  and beta and gamma lipoproteins in guinea pigs exposed to 1,000 ug/m  NO
(mainly NOp),  8  hours/day  for 120 days.   At the  same time,  there was  an  increase  in  serum
alpha (a) lipoproteins.  Blood serum sodium and magnesium were  reduced while liver and  brain
were depleted of  magnesium and zinc as well.  Cell  permeabilities  were changed and ions dis-
placed.    Edema  of the  liver  mitochondria occurred.   At the  same  time, urine  had  increased
secretions of  nitrite,  nitrate,  and coproporphyrin.   Respiratory rate rose significantly with
little or  no excitement or aggressiveness.   Kosmider  also  exposed these animals  to  the same
schedule  of  NO  and added  ammonia.   Nitrogen oxides  reacted with ammonia  (1,000  ug/m  ;  1.4
ppm), reducing  the lipid  and electrolyte disturbances  seen  with NO   exposure  alone.   Blood
serum lipids,  lipoproteins,  and  cholesterol  were not significantly altered from those of con-
trol  guinea pigs  breathing  filtered clean air.   There was a  decrease  in the urinary excretion
of nitrites,  nitrates, and  coproporphyrin  from NO -ammonia  treated  animals.   Blood  serum
                                                    A
sodium and  potassium were  lowered,  while magnesium and calcium were higher than controls.   No
effect on  serum calcium levels  was seen  with  NO   alone.  Liver mitochondria  contracted,  in
contrast to the edematous  state  seen in NO -exposed groups.   Earlier,  Kosmider et  al.  (1973a)
also   reported  a general decrease in  protein  synthesis evidenced by decreased  serum  proteins
and declining body weights  of guinea pigs exposed  continuously to 1,880 ug/m  (1 ppm) N02  for
6 months.
     An interesting observation  of  proteinuria  in  the  guinea  pig was  reported by  Sherwin  and
Layfield (1974) who  found  consistently  higher levels of urinary protein (p < 0.01) in animals

                                             14-67

-------
breathing 940 ug/m   (0.5  ppm)  NO, continuously for 7 to 14 days.   Proteinuria was detected in
                                                                  3
another group of  animals  exposed for 4 hours  per  day to 750 |jg/m   (0.4  ppm) N0? (p < 0.05).
Disc electrophoresis of the  urinary proteins demonstrated the presence of albumin,  and alpha,
beta, and gamma globulins.  The presence of high molecular weight proteins in urine is charac-
teristic of  the nephrotic  syndrome.   Histopathological  studies of  the kidney  were negative.
     The influence of NO,  on pentobarbital  (PEN)-induced sleeping time was investigated in mice.
                                                                              3
(Miller et al.,  1980)   A  3-hour exposure to concentrations as low as 470  ug/m  (0.25 ppm) NCL
caused  a  significant increase  in  PEN-induced  sleeping  time in female mice.   No significant
effects on  PEN-induced  sleeping time  in females were  detected  after 1 or 2 days  (3 hr/day)
                      3
exposure to  235  ug/m   (0.125  ppm) NO,.   None of  the exposure  regimens  affected  the  time
                                                                                             3
required for  the drug  to induce sleep.   Two  or three  days  (3 hr/day) exposure  to 470  ug/m
(0.25  ppm)  N02  caused  no significant  effect  in  female mice.   This trend of  a  reduction or
disappearance of the effect after  repeated  exposure  was  observed at  other,  higher,  con-
centrations also.  When the  effects of repeated daily  exposures  (3  hr/day) to 9,400 (jg/ni  (5
ppm) NO- were  compared in  male and female mice,  the  females had  a significantly increased
PEN-induced sleeping time after 1  and  2 days of exposure.   However,  a significant increase in
PEN-induced sleeping time was  not  observed in males  until  the 3rd day of  exposure.   Since the
duration of  PEN-induced  sleeping  time  is  primarily  determined  by  hepatic  mixed  function
oxidase activity,  it is possible that NO-  may alter some aspects of  xenobiotic metabolism.
     Ozone  (Graham,  1979) also  increased  PEN-induced sleeping time   in female, but not  male,
mice.   Unlike  NO, however,  as  the  concentration was decreased, an  increased number  of  daily
                                                                            3
3-hr exposures were  needed  to  observe  the effect.   For example, at 490 ug/m  (0.25 ppm)  0,, a
significant effect  was  observed only  after 6  and 7 days  (3 hr/day) of  exposure.   Thus,  for
this model  system,  a single exposure of N02 caused more effect than  a single exposure to 0,.
14.2.4.4   Teratogenesis and  Mutagenesis—There is   little  or  no evidence  in  the  literature
demonstrating that exposure  to  NO,  is  teratogenic  or mutagenic in animals.   Shalamberidze and
                                           3
Tsereteli  (1971) exposed rats to 2,360  ug/m  (1.3 ppm) N02, 12 hours/day for 3 months at  which
time exposure  ceased and the  animals were bred.-   Long-term  N02 exposure  had no effect on
fertility.   There was a statistically  significant  decrease  in  litter size  and neonate weight
(p  <  0.001).   J_n  utero  death  due  to  N02  exposure  resulted in smaller  litter sizes, but no
direct  teratogenic  effects  were  observed  in  the  offspring.   In  fact,  after  several weeks,
N02-exposed litters approached weights  similar to controls.  (See Table 14-17.)
     Gooch  et al. (1977) exposed C3H male mice to  190, 1,880, 9,400,  and 18,800 ug/m3 (0.1, 1,
5, and 10 ppm)  N02 for 6 hours.   Blood  samples were obtained at 0 time, and 1 week and 2  weeks
post-exposure.    Mouse   leukocyte  chromosomal  analysis  revealed that  N0?  did  not  increase
chromatid-  or  chromosome-type   alterations.   The analysis of primary spermatocytes showed no
direct  effect  of N02 exposure  on  their  chromosomes.  Therefore, in these  experiments,  N02
exposure did not induce  mutagenesis.  (See Table 14-17.)

                                             14-68

-------
                                                        TABLE 14-17.  STUDIES OF POILNT1AL MUIAGENES1S,  IER/UOGLNLS1S
Pol lutant
Concen tra tion
Pol lutant
NO



NO



1
9
18
9

pg/m •'•
190
,880
,100
,800
,100

ppm
0.1
1
5
10
5

Exposure Species
E
6 hr Mouse 2 wk post-e
or chr
Meet
xposure no


increase-
omosome- type alterat
primary spe
noted.

Continuous, Rat Appearance
to 11 wk shape
of 2
rmatocytes.

No

of hyperplastic
to 4 layer
ions

in
in

chromatid
leukocytes or
Reference
Gooch et a 1 . .
1977
mutagenic effects

loci
pyrami ds

i n
by

the
3 wk.

Rejthar and
Rejthar, J97!>
 i
Oi
            N0
            N0
 9,100 to
18.800
                         18,800
                         18,800
                                          5 to
                                           10
                                           10
                                           10
2 hr/day,
5 day/wk,
  50 wk

2 hr/day,
5 day/wk,
  50 wk
                                                                     Mouse
                                                                     Mouse
                           Continuous  from  Rat
                           pregnancy to
                           3 mo after  delivery
Decreased ciliated cells.
Extensive hyperplasia (3 to 1 layers of
epithelium), cubciidal metaplasia in ad-
jacent alveoli by 6 wk.
Hyperplasia in all bronchioles,
decreased bronch iolar luinina, polymorphous
epithelium extensive by 7 wk.  Terminal
brohchiolar epithelium contained only
2 or 3 irregular  layers, increased number of
ciliated cells by 9 wk.   By 11 wk return to
1 layer epithelium.   Lungs at indefinite state
of repair from week 7 on.

Mice given 1-nitroquinoline-1-oxide and
N0?; N0_ had no  effect on tumor production.


Mice given 4-nitrogutnoline-1-oxide
(carcinogenic agent) + NO, decreased
incidence of  lung tumors.

Decreased litter  size and increased moi—
tality of neonates up to 15 days post
deIivery.
No  teratogenic effects noted.
Ide and Otsu,
1973
                                                                                                          Otsu  and Ide,
                                                                                                          1975
                                                                               Freeman et al .
                                                                               ]971b

-------
TABLE 14-17.   (continued)
Pollutant
Auto Exhaust
CO 58


NO


CO. (0.07 and
Aldehydes


Pollutant
Concentration
ug/m3 ppm Exposure

,000 50 6 hr/day.
5 days/wk,
2.5 mo to
(0.2 2 yr
and
23)

(0.1
and
2.0)
Species Effect Reference

Rat Auto exhaust had no biological effects when Stupfel et al.,
NO was 0.2 ppm. 1973
Exposure to NO (23 ppm) increased number of
spontaneous tuffiors, cutaneous abscesses,
and bilateral renal sclerosis.
No tumors or abscesses in lungs.





-------
14..2.4.5  Effects of NO., on Body Weights—Dogs, rabbits, guinea pigs, rats, hamsters, and mice
have been exposed to 100 to 47,000 |jg/m  N0? (0.05 to 25 ppm) up to 18 months without reported
body weight loss (Nakajima et al., 1972; Shalamberidze, 1969; Wagner et al., 1965).  (See Table
14-18.)  Oda  et  al.,  (1973) however, observed reduced body weights of rats exposed to ambient
                       3
air containing 135 ug/m  (0.07 ppm) NOp amongst other pollutants over a 100-day period.
14.3  DIRECT EFFECT OF COMPLEX MIXTURES
     The oxidation  of organic  substances  contained  in  solid,  liquid, and  gaseous  fuels,  as
well as  the  reaction  of atmospheric oxygen  and  atmospheric nitrogen at furnace temperatures,
are  sources  for complex  mixtures  of nitrogen  oxides in the atmosphere.   Vehicles  and power
plants  release  large  amounts of  nitrogen  oxides into the  atmosphere.  The  biological  and/or
toxicological effects of the combination of these nitrogen oxides with other pollutants is the
scope  of this section.   Much  of  the  research  reported here was  conducted  with  complex pol-
lutant mixtures  and had  no single-pollutant controls.  Thus, the  precise contribution of the
given  level of  N02  to the effects observed  is  not possible to discern.   However,  in  some of
these studies, NO  concentration was varied between groups or NO  was present in one group and
                 A                                              X
absent in another.   In these instances,  the influence of NO  can be elucidated.
     Emik et  al.  (1971)  noted  that males of the C57B1/6 strain of mice exposed to ambient air
in California died  sooner  than  either C57B1/6 females  or  males and females of the  A  and A/J
strains exposed to clean, filtered air.   Guinea pigs and other strains of mice demonstrated no
difference in  survival  when exposed  to clean  or polluted  air.   Concentrations   of  about  40
ug/m   (0.02 ppm)  N0~  were observed during the  study.   A  number of other pollutants were also
present.
     Loosli et  al.   (1972) exposed  specific pathogen-free  mice  to synthetic  smog  23  to  24
                                                                  3                          3
hours/day for 8 to 12  months.   The smog was composed of 1,500 ug/m  (0.8 ppm) N09, 5,750 ug/m
                    •D                               -D                            t-
(5 ppm) CO, 760 ug/m  (0.38 ppm) 03,  and 5,700 ug/m  (2.2  ppm) S02-  The lungs of  mice exposed
for  20  days  had thickened  bronchial   membrane  due  to  cell proliferation.   By  60 days  the
membranes were markedly thickened and appeared to have villus-like hyperplastic folds,  whereas
evidence of  hyperplasia  in control  animals was .absent.   When mice  were removed  from smog
exposure after 4 months,  the hyperplasia regressed.
     Hysell  et  al.   (1975)  studied  the  toxicological   effects   on  animals  of  automotive
emissions,  with  or without  a  catalytic converter  and with  or without  irradiation.   Female
lactating rats and  their  2-week-old  offspring were exposed  for 7  days.   Infant mortality was
increased  following  exposure to  auto  emissions  containing  9,400 ug/m   (5  ppm)   N02  without
catalytic  conversion,  whereas  mortality was  not  affected  in  animals  exposed  to  emissions
modified by catalytic  conversion.   Adult male rats and hamsters  were exposed to these regimens
for 6  days.   An  increase in hemolysis-resistant  RBC  due  to high ambient  CO followed exposure
to raw exhaust with no  catalyst.   Blood eosinophils in rats exposed to converted  exhaust were
not  affected.   Animals  developed  extensive  pulmonary changes when  exposed  to  irradiated,
unconverted auto exhaust.   Hamsters developed purulent bronchitis,  bronchiolitis,  and broncho-
                                             14-71

-------
TABLE 14-18.   EXTRAPULMONARY EFFECTS OF N02:  BODY WEIGHT

N02
Concentration
pg/m3
100
135
1,300 to
1,500
1,900 to
47,000

E 18,800
ro
18,800
24,000
ppm
0.05
0.072
0.7 to
0.8
1 to
25

10
10
12.5
Exposure
90 days
Continuous,
100 days
30 days
18 mo

From birth
to 62 days
Continuous,
90 days
Continuous,
213 days
Species
Rat
Rat
Mouse
Dog, rabbit,
guinea pig,
rat, hamster
mouse
Rat
Cynolmogus
monkey
Rat
Effect
No effect.
Ambient air exposure (6.3 ppm CO, 0.206 ppm NO,
0.047 ppm S0?, 0.0048 mg/m acid mist and 0.88
mg/m dust) Decreased body weight.
No effect.
No effect

Decreased body weight and length of pups.
In combination with heat stress decreased body
weight.
Decreased body weight.
Reference

Shalamberidze, 1969
Oda et al. , 1973
Nakajima et al. ,

1972
Wagner et al. , 1965

Freeman et al . ,
Coate and Badger
1974
Freeman and
Haydon, 1964

1974b
t


-------
pneumonia  when  exposed to  such  exhaust.   An  initial  increase  in  the  number  of alveolar
macrophages  at  the  level  of  the  terminal  bronchioles,  a  proliferation  of  respiratory
epithelium   in  the  ducts,   and   a  thickening  of  the   alveolar  septae  were  observed.
Extramedullary hematopoiesis  in  rat livers resulted from  high CO concentrations.   Occasional
degenerative changes in renal and  hepatic tissue were also seen  in these animals.
      Lee et  al.  (1976)  exposed  lactating rats  24  hours/day for 7 days to auto emissions with
and  without  catalytic  conversion  and  with  and  without   irradiation.    Nitrogen  dioxide
concentrations in  the  unconverted auto exhaust  were 8,650 and 9,780  |jg/m   (4.6  and 5.2 ppm)
for  the irradiated  and non-irradiated  samples,  respectively.   For  exhausts with  catalytic
                                                         3
conversion, N0~  concentrations  were 5,640 and 3,380 ug/m   (3 and 1.8 ppm) for irradiated and
non-irradiated samples,  respectively.   Animals  exposed  to  unconverted  auto exhaust,  whether
irradiated or  not,  had  a significant decrease  in  body  weight by day  7 (p < 0.001).   Exposure
to converted and irradiated exhaust also produced a significant  loss in weight (p < 0.02), but
the  presence  of  the  converter  was  associated with less  weight  loss.   Exposure to  CO (575
mg/m  ;  500 ppm)  did not significantly alter body weight.  Animals exposed only to raw exhaust
or  575 mg/m   (500  ppm) CO  had hematocrit  levels (p  <  0.001) significantly elevated  above
controls  by  day 7.   Exposure to  raw  exhaust  enhanced  serum  lactate dehydrogenase activity
(LDH),  whereas  CO had  no  such effect.   Serum  glutamate-oxaloacetate  transaminase (SGOT) was
not  affected  by  any  exposure  regimen.    Reduction  of  effects in  converted  exhaust-exposed
groups was attributed to the decreased CO levels in the chamber.
     Stupfel  et  al., (1973)  in two separate  experiments,  exposed  specific pathogen-free rats
to  auto exhaust  fumes  6 to  8 hours/day,  5 days/week,  for periods of 2.5 months  to 2 years.
The exhaust gas  contained  either 0.2 or 23  ppm N0x,  0.07 or  0.37  percent C02,  58 mg/m  (50
ppm)  CO and  0.1  or  2  ppm aldehydes.  With  low concentrations of NOX,  no biological  effects
were  observed.   When  NO  was  increased to  23 ppm, body  weight was  reduced  and spontaneous
tumors  and  emphysema  were  increased.  The heart  rate  and  the QRS  wave  of the  EKG were not
affected.   Sound avoidance  reflexes were decreased.
     Cooper et al.  (1977)  exposed  rats  24 hours/day for 38 to 88 days  to automobile  exhaust
with  and  without catalytic converters.   During  three  experiments, N02  levels were  564, 752,
and 9,588  ug/m3  (0.3,   0.4,  and 5.1  ppm);  nitric oxide (NO)  levels  were 8,733,  13,284, and
10,209  (jg/m3 (7.1,  10.8, and  8.3 ppm);  and  total  hydrocarbon levels were 16, 14,  and 50 ppm
(methane).   Spontaneous  locomotor  activity,  as  measured by standard  running wheels,  was 63,
54,  and  64   percent   of  control   values,   respectively.    The  authors   concluded  that  the
suppression  of  activity was  primarily  related  to  either  hydrocarbon  or  nitrogen  oxide
compounds of the exhaust.   However,  it  should be noted that a 10-fold increase in N02 did not
result in a further reduction in activity levels.
     Murphy (1964)  investigated  the effects  of a 4-hour  exposure to irradiated  or raw auto
exhaust on pulmonary function of guinea  pigs.   Since  irradiated exhaust produced  more changes,

                                             14-73

-------
subsequent studies were  performed  with irradiated exhaust maintained at equilibrium values or
at cyclic values.   For the equilibrium group, the following pollutant concentrations were mea-
sured:  2.42 ppm  formaldehyde,  0.2 ppm acrolein, 0.8 ppm oxidant, 5,000 ug/m  (2.66 ppm) NO,,,
and 300 ppm  carbon  monoxide (CO).   For the  "cyclic"  exposure,  concentrations varied:   1.3 to
1.9 ppm formaldehyde, 0.06 to 0.1 ppm acrolein, 0.56 to 0.95 ppm oxidant, 1,485 to 4,079 ug/m
(0.79 to 2.17 ppm) NOp, and 150 to 250 ppm CO.   Flow resistance was increased in both exposure
groups with  the equilibrium condition causing a more  rapid and greater increase.  During the
first 1.5 hours of  exposure,  breathing frequency decreased, with the greater change occurring
under equilibrium  exposure conditions.   For equilibrium exposure  these values  remained  de-
pressed,  whereas  in the  cyclic group  frequency increased.  Increases  in  tidal  volume were
observed  in  both  groups  after  1.5 hours of  exposure;  in the cyclic group  tidal  volumes  had
decreased below control by 2.5 hours.
     Beagles were  exposed  to  auto  exhaust  and pollutant  mixtures,  16  hours/ day,  for 61
months.    Pulmonary function  studies  were  made at 18,  36,  and 61 months of exposure (Lewis et
al.,  1974;  Vaughan et  al.,  1969).   The  animals were allowed to recover for approximately 2
years (Gillespie  et  al. , 1976) and were  then  examined again.  Only those  results  related to
NO  will  be  described  here.   The results  of this study have been described in full by several
                                                                                  3
authors (Stara et  al. ,  eds. ,  1980).   The  high NO, group was exposed to 1,210 ug/m  (0.64 ppm)
                  T                                                            "?
NO, plus  310 ug/m   (0.25 ppm) NO.   The low  N00  group was exposed to 270 ug/m  (0.14 ppm)  N09
                3                                  168
plus  2,050  ug/m  (1.67  ppm)  NO.   Vaughan et  al.     reported no alterations  in CO diffusing
capacity, dynamic  compliance, or total expiratory  resistance to air flow after 18 months of
exposure.   By  36  months,  (Lewis et  al.,  1974) analysis of  variance  indicated  no significant
changes;  however,  a  significant  number  of animals  exposed to  high  N0? and  low NO  had an
abnormally (p < 0.005)  low CO diffusing capacity.   More changes were observed after 61 months
of exposure  (Lewis  et  al., 1974).   In the dogs breathing the low N02 and high NO and raw auto
exhaust,  with and  without SO , residual  volume  was increased (p < 0.05) compared to animals
exposed to air  or  high N0? and  low  NO (p < 0.05).   The  common  treatment factor causing this
effect  appeared  to  be  the  higher  concentration  of  NO.    Irradiated  auto  exhaust  exposure
increased  (p < 0.05)  the mean nitrogen washout  values.    A  significant  number  of  beagles
exposed to high NO,,  and low NO had a lower mean carbon monoxide diffusing capacity/total lung
capacity and a lower peak flow rate compared to control.  A number of alterations in pulmonary
function  were  found in other exposed groups.   The  authors attribute the results observed in
the  dogs  exposed  to high  NO^-low  NO to an alteration of the alveolar capillary membrane.
     After the 61-month  exposure  terminated, the animals were  allowed  to recover for 2 years
before pulmonary function  measurements were  made again  (Gillespie et al.,  1976).  In several
instances, alterations occurred  during this  recovery period.   In  all  pollutant-exposed dogs,
total lung  capacity was  increased relative to  the control  group  of  animals.   Those animals
which received  the NO-  and NO mixtures  experienced modest  increases  in inspiratory volume,
vital  capacity,  and  total  lung  capacity.    Other  groups  of  animals  also  had a  number of
changes.
                                             14-74

-------
     Orthoefer  et al.,  (1976)  utilizing the  same beagles  exposed  for 68  months,  evaluated
biochemical  alterations  2.5  to  3 years after the animals had recovered.  In groups exposed to
irradiated  auto  exhaust  with and without SO   and  high N09 with low  NO,  there was a rise (p
                                            A             £.
<0.05)  in  lung  prolyl  hydroxylase (the rate-limiting  enzyme  for collagen synthesis).   A high
correlation  was  seen between  lung weights and  hydroxyproline  content  in  animals exposed to
NO  .   No  effects were  observed  in  the hydroxyproline/total  ninhydrin  reactive  material.
  A
Histological  and morphological  examinations  revealed  no  significant  differences  in collagen
content  of exposed  tissues.   No  difference was  seen  in  the  collagen/protein ratios  between
tissues.
     Beagle  lung morphology was  evaluated  by Hyde  et al.  (1978)  32 to 36  months  after the
68-month exposure  period terminated.   Several  morphometric parameters were affected, but only
those  relating  to NO  will  be described here.   In  the  high N09 group,  there were increases
                     "                                           £.
(p <0.05)  in  total  lung  capacity and right lung volume and decreases (p <0.05) in the surface
density  of the  alveoli  and  the  volumetric  density  of  parenchymal  tissue.   For  the  high NO
group,  there were no  significant changes in  the morphometric  parameters  examined.   Alveoli
were enlarged  in both  the high N0~ and  high  NO  groups.    In the high NOp but not the high NO
groups,  there  was  increased  ciliary  loss  without  squamous  metaplasia  and  nonciliated
bronchiolar  cell  hyperplasia.   In the high NO group,  there  were lesions in the interalveolar
pores.    In  the  most severely  affected  lungs  of  dogs in the  high  N02  group,  morphological
changes considered to be analogous to human centrilobular emphysema were present.   Since these
morphometric/ morphologic measurements were made  after a 2.5 to 3 year holding period in clean
air, it  is  not  known whether these disease processes  abated or progressed over the clean air
period.
     Coffin  and  Blommer  (1967)  investigated  the effects  of a  4-hour  exposure  to irradiated
auto exhaust  containing  varying concentrations of N09, NO, CO, and oxidant on mice which were
                                                                                   3
also challenged  with S.  pyogenes.   Those mixtures containing greater than 752 ug/m  (0.4 ppm)
N02 and  25  |jg/m3 (0.02 ppm) NO in the presence of 115 ug/m3 (100 ppm) CO and between 0.52 and
0.67 ppm oxidant caused  an increase in mortality (p  < 0.05).   Mixtures of N02 and NO at lower
concentrations were  not  tested.   Other  pollutant combinations  were  also  tested.   Concentra-
tions between 376 and 1,500 ug/m  (0.2 and 0.8 ppm) N09,  0.15 and 0.48 ppm oxidant, and 29 and
         3
115 ug/m  (25 and 100  ppm) CO were  found to  increase  mortality  in the  infectivity  model.
     Using the infectivity model  in which the mortality of  pollutant-exposed mice challenged
with S.  pyogenes  is  measured,  Ehrlich et al.  (1977)  investigated  the effects of combinations
of 03 and NO-.  Mice  were exposed for 3 hours  to  various  concentrations of the gases alone and
in combination.   The  lowest concentrations causing a  significant enhancement of mortality were
                     o                               3
a mixture  of 98 ug/m  (0.05  ppm) 0-,  and 3,760 ug/m   (2 ppm) N09.   The  effect  was  additive.
                                                                       3
This concentration of 0,  alone caused  no significant  change;  3,760 ug/m  (2 ppm) NOp, however,
resulted in a significant enhancement  of mortality.   Multiple 3-hour daily exposures also were
tested.  With the mixture of 98 ug/m3  (0.05 ppm)  03 and 3,760 ug/m  (2 ppm)  N02,  excess
                                             14-75

-------
                                                                    o
mortalities were  evident after  five  daily  exposures.   At  196 ug/m  (0.1 ppm)  0,  plus 2,800
    3
ug/m  (1.5 ppm) N02, there was a significant effect when the mice were examined after 20 daily
exposures, but  not after  10.   In the  latter case,  the author attributed the  effect  to the
presence  of  0,;  in the  former case,  the author suggested a  synergistic  relationship.   When
                                                03
mice were exposed to a combination of 6,580 ug/m  (3.5 ppm) N02 and 980 ug/m  (0.5 ppm) O, for
3 hours,  followed 1  hour  later by challenge with S. pyogenes, bacterial clearance from the
lung was  reduced.   Control  mice  cleared  50  percent bacteria  from the lungs  in  81 minutes.
Exposed animals  took  131  minutes  to clear  the same  amount  of bacteria.   When  the NO., con-
                                    3                                                   e.      .,
centration was reduced to 3,760 ug/m  (2 ppm) and the initial  0^ concentration was maintained,
no distinguishable effect on bacterial clearance was observed.
     Ehrlich  et  al.  (1979)  used another exposure  regimen of  NO^-Og  combinations  to evaluate
effects with  the  streptococcal  infectivity model.   For  1,  2,  3,  and 6 months,  mice were ex-
                               3
posed continuously to  188  ug/m  (0.1 ppm) N02  on  which were superimposed peaks  (3  hr/day,  5
days/wk) of either 940 ug/m3 (0.5 ppm) N02 or 940 ug/m3 (0.5 ppm) N02 plus  196 ug/m3 (0.1 ppm)
0.,.   Other groups received the peak exposures only.   After the indicated exposure period, mice
received S. pyogenes  and were observed  for  mortality  over  a  14-day period in clean air.  For
the 1-  or  2-month  exposures the only significant (p <0.05) change was a decrease in mortality
after 1 mo.  of  peak exposure to the N0? + 0-, mixture.  After 3 mo., the peak exposures to N0?
only  or N02  + 0.,  increased  (p <0.05)  mortality.   At  the  same time,  there was  a decrease
(p <0.05)  in  mortality  in  the group  exposed  to  a  baseline of N02 with peaks  of either N02 or
N02 + On.   However, mortality increased (p  <0.05)  after 6 mo exposure to N02-0.,  peaks, with
or without the baseline of N02.  In another set of experiments using identical exposure regimens,
the mice  were returned  to  their  respective  pollutant exposures over  the 14-day  observation
period  following bacterial  challenge.   In these studies, the  increased susceptibility  to in-
fection occurred earlier compared  to  those animals held  in  clean  air for the  14  day period.
Generally  in  these animals,  the  most changes  occurred in the  group receiving the  N02 + 0^
peak,  and  there was an increased response as exposure length increased. When the peak of NOp
+ 0., was superimposed  on a baseline of N02, the response was reduced, although it did increase
with time.  The effects in the peak of N02 group were roughly equivalent to those in the group
receiving  a   baseline  of N02  with an N02 peak superimposed.   These exposure  regimens also
affected alveolar macrophages.   For  example, the most extensive effect occurred after a 3 mo.
exposure to the peak of 0, + NO,,.   There were decreases (p <0.05) in the number of recoverable
alveolar  macrophages,  their percent  viability  and percent phagocytosis.   Lung morphological
changes  in  infected  mice  were also  observed  using scanning  electron  microscopy.   Marked
changes were  observed after 3. mo. of  exposure to  a baseline  of  N02 or air on which were
superimposed peaks of  N02 + 0,.  Alveolar pores were greatly enlarged in some areas.   Adjacent
to these areas, alveolar walls were thickened and fused with smaller pores.   Peak exposures to
N02 only caused less extensive effects.

                                             14-76

-------
   ,  Goldstein  et  al.  (1974)  found that  mixtures  of N02 and 0.,  would decrease bactericidal
activity of  the lungs.   Mice received S.  aureus  aerosols  before a 4-hour pollutant exposure.
Reductions  (p  <  0.01)  in  bactericidal   activity of  36.9 and  111  percent  were  seen  after
exposure to 7,520 ug/m3 (4 ppm) NO, plus 600 pg/m  (0.36 ppm) 0,, and after 12,860 ug/m  (6.84
                       3
ppm) NO- plus 760  ug/m  (0.39 ppm) 0, respectively.   Lower gas concentrations had no effect.
The protocol  was  then  changed so that mice  were  exposed to pollutants for 17 hours before S.
aureus challenge.   Bactericidal  activity was generally more impaired at higher gas concentra-
tions.   The  lowest gas  concentrations  to cause  a  significant  effect  (p <  0.05)  were  4,320
    3                             3
ug/m   (2.3 ppm) N0~ plus 390 ug/m  (0.2 ppm) 03 which decreased bactericidal  activity 13 per-
cent.   However, decreases  in pulmonary bacterial  deposition were observed at these concentra-
tions.   It  is the authors'  contention that  this  latter effect  is due  to  ventilatory defects
induced by  0,  alone,  whereas  the reduction  in  bactericidal  function  is equivalent to  the
injury that would be expected from each individual gas.
                                                                                       2
     Furiosi   et al.  (1973)  exposed monkeys and  rats to aerosols containing  330  (jg/m  (0.14
ppm) NaCl  and  3,760 ug/m   (2 ppm) N09  continuously  for 14 months in  order  to  delineate  the
                                                                                             3
effect of particulate  aerosols  on NO- toxicity.  Of  the total  NaCl  aerosolized, only 5  (jg/m
('<  0.001  ppm)  had a  particle  size  between  5  and  10.3 microns,  with the  remainder  being
smaller.   NaCl  aerosol  alone  had no effect  on  the  experimental  animals.  Following 14 months
exposure,  the bronchiolar epithelium was  hypertrophic to similar degrees in monkeys exposed to
N02 or N02  in the presence of NaCl.  With only half the concentration  of NaCl  and N02, rats
exposed to  these  agents revealed marginal  results.   Animals  exposed to NO-  with  and without
NaCl developed polycythemia with reductions in mean  corpuscular volumes although mean corpuscu-
lar hemoglobin concentration was normal.
     Kosmider et al. (1973a)  exposed  guinea pigs 8  hours/day  for  6 months to 1 ppm oxides of
nitrogen (NO- + N?0.)  or 1 ppm oxides  of nitrogen  (NO- + N-0.)  plus a somewhat larger quantity
of ammonia.    The oxides  of  nitrogen alone decreased  animal  body weight gain over the 6-month
period; 62 grams versus  395 grams for controls and  120 grams for NO  plus ammonia.   Reduction
in total serum  protein  was  observed with  a  marked  decrease in the levels of albumin, alpha-2
and gamma globulins and  with an increase in alpha-1 and beta fractions.  Higher incidences of
spontaneous   infections  also  were  observed.   Disorders in  acid-base balance were reported.
Increased   appearance   of  urobilinogen,   acid  mucopolysaccharides,   and  hydroxyproline  was
observed.   Hemorrhage  and emphysematous-1ike conditions were noted in the lungs of NO -exposed
animals.   Emik  et al.   (1971) reported  that alkaline phosphatase  activity  decreased in  the
                                                                                 2
lungs  of rats exposed  2.5  years to ambient  air containing  approximately 36 ug/m  (0.019 ppm)
N02, 0.011 ppm NO,  03,  PAN,  etc.
     Antweiler  and  Brockhaus  (1976)  exposed female  guinea  pigs 6 days/week for 6 months to
           o                           '  o
10,000 ug/m   (3.8  ppm)  S02,  10,000 M9/m  (5-3 ppm)  N02,  or  a combination of the  two pollu-
tants.   After 6 months  of exposure, there were no  effects on respiratory frequency,  flow  rate,
or minute volume,  nor  were  there increases  in  mortality or difference in weight gain between
treated and control animals.
                                             14-77

-------
    , Shalamberidze and  Tsereteli  (1971)  reported on the  effects  of low concentrations of S0?
and  NO,  on the  estrous cycle  and  reproductive functions  of rats.   Female  albino rats were
                                                                          3
exposed 12  hours/day  for 3 months to one of the following:  (1) 2,360 ug/m  (1.3 ppm) N02; (2)
5,000 ug/m3 (1.9  ppm) S09; (3) 160  (jg/m3  (0.06 ppm) S09 ; (4)  130 (jg/m3 (0.07 ppm) NO,; (5)
          11
2,500 ug/m  (0.95  ppm)  S02 and 1,130 ug/m   (0.6 ppm)  N02>   Low concentrations of S02 and N02
did not affect the rats' estrous cycle or induce morphological changes in reproductive organs.
Exposure to high  concentrations did alter the  estrous  cycle.   Estrus was less frequent, more
prolonged,   and occurred at  lengthened  intervals.   At  7 months  after exposure,  the estrual
indices  returned  to  normal.   Morphologically,  changes  included a  depletion of glandular
epithelium in the uterus as well as a depletion of thyroid connective tissue between follicles
with a mild cellular degeneration of the adrenals, ovaries,  and uterus.  The number of ovarian
primordial   follicles  was  also decreased.   Long-term  exposure  had  no  effect  on  the  rats'
ability to  conceive,  although  litter size  and average weight  of progeny  were significantly
reduced (p < 0.001).
     Oda et  al.  (1975a; 1975b) exposed female mice and  male rats and rabbits for 1 hour to
13,040 ug/m3  (10.6 ppm) NO containing 1,500 ug/m3  (0.8 ppm)  N02-   Shortly after NO exposure,
mice and rats had increased nitrosylhemoglobin  (NOHb).   Production of NOHb was proportional to
the  concentration  of NO.   Within 20 minutes  equilibrium was  reached,  with  NOHb  being 0.13
percent of  total  hemoglobin.   NOHb levels declined rapidly when mice were placed in clean air
for  1  hour.   NOHb had  a  half-life  of  10  minutes.   NOHb was  not detected  in  rabbits  until
reduced j_n vitro with sodium dithionate.
14.4  NITRIC OXIDE
     The toxicological data base of nitric oxide (NO) is not extensive and most of it has been
done in recent years.   (See Table 14-19.)
                                                                                3
     Azoulay et  al.  (1977) exposed rats continuously for 6  weeks  to 2,460 ug/m   (2 ppm) NO.
Following  exposure,   no  significant  differences  were  seen   in  blood oxygen  saturation,  pH,
oxygen   combining  capacity,   2,3-diphosphoglycerate,   ATP,   glucose,   lactate,   hemoglobin
concentration,  hematocrit, and  red blood  cell cpunt.   Methemoglobin  was  not detected.   No
striking histological  changes were  found  in  the  lungs until  2 weeks of  exposure.   At this
time, 3  of 4  exposed and  1  of 4  controls  appeared to  show inflammatory  changes including
cellular   infiltration   of   alveolar  cells.    Inflammatory  changes,   including  cellular
infiltration of  alveolar walls and areas of intra-alveolar edema,  were observed.   Following 3
weeks  of  exposure to   NO,  animals  evidenced  some emphysemic-like  changes with  increased
incidence until  6  weeks of exposure.  Hugod (1979) exposed rabbits continuously for 6 days to
            •3                               O
52,890  ug/m   (43  ppm)   NO and  6,768 ug/m   (3.6  ppm)  NO^.   No  significant effect  on lung
morphology was observed following exposure.
     Arnold et al. (1977b) and Braughler et al. (1979) exposed various tissues from male rats
iji  vitro to  25 to 250  ul  NO  gas  for 10 seconds.   The  activity  of guanylate cyclase (GC) (an
enzyme that forms  cyclic GMP, an important biochemical regulator  of cells) in various tissues
                                             14-78

-------
                                                                          TABLE  11-19.   NITRIC  OXIDE
Pol 1 ulan I
Concentration
Pollutant jig/in1 ppm
NO 2,160 2.0
Exposure Species
Continuous, Rat
6 wk
Effect
Cellular infiltration of alveolar walls and
areas of intra-alveolar edema observed after
Reference
Azoulay
et al. , 1977
                   NO
                               9,170
                                        7.7
                     8  hr/day,
                     120  days
Guinea pig
2 wk.   After 3~wk exposure, emphysema-1 ike
changes observed until 6 wk.   Melhemoglobin
undetected.   No differences in blood oxygen
saturation,  pH, oxygen combining capacity,
ATP, 2,3-diphosphoglycerate,  glucose, lactate,
hemoglobin concentration, hematocrit, or
RBC count.

Decreased blood sodium, magnesium, and chloride;
decreased Zn and Mg in brain and liver.
Increased blood calcium and urinary
excretion Mg.
Kosmider and
Chorazy, 1975
-p»
1
to
                   NO
                   N00
                   NO
13,010 +  10.6
 1,500     0.8
                              11,800    12
                                                   1 hr
                                                   5 hr
Mice, female;
Rat, male;
Rabbit, male
                                                                 House
NO
NO*
NO.
19,700
61,500
52,890
6,768
to 16 to
50
+ 13 +
3.6
4 hr
Continuous ,
6 days
Guinea pig
Rabbit
Mice and rats showed increased nitrosyl hemoglo-   Oda et al.,
bin (NOHb); NOHb related to concentration of NO.   1975a
By 20 minutes eguiIibratcd, 0.13% total nemo-      Oda et al. ,
globin.   NOHb half-life 10 minutes.   No NOHb       1975b
produced in rabbits exposed to NO until sodium
dithionate added to blood.

Edema and dilation of vessels in submucosal        Udai et al.,
tissue of trachea. Congested alveoli.              1973
24 hr later proliferation of tracheal
mucosal epithelium.
Anomalies in CNS, heart and cell metabolism.

No significant alteration in                       Murphy et  al.
respiratory rate or tidal volume.                  1964

No effect on lung morphology.                      Hugod,
                                                   1979

-------
was, increased  in  proportion  to the dose of  NO.   The levels of this enzyme were increased 19-
to  33-fold  in supernatants  of liver,  lung,  tracheal  smooth muscle,  heart,  kidney,  cerebral
cortex, and  cerebellum with  increases  of 5-  to 14-fold  in  supernatant  of  skeletal  muscle,
spleen,  intestinal  muscle,  adrenal,  and  epididymal  fat pads.   Following NO  activation,  GC
activity decreased with  a  half-life of 3  to  4 hours at 4°C.   When tissue was re-exposed, the
GC  activity  was  reactivated.   Braughler et  al.  (1979)  also found that exposure  of  rat liver
fractions to  165  ul  NO increased GC  activity,  but  purification of the enzyme  resulted in an
apparent loss  of  enzyme  activation by NO.   Restoration of this activity could be accomplished
with the addition of dithiothreitol, methemoglobin,  BSA, or sucrose.   Sodium nitrite increased
GC activity as well.   Nitric oxide increased cyclic  GMP (cGMP) but had no effect on cyclic AMP
(cAMP).  Craven  and  DeRubertis  (1978)  exposed  rat  liver fractions  to  NO at  the rate  of  1
ml/min for 2 seconds and found similar increased activity in liver GC.  They also found that a
nitrosyl-heme complex was formed during exposure.
     Kosmider  and Chorazy  (1975)  reported that following the exposure of guinea pigs to 9,470
ug/m   (7.7  ppm)  NO  8  hours/day  for 120 days,  blood  sodium,  magnesium, and  chloride  were
reduced with a significant rise in calcium.  Liver and brain levels of magnesium and zinc were
reduced while there was an enhanced urinary excretion of magnesium.
14.5  NITRIC ACID AND NITRATES
     Gray et  al.  (1952)  conducted some of the  earliest  experiments  investigating inhalation
toxicity for  rats,  guinea  pigs,  and mice exposed  to N09 generated  from  nitric  acid  (HNO,).
                                                         £.                                 o
(See Table 14-20.)   No measurement of aerosol particle size was made.  Results were expressed
as  evidence  of NO,,  toxicity,  whereas the experimental method could not adequately distinguish
                                                                                      3
the difference between N02 and HN03 effects.   Concentrations of 17,000 and 26,000 ug/m  (9 and
14  ppm) N09  administered 4 hours/day, 5 days/week  for  6 weeks produced lung pathology.  When
                                                3
exposure concentration was reduced to 9,400 ug/m  (5 ppm), no lesions were observed.
     Gardiner  and Schanker  (1976)  investigated the  effects of nitric acid-induced lung damage
on  the  absorption  of drugs from the  lungs.   Rats were given an  intratracheal  injection  of 1
percent nitric acid  solution  (0.15 ml), and drug absorption rates from treated versus control
lungs were measured  with time.  One day following nitric acid exposure, there was significant
bronchiolar inflammation with  inflammatory cell infiltration.   The bronchiolar epithelium lost
its  normal   scalloped  appearance  and  tended  to  have  an  increase  in  cellular  cytoplasm.
Alveolar septae  adjacent to  inflamed bronchioles  appeared  broadened by  enlarged or swollen
alveolar cells.   Wet and  dry weights  of  the exposed  lungs  did  not differ.   Treatment with
nitric  acid   enhanced  the pulmonary  absorption rates  (20  percent)  of  p_-aminohippuric acid,
procaineamide ethobromide, procaineamide, and mannitol.
     Sackner  et  al.  (1976)  exposed dogs  for 7.5 minutes to an  aerosol,  with particles less
than 1 urn in diameter, containing 740 and 4,000 [jg/m  (0.1 and 1 percent) of sodium nitrate in
order  to  observe  potential   effects  on cardiopulmonary  function.   Sodium nitrate  at either
concentration  had no  effect on functional residual  capacity, static  lung compliance, or total
respiratory resistance.
                                             14-80

-------
                                                                 TABLE 14-20.   NITRIC ACID AND NITRATES
J>
I
CD
Pollutant
NO
generated
from HN03
HNO,
J






Sodium
nitrate
Pollutant
concentration
9,400, 17.000 or
26.000 ug/ni
(5, 9 or 14 ppra)
1% solution
(0.15 ml)






0.1 and 1.0% at
740 and ,
Exposure
4 hr/day,
5 days/wk.
6 wk
Intra-
tracheal
injection





7.5 min

Species
Rat, mouse.
guinea pig

Rat







Dog

Effect
No lesions at 9,400 ug/m (5 ppm).
Higher concentrations, increased lung pathology.

24 hr post-injection increased inflammation of
bronchioles; epithelium lost normal scalloped
appearance. Increased cytoplasm in epithelium.
Inflamed alveolar septae.
No difference in lung wet and dry weight.
Enhanced pulmonary absorption rates of
p-aminohippuric acid, procaineamide ethobromide,
procaineamide and mannitol.
No effect on pulmonary function.

Reference
Gray et al. ,
1952

Gardiner and
Schanker, 1976






Sackner et al. ,
1976
Sodium
nitrate
Ammonium
nitrate
Pb(N03)2
NaNO,3 2
KNO,
NH jNO-
0.1
and 1.0% at
740 and
4,000 pg/m
100

2,000
2,800
3,100
4,300
4,500
mM

pg/m,
Mg/m3
M9/"13
pg/m
                                                30 min       Guinea pig      Accounted for 58% of total                         Charles and
                                                                             histamine release.                                 Henzel, 1975
                                                                             Ammonium sulfate released.

                                                 3 hr        Mouse           After 14 days of observation, no effect on         Ehrlich, 1979
                                                                             mortality following challenge with S. pyogenes.
1,250 pg/mj
                                                                             Increased mortality.

-------
     Charles and  Menzel  (1975) incubated 100  mM  ammonium nitrate with guinea  pig  lung frag-
ments  for  30 minutes and measured  the  release of histamine.  Ammonium nitrate released 58.1
percent of the total histamine.
     Ehrlich (1979) investigated the effect of nitrates on resistance to respiratory infection
in mice.   The animals were exposed to the compounds for 3 hr, after which  they were challenged
with a viable  aerosol  of S.  pyogenes, and mortality was determined after  a 14-day observation
period.  No  significant  effects  were observed at the following maximal concentrations tested:
2,000  ug/m3  Pb(N03)2,  2,800  |jg/m3  Ca(N03)2>  3,100  ug/m3 NaN03, 4,300 ug/m3  KN03,  and 4,500
ug/m   NH.NO.,.   However,  zinc  nitrate increased mortality in a  significant  linear concentra-
                                           3
tion-related fashion with about  1,250 ug/m  causing a 20 percent increase in mortality.  This
result was similar to that of zinc sulfate.   Thus, it appeared that the effect was more due to
the cation than the anion.
14.6  N-NITROSO COMPOUNDS
     Reviews   of   the   acute  toxicity,  carcinogenicity,   mutagenicity,  and   detection  of
nitrosamines have  appeared  recently.   (Magee et al.,  1976;  Montesano  and Bartsch, 1976; U.S.
Environmental  Protection Agency,  1977)   These compounds and nitrosamides  are highly toxic and
potent carcinogens.  N-Nitrosamines require metabolic activation to their  mutagenic and carci-
nogenic active intermediates and are most  toxic  to the  liver and  kidneys.   Nitrosamides,  on
the  other  hand,  tend  to  decompose  at physiological  pH,   probably  to  active intermediates
similar to those produced from nitrosamines, and thus often act locally.
     The detection  of  nitrosamines  in food and water  had promoted a broader search for their
presence in the environment.   Evidence for the presence of dimethylnitrosamine in air has been
reviewed in the Scientific and Technical Assessment Report on Nitrosamines (U.S. Environmental
Protection Agency,  1977).   Henschler and  Ross (1966) investigated the possible  formation  of
nitrosamines from  tissue amines  exposed to N09.   Mice were exposed intermittently  to 75,200
    3
ug/m   (40  ppm)  N0? for 38 hours  every  tenth day  for periods up to 1.5 years.   No lung tumors
were found in exposed animals.  In fact, when compared to controls, there  was a slight inhibi-
tion of the  formation  of lung adenomas  and spontaneous skin fibro-adenomas.   The formation of
nitrosamines by  reaction of amines with nitrogen  oxides has been observed  in  the laboratory
but not in the atmosphere (Challis, 1977; Gehlert and Rolle,  1977).   Nitrosamines would not be
expected to  accumulate  to  any great extent in ambient air because they are readily decomposed
by sunlight (Chow, 1973; Polo and Chow,  1976).  Kaut (1970) examined the lungs of rats exposed
for 3 hours to mixtures of 10,000 to 500,000 ug/m  nitrogen oxides for the presence of nitroso
compounds.    None  of the compounds were  found  i_n  vivo,  whereas  they were  found J_n  vitro when
lung homogenates were exposed to high concentrations of nitrogen oxides (15 percent).
     The nitrosamines  are acutely  toxic with  a  single  oral dose  of 27,000  to  41,000 ug/m
being  the  LD50  for dimethylnitrosamine  to  the  rat.   Diethylnitrosamine,  another compound
detected in the air, is much less toxic with an LD50 of 216,000 ug/m3 (Heath and Magee, 1962).
Inhalation toxicity has not been reported.   Industrial use of nitrosamines as solvents suggest
                                             14-82

-------
that  they are  rapidly  absorbed and  exert  their toxic action equally  well  on inhalation and
ingestion.   These  compounds were acutely toxic  to every animal species  tested  and were also
poisonous to humans (Barnes and Magee, 1954; Freund, 1937).
     Nitrosamines  have  caused  hepatotoxicity,  including the formation of "blood cysts", which
are  the  necrotic  areas  of parenchyma  filled  with  recently extravasated  erythrocytes,  and
central  and  sublobular  hepatic necrosis.   Renal tubule  damage  is  the dominant feature of the
kidney  damage.   Dimethylnitrosamine  produces  venous  occlusions in the  liver  (McLean  et al.,
1965).   Ultrastructural  changes in  the  liver after diethyl-  and  dimethylnitrosamine  include
separations  of  the fibrillar  and granular  components  of the hepatocyte  and  the  formation of
electron  dense  plaques  at the  periphery  of  the  nucleolus  (Svoboda  and  Higginson,  1968).
Lysosomal  alterations  occurred within  35  minutes of exposure  to  dimethylnitrosamine  and
reached a maximum at 12 hours  (Svoboda and Higginson,  1968).
     Nitrosamines and nitrosamides (N-nitroso compounds) have induced tumors in a wide variety
of  organs  of experimental  animals,  often at organs distant from  the site  of administration.
Single or repeated inhalation exposures to dimethylnitrosamine resulted  in tumors of the nasal
cavities and kidneys  (Druckrey et al. , 1967).   N-Nitrosoheptamethyleneimine produced squamous
neoplasia of the  lung in rats, histologically similar  to  human lung cancer (Lijinsky et al.,
1969).
     Many N-nitroso compounds  are  mutagenic if  assayed  by  the  appropriate  system.   Bacteria,
in  general,  are  not  capable  of activating nitrosamines,   and  such  assay  systems therefore
require  supplementations  with  animal-derived activating enzymes to detect the mutagenicity of
these  compounds.   Nitrosamides,  which will  spontaneously  decompose  in the  bacteriological
medium, do not require enzyme activation.   More than 20 N-nitroso compounds  have been shown to
be mutagenic in microbial systems (McCann et al., 1975).
     N-Nitroso  compounds  are  also  teratogens.   The nitrosamide, N-nitrosoethylurea,  given to
rats  on the 12th  day of  gestation  (Napalkov and  Alexandrov,  1968) or  N-nitrosomethyl-urea
given on  the 13th  or  14th  (von Kreybig, 1965)  can cause fetal death and resorption and,  for
the progeny which do reach term, a variety  of malformations.
     The  N-Nitroso  compounds,  therefore, are  an important class  of chemical  carcinogens  for
the following reasons:
     Most vital  tissues  are susceptible to  the carcinogenic  action  of  this class of compounds.
Bone  can be  included in  this  list,  based  on  the recent finding that l-(2-hydroethyl)-l-
nitrosourea induced osteogenic osteosarcomas or chondrosarcomas of  the lower vertebrae  in rats
(Pelfrene et al.,  1976).
     In  several  instances,  a  single exposure to  neonatal  animals has  induced tumors  as  the
animals  reached  adulthood  (Druckrey  et  al., 1963; Magee and Barnes, 1959).   Single-exposure
induction of tumors can  also  occur  in adult rats that  are  pregnant (Druckrey et al., 1967) or
recovering from a partial hepatectomy (Craddock,  1971).

                                             14-83

-------
   .  N-Nitroso compounds  can induce  cancers  transplacentally.   Brain and  spinal  cord tumors
(Ivankovic and Druckrey,  1968)  and renal tumors (Wrba  et  al.,  1967) were found in progeny of
pregnant  rats  treated  with  N-nitrosoethylurea.    Diethylnitrosamine  has  transplacentally
induced trachea!  papillomas in rats (Mohr et al.,  1966).
     Small amounts  of carcinogenic nitrosamines have  been detected in some  samples  of urban
air (Fine et al.,  1976) and in the food supply (Crosby and Sawyer,  1976).
     N-Nitroso compounds  could  present a hazard,  not only because  people are exposed to these
compounds but  also because  they  can  be  produced  i_n vivo, at least  in  experimental  animals.
Nitrosation  reactions are  catalyzed   by  acid and  hence  should occur preferentially  in  the
stomach..   Their  reactions  have  been  induced in animals  by feeding  nitrite with  amines  or
amides  (Mirvish,  1972;  1977;  Rounbehler et  al.,  1977).   Also, under these  situations acute
toxic  effects  have  been   observed  and  N-nitroso  compounds  have   been  detected  by  chemical
analysis (Mirvish, 1975).
     A  recent  report by  Iqbal  et al.  (1980)  demonstrates HI vivo  biosynthesis  of N-nitroso-
morpholine from mice  exposed to NCL and  morpholine.   This is the   first and  only  report of a
direct  link  between  NO,  exposure  and  nitrosamine formation  in  vivo.   N-nitrosomorpholine was
                                              3
detected  in  animals with  as low  as  376 ug/m  (0.2 ppm)  NO, exposure for 4  hours.   After 4
                                3
hours of exposure at 94,000 ug/m  (50 ppm) NO,,,  a maximum of 2230 ng N-nitrosomorpholine/mouse
was detected.  These  quantities are extremely small, and  it  is  not known what the biological
significance (in terms of mutation or cancer) is to  this  exposure.  However, the possibility
of  low  level  exposure  to  N02  and   concomitant  biosynthesis  of  nitrosamines  indicates  a
potential  health  hazard.   This  area   of  investigation  requires additional  work  in  order  to
quantitate this potential  health hazard to man (Iqbal et al.,  1980).
14.7  SUMMARY
     The  biological  effects  of  nitrogen  oxides have  been  examined in  a number  of animal
species.  Thus far,  the  most toxic among these  is  nitrogen  dioxide (N09).  A  summary of the
                                         3
research results observed  at 18,800 ug/m  (10.0  ppm) N00 or less is set  forth in Table 14-21.
                                                                                  3
While mechanisms  of action  can be studied by exposures  at  or above 18,800  ug/m   (10.0 ppm)
N02, this concentration  is judged to  be  the  maximum  at which animal studies provide relevant
data to  estimating  the  human health effects of ambient or near ambient concentrations of N02.
     An unusual aspect of the toxicity of N02 is  a delay between  exposure  and  effect.   This
temporal sequence  is  inherent in  understanding the toxicity of N02 and has important implica-
tions  for the  effects of both  short-term  and  long-term exposures  to this  air pollutant.
Despite  the  differences   in  N0~  sensitivity among  animal   species  and  the many  different
endpoints of  toxicity,  illustrated  in Figure 14-4.   A composite  has  been drawn from these
different studies  to  illustrate the relationship with  time  following  a  single short-term ex-
posure  of 4  hours  or less.  These results are drawn primarily from a single species, the rat.
A similar sequence  could  be drawn for other  species.   It is likely that this sequence is the

                                             14-84

-------
                      TABLE 11-21.  SUMMARY OF EFFECTS OF N02  IN ANIMALS AT CONCENTRATIONS OF 10 ppm OR LESS
Concentration of N02   Time of
             pjjin       exposure    Species
                                                                Summary of effects
                                                                                     References
00
en
188
188 + 2
hr daily
spike of
1,880

376
        470
        470
0.1 spike
2 x daily
with 0.05
baseline

0.1 + 2
hr daily
spike
of 1

0.2
0.25
0.25
        560-940    0.3-0.5
                               Continu-   Mouse
                               ous, 15
                               days
                             Continuous   Mouse
                               6 mo
                               3 hrs
                        Rat
                        4 hr/day   Rabbit
                        5 days/wk
                        24 or 36
                        days

                        3 hr/day   Mouse
                        up to 3 d
           Continuous   Mouse
             3 mo
                                         No effect on S.  pyogenes infectivity
                                         Emphysematous alterations
Inhibition of conversion of PGE? to
its metabolite.  No effect on
PGE_ uptake or efflux

Swollen collagen fibers in lung
Increased1 pentobarbital
sleeping time in female mice after
1 day.  No effects after 2 or 3
days.

N0« * influenza virus caused a high
incidence of adenomatous prolifera-
tion of peripheral and bronchial
epithelial cells
                                            Gardner, et al.,
                                            1981
                                                                                                Port, et al.,
                                                                                                1977
                                                                                                Men2el, 1980
                                                                                                Buell,  1970
                                                                                                Miller,  et al. ,
                                                                                                1980
                                                                                                Motomiya,  et al. ,
                                                                                                1973

-------
                                      TABLE  14-21.   (continued)
Concentration of N02
|jg/m3 ppm






i — »
-El
1
CD
cn

600

680
740
740
740
940
940
0.32

0.36
0.4
0.4
0.4
0.5
0.5
Time of
exposure
3 mo

7 days
4 hr/day
7 days
Continuous
1 wk
Continuous
2 wk
6,18 or
24 hr/day
12 mo
8 hr/day
7 days
Species
Rat

Guinea Pig
Guinea Pig
Guinea Pig
Guinea Pig
Mouse
Guinea Pig
Summary of effects
Decreased conditioned reflexes

Increased erythrocyte D-2, 3-
diphosphogly cerate
Increase in lung acid phosphatase
Increase in protein of lung lavage
in vitamin C deficient animals
No effect on protein or lipid in
lung lavage in vitamin C deficient
animal s.
Morphological effects in alveoli
Increase in serum LDH, CPK, SCOT,
SGPT and chol inesterase, and lung
and plasma lysozyme. Decrease in
References
Yakimchuk and
Chelikanov, 1972
Mersch et al . ,
1973
Sherwin et al . ,
1974
Sherwin and
Carlson, 1973
Selgrade et al . ,
1981
Blair et al . ,
1969
Donovan et al . ,
1976; Menzel
et al. , 1977
940
0.5
Continuous   Guinea Pig
  14 days
erythrocyte GSH peroxidase.   No
change in lung GSH peroxidase.

Albumin and globulins in urine
Sherwin and
Layfield, 1974

-------
                                             TABLE 14-21.   (continued)
       Concentration of N02   Time of
        ug/m3     ppm         exposure
                         Species
                                   Summary of effects
                                            References
       1,000 N0>
       (mostly
       N00
       940



       940


       940
-p«

CO
       940 or
       3,760
       940
0.5



0.5


0.5
0.5 or 2
0.5
              8 hr/day   Guinea Pig
              180 days
Continuous   Mouse
30-45 days
  5 days/wk  Mouse
  7 wk

Continuous   Guinea Pig
  8 hr/day
  4 mo
Continuous   Mouse
with 1 hr
peaks of
2 ppm 5
days/wk

Continuous   Mouse
  12 mo
Nitrates and nitrites in urine;  slight
increase in serum cholesterol;  decrease
in total serum lipids; hepatic  edema;
increase in urinary Mg and decrease
in liver and brain Mg

Morphological alterations of tracheal
mucosa and cilia
Increase of injected horseradish per-
oxidase in lung

Decrease in plasma cholinesterase;
erythrocyte or lung GSH peroxidase
unchanged.   Increase in lung acid
phosphatase and plasma and lung
lysozyme

Morphological alterations of alveolar
macrophages; decreased serum neutraliz-
ing antibody to influenza virus immuni-
zation; changes in serum immunoglobulins
At 10 days:  damage to clara cells and
cilia and alveolar edema.  At 35-40
days:  bronchial hyperplasia.  At 6
mo:  fibrosis.  At 12 mo:  bronchial
hyperplasia
                                                                          Kosmider,  1975
Nakajima et al. ,
1972; Nakajima
et al.,  1969

Sherwin et al. ,
1977

Donovan et al.,
1976; Menzel
et al.,  1977
Aranyi et al.,
1976; Ehrlich
et al., 1975
Hattori, 1973;
Hattori and
Takemura, 1974

-------
                                             TABLE 14-21.   (continued)
CD
CO
Concentration of N02
|jg/m3 ppm
940 or 0.5 or 1
1,880
940 or 0.5 or 1
1,880
940 0.5
1,000 0.53
1,030 - 0.55 -
3,000 1.6
1,500 0.8
Time of
exposure Species
Continuous Mouse
1 yr, 5 mo
Continuous Mouse
1 yr, 6 mo
Continuous Mouse
or inter-
mittent
(7-8 hr/day)
180 days Guinea Pig
8 hr/day
Continuous Mouse
5 wk
Continuous Rat
2.75 yr
Summary of effects
No increase in lipofuscin or glutathione
peroxidase
Growth reduced; vitamin E improved
growth
Increased susceptibility to K. pneumoniae
after 90 days continuous or 180 days
intermittent exposure
Alterations in several serum enzymes
Cilia damaged; increased mucus secretion
Increase in respiratory rate
References
Ayaz and Csallany,
1977
Csallany, 1975
Ehrlich and Henry,
1968
Drozdz et al . ,
1975
Miyoshi et al . ,
1973
Haydon et al . ,
1965; Freeman
       1,880
       1,880
Continuous   Guinea Pig
  3 days
Continuous   Rabbit
  2 wk
Increase protein and lipid content of
lavage fluid in vitamin C- depleted
but not normal

Decrease in lung lecithin synthesis
after 1 wk; less marked depression
after 2 wk
et al.,  1966

Belgrade et al. ,
1981
Seto et al.,  1975

-------
                                             TABLE 14-21.   (continued)
       Concentration of NO^   Time of
        ug/m3     ppm         exposure    Species
                                                         Summary  of  effects
                                                                                      References
00
10
       1,880     1-1.5
       2,820
       1,880
       1,880
2,000
1.1
                      Continuous    Mouse
                        1 mo
                      Continuous    Guinea  Pig
                        6 mo
                      Continuous    Monkey
                      493 days
8 hr/day
180 days
.Guinea Pig
       940 + 2 x 0.5 + 2 x   Continuous   Mouse
       daily     daily       15 days
       spikes    spikes
       of 1880   of 1
Hypertrophy of bronchiolar epithelium
after 1-3 mo.   After recovery from
exposure, lymphocyte infiltration

Inhibition of protein synthesis;
decrease in body weight, total serum
proteins, and immunoglobulins

Immunization with monkey-adapted in-
fluenza virus.  Increased serum neutra-
lizing antibody titers at 93 days of
exposure.  No change in hemagglutina-
tion inhibition titers; no effect on
hematocrit or hemoglobin; increased
leukocytes in blood.  Slight emphysema
and thickened bronchial and bronchiolar
epithelium in virus-challenged monkeys

Plasma and liver changes:  decrease in
albumin, seromucoid, cholinesterase,
alanine and aspartate transaminases;
increase in alpha and beta? immuno-
globulins

Increase in mortality due to
S. pyogenes
                                                                                      Chen et al.,  1972
                                                                                      Kosmider et al.,
                                                                                      1973a
                                                                                      Renters et al.,
                                                                                      1973
Drozdz et al.,
1976
                                                                                                Gardner et al. ,
                                                                                                1981

-------
                                             TABLE 14-21.   (continued)
ID
O
Concentration of N02
[jg/m3 ppm
2,300 +
2 x
daily
spikes
of 4,700
2,360
2,400-
5,200
2,800
2,800 +
8,100
spike
2,800 +
8,100
spike
5,600
3,760
1.2 + 2 x
dai ly
spikes
of 2.5
1.26
1.3-3
1.5
1.5 +
4.5
spike
1.5 +
4.5
3
2
Time of
exposure Species
Continuous Mouse
15 days
12 hr/day Rat, prior
3 mo to breeding
2 hr/day Rabbit
15 & 17 wk
Continuous Mouse
or inter-
mittent
(7 hr/day,
7 days/wk)
Continuous Mouse
62 hrs be-
fore & 18 hr
after a spike
for 1,3.5 or 7 hr
14 d; 2 Mouse
daily 1 hr
spike x 5
d/wk x 2 wk
3 hr Mouse
3 hr Mouse
Summary of effects
Increase in mortality due to
S. pyogenes
No effect on fertility; decrease in litter
size and neonatal weight; no teratogenic
effects
Increased leukocytes in blood with
decreased phagocytosis; decreased number
of erythrocytes
After 1 wk, increased susceptibility to
S. pyogenes aerosol greater in continuous
exposure group. After 2 wk, no signifi-
cant difference between modes of ex-
posure
Increased susceptibility to S. pyogenes
aerosol after 3.5 or 7 hr single spike
when bacterial challenge was delayed
18 hrs after spike
Increased susceptibility to S. pyogenes
aerosol
Increased susceptibility to S. pyogenes
aerosol in mice exercising compared to
those not exercising
Increased susceptibility to S. pyogenes
References
Gardner et al . ,
1981
Goldstein et al . ,
1973
Blair et al . ,
1969
Gardner et al. ,
1979
Gardner et al . ,
1981
Gardner et al . ,
1981
11 ling et al. , 198
Ehrl ich et a) . ,
                                                            aerosol
1977

-------
TABLE 14-21.   (continued)
Concentration of N02
ug/m3 ppm
3,760 2

3,760 2
3,760 2
3,800 2
3,800 2
4,280 2.3
5,000 2.7
5,450 2.9
Time of
exposure
Continuous
1-3 wk

Continuous
3 wk
Continuous
43 days
Continuous
14 mo.
Continuous
2 yr.
17 hr
8 wk
Continuous
20 days
Species
Guinea Pig

Guinea Pig
Rat
Rat
Monkey
Rat
Mouse
Rat
Rat
Summary of effects
Increase in number of lactic acid de-
hydrogenase positive lung cells (pre-
sumably Type II cells) with time of
exposure
Type II cell hypertrophy
Between 72 hr - 7 days increasing loss
of cilia and focal hyperplasia; by
14 days, cilia regenerated and recovery
was evident at 21 days
Polycythemia with or without NaCl. Hyper-
trophy of bronchiolar epithelium
Increase in respiratory rate; no change
in resistance or dynamic compliance
Decreased pulmonary bactericidal activity
(no measurable effect at 1 ppm x 17 hr.
or 3.8 ppm x 4 hr. )
Decreased body weight
Decrease in linoleic and linolenic acid
of lung lavage fluid
References
Sherwin et al. ,
1972

Sherwin et al. ,
1973
Stephens et al . ,
1972
Furiosi et al . ,
1973
Freeman et al . ,
1968c
Goldstein et al. ,
1973b
Kaut et al . , 1966
Menzel et al. , 197

-------
                                      TABLE 14-21.   (continued)
Concentration of N02
ug/m3 ppm
5,450 2.9
5,640 3
5,640 3
6,600 3.5
t— >
4=>
10
7,500- 4-7
1,3000
Time of
exposure Species
24 hr/day Rat
5 days/wk
9 mo.
4 hr/day Monkey
4 days
Continuous Guinea Pig
3 days
Continuous Mouse
or Inter-
mittent
(7 hr/day,
7 days/wk)
Continuous Mouse
14 days
Summary of effects
Decrease in lung compliance and volume;
increased lung weight and decreased total
lung lipid; decreased saturated fatty
acid content of lung lavage fluid and
tissue; increased surface tension of
lung lavage fluid
Thickening of basal laminar and alveolar
walls; interstitial collagen
Increased protein and lipid content of
lavage fluid in vitamin C-depleted but
not normal
Increased susceptibility to S. pyogenes
aerosol with increased duration of ex-
posure. No significant difference
between modes of exposure
Increase of injected radio- labeled pro-
tein in lung
References
Arner and Rhoades,
1973
Bils, 1976
Sel grade et al . ,
1981
Gardner et al . ,
1979
Sherwin and Richte
1971
8,100     4.5
9,400
1, 3.5 or    Mouse
7 hrs
  3 hr
Guinea Pig
Increased susceptibility to S.  pyogenes
aerosol proportional to duration of
exposure.   No effect when bacterial
challenge was delayed 18 hrs.

Increase protein and lipid content of
lavage fluid in vitamin C-depleted but
not normal after 18 hrs
                                                             Gardner et al. ,
                                                             1981
Selgrade et al.,
1981

-------
                                                TABLE  14-21.   (continued)
VD
OJ
Concentration of N02
|jg/m3 ppm
9,400-
94,000

9,400
9,400
.9,400
9,400
9,400
9,400
9,400
5-50

5
5
5
5
5
5
5
Time of
exposure Species
3 hr Rabbit

4 hr Guinea Pig
4 hr/day Guinea Pig
5 days/wk
2 mo.
7.5 hr/day Guinea Pig
5 days/wk
5.5 mo.
14-72 hr Mouse
3 days Guinea Pig
Continuous Rat
1 wk
Continuous Monkey
Summary of effects
No measurable effect on benzo(a)pyrene
hydroxylase activity of tracheal
mucosa
Increase in respiratory rate and
decrease in tidal volume
Increased lung tissue serum anti-
bodies
No increase in airflow resistance
Increased lung protein by radio-label
method
50% mortality; histological evidence of
edema; increased protein and lipid con-
tent of lavage fluid in vitamin C
depleted but not normal
Hyperplasia began by 3 wks
Increased susceptibility to
References
Palmer et al . ,
1972

Murphy et al . ,
1964
Balchum et al . ,
1965
Murphy et al . ,
1964
Csallany, 1975
Selgrade et al . ,
1981
Rejthar and Rejthc
1975
Henry et al . , 197C
                                  2 mo.
K.  pneumoniae

-------
                                      TABLE 14-21.   (continued)
Concentration of NO
ug/m^ ppm
9,400-
18,800
5-10
2 Time of
exposure
Continuous
90 days
Species
Monkey
Summary of effects
Infiltration of macrophages, lymphocytes
and some polymorphonuclear leukocytes;
hyperplasia of bronchiolar epithelium
and Type II cells
References
Busey et al . ,
1974
9,400-
18,800

9,400
18,800
190
          5-10


           5
          10
          0.1
Continuous   Monkey
  90 days

Continuous   Monkey
 133 days
                 No significant hematological effects
                                            Coate and Badger,
                                            1974
                 Immunization with mouse-adapted influenza   Matsumura, 1970
                 virus.  Initial depression in serum neutra-
                 lization titers with return to normal by
                 133 days.   No change in hemagglutination
                 inhibition titers or amnestic response
   6 hr
Mouse
No chromosomal alterations in leukocytes
or primary spermatocytes
Gooch et al.,  1977

-------
t


2
u
UJ
UJ
Q
UJ

EC
UJ
CO
m
O
             I   ""I  'I  I
             » EXPOSURE
              CHEMICAL REACTION
   iiiIPM

— SUSCEPTIBILITY TO
     MICROORGANISMS

—— CELL DEATH (max. at 24 hr.)

-— BIOCHEMICAL INDICATORS
     OF INJURY (max. at 1B hr.) .~T

	REPLACEMENT OF DEAD
     AND INJURED CELLS
     AND BIOCHEMICAL
     INDICATORS OF REPAIR
     (max. at 48 hr.)
                                                I     I   I
    (log scale)  4     10    24  48


      I        hours       I
       14
                                    days
30


 I
                 23    6


                    months
   Figure 14-4. Temporal sequence of injury and repair hypoth-
   esized from short-term single exposures of less than 8 hours.
                            12
                              14-95

-------
same  for  all mammalian  species exposed  under  similar conditions.   These reactions will  be
obtained  predominately  with   low  concentrations  of N02.   As  the  concentration  of NCL  is
increased more  than 100-fold  over  ambient concentrations, complications  arise which tend  to
obscure the  sequence  of events.   It  is not  clear,  further,  whether  or  not  these  higher
concentrations are truly relevant to the toxicity of NO,, to man as it occurs  in the atmosphere
of urban  areas.   In any event, the animal studies most important to determining the standards
used in regulating  emissions  are those more closely aligned to ambient concentrations of NCL.
     Studies  of  the reaction  of N02 with  cellular constituents clearly  illustrate  that the
chemical  reactions  are  essentially  instantaneous  (Roehm  et  al.,  1971;  Menzel,  1976)  when
compared  with  the  length of  time  required  for demonstration of a biological effect.   Most
investigators believe  that  the chemical reactions of N0? are dominantly with lipid components
of  the cell   (Menzel,  1976).    The  reaction of  N02 with  the  unsaturated lipids   of  cellular
membranes results in a chemical reaction characterized by the formation of peroxidic products.
This  is  a devastating  event  in terms  of  the organization and  properties  of  the  cellular
membrane  necessary  to  maintain the  integrity of the cell.   Many  of the biological effects can
be ascribed  to  the  peroxidation of cellular membranes,  the most obvious  example  of  which  is
pulmonary edema,  a  commonly  observed phenomenon on  exposure  to high  concentrations of  N02.
The protective role of vitamin E in  the  prevention of N02 toxicity at high  concentrations  is
also supportive of this hypothesis (Menzel, 1976).
     Alternatively,  N0?  could oxidize  a  number of  small  molecular weight compounds such  as
glutathione,   pyridine  nucleotides  and ascorbic acid.   Thiol  oxidation  could be  coupled  to
lipid  peroxidation  through the glutathione peroxidase-glutathione  reductase  cycle  (Chow  et
al., 1974).   The  increased  pulmonary edema found in guinea  pigs mildly depleted  of vitamin C
(ascorbic acid)  suggests that  vitamin  C  also  plays  an  important role in the  maintenance  of
cellular integrity during N02  exposures (Belgrade et al.,  1981).
     Inhaled   NO,, is   rapidly  taken  up  and distributed  throughout  the  lung  as  has  been
                                                      13
determined using short lived radiotracer studies with   NQ2 (Goldstein et al.,  1977b).  A very
significant   fraction  of  N0?  is   retained  in  the  lung.   The fraction  retained  probably
represents that   N0?   which  is  chemically  reactive  with  pulmonary  tissue via   addition  to
unsaturated  fatty acids.
     NOp is  an acid  anhydride  and reacts with water vapor at ambient concentrations in the air
and more  so  at  the  increased  temperature and humidity existing within the respiratory system.
The exact chemical species which reaches the pulmonary surface  to produce the observed lesions
is most likely N02,  but HN02, and perhaps  NO may  be formed in  the  liquid lining the airways
(Goldstein et al.,  1977b).  HN02 and HNO., will  be  rapidly neutralized by the  biological  sub-
stances dissolved in the liquid layer lining the airways of the lung.
     Despite  the hydration of  N02 by water vapor, a significant fraction of N02 is not removed
in the  upper  airways  and penetrates deep within the  lung to produce its toxic effects.   As a
strong  oxidant,  N0?  may  also  oxidize small molecular weight reducing substances  and proteins
                                             14-96

-------
within  seconds  to minutes.   Reaction with  unsaturated  fatty acids to produce peroxidation is
essentially  instantaneous  (Roehm et al., 1971).   It  is not likely, so  far  as  is known, that
NO-  reaching the respiratory portions of the  lung would be able  to  penetrate  the lung cells
and  attain  a significant concentration within  the  blood.   Nitrate is formed as a consequence
of  reactions with  cellular  constituents   and  has been  detected in  the  blood  and  urine  of
animals  exposed to  N02 (Kosmider, 1975).   Levels  of  nitrate attained during NO- exposure are
unlikely  to induce biological  responses  of the nature which have  been  observed.   Because  of
the  high reactivity  of  NO^, the  predominant  response observed  on the inhalation  of NCL  is
direct  injury to  the  tissues of  the lung.   The effects  on organs distal to the lung are likely
to result from  the production of secondary  toxicants in the  lung which are circulated to other
parts  of  the  body.   A  direct  proof  of  this  hypothesis of  circulating  toxins  following
inhalation  of NO- has  not  been  found,  but effects  on organs  other  than the  lung  have been
found  (Miller  et al.,  1980).   The  metabolism of xenobiotic  compounds,  for  example pento-
                                                                       o
barbital,  by the liver  is  inhibited  by  exposure  of mice  to  470 ug/m  (0.25 ppm)  N02 for 3
hours  (Miller  et al.,  1980).   Repeated  exposure  to  N02 resulted  in a  return  to  normal
metabolism  of pentobarbital.   While  the implications  of these observations  are difficult  to
understand, decreased drug metabolism represents the inhibition of an  important detoxification
pathway  in  the  liver for a variety  of  compounds  to  which  man is  exposed  both intentionally
(drugs,  pesticides, and  food additives)  and unintentionally (naturally  occurring or adventi-
tious  toxicants, mutagens,  and  carcinogens).   Inhibition  of  drug  metabolism  is  generally
recognized  as an adverse effect of a  drug, and thus,   these effects are also adverse.   Future
•studies  on  the  effects  of  HQy  inhalation  on other organ  systems  deserve  continued surveil-
lance.
     The major pulmonary effect of N02 is cellular injury among specific cell types within the
lung  (Freeman et al., 1968b).    If the N02  injury is severe, cell  death results.   These events
occur within  24 hours after inhalation.   The  magnitude and site  of the injury resulting from
N02  will  depend  upon the  concentration of  N02 which was  inhaled;   therefore,  the absolute
degree  of  response  will  depend upon both  the  rate and magnitude of  respiration  and  the N02
concentration.   The   moderate  solubility of  N02  in  water  and  the   inability  of  the  upper
respiratory  tract to  remove  all of  the  N0?  which is  inhaled result in  injury  to specific
regions within the lung.   At concentrations near those found in urban environments, the region
of the lung bounded by the terminal and respiratory bronchioles  and adjacent alveoli  are those
which are most  affected  (Freeman et al., 1968,b,c; 1969b,  1974a).   Emphysematous alterations
have been reported in mice exposed for 6 months to 188 ug/m  (0.1 ppm) NO, with a daily 2-hour
                    3
spike of  1,880  (jg/m   (1 ppm) N02  (Donovan  et al., 1976).   The bronchiolar  region represents
the  terminal  portion  of  the lung and  is  intimately  involved  in the exchange  of oxygen and
carbon dioxide.   This  is the region of the  lung which  is most essential for the maintenance  of
life.  Some  differences  may exist between  man  and  rodents  because this region of the lung  is
proportionately much  shorter in the rat than  in man.   At high concentrations of Nt^,  that  is
                                             14-97

-------
above ~9,400 ug/m   (~5  ppm),  segments of the upper airways, as well  as those centering around
the  alveoli,  may be  affected.   As cells  are exposed  to  NOp and begin  to  die,  protein  and
nucleic acid synthesis  is  stimulated  in the surviving stem cells and a wave of mitosis occurs
which reaches  its maximum  at  about 48 hours during or after exposure.   The type I cell of the
lung (a thin, squamous cell across which gases are exchanged) appears to be the most sensitive
and to be injured at lower concentrations than the type II  cell (a cuboidal cell that produces
surfactant) (Evans  et a!.,  1973b).   The nature of this injury can be sufficiently severe that
the cell dies,  sloughs  off,  and leaves  debris within  the  alveoli.   Other  cells  in  the upper
airway,  such  as ciliated  cells,  are  similarly  sensitive  and may  be  replaced by  other stem
cells known  as Clara cells.   These  effects  on  the  lung  result in  dramatic changes  in  its
structure and cell  composition.
     Swollen  collagen  fibers  occur  in  rabbits   exposed  to  470 ug/m  (0.25  ppm)  N02  for  4
hr/day,   5  days/wk  for  24  days  (Buell,  1970).    Presumably, these  swollen  collagen fibers
represent alterations in the  basement membrane or disruptions in collagen synthesis.   One can
not speculate  on the  potential  pathological sequelae of collagen dysfunction, except to note
that collagen metabolism is disrupted  in man and  animals during fibrosis.   Some alterations in
collagen  metabolism  are  suggested  by  the  long-term  exposures of   dogs  to  auto  exhaust
containing NO  and  N02 (Orthoefer et  al.,  1976).   Increased number and size  of interalveolar
pores found  in these dogs  after near  life-time  exposures  (Hyde et al.,  1978) emphasize  the
importance of the emphasematous alterations found in mice on exposure to N02 alone (Donovan et
al., 1976).
     Biochemical indicators of lung  injury  can  provide early evidence of  toxicity.   The  rat
                                                                                             2
lung prostaglandin  dehydrogenase  is sensitive to exposures of as little  as 3 hr  to 376 ug/m
(0.2 ppm) N09  (Menzel,  1980).   In this series of experiments, rats were exposed to 376, 3,760
               3
or 35,720 ug/m   (0.2, 2 or 19 ppm) for  3  hours.   The  lungs  were then removed and used as an
isolated,  ventilated  and  perfused lung preparation  to determine  the  uptake,  release  and
metabolism of  prostaglandin E2  (PGE2),  a natural vasoactive  hormone  secreted by  the lung and
other organs.   N0?  exposure  inhibited  the  metabolism of  PGE2 to  its   inactive  metabolite
13,14-dehydro-15-keto PGE0.   While   there  was  no  difference  in  the amount of  inhibition
                                           3
produced by exposure  to  376  and 3,760 ug/m   (0.2  and  2 ppm) N00,  the time required to return
                                                                             3
to basal levels  of  activity  was greater for those rats exposed to 3,760 ug/m  (2  ppm) than to
376 ug/m  (0.2  ppm).  Rats exposed to 35,720 ug/m  (19 ppm) NO,  required  the longest time for
                                                                                        3
recovery to  basal   levels.   Recovery  required 60  hours following exposure to  376  ug/m  (0.2
                                    3                                              3
ppm), 90  hours following  3,760 ug/m  (2 ppm) and  160  hours following  35,720  ug/m   (19 ppm).
                                                 3
No alteration of the uptake or release of either   H-PGE2 or its metabolites by the exposed rat
lungs was found.  None of the  lungs examined showed any evidence  of  edema  as judged by the wet
weight to  dry weight ratio.   Since  the  prostaglandin system is  intimately  involved  in  the
local regulation  of blood flow  in the  lung,  alterations  in the metabolism  of  these potent

                                             14-98

-------
 hormones  may  have profound effects on  the  perfusion  of the lung and  subsequently  on the gas
 exchange  of the affected lung.
     As pointed  out above, vitamin C appears  to  play an important role in the maintenance of
 the  integrity of the airways to  macromolecules.   Selgrade  et  al.  (1981) repeated in part the
 experiments of Sherwin  and Carlson (1973)  in which guinea pigs were depleted of vitamin C and
 exposed  to N09.    Selgrade et al. failed to  find an  increase  in the  lavage  fluid  protein or
                                                   3
 lipid  content of  guinea  pigs exposed  to 740  |jg/m  (0.4 ppm)  NO,, even after  exposure  for 2
                                                   3
 weeks.   Exposure  to  1,880,  5,640 or  9,400  ug/m  (1,  3  or  5  ppm)  NO,  for 3 days  caused
                                                                                          3
 increased  protein and  lipid content of the lavage fluid.  A single exposure to 9,400 ug/m  (5
 ppm)  for  3 hours also produced similar changes  in the lavage fluid content after 18 hours in
 vitamin  C-depleted guinea pigs,   but  not  in  normal  guinea pigs.   Vitamin C  depletion  also
                                                                       o
 caused  a   50  percent mortality  in the  animals  exposed  to  9,400  ug/m  (5  ppm)  NOp, but no
 mortality  in  animals having normal vitamin C levels.
     The  differences  between  the   Sherwin and  Carlson  and the  Selgrade et al.  studies may be
 explained  by  differences  in the exposure systems, in the vitamin C status  of the guinea  pigs,
 and  in  the methods of analysis.   Sherwin and Carlson exposed guinea pigs to N0? by  the use of
 a  silicon  drip technique  and monitored the N02 concentrations  with a Mast  Meter and intermit-
 tent Saltzman determinations.
     Considerable  improvement has  been made in the methods of analysis for  NOp and exposure of
 animals.   Selgrade et al.   used a  chemiluminescent meter and a Hinners  chamber for exposure.
 Considerable  variation  could have occurred in the chamber NO^ concentration  using  the  older
 methods.  The degree of vitamin C  depletion used by Selgrade et al.  was quite mild,  represent-
 ing  only  a 25 percent reduction of the serum  levels  of the vitamin.   No details are provided
 in the  Sherwin and Carlson study  to allow an assessment of the degree of vitamin C  deficiency
 of  the  animals.   More  completely depleted  guinea  pigs  could have  been more  susceptible.
 Sherwin and  Carlson also  used  disc  electrophoresis  to estimate the  protein  concentration of
 the lavage fluid, while Selgrade et al.  used the direct chemical method of  Lowry et  al.   Addi-
 tionally,   Selgrade  et al.  found another protein not detected by Sherwin and Carlson.   The new
protein was detectable  only on careful  photometric scanning of the gels and could  have  gone
 undetected in  the earlier  study since considerable improvement in  technique has been possible
by advances in the field of protein chemistry,  especially electrophoresis.
     These studies  illustrate that vitamin  C deficiency may lead to greater susceptibility to
ambient levels of N02.   Burch (1961) compared the vitamin C levels  reported in guinea pigs and
 in human autopsy tissue  samples from a number of organs.  Guinea pig tissue ascorbate concentra-
tions reach saturation  levels  on  continued intake of  ascorbate.   Since human leukocytes  also
reach saturation  levels  on high vitamin  C intake,  a similar saturation curve for human tissues
 is likely.  Thus,  the 25  percent   reduction  in  serum  vitamin  C levels that resulted  in  these
major changes  in  susceptibility to N0? represent  conditions likely  to occur in man  with low
vitamin C  intake.   Burch  found  29 percent  of  1,000  subjects  in 8 high  schools  to  have  serum
                                             14-99

-------
ascbrbate  levels  below 0.4  percent,  an  arbitrary  biochemical  deficiency  level,  while  48
percent of 150 students from a poor area had values below 0.4 percent.   Oral contraceptive use
(Wynn,  1975)  and smoking  (Hoefel,  1977) also  lower the  blood  ascorbate  levels  in  man.   At
present the dose  response  curve for vitamin C  intake and changes in lung permeability by NOp
exposure  are   not  known,  so  one  cannot  relate   the  changes  reported  by  Selgrade et  al.
quantitatively to the  present  levels of vitamin C  intake by the U.S.  population and the risk
of persons having  low  vitamin  C to adverse effects associated with NOp exposure.   The subject
is obviously important and should be reviewed as further information becomes available.
     Another  sensitive  measure of  injury  is  the  appearance  of  proteins  in the  airways.
Increased  protein content of  the pulmonary  lavage fluid or  the appearance  of  radiolabeled
serum  proteins  in  the  airways  is taken  as  an indicator  of pulmonary  edema.   Radiolabeled
albumin or rabbit  serum proteins injected into the  blood stream of mice were detected in the
airways  after exposure  to 7,520-13,170  (jg/m  (4-7 ppm) N0?  (Sherwin and  Richters,  1971).
Under  normal  circumstances,  such exudates  of  serum  proteins  do not  occur and  represent  a
major,  deleterious  alteration   in  the  permeability  of  the airways.   While  there  was  a  trend
toward  increased  amounts of  radiolabeled protein  in  the  airways  of  exposed mice,  the results
were  not  statistically  supportable,  mainly  because  of  the large  variation in  the  values.
These  variations  could have been  due to  variations of the  NO,  concentration during  exposure
                                                    3
since the exposure  ranged  from 7,520 to 13,170  ug/m  (4-7 ppm) or to variable recovery of the
radiolabeled protein in tissue extracts.   Since  the time of exposure to discrete levels of N02
is not known and since only trends toward increased levels of proteins  within the airways were
                                                              3
reported, one  must conclude that exposure to 7,520-13,170 |jg/m  (4-7 ppm) NOp does  not produce
pulmonary edema in normal mice.
     The effect  of N02  inhalation on the  metabolism of the carcinogen benzo(a)pyrene by the
lung has been  investigated.  Palmer et al.  (1972)  found no effect on benzo(a)pyrene metabolism
                                                               3
of the tracheobronchial region of rabbits exposed  to 9,400 ug/m  (5 ppm) NO, and greater.   Law
                                                                                         3
et al.  (1975)  found no effect of short-term exposures at even higher levels (75,200 ug/m ;  40
ppm  for  2  hours) on rat  lung  microsomal  benzo(a)pyrene metabolism.   N02 exposure  appears  to
have no effect on these cytochrome P.,-Q~dependent  enzyme systems.
     There is no  reason to suppose that all enzymes are equally sensitive to N0? exposure,  so
lack of an effect on some enzymes is not  indicative of an  absence  of  a  toxic effect at that
N02 concentration.  Further,  some enzymatic changes, such as increased  acid  phosphatase levels
(Sherwin and Carlson, 1973),  may represent changes  in the cell population due to death of some
cells and replacement by a new younger cell  population.
     Pulmonary defenses against infectious agents  are affected by short-term exposures to N02-
The  infectivity model  in which pollutant-exposed  animals  receive an aerosol of live  microbes
has  proven to  be  a particularly sensitive  indicator of pulmonary injury and has been respon-
sible for the  development of most of the data indicating toxicity of N02 at  low concentrations
and  short  times  of exposure (Coffin et  al. ,  1976;  Gardner  and Graham, 1976;  Ehrlich,  1975).
                                             14-100

-------
Mortality  from  exogenous  infectious agents is influenced more in proportion to the concentra-
tion  of  NOp than to the  duration  of exposure.   This observation is consistent with the hypo-
thetical temporal  sequence  of injury.   Pulmonary damage occurs rapidly on exposure to NCL but
the  functional  effects of  pulmonary damage  may  be observed  much  later, depending  upon the
extent  of  damage  and  the system  which  has  been  used to measure the  damage;  e.g., pulmonary
conversion of PGE2 to its metabolites (Menzel, 1980) or susceptibility to airborne infections.
(Coffin et al., 1976; Gardner and  Graham, 1976; Ehrlich, 1975)  The infectivity model  tends to
be an  integral  of many of the defensive mechanisms of the lung and, therefore, to reflect the
overall  damage  which has  occurred.   NCL  concentrations  as low as 4,700  ug/m  (2.5  ppm) may
result in excess mortality from a  single exposure of only 3 hours (Ehrlich et al., 1977).   The.
injury of  a 3-hour exposure appears to  be  repaired within 24 to 36 hours after exposure, but
not by 18 hours (Selgrade et al.,  1981).
     In Figure 14-5 a short-term exposure of constant duration has been given to an animal and
only  one  of the  properties  of intoxication  is  illustrated,  the death of type  I  cells.   In-
creasing concentrations  of N02  are illustrated in  this  figure  on  the z  axis.   Thus,  as the
concentration of NOp is increased, the magnitude of cellular death increases  while the time at
which  cell  death  occurs  is  constant.   The magnitude  of cell  death  is  proportional  to  the
logarithm of the  concentration  of NCL which has been inhaled.   Increasing the total amount of
NOp inhaled by  manipulations  in  the respiratory pattern  will  likewise increase the magnitude
of cell  death,  but not influence  the time  at which cellular death occurs.  Mice  made  to run
and to  inhale  more and more deeply  N0~  are  more  susceptible to airborne  infection than those
resting  (Selgrade et al.,  1981).    Eventually, sufficient  cells will  be injured  to  produce
mortality during  the  peak wave  of death of  alveolar cells.   Death through respiratory  insuf-
ficiency and  pulmonary edema,  however,  does  not  occur  at  concentrations achievable  in  the
urban atmosphere.  Concentrations  greater  than 47,000 ug/m  (25 ppm)  are  necessary to achieve
mortality.   This is not to say,  however, that severe pulmonary damage  is not  achieved  at lower
concentrations  near those which occur regularly in urban areas.
     The delay  between  end of exposure  and observation of biological  effect  complicates the
understanding of  the  effects  of  long-term exposure  to  HO*-   This  is  especially so with expo-
sure regimens resembling  those that occur in the  atmosphere where exposure to relatively high
concentrations  of  NO- may occur  repeatedly over a short time period.   Figure 14-6 illustrates
the sequence of events which is  hypothesized to occur on continuous  long-term exposure to NOg.
The sequence of events is essentially  similar  to  that in short-term  exposure.   The  chemical
reactions between  the inhaled NO- and  cellular constituents are instantaneous  and achieve  a
constant level  throughout the exposure.   During the first 14 days of  exposure, cell death and
replacement of  pulmonary  cells are  the dominant  features.   This  is  expressed as a wave of
mitosis  or  cellular  division  which reaches  its  maximum about  48 hours  after the onset of
exposure.   The extent of  cell  death is illustrated  in  Figure.14-6  and is proportional  to the
concentration of ML.   Likewise,  all of the other  indicators of N02  damage so far examined are
                                             14-101

-------
i
u
it,
e
                                                so  ©o
                TIME AFTER iEGINNIMG 5SPOSJRE

    Figure 14-5.  (Proportionality between effect Ccetl death) ami
    concentration of NC>2 during a constant exposure period.
    The maximum in cell death h reached - 18 hours after sx-
    posurs end the extent is proportional to the dote (concen-
    tration
                           14-102

-------
c
s
t
£
I
U
01
01
D
iu
cc
iu
                               II     I    •
                            CHEMICAL REACTION
                                                    PULMONARY
                                                       FUNCTION
                                                       CHANGES
BIOCHEMICAL
                    REPLACEMENT OF DEAD
                    AND INJUREDCELLS
                    AND BIOCHEMICAL
                    INDICATORS OF REPAIR
                                   INCREASED
                         SUSCEPTIBILITY TO
                        MICROORGANISMS
                                  LEVATED
                                   .CELL
                                 TURNOVER
     INCIDENCE
  OF EMPHYSEMA
LIKE PATHOLOGY
                           HYPOTHETICA
                              TOLERANCE
    1  -
           10
                 24   48
                                   14
                                             6 12  (log scale)
            hours
                                days
                                        months
    Figure 14-6. Temporal sequence of injury and repair hypoth-
    esized from continuous exposure to NO2 as observed in exper-
    imental animals.
                              14-103

-------
dose  dependent.   The  biochemical  and  physiological  functional  indicators  of damage  change
rapidly with injury  and  repair,  reaching a relatively  steady  state  after about a week or two
(Menzel et al.,  1972;  Donovan et al., 1976;  Menzel et  al., 1977).   Several  enzymes have been
                                                                                             o
detected which are  indicative of cellular injury at concentrations of N0? as low as 376 ug/m
(0.2 ppm)  (Menzel,  1980)  or 940 ug/m3 (0.5 ppm)  (Donovan et al., 1976;  Menzel  et al. , 1977)
during  the  injurious phase  of continuous exposure,  that is greater than 7  days.   Pulmonary
macrophages are aggregated within the lung and the degree of aggregation has  been estimated by
a  number  of  biochemical  techniques (Aranyi et  al., 1976; Ehrlich et al., 1975).   Again,  the
infectivity model  is highly  sensitive  to N02  exposure.   The susceptibility  to  infection as
measured  by  this technique  rises  almost  linearly during this period.  The  infectivity model
has  been  used  to illustrate  excess mortalities due to  N0?  exposure  at  concentrations  within
the range of 940-2,820 ug/m3 (0.5-1.5 ppm) N02 (Gardner  et al., 1979;  Ehrlich and Henry, 1968;
Freeman et a!., 1972; Stephens et al. , 1971).
     Long-term exposures  to N02 also result  in major alterations of lung morphology.   These
are very difficult to interpret because  of the fine gradation and slow development of response
once the  initial  phase  of replacement of cells susceptible to NCL has passed (Freeman  et al. ,
1968c,  1972;  Stephens  et al., 1971;  1972).   The development of an emphysema-like  disease in
experimental  animals  requires considerable time  as has been demonstrated in  studies  of rats
and  mice.   The  development  of  obstruction  to airflow,  distension  and  destruction   of  the
alveolar  tissue  in  experimental animals  requires considerable  time  (Freeman  et al.,  1972).
When  compared  to  the  life  span,  the  time  required  for  damage  in  experimental  animals is
equivalent to that required for the development of emphysema in man.   The process of emphysema
development on N02  exposure  is indeed complex, but it is clear that the effects are interpre-
table in  terms of the  changes in the cell populations and structural  alterations concommitant
to that.  A major pathologic change  is an  increase in  the distance between  the air space and
the capillary  in  the respirable  or alveolar  region of  the lung (Henry  et al., 1970; Evans et
al.,  1972,  1974; Buell,  1970).   Other  effects  include the loss of ciliated  cells  which are
responsible for  removing  particles from  the  lung .and narrowing  of  the  airways and alteration
in  the  morphology of the cells lining the junction  between the respiratory  segment  and the
mucous  containing segment (Stephens  et  al.,  1971,  1972).   The cell  type in  the  alveoli most
sensitive to NO^, the  type I cells,  is  replaced by type II cells,  the type I cell progenitor,
but  the appearance  of  the  type I  cells maturing in  the  presence  of  N02  is  significantly
different from those maturing in the absence of  N02  (Evans et al.,  1974).   Other alterations
in  the  lung  include the  appearance  of  collagen in  areas  which are normally  devoid  of this
fibrous protein  and  the   aggregation  of  macrophages  (Stephens et  al.,  1971; Buell,  1970).
                                                                                          2
These effects have been observed in rats  that  have been  exposed continuously  to 3,760 ug/m  (2
ppm) N02 or greater.
     The fatty acid composition of the lung membranes  has also been noted to  change during the
exposure to N02 (Menzel  et al., 1972).   The mortality  from continuous exposure to high  concen-
                                             14-104

-------
trations  of  NOp  is  influenced by  the  level of  vitamin E and  other  free radical scavengers
which  are  included  in  the  diet  (Menzel,   et  al.,  1972).   These  observations  support  the
hypothesis that membrane damage by  chemical  oxidation of unsaturated fatty  acids is a major
mechanism  of toxicity  of  NOp.   These  changes  in  fatty acid  composition  of the  lung  are
accompanied  by  enzyme  changes which in part  may  be protective  and aid  in the destruction of
the peroxidic products formed in the lung on N02  inhalation (Chow et al., 1974; Donovan et al.,
1976).   It should be emphasized that at no point is it possible to provide adequate levels of
vitamin E or other dietary factors that provide complete protection against NOp.  It should be
noted, however, that certain segments of the population may be unusually sensitive to N0? should
their  intake of  vitamin  E  and  other  antioxidants  be marginal.   A similar  conclusion  can be
reached with  regard  to vitamin C intake.   Normal  levels of  vitamin C provide protection when
compared  to  marginal or deficient  levels,  but  still  do not prevent completely NOp toxicity.
The  level  of vitamin C  intake in  some  populations may also be marginal  as  discussed  above.
     The temporal sequence of events suggests that the response  of the animal to inhalation of
NOp returns  to  near  normal  levels during continuous  exposure.   These  results are misleading,
since  it  has clearly  been  observed in  long-term studies  of rats that  the morphology  of  the
lung  has changed  from  its  normal   structure to  that  resembling  emphysema  (Freeman et  al.,
1968c; 1972;  Stephens  et al,  1972).  This  raises  the  question  of tolerance to resistance  and
recovery during continuous exposure.  It is possible that, at some point, the rate of replace-
ment of  dead and injured cells resulting from  the  continuous  inhalation of NO- may return to
levels equivalent to that  found in clean  air  (Stephens  et  al.,  1972).   Tolerant cells,  as
compared to naive cells, may be more resistant to N02 because they are younger or because they
may -have  produced a protective  mechanism  such  as  specific increases  in enzymes  capable of
degrading  the secondary reaction  products  formed  on  NOp inhalation.   Some  enzymes such  as
glutathione peroxidase, glutathione reductase, and glucose-6-phospate  dehydrogenase in the  rat
may  be increased  as a  protective  mechanism  (Chow et  al.,  1974),  or  they  more  likely  may
reflect a proliferation of young cells within the organ which contain  higher enzyme concentra-
tions (Sherwin et al.,  1974).   These cells are younger because all  of  the lung cells are dying
and being replaced at  a more rapid  rate  than that  which would  occur normally  in  the lung in
pollutant free air.   Not all  species exhibit this protective  increase  in  enzymes.   For example,
                                         3
the guinea pig,  when exposed  to 940 ug/m  (0.5  ppm) NOp for  4 months  failed to develop  higher
levels of  these potentially protective enzymes  (Donovan et  al., 1976;   Menzel  et  al.,  1977).
Importantly,   when cultured  lung cells  are  coated with  a  very thin layer  of nutrients  to
resemble the  condition  within  the  lung,  direct exposure to  NOp  is highly toxic.   It is most
likely that  all  cells  are  sensitive to  relatively  low  concentrations  of  NOp  and that  no
adaptation in the true  sense  ever occurs.  The apparent adaptation that may be seen in pul-
monary function  measurements  of people  living  in  polluted  areas  vs.  those who live in  non-
polluted areas may be  artifactual  in the sense that  large changes in  pulmonary tissue  may be
necessary before permanent alterations may be detected in pulmonary function.   In other  words,
                                             14-105

-------
a  major pathophysiologic  change must  occur  before  it is  detected by  pulmonary  physiology
methods.  Biochemical  and morphological  techniques  are more sensitive,  but  so  invasive that
they can only  be  used on experimental animals.  In further support of the idea that all cells
are sensitive  to  concentrations  of  N09 which  are  easily  attainable in inhaled air, when rats
                                3
have been exposed  to  3,760 ug/m  (2 ppm) N02 for long periods of time and then are exposed to
an  abrupt  increase  in  concentration  of  N02,  a  second  wave  of mitosis  and  subsequent
alterations in  biochemical,  physiologic, and  morphologic  indicators of  cell  damage  occur in
exactly  the  same  temporal  sequence  (Evans  et al.,   1972).   Thus,  although  "adaptation"  may
appear to occur, the ultimate development of an emphysema-like condition occurs in the rats on
long-term exposure, and  they remain sensitive to alterations to higher concentrations of NO,,.
     An  important  consideration has  been the  question of tumor formation or  malignant meta-
plasia due to  NCL  exposure.   This concern comes  about due to the  morphology  of  the  lungs of
animals which  have  been  exposed to  NO,,.  Because N02 produces a stimulation or rapid turnover
of cells, a transient hyperplasia of the type II lung cell  and nonciliated bronchiolar cell is
observed.  Such  a hyperplasia .represents a  part  of  the natural repair mechanism.   There  is,
however, no  evidence to  indicate that  such  changes  represent  tumor formation  or malignant
metaplasia.   Thus,  there  is no  data  to  connect the inhalation  of  N02  with  an increased
incidence of cancer at the present time.
     As was  noted in the discussion of  the effects  of  short-term exposure  to  NCL,  the  lag
between  exposure  and  biological  effect represents a potential  situation for  accumulation of
biological  effects.   Such  a cumulative  effect has   been  demonstrated using  the infectivity
                                                                                             2
model   in mice  which  were exposed continuously  or intermittently  (7  hr/day) to  2,820 |jg/m
(1.5 ppm) N02 (Gardner et al., 1979).  Intermittent exposures of mice to 2,820 ug/m  (1.5 ppm)
N02 eventually become equivalent to  continuous exposure when the infectivity model is used.  A
total  of 319 hours  of exposure (13.3 days)  is  required before a  7  hour/day  exposure becomes
equivalent to  continuous  exposure.   The time period  for equivalence between  intermittent and
continuous  exposures will  be shortened relative to the concentration of N09.   The intervening
                                                   3
17 hours between each 7 hour exposure to 2,820 ug/m  (1.5 ppm) N02 are inadequate for complete
recovery.  Excess mortality  upon  challenge  with bacterial  pathogens could be  observed after 7
                                         3                                        3
days of continuous exposure to 2,820 ug/m  (1.5 ppm),  however, or even to  940  |jg/m  (0.5 ppm).
     Considerable differences occur  in  the  response  to N02 when animal species and infectious
agents other than mice and S. pyogenes are used (Purvis and Ehrlich, 1963; Henry et al. , 1970;
Renters  et  al., 1973; Matsumura,  1970a).   Resistance  to  K. pneumoniae  (Purvis  and Ehrlich,
1963)   is less  affected   by  N02 exposure than resistance to  S.  pyogenes.    Squirrel  monkeys
(Henry  et  al.,  1970) were  the  least  sensitive  animals  tested  using  this  end  point,  and
hamsters (Ehrlich,  1975) demonstrated  intermediate  sensitivity when  compared to  mice.   The
quantitative extension of such  data to man  is  difficult  because analogous  human data are not
available.   Even  though   both infectious  agents are  human pathogens, the direct  extension of
this data to man  is difficult,  in part, because of differences in anatomical  structure of the
lung,  and in part, because of differences in native and acquired immunity.
                                             14-106

-------
     The recent work of Gardner et al. (1981) on the effects of short-term exposures to spikes
of  N02  similar to those occurring in the urban atmosphere is particularly important in asses-
sing  the  interaction of NO, and  pulmonary  infections.   Mice were exposed to  spikes  of 8,100
    3
|jg/m   (4.5  ppm)  N02  for 1, 3.5,  or 7  hours,  and increased mortality due  to  exposure to S.
pyogenes was  proportional  to the duration of the exposure.  The mice recovered from the expo-
sure  by 18  hours.   To mimic the  urban  environment,  these same spikes were  superimposed  on a
background  of  2,800  (jg/m  (1.5 ppm)  N0?, which  resulted in a significant (p < 0.05) increase
in mortality with a spike of 3.5 or 7 hours duration, when the bacterial  challenge was delayed
for  18  hours  after  the peak  N0?  exposure.   These results are consistent with the long-term
studies of this group using the same model system where it was found that the magnitude of the
exposure was  more important than  the product of time and concentration.  These  data suggest
that  the  alterations in the  lung leading to increased  susceptibility to  airborne infections
occur with  relatively  brief exposures approaching those encountered in the urban environment.
These experiments provide  an experimental basis for the observations relating increased inci-
dence  of  respiratory infections  with gas  stove  exposure in man  (References  ERC/RTP Review,
1976; Melia  et al. ,  1978;  Spengler et al.,  1979; Speizer et al.,  1980;  Goldstein et al.,  1979
from  Chapter  15).  The effect of  cooking stoves on respiratory infections  is  discussed  more
fully in Chapter  15  (Section 15.2.2.2.2).  Levels of 470 to 1,100 pg/m3  (0.25 to 0.6 ppm) N02
were  found  in  the vicinity of gas stoves for about 2 hours (References  ERC/RTP Review, 1976;
Mitchell et al., 1974 from Chapter 15).
     In terms  of  the probable  temporal  sequence  of  events,  N0? inhalation affects almost all
of the  cell  types within the lung.  Depending,  then, upon the concentration  of N02, different
cells will  be affected  in  addition  to  those which are most susceptible  at lower concentra-
tions.  The mode  of  exposure,  that is the  rate  and depth of respiration,  will  also influence
the specific  cell  types which  are damaged.   Because the rate of chemical  reaction of NO,,  with
cell  constituents  is almost instantaneous  when  compared to the time required  for biological
expression of injury, it may be expected that the concentration of N02 during a given exposure
will have a  greater  effect on determining  the end point used to measure  toxicity than would
the duration of exposure.   Sensitive biochemical  parameters are difficult to  interpret because
of  the  need to correlate  biochemical  changes with pathological processes.  They  are viewed,
then,  as  indicators  of death  or injury of  specific cells  following  N02  inhalation.   Bio-
chemical studies  indicate  that  lung  injury occurs on  inhalation  of N09 at levels as  low as
        3
376 ug/m  (0.2 ppm)  for 3  hours in mice, as  evidenced  by changes  in prostaglandin metabolism
(Menzel, 1980);  as  470 pg/m3  (0-25  ppm) for 3  hr/day  for 1  day as evidenced  by increased
pentobarbital  metabolism in  mice  (Miller et al.,  1980);  as  940 pg/m  (0.5  ppm)  for  8  hr/day
for 7 days  as  evidenced by alterations in serum enzymes in guinea  pigs  (Donovan et al., 1976;
                                  3
Menzel et al.,  1977);  as  940 ug/m  (0.5  ppm) continuous exposure  with 1-hour  peaks  of 3,760
ug/m  (2  ppm) for 5  days/wk  in  mice as evidenced  by morphological alterations  in  alveolar
                                                                                             3
macrophages, decreased serum antibody and immunoglobins (Ehrlich et al.,  1975);  as 1,000 pg/m
                                             14-107

-------
 (0.53 ppm)  for 8  hr/day  for 180  days  in guinea  pigs as  evidenced  by alterations  in  serum
                                                  3
 enzymes  (Drozdz et  al.,  1975);  and as 1,880  ug/m  (1 ppm) continuously for 2 weeks  in rabbits
 as evidenced by  decreased lecithin synthesis (Seto  et  al.,  1975).   Not all effects  have  the
 same  sensitivity;   for  example,  guinea  pigs  exposed  to 740  ug/m   (0.4  ppm)  NO,  have  no
                                                                        3
 alteration in  lung  permeability  to serum proteins  but do  at 1,880 (jg/m  (1 ppm) when  rendered
 slightly deficient in vitamin C  (Selgrade et  al., 1981).
      Because of the  universal toxicity  of NO,, to pulmonary cells, it  is likely that other  air
 pollutants such as ozone,  sulfuric acid, sulfur dioxide,  and particulate matter may  injure  the
 same cells within  the  lung  as are injured by  N02.   In most cases,  following the simultaneous
 inhalation of  NQ2  and other  air  pollutants,  additive,  rather than synergistic,  effects have
 been found.  Tobacco smoking  and  occupational  exposure add very significantly to the  toxicity
 of N02.    At  present, the  data  are  not sufficient  to  provide a detailed evaluation of this
 important variable  in the  response of the human population.   Because  of the delay between  the
 exposure to N02  and effect, the  sequence  of  exposures  to air pollutants may  be particularly
 important.   No synergism  occurs  between 0, and NO,  at  the lowest concentrations examined  for
                             3                                     3
 each pollutant of  100 ug/m  (0.05 ppm) with spikes  of 200  ug/m  (0.1 ppm)  (Gardner et al.,
 1981).   At 940 ug/m3  (0.5 ppm)  N02 with  1,880  ug/m3 (1 ppm) spikes combined with 0.05 ppm 03
 with  0.1  ppm  spikes  or  higher, synergism  between  0,   and  NQ2  occurs  using  mice  in  the
 infectivity experiment (Gardner  et al.,  1981).
      Another area  of possible  toxicity may  be  the formation  of nitroso compounds,   because
 nitrosamides  and   nitrosamines  are  known carcinogens.   Nitrosamines  and  nitrosamides  have
 recently come  into  the public view through their formation in foodstuffs  containing nitrites.
 In this  case,  nitrite  has  been  added to the  foodstuffs to prevent bacterial  contamination  and
 spoilage.   Gas  phase reactions between NOp and amines to form nitrosamines  have been reported,
 and inhaled,  injected or  ingested nitrosamines  produce lung tumors in  exposed animals.  At  the
 moment,  no  evidence exists  that  nitrosamines or nitrosamides  are formed in ambient  air from
 nitrogen oxides.    The  detection of nitrosamines in  the  body of mice   gavaged  morphroline  and
 breathing N02  (Iqbal et  al.,  1980) suggests  that nitrosamine formation in  the lung  can occur.
 The contribution of  inhalation  vs.  ingestion as sources  of nitrosamines remains to  be quanti-
 fied.   Similarly,  the role  of inhaled nitrites  and nitrates  found in  atmospheric particles is
 unknown  and should  be  studied further.   A few experiments  indicate that  inhaled nitrate pro-
 duces biological  effects  through  the release  of histamine and other  intracellular hormones.
-Whether  such effects  occur  in  man is  not known.   Continued surveillance of  these important
 areas is needed.
      While much remains to  be learned about  the toxicity  of N0?, studies  so far conducted in
 animals  indicate that the  biological  effects of N02  are  likely to be displaced from  the time
 of exposure.   As shown in  Figures 14-4  through  14-6, this delay between onset of symptoms  and
 exposure to  N02  may explain many  of  the confounding factors observed  in  epidemiologic  data,
 but complicates further the question  of effects of  transient  episodes of  high N0~  concentra-
                                              14-108

-------
tions  in  the  atmosphere.   It  is  clear  that  the  lowest  concentration  at  which NOp,  in
particular, produces biological effects of a reproducible magnitude so far detected in animals
            3                                             3
is  376  ug/m  (0.2 ppm).   Repeated exposures to  940  ug/m  (0.5 ppm)  also  produce measurable
adverse  effects.   The observation  of  cumulative effects is  especially  important, suggesting
that  under  appropriate circumstances  intermittent  short-term exposure to  N0?  may eventually
become equivalent to  continuous  long-term exposure.   These observations,  when compared to the
data  which  have  been  accumulated  on  the long-term  effects of  NO^,  may  be  particularly
pertinent to the  potential  toxicity of this air pollutant to  man.   There is little doubt that
the inhalation of NO- results  in toxicity,  regardless  of  the species which has been exposed.
Thus,  animal  experiments  are  truly indicative  of  the  hazard of  this air pollutant  to man.
                                             14-109

-------
14.8  REFERENCES

Acton,  J.  0., and  Q.  N.  Myrvik.   Nitrogen  dioxide  effects  on  alveolar macrophages.   Arch.
     Environ. Health 24:48-52, 1972.

Antweiler, H. , and  A.  Brockhaus.   Respiratory  frequency,  flow rate and minute  volume in non-
     anaesthetised guinea-pigs during prolonged exposure to  low concentrations  of  S09  and NO,.
     Ann. Occup.  Hyg. 19:13-16,  1976.                                                *        *

Antweiller,  H,  K.  H. Kompach, and  A.  Brockhaus.   Investigations  on  the influence of N02  and
     SO-2 as  well  as a combination  of  the two gases on  the  production of precipitating  anti-
     bodies  in guinea-pigs.   Zentralbl.  Bakteriol.  Parasitenkd.   Infektionskr.  Hyg.  Abt.  1:
     Orig. Reihe B 160:212-224,  1975.

Aranyi,  C.,  J.  Renters,  R. Ehrlich, and  D. Gardner.  Scanning electron  microscopy of  alveolar
     macrophages  after  exposure to oxygen, nitrogen dioxide  and  ozone.   EHP Environ.  Health
     Perspect. 16:180, 1976.

Arner, E. C.  , and R. A.  Rhoades.  Long-term nitrogen dioxide exposure.   Effects  on lung  lipids
     and mechanical properties.  Arch. Environ. Health 26:156-160,  1973.

Arnold,  W. P.,  R.  Aldred, and F. Murad.   Cigarette smoke activates  guanylate  cyclase and in-
     creases  guanosine  3', 5'-monophosphate  in tissues.   Science  (Washington,  D.C.)  198:934-
     936, 1977a.

Arnold,  W.   P.,  C.  K. Mittal,  S.   Katsuki,  and F.  Murad.   Nitric  oxide  activates guanylate
     cyclase  and  increases guanosine  3':  5'-cyclic monophosphate  levels  in various  tissue
     preparations.  Proc.  Natl.  Acad. Sci. U.S.A.  74:3203-3207, 1977b.

Ayaz,  K.   L.  ,  and  A.  S.  Csallany.  The effect  of continuous,  low  level  nitrogen dioxide.
     exposure  and  dietary vitamin  E upon  lipofuscin  pigment concentrations  and  glutathione
     peroxidase activity in mice.   Fed. Proc. Fed. Am. Soc.  Exp. Biol. 36: 1095, 1977.

Ayaz, K.  L. ,  and  A. S.  Csallany.   Long-term N02  exposure of  mice  in  the presence and absence
     of  vitamin E.   II.  Effect  of  glutathione  peroxidase.   Arch.  Environ. Health 33:292-296,
     1978.

Azoulay, E.,  P. Soler, M.  C. Blayo, and F. Basset.  Nitric oxide effects on lung structure and
     blood oxygen affinity in rats.   Bull. Eur. Physiopathol.  Respir.  13:629-644,  1977.

Balchum,  0.  J.,  R.  D. Buckley,  R.  Sherwin, and M.  Gardner.   Nitrogen dioxide  inhalation  and
     lung antibodies.  Arch. Environ. Health 10:274-277, 1965.

Barnes,  J. M. ,  and P. N.  Magee.   Some toxic properties of  dimethylnitrosamine.  Br.  J.  Ind.
     Med. 11:167-174, 1954.

Bils, R.  F.   The  connective  tissues and alveolar  walls in the lungs of normal  and  oxidant-
     exposed squirrel monkeys.   J.   Cell Biol. 70:  318, 1976.

Blair, W.  H. ,  M.  C. Henry, and  R.   Ehrlich.  Chronic toxicity  of nitrogen dioxide.   II.  Effect
     on histopathology of  lung tissue.  Arch. Environ. Health  19:186-192, 1969.

Blank,  M.  L., W.  Dalbey,  P.  Nettesheim, J.  Price, D.  Creasia,  and  F.  Snyder.    Sequential
     changes  in phospholipid  composition and synthesis  in  lungs  exposed to nitrogen  dioxide.
     Am. Rev. Resp.  Dis.  117:273-280, 1978.
                                             14-110

-------
 Blach,  W.  N.,  Jr.,  S.  Lassiter, J.  F.  Stara, and T.  R.  Lewis.  Blood rheology of dogs chronic-
      ally exposed to air pollutants.   Toxicol.  Appl. Pharmacol. 25:576-581, 1973.

 Braughler, J.   M.,  C.   K.  Mittal, and  F.  Murad.  Effects  of  thiols,  sugars,  and proteins on
      nitric oxide  activation  of guanylate  cyclase.   J.  Biol.  Chem.   254:12450-12454,  1979.

 Buell,  G.  C.    Biochemical  parameters  in inhalation carcinogenesis.   In:   Inhalation Carcino-
      genesis,  Proceedings of  a Conference,  National Cancer  Institute  and Others, Gatlinburg,
      Tennessee, October 8-11,  1969.   M.  G.  Hanna, Jr.,  P.  Nettesheim, and J. R. Gilbert, eds.,
      AEC Symposium  Series  18,  U.S. Atomic  Energy Commission, Oak  Ridge  National Laboratory,
      Oak Ridge, TN,  April  1970.  pp.  209-228.

 Burch,  H.   Methods  for  Detecting and  Evaluating Ascorbic Acid Deficiency in Man and Animals.
      Ann.  N.Y.  Acad.  Sci.  92:268-276,  1961.

 Busey,  W.  M. ,  W. B.  Coate,  and  D.  W.  Badger.   Histopathologic effects  of  nitrogen dioxide
      exposure  and heat  stress  in cynomolgus monkeys.   Toxicol. Appl. Pharmacol. 29:130, 1974.

 Cabral-Anderson,  L.  J. ,  M.  J.  Evans,  and G.  Freeman.   Effects  of  NO, on  the  lungs of aging
      rats.   I.  Morphology.   Exp.  Mol.  Pathol.  27:353-365,  1977.       *

 Campbell,  K.  I.  Effect of  exposure  to  nitrogen dioxide on  swimming endurance in rats.   Clin.
      Toxicol.  9:937-942, 1976.

 Carson,  T.  R. , M. S.  Rosenholtz, F.  T.  Wilinski, and  M.  H.  Weeks.   The  responses of animals
      inhaling   nitrogen  dioxide  for  single, short-term  exposures.   Am.  Ind.  Hyg.  Assoc.  J.
      23:457-462,  1962.

 Challis,  B. C.,  and  S.  A.  Kyrtopoulos.   Rapid formation of  carcinogenic N-nitrosamines  in
      aqueous alkaline  solutions.   Br.  J.  Cancer  3_5:693-696,  1977.

 Charles,  J. M. ,  and D.  B.  Menzel.   Ammonium and sulfate  ion release  of  histamine  from lung
      fragments.   Arch.  Environ. Health 30:314-316, 1975.

 Chen,  C. ,  S.  Kusumoto,  and  T.  Nakajima.   The recovery  processes  of histopathological changes
      in  the respiratory  organs of mice after N02 exposure  with special  reference to chronic
'  ;   trachititis  and bronchitis.   Osaka  Furitsu  Koshu Eisei  Kenkyusho Kenkyu Hokoku Rodo Eisei
    '  Hen  (10):43-49, 1972.

 Chow,  C.  K. ,  and A. L.  Tappel.  An enzymatic protective  mechanism  against lipid peroxidation
      damage to  lungs of ozone-exposed  rats.   Lipids  7:518-524,  1972.

 Chow,  C.  K. ,  C.  J.  Dillard,  and A.  L. Tappel.   Glutathione  peroxidase system and lysozyme in
      rats  exposed to ozone  or  nitrogen dioxide.   Environ.  Res.  Ij.311-319,  1974.

 Chow,  Y.  L.   Nitrosamine photochemistry:   reactions of ammonium radicals.  Accounts of Chem.
      Res.  6:354-360, 1973.

 Coate,  W.  B.,  and D.  W.  Badger.   Physiological   effects of  nitrogen dioxide exposure and heat
      stress in  cynomologus  monkeys.  Toxicol. and Appl.  Pharmacol. 29:130, 1974.

 Coffin,  D.  L. ,  and  E.  J. Blommer.  Acute  toxicity of irradiated  auto exhaust:   its indication
      by  enhancement  of mortality  from streptococcal  pneumonia.  Arch.   Environ.  Health  15:36-
      38, 1967.

 Coffin,  D.  L.  ,  and  D.  E.  Gardner.   Interaction  of  biological   agents and chemical  air
      pollutants.  Ann.  Occup.  Hyg. 15:219-234, 1972.


                                              14-111

-------
Coffin, D.  L. ,  and H. E.  Stokinger.   Biological  effects of  air  pollutants.   Li:   Air  Pollu-
     tion.  Volume  2:   The Effects of Air Pollution.  A. C.  Stern, ed. , Academic  Press,  Inc.,
     New York, NY, 1977.   pp. 231-360.

Coffin, D.  L. ,  D.  E.  Gardner, and E. J. Blommer.   Time-dose  response  for  nitrogen dioxide  ex-
     posure in  an  infectivity  model  system.   EHP  Environ.  Health  Perspect.  13:11-15,  1976.

Coffin, D. L. , D.  E. Gardner, G. I. Sidorenko, and M. A. Pinigin.  Role of time  as a  factor in
     the  toxicity  of chemical  compounds in intermittent and continuous  exposures.  Part  II.
     Effects of intermittent exposure.  J. Toxicol.  Environ.  Health 3:821-828, 1977.

Committee  on  the  Challenges  of  Modern  Society.   North  Atlantic Treaty Organization.   Air
     Quality Criteria for  Nitrogen Oxides.   NATO/CCMS-N. 15,  North  Atlantic Treaty  Organiza-
     tion, Berlin, Germany, June 1973.

Cooper,  G.  P.,  J.  P.   Lewkowski,  L .Hastings,  and  M.  Malanchuk.   Catalytically  and non-
     catalytically  treated  automobile  exhaust:   biological  effects  in  rats.    J.  Toxicol.
     Environ.  Health.  3:923-934, 1977.

Craddock,  V. M.   Liver  carcinomas induced in  rats  by single  administration of  dimethylnitro-
     samine after partial hepatectomy.  J. Natl. Cancer Inst.  U.S. 47:899-907, 1971.

Crapo, J.  D.,  K.  Sjostrom, and R. T.  Drew.   Tolerance and  cross-tolerance  using  N02 and  0^.
     I. Toxicology and biochemistry.   J. Appl. Physiol.:  Respirat. Environ. Exercise Physio!.
     44:  364-369,  1978.

Craven, P.  A. ,  and F.  R. DeRubertis.  Restoration of the responsiveness of purified  guanylate
     cyclase to  nitrosoguanidine, nitric  oxide,  and related  activators  by  heme  and hemepro-
     teins.   J.  Biol.  Chem. 253:8433-8443, 1978.

Creasia,  D.  A.   Stimulation of DNA synthesis in lungs of hamsters tolerant to nitrogen dioxide.
     J. Toxicol.  Environ. Health 4:755-762, 1978.

Crosby, N. T., and R.  Sawyer.  N-nitrosamines:  a review of chemical and biological properties
     and their estimation in foodstuffs.  Adv. Food Res. 22:1-71, 1976.

Csallany,  A. S.   The  effect of nitrogen dioxide on the growth of vitamin  E deficient, vitamin
     E supplemented and  DPPD supplemented mice.  Fed.  Proc.  Fed.  Am. Soc. Exp. Biol. 34:913,
     1975.                                                                             ~~

Csallany,  A. S.,  and  K.  L. Ayaz.  Long-term  N02  exposure of  mice in  the presence and absence
     of vitamin  E.   I.   Effect on body  weights and  lipofuscin in pigments.   Arch.  Environ.
     Health 33:285-291,  1978a.

Csallany,  A.  S.,  and K.  L.  Ayaz.   The effects of intermittent  nitrogen  dioxide  exposure  on
     vitamin E-deficient and -sufficient rats.  Toxicol. Lett. 2:97-107, 1978b.

Dalhamn,   T. ,  and  J.  Sjoholm.   Studies  on  S02, NOZ  and NHa:  effect on  ciliary  activity  in
     rabbit trachea of  single i_n vitro  exposure and  resorption in rabbit nasal cavity.  Acta
     Physiol.  Scand. 58:287-291, 19BT~

Davidson,  J. T., G. A. Lillington, G. B. Haydon, and K. Wasserman.  Physiologic  changes  in  the
     lungs of rabbits continuously exposed to nitrogen dioxide.  Am. Rev.  Respir.  Dis. 95:790-
     796,  1967.

Donovan,  D. H. , M.  B.  Abou-Donia, D.  E.  Gardner,  D.  L. Coffin, C. Roe, R. Ehrlich,  and D.  B.
     Menzel.  Effect  of  long-term low-level  exposures  of  nitrogen  dioxide on enzymatic indi-
     cators of damage.  Pharmacologist 18:244, 1976.

                                             14-112

-------
Drozdz, M.,  E.  Kucharz, K. Ludyga,  and  T.  Molska-Drozdz.  Studies  on  the  effect  of  long-term
     exposure  to  nitrogen  dioxide  on serum  and liver proteins  level  and enzyme activity  in
     guinea pigs.   Eur. J.  Toxicol.  Environ. Hyg. 9:287-293,  1976.

Drozdz, M.,  M. Luciak,  S. Kosmider,  T.  Molska-Drozdz,  K.  Ludyga,  and  J. Pasiewicz.   Brain
     enzymes  activity  and morphological  changes  in  central  nervous  system  of  guinea  pigs
     chronically  intoxicated  with nitrogen dioxide.  Bromat. Chem.  Toksykol. 8:241-249,  1975.

Druckrey,  H.,  R.   Preussmann,  G.  Blum,  S. Ivankovic,  and J.  Afkham.   Producing esophageal
     carcinomas by unsymetrical nitrosamines.  Naturwissenschaften  50:100-101,  1963.

Druckrey, H.,  R.  Preussmann,  S.  Ivankovic, D.  Schmahl,  J.  Afkham,  G.  Blum,  H. D. Mennel,  M.
     Miiller,  P.   Petropoulos,  and   H.  Schneider.   Organotropic  carcinogenic  effects  of  65
     different N-nitroso compounds in BD-rats.   Z.  Krebsforsch. 69:103-201, 1967.

Ehrlich,  R.    Effects  of  air  pollutants   on  respiratory  infection.   Arch.   Environ.  Health
     6:638-642, 1963.

Ehrlich,  R.   Effect  of  nitrogen  dioxide on resistance  to  respiratory infection.   Bacteriol.
     Rev.  30:604-614, 1966.

Ehrlich,  R.    Interaction  between N02  exposure  and respiratory  infection.    In:   Scientific
     Seminar on Automotive  Pollutants, U.S. Environmental Protection Agency, Washington,  D.C.,
     February   10-12,  1975.    EPA-600/9-75-003,   U.S.    Environmental   Protection  Agency,
     Washington, DC,  February 1975.   Section 3h.

Ehrlich,  R.    Interaction  between environmental  pollutants and  respiratory  infections.    In:
     Proceedings of the Symposium on Experimental Models  for  Pulmonary  Research, U.S. Environ-
     mental Protection  Agency,  Hilton Head Island,  South Carolina,  February 5-7,  1979.   D.  E.
     Gardner, E.  P.  C. Hu,  and J.  A.  Graham, eds.,  EPA-600/9-79-022,  U.S. Environmental Protec-
     tion Agency,  Research Triangle  Park, NC, June  1979.  pp. 145-163.

Ehrlich,  R.,  and  J.  D. Fenters.   Influence of  nitrogen  dioxide  on experimental   influenza  in
     squirrel monkeys.  In:  Proceedings of the  Third International  Clean Air Congress, Inter-
     national  Union  of ~A~ir Pollution Prevention Associations,  Dusseldorf,  Germany, October
     8-12, 1973.   Verein Deutscher Ingenieure, Dusseldorf, Germany,  1973.   pp.  A11-A13.

Ehrlich, R., and M.  C. Henry.   Chronic toxicity  of  nitrogen dioxide.  I.  Effect on resistance
     to bacterial  pneumonia.  Arch.   Environ. Health  17:860-865, 1968.

Ehrlich,  R. ,  and  S.  Miller.   Effect  of  N02 on airborne Venezuelan equine encephalomyelitis
     virus.   Appl. Microbiol.  23:481-484, 1972.

Ehrlich, R. , J. C.  Findlay, and D.   E. Gardner.   Effects of repeated  exposures  to  peak concen-
     trations  of  nitrogen  dioxide  and  ozone  on  resistance  to  streptococcal  pneumonia.   J.
     Toxicol.  Environ. Health 5:631-642,  1979.

Ehrlich, R. , J. C.  Findlay, J.  D. Fenters, and D.   E. Gardner.   Health effects of short-term
     exposures to  inhalation of N0p-03 mixtures.  Environ. Res.  14:223-231, 1977.

Ehrlich,  R. ,  E.  Silverstein,  R.  Maigetter, J.  D.   Fenters,  and  D.  E.  Gardner.   Immunologic
     response in vaccinated mice during long-term exposure to nitrogen dioxide.  Environ.  Res.
     10:217-223,  1975.

Emik, L.  0.,  R.  L.  Plata,  K.  I.  Campbell,  and G.  L. Clarke.  Biological effects  of  urban air
     pollution.  Riverside summary.   Arch.   Environ.  Health 23:335-342, 1971.
                                             14-113

-------
Evans, M.  J. ,  L.  J.  Cabral-Anderson, and G.  Freeman.   Effects of N02  on the lungs of  aging
     rats.   II. Cell proliferation.  Exp. Mol. Pathol. 27:366-376, 1977.

Evans, M. J.,  L.  J. Cabral-Anderson, and G. Freeman.  Role of the Clara  cell  in renewal of  the
     bronchiolar epithelium.  Lab. Invest. 38:648-655, 1978b.

Evans, M.  J. ,  L.   J.  Cabral,  R.  J.  Stephens,   and G.  Freeman.   Cell  division of alveolar
     macrophages in rat  lung  following exposure  to NCy   Am.  J.  Pathol. 70:199-208, 1973a.

Evans, M. J.,  L.  J. Cabral, R. J. Stephens, and G. Freeman.  Renewal of  alveolar  epithelium in
     the  rat following exposure to N02-  Am.  J. Path. 70: 175-190, 1973b.

Evans, M. J. ,  L.  J. Cabral,  R.  J.  Stephens,  and G.  Freeman.   Acute  kinetic response and  re-
     newal  of the alveolar epithelium following injury by nitrogen dioxide.   Chest 65:562-565,
     1974.                                                                          ~~

Evans, M. J.,  L.  J. Cabral, R. J. Stephens, and G. Freeman.  Transformation of alveolar Type  2
     cells  to  Type 1  cells following  exposure  to  NCL.   Exp.  Mol.  Pathol.   22:142-150,  1975.

Evans, M. J. ,  N.  P. Dekker, L. J. Cabral-Anderson,  and G. Freeman.  Quantisation of damage to
     the  alveolar  epithelium by  means of type  2 cell proliferation.   Am.   Rev.  Respir.  Dis.
     118:787-790, 1978a.

Evans, M.  J.,  L.   V.  Johnson,  R.  J.  Stephens,  and G.  Freeman.   Renewal  of  the terminal
     bronchiolar  epithelium  in  the   rat  following exposure  to  NO,  or Ov   Lab.  Invest.
     35:246-257,  1976.                                               *       d

Evans, M. J.,  R.  J. Stephens, L. J. Cabral, and G. Freeman.  Cell renewal  in  the  lungs of rats
     exposed to low levels of N02-  Arch. Environ. Health 24:180-188,  1972.

Fairchild,  E.  J.,   II,  and S.  L.  Graham.   Thyroid  influence on  the  toxicity of respiratory
     irritant gases,  ozone  and nitrogen dioxide.  J. Pharmocol. Exp.  Ther. 139:177-184,  1963.

Fairchild,  E.  J. ,  II,  S.  D.  Murphy, and H.  E.  Stokinger.   Protection  by  sulfur compounds
     against the air  pollutants ozone and nitrogen  dioxide.   Science  (Washington, D.C.) 130:
     861-862,  1959.

Fairchild,  G.   A.,  J.  Roan, and J. McCarroll.  Atmospheric pollutants and the pathogenesis of
     viral  respiratory infection.   Sulfur dioxide   and  influenza infection  in  mice.    Arch.
     Environ.  Health 25:174-182, 1972.

Fenters,  J.  D., R.  Ehrlich, J. C. Findlay, J.  Spangler, and V. Tolkacz.   Serologic response in
     squirrel  monkeys  exposed  to nitrogen dioxide and influenza virus.   Am.  Rev. Respir. Dis.
     104:448-451, 1971.

Fenters,  J. D. ,  J.  C.  Findlay, C. D.  Port, R. Ehrlich, and D. L. Coffin.  Chronic exposure to
     nitrogen   dioxide:   immunologic,  physiologic, and  pathologic  effects in virus-challenged
     squirrel  monkeys.  Arch. Environ. Health 22:85-89, 1973.

Fine, D.  H. ,  D. P.  Rounbehler, N. M.  Belcher, and S.  S. Epstein.  N-nitroso compounds:  detec-
     tion in ambient air.   Science (Washington, D.C.) 192: 1328-1330,  1976.

Fletcher, B.  L.,  and A. L. Tappel.  Protective effects of dietary a-tocopherol in rats exposed
     to toxic levels of ozone and nitrogen dioxide.   Environ. Res. 6:165-175, 1973.

Freeman,  G.,  and G. B. Haydon.  Emphysema after low-level exposure to  nitrogen dioxide.   Arch.
     Environ.  Health 8:125-128, 1964.


                                             14-114

-------
Freeman, G., and L. T. Juhos.  Trace  Substances  and  Tobacco Smoke in Interaction with Nitrogen
     Oxides:   Biologic   Effects.   EPA-600/1-76-021,  U.S.  Environmental  Protection  Agency,
     Research Triangle Park, NC, April  1976.

Freeman, G.,  S.  C.  Crane, and N.  J.  Furiosi.   Healing  in rat  lung after subacute exposure to
     nitrogen dioxide.  Am.  Rev. Respir.  Dis.  100:662-676,  1969a.

Freeman, G. ,  N.  J.  Furiosi, and G.  B.  Haydon.  Effects  of continuous  exposure of 0.8 ppm NO-
     on respiration of rats.  Arch. Environ.  Health  13:  454-456,  1966.

Freeman, G. ,  R.  J.  Stephens, and  N.  J.  Furiosi.   The  subacute  nitrogen dioxide-induced lesion
     of the rat lung.  Arch. Environ. Health  18:609-612,  1969b.

Freeman,  G. ,  S.  C.  Crane,  R.  J. Stephens, and  N.  J.   Furiosi.   Environmental  factors  in
     emphysema and a model system  with  NO-.   Yale  J. Biol.  Med. 40:566-575,  1968a.

Freeman, G. ,  S.  C.  Crane,  R. J.  Stephens, and N.  J.  Furiosi.   Pathogenesis  of  the nitrogen
     dioxide-induced  lesion  in  the rat  lung:   a review and presentation of new observations.
     Am. Rev.  Respir. Dis. 98:429-443,  1968b.

Freeman, G. ,  R.  J.  Stephens, S. C. Crane,  and N.  J. Furiosi.   Lesion of the lung in rats con-
     tinuously exposed  to two  parts  per million  of nitrogen  dioxide.    Arch.  Environ.  Health
     17:181-192, 1968c.

Freeman, G., L.  T.  Juhos,  N. J. Furiosi,  R. Mussenden, and T. A.  Weiss.   Delayed maturation of
     rat lung in  an environment containing nitrogen dioxide.   Am.  Rev.  Respir.  Dis. 110:754-
     759, 1974b.

Freeman, G. , S.  C.  Crane,  N. J. Furiosi,  R. J. Stephens,  M.  J.  Evans, and W.  D.  Moore.   Covert
     reduction in  ventilatory  surface  in  rats during  prolonged exposure  to  subacute nitrogen
     dioxide.   Am.  Rev. Respir. Dis.  106:563-579,  1972.

Freeman, G. ,  L.  T.  Juhos,  N.  J.   Furiosi,  R.  Mussenden,  R.   J.  Stephens,   and  M.   J.  Evans.
     Pathology of  pulmonary disease  from  exposure  to interdependent ambient  gases  (nitrogen
     dioxide and ozone).    Arch. Environ.  Health  29:203-210,  1974a.

Freund, H.  A.   Clinical  manifestations  and  studies  in  parenchymatous  hepatitis.   Ann.  Int.
     Med.  10:1144-1155, 1937.

Fukase,  0. ,  K.   Isomura,  and  H.  Watanabe.    Effects  of  nitrogen  oxides  on  peroxidative
     metabolism of mouse  lung.  Taiki Osen  Kenkyu  11:  65-69, 1976.

Furiosi, N.  J.,  S.  C.  Crane,  and G.  Freeman.    Mixed  sodium chloride  aerosol and nitrogen
     dioxide in air:   biological  effects  on  monkeys and rats.   Arch.  Environ.  Health 27:405-
     408,  1973.

Gardiner,  T. H., and L.   S.  Schanker.   Effect of oxygen  toxicity  and nitric acid-induced lung
     damage on  drug  absorption from  the  rat  lung.   Res.  Commun.  Chem.  Pathol.  Pharmacol.
     15:107-120, 1976.

Gardner, D.  E. ,  and J.   A.   Graham.    Increased pulmonary  disease  mediated through  altered
     bacterial defenses.    I_n:   Pulmonary Macrophage and  Epithelial Cells, Proceedings  of the
     Sixteenth Annual  Hanford Biology  Symposium,  Energy Research  and  Development  Administra-
     tion  and  Others,  Richland,  Washington, September  27-29,  1976.   C.  L.  Sanders,  R.  P.
     Schneider,  G.   E.  Dagle, and  H.  A.  Ragan, eds. , ERDA  Symposium Series 43,  Energy Research
     and Development Administration,  Oak  Ridge,  TN,  September 1977.   pp.  1-21.
                                             14-115

-------
Gardner,  D.  E. ,   R.  S.  Holzman,  and  D.  L.  Coffin.   Effects  of nitrogen dioxide  on  pulmonary
     cell population.  J. Bacteriol.  98:1041-1043,  1969.

Gardner, D. E., D. L. Coffin, M.  A. Pinigin, and G.  I.  Sidorenko.   Role  of  time  as a  factor in
     the  toxicity of chemical  compounds in  intermittent and  continuous exposures.    Part I.
     Effects of continuous exposure.  J. Toxicol.  Environ. Health  3:811-820,  1977a.

Gardner, D. E., F. J. Miller, E.  J. Blommer, and D.  L.  Coffin.   Relationships between nitrogen
     dioxide  concentration,  time, and level of effect  using  an animal  infectivity model.   _In:
     International Conference on  Photochemical Oxidant  Pollution and  Its  Control,  Proceedings:
     Volume  I,  U.S.  Environmental  Protection Agency  and Others,   Raleigh,  North  Carolina,
     September  12-17,  1976.   B.  Dimitriades,  ed.,  EPA-600/3-77-001a,  U.S.   Environmental
     Protection Agency, Research  Triangle Park, NC,  January 1977b.  pp.  513-525.

Gardner, D.  E. ,  F.  J. Miller, E. J.  Blommer,  and  D.  L. Coffin.  Influence  of exposure mode on
     the toxicity of  N02-  EHP Environ.  Health Perspect.  30:23-29,  1979.

Gardner,  D.   E. ,  J.   A.  Graham  J.  W.  Illing, E.   J.  Blommer,  and  F.  J.  Miller.   Impact  of
     exposure  patterns  on  the   toxicological  response  to  N02  and modifications  by  added
     stressors.   EHP  Environ. Health  Perspect., in  press, 1982.

Gehlert, P.,  and  W.  Rolle.   Formation of  diethylnitrosamine  by reaction of  diethylamine with
     nitrogen dioxide in the gas  phase.  Experentia 3_3: 579-581,  1977.

Gillespie, J.  R.  , J.  D.  Berry,  and  J.  F.  Stara.   Pulmonary  function  changes in the  period
     following  termination  of air  pollution  exposure  in  beagles.    Am.  Rev.  Respir.  Dis.
     113:92, 1976.

Giordano,  A.  M.,  Jr.,   and  P.  E.  Morrow.   Chronic low-level   nitrogen  dioxide exposure  and
     mucociliary  clearance.  Arch. Environ. Health  25:443-449,  1972.

Goldstein,  B.  D.   Combined  exposure to  ozone and nitrogen  dioxide.   EHP Environ.  Health
     Perspect. 30:87-89, 1979.

Goldstein,  B.  D. ,  S.  J.  Hamburger,  G. W.  Falk,  and M.  A.  Amoruso.   Effect  of  ozone  and
     nitrogen  dioxide on  the agglutination  of rat alveolar macrophages  by concanavalin  A.
     Life Sci. 21:1637-1644, 1977a.

Goldstein, B. D. ,  L.  Y.  Lai, S.  R.  Ross,  and R.  Cuzzi-Spada.   Susceptibility of  inbred mouse
     strains to ozone.  Arch. Environ. Health. 27:   412-413, 1973a.

Goldstein,  E.,  M.  C. Eagle,  and P.  D.  Hoeprich:   Effect  of  nitrogen  dioxide on  pulmonary
     bacterial defense mechanisms.  Arch. Environ.   Health 26: 202-204, 1973b.

Goldstein,  E. ,  D.  Warshauer, W.  Lippert,  and B.  Tarkington.   Ozone  and   nitrogen  dioxide
     exposure.  Murine  pulmonary defense  mechanisms.  Arch.  Environ.  Health 28:85-90,  1974.

Goldstein, E. , N.  F.  Peek,  N. J.  Parks, H.  H. Hines,  E. P.  Steffey, and B.  Tarkington.   Fate
     and  distribution of inhaled nitrogen  dioxide  in  rhesus  monkeys.   Am.   Rev.  Respir.  Dis.
     115:403-412, 1977b.

Gooch,  P.  C. ,  H. E.  Luippold,  D.   A.  Creasia,  and  J.  G.   Brewen.   Observations  on  mouse
     chromosomes   following nitrogen dioxide inhalation.   Mutat.  Res.  48:117-120,  1977.
                                             14-116

-------
Graham, J. A.  Alteration  of  hepatic xenobiotic  metabolism  by  ozone.   Ph.D.  Dissertation,  Duke
     Univ., 1979.

Gray,  E.  L.,  J.  K. MacNamee,  and  S.  B. Goldberg.   Toxicity of  N02  vapors  at very low levels.
     A preliminary report.  AMA Arch.  Ind.  Hyg.  Occup.  Med. 6:20-21,  1952.

Greene,  N. D. ,  and  S.  L.  Schneider.   Effects of  N0j> on  the response  of baboon  alveolar
     macrophages to migration  inhibitory  factor.  J.  Toxicol.  Environ.  Health 4:869-880,  1978.

Guidotti,  T.  L. ,  and  A.   A.  Liebow.    Toxic  inhalation of nitrogen  dioxide  in  canines,   In:
     International Conference  on Photochemical Oxidant  Pollution and  Its  Control,  Proceedings:
     Volume  I,  U.S.  Environmental  Protection  Agency  and Others,   Raleigh,  North  Carolina,
     September  12-17,  1976.   B.  Dimitriades,  ed. ,  EPA-600/3-77-001a,  U.S.   Environmental
     Protection Agency, Research Triangle  Park,  NC,  January 1977.  pp.  545-553.

Hacker,  A. D. ,  N.  El  Sayed,  M.   G.   Mustafa,  J.   J.  Ospital,   and  S.  D.   Lee.   Effects  of
     short-term nitrogen  dioxide  exposure  on  lung  collagen synthesis.  Am.  Rev.  Respir.  Dis.
     113:107, 1976.

Hackett,  N.  A.   Cell  renewal of  Chinese hamster  lung  and   trachea  following  N0?  exposure.
     Annual Meeting Supplement, Am. Rev.  Resp. Dis.  117(4):25, 1978.   (Abstr.)

Hadley, J. G. ,  D.  E.  Gardner, D.  L.  Coffin, and D.  B. Menzel.   Effects  of  ozone  and nitrogen
     dioxide  exposure  of  rabbits  on  the  bindings  of   autologous  red  cells  to   alveolar
     macrophages.  Jn:   International  Conference on Photochemical  Oxidant Pollution and  Its
     Control,  Proceedings:    Volume   I,   U.S.   Environmental   Protection  Agency  and Others,
     Raleigh, North Carolina,  September 12-17,  1976.   B. Dimitriades,  ed.,  EPA-600/3-77-001a,
     U.S.  Environmental  Protection Agency,  Research  Triangle  Park, NC,  January 1977.   pp.
     505-512.

Hatton,  D.  V.,  C.  S.  Leach,  A.  E.  Nicogossian, and N.  Di Ferrante.  Collagen breakdown  and
     nitrogen dioxide inhalation.    Arch.  Environ. Health 32:33-36, 1977.

Hattori, S.  Changes  in  the bronchial  alveoli  due  to polluted  air  (an experimental  inquiry).
     Clinician (219):4-8,  1973.

Hattori,  S. ,  and  K.  Takemura.   Ultrastructural changes  in  the bronchiolar alveolar  system
     caused  by  air  pollution and  smoking.  Nippon  Rinsho Denshikenbikyo  Gakkai Shi  6:350,
     1974.

Haydon, G.  B.,  G.  Freeman, and N.  J. Furiosi.  Covert pathogenesis of  N0? induced  emphysema in
     the rat.   Arch.  Environ.  Health 11:776-783,  1965.                  *

Heath,   D.  F. ,  and P.  N.  Magee.    Toxic  properties  of dialkylnitrosamines  and  some related
     compounds.   Br.  J.  Ind. Med.  19:276-282, 1962.

Henry,   M.  C. ,  R.  Ehrlich,  and W.  L. Blair.   Effect of  nitrogen  dioxide  on  resistance  of
     squirrel  monkeys  to  Klebsiella pneumoniae  infection.  Arch.  Environ.  Health 18:580-587,
     1969.

Henry,  M.  C. , J.  Findlay,  J.  Spangler,  and R.  Ehrlich.  Chronic toxicity  of N02  in  squirrel
     monkeys.   Arch.  Environ.  Health 20:566-570,  1970.

Henry,   M.  C. ,  J.  Spangler,  J.   Findlay,  and  R. Ehrlich.    Effects of  nitrogen  dioxide  and
     tobacco  smoke  on  retention  of  inhaled   bacteria.   Proceedings  Third   International
     Symposium on Inhaled Particles 1:527-533, 1971.
                                             14-117

-------
Henschler, D. , and  W.  Ross.   On the  problem of the carcinogenic  effect  of inhaled oxides of
     nitrogen.  Naunyn Schmiedebergs Arch. Exp. Pathol. Pharmakol.  253:495-507, 1966.

Mine, C.  H.,  F.  H.  Meyers, and R. W. Wright.   Pulmonary changes in animals  exposed  to nitrogen
     dioxide, effects of acute exposures.  Toxicol. Appl. Pharmacol. 16:201-213, 1970.

Hoefel, 0.  S.   Plasma  Vitamin  C  Levels  in Smokers.   Int.  J.  Vitam.  Nutr.  Res.   16:127-137,
     1977.

Hugod, C.   Effect  of exposure to 43  ppm  nitric oxide and 3.6  ppm nitrogen dioxide on  rabbit
     lung.  Int.  Arch. Occup. Environ. Health 42:159-167, 1979.

Hyde, D.,  J.  Orthoefer, D. Dungworth, W. Tyler, R. Carter, and H.  Lum.  Morphometric and morpho-
     logic evaluation  of  pulmonary lesions  in beagle dogs chronically exposed to high ambient
     levels of air pollutants.  Lab. Invest.  38:455-469, 1978.

Hysell, D.  K. ,  W.   Moore,  R. Hinners,  M.  Malanchuk,  R.  Miller, and  J.  F.  Stara.    Inhalation
     toxicology of  automotive emissions  as  affected  by  an oxidation  exhaust catalyst.   EHP
     Environ. Health Perspec. 10:57-62, 1975.

Ide, G. ,  and  H.  Otsu.   A study on the carcinogenic action of pollutants.   In:  Investigations
     of Air  and Water Pollution on Human Health.   Chiga Prefectural Government (Japan), Dept.
     Hyg.  1973.   pp. 99-100.

Illing, J.   W. ,  F.  J.  Miller,  and  D.  E.  Gardner.   Decreased  Resistance  to  Infection in
     Exercised Mice Exposed to N02 and 03-   J.  Toxicol. Envon. Health. 6:843-851, 1980.

Iqbal, Z.  M. ,  K.   Dahl,  S.   S.  Epstein.    Role  of  nitrogen  dioxide in the  biosynthesis of
     nitrosamines in mice.  Science (Washington, D.C.) 207:1475-1477, 1980.

Ito, K.   Effect of nitrogen  dioxide  inhalation on influenza virus infection in mice.   Nippon
     Eiseigaku Zasshi 26:304-314, 1971.

Ivankovic, S., and H. Druckrey.   Transplacental induction of malignant tumours of the nervous-
     system.   I.   Ethyl-nitroso-urea  (ENU)  in BD-IX-rats.  Z.  Krebforsch. 71:320-360, 1968.

Katz, G.  V.,  and S. Laskin.   Pulmonary macrophage  response to irritant gases.  Jji:   Air  Pollu-
     tion  and  the   Lung,  Proceedings  of  the Twentieth Annual  "OHOLO"  Biological  Conference,
     Israel   Institute for  Biological  Research,  Ma'alot,  Israel,  March  16-19, 1975.   E. F.
     Aharonson,  A.  Ben-David,  M.   A.  Klingberg,   and M.  Kaye,  eds., Keter  Publishing House
     Jerusalem Ltd., Jerusalem,  Israel, 1976.  pp. 83-100.

Kaut,  U.   Formation  of  nitrosamines  (in  lung tissue)  after  inhalation of  nitrogen oxides.
     Cesk. Hyg.  15:213-215,  1970.

Kaut, V.,  M.  Tusl,  S. Svorcova,  and M. Tomana.   Some changes in the rat organism following the
     low nitrogen oxides concentrations inhalation.  Cesk. Hyg. 11:479-485, 1966.

Kim, J. C. S.   Virus activation by Vitamin  A and  N0? gas exposures in hamsters.  EHP Environ.
     Health Perspect. 19:317-320, 1977.

Kim, J. C. S.   The effect of dietary vitamin A on N0? exposure on the hamster lung.  Environ.
     Res.  17:116-130, 1978.

Kita,  H. ,  and S.  Omichi.   Effects  of air  pollutants  on cilia movement in airways.   Nippon
     Eiseigaku Zasshi 29:100, 1974.
                                             14-118

-------
Kle.inerman, J.   Some  effects of nitrogen  dioxide  on the lung.   Fed.  Proc.  Fed.  Am.  Soc.  Exp.
     Biol. 36:1714-1718, 1977.

Kleinerman, J. , and M. P. C.  Ip.  Effects  of  nitrogen dioxide  on  elastin  and collagen contents
     of lung.   Arch. Environ. Health 34:228-232, 1979.

Kleinerman, J. ,  and D.  Niewoehner.   Physiological,  pathological, and morphometric studies  of
     long-term  nitrogen dioxide  exposure  and  recovery  in  hamsters.   Am.  Rev.  Respir.  Dis.
     107:1081, 1973.

Kleinerman, J. ,  and D.  Rynbrandt.   Lung  proteolytic activity  and serum protease  inhibition
     after N02 exposure.  Arch. Environ. Health 31:37-41, 1976.

Kleinerman, J. ,  D.  Rynbrandt,  and  J.  Sorensen.   Chronic  obstructive airway disease  in  cats
     produced by NO,.   Am.  Rev. Respir. Dis.  113:107, 1976.
                   C.                          	

Kosmider,  S.    Electrolytes  and  lipid  disturbances  in chronic  intoxication  with  nitrogen
     oxides.   Int.  Arch. Occup. Environ. Health 35:  217-232, 1975.

Kosmider,  S. ,  and  M.  Chorazy.   Electrolyte  disorders  in chronic experimental poisoning  with
     nitrogen oxides.   Patol. Pol.  26:47-53,  1975.

Kosmider,  S. ,  M.  Luciak,  and M.  Drozdz.   The influence of  ammonia  on  some disturbances  in
     protein carbohydrate  and lipid metabolism caused by chronic  intoxication with combustion
     gases.  Int. Arch. Occup. Environ. Health. 35:37-59, 1975.

Kosmider,  S. ,  M.  Luciak,  K.  Zajusz,  A.  Misiewicz, and  J.  Szygula.   Studies on emphysogenic
     action of nitrogen oxides.  Patol. Pol.  24:107-125,  1973a.

Kosmider,  S. ,  A.  Misiewicz,  E.  Felus, M.  Drozdz,  and  K.  Ludyga.   Experimental and  clinical
     studies  on  the effects  of  nitrogen  oxides on  immunity.   Int. Arch Arbeitsmed.  3_l:9-23,
     1973b.

Kuraitis,  K.  V. ,  A.   Richters,  and  R.  P.  Sherwin.  Decrease  in spleen weights  and  spleen
     lymphoid   nodules  following  exposure  to 0.34  ppm  nitrogen  dioxide (N09).   Fed.  Proc.
     Fed.  Am.  Soc.  Exp. Biol. 38:1352, 1979.                                   *

Langloss,  J.  M. ,  E.  A.  Hoover,  and D. E.  Kahn.   Diffuse alveolar damage  in cats induced  by
     nitrogen  dioxide or feline calicivirus.  Am.  J. Pathol. 89:637-644,  1977.

Larsen,  R. I., D. E. Gardner, and D. L. Coffin.  An  air quality data analysis  system  for inter-
     relating  effects,  standards,  and  needed source reductions.   Part  5:   N0? mortality  in
     mice.  J.  Air  Pollut.  Control  Assoc.  29:133-137, 1979.

Law, F.  C. P. ,  J.  C.  Drach,  and J.  E.  Sinsheimer.  Effects of nitrogen  dioxide  and  3-methyl-
     cholanthrene on pulmonary enzymes.  J. Pharm.  Sci.  64:1421-1422,  1975.

Lee, S.  D. , M.  Malanchuk,  and V.  N. Finelli.  Biologic effects of  auto emissions.  I.  Exhaust
     from engine with and without catalytic converter.  J. Toxicol. Environ.  Health 1:705-712,
     1976.

Lewis,  T.  R. ,  W.  J.  Moorman, W.  F.  Ludmann, and K.  I.  Campbell.   Toxicity  of  long-term
     exposure  to oxides of sulfur.   Arch Environ.  Health 26:16-21,  1973.

Lewis,  T.  R., W. J.  Moorman, Y.-Y.  Yang,  and J. F.  Stara.  Long-term  exposure to auto exhaust
     and other pollutant mixtures.   Arch.  Environ.  Health 29:102-106,  1974.
                                             14-119

-------
Lijinsky, W.,  L.  Tomates,  and C.  E.  M.  Wenyar.   Lung tumors  in  rats treated with  N-nitroso-
     heptamethyleneimine  and  N-nitrosooctamethylene.   Proc.  Soc.   Exp.  Biol.  Med.  130:945,
     1969.

Loosli,  C.  G. , R.  D.  Buckley,  M.  S. Hertweck,  J.  D.  Hardy, D. P.  Ryan,  S. Stinson, and  R.
     Serebrin.    Pulmonary  response  of  mice  exposed to  synthetic  smog.   Ann.  Occup.   Hyg.
     15:251-261, 1972.

Lunan,  K.  D.,  P.   Short,  D.  Negi,  and  R.  J.  Stephens.   Glucose-6-phosphate  dehydrogenase
     response  of  postnatal  lungs  to  N02  and 03.   In:   Pulmonary  Macrophage and  Epithelial
     Cells, Proceedings of the Sixteenth Annual Hanford Biology Symposium,  Energy Research and
     Development Administration  and Others,  Richland, Washington,  September 27-29, 1976.   C.
     L.  Sanders,  R.  P.  Schneider,  G.  E.  Dagle,  and H.  A.  Ragan, eds. ,  ERDA  Symposium Series
     43,  Energy Research  and Development Administration, Oak  Ridge, TN, September  1977.  pp.
     236-247.

MacQueen, J.,  and  D.  Plant.   A  review of  the clinical  applications  and methods  for cholines-
     terase.   Am.  J. Med.  Technol.  39:279-287, 1973.

Magee, P. N., and J. M. Barnes.  The experimental production of tumors in the  rat by dimethyl-
     nitrosamine (N-nitroso dimethylamine).   Acta Unio Int. Cancrum  15:187-190,  1959.

Magee, P. N. ,  R.  Montesano,  and R.  Preussmann.   N-nitroso compounds and related carcinogens.
     In:    Chemical  Carcinogens.   C.  E.  Searle,  ed.,  ACS Monograph 173,  American  Chemical
     Society, Washington,  DC, 1976.  pp.  491-625.

Matsumura, Y.   The  effects of ozone,  nitrogen dioxide,  and sulfur  dioxide  on the experiment-
     ally induced allergic  respiratory disorder in  guinea  pigs.   I. The effect  on  sensitiza-
     tion  with an  albumin  through the  airway.   Am.  Rev.  Respir.  Dis.  102:430-437, 1970a.

Matsumura, Y.  The effects of ozone, nitrogen dioxide and sulfur dioxide on  the  experimentally
     induced allergic  respiratory  disorder in guinea pigs.  III. The effect  on  the  occurrence
     of dyspneic attacks.   Am. Rev. Respir. Dis.  102:444-447,  1970b.

Matsumura,  Y. ,  K.  Mizuno,  T.  Miyamoto,  T.  Suzuki,  and  Y.  Oshima.   The  effects of ozone,
     nitrogen dioxide, and  sulfur  dioxide  on experimentally induced  allergic  respiratory  dis-
     order in  guinea  pigs.   IV.  Effects on respiratory  sensitivity to  inhaled  acetylcholine.
     Am.  Rev. Respir.  Dis.  105:262-267, 1972.

McCann, J., E.  Choi, E. Yamasaki, and  B.  N. Ames.  Detection of carcinogens  as mutagens in the
     Salmonella/microsome  test:    assay   of  300  chemicals.   Proc.   Natl.  Acad.  Sci. U.S.A.
     72:5135-5139, 1975.

McLean,  E. ,  G.  Bras,  and  A.  E. M.  McLean.  Venous occlusions  in the  liver  following dimethyl-
     nitrosamine.   Br. J.  Exp. Pathol. 46:367-369, 1965.

Menzel,  D.  B.   Toxicity  of  ozone,  oxygen  and radiation.   Annu.  Rev.  Pharmacol.  10:379-394,
     1970.

Menzel,  D. B.   The  role  of  free radicals  in the toxicity  of  air  pollutants  (nitrogen oxides
     and  ozone).   In:  Free  Radicals  in Biology.   Volume II.   W.  Pryor, ed., Academic Press,
     Inc., New York, NY,  1976.  pp. 181-202.

Menzel,  D. B.   Parmacological  mechanisms in  the toxicity of nitrogen dioxide  and its  relation
     to  obstructive respiratory  disease.    In:  Nitrogen  Oxides  and Their Effect on Health,  A
     Symposium  from a  Joint  Conference,  American  Chemical  Society and Chemical  Society  of
     Japan,  Honolulu,  Hawaii,  April 4-5, 1979.  S.  D. Lee, ed. , Ann  Arbor  Science Publishers,
     Inc., Ann Arbor, MI,  1980.  pp. 199-216.

                                              14-120

-------
Menzel, D. B., J. N.  Roehm,  and  S.  D.  Lee.   Vitamin  E:   the  biological  and environmental  anti-
     oxidant.  J. Agric.  Food  Chem.  20:481-486,  1972.

Menzel, D. B. , M. B.  Abou-Donia,  C.  R.  Roe,  R.  Ehrlich,  D. E.  Gardner,  and D.  L.  Coffin.   Bio-
     chemical  indices of  nitrogen dioxide  intoxication of  guinea pigs following  low  level  -
     long term exposure,   Iji:  International  Conference  on Photochemical  Oxidant Pollution and
     Its  Control,  Proceedings:   Volume II,  U.S.  Environmental  Protection Agency  and  Others,
     Raleigh,  North Carolina, September 12-17,  1976.   B.  Dimitriades  ed. ,  EPA-600/3-77-001b,
     U.S. Environmental  Protection Agency,  Research  Triangle Park,  NC,  January 1977.   pp.  577-
     587.

Mersch, J. ,  B.  J.  Dyce,  B.  J. Haverback and R.  P. Sherwin.   Diphosphoglycerate content of red
     blood  cells.   Measurements  in guinea  pigs  exposed to 0.4 ppm nitrogen  dioxide.   Arch.
     Environ. Health  27:94-95, 1973.

Miller, F.  J. ,  J.  A.  Graham,  J.  W. Illing,  and  D.  E. Gardner.   Extrapulmonary effects of N02
     as  reflected  by pentobarbital-induced  sleeping time  in  mice.   Tox.  Lett.   6:267-274,
     1980.

Mintz, S.   N0£ toxicity  in alveolar macrohpages:   a  mitochondrial  lesion.   Chest 62:382,  1972.

Mirvish, S.  S.   Kinetics of N-nitrosation  reaction  to tumorigenesis experiments with  nitrite
     plus amines  or ureas,   hi:    N-nitroso  Compounds  Analysis and  Formation,  Proceedings  of  a
     Working  Conference,  International  Agency  for  Research on  Cancer,  Heidelberg, Germany,
     October  13-15, 1971.   P.  Bogovski, R.  Preussman,  E.  A. Walker, and  W.  Davis,  eds.,  IARC
     Scientific Publications No.   3,  International  Agency for Research on  Cancer,  Lyon,  France,
     1972.  pp. 104-108.

Mirvish, S.  S.   Formation of  N-nitroso compounds: chemistry,  kinetics  and i_n vivo  occurrence.
     Toxicol. Appl.  Pharmacol. 31:325-351,  1975.

Mirvish,  S.   S.   N-Nitroso  compounds:   their  chemical  and i_n  vitro  formation and possible
     importance as  environmental  carcinogens.  J. Toxicol.  Environ. Health 2:1267-1277,  1977.

Mitina,  L.  S.   The  combined  effects  of  small  concentrations  of nitrogen  oxide  and  sulfur
     dioxide upon an organism.  Gig. Sanit.  27:3-8,  1962.

Miyoshi, Y. ,  F.  Izuchi,  T.   Nakano,  K.  Niijama, and M. Wakabayashi.  Scanning electron micro-
     scopic  observation  of   trachealmucosa  in mice  exposed to  N09  and S09.   Nihon  Kikan
     Shokudoka Gakkai  Kaiho  24:1-8,  1973.                            *         *

Mohr,  U.,  J.  Althoff,   and  A.  Authaler.    Diaplacental  effect  of  the carcinogen  diethylni-
     trosamine in the golden hamster.  Cancer Res. 26:2349-2352, 1966.

Montesano,  R. ,  and  H.   Bartsch.    Mutagenic  and carcinogenic N-nitroso  compounds:  possible
     environmental hazards.  Mutat.  Res. 32:  179-228,  1976.

Moore,   C.   B. ,  R.  Birchall,  H.  M. Horack,  and  H.  M.  Batson.    Changes  in  serum  pseudo-
     cholinesterase levels in  patients with  diseases  of  the heart, liver  or musculo-skeletal
     system.  Am.  J. Med. Sci. 234:538-548,  1957.

Morrow, P.  E.   An evaluation  of  recent  NO   toxicity data and an attempt  to  derive  an  ambient
     air standard for NO  by  established foxicological  procedures.   Environ.  Res.   10:92-112,
     1975.

Motomiya,  K. ,  K.  Ito, A. Yoshida,  S.  Idewara,  Y. Otsu,  and Y.  Nakajima.   The effects  of N02
     gas exposure on influenza virus in mice--long-term low-concentration  experiments.   Kankyo
     Kagaku Kenkyu Hokoku (Chiba  Daigaku) 1:27-33, 1973.

                                              14-121

-------
Murphy,  S.  D.   A  review of  effects  on animals  of exposure to auto  exhaust  and some of  its
     components.  J. Air Pollut. Control Assoc. 14:303-308, 1964.

Murphy S.  D. ,  C.  E. Ulrich,  S.  H.  Frankowitz, and C.  Xintaras.   Altered function in animals
     inhaling  low  concentrations  of  ozone  and  nitrogen dioxide.   Am.  Ind.   Hyg.  Assoc.   J.
     25:246-253, 1964.

Mustafa,  M.  G. , E.  J.  Faeder,  and S. D.  Lee.   Biochemical  effects of nitrogen  dioxide  on
     animal lungs,   Iji:  Nitrogen Oxides and Their  Effects on Health,  A Symposium From a Joint
     Conference, American  Chemical Society  and Chemical  Society  of Japan,  Honolulu, Hawaii,
     April   4-5,  1979.   S.  D.  Lee, ed. ,  Ann  Arbor Science  Publishers,  Inc.,  Ann Arbor,  MI,
     1980.   pp.  161-179.

Mustafa,  M. G. ,  N.  El  Sayed, J. S. T. Lim, E. Postlethwait, and S.  D. Lee.   Effects of nitro-
     gen  dioxide on lung metabolism.   In:   Nitrogenous Air Pollutants, Proceedings of a Sympo-
     sium,  175th National Meeting, American Chemical Society, Anaheim, California, March 12-17,
     1978.   D.  Grosjean,  ed. , Ann  Arbor  Science  Publishers, Inc.,  Ann  Arbor,  MI,  1979.    pp.
     165-178.

Nakajima, T. ,  and S. Kusumoto.  Effect of nitrogen  dioxide exposure  on the contents of reduced
     glutathione in mouse  lung.   Osaka furitsu Koshu Eisei Kenkyusho  Kenkyu Hokoku Rodo Eisei
     Hen  (6):17-21, 1968.

Nakajima, T. , and  S.  Kusumoto.   On carboxyhemoglobin levels in mice continuously exposed to  a
     mixed  carbon   monoxide  and nitrogen  dixoide  gas.    Osaka  furitsu  Koshu  Eisei  Kenkyusho
     Kenkyu Hokoku Rodo Eisei Hen (8):25-28, 1970.

Nakajima, T., S.  Hattori,  R. Tateisni, and T.  Horai.   Morphological  changes in the bronchial
     alveolar system of mice following continuous  exposure  to  low concentrations of nitrogen
     dioxide and carbon monoxide.  Ninon Kyobu Shikkan Gakkai Zasshi 10:16-22,  1972.

Nakajima, T. , S.  Kusumoto,  C. Chen, and K. Okamoto.  Effects of prolonged continuous exposure
     to  nitrogen  dioxide on  the quantity of  reduced glutathione in  lungs  of  mice and their
     histopathological   changes.  Appendix:   effects of  nitrite and  nitrate on  the glutathione
     reductase.   Osaka  furitsu  Koshu  Eisei Kenkyusho Kenkyu Hokoku  Rodo Eisei Hen (7):35-41,
     1969.

Napalkov,  N.    P.,   and  V.   A.  Alexandrov.    Effects   of  blastomogenic  substances  during
     embyryogenesis.  Z. Krebsforsch.   71:31-50, 1968.

National  Research  Council.    Nitrogen  Oxides.   National Academy  of  Sciences,  Washington,  DC,
     1977.

Niewoehner, D.  E. ,  and J.  Kleinerman.  Effects of  experimental emphysema and bronchiolitis  on
     lung mechanics and morphometry.  J.  Appl. Physio!.  35:25-31, 1973.

Oda, H. ,  S. Kusumoto,  and T. Nakajima.  Nitrosyl-hemoglobin formation in the blood of animals
     exposed to nitric oxide.  Arch. Environ.  Health 30:453-455, 1975a.

Oda, H.,  S. Kusumoto,  and T.  Nakajima.   Difference in  nitrosyl hemoglobin  formation among
     animal species.  Taiki Osen Kenkyu ^:714-716,  1975b.

Oda, M.,  S. Yamaoka, M. Fukuda, and T. Kanasaki.  Studies of the effects of urban polluted  air
     on experimental animals.  Part III.   Taiki Osen Kenkyu 8:424, 1973.

Orthoefer,   J.  G.,  R.   S.  Bhatnager,   A.   Rahman,  Y.  Y.  Yang,  S.   D.  Lee,  and J.  F.  Stara.
     Collagen and  prolyl  hydroxylase  levels  in  lungs  of beagles exposed  to  air pollutants.
     Environ.  Res.  12:299-305, 1976.

                                             14-122

-------
Osp.ital, J. J. ,  N.  El Sayed, A. D. Hacker, M. G. Mustafa, and D.  F. Tierney.   Altered  glucose
     metabolism  in  lungs  of rats exposed to  nitrogen dioxide.  Am.  Rev.  Respir.  Dis. 113:108,
     1976.

Otsu, H.,  and G.  Ide.  Effect of nitrogen dioxide on the tumorigenesis  induced  by an  injection
     of 4-nitroquinoline-l-oxide.  Taiki Osen Kenkyu 9:702-707, 1975.

Palmer, M.  S. ,   R.  W.  Exley, and  D.  L.  Coffin.   Influence  of  pollutant gases on  benzypyrene
     hydroxylase activity.  Arch. Environ. Health 25:439-442, 1972.

Pelfrene,   A.,  S. S.  Mirvish,  and  B.  Gold.   Induction  of  malignant  bone tumors  in rats  by
     l-(2-hydroxyethyl)-l-nitrosourea.  J. Natl.  Cancer Inst. U.S.  56:445-446,  1976.

Polo,  J. ,   and  Y.   L.  Chow.    Efficient  degradation  of  nitrosamines  by  photolysis.    In:
     Environmental  N-nitroso  Compounds   Analysis   and  Formation,   Proceedings  of  a  Working
     Conference,  International  Agency for Research on Cancer,  Tallinn, Estonian SSR,  October
     1-3,   1975.    E.  A.   Walker,  P.  Bogovski,   and  L.   Griciute,   eds.,  IARC  Scientific
     Publications No.  14,  International  Agency  for  Research on  Cancer,  Lyon,  France,  1976.
     pp. 473-486.

Port, C. D. ,  K.  V.  Ketels, D. L. Coffin, and  P.  Kane.  A comparative study of experimental  and
     spontaneous emphysema.  J.  Toxicol.  Environ. Health 2:589-604,  1977.

Purvis,  M.  R.,   and  R.   Ehrlich.    Effect   of  atmosphere  pollutants  on  susceptibility  to
     respiratory infection.  II. Effect of nitrogen dioxide.  J.  Infect.  Dis. 113:72-76,  1963.

Ramazzotto, L. T. ,  and L. J. Rappaport.   The effect of nitrogen  dioxide  on aldolase  activity.
     Arch.  Environ.  Health 22:379-380, 1971.

Rejthar, L. ,  and A.  Rejthar.   Histological changes of terminal bronchioles in  rats during the
     exposure to nitrogen dioxide.   Exp.  Pathol.  10:245-250,  1975.

Riddick, J. A.,  K.  I. Campbell, and  D.  L.  Coffin.   Histopathologic changes  secondary to  f^
     exposure in dog lungs.  Am. J. Clin.  Pathol. 59:239, 1968.

Roehm,  J.   N.  , J.  G.  Hadley, and D.  B.  Menzel.   Oxidation of unsaturated fatty acids by  ozone
     and nitrogen dioxide:   a  common mechanism of  action.   Arch. Environ. Health  23:142-148,
     1971.

Rounbehler, D.  P.,  R.  Ross,  D. H.  Fine, Z. M.  Igbal,  and S.   S.  Epstein.   Quantisation  of
     dimethylnitrosamine  in  the whole mouse  after  biosynthesis  i_n  vivo  from trace levels  of
     precursors.   Science (Washington, D.C.) 197:917-918, 1977.

Rynbrandt,  D. , and  J.  Kleinerman.   Nitrogen dioxide and pulmonary proteolytic  enzymes.   Arch.
     Environ.  Health 32:165-172, 1977.

Sackner, M. A.,  R.  D.  Dougherty, and G.  A.  Chapman.   Effect of  inorganic nitrate  and  sulfate
     salts  on cardiopulmonary function.   Am.  Rev. Respir.  Dis. 113:89,  1976.

Samuelsen,  G.  S. , R.  E.  Rasmussen, B. K.  Nair,  and T.  T.  Crocker.   Novel culture and exposure
     system for  measurement of  effects  of airborne pollutants  on mammalian cells.  Environ.
     Sci.  Technol.  12:426-430,  1978.

Schiff, L.  J.    Effect  of nitrogen dioxide  on  influenza  virus   infection  in hamster  trachea
     organ  culture.   Proc. Soc.  Exp. Biol. Med.  156:546-549,  1977.
                                             14-123

-------
Selgrade,  M.  J.  K. ,  M.  L.  Mole,  F. J.  Miller, G.  E.  Hatch,  D.  E.  Gardner,  and  P.  C.  Hu.
     Effect  of  N02 inhalation and  vitamin C deficiency on  protein and lipid accumulation  in
     the lung.  Environ. Res. 26:422-437,  1981.

Seto, K.,  M.  Kon,  M.  Kawakami,  S.  Yagishita,  K. Sugita, and M.  Shishido.   Effect of nitrogen
     dioxide  inhalation on  the  formation of  protein  in  the  lung.    Igaku  to Seibutsugaku
     90:103-106, 1975.

Shalamberidze, 0.  P.   The  joint action  of small concentrations of  sulfurous  gas and nitrogen
     dioxide  on  the estrual  cycle  and  the genital function of animals in experiments.   Gig.
     Sanit. 4:10-14, 1969.

Shalamberidze,  0.   P.,  and  N.   T.  Tsereteli.    Effect of  low  concentrations of  sulfur  and
     nitrogen  dioxides  on  the  estrual   cycle  and  reproductive  functions  of experimental
     animals.  Hyg. Sanit.  36: 178-183,  1971.

Sherwin,  R.   P.,  and  D.  A.  Carlson.   Protein  content  of  lung  lavage fluid of  guinea  pigs
     exposed  to 0.4 ppm nitrogen dioxide.  Arch. Environ. Health  27:90-93, 1973.

Sherwin, R.  P. ,  and L.  J.   Layfield.   Proteinuria  in  guinea pigs  exposed  to 0.5 ppm nitrogen
     dioxide.  Arch. Environ. Health 28:336-341, 1974.

Sherwin, R.  P.,  and V.  Richters.   Lung  capillary  permeability. Nitrogen dioxide exposure and
     leakage of titriated serum.   Arch.  Intern.  Med. 128:61-68, 1971.

Sherwin, R. P., J.  Dibble,  and J. Weiner.  Alveolar wall cells  of  the guinea pig.  Increase  in
     response to 2 ppm nitrogen dioxide.   Arch.  Environ. Health 24:43-47, 1972.

Sherwin,  R.   P.,  K.   V.   Kuraitis,  and  V.  Richters.   Type  2  pneumocyte  hyperplasia  and
     hypertrophy  in  response  to   0.34  ppm  nitrogen  dioxide;  an  image   analyzer  computer
     quantisation.   Fed. Proc. Fed.  Am.  Soc. Exp. Biol. 38:1352, 1979.

Sherwin, R.  P.,  J.  B. Margolick, and  E. A. Aguilar.   Acid  phophatase  in density equilibrium
     fractions of the lungs of guinea pigs exposed intermittently  to 0.4 ppm nitrogen dioxide.
     Fed. Proc.  Fed. Am. Soc. Exp.  Biol. 33:633, 1974.

Sherwin, R. P., J.  B.  Margolick, and S.  P. Azen.  Hypertrophy of alveolar wall cells secondary
     to  an  air pollutant.    A semi-automated quantitation.  Arch Environ.  Health 26:297-299,
     1973.

Sherwin, R.  P.,  D.  Okimoto, and D.  Mundy.  Sequestration of exogenous peroxidase in the  lungs
     of  animals exposed  to continous 0.5  ppm nitrogen dioxide.  Fed. Proc.  Fed. Am. Soc.  Exp.
     Biol.  36:1091, 1977.

Sherwin, R.  P.,  V.  Richters, M.  Brooks, and R.  D.  Buckley.  The phenomenon of macrophage  con-
     gregation in  vitro and  its relationship  to  in  vivo N09  exposure  of  guinea pigs.   Lab.
     Invest.  18:269^2777 1968.                               *

Simons,   J.  R. ,  J.   Theodore,  and E.  D.  Robin.   Common oxidant lesion  of mitochondrial  redox
     state produced by NO,,  0,  and  high oxygen  in  alveolar  macrophages.   Chest 66.-9S-11S,
     1974.                  *    J                                                     ~~

Stara,  J.  F. ,  D.  L.  Dungsworth,  J.   G.  Orthoefer,  and W. S. Tyler,  Eds.  Long-Term Effects  of
     Air  Pollutants:    in  Canine Species.  EPA-600/8-80-014,  U.S.  Environmental  Protection
     Agency,  Cincinnati, OH, July 1980.

Stephens, R.  J.,  G.  Freeman, and M.  J. Evans.  Ultrastructural  changes in connective tissue  in
     lungs of rats exposed to N02.   Arch.  Intern. Med. 127:873-883,  1971.

                                             14-124

-------
 Stephens,  R.  J. ,  G.  Freeman,  and  M.  J.  Evans.   Early response  of lungs  to  low  levels  of
      nitrogen  dioxide--light  and  electron microscopy.   Arch.  Environ.  Health 24:160-179, 1972.

 Stephens,  R. J., M.  F.  Sloan, D.  G.  Groth,  D.  S.  Negi,  and  K.  D.  Lunan.   Cytologic response of
      postnatal  rat lungs  to 0,  or NOp  exposure.  Am.  J.  Pathol.  93:183-200,  1978.

 Stupfel,  M. , F. Romary,  M. H.  Iran, and  J.  P.  Moutet.   Lifelong  exposure of SPF rats to auto-
      motive  exhaust  gas.  Dilution  containing  20  ppm  of  nitrogen  oxides.  Arch.  Environ.
      Health  26:264-269, 1972.

 Svoboda,  D. , and J.   Higginson.   A comparison of ultrastructural  changes in rat  liver  due  to
      chemical  carcinogens.  Cancer Res. 28:  1703-1733,  1968.
*->         \*
 Svorcova  S. , and V.  Kaut.   The  arterio-venous  differences  in the  nitrite and  nitrate  ions
      concentrations  after the nitrogen oxides  inhalation.   Cesk.  Hyg.  16:71-76,  1971.

 Thomas,  H.  V., P.   K.  Mueller,  and  R.  L.  Lyman.    Lipoperoxidation  of lung  lipids in  rats
      exposed to nitrogen  dioxide.   Science  (Washington,  D.C.)  159:532-534,  1968.

 Thomas,  H.  V., P.  K.  Mueller,  and R. Wright.   Response  of  rat  lung mast  cells  to  nitrogen
      dioxide inhalation.   J.  Air  Pollut.  Control  Assoc.  17:  33-35,  1967.

 Trzeciak,  H.  I.,  S.   Kosmider,  K.  Kryk, and  A.  Kryk.  The effects  of  nitrogen oxides and their
      neutralization  products  with ammonia on  the lung  phospholipids  of  guinea pigs.   Environ.
      Res.  14:87-91,  1977.

 Tusl,  M. ,  A.  Vyskocil, and V.  Sesinova.   Changes in plasma-corticosterones  of  rats following
      inhalation of nitrogen oxides.  Staub  Reinhalt  Luft 35:210-211,  1975.

 Tusl,  M. ,  V.  Stolin, M.  Wagner,  and D.  Ast.  Physical  exertion  (swimming)  in rats  under  the
      effect  of  chemical  agents.  J_n:  Adverse  Effects  of Environmental  Chemicals  and Psycho-
      tropic  Drugs:    Quantitative  Interpretation  of  Functional   Tests,  Proceedings  of  the
      I.A.O.H.  Study   Group on  Functional Toxicity,  Volume 1,  Universitas  Carolina,  Prague,
      Czechoslovakia,  1973.   M.  Horvath,  ed. ,  Elsevier,  New  York,   NY,  1973.   pp.  155-160.

 Udai,  G.,  H.  Oda,  and T.  Nakajima.   A pathohistological study of  mice  exposed  to NO,.   Taiki
      Osen Kenkyu 8:423, 1973.                                                .          *

 U.S.  Environmental Protection Agency.   Air  Quality  Criteria  for Nitrogen Oxides.   AP-84,  U.S.
      Environmental Protection Agency,  Washington, DC, January  1971.

 U.S.   Environmental   Protection  Agency.     Scientific  and  Technical   Assessment  Report   on
      Nitrosamines.   EPA-600/6-77-001,  U.S.  Environmental Protection Agency,  Research  Triangle
      Park, NC,  June  1977.

 U.S.  Environmental   Protection  Agency.   Health Effects  of Short-Tenh  Exposures  to  Nitrogen
      Dioxide  (Air Quality Criteria).    Final  Draft.   U.S.  Environmental  Protection Agency,
      Research Triangle Park, NC, May 1978.

 Valand,  S.  B. ,  J.  D. Acton,  and  Q. N. Myrvik.   Nitrogen  dioxide  inhibition of viral-induced
      resistance in alveolar monocytes.  Arch.  Environ.  Health  20:303-309, 1970.

 Vassallo,  C.  L. ,  B.  M.  Domm,  R.  H.  Poe,  M. L.  Duncombe,  and J.  B.  L.   Gee.  N02  gas and  N02
      effects  on  alveolar  macrophage   phagocytosis  and  metabolism.    Arch.  Environ.  Health
      26:270-274, 1973.
                                             14-125

-------
Vaughan,  T.  R. ,  L.  F.  Jennelle,  and T.   R.  Lewis.   Long-term exposure  to  low levels of  air
     pollutants.   Effects on pulmonary function in the beagle.  Arch Environ. Health 19:45-50,
     1969.                                                                           ~~

Voisin, C. ,  C. Aerts,  J.  L. Houdret, A. B. Tonnel and P. Ramon.  Activity of nitrogen dioxide
     on  alveolar macrophages  surviving  in vitro  in the gas phase.   Lille  Med.  21:126-130,
     1976.                                                                         ~~

Voisin,  C. ,  C.   Aerts,  E.  Jakubczak,  J.  L.  Houdret,  and A.  B.  Tonnel.   Effects of nitrogen
     dioxide  on  alveolar macrophages  surviving in  the  gas  phase.   Bull.  Eur. Physiopathol.
     Respir.  13:137-144, 1977.

von Kreybig,  T.   Effect of a carcinogenic  dose of methylnitrosourea on the embryonic develop-
     ment of the rat.  Z.  Krebsforsch. 67:46-50, 1965.

von Nieding,  G.  , H.  Krekeler,  and  R.  Fuchs.  Studies  of  the  acute  effects  of  NO^  on  lung
     function:   influence  on diffusion,  perfusion and ventilation  in  the  lungs.   Int.  Arch.
     Arbeitsmed.  31:61-72, 1973.

Wagner, W. D. , B.  R. Duncan, P. G. Wright, and H. E. Stokinger.  Experimental  study of thres-
     hold limit  of N02.   Arch. Environ. Health 10: 455-466, 1965.

Williams, R.   D. , J.  D.  Acton, and  Q.  N.  Myrvik.   Influence  of nitrogen  dioxide on the uptake
     of para  influenza-3  virus  by alveolar macrophage.  J.  ReticuloendotheT. Soc. 11:627-636,
     1972.                                                                         ~~

World Health Organization.  Oxides of Nitrogen.  Environmental Health Criteria  4, World Health
     Organization,  Geneva, Switzerland, 1977.

Wrba,   H. , K.  Pielsticker,  and  U.  Mohr.   Die displazentarcarcinogene  Workun  von  Diathyl-
     nitrosamin bei  Ratten.   Naturwissenschaften 54:47, 1967.

Wynn,  V.  Vitamins and Oral  Contraceptive Use.  Lancet 1:561-564, 1975.

Yakimchuk, P. P.,  and  K.  N. Chelikanov.   Data for a sanitary basis of the mean daily maximum
     permissible concentration  of  nitrogen dioxide  in atmospheric  air.   In:   AICE Survey of
     USSR Air Pollution  Literature.   Volume XVII:  A  Fourth  Compilation  of Technical Reports
     on  the   Biological   and  the  Public  Health  Aspects  of  Atmospheric Pollutants.    M.  Y.
     Nuttonson,   ed. ,  AICE-AIR-72-17, American  Institute of  Crop  Ecology,  Silver Spring,  MD,
     1972.  pp.   17-23.

Yokoyama,  E.   Uptake of  S02 and  N02 by  the isolated  upper airways.    Koshu  Eiseiin Kenkyu
     Hokoku 17:302-306,  1968.

Yuen,  T. G.  H. ,  and R.  P.  Sherwin.  Hyperplasia of Type 2 pneumocytes and nitrogen dioxide  (10
     ppm) exposure.   Arch. Environ. Health  22:178-138, 1971,

Zorn,  H.  Alveolar-arterial  oxygen pressure difference  and  the  partial  pressure of oxygen in
     tissues  in  relation to nitrogen dioxide.   Staub Reinhalt. Luft 3_5:170-175, 1975a.

Zorn,  H.  The alveolar-arterial oxygen-tension differential and tissue  oxygen partial pressure
     during exposure to N02-  VDI Ber. 247:50-51, 1975b.
                                             14-126

-------
                   15.  EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN

15.1  INTRODUCTION
     The present  chapter  discusses effects of oxides  of  nitrogen  (NO ) on human health, with
major  emphasis on  the effects  of nitrogen dioxide  (NCO  as  the  NO  compound  currently of
greatest concern from a public health perspective.  Human health effects associated with expo-
sure to  nitrogen  dioxide  (N0~) have been  the  subject  of three literature reviews since .1970.
Each focussed mainly on the effects of short-term exposures.
     In the first review,  published in 1971, the Committee on Toxicity of the National Academy
of  Sciences-National  Research  Council  issued guides to  short-term  exposures  of the public to
NO   (National  Academy of  Sciences,  1970).  A  review of the  then  current  literature showed:
(1)  that  the   individuals  most   susceptible  to NO,,  action  are  those  predisposed by  age,
heredity, and preexisting respiratory disease;  (2) that many of these individuals respond most
sensitively at  concentrations  to which healthy individuals  are unresponsive;  and (3) that the
effects of  NOp  are,  within limits, reversible such  that the extent of recovery seems to be a
function of the degree of exposure,   the  length of  the interval  between  exposures,  and the
health and/or  age  of the  exposed  individuals.   This committee acknowledged that too much cri-
tical  information  was missing  to permit  highly  conclusive recommendations  about  short-term
exposure to N09,  but did  conclude that  the  exposure  limit  for the  general  public  for 10
                                                                      3
minutes,  30 minutes, or 60 minutes should be established at  1,880 ug/m  (1.0 ppm).
     A  more complete review  was  published  by the  National  Academy of  Sciences in  1977
(National  Academy  of  Sciences,   1977).  This  document covered  the  medical, biological,  and
physical  effects  of  the  nitrogen oxides  and  made  recommendations  for future  research,  but
included no suggestions for legislative exposure  limitations.
     A task group on  environmental health criteria for oxides of nitrogen,  representing the
World Health Organization,  recommended  in 1978   that  the effects of  pollution designated as
"adverse",   in  addition to  the  morphological and  other changes produced by high  N02 concentra-
tions,  should include:  increased airway resistance, increased sensitivity to  bronchoconstric-
tors, and enhanced susceptibility to respiratory  infections  (World  Health Organization,  1977).
This group  selected  940 ug/m  (0.5 ppm) as  their estimate  of the  lowest concentration  of NOp
at which adverse health effects due to short-term exposure might be expected to  occur, but did
not state their rationale  explicitly.
     The following assessment appraises most of the studies  included in these  previous reviews
plus additional, more  recent,  pertinent publications.   This assessment includes discussion of
controlled   human exposure  studies and  epidemiological  studies of human health effects associ-
ated with  indoor  and outdoor exposures to  NO  compounds.   In addition, studies  on the effects
of accidental and  occupational  exposures to oxides of nitrogen are concisely  reviewed in this
chapter.
                                            15-1

-------
     Placing the present assessment in historical perspective, it should be noted that concern
regarding NO  effects on human health was originally derived from cases of accidental or occu-
pational exposures  to  NO  compounds.   For example, the earliest evidence for potential damage
to  man  due to  NO   exposures occurred in the  chemical  industry where, as early  as  1804,  the
deaths  of  a man and his dog  after  breathing nitric acid fumes were recorded (Raminez, 1974).
Other occupational  exposures have  since  been  seen with the use of  explosives  which generate
NOp  during misfires  and welding  operations  which generate  substantial  quantities  of  NO .
Burning  of  plastics, shoe  polish,  and  nitrocellulose  also results  in  potentially  excessive
quantities of NO .   High concentrations of ambient NO^ were clearly associated with acute .pul-
monary  edema  and death.  Lowry  and Schuman  (1956) were among the  earliest  investigators  who
demonstrated that exposures to NO-  in excess of 200 ppm would induce such effects.  Their des-
cription of  silo fillers'  disease  clearly  implicated  N02 exposure  in  the etiology  of this
disease  as another  potential  occupationally related NO  hazard.   That hazard,  first noted in
                                                       A
1914 (Hayhurst and Scott, 1914), when four individuals died suddenly after entering a recently
filled  silo,  was  earlier  mistakenly  attributed  to  high  concentrations  of carbon dioxide.
     A  fairly typical clinical picture of signs and symptoms associated with exposures to very
high levels of  NO   compounds (especially N02) has emerged from case studies of accidental  and
occupational  exposures, as reviewed by Milne (1969) and Horvath et al.  (1978).   Acute exposure
to  high  concentrations  (>  47,000 ug/m ;  25  ppm)  of NOp produces an almost immediate reaction
consisting usually  of  cough,  dyspnea,  and tightness of the chest and respiratory tract caused
by  acute bronchitis  or  pulmonary edema.   Such exposure may be quickly fatal.   If the exposure
has not  been  overly excessive,  exposed individuals may recover without further complications.
However, if  the exposure  concentration  and duration  are  greater, more intense  symptoms  may
occur after  a  latent  period of 2  to  3  weeks.   These consist of  severe  respiratory distress
usually  occurring  quite suddenly and  can result  in  death within  a  few days.   The cause of
these symptoms is always bronchiolitis fibrosa obliterans.   When symptoms are not sufficiently
severe  to  cause  death,  subjects frequently appear to recover fully.   Such  a biphasic reaction
to  exposure to  N0?  was described by Milne  (1969),  as determined from a literature  review of
clinical case studies.
     Horvath et  al.  (1978)  more recently reviewed  data  accumulated  on 23  patients exposed to
nitrogen dioxide in agriculture or industrial situations.  Their review confirmed that, during
the  acute  phase following  severe  N02  exposures, varying  combinations  of restrictive  and
obstructive ventilatory defects, impaired diffusion capacity and hypoxemia  are found.  However,
Horvath  et al.   (1978)  also  noted  some  evidence  for  pulmonary  dysfunction persisting  after
follow-up periods of 2.5 to 13.5 years,  including diminished exercise tolerances with dyspnea
during  exertion.   Fleming et al. (1979)  recently conducted physiologic studies  on  a patient
exposed to nitric acid fumes during the acute (immediate) and delayed (13 weeks  later) stages.
The  acute  changes  were  as anticipated.   During  the  delayed  stage,  elastic  recoil  and
resistance to  flow were normal.  However,  dynamic compliance was reduced and  dependent upon
                                            15-2

-------
 respiratory  frequency  and,  more significantly, oxygen  transport  was  abnormal  during exercise
 with  P(A-a)0,> of 20 mm Hg.  Dysfunction of small airways was evident.   Many of the individuals
 who were discussed in the above case studies detected a pungent odor when initially exposed to
 NO  compounds in various occupational situations.
  X
      The above types of effects noted in relation to accidental and occupational exposures (as
 discussed  in  more  detail  later in  Section  15.4)  helped to direct attention to possible human
 health effects induced by lower concentrations of N09 and other NO  compounds encountered with
                                                    £             A
 indoor or  outdoor exposures to ambient air pollutants.   Further, the observations made on sub-
 jects  inadvertantly  exposed to clearly toxic  levels of NO  compounds contributed to the con-
 ceptual framework  regarding possible functional  changes associated with lower level NO  expo-
 sures, the physiological  bases of  such changes, and the methodological approaches employed in
 attempting  to  measure such  changes  in  animal  toxicology,  controlled  human  exposure,  and
 epidemiological studies.
 15.2  CONTROLLED HUMAN EXPOSURE STUDIES
      Controlled exposure  studies  are useful  because they can provide accurate measurements of
 the effects  of specific  exposures  to  single or simple combinations  of  pollutants.   However,
 controlled studies usually do not provide definitive evidence of the effects that might be ex-
 pected in  ambient situations.   In the uncontrolled natural environment, exposures are changing
 constantly in regard to both the mixture of pollutants present and the concentrations of each.
 The inability to  extend  controlled exposure studies over  several  months limits the extent to
 which human  studies  have  been useful in determining the effects of repeated, short-term expo-
 sures to the highest levels of pollutants occurring in the natural environment.
      For  these  reasons,  controlled exposure  studies  usually  are  designed to  determine  the
 effects of a short,  single exposure to  a pollutant  at  a concentration believed  to  be high
 enough to  produce  some response.    Obviously,  in  such  studies  the safety of  test  subjects is
 the overriding  factor  in  determining the concentrations and exposure  times that can be used.
 Initial estimates of these factors  are often first obtained from animal studies.   Prudence re-
 quires, however,  that exposure  times  be  limited  to those  causing initial  responses.   When
 effects are detected, additional studies are undertaken to collect evidence of the lowest con-
 centration at which effects can be measured in both healthy and selected, sensitive volunteers.
 As noted above, the  methods and physiological basis for  most  controlled studies are based on
 observations  made  on subjects  inadvertently  exposed to  toxic levels of NO^.   These  include
 controlled human  exposure studies  on  the sensory  effects of  NO   compounds as well  as NO -
                                                                  X                          X
 induced pulmonary function changes discussed below.
 15.2.1  Studies of Sensory Effects
 15.2.1.1   Effects of Nitrogen Dioxide on Sensory Systems--The  significance  of  effects   on
 sensory receptors,  if any, is  unknown.   The  stimulation of  a sensory  receptor  does  invoke
within  an  individual  a  specific  response  resulting  from the  neural   transmission  of  the
 stimulation.
                                            15-3

-------
     Changes in the  intensity  of light to which an individual  is exposed initiate such a bio-
chemically transmitted response.   An impairment of dark adaptation,  then, represents a slowing
of the mechanism by which the eye adjusts to changes in light intensity.   Because the response
to the stimulus is delayed, this effect on dark adaptation must be considered to be an impair-
ment.   Whether or not it is reversible or whether or not the reversibility persists after each
repeated insult, impairment of dark adaptation is reported at lower  concentrations of N0? than
is any other physiologic system tested.
     Shalamberidze (1967)  reported  that  impairment of dark adaptation occurred at NO, concen-
                            3
trations as  low as  140 ug/m  (0.07 ppm) (Table 15-1).   The tests, as reported by the investi-
gator, demonstrated  changes in  ocular  sensitivity to  light by determining  reflex  changes  in
the functional  state of the cerebral cortex.   This study,  however, gave results that conflict-
ed with those  reported by Bondareva (1963) (Table 15-1).   This latter investigator determined
normal dark-adaptation curves  for  five volunteers and then  exposed  them to concentrations  of
                                 3
NOp varying  from  150 to  500 ug/m   (0.08  to  0.26 ppm) to determine  alterations  that might  be
related to  the changed  atmosphere.  While  her results indicated that exposure  to  concentra-
tions of 300 ug/m  (0.16 ppm) had no effect on dark adaptation,  time for adaptation increased
significantly  as  a  result of exposure to  500  ug/m  (0.26 ppm).   Repeated  daily  exposures  to
        3
500 ug/m  (0.26 ppm) NO^ over a period of 3 months, however, induced an apparent physiological
adjustment that largely reversed the initial  increase in the time for adaptation.   It has been
suggested (National  Academy  of  Sciences,  1977) that, since Bondareva did not indicate whether
NOp was used alone  or in combination with nitric  oxide (NO),  the higher value reported to  be
the minimum  effective  concentration may have been due to  differences in  the test atmospheres.
     The  perception  of  odors   is  a  response  to   chemical  stimulation  of  the  olfactory
receptors,   but this  perception  fades  with  adaptation.   The olfactory epithelium  contains
neural tissue  which directly contacts  airborne substances.   Thus,  interference with  normal
olfactory function  could possibly  reflect  either direct  or indirect interruption  of  neuro-
chemical  processes.   Olfactory  insensitivity to  NO- could  reduce  awareness  of  potentially
hazardous situations arising from increasing levels of the pollutant.
     Studies of odor perception  show that sensitive individuals  can detect the characteristic
pungent odor of NO,,  at a concentration of 200 ug/m  (0.11 ppm)   (Table  15-1).   Other studies
have indicated  that,  by  increasing relative humidity in the exposure atmosphere,  odor percep-
tion is improved  and respiratory irritation also  is increased.   Increasing the concentration
gradually in the  controlled exposure atmosphere results in a raising of  the threshold so that
its odor becomes less irritating.
     Henschler  et  al.  (1960) exposed  groups  of  20- to  35-year-old  healthy males  to  N02  to
obtain information  on the lowest concentrations  at  which the odor would  be  detected immedi-
ately.   The  odor  of  NO,  was perceived by  three  of nine volunteers  when  the concentration was
        3                                                                    3
230 ug/m  (0.12 ppm), by 8 of 13 subjects when the concentration  was 410  ug/m  (0.22 ppm), and
by all of eight subjects when the  concentration  of  N02 in the exposure  chamber was 790 ug/m
(0.42 ppm).

                                            15-4

-------
TABLE 15-1.   EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY RECEPTORS IN CONTROLLED HUMAN STUDIES

N0? Concen-
trations
ug/m
790
410
230
230
200
0
to
51,000
2,260
140
150
to
500


ppm
0.42
0.22
0.12
0.12
0.11
0
to
27
1.2
0.07
0.08
to
0.26


Time
No. of until
Subjects effect
8 Immediate
13 Immediate
9 Immediate
14 Immediate
28 Immediate
6 54 minutes
6 Immediate
4 5 and 25
minutes
5 Initial
Repeated
over 3
months
No. of
Subjects
Effects Responding
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
No perception of odor of N0? when
concentration was raised slowly from
0 to 51,000 ug/m
Perception of odor improved when
relative humidity was increased from
55% to 78%
Impairment of dark adaptation
Increased time for dark adaptation
at 500 ug/m (0.26 ppm)
Initial effect reversed

8/8
8/13
3/9
most
26/28
0/6
6/6
4/4
Not
Reported


Reference
Henschler et al . ,
1960
Ibid.
Ibid.
Shal amberidze,
1967
Feldman, 1974
Henschler et al . ,
1960
Ibid.

Shalamberidze,
1967
Bondareva, 1963



-------
The duration of exposure over which odor could be perceived varied considerably among subjects
and was  unrelated  to the concentration of NCL.   At concentrations of up to 20,000 ug/m  (10.6
ppm), perception of  the odor of N02 was lost after periods ranging from less than a minute to
13 minutes.   However,  regardless  of  the concentration, odor  perception  sensitivity returned
within 1 to 1.5 minutes after  subjects  left the exposure chamber.  Some  subjects  exposed to
N02 concentrations as low as 230 ug/m  (0.12 ppm) reported a metallic taste, dryness, and con-
striction in  the  upper  respiratory tract.    Such  symptoms  lessened and eventually disappeared
with repeated  exposures.   When  N02 was added gradually  to the exposure chamber over a period
of approximately  1  hour,  exposed  subjects  did  not  perceive  the odor even when  it  reached a
level of  51,000 ug/m  (27 ppm).  When subjects were exposed to an atmosphere containing 2,260
    2
|jg/m  NOp (1.2 ppm)  at 55 percent  relative  humidity,  after which the  humidity  was  increased
very rapidly  to 78 percent,  a  sharp  increase  in odor  perception occurred along with a corre-
spondingly  sharp increase  in irritation of the mucous  membranes of the respiratory tract.   It
is possible that  the increased  irritation,  and  perhaps  the  increased  odor perception, is  the
result of chemical  reactions between  nitrogen  oxides  and water  in  the  controlled  atmosphere
that increase the  concentrations of nitrogenous acids.
     Odor perception studies were  also conducted by  Feldman  (1974),  who reported that  200
    3
|jg/m  (0.11 ppm) was the lowest concentration at which the odor of NOp was detected.  At this
concentration, 26  of 28 healthy  subjects perceived the  odor immediately.
     In  summary, controlled  exposure  studies indicate  that two types of sensory receptors  .may
be involved in the  initial  response in humans  to  the presence of NO,,.   The  sensory  effects
involved  are   the  impairment of  dark adaptation and  the perception  of  odor.   Effects were
                                            3
reported at levels as low as 140 to 200 ug/m  (0.08 to  0.1 ppm) and occurred almost immediately
upon exposure.
15.2.1.2  Sensory  Effects Due to Exposure to Combinations of Nitrogen Dioxide and Other
 Pollutants—Studies  of the  effects  of  N02 in  combination  with  other pollutants on  sensory
receptors are summarized in Table 15-2.   These studies, all from the Soviet Union, report that
the effects of the test gases,  when  inhaled together,  were  additive,  as they related  to  the
minimum concentrations  causing  impairment  of dark adaptation,  odor perception, and changes in
the amplitude of alpha rhythms in the brain.
     Shalamberidze (1967) exposed 15 healthy subjects for periods of 5  or 25 minutes  to various
combinations of N02 and sulfur dioxide (SOp).  His studies were designed to compare the lowest
concentrations at  which dark adaptation is  impaired by  combinations of  pollutants to  levels of
the individual gases causing impairment.   He reported the minimum levels for impairment of  dark
                                                 3                                 3
adaptation  for  single pollutants  to be 600  ug/m  (0.23  ppm)  for S02 and 140 ug/m  (0.07 ppm)
for N00.  The thresholds for alteration of  odor perception  for subjects exposed to a single
                  3                                  3
gas were  230  ug/m   (0.12 ppm) for N02 and  1,600 ug/m   (0.61 ppm) for  SO,,.   In these studies,
combinations of the gases produced an impairment of dark adaptation or  odor perception  whenever
the  fractional  threshold  concentrations   for  the separate  gases totaled  one or more.   The
                                            15-6

-------
                 TABLE  15-2.   EFFECTS  OF  EXPOSURE  TO  COMBINATIONS  OF  POLLUTANTS  ON  SENSORY  RECEPTORS
                                             IN  CONTROLLED  HUMAN STUDIES
        Pollutant    Subjects
                         Exposure
                 Effects
                                                 Reference
        Various
        Combina-
        tions  of
        N02  and
        otner
           15 healthy
           subjects
5 or 25
min; oral
or nasal
inhalation
              gases
The lowest effective concentration for dark
adaptation was:   N02, 140 ug/m  (0.07 ppm) and
S02, 600 ug/m .(.0.23 ppm).   When inhaled to-
gether, the gases acted additively.  Dark
adaptation was impaired when the sum of the
fractional threshold concentrations for the
separate gases equaled 1.0 or more.
Lowest effective concentration for odor percep-
tion was:  3N02,  230 ug/m  (0.12 ppm) and S02(
1,600 ug/m  (6.16 ppm).  When inhaled togetner
these gases acted additively.  Odor was per-
ceived when the sum of the fractional thresh-
old concentrations equaled 1.0 or more.
Shalamberidze,
1967
en
i
Various
mixtures
of NO
SO   fl SO
aerosoT
and NH,
                     Not
                   reported
   Not
reported
Lowest effective concentrations for odor per-
ception of a combination of gases were reported  1972
to be:  NO  20 ug/nT (0.01 ppm); SQ? 170 ug/rn
(0.06 ppm)? H?SO.,.aerosol ,  110 g/m  (0.03 ppm),
and NH3, 300 flg/m  (0.43 ppm).  When inhaled
together the odor was perceived whenever the
fractional threshold totaled 1.0 or more.
Kornienko,
        Mixture
        of NO
        SO  NH.
           Four
  Not       Threshold for changes in the amplitude of alpha  Kornienko,
reported    rhythms occurred when the sum of the fractional  1972
            concentrations of the individual gases equaled
            1.0 or more.

-------
lowest  N02  concentration causing  impairment of dark adaptation was  approximately 60 percent
lower than the minimum concentration needed for odor perception.  For SO^, dark-adaptation im-
pairment occurred at a concentration about 38 percent below that at which the odor was detected.
     Kornienko (1972)  determined  odor-perception  capabilities in a group  of subjects exposed
to  individual  gases  or  combinations  of NO,,,  SCL,  sulfuric  acid  aerosol,  and  ammonia.   He
reported also that the odor of any gas mixture was perceived whenever the sum of the fractional
threshold concentrations  of  the  component gases totaled one or more.   Kornienko also investi-
gated the  effects of  mixtures  of these  same gases  on  alpha rhythm  in  the  brain.   Again,  he
determined that the earliest decreases in amplitude, in response to combinations of the gases,
occurred whenever the fractional  threshold concentrations for the individual  gases totaled one
or more.
15.2.2  Pulmonary Function
15.2.2.1  Controlled Studies of the Effect of Nitrogen Dioxide on Pulmonary Function in Healthy
Subjects—Controlled experimental  studies in the  laboratory situation  have  been mostly con-
cerned with  exposure  to N02 alone although a few studies have considered effects during expo-
sure to one  or  two additional air pollutants.   These studies have generally been conducted on
young healthy  adults  and/or  on  subjects suspected of being  sensitive,  e.g.,  individuals who
have chronic respiratory problems.   Controlled experimental  studies  on exposures  of  normal
subjects to N02 are summarized in Table 15-3.
     Nakamura (1964) determined the effect of exposure to combinations of NCL and sodium chlo-
ride aerosol  (mean diameter 0.95  urn)  on airway resistance (R.,.,.) measured by  an interruption
                                                              QW
technique (Table  15-3).   Two  groups of  seven and  eight  healthy subjects, 18 to 27 years old,
were exposed for 5 minutes to 1,400 ug/m  sodium chloride aerosol alone.   After resting for 10
to 15 minutes,  individual  subjects were exposed for 5 minutes to different N09 concentrations
                        3
ranging from 5,600 ug/m   (3.0  ppm) to  7,500  (4 ppm).   Nitrogen dioxide  concentrations were
measured by  the Saltzman  method.   Each  individual  in  each group showed  increased R   after
                                                                                      aW
exposure to  the  NO,  alone,  but the sodium chloride  aerosol  alone exerted no effect on airway
                                                                                3
resistance.   Nitrogen  dioxide alone at concentrations of 5,600  and  11,300 |jg/m  (3.0 and 6.0
ppm) caused  increases  in  Rnvi of 16 and 34 percent, respectively, in the one subject tested at
                           3W
each concentration.
      Von Nieding  et  al.  (1970)  reported, at the Second International Clean Air Congress, the
                                                                           3
results of exposures  of 13 healthy subjects to an  NOp  level of 9,400 ug/m   (5.0 ppm) for 15
minutes (Table 15-3).   Concentrations  were measured by the colorimetric Saltzman method.   At
this level,  a significant decrease in arterialized oxygen partial pressure (Pa02) was induced,
but  the  end  expiratory oxygen partial  pressure (Pa02)  remained unchanged.   A  reduced oxygen
pressure in  arterial  blood  would suggest a  reduction in  the transfer of oxygen from inspired
air  to  blood in  the lungs.   The  steady  oxygen  pressure  in expired air  would  indicate that a
constant supply  of  oxygen was delivered to the lungs.   Together, the results suggest that N02
may  have  interfered with  the transfer  of oxygen  from  alveolar air  to  arterial  blood.   This
                                            15-8

-------
             TABLE  15-3.   EFFECTS  OF  EXPOSURE  TO  NITROGEN  DIOXIDE  ON  PULMONARY  FUNCTION
                              IN CONTROLLED  STUDIES  OF  HEALTHY  HUMANS**
Concentration   Pollu-
ug/nT
ppm    tant
 No.  of
 Healthy
Subjects
Exposure
  Time
Effects
Reference
13,000    7.0   N02      Several
                         10-120    Increased R  * in some subjects.   Others    Yokoyama,
                          min.      tolerated 3BVOOO ug/m  (16 ppm) with no     1972
                                   increase in R
                                                aw
 9,400    5.0   N02
                 11       2 hrs.    Increase in R  * and a decrease in AaDO *   Von Nieding
                                   with intermittent light exercise.   No,en-   et al.,
                                   hancement of the effect when,200 ug/m       1977
                                   (0.1 ppm) 0., and 13,000 ug/m  (5.0 ppm)
                                   S0? were combined with N0? but recovery
                                   time apparently extended.
9,400
9,400
7,500
to
9,400
5,600
11,300
5.0 N02
5.0 N02
4.0 N0?
to ^
5.0
3.0 N02
6.0 N02
16 15 min. Significant decrease in DL *
13 15 min. Significant decrease in Pad * but end ex-
piratory 0? * unchanged with significant
increase in systolic pressure in the
pulmonary artery.
5 10 min. 40% decrease in lung compliance 30 min.
after exposure and increase in expiratory
and inspiratory flow resistance that
reached maximum 30 min. after exposure.
1 5 min. Increase in R * compared to pre-exposure
values (enhanced by NaCl aerosol).
1 5 min. More subjects were tested at higher
exposures.
Von Nieding
et al. , 1973
Von Nieding
et al. ,
1970
Abe, 1967
Nakamura ,
1964
                                             (continued)

-------
                                               TABLE 15-3.  (continued)

Concentration Pollu-
ug/m
ppm tant
No. of
Healthy
Subjects
Exposure
Time
Effects
Reference
         14,000     7.5
9,400    5.0
          4,700     2.5
en
i
16       2 hrs.    Increased sensitivity to a bronchocon-
                  strictor (acetylcholine) at this concen-
                  tration but not at lower concentrations.

 8      14 hrs.    Increase in R   during first 30 min.  that
                  was reduced tnrough second hour followed
                  by greater increases measured at 6, 8 and
                  14 hrs.  Also increased susceptibility to
                  a bronchoconstrictor (acetylcholine).

 8       2 hrs.    Increased R   with no further impairment
                  at higher concentrations.   No change in
                  arterial P0?* pressure or PCO? pressure.
                                                                                                 Beil and
                                                                                                 Ulmer, 1976
1,880
1,880
1,300
to
3,800
:1,150
1,880
to
3,760
1.0 N02
1.0 N02
0.7 N0?
to i
2.0
0.6 - N02
1.0 N0?
to
2.0
8 2 hrs. No increase in R
dW
16 2 hrs. No statistically significant changes
in pulmonary function with the exception
of small but statistically significant
changes in FVC; see pp. 15-20.
10 10 mins. Increased inspiratory and expiratory flow
resistance of approximately 50% and 10% of
control values measured 10 mins. after
exposure.
15 2 hrs. No physiologically significant change
in cardiovascular, metabolic, or pulmo-
nary functions after 15, 30 or 60 mins.
or exercise.
10 2h hrs. Alternating exercise and rest produced
statistically significant decreases for
hemoglobin hematocrit, and enythrocyte
acetylchol inesterase.
Beil and
Ulmer, 1976
Hackney, et al
1978
Suzuki and
Ishikawa,
1965
Fol insbee
et al. , 1978
Posin et al . ,
1978
                                                      (continued)

-------
                                          TABLE 15-3.  (continued)
en
i



Concentration
ug/m ppm
1,000
1,000
with
560
1,000
with
560

and
45,000
500
500
with
560

500
with
560

and
45,000
0.50
0.50

0.29
0.50

0.29


30.0
0.25
0.25

0.29

0.25

0.29


30.0

Pollu-
tant
03
°3
J
N02
°3
J
NO,
/
L.
CO
03
°3
O
NO,
L-
0,
3
NO,
}
C-
CO
No. of
Healthy Exposure
Subjects Time Effects Reference
4 4 hrs. With each group minimal alterations in Hackney
p.ulmonary function caused by 0., exposure. et al . ,
Effects were not increased by addition of 1975a,b,c
NO, or NO, and CO to test atmospheres.
L. c.






7 2 hrs. Little or no change in pulmonary function Hackney
found with 03 alone. Addition of NO- or et al.,
of N02 and CO did not noticeably increase 1975a,b,c
the effect. Seven subjects included some
believed to be unusually reactive to
respiratory irritants.






                                                 (continued)

-------
                                       TABLE  15-3.   (continued)


Concea
ug/m
100
with
50
and
300

tration
ppm
0.05
0.025

0.11

Pollu-
tant
N02
°3

SO,
No. of
Healthy Exposure
Subjects Time Effects
11 2 hrs. No effect on R w* or AaDO *; exposed sub-
jects showed increased sensitivity of
bronchial tree to a bronchoconstrictor
(acetylchol ine) over controls not exposed
to pollutants.


Reference
Von Nieding
et al. , 1977




     aw
**
        airway resistance



AaD02:   difference between alveolar and arterial  blood partial  pressure of oxygen



DL_0 :   diffusion capacity of the lung for carbon monoxide



Pa02 :   arterial  partial  pressure of oxygen



P0?  :   partial  pressure  of oxygen



PCO? :   partial  pressure  of carbon dioxide



By descending order of lowest significant effect shown by each  study.

-------
increased difference  between  the alveolar and arterialized  oxygen  partial  pressures  (AaD02)
was' accompanied by  a  significant  increase  in  systolic  pressure  in  the  pulmonary  artery.
However, the significance of the changes in  A-aP02  are questionable in part due to the tech-
niques  employed and  there is apparently  some  question  as to the  conditions  present in their
exposure chambers.   Regardless of these questions,  the potential of high N0? exposure to modify
the  delivery  of. oxygen  to  tissues  remains  unanswered.   As  noted later,  no  evidence  for
increased oxygen uptake during light to moderate exercise has been found.
     Von Nieding  et   al.  (1977)  also  exposed  11 healthy  subjects,  aged 23  to  38  years,  to
9,400 |jg/m  (5.0 ppm) NO^ for 2 hours.   Pulmonary function values, recorded prior to exposure,
when the exposure was terminated, and 1 hour after exposure was terminated,  were compared with
similar  values  from   control  subjects  exposed to  clean air  for  2  hours.   Test  subjects  who
underwent a regimen of intermittent light exercise during the testing period showed significant
increases both in R   and in AaDO^-
     Von Nieding and co-workers (1973)  observed a significant decrease in the lung's diffusion
capacity for CO  (DL~Q)  in 16 healthy  subjects  resulting  from a 15-minute inhalation of 9,400
|jg/m3  (5.0  ppm) NO,  (Table  15-3).   Abe  (1967)  found  that  concentrations of  7,500 to 9,400
    3
|jg/m   (4.0  to  5.0  ppm) for 10 minutes produced increases in both  expiratory and inspiratory
flow resistance  in five healthy  males; these increases  reached a maximum 30 minutes after the
end of exposure.  Effective compliance  (change in lung volume per unit change in air pressure),
observed in this study 30 minutes after cessation of exposure, was decreased by 40 percent when
compared with controls.
     Increases  in the  inspiratory  and  expiratory flow resistance, observed in 10 healthy sub-
                                                                     3
jects exposed  to N02  concentrations ranging from 1,300  to 3,800 ug/m  (0.7 to 2.0 ppm) for 10
minutes, were  reported by Suzuki  and   Ishikawa  (1965)  (Table  15-3).   Ten minutes  after  the
exposure ceased, inspiratory  resistance was increased 53 percent and expiratory resistance 13
percent.  Information  on  variations in the results  at different levels of  exposure  was  not
provided in this report.  Since the exposure levels were reported by the authors to have varied
during the  studies,  results are difficult to interpret.   It is unlikely that concentrations of
NO- would have varied extensively during a controlled exposure of 10 minutes duration.   Results
reported, however, were the  averages  of the  responses of  the  10 test subjects  and may have
reflected a response  averaged  across  several exposure concentrations.   The effect of NO, at a
                           3
concentration of 9,400  ug/m   (5.0  ppm) was not increased by the addition of ozone (0,) to the
                                                        3                                     3
experimental atmosphere at a  concentration of 200 ug/m  (0.1 ppm) or by adding  13,000 ug/m
(5.0 ppm)  S02  to the N02/03  combination.   When 03 or the  03  plus the S02 was  added  to  the
experimental atmosphere,  the  pulmonary  function values,  measured  1 hour  after  exposure  was
terminated,  had  not  normalized  as  much as  had  the  values  in subjects exposed to  N02 alone.
Since subsequent measurements  were  not made,  the only  conclusion to be drawn  from  the study
results  is  that  recovery time  following  exposure  to  the  multiple pollutants  was delayed.
                                            15-13

-------
     Yokoyama (1972) measured airway resistance in volunteers exposed to various concentrations
of N00 for periods of 10 to 120 minutes.  He measured increases in airway resistance at 13,200
    3
ug/m  (7.0 ppm) and higher.  He also recorded wide variations in individual sensitivity.   Some
volunteers tolerated concentrations as high as 30,000 ug/m  (16 ppm) with no increase in airway
resistance.   Because  atropine effectively  blocked  the bronchoconstrictive effect  of  S09 but
not  of  N02,  this  investigator  suggested  that the  mechanism  for the  increase   in  airway
resistance was unrelated to vagal stimulation.
     Folinsbee et  al.  (1978)  concluded from  studies  of  three groups of  five  healthy males,
ranging  in age from 19 to 29 years,  that  no  physiologically  significant alterations in the
measurements of pulmonary,  cardiovascular,  or metabolic factors were produced by 2-hour expo-
sures  to 1,150 ug/m   (0.61 ppm)  NO^ monitored by  a  continuous  chemiluminescence  technique
(Table 15-3).  Pulmonary  measurements included:   ventilatory volume (VV);  tidal  volume  (V-,-);
forced vital  capacity (FVC); forced expiratory volume (FEV) at 1, 2, and 3 seconds,  and forced
expiratory flow  (FEF)  at  50  and  75  percent of vital  capacity exhaled.   Other measurements
included oxygen (02) and carbon dioxide (CO-) percentages  in inspired and expired air,  cardiac
output,  blood  pressure,  heart rate,  steady  state  diffusion capacity of the  lungs  for carbon
monoxide (DL^Q) and closing volume, with slow vital  capacity (VC).
     Hackney et al.  (1978) found no  statisically   significant  changes  in pulmonary function
                                                            o
in.16  healthy  individuals  exposed for 2 hours to 1,800 ug/m  (1.0 ppm)  NO- with the exception
of a marginal  loss  in  forced vital capacity  (FVC).  The  authors question the health signifi-
cance  of this latter  small,  but  statistically  significant change  in FVC.   That  is,  Hackney
et al.  (1978) stated:
              "As indicated, no changes with exposure were apparent except for a
              mean loss of 1.5% in FVC after the second exposure as compared to con-
              trol.   That this change represents other  than a random variation is
              doubtful, due to its small size, its  marginal statistical  significance,
              and the relative large number of statistical comparisons  being made."
Nitrogen dioxide was monitored  by a continuous chemiluminescence  analyzer and  checked by the
Saltzman method.   Pulmonary functions measured included FVC, FEV, peak and maximum expiratory
flow, closing volume (CV), R  ,  and others.
                            aw
     Beil and Ulmer (1976) exposed healthy volunteers (groups of 8 or 16) for 2 hours to 1,880,
4,700,  9,400,  and 14,000  ug/m   (1.0,  2.5,  5.0, and 7.5  ppm) NO,.  Nitrogen  dioxide  concen-
trations were monitored  by the continuous chemiluminescence method.  An  additional  group was
exposed  for 2  hours  to clean air.  Following exposure  to  l^ at concentrations  of 4,700 ug/m
(2.5 ppm)  or  above,  these investigators measured significant increases  in R   compared to the
                                                                            aW
controls,  but no  decrease in   Pa09   or   increase  in   PaC09.    Airway  resistance was  not
                                             3
increased  at  a concentration of 1,880 ug/m   (1.0  ppm).    Nitrogen  dioxide concentrations of
9,400  or 14,000  ug/m  (5.0 or 7.5  ppm) did not produce  significantly greater  increases  than
              o
did 4,700  ug/m   (2.5  ppm).  In these healthy subjects, increased sensitivity to a bronchocon-
strictor  (0.5  percent  acetylcholine  for  1  minute  inhalation  at  the  rate of  0.12  liter per
second) was observed after exposure for 2  hours to  14,000 ug/m  (7.5 ppm) N02 but not after

                                            15-14

-------
                               2
exposure to 4,700 or 9,400 ug/m  (2.5 or 5.0 ppm).  When the duration of exposure was increased
                                3
from  2  to 14  hours,  9,400 |jg/m  (5.0 ppm)  NO,  caused an initial increase  in  R   during the
                                               £.                                  aw
first 30  minutes.   Airway resistance tended to  return toward normal  during the second hour.
This was followed by even larger increases in R   measured after 6, 9, and 14 hours of exposure.
The effect of exposure on two consecutive days was reversible, and R   measured 24 hours after
                                                                    aw
initiation of  exposure  (10 hours after exposure  was  terminated)  had returned to pre-exposure
levels.   Exposure  of  healthy subjects for 14  hours  to 9,400 ug/m  (5.0 ppm) increased sensi-
tivity  to  acetylcholine;  the  effects of  longer exposures  to  lower concentrations  were  not
tested.
     Posin et  al.  (1978) exposed 10 subjects  for 2.5 hours to filtered air on day one and on
two consecutive  days  (days 2 and 3) to  N02.   The subjects  alternated 15  minutes  of exercise
(double resting ventilation) and 15 minutes of rest.   The ambient NO, levels were 1880 or 3760
    3
ug/m  (1 or 2 ppm).  Statistically significant decreases were observed for hemoglobin, hemato-
crit, and  erythrocyte acetylcholinesterase.   Glucose-6-phosphate dehydrogenase was  elevated
after the  second  exposure  to 3760 ug/m   (2  ppm)  NO, and levels of peroxidased red blood cell
                                                3
lipids were elevated after exposure to 3760 ug/m  (2 ppm).   These investigators concluded that
significant blood  biochemical  changes  resulted from N0? inhalation.   However,  there are some
questions  as to  the validity of these conclusions  since  there is considerable variability in
the measurements that were made,
     In contrast,  Horvath  and  Folinsbee  (1979)   in  a study on eight  subjects  exposed  to  940
ug/m  (0.50  ppm)  under  a variety  of ambient temperature  conditions with  one period  of 30
minutes  of exercise during the two hours failed to observe any changes in pulmonary functions.
Also, Kerr et  al.  (1979) studied 10 normal  healthy  subjects exposed for 2 hours to 940 ug/m
(0.5 ppm)  NOp.   One subject  experienced the very mild symptom of slight rhinorrhea.   Although
the authors suggest that the changes reported in  quasi static  compliance may be due to chance
alone, there is  uncertainty  whether these changes were due to daily variation or to N02 expo-
sure  (see  also page 15-27).   No other  significant alteration in  pulmonary  function resulted
from the exposure.
     When  von  Nieding  and  co-workers  (1977) exposed 11 healthy  subjects  to  a  combination
of N02 at  100  ug/m3 (0.05 ppm), 03  at  50 ug/m3  (0.025 ppm),  and  S02 at 300 ug/m3 (0.11 ppm)
for 2 hours,  no effect on R   or AaDO, was reported (Table 15-3).   Exposure to this combination
                           aw        L.
of pollutants did,  however, produce what was interpreted by the investigators as dose-dependent
increases  over  controls  (not exposed to  the pollutants)  in the sensitivity of the  bronchial
tree  to  administered  acetylcholine as  measured  by  increases in  R  .   Constriction  of  the
                                                                     aw
bronchi  is a physiological  alteration similar to  that experienced by many individuals as asthma
attacks.   The suggestion provided by this study is that exposure to air pollutants  may increase
susceptibility to asthma attacks in some individuals.
     Hackney et  al.  (1975a;  1975b;  1975c)  exposed four healthy male volunteers to  0,  (1,000
    •3                                                               3
|jg/m ; 0.5 ppm) and subsequently to mixtures of 03 and NO,, (560 pg/m ; 0.3 ppm) or  03> N02 and
                                            15-15

-------
                2
CO  (45,900  |jg/m ;  30  ppm)  (Table  15-3).   Volunteers were  exposed for 4  hours  plus  about 1
additional hour during which several tests of pulmonary function were performed.  The exposure
regimen was  designed  to  simulate exposure experienced during severe pollution episodes in Los
Angeles on  a summer  day.   The exposure time, however, was about twice that experienced in the
ambient situation.   Under  these  conditions,  minimal alterations  in pulmonary functions (FVC,
FEV,  CV,  R   and  others)  were measured when  test  subjects were exposed to  0-, alone.   These
           3w                                                                  o
alterations  were  not  increased  by  the additions of  N02  or of N02 and CO.   Another group of
seven male  volunteers,  including some believed to  be  unusually reactive  to respiratory irri-
                                                                                             Q
tants, was  exposed under  a similar protocol  with an exposure time of 2 hours and to 500 ug/m
(0.25 ppm)  0-,.   Again,  little or no  change  in pulmonary function was  found  with 0, exposure
                                         3                                         3
alone, or with  addition  of NO- (560 ^g/m ;  0.3 ppm) or of N02 plus CO (45,900 ug/m  ; 30 ppm).
     Schlipkbter and  Brockhaus  (1963) determined,  in three  subjects,  the  effects of exposure
to N09, carbon  monoxide  (CO),  and SO,, on pulmonary deposition of inhaled dusts.  A suspension
                                                                                        3
of homogenized  soot  (particle  sizes 0.07 to 1.0 urn) was combined with either 9,000 [jg/m  (4.8
ppm) N02, 55,000 ug/m3 (50 ppm) CO, or 13,000 ug/m3 (5.0 ppm) S02 and administered to experi-
mental  subjects by  inhalation.   The individual pollutant concentrations  were  the  maximum
acceptable concentrations  in  the Federal  Republic of Germany.   Pulmonary retention was deter-
mined by measuring the differences between the concentrations of dust in the inhaled and exhaled
air.    Under control   conditions  and  with CO  and S02  exposure,  50 percent  of  the  dust  was
retained.   Retention  increased  to approximately 76 percent  when  the  dust  was administered in
                                    3
an atmosphere containing  9,000  (jg/m  (4.8 ppm) N02.  Greater proportions of dust particles in
the range of 0.3 to 0.8 urn were retained than were other size particles.  This study is signi-
ficant  in  that  it demonstrates  a potential  additive or greater  than  additive  mechanism that
could operate  in ambient  situations  involving  significant  N02 exposures  of short duration.
The study suggests that,  as N02 concentrations  in  inhaled  air increase,  the response induced
may result in respiratory retention of larger proportions of inhaled particles.   If the partic-
ulate matter  includes  toxic materials, the additional  impact  on  health could be significant.
     Nakamura's  (1964) studies on the interaction of N02 and sodium chloride aerosol indicated
that sodium  chloride  aerosol  had no influence on R, .  When the sodium chloride aerosol (mean
                                                   aw
diameter 0.95 urn)  was added to the exposure  atmospheres,  the increases in R=l, for the group
                                                                              aW
were approximately 40  percent,  about twice that produced by the gas alone.   A sodium chloride
aerosol comprised of  smaller  particles (mean diameter 0.22 (jm) at 1,400 ug/m , in combination
with the  same concentrations  of N00, produced  no increase  in R=ii over that caused by the gas
                                   L.                            aW
alone.  The  consistent sequential methodology  used  in  this study  tends to  reduce the credi-
bility of this study; nevertheless,  the fact that the final  exposure challenge in the sequence
increased the  R   when the NaCl aerosol  particles averaged  95  |jm in  diameter  but  did  not
                aw
increase R   when they averaged 22 \m in diameter indicates that when used in the same sequence
          61W
the larger  particles  of  NaCl  enhanced the effect of N02 while the smaller particles did not.
                                            15-16

-------
     Von  Nieding  and his  co-workers (1970;1977) ^have  conducted a  number of  studies  of the
effects of  N02  on pulmonary function in healthy and bronchitic subjects.   Some of the methods
used for these studies differ from those employed routinely in the United States, and for this
reason  may  not be directly  comparable.   For example,  von Nieding measured  R    during normal
breathing using a body  plethysmograph with  a  temperature  compensation  mechanism.   Most Amer-
ican  investigators  have  used  constant-volume  body plethysmographs and  measure R    during
                                                                                    aw
panting (DuBois,  1956).   Investigators  in this country also measure arterial partial  pressure
of  oxygen  (PaCL)  in blood  drawn  directly  from  an artery,  as  opposed  to  a drop  of  blood
obtained by pricking the  ear lobe.  In spite of the differences in technique,  and the opinion
offered  here  that  the  American  methodology may be more  accurate  over  the entire  range  of
possible  values,   it  is  generally agreed that,  in  the hands  of competent technicians,  the
methods used by von Nieding provide valid information on directional  changes in airway resist-
ance or changes in PaCL.
     Horvath and  Folinsbee  (1979)  exposed  eight young  adults to either  filtered air  or 980
    3                            3
ug/m  (0.5  ppm) 0., plus 940 |jg/m  (0.5 ppm)  NO^ in filtered air under four different environ-
mental  conditions:   (1) 25°C,  45% RH; (2) 30°C,  85% RH;  (3) 35°C,  40% RH;  and (4)  40°C, 50%
RH.  There  were a total of  eight  exposures  for each subject with a minimum of 1 week between
exposures.  During the  exposures,  the subject first rested for 60 minutes, then exercised for
30 minutes  at  35-40% of his predicted maximum  aerobic  capacity and then  rested for  the final
30 minutes.   Repeat tests  were generally made on each  subject  at the  same time of  the  day.
The pulmonary responses to ozone alone were  as found in previous studies  by the same research
group.   No  additive effect  or  interaction  between  ozone  and nitrogen dioxide was  observed.
     In summary,  studies  on the  effects  of  N0? on pulmonary  functions in healthy  volunteers
(Table  15-3)  indicate that  exposure of 2 hours  or  less  to concentrations of  less  than  4700
ug/m  (2.5  ppm) can induce increases in R   (Beil and  Ulmer, 1976).   The  lowest concentration
                                          aw                                                  o
producing this effect is  somewhat uncertain  but  is  likely  in  the range of 1300 to  3800 ug/m
(0.7 to 2.0 ppm)  (Suzuki  and Ishikawa, 1965).  Other  changes  in pulmonary function  have  been
reported  at higher concentrations.   Exposure to  a  low-level mixture of N02, 03, and  S02 was
also reported  to increase  sensitivity of healthy subjects to a  bronchoconstrictor.
15.2.2.2  The  Effects of Nitrogen Dioxide Exposure on Pulmonary Function in Sensitive
Subjects—Subjects such as patients  with  asthma or chronic bronchitis have  been studied  by
several  investigators,  as summarized in Table  15-4.   For  example,  Von  Nieding  et al.  (1973)
exposed 14 patients with chronic bronchitis  to N02 at a concentration of 9,400  ug/m   (5.0  ppm)
for 15  minutes  (Table  15-4).   Alveolar  partial  pressures  of oxygen measured  before,  during,
and  after  inhalation  of  NO,   were not  altered  significantly  (p >  0.05).   The  earlobe
                                                                                          2
arterialized blood partial  pressure  of  00,  however,  decreased  from an average  of 102  x 10  to
        2
95 x 10   pascals  (76.6  to 71.4 torr) during  exposure to the pollutant.   Accompanying  this was
a significant increase  in  the  difference of partial pressure  of  oxygen in alveoli  (PA02) and
                                            15-17

-------
en
i—•
00
                        TABLE  15-4:   EFFECTS OF  EXPOSURE TO  NITROGEN  DIOXIDE  ON  PULMONARY  FUNCTION
                                         IN CONTROLLED  STUDIES OF  SENSITIVE HUMANS

Concentration
ug/m ppm
9,400
3,800
to
9,400
940
to
9,400
5.0
2.0
to
5.0
0.5
to
5.0
No. of
Subjects
14 chronic
bronchitics
25 chronic
bronchitics
63 chronic
bronchitics
Exposure
Time Effects
60 mins. No change in mean PAD-*, during or after expo-
sure compared with pre-exposure values, but
PaO * decreased significantly in the first 15
mins. Continued exposure for 60 mins. produced
no .enhancement of effect.
lOmins. Significant decrease-in PaCL and increase in
AaDO * at 7,500 ug/m (4.0 ppm) and above; no
significant change at 3,800 ug/m (2.0 ppm).
30 Significant increase in R * above 3,000 ugm/
inhala- (1.63ppm); no signif icantaeffect below 2,800
tions ug/m (1.5 ppm).
Reference
Von Nieding
et al, 1973
Von Nieding
et al. , 1971
Von Nieding
et al. , 1971
940    0.5   10 healthy
             7 chronic
             bronchitics
             13 asthmatics
2 hrs.    1 healthy and 1 bronchitic subject reported
         slight nasal discharge.   7 asthmatics reported
         slight discomfort.   Bronchitics and asthmatics
         showed no statistically significant changes for
         all pulmonary functions tested when analyzed as
         separate groups but showed small but statistically
         significant changes in quasistatic compliance when
         analyzed as a single group.   See pp.  15-28.
                                Kerr, et al.,
                                1978
              190
       0.1   20 asthmatics   1 hr.
         Significant increase in SR  *.   Effect of bron-
         choconstriction enhanced after exposure in 13
         of 20 subjects.  Neither effect observed in 7
         of 20 subjects.
                                Orehek, et al.,
                                1976
          *PA02

           Raw
           SR
             aw
     alveolar partial pressure of oxygen
     airway resistance
     specific airway resistance
                     AaDO
                         2'
                     PaO,
difference between alveolar and arterial
blood partial pressure of oxygen
arterial partial pressure of oxygen

-------
                                                          2            2
in earlobe  arterialized  blood from an average  of  34 x 10  to 43  x  10  pascals (25.5 to 32.3
torr).  When  exposure  was  continued for an additional 60 minutes, further significant distur-
bances of respiratory gas exchange were not observed.
     Von Nieding  et  al.  (1970;1971) also conducted  a  set of studies on NO,  exposure  with 88
                                                                                         3
chronic bronchitics  (Table  15-4).   Of these, 63 were  tested  for R   at 940 to 9400 ug/m  N09
                                                                   cLW                        £-
(0.5  to 5.0 ppm)  and 25 for  Pa02,  PA02,  AaD02, similar measurements for C0?, and other para-
meters at 3700,  7500 and 9400 ug/m3 (2.0, 4.0 and 5.0 ppm).  Significant elevations in R   (p
                                                                    «                    dW
< 0.1) were seen  after exposure to NOp concentrations of 3,000 ug/m  (1.6 ppm) and higher for
30 inhalations  or approximately 3  minutes  (Von Nieding et al.,  1971).  This increase became
                                                     0
more  pronounced   at  concentrations above  3,800 ug/m   (2.0  ppm), and  disappeared  completely
below concentrations of  2,800 ug/m3 (1.5 ppm).   At levels of 7,500 to 9,400 ug/m3 (4.0 to 5.0
ppm), subjects showed >a  significant decrease in Pa02 and an increase in AaD02; no significant
effect was found at 3800 ug/m3 (2.0 ppm).
     Kerr et  al.  (1978)  studied the effects  of  2  hours of exposure to N09 at a concentration
            3
of 940 ug/m  (0.5 ppm) on 7 chronic bronchitic and 13 asthmatic   subjects.   A 15-minute pro-
gram of light to medium exercise on a bicycle ergometer was included in the exposure protocol.
One of seven chronic bronchitics reported a slight nasal discharge associated with the exposure
to NOp.   Seven of 13 asthmatics reported some evidence of slight discomfort,  dyspnea, and head-
ache with exercise.  No  significant changes were found in any of the pulmonary function para-
meters measured   by  spirometry,  plethysmography,  or esophageal  balloon techniques when  the
groups were analyzed separately.   When data  for the  two  groups  were analyzed together, small
but statistically  significant  changes  in  quasistatic compliance were  reported.   However,  the
authors clearly stated:
              "The results of this investigation are in general  negative, which is
              in  itself useful.  Although exposure to higher concentrations of NOp
              have been shown by others to alter function, and very high concen-
              trations  to result in significant damage to the respiratory system,
              it  would  appear that no significant alteration in pulmonary function
              is  likely to result from a 2-hr exposure to 0.5 ppm N02 alone in
              normal  subjects or subjects  with chronic obstructive pulmonary
              disease.   The few significant changes reported here may be due to
              chance alone."
     Several studies have  utilized  a  challenge with acetylcholine in order to further clarify
the pulmonary responses  to  nitrogen dioxide.   Von Neiding  et  al.  (1977) suggested that there
was an  increased  sensitivity  of the  bronchial  tree to administered  acetycholine  in subjects
exposed to  a  very low  level of NO,.   Beil  and  Ulmer (1976) reported an increased sensitivity
                                                          3
to acetylcholine  after a  2-hour exposure  to  14,100  ug/m  (7.5  ppm)  N09 but  not  after 2-hr
                                3
exposures  to  4700 or  9400 ug/m  (2.5 or  5.0 ppm) NO,.    They further found an increased sen-
                                                                       3
sitivity to  acetylcholine in subjects  exposed for 14 hours to 9400 ug/m  (5.0 ppm) N02>
     Orehek  et al.  (1976)  studied  the effects of  low  levels  of NOp exposure on the bronchial
sensitivity  of asthmatic patients  to  carbachol,  a bronchoconstricting  agent.  In  this study
the carbachol was used to induce a response  in asthmatics similar to  the  response occurring

                                            15-19

-------
when  they  are exposed  to  particular  natural  agents to  which  they are  sensitive.   Nitrogen
dioxide  concentrations  were  monitored  by the  Saltzman  method.   For  20 asthmatics,  dose-
response curves were developed for changes in specific airway resistance (SR  ) as a result of
                                                                            aW
the subjects inhaling carbachol after a 1-hour exposure to clean air and, on other occassions,
                                    o
after a 1-hour  exposure to 190 (jg/m   NOp  (0.1  ppm).   Following NOp exposure alone,  slight or
marked increases  in  SR   were observed in only  3  of 20 asthmatic test subjects; however, N09
                       clW                                                                    £
exposure at 0.1  ppm  enhanced  the effect of the  bronchoconstrictor in 13 of 20 subjects.   The
mean  dose  of  carbachol  producing a two-fold  (100%)  increase  in SR   in the 13 sensitive sub-
jects was  significantly decreased from 0.66 mg to 0.36 mg as a result of NOp exposure.   Seven
of the asthmatic subjects showed neither an increase in R   in response to the exposure to N09
                                                         aW                                  L-
alone nor an enhanced effect of NOp on carbachol-induced bronchoconstriction.
     Unfortunately,  the reported  statistical significance  of  some of  the data  is  rendered
difficult to  interpret,  likely  due to the small  sample  size.   For example, the  mean  dose of
carbachol   producing  a  100 percent  increase  in R    was reported  to  be  0.36  mg for  7  non-
                                                  aw
responders and 0.66  mg for 13 responders,  a non-statistically significant difference.   On the
other  hand,  the  mean  doses  of  carbachol  producing  a   100  percent  increase  in R    for 13
                                                                                    aw
responders before  and  after  the NOp  exposure  were 0.66  mg  and  0.36  mg,  respectively;  but,
in  this  instance,  the  same  absolute difference  in  means was  reported to be  statistically
significant.   Similarly,  a 15  percent difference  in  mean R    for 13  responders  before and
                                                             dW
after  NOp  exposure  alone  was  reported to  be  statistically  significant,  but  a 20  percent
difference in the  initial  mean R   between responders and  non-responders was reported to not
                                 aW
be significant.
     The results of  this study are of interest  because  they are suggestive of possible bron-
choconstrictive responses being produced in some asthmatics by very low concentrations of NOp.
These results, however,  do not provide conclusive  evidence  of  adverse responses attributable
to  NOp exposure,  especially  in  view  of some of  the  reported statistically  significant
NOp-induced changes  not  being  markedly  different  in  average  magnitude  to  changes  in R
apparently due to  individual  variations  in lung function  in  the absence of NOp.   The testing
protocol  used  in the  study  was  an  extremely sensitive one, i.e., employing  known  sensitive
subjects,   a potent pharmacologic agent, and  measurements of flow  resistance.   It  is  obvious
from  the  reported responses  of  the  20  subjects to  the  test regimen that only  three  showed
measurable variations as a result of exposure  to NOp alone.   However,  the mean of measurements
of  R    in 13  responders to  the  carbachol  treatment was significantly  higher  after  the N0?
    3W                                                                                       £-
exposure than it  had been  prior to exposure.   The  criticism of this reported change was that
the comparisons  of R    were  made in  subjects selected  not  at  the time  of N0~  exposure, but
                     3W                                                        ^
after the  fact,  following  the carbachol exposure.   There was no report  of the  initiation of
an  asthma  attack,  or even  wheezing, or lack  of  such symptoms in  any  subject,  as a result of
the  combined   insults   of  carbachol  and  NOp,  clouding  interpretation  of  how  the  observed
effects might  relate to asthma  attacks under ambient conditions.  The  study  may have  health
                                            15-20

-------
 implications,  however,  since it  suggests  that those  asthmatics whose  illness  results  from
 vagal  stimulation might  be predisposed  to  have more  severe  attacks  (once  induced by other
 agents)  as  a result of  also  breathing  N0?.  However, such a suggestion  (that the effects  of a
 potent  vagal  stimulus  may  be  increased by  the inhalation of  low levels  of NO- seems to be  at
 odds with the report of  Yokoyama  (1972) discussed earlier, who found  that atropine blocked the
 bronchoconstrictor  effect of SOp but not NCL  and, for  this reason, concluded that NOp did not
 act  by  stimulating the vagus  nerve.   It thus  remains  to be determined  as  to what  concentra-
 tions of N02 may produce  significant broncoconstriction or other pulmonary mechanical effects
 in asthmatics under ambient exposure conditions.
     Another  suggestion  that  measurably greater impact  of  exposure  to  N0?  occurs  in highly
 susceptible  individuals  is  obtained  from the  studies  of Barter and Campbell  (1976).   These
 investigators studied  a  group  of  34 subjects with mild  bronchitis and  showed that decreases  in
 FEV, p,  over  a  period of  5 years,  were  related to the subjects'  degree of reactivity to the
 bronchoconstrictor,  methacholine.  Even minimal cigarette  smoking,  a  source  of significant
 concentrations  of nitrogen oxides (Norman and Keith, 1965), led  to ventilatory deterioration,
 which  the  investigators  believed  to   be  serious  when  methacholine  reactivity   was  high.
 However,  heavy  smoking had little effect on ventilatory function when reactivity to methacho-
 line was slight.  It is  not certain that  the effective  material in the cigarette smoke causing
 the  impairments  in ventilatory function was NOp, although this seems to be a good possibility.
 It also  is  not  known  how  these  study  results  relate to ambient  NOp  exposures  of individuals
 who  are  highly  reactive  to  methacholine.
     Thomas  et  al.  (1972)  showed no  effect  of exposure  to NCL at  concentrations  of 940  to
          3
 6,580 ug/m   (0.5 to 3.5 ppm) on  histamine concentrations in sputum or on total sputum weight,
Jn  five  healthy  subjects,  or four  patients  reported  to  have  chronic  respiratory disease.
     In  summary,  studies of N00 effects on pulmonary function  in  potentially susceptible popu-
                                                                                             3
 lation  groups  show that,  in persons with  chronic bronchitis, concentrations  of 9,400 ug/m
 (5.0  ppm)  produce decreases  in  PaOp  and increases in  AaDOp,  whereas  exposures  to  concentra-
 tions of NOp  above 2,800 ug/m  (1.5 ppm),  for periods  considerably less than 1 hour, produce
 significant increases  in R   (p < 0.1).    Thus,  results  from bronchitic individuals and healthy
                          aW                                                       3
 individuals differ  very  little.   In contrast,  in  one study,  exposures to 190 ug/m  (0.1 ppm)
 N09  for  1 hour  were   reported to have increased mean  R    in  3  of 20  asthmatics  and to have
  £                                                      uW
 enhanced  the effects  of  a bronchoconstrictor  in  13  of the  same 20  individuals.   However,
 in  another  study,  no measurements  of  pulmonary  function were  significantly altered  in  13
 asthmatics as  a  result  of 2  hours  of exposure to  940 ug/m   (0.5 ppm) NOp.   Thus, whereas
 NO-,  exposures sufficient to produce increased R   in healthy  individuals or those with symp-
  £                                              3W
 toms of  chronic  respiratory illness may  indeed produce much greater and more severe responses
 in other highly  susceptible  segments  of the  population  (e.g., asthmatics),  controlled human
 exposure studies  to date do not convincingly demonstrate pulmonary function changes  in suscep-
 tible population  groups  at NOp exposure  levels  below those  affecting normal, healthy adults.
                                            15-21

-------
15.3  EPIDEMIOLOGICAL STUDIES
     Epidemiologies! studies of the effects of community air pollution are complicated because
there are  complex  varieties of pollutants present in the ambient air that exposed populations
breathe.  Thus, the  most that can usually be demonstrated by such studies is that an associa-
tion exists  between observed  health  effects and  a  mixture of air pollutants.   In  order for
inferences to  be  drawn  regarding likely causal  relationships between any individual  pollutant
present  in  such mixtures  and observed effects, consistent  associations  must  be demonstrated
between  variations  in  exposures to  the pollutant  and  particular types  of effects  under  a
variety of circumstances (of course with potentially covarying or confounding variables having
been adequately controlled for or taken into account in the analysis of study results).
     In  attempting to demonstrate  qualitative  or quantitative relationships  between  N02 and
health effects, presently available epidemiological studies have been notably hampered by dif-
ficulties in defining actual exposure levels or durations for study populations.   For example,
many N02-related epidemiological  studies  conducted prior to 1970 are of questionable validity
due to  a  number of instrumental and analytical  problems  inherent in the air monitoring tech-
nique (Jacobs-Hochheiser method) typically employed for measuring atmospheric concentrations  of
NCL.  Still  other  study  results can be questioned on the basis of how representative reported
aerometric results are of  actual  N0? exposures  of study  populations.   For these reasons, the
contributions of pre-1970 community air pollution studies to knowledge concerning N02 exposure
effects  are  highly  limited  at this time  and are,  therefore,  not discussed  in detail  here.
     Rather, only selected pre-1970 studies and other relevant post-1970 studies  are  discussed
below,   together with  notation (as appropriate)  of certain  major  problems affecting  interpre-
tation  or acceptance  of  their results.   The  outdoor pollution  studies  thusly assessed can be
conveniently divided  into  the following categories:   (1) those evaluating  potential  associa-
tions between  N02  exposures and diminished pulmonary functions; and (2) those evaluating pos-
sible increased risks for  acute or chronic respiratory diseases in response to NO,, exposures.
     In addition to  the  outdoor ambient air  pollution studies,  other epidemiological  evalua-
tions of  the effects of  indoor air pollution are  also discussed, with particular emphasis on
possible  relationships between  indoor  exposures to N0? and  respiratory diseases in  children.
15.3.1  Effects of NOp on Pulmonary Function
     Among the  better known studies evaluating NO^-related health effects are those  conducted
by Shy  et al.  (1970a,b;1973) on schoolchildren during 1968-69 in Chattanooga,  Tennessee.   Shy
et  al.  (1970a) reported that values for  0.75-second  forced expiratory  volume  were  lower in
those children  living in areas of apparently high N02 concentrations than for children living
in areas  with  lower  NOp  concentrations.  However, measurements of  N02  concentrations used in
this study were done by  means of the Jacobs-Hochheiser method*,  which was subsequently found  to
"The Jacobs-Hochheiser technique has been withdrawn by EPA and replaced by a new Federal  Refer-
ence Method (chemiluminescence) and other equivalent methods (see Chapter 7).
                                            15-22

-------
be  unreliable  and  not  acceptable for  deriving  quantitative estimates  of  NCL levels present
in  the  1968-69  Chattanooga study areas.   In  view of some overlap between NCL levels reported
for  certain monitoring  sites  in the  "high" NO^  pollution study  areas  and NO,,  levels for
some  monitoring  sites  in  the  lower  N02   pollution  study  areas  (based  on  the  original
Jacobs-Hochheiser  readings),  even  qualitative  comparisons  of  effects  observed  between the
study  areas are  of  questionable value.   This   is  especially  true given  that  differential
effects observed with pulmonary function tests were stated to be small (although statistically
significant) and showed inconsistencies during the testing period.
     Several other  community  health  epidemiological studies in  various  geographic  areas have
attempted to provide quantitative assessments of pulmonary function changes in relationship to
ambient air NCL levels.   These studies, using a more acceptable NCL measurement technique (the
Saltzman  method),   are  summarized in  Table  15-5.   For  example,  Speizer and  Ferris (1973b)
administered pulmonary  function  tests  to 128 traffic  policemen  in  urban  Boston  and  to 140
patrol  officers  in nearby suburban  areas  (Table 15-5)  but  found  no differences  in pulmonary
function between the two study groups.   Mean 24-hour N09 concentrations determined from 1-hour
                                                                 3
sampling data, measured  by the Saltzman technique, were 100 (jg/m  (0.055 ppm) in the downtown
urban area, and  75  (jg/m  (0.04 ppm)  in the suburban area (Speizer and Ferris, 1973a).  Sulfur
dioxide levels averaged 92 ug/m   (0.035 ppm) in the city and 36 ug/m  (0.014 ppm) in the subur-
ban area.
     Cohen et al.  (1972) also found no differences in the results of several ventilatory tests,
including spirometry  and  flow-volume curves,  for nonsmoking adults  living  in the San Gabriel
Valley  of  the  Los  Angeles basin and  similar nonsmokers from  San  Diego (Table  15-5).   The
average N02 concentration  in  the  Los Angeles  basin was  96  ug/m   (0.05  ppm)  based  on the
Saltzman method.   The ninetieth percentile of the daily averages in this area, i.e., the level
exceeded only 10  percent  of the time,  was 188 ug/m  (0.1 ppm).   In San Diego, the average and
ninetieth percentile were, respectively, 43 and 113 ug/m  (0.02 and 0.06 ppm) based on Saltzman
method measurements.
     Linn et al.  (1976)  performed a  variety of pulmonary function tests during the summer and
winter seasons on  205 office  workers of both sexes in Los Angeles and 439 similar individuals
in San  Francisco.   Additional  information about  respiratory symptoms was obtained by means of
personal interviews.  This  study  was undertaken  primarily to determine the effects of oxidant
air pollution,  but information regarding NO- was  provided as well.   Most results of FEV, single
breath Np tests,  and  interviews showed no differences  between  cities.   Los Angeles women did
report nonpersistent  cough  and  phlegm  more often than did San Francisco women, and smokers in
both cities showed  greater  changes  in  pulmonary  function than  did nonsmokers.  Median hourly
oxidant values  (primarily 03)  were 0.07 and 0.02  ppm in  Los  Angeles and San Francisco, respec-
tively.   Ninetieth  percentile oxidant  values were  0.15  and 0.03 ppm.  The  median  hourly NO,
                                                                •3                            t-
concentrations  based on  the Saltzman  method were  130 and 65  ug/m  (0.07 and 0.035 ppm),  respec-
tively, for Los  Angeles  and San Francisco.   The 90th percentile hourly NO, concentrations were
                •3                                                        '
250 and 110 ug/m  (0.13  and 0.06 ppm) for Los Angeles and San Francisco,  respectively.

                                            15-23

-------
                       TABLE  15-5.   QUANTITATIVE  COMMUNITY  HEALTH EPIDEMIOLOGICAL STUDIES ON EFFECTS
                                   OF  EXPOSURE  TO NITROGEN  DIOXIDE ON PULMONARY FUNCTION
en
ro


Measure
High exposure group:
Annual mean
24-hr concentrations

90th percentile
Estimated 1-hr
a
maximum

Low exposure group:
Annual mean
24-hr concentrations
90th percentile
Estimated l~hr
maximum3

Mean "annual" 24-hr
concentrations: high
exposure area

low exposure
area

1-hr mean:
high exposure
area
low exposure area


NO
Conce
ug/m

96


188
480
to
960

43

113
205
to
430
103
92


75
36

260
to
560
110
to
170
Exposure
gtrations
ppm

0.051


0.1
0.26
to
0.51

0.01

0.06
0.12
to
0.23
+ 0.055 +
S0? 0.035
so2

+ 0.04 +
SO,, 0.014
S0?
0.14
to
0.30
0.06
to
0.09

Study
Population Effect Reference

Nonsmokers No differences in several ventil- Cohen et al.,
Los Angeles atory measurements including spi- 1972
(adult) rometry and flow volume curves





Nonsmokers
San Diego (adult)




Pulmonary No difference in various pul- Speizer and
function monary function tests. . Ferris,
tests admin- 1973a,b
istered to
128 traffic Burgess et al.,
policemen in 1973
urban Boston
and to 140
patrol officers
in nearby sub-
urban areas.



-------
                                                     TABLE 15-5.   (continued)
en
i
r-o
en

N09 Exposure

Measure
Los Angeles:
Median hourly N09
^

90th percent! le N0?
t-
Median hourly 0
90th percentile 0
X
San Francisco:
Median hourly N0?

90th percentile N02
Median hourly 0
90th percentile 0
1-hr concentration
at time of testing
(1:00 p.m.)

Concegtrat
ug/m

130

250



65

110


40
to
360

ions
ppm

0.07

0.13
0.07
0.15

0.035

0.06
0.02
0.03
0.02
to
0.19

Study
Population

205 office
workers in
Los Angeles



439 office
workers in
San Francisco


20 school
chi Idren
11 years of
age

Effect

No differences in most tests.
Smokers in both cities showed
greater changes in pulmonary
function than non-smokers.







During warmer part of the year
(April-October) NO SO and
TSP* significantly correlated
with V * at 25% and 50% FVC*
may

Reference

Linn, et
al. , 1976









Kagawa and
Toyama ,
1975

                                                               and with specific airway con-
                                                               ductance.   Temperature was
                                                               the factor most clearly correlated
                                                               with weekly variations in specific
                                                               airway conductance with V    at
                                                               25% and 50% FVC.  Significant
                                                               correlation between each of four
                                                               pollutants (NO   NO, S0? and TSP)
                                                               and V    at 25% and 50% FVC; but
                                                               no clear delineation of specific
                                                               pollutant concentrations at which
                                                               effects occur.
      .Estimated at 5 to 10 times annual mean 24-hour averages
      Mean  "annual" concentrations derived  from 1-hour measurements using  Saltzman technique
      *VEV0.75:
       max

       FVC

       TSP     :
Forced expiratory volume, 0.75 seconds
Maximum expiratory flow rate

Forced vital capacity

Total suspended particulates

-------
     In a Japanese investigation, relationships of ambient temperature and air pollutants (NO-,
NO,' 03, hydrocarbons,  S02,  and participate matter) to weekly variations in pulmonary function
in 20  school  children,  11 years of age, were studied in Tokyo by Kagawa and Toyama (1975) and
Kagawa  et  al.  (1976).  Of  all  the  factors assessed, temperature was  most closely correlated
(p <  0.05) with variations  in  specific airway conductance, and with  maximum expiratory flow
rate (Vmax) at 25 and 50 percent of FVC.  In children believed by the investigators to be sen-
sitive  to  air  pollution,  a significant negative correlation was  observed between exposure to
Og and specific airway  conductance;  other negative  correlations  were  found  between NO- (as
measured by the  Saltzman technique),  NO, SO,, and particulate matter, with V    at 25 percent
                                            c.                                (TlciX
or 50 percent FVC.   At high outdoor temperatures NOp, SOp, and particulate matter were signifi-
cantly  correlated  (negatively)  with both Vm=v  at  25  percent or 50 percent  FVC,  and specific
                                           fTlaX
airway conductance (p < 0.05).
     In the ambient  situation,  however, the above effects were not associated with N0« alone,
but with the combinations of air pollutants, including SOp, particulate matter, and 0.,.   During
the period of high outdoor temperatures, correlations between lung function and N02 concentra-
tions  were calculated using  the pollutant level  in the  ambient  air at  the  time of testing
(1:00  p.m.).   These  hourly  N02 values ranged from 40 to 360 ug/m3 (0.02 to 0.19 ppm), but the
data reported  afforded  no quantitative estimation of specific N02 levels that might have been ,
associated with  the  occurrence  of pulmonary function decrements.   The authors (Kagawa et al.,
1976)  noted that:   "From the relationship between NO,  and V    at 50% FVC in subject No. 16, :
                                                      £-       max
who showed the highest  correlation,  it seems  that  NO,  started  having a  significant  effect
above  a concentration  of 4 pphm."  The basis for this statement,  however, is not obvious from
the published  (Kagawa and  Toyama,  1975;  Kagawa  et  al. ,   1976) data  or  statistical  analyses,
which  do not  appear  to provide sufficient bases for estimating N0~ air concentrations associ-
ated with pulmonary function decrements.
     In other  Japanese  studies measurements  of  pulmonary  function  in  employees exposed  to
diesel  exhausts in railroad tunnels were reported by Mogi  et al. (1968) and by Yamazaki  et al.
(1969).  Results of pulmonary function tests were compared with similar results from employees
in other situations in which exposure was classified as  medium, light, or "no-pollution."  Mean
                                                                                    3
NO, concentrations, measured  by the Saltzman method, ranged from  300 to 1,130 (jg/m  (0.16 to
                                                                •               3
0.60 ppm).  Highest  measured N02 concentrations ranged from 340  to 3,000 ug/m  (0.18 to 1.60
ppm).   Test results [VC, FEV-j^ Q, maximal flow rate (MFR) and mid-maximal  flow rate (MMFR)] from
475 employees  were  highest  in those working in "no-pollution"  areas.   Results obtained on the
remaining  subjects  showed a decrease  in  pulmonary function which did not  correlate  with the
N02 concentrations in their work areas.
     Results of  epidemiological studies on the effects of outdoor ambient  air N0?  exposures
provide no consistent  indication that the mean concentrations  of N02 or of N02 in combination
with other pollutants listed in Table 15-5 had any significant effects on lung function in the
                                            15-26

-------
exposed populations.  One  study  did show some apparent  associations  between Vm,v or specific
                                                                               rnaX
airway conductance  and  concentrations  of NOp and other pollutants at the time of testing, but
the contributions of  individual  air pollutants were difficult  to  disentangle and appeared to
be less than those attributable to temperature variations.
15.3.2  Effects of NO,, on Acute Respiratory Illness
15.3.2.1   Effects Associated With Ambient Exposures—Only  a  few  community  epidemiological
studies  of outdoor  NO   exposures  have  been  reported  as  demonstrating  associations  between
                      A
ambient  air  levels  of  NO   compounds and measurable health  effects.   However,  methodological
problems with  all of  the studies preclude acceptance  of any of the results as clear evidence
for increases in acute respiratory illness due to NO  exposures.
     Shy and co-workers  (Shy,  1970;  Shy et al.,  1970b; 1973) studied the effects of community
exposure to N0?  in  residential areas of Chattanooga on respiratory illness rates in families.
The distances  of three  study  communities from  a large point  source of  N0~ resulted  in  an
apparent gradient of  exposure  over which the illness rates were determined.  The incidence of
acute respiratory disease  was  assessed at 2-week intervals during the 1968-69 school year and
the respiratory  illness rates adjusted  for  group differences  in  family  size and composition
were reported  to  be significantly higher for each family segment (mothers, fathers, children)
in the high-NOp  exposure neighborhood  than in the  intermediate-  and low-NO^ areas.  However,
in this study,  NO- concentrations were  determined by the Jacobs-Hochheiser method and,  as indi-
cated earlier,  this method has since been shown  to  be unreliable (Mauser  and  Shy,  1972; See
Chapter  7  for  a  more complete discussion).   Meaningful quantitative  estimates  of population
N0? exposures were therefore not available for the study areas;  also, overlaps in reported N02
levels between  "high"  N0? area monitoring sites and those for lower NO- study areas make quali-
tative comparisons  between the  study  areas  somewhat problematic.   In addition,  no basis was
provided by which the relative contribution of NOj exposures could be separated from those of
other pollutants present in the study areas.
     Additional data  on acute respiratory disease  rates in the same  Chattanooga study areas
were collected  in 1972-1973,  by which time  no differences in N02 levels  existed between the
study areas  as measured by the  Saltzman  technique.   Preliminary analyses  of these data were
reported by Shy  and Love (1979), but further (final) analyses of these data remain to  be com-
pleted,  peer reviewed, and published.
     In an earlier  retrospective study in the same  Chattanooga areas,  Pearlman et al.  (1971)
investigated the frequency  of  lower respiratory  disease among  first-  and second-grade school
children and among children born between 1966 and 1968.   Responses on 14 percent of the health
status questionnaires were  validated  against  physician  and  hospital  records,  with  overall
accuracy of  parental  reporting  of  illness episodes  being 70.5,  67.9,  and  90.0  percent for
bronchitis, croup, and pneumonia, respectively.  No significant study area differences  in ill-
ness rates  were  found  for croup, pneumonia,  or a  combined "any lower  respiratory disease"
category  in  pre-school   infants  or schoolchildren;  nor  did illness  rates for  these  illness
                                            15-27

-------
categories follow the reported pollutant gradient for any age group classified by period (1,2,
or 3 yrs) of residence in the respective study areas.  Similarly, illness rates for bronchitis
failed  to follow  the  reported  NOp  exposure gradient  (except  for  schoolchildren  of 3  yr
residence), with intermediate area bronchitis rates otherwise generally exceeding those deter-
mined for  the  children  in the high N02 area.  Only bronchitis rates in schoolchildren who had
lived in the area for 3 or more years followed the exposure gradient and were found to be signi-
ficantly higher than for children from the low N02 area.   The validity of this reported differ-
ence, however,  appears to be questionable in view of:  (1) its internal  inconsistency with the
other study results reported; (2) the only moderately high accuracy (70.5 percent) of reporting
of bronchitis  rates  in  comparison to the  accuracy (90 percent) for pneumonia  rates;  and (3)
the  reported  inability  of  parents  to date  precisely the occurrence of  bronchitis episodes,
making  it  impossible to  separate  such  illnesses  occurring  before residence  in  the exposure
areas from those occurring  thereafter.   Also, the same  difficulties  in defining the reported
NOp  exposure  gradient (presumably based on  use  of the Jacobs-Hochheiser N0« method)  for the
study areas  used  in this  study  likely apply  as  noted  above  for  the  Shy et  al.  1968-69
Chattanooga studies.
     Polyak  (1968)  reported  44  percent more health  clinic  visits for  respiratory,  visual,
nervous  symptoms, and skin  disorders by residents living within 1 kilometer of a Soviet Union
chemical works than  by  residents living more than 3 kilometers from the factory complex.   The
study subjects, none  of  whom worked at  the  chemical  plant,  were exposed to  a  combination  of
pollutants.  Concentrations  reported were:   NO.,,  580 to 1,200  vq/tn  (0.31  to 0.64 ppm);  SO,,
        3                                         3
225 (jg/rn   (0.09 ppm);  and sulfuric acid, 400 ug/m  (0.1 ppm).   The report also indicated that
a  NOp concentration  of  1,600 ug/m   (0.85  ppm),  combined with high concentrations  of  S02  and
sulfuric acid, occurred  1 kilometer from the plant.   However,  no information was provided on
the methods used to  measure N02  or  by which to  assess the relative contribution of N02 expo-
sures to the reported health effects.
     In  another study from the Russian literature, Giguz (1968) studied  illness rates and other
factors  in 16- to  19-year-old vocational trainees in  the  Soviet Union.  Individuals training
in fertilizer  or  chemical manufacturing plants  (N=145)  were compared  with 85  individuals  of
the same age not exposed to pollutants found in the manufacturing plants.   Exposure concentra-
tions of N02 and ammonia, gases expected by the investigators to occur in highest concentrations
in this situation, did  not exceed the maximum permissible concentrations (average daily mean:
for  N02,  100  |jg/m3  or  0.053 ppm in  1964)  in the U.S.S.R. (Nikolaeva, 1964).   Subjects  were
exposed  to the pollutants for 3  hours a day for 150 days during  the first year of training,
and for  6 hours a day for 200 days during the second year.   During the second year of training,
exposed  individuals were  reported  to have  an increased incidence of acute respiratory disease
and  increased  serum  levels  of  beta-lipoproteins, cholesterol,  and  albumin.  However,  this
report  lacks important  information  related to air pollutant  sampling  frequencies and methods,
making it difficult to evaluate the reliability of quantitative estimates of NO,, levels associ-
ated with reported  health effects.

                                            15-28

-------
      Petr and Schmidt  (1967)  studied acute respiratory illness among  Czechoslovak!an  school-
 children living  near a  large  chemical  complex.   They found a  disease incidence  twice  that
 observed in  children of  the  same age  living in  a  low-exposure  community of  similar socio-
 economic characteristics.  A greater number of hypertrophied tonsils and cervical  lymph nodes
 also were  found  in  children  from two  towns,  each having  high  pollution but  differing  with
 respect to relative  concentrations  of NCK and  S02.   Children  from  the area having  the  lower
 concentrations of NO  had much lower lymphocytogram values and  higher indices  of proliferation
 and differentiation of monocytes.   The clinical significance of these differences is  not known
 and the results  of  the Petr and Schmidt  (1967)  study are difficult to interpret because  data
 on concentrations of NO and N02 individually were not  presented.   Nor was information provided
 on the sampling frequency or methology for NO or N09 measurements  or on levels  of other pollut-
 ants such  as acid  aerosols,  particulate  nitrates, sulfates,  or total  suspended  particulate
 matter.   It  is probable  that  such a variety of pollutants was  present around  a large chemical
 complex, but  no  basis  was provided  by which  to assess the relative contribution  to reported
 health effects of NO  compounds from among other air pollutants present.
                     /\
 15.3.2.2  Effects Associated With  Indoor Exposures
 15.3.2.2.1  Tobacco smoking studies.    Tobacco smoke is a  major source of nitrogen  oxides,  and
 may include  significant  concentrations  of N09.   Norman and Keith  (1965) demonstrated that the
                                                1              C      T
 concentration of  NO may vary between 492  x 10  and 1.23 x  10  |jg/m  (400 and  1,000  ppm)  in
 cigarette smoke depending on the type of filter included and the extent to  which the  cigarette
 is  smoked,  i.e.,  the  last puff  contained  higher  concentrations  than  did  the fourth  puff.
 Often N09 could not be measured in the cigarette smoke but,  in  other instances,  concentrations
                        3
 as high as 47,000  |jg/m  (25 ppm)  were found.   In confined spaces such as  meeting  rooms,  con-
 centrations of N0~  might build up  to potentially hazardous levels, when  several  individuals
-are smoking.    Smoking  then may represent a  significant source of exposure for  nonsmokers  as
 well as smokers.
      Many adverse  health effects  have  been associated with  smoking, particularly  cigarette
 smoking.   It  has not been possible,  however,  to implicate conclusively any single  factor  in
 cigarette smoke as the one primarily responsible for the effects observed.  Other major pollu-
 tants in cigarette smoke include CO  and  tars.   Each of these materials,  in  experimental  situa-
 tions,  causes a fairly unique  type of  effect.    Consequently,  even  though  no  specific  adverse
 effects can  be attributed conclusively  only to  the N0? in cigarette smoke,  the  increases  in
 some adverse  health  parameters  point strongly  in this  direction.    Specific health  effects
 possibly related  to  exposure to  N02 in  cigarette  smoke  include increased acute  respiratory
 illnesses or  prevalence of chronic respiratory disease.
                                             15-29

-------
15.2.2.2.2   Epidemiological  Studies of Gas Combustion Products.     Combustion  of  natural  or
manufactured gas  within confined  spaces  leads to increases in  N0? concentrations.   Although
some  CO   and other pollutants  may  also  be produced by gas-burning  appliances,  the relative
efficiencies of  the combustion process cause the  largest  quantities of N0? to  be produced
when  CO  production  is  lowest.    This tends  to  suggest  that  increased health  effects,  if
observed in  homes  with gas stoves, are more  likely  the result of  NOp  exposure  than CO expo-
sure; however, effects  due to exposure to  other  potentially  toxic  products  of gas combustion
cannot be ruled out.
     Social   characteristics  of family  life,  as  well  as the  size  and type of  housing,  also
affect exposure  parameters for those  people  living  in homes with pollution  produced  by gas
appliances or other  sources.   For example, a home with a small kitchen containing a gas stove
may represent a  greater hazard for individuals who spend much time  in the kitchen, especially
if the  social  custom  is to  heat  as  little of the home as  possible, and most or  all  of the
family spend considerable  time in or  near the  kitchen.  In  such  homes,  relatively frequent
(almost  continuous)  exposure  periods  to  gas  stove  pollutants may  be  experienced  by  family
members.   In other homes, however, such as those with central  heating, family members may spend
much  less time in  the  kitchen and, therefore,  experience less exposure to gas  combustion pro-
ducts.
     Several studies  show  that homes  with gas  stoves  typically have  higher  N0?  levels  than
those with  electric stoves.   For  example, Wade  et  al. (1975)  reported that, over a  2-week
                                                                                       3
period,  the  average  concentration  of NOp  in kitchens with gas stoves exceeded 94 ug/m  (0.05
ppm)  and that  in  different parts  of the  house,  the  concentrations  fluctuated  with use  of the
stoves.   Nitrogen  dioxide  was monitored by a chemiluminescence method.   Average  levels  of 280
ug/m  (0.15  ppm)  NOp for 2 hours  were  measured  in the kitchen.   Other studies of NOp concen-
trations in  homes during the  preparation  of  meals have demonstrated that gas stoves produce
NOp concentrations  usually within  the  range of 470 to 1100 ug/m  (0.25 to 0.6  ppm) in the im-
mediate vicinity  of the stove (Mitchell  et al., 1974; U.S.  Environmental Protection Agency,
1976).  The  highest level   recorded  was 1,880 ug/m   (1.0  ppm).   The high concentrations are
significantly reduced  within  2 hours  after the  stove  is  turned off.  The  specific time for
reduction of peak  concentrations  by any given percentage  after  the cessation  of stove  usage,
however,  depends  upon  such parameters  as  the  presence  or  absence  of ventilation  devices and
the details  of interior architecture.   Other studies  also indicate NO- is higher  in homes using
gas than those using electricity (Melia et al., 1978;  Goldstein et al.,  1979; Spengler et al.,
1979).
     Observations  of elevated NOp and other air  pollutant  levels in gas stove homes in  com-
parison to electric stove homes have prompted epidemiological  investigations  of possible health
effects associated with  the  higher levels of indoor  air pollutants  in homes  using gas stoves.
The results  of such epidemiological studies are summarized  in Table  15-6.
                                            15-30

-------
  1ABLL 15-6.   EFFECTS OF EXPOSURE [0 N11KOGEN FJIOXIUE  IN  MIL  HOME  ON  LUNG  FUNCTION AND
THE INCIDENCE  OF ACUTE RESPIRA10RY DISEASE IN EPIDEMIOLOGY  STLIULES  OF  HOMES W1III GAS SIOVLS
----- - - ....
Pollutant3
NO;,
Concentration
pg/mj ppm
Study
Population
if feels
Reference
Studies of Children
NO^ plus
other gas stove
combustion products
NO,, plus other gas
stove combustion
products
NO. plus other
gas stove
combustion
products
NO. plus other
gas stove
combustion
products
NO,, concentration
not measured at
time of study
N0« concentration
not measured in
same homes studied
Kitchens:
9-596 (gas) 0.005-0.317
11-353 (elec) 0.006-0.188
Bedrooms:
7.5-318 (gas) 0.004-0. 169
6-70 (elec) 0.003-0.037
(by triethanolamine
diffusion samplers)
95 percentile of 24 hr
avg in activity room
39 - 116 ug/m ( . 02 -
.06 ppm) (gas) vs.
17.6 - 95.2 ug/m
(.01 - .05 ppm)
(electric). Frequent
peaks ~ 1100 ug/m (0.6
ppm)-max peak ~ 1880
ug/m (1.0 ppm) 24 - hr
by modified sodium
arsenite; peaks by
chemi luminescence
2554 children from homes
using gas to cook compared
to 3204 children from homes
using electricity. Ages 6-11
4827 children
ages 5-10
808 6- and 7-year-old
chi Idren
8,120 children 6-10 yrs old in
6 different communities with
data collected on lung function
and history of illness before
the age of 2
Proportion of children with one
or more respiratory symptoms
or disease (bronchitis, day or
night cough, morning cough,
cold going to chest, wheeze,
asthma) increased in homes
with gas stoves vs. electric
stove homes (for girls p -0.10;
boys not sig. ) after controlling
for confounding (actors
Higher incidence of respiratory
symptoms and disease associated
with gas stoves (for boys p -0.02;
girls p -0.15) after controlling
for confounding factors
Higher incidence of respiratory
illness in gas-stove homes
(p ~0.10). Prevalence not
related to kitchen N0? levels,
but increased with NO,, levels
in bed rooms of children in
gas-stove homes. Lung function
not related to NO- levels in
kitchen or bedroom
Significant association between
history of serious respiratory
illness before age 2 and use of
gas stoves (p <.01) and, also,
between lower FEV, FVC levels
and use of gas stoves (p ^.01)
Melia tt al. , 19/7
Melia et al. , 19/9
Florey et al. , 1979
Companion paper to
Melia et dl , 1979,
Goldstein et al . ,
1979
Speizer et al . , 1980
Spengler et al. , 1979

-------
                                                                  TABLE 15-6  (continued)
CO
rsi
Pollutant3
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
N02
Concentration
ug/m3 ppm
Sample of households
24 hr avg: gas (.005 -
. 11 ppm); electric
(0 - .06 ppm); outdoors
(.015 - .05 ppm)- several
peaks > 1880 ug/m (1.0
ppm). Monitoring location
not reported. 24-hr avgs
by sodium arsenite; peaks
by chemi luminescence
Saeiple of same
households as reported
above but no new
monitoring reported
Study
Population
128 children 0-5
346 children 6-10
421 children 11-15
174 children under 12
Effects Reference
No significant difference Mitchell et al., 1974
in reported respiratory See also Keller et al..
illness between homes with gas 1979a
and electric stoves in children
from birth to 12 years
No evidence that cooking mode Keller et al. , 1979b
is associated with the incidence
of acute respiratory illness
Studies of Adults
NO. plus other
gas stove
combustion
products
NO- plus other
ga§ stove
combustion
products
NO. plus other
gas stove
combustion
products
NO- plus other
gal stove
combustion
products
Preliminary measure-
ments peak hourly
470 - 940 ug/g
max 1880 ug/m
(1.0 ppm)
See table above
for monitoring
See table above
for monitoring
See table above
for monitoring
Housewives cooking with
gas stoves, compared to
those cooking with
electric stoves
Housewives cooking with
gas stoves, compared to
those cooking with electric
stoves. 146 households
Members of 441 households
Members of 120 households
(subsample of 441 households
above)
No consistent statistically USEPA, 1976
significant increases in
respiratory illness associated
with gas stove usage
No evidence that cooking with Keller et al., 1979a
gas associated with an increase
in respiratory disease
No significant difference in Mitchell et al., 1974
reported respiratory illness See also Keller et al.,
among adults in gas vs electric 1979a
cooking homes
No significant difference among Keller et al., 1979b
adults in acute respiratory
disease incidence in gas vs
electric cooking homes

-------
     Two independent sets of epidemiological studies, from Britain and the United States, pro-
vide data  suggesting  likely associations between respiratory illness symptoms in children and
residence  in  homes using  gas  stoves  for  cooking versus residence  in  homes  using electrical
stoves.  Much  caution  must be employed, however,  in  interpreting the results of such studies
in  terms  of specifically  implicating NO^  exposures  in the  etiology of the  reported health
effects and in attempting to define pertinent exposure/effect relationships.
     Results of  the British  studies  have  been  reported by Melia et al.  (1977;  1978; 1979),
Goldstein et al.  (1979),  and Florey et al.  (1979).  The initial study,  conducted from 1973 to
1977,  investigated the effects of indoor and outdoor air pollution on respiratory illness in a
large  cohort of  primary school  children from randomly selected areas of England and Scotland.
Results for the  first  year (1973) of  the  study  were reported by Melia  et al.  (1977).  Addi-
tional results from the last year of the study (1977) and from longitudinal  analyses  (1973 to
1977) were reported by Melia et al.  (1979).
     The cross-sectional analysis of  1973 results discussed  by  Melia et al.  (1977),  involved
2,554  children  from  homes with  gas  stoves  and  3,204 from homes  with electric  stoves  and
examined the prevalence  of bronchitis, cough,  colds going to the chest, wheeze, and asthma by
means  of  questionnaires.   Crude prevalences for  each condition were higher  in  children from
homes  where  gas  was used  and statistically significant (p <0.05) for  bronchitis,  cough,  and
colds  going to the chest in both sexes,  and  for  wheeze in girls.   The  authors reported that
this "cooking  effect"  appeared  to be  independent  of  the effects of  age, social  class,  lati-
tude,  population  density,  family size,  overcrowding,   outdoor  levels  of particulate matter
(smoke) and sulfur dioxide,  and  types of fuel  used for heating.   This conclusion was based on
the proportion of  children with  more than  one disease  or symptom being higher for homes with
gas cooking when these various factors were taken into account;  however, when  the factors were
taken  into account, the  main  finding of the proportion of  children with one  or more respira-
tory symptoms  or diseases  remaining  higher in both boys and  girls  from gas  stove  homes only
approached statistical  significance for  girls  (p~ 0.10) but  not  boys.   Furthermore, data for
several of the  variables were missing so that only very small  numbers remained within necessary
subgroups,  prompting the authors  to  state that the results  from these  analyses were not con-
clusive and needed to  be confirmed  by follow-up  data then being collected.   Nevertheless,  the
authors concluded that elevated  levels of nitrogen oxides arising from combustion of gas  might
be the cause of the increased respiratory illness.
     In 1977,  another  cross-sectional  study of  similar design  was conducted  on a different set
of children, 3,017  from  homes with  an electric stove,  and  1,810 from homes with  a gas  stove
(Melia et  al.,  1979).    Crude  prevalences  indicated  that cough  in  boys (p ~0.02),  and  colds
going  to  the  chest in  girls  (p  <0.05)  were significantly  higher  in homes with  gas  stoves.
                                      15-33

-------
When  prevalences  of the  respiratory conditions were  grouped,  an association  of  gas cooking
with  occurrence  of one  or more  respiratory  conditions was  found  in both  sexes  (p  ~0.01 in
boys; p =  0.07  in girls).  When possible confounding or covarying factors considered in 1973,
plus smoking among family members, were taken into account, an association between gas cooking
and respiratory illness was found in urban areas (p <0.005 in boys,  p ~0.08 in girls), but not
rural ones.   In rural  areas  there  only  appeared  to  be an association  for  girls  under eight
years old.   The effect of number of  smokers was significant in rural  areas (p <0.005).
     In  addition  to   results  for   the  1977  cross-sectional  analysis,  Melia et al.  (1979)
reported that  four cohorts of children  from the 1973  study  who  were followed up for  1  to  4
years showed greater risk of having  one or more respiratory symptoms  or diseases in homes  with
gas stoves  relative to homes  with electric stoves  in  1973.   In later years,  however,  as the
cohorts grew older, the relative risk showed considerable variation.   In most groups the  risk
was  greater in  gas  stove  homes,  but there  were  groups with  negligible increased  risk and
groups for  which  the  risk was greater in  homes  with  electric stoves.   The  authors  report no
consistent  change  in  the size of the  relative  risk with time except possibly  a  decline  from
1973 to 1977 for the  youngest cohort.  Comparing the  1973 and 1977  results,  the effect of gas
cooking seemed  to be  smaller in 1977,  at least  among girls.   The  prevalences tended to be
higher in  1973  for children of the  same  age.   The authors stated that differences in weather
conditions  could  not  explain  this observation, but speculated that  past high levels  of atmos-
pheric pollution  may   have  contributed to these  results.   Nevertheless, Melia et al.  (1979)
stated,  in  summary, that they observed an association between respiratory illness  and the use
of gas for  cooking in two different groups  of  children seen 4 years apart  in their national
survey.
     In another  study by  Melia  et  al. (1978)  concentrations of N0? were determined  in the
kitchens of two  gas  cooking homes and two electric cooking homes.   Concentrations  of NO-  were
determined  using TEA  diffusion  tubes (Palmes, 1976) placed  0.6  m and 2.2 m  from  the kitchen
                                                                            0
stove.  The average hourly concentration of N09 in gas kitchens  was  135 ug/m  (0.072  ppm), and
                                     "\
in electric kitchens  it was 17 ug/m  (0.009 ppm);  the difference in  these levels was signifi-
cant at p  <0.05.   This study also established that reproducibility  of the diffusion  tubes was
± 3 percent.
     These  studies by  Melia et al.   provide suggestive  evidence  of  an association between the
use of gas  stoves  and increased  incidence of  acute respiratory disease symptoms in  children,
and between the  use  of gas stoves and  increased  levels of N0«  in the home.   However, because
NCL concentrations were  not directly monitored in  the  homes  used in the health studies,  only
these qualitative conclusions may be drawn regarding their study results.
                                      15-34

-------
     Possible  interrelationships  between  N02  exposures  in  gas  stove  homes  and  increased
respiratory infection and decreased lung function were investigated in a further British study
reported  by Goldstein  et al.  (1979) and  Florey et  al.  (1979).   In these later investigations
levels  of NO-  were determined  in  gas  and  electric cooking  homes,  and  the  prevalence  of
respiratory symptoms among  children in the gas cooking  homes  was  found to be  higher  than  in
the  electric  stove  homes (p -0.10).  The  sample  was  808 children aged  6 to  7 years from 769
different homes  in  a  4-square-km area  in  Cleveland,  UK.   The  study was conducted  for  a two-
week period during  February 1978.   N02 was measured  by  TEA diffusion tubes attached to walls
in the  kitchen  area and in the  children's bedrooms.   In homes with gas stoves, levels of NO-
in kitchens ranged  from 10 to 596  ug/m  (0.005  to 0.317 ppm)  with a mean of 211 ug/m3 (0.112
ppm), and levels in bedrooms ranged from 8 to 318 \jg/m  (0.004 to 0.169 ppm) with a mean of 56
     O
ug/m  (0.031 ppm).   In homes with electric stoves, levels of NO- in kitchens ranged from 11 to
353 pg/m3 (0.006 to 0.188 ppm) with a mean of 34 ug/m3 (0.018 ppm), and in bedrooms NO, levels
                         o                                             n              f.
ranged  from 6  to 70 ug/m   (0.003  to  0.37 ppm)  with a mean  of  26  ug/m  (0.014 ppm).  Outdoor
levels  of N09  were determined  using diffusion  tubes  systematically located  throughout  the
                                                      3
area, and the weekly average ranged from 26 to 45 pg/m  (0.014 to 0.024 ppm).
     Information on  the prevalence  of  respiratory symptoms was collected and  grouped as  in
previous  studies.    Cooking  fuel   was  found  to  be associated  with  respiratory  illness,
independent of   social   class,  age,  sex,  or presence  of a  smoker  in the  house (p =  0.06).
However,  when  social  class was  excluded  from  the regression, the association  was  weaker  (p
~0.11).    For the 6-  to 7-year-old children living in gas stove homes, there appeared to be an
'increase of respiratory illness with increasing levels of NO- in their bedrooms (p ~0.10),  but
no significant relationship was  found between respiratory symptoms in those children or their
siblings  or parents and  levels of NO-  in  kitchens.   Lung function tests (FEVg ^r,  PEFR, MMF)
were also performed on  the 6-  to  7-year-old  children,   but no significant  relationship  was
found between  lung  function and concentrations  of  NO-  in either kitchen  or  bedroom.   These
studies, therefore,  at  most found a weak association between prevalence of respiratory illness
in 6- to  7-year-old  children  and gas cooking in their homes which  may have  been due to levels
of N02  generated by the  use  of  gas.   The authors  note,  however,  that the NO-  levels might
possibly  be a proxy  for some  other factor  more  directly related to respiratory disease, such
as temperature or humidity.
     Results   from   United   States  studies  finding  associations between  gas  stove use  and
increased respiratory  illness  in  children have  also  been published  (Spengler et  al,  1979;
Speizer  et  al,  1980).   Spengler  et al.  (1979)  presented data  on  annual nitrogen  dioxide
concentrations inside  and  outside  electric-  and  gas-cooking  homes in  five  of  six  American
communities  included in a prospective epidemiological  investigation.   In all instances,  houses
                                      15-35

-------
with gas facilities  had  higher levels of NCL  than  were present in the  outdoor  air,  reaching
double the  outdoor concentration  in  some  instances.  'Indoor annual average  values  in these
                               3                                                             3
houses were as  high  as 80 ug/m   (0.04 ppm).   Short-term  peak levels in excess of 1,100 ug/m
(0.58 ppm)  occurred  regularly in  kitchens.   Houses with electric cooking  services  had lower
concentrations than were observed in the outdoor environment.
     Respiratory disease  rates were  evaluated in these same six communities by Speizer et al.
(1980).   Children  from  households with  gas  stoves  had a  significantly greater history  of
serious  respiratory  illness  before age  2  (average  difference 32.5/1000 children).   In  this
study, adjustment  of rates  of illness before  age  2  for  parental  smoking  and  socioeconimic
status led  to  a  clear association with  presence  of  gas stoves  (p  <0.01).  These  findings
corroborate those  reported earlier by Melia et al.   (1977),  but have more importantly removed
the  primary  objection  to the  earlier Melia  studies,  i.e.,  the  role  of  parental  smoking.
Speizer  et al.  (1980)  also  found small but  significantly  (p  <0.01)  lower levels of  FEV-,  and
FVC, corrected  for height,  in children from houses with  gas  stoves.   Although these reported
pulmonary function changes were  statistically significant,  the authors  noted that the changes
are most  likely of relatively minimal  immediate physiological  importance.
     Considerable caution should  be exercised at this  time  before fully accepting findings  of
increased incidence of respiratory disease in children  living in gas  stove homes  and  attribut-
ing  such effects  to  NO^  exposure.   Such  caution  is   warranted  in  view of the following  :
     (1)   The  findings are based  on  initial data analyses from  long-term prospective studies
          and  assume  adequate control for  and exclusion of  contributions  of potential  con-
          founding  factors   (e.g.,  socio-economic   status,   humidity,   temperature)   to   the
          reported associations  between  gas  stove  home  residence  and  increased  respiratory
          illness  history  in young children.   Confidence in  such  findings would be greatly
          enhanced if they were  further  confirmed by analyses of data  subsequently  collected
          in the  studies, analyses  that more  definitively  rule out  effects of  potentially
          confounding factors.
     (2)   The  need to define  better  quantitative exposure/effect or dose-response  relation-
          ships between peak,  24-hr,  weekly or annual  average NOp exposures  and  any  resulting
          increases in respiratory disease  symptoms  in young  children  residing in homes using
          gas  cooking stoves.
     (3)   Results from other  studies  discussed  below,  which  did not  find significant  associa-
          tions between increased respiratory illness and residence  in  gas stove  homes.
     Several  studies, all American, have  failed to  find evidence of  associations between gas
stove usage  and   increased  respiratory  illnesses.    For  example,  in  a U.S.  Environmental
Protection  Agency  study  (Table 15-6) the  incidence of acute respiratory illness among women
                                      15-36

-------
 using gas cook stoves was  compared  with the incidence among women  using electric cook stoves
 (U.S.  Environmental  Protection  Agency,  1976).   Concentrations of NO, as high as 940 ug/m  (0.5
                  3
 ppm)  to  1880  ug/m  (1.0  ppm) were  found for  durations  of 1/2 to 1 hour each time the gas stove
 was  used for the preparation of a meal.  There was  no difference in the incidence of respira-
 tory  disease  in these women.
      Keller  et al.  (1979a) determined  the  incidence of  respiratory  disease  in 209 suburban
 Ohio  middle-class families with gas  stoves  and in 232 similar families with electric stoves.
 Health  data were obtained  through biweekly telephone calls for one year.   In addition, pul-
 monary  function  tests (FEV~ 75 and  FVC) were conducted on a 42 percent sample of the partici-
 pants representative of  both  sexes  and both types  of households.   No differences  in illness
 rates or in the  results  of pulmonary function tests were detected.   Nitrogen dioxide and NO
 levels  were monitored  over 24-hour  periods  in 83  of the homes with gas stoves.   For this
 monitoring, a  sodium arsenite procedure  was  used and continuous chemiluminescence measurements
 were  made for 3-day periods in each of 46 homes.    Reported peak N0«  concentrations  in homes
 with  gas stoves  were as  much  as  8 times higher than  the  24-hour  mean and sometimes exceeded
           0
 1,880 ug/m   (1.0 ppm).   The   location  of  the peak concentrations within  the home  was  not
 reported,  but probably  was within a  few feet of the stove.  On the  basis of the range of mean
 N09  concentrations   reported,  it  can be  determined  that  peak  (15-min)  N09  concentrations in
                                                           3
 most  homes with gas  stoves  ranged  between 75 and 1,650 ug/m  (0.04 and 0.88 ppm).  The average
 peak  value  would  have been approximately 750 ug/m   (0.4 ppm).   In homes with electric stoves,
"the mean  N02 concentration  was  lower  than the mean of 53 outdoor determinations.
      Keller et al.  (1979b) extended  this study of gas versus electric cooking services on 120
 of  the  original  households with  school  age  children.    Reports  of  respiratory  illness  and
 symptoms  were  obtained  by  telephone  interview every 2 weeks for 13 months.  When the onset of
 respiratory illness  occurred  within 3  days  of  a  call, a household  visit  was  made  to examine
 the  ill  person and to obtain a throat  culture.  "Well" controls were also examined.  The only
 significant  difference  (p <0.05) in  the  incidence  of  reported  acute  respiratory  illness
 occurred  among children 12  to 18 years  of age, with a larger percentage occurring in electric-
 stove  households.   Symptoms  of  "tearing  and  redness Of  eye" and frequency  of  consulting
 physicians were higher in homes with  gas stoves.  However, overall,  no significant differences
 were  found between the two  groups  confirming the earlier finding by  Keller et al. (1979a) that
 there was no  evidence that gas or electricity  in households was associated with the incidence
 of acute  respiratory illness.   (A more  detailed account  of  these studies is contained in two
 reports  by Lutz  et  al.,  1974,1977.)   Nitrogen dioxide and NO  concentrations were monitored
 over  periods  of  24 hours using a  sodium arsenite  procedure and continuous chemiluminescence.
                                      15-37

-------
15.3.3  Effects of NO., Pollution on Prevalence of Chronic Respiratory Disease
     Only  a  few  published epidemiological  studies  have  attempted  to investigate  possible
associations  between ambient air exposures to NOp or other NO  compounds and the prevalence of
chronic  respiratory  diseases.   The results  of  such studies  are concisely  assessed  below.
     The prevalence of  chronic  bronchitis among Japanese post office employees in 1962 and in
1967 was investigated by  Fujita et al.  (1969).   Nearly 7,800 employees in  Tokyo,  Tsurumi,  and
Kawasaki,  Japan  were   categorized  on  the  basis  of their  work  sites being "downtown  and
industrial,"  "intermediate," or "suburban."  Chronic bronchitis rates were  higher  in 1967 than
in  1962  for  all  age  groups,  for  all  smoking  categories,  and for employees  who  worked both
indoors  and  outdoors.   Overall  bronchitis  rates associated with  downtown,  intermediate,  and
suburban areas  increased,  respectively,  from 5.0,  3.7,  and  3.7 per 100 employees  in  1962 to
8.4, 8.0,  and  8.1 per  100 employees in 1967.   The investigators speculated that the increases
in  chronic bronchitis were caused  by concomittant increases in the atmospheric concentrations
of  NOp,  NO,   and  SOp,  but the  aerometric data  available  for the  1962-67 study  period  are
insufficient  to establish any such  hypothesized relationships.
     Another  study of chronic bronchitis  among 400 housewives  (30 to 39 years old) living in
six  localities  in  Japan   was  reported  by  the  Central  Council  for Control of  Environmental
Pollution  (1977).   This study,  conducted during the  winter of 1970-71,  reportedly  found an
association between prevalence  rates  for  chronic bronchitis in areas where annual  average  NOp
concentrations were in  the range of 0.02 to  0.03  ppm.   However,  insufficient  information  was
provided by which  to  evaluate the  validity of the reported findings,  and population NOp expo-
sure in  this  study was  likely confounded by high atmospheric particle levels also reported to
be present in the same study areas.
     In  an American study  discussed earlier,  Speizer and Ferris  (1973a)  compared  the  preva-
lence of  chronic respiratory disease among 128  policemen  who patrolled on  foot  in congested
business and shopping areas of central  Boston witti that of 140 suburban patrol  car officers.
The  exposure  of each group to NOp was determined  at several work locations  for  the  central
city officers and  in  the  patrol cars of  suburban  officers.   Nitrogen dioxide  was measured by
the Saltzman  method.   Among urban policemen, small but not statistically significant increases
in  the prevalence  of  chronic  respiratory disease were found among nonsmokers  and stackers  but
not among ex-smokers.   Estimates of annual mean pollution levels,  based on  approximately 1,000
                                                                             j
hourly samples  (Burgess et al. ,  1973),  were, for  the urban area, 103 ug/m  (0.055  ppm)  NO,
                                               o                                              e-
together with  S00  concentrations   of  90  ug/m   (0.05 ppm); the  N00 concentrations for  the
                                3                                                       3
suburban area  averaged  75  ug/m  (0.04 ppm)  and SO-  concentrations  averaged  26  ug/m   (0.01
ppm).
                                      15-38

-------
     Cohen et  al.  (1972) similarly found no differences in the prevalence of chronic respira-
tory disease between a nonsmoking population in the Los Angeles basin and a similar population
in  San  Diego.   The Los Angeles group  was  exposed to concentrations of NO,, between 90 and 100
    3                                                  3
ug/m  (0.05  ppm)  plus  oxidant levels  of about  90 ug/m  (0.045 ppm); the  San  Diego group was
exposed to N09 concentrations of approximately 40 to 45 ug/m  (0.02 ppm) and concentrations of
                                 3
oxidants of approximately 76 ug/m  (0.038 ppm).
     Linn et al.  (1976)  also found no  increase  in  chronic respiratory disease in Los Angeles
women exposed to a median hourly NO,, concentration of 130 ug/m  (0.07 ppm) with a 90th percen-
                        3
tile value  of  250  (jg/m   (0.13 ppm),  over that  occurring in San  Francisco women  where the
                                               3
median  hourly  concentration  of  N00 was 65  ug/m   (0.035 ppm)  and the 90th  percentile  was 110
    3
ug/m  (0.06  ppm).   Median  hourly  oxidant values in the two areas were,  respectively, 0.07 and
0.02 ppm.   These investigators concluded that cigarette smoking was much more significant than
was Los Angeles air pollution in the development of chronic respiratory illness.
     In  summary,   the  epidemiology  studies assessed  above  did  not  establish   any  credible
association between chronic  respiratory disease  prevalence in human  populations  and the con-
centrations of N0£ to which these  populations were exposed.
15.3.4  Extrapulmonary Effects of  Exposure to NO
     Nitrogen  oxides,  as well  as  other components  of  polluted air, have been reported  to be
correlates of  daily mortality,  heart  disease,  and lung cancer, based on certain  epidemiologic
studies reported in the early 1970's.
     For example,  Hickey et al.  (1970)  compared air pollution measurements made at National
Air  Sampling Network  (NASN) stations  with geographical  differences  in mortality  rates for
various categories of  cancer,  cardiovascular  disease, and  respiratory  disease in  38  U.S.
Standard Metropolitan  Statistical  Areas  (SMSAs)  during 1959  to  1961 and  from 1961  to  1964.
Included  in  the  analyses  were  NOp,   S0?,  suspended  sulfates,  total  particulates,  calcium,
chromium,   copper,  iron,  lead,  manganese,  nickel,,  tin, titanium,  vanadium,  zinc,  and  water
hardness.   Mortality rates  were  analyzed both with  and without  regard to  age, sex,  and  race
differences.   Nitrogen  dioxide and SO,, repeatedly were  positively associated with  age-, race-,
and sex-adjusted,  and unadjusted mortality rates  for various cancers,  and for arteriosclerotic
heart disease.    Other  pollutants were variably,  and often negatively,  associated  with  these
mortality  categories.   However,  the  quality of  both  the  monitoring  data  and the  mortality
data, as  well  as  the  fact  that  specific  pollutant exposures  of  individuals dying  of  these
different  diseases could  not be  evaluated,  are such  that the  findings  preclude  more  than
speculative conclusions regarding  possible risk of death or disease due to pollutant exposure.
                                      15-39

-------
     Lebowitz (1971)  studied  variations  in daily mortality in relation to daily air pollution
and weather  variables in  New York City,  Philadelphia and  St.  Louis, from 1962  to  1965 and
reported associations between  air pollution,  weather variables, and  daily  mortality  for each
city.   Multiple  regression  analyses  showed a significant negative  association  between winter
mortality in New York City and daily nitrogen  oxide  concentrations (non-specific for NO, NO-
or other NO  ),  but  no association in summer.   In contrast,  the winter mortality of persons 45
           A
to 64  years  old, 65  years and older, and  all  ages  combined in Los  Angeles,  California, was
significantly and positively  related  to  daily nitrogen oxide concentrations during the period
of 1962 to 1969 but summer mortality was  not.   These results,  therefore, do not provide con-
vincing  evidence of  a   relation  between NO  air  pollution and daily mortality,  given  that
winter mortality results for  New York  City  were  opposite  to  those for Los Angeles  and the
associations  were not consistent across seasons.
     Interactions of  atmospheric  NO   pathways with those of photochemical oxidants, discussed
elsewhere  in  this  document   and  also  in the Air  Quality  Criteria  for Ozone  and  Other
Photochemical Qxidants,  (U.S.  Environmental  Protection Agency,  1978) may lead  to increases,in
the  incidence  of  skin   cancer in certain  population  groups.   Epidemiological  studies  have
demonstrated  that  solar UV  radiation   is  carcinogenic  (Douglas  and  Owen,  1976).   Outdoor
workers, such as farmers or fishermen, have a higher incidence of both basal cell and  squamous
cell   carcinoma   of  the   skin  than do less-exposed  individuals.    Chemical  reactions  in the
atmosphere involving nitrogenous compounds may lead to a decrease in the stratospheric concen-
tration  of  03  and  a  resultant  increase  in  the  amount  of UV  radiation penetrating  to the
earth's surface, but such effects have not yet been conclusively demonstrated.
15.4  ACCIDENTAL AND OCCUPATIONAL EXPOSURES
     As noted earlier  in this chapter,  there are a number of occupational situations  in which
workers  are  intermittently or continuously exposed  to  high concentrations of NQ~  or other
oxides  of nitrogen.   Data  from  such  exposures, or other  accidental  exposures, as  those
encountered with certain fires,  provide some  indications  of N0x  exposure levels  associated
with severe toxic effects in humans.
     There have  been  a  few cases of unusually  high  levels of exposure  for short  periods of
time  which  confirm  a potential  lethal   hazard associated with short-term exposure  to  N02-
Lowry  and  Schuman  (1956)  reported  the  development  of  illness of  four farmers who  entered
freshly-filled  silos  in  which high concentrations  of NO^ had built up.   These  men experienced
cough and dyspnea shortly after entering the silos.   These symptoms disappeared after several
days, but  were  followed  in about 3  weeks by  cough,  malaise,  weakness, dyspnea,  and fever.
Chest X-rays showed multiple  discrete nodules  scattered  in both lungs.  Two of the  patients
died while the  other two improved dramatically after receiving high doses of steroids.
                                      15-40

-------
Concentrations of  N02  were estimated to be in the range of 380,000 to 7,500,000 ug/m  (200 to
4,000 ppm).
     Grayson  (1956)  reported  on two other cases of N02 poisoning from silage gas estimated at
560,000  to  940,000 (jg/m3 (300 to 500 ppm) N02-  Indications from this study are that exposure
to concentrations  in this range is likely to result in fatal pulmonary edema or asphyxia.   The
study further  indicated  that  concentrations in the  range  of  280,000 to 380,000 yq/m  (150 to
200 ppm)  are  likely to produce bronchiolitis; exposure  to 94,000 to 190,000 ug/m  (50 to 100
ppm) are associated with reversible bronchiolitis, and exposure to concentrations in the range
of  47,000  to 140,000  (jg/m   (25 to  75 ppm)  are  associated with  bronchitis or  bronchial
pneumonia with apparent complete recovery probable.
     Gregory  et  al.  (1969)  studied  mortality  of survivors  of a  fire at  Cleveland  Clinic
(Cleveland, Ohio), in May 1929.  At the time of the fire, persons were exposed to high concen-
trations of NO,  N02,  CO, and  hydrogen  cyanide  resulting from the combustion of X-ray film in
which nitrocellulose was  a basic material.   Exposure was such that it caused 97 deaths within
2 hours  and,  over  the next 30 days, 26 died.   Under such extreme condi-tions, several factors,
including various  atmospheric  pollutants,  may have contributed to the  immediate deaths.   The
conditions at  the  time  of the fire, however,  and  the symptoms in many of the individuals who
subsequently  died,  were most  consistent with  symptoms  expected as a result  of inhalation of
very high N0?  concentrations.   In spite of the significant number of deaths within 30 days of
the fire,  the survival  rate  over the  next 30 years  for  exposed clinic  employees,  firemen,
pol.icemen, and  rescue workers  did  not  differ  from that  of  unexposed  similar  groups.   This
suggested an absence of residual effects (excess mortality) due to the intense acute exposure.
     Another study (Lowry and Schuman,  1956),  performed on 70 male chemical  workers exposed to
750 to  5000 (jg/m   (0-4  to 2.7  ppm)  NO,,  in  their work  place daily for 4-6 years,  compared
various blood  lipid  concentrations  in  these subjects to values obtained on a control group of
80 men not exposed to N0?.   They reported that lipid metabolism was impaired subsequent to the
original N0?  exposure.   Adequate  information  to evaluate the significance of this  finding was
not available.  However,  as  discussed  earlier, Horvath et al  (1978)  reviewed case  studies for
acute N02 exposure victims  which also suggest that  certain pulmonary function decrements may
persist for periods up to 13 years after initial  exposure.
15.5  EFFECTS OF  NOX'DERIVED COMPOUNDS
     Many compounds  may be derived  from various  oxides of nitrogen in the  atmosphere,  with
formation mechanisms and  concentrations  depending  on many factors including the concentration
of various nitrogen  and  non-nitrogen  materials present, temperature, humidity,  and sunlight.
The compounds believed to represent the greatest potential  risk to health include nitric acid,
nitrates, nitrites, and nitrosamines.
                                      15-41

-------
15.5.1  Nitrates, Nitrites and Nitric Acid
     Nitrate poisoning occurs  when  a sufficient quantity of nitrate ions is reduced by intes-
tinal bacteria to nitrites, which, in turn, oxidize the iron in hemoglobin from the ferrous to
the ferric  state.   The  resulting substance, termed methemoglobin, cannot function normally in
the  process of  transporting  oxygen  to  tissues.   In  healthy adults,  methemoglobin  usually
accounts for less  than  2.0 percent of the total hemoglobin concentration (National Academy of
Sciences, 1972).   However,  Goldsmith et al. (1975) reported  results  of a study of California
populations  in  which the  mean concentrations  in  populations ranged as high  as  2.11  percent
methemoglobin,   with  1  percent  of  adults  and 8  percent  of infants  exceeding   4.0  percent
methemoglobin.    Infants  usually  carry  higher  concentrations of  methemoglobin and are  more
susceptible  to  nitrate  poisoning  than  are  older  children  or  adults  because  (1)  fetal
hemoglobin  is probably  more susceptible to conversion to  methemoglobin,  (2)  bacteria  capable
of reducing nitrate to nitrite thrive in the less acidic conditions of the infant  stomach,  (3)
the  enzyme  system for reducing  methemoglobin  to  hemoglobin is deficient in  infants,  and  (4)
because  intake  of  wat«£  per  kilogram  body  weight is  higher in  the  infant than  in  adults
(Kravitz  et al.,  1956).    Cyanosis  may  be produced  at  concentrations  of  about  10  percent,
methemoglobin;  however, symptoms  are not likely to become obvious at concentrations less  than
20 percent.
     The  total  weekly  intake of  nitrate  in  the  general populations  of  the United  States
(Ashton,  1970)   and  in  England  (Hill  et  al.,  1973)  has been  estimated to average  about
400,000 to 500,000 (jg.  Because concentrations in water,  in cured meats, and in vegetables  vary
greatly,  as do  the  quantities  of  these materials  consumed by  individuals, the  ingestion
estimates must  be applied with  caution.   However,  since the  worst case  situation would  pro-
bably find  less  than 40 ug/m  nitrate in ambient air (Pitts and Loyd, 1973),  an adult  engaged
                                          o
in heavy exercise,  who  might inhale 20  m  of  air  per day could be expected to inhale  no  more
than 5,600  ug of nitrate  per week,  or  less than 1.5 percent  of  the  lowest  estimate of total
weekly  intake.   Thus, it  is considered  to  be  unlikely that the concentrations of nitrate in
the ambient air contribute significantly to the production of  acute nitrate  poisoning.
     Nitrate aerosols could  be significant from an air  pollution  standpoint  in that they  are
the final stage  in the  atmospheric oxidation of NOX,  a process that includes  the  formation of
various nitrogenous acids.   However, the earlier discussion of measurement techniques (Section
7.4.1)  suggest that  many  of the data  now available relevant  to atmospheric concentrations of
nitrates represent measurements of the atmospheric nitrate plus artifact nitrate formed on  the
collection  filter  by the  reaction between the filter substrate and nitrogen compounds  includ-
ing nitric  acid.   No published epidemiological studies on the effects of atmospheric nitrates
are yet  available  where  the ambient air levels of nitrates were measured following collection
of particulate matter glass filters (which substantially avoids artifact formation).

                                      15-42

-------
      Only a few recent controlled  human  exposure  studies  have  attempted  to  assess  the  effects
 of inhaled nitrates  on  pulmonary functions,  using  acceptable  nitrate  measurement  methods.   For
 example,  Utell et al.  (1979)  studied the effects of  a  nitrate aerosol on  pulmonary function
 and on  the sensitivity  of  test subjects  to  the bronchoconstricting  effects  of  carbachol.
 Included  in these studies were  7 healthy subjects (mean  age 28)  and 13  mild  asthmatics  (mean
 age 25)  selected on  the basis of  a demonstrated abnormal  increase in  R   after inhaling
       i                                                                      3W
 carbachol.   Subjects were  exposed for 16  minutes in a  double-blind manner to  either sodium
 nitrate (NaNO,) or sodium chloride  (aerodynamic  diameters  0.49  urn, ag = 1.7, and  0.46 urn, ag =
                                                    3
 1.7,  respectively)  at a concentration  of 7,000  |jg/m .  Following  exposure,  subjects  inhaled a
 predetermined  quantity of  carbachol  sufficient to  increase  R    20  to 30 percent.  Prior to
 exposure,  after 8 and 16 minutes of exposure, and  again after the  inhalation of carbachol,  the
 following pulmonary  measurements  were made:  functional  residual capacity (FRC),  R  ,  FEV,
 FEV-,  g,  maximum and partial  expiratory flow rates at 60  and 40  percent  total lung  capacity.
 None  of  the tests of pulmonary  function  were affected by  the nitrate exposure although two of
 the asthmatic  subjects did  demonstrate mild potentiation of the  response to  carbachol  after
 nitrate   exposure.   All  subjects  remained  asymptomatic.   These  results   suggested that  in
 healthy   individuals   or in  mild asthmatics, short-term  exposure to  NaNO.,  at concentrations
 approximately  100 times the total  nitrate in ambient  air  exposures,  does  not  affect  pulmonary
 function.   These  investigators  did point out  that their  study results might  have been  quite
 different had  they  (1) used  an  "acidic"  nitrate in their exposure atmosphere rather than  the
 neutral NaN03,  (2)  had the  exposure  time been  extended beyond the 16  minutes, or  (3)  had  the
'study  included symptomatic asthmatics.
     Utell  et al.  (1980)  also  examined the  potential  synergy  between  acute exposure  to a
 pollutant (sodium nitrate  aerosol) and acute respiratory  infections.   The mass median  aerody-
 namic  diameter of the aerosol was  0.49 pm;  the concentration 7,000  ug/m  .  Eleven previously
 healthy adults with uncomplicated  influenza  A (H,NO were  studied  at  the  time  of  acute  illness
 and 1, 3,  and  6 weeks later.  Significant decreases in specific airway  conductance and  partial
 expiratory  flows  at  40% of  total  lung  capacity were observed at the  initial examination  and 1
 week  later.  By the third week,  inhalation of sodium nitrate no longer  produced changes in  air
 way  function.  Control  studies  were  made with  sodium chloride aerosol.   They concluded that
 individuals with  acute  respiratory disease  were susceptible  to bronchoconstriction from this
 air pollutant--one that normally did  not  influence airway  function.
     "Nitric acid  fumes,"  a term used  to designate  the mixture of nitric acid vapor plus  the
 reaction  products of nitric acid and  various  metals  or  organic  material,  has  been known to
 produce varying degrees of upper respiratory irritation within minutes  of exposure.   Prognosis
                                      15-43

-------
for exposed  individuals  depends  upon the concentration of the acid plus its products of reac-
tion and the  duration of exposure.   The clinical picture sometimes is biphasic and similar to
that  shown  by  individuals exposed  to  high  concentrations of  N0? (Treiger  and  Przypyszny,
1947).   In  other instances,  the  picture  is  quite  different and may reflect  the  toxicity of
reaction products, particularly those  produced by,the reaction of nitric acid and some metals
(Danke  and  Warrack,   1958).   Extended  exposure to lower concentrations  of  nitric  acid vapors
have been  postulated as  the  probable  cause  of chronic bronchitis or  a chemical  pneumonitis
(Fairhall,  1957).  Neither  these  effects nor the concentration that might cause them are well
documented.
     There are  no data  available relating to  the  effects  of inhaling  nitric  acid  vapors in
concentrations  likely to occur in the  ambient atmosphere;  however, it  does  seem  likely that
such a  highly  ionized and strongly corrosive  material  would be  a potent respiratory irritant
even at low concentrations. .
15.5.2  Nitrosamines
     A  few  epidemiological studies  have attempted to  link  environmental  nitrates,  nitrites,
and  nitroso  compounds with  human cancer.  The International  Agency  for Research  on  Cancer
(IARC)  investigated  a possible  association between these compounds in the diet and esophageal.
cancer  in specific areas  of Iran and France,  where  these  tumors occur  at  a  high  rate and in
nearby areas where the tumor rates are lower (Bogovski, 1974).   Fifteen of 29 samples of cider
contained 1  to  10 M9/k9  of dimethylnitrosamine and two samples also contained diethylnitrosa-
mine (1 ug/kg).   Benzo(a)pyrene  also occurred  in some  samples.   Correlations  between  dietary
intake  of  N-nitroso   compounds  and  esophageal  cancer  were   not  established  (Bogovski,  1974).
     A  similar  study was  conducted  in the Anyang region  of China, where 20 percent of deaths
from all  causes  reportedly result from esophageal  cancer (Cordination  Group  for  Research on
Etiology of  Esophagal  Cancer  in North China,  1975).   Twenty-three percent of the  food  samples
from, the areas with the highest cancer rates were reported to contain dimethyl-, diethyl-,  and
methylbenzyl-nitrosamine.   Confirmation  of  this analysis  by gas  chromatography and mass spec-
troscopy,  however,  is required before  the finding  can be  accepted.   Dietary  nitrite  levels
were higher  in  the  areas  of high cancer incidence  than in   low  incidence areas.   Chickens in
the area associated with  high esophageal cancer in humans also had a high incidence of  similar
tumors, suggesting an environmental  etiology for the disease.
     Zaldivar and Wetterstand (1975)  and Armijo and Coulson  (1975) have shown some  correlation
between the per capita use of fertilizer and the incidence of stomach cancer in Chile.   It has
been  hypothesized that   nitrate  from  fertilizer  first enters  the  diet  by way  of  meat,
vegetables,   and drinking water.  Nitrates  are then reduced to  nitrites  by  microbial  action,
and are thus  available for j_n vivo nitrosation of secondary amines, contained in  the diet, to
                                      15-44

-------
 form carcinogenic nitrosamines, which  can  induce stomach cancer.  The  suggested  causal  rela-
 tionship remains  highly speculative.   Hill  et al.   (1973)  correlated variations  in  rates  of
 stomach cancer with the  nitrate  content  of drinking water in two English towns.   However,  the
 evidence required to demonstrate  a  causal  role for  nitrate  was not provided.   Gelperin et  al.
 (1976) found no  statistically  significant  differences in death  rates  from  cancers of several
 organs, in three  areas  of  Illinois  each  with different nitrate content in the drinking water.
 It is  doubtful,  however, that the  available  mortality data permitted an analysis  that  could
 have detected an  effect  among  the populations in the  high-nitrate area.   In  Japan, increased
 rates of stomach cancer have been  observed  in population groups having unusually  high  consump-
 tion of salt-preserved  foods (Sato et  al.,  1959).  Reference is made  to Chapter 8  for  a review
 of observed concentrations  of  N-nitroso  compounds in ambient  air.   The  relative  significance
 of the inhalation of the compounds is  unknown.
      There  is  no direct evidence  that atmospheric  nitrogenous  compounds contribute  signifi-
 cantly to the J_n  vivo  formation  of  nitrosamines  in  humans or that inhaled nitrosamines repre-
 sent significant health hazards.   Questions have  been raised as to i_n vivo nitrosation by NCL.
 Iqbal et al.  (1980) have reported that,  indeed,  jjn  vivo  nitrosation of amines does  occur  in
 mice.  There are a number  of  endogenous  and  exogenous  amines  available to  an  organism  for
 nitrosation.   In the preliminary  studies of Iqbal et al., they gavaged mice with  an exogenous
 amine,  morpholine,  and  then  exposed  mice  for 0.5  hour to 50  ppm NO,,.   Production of N-nitroso-
 morpholine  (NMOR) was  measured in the mouse.  Longer  exposures to this  concentration of  NO^
 for  up  to  4  hours  resulted in higher levels  of  the nitrosamine.  They  also  exposed gavaged
.mice  for 4 hours  to NO^ (from  0.2 to  50  ppm)  and  reported increased  levels  of NMOR.   The site
 or mechanisms of the NMOR biosynthesis  were not identified.
      Nitrosation of  amines  in the  stomach has  been demonstrated to occur  in  humans (Sander  and
 Seif, 1969),  in  rodents  (Sander et  al.,  1968), and  in  dogs  (Mysliwy  et al., 1974).  Preformed
 nitrosamines  have been  found  in  tobacco  (Hecht   et  al.,  1974;  Hoffman  et  al.,   1974) and  in
 tobacco smoke (Klus  and Kuhn, 1973;  Neurath,  1967).
 15.5.3   Other Compounds
      Recent  studies  by  Pitts  et al.  (1978)  have  demonstrated that, in sunlight,  very  low
 concentrations  of diethylamine and  triethyl amines behaved like hydrocarbons and  reacted with
 NO,  HOy or  nitrous  acid to form 03,  PAN,  acetaldehyde plus diethylnitramine  and several  amides
 including acetamide. Peroxyacetyl  nitrate (PAN) is a  strong  eye irritant  at  a  concentration  of
 4,945 ug/m   (1.0 ppm).    The  effects  of this compound  are discussed  at length in  Air Quality
 Criteria for  Ozone  and Other  Photochemical  Oxidants  (U.S.   Environmental Protection  Agency,
 1978).   In addition to  nitrosamines, diethylnitramine (Goodall  and  Kennedy, 1976;   Druckey
 et al., 1961) and  acetamide (Jackson  and  Dessau, 1961;  Weisberger, et  al.  1969) have been
 shown to be  carcinogenic in test animals.  However,  the significance of these  materials  as
 human carcinogens is unknown.
                                       15-45

-------
15.6  SUMMARY AND CONCLUSIONS
     Critical N0x  human health  effects  issues include:   (1)  qualitative  characterization of
identifiable health effects associated with exposure to various NO  compounds; (2) delineation
of the  seriousness  of the  identified effects  in  terms  of their reversibility/irreversibility
and their  impact  on normal human functions and activities;  (3) quantitative characterization
of exposure/effect  or exposure/response  relationships  for health effects  of  concern;  and (4)
identification of  sensitive  populations  at special risk  for manifestation of such effects at
ambient air NO,, levels.
     Of the oxides of nitrogen, NOp appears to be  the compound of greatest  concern in terms of
human health effects  documented  as likely to  occur  at  exposure levels within the range of or
approaching ambient air  concentrations  encountered in the United States.   Based on this, the
main  focus of  the present  section  is  on the  summarization  of  key points  and conclusions
regarding  N02  health  effects  and  their  likely significance for protection of public  health.
Brief comments are also provided in regard to  certain NO -derived compounds hypothesized to be
of public health concern.
15.6.1  N02 Effects
     A broad spectrum of human and animal health  effects have been reported to be associated
with N0? exposure.   These range from (1) death or  serious, irreversible lung damage associated
with  very  high  accidental  or  experimental exposures  in  the  range  of 150-300  ppm or  higher;
through  (2)  less  severe but clearly significant  short-term  or  chronic   lung  tissue  damage,
functional  impairment,  or  aggravation of  other disease  processes  at exposure  levels  of  5 to
100 ppm;  to  (3) impairment  of  lung  defense  mechanisms and other,  milder,  temporary effects,
e.g..changes in pulmonary function and sensory system effects,  occurring at N0£ levels  below 5
ppm.   Of most relevance  here is consideration of  the effects occurring at  levels below 5 ppm.
15.6.1.1  Pulmonary Function  Effects—Numerous controlled human exposure studies have examined
the effects  of  single,  short-term NO,,  exposures  on pulmonary  function.   The  most frequently
observed pulmonary  function  effects of  N0« exposure in controlled human  studies (usually at
concentrations higher  than ambient)  include  increases  in  airway resistance  (R  ,) and  changes
                                                                               aW
in susceptibility  to  the effects of bronchoconstricting agents.  Functional  response of human
subjects to N0? are commonly  assessed with measurements of flow resistance  (total respiratory,
pulmonary,  or airway)  and  maximum expiratory  flow rate  (related  to lung volume).  Both types
of measurements are influenced by changes in  diameter of the  laryngotracheobronchial  system.
Airway  narrowing,   or bronchoconstriction,  increases  flow  resistance  and   reduces  maximal
expiratory flow rate.
                                      15-46

-------
      Increased  airway  resistance  (R,.,) and  other physiological  changes  suggesting impaired
                                     QW
pulmonary  function  have been clearly demonstrated to occur in healthy adults with single 2-hr
NO-  exposures  ranging  from  3760  to  13,200  ug/m  (2.5 to  7.0 ppm).   Certain  studies also
indicate that significant effects  occur in healthy subjects with  shorter (5-15 min) exposures
to  the  same or possibly  lower  levels  of N0« administered either  alone or in combination with
NaCl  aerosol.   More specifically, in  regard  to the latter point,  Suzuki  and Ishikawa  (1965)
observed altered respiratory  function after exposure of healthy  subjects to NO,, levels of 1300
             3
to  3760  ug/m  (0.7  to  2.0 ppm) for 10 minutes.  Their data however, preclude a clear associa-
                                                                                             3
tion  of  observed  effects with  any particular concentration in the range of 1300 to 3760 ug/m
(0.7  to 2.0  ppm) NO- exposure.
      In  contrast, Hackney,  et al.  (1978) reported no statistically significant changes  in any
of  the pulmonary functions tested with the exception of a marginal loss in forced vital  capac-
ity after  exposure  to 1880 ug/m  (1.0  ppm)  N02 for 2 hours on  two successive days (1.5% mean
decrease,  P  <0.05).   However, the authors question the health significance of this small, but
statistically  significant change and suggest  that it  may simply  be due  to  random variation.
Also, Beil  and  Ulmer (1976)  and Folinsbee et  al.  (1978) concluded that there were no physio-
logically  significant pulmonary effects at exposure levels of 1880 and 1100 ug/m  (1.0 and 0.6
ppm)  N09,  respectively;  and in a similar study, where  Kerr et  al.  (1979) exposed  10 healthy
                   3
adults to  940 ug/m   (0.5 ppm)  N02 for  2 hours, only small changes  were  found in quasistatic
compliance.   However,   the  authors  again  suggested that  such   results may  be due  to   chance
alone, especially since no  other pulmonary function tests  showed significant changes for the
healthy adult group and only one subject reported mild symptomatic effects associated with NOp
exposure.   In  general,  then,  these  studies appear to have found no observed effect levels for
pulmonary  function changes in healthy adults across a range of 0.5 to 1.0 ppm NO,,.
     Hackney  et  al.  (1975)  and von Nieding et  al.  (1977)  also concluded that  there  were  no
physiologically significant effects  at NO^ levels below 560 ug/m  (0.3 ppm) in the presence of
various other air pollutants, with  the possible exception of increased sensitivity to a bron-
                                                                                 3
choconstrictor  (acetylcholine)  observed by von  Nieding  et  al.   (1977) at 94  ug/m   (0.05 ppm)
N02 in  the  presence  of 49 ug/m   (0.025 ppm)  ozone  and 290  ug/m  (0.11 ppm)  S02.   The von
Nieding  finding,  however, is  difficult to interpret  in view  of:   (1) controversy  over the
health significance  of altered  sensitivity  to  bronchoconstrictors  in  healthy  subjects;  (2)
uncertainties due  to methodological  differences between his techniques  and  other  investiga-
tors'; and (3) no confirmation of von Nieding's et al.  (1977)  findings by other investigators.
Thus,  no presently  available  controlled human exposure study can  be accepted at this time as
providing  conclusive evidence  for  meaningful  pulmonary function changes  occurring at  N09
                      3                                                                      *-
levels below 1880 ug/m  (1.0 ppm) for healthy adult subjects.
                                      15-47

-------
     It is difficult  to  assess the health significance of small  reductions in pulmonary func-
tion, eg.   increased  R  ,  reported for healthy adults with exposures to N09 below 2.0 ppm; nor
                      oW                                                   C.
have controlled  exposure studies  investigated  long-term effects  of repeated  NOo  exposures.
Secondary  effects  of brochoconstriction  can  add to  the biological  significance  of observed
functional alterations.   One such possible secondary effect is the interference with alveolar-
capillary  gas  exchange  (measured  as  an  increase  in alveolar-arterial  PO- gradient, or  as  a
reduction  in arterial PCL  or oxyhemoglobin saturation).  The  relation,  if any, between bron-
choconstriction associated with  a single exposure to NO^ and  possible  development of chronic
respiratory disease  during prolonged  or intermittent  exposure  is unknown.   It  is unlikely,
however,  that  the  slight  increases in airway resistance  which were observed to occur after  a
single exposure to  N0?  at  or below 2.0  ppm  represent a significant adverse health effect for
healthy adults.
     More  difficult to  interpret is  the  health significance  of  NKL exacerbation of pulmonary
function  changes induced by  bronchoconstrictors.   Monitoring  a  subject's  response  to a bron-
choconstrictor is a sensitive experimental approach that utilizes (1) the action of neurotrans-
mitters (e.g.,  acetylcholine)  normally  present  in  the body,  (2)  pharmacologic products  with
similar properties  (e.g., carbachol),  or (3)  nervous system-mediated reflexes.   The purpose of
the bronchoconstrictor is  to  test the response of  the  individual's airways to a standardized
challenge.  This response  in  individual  subjects may be altered  by underlying disease such as
asthma, by respiratory  infection or  by  previous  exposure to  an air  pollutant.   A  reasonable
hypothesis is  that  the  magnitude of  response to a particular experimental  challenge such as  a
synthetic  bronchoconstrictor  may  be   used  to predict  the  individual's   level  of  risk  when
exposed to ambient  pollutants.   However, it  is also  known  that  increases  in bronchial  sensi-
tivity can be produced by sudden changes in temperature or even by emotional stress.  Thus, it
is  believed  to  be unlikely that the relatively  mild  and  inconsistent   bronchoconstriction
produced  by  a  single short  exposure   to  NOp  represents  a  health hazard with  or without the
added  increase  in  constrictive  potential  due  to  any  of  these other  natural   or  induced
influences.
     Increases  in R   and  increased  sensitivity to bronchoconstrictors  are both suggestive of
                   3W
irritation in  the  .laryngo-tracheo-bronchial   system.   The consequence of  repeated  short-term
exposures   has  not  been  determined in  human volunteers;  however,  studies with animals suggest
that repeated  exposures to  N02 levels at or  below those associated with  significant increases
in R,,, can increase susceptibility to  respiratory infections.
    aW
     For purposes of  this  review, the intensity of  the response in test individuals has been
given  little   consideration  in  assessing potential  health  risk.   This  approach  was  taken
because the  intent,  usually,  was to  determine  the  lowest NO- concentration that would cause
                                      15-48

-------
any  increase  in  Rflw  in  healthy  or in  susceptible  individuals  after a  single,  short-term
exposure.   Obviously,  a barely  detectable functional response  has  less  serious implications
than one associated with disability or distress.
     An  assessment  of  the  importance of studies  showing  associations  between exposure to NOp
and increased airway resistance must consider also the known wide variations in susceptibility
within human  populations.   Thus,  an exposure sufficient  to  produce  slightly increased airway
resistance in healthy individuals may produce much greater and more severe responses in, highly
susceptible  segments  of the population,  e.g.,  in those with symptoms  of  chronic respiratory
illness or asthmatics.
     Several  controlled  clinical  studies  have  specifically addressed  the issue   of  whether
detectable respiratory effects  can  be induced by NOp  in  sensitive human subjects at exposure
levels below those affecting healthy human adults.  For example, the studies by von Nieding et
al. (1971; 1973) show that, in persons with chronic bronchitis,  concentrations of 7,500 (jg and
9,400  pg/m   (4.0  and 5.0 ppm) produced  decreases in arterial  partial  pressure  of  oxygen and
increases in  the  difference between alveolar and arterial  partial  pressure of oxygen.   Expo-
sures to concentrations of M^ above 2,800 ug/m  (1.5 ppm), for  periods considerably less than
1  hour,  also  produced  significant increases in airway resistance.   Thus,  results for bronchi-
tic  individuals  and healthy  individuals appear  to  differ  little  and provide  no  particular
support  for  the hypothesis that  chronic  bronchitics  are  more sensitive to  NOo  exposure than
healthy adults.
     In another study (Kerr et al.,  1979), measurements of pulmonary function were not altered
in 13  asthmatics  or 7  bronchitics as a  result  of 2 hours of exposure  to  940 ug/m  (0.5 ppm)
NOp when the  groups were  analyzed separately.   When the data for the two groups were analyzed
together, however,  small but  statistically significant changes   in quasistatic  compliance and
functional  residual capacity were reported.   Nevertheless, the  authors state that the changes
reported may  be due to chance alone.   Seven asthmatics and one  bronchitic  reported some chest
discomfort,  dyspnea, headache,  and/or slight nasal discharge.
     In contrast to  the  above  results,  exposures to  190  ug/m   (0.1 ppm) NOo for  i hour were
reported by Orehek et al.,  (1976) to increase mean airway  resistance (R,..)  in 13 of 20 asthma-
                                                                       dw
tics and to increase the sensitivity to  a bronchoconstrictor (carbachol) in these same individ-
uals.   However, considerable controversy exists regarding interpretation of the Orehek (1976)
study and the  health  significance of the  increased  response to a bronchoconstrictor observed
in the study.  Also, its basic findings remain to be independently replicated.
     Based on  the above results,  conclusive statements  regarding the possible  special  risk
status of asthmatics in response to NO^  exposure cannot be made  at this time.   The Kerr et al.
(1979) study results do suggest,  however, that increased occurrence of personal  discomfort and
symptoms may  occur  in  asthmatics  as the result of short-term (2 hr) exposures to 0.5 ppm Nt^.

                                      15-49

-------
     The above clinical studies provide important data concerning the effects of single short-
term NOo exposures on healthy young adults and certain groups defined a priori  as "sensitive",
i.e., bronchitics and  asthmatics.   However,  members of other presumed  sensitive populations,
e.g., children,  the elderly,  and  individuals with  chronic  cardiovascular  disease,  have  not
been tested  in controlled  clinical  studies and  are not  likely  to be tested  in  the future.
because of  medical  ethics  limitations  on the  use  of such subjects  in experimental  studies.
Therefore,  statements  on  whether  such  individuals  are  at  greater  risk  than  healthy  young
adults  for  experiencing  respiratory  effects  with  single  short-term NOp  exposures  cannot  be
made based on controlled human exposure studies.
     It  is  informative  to compare  the  above  controlled human  exposure  study results  with
findings  from  epidemiological  studies investigating possible effects of ambient air NOp expo-
sures  on  pulmonary  function   parameters  in  human  adults  and children.   In that  regard,  no
evidence  of  pulmonary  function decrements  was obtained  in  several epidemiological  studies
(Cohen et al.,  1972;  Speizer  and Ferris  1973a,b; Burgess  et  al., 1973; Linn et al.,  1976)  of
adults exposed  to ambient  maximum  hourly N(L levels as high  as  0.50 ppm or annual  average  NO-
levels  up to 0.06  ppm.   These results appear  to be consistent with no observed  effects  for
pulmonary function  changes  in healthy adults generally obtained in the above controlled human
exposure  studies  with exposures to  NO^  levels  of  1.0 ppm  or  below.  None of  the presently
available  epidemiological   studies,   however,  provide  information  regarding  NOp  effects  on
pulmonary functions  in bronchitis or asthmatics.  Also, critical  evaluation  of  other epidemio-
logical studies, on  children,  reveals that such studies to date do not provide useful quanti-
tative  information  upon  which  to  base estimates of ambient N02 levels associated with  pul-
monary function decrements in children.
15.6.1.2  Acute Respiratory Disease Effects—Epidemiological  studies of outdoor and indoor  air
pollution  have also  been  employed  in  an effort  to demonstrate  an association  between  NO 2
exposures and the occurrence of acute respiratory disease symptoms and illnesses in both human
adults and children.   Such studies only provide relatively limited evidence for such associa-
tions possibly existing at ambient  air N(L levels.
     Only  a  few  American  community  air  pollution studies on  the effects  of hK^  on  acute
respiratory disease  are  available,  but all were  found  to be of  questionable  validity  due  to
the  use  of the  Jacobs-Hochheiser  technique in  measuring atmospheric concentrations  of  ^2-
     A  few  reports  on other  outdoor air  pollution  studies  on  the subject were found  in  the
foreign  literature,  but  were  such  as to preclude  confident  evaluation  of  the  methodology
involved  or  contained  information which  precluded  reliable attribution  of  observed  health
effects to ambient air N0? exposures.
                                      15-50

-------
     Certain other epidemiclogical studies on indoor air pollution, in contrast to the outdoor
pollution  studies,  appear to  provide useful  information  regarding associations  between N0?
exposures  and  acute  respiratory disease effects.  More specifically, some support for accept-
ing  the hypothesis  that  children  are at  special  risk from  NCL-induced increases  in  acute
respiratory  illnesses  might be  derived from  certain  British  and  American  studies  on indoor
pollution  effects summarized above in Table 15-6.
     The British  studies  by  Melia  et  al.  (1977,  1979) provided  initial  evidence suggesting
that  increased acute respiratory symptoms  and illness rates may  occur  among school  children
living  in  homes  using  gas  stoves  for cooking  in  comparison to  children   from  homes  using
electric ranges.   High  temperature  gas combustion is  a source  of NOo.  However,  the  first
study (Melia,  1977) did  not take parental  smoking into account, and, when socioeconomic status
was  controlled for  in the statistical  analyses  for  each of the two  studies,  only relatively
weak associations (p=.10) were found for some subgroups of children but not others.  Also, N0?
levels  were  not monitored  in  the study  homes.   In  later  British studies,   by  Florey et al.
(1979)  and Goldstein  et  al.  (1979),  NO^ levels  were  measured  in  the kitchens and bedrooms of
children residing  in gas  stove homes; but  no  significant  relationships were  found between
weekly  NCL levels  in  the  kitchen and acute respiratory  illness  symptoms in 6  to 7  year old
children or  their  siblings or  parents.   Nor were any significant  associations  found between
N02  levels and pulmonary function measures in the 6  to  7 year old  children.   Only  some weak
associations (ps  .10)  were found between  increased  respiratory illness  in  the  same  children
and N02 levels  in their bedrooms.  The authors  suggest, however,  that the apparent association
may  be  due to  NOg  serving as  a proxy for  some other variable  (humidity,  temperature)  more
important  in the etiology  of  acute respiratory infections  in the  children.   The later British
studies,therefore,  do  not  appear to  have  provided  convincing evidence to   substantiate  the
initial  hypothesis of possible  NCL  -induced increases in acute respiratory disease effects in
children residing in gas-stove  homes.   Consistent with this,  United  States  studies  by Keller
et al.  (1979  a,b) failed  to  find any  evidence  supporting  the existence of the hypothesized
relationship between  NOp  and acute respiratory  illness in school-aged American children living
in gas stove homes.
     On the other hand in  the United States  study recently  reported by Speizer et al. (1980),
children from  households with  gas stoves were reported  to  have a greater history of serious
respiratory illness before age  2.   In this study,  adjustment of rates of illness before  age 2
for parental smoking and socioeconomic status  led to  a  clearly  significant  (p <.01)  associa-
tion  with  the  presence  of  gas-cooking devices.   Also  found were  small   but  statistically
significant  lower  levels  of  two  measures  of  pulmonary function,  corrected for height,  in
children from  houses with  gas  stoves.   In  all  instances  in  the subset of study homes  with gas
                                      15-51

-------
facilities where  NO^  levels  were monitored (Spengler et al., 1979), NOp was present in higher
concentrations than was  present  in the outside air.   Indoor values monitored in one gas stove
                                 3
home averaged  as  high as 54 ug/m   (0.03  ppm)  over a two-week period; and short-term (lasting
                                                    o                              q
minutes to hours)  N02 levels in excess of  500 ug/m   (.25 ppm) and even 1,000 [jg/m  (0.5 ppm)
occurred in the kitchen during cooking.
     The Speizer/Spengler  findings  tend  to support the original hypotheses initially advanced
by Melia et  al.  (1977) regarding associations between exposure to N0? produced by gas combus-
tion and increased  acute respiratory disease  in children  residing  in homes using gas stoves.
Also,  the  small  but  significant decrements  in pulmonary function observed by  Speizer  et al.
(1980)  in  the children  at age  6  to 7,  while not likely of much  immediate  physiological  or
health  consequence,  may be  indicative of persisting residual effects of  the  early childhood
respiratory infections  on  lung  development and growth.  Furthermore,  other  studies by Colley
et  al.  (1973),  Kiernan et  al.  (1976),  and  Tausseg (1977)  suggest  that increased  rates  of
respiratory  illness  in young pre-school  children  may result in  increased susceptability for
respiratory  infection lasting  into  early adulthood.  Such  considerations regarding possible
long-term  health  consequences,  together  with  the  obvious  immediate health  significance  of
respiratory  infections  in  young  children,  argue  for  treating any such  effects as  being
sufficiently adverse as to be of clear concern in terms of public health protection.
     Certain  factors  as noted  earlier (page  15-36),  however,  should  be taken  into  account
before fully accepting at this  time the above findings and their potential implications.   This
includes an apparent  inconsistency  between the Speizer findings and the results of the Keller
studies, which found no association between residence in gas-stove usage homes and respiratory
illness rates  in  American  school children.   Several  explanations for the apparant discrepancy
can be  advanced.   For example,  the sample  sizes for children used in the Keller studies were
approximately  10  times smaller  than  the  sample  size employed in the  Speizer  study,  thereby
reducing the likelihood of Keller demonstrating statistically significant associations between
gas stove usage  and  increased  respiratory illness  .among children from gas stove homes.   Also,
the associations  reported  by Speizer were for  increased respiratory  illness  rates before the
age of two,  whereas the Keller  findings apply to older, school-aged children 6 to 7 years old.
If  both sets  of  findings are  accurate,  however,  then  they may  suggest that  the increased
respiratory infections  observed  before the  age of  two  by Speizer are  not  associated,  after
all, with long-term,  persisting  consequences of the  type  hinted  at by the Colley and Kiernan
findings (vida supra).
     If one  does accept  the Speizer  findings as  being  indicative of  increased respiratory
infections  occurring in young children living in gas  stove homes,  then the question remains as
to  what N02  exposure levels and  durations might be associated with  the induction of  such
                                      15-52

-------
effects.   Unfortunately,  no clear  resolution  of  this  issue  is  presently  available.   The
authors  themselves  (Speizer  et  al.,  1980) speculate that repeated exposures to intermittently
high peak  levels  of NC^ may be  most  important in contributing to the  increased  incidence of
respiratory  illness.   This  hypothesis  is based primarily on their  observations  (Spengler et
al., 1979)  of  long-term NO- annual averages levels in gas stove homes not differing much from
those found in electric  homes, and of the latter lacking the occurrence of intermittent marked
1-  or 2-hr indoor air NC^ peak  concentrations  associated with  periodic use of the gas stoves
for cooking.
     Estimates  of  specific  NO,,  levels,  either  for  1-2  hr  peaks  or  for long-term  (24  hr,
weekly,  annual) average  levels  that  might be associated with increased respiratory illness in
young children  cannot  be clearly derived based  alone  on  the  limited monitoring data reported
by Spengler et al.  (1979).   Rather, additional  data from other studies of ML levels typically
encountered in  American  homes  using  gas stoves may also be of value in attempting to estimate
the effective NO^  exposure parameters.   The results of several  such studies are summarized in
Table 15-7, along  with the Spengler  et al.  (1979)  findings.   Collectively, the studies found
daily peak 1-2 hr ^ levels generally to average between 0.04 and 0.50 ppm (depending on room
of  house monitored) but some instantaneous peak  levels  in  kitchens  were at times  as  high as
1.0 ppm);  whereas  24-hr and annual average  levels  fell  in the  range of 0.02 to 0.07 ppm,  and
0.02 to  0.06  ppm,  respectively.   Reported increases in  respiratory  disease symptoms in young
children  residing  in  gas  stove  homes could  be associated  with any  of these  NO-  exposure
levels/durations.
     Placing  such  levels  in  perspective  against reported  ambient  air  levels in  the  United
States,   examination of  selected  nationwide  monitoring  data  for  1975  to 1980 (discussed  in
Chapter 8)  reveals  that  peak 1-hr N02 concentrations  only  occassionally equalled or exceeded
0.4 ppm  in a few locations nationwide  (e.g.,  Los Angeles;  several other  California  sites;
Ashland,  Kentucky;  and  Port   Huron,   Michigan).    Similarly,   annual   average   NO,,  levels
during  the  1975  to 1980  period  exceeded  0.05  ppm   in  some areas,  including  such  heavily
populated locations as Anaheim and San Diego, California,  and  Chicago,  Illinois.
15.6.1.3  Chronic Respiratory Disease Effects—A  number  of investigators have  failed  to find
an  association  between  long-term mean  ambient  NO/,  exposure and  the  prevalence  of  chronic
respiratory disease  in  adults.   In contrast, long term NO^ concentrations  have been reported
to  be  associated  with  mortality,  various cancers,  and arteriosclerotic  heart disease.   Such
epidemiologic results,   however,  are  not  consistent   in  their findings;  one  even  showed  a
significant negative correlation  between  N0~ and mortality.   In addition, the  quality of data
available for such long-term studies  is such  that the  results  must be viewed with  much skepti-
cism until  they  can be substantiated  by additional research.
                                      15-53

-------
                                         TABLE 15-7.   NITROGEN DIOXIDE LEVELS REPORTED  IN  GAS AND ELECTRIC STOVE HOMES
ui
-p-
Site and conditions
Parameter
NO, concentration
(ppm)
Home 1: 2000 ft.
split-level with
well ventilated
kitchen.
range (mean)
Kitchen, 1 meter froa stove

Living room

Bedroom

Outdoors

Study simulated typical
gas stove use patterns
Kitchen

Living room

Bedroom

Outdoors

Daily peak
24-hr avg
Dai ly peak
24-hr avg
Daily peak
24-hr avg
Daily peak
24-hr avg


Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
2-hr avg

2-hr avg

2-hr avg

2-hr avg



avg

avg

avg

avg

.04-.
.01-.
.01-.
.01-
.02-.
.02-.
.02-.
.01-










28
08
.17
Ob
.09
04
.08
.05










(-10)
(.04)
(4)6)
(-03)
(.05)
(-03)
(.04)
(.02)










Measurement Reference
method

Hone 3: 2- story Home 4: 1500 ft2
apartment with ranch style with
small, unventi- kitchen open to
lated kitchen. other rooms.
range (mean) range (mean)
.03-.
.03-.
.01-
.01-
.02-
.03-.
.01-
.02-.










.31
.13
.06
.04
.19
.05
.09
.03










(.
(.
(.
(-
(.
(.
(.
(-


45
.07
40
07
24
.05
07
.04
10) .05-. 41 (.18)
06) .04-. 11 (.06)
04) .04-. 35 (.11)
03) .03-. 07 (.04)
07)
03)
04) .02-. 12 (.05)
02) .01-. 04 (.02)


Chemi luminesent Cote, Wade, and
Analyzer Yocom, 1974
Suburban homes
in Connecticut




Chemi luminesent Hollowel et al.
Analyzer 1980










Energy efficient

research house,

.33-. 44 air changes





per hour (ach).










-------
                                                                        TABLE  15-7.  (continued)
en
in
Site and conditions

Kitchen with a gas oven on for
1-hr at 350°F
0.25 ach (no stove vent)
1.0 ach (hood vent
above stove)
2.5 ach (hood vent with fan
at 50 CFH)
7.0 ach (hood vent with fan
at 140 CFM)
Outside during test
83 gas stove homes
50 electric stove homes
53 outdoor samples in
vicinity
46 gas stove



Activity room (gas stove
homes)
Activity room (electric
stove homes)
Outdoors

Kitchen, 3^ ft from gas
stove home



Parameter



1-hr average
1-hr average

1-hr average

1-hr average

1-hr average
24-hr average
24-hr average
24-hr average

continuous measurement
over 3 day periods


95th percentile of 24-hr
averages measured over a
1 year period



continuous




NO- concentration
(ppm)


1.20
O.BO

0.40

0.10

0.03
range (mean)
.01-. 11 (0.05)
0-.06 (.02)
.02-. 05 (.03)
peak values in some homes
exceeded 1 ppm; peaks during
cooking reached as high as
8 x 24-hr average
.02-. 06

.01-. 05

.01-. 06

peak concentrations
in the range of 0.25-
0.50 were observed for
10-15 minute periods
during oven or stove use.
Measurement
method
Chemi luminescent
Analyzer








Modified Jacobs-
Hochheiser
(arsenite modified)

Chemi luminescent
Analyzer


Modified Sodium
Arsenite




Chemi 1 umi nescent
Analyzer



Reference

Hollowel et al. ,
1978
Test kitchen (27m3)







Kel ler et al. , 1979
Gas and electric
stove homes in
Columbus, Ohio




Speizer et al. , 1980
Activity room in
5-11 gas and
electric stove
homes in each of
six communities.
Also monitored in
1 kitchen of a gas
stove home for 2 wks.



-------
15.6.1.4  Sensory System  Effects--In  addition to  pulmonary  function and  respiratory disease
effects, NO,  exposures have  been  shown to  exert effects on sensory systems.   This  includes
                                                                           3
detection of  NO- as  a pungent odor at concentrations  as  low as 210 ug/m   (0.11  ppm)  of N0?
immediately upon exposure.   Under  higher  exposure conditions (10 ppm) impaired odor detection
occurs.   Both of these sensory effects, however, appear to be of negligible health concern in
view  of their temporary,  reversible nature  and  generally minor impact on  normal  human func-
tions and activities.   Probably  of somewhat greater importance  are  certain other NO- sensory
effects, especially   impairment  of dark  adaption which  can  occur  in  human subjects  at NO,
                                  3
levels  as  low as 130  to  150 ug/m  (.07 to  .08  ppm).   It is difficult to  appraise  fully the
health  significance of such  an effect, however;  but it appears to be of generally negligible
health  concern  except, perhaps,  for  certain occupational  or public safety situations where
rapid dark adaptation may  be important.
15.6.2  Effects  of  NO -Derived Compounds
     Nitrate poisoning  (i.e.,  the  formation of sufficient methaemoglobin to produce cyanosis)
occurs  not  infrequently  in  the  United States,  most often in children.   It  is  not  believed,
however, that the  inhalation of  atmospheric nitrates is important in producing symptoms since
the  quantity  absorbed from  the  air  would  represent  a  relatively small  fraction  of  that
ingested by other routes (e.g., food and water).   Even  if absorption from the lung was several
times that  from the  gut,  atmospheric  nitrates  probably would  still  be  unimportant  in this
regard.
     Nitrate aerosols  and nitric  acid  vapor may  represent  significant  respiratory irritants.
Two  studies  have suggested  that  increases  in atmospheric nitrate  concentrations  or  combined
nitrate  and  sulfate   concentrations  were  associated  with  increases  in  asthma  attacks.   A
laboratory study, however,  indicated  that  short-term exposure to sodium nitrate at concentra-
tions at  least  100 times the total nitrate  in  ambient exposures had no  effect on  pulmonary
function in healthy individuals or in  asthmatics. .
     Chemical  reactions in  the atmosphere  involving N02 and  hydrocarbons  can produce peroxy-
acetyl nitrate (PAN),  a strong eye irritant.   The effects of PAN have been thoroughly reviewed
recently in the  document Air Quality Criteria for Ozone and Other Photochemical Oxidants (U.S.
EPA, 1978)  and reference is  therefore  made to this document for further  information.
     Although the existence  of a  mechanism for the m'trosation i_n vivo  of an exogenous amine,
morpholine,  by  inhaled NO-  has recently been demonstrated  in mice, there  is  no evidence,  to
date, that  nitrogenous  atmospheric  pollutants contribute to the i_n vivo formation of nitrosa-
mines in humans  or  that nitrosamines inhaled from the ambient air represent significant health
hazards.
                                      15-56

-------
15.7 REFERENCES

Abe, M.   Effects  of mixed N0?-S0,,  gas  on human pulmonary  functions.  Effects  of  air pollution
     on the human body.  Bui if Tofeyo Med. Dent. Univ. 14(4): 415-433,  1967.

Armijo, R., and A. N.  Coulson.  Epidemiology  of stomach  cancer  in  Chile.   The  role  of nitrogen
     fertilizer.  Inter. J. Epidemiol.  4: 301-309,  1975.

Ashton, M. R.  The occurrence of  nitrates and nitrites in  foods.   BFMIRA  Literature Survey  No.
     7, 1970.  pp. 32.

Barter,  C.  E. ,  and  A.  H.  Campbell.    Relationship  of  constitutional  factors and  cigarette
     smoking  to  decrease  in  1-second  forced  expiratory volume.   Am.  Rev. Resp.  Dis.  113(2):
     305-314, 1976.

Beil,  M.,  and   W.   T.   Ulmer.    Wirkung   von   N0~  in   MAK-Bereich auf  Atemmechanik   und
     Acelytcholinempfindlichkeit  bei  Normalpersonen.  (Effect  of N02 in workroom concentra-
     tions on respiratory mechanics  and bronchial  susceptibility tcr acetylchol ine  in  normal
     persons.)  Int. Arch. Occup. Environ. Health.  38: 31-44, 1976.

Bogovski, P.   Organizational and  research activities of  the analysis of N-nitroso compounds of
     the  IARC.    N-Nitroso compounds   in  the environment.   Scientific  publication  No.   9.
     International Agency  for Research  on Cancer,  Lyon,  France, 1974.

Bondareva,  E.  N.    Hygienic  evaluation  of  low concentrations  of nitrogen  oxides  present  in
     atmospheric  air.   In:   USSR  Literature  on  Air  Pollution  and  Related  Occupational
     Diseases.  A  Survey, Vol.  8.,  B.  S.  Levine,  ed. ,  Washington,  D.C., U.S. Public  Health
     Service, 1963.   (Available from the National  Technical Information Service.  Springfield,
     VA, as Publication TT-63-11570).   pp. 98-101.

Burgess,  W. ,  L.  Di  Berardinis,  and  F.  E.  Speizer.  Exposure to  automobile exhaust.   III.  An
     environmental assessment.  Arch. Environ. Health. 26:  325-329, 1973.

Case,  G.  D. ,  J.  C.  Schooley,  and  J.   S.  Dixon.   Uptake  and metabolism  of nitrogen oxide  in
     blood.   Presented at the  20th Annual Meeting,  Biophysics Society,   Seattle,  Washington,
     February, 1976.  Report no.  LRL-4417.

Case,  G.  D. ,  J.  S.  Dixon, and  J.  C.  Schooley.    Interactions  of Blood  Metal loproteins with
     Nitrogen Oxides and Oxidant Air Pollutants.    Environmental Research  20:43, 1979.

Central  Council  for  Control  of  Environmental  Pollution.   Long-term  plan  for environmental
     protection.   Environment Agency, Tokyo,  1977.  (In Japanese)

Cohen,   C.  A.,  A.  R.  Hudson,   J.   L.   Clausen,   and  J.   H.  Knelson.    Respiratory  symptoms,
     spirometry, and  oxidant  air  pollution  in  nonsmoking adults.  Amer.  Rev. Resp.  Disease
     105:251-261,  1972.

Colley, J.  R.  T.,  J.  W.  B.  Douglas,   and  D. D.   Reid.   Respiratory  disease in young  adults:
     Influence of  early childhood  lower respiratory tract illness,  social  class,  air  pollu-
     tion, and smoking.  Brit. Med.  J.   (July  28),  pp. 195-198,  1973.

Committee  on  Medical  and  Biological  Effects  of  Environmental  Pollutants,  National  Research
     Council.   Nitrogen Oxides.   Washington,  D.C., National Academy of Science, 1977.   333  pp.
                                           15-57

-------
Committee on Toxicology of the National Academy  of  Sciences,  National  Research  Council.   Guide
     for  Short-Term  Exposures  of  the Public  to  Air Pollutants.   I.   Guide  for Oxides  of
     Nitrogen,   Prepared  under  EPA Contract No.  CPA 70-57.   Washington,  D.C., April,  1970.

Coordination Group for Research on  Etiology  of Esophageal Cancer  in  North China.  The  epidemi-
     ology  and  etiology  of  esophageal cancer  in North  China.   Chinese Med.  J.   1:  167-183,
     1975.  (In Chinese)

Cote, W.  A.,  W.  A.  Wade,  III,  and  J.  E.  Yocom.  A study of  indoor  air  quality.  Final  Report
     under EPA Contract No. 68-02-0745.  EPA-650/4-74-042.  September, 1974.

Danke,  C.  S. , and  A.  J.   N.  Warrack.   Broncholitis  from nitrous fumes. Thorax. 13:  327-333,
     1958.                                                                        ~~

Douglas,  D. B.,  and R.  Owen.  Occupational  Cancer.   I.n:  The  Physiopathology of Cancer.   Vol.
     2.    Diagnosis,  Treatment,  Prevention.   M.   J.  Brennan and  I.  H.  Krakoff, eds.   Karger,
     Basel.  Third edition, 1976.   pp. 323-344.

Druckrey, H.,  R.  Preussmann, D. Schmahl, and M.  Muller.  Chemical  constitution  and  carcinogenic
     action of nitrosamines.  Naturwissenschaften 48:  134,  1961.

DuBois,   A.  B. ,  S.   Y.  Botelho,  and  J.  H.  Comroe,  Jr.    A  new method  for  measuring  airway
     resistance in man using a body plethysmograph:   values in  normal  subjects  and  in  patients
     with respiratory disease.  J.  Clin.  Invest.  35:  327-335, 1956.

Fairhall,  L.  T.   Industrial  Toxicology.   Second  ed.   Williams  andWilkins Co.,  Baltimore,  Md,
     1957.  pp.  83-84.

Feldman,  Y.  G.   The  combined  action on a human body of a mixture  of  the  main components  of
     motor traffic exhaust gases  (carbon monoxide,  nitrogen dioxide, formaldehyde and  hexane).
     Gig. i Sanit.  10: 7-10, 1974.  (In Russian)

Fleming,  G. M. ,  E.  H. Chester,  and H.  D.  Montenegno.  Dysfunction  of small airways following
     pulmonary injury due to nitrogen dioxide.    Chest  75:720-721,  1979.

Florey,  C. duV.,  R.  J. W.  Melia,  S.  Chinn, B. D.  Goldstein, A.  G.  F. Brooks, H.  H.  John,  I.  B.
     Craighead,  and  X.  Webster.  The relation  between respiratory  illness  in  primary  school
     children and the use of gas  for cooking.  Ill -  Nitrogen dioxide, respiratory  illness  and
     lung infection.  Int. J. Epid.  8:347, 1979.

Folinsbee, L.  J. ,  S.  N.  Horvath, J.  F.  Bedi,  and J.  C.  Delehunt.   Effect of  0.62 ppm  NO, on
     cardiopulmonary  function  in young male non-smokers.   Environmental Research 15:  199-205,
     1978.

Fujita,  S., M. Tanaka, S.  Kawame, I. Yoshioka, T. Furuya, S. Shibata, T. Kosoda, M. Makita,  Y.
     Fujiwara, Y. Ueda,  and K.  Tokuda.  Studies  on chronic bronchitis—epidemiological  survey
     (second report).  Commun. Med.  21: 197-203,  1969.  (In Japanese)

Gelperin, A., V.  K.  Moses, and  G.  Fox.   Nitrate in water  supplies  and  cancer.  111.  J.  Med.
     149: 251-253,  1976.

Giguz,  T.  L.    Effect of low concentrations  of ammonia and  nitrogen  oxides  on  adolescents
     undergoing  vocational  training  in the chemical  industry.   Hyg.  Sanit.   33(9):431-434,
     1968.


                                           15-58

-------
Goldsmith,  J.  R. ,  S.  N.  Rokaw,  and L.  A.  Shearer.   Distributions of methemoglobin in several
     population groups  in  California.    Inter.  J.  Epidemiol.  4:  207-212,  1975.

Goldstein,  B.  D. , R. J.  W.  Melia, S.  Chinn,  C.  DuV. Florey, D.  Clark,  and H.  H.  John.   The
     relation  between  respiratory  illness in  primary schoolchildren  and  the use  of gas for
     cooking.   II  -  Factors  affecting nitrogen  dioxide  levels in the  home.   Int.  J.  of Epid.
     8:339,  1979.

Goodall,  C.  M. ,  and T.  H.  Kennedy.   Carcinogenicity of dimethylnitramine  in NZR rats and NZO
     mice.   Cancer Lett.  1(5): 295-298,  1976.

Grayson,  R.  R.   Silage  gas poisoning:   nitrogen dioxide pneumonia,  a  new  disease in  agricul-
     tural  workers.  Ann.  Inter. Med. 45(3): 393-408,  1956.

Gregory,  K.  L. ,  V.  F.  Malenoski,  and C.  R. Sharp.   Cleveland Clinic fire  survivorship study,
     1929-1965.  Arch.  Environ.  Health  18:  508-515,  1969.

Hackney,  J.  D. ,  W.  S.  Linn,  D.  C.  Law,  S. K.  Karuza,  H.  Greenberg,  R.  D.  Buckley, and E.  E.
     Pedersen.   Experimental  studies on  human health effects on air  pollutants.   III.   Two-
     hour  exposure to  ozone  alone  and  in combination with other  pollutant  gases.   Arch.
     Environ. Health. 30:  385-390,  1975a.

Hackney,  J.  D. ,  W.   S.   Linn,  J.   G.  Mohler,  E.  E.  Pedersen,  P.  Breisacher,  and A.  Russo.
     Experimental  studies  on  human health  effects  of air pollutants.   II.   Four-hour  exposure
     to ozone alone and in combination with other pollutant  gases.   Arch.  Environ.  Health.  30:
     379-384, 1975b.

Hackney,  J.  D. ,  W.  S.  Linn,  R.  D.  Buckley, E.  E. Pedersen,  S. K.  Karuza,  D.  C.  Law, and D.  A.
     Fischer.   Experimental  studies  on  human  health  effects of  air  pollutants.   I.   Design
     considerations.  Arch. Environ.  Health. 30: 373-378, 1975c.

Hackney,  J.  D. ,  F.  C. Thiede, W.  S.  Linn, E.   E.  Pedersen,  C. E. Spier, D.  C.  Law, and D.  A.
     Fisher.  Experimental studies  on human health  effects of  air pollutants.   IV.   Short-term
  1  physiological and clinical  effects.  Arch.  Environ. Health 33(4):  176-181,  1978.

Hauser, T.  R. ,  and  C.  M.  Shy.   Position  paper:   nitrogen  oxide measurement.   Environ.  Sci.
     Techno!. 6(10):890-894, 1972.

Hayhurst,   E.  R. ,  and E.  Scott.    Four  cases  of  sudden death in a silo.  JAMA  63:1560-1562,
     1914.

Hecht,   S.   S. ,  R.  M.  Ornaf,  and  D.  Hoffman.   Chemical  studies   in  tobacco smoke.   XXXIII.
     N-Nitrosonornicotine  in  tobacco:   analysis of  possible contributing factors and  biologic
     implications.   J. Nat. Cancer  Inst.  54: 1237-1244,  1974.

Henschler,  D. ,  A.  Stier, H.  Beck,  and  W. Neumann.  Olfactory  threshold  of some important
     irritant gases and effects  in man at  low  concentrations.  Arch.  Gewerbepath.  Gewerbehyg.
     17(6):  547-570, 1960.  (In German)

Hickey, R.  J. ,  D.  E.  Boyce, E.  B. Harner,  and  R. C.  Clelland.  Ecological  statistical studies
     on environmental pollution  and chronic disease  in metropolitan  areas of  the  United States.
     RSRI   Discussion  Paper Series No. 35.  Regional  Science Research  Institute,  Philadelphia,
     Pennsylvania, 1970.  Ill pp.
                                           15-59

-------
Hill,  M.  J. ,  G.   Hawksworth,  and G.  Tattersall.   Bacteria,  nitrosamines and  cancer of  the
     stomach.  Br. J. Cancer 28(6): 562-567, 1973.

Hoffman, D. ,  S.  S. Hecht, R.  M.  Ornaf,  and E. L.  Wynder.   N-Nitrosonor-nicotine in  tobacco.
     Science 186:  265-267, 1974.

Hollowel, Craig D.  et al.   Indoor air quality in residential buildings.  Presented at  Inter-
     national Congress  on  Building Energy Management.   Poroa de Varzim,  Portugal, May  12-16,
     1980.   Lawrence Berkeley  Lab Report No. LBL-10391.

Hollowel, Craig D. ,  and G.  W.  Traynor.  Combustion-generated  indoor air pollution.  Presented
     at the  13th  International Colloquium on  Polluted Atmospheres.  Paris, April  25-28,  1978.
     Lawrence Berkeley Laboratory Report No. LBL-7832.

Horvath, E.  P., G. A. doPico,  R. A. Barbee, and H. A. Dickie.  Nitrogen dioxide  induced  pulmo-
     nary disease.  J. Occup.  Med. 20:103-110, 1978.

Horvath, S.  M. ,  and  L.  J.   Folinsbee.   Effects  of  pollutants  or  cardiopulmonary function.
     Report   to   U.S.   Environmental   Protection   Agency,   EPA   Contract  68-02-1723,   1979.
     (Manuscript submitted)

Iqbal,   Z.  M. , K.   Dahl,  and S. S. Epstein.   Role of nitrogen dioxide  in  the biosynthesis  of
     nitrosamines  in mice.   Science 207:1475-1476, 1980.

Jackson, B. ,  and   F.  I.  Dessau.   Liver  tumors in rats  fed  acetamide.   Lab.  Invest.  10:  909,
     1961.

Kagawa, J. ,  and T.  Toyama.   Photochemical air pollution:  Its effects on  respiratory  function
     of elementary school children.  Arch. Environ. Health ^0:117-122, 1975.

Kagawa, J. ,  T.  Toyama,  and  M. Nakaza.   Pulmonary function test in  children exposed to  air
     pollution.   _In:   Clinical Implications  of Air Pollution Research  Action,  A. J.  Finkel,
     Jr., and  W.   C.  Duel  (eds.)  Acton,  MA,   Publishing Sciences Group,  1976.    pp.   305-320.

Keller, M.   D. ,  R.  R.  Lanese,  R.  I.  Mitchell,  and R. W.  Cote.   Respiratory illness in  house-
     holds  using gas and electric cooking.  I.  Survey of Incidence.  Environ. Res. 19:495-503,
     1979a.

Keller, M.   D. ,  R.  R.  Lanese,  R.  I.  Mitchell,  and' R. W.  Cote.   Respiratory illness in  house-
     holds   using  gas and  electric cooking.    II.    Symptoms  and  Objective Findings.   Environ.
     Res.  19:504-515, 1979b.

Kerr,  H. D. , T.  J.  Kulla,  M.   L.  Mcllhany,  and P. Swidersky.   Effect  of  nitrogen dioxide  on
     pulmonary function  in human  subjects:   An  environmental  chamber  study.   Environ.  Res.
     19:392-404, 1979.

Kerr,  H. D. , T.  J.  Kulla,  M.   L.  Mcllhany,  and P. Swidersky.   Effect  of  Nitrogen Dioxide  on
     Pulmonary Function in Human Subjects.  An Environmental  Chamber Study.  EPA-600/1-78-025.
     U. S.   Environmantal  Protection  Agency, Office of Research  and Development  Health Effects
     Research Laboratory.  Research Triangle Park.  April, 1978.

Kiernan, K.  E. ,  J. R.  J.  Colley,  J.  B.  W. Douglas,  and D.   D.  Reid.   Chronic cough in  young
     adults in relation  to  smoking habits, childhood environment and chest illness.   Respira-
     tion 33: 236-244, 1976.


                                           15-60

-------
Klus,  H. ,  and H.  Kuhn.   Determination of  nornicotine  nitrosamine in the smoke  condensate of
     nornicotine-rich  cigarets.    Fachliche   Mitt.  Cesterr.  Tabakregie  14:  251-257,  1973.
     Chemical Abstracts 80:  11012h.

Kornienko,  A.  P.   Hygienic  assessment  of a  mixture  of  sulfuric  acid  aerosols,  sulfurous
     anhydride,  nitrogen  oxides  and ammonium  as  atmospheric pollutants.   Gig.  Sanit.  37(4):
     8-10,  1972.   (In Russian)   Translation  available from Air  Pollution  Technical  Center,
     Research Triangle Park,  North  Carolina,  as APTIC No. 40655.

Kravitz, H., L. D. Elegant,  E. Kaiser,  and  B.  M. Kagan.  Methemoglobin values in  premature and
     mature infants and children.   A.M.A.J. Dis. Child., 91:  1-5,  1956.

Lebowitz,  M. D.   Comparative urban  daily mortality in  relation to  air pollution and weather,
     PhD.  Thesis.  University of  Washington,  Seattle, 1971.

Linn,  W.  S. , J.  D. Hackney,  E.  E.  Pedersen,   P. Breisacher,  J.  V.  Patterson, C.  A.  Mulry, and
     J.  F.  Coyle.  Respiratory  function  and  symptoms  in urban  office workers in  relation to
     oxidant air pollution exposure.  Amer. Rev. Resp.  Disease.  114:  477-483,  1976.

Lowry.   T. ,  and  L.  M.  Schuman.   Silo fillers  disease:   A syndrome caused  by  nitrogen dioxide.
     JAMA  126:153-160, 1956.

Lutz,  G. A., R. I. Mitchell,  R. W.  Cote,  and  M.  D.  Keller.   Indoor epidemiology study.   Report
     prepared for the American Gas  Association.  Battelle Columbus Laboratories,  1974.

Lutz,  G. A., R. I. Mitchell,  R. W.  Cote,  and  M.  D.  Keller.   Respiratory disease symptom study.
     Report prepared  for  the American  Gas  Association.  Battelle  Columbus Laboratories,  1977.

Melia,   R.  J.  W. ,  C.  Du  V.   Florey,  D.  S.  Altman,  and A.   V.  Swan.  Association  between gas
     cooling and respiratory  disease  in children.   Brit. Med. J. 2:  149-152,  1977.

Mel-ia,   R.  J. W. ,  C.  du V.  Florey,  and S.  Chinn.   The  relation  between respiratory illness in
   :  primary schoolchildren  and  the  use  of  gas  for  cooking.    I  -  Results from a  national
     survey.  Int. J.  Epid. 8:333,  1979.

Melia,   R. J. W., C. du V.  Florey, S.  C. Darby,  E.  D. Palmers, and  B.  D.  Goldstein.   Differences
     in N02  levels  in kitchens with  gas  or electric cookers.   Atm.  Env.  12:  1379-1381,  1978.

Milne,   J.  E.  H.   Nitrogen  dioxide  inhalation and bronchitis  obliterans.   A review of  the
     literature and report of a case.  J. Occup. Med. 11: 538-547,  1969.

Mitchell, R. I., R. Williams, R.   W. Cote, R.  R.  Lanese, and  M. D.  Keller.  Household  survey of
     the  incidence of  respiratory  disease   in  relation  to environmental  pollutants.    WHO
     International  Symposium Proceedings:   Recent  Advance  in  the Assessment of the  Health
     Effects of Environmental Pollutants.   Paris,  June  24-28, 1974.

Mogi,  T. ,  M. Shimizu,  N.  Kondo,  K.  Yamazaki,  and S. Jinguji.   The effects  of diesel  exhaust
     gas on  the body.   Report No.  1.   Environmental  Survey.   Railway Labor  Sci.  22:  1-25,
     1968.   (In Japanese)

Mysliwy, T.  S. ,  E. L.  Wick,  M.  C.  Archer,  R. C.  Shank,  and  P.  M.  Newberne.   Formation of
     N-nitrosopyrrolidine in  a dog's  stomach.    Brit. J.  Cancer 30:  279-283, 1974.
                                           15-61

-------
Nakamura, K.   Response  of pulmonary airway resistance by interaction of aerosols and gases of
     different physical  and  chemical  nature.   Jap. J.  Hyg.  19:  322-333, 1964.  (In Japanese)
     Translation available from  Air Pollution Technical Information Center, Research Triangle
     Park, North Carolina as APTIC No. 11425.

National Academy of Sciences.  National Research Council.  Accumulation of nitrate.  Committee
     on  Nitrate  Accumulation,  Agricultural   Board,  Division  of  Biology  and  Agriculture,
     Washington, D.C., National Academy of Sciences, 1972.

National Academy of Sciences.  National Research Council.  Committee on Medical and Biological
     Effects  of  Environmental  Pollutants,  Nitrogen Oxides.   Washington,  DC,   1977.   333 pp.

National  Academy of  Sciences,  National  Research  Council.    Committee  on Toxicology  of the
     National  Academy of  Sciences.    Guide  for  Short-term  Exposures  of the Public  to Air
     Pollutants.    I.   Guide  for  Oxides  of  Nitrogen.   Prepared  under  EPA Contract  No.  CPA
     70-57.   Washington, DC,  April-, 1970.

National  Academy of  Sciences.    National  Research  Council.   Environmental  Impact  of Strato-
     spheric  Flight:   Biological  and  Climatic Effects  of  Aircraft Emissions  in  the Strato-
     sphere.  Climatic Impact Committee, Washington, DC, 1975.

Neurath,  G.   Zur Frage  des  Vorkommens von N-nitrosoverbindungen  im Tabakrauch.   Experientia
     23: 400-404, 1967.

Nikolaeva, T.  Maximum  permissible concentrations of harmful substances in atmospheric air of
     populated places.  Hyg.  Sanit. 29(5): 166-158, 1964.

Norman,  V.,  and C.  H.  Keith.   Nitrogen oxides in tobacco  smoke.   Nature  205(4974):  915-916,
     1965.

Orehek,  J. ,  J.  P.  Massari,  P.  Gayrard,  C.  Grimaud,  and  J.  Charpin.  Effect  of  short-term,
     low-level nitrogen  dioxide  exposure  on bronchial sensitivity  of  asthmatic patients.   J.
     Clin. Invest.  57: 301-307, 1976.

Palmes,  E.  0.   Field  Comparison of Two Methods  for N0? Measurement in Air.   Amer.  Ind.  Hyg.
     Assoc.  J. 40:   April, 1979.

Pearlman, M.  E. , J.  F.  Finklea, J. P.  Creason,  C.  M. Shy,  M.  M.  Young,  and R. J. M. Horton.
     Nitrogen dioxide and lower respiratory illness.  Pediatrics 47(2):  391-398, 1971.

Petr, B. , and P.  Schmidt.  Der Einfluss der durch Schwefeldioxid und nitrose Gase verunreinigten
     Atmosphere  auf den  Gesundheitszunstand der Kinder.  Z.  Gesamte  Hyg.  13(1):  34-38, 1967.
     (In German)

Pitts,  J. N., Jr.,  and A. L.  Loyd.   Discharges into the atmosphere.  J_n:   Nitrogenous Compounds
     in  the  environment.   EPA-SAB-73-001.  U.S.  Environmental  Protection  Agency,  Washington,
     DC, 1973.

Pitts,   J.  N. , Jr.,  D.  Grosjean,  K. Van  Cauwenberghe,  J.  P. Schmid, and D.  R. Fitz.  Photo-
     oxidation  of   aliphatic  amines  under simulated atmospheric  conditions:  formation  of
     nitrosamines,  nitramines, amides,  and  photochemical oxidant.   Envir.  Sci. and Technology
     12: 946-953, 1978.
                                           15-62

-------
Polyak,  V.  E.  Air  pollution around  a chemical  works  and  the  effects of  its discharge  on
     sanitary living conditions.  Hyg.  Sanit.  35:  117-118,  1968.

Posin, C., K. Clark, M. P. Jones, J. V.  Patterson,  R. D. Buckley,  and  J.  D. Hackney.   Nitrogen
     dioxide  and   human  blood biochemistry.   Arch. Environ.  Health (Nov/Dec):318-324,  1978.

Raminez,  R. J.  The first death  from nitrogen  dioxide fumes.   JAMA 229:  1182,  1974.

Sander,  J. ,  and F. Self.   Bakterielle  reduktion von Nitrat  im Magen  des Menschen  als  Ursache
     einer Nitrosaminbildung.  Arzneimittel-Forsch.  19:  1091-1093,  1969.

Sander,  J. ,  F.  Schweinsberg, and J. P.  Menz.  Untersuchungen iiber die  Entstehung  Kanzerogener
     Nitrosamine im Magen.   Hoppe-Seyler1s  Z.  Physio!. Chem.  349:  1691-1697,  1968.

Sato,  R. ,  T.  Fukuyama, T. Suzuki, J. Takayanagi,  T. Murakami, N.  Shiotzuki,  R.  Taraka,  and  R.
     Tsuji.   Studies  of  the causation  of gastric  cancer.   The relation between gastric  cancer
     mortality  rate  and  salted  food   intake  in several places  in Japan.   Bull.  Inst.  Pub.
     Health (Japan) 8: 187-198,  1959.

Schlipkdter,   H.   W. ,   and  A.   Brockhaus.    Versuche   uber    den   Einfluss   gasformiger
     Luftverunreinigungen  auf die Deposition  and  elimination inhalierter Staube.  Zentralbl.
     Bakteriol.   Parasitenkd.  Infektionskr.  Hyg.   Abt.  1.  191:   339-344,  1963.   (In  German)

Shalamberidze, 0.   P.    Reflex effects of mixtures of sulfur  and nitrogen dioxides.   Hyg.  Sanit.
     32:  10-15,  1967.

Shy,  C.   M.   The   Chattanooga study.    J.  Air Pollut.  Control Assoc.  20(12):  832-833,  1970.

Shy, C.  M.,  and G. J. Love.  Recent evidence  on the human  health  effects of  nitrogen  dioxide.
     Proceedings  of  the  Symposium  on   Nitrogen  Oxides, Honolulu, Hawaii,  April  4-5,  1979.

Shy, C.  M. ,  J.  P.  Creason, M. E. Pearlman, K. E.  McClain,  F.  B. Benson,  and  M.  M.  Young.  The
   '  Chattanooga  school  children study:   effects   of community  exposure of  nitrogen  dioxide.
     I.   Methods,  description of pollutant exposure and results of ventilatory function test-
     ing.  J. Air  Pollut.  Control Assoc. 20(8):  539-545, 1970a.

Shy, C.  M. ,  J.  P.  Creason, M. E. Pearlman, K. E.  McClain,  F.  B. Benson,  and  M.  M.  Young.  The
     Chattanooga  school   study:   effects   of  community  exposure  to   nitrogen  dioxide.  II.
     Incidence  of  acute  respiratory  illness.   J.'Air Pollut.  Control  Assoc.  20(9):   582-588,
     1970b.

Shy  C.   M. ,  Niemeyer,  L  Truppi,  and  J.  English.   Reevaluation of  the  Chattanooga  School
     Children Studies  and the  Health   Criteria  for NO^ Exposure.   Inhouse  technical  report.
     Health  Effects  Research  Laboratory,   Environmental  Research  Center,  U.S. Environmental
     Protection  Agency, Research Triangle Park,  NC.  March, 1973.

Speizer,  F.   E.  ,  and  B.   G.  Ferris,  Jr.   Exposure to  automobile   exhaust.    I.  Prevalence  of
     respiratory symptoms and disease.    Arch.  Environ.  Health. 26:  313-318, 1973a.

Speizer,  F.   E.  ,   and  B.  G.  Ferris,  Jr.   Exposure  to automobile exhaust.    II.   Pulmonary
     function measurement.  Arch. Environ.   Health.   26(6): 319-324,  1973b.
                                           15-63

-------
Speizer,  F.  E. ,  B.  G.  Ferris,  Jr.,  Y.  M.  M.  Bishop,  and  J.  Spengler.  Respiratory  disease
     rates  and  pulmonary  function  in children associated with  NO,  exposure.   Am. Rev.  Resp.
     Dis. 121:3-10, 1980.                                          "

Spengler, J. D. ,  B.  G.  Ferris,  Jr.,  and D.  W.  Dockery.   Sulfur dioxide and nitrogen  dioxide
     levels inside and outside homes  and  the implications  on health  effects  research.   Environ.
     Sci. Tech.  13:1276-1271, 1979.

Suzuki, T. , and  K.  Ishikawa.  Research  of  effect of smog on human  body.  Research and Report
     on Air Pollution Prevention 2: 199-221, 1965.   (In  Japanese)

Thomas, H.  V.,  R.  L.  Stanley, S.  Twiss,  and P.  K.  Mueller.   Sputum histamine and inhalation
     toxicity.  .Environ. Lett. 3: 33-52,  1972.

Treiger,  B. ,  and C.  Przypyszny.  Nitric  acid  fume pneumonia--a  case  report.   Ind.  Med.  16:
     395-397,  1947.                                                                         ~

Tuasseg,  L. M.   Clinical  and physiologic evidence for the persistence of pulmonary abnormali-
     ties  after  respiratory  illnesses  in infancy  and  childhood.   Pediat.  Res.   11:  216-218,
     1977.                                                                         ~~

U.S. Environmental  Protection Agency.  Air Quality  Criteria for Ozone and Other Photochemical
     Oxidants.   EPA-60/8-78-004.   Washington, D.C.,  1978.

U.S.  Environmental  Protection  Aency.   Scientific  and   Technical  Data  Base  for  Criteria  and
     Hazardous  Pollutants.    1975   ERC/RTP  Review.    EPA-600/1-76-023,  U.S.  Environmental
     Protection Agency, Research Triangle Park, NC.  May,  1976.

Utell,  M.  J., A.  T.  Aquilina, W. J.  Hall, D. M.  Speers, R. G. Douglas, Jr., F. R. Gibb,  P.  E.
     Morrow, and R.  W.  Hyde.  Development of  airways  reactivity to nitrates in subjects with
     influenza.   Am. Res. Resp.  Dis.  121:233-240, 1980.

Utell, M. J. ,  A.  J. Swinburne, R. W.  Hyde, D. M.  Speers, F. R. Gibb, and P.  E. Morrow.   Airway
     reactivity  to  nitrates  in normal  and  mild  asthmatic subjects.   J.  Appl.   Physiol.:
     Respirat.  Environ.  Exercise Physiol. 46: 189-196, 1979.

Von Nieding,  G. ,  H.  Krekeler,   R.   Fuchs,  H.  M.  Wagner,  and K.  Koppenhagen.   Studies  of  the
     acute  effect  of  N0? on  lung function:  influence on  diffusion, perfusion and ventilation
     in the lungs.   Int. Arch. Arbeitsmed. 31: 61-72, 1973.

Von Neiding, G.,  H. M. Wagner, H. Krekler, U. Smidt, and K. Muysers.  Absorption of NO, in  low
     concentrations  in  the  respiratory  tract  and  its acute  effects  on   lung   funcrion  and
     circulation.    Paper No.  MB-15  G  Second  International  Clean  Air  Congress,  Washington,
     D.C., 1970.

Von Nieding, G., H.  M.  Wagner,  H.  Krekeler, U. Smidt, and K. Muysers.  Minimum concentrations
     of  N0? causing acute  effects  on  the  respiratory  gas exchange and airway resistance  in
     patierfts with  chronic  bronchitis.   Int.  Arch.  Arbeitsmed.  27:  338-348, 1971.  Translated
     from  German  by Mundus  Systems for Air  Pollution  Technical  Information  Center, U.S.
     Environmental  Protection Agency, Research Triangle  Park, North  Carolina.

Von Neiding, G. ,  H.  M.  Wagner,  H.  Lbllgen,  and  K.  Krekeler.  Acute effects of ozone  on lung
     function of men.  VDI-Ber.  270:123-129, 1977.
                                           15-64

-------
Wade, W. A., Ill, W. A. Cote, and J. E. Yocom.  A study of  indoor  air  quality.   J.  Air  Pollut.
     Control Assoc. 25: 93-939, 1975.

Weisburger,  J.  H., R.  S.  Yamamato, R.  M.  Glass,  and H. H.  Frankel.   Prevention  by arginine
     glutamate of the carcinogenicity of acetamide in rats.   Toxicol.  App.  Pharmacol. 14:  163,
     1969.                                                                            ~~

World Health Organization.  Oxides of Nitrogen, Environmental Health Criteria  4.  World Health
     Organization, Geneva, Switzerland, 1977.  79 pp.

Yamazaki, K. T.  Mogi,  Y.  Nishimoto, and  T.  Komazawa.   The effect of  disel  exhaust gas on the
     body.   Report No.  2.    An  analysis  of  pulmonary  function  tests.    Railway  Labor  Sci.
     23:1-11, 1969  (In Japanese)

Yokoyama, E.   The respiratory  effects  of  exposure  to S09-N09  mixtures  on healthy subjects.
     Japan.  J.  Ind. Health 14: 449-454, 1972.  (In Japanese)  *

Zaldivar,  R.,  and  W.   H.  Wetterstand.    Further evidence  of  a positive  correlation  between
     exposure  to  nitrate  fertilizers   (NaNOU and  KNO,)  and  gastric  cancer  death   rates:
     nitrites and nitrosamines.   Experientia 31:  1354-1355,  1975.
                                           15-65

-------

-------
                                   GLOSSARY
AaDOy  Alveolar-arterial difference or gradient of the partial pressure of
     oxygen.  An overall measure of the efficiency of the lung as a gas ex-
     changer.  In healthy subjects, the gradient is 5 to 15 mm Hg (torr).

A/PR/8 virus:  A type of virus capable of causing influenza in laboratory
     animals; also, A/PR/8/34.

Abscission:  The process whereby leaves, leaflets, fruits, or other plant
     parts become detached from the plant.

Absorption coefficient:  A quantity which characterizes the attenuation with
     distance of a beam of electromagnetic radiation (like light) in a substance.

Absorption spectrum:  The spectrum that results after any radiation has
     passed through an absorbing substance.

Abstraction:  Removal of some constituent of a substance or molecule.

Acetaldehyde:  CH3CHO; an intermediate in yeast fermentation of car-
     bohydrate ana in alcohol metabolism; also called acetic aldehyde,
     ethaldehyde, ethanal.

Acetate rayon:  A staple or filament fiber made by extrusion of cellulose
     acetate.  It is saponified by dilute alkali whereas viscose rayon remains
     unchanged.

Acetylcholine:  A naturally-occurring substance in the body which can
     cause constriction of the bronchi in the lungs.

Acid:   A substance that can donate hydrogen ions.

Acid dyes:   A large group of synthetic coal  tar-derived dyes which
     produce bright shades in a wide color range.   Low cost and ease
     of application are features which make them the most widely used
     dyes for wool.   Also used on nylon.   The term acid dye is derived
     from their precipitation in an acid bath.

Acid mucopolysaccharide:   A class of compounds composed of protein
     and polysaccharide.   Mucopolysaccharides comprise much of the
     substance of connective tissue.

Acid phosphatase:   An enzyme (EC 3.1.3.2) which catalyzes the disassociation
     of phosphate (PO.) from a wide range of monoesters of orthophosphoric
     acid.   Acid phosphatase is active in an acidic pH range.

Acid rain:   Rain having a pH less than 5.6,  the minimum expected from
     atmospheric CO
                                      G-l

-------
Acrolein:   ChL=CHCHO; a volatile, flammable, oily liquid, giving off
     irritant vapor.  Strong irritant of skin and mucuous membranes.  Also
     called acrylic aldehyde, 2-propenal.

Acrylics (plastics):  Plastics which are made from acrylic acid and are
     light in weight, have great breakage resistance, and a lack of
     odor and taste.  Not resistant to scratching, burns, hot water,
     alcohol or cleaning fluids.  Examples include Lucite and Plexiglass.
     Acrylics are thermoplastics and are softened by heat and hardened
     into definite shapes by cooling.

Acrylic fiber:   The generic name of man-made fibers derived from acrylic
     resins (minimum of 85 percent acrylonitrite units).

Actinic:  A term applied to wavelengths of light too small to affect
     one's sense of sight, such as ultraviolet.

Actinomycetes:   Members of the genus Actinomyces; nonmotile, nonspore-
     forming, anaerobic bacteria, including both soil-dwelling saprophytes
     and disease-producing parasites.

Activation energy:  The energy required to bring about a chemical reaction.

Acute respiratory disease:  Respiratory infection, usually with rapid
     onset and of short duration.

Acute toxicity:  Any poisonous effect produced by a single short-term
     exposure,  that results in severe biological harm or death.

Acyl:  Any organic radical or group that remains intact when an organic
     acid forms an ester.

Adenoma:  An ordinarily benign neoplasm (tumor) of epithelial tissue;
     usually well circumscribed, tending to compress adjacent tissue rather
     than infiltrating or invading.

Adenosine monophosphate (AMP):  A nucleotide found amoung the hydrolysis
     products of all nucleic acids;  also called adenylic acid.

Adenosine triphosphatase (ATPase):  An enzyme (EC 3.6.1.3) in muscle
     and elsewhere that catalyzes the release of the high-energy, ter-
     minal phosphate group of adenosine triphosphate.

Adrenalectomy:   Removal of an adrenal gland.  This gland is located near
     or upon the kidney and is the site of origin of a number of hormones.

Adsorption:  Adhesion of a thin layer of molecules to a liquid or solid sur-
     face.

Advection:  Horizontal flow of air at the surface or aloft; one of  the
     means by which heat is transferred from one region of the earth
     to another.
                                      G-2

-------
Aerodynamic diameter:  Expression of aerodynamic behavior of an irregularly
     shaped particle in terms of the diameter of a sphere of unit density
     having identical aerodynamic behavior to the particle in question.

Aerosol:  Solid particles or liquid droplets which are dispersed or sus-
     pended in a gas.

Agglutination:  The process by which suspended bacteria, cells or similar
     particles adhere and form into clumps.

Airborne pathogen:   A disease-causing microorganism which travels in the
     air or on particles in the air.

Air pollutant:  A substance present in the ambient atmosphere, resulting
     from the activity of man or from natural processes, which may cause
     damage to human health or welfare, the natural environment, or
     materials or objects.

Airway conductance:   Inverse of airway resistance.

Airway resistance (R,w):   The pressure difference between the alveoli
     and the mouth required to produce an air flow of 1 liter per second.

Alanine aminotransferase:   An enzyme (EC 2.6.1.2) transferring amino
     groups from L-alanine to 2-ketoglutarate.   Also known as alanine
     transaminase.

Albumin:  A type of simple, water-soluble protein widely distributed
     throughout animal  tissues and fluids, particularly serum.

                                                           0
                                                           M
Aldehyde:   An organic compound characterized by the group -OH.

Aldolase:   An enzyme (EC 4.1.2.7) involved in metabolism of fructose
     which catalyzes the formation of two 3-carbon intermediates in the
     major pathway of carbohydrate metabolism.

Algal  bloom:   Sudden spurt in growth of algae which can affect water
     quality adversely.

Alkali:   A salt of sodium or potassium capable of neutralizing acids.

Alkaline phosphatase:   A phosphatase (EC 3.1.3.1) with an optimum pH of
     8.6,  present ubiquitously.

Allergen:   A material  that,  as a result of coming into contact with appro-
     priate tissues  of  an animal  body,  induces a state of sensitivity result-
     ing in various  reactions; generally associated with idiosyncratic
     hypersensitivities.

Alpha-hydroxybutyrate dehydrogenase:   An enzyme (EC 1.1.1.30),  present
     mainly in mitochondria,  which catalyzes the conversion of hydro-
     xybutyrate to acetoacetate in intermediate biochemical  pathways.
                                      G-3

-------
Alpha rhythm:  A rhythmic pulsation obtained in brain waves exhibited
     in the sleeping state of an individual.

Alveolar capillary membrane:  Finest portion of alveolar capillaries,
     where gas transfer to and from blood takes place.

Alveolar macrophages (AM):  Large, mononuclear, phagocytic cells found
     on the alveolar surface, responsible for the sterility of the lung.

Alveolar oxygen partial pressure (PACL):  Partial pressure of oxygen in the
     air contained in the air sacs of the lungs.

Alveolar septa:  The tissue between two adjacent pulmonary alveoli, con-
     sisting of a close-meshed capillary network covered on both surfaces
     by thin alveolar epithelial cells.

Alveolus:  An air cell; a terminal, sac-like dilation in the lung.   Gas
     exchange (0?/CO?) occurs here.

Ambient:  The atmosphere to which the general population may be exposed.
     Construed here not to include atmospheric conditions indoors,  or in
     the workplace.

Amine:   A substance that may be derived from ammonia (NH,) by the re-
     placement of one, two or three of the hydrogen (H) atoms by hydro-
     carbons or other radicals (primary, secondary or tertiary amines,
     respectively).

Amino acids:  Molecules consisting of a carboxyl group, a basic amino
     group, and a residue group attached to a central carbon atom.   Serve
     as the building blocks of proteins.

p-Aminohippuric acid (PAH):   A compound used to determine renal plasma
     flow.

Aminotriazole:   A systemic herbicide, C^H.N., used in areas other than
     croplands, that also possesses some anlithyroid activity; also called
     amitrole.

Ammonification:  Decomposition with production of ammonia or ammonium
     compounds, esp.  by the action of bacteria on nitrogenous organic
     matter.
Aminonium
     with
     lizers.
urn:   Anion (NH.) or radical  (NH.)  derived from ammonia by combination
ith  hydrogen.   Present in rainwater,  soils and many commercial  ferti-
Amnestic:  Pertains to immunologic memory:   upon receiving a second
     dose of antigen, the host "remembers"  the first dose and responds
     faster to the challenge.
                                      G-4

-------
Anaerobic:  Living, active or occurring in the absence of free oxygen.

Anaerobic bacteria:  A type of microscopic organism which can live in
     an environment not containing free oxygen.

Anaphylactic dyspneic attack:  Difficulty in breathing associated with
     a systemic allergic response.

Anaphylaxis:  A term commonly used to denote the immediate, transient
     kind of immunological (allergic) reaction characterized by contraction
     of smooth muscle and dilation of capillaries due to release of
     pharmacologically active substances.

Angiosperm:   A plant having seeds enclosed in an ovary; a flowering plant.

Angina pectoris:  Severe constricting pain in the chest which may be
     caused by depletion of oxygen delivery to the heart muscle; usually
     caused by coronary disease.
          o              _o
Angstrom (A):   A unit (10   cm) used in the measurement of the wavelength
     of light.

Anhydride:  A compound resulting from removal of water from two molecules
     of a carboxylic (-COOH) acid.  Also,  may refer to those substances
     (anhydrous) which do not contain water in chemical combination.

Anion:   A negatively charged atom or radical.

Anorexia:   Diminished appetite; aversion to food.

Anoxic:  Without or deprived of oxygen.

Anthraquinone:   A yellow crystalline ketone,  C-w-HgOp, derived from
     anthracene and used in the manufacture of ayes.

Anthropogenic:   Of, relating to or influenced by man.  An anthropogenic
     source of pollution is one caused by man's actions.

Antibody:   Any body or substance evoked by the stimulus of an antigen
     and which reacts specifically with antigen in some demonstrable way.

Antigen:   A material such as a foreign protein that,  as a result of
     coming in contact with appropriate tissues of an animal, after a
     latent period, induces a state of sensitivity and/or the production of
     antibody.

Antistatic agent:   A chemical compound applied to fabrics to reduce or
     eliminate accumulation of static electricity.

Arachidonic  acid:   Long-chain fatty-acid which serves as  a precursor
     of prostaglandins.
                                      G-5

-------
Area source:  In air pollution, any small individual fuel combustion
     or other pollutant source; also, all such sources grouped over a
     specific area.

Aromatic:   Belonging to that series of carbon-hydrogen compounds in
     which the carbon atoms form closed rings containing unsaturated
     bonds (as in benzene).
Arterial partial pressure of oxygen (PaO^):  Portion of total pressure of
     dissolved gases in arterial blood as measured directly from arterial
     blood.

Arterial ized partial pressure of oxygen:   The portion of total pressure
     of dissolved gases in arterial blood attributed to oxygen, as
     measured from non-arterial (e.g., ear-prick) blood.

Arteriosclerosis:  Commonly called hardening of the arteries.  A condition
     that exists when the walls of the blood vessels thicken and become
     infiltrated with excessive amounts of minerals and fatty materials.

Artifact:   A spurious measurement produced by the sampling or analysis
     process.

Ascorbic acid:   Vitamin C, a strong reducing agent with antioxidant proper-
     ties.

Aspartate transaminase:  Also known as aspartate ami notransf erase
     (EC 2.6.1.1).   An enzyme catalyzing the transfer of an amine group
     from glutamic acid to oxaloacetic, forming aspartic acid in the
     process.  Serum level of the enzyme is increased in myocardial in-
     farction and in diseases involving destruction of liver cells.

Asphyxia:   Impaired exchange of oxygen and carbon dioxide, excess of
     carbon dioxide and/or lack of oxygen, usually caused by ventilatory
     problems.

Asthma:  A term currently used in the context of bronchial asthma in
     which there is widespread narrowing of the airways of the lung.
     It may be aggravated by inhalation of pollutants and lead to
     "wheezing" and shortness of breath.

Asymptomatic:  Presenting no subjective evidence of disease.

Atmosphere:  The body of air surrounding the earth.   Also, a measure of
     pressure (atm. ) equal to the pressure of air at sea level, 14.7 pounds
     per square inch.

Atmospheric deposition:  Removal of pollutants from the atmosphere onto
     land,  vegetation, water bodies or other objects, by absorption,
     sedimentation, Brownian diffusion, impaction, or precipitation in rain.
                                      G-6

-------
Atomic absorption spectrometry:  A measurement method based on the
     absorption of radiant energy by gaseous ground-state atoms.   The
     amount of absorption depends on the population of the ground state
     which is related to the concentration of the sample being analyzed.

Atropine:  A poisonous white crystalline alkaloid, C-^HpoNO.,, from
     belladonna and related plants, used to relieve spasms and to dilate
     the pupil of the eye.

Autocorrelation:   Statistical interdependence of variables being analyzed;
     produces problems, for example, when observations may be related
     to previous measurements or other conditions.

Autoimmune disease:   A condition in which antibodies are produced against
     the subject's own tissues.

Autologous:  A term referring to cellular elements, such as red blood cells
     and alveolar macrophage, from the same organism; also, something
     natually and normally ocurring in some part of the body.

Autotrophic:   A term applied to those microorganisms which are able to
     maintain life without an exogenous organic supply of energy, or which
     only need carbon dioxide or carbonates and simple inorganic nitrogen.

Autotrophic bacteria:   A class of microorganisms which require only
     carbon dioxide or carbonates and a simple inorganic nitrogen com-
     pound for carrying on life processes.

Auxin:   An organic substance that causes lengthening of the stem when
     applied in low concentrations to shoots of growing plants.

Awn:   One of the slender bristles that terminate the glumes of the
     spikelet in some cereals and other grasses.

Azo dye:   Dyes in which the azo group is the chromophore and joins
     benzene or napthalene rings.

Background measurement:  A measurement of pollutants in ambient air due
     to natural  sources; usually taken in' remote areas.

Bactericidal  activity:   The process of killing bacteria.

Barre:   Bars or stripes in a fabric, caused by uneven weaving, irregular
     yarn or uneven dye distribution.

Basal cell:  One of the innermost cells of the deeper epidermis of the
     skin.

Benzenethiol:   A compound of benzene and a hydrosulfide group.
                                      G-7

-------
Beta (p)-lipoprotein:  A biochemical complex or compound containing both
     lipid and protein and characterized by having a large molecular
     weight, rich in cholesterol.   Found in certain fractions of human
     plasma.

Bilateral renal sclerosis:  A hardening of both kidneys of chronic
     inflammatory origin.

Biomass:   That part of a given habitat consisting of living matter.

Biosphere:  The part of the earth's crust, waters and atmosphere where
     living organisms can subsist.

Biphasic:  Having two distinct successive stages.

Bleb:   A collection of fluid beneath the skin; usually smaller than
     bullae or blisters.

Blood urea:   The chief end product of nitrogen metabolism in mammals,
     excreted in human urine in the amount of about 32 grams (1 oz.)
     a day.

Bloom:   A greenish-gray appearance imparted to silk and pile fabrics
     either by nature of the weave or by the finish; also, the creamy
     white color observed on some good cottons.

Blue-green algae:   A group of simple plants which are the only N^-fixing
     organisms which photosynthesize as do higher plants.

Brightener:   A compound such as a dye, which adheres to fabrics in order
     to provide better brightness or whiteness by converting ultraviolet
     radiation to visible light.   Sometimes called optical bleach or
     whitening agent.  The dyes used are of the florescent type.

Broad bean:   The large flat edible seed of an Old World upright vetch
     (Vicia faba), or the plant itself, widely grown for its seeds and
     for fodder.

Bronchi:   The first subdivisions of the trachea which conduct air to
     and from the bronchioles of the lungs.

Bronchiole:   One of the finer subdivisions of the bronchial (trachea)
     tubes,  less than 1 mm in diameter, and having no cartilage in
     its wall.

Bronchiolitis:   Inflammation of the smallest bronchial tubes.

Bronchiolitis fibrosa obliterans syndrome:  Obstruction of the bronchioles
     by fibrous granulation arising from an ulcerated mucosa;  the condition
     may follow inhalation of irritant gases.
                                      G-8

-------
Bronchitis:  Inflammation of the mucous membrane of the bronchial tubes.
     It may aggravate an existing asthmatic condition.

Bronchoconstrictor:  An agent that causes a reduction in the caliber
     (diameter) of a bronchial tube.

Bronchodilator:  An agent which causes an increase in the caliber (diameter)
     of a bronchus or bronchial tube.

Bronchopneumonia:  Acute inflammation of the walls of the smaller bronchial
     tubes, with irregular area of consolidation due to spread of the in-
     flammation into peribronchiolar alveoli and the alveolar ducts.

Brownian diffusion:  Diffusion by random movement of particles suspended
     in liquid or gas, resulting from the impact of molecules of the
     fluid surrounding the particles.

Buffer:  A substance in solution capable of neutralizing both acids
     and bases and thereby maintaining the original pH of the solution.

Buffering capacity:  Ability of a body of water and its watershed to
     neutralize introduced acid.

Butanol:  A four-carbon, straight-chain alcohol, C,HqOH, also known as
     butyl alcohol.                               ^ 3

Butyl ated hydroxytoluene (BHT):   A crystalline phenolic antioxidant.

Butylated hydroxyanisol (BHA):   An antioxidant.
14
  C labeling:   Use of a radioactive form of carbon as a tracer, often
     in metabolic studies.
14
  C-proline:   An amino acid which has been labeled with radioactive carbon.

Calcareous:  Resembling or consisting of calcium carbonate (lime), or
     growing on limestone or lime-containing soils.

Calorie:  Amount of heat required to raise temperature of 1 gram of
     water at 15 C by 1 degree.

Cannula:  A tube that is inserted into a body cavity, or other tube
     or vessel, usually to remove fluid.

Capillary:   The smallest type of vessel;  resembles a hair.   Usually
     in reference to a blood or lymphatic capillary vessel.
Carbachol:   A chemical compound (carbamoylcholine chloride, CgH-icClN^Op) that
     produces a constriction of the bronchi; a parasympathetic stimulant
     used in veterinary medicine and topically in glaucoma.
                                      G-9

-------
Carbon monoxide:  An odorless, colorless, toxic gas with a strong affinity
     for hemoglobin and cytochrome; it reduces oxygen absorption capacity,
     transport and utilization.

Carboxyhemoglobin:  A fairly stable union of carbon monoxide with hemo-
     globin which interferes with the normal transfer of carbon dioxide
     and oxygen during circulation of blood.  Increasing levels of
     carboxyhemoglobin result in various degrees of asphyxiation, in-
     cluding death.

Carcinogen:  Any agent producing or playing a stimulatory role in the
     formation of a malignancy.

Carcinoma:   Malignant new growth made up of epithelial  cells tending to
     infiltrate the surrounding tissues and giving rise to metastases.

Cardiac output:  The volume of blood passing through the heart per unit
     time.

Cardiovascular:  Relating to the heart and the blood vessels or the
     circulation.

Carotene:   Lipid-soluble yellow-to-orange-red pigments  universally
     present the photosynthetic tissues of higher plants, algae, and the
     photosynthetic bacteria.

Cascade impactor:   A device for measuring the size distribution of particulates
     and/or aerosols, consisting of a series of plates  with orifices of
     graduated size which separate the sample into a number of fractions
     of decreasing aerodynamic diameter.

Catabolism:  Destructive metabolism involving the release of energy and
     resulting in breakdown of complex materials in the organism.

Catalase:   An enzyme (EC 1.11.1.6) catalyzing the decomposition of hydrogen
     peroxide to water and oxygen.

Catalysis:   A modification of the rate of a chemical reaction by some
     material which is unchanged at the end of the reaction.

Catalytic converter:   An air pollution abatement device that removes
     organic contaminants by oxidizing them into carbon dioxide and
     water.

Catecholamine:   A pyrocatechol with an alkalamine side  chain, functioning
     as a hormone or neurotransmitter, such as epinephrine, morepinephrine,
     or dopamine.

Cathepsins:  Enzymes which have the ability to hydrolyze certain proteins
     and peptides; occur in cellular structures known as lysosomes.

Cation:  A positively charged ion.
                                      G-10

-------
Cellular permeability:  Ability of gases to enter and leave cells; a
     sensitive indicator of injury to deep-lung cells.

Cellulose:   The basic substance which is contained in all vegetable
     fibers and in certain man-made fibers.   It is a carbohydrate and
     constitutes the major substance in plant life.   Used to make cellulose
     acetate and rayon.

Cellulose acetate:  Commonly refers to fibers or fabrics in which the
     cellulose is only partially acetylated with acetate groups.   An
     ester made by reacting cellulose with acetic anhydride with SO.
     as a catalyst.

Cellulose rayon:   A regenerated cellulose which is chemically the same
     as cellulose except for physical differences in molecular weight
     and crystallinity.

Cellulose triacetate:   A cellulose fiber which is completely acetylated.
     Fabrics of triacetate have higher heat resistance than acetate and
     may be safely ironed at higher temperature.   Such fabrics have improved
     ease-of-care characteristics because after heat treatment during
     manufacture, a change in the crystalline structure of the fiber
     occurs.

Cellulosics:  Cotton,  viscose rayon and other fibers made of natural fiber
     raw materials.

Celsius scale:   The thermometric scale in which freezing point of water
     is 0 and boiling point is 100.

Central hepatic necrosis:   The pathologic death of one or more cells,
     or of a portion of the liver, involving the cells adjacent to the
     central veins.

Central nervous system (CNS):   The brain and the spinal' cord.

Centroacinar area:  The center portion of a grape-shaped gland.

Cerebellum:   The large posterior brain mass lying above the pons and
     medulla and beneath the posterior portion of the cerebrum.

Cerebral cortex:   The layer of gray matter covering the entire surface
     of the cerebral hemisphere of mammals.

Chain reaction:  A reaction that stimulates its own repetition.

Challenge:   Exposure of a test organism to a virus,  bacteria,  or other
     stress-causing agent, used in conjunction with exposure to a pollutant
     of interest, to explore possible susceptibility brought on by the
     pollutant.
                                      G-ll

-------
Chamber study:  Research conducted using a closed vessel in which pollutants
     are reacted or substances exposed to pollutants.

Chemiluminescence:   A measurement technique in which radiation is pro-
     duced as a result of chemical reaction.

Chemotactic:   Relating to attraction or repulsion of living protoplasm
     by chemical stimuli.

Chlorophyll:   A group of closely related green photosynthetic pigments
     occurring in leaves,  bacteria, and organisms.

Chloroplast:   A plant cell inclusion body containing chlorophyll.

Chlorosis:   Discoloration of normally green plant parts that can be
     caused by disease, lack of nutrients, or various air pollutants,
     resulting in the failure of chlorophyll  to develop.

Cholesterol:   A steroid alcohol CpyH.cOH; the most abundant steroid in
     animal cells and body fluids.

Cholinesterase (CHE):   One (EC 3.1.1.8) of a family of enzymes capable
     of catalyzing the hydrolysis of acylcholines.

Chondrosarcoma:   A malignant neoplasm derived from cartilage cells,
     occurring most frequently near the ends of long bones.

Chromatid:   Each of the two strands formed by longitudinal  duplication
     of a chromosome that becomes visible during an early stage of cell
     division.

Chromophore:   A chemical group that produces color in a molecule by absorbing
     near ultraviolet or visible radiation when bonded to a nonabsorb-
     ing, saturated residue which possesses no unshared, nonbonding valence
     electrons.

Chromosome:  One of the bodies (46 in man) in the cell nucleus that is the
     bearer and carrier of genetic information.

Chronic respiratory disease (CRD):  A persistent or long-lasting intermittent
     disease of the respiratory tract.

Cilia:   Motile,  often hairlike extensions of a cell surface.

Ciliary action:   Movements of cilia in the upper respiratory tract, which
     move mucus and foreign material upward.

Ciliogenesis:   The formation of cilia.
                                      G-12 .

-------
Citric acid (Krebs) cycle:  A major biochemical pathway in cells, in-
     volving terminal oxidation of fatty acids and carbohydrates.  It
     yields a major portion of energy needed for essential body functions
     and is the major source of CO-.  It couples the glycolytic breakdown
     of sugar in the cytoplasm witn those reactions producing ATP in the
     mitochondria.  It also serves to regulate the synthesis of a number
     of compounds required by a cell.

Clara cell:  A nonciliated mammalian cell.

Closing volume (CV):  The lung volume at which the flow from the lower
     parts of the lungs becomes severely reduced or stops during expiration,
     presumably because of airway closure.

Codon:   A sequence of three nucleotides which encodes information re-
     quired to direct the synthesis of one or more amino acids.

Coefficient of haze (COM):  A measurement of visibility interference in the
     atmosphere.

Cohort:   A group of subjects included in a test or experiment; usually
     characterized by age, class or other characteristic.

Collagen:   The major protein of the white fibers of connective tissue,
     cartilage, and bond.   Comprises over half the protein of the mammal.

Collisional deactivation:   Reduction in energy of excited molecules
     caused by collision with other molecules or other objects such
     as the walls of a container.

Colorimetric:   A chemical  analysis method relying on measurement of the
     degree of color produced in a solution by reaction with the pollutant
     of interest.

Community exposure:   A situation in which people in a sizeable area are
     subjected to ambient pollutant concentrations.

Compliance:  A measure of the change in volume of an internal organ (e.g.
     lung,  bladder)  produced by a unit of pressure.

Complement:   Thermolabile substance present in serum that is destructive
     to certain bacteria and other cells which have been sensitized by
     specific complement-fixing antibody.

Compound:   A substance with its own distinct properties, formed by the
     chemical  combination of two or more elements in fixed proportion.

Concanavalin-A:   One of two crystalline globulins occurring in the jack
     bean;  a potent  hemagglutinin.

Conifer:   A plant, generally evergreen,  needle-leafed,  bearing naked seeds
     singly or in cones.
                                      G-13

-------
Converter:  See catalytic converter.

Coordination number:  The number of bonds formed by the central atom in
     a complex.

Copolymer:  The product of the process of polymerization in which two or
     more monomeric substances are mixed prior to polymerization.   Nylon is
     a copolymer.

Coproporphyrin:  One of two porphyrin compounds found normally in feces
     as a decomposition product of bilirubin (a bile pigment).  Porphyrin
     is a widely-distributed pigment consisting of four pyrrole nuclei
     joined in a ring.

Cordage:   A general term which includes banding, cable, cord, rope, string,
     and twine made from fibers.   Synthetic fibers used in making cordage
     include nylon and dacron.

Corrosion:  Destruction or deterioration of a material because of reaction
     with its environment.

Corticosterone:  A steroid obtained from the adrenal cortex.   It induces
     some deposition of glycogen in the liver, sodium conservation, and
     potassium excretion.

Cosmopolitan:   In the biological  sciences, a term denoting worldwide
     distribution.

Coulometric:  Chemical  analysis performed by determining the amount of a
     substance released in electrolysis by measuring the number of
     coulombs used.

Coumarin:  A toxic white crystalline lactone (CgHgO-) found in plants.

Coupler:   A chemical used to combine two others in a reaction, e.g.  to
     produce the azo dye in the Griess-Saltzman method for NOp.

Crevice corrosion:   Localized corrosion occurring within crevices  on metal
     surfaces exposed to corrosives.

Crosslink:  To connect, by an atom or molecule, parallel chains in a complex
     chemical  molecule, such as a polymer.

Cryogenic trap:  A pollutant sampling method in which a gaseous pollutant
     is condensed out of sampled air by cooling (e.g.  traps in one method
     for nitrosamines are maintained below -79 C, using solvents maintained
     at their freezing points).

Cuboidal:  Resembling a cube in shape.

Cultivar:  An organism produced by parents belonging to different  species
     or to different strains of the same species, originating and  persist-
     ing under cultivation.
                                      G-14

-------
Cuticle:  A thin outer layer, such as the thin continuous fatty film
     on the surface of many higher plants.

Cyanosis:  A dark bluish or purplish coloration of the skin and mucous
     membrane due to deficient oxygenation of the blood.

Cyclic GMP:  Guanosine 5'-phosphoric acid.

Cytochrome:  A class of hemoprotein whose principal biological function
     is electron and/or hydrogen transport.

Cytology:  The anatomy, physiology, pathology and chemistry of the cell.

Cytoplasm:  The substance of a cell exclusive of the nucleus.

Dacron:  The trade name for polyester fibers made by E.I. du Pont de Nemours
     and Co., Inc., made from dimethyl terephthalate and ethylene glycol.

Dark adaptation:   The process by which the eye adjusts under reduced
     illumination and the sensitivity of the eye to light is greatly in-
     creased.

Dark respiration:   Metabolic activity of plants at night; consuming oxygen
     to use stored sugars and releasing carbon dioxide.

Deciduous plants:   Plants which drop their leaves at the end of the grow-
     ing season.

Degradation (textiles):  The decomposition of fabric or its components
     or characteristics (color, strength, elasticity) by means of light,
     heat, or air pollution.

Denitrification:   A bacterial process occurring in soils, or water, in
     which nitrate is used as the terminal electron acceptor and is re-
     duced primarily to Np.   It is essentially an anaerobic process; it
     can occur in the presence of low levels of oxygen only if the micro-
     organisms are metabolizing in an anoxic microzone.

De novo:  Over again.

Deoxyribonucleic acid (DNA):   A nucleic acid considered to be the carrier
     of genetic information coded in the sequence of purine and pyrimidine
     bases (organic bases).   It has the form of a double-stranded helix
     of a linear polymer.

Depauperate:   Falling short of natural development or size.

Derivative spectrophotometer:   An instrument with an increased capability
     for detecting overlapping spectral  lines and bands and also for
     suppressing instrumentally scattered light.
                                      G-15

-------
Desorb:   To release a substance which has been taken into another substance
     or held on its surface; the opposite of absorption or adsorption.

Desquamation:   The shedding of the outer layer of any surface.

Detection limit:   A level below which an element or chemical compound
     cannot be reliably detected by the method or measurement being used for
     analysis.

Detritus:   Loose material that results directly from disintegration.

DeVarda alloy:  An alloy of 50 percent Cu, 45 percent Al, 5 percent Zn.

Diastolic blood pressure:  The blood pressure as measured during the period
     of filling the cavities of the heart with blood.

Diazonium salt:  A+chemical compound (usually colored) of the general
     structure ArN?Cl , where Ar refers to an aromatic group.

Diazotizer:   A chemical which, when reacted with amines (RNHL,  for example),
     produces a diazonium salt (usually a colored compound).

Dichotomous sampler:   An air-sampling device which separates particulates
     into two fractions by particle size.

Differentiation:   The process by which a cell, such as a fertilized egg,
     divides into specialized cells, such as the embryonic types that
     eventually develop into an entire organism.

Diffusion:   The process by which molecules or other particles intermingle
     as a result of their random thermal motion.

Diffusing capacity:  Rate at which gases move to or from the blood.

Dimer:   A compound formed by the union of two like radicals or
     molecules.

Dimerize:   Formation of dimers.

1,6-diphosphofructose aldolase:  An enzyme (EC 4.1.1.13) cleaving fructose
     1,6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde-
     3-phosphate.

D-2,3-diphosphoglycerate:  A salt or ester of 2,3-diphosphoglyceric acid,
     a major component of certain mammalian erythrocytes involved in the
     release of CL from HbO?.  Also a postulated intermediate in the bio-
     chemical  patnway involving the conversion of 3- to 2-phosphoglyceric
     acid.

Diplococcus pneumoniae:  A species of spherical-shaped bacteria belonging
     to the genus Streptococcus.  May be a causal agent in pneumonia.
                                      G-16

-------
Direct dye:  A dye with an affinity for most fibers; used mainly when
     color resistance to washing is not important.

Disperse dyes:  Also known as acetate dyes; these dyes were developed
     for use on acetate fabrics, and are now also used on synthetic
     fibers.

Distal:  Far from some reference point such as median line of the body, point
     of attachment or origin.

Diurnal:   Having a repeating pattern or cycle 24 hours long.

DL-Q:  The diffusing capacity of the lungs for carbon monoxide.   The ability
     of the lungs to transfer carbon monoxide from the alveolar air into the
     pulmonary capillary blood.

Dorsal hypnosis:   Abnormal curvative of the spine; hunch-back.

Dose:  The quantity of a substance to be taken all at one time or in
     fractional amounts within a given period; also the total  amount of a
     pollutant delivered or concentration per unit time times  time.
                                                                  o
Dose-response curve:   A curve on a graph based on responses occurring
     in a system as a result of a series of stimuli intensities or doses.

Dry deposition:  The processes by which matter is transferred  to ground
     from the atmosphere,  other than precipitation; includes  surface ab-
     sorption of gases and sedimentation, Brownian diffusion  and impaction
     of particles.

Dyeing:  A process of coloring fibers,  yarns, or fabrics with  either
     natural  or synthetic  dyes.

Dynamic calibration:   Testing of a monitoring system using a  continuous
     sample stream of known concentration.

Dynamic compliance (C,.  ):   Volume change per unit of transpulmonary
     pressure minus tne^pressure of pulmonary resistance during airflow.

Dynel:   A trademark for a  modacrylic staple fiber spun from a  copolymer
     of acrylom'trile and  vinyl  chloride.   It has high strength, quick-
     drying properties, and resistance  to alkalies and acids.

Dyspepsia:   Indigestion,  upset stomach.

Dyspnea:   Shortness of breath; difficulty or distress in breathing;  rapid
     breathing.

Ecosystem:   The interacting system of a biological community  and its
     environment.

Eddy:  A current of water  or air running contrary to the main  current.
                                      G-17

-------
Edema:   Pressure of excess fluid in cells, intercellular tissue or cavities
     of the body.

Elastomer:   A synthetic rubber product which has the physical properties
     of natural rubber.

Electrocardiogram:   The graphic record of the electrical currents that
     initiate the heart's contraction.

Electrode:   One of the two extremities of an electric circuit.

Electrolyte:   A non-metallic electric conductor in which'current is carried
     by the movement of ions; also a substance which displays these qualities
     when dissolved in water or another solvent.

Electronegativity:   Measure of affinity for negative charges or electrons.

Electron microscopy:   A technique which utilizes a focused beam of electrons
     to produce a high-resolution image of minute objects such as particu-
     late matter,  bacteria, viruses, and DMA.

Electronic excitation energy:  Energy associated in the transition of
     electrons from their normal low-energy orbitals or orbitals of higher
     energy.

Electrophilic:  Having an affinity for electrons.

Electrophoresis:  A technique by which compounds can be separated from a
     complex mixture by their attraction to the positive or negative
     pole of an applied electric potential.

Eluant:   A liquid used in the process of elution.

Elute:   To perform an elution.

Elution:   Separation of one material from another by washing or by dissolving
     one in a solvent in which the other is not soluble.

Elutriate:   To separate a coarse, insoluble powder from a finer one by
     suspending them in water and pouring off the finer powder from the
     upper part of the fluid.

Emission spectrometry:   A rapid analytical.technique based on measurement
     of the characteristic radiation emitted by thermally or electrically
     excited atoms or ions.

Emphysema:   An anatomic alteration of the lung, characterized by abnormal
     enlargement of air spaces distal to the terminal bronchioles, due
     to dilation or destructive changes in the alveolar walls.

Emphysematous lesions:   A wound or injury to the lung as a result of
     emphysema.
                                      G-18

-------
Empirical modeling:  Characterization and description of a phenomena
     based on experience or observation.

Encephalitis:  Inflammation of the brain.

Endoplasmic reticulum:  An elaborate membrane structure extending from the
     nuclear membrane or eucaryotic cells to the cytoplasmic membrane.

Endothelium:  A layer of flat cells lining especially blood and lymphatic
     vessels.

Entropy:  A measure of disorder or randomness in a system.   Low entropy
     is associated with highly ordered systems.

Enzyme:  Any of numerous proteins produced by living cells which catalyze
     biological reactions.

Enzyme Commission (EC):   The International Commission on Enzymes,  established
     in 1956, developed a scheme of classification and nomenclature under
     which each enzyme is assigned an EC number which identifies it by
     function.

Eosinophils:  Leukocytes (white blood cells) which stain readily with the
     dye, eosin.

Epidemiology:  A study of the distribution and determinants of disease
     in human population groups.

Epidermis:  The outermost living layer of cells of any organism.

Epididymal fat pads:   The fatty tissue located near the epididymis.   The
     epididymis is the first convoluted portion of the excretory duct
     of the testis.

Epiphyte:   A plant growing on another plant but obtaining food from the
     atmosphere.

Epithelial:   Relating to epithelium,  the membranous cellular layer which
     covers free surfaces or lines tubes or cavities of an animal  body,
     which encloses,  protects,  secretes, excretes and/or assimilates.

Erosion corrosion:   Acceleration or increase in rate of deterioration
     or attack on a metal because of  relative movement between a corrosive
     fluid and the metal  surface.   Characterized by grooves,  gullies,  or
     waves in the metal  surface.

Erythrocyte:   A mature red blood cell.

Escherichia coli:   A short,  gram-negative, rod-shaped bacteria common
     to the human intestinal  tract.   A frequent cause of infections in
     the urogenital  tract.
                                      G-19

-------
Esophageal:   Relating to the portion of the digestive tract between the
     pharynx and the stomach.

Estrus:   That portion or phase of the sexual cycle of female animals
     characterized by willingness to permit coitus.

Estrus cycle:  The series of physiologic uterine, ovarian and other
     changes that occur in higher animals.

Etiolation:   Paleness and/or altered development resulting from the
     absence of light.

Etiology:   The causes of a disease or condition; also, the study of
     causes.

Eucaryotic:   Pertaining to those cells having a well-defined nucleus
     surrounded by a double-layered membrane.

Euthrophication:   Elevation of the level of nutrients in a body of water,
     which can contribute to accelerated plant growth and filling.

Excited state:   A state of higher electronic energy than the ground state,
     usually a less stable one.

Expiratory (maximum) flow rate:   The maximum rate at which air can be
     expelled from the lungs.

Exposure level:   Concentration of a contaminant to which an individual
     or a population is exposed.

Extinction coefficient:  A measure of the space rate of diminution, or
     extinction,  of any transmitted light,  thus, it is the attenuation
     coefficient applied to visible radiation.

Extramedullary hematopoiesis:   The process  of formation and development
     of the various types of blood cells and other formed elements not
     including that occurring in bone marrow.

Extravasate:  To exclude from or pass out of a vessel into the tissues;
     applies to urine,  lymph,  blood and similar fluids.

Far ultraviolet:   Radiation in the range of wavelengths from 100 to 190
     nanometers.

Federal  Reference Method (FRM):   For NOp, the EPA-approved analyzers based
     on the gas-phase chemiluminescent measurement principle and associated
     calibration procedures; regulatory specifications prescribed in Title
     40, Code of Federal Regulations, Part 50,  Appendix F.

Fenestrae:   Anatomical  aperatures often closed by a membrane.

Fiber:   A fine,  threadlike piece, as of cotton, jute, or asbestos.
                                      G-20

-------
Fiber-reactive dye:  A water-soluble dyestuff which reacts chemically
     with the cellulose in fibers under alkaline conditions; the dye
     contains two chlorine atoms which combine with the hydroxyl groups of
     the cellulose.

Fibrin:  A white insoluble elastic filamentous protein derived from fibrino-
     gen by the action of thrombin, especially in the clotting of blood.

Fibroadenoma:  A benign neoplasm derived from glandular epithelium, in-
     volving proliferating fibroblasts, cells found in connective tissue.

Fibroblast:   An elongated cell with cytoplasmic processes present in
     connective tissue, capable of forming collagen fibers.

Fibrosis:  The formation of fibrous tissue, usually as a reparative or
     reactive process and not as a normal constituent of an organ or
     tissue.

Flocculation:  Separation of material from a solution or suspension by
     reaction with a flocculant to create fluffy masses containing the
     material to be removed.

Fly ash:  Fine,  solid particles of noncombustible ash carried out of a
     bed of solid fuel  by a draft.

Folded-path optical system:   A long (e.g.,  8-22 m) chamber with multiple
     mirrors at the ends which can be used to reflect an infrared beam through
     an ambient air sample many times;  a spectrometer can be used with such
     a system to detect trace pollutants at very low levels.

Forced expiratory flow (FEF):   The rate at which air can be expelled from
     the lungs;  see expiratory flow rate.

Forced expiratory volume (FEV):   The maximum volume of air that can be
     expired in a specific time interval when starting from maximal
     inspiration.

Forced vital  capacity (FVC):   The greatest volume of air that can be
     exhaled from the lungs under forced conditions after a maximum
     inspiration.

Fractional  threshold concentration:   The portion of the concentration
     at which an event  or a response begins to occur,  expressed as a
     fraction.

Free radical:   Any of a variety of highly-reactive atoms or molecules
     characterized by having an unpaired electron.

Fritted bubbler:   A porous glass device used in air pollutant sampling
     systems  to  introduce small  bubbles into solution.
                                      G-21

-------
Functional residual capacity:  The volume of gas remaining in the lungs
     at the end of a normal expiration.   It is the sum of expiratory
     reserve volume and residual volume.

Gas exchange:   Movement of oxygen from the alveoli into the pulmonary
     capillary blood as carbon dioxide enters the alveoli from the blood.

Gas chromatography (GC):  A method of separating and analyzing mixtures
     of chemical substances.   A flow of gas causes the components of a
     mixture to migrate differentially from a narrow starting zone in a
     special porous, insoluble sorptive medium.   The pattern formed by
     zones of separated pigments and of colorless substances in this
     process is called a chromatogram, and can be analyzed to obtain the
     concentration of identified pollutants.

Gas-liquid chromatography:  A method of separating and analyzing volatile
     organic compounds, in which a sample is vaporized and swept through
     a column filled with solid support material covered with a nonvolatile
     liquid.  Components of the sample can be identified and their con-
     centrations determined by analysis of the characteristics of their
     retention in the column, since compounds have varying degrees of
     solubility in the liquid medium.

Gastric juice:   A thin watery digestive fluid secreted by glands in the
     mucous membrane of the stomach.

Gastroenteritis:  Inflammation of the mucous membrane of stomach and
     intestine.

Genotype:   The type of genes possessed by an organism.

Geometric mean:  An estimate of the average of a distribution.   Specifically,
     the nth root of the product of n observations.

Geometric standard deviation:  A measure of variability of a distribution.
     It is the antilogarithm of the standard deviation of the logarithms
     of the observations.

Globulins (a,  b, q):  A family of proteins precipitated from plasma (or
     serum) by half-saturation with ammonium sulfate, or separable by
     electrophoresis.  The main groups are the a, b, q fractions, differ-
     ing with respect to associated lipids and carbohydrates and in their
     content of antibodies (immunoglobulins).

Glomular nephrotic syndrome:   Dysfunction of the kidneys characterized
     by excessive protein loss in the urine,  accumulation of body fluids
     and alteration in albumin/globulin ratio.

Glucose:  A sugar which is a principal source of energy for man and other
     organisms.

Glucose-6-phosphate dehydrogenase:  An enzyme (EC 1.1.1.49) catalyzing
     the dehydrogenation of glucose-6-phosphate to 6-phosphogluconolactone.
                                      G-22

-------
Glutamic-oxaloacetic transaminase (SGOT):  An enzyme (EC 2.6.1.1) whose
     serum level increases in myocardial infarction and in diseases in-
     volving destruction of liver cells.  Also known as aspartate
     aminotransferase.

Glutamic-pyruvic transaminase (SGPT):  Now known as alanine aminotransferase
     (EC 2.6.1.2), the serum levels of this enzyme are used in liver function
     tests.

Glutathione (GSH):  A tripeptide composed of glycine, cystine, and glutamic
     acid.

Glutathione peroxidase:   An enzyme (EC 1.11.1) which catalyzes the destruction
     of hydroperoxides formed from fatty acids and other substances.
     Protects tissues from oxidative damage.   It is a selenium-containing
     protein.

Glutathione reductase:   The enzyme (EC 1.6.4.2) which reduces the oxidized
     form of glutathione.

Glycolytic pathway:  The biochemical pathway by which glucose is con-
     verted to lactic acid in various tissues, yielding energy as a
     result.

Glycoside:   A type of chemical compound formed from the condensation of
     a sugar with another chemical radical  via a hemiacetal linkage.

Goblet cells:   Epithelial  cells that have been distended with mucin and when
     this is discharged as mucus, a goblet-shaped shell remains.

Golgi apparatus:   A membrane system involved with secretory functions
     and transport in a cell.   Also known as a dictyosome.

Grana:   The lamellar stacks of chlorophyll-containing material in plant
     chloroplasts.

Griege carpet:   A carpet in its unfinished state, i.e.  before it has
     been scoured and dyed.   The term also is used for woven fabrics
     in the unbleached and unfinished state.

Ground state:   The state of minimum electronic energy of 'a molecule or
     atom.

Guanylate cyclase (GC):   An enzyme (EC 4.6.2.1) catalyzing the trans-
     formation of guanosine triphosphate to guanosine 3':5'-cyclic phosphate.

H-Thymidine:   Thymine deoxyribonucleoside:   One of the four major nucleosides
     in DNA.    H-thymidine has been uniformly labeled with tritium, a radio-
     active form of hydrogen.

Haze:  Fine dust, smoke or fine vapor reducing transparency of air.
                                      G-23

-------
Hemagglutination:   The agglutination of red blood cells.   Can be used as
     as a measurement of antibody concentration.

Heuiatocrit:   The percentage of the volume of a blood sample occupied by
     cells.

Hematology:   The medical specialty that pertains  to the blood and blood-
     forming tissues.

Hemochromatosis:  A disease characterized by pigmentation of the skin
     possibly due to inherited excessive absorption of iron.

Hemoglobin (Hb):  The red, respiratory protein of the red blood cells,
     hemoglobin transports oxygen from the lungs  to the tissues as oxy-
     hemoglobin (HbO-) and returns carbon dioxide to the lungs as hemoglobin
     carbamate, completing the respiratory cycle.

Hemolysis:  Alteration or destruction of red blood cells, causing hemoglobin
     to be released into the medium in which the  cells are suspended.

Hepatectomy:   Complete removal of the liver in an experimental animal.

Hepatic:   Relating to the liver.

Hepatocyte:   A liver cell.

Heterogeneous process:   A chemical reaction involving reactants of more
     than one phase or state, such as one in which gases are absorbed into
     aerosol  droplets, where the reaction takes place.

Heterologous:  A term referring to donor and recipient cellular elements
     from different organisms, such as red blood  cells from sheep and
     alveolar macrophage from rabbits.

Hexose monophosphate shunt:  Also called the phosphogluconate oxidative
     pathway of glucose metabolism which affords  a total  combustion of
     glucose independent of the citric acid cycle.   It is the important
     generator of NADPH necessary for synthesis of fatty acids and the
     operation of various enzymes.  It serves as  a source of ribose and
     4- and 7-carbon sugars.

High-volume sampler (Hi-vol):  Device for taking  a sample of the particulate
     content of a large amount of,air,  by drawing air through a fiber filter
     at a typical  cate of 2,000 m /24 hr (1.38 m  /min), or as high as 2,880
     mV24 hr (2 nT/min).

Histamine:  An amine derived from the amino acid, histidine.  It is a
     powerful stimulant of gastric secretion and  a constrictor of bronchial
     smooth muscle.   It is a vasodilator and causes a fall in blood
     pressure.
                                      G-24

-------
Homogenate:  Commonly refers to tissue ground into a creamy consistency
     in which the cell structure is disintegrated.

Host defense mechanism:   Inherent means by which a biologic organism
     protects itself against infection, such as antibody formation,
     macrophage action,  ciliary action, etc.

Host resistance:  The resistance exhibited by an organism, such as man,
     to an infecting agent, such as a virus or bacteria.

Humoral:  Relating to the extracellular fluids of the body, blood and
     lymph.

Hybrid:  An organism descended from parents belonging to different
     varieties or species.

Hydrocarbons:   A vast family of compounds containing carbon and hydrogen
     in various combinations; found especially in fossil fuels.  Some
     contribute to photochemical smog.

Hydrolysis:  Decomposition involving splitting of a bond and addition
     of the H and OH parts of water to the two sides of the split bond.

Hydrometeor:   A product of the condensation of atmospheric water vapor (e.g.
     fog,  rain, hail,  snow).

Hydroxyproline:   An amino acid found among the hydrolysis products of
     collagen.

Hygroscopic:   Pertaining to a marked ability to accelerate the condensation
     of water vapor.

Hyperplasia:   Increase in the number of cells in a tissue or organ ex-
     cluding tumor formation.

Hyperplastic:   Relating to hyperplasia; an increase in the number of
     cells.

Hypertrophy:   Increase in the size of a tissue element, excluding tumor
     formation.

Hypertension:   Abnormally elevated blood pressure.

Hypolimnia:  Portions  of a lake below the thermocline, in which water
     is stagnant and uniform in temperature.

Hypoxia:  A lower than normal  amount of oxygen in the air, blood or tissues.
                                      G-25

-------
Immunoglobulin (Ig):   A class of structurally related proteins consist-
     ing of two pairs of polypeptide chains.   Antibodies are Ig's and
     all Ig's probably function as antibodies.

Immunoglobulin A (IgA):  A type of antibody which comprises approximately
     10 to 15 percent of the total amount of antibodies present in normal
     serum.

Immunoglobulin G (IgG):  A type of antibody which comprises approximately
     80 percent of the total amount of antibodies present in normal serum.
     Subfractions of IgG are fractions G-,, and G~.

Immunoglobulin M (IgM):  A type of antibody which comprises approximately
     5 to 10 percent of the total amount of antibodies present in normal
     serum.

Impact!on:   An impinging or striking of one object against another; also,
     the force transmitted by this act.

Impactor:   An instrument which collects samples of suspended particulates
     by directing a stream of the suspension against a surface, or into a
     liquid or a void.

Index of proliferation:  Ratio of promonocytes to polymorphic monocytes
     in the blood.

Infarction:  Sudden insufficiency of arterial or venous blood supply
     due to emboli, thrombi, or pressure.

Infectivity model:   A testing system in which the susceptibility of
     animals to airborne infectious agents with and without exposure to air
     pollutants is investigated to produce information related to the
     possible effects of the pollutant on man.

Inflorescence:   The arrangement and development of flowers on an axis;
     also,  a flower cluster or a single flower.

Influenza A^/Taiwan Virus:   An infectious viral  disease, believed to
     have originated in Taiwan, characterized by sudden onset, chills,
     fevers, headache,  and cough.

Infrared:   Light invisible to the human eye,  bgtween the wavelengths
     of 7x10"' and lO'^m (7000 and 10,000,000 A).

Infrared laser:   A device that utilizes the natural oscillations of atoms
     or molecules to generate coherent electromagnetic radiation in the
     infrared region of the spectrum.

Infrared spectrometer:   An instrument for measuring the relative amounts
     of radiant energy in the infrared region of the spectrum as a function
     of wavelength.
                                      G-26

-------
Ingestion:  To take in for digestion.

In situ:  In the natural or original position.

Instrumental averaging time:   The time over which a single sample or
     measurement is taken, resulting in a measurement which is an average
     of the actual concentrations over that period.

Insult:  An injury or trauma.

Intercostal:  Between the ribs, especially of a leaf.

Interferant:  A substance which a measurement method cannot distinguish
     completely from the one being measured, which therefore can cause some
     degree of false response or error.

Interferon:   A macromolecular substance produced in response to infection
     with active or inactivated virus, capable of inducing a state of
     resistance.

Intergranular corrosion:  A type of corrosion which takes place at and
     adjacent to grain boundaries, with relatively little corrosion of
     the grains.

Interstitial edema:   An accumulation of an excessive amount of fluids
     in a space within tissues.

Interstitial pneumonia:   A chronic inflammation of the interstitial tissue
     of the lung,  resulting in compression of air cells.

Intraluminal mucus:   Mucus that collects within any tubule.

Intraperitoneal injection:   An injection of material into the serous
     sac that lines the abdominal cavity.

In utero:   Within  the womb; not yet born.

In vitro:   Refers  to experiments conducted outside the living organism.

In vivo:  Refers  to experiments conducted within the living organism.

Irradiation:  Exposure to any form of radiation.

Ischemia:   Local  anemia due to mechanical  obstruction (mainly arterial
     narrowing) of the blood supply.

Isoenzymes:   Also  called isozymes.   One of a group of enzymes that are
     very similar  in catalytic properties, but may be differentiated by
     variations in physical properties, such as isoelectric point or
     electrophoretic mobility.   Lactic acid dehydrogenase is an example
     of an enzyme  having many isomeric forms.
                                      G-27

-------
Isopleth:   A line on a map or chart connecting points of equal value.

Jacobs-Hochheiser method:   The original Federal Reference Method for N02,
     currently unacceptable for air pollution work.

Klebsiella pneumoniae:   A species of rod-shaped bacteria found in soil,
     water, and in the intestinal tract of man and other animals.  Certain
     types may be causative agents in pneumonia.

Kyphosis:   An abnormal  curvature of the spine, with convexity backward.

Lactate:   A salt or ester of lactic acid.

Lactic acid (lactate) dehydrogenase (LDH):   An enzyme (EC 1.1.1.27) with
     many isomeric forms which catalyzes the oxidation of lactate to
     pyruvate via transfer of H to NAD.  Isomeric forms of LDH in the
     blood are indicators of heart damage.

Lamellar bodies:   Arranged in plates or scales.  One of the characteristics
     of Type II alveolar cells.

Lavage fluid:  Any fluid used to wash out hollow organs, such as the lung.

Lecithin:   Any of several  waxy hygroscopic phosphatides that are widely
     distributed in animals and plants; they form colloidal solutions in
     water and have emulsifying, wetting and hygroscopic properties.

Legume:  A plant with root nodules containing nitrogen fixing bacteria.

Lesion:  A wound, injury or other more or less circumscribed pathologic
     change in the tissues.

Leukocyte:  Any of the white blood cells.

Lewis base:  A base, defined in the Lewis acid-base concept, is a sub-
     stance that can donate an electron pair.

Lichens:   Perennial plants which are a combination of two plants, an alga
     and a fungus, growing together in an association so intimate that they
     appear as one.

Ligand:  Those molecules or anions attached to the central atom in a
     complex.

Light-fastness:  The ability of a dye to maintain its original color under
     natural or indoor light.

Linolenic acid:  An unsaturated fatty acid essential in nutrition.

Lipase:  An enzyme that accelerates the hydrolysis or synthesis of fats
     or the breakdown of lipoproteins.
                                      G-28

-------
 Lipids:  A heterogeneous group of substances which occur widely in bio-
      logical materials.  They are characterized as a group by their
      extractability in nonpolar organic solvents.

 Lipofuscin:  Brown pigment granules representing lipid-containing residues
      of lysosomal digestion.  Proposed to be an end product of lipid
      oxidation which accumulates in tissue.

 Lipoprotein:  Complex or protein containing lipid and protein.

 Loading rate:  The amount of a nutrient available to a unit area of body
      of water over a given period of time.

 Locomotor activity.  Movement of an organism from one place to another
      of its own volition.

 Long-pathlength infrared absorption:  A measurement technique in which a
      system of mirrors in a chamber is used to direct an infrared beam
      through a sample of air for a long distance (up to 2 km); the amount
      of infrared absorbed is measured to obtain the concentrations of
      pollutants present.

 Lung  compliance (C.):   The volume change produced by an increase in a
      unit change in pressure across the lung, i.e., between the pleural
      surface and the mouth.

 Lycra:  A spandex textile fiber created by E.  I.  du Pont de Nemours & Co.,
      Inc., with excellent tensile strength, a long flex life and high
      resistance to abrasion and heat degradation.   Used in brassieres,
      foundation garments, surgical  hosiery, swim suits and military and
      industrial uses.

 Lymphocytes:   White blood cells formed in lymphoid tissue throughout the
      body, they comprise about 22 to 28 percent of the total number of
      leukocytes in the circulating blood and function in immunity.

 Lymphocytogram:   The ratio,  in the blood,  of lymphocyte with narrow
     cytoplasm to those with broad cytoplasm.

 Lysosomes:   Organelles found in cells of higher organisms that contain
     high concentrations of degradative enzymes and are known to destroy
      foreign substances that cells engulf by pinocytosis and phyocytosis.
     Believed to be a major site where proteins are broken down.

 Lysozymes:   Lytic enzymes destructive to cell  walls of certain bacteria.
     Present in some body fluids,  including tears  and serum.

Macaca speciosa:   A species  of monkeys used in research.

Macrophage:   Any large, ameboid,  phagocytic cell  having a nucleus  without
     many lobes,  regardless  of origin.
                                      G-29

-------
Malaise:  A feeling of general discomfort or uneasiness, often the first
     indication of an infection or disease.

Mai ate dehydrogenase:  An enzyme (EC 1.1.1.37) with at least six isomeric
     forms that catalyze the dehydrogenation of malate to oxaloacetate
     or its decarboxylation (removal of a COj group) to pyruvate.   Malate,
     oxaloacetate, and pyruvate are intermediate components of biochemical
     pathways.

Mannitol:   An alcohol derived from reduction of the sugar, fructose.
     Used in renal function testing to measure glomerular (capillary)
     filtration.

Manometer:  An instrument for the measurement of pressure of gases or
     vapors.

Mass median diameter (MMD):   Geometric median size of a distribution of
     particles based on weight.

Mass spectrometry (MS):   A procedure for identifying the various kinds of
     particles present in a given substance, by ionizing the particles
     and subjecting a beam of the ionized particles to an electric or
     magnetic field such that the field deflects the particles in angles
     directly proportional to the masses of the particles.

Maximum flow (V   ):   Maximum rate or expiration, usually expressed at
     50 or 25 percent of vital capacity.

Maximum mid-expiratory flow rate (MMFR):  The mean rate of expiratory gas
     flow between 25 and 75 percent of the forced expiratory vital capacity.

Mean (arithmetic):  The sum of observations divided by sample size.

Median:  A value in a collection of data values which is exceeded in
     magnitude by one-half the entries in the collection.

Mesoscale:  Of or relating to meteorological phenomena from 1 to 100
     kilometers in horizontal extent.

Messenger RNA:   A type of RNA which conveys genetic information encoded
     in the DNA to direct protein synthesis.

Metaplasia:   The abnormal transformation of an adult, fully differentiated
     tissue of one kind into a differentiated tissue of another kind.

Metaproterenol:   A bronchodilator used for the treatment of bronchial
     asthma.

Metastases:   The shifting of a disease from one part of the body to another;
     the appearance of neoplasms in parts of the body remote from the seat
     of the primary tumor.
                                      G-30

-------
Meteorology:  The science that deals with the atmosphere and its phenomena.

Methemoglobin:  A+form of hemoglobin in whiclj! the normal reduced state
     of iron  (Fe  ) has been oxidized to Fe  .   It contains oxygen in
     firm union with ferric (Fe  ) iron and is not capable of exchanging
     oxygen in normal respiratory processes.

Methimazole:  An anti-thyroid drug similar in action to propylthiouracil.

Methyltransferase:  Any enzyme transferring methyl groups from one compound
     to another.

Microcoulometric:  Capable of measuring millionths of coulombs used in
     electrolysis of a substance, to determine the amount of a substance
     in a sample.

Microflora:   A small or strictly localized plant.

Micron:  One-millionth of a meter.

Microphage:   A small phagocyte; a polymorphonuclear leukocyte that is
     phagocytic.

Millimolar:   One-thousandth of a molar solution.   A solution of one-
     thousandth of a mole (in grams) per liter.

Minute volume:  The minute volume of breathing;  a product of tidal  volume
     times the respiratory frequency in one minute.

Mitochondria:   Organelles of the cell cytoplasm which contain enzymes
     active in the conservation of energy obtained in the aerobic part
     of the breakdown of carbohydrates and fats,  in a process called
     respiration.

Mobile sources:   Automobiles,  trucks and other pollution sources which are
     not fixed in one location.

Modacrylic fiber:  A manufactured fiber in which the fiber-forming  sub-
     stance is any long chain synthetic polymer composed of less than 85
     percent but at least 35 percent by weight  of acrylonitrite units.

Moeity:  One of two or more parts into which something is divided.

Mole:   The mass, in grams, numerically equal to the molecular weight of
     a substance.

Molecular correlation spectrometry:   A spectrophotometric technique which
     is used to identify unknown absorbing materials and measure their
     concentrations by using preset wavelengths.

Molecular weight:  The weight of one molecule of a substance obtained
     by adding the gram-atomic weights of each  of the individual atoms
     in the  substance.
                                      G-31

-------
Monocyte:  A relatively large mononuclear leukocyte, normally constituting
     3 to 7 percent of the leukocytes of the circulating blood.

Mordant:   A substance which acts to bind dyes to a textile fiber of fabric.

Morphological:   Relating to the form and structure of an organism or any
     of its parts.

Moving average:  A procedure involving taking averages over a specific
     period prior to and including a year in question, so that successive
     averaging periods overlap; e.g.  a three-year moving average would
     include data from 1967 through 1969 for the 1969 average and from
     1968 through 1970 for 1970.

Mucociliary clearance:  Removal of materials from the upper respiratory
     tract via ciliary action.

Mucociliary transport:  The process by which mucus is transported, by
     ciliary action, from the lungs.

Mucosa:  The mucous membrane; it consists of epithelium, lamina  propria
     and, in the digestive tract, a layer of smooth muscle.

Mucous membrane:   A membrane secreting mucus which lines passages and
     cavities communicating with the exterior of the body.

Murine:  Relating to mice.

Mutagen:   A substance capable of causing, within an organism, biological
     changes that affect potential  offspring through genetic mutation.

Mutagenic:   Having the power to cause mutations.  A mutation is  a change
     in the character of a gene (a sequence of base pairs in DNA) that
     is perpetuated in subsequent divisions of the cell  in which it occurs.

Myocardial  infarction:  Infarction of any area of the heart muscle usually
     as a result of occlusion of a coronary artery.

Nares:   The nostrils.

Nasopharyngeal:   Relating to the nasal cavity and the pharynx (throat).

National  Air Surveillance Network (NASN):  Network of monitoring stations
     for sampling air to determine extent of air pollution;  established
     jointly by federal and state governments.

Near ultraviolet:   Radiation of the wavelengths 2000-4000 Angstroms.

Necrosis:  Death of cells that can discolor areas of a plant or  kill
     the entire plant.

Necrotic:  Pertaining to the pathologic death of one or more cells, or
     of a portion of tissue or organ, resulting from irreversible damage.
                                      G-32

-------
Neonate:  A newborn.

Neoplasm:  An abnormal tissue that grows more rapidly than normal; synonymous
     with tumor.

Neoplasia:  The pathologic process that results in the formation and
     growth of a tumor.

Neutrophil:   A mature white blood cell formed in bone marrow and released
     into the circulating blood, where it normally accounts for 54 to 65
     percent of the total number of leukocytes.

Ninhydrin:  An organic reagent used to identify amino acids.

Nitramine:  A compound consisting of a nitrogen attached to the nitrogen
     of amine.

Nitrate:  A salt or ester of nitric acid (NO/).

Nitrification:   The principal natural source of nitrate in which ammonium
     (NhL-t-)  ions are oxidized to nitrites by specialized microorganisms.
     Other organisms oxidize nitrites to nitrates.

Nitrite:  A  salt or ester of nitrous acid (N0~~).

Nitrocellulose:   Any of several  esters of nitric acid formed by its action
     on cellulose, used in explosives, plastics, varnishes and rayon;
     also called cellulose nitrate.

Nitrogen cycle:   Refers to the complex pathways by which nitrogen-containing
     compounds are moved from the atmosphere into organic life, into the
     soil, and back to the atmosphere.

Nitrogen fixation:   The metabolic assimilation of atmospheric nitrogen by
     soil microorganisms, which  becomes available for plant use when the
     microorganisms die;  also, industrial conversion of free nitrogen into
     combined forms used in production of fertilizers and other products.

Nitrogen oxide:   A compound composed of only nitrogen and oxygen.   Components
     of photochemical  smog.

Nitrosamine:   A compound consisting of a nitrosyl  group connected to the
     nitrogen of an amine.

Nitrosation:   Addition of a nitrosyl  group.

N-Nitroso compounds:   Compounds  carrying the functional  nitrosyl group.

Nitrosyl: A group composed of one oxygen and one nitrogen atom (-N=0).

Nitrosylhemoglobin (NOHb):   The  red,  respiratory protein of erythrocytes
     to which a nitrosyl  group is attached.
                                      G-33

-------
N/P Ratio:  Ratio of nitrogen to phosphorous dissolved in lake water,
     important due to its effect on plant growth.

Nucleolus:  A small spherical mass of material within the substance of the
     nucleus of a cell.

Nucleophilic:   Having an affinity for atomic nuclei; electron-donating.

Nucleoside:  A compound that consists of a purine or pyrimidine base com-
     bined with deoxyribose or ribose and found in RNA and DNA.

5'-Nucleotidase:   An enzyme (EC 3.1.3.5) which hydrolyzes nucleoside 5'-
     phosphates into phosphoric acid (HjPO,) and nucleosides.

Nucleotide:  A compound consisting of a sugar (ribose or deoxyribose),
     a base (a purine or a pyrimidine), and a phosphate; a basic structural
     unit of RNA and DNA.

Nylon:   A generic name chosen by E.  I.  du Pont de Nemours & Co., Inc.
     for a group of protein-like chemical products classed as  synthetic
     linear polymers; two main types are Nylon 6 and Nylon 66.

Occlusion:  A point which an opening is closed or obstructed.

Olefin:   An open-chain hydrocarbon having at least one double  bond.

Olfactory:  Relating to the sense of smell.

Olfactory epithelium:  The inner lining of the nose and mouth  which contains
     neural tissue sensitive to smell.

Oligotrophic:   A body of water deficient in plant nutrients; also generally
     having abundant dissolved oxygen and no marked stratification.

Oribitals:  Areas of high electron density in an atom or molecule.

Orion:   An acrylic fiber produced by E. I.  du Pont de Nemours  and Co., Inc.,
     based on a polymer of acrylonitrite;. used extensively for outdoor
     uses, it is resistant to chemicals and withstands high temperatures.

Osteogenic osteosarcoma:   The most common and malignant of bone sarcomas
     (tumors).  It arises from bone-forming cells dfid affects  chiefly
     the ends of long-bones.

Ovarian primordial follicle:  A spheroidal  cell aggregation in the ovary
     in which the primordial oocyte (immature female sex cell) is surrounded
     by a single layer of flattened follicular cells.

Oxidant:  A chemical compound which has the ability to remove  electrons
     from another chemical species,  thereby oxidizing it; also, a substance
     containing oxygen which reacts in air to produce a new substance, or
     one formed by the action of sunlight on oxides of nitrogen and hydro-
     carbons.
                                      G-34

-------
Oxidation:  An ion or molecule undergoes oxidation by donating electrons.

Oxidative deamination:  Removal of the NH~ group from an ami no compound
     by reaction with oxygen.

Oxidative phosphorylation:  The mitochondrial process by which "high-
     energy" phosphate bonds form from the energy released as a result of
     the oxidation of various substrates.  Principally occurs in the tri-
     carboxylic acid pathway.

Oxyhemoglobin:  Hemoglobin in combination with oxygen.  It is the form
     of hemoglobin present in arterial blood.

Ozone layer:  A layer of the stratosphere from 20 to 50 km above the
     earth's surface characterized by high ozone content produced by ultra-
     violet radiation.

Ozone scavenging:   Removal of 0, from ambient air or plumes by reaction with
     NO, producing NO- and 0^-

Paired electrons:   Electrons having opposite intrinsic spins about their
     own axes.

Parenchyma:   The essential and distinctive tissue of an organ or an ab-
     normal  growth, as distinguished from its supportive framework.

Parenchymal:  Referring to the distinguishing or specific cells of a
     gland or organ.

Partial  pressure:   The pressure exerted by a single component in a mixture
     of gases.

Particulates:   Fine liquid or solid particles such as dust, smoke, mist,
     fumes or smog, found in the air or in emissions.

Pascal:   A unit of pressure in the International System of Units.   One
     pascal  is equal  to 7.4 x 10   torr.   The pascal is equivalent to one
     newton  per square meter.

Pathogen:   Any virus, microorganism,  or other substance causing disease.

Pathophysiological:  Derangement of function seen in disease; alteration
     in  function as distinguished from structural defects.

Peptide  bond:   The bond formed when two amino acids react with each other.

Percentiles:   The  percentage of all  observations exceeding or preceding
     some point;  thus, 90th percentile is a level below which will fall 90
     percent of the observations.

Perfusate:   A liquid, solution or colloidal  suspension that has been passed
     over a  special surface or through an appropriate structure.
                                      G-35

-------
Perfusion:   Artificial passage of fluid through blood vessels.

Permanent-press fabrics:   Fabrics in which applied resins contribute to the
     easy care and appearance of the fabric and to the crease and seam
     flat-
     ness by reacting with the cellulose on pressing after garment
     manufacture.

Permeation  tube:   A tube which is selectively porous to specific gases.

Peroxidation:   Refers to the process by which certain organic compounds
     are converted to peroxides.

Peroxyacetyl nitrate (PAN):   Pollutant created by action of sunlight on
     hydrocarbons and NO  in the air; an ingredient of photochemical smog.
                        /s.

pH:   A measure of the acidity or alkalinity of a material, liquid, or solid.
     pH is  represented on a scale of 0 to 14 with 7 being a neutral  state,
     0 most acid, and 14 most alkaline.

Phagocytosis:   Ingestion, by cells such as macrophages, of other cells,
     bacteria, foreign particles, etc.; the cell membrane engulfs solid or
     liquid particles which are drawn into the cytoplasm and digested.

Phenotype:   The observable characteristics of an organism, resulting from
     the interaction between an individual genetic structure and the
     environment in which development takes place.

Phenylthiourea:  A crystalline compound, C^HgN^S, that is bitter or tasteless
     depending on a single dominant gene in the tester.

Phlegm:   Viscid mucus secreted in abnormal quantity in the respiratory passages.

Phosphatase:  Any of a group of enzymes that liberate inorganic phosphate
     from phosphoric esters (B.C. sub-subclass 3.1.3).

Phosphocreatine kinase:   An enzyme (EC 2.7.3.2) catalyzing the formation of
     creatine  and ATP, its breakdown is a source of energy in the contraction
     of muscle; also called creatine phosphate.

Phospholipid:   A molecule consisting of lipid and phosphoric acid group(s).
     An example is lecithin.   Serves as an important structural factor
     in biological membranes.

Photochemical  oxidants:   Primary ozone, NO,,, PAN with lesser amounts of
     other  compounds formed as products of atmospheric reactions involving
     organic pollutants,  nitrogen oxides, oxygen, and sunlight.

Photochemical  smog:  Air pollution caused by chemical reaction of various
     airborne  chemicals in sunlight.

Photodissociation:  The process by which a chemical compound breaks  down into
     simpler components under the influence of sunlight or other radiant energy.
                                      G-36

-------
Photolysis:  Decomposition upon irradiation by sunlight.

Photomultiplier tube:  An electron multiplier in which electrons released
     by photoelectric emission are multiplied in successive stages by
     dynodes that produce secondary emissions.

Photon:  A quantum of electromagnetic energy.

Photostationary:  A substance or reaction which reaches and maintains a
     steady state in the presence of light.

Photosynthesis:  The process in which green parts of plants, when exposed to
     light under suitable conditions of temperature and water supply, produce
     carbohydrates using atmospheric carbon dioxide and releasing oxygen.

Phytotoxic:  Poisonous to plants.

Phytoplankton:   Minute aquatic plant life.

Pi (Fl) bonds:   Bonds in which electron density is not symmetrical about a
     line joining the bonded atoms.

Pinocytotic:   Refers to the cellular process (pinocytosis) in which the cyto-
     plasmic membrane forms invaginations in the form of narrow channels
     leading into the cell.   Liquids can flow into these channels and the
     membrane pinches off pockets that are incorporated into the cytoplasm
     and digested.

Pitting:   A form of extremely localized corrosion that results in holes in
     the metal.  One of the most destructive forms of corrosion.

Pituary:   A stalk-like gland near the base of the brain which is attached
     to the hypothalmus.   The anterior portion is a major repository for
     for hormones that control  growth,  stimulate other glands, and regulate
     the reproductive cycle.

Placenta:   The  organ in the uterus that provides metabolic interchange between
     the fetus  and mother.

Plasmid:   Replicating unit,  other than a nucleus gene, that contains
     nucleoprotein and is involved in various  aspects of metabolism in
     organisms; also called paragenes.

Plasmolysis:   The dissolution of cellular components, or the shrinking
     of plant cells by osmotic  loss  of cytoplasmic water.

Plastic:   A plastic is one of a large group of organic compounds synthesized
     from cellulose,  hydrocarbons,  proteins or resins and capable of being
     cast,  extruded,  or molded  into  various shapes.

Plasticizer:   A chemical  added  to  plastics to  soften, increase malleability
     or to make more readily deformable.
                                      G-37

-------
Platelet (blood):   An irregularly-shaped disk with no definite nucleus;
     about one-third to one-half the size of an erythrocyte and containing
     no hemoglobin.   Platelets are more numerous than leukocytes, numbering
     from 200,000 to 300,000 per cu.  mm.  of blood.

Plethysmograph:   A device for measuring and recording changes in volume of
     a part, organ or the whole body; a body plethysmograph is a chamber
     apparatus surrounding the entire body.

Pleura:  The serous membrane enveloping the lungs and lining the walls of
     the chest cavity.

Plume:  Emission from a flue or chimney,  usually distributed stream-like
     downwind of the source, which can be distinguished from the surrounding
     air by appearance or chemical characteristics.

Pneumonia (interstitial):  A chronic inflammation of the interstitial  tissue
     of the lung,  resulting in compression of the air cells.   An acute, infec-
     tious disease.

Pneumonocytes:  A nonspecific term sometimes used in referring to types of
     cells characteristic of the respiratory part of the lung.

Podzol:  Any of a group of zonal soils that develop in a moist climate,
     especially under coniferous or mixed forest.

Point source:   A single stationary location of pollutant discharge.

Polarography:   A method of quantitative or qualitative analysis based  on
     current-voltage curves obtained by electrolysis of a solution with
     steadily increasing voltage.

Pollution gradient:   A series of exposure situations in which pollutant con-
     centrations range from high to low.

Polyacrylonitrile:   A polymer made by reacting ethylene oxide and hydrocyanic
     acid.   Dynel  and Orion are examples.

Polyamides:   Polymerization products of chemical compounds which contain
     ami no (-NH2)  and carboxyl (-COOH) groups.   Condensation reactions
     between the groups form amides (-CONH?).   Nylon is an example of
     a polyamide.

Polycarbonate:  Any of various tough transparent thermoplastics characterized
     by high impact strength and high softening temperature.

Polycythemia:   An increase above the normal in the number of red cells in the
     blood.

Polyester fiber:  A man-made or manufactured fiber in which the fiber-
     forming substance is any long-chain synthetic polymer composed of
     at least 85 percent by weight of an ester of a dihydric alcohol and
     terephthalic acid.  Dacron is an example.
                                      G-38

-------
Polymer:  A large molecule produced by linking together many like molecules.

Polymerization:  In fiber manufacture, converting a chemical monomer (simple
     molecule) into a fiber-forming material by joining many like molecules
     into a stable, long-chain structure.

Polymorphic monocyte:   Type of leukocyte with a multi-lobed nucleus.

Polymorphonuclear leukocytes:  Cells which represent a secondary non-
     specific cellular defense mechanism.  They are transported to the lungs
     from the bloodstream when the burden handled by the alveolar macrophages
     is too large.

Polysaccharides:   Polymers made up of sugars.  An example is glycogen which
     consists of repeating units of glucose.

Polystyrene:   A thermoplastic plastic which may be transparent, opaque,
     or translucent.   It is light in weight, tasteless and odorless, it
     also is resistant to ordinary chemicals.

Polyurethane:   Any of various polymers that contain NHCOO linkages and are
     used especially in flexible and rigid foams, elastomers and resins.

Pores of Kohn:   Also known as interalveolar pores; pores between air cells.
     Assumed to be pathways for collateral ventilation.

Precipitation:   Any of the various forms of water particles that fall from
     the atmosphere to the ground, rain, snow, etc.

Precursor:   A substance from which another substance is  formed; specifically,
     one of the anthropogenic or natural emissions or atmospheric constituents
     which reacts under sunlight to form secondary pollutants comprising
     photochemical  smog.

Probe:   In air pollution sampling, the tube or other conduit extending
     into the atmosphere to be sampled,  through which the sample passes
     to treatment,  storage and/or analytical equipment.

Proline:  An amino acid,  CrHgNCL, that can be synthesized from glutamate
     by animals.

Promonocyte:   An immature monocyte not normally seen in  the circulating
     blood.

Proteinuria:   The presence of more than  0.3 gm of urinary protein in a
     24-hour urine collection.

Pulmonary:   Relating to the lungs.

Pulmonary edema:   An accumulation of excessive amounts of fluid in the lungs.
                                      G-39

-------
Pulmonary lumen:   The spaces in the interior of the tubular elements of
     the lung (bronchioles and alveolar ducts).

Pulmonary resistance:   Sum of airway resistance and viscous tissue resistance.

Purine bases:  Organic bases which are constituents of DMA and RNA, including
     adenine and guanine.

Purulent:  Containing or forming pus.

Pyrimidine bases:   Organic bases found in DNA and RNA.   Cytosine and
     thymine occur in DNA and cytosine and uracil are found in RNA.

QRS:   Graphical representation on the electrocardiogram of a complex of three
     distinct waves which represent the beginning of ventricular contraction.

Quasistatic compliance:   Time dependent component of elasticity; compliance
is the reciprocal  of elasticity.

Rainout:  Removal  of particles and/or gases from the atmosphere by their
     involvement in cloud formation (particles act as condensation nuclei,
     gases are absorbed by cloud droplets), with subsequent precipitation.

Rayleigh scattering:   Coherent scattering in which the intensity of the
     light of wavelength A., scattered in any direction making an angle
     with the incident direction, is.directly proportional to 1 + cos 9
     and inversely proportional to A. .

Reactive dyes:  Dyes which react chemically with cellulose in fibers under
     alkaline conditions.   Also called fiber reactive or chemically
     reactive dyes.

Reduction:  Acceptance of electrons by an ion or molecule.

Reference method (RM):   For N02> an EPA-approved gas-phase chemiluminescent
     analyzer and associated calibration techniques; regulatory specifications
     are described in Title 40, Code of Federal Regulations, Part 50,
     Appendix F.   Formerly, Federal Reference Method.

Residual capacity:   The volume of air remaining in the lungs after a maximum
     expiratory effort;  same as residual volume.

Residual volume (RV):   The volume of air remaining in the lungs after a
     maximal expiration.   RV = TLC - VC

Resin:   Any of various solid or semi-solid amorphous natural organic sub-
     stances, usually derived from plant secretions, which are soluble in
     organic solvents but not in water; also any of many synthetic substances
     with similar properties used in finishing fabrics, for permanent press
     shrinkage control  or water repel!ency.

Ribosomal RNA:  The most abundant RNA in a cell and an integral constituent
     of ribosomes.
                                      G-40

-------
Ribosomes:  Discrete units of RNA and protein which are instrumental in the
     synthesis of proteins in a cell.  Aggregates are called polysomes.

Runoff:  Water from precipitation, irrigation or other sources that flows
     over the ground surface to streams.

Sclerosis:  Pathological hardening of tissue, especially from overgrowth
     of fibrous tissue or increase in interstitial tissue.

Selective leaching:   The removal of one element from a solid alloy by
     corrosion processes.

Septa:   A thin wall  dividing two cavities or masses of softer tissue.

Seromucoid:   Pertaining to a mixture of watery and mucinous material such
     as that of certain glands.

Serum antiprotease:   A substance, present in serum, that inhibits the activity
     of proteinases  (enzymes which destroy proteins).

Sigma (s) bonds:   Bonds in which electron density is symmetrical about a
     line joining the bonded atoms.

Silo-filler's disease:   Pulmonary lesion produced by oxides of nitrogen
     produced by fresh silage.

Single breath nitrogen elimination rate:   Percentage rise in nitrogen fraction
     per unit of volume expired.

Single breath nitrogen technique:   A procedure in which a vital  capacity
     inspiration.of  100 percent oxygen is followed by examination of nitrogen
     in the vital capacity expirate.

Singlet state:   The  highly-reactive energy state of an atom in which certain
     electrons have  unpaired spins.

Sink:   A reactant with or absorber of a substance.

Sodium arsenite:   Na-jAsO.,,  used with sodium hydroxide in the absorbing solu-
     tion of a 24-hour integrated manual  method for N02-

Sodium dithionite:   A strong reducing agent (a supplier of electrons).

Sodium metabisulfite:   Na9S?Or,  used in absorbing solutions of NO-, analysis
     methods.             6 * D                                   *

Sorb:   To take up and hold by absorption  or adsorption.
                                      G-41

-------
Sorbent:  A substance that takes up and holds another by absorption or
     adsorption.

Sorbitol dehydrogenase:   An enzyme that interconverts the sugars, sorbitol
     and fructose.

Sorption:   The process of being sorbed.

Spandex:  A manufactured fiber in which the fiber forming substance is a
     long chain synthetic elastomer composed of at least 85 percent of a
     segmented polyurethane.

Spectrometer:   An instrument used to measure radiation spectra or to deter-
     mine wavelengths of the various radiations.

Spectrophotometry:   A technique in which visible, UV, or infrared radiation
     is passed through a substance or solution and the intensity of light
     transmitted at various wavelengths is measured to determine the spectrum
     of light absorbed.

Spectroscopy:   Use of the spectrometer to determine concentrations of an
     air pollutant.

Spermatocytes:  A cell destined to give rise to spermatozoa (sperm).

Sphingomyelins:   A group of phospholipids found in brain, spinal cord, kidney
     and egg yolk.

Sphygomenometer:  An apparatus, consisting of a cuff and a pressure gauge,
     which is used to measure blood pressure.

Spirometry:   Also called pneometry.   Testing the air capacity of the lungs
     with a pneometer.

Spleen:  A large vascular organ located on the upper left side of the abdominal
     cavity.   It is a blood-forming organ in early life.   It is a storage
     organ for red corpuscles and because of the large number of macrophages,
     acts as a blood filter.

Sputum:  Expectorated matter, especially mucus or mucopurulent matter expec-
     torated in diseases of the air passages.

Squamous:   Scale-like, scaly.

Standard deviation:   Measure of the dispersion of values about a mean
     value.   It is calculated as the positive square root of the average of
     the squares of the individual deviations from the mean.

Standard temperature and pressure:  0°C, 760 mm mercury.

Staphylococcus aureus:  A spherically-shaped,  infectious species of bacteria
     found especially on nasal mucous membrane and skin.
                                      G-42

-------
Static lung compliance (Cistat):  Measure of lung's elastic recoil  (volume
     change resulting from cnange in pressure) with no or insignificant air-
     flow.

Steady state exposure:  Exposure to air pollutants whose concentration
     remains constant for a period of time.

Steroids:  A large family of chemical substances comprising many hormones and
     vitamins and having large ring structures.

Stilbene:  An aromatic hydrocarbon C-./.H-,- used as a phosphor and in making
     dyes.                          I4 u

Stoichiometric factor:  Used to express the conversion efficiency of a non-
     quantitative reaction, such as the reaction of NCL with azo dyes in air
     monitoring methods.

Stoma:   A minute opening or pore (plural is stomata).

Stratosphere:   That region of the atmosphere extending from 11 km above the
     surface of the earth to 50 km.   At 50 km above the earth temperature
     rises to a maximum of 0 C.

Streptococcus pyogenes:   A species of bacteria found in the human mouth,
     throat and respiratory tract and in inflammatory exudates, blood stream,
     and lesions in human diseases.   It causes formation of pus or even fatal
     septicemias.

Stress  corrosion cracking:   Cracking caused by simultaneous presence of
     tensile stress and a specific corrosive medium.   The metal or alloy is
     virtually unattached over most of its surface, while fine cracks progress
     through it.

Strong  interactions:   Forces or bond energies holding molecules together.
     Thermal energy will  not disrupt the formed bonds.

Sublobular hepatic necrosis:   The pathologic death of one or more cells, or
     of a portion of the liver,  beneath one or more lobes.

Succession:   The progressive natural development of vegetation towards
     a  climax,  during which one community is gradually replaced by others.

Succinate:   A salt of succinic acid involved in energy production in the
     citric acid cycle.

Sulfadiazine:   One of a group of sulfa drugs.   Highly effective against
     pneumococcal, staphlococcal,  and streptococcal infections.

Sulfamethazine:   An antibacterial  agent of the sulfonamide group, active
     against homolytic streptococci, staphytococci, pneumococci and meningococci,

Sulfanilimide:   A crystalline sulfonamide (CcHgO^S),  the amide of sulfanilic
     acid and parent compound of most sulfa arugs.
                                      G-43

-------
Sulfhydryl group:  A chemical radical consisting of sulfur and hydrogen
     which confers reducing potential to the chemical compound to which it is
     attached (-SH).

Sulfur dioxide (SQ2):  Colorless gas with pungent odor released primarily from
     burning of fossil fuels, such as coal, containing sulfur.

Sulfur dyes:   Used only on vegetable fibers, such as cottons.   They are
     insoluble in water and must be converted chemically in order to be
     soluble.  They are resistant (fast) to alkalies and washing and fairly
     fast to sunlight.

Supernatant:   The clear or partially clear liquid layer which separates
     from the homogenate upon centrifugation or standing.

Surfactant:   A substance capable of altering the physiochemical nature of
     surfaces, such as one used to reduce surface tension of a liquid.

Symbiotic:  A close association between two organisms of different species in
     which at least one of the two benefits.

Synergistic:   A relationship in which the combined action or effect of two
     or more components is greater than that of the components acting separately.

Systolic:  Relating to the rhythmical contraction of the heart.

Tachypnea:  Very rapid breathing.
                                            12
Terragram (Tg):   One million metric tons, 10   grams.

Teratogenesis:  The disturbed growth processes resulting in a deformed
     fetus.

Teratogenic:   Causing or relating to abnormal development of the fetus.

Threshold:  The level at which a physiological or psychological effect begins
     to be produced.

Thylakoid:  A membranous lamella of protein and lipid in plant chloroplasts
     where the photochemical reactions of photosynthesis take place.

Thymidine:  A nucleoside (C^H^Ot-) that is composed of thymine and
     deoxyribose; occurs as a strnctural part of DMA.

Tidal volume (Vj):   The volume of air that is inspired or expired in a single
     breath during regular breathing.

Titer:   The standard of strength of a volumetric test solution.  For example,
     the titration of a volume of antibody-containing serum with another
     volume containing virus.
                                      G-44

-------
Tocopherol:  a-d-tocopherol is one form of Vitamin E prepared synthetically.
     The a form exhibits the most biological activity.  It is an antioxidant
     and retards rancidity of fats.

Torr:  A unit of pressure sufficient to support a 1 mm column of mercury;
     760 torr = 1 atmosphere.

Total lung capacity (TLC):  The sum of all the compartments of the lung, or
     the volume of air in the lungs at maximum inspiration.

Total suspended particulates (TSP):  Solid and liquid particles present in
     the atmosphere.

Trachea:  Commonly known as the windpipe, a cartilaginous air tube extending
     from the larnyx (voice box) into the thorax (chest) where it divides,
     serving as the entrance to each of the lungs.

Transaminase:  Aminotransferase; an enzyme transferring an amino group from
     an a-amino acid to the carbonyl carbon atom of an a-keto acid.

Transmissiyity (UV):   The percent of ultraviolet radiation passing through a
     a medium.

Transmittance:   The fraction of the radiant energy entering an absorbing
     layer which reaches the layer's further boundary.

Transpiration:   The process of the loss of water vapor from plants.

Triethanolamine:   An amine, (HOCH?CH?)qN, used in the absorbing solution
     of one analytical  method for NO^.

Troposphere:   That portion of the atmosphere in which temperature decreases
     rapidly with altitude, clouds form,  and mixing of air masses by convection
     takes place.   Generally extends to about 7 to 10 miles above the earth's
     surface.

Type 1 epithelial  cells:   Squamous cells  which provide a continuous lining
     to the alveolar surface.

Type I pneumonocytes:   Pulmonary surface  epithelial  cells.

Type II pneumonocytes:   Great  alveolar cells.

Ultraviolet:   Light invisiblebto the human eye of wavelengths between 4x10
     and 5xlO"9 m (4000 to 50A).
Urea- formaldehyde resin:   A compound composed of urea and formaldehyde in
     an arrangement that conveys thermosetting properties.
                                      G-45

-------
Urobilinogen:  One of the products of destruction of blood cells; found in
     the liver, intestines and urine.

Uterus:  The womb; the hollow muscular organ in which the impregnated ovum
     (egg) develops into the fetus.
Vacuole:  A minute space in any tissue.

Vagal:  Refers to the vagus nerve.  This mixed nerve arises near the medulla
     oblongata and passes down from, the cranial cavity to supply the larynx,
     lungs, heart, esophagus, stomach, and most of the abdominal viscera.
Valence:  The number of electrons capable of being bonded or donated by
     an atom during bonding.

Van Slyke reactions:  Reaction of primary amines, including amino acids,
     with nitrous acid, yielding molecular nitrogen.

Variance:  A measure of dispersion or variation of a sample from its
     expected value; it is usually calculated as the square root a sum of
     squared deviations about a mean divided by the sample size.

Vat dyes:  Dyes which have a high degree of resistance to fading by light,
     NO  and washing.  Widely used on cotton and viscose rayon.   Colors are
     brilliant and of almost any shade.   The name was originally derived
     from their application in a vat.

Venezuelan equine encephalomyelitis:   A form of equine encephalomyelitis
     found in parts of South America, Panama, Trinidad, and the United States,
     and caused by a virus.  Fever, diarrhea, and depression are common.  In
     man, there is fever and severe headache after an incubation period of  2
     to 5 days.

Ventilatory volume (Vr):   The volume of gas exchanged between the lungs and
     the atmosphere that occurs in breathing.

Villus:  A projection from the surface,  especially of a mucous membrane.

Vinyl chloride:  A gaseous chemical suspected of causing at least one type
     of cancer.  It is used primarily in the manufacture of polyvinyl
     chloride, a plastic.

Viscose rayon:  Filaments of regenerated cellulose coagulated from a solution
     of cellulose xanthate.  Raw materials can be cotton linters or chips
     of spruce, pine, or hemlock.
                                                            6
Visible region:  Light between the wavelengths of 4000-800Q A.

Visual range:  The distance at which an object can be distinguished from
     background.

Vital capacity:  The greatest volume of air that can be exhaled from the
     lungs after a maximum inspiration.
                                      G-46

-------
Vitamin E:  Any of several fat-soluble vitamins (tocopherols), essential
     in nutrition of various vertebrates.

Washout:  The capture of gases and particles by falling raindrops.

Weak interactions:  Forces, electrostatic in nature, which bind atoms and/or
     molecules to each other.   Thermal energy will disrupt the interaction.
     Also called van der Waal's forces.

Wet deposition:  The process by which atmospheric substances are returned
     to earth in the form of rain or other precipitation.

Wheat germ lipase:  An enzyme, obtained from wheat germ, which is capable
     of cleaving a fatty acid from a neutral fat; a lipolytic enzyme.

X-ray fluorescence spectrometry:   A nondestructive technique which utilizes
     the principle that every element emits characteristic x-ray emissions
     when excited by high-energy radiation.

Zeolites:   Hydrous silicates analogous to feldspars, occurring in lavas
     and various soils.

Zooplankton:   Minute animal life floating or swimming weakly in a body of water.
                                      G-47

-------
TECHNICAL REPORT DATA
(Please read Insrructions on the reverse before completing)
EPA- 600/8-82- 026F
4. TITLE AND SUBTITLE
AIR QUALITY CRITERIA FOR
Report
7. AUTHOR(S)
See list of Contributors
2.
OXIDES OF NITROGEN: Final
and Reviewers
9. PERFORMING ORGANIZATION NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Research and Development
Environmental Criteria and Assessment Office (MD-52)
Research Triangle Park, N.C. 27711
12. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
,401 M Street, S.W., Washington, D.C. 20460
3. RECIPIENT'S ACCESSION NO.
PB-83-163337 "
5. REPORT DATE
December 1982
6. PERFORMING ORGANIZATION CODE
8. PERFORMING ORGANIZATION REPOR'
10. PROGRAM ELEMENT NO.
A9DA1A
11. CONTRACT/GRANT NO.
13. TYPE OF REPORT AND PERIOD COVE
Final
14. SPONSORING AGENCY CODE
EPA/600/21
15. SUPPLEMENTARY NOTES
16. ABSTRACT
   This criteria document focuses  on  a  review and assessment of the effects on  human
   health and welfare of the  nitrogen oxides, nitric oxide (NO) and nitrogen dioxide
   (NOp), and the related compounds,  nitrites, nitrates, nitrogenous acids, and
   nitrosamines.  Although the  emphasis is  on presentation of health and welfare
   effects data, other scientific  data  are  oresented in order to provide a better
   understanding of these pollutants  in the environment.  To this end, separate
   chapters are included which  discuss  the  nitrogen cycle, sources and emissions,
   atmospheric chemical processes  which transform emissions of nitrogen oxides  into
   related airborne compounds,  transport and removal processes, measurement methods,
   and atmospheric concentrations  of  nitrogenous pollutants.
                               KEY WORDS AND DOCUMENT ANALYSIS
                 DESCRIPTORS
                                             b.IDENTIFIERS/OPEN ENDED TERMS  t.  COSATI I Icld/Groi
8. DISTRIBUTION STATEMENT

   Release  unlimited
19. SECURITY CLASS t'fliis Report)

  Uncla s_s_rfie
-------