EPA
             United States
             Environmental Protection
             Agency
              Environmental Criteria and
              Assessment Office
              Research Triangle Park NC 27711
EPA-600/8-82-026
September 1982
             Research and Development
Air Quality
Criteria for
Oxides of Nitrogen

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                                    EPA-600/8-82-026
                                    September 1982
AIR  QUALITY CRITERIA
               FOR
OXIDES OF NITROGEN
     Environmental Criteria and Assessment Office
       Office of Research and Development
       U.S. Environmental Protection Agency
        Research Triangle Park, NC 27711

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                     NOTICE

Mention of trade names or commercial products does not
consititute endorsement or recommendation for use.
                         11

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                                 FOREWORD

     This document  has  been prepared in compliance with  Section 108(c) of
the Clean Air Act, 42 U.S.C. §7408 (c), which requires that the Administra-
tor from  time  to time review, and,  where  appropriate,  revise  and reissue
criteria.  This  document  has also been prepared in compliance with Section
109(d)(l) of the Act, 42 U.S.C. §7409(d)(l) which requires that by December
31,  1980,  the  Administrator  thoroughly  review  and,  where  appropriate,
revise criteria in accordance with Section 108.  Section 108(a)(2) requires
that   upon  issuance the criteria reflect  accurately  the  latest scientific
information available  relative to all identifiable effects  on the  public
health or welfare  from the presence of the pollutant  in  the  ambient air.
     These health  and welfare  criteria  fulfill the  regulatory purpose of
serving as the  basis upon which the  Administrator will  consider promulga-
tion of a short-term (three hours or  less)  standard  for nitrogen dioxide,
and standards  for other  nitrogenous compounds  (nitric and  nitrous  acids,
nitrites, nitrates, nitrosamines and certain other derivatives of oxides of
nitrogen).  Criteria related  to nitrogen dioxide will  also  be used  to
determine the  need to  promulgate  a  revised  annual  standard  for nitrogen
dioxide.   The proposed  standards  are being published concurrently with the
publication of this criteria document.
     Although the preparation  of  a  criteria document requires a comprehen-
sive review  and evaluation  of the   current  scientific  knowledge regarding
                                    iii

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the air pollutant  in question.   The  references cited  do not constitute a
complete bibliography.   The objective  is to  evaluate  the scientific data
base and to  formulate criteria which may  serve  as  the basis for decisions
regarding  the  promulgation of  national  ambient air  quality standards for
the subject  compounds.    Scientific work  of  marginal  significance to this
end may not be included in the document.
     The Agency  is  pleased to acknowledge the efforts and contributions of
all persons  and groups  who have  participated as  authors  or reviewers to
this document.   In the last analysis, however, the Environmental Protection
Agency is responsible for its content.
                                    iv

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                                  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  (NO-),  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
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 NQo  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 N0_ is a significant component, but the exact effective concentra-
tions and exposure tiroes are difficult to determine.
     Animal studies provide  support for the mechanism of increased suscep-
tibility to some respiratory pathogens as a consequence of NO, exposure but
cannot provide quantitative  data.    Increases in animal susceptibility due

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to repeated  short-term  exposure 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  in
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.   NO-
acts as  a blue-minus  filter for transmitted light.  The  strength of this
filter effect is   theoretically  determined by the integral  of NO- 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 N02 in ambient air.
     Nitrogen  dioxide  and  particulate  nitrates  may  also  contribute  to
pollutant haze.   The discoloration of the horizon sky due to NO. 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/m3) N02 can color
the horizon noticeably.   At a visual range of 10 km, typical  of urban haze,
at least  0.03  ppm (60 ug/m )  NO.  would  be required  to  produce the same
effect.  Estimates  of the  possible role played by particulate nitrates are
currently hampered by the lack of high quality data on their concentrations
in ambient air.
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     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 lakes 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
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ambient concentrations producing measurable injury are above those normally
occurring  in  this   country.    Exceptions  to  this  generality   have  been
observed: the  growth of Kentucky bluegrass was reduced about 25 percent by
exposures to 210 ug/m  (0.11 ppm) NO, 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 cases
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 pg/m   (0.15  ppm)  NO, in combination
with 260  (jg/m   (0.1  ppm) SO^.  Similar results were observed in green peas
and swiss chard.
 Kentucky bluegrass  showed reductions in yield parameters  ranging from 30
to 90  percent  upon  exposure for 20  weeks  to 210 ug/m   (0.11  ppm) NO. in
combination with 290 ug/m  (0.11 ppm) S02 for 103.5 hours per week.
     Nitrogen dioxide has been found to cause deleterious effects on 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
exposure  to  94 Mg/m   (0.05  ppm)  NOj 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/rn  (0,1 ppm).  Yellowing of several white
fabrics  has  been shown  in exposure  to  376 pg/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.
                                   viii

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                                 ABSTRACT

     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  carbon  monoxide and its
effects 1n 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.
                                    ix

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                               TABLE OF CONTENTS
                                                                         Page

FOREWORD.	       ifi
PREFACE	         v
ABSTRACT	,  .        ix
LIST OF FIGURES	     xviii
LIST OF TABLES  	      xxil
LIST OF ABBREVIATIONS, ACRONYMS AND SYMBOLS	  .     xxvfi
CONTRIBUTORS AND REVIEWERS  .	     xxxvi
SCIENCE ADVISORY BOARD COMMITTEE	      xliv

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	       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 Toxicology Studies ........       1-20
          1.3.2  NO, 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 NOV AND NO -
     DERIVED POLLUTANTS	*.  .  .  .*.  .  .  .       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  UnsymmetricaT Nitrogen Trioxlde (OONO)  	       3-10
          3.2.5  Symmetrical Nitrogen Trioxide (NO,)  	       3-10
          3.2.6  Dinitrogen Trioxide (N90,) ... 7	       3-11
          3.2.7  Dinitrogen Tetroxide (fuL)	       3-11
     3.3  NITRATES, NITRITES,  AND NITR06EN*ACIDS  	       3-11
     3.4  AMMONIA (NH,)	       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

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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  AHMQNIA 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  *	        5-2
          5.2.2  Sources of NO  in thi United States  .	        5-2
     5.3  EMISSIONS OF AMMONIA*	        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 N0?-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

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     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 .......       6-27
                 6.3.2,3  Wet Deposition  	       6-27
          6.3.3  Source-Receptor Relationships  	       6-28
     6.4  MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION 	       6-30
          6.4.1  Non-Photochemical Reaction of Gaseous Amines
                 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 NOv	       7-5
          7.2.1  The Reference MethSd for NO.:
                 Gas-Phase Chemiluminescence  	       7-5
          7.2.2  Other Analytical  Methods for N0?	       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
                 7.2.2.4  Sodium Arsenite Method  	       7-10
                 7.2.2.5  TGS-ANSA Method	       7-11
                 7.2.2.6  Other Methods 	       7-12
                 7.2.2.7  Summary of Accuracy and Precision
                          of NO, 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 RO 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
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          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 NO  AND OTHER
     NITROGENOUS COMPOUNDS	?	       8-1
     8.1  ATMOSPHERIC CONCENTRATIONS OF NO	       8-1
          8.1.1  Background Concentrations of NO	       8-2
          8.1.2  Ambient Concentrations of NO   7	       8-3
                 8.1.2.1  Monitoring for NO   	       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 N02 Concentrations  	       8-14
          8.1.5  Seasonal Variations in NO- 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 N0_ 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 N0_	       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
                                    xiii

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                                                                             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	10-10

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   	   11-12
          11.2.1    Emissions of Nitrogen and Sulfur Oxides 	   11-12
          11.2.2    Transport of Nitrogen and Sulfur Oxides 	   11-13
          11.2.3    Formation 	 .........  	   11-21
                    11.2.3.1  Composition and pH of Precipitation 	   11-22
                    11.2.3.2  Seasonal Variations In Nitrates and Sulfates.   11-25
                    11.2.3.3  Geographic Extent of Acidic Precipitation .  .   11-31
          11.2.4    Acidic Deposition 	   11-35
     11.3 EFFECTS OF ACIDIC DEPOSITION	11-35
          11.3.1    Aquatic Ecosystems	11-37
                    11.3.1.1  Acidification of Lakes and Streams  	   11-37
                    11.3.1.2  Effects on Decomposition  ..........   11-47
                    11.3.1.3  Effect on Primary Producers and Primary
                              Productivity	   11-49
                    11.3.1.4  Effects on Invertebrates	11-55
                    11.3.1.5  Effects on Fish	11-58
                    11.3.1.6  Effects on Vertebrates Other Than Fish  .  .  .   11-64
          11.3.2    Terrestrial Ecosystems	11-66
                    11.3.2.1  Effects on Soils  	   11-66
                    11.3.2.2  Effects on Vegetation 	  ....   11-76
                              11.3.2.2.1  Direct Effects on Vegetation  .  .   11-77
                    11.3.2.3  Effects on Human Health 	   11-87
                    11.3.2.4  Effects of Acidic Precipitation on Materials.   11-87
     11.4 ASSESSMENT OF SENSITIVE AREAS 	   11-90
          11.4.1    Aquatic Ecosystems  	   11-90
          11.4.2    Terrestrial Ecosystems  	  .  	   11-96
     11.5 SUMMARY	11-100
     11.6 REFERENCES	11-104

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
                                   xiv

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           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  NO- 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  SUMHARY	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	x	13-15
           13.1.2  Yellowing of White Fibers by NO	   13-15
           13.1.3  Degradation of Textile  Fibers bj  NO  	   13-19
     13:2  EFFECTS OF NITROGEN DIOXIDE  ON  PLASTICS AND
           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

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                                                                             Page

14.  STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS  	 .  .   14-1
     14.1  INTRODUCTION	14-1
     14.2  NITROGEN DIOXIDE 	 ;..... 	   14-1
           14.2.1  Respiratory Tract Transport and Absorption 	   14-1
           14.2.2  Mortality  	   14-3
           14.2.3  Pulmonary Effects  	   14-3
                   14.2.3.1  Host defense mechanisms  	   14-3
                             14.2.3.1.1  Interaction with
                                         infectious agents  	   14-3
                             14.2.3.1.2  Mucociliary transport  	   14-18
                             14.2.3.1.3  Alveolar macrophage  .......   14-18
                             14.2.3.1.4  Immune system	14-24
                   14.2.3.2  Lung Biochemistry	14-28
                             14.2.3.2.1  Introduction 	   14-28
                             14.2.3.2.2  Lipid and diet effects 	   14-28
                             14.2.3.2.3  Sulfhydryl compounds and
                                         pyridine nucleotides 	   14-38
                             14.2.3.2.4  Effects on lung amino
                                         acids, proteins, and
                                         enzymes	14-38
                             14.2.3.2.5  Potential defense
                                         mechanisms ..... 	   14-40
                   14.2,3.3  Morphology Studies 	   14-41
                   14,2,3.4  Pulmonary Function 	   14-49
                   14.2.3.5  Studies of Hyperplasia 	   14-54
                   14.2.3.6  Edemagenesis and Tolerance 	   14-57
           14.2.4  Extrapulnonary Effects .... 	   14-59
                   14.2.4.1  Nitrogen Dioxide-induced Changes in
                             Hematology and Blood Chemistry 	   14-59
                   14.2.4.2  Central Nervous System and
                             Behavioral Effects	14-63
                   14.2.4.3  Biochemical Markers of Organ Effects 	   14-63
                   14.2.4.4  Teratogenesis ancTMutagenesis	14-68
                   14.2.4.5  Effects of NO, on Body Weights ........   14-71
     14.3  DIRECT EFFECT OF COMPLEX MIXTURES  	   14-71
     14.4  NITRIC OXIDE	14-78
     14.5  NITRIC ACID AND NITRATES	14-80
     14.6  N-NITROSO COMPOUNDS  	   14-82
     14.7  SUWIARY	14-84
     14.8  REFERENCES FOR CHAPTER 14	14-110

15.  EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN 	   15-1
     15.1 INTRODUCTION	15-1
     15.2  CONTROLLED HUMAN EXPOSURE STUDIES  	   15-3
           15.2.1  Studies of Sensory Effects .....  	   15-3
                   15.2.1.1  Effects of Nitrogen Dioxide on
                             Sensory Systems  	   15-3
                   15.2.1.2  Sensory Effects Due to Exposure to
                             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

                                   xvi

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                                                                         Page

                   15.2.2,2  The Effects of Nitrogen Dioxide
                             Exposure on Pulmonary Function in
                             Sensitive Subjects 	   15-17
     15.3  EP1DEMIOLOGICAL STUDIES	15-22
           15.3.1  Effects of NO, on Pulmonary Function 	   15-22
           15.3.2  Effects of Nflf 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 NO, Pollution on Prevalence of
                   Chronic Respiratory Disease  	  ...   15-38
           15.3.4  Extrapulmonary Effects of Exposure to N0?  	   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  NO- Effects	15-46
                   1576.1.1  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

APPENDIX A:  GLOSSARY	   A-l
                                   xv 11

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                              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"	    1-32

 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 RO  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 NO,, ANO,, for 10 Seconds in Dark Sampling
          Line	f .  .	    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 NO. 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 N02 (4-Year Running
          Mean)  in the Los Angeles Basin	    8-20
 8-10.     Seasonal N0? Concentration Patterns of Three U.S.  Urban
          Sites  (Montnly Averages of Daily Maximum 1-Hr Concentrations).   8-22
 8-11.     Seasonal N0_ Concentration Patterns of Four U.S.  Urban
          Sites  (Montnly Averages of Daily Maximum 1-Hr Concentrations).   8-23
 8-12,     Distribution of Maximum/Mean NO,, Ratios for 120 Urban
          Locations Averaged Over the Years 1972, 1973, and 1974  .  . .    8-41

                                   xviii

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Figure                                                                     Page

8-13.    Trends in the Maximum Mean NO- Ratio for Two Groups of Sites. .    8-42
8-14.    Average Diurnal Pattern for tne Month During Which the
         Highest 1-Hour NO, Concentrations were Reported 	 ...    8-44
8-15.    One-Hr Average Concentration Profiles on Day of Peak NO-
         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 NO,, Daily Maximum Hourly Concentration
         Above the California One-Hour Standard at Various Frequencies .    8-69
8-22.    Population Exposed to NO, Hourly Average Concentration Above
         the California One-Hour Standard at Various Frequencies ....    8-71

10-1.    Transmittance of NO- 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

                                     xix

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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
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 	    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

                                     xx

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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 NO, 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 ug/m  (3.5
         ppm) NO, Prior to Challenge with Streptococci	    14-13
14-3.     Percent Mortality of Mice Versus Lengtb of Either Continuous
         or Intermittent Exposure to 2,800 ug/ro  (1.5 ppm) NQ«
         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 Injury and Repair Hypothesized from
         Continuous Exposure to N0_ as Observed in Experimental
         Animals	    14-103
                                     xxi

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                                  LIST OF TABLES

Table                                                                      Page

 1-1.  Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
       in Controlled Studies of Healthy Humans Adults .  	       1-6
 1-2.  Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
       in Controlled Studies of Sensitive Humans Adults 	       1-11
 1-3.  Quantitative Community Health Epidemiological Studies on
       Effects of Exposure to Nitrogen Dioxide on Pulmonary Function       1-14
 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 .......       1-17
 1-5.  Summary of Studies Demonstrating Health Effects in Animals at
       Low (< 2.0 ppm) NO- Exposure Levels	       1-22
 1-6.  Effects of Exposure to Nitrogen Dioxide on Sensory Receptors
       in Controlled Human Studies  	       1-25

 3-1.  Theoretical Concentrations of Nitrogen Oxides and Nitrogen
       Acids Which Would be Present at Equilibrium with Mglecular
       Nitrogen, Molecular Oxygen, and Water in Air at 25 C, 1 ATM,
       50 Percent Relative Humdfity  	       3-3
 3-2.  Some Physical and Thermodynamic Properties of the Nitrogen
       Oxides	       3-4
 3-3.  Theoretical Equilibrium Concentrations of Nitric Oxide and
       Nitrogen Dioxide in Air (50 Percent Relative Humidity) at
       Various Temperatures  ...... 	       3-8
 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.  .  .       3-12

 4-1.  Distribution of Nitrogen in Major Compartments	       4-5
 4-2.  Estimates of Global Nitrogen Fixation in the Biosphere  .  .  .       4-6
 4-3.  Estimates of Global Emissions and Fluxes of Oxides of
       Nitrogen and Related Compounds  .... 	       4-7
 4-4.  Estimates of the Global Flux of Nitrates and Nitrites ....       4-9
 4-5.  Estimates of Global Flux of NO	       4-10
 4-6.  Estimates of the Global Flux of Nitrous Oxide	       4-13
 4-7.  Estimates of.the Global Flux of Ammonia and Ammonia Compounds.       4-16
 4-8.  Estimates of Global Denitrification 	       4-17

 5-1.  Estimated Annual Global Emissions of Nitrogen Dioxide
       (Anthropogenic) 	       5-2
 5-2.  Historic Nationwide NO  Emission Estimates 1940-1970  ....       5-3
 5-3.  Recent Nationwide NO  Emission Estimates 1970-1976  	       5-5
 5-4.  NO/NO  Ratios in Emissions from Various Source Types  ....       5-13
 5-5.  Estimated Ammonia Emission from Fertilizer Application and
       Industrial Chemical Production in U.S. (1975) 	       5-15
                                      xxn

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Table                                                                      Page

 5-6.  Nitrogenous Compounds Applied as Fertilizer 1n 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 Triethylamlne  	  ....        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 Colorfmetric 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 N09 Concentrations at
       Various Sites in U.S. Urban Areas . . . ,	        8-27
                                     xxiii

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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
       N0_ Concentrations at Various Sites in U.S.  Urban Areas ....      8-32
8-11.  Distribution by Time of Day of One-hour Maximum N02
       Concentrations for One Month in 1975 for Selected urban
       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 N0_ Concentrations
       During a Period of High NO, Concentrations	      8-56
8-14.  High Concentrations of Nitrogen Oxides, St.  Louis,
       Missouri, 1976.	      8-60
8-15.  Monthly Trends in Hourly NO and NO- 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 STte 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 NO. Hourly
       Ambient Concentrations	      8-72

11-1.  Composition of Ecosystems 	      11-7
11-2.  Hean 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 Basejl on Buffer
       Capacity Against pH-Change, Retention of H , and Adverse
       Effects on Soils	      11-98
                                      xx iv

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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 NO, Exposures for 5 Percent Injury Levels on
        Selected Vegetation  	 ...... 	     12-35
12-8.   Effect of Chronic NO, Exposures on Plant Growth and Yield   . .     12-36
12-9.   Plant Response to Sulfur Dioxide and Nitrogen Dioxide
        Mixtures	     12-42
12-10.  The Effects of NO- and SO, Singularly and in Combination on the
        Growth of Several Grassesf ............. 	     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 NO. 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 NO, on Lung Biochemistry	     14-29
14-9.   Effect of NOj 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 NO,	     14-58
14-13.  Tolerance to N02 Exposures ...... 	     14-60


                                       xxv

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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 NO-:  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
        Hones	      15-54
                                      xx vi

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     ABBREVIATIONS, ACRONYMS, AND SYMBOLS
"A" strain
AAS
AATCC
Ad
AICHE
AM
AMP
ANSA
APCD
APHA
A/PR/8
A/PR/8/34
AQCR
AQSM
ASTM
atm
ATP
avg
BAKI
BHA
BHT
BP
            _
Angstrom (10    meter)
A particular type of influenza virus
Difference between alveolar and arterial ized partial
pressure of oxygen
Atomic absorption spectroscopy
American Association of Textile Chemists and Colorists
A particular strain of laboratory mouse
American Institute of Chemical Engineers
Alveolar macrophage
Adenosine monophosphate; adenosine 5' phosphate
8-anilino-l-naphthalene-sulfonic acid
Air Pollution Control District
American Public Health Association
A particular strain of influenza virus
A particular strain of influenza virus
Air Quality Control Region
Air Quality Simulation Model
American Society for Testing and Materials
One atmosphere, a unit of pressure
Adenosine triphosphate
Average
Potassium iodide solution acidified with boric acid
Butyl ated hydroxyanisole
Butyl ated hydroxy toluene
Blood pressure
                     xxvii

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"scat
C3H
C57BL
C57BL/6
cAMP
CAMP
CO-1
cGMP
°C
14C
CHE
CL
CLdyn
CLstat
cm
CMS
CO
C02
CoA
COH
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
                                   xxvln

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DEN            Diethylnitrosamine (also OENA)
DIFKIN         Diffusion Kinetics Model
DL-Q           Diffusion capacity of the lung for carbon monoxide
DMN            Dimethylnitrosanrine
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
FEV0 75        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

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GMP            Guanos ine 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
HbOp           Oxy hemoglobin
HN02           Nitrous acid (also HONO)
HN03           Nitric acid (also
HO'            Hydroxyl free radical (also OH)
H02'           Hydroperoxyl free radical
HO-NO          Pernitrous acid
H02N02         Pernitric acid (also HOONOg)
hr             Hour
HR             Heart rate
hv             Planck's constant (h) times the frequency of radiated
               energy (v) = Quanta of energy (E)
H«02           Hydrogen peroxide
H2S            Hydrogen sulfide
H2S04          Sulfuric acid
IARC           International Agency for Research on Cancer
Ig             Immunoglobulins
IgA            Immunoglobulin A fraction
IgG            Immunoglobulin G fraction
IgG,           Immunoglobulin G, fraction
IgG2           Immunoglobulin G- fraction
IgM            Immunoglobulin M fraction
                                    xxx

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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
L050           Lethal dose 50%; dose which is lethal to 50 percent of
               the subjects
LTSO           The time required for 50 percent of the test animals
               to die when given a lethal dose
LOH            Lactic acid (lactate) dehydrogenase
LPS            Bacterial lipopolysaccharide
m              Meter
M              Molar
H              Third body (in a reaction)
MAK            Maximum permissible concentration (in Germany)
max            Maximum
MFR            Maximal flow rate
ug/m           Micrograms per cubic meter
mg/m           Milligrams per cubic meter
Mg             Magnesium
ml             Milliliter
mM             Millimoles
HMD            Mass median diameter
MMFR           Mid-maximal flow rate
mo             Month
                                   xxxi

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MPC            Maximum permissible concentration (in the U.S.S.R.)
HT             Metric Ton
N              Nitrogen
N              Normal
  N            A radioactive form of nitrogen
N-6-MI         N-nitrosoheptamethyleneimine
NA             Not applicable
NAAQS          National Ambient Air Quality Standard
NaCI           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-Naphthy1)-ethylenediamine dihydrochloride
NEOS           National Emissions Data System
NEIC           National Enforcement Investigations Center
ng             Nanogram
NH.            Ammonium ion or radial
rim             Nanometer
NO             Nitric oxide
NOHb           Nitrosylhemoglobin
                                    xxx n

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NO             Nitrogen oxides
N,0            Nitrous oxide
NO,            Nitrogen dioxide
NjO,           Dinitrogen trioxide
N_0,           Dinitrogen tetroxide
NSF            National Science Foundation
0              Atomic oxygen
0( D)          Excited atomic oxygen
0,             Ozone
OH             Hydroxyl group
0( P}          Ground state atomic oxygen
32
  P            A radioactive form of phosphorus
 PaCO,         Alveolar partial pressure of carbon dioxide
PaCQ-          Arterial partial pressure of carbon dioxide
PAH            p-Afwniohippurie acid
PAN            Peroxyacetyl nitrate
PaO,           Arterial partial pressure of oxygen
PAD™           Alveolar partial pressure of oxygen
pH             Log of the reciprocal of the hydrogen ion concentration
PHA            Phytohemagglutinin
PO,            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
                                   xxxiii

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RAMS           Regional Air Monitoring System



RAPS           Regional Air Pollution Study



R              Airway resistance
 oW


RBC            Red blood cell; erythrocyte



RH             Reference method for air quality measurement



RNA            Ribonucleic acid



RV             Residual volume



SAI            Science Applications, Inc.



SO             Standard deviation



SGOT           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


SRH            Standard reference material



SS             Suspended sulfates



STP            Standard temperature and pressure



TEA            Triethanolamine



Tg             Terragram; 10  metric tons or 10   grams



TGS-ANSA       A 24-hour method for the detection of analysis of N02

               in ambient air



TLC            Total lung capacity



TPTT           20 percent transport time



TSP            Total suspended particulate
                                   xxxiv

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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
 rndx
V_             Total volume
V/V            Volume per volume
WBC            White blood cells
wk             Week
yr             Year
Zn             Zinc
Mg             Microgram
Ml             Microliter
Mm             Micrometer
>              Greater than
<              Less than
~              Approximately
                                  xxxv

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                        CONTRIBUTORS AND REVIEWERS
Principal authors:
Dr. Charles E. Anderson, Department of Botany, North Carolina State Univer-
    sity, Raleigh, North Carolina.
Or. Paul J. Crutzen, National Center for Atmospheric Research, Boulder,
    Colorado.
Or. 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 H. 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.
Dr. 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.
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.
                                   xxxv i

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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 Laboeatory, 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 Analaysis 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.


                                    xxxvii

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

Or. David J. McKee, 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.
    Environmental Protection 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. Hark R. Antell, Division of Stationary Source Enforcement, U.S. Inviron-
    •ental Protection Agency, Washington, D.C.

Hr. John 0. 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.


                                   xxxviii

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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.

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.

Or. 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 1, 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.

                                 xxx ix

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Or. 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.

Hr. 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.

                                    xl

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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.
    Environmental Protection Agency, Research Triangle Park, North Carolina.

Mr. Grin 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.

                                   xli

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

Hr. 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.
                                   xlii

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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
     Or. 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 Chappell
     Ms. Constance Van Oosten
     Ms. Evelynne Rash
     Ms. Donna Wicker
                                    xliii

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                   CLEAN AIR SCIENCE ADVISORY COMMITTEE
                        SUBCOMMITTEE ON AIR QUALITY
                      CRITERIA FOR OXIDES OF NITROGEN
Dr, Mary 0. Amdur
Department of Nutrition and Food Science
Massachusetts Institute of Technology
Cambridge, MA

Dr. Domingo M. Aviado
Allied Chemical
Morristown, NJ

Dr. Judy A.   Bean
Associate Professor
Department of Preventive Medicine
College of Medicine
University of Iowa
Iowa City, IA

Dr. Robert Dorfman
Department of Economics
Harvard University
Cambridge, MA

Dr. Sheldon K. Fried!ander
Professor of Chemical Engineering and
Environmental Health Engineering
H, M, Keck Laboratory
California Institute of Technology
Pasedena, CA

Mr. Harry H. Hovey, Jr.
New York State, Department of
Environmental Conservation
Albany, NY

Dr. Donald H. Pack
Consulting Meteorologist
McLean, VA
                                      xliv

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

I.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  (NOy)  and  nitric oxide
(NO), and other nitrogenous compounds which may be derived from NO  through atmospheric  trans-
formations.   Since  NO^  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

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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 NOX  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, NO, 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 NO-  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  N0_  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  N02  are  complex and
involve other  atmospheric  constituents such as  hydrocarbons and  ozone.   Also, NO,, 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 NO^ concentrations is neither direct
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

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     In general, adequate methodology  now exists for sampling and  analysis  of NO, concentra-
tions 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 NO, for some  time.   The following
summary of  recent  ambient  levels  of N02 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  N02  concentrations cited.   Moreover, considering  the likelihood  that  fixed
monitoring  sites may  not intercept the maximum N02 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 NOj concentrations equalling or exceeding 750 wg/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  yg/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/ n>  (0.14 ppm) were quite common nationwide in 1975 to 1980.
     Annual arithmetic means  for  NO,  concentrations in 1976 exceeded 100 pg/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  pg/ra   (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 vg/m  in that year (except for one in
San Diego; 114
l',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 (N02), 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

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     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 N0»  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  N0_ most  definitively  characterized to date,  the effects  of NO-  on  the
respiratory system  have  been  most extensively delineated and appear  to  be of most concern in
terms of  both acute and  long-terra  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 NO,.
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  NOg effects  ranges from  (1)  death  or  irreversible  pulmonary  damage  seen  with
accidental high exposures  to  NOg 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 N0_
levels.
     Acute  high level exposures  to NO, that  have  occurred  accidentally or in  occupational
                                                                     3
settings demonstrate that concentrations in the range of 560,000 Mg/m  (300 ppm) or higher are
Hkely 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) NO,  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 NO™ 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 NO, exposures,  how-
ever, a variety of  respiratory system effects have  been reported  to  be  associated with expo-
sures to  lower  concentrations  of NOg.   Extensive literature characterizing  such effects  has
                                              1-4

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resulted  from three  general  approaches:   (1)  controlled human  exposure studies;  (2)  human
epidemiological  studies;  and  (3)  animal  toxicology studies.   The major  types  of NO^-induced
respiratory effects characterized by these different approaches include:   (1) increased airway
resistance (R  ) and other indications of altered pulmonary function as observed in controlled
             3W
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  NO, concentrations  approaching or falling within the
range of recorded ambient air NQg 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 NO, 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  NO- 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 NO- 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 NO™  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
jjg/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 \tg/m  (0.7 to
2.0 ppm) NO- 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 pg/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

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      TABLE 1-1.   EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON
PULHONARY FUNCTION IN CONTROLLED STUDIES OF HEALTHY HUMAN ADULTS**
Concentration Pollu-
M9/n3
13,000
9,400
9,400
9,400
7,500
to
9,400
5,600
11,300
ppn tant
7.0 N02
5.0 H02
5.0 N02
5.0 N02
4.0 NO,
to i
5.0
3.0 N02
6.0 N0?
No. of
Healthy
Subjects
Several
11
' t
16
13
5
•1
1
Exposure
Tine
10-120
min.
2 hrs.
15 min.
15 min.
10 rain.
5 min.
5 min.
Effects
Increased R * in some subjects. Others
tolerated 30,000 yg/m (16 ppm) with no
increase in R,, .
QW
Increase in R * and a decrease in AaDO,*
with intermittent light exercise. No,en-
hancement of the effect when 200 ug/m
(0.1 ppm) 0, and 13,000 n/ra (5.0 ppm)
SO. were combined with NO- but recovery
time apparently extended.
Significant decrease in DL-Q*
Significant decrease in PaO«* but end ex-
piratory P0«* unchanged witn significant
increase in systolic pressure in the
pulmonary artery.
40% decrease in lung compliance 30 min.
after exposure and increase in expiratory
and inspiratory flow resistance that
reached maximum 30 min. after exposure.
Increase in R * compared to pre-exposure
values (enhanced by NaCl aerosol).
More subjects were tested at higher
Reference***
Yokoyama,
1972
von Nieding
et al.,
1977
von Nieding
et al., 1973
von Nieding
et al.,
1970
Abe, 1967
Nakamura,
1964
                         exposures.

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TABLE 1-1.   (continued)
Concentration Pollu-
ug/mj
1,880
4,700
14,000
9,400
1,300
to
3,800
1,880
1,150
ppra tant
1.0 N02
2.5 N02
7.5 N02
5.0 N02
0.7 NO,
to *
2.0
1.0 N02
0.6 N02
No. of
Healthy Exposure
Subjects Time Effects
8 2 firs. No Increase in R,^.
3W
8 2 hrs. Increased R with no further impairment
at higher concentrations. No change in
arterial PO, pressure or PCO, pressure.
16 Z hrs. Increased sensitivity to a bronchocon-
strlctor (acetylcholine) at this concen-
tration but not at lower concentrations.
8 14 hrs. Increase in R during first 30 min. that
was reduced through second hour followed by
greater increases measured at 6, 8 and 14
hrs. Also increased susceptibility to a
bronchoconstri ctor ( acety 1 chol i ne) .
10 10 mins. Increased inspiratory and expiratory flow
resistance of approximately 50% and 10% of
control values measured 10 mins. after
exposure.
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).)
15 2 hrs. No physiologically significant changes
in cardiovascular, metabolic, or
Reference
Beil and
Ulraer, 1976
Suzuki and
Ishikawa,
1965
Hackney et al.
1978
Folinsbee
et al., 1978
      pulmonary functions after 15, 30
      or 60 mins.  of exercise.

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                                                TABLE 1-1.   (continued)
00


Concentration
ug/m-1
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

ppia
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
j
0,

N02
°3
**
NO,
£
CO
°3
3
°3
J
NO,
t.
0,
•*
NO,
£.
CO
NO,
£.


No, of
Healthy Exposure
Subjects Tine Effects
4 4 hrs. With each group minimal alterations in pul-
monary function caused by 0, exposure.
Effects were not increased By addition of
NO, or NO, and CO to test atmospheres.
t. c.





7 2 hrs. Little or no change in pulmonary function
found with 0, alone. Addition of NO, or
of NO, and CO did not noticeably increase
the effect. Seven subjects included some
believed to be unusually reactive to
respiratory irritants.





10 2 1/2 hrs Alternating exercise and rest produced
significant decrease for hemoglobin,
hematocrit, and erythrocyte acetyl-
cholinesterase.


Reference
Hackney
et al,,
1975







Hackney
et al.,
1975








Posin et al. ,
1978



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                                    TABLE  1-1.   (continued)


Concentration
M9/n>3
100
with
50
and
300
ppm
0.05
0.025

0.11

Pollu-
tant
N02
0,

SO,
No, of
Healthy Exposure
Subjects Time Effects
11 2 hrs. No effect on R or AaD02; exposed sub-
jects showed increased sensitivity of
bronchial tree to a bronchoconstrictor
(acetylcholine) over controls not exposed
to pollutants.


Reference
von Nieding
et al., 1977



*R    :   airway resistance
 AaDtk:   difference between alveolar and  arterial blood partial  pressure  of  oxygen
 DU0 :   diffusion capacity of the  lung for  carbon monoxide
 PaO, :   arterial  partial  pressure  of oxygen
 PO,  :   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.

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     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)  N02 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  N0_ 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 NO,.   The results of the Kerr study concerning
asthmatics and chronic bronchitics are discussed later.
     Bell  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 NO.  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                                          33
94 pg/m  (0.05 ppm) N02 in the presence of 49 pg/m  (0.025 ppm) ozone and 290 ug/m  (0.11  ppm)
sor
     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  NO-  concentrations substantially below 1880 pg/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 NQ« in sensitive human subjects at exposure levels below
those affecting healthy human adults.  Key clinical  studies  of the  effects of exposure to NO,
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-
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
arterial partial  pressure of  oxygen.   Exposures  to  concentrations of NO,  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.
     In contrast  to the above results  for  bronchitics,  exposures to 190 pg/m (0.1 ppm)  N02
for 1 hour were reported by Orehek (1976) to increase mean airway resistance (R_w) in 3 of 20
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

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                           TABLE  1-2.   EFFECTS OF EXPOSURE TO  NITROGEN  DIOXIDE  ON
                     PULMONARY FUNCTION IN  CONTROLLED  STUDIES  OF  SENSITIVE  HUMAN ADULTS
Concentration
MtJ/m3 ppm
9,400
3,800
to
9,400
940
to
9,400
940
5.0
2.0
to
5.0
0.5
to
5.0
0.5
No. of Exposure
Subjects Time
14 chronic 60 mins.
bronchitics
25 chronic 10 mins.
bronchitics
63 chronic 30
bronchitics inhal-
ations
10 healthy 2 hrs.
7 chronic
bronchitics
13 asthmatics
Effects* Reference
No change in mean PAO-, during or after expo- von Nieding
sure compared with pre-exposure values, but et al, 1973
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 von Nieding
AaDO- at 7,500 ug/m (4.0 ppm) aqd above; no et al., 1971
significant change at 3,800 ug/m (2.0 ppm).
Significant increase in R above 3,000 ugm/ von Nieding
(1.6-ppm); no significant effect below 2,800 et al., 1971
ug/m (1.5 ppm).
1 healthy and 1 bronchitic subject reported Kerr, et al.,
slight nasal discharge. 7 asthmatics reported 1979
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
*PA02

 Raw
 SR
   aw
alveolar partial  pressure of oxygen

airway resistance

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

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function were not altered in 13 asthmatics or 7 bronchltics as a result of 2 hours of exposure
to 940  ug/m  (0.5 ppm) NO, 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 bronchi tic 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
be affected at NQ2 levels of 940 ug/m3 (0.5 ppm) or below.
     The above controlled human exposure studies provide important data concerning the effects
of single short-term NOg 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

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     It  is  important  to  note  that community  epidemiological  studies prior  to 1973  on  the
effects of  HOy  exposure are of questionable validity  due to the use of the Jacobs-Hochheiser
technique in measuring atmospheric concentrations of NO-.*  For this reason, the contributions
of  those  community  studies to  knowledge  concerning  the  effects  of  NO- 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  NO, effects on pulmonary function and providing
quantitative data on  associated  ambient air levels of NO-  are  summarized in Table 1-3,  Most
of these studies consistently tend to indicate that reported daily mean concentrations of peak
levels  of  NOp,  or NO,  in  combination with  other pollutants  (all less  than  1.0  ppm NO,)
typically had no significant effects on lung function in the exposed study populations.
     An exception is  the Kagawa  and Toyaroa (1975)  study  which  showed some correlations in 20
Japanese schoolchildren, 11  years  of age, between decrements in  maximum expiratory flow rate
$m**y  or specific airway conductance  and  concentrations of NO,  or other specific pollutant
  HlaX                                                           £.
levels  at the time of testing.  One-hr.  NO,  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 N02  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  NO, alone,  but  rather  with   various  combinations  of  air
pollutants,   including SO,,  particulate matter,  and  0,.    In addition,  weekly  variations in
specific airway  conductance  and  in V     at 25 percent FVC were  most closely correlated with
                                     fll3X
outdoor temperature  levels.   These  results emphasize that  the observed  respiratory effects
resulted from  a complex  interaction of pollutants  including N0» and do  not  allow for clear
attribution of an association of decreased lung function with any specific ambient air concen-
tration of NO,.
     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  epidetniological studies  also evaluated  relationships
between ambient  air exposures to  NO.  at  levels reported  in  Table  1-3 and  the occurence of
chronic respiratory  diseases,  but  found  no significant associations between  the  ambient  NOg
exposures and the  health endpoints measured.   A few other community epidemiology studies have
been  published   which  report  quantitative  associations   between ambient  NOg  exposures  and
increased acute respiratory disease incidence,  but the methods employed in those studies (e.g.
use of  the  Jacobs-Hochheiser  method for monitoring NO,  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

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TABLE 1-3,   QUANTITATIVE COWUNITY HEALTH EPIDEMIOLOGICAL STUDIES ON  EFFECTS
            OF EXPOSURE TO NITROGEN DIOXIDE OH PULMONARY FUNCTION


Measure
High exposure group:
Annual nean
24-hr concentrations

90th percent! lei
Estimated 1-hr
maximum

Low exposure group:
Annual mean
24-hr concentrations
90th percent! le
Estimated 1-hr
maximum

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

low exposure
area

1-hr nean:
high exposure
area
low exposure area


N0?
Conce
iV*

96


188
480
to
960

43

113
205
to
430
103
92


75
36

260
to
560
110
to
170
Exposure
ntrations
I ppM

0.051


0.01
0.26
to
0.51

0.01

0.06
0.12
to
0.23
«• 0.055
SO, 0.035
2 SO-
*
+ 0.04 <
SO, 0.014
i SO,
0.14
to
0.30
0.06
to
0.09

Study
Population Effect Reference

Nonsraokers 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.



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                                               TABLE 1-3.  (continued)

NO, Exposure
Concentrations
Measure
Los Angeles:
Median hourly NO,
e.
90th percentile NO,
e.
Median hourly 0
90th percentile DX
San Francisco:
Median hourly NO-

90th percentile NO-
Median hourly 0
90th percentile Ox
1-hr concentration
at time of testing
(1:00 p.m.)

US/Hi"

130

250



65

110


40
to
360

ppm

0.07

0.13
0.15
0.15

0.35

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
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) N0~, S0? and
TSP* significantly correlated
with V * at 25% and 50% FVC*
Reference

Linn, et
al., 1976









Kagawa and
Toy ana ,
1975

                                                         and wiffl 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, SO, 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
*F,£VQ ^c:   Forced expiratory volume, 0.75 seconds
  max'   :   Maximum expiratory  flow  rate
 FVC    :   Forced vital  capacity

 TSP    :   Total suspended particulates

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     As for the results of other epidemiologycat studies, some support for accepting the hypo-
thesis that children  are  at special risk for  NQ,-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 NO, levels accumulate in homes using gas stoves
in comparison to N02 levels found in homes with electric stoves.   Melia et al.  (1978) reported
that average NO, 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 ug/m  (0.01
ppm) in 2 other  homes where electricity was used.   In this study the NO, 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 NO, 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
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, Helia  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

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  TABlE 1-4,   EFFECTS OF EXPOSUBl  TO NITROGEN  DIOXIDE  IN IHE HOME  ON LUNG FUNCTION AND
THE INCIDENCE OF ACUTE RESPIRATORY DISEASE  IN  EPIDEMIOLOGY STUDIES OF HOMES WITH GAS STOVES
Pollutant*
m-i
Concentration
MgAn3 pp«
Study
Population
Effects
Reference

Studies of Children
NO. plus
otner gas stove
combustion products
NO. plus other gas
stove combustion
products
NO, plus other
gas stove
C embus lion
products
HO, plus other
gal stove
combustion
products
HO, concentration
not Measured at
tine of study
NO, concentration
not measured in
sane hones studied
Kitchens:
9-596 (g«) 0,005-0.31?
11-353 (elec) 0.006-0.168
Bedrooms:
7.5-318 (gas) 0.004-0.169
6 - 70 (elec) 0.003-0.037
(by triethanolaaine
diffusion samplers)
95 percent! le of 24 hr
avg in activity room
39 - 116 ug/aj (.02 -
.06 ppn) (gas) vt.
17,6 - 95.2 M9/m
(.01 - .05 pp«)
2554 children from hones
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 coamunities with
data collected on lung function
and history of illness before
the age of 2
Proportion of children with one
or «ore respiratory symptoms
or disease (bronchitis, day or
night cough, corning cough,
cold going to chest, wheeie,
asthma) increased in hones
with 
-------
IMll 1-4 (continued)
Pollutant*
H02 plus other
gas stove
coafiustion
products
HO, plus other
gas stove
coebustion
products
HOj
Concentration
(igTP pp»
Saaple of households
24 hr avg: gas (.005 -
.11 pp»); electric
(0 - .06 pp«); outdoors
(.015 - .OS pp«); .several
peaks > 1880 pg/« (1.0
pp»). Monitoring location
not reported. 24-hr avgs
by soditM ar senile; peaks
by cheniluaineseence
Saiple of sine
households as reported
above but no new
•on it or ing reported
Study
Population
128 children 0-5
345 children 6*10
421 children 11-15
174 children under 12
Effects
Ho significant difference
in reported respiratory
illness between hoaes with gas
and electric stoves in children
frog birth to 12 years
No evidence that cooking node
is associated with the incidence
of acute respiratory illness
Reference
Hitched et •!., 1974
See also Keller et al. ,
19?9a
Keller et al., 1973b
Studies at Adults
HO, plus other
gas stove
coabustion
products
NO, plus other
gas stove
coobuition
products
NO. plus other
gas stove
cMbustion
products
NO, plus other
gal stove
combustion
products
Preliminary measure-
ments peak hourly
470 - 940 |ig/
-------
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 Spongier- et al.
(1979).  Continuous NO, measurements in a residence with gas stoves showed that  levels exceed-
            3                   3
ing 500 ug/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 NO,
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  HO, 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
NO. 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  N02  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  epldemiological  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

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(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
NOg 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 NO, 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  N02-   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.
     Horphological 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
(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  NOg exposure
nay 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 ppm) far
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 NO- 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
KOy,   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 NO, (see Section 14.2.3.1.1).   NO, exposures caus-
ing increased  infectivity  in animals have been observed across a wide range, beginning at 940
    3                                                                         3
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 NO, has more importance than time of exposure in producing increased susceptibility to
bacterial  infection.  Of interest,  the lowest N0«  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  NOg Sensory System Effects
     In addition to the  effects  of NO^  on pulmonary functions  and  its  possible  association
with  increased  acute  respiratory  disease  in  young  children,  NO-  also exerts  discernible
effects on  sensory  receptors (Table 1-6).   This  includes  the detection of NO, as  a noxious
                                                                     3
pungent  odor starting  at concentration  levels as  low as 210  ug/m  (0.11  ppm)  of N0£ and
occurring immediately upon  exposure.   Under some exposure conditions, however,  impairment of
odor detection occurs.   For  example, impaired detection of NO* 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

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                   TABLE 1-5.   SUHHARY OF STUDIES OEHONSTRATIHG HEALTH EFFECTS IN AHIHALS
                                   AT LOW (<2.0 ppw) NO  EXPOSURE LEVELS
     N02
 Concentrations
                                   Effects
                                                 NO, measurement method     Reference
 3,760      2.0
             A single 3-hr exposure caused
             increased mortality following
             challenge with an infectious
             agent in mice.
                                     Cheffliluminescence      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 e.t al., 1979
                                     minescence procedures
 1,880      1.0
(daily 2 hr spike)
   188      0.1
  (continuous)
             Emphysematous alterations in
             mice after 6 mo exposure.
                                     Saltzman
                       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.
Saltzman
Ehrlich and
Henry, 1968

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                                                 TABLE  1-5.   (continued)
    ND2
Concentrations
           ppm
                                   Effects
                                                 NO, measurement method     Reference
  940
0,5
                        A 7-day intermittent exposure
                        caused enzymatic alterations
                        in lungs and blood of guinea
                        pigs.
Saltzman
Donovan  et al., 1976
  940
0.5
                        Intermittent exposure for  6
                        hr/day for up to 12 mo caused
                        morphological changes in lung
                        alveoli  of mice.
                       Blair et al., 1969
  940
0.5
                        Increased susceptibility to
                        influenza infection in mice.
Saltzman
I to, 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.
 1880       1.0
  (max peak
  reported)
50-350* 0.03-0.19
  (2-hr avg)
             Swollen collagen fibers
             after an intermittent 24
             or 36 day exposure of
             rabbits
                                                                                    Buell, 1970
667
to
94

0.36
to
0.05

Hemato logical effects
observed in guinea pigs
, after 7 days of»exposure to
690 or 940 ng/nr (0.36 or
0.5 ppm).
Donovan et al.
Menzel et al, ,
Hersch et al. ,

, 1976
1977
1973


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                                                  TABLE 1-5.   (continued)
     N02
 Concentrations
 jig/n3      pfwf                   Effects                   NO- measurement method     Reference


  470      0.25          Increased pentobarbital-                                    Miller etal,, 1980
                         induced sleeping time in
                         female mice after a 3 hr
                         exposure.  No effects after
                         2 or 3 days.


  376      0.2           Inhibition of meta-                                         Menzel, 1980
                         holism of prostaglandin
                         E, in rats to its inactive
                         15-keto metabolite.


aSaltzman, 1954 (See Chapter 7.)

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        TABLE 1-6.  EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY RECEPTORS  IN CONTROLLED HUMAN STUDIES
 I
ro
01
N02 Concen-
trations
ug/m-5
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
Effects
Perception of odor of NO,
£.
Perception of odor of N02
Perception of odor of N02
Perception of odor of NO-
Perception of odor of NOp
No perception of odor of NO,, when
concentration was raised slowly from
0 to 51,000 pg/nr
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


No. of
Subjects
Responding
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 amber idze,
Feldman, 1974
Henschler et al. ,
1960

Ibid.


Shal amber idze,

Bondareva, 1963






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     NO- exposures  also exert  effects  on other sensory perception  functions.   Probably  most
significant is the N02 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 N02  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-
ration  in  decision-making regarding  primary  National Ambient  Air Quality  Standards  for N0x
compounds can be summarized as follows:
              (1)  At concentrations of 9,400 ug/m  (5.0 ppm) or above,  exposure to
                   NOp 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) N02 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
                   pg/rn  (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
                   NOp 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 NO- 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) N0_ exposure levels.

                                              1-26

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              (S)  Prospective studies of th* 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  NO, 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 NO- 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 NO.
                   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 NO.  concentrations  rarely
exceed  0.4 to  0.5 ppm.   Such peaks  occurred during 1S75  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 NO- 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,
visibility, climate,  and man-made  materials—effects which may  impact negatively  on  public
                                              1-27

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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
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 wade 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  raanmade 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  NOX  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,   1976;  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

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     Sulfates and  nitrates are among  the products of the chemical  transformations  of sulfur
oxides  (especially SO-)  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 (H-SO.) and
nitric (HNO,) 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
1-1).
     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, 1978).
     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

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CO
O
                          Figure 1-1. Average pH isopleths as determined from laboratory analyses of precipitation
                          samples, weighted by the reported quantity of precipitation.

                          Source: Wisniewski and Keitt (1981).

-------
     Although acidic precipitation  (wet deposition) is usually emphasized, it is not the only
process by which  adds  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 Hountains  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.,  1980).  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

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     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; Koran et a!.,  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.
                iow«-
                                            -GRA01ENT-
                                                                            -*-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

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     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 Hountains of New York State, 1n 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 paniculate 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

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        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.
        S.   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, 1§8Q).
     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 (S0.~)  and nitrate (NO,) ions on vegetation and have caused necrotic lesions in a wide

                                              1-34

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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 seasonality of their
contributions; (7)  the  existence  and significance of anthropogenic, non-combustion sources of
SOX, N0x  and HC1;  (8)  the dry deposition rates  for SOX,  N0x, sulfate,  nitrate  and HC1 over
various terrains and seasons of the  year;  (9)  the existence and reliability  of long-term  pN
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
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 NO  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
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  EffectsOf NOon Ecosystems and Vegetation
     Chapter  12  discusses  NO  effects on ecosystems and vegetation.   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 systems  their value cannot be fully  quantified  in economic terms.
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     Ecosystems  are iaportant  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) nay  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.
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     When  exposures  to  NO- 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 eseulentum)  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 Mi/m   (1-0 ppm).   Other
reports cited no injury in beans (Phaseolus vulgaris), tobacco (Nicotiana tabacum) ,  or petunia
(Petunia multl flora) 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) NO,  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  (  Pi sum  sativum) seedlings  from  5 to  10  percent.   The
significance  of  the increased chlorophyll is  not known.   Some species of  lichens  exposed to
3,760 Mg/rn  (2.0 ppm) for 6 hours showed  reduced chlorophyll content.
     In contrast to studies cited on the  effects of NO, alone, a number of studies on mixtures
of NO. and  SO,  showed that the NO,  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 NO- and  SO,  occurring in some  areas  of the U.S.   A combination of 188 ug/m  (0.1 ppm) NO,
and 262 pg/m   (0.1  ppm) SO^ 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) NO, in
                                                                                          ^
combination with 262  MS/IB   (0^1 ppm) SO, 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 gg/m  (0.11 ppm) NO- and 290 ug/m  (0.11
ppm) SO,  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
NO,, 0,, and  S0_.   These exposures were  carried out in ambient air and protected against sun-
light.   Chamber  studies using  individual  pollutants  NO,,  0., and S02  have  shown  that some
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Individual  dye-fiber combinations  exhibit  color fading  only in  response to  NO, exposure,
whereas others  are susceptible to 0,, as  well  as combinations of NO- and 0,.   SO, 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  (O.S  ppm) NO.  under high  humidity  (90 percent)  and high
temperature  (90°F) conditions.   Significant fading  is observed  on  12  weeks  exposure  to 94
ug/»  (0.05 ppm) NO, under high humidity and temperature conditions (90 percent, 90°F).
                                                                            3
     Acid dyes on nylon fade on exposure to NO, at levels as low as 188 pg/m  (0.1 ppm), under
similar conditions.  Dyed polyester fabrics are highly resistant to N0,"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 SO, showing no
                                                               3          a       £
affect.   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
(-NH,) of nylon to the degree  that  the  fiber  has less affinity for acid-type dyes.  Nylon 66
                                                               3
nay suffer chain scission when exposed to  1,880  to  9,400 ug/m  (1.0 to 5.0 ppm) NQ2<  Field
exposures of fibers emphasize the action of acids  derived from SO,, although NO, may also be
present  in  high  concentrations  in  urban  sites.   Information on  the contribution of NOg 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 N0_ 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,, 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
ug/ra  (1.0 to 5.0 ppm).
     The extensive  data on corrosion of metals in polluted areas relate the corrosion effects
to the SQy  concentrations.   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
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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
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, NO,  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 NO,  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  NO, or  a  0.1 kilometer-wide plume containing 1.0 ppm (1,900
    3
yg/m ) of  NO,.  Less than  0.1 ppm-km  NO, is  sufficient  to produce  a color shift which is
distinguishable in  carefully  controlled,  color-matching tests.  Reports  from one laboratory
using N02-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 NO- plumes from
nitric acid manufacturing plants  under varying operating conditions.   The value cited refers
to the  effect of  N02 in the  absence of atmospheric aerosol.   Empirical  observations  under a
variety of conditions are needed  to determine the perceptibility of NO, in ambient air.
     Plume coloration due to  NO, 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.   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  the plume tends  to washout the brownish  light  transmitted from  beyond.   Under these
conditions,  light   scattering  by particles  diminishes  the   plume  coloration caused  by N0£.
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.

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     The discoloration of the horizon sky in an urban, or more extensive regional  area, due to
NO- absorption,  is  determined by the relative concentrations of NO^ 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 ppra (6 ug/m ) N0« 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 )
HO- would be  required  to produce the sane 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.
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                                       2.   INTRODUCTION

     Molecular nitrogen  (N-)  and oxygen (Op)  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
(NO,), 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-
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 polluted 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-OQ4.
     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 NOX
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, N0£ 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
NO- 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.
                                            2-1

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     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 NQ~ 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 NO, 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 epidemic-
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 epidetniological  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 NOX of individuals or populations in ambient situations.  Because
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.  NOX 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
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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

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                     3,   GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NO
                                  AND NOX-OERIVEO POLLUTANTS            x
                                                                           V
3.1  INTRODUCTION AND OVERVIEW
     In this  chapter some  general  chemical and  physical  properties of NO *  and NO -derived
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  (NyO),  unsymmetrical  nitrogen  trioxide
(OONO),  symmetrical  nitrogen  trioxide  (ON(O)O),  dinitrogen  trioxide  (N-0,),  dinitrogen
tetroxide (N^O.), and dinitrogen pentoxide (N-Oc).
      Of these, NO and NO- 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-0., and N20,- 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 NH, 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, NO  is the sum of nitrogen dioxide (NO,) and nitric oxide (NO).

                                            3-1

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              where  R  represents  any one  of a  large  variety  of  possible  organic  groups)
(Chapter 8).
     The peroxyacyl  nitrates,  of which peroxyacetyl nitrate (CH-C(0)QQNO_, or PAN) is of roost
concern in  terms of atmospheric  concentrations,  have been thoroughly reviewed  in the recent
EPA document, Air  Quality Criteria for Ozone and Other Photochemical Qxidants (1978) and wi11
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 (HNQ,).  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 1s 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

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   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)
Concentrations in Hypothetical Atmosphere, ppm
Compound
°2
N2
H20
N02
NO
N03
N2°3
N2°4
N2°5
HONO (cis)
HONO (trans)
HON02
At Equilibrium
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
In Typical Sunlight-irradi-
ated, Smoggy Atmosphere
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
10"3
10"3
io"2-io"3
theoretical estimates made using computer simulations of the chemical
 reactions rates in a synthetic smog mixture.
                                   3-3

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                       TABLE 3-2.  SOME PHYSICAL AND THERHODYNAMIC PROPERTIES OF THE NITROGEN OXIDES
U)
I
Thermodynamic Functions
(Ideal Gas, 1 atm, 25°C)C
Oxide
NO
N02
N2°4
N20
N2°3
N2°5
Molecular Halting Boiling
Weight, Q^iRt §°infc
30.01 -163.6 -151.7
46.01 Liquid, solid
forms largely
as N204
92.02 -11.3 21.2
44.02 -102.4 -89.5
76.02 -102 3.5
(decomposes)
108.01 30 32.4
(decomposes)
Solubility in Enthalpy of
,H,Q(Q°C), . Formation,
cnT CSTP)/100 ga kcal/mol
7.34 21.58
Reacts with H?0 7.91
forming HONO/and
MONO £
Reacts with H?0 2.17
forming MONO, and
MONO z
130.52 19.61
Reacts with H?0 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
        fMatheson Gas Data Book (Matheson, 1966).
        "Handbook of Chemistry and Physics (Chemical Rubber Company, 1969-1970).
         JANAF Thermochemical Tables (U. S. Department of Commerce, 1971).

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 •i50
 n

 I  40
 »"•"
 UJ
 i  so
 o
 u  20
 CC
 O
 I/)
 ce
 <£
    10
     1500
                   1700
                                                 i
A      A
                                 1900


                            WAVE LENGTH,&
                                               2100
                                                             2300
Figure 3-1. Absorption spectrum of nitric oxide (McNesby and Okabe,
1964).
                            3-5

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It has an uneven number of valence electrons, but, unlike NQg, 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 NO ."
     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 N, bond through reactions such
as (Fenimore, 1976):
               CH + N2 •» CHN f 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 N«  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

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     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 Z 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.
In practice, only a portion of these nitrogen compounds is converted to NO , with the remainder
being  converted  to molecular nitrogen  (Ng).   Tests designed to determine the  percent of the
NOX 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 al.,  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
N-, 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  NO   emissions are defined by  the kinetics of the
process  rather  than  being an equilibrium  phenomenon  is  that NOX 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

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TABLE 3-3.  THEORETICAL EQUILIBRIUM CONCENTRATIONS OF NITRIC OXIDE
    AND NITROGEN DIOXIDE IN AIR (50 PERCENT RELATIVE HUMIDITY)
     AT VARIOUS TEMPERATURES (NATIONAL RESEARCH COUNCIL,  1977)
                                 Concentration,
 Temperature,  K ( C)                 NO                N0
                                                          2
    298 (24.85)                  3.29 x 10~"j       3.53 x 10"1
                                (2,63 x 10~1U)     (1.88 x 10 1

    500 (226.85)                 8.18 x 10~*        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

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are  flue  gas recirculation,  reduced  load,  reduced combustion air  preheat  temperature,  water
injection and reduced excess air (Proceedings, 1976; Proceedings, 1977).
     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 (Proceedings, 1976).
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  NO- in  the atmosphere
prevents condensation.   Nitrogen  dioxide  is  corrosive and highly oxidizing.  It has an uneven
number  of  valence  electrons and  forms  the dimer  N-0. at  higher concentrations  and  lower
temperatures, but the  dimer is  not important at ambient concentrations.   In the atmosphere NO
can be oxidized to NO-  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 NO
from combustion sources is  in the form of NO,, although substantial variations from one source
to  another  have  been  observed.   Under  more dilute  ambient conditions,  photochemical  smog
reactions involving hydrocarbons convert NO to NO- (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 NO- at ground level is, therefore, 290 nm to 430 nm.   Because of
its absorption properties,  NO,  produces discoloration and  reduces  visibility in the polluted
lower troposphere.
3.2.3  Nitrous Oxide (N20)
     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
group  of bacteria  that use  nitrate  as  their  terminal  electron  acceptor  in the  absence of
oxygen (denitrification) (Brezonik, 1972;  Oelwiche, 1970; Focht and Verstraete; Kenney, 1973).

                                            3-9

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     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  N_ and  singlet oxygen
(Johnston and Selwyn, 1975):
                   HyO + hv •» N~ + 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 ozonel
               NO + 03 •» N02 + 02
               0, + hv -» 0, + 0
               N02 + 0 + NO + 02
     These  reactions are of concern because of the possibility  that  increased N20 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)
     Unsynnetrical  nitrogen trioxide is thought  to be an intermediate in  the  reaction of NO
with 0,,
     "2*
               NO + 02  *  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 NO/O- reaction accounts for very little of the NO oxidized.
3.2.5  Symmetrical Nitrogen Trioxide (N03)
     Symmetrical nitrogen trioxide has been identified in laboratory systems containing N02/0.j,
NQ-/Q,  and N,0C  as an  important  reactive transient  (Johnston, 1966).   It is  likely  to be
  £,           t, O
present in photochemical snog.  This compound can be formed as follows:

               0 + N02  (+ H) * N03 (+ H)
               N 0  (+ M^ •* NO  + Nfl  f+ M^
(where H represents any third molecule  available  to remove a fraction of the energy involved
in the reaction.)
                                            3-10

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     Symmetrical nitrogen  trioxide  is highly reactive towards  both  nitric oxide and nitrogen
dioxide.
               N03 + NO + 2N02
               NO, + NO, (+ M) - N,0, (+ M)
                                                                       -6      3      -9
     Its  expected  concentration in polluted air  is  very low (about 10    ug/m  or 10   ppm).
3.2.6  Dinitrogen Trioxide (N^O^) (Also Known as Nitrogen Sesquioxide)
     In  the  atmosphere, N203  is in  equilibrium  with NO  and NO- according  to the following
equation:
              NO + NO,  -»  N,0,
                     '      ' J                                                             -4
The  equilibrium  concentrations  at  typical  urban  levels of NO and NO,  range from about 10
    n     _ -j           ^r     O     «Q                                ^
ug/m  (-^10   ppm) to 10   ug/m   (-^10   ppm) (Table 3-4). N-0, is the anhydride of nitrous acid
and reacts with liquid water to  form the acid:
               N2°3 * H2° "* 2HONO
3.2.7  Dinitrogen Tetroxide (NpO,.) (Also Known as Nitrogen Tetroxide)
     Dinitrogen tetroxide  is  the dimer of NO- formed by the association of NO- molecules.  It
also readily dissociates to establish the equilibrium:
               2N02  ?  N204
Table 3-4 presents  theoretical  predictions of concentrations of  NgO^  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 + NO- -» HNO,    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 (NH,)  to neutralize  the acid, producing  particulate nitrates  (Chapter 6).
     The nitrate ion (NOl) 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

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TABLE 3-4.  THEORETICAL CONCENTRATIONS OF DINITROGEN TRIOXIOE AND
     DIN1TROGEN TETROX1DE IN EQUILIBRIUM WITH VARIOUS LEVELS
       OF GASEOUS NITRIC OXIDE AND NITROGEN DIOXIDE IN AIR
            AT 25°C (NATIONAL RESEARCH COUNCIL, 1977)
Concentration, ppm

NO              N02             N203            N204


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

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     The nitrite ion is the Lewis base of the weak acid, nitrous acid (HNO-).  When NO and N02
are present in the atmosphere, HNO- 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 (NHg)
     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,  NOl, NO,, halogen, tetrafluoroborate, hydrogen sulfate or OHp .  The
equilibrium reaction of nitrosonium ion (ON ), nitrous acid and nitrite ion:
               ON*  +  OH"  j  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 (OMN) 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

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     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  \im.    Nuclear magnetic  resonance  (NMR),  infrared  (IR),
ultraviolet (UV), and mass spectrometry (MS) spectra have been reviewed  by Hagee 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  (N-0),  unsymmetrical  nitrogen  trioxide (OONO),
symmetrical  nitrogen trioxide  (O-N(O)-O), dinitrogen  trioxide (N-0,),  dinitrogen  tetroxide
(N20.), and dinitrogen pentoxide (N-0,.).
     Of these,  NO and NO- are generally considered the most important in the lower troposphere
because  they may  be present  in significant  concentrations  in polluted  atmospheres.   Their
interconvertible ity  in  photochemical  smog  reactions  has  frequently  resulted in  their  being
grouped  together under  the  designation  NO ,  although  analytic  techniques can  distinguish
clearly between them.  Of the two, NO- 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, N-0,, N-0., and N-0,- 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 (NH,) 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)OON02L 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  [CH_C(0)OONO-]  or  PAN is of most
concern  in  terms of atmospheric  concentrations,  have been thoroughly reviewed  in the recent
EPA document, Air Qua!1ty Criteria for Ozone and Other Photochemical  Oxidants.

                                            3-14

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     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 (NO,)  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,  NO,  arises mainly from the conversion of NO to NOy 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), NQg can
cause  visibility reduction and affect the  spectral distribution  of solar  radiation  in the
polluted, lower atmosphere.
3.6.2  Nitrates, Nitrites, and NitrogenAcids
     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

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3-6.3  N-Nitroso Compounds
     The N-nitroso family comprises a wide variety of compounds all containing a m'troso 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 NO -derivatives in gas
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

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CHAPTER 3

Axworthy, A. E., and M. Schuman,  Investigation of the mechanism and chemistry of fuel nitrogen
     to nitrogen oxides  in combustion.   Rocket-Dyne Corp.   Paper  presented at the Pulverized
     Coal Combustion  Seminar,  Research  Triangle Park, North Carolina.   June 1973.  pp. 9-43.

Bowman,  Craig  Thomas.    Kinetics  of  nitric  acid  formation  in  combustion  processes.    In:
     Fourteenth Symposium  (International)  on Combustion.   The Combustion Institute, 1973.  p.
     729.

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

Burns, R. C., and R. W. F. Hardy.  Nitrogen Fixation in Bacteria and Higher Plants.  Springer-
     Verlag, Berlin-Heidelberg, Berlin.   1975,

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

Council for Agricultural Science and Technology (CAST).  Effect of  increased  nitrogen  fixation
     on stratospheric ozone.  Report No. 53.  January 1976.  33 pp.

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

Delwiche, C. C.  The nitrogen cycle.  Scientific American 223(3): 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, 1976.

Fenimore, C.  P.   Formation  of  nitric oxide in premixed  hydrocarbon flames.   In;  Thirteenth
     Symposium (International) on Combustion. The  Combustion Institute.   1971,

Focht, D., and W.  Verstraete.  Biochemical ecology of nitrification and denitrification.   Ann.
     Rev. Hicrobial Ecol. (In press).

Johnston, H. S.  Experimental chemical kinetics.   In;  Gas Phase Reaction Rate Theory.  Ronald
     Press, New York, 1966.  pp. 14-35.

Johnston, H.  S,.  and  6.  Selwyn.  New  cross sections for the  absorption of near ultraviolet
     radiation by nitrous oxide (NyO).   Geophys. Res. Lett. 2: 549-551, 1975.

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

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

Magee,  P. N.,  R.  Montesano, and R.  Preussman.   Chapter 11.   In: Chemical Carcinogens.  C. E.
     Searle, ed.  American Chemical Society, Washington, O.C., 1976.
                                                 3-17

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Hartln, 6. B.,  D.  W. Pershing and  E,  E.  Berkau.  Effects of  fuel  additives on air pollutant
     emissions  from  distillate  oil-fired furnaces. Publ. No.  AP-87;  NTIS No. PB 213-630.  U.
     S. Environmental Protection Agency, Research Triangle Park, North Carolina, 1971.  82 pp.

Hatheson of Canada, Ltd.  Hatheson Gas Data Book.  Fourth edition. Whitby, Ontario, 1966.  SOO
     pp.

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

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

Hirvlsh, S. S.  Kinetics of dimethylamine nitrosation in relation to m'trosamine carcinogenesis.
     J. Nat.  Cancer Inst. 44: 633-639, 1970.

National Research  Council,  National Academy of  Sciences.   Nitrogen Oxides.   Washington, D.C.
     1977.

Pershing,  D.  W., and J.  0.  L.  Wendt.  Pulverized  coal combustion:   the influence of  flame
     temperature  and   coal   composition  on  thermal  and  fuel  NO  .    Sixteenth  Symposium
     (International) on Combustion.  The Combustion Institute, 1976.  p.  389.

Proceedings  of  the  First Stationary Source Combustion  Symposium.  EPA-600/2-76-150 (a, b, c).
     U.  S.   Environmental  Protection  Agency,  Research  Triangle Park, North Carolina,  1976.

Proceedings of  the Second Stationary Source Combustion Symposium.  EPA-600/7-77-073 (a-e).  U.
     S. Environmental Protection Agency, Research Triangle Park, North Carolina, 1977.

Rao, C.  N.  R., and  K.  R.  Bhaskar.  Chapter  3.   In;   The Chemistry of  the  N1tro and  Nitroso
     Groups.   Part 1.  H. Feuer, ed. Inter-science, New York,  1969.

Soderlund, R.,  and  B.  H. Svensson.  The global  nitrogen cycle.  In:  Nitrogen, Phosphorus, and
     Sulfur - Global Cycles.  SCOPE Report No. 7.  B. H. Svensson and R.  Soderlund eds.   Ecol.
     Bull. (Stockholm) 22: 23-73, 1976.

Turner,  D. W., and  C.  W.  Siegmund.   Staged combustion and flue  gas  recycle:  potential for
     Minimizing NO   from fuel oil combustion.   Exxon Research and Engineering Company.   Paper
     presented  at The  First American  Flame Days.   Chicago,  Illinois,  September 5-7, 1972.   8
     PP-

U.  S.  Department  of Commerce,  National Bureau of Standards.  JANAF Thermochemical  Tables.
     Second  edition. NBS 37.   U. S. Government  Printing Office, Washington,  D.C., 1971.  1141
     pp.

U.S. Environmental  Protection Agency.   Air Quality Criteria for Ozone and Other Photochemical
     Oxidants.   EPA-600/8-78-004.   U.S. Environmental  Protection Agency, Office of Research
     and Development, Washington, D.C., April 1978

Zeldovich, Y. B.   Acta Physiochem. URSS. 21: 577, 1946.
                                              3-18

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                                    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;  Kenney,  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 NH.)  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 ami no 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

-------
               ff
               NZ
               IN
           ATMOSPHERE
                             BIOLOGICAL FIXATION  j: ''''.
                           iOF MOLECULAR NITROGEN:   ;
  ELECTRICAL
     AND
PHOTOCHEMICAL
   FIXATION
   NITROGEN
   OXIDESt
   NO, NO2
                 VOLCANIC
                 ERUPTION
                                      WEATHERING
                                       OF ROCKS
                                                   FOREST & GRASSLAND FIRES
                                   STORAGE OF
                                  NITROGENOUS
                                  COMPOUNDS IN
                                SEDIMENTS, SOILS,
                                AND SEDIMENTARY
                                     ROCKS
ANIMALS IN GRAZING
    FOOD CHAIN
                                        NITRATE /—| NITRITE/ - 1 AMMONIA / - , NI
                                           ~   ^ - «N02~  \f - 1   NH3    \, - 1  R « NH2
____    _____ A _________
          ^           r
                                                                                          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 (NH3).   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  (NO,~)  and  then to  nitrate (NO,").   Nitrates  may be
                               mnmnninnnninnnnn-       ^                 nnn	"iniiminr-    ^
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 dem'trification converted into atmospheric nitrogen  (N,).
     5.  Denitrification — Nitrates,  through bacterial action, are converted into atmospheric
nitrogen.    Denitrification  is an  anaerobic process.   Nitrates  (NO,   )  are  converted  into
nitrites (NOp ), to nitrous oxide (N-O) and finally into nitrogen gas (N,) 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  N^O 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

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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.  So'derlund  and Svensson (1976)
have hypothesized  that a net flow of NO  prevails from terrestrial to aquatic systems; losses
of  NOX  from  aquatic system  to  the atmosphere  were considered  insignificant.   Nitrogenous
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.   Delwiche1s figures are at variance with those of Soderlund and Svensson
(1S76)  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 Soderland and Svensson
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.  Host 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

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                   TABLE 4-1.   DISTRIBUTION OF NITROGEN IN MAJOR COMPARTMENTS
Compartment Tg* N
q
Atmosphere 3.9 x 10
Plants and animals 1.0 x 10
Organic, soil 1.7 x 105
Organic, set 8.9 x 105
Inorganic, soil 1.6 x 10
Inorganic, sea 9.9 x" 10
Sediments 2.0 x 10®
Reference
Carrels et al. ,
Delwiche, 1970
Oelwiche, 1970
Delwiche, 1970
Del wi che, 1970
Delwiche, 1970
Carrels et al. ,

1975



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 (N^O), 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

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


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
Soderlund
and Svensson
(1976)
224-324
139
169-269 .
30-130
19
36
N/A
Robinson
and Bobbins
(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

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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 denitrfflcation
( 1 and and sea ) 	 ......
NO emissions fron land
to atmosphere. . 	 	
NO emissions from land
and sea 	
NO^ formed by combustion...
NO formed by industrial
processes 	
Atmospheric HH, trans-
formation to HO . . ......
KHj emissions to atmosphere
Atmospheric production of
NO., bv liahtnina 	
Oelwtche
(1970)
54
83
(H?,H20)
HA
NA
HA
30
NA
NA
NA
Burns Soderlund Robinson
and Hardy and Svensson and Robbins Liu et a).
(1975) (1976) (1975) (1977)
175
190(H.)
20(Np)
NA
HA
15
30
30
165(1 and
and sea)
10
169-269
96-191(H,)
36-l«(Np)
40-108
HA
19
36
3-8
113-244
(land)
NA
117
338
(N20)
NA
210(NO)
15
NA
NA
870(land
and sea)
NA
240
270
(N2,H20)
HA
HA
NA
40
NA
NA
NA
Sze
and Rice
(1976)
260
260
NA
NA
NA
NA
NA
NA
NA
CAST
(1976)
171-200
(N2,H20)
NA
NA
NA
NA
NA
NA
NA
CKaiwides
et al.
(1977)
NA
NA
NA
NA
NA
NA
NA
HA
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 theibautii.  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
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 raonatomic
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).
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, N02, NH, 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 NOg-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 NQg-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 NOj-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 N05 	
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
Soderlund
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 (NQ,-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
million tons  in 1980  (Parr, 1973).  The  impact  of  this environmental loading  has  not, until
very recently, been considered.
4.4  AMHONIFICATION 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
(NH,) 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 transfornation (Chameides et  al.,  1977; National
Research Council, 1978).
4.5  NITRIC OXIDE, NITROGEN DIOXIDE AND THE NITROGEN CYCLE
     Total NO  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 NOV
                                                          (NO AND NO,)               *
                                                             TgN/yr l
                                             Burns
                                           and Hardy
                                             (1975)
Sb'derlund and
   Svensson
    (1976)
 Robinson
and Bobbins
   (1975)
 Crutzen
and Ehtialt
  (1977)
Chameides
  et al.
  (1977)
    Natural emissions from land to
      atmosphere	      N/A
    Natural emissions from land and sea
      to atmosphere	      N/A
    Tropospheric production by lightning       10
    Stratospheric production from NpO...        5
    Atmospheric production from NH,	      N/A
4*                                J
5  Production during combustion	       15
    Other industrial production	       30
    Total land deposition..	       31
    Total aquatic deposition.	       18
    Total wet deposition (as nitrates;
      land and sea)	       49
    Total dry deposition (land and sea).       11
   21-89

    N/A
    N/A
    0.3
    3-8
     19
     36
   32-83
   11-33
   18-46
   25-70
    N/A

    210
    N/A
      2
    N/A
     15
    N/A
    N/A
    N/A

     75
    151
   N/A

   N/A
  8-40
   N/A
   N/A
   N/A
   N/A
   N/A
   N/A

   N/A
   N/A
   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
troposphere (Soderlund  and Svensson,  1976).    Hill  (1971)  has reported that  NO  and  N02 are
absorbed from  the atmosphere  by plants.  Using data  obtained from the experiments of Marakov
(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  NOg  can  be  produced through  photolysis  and transformation
reactions  involving  N20 and  0.,.   Small amounts of  these  products  (about 0.3 Tg annually) are
expected to reenter the troposphere, mainly as  N02 and HN03.
     Tropospheric ammonia may be  converted  to NO,  and  indirectly to  NO-,  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
reported by Chameides and co-workers (1977).
     Tropospheric production of NOX during lightning discharges has been estimated to account
for 8 to 40 Tg NOX~N per year (Chameides et al., 1977; Griffing, 1977; Noxon, 1976).
     The work  of Chameides et al.   (1977)  suggests  that  lightning is a significant source of
NOX,  producing about 30 to 40 Tg NO -N per year.  If this estimate is correct, lightning could
account for as much as 50 percent of the total  atmospheric production of NO  on a global basis
(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 NO- 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  NOX 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 N0x (National Research
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, N.O 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 N~0.
     From  a  review of  the  literature,  Sb'derlund  and Svensson  (1976) estimated  the N20 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 N^O production in
soils at 7 Tg N per year.
     Total annual marine production and release to the atmosphere of N,0 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 N,0.
     Sb'derlund and  Svensson  (1976),  using data obtained  by  Junge (1972), estimate that 18 Tg
NoQ-N per year is conveyed  from the  troposphere  to the stratosphere and converted to N-, Qj,
and NO...   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  N20 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 N^O.  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.
     Han's agricultural  activities have been reported  to be a cause of  depletion of organic
matter in soils  (Paul,  1976;  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 (Soderlund 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 (Soderlund and Svensson, 1976).
4.8  AMMONIA AND THE NITROGEN CYCLE
     There is  considerable  uncertainty  as to the sources of atmospheric NH-.  A global source
strength of  113 to 224 Tg-N per year has been estimated (Soderlund and Svensson, 1976), based
on balancing  of estimated  total deposition.  Sources such as excreta from  wild and  domestic
animals and humans (Oenmead et al., 1974; Healey et al., 1970; Luebs et al., 1973; Stanford et
al.,  1975) and coal  combustion (Burns and Hardy, 1975; Georgii, 1963; Soderlund 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  (Soderlund  and
Svensson,  1976)  volatilization  from oceans  (Bouldin  et al.,  1974),  and possibly  from the
senescing leaves of  living  plants  (Fargahar 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  (Oenmead
et al., 1976).
     It has been  proposed  that atmospheric NH, may  be converted to NO   by  reaction  with -OH
                                              j                        X
radicals  (McConnell,  1973;  McConnell  and McElroy,  1973).   A  recent  estimate of  the annual
magnitude of  this source is  20 to  40 Tg  NO -N  (Chameides et  al.,  1977).   McConnell (1973)
concluded that this reaction and heterogeneous losses are the dominant tropospheric NH, removal
mechanisms.  Atmospheric NH,  returns  to terrestrial and aquatic systems via precipitation (as
ammonium salts), by dry deposition of gaseous NH, and particulate ammonium compounds (Soderlund
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  OENITRIFICATION
     In contrast to  nitrogen  fixation,  denitrification results  in  the  release of fixed forms
of nitrogen,  principally NgO  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 (Oelwiche, 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  (Soderlund  and Svensson,
                                            4-14

-------
1976).   The ratio  of  N2 to N20 produced is an area of current interest because of the role of
N20 in the destruction of stratospheric ozone (Chapter 9).
     Delwiche (1970) estimated  that  83 Tg of N20-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 N2 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-0 from  nitrates  include  high  soil  acidity  (low pH),
presence  of  02,  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  N2 and  N20  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)
              Soderlund
             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 NH. (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 (N2), 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 (NOX) 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  NOX
                                            4-16

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


Biological denitrification
(total) 	
terrestrial ., 	 	
aauatic. 	

Delwiche
(1970)
83
43
40
Burns and
Hardy
(1975)
210
140
70
SSderlund
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
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

-------
CHAPTER 4

Alexander, H.   Introduction to 2nd  ed.,  Soil Microbiology.  John  Wiley and Sons.  New  York,
     1977.  472p.

Bolin,  B.,   and  E.  Arrhenius,  eds.   Nitrogen  -  An  Essential  Life  Factor and  a  Growing
     Environmental  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.  Qua!.  3(2):107-114,  1974.

Bowen,  J.  J., Jr.   Trace Elements  in Biochemistry.  Academic Press.  London, 1966.   p.  241.

Bremner, J.  M., and A. M. Blackmer.  Nitrous  oxide:  emissions  from soils  during nitrification
     of fertilizer nitrogen.  Science.  199:295-296, 1978.

Broadbent, F,  F., and F. Clark.  Denitrification.   In:  Soil Nitrogen.  W. V.  Bartholomew and
     F. E.  Clark,eds.  Am.  Soc. Agron.  Inc. Pub.,  Hadison,  WI, Agronomy.  10:344-359,  1965.

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, Berlin-Heidelberg-New York, 1975.

Cady,  F.  B.,  and W,  V.  Bartholomew.   Sequential  products  of  an  aerobic denitrification  in
     Norfolk soil material.  Soil  Sci. Soc. Amer.  Pro.   24:477-482,  1960.

Carpenter, F.  J., and C. C. Price,  IV.  Marine Oscillatoria  (Trichodesmiurn):   explanation for
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Chameides, W. L., D. H.  Stedman, R.  R. Dickerson,  D. W.  Rusch,  and  R. J. Cicerone.   NO   produc-
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Chapham, W.  B., Jr.  Natural Ecosystems.  The MacMillan  Co.,  New York/Collier-MacMi11 an Limited,
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Chen, R. L., D. R. Kenney, and J.  A. Konrad.  Nitrification in  Sediments of Selected Wisconsin
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Cohen,  Y.,   and   L.  I.  Gordon.   Nitrous  oxide  production  in  the  ocean.   J. Geophys.  Res.
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Council for  Agricultural Science  and Technology.   Effect of  increased nitrogen fixation  on
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Crutzen,  P.  J.   Estimation  of possible  variations in total ozone due  to natural  causes  and
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Crutzen,  P.  J.,  and D.  H.  Ehhalt.   Effects of  nitrogen  fertilizers and  combustion  in  the
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Crutzen, P.  J. ,  I.  S. A. Isaksen,  and J.  R. McAfee.  The impact of the chlorocarbon industry
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                                            4-19

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Delwiche, C. C.  The nitrogen cycle.  Scientific American.   223(3):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.
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Denraead, 0. T., J. R. Simpson, and J, R.  Freney.  Ammonia flux  into the atmosphere from grazed
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Fargahar, G.  D.,  R.  Wetselaar, and  P. M. Firth.  Ammonia volatilization  from senescing leaves
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Focht, D.  D.   The effect of temperature, pH  and aeration  on  the production of nitrous  oxide
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Focht, D.  D., and  W.  Verstraete.   Biochemical ecology of  nitrification and  denitrification.
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Cartels,  R.  H.,  F.  T.   Mackenzie,  and  G. Hunt.  Chemical  Cycles and the Global  Environment.
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Georgii,  H.-W.   Oxides  of  nitrogen  and  ammonia   in the   atmosphere.    J.  Geophys.   Res.
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Griffing,  G.  W.   Ozone  and  oxides  of nitrogen production  during thunder-storms.   J.  Geophy.
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Hahn, J.   The North Atlantic Ocean as a source of atmospheric N,0.   Tellus.   26:160-168,  1974.

Hahn, J., and C. E. Junge.  Atmospheric nitrous oxide:   a critical  review.   Zsche.  Naturforsch.
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Hardy,  R.  W.  F.,  and   F.  Knight,   Jr.   Reduction  of  N_0 by  biological  N_-fixing  systems.
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Healy, T,  V.,  H.  A.  C.  McKay,  A.  Pilbeam,  and D.  Scargill,   Ammonia and ammonium  sulfate in
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Junge,  C.   The  cycles  of atmospheric   gases  -  natural  and  man-made.   Quarterly  J.  Royal
     Heteorol. Soc.  98:711-728, 1972.

Keeney,  D.  R.,  R.  L.   Chen,  and D.  A.  Graetz.   Importance   of  denitrification  and  nitrate
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     1973.
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Kim,  C.  M.   Influence  of vegetation  type in  the  intensity  of  ammonia and nitrogen  dioxide
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Luebs,  R.   E.,  K.  R.  Davis,  and  A.  E.  Laa§.  Enrichment of the atmosphere with  nitrogen
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McDonnell, J. C.   Atmospheric  ammonia.   J. Geophys. Res.   78:7812-7820,  1973.

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      ^                               ~""~  f
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                                              4-21

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     1975.  p. 385.
                                             4-22

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                                   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) NO, is  a  pollutant  of major concern  for  human  health (Chapter 15)
and (2)  atmospheric  transformation products of NO  such as nitric acid (HNO,) and particulate
nitrates are of  concern  both for their effects on human health and their role in the acidifi-
cation of precipitation  (Chapter II).   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 HNO, 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 (N,0) (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 NO-
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 NQ^ 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 NO™.  This method of presentation serves the purpose of allowing ready comparison
of different sources.  Because  of the interconvertibi1ity 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 NO/NO, being emitted by different sources.   Two points, however,

                                          5-1

-------
should be noted:   (1)  although NO is the  dominant NOX compound emitted by  most  sources,  NO-
fractions from  sources  do vary somewhat with source  type  and (2) conversion of NO  emissions
to NO. 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 NO, 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.
Statistical Abstract, 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 NO-).  These authors also estimated the ratio
of natural emissions of NOX from terrestrial and aquatic  sources to those from anthropogenic
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 1.  The downward revision was
based on a 55 percent lower estimate of the amount of NO- emitted by natural sources.

          TABLE 5-1.  ESTIMATED ANNUAL GLOBAL EHISSIONS OF NITROGEN DIOXIDE (ANTHROPOGENIC)
                           (10  metric tons per year, expressed as N0_)
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 NO  in the United States
     Table 5-2  and Figure  5-1  provide  historical  data on estimated emissions  of NOX 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 NO  EMISSION
                               6         ESTIMATES 1940-1970  x
                            (10  metric tons per year, expressed as NOp)
Source Category
TRANSPORTATION
Motor vehicles
Aircraft
Rai 1 roads
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:   U.S. EPA, 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.
population in 1970 (U.S.  Bureau of the Census, 1973).

                                          5-3

-------
    20
1  16
    10
              I
             1940
                         ALL OTHER SOURCES

                         (INDUSTRIAL. SOLID WASTE)
                                               STATIONARY FUEL

                                               COMBUSTION
                                 TRANSPORTATION SOURCES
                           1950
                                         1960
                                                       1970
                                YEAR
   Figure 5-1. Historic NOX emissions by source groups (U.S. EPA,
   1973).  (Values shown for each year are cumulative over source
   groups.)
                                5-4

-------
TABLE 5-3.g RECENT NATIONWIDE NO  EMISSION ESTIMATES
       (10  metric tons/yr, expressed as NO,,)

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
f Oil and gas production
01 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
HISCELLANEOUS
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
197S
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, 1977b.
i
OV

-------
 5
1

 «A*
 o

 (A
 I
 26
 20
  IS
  10
            ALL OTHER SOURCES (INDUSTRIAL.COLID WASTE!
                     TRANSPORTATION SOURCES
          J_
                     _L
J_
_L
_L
          1970    1971    1972    1973   1974    1975    1876

                             VEAR

Figure 5-2. Recent NOX emissions by source groups (U.S. EPA,
1976). (Values shown (or each year are cumulative over source
groups.)
                              5-7

-------
AQCR Urbanization'
Large Urban
Medium-iiztd Urban
Small Urban
Rural
Total
imiHiom,
10G tom/yr
11,71
5.30
2.36
2.88
22.25
       a. Urbanization » bated on largest SMSA population
          in in AQCR:
             Large Urban - SMSA 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. Miicelfaneoul 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
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 indus-
trial  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
considered.   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 Figure 5-4 reveals that, in general, major point sources make a significant contri-
bution to total NO  emissions in those areas where NO  emissions are high.  (In this discussion,
a major 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.  Exami-
nation 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 NO,.   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 Board of Air  Sanitation,  1966).  In San
Francisco, California, they are estimated to contribute about 56 percent  (California Board of
Air Sanitation,  1966), while  in  northwestern  Indiana the estimate is  8 percent (Ozolins and
Rehmann,  1968).  Motor vehicle emissions in Los Angeles  County,  California, increased 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
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

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  or
  o:
      O O & E3 E3
      *» O O O O
      O O O O O
<^\/% *v/ %^
                                        00
                                        h«
                                        0)
                                        M
                                        3
                                         X
                                        J3

                                        .s
                                         s

                                         0!

                                        Q
5-10

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I
 

        !

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Ul
I
                                    %p; X/;^p^;^

                                        \  A s /f S*f- •'
                                                                                      PERCENT
                 Figure 5-6. Percent NO, Bmissiom contributed by major point sources, by county (over 100 tom/yr)

                 (U.S. EPA, 1978).

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     TABLE 5-4.
NO/NOX RATIOS IN EMISSIONS FROM VARIOUS SOURCE TYPES
 Source Type
                           NO/N(3
Reference
Uncontrolled tall-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—
 K fuel oil
Industrial boilers—natural gas
Industrial boilers—#2 fuel oil
Industrial boilers—PS 300 fuel
Industrial boilers—#6 fuel oil
Industrial boilers—coal
Industrial boilers—refinery gas
Industrial boilers—natural gas and
 #6 fuel oil
Industrial boilers—natural gas and
 refinery gas
Diesel-powered passenger cai—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)
                                         Gerstle and
                          •v 0.50         Peterson, 1966
                                         Hunter et al.,
                         0.93-1.00       1979
                         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 Ioad)-(ful1 load)
                         0.90-1.00
                         0.95-0.99
                          •v 0.96
                         0.96-1.00
                         0.95-1.00
                          •v 0.95

                          •v 1.00

                          •v 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
Winuner and
Reynolds, 1962
Campau and
Neerman, 1966
                         0.13-0.28(idlerSouza and
                         0.73-0.92       Daley, 1978
                      (takeoff & cruise)
Earlier studies (Lozano et al., 1968; Chase and Burn, 1970) did not report
such high idle concentrations of HQ--
                                5-13

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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 NQ-/NO  ratios occur
                                                                            £.   X
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
percent 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  Board of Air Sanitation, 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 distribution
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 para-
meters 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
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 NH,-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 (U.S.  EPA,  1977a) has reported estimated NH, emissions for the United States at
                                          5-14

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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 NH, emissions resulting from fertilizer usage.
                 TABLE 5-5.   ESTIHATED 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
Ammoniator-granulators
Urea
Miscellaneous emission from
fertilizer production
Beehive coke ovens
Total
Ammonia
tons/yr
19,000
168,000
59,000
32,000
14,000
10,000
10,000
4,000
2,000
1,000
319,000
Emission 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
           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:  (U.S. EPA, 1977a).


     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,  1977).   As urea  is. rapidly
from feedlot-generated urine of
                           e
hydrolyzed  into  NH- and CO,, atmospheric contributions of NH.
                   •5       £                                 4
an  estimated  cattle population of 132 million in the United States could amount to 2 x 10  to

4 x 10  metric tons NH,-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

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S.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 contri-
buting an anthropogenically produced burden to stratospheric concentrations of N-O with conse-
quent potential  for  attenuation of the  ozone  layer (see Chapter 9) and  (b)  by contributing,
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
historical perspective.  Examination  of Table 5-6  reveals  that  the total nitrogen applied as
fertilizer 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-m'troso 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 (Federal
Register,  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, 1968; Marquardt, 1971; Hoffman et al., 1974).  Release of small quantities of N-nitroso
compounds may  occur  in the processing  of such products.   Emissions occurring as a result of
certain combustion processes have also been suspected.  Analysis for emissions of nitrosamines
(usually only N-nitrosodimethylamine) has been carried out as part of research programs
                                          5-16

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Ul
s
                                                I

                                            AMMONIUM NITRATE

                                            NITROGEN SOLUTIONS

                                            ANHYDROUS AMMONIA
                                            UREA
    1955
                   1960
                                1965


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

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

Haterial 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

  Numbers are rounded to two decimal  places.

Source:  HARGETT, 1977.

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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,  1977e),   although   Fine  et  al.  (1975)  reported  the  presence  of  several  unidentified
N-nitroso compounds in the exhaust of a truck diesel engine and an automobile internal combus-
tion 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 de
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 jr\ 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,  1977e;  U.S. EPA,  1975).   A  study, however, reported no detec-
tion  of  nitrosamines  in  emissions  from a  power plant using such  amine  additives  (U.S.  EPA,
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, 1977e).  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,  1972j  U.S.  EPA,   1977e).   Volatility and
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.
                                          5-19

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5.5.4  N-Nltrosamlnes In Food. Water and TobaccoProducts
     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).  Scanlon (1975)
has  summarized  a  number of the studies reported since 1970.  These recent studies concentrate
on processed meats  and  fish,  in which  m'trosamines,  nitrosopiperldine  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, I to 94 ppb DMN, 2 to 25 ppb diethylnitrosamine (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,
1977c,1977d,1977e).   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., 1975a,1975b).
     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).  N1-nitrosonornicotine  found in a variety of chewing tobacco products
indicates that  such  unsmoked  products may also be  sources of  exposure to N-nitroso compounds
(Hoffman et al., 1974).
                                          5-20

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5.6  SUMMARY
5.6.1  Sources and Emissions of NO
     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,
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.
     In most ambient  situations  nitrogen dioxide (NOg),  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 NO,).   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 NO-.
     In general,  the relationship between the magnitude of NO  emissions and resulting ambient
NO- 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
and area sources  contribute significantly in those places where total N0x emissions are high.
There are,  however,  considerable local or regional differences in the relative amounts of NOX
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
corresponding statistic in northwestern Indiana is only 8 percent.  Emissions may also exhibit
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
                                          5-21

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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 NQ"X in the atmosphere) include coal combustion, inefficiencies in handling and apply-
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 (NgO is not included in this estimate).
     The use of nitrogen-based fertilizer (which some researchers have implicated in increased
NpO  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 N0x, 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

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CHAPTER 5

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 97: 915, 1972.

Ashby,  H.  A., R.  C.  Stahman, B. H.  Eccleston and R. W.  Hum.   Vehicle emissions—summer to
     winter.  SAE  Paper  741053.   SAE Automobile Engineering Meeting, Toronto, Canada, October
     21-25, 1974.

Ayanaba, A.  and M.  Alexander.   Transformation  of methyl amines and  formation of a hazardous
     product, dimethylm'trosamine,  in  samples of treated  sewage  and  lake water.   J. Environ.
     Quality 3: 83-89, 1974.

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                        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 nitrosanu'ne 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 photo-
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,  1977), as are detailed discussions of reaction mechanisms (Baldwin
et al.,  1977; Carter et a!., 1978; Demerjian  et al., 1974; Falls and Seinfeld, 1978; Whitten
and  Hogo, 1977)  and  rate constants (Hampson and Garvin,  1975).  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
states of the oxygen atom, triplet-P oxygen atoms [0( P)], and singlet-D oxygen atoms [0( D)];
ozone (O,); symmetrical  nitrogen trioxide (NO,); dinitrogen pentoxide (N^O^); hydroxyl radicals


                                             6-1

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(HO);  alkylperoxyl  radicals  (R02);  acylperoxyl  radicals  RC(0)02;  and other  less important
species.  In the formulas, R represents a methyl (CH3), ethyl (CpH.,), 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 (N02) through oxidation by
the oxygen in air:
               2ND + 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
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 (HONO,):
                        N,0, * NO, + NO,                  *          (6-7)
                   or    2 5     3     2
                        N205 + H20 -»• 2HON02                          (6-8)
The following reactions may take place between oxygen atoms and N02 and NO:

                        N0? + 0(3P) - NO + 0?                        (6-9)
                   or     L     ,
                        NO, + OrP) + M - N03 + M                    (610)
                   or          ,
                        NO + or?) •»• M -» N02 + M                     (6-11)
         Also, NO and NO, may react to regenerate NO,:
                        N03 + NO -» 2N02                              (6-12)
              Nitrous acid is produced by:
                        NO + N02 + H£0 -» 2HONO                       (6-13)
         and may react bimolecularly to regenerate the original reactants:
                        HONO + 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                          ,
               3               450-700 nm .  •» 02 •»• 0(JP)             (6-15b)
              The singlet-D oxygen [0( D)J atom is much more reactive than the
         ground state triplet-P oxygen [0(-P)J 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:
                        O^D) + 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 N02 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  R024:
               R- + 02 $ R02-                                 (6-21)
Typically, the next  reaction  in the  series  converts NO to  NO. and produces  an oxyl  radical,
RO-:                                                       i
               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 (HO.) can react with a second NO to form N02 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 N02 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-
ple, 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 alkanes,
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,CH,CH,+ OH- •» CH,CH,CH,CH,- + H,0           (6-26a)
                     *  t  t  6     and  3  l  l  l     i
                                     •» CH3CH2tHCH3 + 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,
                                    ,   0.
                   CH,CH,CH,CH, + 0(4P) -^OH- + CH,CH,CH,CH,Q,-      (6-28a)
                     3223        and        32222
                                        0             ?°*
                                        -2QH- + CH3CH2CHCH3          (6-285)
The importance of both the OH and 0( P) reactions with alkanes is the generation of the peroxy-
alkyl radical  RQ^*,  which plays a substantial role in the conversion of NO to N02>  Rate con-
stants for alkane reactions are summarized by Hampson and Garvin (1975).
     The atmospheric  chemical  reactions  involving olefins have been widely studied (Carter et
al., 1978; Demerjian et al., 1974; Niki,  1978).  The most important reactions in which olefins
participate are with OH radicals, ozone,  and atomic oxygen, in that order.  The reaction of OH
with an  olefin, such as propylene,  may  proceed by addition  of OH  to the double bond or by
abstraction of  a H-atom from the olefin.   For propylene, for example, the reaction paths with
OH are:
                   CH3CH = CH2 + OH- •» CH3£HCH2OH                    (6-29a)

                                          OH
                                     -> CH3CHCH2-                     (6-29b)
                                     •*• CH2£H = CH2 + H20             (6-29c)

                                             6-5

-------
In each  case the  free radical product  will  quickly  react  with 0, to  produce  a peroxyalkyl
radical that is capable of converting NO to NCL.
     Ozone-olefin reactions are a source of free radicals and stable products in air pollution
chemistry.  The initial attack of 0, on an olefin produces an unstable intermediate, which may
decompose by  several  pathways  (Niki,  1978;  O'Neal  and Blumstein, 1973).   For  propylene,  for
example, the initial step in the reaction with 0, is believed to be:
         CH3CH-CH2
                                                      0.
                                                    0  0.
                                              CH3CH = CH2 + 03 -* CH3CH-CH2
         (6-30)
                                                   •0  0
                                                 CH3CH-CH2
Subsequent composition 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:
                   CH,CH = CH, + 0(3P) •»• CH,CH,- + HCO              (6-31a)
                     J       l         or  J  i
                                       •* CHgCO + CH-'               (6-3 Ib)
                                       or
                                       + 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,  1978;  Perry  et  al.,  1977).   For aromatic-OH
reactions, 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 0, or NO^, 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,  1978).   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 Q(3P), O^D), 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 * H,0 * ECO                        (6-32)
                            •                     C             _T
If one assumes  an  atmospheric concentration of 10   radicals  cm  ,  the rates of decay of HCHO
and CH,CHQ by reaction with OH are approximately 4.2 percent and 5.8 percent per hour, respec-
tively (Lloyd, 1978).
     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 * B + HtO                          (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.  Ihere appears to be general  agreement that the primary paths are:
                        HCHO + hv + H- + HCO                         (6-34a)
                                 and
                                  -» H2 + CO                          (6-34b)
     Moortgat and  Warneck (1919)  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- 	•»  H20 + 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).
     Eormaldehyde  photolysis represents  an  important  source  of radicals in  smog chemistry
through  reaction  of  the products  with 0,  yielding the  hydroperoxyl radical,  H02-.   Ihus:
                         H. + 02 + H	f  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-—O^T    H20 + H02- + CO                 (E)
                                         *"  6-7

-------
     A rate  constant  for reaction E was recently recommended by the NASA Panel for Data Eval-
uation (NASA, 1979).
     Acetaldehyde, CHjCHO, 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 	+  CHj + HCO-                      (E)
     Another primary reaction is the abstraction of hydrogen by the OH radical:
                         CH3CHO + OH- 	».  CH3 C(0)- + H20                (G)
     Subsequent reactions of the product radicals of reactions E and G with atmospheric 02 are
very fast so that one may write:
                         CH3CHO + hv  202    CH3Oj + HOj + CO                (H)
                         and CH3CHO + OH- * 02     CH3C(0)02« + H£0          (I)
     Acetaldehyde chemistry  thus introduces  thl chemistry of alkylperoxy  radicals (SOj) via
the methylperoxy radical, CH30*; and the chemistry of peroxyacyl  nitrates [BC(0)02N02] via the
formation of peroxyacetyl nitrate (PAN) from the acetylperoxy radical, CH3(CO)OA (see reaction;;
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).
     Ihe interaction with NO and N02 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.  Ihe radicals can be classed according to:
                   8-         alky]               0
                                                 it
                   BO-       alkoxyl            SC<         acyl
                   BOO-      peroxyalkyl         0
                                                RCO-        acylate
                                                 0
                                                 ii
                                                BCOO-       peroxyacyl
In  air  it can  be assumed that combination with 02  is the sole fate of alky]  (B-) and acyl
(RCO-) radicals and that the reaction is essentially instantaneous.  Consequently, in reaction:;
with alky] or acyl radicals as products, these products are often written as the corresponding
peroxy radicals.  Also,  acylate radicals will decompose  rapidly  to give an alky] radical and
C02-   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
                          A
are important between these radicals and NO and N02.
     The reactions  of  OH with NOp 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, 1975).
     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

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

I


NO
Free Radical Reaction Reference
OH

HO,


RO

R02

RCO,


OH + NO •+ HONO Hampson and
Garvin, 1978
HO, + NO -> NO, + OH Howard and
i Evenson, 1977

RO + NO -» RONO Batt et al.,
(RONO + hv -» RO + NO) 1977
R02 + NO -f N02 + RO
-» RON02
RC03 + NO -» N02 + RC02 Cox and Roffey,
Aendry and
Kenley, 1977
N02
Reaction Reference
OH + NO, •» HONO, Tsang et al.,
i i 1977
on
H0? •*• N0? -> HONO + Op Howard, 1977*
-» HO,N05 Graham et al . ,
(HO,NO, -» HO, * N6,) 1977
£ £. £. £-
m + NO, -» RONO, Wiebe et al. ,
6 -» RCHO*+ HONO 1973
RO, + N02 * R02N02
(RO,NO, -> RO, + NO,)
c. C. £. L
RC03 + N02 -» RC03N02 Cox and Roffey,
(RCO^NO, ->• RCO. + NO,) Re'n'ary and
J * J ^ Kenley, 1977

-------
1977).  The HO--NO reaction, as noted earlier, is a key reaction in the atmospheric conversion
of NO to N02.
     The  reaction  of HO,  and N02  has  the following  two  possible mechanisms (Howard, 1977).
Reaction 6-35b is not considered to be important in atmospheric chemistry:
                        H02 + N02 ->• H02N02                           (6-35a)
                        H02 + N02 •» HONO + 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 N02 because of the rapid
thermal  decomposition reaction 6-36.  At lower temperatures HOgNO, will achieve higher concen-
trations and its importance as a sink for NO, increases.
     The  reactions of RO,  RO, 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 N02 are:
                        RO- -»- NO -» RONO                              (6-37a)
                                 or
                                 -» RCHO + HNO                        (6-37b)
                                and
                        RO- + N02 •» RONO£                            (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 N02 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
                        R02N02 •* R02« + N02                          (6-41)
Measured  rate  constants for  the RQ2~NO,  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
                        CHjCOO- + N02 J CH3CQON02                    (6-42)
         There exists a competition between NO and N02 for the peroxyacyl radical
         through:
                           0              0
                        CHgCOO- + NO -»• CH3CO- + 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 * CH3Q- + N02                    (6-22)
                        CH30- + 02 •» HCHO + H02-                     (6-23)
                        H02-> + NO •» OH- + N02                        (6-24)
Thus, PAN chemistry  is intimately interwoven  in  the NO to N02 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 NO- is accompanied by accumulation of 03-  NO- serves as both an initiator
and terminator  of  the chain reactions that  result  in conversion of NO  to  N02 and  buildup of
03-  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
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 N02 are created, photodissociation
of  HO2  will   be diminished and  less ozone will  accumulate on that  day.   At moderately high

                                             6-11

-------
(HC]/[NQX) 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 1 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 N02 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, W^NOp, is  unknown, and rate constants for the key
reactions in the series, R02 + NO, are yet to be determined.
6.1.2  Laboratory Evidence of the NOp-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., 1978; Demerjian et al., 1974; Falls and  Seinfeld, 1978; Whitten and Hogo, 1977).
Smog chambers have been used extensively to determine how concentrations of NOX and other photo-
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 NQp 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 m3) 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)
   • 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.,
     1975)
   • 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
   • 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 (1978,1979) 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 N02 and average N02 on NO  input.  With other factors held constant,
maximum NO- 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 NO--
     There   is  less  agreement among  the  chamber  studies  concerning the  dependence of N02 on
initial hydrocarbon  concentrations.   With  respect  to  maximum NO-,  the  Bureau  of  Mines study
indicates essentially no dependence on hydrocarbons.   However, three other studies suggest that
hydrocarbon  reductions decrease maximum NO- concentrations.   The UNC,  General  Motors, and UC
Riverside studies indicate  that  50 percent hydrocarbon control  tends  to decrease maximal HQ^
by 10-20 percent, 25 percent, and 10-15 percent, respectively.
     With respect to  average NO-,  the Bureau of Mines study indicates that hydrocarbon reduc-
tions would tend to increase NO- dosage.  This result is consistent with the theoretical argu-
ment of  Stephens (1973), who hypothesized that hydrocarbon  reduction  would increase average
NO- 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 N02
concentrations.  The UNC experiments imply that a 50 percent reduction in hydrocarbons produces
about a 20  percent  decrease in  average NO-.  There is some question about the UNC conclusion,
however, because the UNC chamber runs were of a 10-hour duration and the NO- levels at the end
of the experiments were greater when hydrocarbons were reduced.  The extra N0  remaining after
                                             6-13

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                            TABLE 6-2.  SUMMARY OF CONCLUSIONS FROM SMOG CHAMBER EXPERIMENTS
0>
I

CHAMBER STUDY
University of North
Carolina (Jeffries
et al., 1975)
Bureau of Mines
(Dimitriades,
1972,1977)
General Motors
(Huess, 1975)
UC Riverside
(Pitts et al.,
1975)
new, Auto exhaust
(Korth et al.,
1964)
ntw, loiuene
(Altshuller et
al., 1970)

MAXIMAL
Dependence
on NOX
Proportional
or slightly
less than
proportional
Proportional
Slightly less
than propor-
tional
Proportional



N02
Dependence
on HC
50% HC reduc-
tion reduces
maximal NO,
by 10% to 20%
No effect
50% HC reduc-
tion reduces
maximal NO,
by -25% i
50% HC control
reduces maximal
N09 by 10% to
15%



AVERAGE
Dependence
on NOX
Proportional
or slightly
less than
proportional
Proportional
Proportional
to slightly
less than
proportional
Proportional
Proportional


N02
Dependence
on HC
Uncertain, 50% HC
reduction may de-
crease average
N02 by 20% or may
increase average
N02
50% HC reduction
increases average
N02 by 10% to 30%
No effect
No effect
No consistent
effect
No offnrf


-------
the 10-hour period could cause an increase in 24-hour average NO-, 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  NO, 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.
     Some additional  support  for these conclusions was provided recently by studies of actual
ambient data on NOX and hydrocarbon levels from a number of cities in the U.S.   Using empirical
modelling and  historical  trend  analysis,  Trijonis (1978,1979) concluded that the ambient data
were  generally consistent  with  the  consensus  of chamber  results.   The  exact form  of the
N0-/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,
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 example, 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 vehicle, the relatively high NO concentrations which may be present can pro-
duce NO, in significant amounts through reaction 6-1 given sufficient 0-.  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 Oj
is entrained  into  the plume by turbulent mixing (Hegg et al., 1976;  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  NO,  with N03  and t^O
(reactions 6-10  and 6-8).  The generation  of  nitrous acid is also probable since the stack
gases will contain  NO,  NO,, and H-0 (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 be 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., 1976; 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.,  1978; Denterjian 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 HO, with NO and
NOn,  the  inorganic portion  of the photochemical  smog mechanism  is now, by and large,  well
understood.  Uncertainties remaining include
        • photolysis rates
        « alkane-QH 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:
                    OS
               Kj = I aj(A)4.J-(A)I(A) dA                     (6-45)
                    o

                                             6-16

-------
where
               K.    = photolysis rate constant for species j
               iW = quantum yield for the photolysis of species j
               I(M  = actinic irradiance
Data applicable to some atmospheric systems have been compiled by Schere and Demerjian (1977). '
For  species  such as  NOp,  HOMO,  and  0,, 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 0, to form peroxyalkyl (RO,)
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 f^,
the  reaction  mechanism  becomes  uncertain.   Alkoxyl  radicals  can  decompose,  react  with  0^,
isomerize, 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, isonerization, and reaction with 0-, NO, and NO, 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.  Qlefin-QH reactions may proceed by addition or  abstraction.  For smaller ale-
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  0.  to  form hydroxy-peroxyalkyl  radicals  and thereafter  react with  NO to  give  N02  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 Q~ are most  likely possibilities.
     The inherent uncertainty of the decomposition, reaction with 0-, and isomerization of the
alkoxyl and hydroxy-alkoxyl radicals class  can be represented by  the generalized  reaction step:
               RO -> aH02 •*• (l-ci)R02 + pHCHO + yRCHO         (6-46)
                                             6-17

-------
From the  earlier discussions of alkoxyl  radical  behavior,  RO always gives rise to either HO,
or R02  in any of the decomposition, isomerization, or 0, reaction pathways.  Hence, the stoi-
chiometric coefficients  representing the fraction of HO- and RO- found in the lumped RO reac-
tion should sun 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, o
can have a value in the range 0 to 1.  Many RO reaction routes produce aldehydes.  Thus, 0 < p
< 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 unc
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:
          HONO           nitrous acid
          HONO-          nitric acid
          HOgNO-         peroxynitric acid
          RONO           alkyl nitrite
          RONO,          alkyl nitrate
                    0
                   RCOON02        peroxyacylnitrate (PAN)
          ROjNO,         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-NQ  chemistry.  Table 6-3 lists calculated concentrations of HONO,
HON02, HOoNO,, RONO,  RON02> RC(0)OON02, and R0-N02 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- 03, 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
HO,NO,
2 2
RONO
RON02
0
11
RCOON02
R02N02

60 min.
0.0061
0.067
0.00083

0.0030
0.0041


0.025
0.034
Concentration, ppm
180 min.
0.00040
0,22
0.0019

0.00054
0.0070


0.089
0.075

300 min.
0.00036
0.29
0.0025

0.000080
0.0072


0.13
0.098

         Conditions of the experiment:   T = 303°K,  k, = 0.3 min  ,  [NO,]   = 0.106,
              [NO], = 0.377,  [H,0]  = 2.4 x 10*,  [CQP= 0.96, [Aldehyde!]" = 0.0012,
              [Alkinesl  = 1.488, (Non-ethylene  OlefinsL = 0.15,  {C,H.]° = 0.875,
              [Aromatici]  = 0.177, [HONO]  (assumed},= 8.1 (All  concentrations in
              ppm).  Dilution rate  = 2.93 8 10   min

     The concentrations  of HONO, H02N02, and RONO  are predicted  to be small relative to those
of NO and NO,.   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,
HOJW, may accumulate.
     Under daytime conditions the reactions that govern the concentration of KONO 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][NQ2][H201
                       [HONO] =         R^                          (6-48)


At  [NO] = [N02]  = 0.1 ppm,  [H20]  = 2.4 x 104 ppm (50 percent relative humidity), the equili-
brium HONO concentration calculated from equation 6-48 is 1.9 x 10   ppm.
     Like HONO,  HOgN02  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 NO, 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  H02N02
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,N02  and  PAN.  Assessment  of the
importance of  ROgNOg  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 NO,.  Beth 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 nucle
ate to form particles.
     Figure 6-1 depicts the potential paths by which particulate nitrate species may be formed
from NO and N02.   Path 1  involves  the  formation of gaseous nitric acid  by reactions S-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.NQ, (path 2), which at standard temperature and pres-
sure,  exists as a solid.   Alternatively, the nitric acid vapor may be absorbed directly into a
particle  (path 3),  although thermodynamic and kinetic  considerations  favor reaction with NHj
to form NH^NO, as the path of conversion of gaseous nitric acid to nitrate in particulate form
(Bradner  et  al., 1962;  Morris and Niki, 1971;  Stelson et al.).   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

-------
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-
merits have identified the participate nitrate as NH.NO,, suggesting that the aerosol may consist
                     +       •                     Ho
of solid NH.NO, or NH. and NO, 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 (Bradner et  al., 1962;.  Morris  and Niki,  1971; Stelson  et al.).

               NH3(g) * HON02(g) j NH4N03(S)                (6-49)

Second, the rate of absorption of NO and N0» 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  of NH,  is  required, either  to  form  NH.NO,  or to neutralize the
acidity of a liquid droplet in which NO and N02 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  N02 into aqueous droplets.   The relative rates of these two paths cannot
be  determined  in  general.   Although measurements of participate  organic nitrate levels have
been reported (Grosjean,  1979),  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, N02 is converted to nitric acid vapor and
NO  and N02 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 N02 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 participate 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 conc.en-
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 among
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, NO,,  and HNO, 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

-------


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-J^5^
^, XS°X' CIRCUMFERENCE
^ -^ ^ "^ OF EARTH
^^ r ^ ~ i
(Is I I i I I I
1m 10m 100m 1km 10km 100km 1000km 10,000km 100,000km

1 	 1
I 	 ,1
   MICROSCALE
METfOROLOGICAL
     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

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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. (micrograms per cubic meter) is removed across a horizontal surface of unit area at
an elevation  z   is often expressed as CjV. 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 NCL and NO from the
atmosphere.  Tingey (1968) showed that alfalfa and oats absorbed N00 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  N02 (or 1 x 10   moles per cubic meter).  More recent work by Rogers et al. (1977), using
a continuous  reactor technique,  indicated that the  NO,  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  NOp  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 HOy from the
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
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 N20) have long been known to be produced by biological action
in soils.  Recently,  however,  Abeles  et al. (1971) found that soils could absorb NQ2 from the
atmosphere as well.   They found that when air  containing N00 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
pg/m  (100 ppm) to 5.7 x 10  M3/m  (3-° PPm) over a 24-hour period.   When soil was autoclaved,
the total NO, present over the same  time period  was reduced from 186 x 10  vg/m  (97 ppm) to
only 25 x  10   pg/m  (13 ppm).   This result would point to a biological sink for N0« 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 N02 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 NOg.
Hortland  (1965) has noted that transition metal  ions  in the soil  promote  NO absorption.   If

                                             6-26

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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 nitrogen
oxides by soil is unknown.
6.3.2.2   Dry  Deposition of  Particles—The  deposition  of particles  can  occur  through sedimen-
tation, Browm'an  diffusion, or  impaction.   Impact ion occurs when,  because of  its  inertia,  a
particle  is unable  to  follow the streamlines of  air  around an obstacle and is intercepted by
the object.   The  removal  of* particles through impaction  on an object can be defined in terms
of a pseudo-deposition velocity, v .   The loss of particles per unit surface area of the object
per unit time can then be expressed as:
               Lj  =  -vgN,                                 (6-48)
where N is  the number density of particles  in  the size range corresponding to the deposition
velocity,  v .
     The transfer of aerosol particles from the turbulent atmosphere to an underlying boundary
depends upon  the flow  near the  surface,  as well  as upon the nature  of  the surface itself.
Particles are transferred through a turbulent boundary layer, the transport properties of which
depend on  the eddy motion of the turbulence.  Near the surface, the particles move through a
laminar sublayer, where the thermal  motion of the particles becomes  important.
     Particle  removal  from  the atmosphere by deposition strongly depends on the properties of
the  surface on which material deposits, the  surface  roughness, and the wind speed.   For the
purposes  of  an order-of-magnitude estimate  of deposition  rates, one  can  use  the  results of
Chamberlain (1967) to estimate v
6.3.2.3  Wet  Deposition—Precipitation can  remove gases and particles by two methods, rainout
and washout.   Rainout  involves the  various processes taking place within a cloud that lead to
the  formation of raindrops.   Washout refers to  the  removal  of.aerosols  below  the cloud by
falling raindrops.   Wet  deposition  removal  effectiveness probably varies with the form of the
precipitation, e.g., liquid versus  solid forms.   Rainout and washout, together with dry depo-
sition, are the major sinks for atmospheric nitrogen-containing species.
     Particles are  removed  by rainout through their  serving  as condensation nuclei for cloud
formation.  The extent of absorption of gases by cloud droplets depends on the chemical compo-
sitions of  both  the gases and the droplets.   Whereas the removal of SCL by cloud droplets has
received  considerable  attention, the  processes  taking place during the absorption of NO and
N02  by  water  droplets  have not yet  been  thoroughly  studied.   In  a study  of aerosol nitrate
formation routes, Orel and Seinfeld (1977) elucidated many of the chemical processes that occur
when  NO  and  N02  are absorbed  in water droplets.  The most  important factor  in the overall
efficiency of rainout  in removing oxides of  nitrogen from the atmosphere is the frequency of
rains.  Because  of  the difficulty in  describing  the  detailed processes occurring  in rainout,
it is generally assumed that removal  of pollutants by rainout can be described adequately by a
characteristic mean  residence time, and that the amount of pollutant removed by rainout at any
one place is  proportional to the ambient concentration of that pollutant.

                                             6-27

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     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 NOX by
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. (1973) suggests that for SO- 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  NOX 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 NO^ concentration experienced by a receptor, such as a human being,  due to given
emissions of NOX (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  N02 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.
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

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              (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 NOp 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 NO- concentrations.
     Assessment of the  specific impacts on air quality of the various source types in the NO,
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 NO,  problem,  currently underway at the USEPA 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 NO- con-
centrations very  close  to  a highway in  the absence  of all other NOX  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 NO, 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

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     In summary, it may be stated that the prospects for estimating NO- 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 nitrosaraine 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 terns 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 NO,.   The authors also report
that nitrosamine formation can be catalyzed by SO-.
     A fast reaction between diethylamine and NO- 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(NO,)/dt = k (dimethylamine) (NO,)2        (6-51)
                                      82-2  -1
with  a  rate constant  kc,  = 6,5  x  10  £  Mol    s  .   Initial  reactant concentrations ranged
            -fi            —*5      —1
from  4  x 10    to 6 x 10   Mol  i  .  The other major product of the  reaction  was the amine
nitrate (aerosol), corresponding to the overall equation:
          2 N02 + 2(C2H5)2NH •» (C2Hg)2NNO + (^Hg^NHgNOg   (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 + HgO                (6-54)
where R  =  alkyl group.  Addition of  tertiary  amines  (trimethyl, diethyl-methyl, and N-methy1
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 diethylamine 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.
     Oushumin and  Sopach (1976)  also report a rapid  reaction  between dimethylamine, N^O^ (in
equilibrium  with  NO,)  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 [(CH^JJNO^J, 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. (1977), and Pitts et al.  (1978) in experiments involving
dark reactions of ppm levels of alkylamines and nitrogen oxides in humid air.
     Hanst, Spence and Miller (1977), using long path infrared spectroscopy, followed the reac-
tion of  1  ppm dimethyl amine with  0.5 ppm HONO (in equilibrium  with  2 ppm NO,  2  ppm NO- and
13,000 ppm water vapor) in air in a 9 x 0.3 m diameter cylindrical glass cell.  Dimethylnitro-
samine was  formed  in yields of 10 to 30 percent, and the  rate  of  amine disappearance was ~4
percent min  .
     Grosjean et al. (1977) 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. (1967),  Hanst et al.  (1977) estimated an amine dis-
                              •*» 1
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  (1976/77) 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

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They found  the  reactions to be heterogeneous  under  all  surface conditions tested.  They also
estimated upper limits for the homogeneous rate constants:
               k, < 4.4 x 10"40 cm6 molecule"2 s"1
                •*• ~       -9fl   7         -1  -1
               k2 < 1 x 10 ^U cnT molecule l s l
which are more than 100 times slower than those of Chan et al. (1967).  Thus, homogeneous (gas
phase) formation of  nitrous  acid seems too  slow  to  account for MONO formation in the studies
of Hanst  at al.  (1977) and Grosjean and Pitts (1977,1978), 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 m'trosamines 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 (Onshima 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  NgOg (Mirvish, 1975; Ridd, 1961; Scanlan, 1975) according to the
reactions:
               2 HONO j N203 + H20                          (6-57)
               N2°3 + 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 NgO.,   (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 NO, in dry nitrogen  (i.e.,  under conditions not conducive  to the formation of
nitrous acid) was comparable to  that measured in the amine-HONO-NO  -water  mixture  in air (1
            -i                    _i                                  *
percent min  and 4  percent  min  , respectively).   Thus,  the  conflicting evidence currently
available does not permit fin 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., 1977;
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  [(CgHjJgNNO,]  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, dime thy! nitramine  ((CH-j^NNQ-]  and  several  methyl substituted amides in tlie 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

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     TABLE 6-4.   MAXIMUM CONCENTRATIONS  AND YIELDS OF THE PRODUCTS OF
DIETHYLAMINE AND TRIETHYLAMINE  (GROSJEAN ET AL.,  1977; PITTS ET AL.,  1978)

Product
GAS PHASE
Ozone
Acetaldehyde
PAN
GAS PHASE (by GC-MS)
Dark
Diethylnitrosaminec
Sunlight
Diethylnitrosaminec
Diethylnitramine
Diethylfornamide
Diethylacetamide
Ethylacetamide
A
Unidentified, MW=87a
Diacetamide

Frnm (T? 1'?

Maximum
Concentration
Formula jjg/m ppb

03 290
CH3CHO 300
CH3CO-OON02 41


(C2H5)2NNO 59 14

(C2H&)2NNO (destroyed)
(C2H5)2NN02 780 162
(C2H5)2NCHO 29 7,0
(C2H5)2NCOCH3 3.6 0.8
C2H5NHCOCH3 42 12
--
(CH3CO)2NH

NH

From (C0
Molar
Conversion Maximum
Yield, Concentration
%a Mg/irT ppb


30b
4b


2.8 17

38
32 177
1.4 178
0.2 15
2.4 48
41
trace

260
700
72


4.1

9.1
37
43
3.2
13
12


Hs¥
Molar
Conversion
Yield,


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)
TSP
Acetamide
D iethy 1 hydroxy 1 ami ne
Nitrates
Formula


CH3CONH2
(C2H5)2NOH
N03
From (C2-5-*2
Maximum
Concentration
Mg/B ppb
4 x 10'V1
60
3
42
NH
Molar
Conversion
Yield,
%a
46

0.2
From
Maximum
Concentration
M9/m ppb
x 10'V1
370
8.7
7.6
158
(C,H,)3N
Molar
Conversion
Yield,
r


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.
cNot corrected for artifact formation (maximum ~ 10% of the observed concentration).
 Assuming same mass spectrometer response as  diethyl acetamide.
eBased on volumes sampled:   27.9 m3 (DEA) and 30.8 ro3 (TEA).
d

-------
Sopach, 1976; Hanst et al., 1977), dime thy Irtitramine (Dushumin and Sopach, 1976; Tuazon et al.,
1978), and  the amine  nitrate  aerosol  (Dushurain  and Sopach, 1976; Gehlert  and Rolle, 1977).
     In the experiments conducted with secondary amines (diethyl and dimethyl), the m'trosamine
formed in the dark was progressively destroyed in sunlight, as was reported before for dimethyl-
nitrosamine  (Bretschneider  and Matz,  1973,1976;  Hanst et al.,"197?)  and diethyl m'trosamine
(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., 1977; 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 -» (C2Hj)2NCHCH3                (6-59)
followed by the well-known sequence ft + 0  •*• R6 , Rfl  + NO -* NO  + RO (Demerjian et al., 1974.
The alkoxy  radical RO  then decomposes  to  give two  of the major products, acetaldehyde and
diethylacetamide:
                        0
               (C2H5)2 NCHCH3 - CH3CHO  (C2H5)2N            (6-60)
                              •* (C2Hg)2NCHO + CH3           (6-61)
     Further reactions  of  acetaldehyde lead to PAN,  another major product.  • The diethylamino
radical, (C2Hr)2N,  reac-ts  with  NO  and  NO-  to form  diethylnitrbsamine 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
(CjHgJ-N with oxygen is very slow [this has received confirmation very recently in the case'of
NH, (Lesclaux and Oemissy,  1978)].
     A recent study by Calvert et al. (1978) of the photolysis of dimethylnitrosamine has shown
that the dimethy!amine radical,  (CH,),N, can  react  with  NO almost 10  times faster than with
                                 7
02 and with  NO, approximately 10  times  faster  than with 02-   Nitrous acid and CH,N=CH2 were
also identified as major products.   These results  suggest that dimethylamine radicals formed
in a NO-NOg-polluted atmosphere have a good chance of forming nitrosamines and nitramines even
though the concentrations of NO and NO- 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

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iU
I
5  5
t-
UJ
60
       40
       20
                             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

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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., 1977; Pitts et al., 1978).   In contrast, nitrosamines
photodecornpose readily:
                                   hv
                             R£NNO + 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,  19765; 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, 1976a) 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 *• I) 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 (Reefer,  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

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     Nighttime production of nitrosamines:  Conflicting results are presented in the literature
concerning nitrosaraine 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., 1977; Hanst et al.,
1977; Pitts et al., 1978) and tertiary amines (Grosjean et al., 1977; 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. (1977), 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,  nitraiaines,  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 nitrosantine
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.,  nitraniines  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  liO 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-dimethy1-acetamide,  has  been identified in
diesel  crankcase emissions (Southwest Research Institute, 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 NOX 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

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     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 N02 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
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  NOX and hydrocarbon  inputs  and resulting
N02 concentrations.   The results show that, with other factors held constant,  both average and
maximum N02 concentrations tend to be proportional to initial NO  inputs.   While some disagree-
ment is reported from different chamber studies on the precise effect of hydrocarbon reduction
on N02  concentrations,  a  consensus  would seem  to be as  follows:   Fifty percent hydrocarbon
reduction would have little effect on  average  NO- 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 NOX into aqueous droplets
                                             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 NCL 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.
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

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     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 -v 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 NQ~ 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 N0« 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

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CHAPTER 6

Abeles, F. B., L. E. Cracker,  L.  E.  Forrence,  and G.  R.  Leather.   Fate of afr pollutants:
     removal of ethylene,  sulfur  dioxide,  and  nitrogen dioxide  by soil.   Science 173:  914,
     1971.                                                                        	

Altshuller, A. P., S. L. Kopczynski, W.  A.  Lonneman,  F.  D,  Sutterfield,  and D.  L.  Wilson.
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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,  O.C.  20037.   EF78-32R,  May
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Atkinson, R., R.  A. Perry, and J. N. Pitts,  Jr.   Rate constants for  the reaction of the OH
     radical with CH,SH and CH,NH, over  the temperature range 299-426 K.   J.  Chem.  Phys.  66:
     1578, 1977.     332                                                        —

Atkinson, R., R.  A. Perry  and  J.  N.  Pitts,  Jr.   Rate  constants  for the reactions of the OH
     radical with (CH,),NH, (CH,)~N and  C9HcNH,  over  the temperature range 298-426°K.   J,
     Chem. Phys.  68: 1850, 1978T  4       * 5  i

Baldwin, A. C., J. R. Barker,  0.  H. Golden,  and  D.  6.  Hendry.   Photochemical  smog.   Rate
     parameter estimates and computer simulations.  J.  Phys.  Chem. 81:  2483,  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.
     Inter J. Chem. Kinetics Syinp. 1: 441,  1977.

Bradner, J. 0., N. M. Junk, J. W. Lawrence,  and  J,  Robins.   Vapor pressure of ammonium nitrate.
     J. Chem. Eng. Data 7: 227, 1962.

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

Bretschneider, K., and J.  Matz,   (Nitrosamines (NA) in the  atmospheric air and in the air at
     the workplace). Arch. Geschwulstforsch.,  42;  36,  1973.   (In  German).

Bretschneider, K., and J.  Matz.   Occurrence and  analysis of nitrosamines  in air.   Int.  Agency
     for Research on Cancer (IARC) Scientific  Publication No. 14:  395.   Lyon, France, 1976.

Calvert, J. G. and J. N. Pitts, Jr.  Photochemistry.   John  Wiley  and Sons, New York, New York,
     1966.

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.
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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 photooxielation  of
     propene and n-butane in photochemical smog.   Int. J. Chem. Kinetics, XX:  XXX, 1978.

Challis, 8. C., and S. A, Kyrtopoulos.  Rapid formation of carcinogenic  N-nitrosaraines in
     aqueous alkaline solutions.  Brit. J. Cancer  35: 693, 1977.

Chamberlain, A. C.  Radioactive aerosols and vapors.  Contemporary Physics 8:  561, 1967.

Chan, W. H., R. J. Nordstrom, J. G. Calvert, and J. H. Shaw.  Kinetic study of MONO formation
     and decay reactions in gaseous mixtures of HONO, NO, NO-,  H,0,  and  N,.   Environ. Sci.
     Technol. 10:  674, 1967.                               z   z        z

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

Cole, H. S., and 0. E. Summerhays.  A  review of techniques available for estimating short-term
     NO, concentrations.  Submitted for publication to J. of Air Pollut. Control  Assoc.,
     FeDruary 1979.

Cox, R. A., and R. G. Derwent.  J. Photochem. 6: 23, 1976/77.

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

Dana, M. T., J. H. Hales, and H. A. Wolf.  Rain scavenging of SO, and sulfate from power plant
     plumes.  J. Geophys. Res. 80: 4119, 1973.                  *

Darnall, K. R., W. P. L. Carter, A. H. Winer, A. C.  Lloyd, and  J. N. Pitts, Jr.   Importance of
     R0? + NO in alkyl nitrate formation from C4~C& alkane photooxidations under simulated
     atlospheric conditions.  J. Phys. Chem. 80? 1948, 1976.

Davis, 0. 0., G. Smith, and K. Klauber.  Trace gas analysis of  power plant plumes via aircraft
     measurement:  0,, NO , and SO, chemistry.  Science 186: 733-736, 1974.
                    4    X        £,                     ——

Demerjian, J., J. A. Kerr, and J. G. Calvert.  The mechanism of photochemical smog  formation.
     In:  Advances in Environmental Science and Technology, Vol. 4.  J.  N. Pitts, Jr.,  R.  L.
     Metcalf, and A. C. Lloyd (eds.).  John Wiley  and Sons, New York, 1974.

Dimitriades, 8.  Effects of hydrocarbons and nitrogen oxides on photochemical smog  formation.
     Environ. Sci. Technol. 6: 253, 1972.

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

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

Dushumin,  K.  K., and E. D. Sopach.  The role of reactions  of dimethylamine with nitrogen
     tetraoxide and ozone in atmospheric pollution.  Gig.  Sanit. 7:  14,  1976.

falls, A.  H., and J. H. Seinfeld.   Continued development of a  kinetic mechanism for  photo-
     chemical smog.  Environ. Sc1. Technol., 12: 1398, 1978.
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Falls, A. H:, G. J. HcRae, and J. H. Seinfeld.  Sensitivity  and  uncertainty  of  reaction
     mechanisms for photochemical air pollution.   Int. J. Chem.  Kinetics,  XX: XXX,  1979.

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

Gehlert, P., and W. Rolle.  Formation of diethylnitrosamine  by reaction of diethylanrine with
     nitrogen dioxide in the gas phase.  Experientia 33:  579,  1977.

Ghiorse, W.   C., and M. Alexander.  Effect  of microorganisms  on the sorption  and fate of sulfur
     dioxide and nitrogen dioxide in soil. J, Envir. Qual. f>:  227-230, 1976.

Goodall, C.  M., and T. H. Kennedy. Carcinogenicity of dimethylnitramine in NZR  rats and NZO
     mice.   Cancer Lett. 1: 295, 197i.

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.  Lutt.  51:
     215, 1977.

Grosjean, D.  Formation of organic aerosols from cyclic olefins  and  diolefins.   Chapter 19 in
     the Character and Origins of Smog Aerosol, Adv. in Environ.  Sci.  Technol., Wiley,, New
     York, 1979.

Grosjean, D., K. Van Cauwenberghe, J. Schmid, and  J. N. Pitts, Jr. Formation of nitrosamines
     and nitramines by photooxidation of amines under simulated  atmospheric  conditions;.   Paper
     No. 54, Proc. of 4th Joint Conf. on Sensing of Environmental Pollutants, New Orleans,
     Louisiana, November 6-11, 1977.  pp.  196-199.

Hampson, R.  F., Jr., and D. Garvin.  Reaction Rate and Photochemical Data for Atmospheric
     Chemistry—1977.  National Bureau of  Standards Special  Publication 513.  National Bureau
     of Standards, Washington, D.C., 1975.

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

Hegg, D., P. V. Hobbs, L. F. Radke, and H. Harrison.  Ozone  and  nitrogen  oxides in  power  plant
     plumes.  Paper 5-2. Proc. Int. Conf.  on Photochemical Oxidant Pollution and its Control.
     EPA-600/3-77-001a.  U.S. Environmental Protection Agency, 1976.

Heiklen, J.   Atmospheric Chemistry.  Academic Press, Inc., New York, 1976.

Hendry, D. G.  Reactions of aromatic hydrocarbons  in the  atmosphere. Workshop on Chemical
     Kinetic Data Needs for Modeling the Lower Troposphere,  U.S.  Environmental  Protection
     Agency and the National Bureau of Standards,  Reston, Virginia,  May 15-17,  1978.

Hendry, D. G., and R. A. Kenley.  Generation of peroxy radicals  from peroxy  nitrate (RO,NO_)
     decomposition of peroxyacyl nitrates.  J. Am. Chem.  Soc.  99: 3198, 1977.

Herron, J. T., and R. E. Huie.  J. Am. Chem. Soc.  99: 5430,  1977.

Heuss, J. M.  Smog Chamber Simulation of the Los Angeles  Atmosphere.   General Motors Research
     Publication GMR-1082, 1975.
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Hill, A, C.  Vegetation:  a sink for atmospheric pollutants.  J.  Air Pollut.  Control  Assoc.
     21: 341, 1971.

Horowitz, A., and J. 6. 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 NOg.   J.  Chem.  Phys.  67:5258-5262,  1977.

Howard, C. J., and K. H. Evenson.  Kinetics of the reaction of HO,  with NO.   Geophys.  Res.
     Lett. 4: 437, 1977.                                          £

Jackson, B., and F. I. Dessau.  Liver tumors in rats  fed  acetamide.   Lab.  Invest.  10:  §09,
     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,
     1975.

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

Keefer, L. K.  Promotion of N-nitrosation reaction by metal complexes.   Int.  Agency for
     Research on Cancer (IARC) Scientific Publication No.  14: 513.   Lyon,  France, 1976.

Keefer, L. K., and P. P. Roller.  N-nitrosation by nitrite ion in neutral  and basic medium.
     Science 181: 1245, 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, 1978.

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

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

Lesclaux, R., and M. Demissy.  On the reaction of  NH, radical with  oxygen.   Nouveau J.  de
     Chimie 1: 443, 1978.                           i

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

Liu, M., and D. R. Durran.  The Development of a Regional  Air Pollution Model  and Its Applica-
     tion to the Northern Great Plains.  EPA-908/1-77-001.  U.S.  Environmental Protection
     Agency, Research Triangle Park, North Carolina,  June 1977.

Lloyd, A. C.  Tropospheric chemistry of aldehydes.  Workshop  on Chemical Kinetic Data Needs
     for Modeling the Lower Troposphere.  U.S. Environmental  Protection Agency and the
     National Bureau of Standards, Reston, Virginia,  May  15-17, 1978.

Mirvish, S.  S.  Formation of N-nitroso compounds:  chemistry, kinetics and |n vivo occurrence.
     Appl. Pharm. 31: 325, 1975.
                                    6-45

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

Morris, E. D.,  and H. Niki.  Mass spectrophotometric  study  of the  reactions  of  nitric acid
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     514, 1965.                                                                        ~~

NASA,  Update of rate constant tables  in:  Upper Atmospheric Programs  Bulletin  Ho.  79-4,  9,
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     Data Needs for Hodeling the Lower Troposphere,   U.S. Environmental  Protection  Agency and
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Niki, H., P, D. Maker, C. M. Savage, and L. P. Breitenbach.  Chem.  Phys.  Lett.  46:  327,  1977.

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Perry, R. A., R. Atkinson, and J. N. .Pitts, Jr.  Kinetics and mechanism  of the  gas  phase
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Peterson, T. W., and J. H. Seinfeld.   Mathematical model  for transport,  Intel-conversion,  and
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                                            6-46

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Pitts, J. N., Jr., 0. Grosjean, K. Van Cauwenberghe, J, P. Schmid, and 0. R.  Fiti.   Photo-
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Pitts, J. N, Jr., A. M. Winer, K. R. Darnell, G. J. Doyle, and J. M. McAfee.  "Chemical
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Polo, J., and Y. L. Chow.  Efficient degradation of nitrosamines by photolysis.   Int.  Agency
     for Research on Cancer (IARC) Scientific Publication No. 14: 473.  Lyon,  France,  1976.

Ridd, J. H.  Nitrosation, diazotisation and deanrination.  Quart. Rev. Chem.  Soc.  (London) 15:
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Robinson, E., and R. C. Robbins.  Gaseous nitrogen compound pollutants from urban and  natural
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Scanlan, R. A.  Nitrosamines in food.  C. R. C. Critical Reviews in Food  Technology, 1975.  p.
     357

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Smith, P. A. S., and R. N. Loeppky.  Nitrosative cleavage of tertiary amines.  J. Amer, Chem.
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Southwest Research Institute.  Diesel Crankcase Emissions Characterization,  San Antonio,
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                                           6-47

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Tingey, D. T.  Foliar  absorption of  nitrogen  dioxide.   M.  A. Thesis,  Department of Botany,
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Trijonis, J.  Empirical Relationships Between Atmospheric Nitrogen Dioxide and its Precursors.
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Trijonis, J.  Dependence  of ambient  N02  on precursor control.   Session on Secondary Pollutant
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     Technical Symposium  on the  Implications  of a Low NO   Vehicle Emission Standard.   Reston,
     Virginia, May 1979.                                x

Tsang, W., D. Garvin,  and R.  L.  Brown.   NBS Chemical  Kinetics  Data Survey—The Formation of
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Tuazon, E. C., A. M. Winer, R. A.  Graham,  J.  P. Schmid, and  J.  N.  Pitts, Jr.   Fourier trans-
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Walker, P., J. Gordon, L. Thomas,  and R. Oulette.   Environmental  Assessment of Atmospheric
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Wartheson, J. J., R. A. Scanlan, D.  P. Bills, and L.  M. Libbey.   Formation of heterocycllc
     nitrosamines from reaction  of nitrite and  selected primary diamines and  ami no acids,   J.
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     163, 1969.
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White, W. H.  NO -0, photochemistry  in power plant plumes:   comparison  of theory with observa-
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     Carolina, January 1977.
                                    6-49

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             7.   SAMPLING AND ANALYSIS FOR AMBIENT NOX AND NOX-DERIVED POLLUTANTS

7,1  INTRODUCTION
     This chapter summarizes  a  variety of methods used for measuring oxides of nitrogen (NO )
and other pollutants which may be derived from NO  through atmospheric transformations (Chapter
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 r.
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.  Environmental
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 N02
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

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     A critical  analysis  of techniques for measuring  nitrogen  oxides in ambient air has been
reported  very  recently by  Saltzman (1979).   In  addition, a  historical  review  of  USEPA NO,
monitoring methodology requirements has been given by Purdue and Hauser (1979).
     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  NO-.  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-m'troso 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 NOg, 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,  1976)  upon  which  a
number of chemiluminescent  analytical  instruments are based.   These  analyzers,  once approved
by the U.S. EPA  (1975a)  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

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                  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,
ppm NO-
Low 0.02 to 0.08
Medium 0.10 to 0.20
High 0.25 to 0.35
Maximum Discrepancy
Specification, ppm
0.02
0.02
0.03
                                            7-3

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     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-
nodified 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  NO-
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  NOg
and/or nitric acid  (HNO,) 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 NOX
     Many methods  have  been used to measure NO  concentrations in air.   Some of these methods
                                               X
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 NCL 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 NO, 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.WO 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 NOg molecules, the
number of which  is proportiona.l to  the  NO concentration.  Some of  the  excited NOg 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 NO, 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 NO- concentrations.
     Catalytic reduction of NO, to NO is commonly employed in chemiluminescence NQ-NOX  instru-
ments.  These instruments  measure  NO  alone by passing  the  sample  directly to the detector.
The total concentration of NO and N02 (NOX) is measured by drawing the sample through a cataly-
tic reduction unit prior to entering the detector.  N02 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 NO,  but  peroxyacetyl  nitrate  (PAN) and a
                                            7-5

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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 (NH,) to NO  (U.S. EPA, 1973).    This  can  be of importance in measuring NO, exposures
in animal studies, where  elevated levels of NH, 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  NO, concentrations
                            3
ranging from 50  to 300 ug/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-Saltznian Method
7.2.2,1.1  General  description of method.  This chemical  method for collection and analysis of
NO- 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 N02 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.
     Hany 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, 1974).   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

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     If an extended  sampling  time is required in  the  manual  version,  the azo dye  may  suffer
bleaching by SO,-  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  NO, 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
Saltzman's  original  formulation  (1954)  or  his modified  version  (1960) the  stoichiometric
factor  has .been   reported   to be  0.72  (Saltzman,  1954,  1960; Saltzraan  and Wartburg,  1965;
Shaw, 1967).  Scaringelli  et  al.  (1970)  obtained  a  value  of  0.764.    However, recent work by
two California groups,     the California Air Resources Board (CARB) and the Air and Industrial
Hygiene Laboratory (AIHL) has shown that measurements performed by the  manual  Saltzman techni-
que are sensitive to the exact concentration of the coupling compound NEDA used in the reagent.
Careful evaluation 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
sensitive 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,  N02 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 NO, 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  EPA  (1975b).   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  procedures  by
means of a  reliable  NO- 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,  Aderaa  (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

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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 alky!
nitrites,  ethyl,  n-butyl, and  isoamyl  have  been  reported in  a manual  procedure  using this
solution  (Thomas  et a!.,  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 ug/m  (0.01 to B.O ppm).  Results of the
USEPA's quality assurance testing over the range 90  to 370 (ig/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 a!., 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  ManualSaltzman Procedure.   In  this  method, NO, 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 contajn-
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 N02 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
                         3
range of 10 to 9,400 pg/ro  (0.005 to 5.0 ppm).  A precision of 1 percent  of the mean concentra-
tion is obtainable (Intersociety Committee, 1977c).
     ASTH  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 NO,, with additional, accurately known, concentrations of NOg 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

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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 NOg 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 NO, concentration  range,  expected in health-related studies
                                                                                  3
which use  ambient air.  Maximum ambient NO,  concentrations were about 250  ug/m  during the
test and maximum total NO, (ambient plus spike) concentrations used in the test were about 400
    3
gg/in .   Extrapolation  of the test results  to  situations where high NO,  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  NO-, 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  Saltzman1 s  original  stoichioaetric 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 SOg 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 SO, 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).
     The National  Academy  of Sciences document on nitrogen oxides (National Research Council,
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

                                            7-9

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level, sampling-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
NOg  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  a!.,  1970; Huygen and Steerman,  1971;  Morgan et a!., 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 SO 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/m3 (0.01-fo 0.4  ppm) NO, (Katz, 1976).  Katz (1976) reported relative
                                                                                       3
standard deviations of  14.4  and 21.5 percent at NO, concentrations of 140 and 200 ug/m  (0.07
and 0.11 ppm), respectively.
     Because the  sampling  efficiency  and stoichionetric factor are  significantly affected by
the  details of the method employed, by  NO™  concentration, and by constituents  of the sample
other than NO,,  the use of many  modifications of the Jacobs-Hochheiser method in air quality
and  epidemic!ogical 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 spectrophoto-
metric  measurements.    Sampling   efficiencies  up  to  95  to   99  percent  have  been  reported
(Intersociety  Committee,  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 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 USEPA 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,  0,,  or NO at  ambient levels and the sample solutions are stable for three
weeks after  sampling.   The  accuracy  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 (Na,As0.j)
to absorb  NO,  was described by Christie  et  al. (1970) and Merryman et  al.  (1973).  Christie
                                            7-10

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et al. reported  a collection  efficiency of 95  percent using an orifice  bubbler.   The USEPA
recently  has  evaluated  the  sodium-arsenite procedure  (Beard  and  Margeson,  1974) and  has
designated 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
efficiency for NO,  of 82 percent over the  recommended useful concentration  range,  20  to 750
    3
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., 1975c).  EPA concluded that the
measurement errors were essentially uniform for all collaborators,  although some dependence on
NO, level was noted.   Eight of ten collaborators exhibited a uniform percent bias over all N0~
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  sulfanilainide 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 percent  of the NO,  actually present.  Carbon dioxide,  in  excess of  typical  ambient
concentrations,  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 CO,  interferences (Beard et
                                                           •3         '
al., 1975).  Results show that, in the range 50 to 310 ug/m  (0.04 to 0.25 ppm) NO and 360,000
to 900,000 ug/m  (200 to 500 ppm) CO,,  the average effect of these interferents is to increase
                                      3                              T
the indicated  NO, response  by 10 ug/m  over the range 50 to 250 ug/m  NO, (0.03 to 0.13 ppm).
7.2.2.5   TGS-ANSA Method—A  24-hour manual  method for  the  detection and analysis  of  NO, in
ambient  air,  the TGS-ANSA  method  was  first  reported by Mulik et  al.  (1973).   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 (NOg)
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-
                 •j                                                                 *
tion  of  100  ug/m  (0.05 ppm) for the following pollutants at the levels shown in parentheses:
                                            7-11

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ammonia  (205  ug/m3 or  0.29 ppm); CO  (154,000  ug/m3  or 134 ppm); formaldehyde  (750  ug/m3  or
0.61 ppm);  NO  (734 ug/m  or 0.59 ppm),  phenol  (150 ug/m  or 0.04 ppm);  0, (400 ug/m3 or 0.2
                       ^
ppm); and SO. (439 ug/m  or 0.15 ppm).  The absorbing reagent is stable for three weeks before
sampling  and  the  collected samples  are stable  for  three weeks  after sampling  (Fuerst  and
Margeson, 1974; Hulik et al., 1973).
     Results  of  USEPA's collaborative  quality  assurance  testing  (Constant  et al.,  1974)
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-
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 N02 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 NO-
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. reported an
extensive comparison of both intra- and intermethod accuracy and precision of.the chemilumines-
cent, sodium arsenite,  TGS-ANSA and  continuous colorimetric (Lyshkow modification) procedures
for NO- measurement (Purdue et al., 1975).   The study was conducted under carefully controlled
laboratory conditions using  skilled  technicians.  Ambient air  spiked  with NO- was sampled by
two identical   instruments for  each method tested.  In the case of manual methods four samples
were taken.   The NO, spikes  were varied randomly from day to day over a 20-day sampling sched-
                                          3
ule.  Spikes  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  NO,.  The worst case of intramethod differences occurred with
                                                                             3
the continuous colorimetric  method where there was a  small  bias of 7.5 ug/m  NO- 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 NO, 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 ug/m , no interference was detected.   At NO concentrations as high as 302 ug/m
no  interference was  found in the sodium arsenite procedure,  although NO  has  been  cited as a
positive interferent in the method.

                                            7-12

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   TABLE 7-3.  STATISTICAL ANALYSIS OF N00 MEASURING METHOD  DIFFERENCE
(M9/m3)
Sampling Spiked Ambient Air

Comparison
Intramethod
Chemil/Chemil
. Color/Color
ARS/ARS (A)
ARS/ARS (B)
TGS/TGS (A)
TGS/TGS (B)
ARS (A)/ARS (B)
RGS (A)/TGS (B)
Intermethod
Cheinil/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
(Mi/nO

1.3
7.5
0.6
0.2
-0.9
0.2
-2.6
0.6

3.8
-1.9
5.6
-3.8
3.8
7.5
95%,
Standard
Dew.

5.6
7.5
5.6
5.6
3.8
9.4
5.6
7.6

7.5
9.4
9.4
11.3
11.3
7.5
C.
Lower

-1.1
3.8
-1.9
-1.9
-1.9
-3.8
-5.6
-3.8

0.0
-5.6
+0.9
-9.4
-1.9
+3.8
I.u
Upper

3.3
11.3
+3.8
1.9
0.8
+3.8
+0.1
+3.8

+7.5
+1.9
9.4
1.5
9.4
11.3
Corr.
Coeff.

0.999
0.995
0.997
0.996
0.999
0.992
0.997
0.996

0.994
0.991
0.990
0.989
0.985
0.994

Extracted from Purdue
1>C ' A' ft
et al.,

1975.









€Standard deviation.
 95 percent confidence interval  of mean difference.
Correlation coefficient between paired values  in calculating  mean
 difference.
                                  7-13

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     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.,
1974, 1975a,  1975b,  1975c).  In this  type  of testing,  a number of  collaborators,  following
analytical procedures according to  specified guidelines, sample the  same  ambient  air spiked
with known N02 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 NCL  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 ug/m  NOp.  "Acceptable"  limits for the difference between measured NO-
values and  known  audit NOp  concentrations were  established for the purposes  of the study at
+19, +30,  and  +71  ug/m3  respectively.  At  the   0 audit level all  23 analyzers were within
limits;  at an  audit level of 150 ug/m , three analyzers were  found to "very narrowly" exceed
specified  limits;  at 355  ug/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 N02 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 NO
     Sampling  technique is   a particularly  important consideration for the  measurement of NO
and NOp.   Nitric  oxide  and NO* in the atmosphere during the  day are involved  in  very rapid

                                            7-14

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  TABLE 7-4.   SUMMARY OF RELIABILITY OF  NO, ANALYTICAL  METHODS  IN  COMMON USE  AS OBTAINED BY COLLABORATIVE TESTING
              (CONSTANT ET AL.,  1974, 1975S, 1975b.  1975c)
Method
Chemi luminescence
(Reference Method)
Sodium Arsenite
(Equivalent Method)
TGS-ANSA
(Equivalent Method)
Range of NO.
Concentrations
Used in,Test
(ug/«3)
80-300
50-300
50-300
Griess-Saltznan 90-370
(Continuous Colorimetric
with dynamic calibration;
both variants cited in
7.2.2.1)
Bias
(Average
for all
Tests)*
-8 ug/m
or
-5X
6.2 ug/m3
or
1.3X
9. 5 ug/m3
or
i. -5X
16.1 ug/m
or
v 6X
Standard
Deviation
(Average
for all
Tests)4
14X
11 M9/n3
11.6 M9/m3
32. 7 ug/m3
Practical
Lower
Detection
Limit
(ug/m ) Comments (Reference)
<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)
< 9 Measurement errors were essentially uniform
for all collaborators, although some depen-
dence on NO. level was noted. 8 ef 10 col-
laborators exhibited a uniforn percent bias
over all NO, levels tested. (Constant et. al.,
1975c) 2
<15 Errors were essentially uniform for all col-
laborators. The biases shown were nearly
independent of NO. level for range tested.
(Constant et al./1974)
<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)
aOepends in detail  upon NO^ concentration.
Depends significantly on laboratory performing test.

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                     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
(ug/m )
0
150
355
"Acceptable"
Limits for
Difference
(ug/ni )
+19
+30
+71
Number
Outside
Limits
0
3
1
Average
Difference
for Network
(ug/m3)
+2
-11
-28
Standard
Deviation
for Network
(ug/m )
6
15
26
reactions which keep 03 in a photostat!onary state.  The rate of photolysis of NO- (forming NO
and 0  and thus  03)  is nearly  equal to  the reaction of  the  NO and 0, to  form  NO-.   When a
sample is drawn  into a dark sampling line, photolysis ceases while NO continues to react with
0,  to  form NCL.   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 NO- 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 NO-, it is necessary
to  remove  NO- from  the  sample, then oxidize NO  to NO-  and  measure the  NO- concentration.
Several selective absorbers for NO- have been employed, but some of the NO- is converted to NO
in  all  the absorbers  tested.   Absorbents include Griess-Saltzman  reagent (Huygen,  1970) and
granules  impregnated with  triethanolamine  (Intersociety  Committee,  1977c;   Levaggi  et al.,
1972).   The triethanolamine is reported to be the best absorbent, with only two to four percent
of the incoming NO- converted to NO.
     When NO  is  to be measured by a method specific to NO-, either with or without removal of
NOp  from the  sample,  it  is necessary   to  oxidize NO  to  N02 in  the  gas  phase.   The most
frequently  used  oxidizer  is chromic oxide  on a  fire  brick   granule  support (Intersociety
Committee, 1977c;  Levaggi  et al.,  1974).  This material  gives  over 99 percent oxidation when
the relative  humidity in  the  sample  is  between 20  and  80 perce.it.  The chromic oxide also
removes S02-
     Considerations  relating to the reduction of N02 to NO have  been discussed in Section 7.2.1.
7.2.5  Calibration of NO and NO,, 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

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    1.0 oh—|
               t HUH    i ii iimi    I  i
0.002h

0.001
   0.001
                   0,01          0.10


                 NO CONCENTRATION, ppm
Figure 7-1.  Absolute error in NO2 and AND? for 10
seconds in dark sampling line (Batcher and Ruff, 1971).
                         7-17

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     Standard gas  sources  are the principal means by which NO and NO. 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),     nhotolvsis of
known N02 concentrations and rapid dilution (Guicherit, 1972).
     The permeation  tube is the only direct  source  of dilute NO2 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 NO- 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, 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, N02, PAN, H2S04, 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 N02 concentrations
(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 microcoulometrlc 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 NO, were reported over a range of NO, concentrations up to 15,000
    3                                                    3
Hg/m  {8.0  ppm).   The  equivalent of about  1 ug NO,-N/m  of artifact gaseous  nitrate corre-
                    3
sponded to 188  pg/m  (0.1 ppm) NO, 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 yg/m  (0.73 ppm) NO,.  Interferences from PAN and n-propyl
nitrate were  cited as  negligible or very small.   Nitrate  formation from  NO-  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 forNitrate 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 (Federal Register, 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.  SWtttRY OF NITRIC ACID DETECTION TECHNIQUES*
 I
rj
o
Technique
Cheai luminescence
Chenlliminescence
Fourier Transforn
Spectrometer
Hlcroeoylometry
Colorfaetry
Colorinetry
Electron Capture
Gas Chro«atography
Procedure
Staple Modification of cheiilunin-
escence procedure used for NO
Adaptation of sensitive che«i1liMln-
escence NOX monitor described by
Hitter et al, , 1978
Long path infrared speetranetry
Sample conditioning with ethylene to
remove ozone interference; differ-
ence method using direct reading
and reading after nylon trap which
removes UNO,
Reduction to KH* of fixed organic
nitrogen collected on nylon filter,
followed by tndaphenol ammonia
test. Teflon pref liter.
Collection of HNO, on NaCl impreg-
nated filters, followed by extrac-
tion and hydrazine reductlon-
diazotization analysis of nitrate
Collection of HNO, on nylon or cot-
ton, extraction, conversion to
nitrobenzene analysis by gas
chronatography
Minium
Detectable
level (ppbv)
5.0
0.3
S.O
5.0
<0.1
0.1
0.1
Interferences
Tested
For, To Datt
NO, HO,, PAH, organic
nitrates
NO, NO., PAN, organic
nitrates
Host gaseous species in
noraa) ambient air
0,, NO., SO,, H2SO,,
HC1, HCHO, PAVHCOOH,
HN02
NH!, particulate
nitrate
NO,, partlculate
nitrate
NO., particulate
nitrate
Reference
Joseph and Sptcer, 1978
Kelly and Steiten, 1979
Likens, 1976
Tuajon et al.,
1979, 1978
Miller and Spicer, 1975
Spictr et at., 1978a, »78b
Lazrus et al. ,
1968, 1979
Okita et al., 197670
Forrest it at., 1979
Hare tt al., 1979
Tesch and Slevers, 1979
(toss et al., 1975
           'Adapted from Stevens and HcClenny, 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  (1976, 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, N00 as nitrate.  Cellulose acetate and nylon filters
                                            C      f
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  NO- concentra-
                 3
tions of 592 ug/m  (0.315 ppm).  When a variety of quartz filter types were tested, the great-
est quantity  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 ug/m   (2.4 ppm)  NO-  through the  filters.  The  relative  humidity was 30 + 10 percent.
     Most recently,  Spicer  and Schumacher (in press)  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

-------
-J
I
ro
ro
                       TABLE 7-7.  COMPARISON OF NITRATE COLLECTED OH VARIOUS FILTER3 TYPES
                                   (SPICER AND SCHUMACHER, IN PRESS; SPICER ET AL., 1978a)

Date
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.

15
18
19
20
21
22
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
m~
ugfw
1.6
1.6
14.4
0.39
17.0
1.2
28.7
2.3
18.8
0.82
11.2
0.49
38.4
0.78
Date
Oct. 26
Oct. 27
Oct. 28
Oct. 29
Nov. 1
Nov. 2
Nov. 3
Filter
Quartz 1
Quartz 2
Glass 2
Quartz 2
Glass 1
Quartz 2
Quartz 1
Quartz 2
Quartz 2
Quartz 2
Glass 2
Quartz 2
Quartz 1
Quartz 2
N03'3
ug/n 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
Filter
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"
ug/«
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
        aGlass 1 - "EPA Type" Gelman AA.

         Glass 2 - Gelnan A.

         Quartz 1 - High purity quartz filter developed by Arthur D. Little under contract to EPA.

         Quartz 2 - Pal Iflex 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,  in
press) have conducted several  studies  bearing on both positive artifact formation and loss  of
nitrate  from  a variety of  filter media (Appel et al.,  1979,  Appel et al.,  in  press).   They
concluded that gaseous HN03 is the principal source of artifact nitrate formation, NO- collec-
tion only became substantial at high ozone levels.  Ambient participate nitrate values (at San
Jose and Los  Alamitos,  California)  differed 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 (in press).  Fluoropore (Teflon) filters in low volume samplers were subject to
small error although, under laboratory conditions, passage of  NH,-  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 pressure of ammonium nitrate (see page 6-49).   They
also reported that at low HNO, 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  (C-jH-gN-O^)  (Intersociety
Committee, 1977a, Jenkins and Medsker, 1964; Lunge and Lwoff, 1894; Robinson et al., 1969) or
phenoldisulfonic acid (ASTM, 1968; Beatty et al., 1943; Easthoe and Pollard, 1950; Intersociety
Committee, 1977d; Taras,  1950). Newer procedures  extensively used to analyze nitrate in atmos-
pheric particulate matter extracts involve the nitration of xylenols [(CH-jKCgH^OH] and separa-
tion  of  the  nitro-derivative  by  extraction or  distillation (Andrews, 1964;  Buckett et al.,
1955;  Hartley and Asai,  1960; Holler  and Huch,   1949;  Intersociety  Committee,  1977b; Swain,

                                            7-23

-------
1957; Yagoda  and Goldman,  1943).  Recent comparison  of a 2,4-xylenol procedure (Intersociety
Committee  1977b)  with  the  automated  copper-cadmium  reduction  and  diazotization  method
(Technicon, 1973)  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,QH.(QH)2(S03H)2]  (West  and Ramachandran,  1966)  and
couaiarin  (CgHgO,) analogs  (Laby and Morton,  1966;  Skujins,  1964)  also have  been reported.
Snail amounts  of nitrate can be assayed by  the quenching of the fluorescence after nitration
of  fluorescein  (^20^12^5^  (Axelrod et al., 1970).  Nitrate  analysis can also be accomplished
through reduction with Devarda alloy to ammonia (NH,) (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 (NHgNHg)  (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 [Sb2(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
(Intersociety Committee,  1977a).
     Kitrate 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 alkaline
absorbent (Altshuller  and Wartburg, 1960)  or nitrate  (Cawse,  1967)  obtained  after oxidation
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 measurement
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  conductometrie 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

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       was  reported.   The related  standard deviation  was 1  percent  (95 percent  confidence
level) for  ten replicate  injections  at the S  ug/m£  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 Hoffsomtner (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 chroraatographic 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 KNO, and KNO».
     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 Hoi ley, 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
(Kenney et  al.,  1970;  Langmuir and Jacobson, 1970).  The method, however, is not currently in
widespread  use.
                                            7-25

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             TABLE 7-8.  ANALYTICAL METHODS FOR NITRATE IN WATER
Method
                           Range
                           (mg/A
                     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
    cadmi urn
                          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. Oevarda's alloy
                            2 ->200
Szekely, 1975
O'Brien and
Fiore, 1962
APHA, 1976
Technicon, 1973
EPA, 1974
APHA, 1976
Strickland and
Parsons, 1972

Kemphake,
1976

APHA, 1976
                                   7-26

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     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 NO^ 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,  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 (NO^)
ion (Section  7.2.1).   Although nitrate is  readily  reduced by a variety  of  agents "including
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, 1973;  U.S.  EPA, 1974).  Techniques presently  recommended  to avoid
these difficulties  have  been  documented by the  American  Public  Health Association (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 quantitatively to ammonia by
Devarda's alloy and subsequently analyzed by titration or colorimetrically.
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., K-SO.  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

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                                TABLE 7-9,   METHODS  FOR DETERMINATION OF NITRATE IN SOILS
              Method
                        Range,
       Interferences
References
          1,  Ion electrode
                           2 -1400
ro
CD
          2.  Phenoldisulfonk      0.1-2
             acid

          3.  Brucine               0.1-2
4. Reduction of NO*      0.02-0.1
   by Cd Griess-  £
   Illosvay method

5. Reduction to NH~ by     1 -1000
   Devarda alloy, stean
   distillation of NH3

6. UV absorbance
Chloride, bromide, nitrite, iodide,  Carlson and
sulfide, ionic strength              Keeney, 1971

Chloride, organic matter, nitrite    Brenner, 1965
                                                   None
                                     Bri»ner, 1965; Brenner
                                     and Keeney, 1965,
                                     APHA, 1976

                                     Brenner, 1965; Brenner
                                     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.

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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  chrontatograph  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 (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 diehloromethane.   Before evaporative concentration,
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/mfi.   The TEA detector operates by
splitting the nitrosyl radical  off N-nitroso compounds coming  from  a chromatographic column.
                                            7-29

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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-m'troso responses (Hansen et al,, 1979; Krull et a!., 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 (Walter, 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-HS) 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 nitrosatnines.
     GC-HS  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 Vtestcott,
1976).
7.6  SUMMARY
     Since the  publication  in  1971 of the original document Ajr 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.

                                            7-30

-------
     With regard to the measurement of NO-, 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 Wy 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 NO,.   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

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CHAPTER 7

Adema, E. H,  Ozone  interference  in  the  determination  of  nitrogen  dioxide  by  a  modified manual
     Saltzman method.  Anal.  Chera. 51:1002-1001,  1979.

Afghan, B. K., and J. E.  Ryan.  Substituted  benzophenone  as  a  fluorometric reagent in  automa-
     tic determination of nitrate.   Anal.  Chem. 47:  2347,  1975.

Allen, S. E., and H. M. Griroshaw.  Effect  of low-temperature storage on  the extractable
     nutrient ions in soils.  J.  Sci. Food Agric.  13:  525-529, 1962.

Altshuller,  P. A., 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
     Wastewater,  14th edition, New  York,  N.Y., 1976.

Andrews, D.  W. W.  A sensitive method for  determining  nitrate  in water with 2,6-xylenol.
     Analyst 89: 730-734, 1964.

Appel, B. R,, E. H. Hoffer, E. L. Kothny,  and S.  M.  Wall.  Interference  in 2,4-xylenol
     procedure for nitrate determination in  atmospheric aerosols.  Environ. Sci. Techno!.  11:
     183, 1977.                                                                            ~~

Appel, B. R., S. H. Wall, Y.  Tokiwa, and H.  Haik.  Interference effects  in sampling particu-
     late nitrate in ambient  air.  Atm.  Envir. 13:319-325, 1979.

Appel, B. R., S. H. Wall, Y.  Tokiwa, and M.  Haik.  Simultaneous nitric acid,  particulate
     nitrate and acidity  measurements in ambient  air.  Atmospheric Environment:  in press.

American Society for Testing  and  Materials,  Committee  0-22 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:  0 1608-60  (Reapproved
     1967).  In:  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
     Atmospheres.  Standard method of test for nitrogen dioxide content  of the  atmosphere
     (Griess-Saltzman reaction) ASTM Designation:  01607-69.   In:  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
     Precision and Accuracy of the Measurement of Nitrogen Dioxide Content in the  Atmosphere
     Using ASTM Method 01607.  ASTM  Data Series Publication  OS55,  1974b.

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.  Die Bestiiwnung von nitrat in Tabak  durch  UV-spektrometrie.   Beitrage zur
     Tabakforschung 3(7): 455-459, 1966.
                                            7-32

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Bastian, R., R. Weberling, and F. Palilla.  Ultraviolet spectrophotometric determination of
     nitrate.  Application to analysis of alkaline earth carbonates.  Anal. Chem. 29: 1795,
     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.  Anat. Chem.
     47:515-521, 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, North Carolina, 1974.

Beard, M. E., J. C. Suggs, and J. H. Hargeson.  Evaluation of effects of NO, CO.  and sampling
     flow rate on arsenite procedure for measurement of NO- In ambient  air.  EPR-650/4-75-019.
     U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, 1975.

Beatty, R. L., L. B. Bergern, and H. H. Schrenk.  Determination of the  Oxides  of  Nitrogen  by
     the Phenoldisulfonic Acid Hethod.  U.S. Department of the Interior, Bureau of Mines.
     Report of Investigations 3687.  Pittsburgh, U.S. Bureau of Mines,  1943.   pp. 17.

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  NO* and NH,  by
     NO-measuring instrument.  J. Air Pollution Control Assoc. 23: 128-131, 19737

Bremner, J. H.  Inorganic forms of nitrogen.   In:  Methods of Soil Analysis.   Part 2.  C.  A.
     Black, ed. Agronomy 9: 1179-1237, Araer. Soc. Agron., Inc., Madison, Wisconsin, 1965.

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:
     Environmental N-Nitroso Compounds Analysis and Formation.  IARC Scientific Publication
     14: 395-399, 1976.

Brezonik, P. L., and B. 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. Ouffield, and R. F. Milton.  The determination of nitrate and  nitrite  in
     soil.  Analyst 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.   In:  Instrumental Methods for the Analysis of  Soils and Plant
     Tissue.   L. M. Walsh, ed. Amer. Soc. Agron., Madison, Wisconsin, 1971.

Cawse, P. A.   The determination of nitrate in  soil solutions by ultraviolet spectrophotometry.
     Analyst 92:  311-315, 1967.

Chow, T. J., and  M. S. Johnstone.  Determination of nitrate in sea water.  Anal.  Chim. Acta
   ' 27: 441-446, 1962.
                                            7-33

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Christie, A. A., R. G, Lidzey, and D. W. F, Radford.  Field methods for the determination of
     nitrogen dioxide in air.  Analyst 95: 514-519, 1970.

Clough, P. N., and B. A. Thrush,  Mechanism of chemiluminescent reaction between nitric oxide
     and ozone.  Trans. Faraday Soc. 63: 915, 1967.

Constant, P. C., Jr., H, C, Sharp, and 6. 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, North Carolina, 1974.

Constant, P. C., Jr., H. C. Sharp, and G. W. Scheil.  Collaborative test of the continuous
     chemiluminescent method for measurement of N0» in ambient air.  EPA-iSO/4-75-013.  U.S.
     Environmental Protection Agency, Research Triangle Park, North Carolina, 1975a.

Constant, P. C., Jr., H. C. Sharp, and G. W. Sheil.  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, North Carolina, 1975b.

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     Compounds:  Analysis and Formation.  P. Bogovski, R. Preussman, and E. A, Walker, eds.
     IARC Scientific Publication 3: 10-15.  Lyon, France, 1972.

Wegner, T. N.  Simple, sensitive procedure in 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
     chromotropic acid.  Anal. Chim.  Acta 35: 317-324, 1966.

Williams, D. T., and B. L. Kolitz.  Molecular correlation spectrometry.  Appl. Opt. 7:607-616,
     1968.
                                            7-42

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Winer, A. M., J. M. Peters, J. P.  Smith,  and  J.  N.  Pitts,  Jr.   Response of commercial
     chemiluminescent NO-NO, analysis  to  other  nitrogen-containing compounds.   Environ.  Sci.
     Techno!. 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 nitrate.   J. Marine  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

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                        8.  OBSERVED ATMOSPHERIC CONCENTRATIONS OF NO
                                AND OTHER NITROGENOUS COMPOUNDS      x

8.1  ATMOSPHERIC CONCENTRATIONS OF NOX
     In  this  section,  selected  examples of  ambient concentrations of  NO  are presented  in
order to place possible  human exposure  in  nationwide perspective.  NO.  is  given particular
emphasis since it is the oxide of nitrogen of most concern to human health.  The data presented
are  not  intended   to  be  a  compendium  of  ambient  monitoring activities.   They have  been
summarized to give a representative picture of NO- concentrations in the United States and,  in
particular, to provide  a  rational  basis for  deciding  whether or  not existing  ambient  NO,
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 NO. 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 NO, concentrations exists
nationwide is discussed.  This question has bearing on the problem of estimating human exposure
to  ambient NO- concentrations.   Other  considerations  bearing  on human  exposure  are  also
illustrated with recent data on the temporal and spatial variability of NO- concentrations in
a single airshed.   Data are also presented to illustrate certain general types of atmospheric
mechanisms potentially  leading to high short-term NO, concentrations.   An example is given of
late morning NO. 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 NO, by ambient ozone.  This mechanism is
of interest because of its potential for producing high NO, 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 NO, 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  (GARB)  Air Monitoring Technical Advisory  Committee (AMTAC)
composed of the  CARB", the Air Industrial  Hygiene Laboratory, IPA Region IX,  and the local  air
pollution  control  districts,  have  reported  NO ,  NO,  and  NO, concentrations  to  be on  the
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 NEOA (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 NO,  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 yg/m  (0.004
ppm), respectively.   The measurements cited for North  Carolina  and  Pike's  Peak indicate that
background concentrations  of NO and NO, 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 NO, concentrations  at   a  remote  site  in
                                        3
Colorado  mountains  of  up  to  O.ZO  pg/m   (0.0001  ppfli) 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-
                                     3
logy with  a  sensitivity  of 0.03 ug/m  (0.015 ppb) at sea level.  The author concludes that in
                                                                                 14
the truly  unpolluted  troposphere  the column abundance of NO, 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  yg/m   (0.5 ppb) would  be Implied.  In addition,  Noxon reports that the
ground  level NO. 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.  (1379)  using chemiluminescence analyzers at a site in Michigan showed NO  long-
term average concentrations  in presumably clean air coming  from Canada to be in the range of
0.56 to 0.94 M9/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 NOX MEASUREMENTS (RITTER ET AL., 1979)

Author
Junge (1956)
Lodge and Pate (1966)
Breeding et al. (1973)
Moore (1972)
Drummond (1976)
Cox (1977)
Galbally (1977)
Ritter et al. (1979)
Ambient Concentrations of
. Monitoring for NO — Data
Location
Florida
Panama
Central U.S.
Boulder, CO
Wyomi ng
Ireland
S. Australia
Rural MI
Fritz Peak, CO
N0x
from stationary
Date
1956
1966
1973
1974
1976
1977
1977
1977
1977
monitoring
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
sites may be used to estim
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 NO,, 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 NO, 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 NOg 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 NOg)  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  (Federal  Register,
August 7, 1978).
                                            8-4

-------
8.1.2.2  Sources of Data—The emphasis  in  monitoring NO  has been primarily  on NO,, 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  NO-  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
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  (NO,) 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 ttO^
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 NO, 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

-------
TMl£ 8-2.   YEARIY AVERAGE AKO (WXIHUH CONCMTRATIOHS OF NITRIC OXIDE AT CWff STATIONS,
              MEASURED BY THE CONTINUOUS  SALT2KAN COLORIHETRIC METHOD (U.S. EPA. 19?5l)
Concentration,
Denver
Year
1962
1963
1964
1965
1966
1967
1968
1969
Hean
—
—
—
37
(30)
49
(39)
49
(39)
49
(39)
49
(39)
Max
--
—
--
652
(522)
627
(502)
590
(472)
738
(590)
677
(542)
Washington
Hean
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)
, (ig/« (PF*), 2iDC
Chicago
Hean
123
(.98)
123
(98)
123
(98)
123
(98)
123
(98)
98
(78)
86
(77)
135
(108)
Max
539
(704)
615
(492)
1,105
(884)
750
(600)
775
(620)
763
(610)
739
(591)
1,920
(1,536)
St. Louis
Mean
—
—
(39)
37
(30)
37
(30)
49
(39)
3?
(30)
37
(30)
Max
—
--
923
(738)
443
(354)
688
(550)
393
(314)
492
(394)
873
(698)
Cincinnati
Hean
37
(30)
37
(30)
49
(39)
37
(30)
49
(39)
37
(30)
74
(60)
49
(39)
Hax
702
(562)
615
(492)
787
(630)
750
(600)
1,230
(984)
1.685
(1,348)
1,242
(994)
861
(689)
Philadelphia
Hean Hax
25 431
(20) (345)
62 1,845
(SO) (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 1.73S
(50) (1,388)
49 1.083
(39) (866)
                                         (continued)

-------
TABLE 8-2.  (continued)
Concentration, |ig/n (ppb).
Denver
Year
1970
1971
1972
1973
Mean
62
(50)
62
(50!
74
(60)
74
(60!
Max
750
(600)
677
(542)
788
(630)
652
(522)
Washington
Hean
62
(50)
49
(39)
86
(69)
123
(98)
Max
1,430
775
(620)
825
(660)
640
(512)
Chicago
Mean
172
(137)
13S
(108)
160
(128)
221
(177J
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)


Philadelphia
Mean
74
(60)
49
(39)
62
(50)
	
Mix
1,672
(1,338)
93S
(748)
BOO
(640)
—

-------
Ml

I
2

O
200

100

  e
100

 to

  e
100

 w

  0
100

 60

  0
100

 CO

  6
                                                 CHICAGO CAM*
                                                 I	I
             i    I    i    t    i    i    i
1   1
             I    t     I    I   I    I
I   I
                                     BEMVCII C«*M>
                                    lit
             Jill
             I    I    I    I    I    t    t
                                PHH.A0CI.rMIA CAMT
                               til    I
                                                 rr. LOUIS CAMf
                                                      I	1	
            •62  '63  '64  "65  '66  *C7  *6£  *CS  *70  71
                                  YEAR
      Figure 8-1. Trend lines for nitric oxide annual averages in five
      CAMP cities. —O— :daia satisfying NADB minimum sampling
      criteria; —o~ : invalid average (based on incomplete data).
      •Note change in ordinate scale for these data (U.S. EPA, 1973!.
                             8-8

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                  TABLE 8-3.   FIVE-YEAR AVERAGES OF NITRIC OXIDE  CONCENTRATIONS AT CAMP STATIONS,

                              MEASURED BY CONTINUOUS SALTZMAN  COLORIMETRIC  METHOD (U.S.  EPA,  (1973)

Average-Concentration ,
MO/m4 (ppb), 25°C
Station
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
CAMP average
1962-1966
122.6 (98.1)
43.8 (35.0)
44,9 (35.9)
55.2 (44.2)
39.8 (31.8)
61.2 (49.0)
1967-1971
125.4 (100.3)
53.6 (42.9)
54.4 (43,52)
65.4 (52.3)
47.6 (38.1)
69.3 (55.4)
Change, %
+ 2
+22
+21
+18
+19
+13
Average of Annual
2nd Highest Value.
Mfl/m3 (ppb), 25°C
1962-1966
731 (584.8)
782 (625.6)
633 (506.4)
1,331 (1,064.8)
541 (287.8)
804 (643.2)
1967-1971 Change, X
969 (775.2)
1,067 (853.6)
620 (496.0)
1,391 (1,116.0)
578 (462.4)
926 (740.8)
+32
+36
- 2
+ 5
+ 7
+15
00
I

-------
                                TABLE 8-4.  YEARLY AVERAGE AND KW1HUH CONCEHTRATIOHS Of NITROGEN DIOXIDE AT  CAW  STATIONS,

                                            MEASURED BY THE  CONINUOUS SALTZKAN COLORIHETRIC METHOD (U.S. EPA.  1975a)
CO
i
Concentration, |ig/n , at 25 C
Denver
Year
1962
1963
1364
1965
1966
196?
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
n
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
86S
319
564
470
319
358
395
1,090
413
676
St. louts
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
Mix
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
..

-------
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c
U)
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200


100

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100

 50

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100

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100


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100

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                                           I     I    I    I
                                   I

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                                                        '
                                              CINCINNATI CAMP

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                          1    1
                                      n
 1
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1    I
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                                                 DENVER CAMP
                                                III!
                                  J	I
                                            PHILADELPHIA CAMP

                                            I    I    I    I
                    _£.
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                        TT
                          I
                              i
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                             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. -O- :  data satisfying NADB minimum sampling cri-
 teria;-O-: invalid average (based on incomplete data). "Note change
 in ordinate scale for these data (U.S. EPA. 1973).
                               8-11

-------
TABU 8-5.   FIVE-YEAR AVERAGES OF NITROGEN DIOXIDE CONCENTRATIONS AT CAMP STATIONS,
            MEASURED BY THE CONTIHUOUS SM.TIHAH COIORIHETR1C (CTHOO (U.S. EM,  1973)
Ave rags ,Co nc«n t n t lo n ,
«/«.» (ppb), 2S*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, X
US
- 3
* 3
U5
- 7
« 6
Average, of Annual
2nd Highest Value.
WflAT (PPb). 25aC
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, X
U2
- 6
- 1
*15
-16
+ 1

-------
 AVERAGE NO, CONCENTRATION CHANGE (11 STATIONS): +20%

                                                 \
Figure 8-3.  Trends in NOj air quality. Los Angeles Basin, 1965-1974
(Trijoniset al., 1976).
                               8-13

-------
8.1.4  Recent Trends In NO,, Concentrations
     Examination of  data  on trends in NO-  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 NO. 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 NO,  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),
NO.  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 Table
8-6 generally experienced declines in NOg levels.
8-1-5  Seasonal  Variations in NO, Concentrations
     In  this section, a  few  examples  of  seasonal   variations   in  NO,   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  NO™ 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  NO- 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  publish 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 NO,  in  recent
years are presented.   In summary,  the data cited illustrate the following points:
                                            8-14

-------
1100
                                                                      ANNUM. STATISTICS
                                                                « * . . . >V£AR MOVING AVERAGES

                                                                — X — INCOMPLETE DATA
                    MAXIMUM ONE-HOUR OBSERVATION
                         ARITHMETIC MEAN
                       CQLORIMETRIC SRIESS SAITZMAN
     •68
                                                                                              •80
                                            YEAR
Figure 8-4. Annual air quality and 3-year moving averages at Camden, New Jersey. [Oala adapted from Trijoni:.
[1978], augmented with data from SAROAD.j
                                                  8-15

-------
                                                             ANNUAL STATISTICS


                                                        • « ... o-YEAR MOVING AVERAGES
                                               MAXIMUM ONE-HOUR OBSERVATIONS
                                                                                O
                                                                                u
                                                                                O

                                                                                5


                                                                                9
                             -COLORIMETRIC - LYSHKOW |14-, POSITIVE BIAS



                                I    I    I    I    I    I    I    I
•83  -84 -65  -66  '67  '68
                                        70  '71  72  73  74  75  76  77  78  79 '80



                                             YEAR
Figure 8-5. Annual air qualify statistics and 3-year moving av.eragcs at downtown Los Angeles.

California. [Data adapted from Trijonis (1978], augmented with data from SAROAD.]
                                            8-16

-------
I
            1    1    i


MAXIMUM ONE-HOUR OBSERVATIONS
                                                         —O- ANNUM. STATISTICS

                                                         • • • * J-YEAR MOVING AVERAGES

                                                         -X- INCOMPLETE PAT*
         _ 900s PERCENTILE
            ARITHMETIC MEAN
                                     COLORIMETRIC - LYSMKOW !•'-; POSITIVE BIAS


                                                     If    I     I    I
                             70   71  72  73  74  75  76  77   78  79  '80
Z  7BOJ--
<
(E
 O
 U
 X

 S
 D
 m
 IS
        «3  «4  «5
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
    500 —
I
5?

w

o
ui
o


I
UI
g
«c
O
S

IU
o
o
c

z
    400 —
300
    200
                                                                —O— ANNUAL STATISTICS

                                                                ...... J-YEAP MOVING AVERAGES

                                                                — X — INCOMPLETE DATA
                              MAXIMUM ONE-HOUR OBSERVATION
                                      ARITHMETIC MEAN
                              COLOR1METR1C  SRIESS  SALTZMAN
                   •68    '69    70    71    72    73    74    75    76    77    78    79    '80
    100 —
  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

-------
    500
    400  -'
I

(A

g


a:
LJ
u

o
u
tu
g
X
O
5
z
tu
O
O
300  —
                                                     ANNUAL STATISTICS

                                                 • * •  3-YEAR MOVING AVERAGES

                                                X —  INCOMPLETE DATA
200  —
       '70
                                               YEAR
   Figure 8-8.  Annual air quality statistics and 3-year moving averages at Portland, Oregon. (Data
   adapted Irom Trijonis [1978], augmented wtlh data from SAROAD.)
                                                8-19

-------
   340
   320
   300
   280
1
   260
UJ

z
o
u
   220
   200
   180 -
                                 HIGHEST AVERAGE
                           BAS1NWIDE MEAN IS SITES!
                                  LOWEST AVERAGE
                                I
             1970     1971
                               1972     1973



                               YEAR
                                                 1974    1975
Figure 8*9.  Annual average of daily maximum 1-hour NOj (4-year


running mean) in the Los Angeles Basin (U.S. EPA, 1976a).
                             8-20

-------
TABLE 8-6.  FIVE-YEAR CHANGES IN AMBIENT
                                                   CONCENTRATIONS
                                                                 a
NET PERCENTAGE CHANGE IN NO- CONCEN


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
Salinas
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
TRATIONS
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%
FROM 1969
90th
Percenti le

+ 5%
+60%
+33%
+ 7%
-11%
- 2%
+11*
-10%
- 1%

- 9%
- 4%
-25%
- 1%
0%
-24%
-44%
-15%

-18%
- 7%
0%
- 8%

+51*
+44%
TO 1S74
Yearly
Maximum

+13%
+72%
+43%
+ 6%
+ 1%
-28%
+32%
-13%
- 1%

-14%
-12%
- 9%
+27%
0%
r27%
-21%
- 8%

-36%
-52%
0%
-24%

+94%
- 3%
Adapted from Trijonis (1978).
                                  8-21

-------
g



K
t-
z
UJ
0


O
o
O
u

1
z
o
(£

H

2
122
U


O
u
10





 8





 6




 4
      IS
      10
                                            I     I     I
              HOUSTON/MAE 1975 1976
                                       I	I
                                              J	I
         123456783    10   11   12



                                 MONTH
                                                          T
              DENVER 1967-1973
         1   2    3    4    S
                                 $    7    8    9    10   11   12



                                 MONTH
              CHICAGO 1369-1973



              !_..  I     1
 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

-------
IV3

C.J
            25
            20
        I   15
        oc

        z
        U

        Z
            10
                                               1     I     I    I
                   AZUSA 1969-1974
               1    2    3    4     5    6    7    8    9    10   11   12
                                                              J>




                                      MONTH
            20
|   15
a


g


i   10

z
ui
U
                                        I     I     I
                   POMONA 1869-1974
                                  I	I
              1234    56789    10   11   12



                                     MONTH
                                                                  I
                                                                  z*
                                                                  Ul
                                                                  u
                                                                  z

                                                                  8
                                                                              20
                                                                              15
                                                                              10
                                                                                     LOS ANGELES  1969-1974

                                                                                     I     I     I     I    I    I
                                                                         1234667



                                                                                                MONTH
                                                                              15
                                                                           ,
                                                                         O
                                                                         U    S


                                                                         O
                                                                         U
                                                                                                                  8    9    10    11    12
                                                                                                                              NO-
                                                                             LENNOX 1969-1974 |SEf TiXTI
                                                                        123456789    10   11   12



                                                                                                MONTH
         Figure 8-11.   Seasonal NO2 concantration patterns of four U.S. urban sites (monthly averages  of daily maximum 1-hr concentrations).


        Adapted from Trijonii (1978).

-------
        • Annual average concentrations of N02 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 NO, 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 NO, 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,  Hew  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 ug/m   in 1980.   As shown in Tables 8-7 to 8-9 recurrent NO, hourly concentra-
                            3
tions in excess of  250 yg/m  (0.14 ppm)  were  quite common nationwide in both 1975 and subse-
quent years, but  very  few exceeded 750 yg/m  (0.4 ppm).   Table 8-10  presents  data  for 24-hr
average N0_  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  (NAOB)  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  occassional  peak NO,
concentrations of possible concern for human health (see Chapter 15) occurred in the nation in
the raid-1970s.   More recently available data for 1976-1980 from the SAROAO system suggest that
basically the same patterns of occassional peak NO, 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 noncontiguous 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*



State
California












Colorado
Georgia
Illinois



Kentucky




Location
Anaheim
Azusa
Costa Mesa
Los Angeles

Lynwood
San Bernadino
Napa
San Francisco
Barstow
Fontana
Chula Vista
Visalia
Denver3
Atlanta
Chicago3


East St. Louis
Paducah
Louisville
Ashland
Mi/™
Maximum hourly concentration -
Method Ab
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
-
-
-
-
-
-
-
-
-
714/66 =10.8
-
895/85 =10. 5

yearly arithmetic mean
Method Bc
«,
-
.
-
-
-
-
-
-
-
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)

ug/«3
Maximum hourly concentration - yearly arithmetic mean
State
Maine
Maryland
Michigan
Oregon
Texas
Location
Bangor
Essex
Grand Rapids
Detroit
Portland
Dallas
Method Ab
270/49 * 5.5
-
279/67 =4.2
207/50 = 4.1
-
Method Bc
-
282/53 =5.3
338/58 = 5.8
-
432/32 =13.5

 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, note that:  1.0 ppn NO- s 1880 ug/m ; 0.5 ppm s 940
 ug/in ; 0.1 ppm £ 188 ug/m ;  0.05 ppn s 94 vg/m; and 0.01 ppm s 18.8 ug/m .

-------
    TABLE 8-8.   FREQUENCY DISTRIBUTION OF 1975 HOURLY N0_ CONCENTRATIONS
           AT VARIOUS SITES IN U.S. URBAN AREAS (U.S. EPA, 1977a)*
                                Concentrations (ug/m )          Maximum
                                equalled or exceeded by         observed
                             stated percent of observations   concentration
Location
Arizona
Phoenix3
California
Los Angeles
Redlands.
Redlands
Riverside3
Riverside
San Diego.
San Diego
Colorado
Denver.
Denver
Kentucky
Ashland3
Michigan.
Detroit0
Missouri
St. Louis3
New Jersey
Newark^
Newark0
New York .
New York City0
Ohio .
Cincinnati0
Pennsylvania .
Philadelphia0
Texas h
Dallas0
1%

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
aObtained by Instrumental Colorimetric-Lyshkow (Mod) method, a variation
 of the Griess-Saltzman method.

 Obtained by Chemiluminescence Method.

C0btained by Instrumental Colorimetric-Griess-Saltzman method.
*For comparison purposes, note that: 1.0 ppm NO, = 188" •—'-  -
 = 940 ug/m i 0.1 ppm = 188 ug/m ; 0.05 ppm = 94 ug/m
 = 18.8 ug/m .
= 1880 ug/m ; 0.5 ppm
••-'- - and 0.01 ppm
                                   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 SAROAO Site ID Method
Arizona
Phoenix 030600002G01 Instrumental
Chenil 1 un< nescence

Tucson 030860002601 Instrumental
00 , Chemf luminescence
I
rsi
» California
Anaheim 050230001101 Grless-Saltznjn*
(Lyshkow)

Chlno 051300001101 Instrucental
Chemi luminescence

Costa H«sa 051740002101 Grfess-Sattinan*
(lyshkow)

£1 Cajon 055300002101 InstrunenUl
Cheml luminescence

Fontana 052680001101 Instrumental
Chemi 1 uffl i nescence

Fremont 052780001101 GHess-Semman"
(lyshkoMj

La Habra 053620001101 Gries*-$aH»an*
Uyrtkow)

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
wao
Concentrations equalled or
exceeded by stated percent
of observations (ug/« )
a in sox

226
150
94
132
ISO
301


39S
338
226
414
226
-
301
263
263
320
301
244
244
-
207
301
207
-
320
-
"

150
75
38
94
100
ISO


188
ISO
132
132
ISO
-
132
113
113
188
169
169
132
-
132
ISO
113
*
169
•
*

56
38
5
56
56
56


94
75
56
19
94
-
19
38
38
94
94
94
56
-
56
56
56
"
75
-
"
HaxlMM 2nd Highest Yearly
observed observed arHhuetlc
concentration concentration dean,
(M3/«3)  (IIS/"3)

451
226
132
451
432
414


B6S
564
470
602
301
-
639
564
583
545
508
338
564
-
470
S26
320
~
526
-
"

432
207
132
357
301
414


752
545
395
563
282
-
639
545
S26
489
432
282
508
-
432
526
282
™
508
-
"

60
Mb
17°
5L
61b
69


103.
90°
71°
54
94°
-
53b
53°
so"
108b
»«b
95*
63
k
73°
80
£6
"
91
*


-------
                                                         TABLE 8-9. (continued)
oo
i
location
SAROAD Site 10 Method
Year
Concentrations equalled or Haximum 2nd highest Yearly
exceeded by stated percent observed observed arithmetic
of observations (ug/m ) concentration concentration mean,
~I5 IB! so* (MS/I ) (MB/" ) (C9/» )
California (cont.)
Oakland


Oceans Ide


(tea-lands


Riverside


San Oiego


San Diego


San Jose


Sao Jose


0553000MF01 Instrumental
Che*! luminescence

055320003101 Instrument!!
Che«l IiMinescf nee

056200001101 Instrwental
Cheniluainescence

056400005F01 Instrumental
Chemi luminescence

056800006101 Instrumental
Ctitnf luminescence

OS6800004I01 Instrumental
Che*t luminescence

OS6980004A05 Instrumental
Cheat luminescence

056980004101 Griess-Sattnufl*
(lyshkow)

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
301
-
-
263
»4
207
169
-
-
338
301
282
244
226
226
357
376
320
301
-
-
320
244
207
ISO
-
-
113
113
75
75
-
-
207
169
150
113
132
113
108
207
207
169
-
-
169
132
132
56
-
-
38
56
38
38
-
•
94
94
75
56
56
38
94
94
94
66
-
,;, . T. .
75
75
75
545
-
-
620
602
357
470
-
-
564
564
414
451
432
357
585
940
470
479
-
•
526
414
301
489
-
-
620
545
338
451
-
-
526
489
395
451
395
357
564
846
451
461
-
-
507
414
'282
77
-
-
"t,
S8°
40
47
-
-
113b
101b
90b
63b
?*b
55D
105
HZ*
114°
86
~
*
86
78b
79

-------
IABIE 8-9.  (continued)
Concentrations equalled 01
exceeded by stated percent
of observations (M

244
348
301
461
461
519
239

572
306

832
450
643
649
189
645
365
2nd highest Yearly
observed arithmetic
concentration mean.

216
292
273
442
442
293
205

464
275

815
438
622
629
180
585
361

"b
61b
116
108
40b

41b

"H
79b
94b
48b
100.
106b

-------
                                                   TABLE 8-9.  (continued)
Concentrations equalled or
exceeded by stated percent
of observations (uq/« )
location
New Jersey
Newark


Ohio
oo Cincinnati
i
CO
t— »
Pennsylvania
Philadelphia


Utah
Salt lake City


Salt lake City


SAROAO Site 10 Method

313480002A05 Instrumental
Chemi luminescence


361220019A05 Instrumental
Chemi luminescence


397140023H01 Greiss-Saltzmana
(lyshkow)


460920001F01 Instrumental
Chemi luminescence

460920001A05 Instrumental
Chemi luminescence

Year

1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
IX

226
_
167

147
ISO
103

188
-
-

244
188
207
226


10%

122
„
117

94
98
70

113
-
-

132
113
113
132
-

SOX

75
.
66

56
47
38

75
-
•

75
56
56
75
-

Haxlnun 2nd highest Yearly
observed observed arithmetic
concentration concentration Mean..
(ug/m ) (vgf" ) (vgft )

338
_
196

677
254
150

451
-
-

470
263
357
470
-


320
_
192

508
235
145

451
-
•

451
263
357
432
-


80
.
70b

60
55
41

74
-
•

80b
65b
61b
75
-

 Data obtained using dynamic  calibration procedures.

 Data not satisfying NAOB minimum sampling criteria.

*For comparison purposes, note thai:   1.0 ppm NO  "* 1880 uq/m ;  0.5 ppm f  ppm940 pq/m  0.1 ppm " 188 ug/m  ; 0.05 pp« - 94 \tg/n  ; and 0.01
 ppm " 1R.8 pq/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 S001UK ADSENITE KOHOO) (U.S.  EM,  19?6c.  1979, 198])*
00
k)
ISS
Location
AiabaM
aimingna*


Alaska
Fairbanks


Arizona
Tucson


Arkansas
Little Rock


California
Fresno


long Beach


Sin Bernadino


Colorado
Denver


Site Code
010380003POI
w
*

020160001P01
H
W

Q38S60001F01
M
H

041440003F01
It
M

052800002F01
M
"
054100001F01
"
"
056680001F01
11
11

060S80001P01
"
" '
Year
1976
1978
1980

1976
1978
1980

1976
J978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
HiXimp
12?
-
-

110
-
-

12?
-
-

105
93
79

147
-
-
339
-
-
156
-
-

163
-
-
Concentrations (ny/« } equalled
Second or exceeded by stated percent
highest of observations
(M9/» )
117
-
•

103
-
-

96
-
-

100
72
76

133
-
-
285
-
-
154
-
-

140
-
-
10X
107
»
-

85
-
-

69

-

65
58
53

118
-
-
215
-
-
124
-
-

102
-
-
50*
66
-
-

59
-
-

45
-
-

32
28
2?

49
-
-
101
-
-
78
-
-

46
-
"
Annual
• HthKtiC
«an3
69
-
-

59
-
-

47
-
-

37
31
30

58
-
-
119
-
-
85
-
-

55
-
*

-------
                                                     TABLE  8-10.  (continued)
00

u>
u>
Location
Connecticut
Bridgeport


Greenwich


Florida
Jacksonville








Orlando


Georgia
Atlanta











Macon


Site Code

070060123F01
II
H
070330008F01
070060004F01
070330004F01

101960033H01
"
11
101960002P01
H
"
101960032H01

H
103260004F01
"
ii

110200038G02
M
"
110200001P01
"
M
110200039G01
"
11
11020004 1G01
"
M
113440008F01
113440007F02
113440007F02
Year

1976
1978
1980
1976
1978
1980

1976
1976
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1976
1980
1976
1978
1980
1976
1976
1980
1976
1978
1980
1976
1976
1980
MaxioHjm

143
134
207
101
93
123

138
-
-
100
-
.
93
SO
-
91
71
74

133
60
106
123
73
-
120
99
96
100
74
.
109
84
92
Concentrations (pg/a ) equalled
Second or exceeded by stated percent
highest of observations

-------
IMIU 8-10. (continued)
Location
Idaho
Boise City


Illinois
Chicago





Peorta


Indiana
Indianapolis




Iowa
Bel Icvue


Kentucky
Ashland





Paducah


Site Code

130220007F01
11
11

141220002P01
"
11
141220001P01
11
"
146080001P01
ii
"

1S204002SH01
11
"
152040015X01
M
"
280180002F01
**
11

180080003F01
11
"
1B0080008F01
M
*'
183180020F01
"
"
Year

1976
1978
19SO

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
Haxl«u»
(MS/*3)

96
-
-

172
-
-
117
-
-
94
-
-

308
-
-
128
-
92
126
-
-

94
173
92
93
84
-
90
-
-
{
Second
highest

83
-
-

140
-
-
113
-
-
72
-
-

132
-
-
122
-
90
97
-
-

93
123
87
89
79
-
82
-
-
:oncentrations (jig/« ) equalled
or exceeded by stated percent
of observations
IDS

66
-
-

130
-
-
99
-
-
68
-
-

86
-
-
89
-
90
87
-
-

79
72
65
76
76
-
71
-
-
SOX

"17
-
-

91
-
-
70
-
-
52
-
-

SO
-
-
S3
-
SI
41
-
-

46
30
42
43
38
-
40
-
-
Annual
arflNuUc
•ean,


SO
-
-

91
-
-
73
-
-
51
-
-

56
-
-
54
-
55
46
-
-

48
35"
41
47
41
-
44
-
-

-------
                                                    TABLE 8-10.  (continued)
CO
en
Location
Louisiana
Baton Rouge


Maine
fiangor


Maryland
aaUinore





Silver Spring


Michigan
Detroit








Minnesota
St. Paul


Site Code

190280002F01
*
"

200100001F01
W
**
21012M18F01
II
"
210120007H01
w
11
HW80005G01
ii
H

231180001P01
'*
"
231180018F01
II
II
231180016f01
H
"

243300031P01
M
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
1980
Maxinua

-------
                                                        TA3LE 8-10, (canlinued)
00
(A)
91
Location
Hltiourl
Kansas City


St. Louis





Hebrasfca
Lincoln


Hew HuasMre
Nashua


North Carolina
BelMnt


Charlotte


Winston-Sale*


Site Code

171800012P01
H
M
264280072P01
H
«
264280001P01
*
"

281560004G01
"
281560012G01

300480005F01
"
•"

340300001F02
«
340300003F02
340700001C01
"
"
344460002G02
"
H


1976
1978
1980
1976
1973
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
(|ifl/«r)

147
-
-
136
-
.
Ill
-
-

112
120
86

1S1
•
-

107
_
84
84
112
154
80
95
148
(
Second
highest

147
-
.
127
-
-
105
-
-

91
59
86

116
-
-

103
.
57
80
103
132
68
91
94
;oncentratlons (|ig/n ) equalled
or exceeded by stated percent
of observations
10X

69
-
.
109
-
-
94
-
-

70
21
69

76
-
-

96
.
57
67
88
91
65
76
55
SOX

49
-
-
71
-
-
64
-
-

45
11
48

46
-
-

67
h
28
46
54
54
43
39
24
Annual
arithmetic
(M^3)

SO
-
-
73
-
.
59
-
-

46
14
47

54
-
-

73
-
31b
48
57
58
45
43
33

-------
                                                     IA8LE  8-10.  (continued)
to
CO
Location
Ohio
Akron





Caopbel 1


Cincinnati





Cleveland





Moraine


Toledo


Okl show
Tulsa


Oregon
Portland


Site Code

360060006H01
M
"
360060004HOI
»
"
360960001101
M
»
3612200 18H01
»
"
361220019P01
»
w
361300033H01
»
"
361300012N01
"
"
364S50001G01
»
"
366600007H01
"
M

3730001 12F01
11
**

38 146000 1P01
"
"
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
1980
Maximum
ClH/« )

96
139
93
100
135
86
128
110
103
158
105
-
121
-
-
193
259
136
189
222
132
126
-
-
117
162
102

193
-
-

102
-
-
(
Second
highest

91
109
93
91
126
83
12S
100
90
139
100
-
98
-
.
181
247
126
175
207
121
91
-
-
115
116
101

157
-
-

98
-
-
;oncentratioris (iig/n ) equalled
or exceeded by stated percent
of observations
10X

70
87
75
82
82
76
92
79
84
106
105
-
89
-
-
127
197
112
127
135
115
84
-
-
80
92
90

119
-
-

90
-
-
SOX

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
arithmetic
mean.
(M9/« )

46
57
54
53
53
52
63
54
51
70b
93°
-
62
-
«
88
109b
66
87
99
78
53
-
-
56
64
59

.74
-
-

57
-
-

-------
(A8U 8-10.  (continued)
location
South Carolina
Mount Pleasant


Spartanburg


Tennessee
Chattanooga


Eastridge


tinoxville


Nashville


Texas
Austin





Dallas








Site Code

421700001F01
**
»
422040001F01
(i
"

440380025G01
**
"
440900001G01
H
"
441740005G01
"
"
442540002G01
«
*

4S0220004F01
"
"
450220012F01
"
»
451310023HOI
"
»
4S1310002F01
M
II
451310002H01
"
"
Year

1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
197B
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Haxlny*


118
43
63
121
US
119

94
™
-
124
-
-
119
-
-
145
125
156

117
94
75
93
106
-
31
231
-
97
238
265
108
133
-
(
Second
highest

74
34
40
90
99
4S

92
-
-
95
-
-
114
-
-
US
124
140

71
86
70
79
77
-
88
190
-
96
165
202
105
131
-
Concentrations (MS/* ) equalled
or exceeded by stated percent
at observations
IBS

37
29
32
74
83
43

74
-
-
64
-
-
101
*
.
97
108
113

47
86
55
58
57
-
77
112
-
83
127
183
80
104
-
SOX

16
14
9
38
28
3

48
-
.
46
-
-
70
-
-
64
58
54

27
44
32
20
17
-
50
54
-
52
74
84
57
62
-
Annual
arithmetic
•ean,
(MAO

20
16.
15b
42
33.,
18b

51
*
.
47
-
.
70
-
-
69.
,.i>
60b

30
46b
35
24
22
-
51
£3
-
52
77.
98b
5?
63
-

-------
                                                         TABLE 0-10. (continued)
Co
to
Location
Fort Worth





Houston


Utah
Salt Lake City


Washington
Seattle


Wisconsin
HI Iwaukee


Site Code
4S1880Q21H02
"
"
451880022H02
»
"
452560009H01
"
"

46092000 1P01
'*
11

491840001P01
it
ii

512200G4SF01
"

Year
1976
1978
1980
1976
1978
1980
1976
1978
1980

1976
1978
1980

1976
1978
1980

1976
1970
19BO
Maximum
153
94
-
138
91
-
162
170
128

364
-
-

119
139
-

148
133
81
(
Second
highest
143
94
-
124
66
-
137
116
101

182
-
-

114
113
-

115
125
76
:oncentratioi» (MQ/I* ) equalled
or exceeded by stated percent
of observations
10X
102
94
-
95
91
-
127
102
99

120
-
.

91
113
-

88
95
76
SOX
74
65
-
63
61
-
56
66
30

57
-
-

66
90
-

62
65
54
Annual
arithmetic
mean,
(N9/» )
"b
74b
-
61h
59b
-
64
64
46b

70
-
-

65K
93b
-

60
67
57b
               'For comparison purposct, note that:  1.0 ppn NO. ~ 1880 ug/n ;  0.5 PP« s 940 ug/«  ; 0.1 ppn  =  186 ug/m ;  0.05 ppn

                s 94 MQ/« ! *i«l 0.01 ppn s 18.8 M9/«          '
                Data do not satisfy NAU8 «ini»u» sanpling criteria.

-------
     Since the  National  Ambient Air Quality Standard for NO, 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 NOg 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 NO,  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 NO,  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 1n the maximum-to-mean NO, 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 1s, 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 NO, 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),
and  113 ug/m   (0.06  ppm)  respectively.   St. Louis,  Missouri,  on  the other hand,  had the
moderate median value of  7S 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 NO, even  higher than  those observed in
center-city  locations  in major metropolitan areas.  Ashland,  Kentucky, reported a maximum of
895  pg/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  NO- 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 NO,  in the morning as  the  result of NO emissions and photo-
chemical conversion to NO,.  This is followed  by  a decrease  of NO, in the midmorning  hours due
to  advection and increasing vertical  dispersion  and also loss of N02 in various atmospheric

                                             8-40

-------
fc
5

I
I
    10
                    4       C      •     10

                        MAXIMUM/MEAN RATIO
                                                 12
                                                        14
  Figure 8-12.  Distribution of maximum/mean NC>2 ratios for 120
  urban locations averaged over the years 1972, 1973. and 1974
  (adapted from Trijonis, 1978).
                                        8-41

-------
tc
 CM
o


<
Ul
E
O
J_
      I
           I
    _L
                         I
                                   I
                         I	I
'54   '65   '66   '87  '68  '68  "70  'Tl   "72  73  74

                     YEAR
           I
      I
I
I
I
I
I
                                                  T
              b

          J	I
          ±
     1
     I
     I
     I
                                   T
          '64  '65  '66   '67   '68   '69  70   71   72   73   74

                                YEAR


     Figure 8-13.  Trends in the maximum mean NO? ratio for two
     groups of sites:  (a) average of five locations witnin 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 NO- 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 NO,, concentration data from the month of the highest observed
1-hr HQ-  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 NO,,  levels  in Los Ageles 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  NO, 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 N0_ concentration  data  are plotted versus time for periods
of 3 days  during  which high N0_ 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
NO- 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 NQ? concentration did not take place until 5:00 or 6:00 p.m.
     Figure  8-17  shows  the  NO,  and  NO concentration profiles  obtained  from  a center-city
station in St.  Louis,  Missouri, and the  NO,  concentration from a rural  site,  45 km north of
                          12
the center-city  location.     The  center-city site  showed a rapid  buildup of NO  during the
morning with a  slower  rise in the  N02 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 northwest.
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 other

                                            8-43

-------
00
-c.
                                                                                                           LOS ANOELES. JANUARY 1975

                                                                                                           DENVER, APRIL 1975

                                                                                                           CHICAGO, JUNE 1975
       Figure 8-14. Average diurnal pattern for the month during which the highest 1-hour NC>2 concentrations were reported (U.S. EPA, 1975b).

-------
•t*
01
                                                                                                   UK ANOELES, CALIFORNIA, JANUARY 17. 1975


                                                                                                   DENVER,COLORADO. APRIL S. 1975


                                                                                                   CHICAGO. ILLINOIS. Jurt« 21,1975
                24
              Figure 8-15. One-hour average concentration profiles on day of peak NO2 concentration for three U.S. cities (U.S. EPA, 1975b).

-------
00
I
                        8U*U __^


                    _   <>«!
                                                                                                                          NOON          MIDNIGHT
                              F.quts B 16. Om hour NO; conconligtioni during IhrM diyi ol high pollution in 
-------
03
I
-fa.
 0.10
(188.0)
    AT RAMS STATION S (CENTER CITY)
    AT RAMS STATION ZZ US km NORTH OF CENTER CITYI
NO AT RAMS STATION S (CENTER CITV)
                                                                                                                                 0.22
                                                                                                                                 12711

                                                                                                                                 0.20
                                                                                                                                 1246)
                                                                                                                24
     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, 1976bl.

-------
monitoring sites  in  and around St. Louis  did  not show a consistent, concomitant variation of
NO„ concentrations,  the most likely explanation for the data presented is dispersion or plume
impietion  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 NO, 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 NO-  levels  are apparent from 9:00  a.m.  to 7:00
p.m.  In  II  Paso, Texas, both morning  and early evening elevations in NO, concentrations are
apparent.  It  also  can  be seen that,  for  all  hours on at least one day during the month, NO,
concentrations exceeded the monthly mean.
     To summarize, the  above data indicate  that  very  high  NO- 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  NO. 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,
N0_, 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 03 concentration is quite Tow,  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 NO- formation.  After sunrise, the NO, concentra-
tion increased sharply  as  a result of photochemical  reactions.   Photochemical  generation of
HOy Is  followed by a concomitant  rapid  increase in  0, 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 NO, CONCENTRATIONS3
        FOR ONE MONTH IN 1975 FOR SELECTED URBAN SITES (U.S. EPR, 1976b)


12 an
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
California
(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
Illinois
(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



aData presented to two significant figures only.

bNo 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 NO- 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 NO- concentrations.   It may be  postulated  that
this mechanism is  operative  also in  other localities exhibiting  elevated NO.  levels  after
photochemical  activity,  including  NO, photodissociation,  decreases  in   the  evening.   Rapid
reaction of  NO and 0, 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 NO- levels  in the  late evening
hours  are  a  fairly  common phenomenon in the Greater St.  Louis area.  Fifty-three of the 89
high NO,  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 NO., 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  (SAROAO  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 NOj
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 NO, 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 NOg
concentrations on a nationwide basis is lacking in the literature.
                                            8-50

-------
E

S   0.20
cc
t~
z
Ui
o

o
           NO FORMAT ION


           OF NO,
        _,.
3
_J
_l
O
    0.10
                                                                                                       3


                                                                                                     • NO
. PHOTOCHEMICAL FORMATION OF NO-
OZONE SCAVENGING


FORMATION OF NO,
          NIGHTTIME NO-CARRYOVER
         	L	jX
                       SUNRISE
                                               10            12            14
                                                        TIME OF DAY (CSTf
                                                                                      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 photochnmical and ozone se,wenqin«j formation of NOj (U.S. EPA, 197BHI.

-------
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)

Site Number
101
(Center-city)



104




105




107




108




Date of
Measurement
Nov.
Nov.
Nov.
Nov.
Nov.
Hay
Oct.
Hay
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
I
1
1
1
1
2
25
2
. 1
30
26
30
2
Time of
Measurement
10 pm
9 pm
8 pm
7 pm
11 pm
7 am
6 pm
8 am
5 pm
6 pm
,
--"-first value
7 pm
10 pm
8 pm
9 pm
6 pm
7 pn
7 pm
9 am
8 am
7 am
8 am
11 am
9 am
8 am
Distance from
Concentration Arithmetic Mean Site 101
\tg/m ppm ug/m ppra
481
454
443
434
411
293
291
287
284
284
invali
350
337
334
332
358
353
271
266
263
636
566
321
312
291
0.2556 53 0.0282
0.241B
0.2358
0.2310
0.2187
0.1559 48 0.0253
0. 1549
0. 1526
0. 1512
0. 1509
J-*_.| ___ _«™«to»™— w
dated — ~ —
0.1864 44 0.0235
0. 1795
0. 1776
0. 1768
0.1907 57 0.0305
0. 1880
0. 1441
0. 1413
0. 1400
0.3383 33 0.0174
0. 3010
0. 1707
0. 1659
0.1548
(km)
0




<4





<4



<4




<20




                                    (continued)

-------
                                                   TABLE 8-12. (continued)
CD
I
cn

Site Number
109




114




115




116




102




Date of
Measurement
Apr. 30
Oct. 1
Oct. 1
Oct. 1
Apr. 7
Oct. 2
Oct. 2
Oct. 2
Oct. 1
Oct. 2
Dec. 4
Oct. 2
Hay 10
Sept. 22
July 6
Hay 7
Hay 7
Oct. 2
Oct. 1
Oct. 1
Oct. 1
Oct. 2
Oct. 2
Oct. 1
Oct. I
Time of
Measurement
8 am
6 pm
7 pm
8 pin
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
Conce
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
ntration Arithmetic Mean
ppm (jg/Hi" 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
(ta)
<20




<20




<20




<20




<10




                                                         (continued)

-------
                                                  TABLE 8-12.  (continued)
CO
I

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
Tine of
Measurement
10 pm
9 pm
11 pra
7 pm
8 pm
7 an
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
Concc
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
Distance from
ntration Arithmetic Mean Site 101
ppn pg/m ppffl (km)
0.2449 56 0,0298 <10
0.2375
0.2352
0.2169
0.2156
0.2155 34 0.0182 <10
0. 1398
0.1366
0.1069
0. 1067
0.2230 45 0.0241 <10
0.2161
0. 2121
0.2060
0. 1956
0.1689 52 0.0275 <10
0.1686
0.1677
0.1637
0. 1636
0.3594 21 0.0110 <20
0.3008
0.2891
0.2450
0.1914
                                                             (continued)

-------
                                                  TABLE 8-12.  (continued)
00
I

Site Number
118




119




120




Date of
Measurement
Sept. 17
Sept. 15
Nov. 6
Nov. 6
Nov. 6
Feb. 3
Feb. 3
Feb. 3
Feb. 3
Feb. 3
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 pin
9 pm
7 pm
6 pm
7 am
8 am
7 pm
8 am
Conce
MS/'m
149
136
134
132
127
360
343
336
336
316
360
296
258
248
236
ntration 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)
                                                          ISt.  louii,  October I  and  2, 1976  (pp»)J         '
oo

o>
nuts
Stat
101
102
103
104
106
107
108
109
110
111
112
113
' Hour of Day ,
Ion
0,07
0.07
O.OS
O.OS
0.07
0.07
0.06
ft
0.03
O.OS
O.OS

7
0.12
0.12
0.10
0.07
0.11
0.08
0.10
*
0.04
0.07
0.06

8
0.12
0,17
0.15
0.12
0.10
0.08
0.09
A
o.oa
0,08
O.OS

9
0.18
0.11
0.12
0.14
0.08
0.08
0.08
*
0.07
0.06
0.06

10
0.14
0.12
0.10
0.07
0.08
0.11
0.05
0.02
0.04
0.04
O.OB

11
0.08
0.10
0.07
0.04
0.06
0.09
0.05
0.01
0.01
0.04
0.05

12
0.09
0.08
0.06
0.07
O.OS
0.06
0.07
0.02
0.02
0.02
0.03
0.04

13
0.09
0.06
0.04
0.07
0.07
O.OS
O.OS
0.03
0.03
0.04
0.03
0.02

14
0.10
O.OS
0.02
0.07
0.10
0.06
0.07
0.02
0.02
0.06
0.04
0.03

15
O.OS
0.07
0.03
0.08
0.06
0.10
0.08
0.02
0.02
0.05
0.06
0.06

16
0.12
0.13
0.06
0.15
0.08
0.11
0.14
0.04
0.04
0.08
0.11
0.16

17
0.19
0.19
0.15
0.15
0.17
0.17
0.19
0.10
0.11
0.14
0.21
0.15

IB
0.10
0.20
0.16
OJ5
OJJ
0.22
0.19
0.04
0.10
0.14
0.22
0.16

19
0.19
0.18
0.13
0.15
0.18
0.22,
0.09
0.10
0.10
0.22
0,16

20
A
0.1?
0.14
0.13
0.18
0.24
0.11
0.08
0.10
0.21
0.16
0.21
21
0.18
ft
0.15
0.13
0.18
0.24
0.12
0.08
0.11
0.20
0.17
0.20
22
0.16
0.13
0.13
0.11
0.13
0.2«
0.11
0.07
0.11
0.17
0.17
0.21
23
0.17
*
0.12
0.09
0.11
0.20
0.11
0.05
0.09
0.13
0.15
0.21
24 1 2
ft ft
ft *
0.09 0.08
0.08 0.07
0.08 0.08
0.17 0,15
0.09 0.10
0.04 0.04
0.07 0.07
0.12 0.08
0.15 0.13
0.18 0.17
(continued)

-------
                                                  TABLE 8-13.  (continued)
                                                          Hour of Day
RAHS
Station       7     8     9     10     11    12    13    14    IS    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

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

120*     *     *     *      *    *     *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 NO- concen-
trations varied from  0.15 to 0.20 ppra; 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
N0« 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  NQ/NOj 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,  O.C.   These stations are  located  in an urban complex dominated by
area sources  (70  percent of NO   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  NO,,  suggesting a considerable  variation  in  local NO area emissions
or  in  monitor siting.   Nevertheless, it is important  to  note  that  the highest  hourly W^
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,  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

-------
Ul
to
                           NO If  Silnwx
                                                               titiic £irctu ol •, 19, 20. iml 40 hm. »



                                                                8 19, Si. Louli RAMS itMion loeMiont,

-------
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
Apri 1
May
June
RAMS STATION 111
January
February
March
April
May
June
Highest-NO
(ug/m3)

329
475
260
500
179
303

362
474
303
406
276
228

644
617
456
434
267
226
Corresponding
N02 (ug/m3)

126
59
147
199
*
190

111
103
99
91
*
99

76
*
134
128
*
152
Highest,NQ-
(ug/m )

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

-------
     MASSEY
TABLE 8-15.  MONTHLY TRENDS IN HOURLY NO AND NO, CONCENTRATIONS,
EY BUILDING STATION, FAIRFAX COUNTY, VIRGINIA, I977a (KEYES ET AL.)

Month
January
February
March
Apri 1
May
June
July
August
September
October
November
December
Highest NO
655
650
350
230
40
80
20
70
125
420
680
645
Corresponding
N0_ {(jg/ra )
140
105
105
120
20
85
65

95
75
43
120
Highest3
160
190
140
160
180
170
85
95
115
225
115
120
2nd Highest
150
170
130

130
160
75
75
105
130
105
115
Annual Average NO-:  40 \jg/m
Second Highest N02:  190 pg/m3
Peak/mean = 4.8
30ata from Fairfax County (Va.) Air Pollution Control Agency.
                                   8-61

-------
TABLE 8-16. MONTHLY TRENDS IN HOURLY NO AND NO,
LEWINSVILLE STATION, FAIRFAX COUNTY, VIRGINIA, 197
CONCENTRATIONS,
7a (KEYES ET AL. )

Month
January
February
March
Apri 1
May
June
July
August
September
October
November
December
Highest NO
(N9/» )
680
630

615
380
290
290
650
515
580
700
680
Corresponding
N02 (Hg/irr)
65
65

95
120
180
75
10
75
40
45
75
Highest-
N02 (Hg/ni }
130
290

190
290
225
170
280
280
160
140
130
2nd Highest
N02 ((jg/RO
125
225

180
255
205
140
265
235
150
130
120

Annual Average N02:  56 ug/m
Second Highest N02:  280 ug/m3
Peak/mean =5.0
aData from Fairfax County (Va.) Air Pollution Control Agency.
                                   8-62

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TABLE 8-17.  MONTHLY TRENDS IN HOURLY NO AND NO, CONCENTRATIONS,
VEN CORNERS STATION, FAIRFAX COUNTY, VIRGINIA, 1977a (KEYES ET AL.)
SEVEN

Highest NO
Month (u9/m )
January
February
March
Apri 1
May
June
July
August
September
October
Annual Average NO-:
Second Highest NO.:
Peak/mean = 5. 1
a
630
620
540
665
240
170
185
320
505
420
46
235


Corresponding
N02 (M9/m )
10
50
0
0
40
20
55
105
105
85




Highest,
N02 (MS/IT )
150
205
120
265
190
140
170
235
205
160




2nd Highest
N00 (M8/m )
£
120
145
110
195
170
130
150
150
170
150




                           8-63

-------
stacks, 42 in  apart,  each 138 ra 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
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 soma bearing on  the question of estimating human exposure
to  this pollutant.   Such an estimation might  include a study of the spatial variation of NO.
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
HQy concentrations which 1s 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 N0_ 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
                                                            3
California Ambient Air  Quality  Standard  (CAAQS) (470 \sg/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  A1r  Quality  Standard  but  is included  only  to  illustrate   an  existing  exposure
methodology.
                                            8-64

-------
Figure 8-20. Location and elevation of Clinch River Power Plant monitoring stations (Pickering, 1980).

-------
      TABLE 8-18.  MEAN NOV CONCENTRATIONS FOR ISOLATED POINT SOURCE
  IN COMPLEX TERRAIN (CLINCH RIVER POWER PLANT) (ppb) (PICKERING, 1980)
Station                    N0x             NOg                NO
Tower                      29              15                 15
Munsey                      7               S                  1
Hockey                      S3                  2
Lambert                     -
Johnson                     -
Castle                     25              11                 13
Kents                      11               7                  3
Nashs                      15               9                  6
                                8-66

-------
                        TABLE  8-19.   TEN  HIGHEST  HOURLY AVERAGE NO   CONCENTRATIONS OBSERVED AT EACH
                     MONITORING  SITE  FOR  ISOLATED SOURCE (CLINCH  fifVER  POWER PLANT) (PICKERING, 1980)
00

-j




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
V
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
6/7/77
8/10/77
2/10/77
7/8/77
2/10/77
7/12/77
2/11/77
6/7/77
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
Con2.
(PPb)
816
589
464
435
410
394
371
365
350
290
Hockey


Date
6/30/77
7/5/77
8/15/77
6/30/77
7/6/77
7/2/77
A/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
ConS.
(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, N0_ 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  NO-  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  NOg 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 or  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

-------
a
<
t-
X
K

Z
1C
o


a
Ul
o
o
z
o
<
cc
0.1
    0.01
             I  I  I  I  I  1  I  I  I I t  I  I  1  I  I  II I  I  I  I  I  I  I  I   L.
                                       	 ALL TIME

                                       	 WEEKDAY

                                       __._ WEEKEND
          I  I  I  I  I  I  I  I  I I  I \'\  M \ I  I \\  I  I  I  I  I  I  I I  I
       0                    5                    10


                PERCENT OF DAYS ABOVE THE CALIFORNIA STANDARD



        Figure 8-21.  Population exposed to MOj daily maximum hourly

        concentration above the California one-hour standard at various

        frequencies (Horieet al., 1977).
                                                                      15
                                        8-69

-------
  TABLE 8-20.  REGIONWIOE 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
Percent of Days Exceeded3
3,7 (3.8)
4.4 (4.5)
2.1 (2.1)
Percent of Hours Exceeded3
0.46 (0.50)
0.57 (0.63)
0.18 (0.18)
  Weekday/Weekend
  Difference                  +2.3 (+2.4)                 +0.39 (+0.45)
Percentages in parentheses computed based on the mobile population assumption.
                                   8-70

-------
u

u


o
ui
cc
u.

Q
IU
O
IU
cc
O


o

8
o

X
IU


O
 .
O


O
0.1
   0.01
               I  I  I  I  I  I  I   I  I  I  I  I  I  I I 1  I  I  I  I  I  I I  I  I
                                    	  ALL TIME

                         \           _ —-  WEEKDAY


                         V         — •—.  WEEKEND
         I  I  I  I  I  I  I  I  I  I  I  I  I  M  I I  Pi>J  I  I  I  l\l  I  I  I  I
                           0.5                    1


              PERCENT OF HOURS ABOVE THE CALIFORNIA STANDARD
                                                                      1.5
      Figure 8-22. Population exposed to NO7 hourly average concentration

      above the California one-hour standard (470 pg/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 NO-  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  NO. concentration reported in the county, provided that the moni-
toring site reporting  was  located  specifically to monitor population exposure (SAROAO 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 N02 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  NO. 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 NO, concentra-
                              3                                                   ^
tions which exceeded  500  ug/m  at least twice during the year; and 14 percent to one-hour NO.
                                        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 NO. 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
1974 Second Highest
County 1-hour NO.
Count Concentration (ug/m
68 250
24 500
6 750
% Monitored
, Total 1970 Population Population Potentially
J) Potentially at Risk at Risk
41,837,864
21,341,617
10,106,698
57
29
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 ug/m  in the fine particle fraction (<2.4|j) of a sample collected
by  a dichotomous  sampler using  Teflon filters  (Ozubay 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  ug/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 M and 16 u) range from 0.06 to 0.83
Mg/m  with a mean  of 0.22 ug/m  .   Measurements at  a  number of  sites near  freeways in Los
Angeles gave fine  fraction  nitrate concentrations up to  2.0  ug/m  and similar readings up to
2.1 MS/i"  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)  HNO,   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
23-hr average  HNO- 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
23-hr average  values  up to 65 ug/m   (26  ppb)  and a 1-hr maximum of 78 pg/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  M9/m   (6 PPb)  in Riverside, California,  during approximately  one day of
monitoring  in October 1976.
                                            8-73

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     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  (1975a,b)  first  reported  dimethylnitrosamine  (DMN)  in ambient  air in 1975.   Levels
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  (1975a,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) (1977b) showed  little indication  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  (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 atmosphere.   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 concen-
tration  (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 NO2 concentra-
tions.  In summary,  the data cited illustrate the following points.
                                            8-74

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        • Annual average concentrations of NO. 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 NO- 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 NO. concentrations also tend to be
          area-specific.
        • The  oxidation  of NO to NO.  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 NO. 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 pg/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 NO. 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 NO. concentrations exceeded 150 ug/m  (0.08 ppm).
                                                                              3
     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,  by 1980 virtually none of  the  still operating
monitoring  sites reported  annual  average  levels over 100  pg/m   (except  one  in  San  Diego;
114 ug/m3).

                                            8-75

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8.4.2  Atmospheric Concentrationsof 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
from 0.18 pg/m  in Philadelphia, Pennsylvania, to 2.1 yg/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 (OMN) ranged up to  32  vg/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

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CHAPTER 8


Breeding, R. J., J. P. Lodge, Jr., J. B. Pate, D. C. Sheesley, H. B. Klom's, B. Fogle, J. A.
     Anderson, T, R. Englert, P. L. Haagenson, R. B. McBeth, A. L. Horn's, R. Pogue, and A. F.
     Wartburg.  Background trace gas concentrations in the central United States,  J. Geophys.
     Res. 78(30): 7057-7064, 1973.

Chameides, W. L. Tropospheric odd nitrogen and the atmospheric water vapor cycle.  J. Geophys.
     Res. 80: 4983, 1975.

Cox, R. A.  Some measurements of ground level NO, NO, and 0, concentrations at an unpolluted
     maritime site.  Tellus 29:  356-362, 1977. '    l      *

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

Drununond, J. W.  Atmospheric Measurements of Nitric Oxide Using a Chemiluminescent Detector.
     Ph.D. thesis, University of Wyoming, 1976.

Dzubay, Thomas G., and R. K. Stevens.  Ambient air analysis with dichotomous sampler and x-ray
     fluorescence spectrometer.   Environmental Science and Technology 9(7): 663-668, 1975.

Dzubay, T. 6., R. K. Stevens, and L. W. Richards.   Composition of aerosols over Los Angeles
     freeways.  Accepted for publication in Atin. Env., Hay 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 freeway.
     In;  The Los Angeles Catalyst Study Symposium.  EPA-600/4-77-034.  U.S. Environmental
     Protection Agency, Research Triangle Park, North Carolina, June 1977.

Federal Register.  40 CFR Parts 51, 52, 53, 58, 60.  August 7, 1978.

Fine, D. H.  Final Report of Honitoring 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-nitroso compounds in the
     environment.  Paper presented in Int'l. Conf. of Environmental Sensing and Assessment,
     Las Vegas, Nevada, September 22-26, 1975a.

Fine, D. H., D. P. Rounbehler, N. B. Belcher, and S. S. Epstein.  N-nitroso compounds in air
     and water.   Paper presented at the Fourth Meeting of the  Int'l. Agency for Research on
     Cancer, Tallinn, Estonia, USSR, October 1-2, 1975b.

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.
     Environmental Protection Agency, Research Triangle Park,  North Carolina.  June  1978.
     This data base is maintained at the Statistics and Data Management Office, Health Effects
     Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North
     Carolina  27711.
                                           8-77

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Galbally, I. E.   In:  Air  Pollution  Measurement Techniques,  Special  Environmental  Report No.
     10, World Meteorological Organization  No. 460, WHO,  Geneva,  1977.   pp.  179.

Hanst, P. L., E.  W. Wilson,  R.  K.  Patterson,  B, 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, North Carolina,  1975.

Marker, A. B., L.  W. Richards,  and W.  E.  Clark.   The  effect  of  atmospheric  SO- photochemistry
     upon observed nitrate concentrations in  aerosols.  Atm.  Env.  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-450/3-77-0046.  U.S. Environmental Protection Agency,  Research  Triangle Park,  North
     Carolina, January 1977.

Huebert, B. J,, and A. L.  Lazrus.  Global tropospheric measurements  of nitric acid vapor and
     particulate  matter.   Geophys. Res. Lett. 5:  557-589,  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 partieulates in Panama.   Sciences
     153: 3734, 408-410, 1966.

Ludwig, F. L., and E. Shelar.   Site  Selection for the Monitoring  of  Photochemical  Air
     Pollutants.   EPA-450/3-78-013.   U.S. Environmental Protection Agency,  Research Triangle
     Park, North  Carolina, 1978.

Miller, D. F., and C. W. Spicer.   A  continuous analyzer for  detecting nitric  acid.  Presented
     at Air Pollution Control Association 67th Annual Meeting,  Denver, Colorado, June  9-13,
     1974.

Moore, H. E.  Isotopic measurement of atmospheric nitrogen compounds. Tellus  26: 169-174,
     1974.                                                                    ~™

Nelson, E.  Regional Air Pollution Study  (RAPS).  Final Report:   High Volume  Filter Measure-
     ments of Suspended Particulate  Matter.   EPA  Contract No. 68-02-2093.   U.S. Environmental
     Protection Agency, Research Triangle Park, North Carolina, September 1978.

Noxon,  J. F.  Nitrogen dioxide in the stratosphere and the  troposphere  measured by ground-
     based absorption spectroscopy.   Science  189;  547-549,  1975.
Noxon
,  J.  F.   Tropospheric NO,.   J. Geophys. Res. 83: 3051-3057, 1978.
Pellizzari, E. D.  The Measurement of Carcinogenic Vapors  in Ambient Atmospheres.
     EPA-600/7-77-055.  Environmental Sciences Research  Laboratory, U.S.  Environmental
     Protection Agency, Research Triangle Park, North Carolina, June 1977.

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.
     Environmental Protection Agency, Research Triangle  Park, North Carolina, January 1980.
                                           8-78

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Ritter, R. A., 0. H. Stedman, and T. J. Kelly.  Ground level measurements of NO, NO- and 0,  in
     rural air.  In:  Nitrogenous Air Pollutants.  D. Grosjean, ed. p. 325.  Ann ArBor  Science.
     Ann Arbor, Michigan, 1979.

Robinson, E., and R. C. Robbins.  Emissions, concentrations, and fate of gaseous atmospheric
     pollutants.  In:  Air Pollution Control Part II. W. Strauss (ed.).  Wiley-Interscience,
     New York, 1972.  pp. 193.

Spicer, C. W.  The fate of nitrogen oxides in the atmosphere.  In: Advances in Environmental
     Science and Technology, Vol. 7.  J. N. Pitts, Jr. and R. L. Metcalf (eds.).  John  Wiley
     and Sons, New York, 1977.

Spicer, C. W., P. M. Schumacher, J. A. Kouyoumjian, and D. W. Joseph.  Sampling and Analytical
     Methodology for Atmospheric Particulate Nitrates.  EPA-600/ 2-78-067.  Environmental
     Sciences Research Laboratory, U.S. Environmental Protection Agency, Research Triangle
     Park, North Carolina, April 1978.

Stevens, Robert K., T. G. Dzubay, D. J. Mage, R. Burton, G. Russwurm, and E. Tew.  Comparison
     of nitrates and sulfates collected by Hi-vol and dichotomous samplers.  Presented  to
     American Chemical Society, Division of Environmental Chemistry, Miami, Florida, September
     1978a.

Stevens, Robert K., T. G. Dzubay, 6. Russwurm, and D. Rickel.  Sampling and analysis of atmos-
     pheric sulfates and related species.  Atm, Env. 12: 55-68, 1978b.

Trijonis, J.  Empirical Relationships Between Atmospheric Nitrogen Dioxide and Its Precursors.
     EPA-600/3-78-018.  Environmental Sciences Research Laboratory, Office of Research  and
     Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina,
     February 1978.

Trijonis, J. C., et al.  The Relationship of Ambient NO- 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, North Carolina.

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.  Atm. Env. 12: 867-875, 1978.

U. S. Environmental Protection Agency.  The National Air Monitoring Program: Air Quality and
     Emissions Trends—Annual Report.  Volume 1, Chapter 4.  EPA-450/1-73-001.  Washington,
     D.C., 1973.  pp. 26-28.

U. S. Environmental Protection Agency.  National Aerometric Data Bank, 1975a.

U. S. Environmental Agency.  SAROAD, 1975b.  Data reported were abstracted from the 1975
     SAROAO raw data file maintained at the National Air Data Branch, Durham, North Carolina.

U. S. Environmental Protection Agency.  National Air Quality and Emissions Trends Report,
     1975.  EPA-450/1-76-002.  Office of Air Quality Planning and Standards.  Research
     Triangle Park, North Carolina, November, 1976a.

U. S. Environmental Protection Agency.  RAPS, 1976b.  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, North Carolina.


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U. S. Environmental Protection Agency.  SARDAD, 1976c.  Data reported were abstracted from the
     1976 SAROAO raw data file maintained at the National Air Data Branch, Durham, North
     Carolina.

U. S. Environmental Protection Agency.  Air Quality Data - 1975 Annual Statistics including
     suramaries with reference to standards.  EPA-450/2-77-Q02.  I977a.

U.S. Environmental Protection Agency.  Air Quality Data - 1978 Annual Statistics including
     Summaries with Reference to Standards.  EPA-45Q/4-79-037.  U.S. Environmental Protection
     Agency, Research Triangle Park, North Carolina, November, 1979.

U.S. Environmental Protection Agency.  Air Quality Data - 1980 Annual Statistics Including
     Suramaries with Reference to Standards.  EPA-450/4-81-027.  U.S. Environmental Protection
     Agency, Research Triangle Park, North Carolina, August 1981.

U. S. Environmental Protection Agency.  Reconnaissance of Environmental Levels of Nitrosamines
     in the Central United States.  EPA-330/1-77-001.  National Enforcement Investigations
     Center, Office of Enforcement, Denver, Colorado, August 1977U.

U. S. Environoental Protection Agency.  Reconnaissance of Environmental Levels of Nitrosamines
     in the Southeastern United States.  EPA-330/1-77-009.  National Enforcement Investigations
     Center, Office of Enforcement, Denver, Colorado, August 1977c.
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                      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 NOX (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 ran)
                        0   + N02 •+ NO  + 02                                   (9-2)
                        NO  + 0   •» N0  + 0                                    (9-3
                            2 03  * 3 02                                       net
     The main  source 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):
                   03    + hv  + 0(1D) + 02                                    (9-4)
                                            (wavelengths shorter than 310 nm)
                        0(1D) + 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 N02  into the  stratosphere  from  the  earth's surface is strongly  prohibited  by wet
removal of  NQ2 and  especially its oxidation product HNO,,  which is formed  by  the reaction:
                        OH + N02 (+M) + HN03 (+M)                              (9-S)
     The hydroxyl  radical (OH)  is  primarily formed by the  attack  of 0( D)  on  water vapor,
following reaction 9-4, above:
                        0(1D) + 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 0-18
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

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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, NO , play a remarkable catalytic role in the ozone balance of the
atmosphere.  Above  about 24 km, the  net effect  of NOX 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
                        N02 + hv •* NO + 0
                        0   + Q2 •*• M  -» 03 + M
                        R02 + 02 •* RO + 03

     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
CH,CO  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 0- •* CO, + 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 (Fishraan
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   (X < 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

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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 NO  volume mixing ratios
                       "11
are not too small (> 10   ), because of the fast rate of reaction 9-8.
     In the lower  stratosphere (-10-24 ton) 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)

         by deferring it into the sequence
                        OH  + 03 •» H02 + 02
                        H02 + NO •» OH + N02
                        N02 + hv -» NO + 0
                        0   •*• 02 + M -»•  03 + M
                        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 NOX additions from high-flying aircraft.  As a result of the peculiar photochem-
ical action  of  NO , 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 N20  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

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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  + H -» C10N02 + H                             (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 CIQNO,
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 TOJ 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  interferring 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

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by  the  increased absorption of  ultraviolet solar radiation and enhanced  trapping  of thermal
9.6 Mffl 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 HO  via  reactions  9-4 and 9-5.  Because of its absorption bands at about 7.8 urn
and  17,0  urn,   nitrous  oxide  (N,0)  likewise  contributes  significantly  to  the  atmospheric
"greenhouse" effect by trapping outgoing terrestrial radiation.   It has, therefore,  been esti-
mated that a doubling of the atmospheric N,0 content could cause an increase in surface temper- •
atures by  as much  as 0.7°K (Wang et al., 1976).  Several recent studies have been designed to
estimate the possible extent of future atmospheric N^O build-up due to increased use of nitro-
gen  fertilizer  (CAST,  1976; Crutzen, 1976;  Crutzen  et al., 1976; 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 N20 front soil arid water to the atmosphere are the following:
     1.   The release  of N-O  in the denitrification  process.   This  microbiological process,
          which is  currently considered  to be the main source of atmospheric N20, takes place
          in anaerobic  microenvironments, and  involves  the reduction  of nitrate  to HJ3 and
          molecular  nitrogen  (N«).   It  is  this process  which presumably  balances nitrogen
          fixation,  i.e., the  conversion of N~ to fixed nitrogen.  A growing mount of obser-
          vational evidence is  now accumulating, which indicates that the yield of N-O versus
          N, 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 conversions in the atmo-
          sphere, 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), HcElroy et al. (1977), and Crutzen and Ehhalt (1976).
     3.   The role of the oceans in the worldwide N^Q budget.  While initial studies indicated
          a large source of N^Q in the oceans (National Academy of Sciences, 1978), recent in-
          vestigations  point  towards a much  smaller role of oceans in  the  global  N^O budget
          (Hahn, 1974; Weiss, 1977).
     The scientific  problems connected with possible future increases in atmospheric HJ3 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  Academy of Sciences
(1978).  The  issue  is further complicated  by  the  fact that the  nitrogen  cycle  is  coupled to
                                             9-5

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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
nitrous  oxide (NgO).  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  dem'trification 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 N-O,
with most of the rest returned to the atmosphere as N--  Since N,0 is not believed to take part
in any  atmospheric chemical  reactions below  the  stratosphere,  all the  N«0 produced terres-
trially  is  available for  stratospheric  reactions.   The concern expressed  by  some  authors in
the recent  past,  that  NgO arising  from  excess fertilizer  might  decrease  the  total strato-
spheric ozone by  as  much as 20 percent  for a 100 percent increase in total N^O, 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
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.  Nitrous oxide like-
wise contributes to the atmospheric "greenhouse" effect by trapping outgoing terrestrial radi-
ation.   One author recently estimated that a  doubling  of  the atmospheric burden of NgO 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 ferti-
lizer 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
definitive conclusions can prudently be drawn.
                                             9-6

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CHAPTER 9


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.  Hem. Royal Meteorological Society 3:103-125,
     1930.

Cohen, Y., and L. I, Gordon.  Nitrous oxide production  in the ocean.  J. Geophys.  Res. 84(C1):
     347-353, 1979.

Council for Agricultural Science and Technology (CAST).  Effect of  increased nitrogen fixation
     on atmospheric ozone.  Report No. 53, Iowa State University, Ames,  Iowa, January 1976.
     33 pp.

Crutzen, P. J.  The influence of nitrogen oxides on the atmospheric ozone content.  Quart. 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, 1976.

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

Oanielsen, E. F., and V. A. Hohnen.  Project dustorm report:  ozone transport, in  situ
     measurements and meteorological anlyses of tropopause  folding.  J.  Geophys. Res. 82(37):
     5867-5877, 1977.

Delwiche, C. C.  Nitrous oxide and denitrification.  Presented at Oenitrification  Seminar,
     Oct. 1977, San Francisco.  The Fertilizer Institute, Washington, D.C.

Fishman, J., and P. J. Crutzen.  The origin of ozone in the troposphere Nature 274: 855-858,
     1978.

Hahn, J.  The North Atlantic Ocean as a source of atmospheric N-O.  Tell us 26: 160, 1974.

Hampson, R. F., and D. Garvin.  Chemical kinetic and photochemical  data for modelling atmos-
     pheric chemistry.  Nat. Bur. Standards, Tech. Note 866, U.S. Dept.  of Commerce,
     Washington, O.C., 1975.

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

Johnston, H. S.  Reduction of stratospheric ozone by nitrogen oxide catalysts from SST exhaust.
     Science 173: 517-522, 1971.
                                            9-7

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Liu, S. C., R, J. Cicernone, T. M. Donahue, and W. C. Chameides.   Limitations  of  fertilizer
     induced ozone reduction by the long lifetime of the reservoir of  fixed nitrogen.  Geophys.
     Res. Letter 3: 157-160, 1976.

McElroy, H. B.  Testimony presented to the Committee on Interstate and Foreign Commerce,  U.S.
     House of Representatives, Washington, O.C., December 11, 1974.

McElroy, H. B., and J. C. HcConncll.  Nitrous oxide:  a natural  source of  stratospheric NO.
     J. Atmos. Sci. 28: 1095-1098, 1971.

McElroy, M. B., S. C. Wofsy, and Y. L. Yung.  The.nitrogen  cycle:  perturbations  due to man
     and their impact on atmospheric N,0 and 0,.  Phil. Trans. Roy.  Soc. London,  B. Biological
     Sciences 277: lSi-181, 1977.     *       *

Molina, M. J., and S. S. Rowland.  Stratospheric sink for chlorofluromethane;  Chlorine atom-
     catalysed destruction of ozone.  Nature 249: 810-812,  1974.

National Academy of Sciences.  Nitrates:  an environmental  assessment.  Washington,  D.C.,  1978.

Nicolet, M., and E. Vergison.  L'oxide azoteux deus la stratosphere. Aeronimica Acta 90:  1-16,
     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. 0. Sze.  The analysis of fertilizer impacts on  the  ozone  layer.  Environmental
     Research and Technology, Inc., Document P-2123, 1976.

Rolston, D. E.  Field-measured flux of nitrous oxide from soil,  presented  at Denitrification
     Seminar, Oct. 1977, Sao Francisco.  The Fertilizer Institute, Washington, D.C.

Simpson, H. J., et al. "Han and the global nitrogen cycle.  Group Report,  in  Global Chemical
     Cycleis and Their Alterations by Han, ed. W. Stumm, pp. 253-274, Berlin:   Dahlem
     Konferenzen, 1977.

Sze, N. D., and H. Rice.  Nitrogen cycle factors contributing to N_0 production from
     fertilizers.  Geophys. Res. Letter 3: 343-386, 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 194: 685-690, 1976.

Weiss, R. F.  Nitrous oxide in the atmosphere and the sea.  Presented  at Denitrification
     Seminar, Oct. 1977, San Francisco.  The Fertilizer Institute, Washington, D.C.
                                            9-8

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                         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 responsible 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 contribute to the
reduction of visual range (White and Roberts, 1977; Trijonis and Yuan, 1978b).  (See Chapter 6
for a discussion of  atmospheric  processes resulting in ambient burdens of NO, 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        S
which a beam of  light is attenuated in passing through the atmosphere:  •
               dl/l  =  -b dx,  and  dl /I  =  -b dx,
                 9         a            S         5
where I  is  the intensity of the  beam,  and dl  and dl  are the changes in I due to absorption
                                              2       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    b
     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 participates):
                    b  -  ba  + bs
                       =  b+b+b+b
                          uag     "ap     usg      sp
In polluted atmospheres, the term b   is dominated, at visible wavelengths, by the contribution
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  (U.S. DHEW, 1969).  Nitrate compounds may constitute a significant fraction in
the optically important particle size range, but current information on ambient nitrate concen-
trations is insufficient to make any conclusive assessment.

                                              10-1

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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 N02  can  be
used to calculate the visual impact of NO, in the atmosphere (Dixon, 1940).
10.2.1  Nitrogen Dioxide and ...Plumes
     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 integral of NQ2 concentration
along the sight  path;  e.g., theoretically similar effects would be produced by a 1 kilometer-
wide plume containing 0.1 ppm (190 ug/n ) NO- or a 0.1 kilometer-wide plume containing 1.0 ppm
(1,900 ug/m3} N02.
     Figure  10-1  shows the  calculated  transmittance of particle-free  NO- plumes  for several
values of the  concentration-distance product.   Less than 0.1 ppm-km NO- is sufficient to pro-
duce  a  color  shift which  is distinguishable  in carefully-controlled, color-matching tests
(HacAdan, 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 N02 plumes  from nitric acid manufacturing plants  under varying
operating conditions  (Hardison,  1970).   The  value cited  refers to the effect of N02  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 NO,  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 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.  NO-  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 observer, 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 diminishes  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  NO- absorption  is  determined  by  the relative concentrations  of  N02 and  light-

                                             10-2

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  4000

    BLUE
500C>              6000

    WAVELENGTH. X
 7000

RED
Figure 10-1. Transmittance expfbpjOj*^ °* ^^2 plurnes for
selected values of the concentration-distance product (Adapted
from Hodkinson, 1966.)
                              10-3

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scattering  particles.   In a uniform atmosphere,  the  effect of NO, at any given wavelength is
described by the following  relationship (Robinson, 1968):
where Bhnrizon anc* ^horizon^^^ = ^ are ^e Brightness of the horizon sky, with and without
N02.
     The ratio bN02/bs is more easily related to experience when expressed in terms of concen-
tration, [NO,], 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 measurements
and  found  indications  that  VR and b  are  related by the formula, VR = (3 + l)/b .  Since, in
                                    s                                      -*•     s
addition,  b,,n2  is  proportional  to [NQ2], it follows that the ratio buno/kg 1S proportional to
the  product  [NO,]  VR.   Figure 10-2 shows, for  several  values of this product, the calculated
alteration contributed  by NQ2  to horizon brightness  which is in turn a  function of aerosol
scattering.   It  should be noted  that this calculation neglects  the  wavelength dependence of
the  scattering, which can be substantial in relatively clean air and mitigates the discoloring
effects of N02.
     The  interpretation  of Figure 10-2  is similar to that of Figure  10-1.   A concentration-
visual range product of 0.3 ppm-km N02 corresponds to  a color shift which should be detectable
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 ug/m ) N02
night suffice to color the horizon noticeably.  At a visual range of 10 kilometers, typical of
urban haze,  0.03  ppm  (60 pg/rn ) N02  might be required to produce the  same  effect.   However,
quantitative theoretical  calculations of human  perception of  N02  are  not fully developed and
experimental observations are needed to evaluate the actual effect.
     Independent of absorption  by N02,  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

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  4003

   BLUE
6000              6000

    WAVf LENGTH, A
 7000

RED
Figure 10-2. Relative horizon brightness, bs/(bs + bpgQ-), 'or
selected values of the concentration-visual product, assimung
bj = 3/(visual range).  (Adapted from Hodkinson, 1966.)
                          10-5

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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  -i                                         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 O.S 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  (sych  as  in secondary aerosols)
should exhibit  extinction  coefficients  per unit mass  on the  order of 0.06 +  0.03,  where  the
units  are (10 m)~  /(pg/m )  (Latimer  et al., 1978; 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, 1976; Whitby  and Sverdrup 1978),
should exhibit much lower extinction coefficients, per unit mass, on the order of 0.006 + 0.003
where  the units are (10*m)~l/(pg/m3)  (Latimer et al., 1978; Ursenback et al., 1978; White  and
Roberts, 1977).   These results are confirmed  by empirical  studies  (Cass, 1976;  Trijonis  and
Yuan,  1978a,1978b; Waggoner et al.,  1976; White  and  Roberts,  1977), which typically find  ex-
tinction coefficients per  unit mass  of sulfates (a prevalent secondary aerosol) to be 0.04 to
0.10 (10 m)  /(pg/m ).  For the remainder of TSP (mostly coarse particles), the extinction  co-
efficient per unit mass is 0.004 to 0.01 (104m)"1/(Mg/m3).
     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 especially
                                             10-6

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i   °-10
>-
z
K""0'08
si
« 3-
Z^T- 0.06
21
<  -0.04
2    0-02
              III
                           1    I
i   i    r
                                                           I   I
              I
        0.030.050.070.10   0.20.3   0.50.71.0    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

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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 aug-
mented 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 contrast due
to haze  and plumes  may  impede  air  traffic.   N02  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 N02 concentration along the sight
path;  i.e., theoretically  similar  effects  would be  produced  by a 1 kilometer-wide plume con-
taining 0.1  ppm (190  u'g/m )  of NO,  or  a  0.1 kilometer-wide plume containing  1.0  ppm  (1,900
    3
pg/m ) of  NO,.   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  ab.out  0.06 ppm-km.  Empirical observations under  a  variety of
conditions are needed to determine the perceptibility of N02 in ambient air.
     Plume coloration due to NO, 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
tha  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.   N02  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

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Under these conditions, particle scattering diminishes the plume coloration.  Estimates of the
magnitude of  this effect attributable  to participate 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 dis-
coloration of  the horizon  sky due to  NO, absorption  is  determined by  the relative concen-
trations of NO,  and  light-scattering particles.  A concentration-visual  range product of 0,3
ppra-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
plains, 0.003  ppm (6  u/m  ) NO, 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 ) NO,  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

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CHAPTER 10


Ahlquist, M. C., and R. J. Charlson.  Measurement of the wavelength dependence of atmospheric
     extinction due to scatter.  Atmos. Environ. 3: 551, 1969.

Bradway, R. H., and R. A. Record.  National Assessment of the Urban Particulate Problem,
     Volume II Particulate Characterization.  EPA-450/3-76-025.  U.S. Environmental Protection
     Agency, 1976.

Cass, G. R.  The Relationship between Sulfate Air Quality and Visibility  in  Los Angeles.
     Caltech Environmental Quality Laboratory Memorandum No. 18, California  Institute of
     Technology, Pasadena, California, 1976.

Charlson, R. J., A. P. Waggoner, and J. F. Thielke.  Visibility protection for Class I areas.
     The technical basis.  Report to Council of Environmental Quality, Washington, DC, 1978.

Covert, D. S.  A Study of the Relationship of Chemical Composition and Humidity to Light
     Scattering by Aerosols, Ph.D. Dissertation, University of Washington, Seattle,
     Washington, 1974.

Dixon, J. K.  Absorption coefficient of nitrogen dioxide in the visible spectrum.  J. Chem.
     Phys. 8: 157, 1940.

Hardison, L. C.  Techniques for controlling the oxides of nitrogen.  J. Air  Pollut. Control
     Assoc. 20:377, 1970.

Hidy, G. M., et al.  Characterization of Aerosols in California (ACHEX),  Volume IV:  Analysis
     and Interpretation of Data.  Report to the California Air Resources  Board by Rockwell
     International Science Center, 1974.

Hodkinson, J. R.  Calculations of colour and visibility in urban atmospheres polluted by
     gaseous N02-  Intern. J. of Air and Water Pollut. 10: 137, 1966.

Horvath, H., and K. E. Noll.  The relationship between atmospheric light  scattering
     coefficient and visibility.  Atm. Env. 3:543, 1969.

Husar, R. B., N. V. Gillam", J. D. Husar, and D. E. Patterson.  A study of long range transport
     from visibility observations, trajectory analysis, and air pollution monitoring data.
     In:  Air Pollution:  Proceedings of the Seventh International Technical Meeting 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. 19:
     199-204, 1976.

Latimer, D. A., et al.  The Development of Mathematical Models for the Prediction of
     Anthropogenic Visibility Impairment.  Draft Final Report, EPA Contract  No. 68-01-3947.
     U.S. Environmental Protection Agency, 1978.

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, 1969.
                                            10-10

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MacAdam, D. L.  Visual sensitivities to color differences  in daylight.  J. Opt. Soc. Amer. 32:
     247, 1942.

Halm, W.  Considerations 1n the measurement of visibility.  J. Air Pollut. Control Assoc.
     29:1042, 1979.

Middleton, W. E. K.  Vision Through The Atmosphere.  University of Toronto Press, Toronto,
     Canada, 1952.

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, 19S7.

Robinson, E.  Effect on the physical properties of the atmosphere.  In:  Air Pollution.  A. C.
     Stern (ed.).  Academic Press, Inc., New York, 1968.

Samuels, J. J., S. Twiss, and E. W. Wong.  Visibility, light scattering and mass concentration
     of particulate matter.  A report of the California Tri-City Aerosol Sampling Project,
     California Air Resources Board, 1973.

Trijonis, J., and K. Yuan.  Visibility in the Northeast:   long-term visibility trends and
     visibility/pollutant relationships.  EPA-600/3-78-075.  U.S. Environmental Protection
     Agency, 1978a.

Trijonis, J., and K. Yuan.  Visibility in the Southwest—an exploration of the historical data
     base.  EPA-600/3-78-039,  U.S. Environmental Protection Agency, 1978b.

Ursenbach, W. 0., et al.  Visibility models for the arid and semiarid western United States.
     Paper presented at the Seventy-First Annual Meeting of the Air Pollution Control
     Association, 1978.

U.S. Department of Health, Education and Welfare.  Air Quality Criteria for Particulate Matter.
     NAPCA Publ. No. AP-49, Public Health Service, Environmental Health Service, National Air
     Pollution Control Administration, Washington, D.C., January 1969.

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 261: 55-56, 1976.

Whitby, K. T., and G. M. Sverdrup.  California aerosols:   their physical and chemical
     characteristics.  To Be Published in ACHEX Hutchinson Memorial Volume.  Particle
     Technology Laboratory Pub. No. 347.  University of Minnesota, 1978.

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,  1977.
                                           10-11

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                                    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
elements 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
discussion which follows to the main topic of this document, nitrogen oxides.
     Chapter 12 emphasizes  the effects qf 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
                                           11-1

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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
•Jihje  chemical  processes that  form  them.   When sulfates and  nitrates combine with atmospheric
water, dissociated  forms  of sulfuric  (H-SO.) 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 valye has been selected because precipitation formed in a geochemically clean environment
would have a pH of approximately  i.S  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.  Oust 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
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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

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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  bedrocks.
     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 emphasized
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 reduction  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 decomposition 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 W 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

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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 (S0.~)  and  nitrate (NOl) 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 sources; (4)
                                           11-5

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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; 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
responses 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
because  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, grasslands,
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 atmosphere 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 environment, the litho-
sphere,  hydrosphere  and atmosphere, make up the ecosystem that  is the planet Earth (Billings,
1978; Boughey, 1971; Qdunt, 1971; Smith,  1980).
     Ecosystems are basically energy processing systems "whose components have evolved  together
over a  long  period of time.  The boundaries  of the system are  determined by the environment,
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.
Energy  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

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                   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)
                                      11-7

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     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

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         •S03
   Inorganic A
    Sulfate  V
     so,-
Weathering
 of Rocks
                    Photochemical
                      Oxidation
                                        Direct Utiliiation
                                     . of Atmospheric S02
                                           by Plants
                                             fidt Jf    o*idatio
                                                          Elemental
                                                           Sulfur
1        I
                                            Storage of Sulfur or
                                           Sulfur Compounds in
                                         • Sediments. Fuels, Soils,
                                          and Sedimentary Rocks
                          Volcanic
                         Eruptions
-H,S

  1 ,
                              Combustion
                                  of
                          " Sulfur-Containing
                                 Fuels
                          Figure 11-1.  The sulfur cycle (organic phase shaded).

                          Source: Clapham (1973).
                                                     11-9

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     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;
Horan et al.,  1980;  Qdun, 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, 1378;
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

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  ZONE Of
INTOLERANCE
              ZONE OF
            PHYSIOLOGICAL
               STRESS
                                   TOLERANCE RANGE
RANGE Of OPTIMUM
   ZONE Of
PHYSIOLOGICAL
   STRESS
                                          ZONE OF
                                        INTOLERANCE
              ORGANISMS
             INFREQUENT
 ORGANISMS
  ASSENT
                                       GREATEST
                                      ABUNDANCE
                            ORGANISMS
                            INFREQUENT
                                        ORGANISMS
                                          ABSENT
   LOW4-
                                     -GRADIENT-
                                                                           -»HIGH
                           Figure 11-2. Law of tolerance.
                                        11-11

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     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
because 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 (Holling,  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

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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  manniade 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 (National Research Council,  1978)  were used 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
1960, 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 11-58 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
(U.S.  Environmental Protection Agency, 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

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CO
    so
    40
    30
to

I   20
a
tr
     1850
                            n  n   r
                                         fOIL
                  1900
                                1910

                               YEAR
                                             2000
2050
  Figure 11-3.  Historical patterns of fossil fuel consumption in the
  United States (adapted from Hubbert, 1976).
                       11-14

-------
o
£

(ri

O
o
-J
<
O
u
ce

lu
>•
800



700




600



600




400



300




200



100
                            TOTAL
- OTHER



-OVENCOKE
 ELECTRIC

 UTILITIES
                                                  I
                                                       I
      1900  10    20   30   40   SO    60   70   80   90   2000


                                YEAR


    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

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I

1
s
111


8*
35





30





25





20





15





10





 5





 0
      1940
tn

a
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35




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10
     TRANSPORTATION






    	I
                  1950
                                1960




                               YEAR
                                 I
TOTAL
                                              _L
                                             1970
                                                          1S80
       —  __„.— —*""   TRANSPORTATION
     1940
                  1950
                                1960



                               YEAR
                                             1970
                                                     1980
  Figure 11-5a. Trends in emissions of sulfur dioxides.



  Figure 11-5b. Trends in emissions of nitrogen oxides.



  Source: U.S. Environmental Protection Agency (1978).




                           11-16

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 I
M
•si
            KEY

   EMISSION  DENSITY, fon«/mi*
       3*10
   nil 10- 20
 20-50-


!>50
                   Figure 11-6. Characterization of U.S. SOX emissions density by stata (U.S. Dept. of Energy, 1980).
                   (Roman numerals indicate EPA Regions.)

-------
 I
£
       EMISSION OCNS1TV, lo«»/mi2
                         Figure 11-7. Characterization of U.S. NOX emissions density by state (U.S. Dept. of Energy, 1980).
                         (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; Cogbill 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 andt 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 (Sinclair, 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  SO*  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.  (1973)
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 (HNO,)  and  sulfuric  (H,SO,)  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

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                   Figure 11-8. The transport and deposition of atmospheric pollutants, particularly oxides of sulfur and
                   nitrogen, that contribute to acidic precipitation.

-------
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 II 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 (H.CO,) is formed.  Carbonic
acid  is a weak acid and in  distilled  water only dissociates slightly,  yielding hydrogen ions
and bicarbonate  ions  (HCO,  ).   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.   Oust 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
   Jj.                A,                  A,
(Mg  ), potassium  (K ), and sodium (Na )  into  solution.  Bicarbonate  usually  is  the  corre
spending  negative  ion.   Decaying  organic matter adds  gaseous  ammonia  to the atmosphere.
Ammonia gas  in rain  or snow forms  ammonium  ions  (NH.*) and  tends  to increase  the pH.   In
coastal areas  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 (Cl  ) and sulfate (SO,  )--are also those most abundant in ocean water (Likens,  1976;
Likens et al., 1979).
     Gases,  in  addition to CO-, which enter  precipitation, are sulfur  dioxide (SO,) 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 SCL and HUS
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 aqueous
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  (SQ.T), sulfate SO/"), nitric oxide (NO), nitrogen dioxide (NO^),
nitrite (NO,"),  nitrate  (NO,"), ammonium (NH^*),  chlorine  (Cl")  hydrochloric acid (HC1), and
Briinsted acids [e.g., dissolved iron (Fe) and ammonium (NH. )} (Whelpdale, 1978).

                                           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 nay 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
responsible 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.)  Cogbill
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 H2S04,  30  percent to HNO,, 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  (1958)  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
occurred  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) concluded that, despite deficiencies in the historical  data and questions

                                           11-22

-------
     ;£
     M

     f
     z
     f
     <
     >-
     z
-A*
            I
               I  I  I   I  I  I   I  I  I
           1920 1830
                    1940  1950 1860


                     ViAB
                                  1970
           1920 1930  1940  19SO  1960  1970

                      YEAR
Z
I
                                              1 -]
                                      1920  1930 1940  19SO  1960 1970


                                                YEAR
                                   0.6

                                   O.S


                                   0.4


                                   0,3


                                   0.2


                                   0.1

                                    0
                                                  I  I   I  I  1   I  I
                                                   1968
                                             1970  1972 1974


                                             ViAR
      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 (Ah 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 H-SQ. 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  NOj,  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 , MH.,  K  , Ca   and
  ?+                                 —      —        ?—
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 (SOt  )  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 SO, (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  VariationsIn 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 SQ^,   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.  (1976) and Miller et al.  (1978) both stated that
a sunnier  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 Nitrogen Oxides, 1980),   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 varia-
tions,  but  relatively small  seasonal variations, for nitrogen forms in wet-only precipitation
at Sapelo Island, Georgia; nitrogen concentrations were  lowest during the rainy months of July
and  September.   The  highest'nitrogen  loadings occurred  during July and  were asosciated with

                                            11-25

-------
ID

44


12

1O

~
CP
I 8
•o*
6

4
«
1 1 1 1 I 1 I 1 111
* WBW 9,
- :?^ACEl'-AP3s i
ii-7,1, «~TATIT PRECIPITATION !
* PENN STATE NETWORK
0 VIRGINIA J |

f • I |

*/ \ *
• / A I '
I/ 'l\ *
/ / Vl
AJ/A/A -
•f W\ K l
Jt/t\^\y/\ v\ \
7^\_A.J$' ^' V^V"
M   A    M    J    J
           1977
                                                             SON
Figure 11-10, Comparison of weighted mean monthly concentrations of sulfate
in incident precipitation collected in Walker Branch Watershed, Term. (WBW)
and four MAP3S precipitation chemistry monitoring stations in New York,
Pennsylvania, and Virginia (Lindberg et at., 1979).
                                11-26

-------
the  lowest  range in  pH,  4.2-4.8,  Hendry  (1977)  and Hendry and Brezonik  (1980)  found rela-
tively 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 concentration 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 (S0.~)],  inorganic  forms of  nitrogen [nitrate
    "                     4-
(NO, )  and  ammonium  (NH. )],   total  phosphorus and pH  were  measured  in rain  collected  in
5-minute  segments  within  three  individual  rainstorms.    Initially,   rapid  decreases  were
observed 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  Mew 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

-------
I
11
4.80


4.60


4.40


4.20




0.40


0.30


0.20


0.10
                                              MAM
                A   S   O

               	1376	
                                              M
                                                       M
                                 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
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
Mean pH
4.32
4.25
4.34
4.31
4.29
4.25
4.63
4.60
4.28
SD
0.26
0.36
0.34
0.37
0.25
0.30
0.35
0.19
0.32
No. obsd
50
64
48
57
39
25
20
21
72
Range
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.C
      4.5
      4.4
      4.3
      4.2
      4.0     JFM     AUJ     JAS     ONO

          MONTHS OP  THE  VEAA (IVTS
Figure 11-12.  Seasonal variation of precipitation pH in the
New York Metropolitan Area (Wolff et al, 1979).
                     U-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 (Hendrey 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 a!.,  1976),  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 NO,  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  (Lipske,  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

-------
  1.0


  t,0
                                                AtSANV.NEWYOKK
  7.01—
  40

  J.O

  an*
                                         ALLEGHENY STATE PARK. NEW YORK
 e.«n
                                               ATHENS. PENNSYLVANIA
 1.0

 50
                                                CANTON. NEW YORK
                                  1K7      1KI
                                                      19S»

                                                     YEAR
                                                                          W1       1S72
Figure 11*13.  History of acidic precipitation at various sites in and adjacent to State of New York
(Harr and Coffey, 1975).
                                               11-32

-------
   7.0

   60


   S.O


   4.0

   o.e"




   7.0


   it


   SO

   40

   oo"
   HINCKLEY, NtW YOU*
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      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

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11-34

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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  participate 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 (1974) 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  SO™,  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 , SOt , and NO, ions on aquatic and terrestrial receptors.
     The effects of the  dry deposition of SO- 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

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                   IN CLOUD
                PRECIPITATION
                 SCAVENGING
                     25%
                                           TOTAL DRY
                                           DEPOSITION
                                              13%
                 BELOW CLOUD
                 PRECIPITATION
                 SCAVENGING
                      2%
                                TO LEAFY
                                CANOPY
I                  TO GROUND
               {DORMANT PERIOD)
                      l%>
  • iX ,'':,.'•'. •'•',«
INCIOENT'PR'ECIPITATION
                                                               TO BRANCHES
                                                             [DORMANT PERIOD]
                                                                    IK
                                                         m  A
                                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

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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.,  1980),
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,
1976), 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 life.   The disappear-
ance  of  fish  populations from  acidified  freshwater lakes  and streams  was  first noted  in
southern Norway in the 1920's.   In 1959,  Dannevig  (1976) proposed  that acidic  deposition was
the probable cause for acidification  and  thus  far  the  loss of fish populations (Lievestad 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
Scotland (Wright  et  al.,  1980a), the  Adirondack  Region  of New  York  State (Schofield,  1976),
and   the   LaCloche  Mountain   Region   in  southern  Ontario  (Beamish   and  Harvey,   1972).
Acidification  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
retention 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
sensitive  to  surface  water  acidification are  discussed in more  detail  in Section  11.4.1.

                                           11-37

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     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  (Hornstrom et  al.,  1976),  and
west-central  regions of Sweden  (Grahn et al., 1976),  the  LaCloche  Mountains  of southeastern
Ontario (Beamish, 1976), and the vicinity of  Sudbury, Ontario (Scheider et al., 1976), 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 rag/liter) relative to world-wide averages
[15  rag/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,  1976;  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
(Armstrong and Schindler,  1971).   Of 155 lakes  systematically surveyed  in southern Norway in

                                           11-38

-------
     ALLOCHTHONOUS SOURCES OF HYDROGEN ION
           PRECIPITATION,
           DRY DEPOSITION,
           DRAINAGE WATER
     — 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-UGANDS,
              ORGANIC AN1ONS
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 Srfrlandet  Region of southern
Norway surveyed  in  1974 to 1975 (May-November), 65 percent had pH levels below 5.0  (Wright ad
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
(Oickson, 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 consumed 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
significant  acidification  of  lakes  has  occurred  in  areas receiving  precipitation  with
volume-weighted  average  concentrations of  H   above 20-25 ueq/liter  (pH  4.7-4.6) and sulfate
concentrations 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

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ISBIE 11-4,  CHIH1CAL COWOSmOH (MIAN I SIANflSPO OEKIAIION)  OF  ACID  IAKIS  (rH -4) IK BfCIONS  RECEIVING HIGIIlt
 ACIDIC  MlClPHAflON (pll «.4,S), AND 01  Utl-UAItR lAKB IN AREAS NO!  MIB.KCI  1(1 III GUI* ACIDIC PREC1PIIAIIW
                                                  **: 22 2l»
North AmPrtC*
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OnUrin lest 5 »": 20 9
'.mllniry, Keaiurnl: 4 120:40 36*5 (4.5) 100*30
Ontario less * «*: 16 50
LAKES IN UWrrtCltO ARfAS



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Wrjqht .in.) Ujessimi (1976).
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280
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-------
     4.0
                  1
                  50
 2
100
 3
150
 4
200
 5     Cmg 1"1)
250    fjiEq T1)
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

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                                                                        CURVE 2
                                                            I
        0123

                               EXCiSS S W LAKE WATER, g/m2/y*«r

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

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       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;
Schofield 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
between  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,
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 1ri 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 approx-
imately  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, 1976; 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
         _       I         I
%
a.   100
   10
                        SOUTH NORWAY 1B74
                            154 LAKES
                         I          1
                                                1000
                                              3  100
1000
t 100
5
10
4
WEST COAST SWEDEN
	 ° 37 LAKES 	
•
*
__ *" .« _.
i
* *
* ** * * *
* *
1 1 " * 1
1 5 6 7 £
PH
                                                  10
                                                1000
                                                                                 SCOTLAND
                                                                                  72 LAKES
                                                                 I          i
                                                                        6

                                                                        PH
                                                 100
                                                  10
                                                                           ADIRONDACK* USA

                                                                               134 LAKES
                                                        **£**. '
                                                        •• 1S1  ".
                                                               1          I
                                                                        6

                                                                        pH
Figure 11-19. Total dissolved Al m a function  of pH level in lakes in acidified areas in Europe and
North America (Wright et at.. 1980b).
                                            11-45

-------
1
                                            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  (Oriscoll,  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,
minerals and other compounds  stored in the organic natter 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 microbia) activity and decomposition.  On
the  other  hand,  increased accumulations  of dead  organic  matter  (as  a result  of  decreased
decomposition  rates) are commonly noted  in acidic lakes and streams.
     Abnormal  accumulations of  cjoarse 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.,   1978;  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

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neutral   waters   (Lelvestad   et   al.,   1978;   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  nicrobial respiration  between  the
streams.    The  acidic  stream  did show a  reduction in  the  invertebrate  functional  group that
specializes  in, processing  large particles   (shredders).    Gahnstrom et  al.   (1980)  found  no
significant  differences  in oxygen  consumption by  sediments  from acidified and non-acidified
lakes.   Rates  of  glucose  decomposition 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  Hogsjon in Sweden also  increased  rates of  glucose processing.
However  in a humic lake, the maximum  rate  of glucose  transformation occurred  at  the j_n si tu
value pH 5 (Gahmstrom et al., 1980).
     Laboratory  and field experiments involving  decomposition  rates have  fairly consistently
found  decreasing microbial activity  with increasing acidity.  Traaen and  Laake (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.
B1ck 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,  de-
composition  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

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been formulated into  the  hypothesis  of "self-accelerating oligotrophication" by  Grahn  et al.
(1974),
11.3.1.3   Effecton PrimaryProducersand PrimaryProductivity—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
phytoplankton 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).    Dinoflagellates  constituted  the  bulk of the
phytoplankton  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 productivity

                                           11-49

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      r//
    80

    70

w  60
IU
o
I  M
u.
2  «
ui

1  3°
    20

    10
I     I     I     I     I     I
I     I     I     I     I     I     I
 PMYTWLANKTON SPECIES IN «0 LAKES
 ON THE SWEDISH WEST COAST
 AUGUST 1976
      pH  4.1   4.3   4.5   4.7   4.9   5.1   5.3   S3   5.7   S3   6.1   6,3   6.5   6.7   6.9   7.1
 NUMBER  110432433121033100203S0541231011
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

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           pH 4.60-5.45
                                                    pH 6^5-7.70
                                 BIOMASS
                                  SPECIES
                |'||;|:j OIATOMEAE


                [  ^_J GHLOROPHYCEAE


                PH3 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 at al., 1978).
                                   11-51

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regardless of algal species involved.  In ffeld surveys and experiments, relationships 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 productivity
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 measure-
ments 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
Carlyle 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 in 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 J£ vitro.   They  found that, although the total rate, of
photosynthesis 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
between 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
bionass 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 Tabellaria 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., 1980).  As noted in Section 11.3.1.1, aluminum  concentrations increase with decreasing
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).  In

                                            11-52

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oligotrophic lakes, phosphorus is most commonly the limiting nutrient for primary productivity
(Schindler, 1975; Wetiel,  1975),   Therefore,  chemical  interactions between aluminum and phos-
phorus 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.   Qickson (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.

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     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 (1976) 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 wore 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 (National  Research  Council,  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,  1976).  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,  1976;  Grahn et a.,  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

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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 zooplankton) 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 dominance of small-
bodied  herbivores  in the zooplankton community (Hendrey et al., 1980).   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 decreases 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  Kvdatkowski,  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 (Okland, 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 (Okland, 1980).  Experimental investigations

                                           11-55

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 o

 cc
 UJ
 m

 3
 z

 z
m
          4,0-4.49     4.5-4.99     5.0-5.49    5.5-5.99    6,0-6.49      >6,5   pH INTERVAL


            2           9         16          7         11          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

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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 parti-
cularly 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 macroinvertebrates to
low  pH  levels.   Tolerance  seems  to  be in  the  order  caddisflies  > stoneflies  >  mayflies
(Hendrey et al., 1980).
                                                                                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.  (1980), 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., 1980).
     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  many 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

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algal accumulations  in acidic  streams  and benthic  regions  of acidic lakes  (Hendrey  et  al.,
1980).   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 haa 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
commercial  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 (National  Research Council, 1978).
     Declines  in fish  populations have  been related to acidification of  surface waters in the
Adirondack Region  of New York  State (Schofield,  1976), 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  (1976)  estimated  that  in  1975  fish populations  in  75  percent  of
Adirondack  lakes  at  high elevation  (<610  m)  had been  adversely affected  by  acidification.
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 indicated
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 cyprim'd 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,  Salmo  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

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    20
 o
 c
 S  10
 s
 z
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 (Schofield, 1976b).
                                                 11-59

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       20
       10
       10
                                        I         I
                                           1975

                                 NO FISH PRESENT


                                 FISH PRESENT
                                            1930s
                               6

                               PH
Figure 11-25.  Frequency distribution  of  pH end fish pop<
ulation status in 40 Adirondack lakes greater than 610 meters
elevation, surveyed during the period 1929-1937 and again in
1975 (Schofield, 1976b).
                               11-60

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salmon  (Salmo 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  (Oickson,  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 Scandinavia 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.
     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
generalize 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;  Oickson,  1978;  Oriscoll
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,
magnesium, 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 se, 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

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  STAVANGER
                           RIVER TOVDAL
        380
        250
    O  200
        160
            1900
                        1920
                                     1940
                                                  1060
                                                               1980
    in
    §
         30
         20
         10
            1900
                                 I      I      I      I      I
                                              7 AGIO 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

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                       TABLE 11-5.   pH LEVELS IDENTIFIED IN FIELD SURVEYS  AS
                        CRITICAL TO LONG-TERM SURVIVAL OF FISH POPULATIONS

Fami 1y
Salmonidae

Species
Brook trout (Salvelinus
fontl nails)
Lake trout (Salve! inus
namaycush)
Critical pH
5,0
5.1
5.2-5.5
Reference
Schofield, 1976c
Schofield, 1976c
Beamish, 1976
                  Brown trout (Salmo trutta)             5.0
                  Arctic char (Salvelinus alpinus)
                                                          5.2
   Percidae
   Catostomidae
   Ictaluridae
   Cyprim'dae
               Perch (Perca fluviatilis)           4.4-4,9
               Yellow perch (Perca flavescens)     4.5-4.7
               Walleye (Stigostedion yjitreum)      5.5-6.0-*-

               White sucker (Catostomus            4.7-5.2
                 commersoni)                         5.1

               Brown bullhead (Icaturus            4.7-5.2
                 nebulosus)                          5.0
               Minnow (Phoxinus phoxinus)
               Roach (RutiTus rutilus)
               Lake chub (Couesius plumbeus)
                                      5.5
                                      5.5
           	4.5-4.7
Creekchub (Semotilus atromaculatus)   5.0
Commonshiner (Notrppis cornutas)      5.5
                  Goldenshiner (Notemigonus
                    crysoleucas)
                                                     4.9
                                                      5.5-6.0+
Centrarchidae  Smallmouth bass (Mlcropterus
                 dolomleui)
               Rock bass (Ambloplites rupestris)   4.7-5.2
   Esocidae
               Pike (Esox lucius)
                                    4.4-4.9
Aimer et al.,  1978
Aimer et al.,  1978

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  j_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 rag/liter in
                                           11-63

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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 a!., 1980;  Wright
and  Snekvik,  1978).    Field  observations  (Aimer et  al.,  1974;  Beamish,  1974; Jensen  and
Snekvik, 1972; Schofield, 1976) indicate changes in population structure over time with acidi-
fication.   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
decreased egg deposition  may be associated with disrupted spawning behavior and/or effects of
acidification on reproductive physiology in maturing adults (Lockhart and Lutz, 1976).   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 immediateTy 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 blotic, 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-
     194
tion.     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  and  frogs  in the
                                           11-64

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United States  regularly breed in  ephemeral  pools;  about one-third of  the  salamander 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,  Pough.
and Wilson (1976)  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  permanent ponds was
6.1 (range  5.5  to  7.0).   Amphibian eggs and  larvae  in temporary pools are exposed  to these
acidic conditions.
     Pough and Wilson  (1976) and  Pough  (1976)  studied the  effect  of pH  level  on embryonic
development of  two common  species  of  salamanders:   the spotted  salamander (Ambystoma macu-
latum) 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,  Pough and Wilson  (1976)  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 (Hogstrb'm,  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 lana 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
vertebrates.    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

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     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.    COy produced by plant roots and micro-organisms;
     3.    oxidation of NH4* and S, FeS2> and HgS to HNOj and H2S04;
     4.    very acid litter in coniferous forests, the main acidifying
          source for the A and B horizons;
     S.    atmospheric deposition of H-SO,  and some HNO,, NO , 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  (N03~)  and  hydrogen ions  (H  )  (Donahue et a!., 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

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       SOIL PARTICLES
          ACID RAIN

               I
          SOIL SOLUTION
WEATHERING-
K*
Na*-

NH/
SOf
                            Na*
                                  NO
                          CAN BE LEACHED
      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

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         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.
                                                      o-        -
     Acidic precipitation increases the amounts of SO.   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
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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
                                        -      »      p        «
leaching was in the following order:   Cl  ~ NO,  < SO' < H-PO,  (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  a!,,  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.
                                        2™
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+
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
                                                                             2
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.  These 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 Oollard,
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
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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).
     The effects  of acidic  precipitation on  soils  potentially could  be  long-lasting.   Oden
                                                                                        +2
(1971) has estimated that  rainfall  at pH 4.0 would be the cation equivalent of 30 kg Ca  /ha,
which represents a considerable potential loss of  cations  essential  for  plant growth as well
as base saturation.   HcFee et al.  (1976) 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  (Halmer,  1976).   Baker et al..
(1976) 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  (1976).   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
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deposited in rainfall and dustfall were nickel, copper, cobalt, iron, zinc, and lead.   Most of
these metals  are retained  irr 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  Bollard,
1979; Alexander,  1980;  Halmer,  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,
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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
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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
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(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  Laflin (1976)  found that
SOVj-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 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).
Particularly 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 bene-
fit chiefly to plants growing on lands with a low sulfur content (Brezonik, 1975).
     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 SO, (Turner and
Lambert, 1980).
     When  discussing the  effects  of  acidic  precipitation,  or  the  effects  of  sul fates  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
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.
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     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,  1975; Hutchinson and
Whitby,  1976) mercury,  (Brezonik,  1975) and cobalt (Hutchinson  and Whitby, 1976).   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, and  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 CaCO, and other
                                                                                   J
          unstable minerals and by. cation exchange,
     2.    At  soil  pH  F 5.5 the efficiency  of the proton to  decompose minerals and to replace
          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 Tow  nutrient  level is a  crucial   factor which limits
                                           11-75

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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
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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,
decomposition, 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,  1980).  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,
1980) and Canada (Linzon personal communication).
11.3.2.2.1   Direct effects on vegetation.    Hydrogen  ion  concentrations  equivalent to  that
measured  in  more acidic  rain events  (5 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

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         TABLE 11-7.   TYPES OF  DIRECT, VISIBLE INJURY REPORTED IN RESPONSE TO ACIDIC WET DISPOSITION

Injury Type
Pitting, curl
shortening, death
1-mm necrotic lesions,
premature abscission



Cuticular erosion
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
Reference
Remarks
Wood and Bormann (1974)

Shriner et al.




Shriner (1978a)

(1974)





Lang, et al. (1978)
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-irw bifacial necrosis
due to coalescence of
smaller lesions, total
tissue collapse.
Wrinkled leaves, excessive
adventitious budding, pre-
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

Evans et al.
(1977)
Evans et al.
(1977)


Evans et al.
(1977)


Evans et al.
(1977)
Evans et al.
(1977)


Ferenbaugh
(1976)


More frequent near
veins. (A) - (0)
represent sequential
stages of lesion
development, through
time, up to 72 h (one
6-rain rain event daily
for 3 d)








mature abscission

-------
                                               TABLE  11-7  (Continued).

Injury Type
Incipient bronzed spot

Bifacial necrotic pitting
'

Necrotic lesions,
premature abscission



Harginal and tip necrosis


Galls, hypertrophy,
hyperplasia
Dead leaf cells
Necrotic lesions
Species
Bean

Bean


E. white pine,
scotch pine,
spinach,
sunflower,
bean
Bean, poplar,
soybean, ash
birch, corn,
wheat
Hybrid poplar

Soybean
Citrus
pH Range
2.0-3.0

2.0-3.0


2.6-3.4




Submicron
H2SO.
aerosol

2.7-3.4

3.1
0.5-2.0
Reference
Hindawi et al.
(1980)
Hindawi et al.
(1980)

Jacobsen and
van Leuken
(1977)


Lang et al.
(1978)

Evans et al.
(1978)
Irving (1979)
Heagle et al.
Remarks

After first few hours


After 24 h (reported
pooling of drops
more injury)
Injury associated
droplet location
within 24-48 h.








(1978)
=

with












Shriner (1980).

-------
thefr 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 , NO,  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. (1977), 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.   By
comparison,  studies with  the  very waxy leaves of citrus  (Heagle  et  al.,  1978)  reported  a
threshold for visible symptoms to be near pH 2.0.   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

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TABLE 11-8.   THRESHOLDS  FOR VISIBLE INJURY AND GROWTH EFFECTS ASSOCIATED WITH  EXPERIMENTAL
         STUDIES OF WET  DEPOSITION OF ACIDIC SUBSTANCES  (AFTER JACOBSON, 1980a,  b)

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,
1 ncreased/decreased
nutrient content
Reduced growth
Reduced yield
Reduced growth
Reduced yield
Species
Yellow birch
Bean
Bean, sunflower
Bean
Hybrid poplar
Sunflower
Soybean
Lettuce
Pinto bean
Pinto bean
Soybean
Soybean
Threshold1
pH 3.1
pH 2.5
pH 3.1
pH 3.2
pH 3.4
pK 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.
(1977a)
Sbriner (1978a)
Evans et al.
(1978)
Jocobson and
Van Leuken (1977)
Jacobson (1980b)
Jacobson (1980b)
Jacobson (1980b)



Remarks
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse (varied
with S04" & N03~)
greenhouse




-------
                                                  TABLE 11-8 (Continued).
I
CO

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
Threshold1
pH 3.1
pH 3.0
pH 3.0
pH 3.0
pH 3.0
pH 3.1
pH 2.8
pH 2.8
pH 2.8
pH 3.0
pH 3.0
Reference Remarks

Jacobson (1900b) greenhouse



Irving (1979) field
Jacobsen (1980b) field, low ozone
field, high ozone
field, low ozone
Jacobson (1980b) field
field

        Highest pH to elicit a negative response, or lowest pH to elicit a positive response


       Shriner (1980).

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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 Do!lard (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 Phaseo1 us 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 SOy-  Shriner
(1978b), however,  reported  no significant interaction between  multiple  exposure to simulated
rain at p  4.0 and four SO*  exposures (3 ppm  peak  for  1  hr.) upon the  growth  of  bush beans.
Shriner (1978b) also exposed plants to 0.15 ppffl 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 fusiforine.  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 (1976, 1980) also observed that root nodulation by
Rhizobi'um 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.   Host
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 Oollard, 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
mH) decreased fertilization  at least 50 percent at all pH values observed.   In another study,
Evans and Bozzone  (1978) observed that both  sperm  aotility and fertilization in gametophytes
°f Pteridiun  aguil I'num 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 NO,: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 SO, 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  SO,  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 NO," 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, Taram 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, 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,  1975;  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
Jernelov,  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,   19765).   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  Oochinger,   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

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                    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
(pg/D

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 (SO,  ) 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/ra  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

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     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  haii—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 (SOp) 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 SO- 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 (Anderson,
1978).   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

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           TABLE 11-10.  COMPOSITION OF RAIN AND HOARFROST AT HEAOINGLEY,  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-Og
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

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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, 1979;
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 Adirondack*, as pointed out by Scho-
field  (1975),  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., 1980).
     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 HCO^/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. (1980)  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

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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  (1979) 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  SQ./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 SQ,/ha/yr.  The amount of precipitation must also
be considered since it affects total sulfate additions.
     The  report by Hendrey et al. (1980) 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  inflow is  minimal  have  become  acidified (Hendrey
et al.,  1980).   Conversely, there  are  areas in  Maine with  granitic bedrock where lakes have
                                           11-93

-------
o
cc
01
a.


u

IU
IU

EC
                  20
                                                                       HC03-'
                               40           60


                           EQUIVALENT PERCENT
                                                        BO
    Figure 11-29. Equivalent percent composition of major ions in Adirondack lake

    surface waters (215 lakes) sampled in June 1975 (Schofield, 1979).
                                   11-94

-------
   10
   10
LU
o
IT
LU
a.
   30
   70
    to
                                               NW Norway
                                                         (58)
                                                 SE  Norway
                                                         (57)
Adirondacks
        (1845
        ELA
        (102)
                50
                            100         liO

                             SO4, fi Ml/liter
                                                  200
                                                              250
Figure 11-30.  Percent frequency distribution of sulfate concentrations in surface
water from lakes in sensitive regions (Schofield, 1979).. (EUA refers to Experimen-
tal Lake Area. Figures in parentheses refer to number of lakes.)
                                11-95

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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

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                                                  Rf G1ONS WITH SIGNIFICANT

                                                  AREAS OF SOILS THAT ARE
                                                      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 soi Is
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

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probably  release  Al *  ions into  the  leachate  (HcFee,  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  on 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

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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.
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     Ecosystems  can  respond to  environmental  changes  or  perturbatiojis  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.
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     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 (S04~) and nitrate (NOg) ions on vegetation and  have caused necrotic  lesions in a wide
                                           11-102

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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

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CHAPTER 11

Abrahamsen, G.,  K.  Bjor, R. Horntvedt, and 8. Tveite.  Effects of acid precipitation on  coni-
     ferous forest.   lr\:   F. H. Braekke, ed., Research Report FR-6.  SNSF Project, NISK, Aas,
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Abrahamsen, G.,  Horntvedt,  R.,  and Tveite,  B.   Impacts  of  acid precipitation on coniferous
     forest ecosystems.  Water, Air Soil Pollution 8:57-73, 1977.

Abrahamsen, G.,  and  G.  J.   Dollard.   Effects of Acid  Deposition on  Forest Vegetation.   In:
     Wood, H.  0. (ed.).  Ecological Effects of Acid Precipitation.  Report of workshop  held at
     Galley Hotel,  Gatehouse-of-Fleet, Galloway, U.K., 4-7 Sept. 1978.  EPRI SOA77-403,  Elec-
     tric Power Res.  Institute, 3412 Hillview Ave., Palo Alto, California 94303, 1979.

Alexander, H.   Effects  on Acidity on  Microorganisms and Microbial Processes in the Soil.   In:
     Effects of  Acid  Precipitation on Terrestrial Ecosystems.  T. C. Hutchinson and M. Havas,
     eds., Plenum Press, NY, 1978.  pp. 341-362.

Alexander, H.   Effects of Acidity  on  Microorganisms  and  Microbial Processes  in  a Soil.   In:
     Effects  of  Acid  Precipitation  on  Terrestrial  Ecosystems,  Proceedings of  the  NATO
     Conference  on  Effects  of  Acid Precipitation on Vegetation  and  Soils,  National  Atlantic
     Treaty Organization, 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.,  C.  Dickson, C. Ekstrom, and E. HornstrSm.   Chapter 7.  Sulfur Pollution and  the
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Aimer, B., W.  Dickson,  C.  Ekstrom, E.  Hb'rnstrom,  and U.   Miller.  Effects of acidification on
     Swedish lakes.   Ambio 3:30-36, 1974.

Altshuller, A.  P.,  and  G.  A. McBean,  Chairmen,  1979.   The LRTAP Problem in North America:  a
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Amundsen, T.,  and K. Lunder.  Report on fishery-biological surveys in Tjagevatn and Sonstevatn
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Andersson,  I.,  0.06rahn, H.  Hultberg,  and  L.  Landner.   Jamfb'rande  undersb'kning  av olika
     tekniker for aterstallande  av forsurade sjoar.  STU  Report 73-3651.   Stockholm:   Insti-
     tute  for  Water  and  Air Research,  1975.  Cited  in:   National Research  Council,  Sulfur
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Anschutz, J.,  and F. Gessner.  Der loneraustausch bei  torfmoosen (Sphagnum).  Flora 141:178-236,
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Armstrong, F.  A.  J.,  and D. W. Schindler.  Preliminary chemical characterization of waters in
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Arnold, D.  E.,  R.  W.  Light,  and  V.   J.  Dymond.   Probable Effects  of Acid  Precipitation on
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                                          11-104

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Baker,  J.,  0.  Hocking,  and  M.  Nyborg.   Acidity  of open  and intercepted  precipitation in
     forests  and  effects on forest soils  in  Alberta, Canada.  In:   Proceedings  of the First
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     Technical  Report NE-23,  U.S.  Department  of  Agriculture,  Forest  Service,  Northeastern
     Forest Experiment Station, Upper Darby, PA, 1976.  pp. 779-790.

Baker, J.,  and  C.  Schofield.   Aluminum toxicity to  fish as  related to acid precipitation and
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     Tollan, eds.   SNSF-project report, Oslo, Norway, 1980, pp. 292-293.

Beamish,  R. J., and H.  H.  Harvey.  Acidification of the La Cloche Mountain Lakes, Ontario and
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Beamish,  R. J.  Growth  and survival of white  suckers (Catostorous commersoni) in an acidified
     lake,  J. Fish Res.  Board Can.  31:49-54, 1974.

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.

Beamish,  R.  J.   Acidification  of  Lakes  in  Canada By  Acid  Precipitation  and  the Resulting
     Effects of Fish.  Water, Air and Soil Poll. 6:501-514, 1976.

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.

Bell, H.  L.   Effect of  low pH  on the survival  and emergence  of  aquatic insects.  Water  Res.
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Bick,  H.,  and  E.  F.   Drews.   Selbstreiningung  und  ciliatenbesiedlung  in  saurem milieu
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Billings, W.  D.   Plants  and the Ecosystem.  3rd ed.  pp.  1-62.  Wadsworth Publishing  Company,
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Bolin,  B.   Sweden's  Case  Study for  the  United Nations  Conference on  the Human Environment:
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Boughey,  A. S.   Fundamental  Ecology.   Scranton, Pa.,  Intex  Educational Publishers, 1971.  p.
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Brady,  N.  C.   The  Nature and  Property  of  Soils.   McMillan  Publishing Co.,  New York.   p.
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Braekke,  F.  H.,  ed.   Impact of Acid  Precipitation on  Forest and  Freshwater Ecosystems in
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Brezonik,  P.  L.   Nutrients and Other Biologically Active  Substances  in Atmospheric Precipita-
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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 2:2-8, 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.  Effect!?
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Chamberlain, A.  C.   Dry  deposition of  sulfur dioxide.  In:   Atmospheric Sulfur Deposition,
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Chapham,  W,   B.,   Jr.   Natural  Ecosystems.    The MacMillan  Co.,  New York/Collier-MacMillari
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Cholonky, B. J.   Die Okologie der diatomeen  in  Binnengewasser.   Cramer, Weinheim, 1968.  699
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Cogbill,  C.  V.   The History  and Character  of  Acid  Precipitation  in  Eastern North America,
     Water, Air and Soil  Pollution 6:407-413,  1976.

Cogbill,  C.  V.   The  effect of  acid  precipitation on  tree growth in eastern North America,
     Water, Air and Soil  Pollution 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-
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Comerford, N. B.,  and E.  H.,  White.  Nutrient content of throughfall  in  paper birch and red
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Conroy, N., K.  Hawley, W.  Keller, and C.  Lafrance.   Influences of the atmosphere on lakes in
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Cowling,  E. B., and  L.  S.  Dochinger.  The Changing Chemistry  of Precipitation and Its Effects
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Crisman, T. L., R.  L. Schulze,  P.  L.  Brenzonik, C.  D.  Hendrey,  and  S.  A.  Bloom.  The biotic
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                                          11-106

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Oonan, C.  S.   Consequences  of Sulfuric Acid  Inputs to  a Forested  Soil.   In:  Atmospheric
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Cronan,  C.   S.   Solution  chemistry  of  a  New Hampshire  subalpine  ecosystem:   biochemical
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Eaton,  J.  S.,  G.   E.  Likens,  and F. H.  Bormann.   Throughfall  and Stemflow  Chemistry  in a
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     In:   Effects  of  Acid  Precipitation  on Terrestrial Ecosystems.  T.  C.  Hutchinson and H.
     Havas, eds.   Plenum Press, New York, NY, 1980.  pp. 239-254.

Wiklander,  L.  Leaching  and  Acidification of  Soils.   In:   Wood,  M.   J. (ed.).   Ecological
     Effects  of  Acid  Precipitation.   Report of workshop  held at Cally  Hotel,  Gatehouse-of-
     Fleet,  Galloway,  U.K.    4-7  Sept.  1978.  EPRI  SOA77-403,  Electric Power Res.  Institute,
     3412 Hillview Ave. , Palo Alto, California 94303, 1979.

Williams,  Wayne  T.   Acid  Rain:   The California  Context.   Citizens for  Better Environment.
     Environmental Review, May 1978.  p.  6-8, 10.

Winkler, E.  M.   Important Agents of Weathering For  Building  and Monumental  Stone.   Eng. Geol.
     1:381-400, 1966.

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.  and Tech.
     13:209-212, 1979.

Wood,  T.   Acid Precipitation.  In:  Sulfur  in  the Environment.  Missouri Botanical  Garden in
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Wood,  T.,  and F.  Bormann.    Increases  in foliar  leaching  by  acidification  of  an  artificial
     mist.  Ambio 4:169-171,  1975.

Wood,  T.,  and F.  H. Bormann.  Short-term effects  of a  simulated acid rain upon  the  growth and
     nutrient relations of Pinus strobus  L.  Water,  Air Soil  Pollut.  7:479-488,  1977.

Wood,  T., and F. H. Bormann.  The effects of an artificial acid mist  upon  the growth of Betula
     alleghaniensis.   Brit. Environ. Pollut. 7:259-268, 1974.

Woodwell,   G. M.    Effects  of  ionizing   radiation   on   terrestrial   ecosystems.   Science.
     138:572-577, 1962.
                                           11-121

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     168:429-433, 1970.

Wright,  R.  F.,  R.  Harriman,  A.  Henriksen,  B.  Morrison,  and  L.  A.   Caines.   Acid lakes  and
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Wright, R. F., and A. Henriksen.  Chemistry of small  Norwegian lakes with special  reference  to
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Wright,  R.  F.,  and  E.  T.  Gjessing.   Changes  in the chemical  composition of  lakes.   Ambfo.
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Wright,  R.  F.,  N.  Conroy,  W.  T.  Dickson, R.  Harriman, A,  Henriksen,  and  C.  L.  Schofield.
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Wright, R. F.,  T.  Dale, E.  T. Gjessing, G. R. Hendry, A. Henriksen, M. Johannessen, and I.  P.
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     Alterations of pH.  Environ. Conservation 5:93-100, 1978.
                                          11-122

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     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
organisms 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 non-
living components  together  into a stable system, i.e.,  the interactions between organisms or
communities 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, physicochemical, or  biological  changes,  regardless of  their source  or 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 organisms
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 integrity
of the biosphere.   They  are important: (1)  in  the  production of food; (2) the maintenance of
forests;  (3)  as global support systems for  the  regeneration of essential  nutrients and atmo-
spheric components;  (4)  for their aesthetic value  in  maintaining natural vegetative communi-
ties;  and (5) in  the  assimilation  or destruction  of many pollutants from  the air, water, and
soil.

                                            12-1

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     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 entirely
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 suc-
cessively 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  ion  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 NH3 and collectively
for NH.+ plus NH,,  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  organism (food or prey) to another
organism (consumer or predator).   Nitrogen  is  bound in plant   or animal  protein until the
organisms die or as in 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

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                                                 (4!
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

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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 way be transformed into atmospheric
nitrogen or reduced to ammonia.
5.  Denltrification. implies the gaseous loss of nitrogen, usually as molecular nitrogen (N2),
nitrous oxide (N«0) or nitric oxide (NO), to the atmosphere as a result of microbial reduction
of  nitrate.   Nitrate  is reduced  to  nitrous  oxide (N,Q) and  molecular nitrogen  (N,)  under
anaerobic conditions.  Nitrates (NO,") are converted into nitrites (NO."), to nitrous oxide (a
gas) (NpO) 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 N«
(Alexander, 1977; 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.
     Ammonification  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 further
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, denitrif1cation is considered a  nitrogen  sink since the products
(N, and N«G) 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

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     Nitrogen fixation is important as a source 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 process
is important in global nitrogen balances, and in the current controversy over the depletion of
stratospheric ozone by N20.   (See Chapter 9).
     Numerous  texts,  monographs,  and papers  review the nitrogen  cycle,  (Alexander,  1977;
Bartholomew  and Clark,  1965;  Brezonik,  1972,  Brock, 1970;  Delwiche,  1970;  Delwiche,  1976;
Delwiche,  1977,   Hutchinson,   1944;   Hutchinson,  1954;  Hutchinson,   1957;   Keeney,  1973;
Soderlund 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 transformations 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
very important  nutrient.  Any  effect, environmental  or biological,  which  interferes with the
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
injections.   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 nitrogen
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 significant
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

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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
terrestrial  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
approximate 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 precipi-
tation (rain plus snow)  is usually equivalent to only a few percent of the total nitrogen assi-
milated 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

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AIR
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Figure 12-2. Schematic presantation 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 ni-
trogen in the soil.  In nutrient-impoverished ecosystems, such as badly eroded abandoned crop-
lands or soils  subjected  to prolonged leaching by acid precipitation,  nitrogen additions from
atmospheric fluxes are  certainly important to biological  productivity.  Such sites,  however,
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 in-
creased production must come either from biological fixation or from atmospheric influxes.  It
seems possible, therefore, that man generated contributions could play a significant 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  Terrestri al PI ant Communlties—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; Wood-
well, 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 fixation will in-
fluence  the  animal  populations  in the  vicinity and microorganisms  in the  underlying soil.
These changes,  in  their turn, will modify the  behavioral  patterns or alter competition 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

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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 a!., 1971).  It is the general conclusion of these
investigations  that further  research on  the influence of nitrogen oxides on plant communities
is required.   The  available  information  clearly is  too small  to warrant meaningful generali-
zations at this time;  however, there is  information detailing the effects on individual 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 dif-
fer 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.

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     Beyond this limited amount of knowledge, the literature concerning the effects of nitrogen
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 Hicrobial  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.
Hicrofloras 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 solely
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 (National Academy of Sciences, 1977).
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 undesirable.  Phosphorus and nitrogen are  the most important nutrients that stimulate eutro-
phication, 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 pro-
ductivity  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)
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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  nitrogen
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  a  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 summarizes
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,
however,  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  survive 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 recreational
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
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                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)
                     o
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 CD)


 (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

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       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
   •  Transim'ssibility 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

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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 biosphere 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 ratio (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
limitation  was  lower among lakes  that were more productive.  The same  relationship has been
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 the 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  eutrophication 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 single
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 of 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 denitrifi-
cation of the nitrate that diffuses into anoxic sediments limits the amount of available nitro-
gen 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

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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  (1947) 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 Vollenweiger's 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 limit-
ing 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

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   10.0
Z   2.0
5

5
z
tu
§   1'°
e
2   0.5
    0.2
             EUTROPHIC LAKES
                              J_
OLIGOTROPHIC LAKES
                                         I
                              10        20


                           MEAN DEPTH, meters
                                                      50
                                                              100
  Figure 12-3. Areal loading rates for nitrogen plotted against mean
  depth of lakes (Vollenweider, 1968).
                        12-16

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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 cases 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 contribution
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,
Nitrates,  1978).   Denitrification also occurs  in the anoxic sediments  of  lakes.   The source
of nitrate for  sediment  denitrification may be upward seepage of groundwater, downward diffu-
sion 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, 1968) 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 Total
N as N03"-N
40
22
96
13
*"**
47
            SOURCE:  (National Research Council, 1978).

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     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  compositon, 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:  NH3~H, 0.44 mg/liter; NQ3~-N, 0.51 ing/liter;  organic nitrogen,
2.0 rag/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  succession,  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 relationships
among these factors.
12.2.5  The Value of a NaturalEcosystem
     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 dependent 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 decision
makers.  Gosselink,  Odum,  and Pope (1975) have, however,  placed a value on a tidal  marsh by
assigning  monetary  values   to the  multiple  contributions  to  man's  welfare  such  as  fish
nurseries, food suppliers, and waste-treatment functions of the marsh.  They estimate the total
social values to range from $50,000 to $80,000 per acre.
     Using  four  different categories, Gosselink,  Odum and  Pope (1975)  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

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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.  ISO,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., 1975).   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., 1975).
     Westman (1977)  also evaluated  the benefits of natural ecosystems by estimating the mone-
tary  costs associated with the loss  of  the free services  (absorption  of  air pollution, pro-
duction of oxygen, regulation of global climate and radiation balance, and soil binding) 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 benefit 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
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                 accrue to the 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 dollar
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 (NGX) in the ambient air (Chapter 8) only nitric oxide (NO)
and nitrogen dioxide (NO,) are considered important phytotoxicants.   The direct effects of NO
on  vegetation  are  usually associated  with  and confined  to  areas   near  specific  industrial
sources.  For  example, vegetation injury  from exposure  to NOg 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  NOX on vegetation are reviewed in this  chapter  with  emphasis on
studies relating NO  effects to known exposure concentrations and durations.  Since most avail-
able  data pertained to NQ2, this pollutant  receives the most attention.   Also, when NO- was
experimentally combined with other pollutants such as SOy, injury occurred at much lower doses
than had been found in earlier studies with NO- alone.  This suggests that, in certain circum-
stances  HQy in conjunction 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.
12.3.1  Factors Affecting Sensitivity of Vegetation to Oxides of Nitrogen
     A notable feature  of the response of vegetation  to N02 stress  is  the varied  degrees of
NOg-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 N02  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 of 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 N02
exposures.
     Information on relative sensitivity (differential response) to NO* is summarized in Table
12-4.   The  three classes - susceptible, intermediate, and  tolerant  - are approximate because
                                            12-20

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                      TABLE  12-4.  RELATIVE SENSITIVITY OF SEVERAL PLANT SPECIES TO NITROGEN DIOXIDE (HECK AM) 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
Field Crops & Grasses
Fruit Trees
                              LaHx decidua Hill.
                                ^European Larch)
                              LaH« leptolepis Gord,
                                ^Japanese larch)
Avena saliva I.  (Oats)
cv. Clint land 64
cv. 3J9-80
cv. Pendek
Brofim* ine rials,  L.
  (Bromegrass)
cv. Sac Smooth
HordeuB distichon I,
   ___
Medicaqo saliva, L.  (Alfalfa)
Hicqljana gjullnpsa I.  (Tobacco)
Nicgljana tgbacui'i L.  (Tobacco)
Scorionera hispanica L.
  (Viper's grass]
li- inCfrnatuB L. (Crimson or
  Italian Clover)
TrifoUai pratense I.  (Red clover)
Triticua vulaare. VHI.  (Wheat)
cv.  Hells
Victa saliva I.  (Spring vetch)

Hal us sj>. (Showy apple)
Abies alba Mill. (White Fir)

Abies hoaolopls Sltb, 4 luce.
   CNikko or Japanese fir)
Abies pectlnata OC (Connon
   SiIver Fir)
Chamaecyparis Uwsontana (Hurr.]
   Parl (Lawson's cypress)
Plcea glauca [Hoench] Voss
   ?Bhite Spruce)
Picea pungens glauca, Regel
 (Colorado Blue Spruce)

Cossyplua hirsulun, I. (Cotton)
cv. Acala 4-42
cv. Payaasler
Hlcotiana labcacun, I. (Tobacco)
cv. White dold
cv. Bel-B
cv. Bel W3
Poa annua, I. (Annual bluegrass)
Secale cereale L. (Rye)
TriticuiTaestTvuin L.  (Wheal)
|ea Hays I. (Sweet Corn)
                                                                Citrus sj>.  (Orange, grapefruit,
                                                                   tangelo)
                                                                        Pi mis Hugo Turra (Knee pine or
                                                                           dwarf  mountain pine)
                                                                        Plnus nlgra Arnold (Austrian pine)
                                                                        Taxus baccata I.  (English yew)
NIcoIIana labaom, t. (Tobacco)
cv.  Hurley 21
Poa pralensis I. (Kenlucky bluegrass)
Sorghum sp.  (Sorghua)
cv.  Marlln
leu Hays I.  (Corn)
                                                                                                     lea Hays
                                                                                                     cv.  Pioneer 509-W
                                                                                                     cv.  Golden Cross
                                     Hosla planlaginej (Lan.) Aschers
                                        ffragrant plantian lily)

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                                                             TABU 12-4 {continued)
             Plant Type
     Susceptible
                                                                             Intermediate
                                                                                                                Tolerant
        Cirden Craps
        Ornamental  Shrubs
           and Flowers
N)
I
Is)
H«lus sylvestris Hill.
"Tipple)
Pyrus conaunis L. (Mild Pear)

A|Hu» parrot I. (Leek)
Apian qraveolens L.  (Celery)

Brasslca oltraeea botrytis, L.
  (Broccoli) cv. Calabrese
Daucus carota L. (Carrot)
Laetuca~sattvai L. (Lettuce)
Petrosellmm hortense Nym.
  (Parsley)
Phaseolus yulgaris.  L.  (Bean)
cv. Pinto
Pi sum satlvua L. (Pea)
Raphanus satlvus L.  (Radish)
cv. Cherry Bell*
Rheum rhaponticua L.  (Rhubarb)
Slnapisalba (White  nustard)

Antirrhimia aaj'us I.
  (Giant Snapdragon)
Begonia nultHlora (Tuberous-
  rooted begonia)
Begonia rex, Pull. (Begonia)
  cv. Thousand Wonders  White
flougainvillea spectabllis
  Willd. (BougainvUlea)
CalHstephus chlnensls  I L.I
  Nees (China aster)
Chrysanthemum sj>. (Chrysan-
  santhenufn)
  cv. Oregon
Hibiicus Boja-sinensis  L.
  (Chinese hibiscus)
liBsatiens sultanif Hook.
  (Sultana) cv.White I»p
                                                                        Citrus slnepli (L, ) Osbeck
                                                                             Navel Orange)
Aplim nraveolens rapaceua
   (Celery?
Cichorlu* Endlvia, L. (Endive)
  Ruffee
Fraqarla chlloensls
  qrandi flora (Pine striwberry)
lycoptrsicon escultntua. Hill
  (lomato)
cv. Boea
Phaseolus vulgaris hunlHs
  Alef.  (Bush bean)
Solanun tuberosum L.  (Potato)
Oahlla vaHablUs Hllld.
       -
Fuchsia hybrtda Voss (Fuchsia)
       a jasiiii nn
                                                                        Gardenia jasiiii nn Ides Ellis
                                                                          (Ctpe Jasnine)
                                                                        Gardenia radtcans Thunb.
                                                                        Ixora cocci noa L.  (Ixora)
                                                                        Ligustrum Itciiium Alt.
                                                                          (LiguitruSl
                                                                        Petunia X hybrlda Hort.
                                                                          Volm.'Andr. (Comon
                                                                          Garden Petunia)
                                                                        PiUosporum toblra Ait.
                                                                          (Japanese pittosporua)
                                                                        Rhododendron eatawbiense Hichx.
                                                                          (Catawaba rhododendron)
All tun eepa L.  (Onion)
Asparagus offlclnalls L.  (Asparagus)
Brasslca eaulorapa Pasq.  (Kohlrabi)
Brassjca oleraeea acephala DC (Kale)
Brass lea oleraeea capitata L,
   (Cabbagel
Brass lea oleraeea capltlata rubra L.
   (Red cabbage)
Cucuaii s satlvus, L.  (Cucunber)
cv. Long Harketeer
Phaseolus vulflarls.  L.  (Bush Bean)
Carlsta earandas L.  (Carlssa)
Codlaeufn varieqitun Bluae (Croton)
Chrysanthemun 1i-ucanthe«iu» L, (Daisy)
Comiallarl najaljs L.  (Lily-of-the-vaHty)
trica carnea L.  (Spring heath)
Gladiolus comaunls L.  (Gladiolus)
EricaSp7 (Heath)
Hosta sg. (PUntiin Illy)
junlperiis conferta Parl.  (Shore juniper)
Rhododendron sj>. (Alaska)

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                                                      TABU  12-4 (continued)
     Plant Type
     Susceptible
                                                                      Intermediate
                                                                                                         Tolerant
Trees & Shrubs
Weeds
lathyfus odoratus I. (Sweet pea)
JMpinus augustifolJus L,  (Lupine)
Nenuin oleander L. (Oleander)
Pyracantha coccinea Roes.
  (fire thorn?
Rhododendron canesjens [Htchx.|
  Sweet(Hoary Azalea)
Rosa sp. (Rose)
Vinea minor L. (Periwinkle)
  cv. Bright lye*

Betula pendula Roth. (European
  white birch)
Helaleuca Itucadendra (1.)  L.
  (Brittlewood)
                              Brassica  sp.  (Hustard)
                              He Ilanthus annuus L.
                               (Common Sunflower)
                                                                Acer platanoides I. (Norway
                                                                  naple^
                                                                Acer palmatua Thunb.
                                                                  (Japanese naple)
                                                                Tijia grandiflofa (Summer)
                                                                Tilia cordata Hill. (Small-
                                                                  leaved European linden)
                                  Halya parviflora  L.
                                     CcKeeseweed)
                                  Stellarla media {L.J Cyrill
                                     (Chickweed)
                                  Taraxacum officinale Weber
                                     (Dandelfonl
Carpinus betylus L. (European hornbean)
fagui sylvatica I. (Beech)
Fagus sylvatica atropurpurea Klrchn.
  (PurpI•-1eaved beech)
Cingkn blloba I. (Gingko)
Quercus robur I. (English oak)
Rut i at a pboudoacacia i. (Black locust)
Sambucus niara I. (European elder)
Ulmus glabra Huds. (Scotch ela)
ylmus ingntana With. (Hountain ell)

Anaranthys retroflexus I. (Pigweed)
ChenopodTilji album I. (Lamb1 s-«)uarters)
Chennpodium sp.  (Meetle-leaved goosefoot)

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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 N0_
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 NOj
sensitivity of species or cultivars within species can change.
     A  given  plant and its  individual  leaves,  will  vary in  sensitivity  to NO-,  depending on
the  stage  of  development.   In tobacco  (Nicotiana SJB. ) the  oldest  leaves became chlorotic,
middle  age leaves  became  chlorotic with  necrotic lesions, and injury to the  younger leaves
was  limited to necrosis (VanHaut and Stratmann, 1967).  In Ixora (Ixora coccinea) (Maclean et
al., 1968) mustard  (Brassica sg.), (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 sp.) 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
NO..  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  N0_  and  nitrogen metabolism, the
influence of soil  nitrogen on the plant response to NO, has been studied.   Rogers et al. (1979)
was  unable to show differences in N0«  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.
(1975)  reported that  NO,  uptake in bean (Phaseolus vulgaris) decreased with increasing levels
of soil nitrogen.   They also reported that NQg-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  N0,-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  NOg"induced  injury  and contained higher levels
of  foliar  nitrite  after  NO,  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

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the nutrient  solution contained  less  nitrite in  the foliage following a 3-hour  exposure  to
7.52 mg/m  (4 ppm) ^ 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/m  (0.3  ppm) NO,  for  2 weeks.   Plant growth was  depressed
between 0 and  approximately 21% with no clear trend between the nitrogen concentration 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 exposed
to  a  concentration range 0 to  0.98 mg/m   (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 0.98 mg/m  (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 con-
trols.
     Several researchers have studied the effect of light and time of day on plant sensitivity
to NO,.  Zahn (1975) noted that alfalfa (Medicago sativa) exposed to NO, 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/m  (100 ppm) than at night,
18.8 mg/m   (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  NO,  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/m  (3 ppm) NO, in the darkness and that this
                                                                £
dose caused as much damage as 11.3 mg/nt  (6 ppm) NO, in the light.  Zeevaart (1976) exposed 9
plant species to NO, 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 expressed
cell sap pH;  fumigation  of the plants with NH,  + NO,  reduced  injury.   However,  with tobacco
(Nicotiana  glutinosa)  light was required for injury  to develop and  there was no association
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  NO, in  the  dark.   Also
leaves treated with the  photosynthetic inhibitor OCHU were very sensitive to NO- exposures 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  N0,-induced  perturbations  occur  at  cellular  sites  within mesophyll  tissue, N02
uptake into the leaf is  required.  Absorption  is governed by factors regulating gaseous exchange
                                            12-25

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between  the  atmosphere  and  the leaf  (Nobel,  1974),   The  NO, diffuses  from the  boundary
layer—bulk  air interface and  terminates with extraction onto  mesophyll  cell  surfaces.   The
driving force  for NO, uptake is a concentration gradient and net movement along this gradient
is  Impeded  by  several  leaf  resistances:   boundary  layer,  stomatal  and nesophyll  (residual)
resistance.
     Rodgers et al.  (1979) suggested that  NO,  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
— 2                                                       ^
mg/m  (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  NO, concen-
   .                                               _____                         ^
trations  over  the range  of 0 to 13.16 mg/m  (7 ppm), NO, uptake was controlled more by inter-
nal  leaf  factors  (mesophyll  resistance) than stomatal  resistance  (Srivastava  et  al.,  1975a,
1975b); N02 uptake was also reported to increase with concentration and decline with increasing
exposure  time.   The  NO,  uptake rate in  the  dark was approximately one-half the  rate  in the
light.    Sunflower (Helianthus  annuus)  leaves  absorbed approximately.14% as much  NO-  in the
dark as in the  light  (Yoneyama et al., 1979),   Eventhough NO- uptake in the dark is lower, NQ-
exposures in the dark cause greater injury  (see 12.2.1).
     Nitrogen  dioxide reacts in water to  produce nitrate, NO, ,  and nitrite  NO-  in  dilute
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 NO-  exposures induced  nitrate  reductase activity and  enzyme
activity  increased with NO, concentration  and duration of exposure.  Yoneyama et al.  (1979)
                                 3
showed that exposure  to 7.52 mg/m  (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/m  (3.2 ppm).
The control  plants showed  severe signs of nitrogen deficiency and restricted growth.  However,
the  symptoms  of nitrogen  deficiency  decreased and.plant growth increased as  the  ttO^ concen-
tration 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
(jLycgpersjcorj esculentum), sunflower  (Helianthus annuus). and corn  (Zea mays) derived approxi-
mately 16,  22 and 14% of  their  nitrogen,  respectively, from NO- when the plants were exposed
             3
to  0.56  mg/m   (0.3  ppm)  for 2  weeks  (Hatsumaru et  al., 1979).  The absorption rate of N02,
based on  plant  dry weight, showed little change with soil nutrition and ranged  around approxi-
mately 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

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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).   Exposures
also  increased  the  soluble amino  (NH-)  groups  in  several  plants  and the  protein  content
increased by  10-20 percent.  Troiano  and  Leone (1977) reported that  NO-  exposures increased
the organic nitrogen content of tomato plants (Lycopersicon esculentum).
     Matsushima (1972)  found that exposure to 75.2 mg/m  (40 ppm) NO, 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   NO- (0.01-5 percent by volume) Durmishidze
and Nutzsubidze (1976)  showed  that 10 species  of decidious trees, 5 species of grasses and 5
species of coniferous trees readily assimilated isotopically-labeled   NO, and incorporated it
                                                                       ^         1C
into arm"no acids.   Spinach (Spinacia oleracea) was exposed to 7.52 mg/m  (4 ppm)   NO- for 2.5
hours to  determine the metabolic fate of  the nitrogen from the  NO,  (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  accumulated isotopically
labeled nitrogen proportional to the ambient NO- concentration over  at range of 0.19 to 0.75
    3                                                            3
mg/m  (0.1 to 0.4 ppm).  Following a 3-hour exposure to 0.60 mg/m  (0.32 ppn) NO-, over 97% of
             15
the absorbed   NO, 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 NO, the injured leaves frequently exhibit a waxy
or water-soaked appearance  prior to necrosis.  This  suggests  that cell  membranes  were  dis-
rupted, possibly beyond repair.   Berge (1963) suggested that NO- may cause cellular plasmolysis
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 pro-
posed to  be components of biological membranes.  The work of Estefan et al. (1970) suggested
that  the  products  of NO- action  on  lipid  monolayers 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.
     Wellburn et  al.   (1972) studied the  effects  of NO-  exposures on  the ultrastructure of
chloroplasts in vivo.   Broad bean (Vicia faba) plants were exposed for 1 hour to 1.9, 3.8, or
5.6 mg/m   (1.0,  2.0,  or 3.0 ppra).   The leaves were  harvested  immediately  after exposure and
prepared  for  electron microscopy.   Examination of  the chloroplasts showed  that NO-  caused a
swelling  of  the thylakoids  associated with the stroina.  These swellings appeared to be rever-
sible since thylakoid swelling was not observed in chloroplasts of leaves exposed to unpolluted
air immediately following NO, fumigation.
     Kandler and Ullrich  (1964) demonstrated that there was  a reduced amount of carotene and
chlorophyll in leaves after acute NO- exposure.  Some species of lichens exposed to 3.76 mg/m


                                            12-27

-------
                                                                               "5
(2.0 ppm)  NO,  for 6 hours had reduced chlorophyll content; a dose of 7.52 mg/m  (4.0 ppm) NO,
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  N02.
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).
     In vivo experiments performed by Hill and Bennett (1970) showed that both NO and NQ2 inhi-
bited  apparent photosynthesis of oat  (Avena sati'va) and alfalfa (Hedicago  satiya)  plants at
concentrations  below  those  that cause foliar lesions.  The threshold dose for this inhibition
                 3                               1
was     0.74 mg/m  (0.6 ppm) for NO and 1.13 mg/m  (0.6 ppm) for NO, in 90 minute fumigations,
but the inhibition  occurred faster for NO than  N02<   The N0x-induced inhibition of photosyn-
thesis was  not permanent.   The rate of  recovery for a given NO-induced  inhibition  level was
faster than  for N02-   Recovery from NO-inhibited photosynthesis was generally complete within
1 hour.  Full  recovery from NQg-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/m  (0.25 ppm)  N02,  0.31 rag/m  (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 NO, on the gas exchange of the primary leaves of bean (Phaseolus vulgaris).  Apparent photo-
synthesis and dark respiration were both inhibited by N00 concentrations between 1.88 and 13.5
    3
mg/m  (1 and 7 ppm).  The degree of inhibition increased with increasing N02 concentration and
exposure time.    In  exposures  to NCL,  transpiration rate was effected less than photosynthesis
or respiration.  Hence, it was proposed that the principal effects of NO, on leaf gas exchange
occurred in the leaf inesophyll cells and not on the stomata (Hill and Bennett, 1970; Srivastava
et al., 1975a).
12.3.3  Visible Symptoms of N0.> 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
SOj-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  NO,  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 NO. 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 NO, 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 NO, exposure but is nonspecific and can be a symptom
of  injury  caused by other pollutants.   For many chronic  exposures,  chlorosis  precedes  the
appearance of  chronic  lesions.   Cereal,  grains, and  corn leaves  often develop longitudinal
chlorotic bands before necrosis develops.   In monocots, chlorosis may occur as transition zones
between healthy tissue and the necrotic tips.  In some broad leaf plants, chlorosis from chronic
NO. 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
exposure (doses) for acute and chronic exposures have not been defined.   Most botanic investi-
gators would designate NO, exposures of 3 to 5 mg/m  (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 recognize
the importance  of  NO,,  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  NO.  at 0.75 mg/m  (0.4 ppm) on 5 species but observed no injury.  Middleton
(1958), Middleton et al.  (1958)  and Thomas  (1961)  all  recognized that NO,, appeared in photo-
chemical^ 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 (Nlcotiana tabacum),
                                             		
and petunia  (Petunia multiflora)  were not  injured by  1.88  mg/m  (1.0 ppm)  NOg  for 2 hours.

                                            12-29

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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 NCL in the
laboratory  and in  small  greenhouses.   Rape  (Brassica  napus),  wheat (Triticum satuvini),  oats
(Avena sativa), peas  (Pisum  S£.), potatoes  (Solanurn tuberosurn), and beans (Phaseolus vulgaris)
showed little or no  injury from 56.4 mg/m   (30 ppm) N02 for 1 hour.  Alfalfa (Hedicago sativa),
sugar beets (Beta  vulgar!s). winter rye (Secale cereale). and  lettuce (Lactuca sativa) showed
some effects.  Fujiwara (1973) reported that  37.6-94 mg/m3 (20-50 ppm) N02 for 30 to 60 minutes
injured most plants  studied.
     Heck  (1964) fumigated  cotton (Gossypium hirsutum), pinto  beans  (Phaseolus  vulgan's) and
endive (Cicorium endlvia) under controlled  conditions with 1.88 mg/m  (1.0 ppm) N02 for 48 hours
and  observed slight  but  definite spotting of  leaves.   There was no  injury  produced  at 1.88
mg/m  (1.0  ppm) NO-  for 12 hours.  In another study, the same species were fumigated with 0.94,
3.76 and 6.58 mg/m   (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
vulgan's) leaves and  the endive leaves (Cicorium endiyja) 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/m  (10
ppm) NO,  for 90  minutes suffered little or no  injury;  but in tomato, a 90-minute exposure to
          3
28.20 mg/rs   (15 ppm) increased the extent of injury by 90 percent.   They  concluded  that the
                                                                      o
injury threshold for several field crops would be 18.80 to 28.20 mg/m  (10 to 15 ppm) N02 for
90 minutes.
     Maclean  et  al.  (1968)  exposed  14  ornamental  and 6 citrus species  to  NO, concentrations
                              3
ranging from 18.8  to 470 mg/m  (10  to  250 ppm) for 0.2 to 8 hours.   Necrosis occurred in the
citrus species  when  the leaves were  exposed to 376 mg/m  (200 ppm)  for 4 to 8  hours  or 470
mg/m  (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 NO, concentrations.   In one  experiment 10 field and vegetable
                                                    3
species were exposed to  15.04, 30.08, or 60.16 mg/m  (8,  16, or 32 ppm) NO, for 1 hour (Table
                      3
12-5).  At  60.16 mg/m  (32 ppm) levels of  NO,,  all species showed visual injury.   However, at
          3
15.04 mg/m   (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 concentration treatments.  Exposure duration varied from 0.5 to 7 hours and
NO, concentrations  ranged  from 3.76 to 37.6 mg/m  (2-20 ppm) (Table 12-6).   An important con-
clusion from these  experiments  was  that the extent of injury was greatest when the NO, levels
                                                                                3
were high,  even for short time periods.   For example,  cotton exposed 28.2 mg/m  (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/m  (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

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               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 esculenturn)
Wheat, Wellsc
(Triticum durum)
Soybean, Scott
(Glycine max)
Tobacco, Bel W3b
(Nicotiana tabacum)
Bromegrass, Sac Smooth
(Bromus Inermis)
Swiss Chard, Fordhook Giantc
(Beta vulgar is cicla)
Tobacco, White Goldb
(Nicotiana tabacum)
Cotton, Acala 4-42c
(Gossypiun) hirsutum)
Beet, Perfected Detroit0
(Beta y u 1 ga r i s )
Orchard Grass, Potomacc
(Dactyl is glomerata)
Tobacco, Bel W3C

8 ppa
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, Ohto.

 Plants were exposed in August with light intensity at 2200 ft-c,
     temperature 28°C, humidity 75 percent.

cPlants were exposed in January with light intensity at 1400 ft-c,
     temperature 21°C, humidity 70 percent.

 Scientific name is given only when plant is first listed.
                                   12-31

-------
              TABLE 12-6.  PERCENT LEAF AREA INJURED BY DESIGNATED DOSAGE OF HITROGEN DIOXIDE (HECK AMD TINGEY,  1979}
M
I
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 Impd *
(Impatiens sultani)
Oats, 329-80b
(Avena sativa)
Cotton, Paymaster
(Gossypium hirsuturo)
Wheat, Wells
Cotton, Acala 4-42
Periwinkle, Bright Eyes *
(Vinca minor)
Oats, Pendekc
(Avena sativa)
Dosage (ppm x hr) 2.5
(ppm) 5
(hr) 0.5
0

0

0
0
1

0

2

0

3
0
0

1

4
4
1
0

0

0
1
1

0

2

0

2
0
0

2

6
3
2
0

0

0
0
1

0

1

6

1
0
0

0

10
20
0.5
80

95

69
26
34

51

32

50

31
28
13

39

14
7
2
2

0

0
0
0

0

1

0

3
0
0

0

15
15
1
84

90

50
35
41

26

18

27

34
28
20

2

20
5
4
0

1

1
4
4

0

9

2

3
0
1

1

20
10
2
39

31

26
49
25

24

14

2

2
1
23

2

35
5
7
21

2

0
5
1

0

14

1

1
1
1

2


-------
                                                 TABLE  12-6 (continued)
Plants
(Common, Cultivar, Scientific)
Broccoli, Calabreese
(Brassica oleracea botrytis)
Tobacco, Bel B
(Nicotiana tabacun)
Tobacco, White Gold
Tobacco, Bel VL
Tobacco, Bur ley 21
(Nicotiana tabacum)
Corn, Pioneer 509-W
(Zea jnay_s)
Corn, Golden Cross
(Zea fflayj.)
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

1
6
0

0

0

0

0

0

10
20
0.5
19

18

18
15
a

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 NO- exposures
using the following model:
                   C = Ao * A1Z * A2/T
              C = Concentration ppm
              AQ, A^, A- = 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 NO-
exposure durations and concentrations necessary to produce injury on susceptible, intermediate,
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/m  (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/m  (0.6 ppm) N02 for 30 days reduced the growth of buckwheat (Fagopyrum esculentum) and egg-
plant (Solanum melongana)  (Fujiwara, 1973).  The same concentration for 51 days increased 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/m  (1.0
ppm)  N02  for 14  days.   He suggested that  a  likely threshold dose for  injury would  be 0.752
mg/m  (0.4 ppm) NOp 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/m  (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/m  (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
(Lycopersicon esculentum)  to  0.47  mg/m  (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
substantial  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/m  (0.5 ppm) for 10 days or
0.47  mg/m   (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

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                         TABLE  12-7.   PROJECTED NO, EXPOSURES THAT HAY  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
Susceptible3
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
Intermediate3
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
"Plant type.

-------
  TABLE 12-8.  EFFECT OF CHRONIC N02 EXPOSURES ON PLANT BRQWTH AND YIELD (ZAHN, 1975)
Plant Type
                    NO  Concentration
  Duration
of Exposure
  (hours)
Effect
Wheat
Bush Bean
    334        No effect on grain yield,
               but the straw yield was
               reduced 12%.

    639        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 N02 continuously for 290 days.   When
compared to trees exposed to filtered air, those fumigated with NO- concentrations ranging from
0.12 to 0.47  mg/m   (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/m   (0.25 ppm) or  less  of  HQy 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/m   (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/m  (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/m  (0.1 ppm)  NO,,  had  no effect on
                                          3                             3
plant growth  and the mixture of 0.19  mg/m  (0,1 ppm) NO, and 0.49 mg/m  (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/m
(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/m  (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
relationship  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  NO, doses.   The threshold  curve  for N02 doses that result in  the death of
plants is short because .it is based on limited information.   NO- doses approaching this thres-
hold result in complete defoliation of some  species  but  are not lethal.   The threshold curve
for  leaf  injury is  based on observations at  many  NO, doses.   The shift  in  leaf  injury from
necrosis  to  chlorosis  for  NO,  doses  along this curve generally occurred between 10 and 100
hours.   Because  no measurable effects have been reported for NO, doses below the  lower curve,
it can be considered as the threshold for metabolic and growth effects.  NO, 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 vegetation
in general, can  serve as points of reference to evaluate air quality standards for NO, in the
                                            12-37

-------
    1000
     100
EC

I
X
IU
10
     1.0 —
                                   o1
                         0E
                                                  cO
                         1.0
                                           10
                                                           100
Figure 12-4. Summary of effects of NO2 on vegetation.  The points
describe a dosage tine 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., 1974; (C) Czech and Northdurft.
1952;  (D) H. Strattman (in Taylor et al., 1975);  (E) Heck, 1964;
(F> Taylor and Eaton, 1966; (GJ Thompson et al., 1970; and (H)
Matsushima, 1976.
                            12-38

-------
                              DAYS



          ,0.01      0,1       1.0       10       100
o
u
O
 (M
O
    1000
     100
      10
     1.0
     0.1
THRESHOLD FOR

FOLIAR LESIONS
       0.1       1.0        10       100       1000



                  DURATION OF EXPOSURE, hours
                                                         1000
                                                         100
                                                         10
                                                         1.0
o


c


u
U


8
 N
O
                   10,000
 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 (McLean, 1975).
                        12-39

-------
atmosphere in the absence of other gases and they can be viewed with respect to NO, concentra-
tions 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
N02 with sulfur  dioxide  (SO,) and/or ozone  (0,).   Reinert  et  al.  (1975)  reviewed information
on these types  of  pollutant combinations.  Earlier the assumption was made that NOX 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 NO, 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 pollution
on vegetation, NO, and SO, have been evaluated for their combined effects.
                                                      •)                            2
     Tingey et al.  (1971) found that neither 3.76 mg/m  (2.0 ppm) NO, nor  1.31 mg/m  (0.5 ppm)
                                                                   3
SO, alone caused  foliar  injury.  However, a mixture  of  0.188  mg/m  (0.10  ppm)  N02  and  0.262
mg/m   (0.10  ppm)  SO- administered for 4 hours caused foliar injury to pinto  bean (Phaseolus
vulgaris),  radish (Raphanus sativus). soybean (Glycine max), tomato (Lycopersi con esculentum),
oat (Avena sativa) and tobacco (Nicotiana tabacyro).  Exposure to 0.282 mg/m  (0.15 ppm) NO- in
     *     '                  ^
combination with 0.262 mg/m  (0.1 ppm)  SO-  for  4-hours  caused greater foliar injury.  Traces
of foliar injury were observed at 0.094  rag/m3 (0.05 ppm) N02  and 0.131 rng/m  (0.05 ppm) S02-
     Hatsushima  (1971)  observed more leaf  injury  on several  plant species from a mixture of
N02 and SO,  than that caused by  each  pollutant alone.   He also tested different sequences of
exposure.   When  N02  exposure preceded  SO-, the degree of injury was similar to that resulting
from individual exposures to either gas.   But when SO, exposure was followed by N02 the degree
of leaf  injury increased  as would  be  typical of simultaneous exposures  to  both pollutants.
Fujiwara et  al.  (1973)  found  greater-than-additive effects when  peas (Pisum  sativum)  were
exposed to  0.188 mg/m   (0.1 ppm) NO,  in combination with 0.262 mg/m  (0.1  ppm) SOg.   When
0.376  mg/m3  N02 and  0.524 mg/m3  S02  (0.2 ppm  of each  gas)  were used,   the  effect  was only
additive.
     When a  large  number of desert  species were  exposed to either S02 or combinations of S0?
and NO, (ratio  approximately 4:1) injury from S02 and mixtures of S02 + N02 was similar (Hill
et al.,  1974).   N02  decreased the  foliar  injury threshold of S02  on tomatoes (Lycopersicon
esculentum),  geranium  (Pelargonium s_g.), and petunia (Petunia  sp.) (de Cormis and Luttringer,
1976).  Exposure to 0.79 mg/m  (0.3 ppm) SO, caused no foliar injury but the same concentration
                                    •3      L.
of SO, in conjunction with 0.94 mg/m  (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 NQ2 and
S0? 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 NOX was 0.585
                                            12-40

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ppm and  2-hour  maximum for S02 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 mix-
tures of N02 and S02 may reduce plant growth (Stone and Skelly, 1974).
     Bennett et al,  (1975)  studied  the effects  of NO- and S02 mixtures  on radish (Raphanus
sati'vus). swiss chard  (Beta yulgari's), oats (Avena  sativa)  and  peas (Pi sum sativum).   Treat-
ments consisted of  1-  and 3-hour fumigations with  the pollutants  separately and with SO, and
N02 (1:1) mixtures  in  concentrations ranging from 0.33-2.62 mg/m3 SO, and 0.23-1.88 mg/m  NO,
(0.125 to 1.0 ppm).   No visible injury occurred on experimental  plants treated with NO, alone
                                                                             3
or from  exposures  to  SO, concentrations of  less  than  or equal to 1.31  mg/m  (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/m  N02 and 1.31 mg/m  S02 (0.5 ppm of each gas) or to 1.95 mg/m  (0.75 ppm)
S02 alone.  The data  indicated that S02 and  N02  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 NO- and S02 may inter-
act 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/m  (0.11 ppm) N02, 0.29 mg/m  (0.11 ppm)
SO, or  a mixture  of  both  gases  at these  same concentrations.   The plants  were exposed for
  £•                                                                              3
103.5 hours per week,  which resulted  in weekly mean concentrations of 0.13 mg/m  (0.068 ppm)
N02 and 0.18 mg/m  (0.068 ppm) SO,.  The plants were harvested monthly and various growth para-
meters 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 SO-.   The combination of NO, 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 toxicity.  However,
the data clearly show  that intermittent  exposures to ambient concentrations of  N02  and SO,
singly  and in  combination can  significantly  depress yield  parameters of  important forage
grasses.
     Alfalfa (Medjcago sativa) exhibited  a  greater-than-additive  response,  i.e.,  a greater
inhibition of apparent photosynthesis  (C02 uptake) when NO, and S02 were applied together for
2 hours  at  0.47 mg/m3 (0.25 ppm)  NO,  and  0.655 mg/m3 (0.25 ppm) SO, (White et al., 1974).  A
                       1                                3
mixture  of  0.282 mg/m   (0.15  ppm) NO,  and 0.393 mg/m  (0.15 ppm)  S02  for 2-hours decreased
apparent photosynthesis  7  percent more than when the total of the two gases was applied inde-
pendently.  At  higher concentrations, 0.5 ppm of each gas,  the effects were not greater-than-
                                            12-41

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                                TABLE 12-9.  PLANT RESPONSE TO SULFUR DIOXIDE AHO KITROCEH DIOXIDE MIXTURES
                             (TIHGW IT AL. M71s HMSUSHIKA, 1911; KWETT ET At,, 1975; HILl ET At., 2974)
Plant Species
Avena saliva L.
Beta vulgaris vir. clcla L,
lathyrus odoratus L,
Raphanus sativus L
A. saliva
R. sativus
Phaseolus vulgaris L,
R sativus
Nicotiana Ubacua L.
Oriopsis hyaendoides (RiS) Ricker
Populus treiuloidcs Hichx.
Sphaeralcea nunroana Spach.
P. vulgaris
lycopers icon esculentin Hill.
Cucunis sativus L.
A, satlva
Capsicum frutescens L.
P. vulgaris Pinto
A, sativa
R. sativus
Glycine aax (L.) Here.
N. tabacun
L, esculentu*
Exposure
Chaitera'c
CE
CE
CE
CE
CE
CE
CE
CI
GH
f
f
f





GH
6H
GH
GH
GH
GH
S0,/K0,
(tip"}2
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)
lor 3
1 or 3
1 or 3
1 or 3
4
4
4
1 or 3
4
2
2
2
l.W
1
0.67
1
1
4
4
4
4
4
4
Plant
Response
(X injury)
0-5
0-1
0-5
5-8
0
0
0
0-5
0-10
16
I
31
70-75
35-85
50-100
4J-75
10-58
0-24
0-27
0-27
0-35
0-18
0-17
MIxtureh
Response '
»
*
+
*





0
0
0
+
*
+
-
4-
+
+
*
»
+
+
Plant
Age
(weeks)
4-5
4-5
4-5
4-5
2-3
2-3
2-3
4-5
7-8
A
It
ft
3-4
3-5
3-4
3-4
5-6
3-4
3-4
3-4
3-4
7-8
5-6
 CE, Control environment; GH, greenhouse; F,  field.
 •. Greater than additive; 0, additive;  -,  less than additive.
c* Hot defined.

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            TABLE 12-10.  THE EFFECTS OF N02 AND S02 SINGULARLY AND IN COMBINATION ON THE GROWTH OF SEVERAL GRASSES1
N)
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
M2
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*
NO, + SO,
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 12?b.
        The exposures were for 20 weeks (140 days).  Plants were exposed for 103.5 hr/week.  The concentrations
        of N0« and SOp during exposure were 0.11 ppm which resulted in a weekly average concentration of 0.068
        ppm.

        2
        The scientific names are:  Orchard grass, Dactylis glgnerata; Kentucky bludgrass, Poa pratensis; Italian
        ryegrass, Lolium multiforum; Timothy, Phleum pratense.
        3
        Numbers followed by + indicate increase above the control and * indicates significant reductions of the
        5% significance level or greater.

-------
additive.  Exposures  of  alfalfa (Medicago sativa) to 0,62 mg/m  (0.33 ppm) NO, and 2.62 mg/m3
(1 ppm)  SO-  at an ambient CO,  concentration  for 1 to 3 hours reduced the photosynthetic rate
approximately  SOX (Hou  et  al.,  1977).   When the ambient  carbon dioxide  concentration  was
increased  645  ppm, the  inhibitory effect of NO, and  S02 on photosynthesis was  only  50% as
large as at ambient CO, levels.  In studies with pea (Pisum sativum) Bull  and Mansfield (1974)
                      ^                                                             ^         .
reported that  over the concentration range of 0-0.47  mg/m  (0.25 ppm) NO-  and  0-0.655 mg/m
(0.025) SO-, 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/m   (0.10 ppm)  NO, and 0.262 mg/m  (0.10 ppm) SO, were applied individually the
pollutants stimulated short-term  increases  in transpiration, but the  combination  of  NO,  and
SO- decreased the transpiration rate (Ashenden, 1979b).
     Horsman and Wellburn (1975) studied the effects of NO- and SO- mixtures on several  enzyme
systems  in peas  (Pisum sativum).   Peroxidase  activity  was  enhanced somewhat by SO, alone but
                                  3                                3
not by  NO,.   However,  0.188 mg/m   (0.1  ppm)  NO, plus 0.524 mg/m  (0.2 ppm) SO,  for  6 days
          C                                      £                               C,      m
increased  the activity by 24 percent.   A  100 percent  increase occurred when 0.188 mg/m  (0.1
ppm) NO- plus 5.24 mg/m  (2.0 ppm) SO, 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
greater-than-additive response by mixtures of NO, and SO- (Wellburn et al., 1976).
12.3.5.2  Nitrogen Dioxide with Other Pollutants—Matsushima (1971) reported that combinations
of NO,  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-
raore (Platanus  occidentalis) were exposed to either  0.10 mg/m  (0.05  ppm)  ozone  and/or 0.19
mg/m  (0.10  ppm) NO,  for  6  hours  per  day for 25  days and effects on  injury  and  growth were
determined.  At  this concentration NO, had  no deletrious effects on  plant  growth or injury.
The combination of 0- plus NO, 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 NO,, SO, or 0, were less injurious when used individually than when in combinations
             b    £     «3
of NO, + SO,, NO, +  0,,  or SO, + Q-.  de Corrals and Luttringer (1976) found that a mixture of
     it   •» i-     fm     3       £.    **Q                           *3
0.31 mg/m  (0.12 ppm) SO,, 0.56 mg/m  NO- (0.3 ppm) and 0.2 mg/m  (0.1 ppm) 0^ caused extensive
leaf necrosis in tomato (Lycopersicon esculentum) within 2 hours.
     It  is clear from  these limited data that levels of NO- 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/m  (0.1 ppm) to 0.47 mg/m  (0.25 ppm) can cause direct
effects on vegetation in combination with certain other pollutants.
                                            12-44

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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 pollutants
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 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 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 calcu-
lations.  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 exten-
sive, 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.
     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.
                                            12-45

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12.4.2  Effects on Vegetation
     Sensitivity  of  plants to NO, varies with species, time of day, light, stage of maturity,
type of injury assayed, soil moisture, and nitrogen nutrition.
     When  exposures   to  NOg  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/m  (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/m  (0.25  ppm)  continuously for 8
months.  Pinto beans  (Phaseolus  vulgari's).  endive  (Cicorium  endivia) and  cotton  (Gossypium
hirsutuw) exhibited  slight leaf spotting after  48 hours  of exposure to 1.88 mg/m  (1.0 ppm).
Reduced growth in bush beans (Phaseolus vulgaris) was reported after a 14-day exposure to 1,88
mg/m   (1.0  ppm).   Other reports cited no injury in beans (Phaseolus vulgaris), tobacco (Nico-
tiana  tabacunO,  or petunia  (Petunia  multiflora) after a 2-hour exposure of the  same concen-
tration.
     Exceptions to this  generality,  however, have been observed.   For example, the growth of
Kentucky bluegrass  was significantly  reduced (approximately 25%) by  exposures to  0.21 mg/m
(0.11  ppm)  NO,  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/m   (0.1  to  1.0  ppm)
increased chlorophyll  content  ifi  pea (Pisum sativum)  seedlings  from  5  to 10 percent.   The
significance  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/m  (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
mixtures of NO, with SO,  showed that the NO^ 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 NO, and SO,  occurring in some areas  of the United States.   Neither  3.96
    31
mg/m   (2.0  ppm) N02  nor 1.31 mg/m  (0.5  ppm)  SO, alone caused foliar  injury.   Research  data
from grass species exposed for 20 weeks to concentrations of 0.21 mg/m  (0.11 ppm) NO, and 0.29
    3
mg/m  (0.11 ppm)  SO, for 103.5 hours per week showed significant reductions in yield parameters
ranging from  30  to  90% indicating that  concentrations of  these  two gases  occurring simul-
taneously can have major deletrious effects on plant growth.
                                            12-46

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CHAPTER 12

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Anderson, L. S.,  and T. A. Mansfield.  The effects of nitric oxide pollution on the growth of
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Ashenden, T. W.  The effects of long-term exposures to SO, and NO- pollution on the growth of
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Ashenden, T. W.  Effects of SO. and N0_ pollution on transpiration in Phaseolus vulgaris L.
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Ashenden, T. W.,  and T. A. Mansfield.  Extreme pollution sensitivity of grasses when SO- and
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Bartholomew, W. V., and F. E. Clark,  eds.  (1965)  Soil Nitrogen.  Agronomy, Vol. 10.
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Bennett, J. H., A. C. Hill, A. Soleimani, and W. H. Edwards.  Acute effects of  combination of
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Berge, H.  Phototoxische Immissionen.  Parey Verlag, Berlin.  1963.

Botkin, D. B.  The role of species interactions  in the response of a forest ecosystem to
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Boughey, A. S.  Fundamental Ecology.  Scranton,  Pa., Intex Educational Publishers.  1971.  p.
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Brezonick, P.  Nitrogen fixation in  some anoxlc  lacustrine environments.  Science.
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Brezonik, P.  L.  Nitrogen:  sources  and transformations in natural waters.  Pages 1-50,
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                                            12-47

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Brock, Thomas D.  Biology of Microorganisms,   Prentice-Hall,  Englewood  Cliffs,  N.J.   1970,  p.
     470-471, 485-487.

Bull, J. N., and T. A. Mansfield.   Photosynthesis  in  leaves exposed  to  SO, and  NO,.   Nature
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Capron, T. M., and T. A. Mansfield.   Inhibition of growth  in  tomato  by  air polluted  with
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Capron, T, M., and T. A. Mansfield,   Inhibition of net  photosynthesis in  tomato in air polluted
     with NO and NOg.  J. Experimental Botany  27:1181-1186, 1976.

Chen, R. L, D. R. Keeney, D. A. Graetz, and A. J.  Holding.   Dentrification and nitrate reduc-
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Czech, M., and W. Nothdurft.  Investigations of the damage to field  and horticultural  crops by
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de Cormis, L., and M. Luttringer.   Effets sur  les  vegetaux des  pollutants de 1'atmosphere
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                         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 (N0?).   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
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 N0x,
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

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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.
These dyes include Disperse Blue 7, Disperse Blue 3, Disperse Red 11 and Disperse Red 55.  Tho
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  N0» 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,  1976;
Salvin, 1974a; Seibert, 1940).  Selected anthraquinone-b and blue dyes exhibit high resistance
to fading by NOX (Salvin, 1959; Seymour and Salvin, 1949;  Straley and Dickey, 1953).
     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
pg/m   (0.2 ppm) (Hemphill, 1976).    Also,  the additional acid  introduced  by  SO-,  frequently
present  in significant  concentrations in ambient air, appears to accelerate the fading by NO,
even though S02> by itself, produces no change.  (See Table 13-1.)
13.1.1.2  Fading of Dyes on Cotton and Viscose Rayon (Cellulosics)—Although  the  effects  of
NO  on dyed  acetate are well  documented, the  effects on  dyes used for  the cellulosic fibers
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 pf 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  , 0. 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 burning
of coal; ozone concentrations  were low.  The concentrations of NO  are high in both Los
                                           13-2

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TABLE 13-1.   FADING OF DYES ON  CELLULOSE  ACETATE AND CELLULOSICS
                       (COTTON  AND  RAYON)
Concentration
of Pollutant
Dyed Fiber
Acetate
Acetate
Acetate
Acetate
Cotton- Rayon
Acetate-
Cotton, Rayon


Exposure Pollutant
Gas heated N02
rooms
Chamber NO,
Pittsburgh- N09-0,
Urban, i 4
Ames -Rural
Chamber N02
Clothes dryer NOp
Los Angeles3 NO.
*so2
Chicago3 N02
+ °3
ug/rn
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
N/A
16 hr
6 mo
16 hr
1 hr
cycle
30 to
120
days

Effect
Fading
Fading
Fading
Fading
Fading
Fading


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)
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~N02
S02-N02
and 03
S02-N02+03
N02
N02 •«• Xenon
arc radiation
NO,
N0?,
en' U <:
jU^, n«a
Concentration
of Pollutant
pg/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, 1969
Ajax et al., 1967

Beloin, 1972
Beloin, 1973
Hemphill
et al., 1976
Upham
et al . , 1976
Upham and
Salvin, 1975

Concentrations also shown in Table 13-3

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         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
Disperse Yellow 37
POLYESTER
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

Phoenix

4.5Y
3.0W


3.5
3,0





4.1
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

Los Angeles

4.0Y
2.0W


1.5R
1.5





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
(continued)
Chicago

4.5Y
2.5W


2. OR
3.5





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

Sarasota

4.5Y
2.0W


3.5
2.5





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

SOURCE:   Salvin, 1964.
                                      13-5

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                           TABLE 13-2 (continued)
Code Index No.
Phoenix    Los Angeles
             Chicago
          Sarasota
  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
 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
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
4.5
4.5
3. OR
4.0
4.0
4.5
4.0
1R
1.5G
3,5
3. SB
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
4.5
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
ORLON
Basic Yellow 11
Basic Red 14
Basic Blue 21
Disperse Yellow 3
Disperse Red 59
Disperse Blue 3

5.0
5.0
4.5
4.0
5.0
5.0

4.0
5.0
4.5
5.0
5.0
5.0

4.0
4.5
4.0
4.5
4.5
4.0

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

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          TABLE 13-3.  TYPICAL CONCENTRATIONS3 OF ATMOSPHERIC CONTAMINANTS IN EXPOSURE AREAS


Oxides of Nitrogen
Sulfur Dioxide
Carbon Monoxide
Ozone
Aldehydes
(PhoenilMarasota) Los A"9eles
(ppm) (ug/m ) (ppra) (ug/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
(ppra) (ug/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 r«acts 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
in its shade  card  of Procion Dyes.  The vulnerability of certain reactive dyes  on cotton to
NO  also has been reported by Hertig (1968) in his critical study of the International Standard:
Organization test procedure  (Rabe  and Dietrich,  1956) for color fastness to NOX.  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   SO-  were added  over a  54-hour period.
Neither the  auto exhaust  nor SO,  produced  significant fading.  However,  irradiation of the
auto exhaust, which contains  both  hydrocarbons   and  oxides  of nitrogen,  gave products which
caused significant  fading.   The addition of  SO, at  a concentration of 2,620  pg/ffl   (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

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                 TABLE 13-4.  EXPOSURE SITES
City
Washington, DC
Pool esvi lie, MD
Tacoraa, 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

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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 0,, NO,  and SO,,.   The  gas fading control (Disperse Blue 3 on
cellulose acetate)  showed high  correlation with  NO  concentration.   Fadings on  the 0, test
                                                    X                                   
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                TABLE 13-5.   AVERAGE FADING OF 20 DYE-FABRIC  COMBINATIONS'' AFTER 12 WEEKS EXPOSURE TO NITROGEN DIOXIDE
                                                   Hunttr Color Units"
Material
Cotton
Rayon
Wool
Cotton
Acryl ic
Cotton
Nylon
Wool
Acrylic
Cotton
Wool
Oyc
Direct
Direct
Acid
Reactive
Basic
Azoic0
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
12.78BC
7.2
3.4
T
T
T
T
5.6
T
T
T
T
94 tig/
High Temp,
Average
32.22°C
8.0
T
T
T
T
T
17.0
T
T
3.3
T
m3 NO,
Low
Humidity
Average
(SOS RH)
7.4
T
T
T
T
T
10.1
T
T
T
T
940 ug/rn3 NO,
High
Humidity
Average
(90S 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
High Temp.
Average
32.229t
20.4
16.3
T
6.9
T
T
27.9
T
T
6.6
T
Low
Humidity
Average
(SOS RH)
16.1
12.6
T
9,7
T
T
24.1
T
T
6.1
T
High
Humidity
Average
(90% RH)
22.3
17.0
T
7.8
T
T
25.1
T
T
7.1
4.1
SOURCE:   Beloin.  1973.
                                                                 (continued)

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                                                          TABLE  13-5.   (continued)
94 ug/«3 HO,
HaUrial
Cotton
Cellulose
Acetate
Nylon
Cellulose
Acetate
Polyester
Cotton
Cotton
Cotton
Acetate
Dye
Direct
Disperse
Disperse
Disperse
Disperse
Reactive
Reactive
Vat
	 d
Color Index No.
Blue BG
Blue 3
Blue 3
Slue 27
Blue 27
Blue 1
Blue 2
Blue 14
AATCC Ozone
Ribbon
Low Te*p.
Average
12.7fl°C
5.9
29.0
5.5
6.4
T
3.9
6.4
6.3
T
High Te»p.
Average
32.22 C
9.5
42.3
14.7
4.9
T
13.6
10.6
6.7
T
Low
Kunidtty
Average
(SOX RH)
9.4
37.7
5.9
3.8
T
9.6
8.2
3.3
T
High
Hiwidity
Average
{90% RH)
6.0
33.6
14.2
7.5
T
7.9
8.9
9.7
T
Low Te«p.
Average
12.78aC
14.1
86.9
39.6
20.5
T
31. 8
30.5
34.3
5.7
940 pg/B3 NO,
High Te*p-
Average
32,22 C
17.2
75.6
45.5
26.8
T
41.7
41.6
30.4
11.7
low
Hunidity
Average
(SOX RH)
14.2
83.0
34.0
17.0
T
35.4
33.8
23.4
5.7
High
Hunidity
Average
(90S RH)
17.1
74.4
51.1
29.6
T
38.1
38.4
41.3
11.7
 Each average, e.g.  the low temperature average,  was calculated by averaging the color change of duplicate staples fron both  the  low
 temperature-low humidity and low temperature-high hinidity exposure periods.
 T=trace (less than 3 units of fading).   The higher the number, the greater the fading.   Hunter Color Units approximate the NBS color scale.
 Coupling Component 2, Azoic Oiaio Conponent 32.
dC.I.  Disperse Blu* 27, C.I.  Disperse R«d 35, C.I.  Disperse Yellow 37.

-------
(131  and  1310 ug/m3),  03 (98 and  980 ug/m3),  and N02  (94  and 940  \ig/m3)  under Xenon  arc
irradiation, at  various humidities.   The effect of NO, was pronounced, especially on  a  vat-
                                                                           3
dyed  drapery  fabric.   The most  noticeable color changes were  at 940 ug/m  (O.S pptn)  and 90
percent relative humidity.
     In summary, the  investigations  by ieloin both  in  the  field study (1972)  and the chamber
study (1973) show that,  at concentrations of NO, present in urban atmospheres, representative
dyes  for  cotton  and  rayon  will  suffer  serious  fading.  NO,  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  increased 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 NO,, 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 (NO,, SO, and
0«), 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  0-  in the presence of high humidity (Salvin, 1974b).
Acid dyes, which  are  more resistant to 0,, 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 NO,,  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 NO.  from gas burner fumes.
     Acid dyes  on  nylon were included in the range of dyes exposed to visible  light radiation
and N09 by Hemphill in the AATCC study (Hemphill et al., 1976).   Under high humidity conditions
                                        3
and at  an  NOp 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  NOj  were
present than in the control exposure with Xenon arc  irradiation and NQ_-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

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TABLE 13-6.   EFFECT OF NITROGEN DIOXIDE ON  FADING OF DYES  ON  NYLON AND POLYESTER
Concentration
of Pqllutant
Dyed Fibers
Nylon
Polyester
Nylon
Polyester
Nylon
Polyester
Nylon
Nylon
Polyester
Permanent
Press
Polyester
Textured
Double Knit
Exposure
Chicago
Los Angeles -
Chicago
Los Angeles
Urban Sites
Urban Sites
Chamber
High Humidity
Chamber
High Humidity
Chamber
High Humidity
Chamber
High Humidity
Xenon Arc
Chamber
Chamber
Pollutant ug/m"
NO, 188
* 282
NO, 376
i 282
N02 376
N02 376
NO, 188 to
* 1,880
NO- 188 to
£ 1,880
N02 376
N02 940
N02 940
N02 940
pp.ra
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
Sal vi n, 1964
Ibid.

Beloin, 1972
Ibid.
Beloin, 1973
Ibid.

Imperial Chemical
Industries, 1973
Hemphill et al., 1976
Salvin, 1966
Urbanik, 1974

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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 polyestei—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 NO- or 0,, 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 0,.  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 NO,  or 0,.   The fading
attributed  to  NQg 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.
1.3.1.1.5  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
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 NO  action
are discussed  in  Chapter  8, "The Effects  of  Nitrogen Oxides on Materials," in the National
Academy of Sciences report on nitrogen oxides (National Academy of Sciences, 1976a).
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

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TABLE 13-7. ESTIMATED COSTS OF DYE FADING IN TEXTILES
Pollutant Effect $
NO Fading on acetate and triacetate
Fading on viscose rayon
Fading on cotton
Yellowing of white acetate-nylon-Spandex
Subtotal
0, Fading on acetate and triacetate
Fading on nylon carpets
Fading on permanent-press garments
Subtotal
million3
73
22
22
6
122
25
42
17
84

Total
206
aA11 costs rounded to nearest million, therefore some totals do not agree.
SOURCE:  Barrett and Waddell, 1973.
                                    13-16

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     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,,  SO,,  or hydrogen sulfide (H-S).
     The standard AATCC test procedure  (conducted in low humidity) for effects of NO,, 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
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  NO,  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 N0_ 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 N0?.   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 AATCC (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 NO,,.   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

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TABLE 13-8.  YELLOWING OF WHITES BY NITROGEN DIOXIDE

Concentration
of Pollutant
Fiber
Survey
Rubberized
Cotton
Rubberized
Cotton
,_. Spandex
w
H*
00
Acetate
Optical
brightener
Nylon
Optical
brightener
Nylon
Anti-stat
finish
Cotton
Cationic
softener
Exposure Pollutant jig/m
Service N/A
Complaints
Chamber N02 376
Chamber N02 376
Chamber N02 376
Chamber NO. 376
Chamber NO- 376
High Humidity
Chamber NO, 376
High Humidity i
Chamber N02 376
ppm Time Effect
N/A Yellowing
0.2 16 hr Yellowing
0.2 16 hr Yellowing of
anti-oxidant
0.2 8 hr Action on
fiber
0.2 8 hr Yellowing
0.2 16 hr Yellowing
0.2 16 hr Yellowing
0.2 16 hr Yellowing
Reference
Up ham and
Salvin, 1975
Burr and
Lannefeld,
1974
Salvin, 1974c
jbid.
Ibid.
Ibid.
Ibid.
Ibid.


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13.1.3  Degradation of Textile Fibers by Nitrogen Oxides
     Cotton and nylon are the two fibers whose strength 1s 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  NO,  and light on  cotton  did  demonstrate that
NO, 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 0,  and NOg.
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  NOX
gave increased deterioration  over  sunlight  alone.   The contributions of 0, 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
al., 1968;  Morris,  1966; Travnicek,  1966).   The effect  of  NO, on fiber degradation of cotton
requires further investigation.
     Inconclusive results  were  shown by Zeronian et al.  (1971) in a study  of  the effect of
NO-, 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 ug/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 NO,-   Modacrylic (Dynel), acrylic (Orion), and polyester showed only slight
differences in degradation  in exposures with and without NO-.  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
NQ_ 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 Engineer!ng 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

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     Ageing 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 NO*, have been assessed 1n 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 SO-, NO,, and ozone obtained by action of
UV  radiation  on  the  oxygen-containing mixture.   These  combinations of  SO-, N02,  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 SO, and NO,
than other polymers.   However,  the effect of 0,  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  NO, at  concentrations  of 1,880 to 9,400  ug/m  (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 SO- and NO, took place in the  presence of air and UV radiation.
     The action  of NO,  and 0.  on polyurethane  also was  investigated by Jellinek (1974).  The
tensile strength of   linear polyurethane was reduced  by NO-  alone and also  by NO, plus 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 SOg,
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 NO-  to  corrosion   in  the review  by  the National  Research Council
(National Academy of Sciences,  1976b).
     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 NO- and  nitrate

                                    13-20

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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 (1S73) estimated costs
at $7.5 billion in 1958.
     Material  damage due  to air pollutants emphasizes SO, 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  N02  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  SO.,  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 ug/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-

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     A field study was  made of the Incidence  of  breakage as related to the nitrate accumula-
tion.   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
hygroscopic  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 electro-
lyte 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
nHrates,  forming bright greenish  corrosion products which gradually crept over the palladium
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 N02  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. SO^. H.S and  dust were monitored.   This study did not isolate the specific contribu-
tion of NO- 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
ASIH of various  metals in different locations sought  to establish which  metal or alloy was
•ost resistant.   The case of the telephone  equipment failure as investigated  by Hermance et
 »'   (1971) did show that  nitrates were  a contributory  factor,  although  no  relation  to the
 concentration of N02 in the air was established.
     Gerhard and  Haynie (1974)  examined the cases  of catastrophic  failure of metals in which
 itructures  failed unexpectedly,  leading  to  loss of  life  as  well  as well  as  collapse  of the
 •»i4%  structure.   Their conclusion  was that air pollutants were a probable contribution  to the
 c-.-*osion  that  was the cause  of failure.   However,  there is no finding  that determined the
 '•'•'.lonship between levels of particular pollutants and the occurrence of the failure.
      Httroqenous  compounds, however, were implicated in a situation in which steel cables on a
 &--i;« (n Portsmouth,  Ohio failed  after 12 years of service.   The cause of failure was  traced
 ':  --.»-  water contaminated with ammonium  nitrate  that had  concentrated  at  natural  crevices
   '••»•-•.. 1965). Nitrogen dioxide was not considered a factor.
                                    13-22

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     A review of  the  voluminous literature on corrosion has produced no further references to
investigations of  NO, action,  in  the absence  of S0~.   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 NO,, 0,,  and SO,.   These
exposures were  carried out  in  ambient air  and protected  against  sunlight.   Chamber studies
using  individual   pollutants N02,  0,,  and SO,  have  shown  that  some  individual  dye-fiber
combinations exhibit color fading only in response to NOj exposure, whereas others are suscep-
tible  to  0-,  as  well  as combinations  of  NO^  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  yg/m  (0,05 ppm)  HO* 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 N0,-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 Og  and SO,
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 amihe group
(-NH,) 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) N02.   Field
exposures of  fibers  emphasize the action of acids derived from SO,, although NO, may also be
present  in  high  concentrations  in  urban  sites.   Information on  the   contribution  of  NOg to
degradation is incomplete.
                                    13-23

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                             TABLE  13-9.   CORROSION OF METALS BY NITROGEN DIOXIDE
Metal
Mechanics of
Nickel Brass
Nickel Brass
Nickel
Tungsten
Electronic
contacts
Metal parts
Exposure
Corrosion - Function of
Los Angeles
Los Angeles
Los Angeles
New York
Chamber
Field
Field
Pollutant
Nitrates
Nitrates
Nitrates
Nitrates
N02
N02-S02-H2S
N02-S02-03
Effect

.Strength
Loss
Strength
Loss
Corrosion
Change oxide
surface
Corrosion
film
Failure
Reference
National Academy of
Sciences, 1976a


Hermance et al . , 1971
McKinney and
Hermance, 1967
Hermance, 1966
Lazareva, 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
dioxidt 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  SO- concentrations.   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

-------
CHAPTER 13

Ajax, R. W., C. J. Conlee, 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.  AATCC Technical Manual.   Volume 48.
     Research Triangle Park, North Carolina. 1972, 370 pp.

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.

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. £. Waddell.  Cost of air pollution damage.  A status report.  NTIS
     Publication No. PB-22Q-040.  U.S. Environmental Protection Agency, AP-85,  February  1973.

Beloin, N. J.  A chamber study—fading of dyed fabrics exposed to  air pollutants.   Textile
     Chem. and Color. 5: 29-33, 1973.

Beloin, N. J.  A field study—fading of dyed fabrics by air pollution.  Textile Chem.  and
     Color. 4: 43-48, 1972.

Brysson, R. J., B. J. Trask, and A. S. Cooper, Jr.  The durability of cotton  textiles—the
     effects of exposure in contaminated atmospheres.  Amer.  Dyestuff Reporter  57:  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.  November 7, 1977.

Chiaranzelli, R. V., and E. L. Joba.  Effect of air pollution on electrical contact materials.
     J. Air Pollut. Control Assoc. 16:  123, 1966.

Couper, M.  Fading of a dye on cellulose acetate by light and gas  fumes:  1,4 bis methyl amino-
     anthraquinone.  Textile 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.  Economic costs of corrosion.  NTIS Publication
     No. PB 198 453, EPA Publication No. APTD 0654.  February 1971.  160 pp.

Gerhard, J., and F. H. Haynie.  Air pollution effects and catastrophic  failure  of metals.
     NTIS Publication No. PB 238-290.  November 1974.

Gillette, D. G.  SO, and material damage.  J. Air Pollut. Control  Assoc. 25:  1238, 1975.



                                             13-26

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Haynie, F. H., J. W. Spence, and J. B. Upham.  Effect of gaseous pollutants on materials—a
     chamber study.  NTIS Publication No. PB 251-580 7 ga.  EPA-600/3-76-015,  February 1976.
     98 pp.

Hemphill, J. E., J. E. Norton, 0. A. Ofjord, and R. L. Stone.  Color fastness to light and
     atmospheric contaminants.  Textile Chem. and Color. 8:60-62, 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. Sc1. Tech, 5_;781-789, 1971.

Hertig, J.  Prufung der Stickoxidechtheit-Erfahrungen und Vorschlage.  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 (1-5 ppm) of sulfur
     dioxide and nitrogen dioxide, respectively, in the presence of air and near UV radiation.
     J. Air Pollut. Control Assoc. 20:672-674, 1970.

Jellinek, H. H.  G.  Degradation of polymers at low temperatures by NO-, 0_, and near-
     ultraviolet light radiation.  Cold Regions Res. Eng. Lab., Hanover, New Hampshire.  USN
     TIS AD 782950/OGA, 1974.  31 pp.

Jellinek, H. H.  G., F. Flajeman, and F. J. Kryman.  Reaction of SO, and N0? with polymers.  J.
     App- Poly Sci, 13(1):107-116, 1969.                          *       i

Lazareva, I. Y., D. A. Prokoshkin, E. V. Vasileva, and S. A. Skotnikov.  Reactional diffusion
     during oxidation of tungsten alloys in an atmosphere with a high concentration of NO,,
     Protective Coating Metals §: 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, ASTM STP 425, Amer. Soc. Testing
     Mat., Philadelphia, Pennsylvania, 1967.  pp. 274-291.

McLendon, V., and F. Richardson.  Oxides of nitrogen as a factor in color changes of used and
     laundered cotton articles.  Amer. Dyestuff Reporter §4(9):15-21, 1965.

Morris, M. A.  Effect of weathering on cotton  fabrics.  California Agricultural Experiment
     Station Bulletin 823, Davis, California, 1966.  29 pp.

National Academy of Sciences.  Effects of NO, on materials.  In:  Nitrogen Oxides.  Chapter 6.
     National Research Council, Subcommittee on Nitrogen Oxides, Washington, D.C., 1976a.

National Academy of Sciences.  Nitrogen Oxides.  National Research Council, Committee on
     Medical and Biological Effects of Environmental Pollutants, Subcommittee on Mitrogen
     oxides.  Washington, D.C. 1976b.
                                              13-27

-------
Rabe, P., and R. Dietrich.  A comparison of methods for testing the fastness to gas fading of
     dyes on acetate.  Amer. Dyestuff Reporter 45:737-740, 1956.

Romans, H. 8.  Stress Corrosion Test,  Environments and Test Periods Report of ASTM Task Group
     B.  January 1965.  p. 58.

Rowe, F. M., and K. J. Chamberlain.  The fading of dyeings on cellulose acetate rayon.  J.
     Soc. Dyers Colour. 52:268-278, 1937.

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.  Relation of atmospheric contaminants and ozone to  light fastness.  Amer.
     Dyestuff Reporter 53:33-41, 1964.

Salvin, V. S.  Testing atmospheric fading of dyed cotton and rayon.  Amer. Dyestuff Reporter
     5:8-29, 1969.

Salvin, V. S.  The effect of dry heat on disperse dyes.  Amer. Dyestuff Reporter  55:490-510,
     1966.

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., W. D. Paist, and W. J. Myles.  Advances in theoretical and practical studies of
     gas fading.  Amer. Dyestuff Reporter 41:297-302, 1952.

Salvin, V. S., and R. A. Walker.  Relation of dye structure to properties of disperse dyes.
     Amer. Dyestuff Reporter 48:35-43, 1959.

Salvin, V. S., and R. A. Walker.  Service fading of disperse dyes by chemical agents  other
     than oxides of nitrogen.  Textile Res. J. 25:571-585, 1955.

Schraitt, C.  H. A.  Light fastness of dyestuffs on textiles.  Amer. Dyestuff Reporter
     49:974-980, 1960.

Seibert, C.  A.  Atmospheric (gas) fading of colored cellulose acetate.  Amer. Dyestuff Reporter
     23:366-374, 1940.

Seymour, G.  W., and V. S. Salvin.  Celanese Corporation.  Process of reacting a nitro hydroxy
     anthraquinone with a primary amine and a product thereof.  U.S. Patent 2,480,269.  August
     30, 1949.

Straley and Dickey.  Eastman Kodak.  U.S. Patent 2,641,602.  June 9, 1953.

Travnicek, Z.  Effects of air pollution on textiles especially synthetic fibers.  International
     Clean Air Congress Proceedings, London, 1966.  pp. 224-226.

Upham, J. B., F. H. Haynie, and J. W. Spence.  Fading of selected drapery fabrics by  air
     pollution.  J. Air Pollut. Control Assoc.  2S(8):790, 1976.


                                             13-28

-------
Upham, J. B.,  and V.  S.  Salvin.  Effects of Air Pollutants on Textile Fibers and Dyes.
     Ecological Res.  Series.   EPA-650/3-74-008.  U.S. Environmental Protection Agency,
     Washington, O.C.  1975.

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, O.C.,
     1967.

Waddell, T. E.  Economic damage of air pollution.  NTIS Publication No. PB 235 761 PGF,  1974.

Yocum, J. E.,  and N.  Grappore.   Effects of power plant emissions on materials.  NTIS
     Publication PB 257-537 7 ga.   July 1976.  92D.  EPRI EC 139.  EPRI RB 575.

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.  Proceedings  of  the
     Second International Clean Air Congress, Washington, O.C., December, 1970.  Academic
     Press, Inc., New York, 1971.   pp. 468-476.
                                             13-29

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                 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 (National
Academy of  Sciences,  1977),  the  North Atlantic Treaty  Organization  document (North Atlantic
Treaty Organization,  1973)  and the USEPA document concerning short-terra effects of NO, (U.S.
Environmental Protection  Agency,  1978).   A World Health Organization monograph has been re-
cently 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 publica-
tions 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  (NO.) 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-
                       3                    *
tions below  9,400 pg/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  RespiratoryTract Transport and Absorption
     Nitrogen  dioxide  is   soluble  and  can  be  absorbed  in  the  mucous  lining  of  the
riasopharyngeal  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 NO. removal,
which amounted to 42.1  percent of the incoming NQ_ concentration.  Dalhamn and SjSholin  (1963)
measured the  concentration  of NO. in a  stream of water-saturated air before and after  it had
been  passed  through  the nose and  out  a trachea! 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 ug/m3  (0.3 to 0.91
ppm) NOg plus   NO,.   During quiet respiration, 50 to 60 percent of the  inspired pollutant was
retained  by  the animal;  radioactivity was  distributed  throughout  the lungs.   Once absorbed,
NO,  or  chemical  intermediates derived from  NO, remained within the lung for prolonged periods
                      13
following  exposure.     N-radioactivity was  detectable   in extrapulmonary  sites  as well.  The
authors postulated that NO- 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
MS/™3
Not
Reported
560
1,710
188,000
ppiti
Not
Reported
to 0,3 to
0.91
100
Duration
(win)
Not
Reported
9
< 45
Species
Dog and
rabbit
Monkey
Rabbit
Effect
Removal of 42.1% by isolated upper airways.
Concentration and flow rates not given,
13
Concurrent exposure to NO, demonstrated that
N02 was evenly distributed fn the lungs and
absorbed into the blood.
Absorption of approximately 50% N0_ in the
nasopharyngeal cavity.
Reference
Yokoyaraa, 1968
Goldstein e't
al., 1977b
Dalhatnn and
Sjohfilm, 1963

-------
     Observed effects  of exposure to  much  higher concentrations of NO.  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
Hine et al.  (1970)  found that concentrations below 94,000 ug/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 NOg include cold stress
and adrenalectomy.
     Dietary supplementation  of Vitamin E  (45  to 100 mg d.l-ortocopherol)  has been shown to
protect against mortality and  increase mean survival of  animals exposed, for long periods of
time, to  high  concentrations  of  NO-  (37,600  to  62,000  ug/ro ;  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  SQg
(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  NO,, 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  EHr'Hch
                                             14-3

-------
                         TABLE 14-2.   MORTALITY  FROM N02  EXPOSURE  FOR  1  TO 8 HOURS

W2
Concentration
ug/ma
94,000
to
141,000
141,000
141,000
141,000
141,000
141,000
173,000


ppin
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
House
.House (


Effect
Increased mortality with cold stress,
adrenalectomy, and exercise.
No increase with heat or prior NO-
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. ,


Hine 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.

-------
(1375), 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 N0_) 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), Klebs iella pneumoniae (K^  pneumoniae),  Diploccoecus
pneumonias (0. 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-
centrations of N02 were  varied from 1,880 to 26,320  pg/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 NO,  for brief periods of time resulted in more
severe infections and in greater mortality than did prolonged exposures to lower concentrations
of NO,.  This  indicated  that susceptibility to infection was influenced more by concentration
of NO, 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-
                                                      3                3
posed  to  6  constant concentrations  of NO, (940 ug/m  to  52,670 ug/m  ; 0.5  to 28  ppm).   S.
                                                              3                            ~
pyogenes  was  used  for  all  concentrations,  except  940 MS/"1  (0-5 ppm),  in which  case K.
pneumoniae was  used.   A  linear dose-response  (p <  0.05)  indicated that mortality increases
with increasing length of  exposure to a given concentration of NO,.  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.
x  T of  approximately  21  (ppm  x hour),  a 14-hour  exposure  at  2,800  pg/m   (1.5  ppm) NO,
                                                                                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 1s  more  important than time in determining  the degree of Injury induced by NO,
in this  model.   According  to Larsen et  al.  (1979),  NO, modeling  studies have  shown that the
concentration (c)  of NO. 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  NO,  followed  by bacterial  challenge with  S.  pyogenes  (Figures 14-2,   14-3).   Mice  were
      f_                                         —
exposed  either continuously or  intermittently  (7  hours/day,  7 days/week)  to  2,800 pg/m  or
6,600  ug/m   (1.5  or 3.5  ppm)  NO-.   Figure  14-2  illustrates the results  of  continuous and

                                             14-5

-------
                                          TABLE 14-3.   INTERACTION WITH INFECTIOUS AGENTS

NOj,
Concentration
Mi/n3
560
to
940


940
940
to
1,880
18,800
1,880
4,320
12,400
ppra
0.3
to
0.5


0.5
0.5
to
1
10
1
2.3
6.6
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
17 hr Mouse


Infective
Agent Effect Reference
A/PR/8 virus High incidence of adenomatous Motonriya et al.,
proliferation of peripheral 1973
and bronchial epithelial cells.
NO, alone & virus alone caused
lets severe alterations.
No enhancement of effect of NO,
and virus.
K- pneumoniae Increased mortality after Ehrlich and
~ 6 mo intermittent exposure Henry, 19S8
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.

S. aureus Bactericidal activity unchanged. Goldstein et al.,
after N02 1973b
6% decrease in bactericidal
activity (p<0.05).
35% decrease In bactericidal
2820 to    1.5 to  (See Figure 14-1} Mouse      S.  pyogenes
52,670     28
activity (p<0.01).

Increased mortality with in-
creased time and concentration.
Gardner et al.,
1979

-------
TABLE 14-3,   (continued)

N02
Concentration
jjg/m3 ppni
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-
mi ttent
7 hr/day,
7 days/wk,
to 15 days
1, 3.5 or Mouse
7 hrs
Cont. 62 hrs. House
then spike for
1, 3.5 or 7 hr, ,
then cont. 18
hrs.
Infective
Agent Effect Reference
S. pyogenes Exercise on continuously moving llling 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 (1981)
was immediately, but not 18
hrs post exposure
S. pyoqenes Mortality increased with 3.5 Gardner et al.,
and 7 hr. single spike when (1981)
bacterial challenge was
immediately or 18 hrs post
exposure

-------
TABLE 14-3.   (continued)
N02
Concentration
|jg/ra3 ppm
Exposure Species
2,800 1.5 Cont, for 14 d House
(8,100 4.5) spike 2x1 hr/d
5 days/wk x 2 wk
continuous:
100 0.05+ Cont. House
100 0.05 03
with spikes 2x per day:
200 0.1+ 15 days
200 03 0.1 0, (spikes-1 hr,
twice/day, 5
days/wk)
continuous:
940 0.5 House
100 03 0.05 03
with spikes 2 x per day:
1,880 1.0+
200 03 0.10,
continuous:
2,300 1.2+ Cont. 15 days House
200 0.1 03 (spikes-1 hr,
twice/day, 5
days/wk)
with spikes 2 x per day:
4,700 2.5
600 0, 0.3 03
2,800 1.5 Cont. Mouse
Infective
Agent Effect
$' 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. pyopenes Increased mortality with NOj
alone; no effect 0, alone;
synergistic effect 0, + NO,
S. pyogenes Increased mortality with NO-
alone and 03 alone; additive
effect of 03 + H0?
S. pyogenes Elevated temp. (32° C) in-
creased mortality
Reference
Gardner et al . ,
(1981)
Gardner et al . ,
(1981)
Gardner et al . ,
(1981)
Gardner et al. ,
(1981)
Gardner et al . ,
(1981)

-------
                                             TABLE 14-3.  (continued)
    N02
Concentration
JjgTff3     ppi    Exposure
                                  Species
                                               Infective
                                                 Agent
                                     Effect
                                                  Reference
 3,570     1.9    4 hr

 7,140     3.8


13,160       7


17,200     9.2


27,800    14.8


 3,760     2      3 hr
 4,700     2.5    2 hr
47,000    25
 9,400       5

18,800      10

28,200      15


 6,580     3.5    2 hr

65,830      35    2 hr
                                   House
House


Mouse
                                   House

                                   Hamster
            Infected with Physical  removal  of bacteria
            S.  aureus     unchanged at 3,570 and 7,140
            prior to NO-  ug/m  (1.9 and 3.8 ppm).
            exposure

                          7X lower  bactericidal activity
                          (p<0.05).

                          14X lower bactericidal activity
                                                             50% lower bactericidal activity
                                               S. pyogenes   Increased mortality (p<0.05)
                                               Challenge
                                               with K.
                                               pneumoniae
                                               before and
                                               after ex-
                                               posure
              No effect on mortality. At
              47,000 ug/m  (25 ppm) effect
              when bacterial challenge was
              up to 72 hrs. but not later,
              after NO^ exposure ceased.
            K.  fi
            chal
   llenge
after
exposure
                                                            creased mortality.  Each species
                                                            had decreased resistance to NO-
                                                            and bacteria.
                                                  Goldstein et al.,
                                                  1973b
                                                                                                Ehrlich et al.,
                                                                                                1977

                                                                                                Purvis and
                                                                                                Ehrlich, 1963
              Significant increase in
              mortality on K. pneumoniae
              challenge 1 and 6 hr post NO*.
              When K. pneumoniae challenge
              27 hr~post HO- effect only at
              28,200 ug/m  fl5 pprn).

K- Pneumoniae NO, toxic to all species and in-    Ehrlich, 1975

-------
                                             TABLE 14-3.   (continued)

N02
Concentration
pg/ra3
94,050
9,400
19,000
9,400
ppni
50
5
10
5
Exposure
2 hr
Continuous,
2 mo
Continuous
1 ino
2 mo
Species
Squirrel
monkey
Squirrel
monkey

Squirrel
monkey
Infective
Agent Effect Reference

K. pneumoniae One-third died after infection. Henry et al.,
and A/PR/8 1970
virus
Death within 2-3 days after in-
fection. Increased susceptibil-
ity to infection. Decreased lung
clearance of viable bacteria.
K- pneumoniae Mortality 2/7. Bacteria present Henry et al.,
in lung of survivors upon 1969
19,000
10    1 mo
autopsy.

Mortality 1/4.  Bacteria present
in lungs of survivors at
autopsy.
94,000      50    2 hr
                                                  Mortality 3/3.

-------
        TABLE 14-4.  THE INFLUENCE OF CONCENTRATION AND TIME ON ENHANCEMENT
             OF MORTALITY RESULTING FROM VARIOUS N02 CONCENTRATIONS3

Concentration x time
7
Concentration
fjg/m3 ppm
2,820
6,580
13,160
26,320
52,640
1.5
3.5
7
14
28
Time %
(hrs) Mortality
4.7
2.0
1.0
.5
.25
6.4
18.7
30.2
21.7
55.5
Time
(hrs)
9.3
4.0
2.0
1.0
.5
14
%
Mortality
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

-------
•*    >-
ii    2
ro    ui
     O
     cc
     UJ
     a.
    go
uj   BO
 cc 50


il4°

is130
5 -
     10
    -10
                                                                                  I      II      III
                                                                                  III      II
       6       15  253035   1     2357    14   24    48    96   7    1416   30    23     6  9 12

       p*     minutm	* j*'	hours	* | —	days "	* | *•     months    **f

                                                   TIME
      Figure 14-1. Regression linns of percent mortality ol mice versui length of continuous exposure to various N(>2 concentrations prior to

      chalNnqe with bacteria (Gardner Bt al.. 1977h|.

-------
   80
   70
   60
<   50
i-
tr
O



Z   40
L&l
O
cc
Ul

°-   30
   20 —
   10 —
      -O
        o
                o
                a
                        o
                        D
                                 O


                                 a
                                                                  i      n      n     n      n      r
                                                         O CONTINUOUS
                                                         D INTiBMITTENT
                                                                                                                         TT

                                                                                                                           CH
                                                                                                                          cr~
                                                  INrERMirreNTNOjEXPOSURC'
                                                                       v/
      0  7
                                                                                         247
                                                                                                  271
                                                                                                          295
                                                                                                                           343
                                                             TlME.houfi
Figure 14-2.  Percent mortality of mice versus the length of either continuous or intettnittent exposure to 6,800 Mfl^m' (3-5 ppm) NOj prior

to challenge with streptococci (Gardner et «!., 1977h; Gardner et al.( 1977a;  Coffin et al., 1977).

-------
O
(C
H


8
O
o
30
    20
t   10
en
O
o
en
                                             O* CONTINUOUS
O



a
        8
                     o*
                 a
                                             O   INTERMITTENT
                                                                                         * CONTINUOUS AND INTERMITTENT

                                                                                          TREATMENT MEANS ARE SIGNIFICANTLY

                                                                                          DIFFERENT AT p<0 05
                                                  J-INTERMITTENT NOpFXfOSUHt
      0 7
                                            151
                                                                                      319
                                                               TIME.houn
                                                                                                                                187
 Figure 14-3. Percent mortality of mice versus length of either continuous or intermittent exposure to 2.800 )ig/m^ (1.5 ppm) NC^ prior to

 challenge with streptococci (Gardner et al.. 1977b;  Gardner et al., 1977a; Coffin et al., 1977).

-------
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 es-
sentially the  same for  the continuous and Intermittent groups.   The  continuous  exposure of
mice to 2,800 ug/m   (1.5 ppm} NO, increased mortality after 24 hours of exposure.   During the
first week of exposure, the mortality was significantly higher in mice exposed continuously to
NO. 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) NO.  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 NO- showed significant (p < 0.1) increases
in mortality over that of controls (18%).  After 12 months exposure to NO., 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 £._ pyogenes  to  those using ]C_ pneumoniae,  the data suggest
that as  the concentration  of  NO. 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.  (1981)  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 NO, 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 \ig/m  (4.5 ppm) for 1, 3,5 or 7 hrs  and exposed to S. pyogenes
either  immediately  or 18 hrs  afterwards.   Hortality 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 vg/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 im-
paired  by  the  continuous exposure  to  NO,.  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 pg/m
(4.5 ppm)  superimposed  to a continuous background  of  2,800 pg/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-
lent to continuous exposure to 2,800 pg/m  (1.5 ppm).
     In this same study, Gardner et al. (1981) also examined the effects of exposure to spikes
of 0, and NO,, and heat stress.*  At the lowest concentration of 0, and NO, examined, 100 ug/in
(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 NO, with 1.0 ppm
spikes and 0.05 ppm 0, with 0.1 ppm spikes) or high (1.2 ppm NO- with 2.5 ppm spikes and 0.1 ppm
0, with  0.3  ppm  spikes)  doses,  mortality was increased synergistically;  e.g.,  mortality 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/o  (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.  (1981)  concluded that while  a  simple  log-log relationship exists for the
mortality associated with  a given exposure-time product with mice continuously exposed to NO-
or given  intermittent  regular  exposures,  no  such  relationship exists  for mice continuously
exposed to a constant  concentration of N0» 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 NO^ 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 dif-
fering  sensitivity to  either the pathogen  or NO-,  or  a combination  of both.   All  three
                                        3
squirrel monkeys exposed  to 94,050 ug/m  (50  ppm)  NO, died from the pneumonia (Henry et al.,
                                                         3
1969).   Lower concentrations tested (9,400 to 65,830 ug/m  ; 5 to 35 ppm) had no effect in mon-
keys.   The hamster model,  which  exhibited  enhanced mortality  due  to NO,  at concentrations
             3                                            3
> 65,830  ug/m   (35 ppm)  but not  at  9,400 to  47,000  pg/m   (5 to 25  ppm), had intermediate
sensitivity.   The mouse model was  sensitive to NO- exposure as evidenced by enhanced mortality
                                 3                                          3
following exposure  to  6,580 ug/m  (3.5 ppm) but not to 2,820 to 4,700 ug/m  (1.5 to 2.5 ppm)
NO-  for  2 hours  (Ehrlich, 1975).  No  effect  on mortality was observed  in mice  exposed for 2
                    3
hours to  4,700 ug/m  (2.5 ppm) (Purvis and Ehrlich, 1963).  However, when S. pyogenes was the
infectious agent,  a 3-hour exposure to 3,760  ug/m  (2 ppm) N02 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 NO, before  or  after an aerosol challenge with K. pneumom'ae.   At
9,400,  18,800,  28,200 and  47,000  ug/m3 (5, 10,  15,  or 25 ppm) N02,  there  was  a significant
enhancement of  mortality in mice  challenged with  bacteria 1  and 6  hours  after  the  NO™  ex-
posure.  When bacterial .challenge  was delayed for  27  hours,  there was an effect  only in  the
group exposed to 28,200 gg/m  (15 ppm).  Exposure to 4,700 ug/nt  (2.5 ppm) caused no effect at
any of the bacterial challenge times tested.  Exposure of 47,000 ug/m  (25 ppm) N02 for 2 hours
with  subsequent K.  pneumom'ae  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
ppn)  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  gg/m  (3.5 ppm) had  a significant effect; exposure concentrations
of 2,820 and 4,700 ug/m  (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 Mg/m  (3 ppm) NO,, but not 1,880
    3
ug/rn   (1  ppm),  for  3  hours showed  enhanced mortality over nonexercised NOg exposed mice (p <
0.06)  using the infectivity model  (Illing et a!,, 1980).  The presence of other environmental
factors, ozone  (0,) (Ehrlich  et al.,  1977, Gardner et a!., 1981)  or  tobacco smoke (Henry et
a!.,  1971),  also  augments  the  deleterious effect  of NO, on host resistance to experimental
infection (see Section 14.3).
     Squirrel  monkeys exposed continuously  to NO-  levels  of  18,800 gg/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. pneumom'ae or influenza  A/PR/8 virus and reduced lung  clearance of viable
bacteria (Henry et al., 1970).   All six animals exposed to 18,800 Mg/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 NO, exposure occurred 24
                                                            3
hours  after infectious  challenge.   Exposure to  94,000  yg/m   (50 ppm)  NO, 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.  pneumom'ae. two of seven
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  HQy  alone
caused  less severe  alterations  than the combination  of N0_ plus virus.   Continuous NO, expo-
sure  for  an  additional  3 months did  not enhance further the effect of  NO,  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/m   (0.5 to 1 ppm)  NO,  for 39 days and  to  18,800 ug/m  (10 ppm)  NO,  for 2 hours
                                                                             3
daily for  1, 3,  and 5 days.  Acute and intermittent exposure to 18,800 pg/m  (10 ppm) NO, as
                                                  3
well as continuous  exposure to 940 to  1,880  ug/m  (0.5 to 1 ppm) NO. 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
                                                                     _
radioactive  phosphorus (   P)  and  were then  exposed to  NO-  for  4  hours  (Goldstein  et al.,
1973b).   Physical  removal  of the bacteria was  not affected by any of the NO, 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)  NO. 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 ^.  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 NO,  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 pg/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 NO. exposure on  the  function  of
alveolar macrophages are presented in Section 14,2.3.1.3.
14.2.3.1.2    Hucociliary transport.   Mucociliary   transport   is  the  principal mechanism  for
removal  of  inspired and aspirated particles from the tracheobronchial tree.  Concentrations of
NO.  greater than  9,400 ug/m  (5 ppm)  decrease  rates of ciliary beating as  measured in vitro
(Kita and  Omichi, 1974) and of mucociliary transport in vivo (Giordano and Morrow,  1972).  The
effect of  lower  concentrations of  NO,  on mucociliary function is unknown.   (See  Table 14-5)
                                                                         3
     Schiff (1977)  exposed  hamster  trachea!  ring cultures  to 3,760  ug/m  (2 ppm) NO, for 1.5
hours/day,  5 days/week,  for 1,  2,  and 3 weeks.    Trachea!  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 NO,  exposure showed
decreased   ciliary  activity and morphological  changes  compared  tu controls' held  in filtered
air.  After  14  days  exposure  to  NO. 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, trachea! organ cultures exposed
to NOg exhibited a more rapid production of virus  than explants held in filtered air.
14.2.3.1.3    Alveolar  macrophage.   Exposures  of  animals  to  NO,  concentrations ranging from
                      3
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
pg/m3
11,280
ppm Exposure Species
6 7 days/wk, Rat, female
6 wk
Effect
Increase in TPTT and FETa: decrease 1n muco-
ciliary velocity, p<0.02. Functional
impairment reversed within 1 wk.
Reference
Giordano and
Morrow, 1972
      TPT7 = Twenty percent transport time.
      FET  = First-edge time.
I
I"*
to

-------
abnormalfties in  alveolar  maerophages.   (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,  1975) 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 AH, (Hadley et al.,
1977) increased in  vitro penetration of AH by virus,  (Williams et al.,  1972) reduced jn vitro
production  of interferon,  (Valand et  al.,  1970) and  increased mitochondria!  and  decreased
cytoplasmic  NAQ+/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  NO-  on  the anatomic  integrity  of mouse alveolar macrophages which were lavaged
from the lung.  No  changes in the AH 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 pg/m  (0.1 ppm) NO, with
                             3                                                           £
3-hour  peaks at  1,880  ug/«i  (1 PPm)  for 5  days/week.   Macrophages from  mice continuously
exposed to 3,760  ug/m   (2 ppm) without  peaks  or 940  ug/m  (0.5 ppm) NO- with 1-hour peaks of
          3
3,760 pg/m  (2 ppm) NO, 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 eel Is.were seen.
Structural  changes were  still  observed  at the  same NO,  concentrations  after continuous expo-
                               's                                    3
sure to a  baseline  of 940 pg/m   (0.5 ppm) with peaks of 3,760 ug/m  (2 ppm) NO, for 28 or 33
weeks.  These  observations appear to correlate  well  with a reduction  in  jjn 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 pg/m  (5,  15, 25,  or
50 ppm)  NO,.  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
48 hours  following exposures  to 28,200  ug/m   (15 ppm)  NO,.   No  decrease  in resistance was
                         3                                 '
observed with  9,400 Mi/1"   (5 ppm) NO,.   Phagocytic  capabilities  were  adversely affected in
                                                           3
macrophages  from  animals exposed to 28,200 to  94,000 ug/n>  (15 to 50 ppm) NO,.  At & concen-
                       3
tration of  94,000 pg/m  (50 ppm), N0» 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
that jjj vitro exposure  of rat alveolar macrophages  to  4,512 pg/m   (2.4  ppm)  NO,  for 1 hour
resulted  in a  64 percent  increase  in agglutination  by concanavalin  A (Goldstein  et al.,
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) NO,  for  1  hour,  Incubation of macrophages

                                             14-20

-------
                                      TABLE 14-6.   ALVEOLAR MACROPHAGES

N02
Concentration
ng/w3 ppm
940 0.5
188 0. 1
[with 3
hr peaks
of 13880
(1 ppm)]
3,760 2
940 0. 5
[with 1
hr peaks
of 33760
(2 ppm)]
6,768 3.6
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

1 hr Rat
Effect Reference
Alveolar macrophage (AM) surface Aranyi et al.,
unchanged. 1976


Distinct morphological altera- Aranyi et al.,
tlons 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.

Incubation of macrophages with Goldstein et al.,
22,748   12.1   2  hr
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.
                                                                                           1977a

-------
                                           TABLE 14-6.   (continued)
     N02
Concentration
jjgTB3     ppi   Exposure
                             Species
                                                      Effect
                                                    Reference
 9,400      5   3 hr exposure
                after infection
28,200     15   with parainfluenza-3
                virus.  Challenge
                with rabbit pox virus.

47,000     25
94,000     50
                             Rabbit
                                                                            Acton and Myrvik,
                                                                            1972
13,200

15,000
  to
112,800


18,800

47,000
18,800
 8
to
60


10

25
10
24 hr

3 hr




24 hr
7 wk
continuous
Rabbit

Rabbit




Rat





Guinea pig
Control AM had increased
resistance (75%) to pox virus.
Partial loss of resistance,
following 28,200 ug/m  (15 ppm)
N02.

Decreased phagocytic capabilities
at all concentrations except
9,400 ug/m  (5 ppm).

Reduction in resistance,
decreased phagocytic
capabilities, stimulation
of Oy uptake plus hexose-
monophospate shunt activity.

Increased rosette formation in AM  Hadley et al.,
treated with wheat germ lipase.    1977
Increased number of poly-          Gardner et al.,
morpho-nuclear leukocytes in       1969
lavage fluid persisted for more
than 72 hr.
Phagocytic activity was unchanged. Katz and Laskin,
                                   1975
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 AH
on a single epithelial cell-2,5
times more frequent.
Sherwin et al.,
1968

-------
                                                  TABLE 14-6.   (continued)
-C.

IV
tj

N02
Concentration
jjg/ra3 ppm Exposure
19,000 10 3 hr

43,300 23 1 hr


47,000 25 3 hr








Species Effect
Rabbit 50% inhibition of phagocytlc
activity.
Rabbit Increased mitochondria! and
decreased cytoplasraic NAD /NAOH
were observed.
Rabbit 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.


Reference
Gardner et al. ,
1969
Mintz, 1972


Valand et al. ,
1970





47,000     25
3 hr
Rabbit
Viral uptake not affected
when infected with para-
influenza-3 virus after NO,
exposure.  No inhibition of
viral RNA synthesis.  Twice
as many virus attached and
penetrated exposed AH.
Williams et al.,
1972

-------
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) NO,  for  8 hr/day, 5
days/wk for  6 months and examined the  response of their  alveolar macrophages  to migration
inhibition factor  (HIF).  HIF is a substance produced by lymphocytes which inhibits migration
of Macrophages  and thus influences their protective functions.   Two of three of the antigen-
sensitized, N0,-exposed animals did  not respond to  MIF.   Macrophages  from 3 of the 4 NO--
exposed baboons had diminished responsiveness to HIF.
     Voisin et  al.  (1976;  1977}  exposed guinea pig  macrophages,  in  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-
duction in ATP  content  and  changes in morphology.  Following exposure to 188 ug/m  (0.1 ppm)
NO,, the alveolar  inacrophage  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
and 2 ppm) HOy*  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 in vitro exposure  to NO, for 15 to  20  minutes could
                                         vv    ;~~~ • •                  £
damage the AH.  Phagocytosis  and bactericidal capability were adversely affected by NO- con-
centrations at  15  mH  (690 ppm) (p <  0.05).   Both 5 and 10 mH  (230 and 460 ppm) NO, increased
14                      14          14                      14
  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 CO- 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 NO, alone did not
inhibit its activity.
14.2.3.1,4  Immune system.  The  effects  of exposures of animals to NO- 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;  Ehrlick 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 \ig/m
(0.5 ppm) NO, with daily 1-hour peaks of  3,760  jig/ffl  (2 ppm)  for 5 days/ week for 3 months.
After exposure,  all mice were vaccinated with influenza A,/Taiwan/1/64.  Mean serum neutraliz-
ing antibody titer was  four-fold lower with NO- exposure (p <  0.05) than with controls.  Con-
trol nice 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
increased serum IgG^^  (p < 0.05).  Mice  breathing 940  ug/m3 (0.5 ppm) N02 with peaks of 3,760

                                             14-24

-------
                      TABIE 14-?.   ItWUNOLOClCAl EFFECTS
Pollu-
tant
HO.
£.




NO,
£



NO.
£.


N02




H02



N02
NO,,


Pollutant Concentration
ug/«3 PP«
3,760

940 with
daily 1 hr
3,760

1,860




1,880



9,400




9,400

9,400
28,?00
10,000
37,600
75,200
131,700
2

0,5 with
dally 1 hr
2

I




1



5




S

5
15
5,3
20
40
70
Exposure Specks
24 hr/day, 5 dayi/wk, Mouse,
3 no followed by vied* Hale
nation with Influenza
A,/T«iwan/l/64 virus
t.

Continuous, 493 days; Monkey
challenge 5 tines with
monkey adapted Influenza
A/W/8/34 virus during
exposure
6 no followed by intra- Guinea pig
nasal challenge with
0. pneuflionlae

Continuous, to 169 days; Monkey
challenge with mouse
adapted influenza
A/PB/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 Bin, then aerosol Guinea pig
of egg albumin or bovine
serum albumin for 45 nln.
Effects
4-fold decrease in sen* neutralizing antibody
tlter. Hemagglutlnatlon Inhibition tilers
unchanged. Before viral challenge, decreased
seruo IgA and increased serum IgG,. Increased
IgM and IgG. (p < 0.05). Serum IgA unchanged,
IgH increased (p < 0,05) after virus.
Heiugglutinalion inhibition tlters unchanged.
Increased mean serum neutralizing antibody
titers after 493 days exposure, Titeri
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 Imunoelectrophoretlc fractions. In-
creased mortality following 0, pneuaoniae.
Heaagglutination Inhibition tlters or amnestic
response unchanged. Initial depression In serum
neutralization liters with return to normal by
133 days.

Lung tissue serum antibodies increased
with intensity and duration of exposure.


No effect on antibody production.
Anaphy lactic attacks in SOX exposed initials by
5th aerosol administration at highest concentra-
Reference
Ihrllch tt «!.,
1975




Fenlers el al. ,
1973



Kosnider el al . .
1973b


Fenlers et al. ,
1971



BalcnuB et al. ,
1965


AntvelHer, 197S
MalsMura, 1970s

tion. No effect at lower levels. Hemagglutinatlon
repeated 5-7 timet on
different days
tests unchanged.  Less antigen needed in active
cutaneous anaphylaxls test at highest levels
(p < 0.05).

-------
TABLE 14-7.   {continued)
Pollu- Pollutant Concentration
tant ug/nr1
NO, 56,400
1 75,200
64,600
94,000
HO, 75,000
* 150,000




PP«
30
40
45
50
40
80




Exposure Species
Exposure 30 ntn then Guinea pig
nebulized acetylcnollne.


Sensitized to egg and Guinea pig
bovine serum albumin by
Intraperttoneal Injection;
3 days later exposure for
30 nln to pollutants then
antigen 30 mln later.
Effects Reference
HortaTlty Increased at NO, Hatsunura et a).,
> 94,000 US/" <50 ppin). * 1972


Mortality; 2M Hatsnura, 1970b
37X





-------
ug/m  (2 ppm)  also  had increases in  IgH  and  IgG- (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 ug/m  (0.5 or 2 ppm) NO,.  Immunoglobulin
M (IgM) concentrations  were  elevated in all NO,-exposed  groups.   A significant increase (p <
                                                                                             3
0.05) took place  in  only the following groups:   (a) continuous exposure to 940 or 3,760 ug/m
(0.5 or 2 ppra), (b) continuous exposure to 940 or 3,760 pg/m  (0.5 or 2 ppm) or to 3,760 pg/m
(2 ppm),  pre-vaccination and  clean air afterwards,  and  (c) 3 months  filtered  air  and 3,760
ug/m  (2 ppm)  NO, post-vaccination.  Similar results were observed for  IgG,  and  IgG,  deter-
minations.
     The  immune  system  of monkeys  exposed  to  NO,  was  studied  in  an additional  series  of
experiments (Ehrlich and  Fenters,  1973;  Fenters 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 exposure  to 9,400  ug/tn   (5 ppm)  NOp.   Hemagglutination  inhibition  titers  to in-
fluenza titers were not changed.  Initially serum neutralization titers were depressed by NQ2-
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)
NO™ for 493  days  on  monkeys challenged five times via intratracheal injection to live monkey-
adapted  influenza  virus  A/PR/8/34  during  NO-  exposure.   Again,  hemagglutination  inhibition
titers were not significantly affected by NQ2 exposures.  However, the mean serum neutralizing
antibody titers were significantly  higher in animals exposed to NCL for 493 days.   Twenty-one
days post-vaccination,  animal titers were increased 7-fold over controls.  Forty-one days post-
challenge,  NOp-treated  animals  exhibited  an 11-fold  enhancement.   Even  after 266  days of NO,
exposure,  titers were  higher  when compared to controls.  Again, the authors hypothesized that
N0~  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) NOj.
     On the  basis  of  experiments  in which  the  continuous  exposure  of  guinea  pigs to 1,880
ug/m  (1 ppm)  NO,  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
function (Kosmider et al., 1973b).  These investigators also claimed that NO, causes decreases
in complement  concentrations when  measured by a  hemolysis assay; reductions  in  all  immuno-
globulin  fractions  when  tested  by  immunoelectrophoresis;  and   increased  mortality in  mice
exposed to 1,880 ug/m   (1 ppm) of NO- when infected  intranasally with 0. 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) NO, for 4 hours/day, 5
                            •5                              \
days/week and  to  9,400 ug/m  (5 ppm) NO, or to 28,200 ug/m  (15 ppm) N02 for 7-1/2 hours/day,
5 days/week.   There  was a noticeable  increase  in  the titer of  serum  antibodies against lung
                                               «3                       a
tissue in all guinea pigs exposed to 9,400 pg/m  (5 ppm) or 28,200 ug/m  (15 ppm) N0~ as early
as  160  hours  after N02  inhalation.   The  antibody titers  increased  with the  intensity and
duration 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 NO.  exposure.   Two theories of  action  of N02 on
biological systems have evolved as a result of these studies.  The dominant theory is that NO.
initiates lipid peroxidation,  which subsequently causes cell injury or death and the symptoms
associated with N02  inhalation.   The second theory  is  that NO- 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  NO. or to
responses to NO.  intoxication have been proposed.   The effects of NO. 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 NO. 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 NO. exposure.  Roehm et al. (1971) studied the jn vitro
oxidation of  unsaturated  fatty  acids  by 0. and  NO..   A common mechanism  of action was sug-
gested for these  two  oxidizing air pollutants.  Both  NO. and 0,  initiated  the oxidation of
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) N02-   The addition of free radical  scavenging agents such as vitamin E, butylated hydroxy-
toluene (BHT), or butylated  hydroxyanisol  (BHA) delayed the onset of oxidation uj vitro.  The
rate  of oxidation of linolenic acid in thin  films  was proportional  to  concentrations of NO.
                               3
ranging from 940 to 10,200 jjg/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   +  NO.  -» -C-C-NO,  -»2  -C -C-NO.
                  '   *       £•     i i    (•       i   i   f-

                    00-                  OOH
                   -C -C-NO.  +  RH -»   -C -C-NO.  +  R-
                    \  \   f.             i   i    e.
                   R-  +  02  •»  ROO-  ->  ROOM
Nitrohydroperoxides  and  fatty  acid  hydroperoxides  are  produced  from  the  oxidation  of
unsaturated fatty acids by NO..  Phenolic antioxidants prevent the autoxidation of unsaturated
                                             14-28

-------
                             TABLE 14-8.
                                 EFFECTS OF N02 ON  LUNG BIOCHEMISTRY

N02
Concentration
|jg/ra3 ppm Exposure
94 0.05 8 hr/day,
940 0.5 122 days

94 0.05 or
or 940+ 0.5+
equal equal
amount amount
ammonia ammonia
376 0.2 3 hr
3.760 2
35,720 19




Species Effect Reference
Guinea No effect on total weight of phospholipid. Trzedak et al.,
Pig Significant alterations (p <0.05) in 1977
individual phospholipid classes.





Rat At 376 ug/m3 (0.2 ppm) inhibition of Menzel,
conversion of prostaglandin E, (PGE,) 1980
to its metabolite (15-keto PGE.) IB*
hr post exposure. No effect on uptake
or efflux of PGE,.
  750
 ,880
 ,640
 ,400
0.4
1.0
3.0 or
5.0
9,400    5.0
72 hr
        3 hr
            At 3,760 and 35,720 ug/nr (2 and 19 ppm),
            no effect on uptake of PGE-.   Efflux
            altered 18 hr post-exposure.   Conversion
            of PGE» to 15-keto PGE- inhibited 18 and
            60 hr post-exposure.

Guinea Pig  No effect at 750 |jg/m .  Increase in lung
            lavage protein and lipid content in
            vitamin C depleted but not normal
            at 1,880 ug/nt •   (See Edema Section
            4.2.3.6)

Guinea Pig  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)
              N02
         Concentration
                  ppni
 Exposure     Species
                                                                Effect
 Reference
CO
o
          750    0.4     72 hr or
                           1 wk
          750    0.4     Continuous,
                           1 wk
   750    0.4      4 hr/day,
                    7 days

750 to    0.4 to Continuous
940       0.5      1.5 yr

1,790 to  0.95 to
1,880     1
   940    0.5
8 hr/day,
 7 days
8 hr/day,
  4 mo
              Guinea Pig  No mortality or effect on lung lavage
                          fluid composition.   (See Edema Section
                          4.2.3.6)

              Guinea      Increase in lung protein content of guinea
                pig       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.

              Guinea      Increase in acid phosphatase  (EC 3.1.3.2).
                pig

              House       Growth reduced; vitamin E (30 or 300 wg/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.
                                                                                          Selgrade et al.,
                                                                                          1981
                                                                                          Sherwin and
                                                                                          Carlson,
                                                                                          1973
Sherwin et al.,
1974

Csallany,
1975
 Menzel et al.,
 1977

-------
                                               TABLE  14-8.  (continued)
      N02
 Concentration
 pg/m3ppm
                   Exposure
                Species
                               Effect
                                              Reference
  940    0.5    Continuous,
1,880    1         17 no
                                Mouse
         0.5
         0.5
         1
  940
1,880

  940
1,880
1,880
 1,880   1
 4,330   2.3
11,560   6,2
 3,760   2
Continuous,
   17 mo
 Continuous,
 17 mo
                 Continuous,
                    2 wk

                 Continuous,
                   4 days
 House
Mouse
                Rabbit
                Rat
                 Continuous      Guinea
                   1  to  3  wk      pig
Decreased body weight with vitamin E         Csallany and
deficient, vitamin E supplemented (30 and    Ayaz, 1978
300 ppm) and DPPO 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   Ayaz and
activity.                                    Csallany, 1978

Suppression of GSH-peroxidase activity.

No increase in lipofuscin or glutathione     Ayaz and
peroxidase.   Vitamin E (30 or 300 ing/kg)     Csallany,
prevented lipofuscin accumulation            1977
(EC 1.11.19).

Decrease in lecithin synthesis after 1 wk;   Seto et al.,
Less marked depression after 2 wk.            1975

Activities of GSH reductase (EC L6.4.2)     Chow et al.,
and glucose-6-phosphate dehydrogenase        1974
(EC 1.1.1.49) increased at 11,560
pg/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 pg/nT (1 or 2.3 ppm).

Increase in number of lactic acid dehydroge- Sherwin et al.,
nase (EC 1.1.2.3) positive cells with time   1972
exposure.  Suggest Type I (LOH negative)
cells decrease as Type II (LDH positive)
cells increase.

-------
                                                        TABLE 14-8.   (continued)
              N02
         Concentration
         ug/m3
ppm
Exposure     Species
                                                     Effect
 Reference
I
CO
ro
         5,450    2.9    Continuous,
                         5 days/wk,
                            9 mo
                      Rat
         5,640    3      Continuous,    Rat
                           17 days

        18,800   10       Continuous
                             4 wk
5,640
5,600
13,200
3
3
7
4 hr/day,
4 days
7 days
4 days
Squirrel
monkey
Rat

        18,800   10
        28,200   15
         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,l-crtocopheryl  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, DNA
                         content, G-6-PO, 6-P-gluconate dehydro-
                         genase,  glutathione reductase, disulfide
                         reductase, glutathione peroxidase,
                         succinate oxidase, cytochrome oxidase;
                         no effect on lung protein.
Arner and
Rhoades, 1973
                                                                               Henzel  et al.,
                                                                               1972
                                                                                                 Bils,  1976
                                                                                                 Mustafa et al.,
                                                                                                 1979a,  b

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                                                      TABLE 14-8.  (continued),
i
CJ

NOZ
Concentration
pg/m3
9,400
9,400
9,400
9,400
37,600
94,000
11,000
15,000
18,800
PPM
5
5
5
5
20
50
6
8
10
Exposure
14 to 72 hr
12 hr
0,33, 1, 2
and 4 days
3 hr
4 hr/day,
30 days
Continuous
14 days
1 hr
once a week
4 to 8 wk
Species
Mouse
Rat
Rat
Rabbit
Mouse
Mouse
Hamster
(Vitamin
A defi-
cient)
Effect
Increase in lung protein (14 to 58 hr) by
radio- label.
Incorporation of l*C-proline into
insoluble collagen increased (58%).
Increase in glucose utilization and lactate
production. Lesser increase in pyruvate
production.
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.
Lipid droplets in alveolar walls. Alveolar
necrosis and thickening of epithelial base-
ment membrane with calcium deposits on inner
and outer surfaces. Presence of virus par-
Reference
Csallany, 1975
Hackner et al. ,
1976
Ospital et al. ,
1976
Palmer et al. ,
1972
Csallany,
1975
Csallany,
1975
Kim, 1977; 1978
                                                  tides 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
                                                  mitochondria! damage.

-------
                                                TABLE  14-8.   (continued)
      N02
 Concentration
 ug/«3
ppn
        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,        Csallany,  1975
                                            glucose-6-phosphate  dehydrogenase,  and  GSH
                                            peroxidase.

                                            Increase  in lung proteolytic activity and     Kleinerman and
                                            in serum  antiprotease  at 2 days.              Rynbrandt,
                                            Declined  to normal values at 50 days.         1976

                                            Increase  in lung proteolytic activity at      Rynbrandt  and
                                            2 and 5 djys,  but the  optimum pH was acidic   Kleinerman,
                                            (3.0).  Not active at  physiological pH  of     1977
                                            7.2.   Attributed to  cathepsins, A,  B.,  By,
                                            C,  D,  and E.                        1   *
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

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                                                TABLE 14-8.  (continued)
       N02
  Concentration
  jlgTiPppm      Exposure      Species                         Effect                      Reference


 75,200     40        2  hr       Rat         Benzo(a)pyrene hydroxylase  (EC  1.14,12.3),    Law et al.,
132,000     70                              phenol-0-methy1 transferase (EC 2.1.1.25)     1975
                                            and catechol-0-methyl  transferase
                                            (EC 2.1.1.6) not affected.

-------
fatty  acids  by  NO-  by  reacting  with  both  fatty  acid  hydroperoxyl   free  radicals  and
nitrohydroperoxyl  free radicals  generated  by  addition  of NO,  to unsaturated  fatty acids:

                   00-                   OOH
                  -C -C-NO,  +  AOH  •»  -C -C-NO,  +  AO-
                   i    i   £              i    i   £

                  ROO-  +  AOH  *  ROOH  +  AO-
where AOH represents a phenolic antioxidant.
     Rats evidenced  increased  mortality (Fletcher and Tappel,  1973; Menzel et a!., 1972) and
decreased content of unsaturated fatty acids in lung lavage fluid (Menzel et al,,1972; Thomas
et al,, 1968) when exposed to NO, concentrations ranging from 18,800 to 62,000 \ig/n  (10 to 33
ppm).  The effect was greater in animals fed diets depleted in vitamin £.
     The effect  of NO- exposure on the metabolism of vasoactive compounds by the rat  lung was
                                                                      33
studied by Menzel  (1980).   Rats were exposed for  3 hours to 376 (jg/m  (0.2 ppm), 3,760 yg/m
(2 ppm), and 35,720 fjg/m  (19 ppm) NO, and their lungs were excised and perfused with  H-Prosta-
            3
glandin E, ( H-PGE,),  a natural product of the lung that acts on smooth muscles, up to 6 days
                                                                              3
at various tines,  NO, exposure did not affect  the unidirectional  uptake of  H-PGE,, at 0 or
                                     3
18 hr post-exposure,  while efflux of  H-PGE, and its metabolites from the lung were altered 18
                                             3
hours post exposure  to 3,760 and 35,720 \tq/m   (2  and 19 ppm)  NO,,  Eighteen hours following
376, 3,760, and  35,720 ug/m3 (0,2, 2, and 19 ppm) N02> the conversion of the perfused P6E2 to
its  15-keto  metabolite was  inhibited by 37, 41, and 62  percent, respectively.   Recovery was
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 pg/m   (19 ppm)
NO,  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  (jg/m  (2.9 ppm) NO,  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.
     Trzeciak et al.  (1977)  exposed guinea  pigs to  940  |jg/m  (0.5 ppm), 94 ug/m  (0.05 ppm),
or these  same NO^ concentrations plus an equaFamount 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)
wer«  found in  the  individual  phospholipid classes.   Decreases were noted  in  phosphatidyl"
ethanolamine,  sphingomyelin,  phosphatidyl  serine,  phosphatidyl  glycerol-3-phosphate,  and

                                             14-36

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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.
     Lecithin synthesis appeared  to be depressed in the lungs of rabbits exposed to 1,880 pm
(1 ppm) NO- 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.
     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 ing/kg of  diet.   The author
indicated that  NO.  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,  1978)  female  weanling  mice were exposed to  940  or 1,880
pg/m  (0.5 or  1 ppm)  NO,  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 N02 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) NO.,  5  hours once a
week for 4 to  8 weeks caused lung  damage as compared to N02~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
NO, toxicity (Belgrade  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)  NO./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
the exception of  those guinea pigs  exposed to 752 ug (0.4 ppm) NO./m .  Exposure of normal or
                                                    3
vitamin C  depleted guinea pigs exposed  to  752 MS/™   (0.4  ppm)  for as long as 1 week had no
effect on  the  composition of the lavage fluid.   At 9400 ug (5 ppm) NO./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) NQ./m  for 3 hrs, increased
protein and  lipid  contents were not observed until 15 hrs after exposure.  These results con-
flict  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 NO, 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 a!., 1974)
but little evidence has been reported for NQ-.
                                                                          3
     In experiments involving exposure of mice to very high (>143,000 ug/m ; 76 ppm) concentra-
tions of NO*, several investigators reported that a wide variety of sulfur-containing compounds
reduced the toxicity of NO- (Fairchild et a!., 1959; Fairchild and Graham, Ii63).   For example
when mice were  first exposed to benzenethiol (14 ppm) for 24 to 72 hours prior to 4 hours of
NO, exposure  only  1/20 died, whereas 10/20  of  the  NO^-exposed mice not  pratreated  with ben-
zenethiol died.  Inferences  drawn from the protective effect  of these compounds suggest 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.
     Ospital   et  al.  (1976)  reported that exposure  to 9,400  ug/m  (5 ppm)  N02 for 8 hours
altered  the   glucose  metabolism  of slices  made from the  lungs of  exposed  rats.   Glucose
utilization and  lactate production  were  increased  by 28 and 43  percent,  respectively, while
pyruvate production  rose by 6 percent.  Exposure of rats to 9,400 ^g/m  (5 ppm) NO. 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 NO- 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 ami no acids, proteins, and enzymes.   Concentrations  of NO,  >9,400
    2                                   —                  	                        (.
ug/ra  (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  ug/m  (2 ppm)  NO, 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 NO- 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)
NO, 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  NQ.-exposed guinea pigs,  but was  statistically significant only  in liver samples.
Values for the lung and exposure levels were not reported.
     The effect of N0« 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/m  (5, 20,  or 50 ppn) NO, for
3 hours.  No effect was observed on the benzpyrene hydroxylase activities in NO, exposure, but
                                   3
0, exposure of 1,400 to 19,600 ug/m  (0.75 to 10 ppm) markedly decreased benzpyrene hydroxylase
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-methylcholanthrene,
exposure to 75,200  or  132,000  M9/«i3 (40  or  70 ppm) NO, for 2 hours had no effect.   Thus, the
studies  of Palmer et al. and Law et al.  agree that NO- 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 cateeholantine hormones.   This metabolism does
not appear to be affected by NO- treatment.
                                                                       3
     Menzel et  al,  (1977)  exposed  guinea pigs  8  hr/day to  940 pg/m   (0.5  ppm)  NOj  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  pg/m  (3 ppm) N0«  for 4 hours/day
for 4 days.   Kosmider  et al. (1973a) reported that the urinary hydroxyproline and acid rouco-
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) NO- for 12 hours.  Incorporation


                                             14-39

-------
of   C-proline  into insoluble collagen was 58 percent greater in the NOg-exposed animals than
in air-exposed control groups, supporting the biochemical evidence for greater collagen turnover
in NQ,-exposed animals.
     Enzymes observed  to  have increased activity following exposure to high concentrations of
NO,  included aldolase  (in vitro) (Ramazzotto and Rappaport,  1971}  and serum antiprotease (j_n
vivo) (Kleinerman and Rynbrandt, 1976).  Plasma lysozytne activity was reported to be unaffected
(la ylyg) (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 NO,  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 peroxi-
dation damage by ozone.  They proposed the following scheme:

         p-oxidation
               t
               ROH   .          GSH               NADP       >   Glucose-6-P04
                      11  GSH Peroxidase 1  I  GSH Reductase | [ G-6-P Dehydrogenase
              °3      A               J\              A
         RH   +4 ROOM          GSSG    r        NADPH          6-Phosphogluconate
                          where R is an aliphatic organic radical
Chow et  al.  (1974)  exposed rats to  1,880, 4,330,  or 11,550 ng/nt3 (1, 2.3,  or  6.2 ppm) NO,
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 cor-
relation between the  HO, 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 pg/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) N02 and fed the animals a basal diet which was either deficient in vita-
min E  or supplemented with 30 or  300 rag/kg  of diet.  Blood,  lung, and  liver  tissues were
                                                                     2
assayed  for  glutathione  peroxidase  activity.   Exposure to  940 ug/m   (0.5 ppm)  NO,  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 (jg/rn  (1 ppm) N02 exposure
resulted in the  lowest  GSH peroxidase in blood and lung.   Liver GSH-peroxidase was unaffected
by either vitamin deficiency or NO, exposure.

                                             14-40

-------
     Donovan et  al.  (1976)  and Menzel et  al.  (1977) exposed guinea pigs  continuously  to 940
ug/m3 (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 HO. 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 NO, and 0, 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 0, 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  NOn-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
high  levels  of  N02  exposure,  9400  ug  (5.0 ppm)  N0,/m   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 yg/nt   (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
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 N02.   Since  vitamin C is readily oxidized and reduced, it could serve to detoxify oxidative
products formed by N0_ or to maintain the intracellular redox potential.
14.2.3.3  Horphology 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.,  19S6; 1968c; 1972; Stephens et al., 1971; 1972)  The earliest altera-
tions resulting  from exposures to concentrations above 22,600 ug/m  (12 ppm) were seen within
24 hours of continuous exposure.  These alterations  Included increased macrophage 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 parenchyma  into a
"gland-like" tissue  in  the  region of the  ducts.    Incorporation  of   H-thym1dine  by  Type II

                                             14-41

-------
                                        TABLE 14-9.   EFFECT OF
                                                                           ON LUNG MORPHOLOGY
£»
I

I-O

N02
Concentration
ug/m3
188 +
daily 2-hr
spike of
1,880
470



553



940



ppm
0.1 +
dai ly
spike
of 1
0.25



0.34



0.5



Exposure
Continuous,
6 mo


4 hr/day,
5 days/wk,
24 or 36
days
6 hrs/day,
5 days/wk
6 wk

Continuous,
12 mo


Species
Various
species


Rabbit



Mice



Mouse



Effect
Eraphyseraatous 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
Reference
Port et al. ,
1977


Buell, 1970



Sherwin et al. ,
Kuraitis et al.


Hattori, 1973

Hattori and
Takemura, 1974









1979
, 1979






          940
  940
1,880

  940
   to
1,500
            0.5
 0.5
 1

 0.5
 to
0.8
 6. 18, or
 24 hr/day,
 to 12 mo
   4 hr
   1 hr
Continuous,
   1 mo
                     Mouse
                                        Rat
                                        Mouse
  and epithelium
At 35 to 40 days:
  Bronchial hyperplasia
At 6 mo:
  Fibres is
At 12 mo:
  Bronchial hyperplasia

Alveolar damage.  Interstitial pneumonia
may have confused interpretation.
Degranulation of mast cells.
seemed reversible.
                              Response


Damage to tracheal mucosa and cilia.
        1,030 to   0.55   Continuous,   Mouse
        3,000     to 1.6     5 wk
                                            Damaged cilia, increase in mucus secretion
                                            by nonciliated cells.
                                                  Blair et al.,
                                                  1969
Thomas et al., 1967

Hattori et al.,
1972
Nakajima et al.,
1969
Miyoshi, 1973

-------
                                        TABLE  14-9.   (continued)

N02
Concentration
ug/m3
1.500
ppm
0.8
Exposure
Continuous,
Species
Rat
Effect
Normal growth. Decreased respiratory rate
Reference
Freeman et al.

, 1966
 1,880
 1,880 to
 2,820
 3.760
32,000



 3,760

 3,760

 3,800



 3,760



32,000
17
                    to 33 mo
 1     Continuous,
        493 days


 1 to  Continuous,
 1.5      1 mo
 2     Continuous,
        43 days
17
Continuous,
   3 wk
Continuous,
   3 wk
Continuous,
   14 mo


Continuous,
to 360 days


Continuous,
  7 days
              Monkey



              Mouse

              Rat
                     Guinea
                      pig
                     Guinea
                       pig
                     Monkey
                     (Macaca
                     speciosa)
                     Rat
                                 (~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.

Sane 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 days.

Earlier and greater injury of same type
and sequence as at lower level with loss
of Type I cells.
Renters et al., 1973
Chen et al.,
1972
Stephens et al.,
1972
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.

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.
Sherwin et al.,
1972
Sherwin et al.,
1973
Furiosi et al.,
1973


Evans et al.,
1972; 1978a

-------
                                               TABLE 14-9.  (continued)
*»
i
-C.
*»
N02
Concentration
iiqTi3 ppm Exposure Species
32,000
5,640

9,400
18,800
18,800
28,200
18,800
18,800 to
47,000
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
10 Continuous, Guinea
6 wk pig
10 to 6 mo Dog
25
Effect
Type II cell proliferation.
Thickening of alveolar wall and basal lamina.
Interstitial collagen.

Infiltration of macrophages, lymphocytes, and
occasionally polymorphonuclear leukocytes.
Hyperplasia of bronchiolar epithelium and Type
II cells.
Decrease in length and weight of neonates
exposed, delivered and reared 1n NO™.
Delayed lung development in progeny exposed
in utero and raised in NO,,. 75 days required
to make up deficit.
Type II cell hypertrophy, 1 to 6 wk exposure
with Increased lamellar bodies within Type II
cells.
Emphysema and death.
Reference

Bils, 1976

Busey et al . ,
1974
Freeman et al . ,
1974b

Yuen and Sherwin,
1971
Riddick et al. ,
1968
        19,100 to  10.2 to   12 mo
        21,500      11.4
Cat         Intraluninal mucus.  Increase in goblet cells.
            Thickening gf epithelium.  Fly ash (9,950 to
            10,200 ug/m ) had no effect.
Kleinerman et al.,
1976

-------
                                                 TABLE 14-9.   (continued)
N02
Concentration
vg/m*
ppm Exposure
Species Effect
Reference
        28,000
14
48 hrs
        28,000 to   15 to
        32,000       17 '
        28,200       15
        28,200
4»
I

cn
        28,000



       ^28,000


        28,200
       24 hr

       48 hr

15    4 days/wk,
     5 wk, total
      31.5 hr

      5 days/wk,
      18 wk,
     total 93.5
       hr
15   Continuous,
     1,4,10,16
      and 20 wk


15    Subacute


15      24 hr
Rat         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.

Rat         Division  of Clara cells replaced damaged
            ciliated  cells.
Rat         Increased cell division, especially Type II
            cells.
Rat         No effect on  blood metheinoglolxin.
Stephens et al.,
1978
                                                                          Evans et al.,
                                                                          1976
                                                                          Evans et al.,
                                                                          1974
                                                                          Csailany and Ayaz,
                                                                          1978
                        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 NO- exposure or
                        dietary Vitamin E.   Lung lipid extract distri-
                        bution not affected by NO, exposure.
            Rat         Hyperplasia of terminal bronchiolar and
                        alveolar epithelium reversible on discontinu-
                        ation of exposure;  alterations of interstitial
                        structural features of alveoli not reversible.
            Rat         Newborn rats up to age 3 wk relatively resis-
                        tent to exposure compared to mature rats.

            Hamster     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.
                                                              Freeman et al.,
                                                              1969
                                                              Lunan et al., 1977

                                                              Hackett, 1978

-------
TABLE 14-9.  (continued)

N02
Concentration
|jg/m3
28,200
to
32,000
28,200
to
32,000

28,000
to
31,960
32,000

^ 69,000
4U
1
£ 150,000












ppm
15
to
17
15
to
17

15
to
17
17

37.2

80












Exposure Species
48 hr Rat


Continuous, Rat
lifetime


12 and 24 hr Rat


Continuous, Rat
90 days
4 hr Dog

3 hr Cat












Effect
Alveolar macrophage division seen with DNA
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-NO., 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












-------
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   H-thymidine,
indicative of cell replication,  was documented at 3,760 vg/m  (2 ppm) NO, as well  as at 32,000
    3 •
MS/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 nonciliated (Clara) cells and
the exfoliation of ciliated  cells  (Evans et al., 1978b).   Later,  aberrations  in  ciliogenesls
occur and cilia often appear within vacuoles surrounded by cytoplasm.
     Fenters  et al.  (1373) exposed monkeys to 1880 ug/m  (I ppm) NO, continuously  for 493 days.
Four monkeys  wtre challenged with influenza A/PR/8/34  virus one  day before and  41,  83,  146,
and 266  days  after  initiation  of NO, exposure.  Monkeys exposed to NO,  and  virus developed
moderate  emphysema   with  thickened  bronchial  and  bronchiolar  epithelium.   No  effect  was
observed in monkeys  exposed to NO- alone or controls.
     Age  is a  factor in determining the response of the lungs to NO-.   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 NO, (Evans et al. , 1977).
     Sherwin  and  co-workers  (Kuraitis  et al., 1979; Sherwin et al., 1979) exposed mice to 553
pg/m   (0.34  ppm)  NO- 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 NO,.
     Buell (1970) reported  the  isolation of swollen, damaged,  insoluble collagen fibers from
the lungs of  rabbits exposed to 470 ug/rn  (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
discontinuation of exposure  to  28,000 pg/m  (15 ppm) NO-, 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/m3 (0.8 ppm) NO- (Freeman et al., 1968c).
                                                                                      3
     Embryonic and adult hamster trachea! cells were exposed as cultures to 1,880  ug/m  (1 ppm)
N02 for 6 hours (Samuelson et al., 1978).   Cells so treated lost their ability to  grow and form
colonies.  Hamster  lung fibroblasts  (V-79), when exposed in vitro to 216 ug/m3 (0.12 ppm) N02
for periods up to 6 hours, also failed to divide and form colonies.
     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

                                             14-47

-------
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 nonocytes.   (Hattori, 1973; Hattori and Takemura, 1974; Hattori et
a!., 1972;  Nakajima et  al.,  1969)  Mice exposed  continuously for 5 weeks  to 1,030 to 3,000
u§/ra  (0.55 to 1.6  ppm) N0« exhibited  damaged  cilia  and an increase  in mucus secretion by
nonciHated cells.
     Furiosi et  al.  (1973)  investigated the influence  of a  14-month  continuous  exposure to
          3                           3
3,800 ug/m   (2 ppm) N02 and 330  ug/m  (0.1 ppn) Nad  (0.1  to 10.3 M»).  alone  and in com-
bination,  on  monkeys   (Macaca  speciosa).   Rats  were  exposed  simultaneously  but  received
approximately  1,880  ug/m   (1 ppm) N02  due  to  differences  in the exposure cages.   The NaCl
exposure alone caused no effects.   In monkeys, the NO- 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 NO,, 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
                           3
exposed to about 1,500 ug/m  (0.8 ppm) NO- 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).
                                                         3
In mice  sacrificed after exposure to 1,880 to 2,820 Mg/m  (1 to 1,5 ppm) NO. 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 NO, 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
ug/m   (3 ppm) NO, 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
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.

                                             14-48

-------
     Port et  al.  (1977)  investigated  the effects  of  NO- on several species using  light and
                                                    3
scanning electron  microscopy.   Exposure to 188  \ig/m   (0.1 ppn) was continuous  for  6 months.
Upon this regimen were  superimposed daily 2-hour peaks  of 1,880 pg/m  (1 ppm)  N0_.   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  pg/m  (0.5 ppm) for  4  hours or 1,880 pg/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 NO- inhalation to signify  the potential  onset of  an  acute inflammatory
reaction.
14.2.3.4  Pulmonary  Function—Exposures  of  animals to 9,400 pg/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
were exposed to  1,500 pg/m   (0.8 ppm)  NO- for periods up to 2.75 years (Freeman et al., 1966;
Haydon et al., 1956).
     Rats exposed  to 5,400 (jg/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
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 pg/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 NQ« between 9,780
                3                                   3
and 24,440 M9/
-------
TABLE 14-10.   PULMONARY FUNCTIONS
NO,
Concentration
Pollutant ugTm3 jiprn
N02 940 to 0.5
38,000 20
N02 1,500 0.8
_
ij N02 1,880 1
N0? 3,800 2
N02 3.800 2
16.900 9
N02 5.400 2.9
N02 9.400 5
N02 9.400 5
Exposure
to Continuous
Continuous,
to 2.75 yr

16.5 no. NO.
alone or with
subsequent In-
fluenza virus
A/PR/B/34
challenge.
- 2 yr
10 yr
Syr
Continuous,
5 days/wk,
9 mo
6 hr/day,
18 mo
7.5 hr/day,
5 days/wk,
5.5 mo
Species
Rat, cat
Rat

Squirrel
monkey
Rat
Monkey
(Hacaca
speclosa).
Pregnant and
offspring
Rat
Rabbit
Guinea pig
. Effect
Increased respiratory rates.
Decreased arterial oxygen pressure.
Impaired 0. 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 (13X, 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)
 I
U>
Concentration
Pollutant
NO,
£




NO,
f.








NO


NO
SO*
NO* +
so2
NO

pg/m3
9,400
18,800




9,400




18,800




9,780


10,000
10,000
10,000 »
10,000
15,000 to
22,600
PP»
5
10




s




10




5.2


5.3
3.8
5.3 »
3.8
8 to
12
Exposure Species
Continuous, Cynomologus
90 days monkey




Continuous, Squirrel
2 mo, monkey
K. pneu-
moniae
challenge
Continuous,
1 mo.
K. pneu-
loniae
chal lenge
4 hr Guinea pig


6 days/vk, Guinea pig
6 mo


continuous, Rabbit
12 wk
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 volunie.
Increased respiratory rate. Minor
changes In minute respiratory volume.
After challenge, Minute volumes decreased
and remained depressed.
Elevation in nlnute respiratory volunie
due to Increased tidal volume and respira-
tory rate by 2 wk and throughout exposure.
3 days after challenge, narked reduction
1n 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

AntMCiler and
Brockhauser, 1976


Davidson et al. ,
1967
                                                                          •Static lung compliance unchanged.

-------
                                                                  TMIE 14-10.  (continued)
*•
i
Pollutant
NO,
£.















NO
£.


fly ash

elutriated
dust of
fly ash
N02

HO,
Concentration
ug/«J ppn
18,800 10
28,200 15

65,800 35 •

94,000 50


94,000 50



94,000 50




19,200 to 10.2 to
21,400 11.4


10,000 to
10,200
2,100 to
1,600

28,200 15

Exposure
2 hr, K.
pneimonlae
challenge





2 hr, chal
with j. Egeu-
noniae after
24~hr
2 hr




Continuous,
12 mo







Continuous,
lifeline
Species Effect Reference
Squirrel Decreased tidal volume. Increased resplra- Henry et «!,, 1969
•onkey, itale lory rate 2 to 4 hr post exposure.
and female No enhancement by K. pneumoniae.
Ho iiartal fty. Less drastic effects
on respiratory function.
Tidal and nlnute volume decreased by 4 hr.
Mortal Ity: 2/3 wfthin 5 to 72 hr.
Increased respiratory rate.
Tidal volume decreased.
Respiratory rale Increased.
Death within 72 hr.

Respiratory rate Increased 2-fold.
Decreased tidal volumes.
Minute volumes constant.
Respiratory rates high for 72 hr,
return to normal by 7 days.
Cit Increased total airway resistance and Klelnenun et at.,
upstream resistance. 1976
Decrease In static lung corp! lance.
Internal surface area unchanged.
No effect due to fly ash.




Hal Increased tidal volumes SO to 3SOX. Freeman et al..
Minor Increased resistance and de- 1972
                                                                           creased compliance 15 to 20 «k.

                                                                           Increased emphysema.

-------
TABU 14-10.   (continued)
Pollutant
N02
N02
NO,
Concentration
MgTS1 pp»
38,400 20.4
56.000 30
56,400 to 30 to
65,800 35
Exposure Species
20 to 22 Hamster
hr/day,
7 days/wit.
12 to 14 KO
IS «ln Rabbit
7 to 10 days, Hamster
followed by
papain
Effect
Increased total pulmonary resistance
during passive ventilation am) naxtml
airflow with concurrent decreased flow
values. Return to nornal within 3 no.
Static lung coopl lance unchanged.
Decreased surface area.
Redistribution of lung perfuslon resulting
In reduced storage activity in peripheral
zones of lung.
NO, * papain increased lung volumes.
NO, * papain Increased pulmonary
resistance (p < 0,05). Pulmonary
Reference
Kleineraan, 1977
von Niedfng et al. ,
1973
Nievoehner and
Kleineroan, 1973
         resistance unchanged by papain.

-------
     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
throughout exposure to 18,800  pg/m  (10 ppm) N02<   At the end of the exposure period, monkeys
were challenged  with  K.   pneumom'ae;  3 days  later minute volume was markedly reduced.   Only
ninor  changes  in minute  respiratory volumes were  noted in monkeys exposed to  9,400  \tg/m  (5
ppra) NO- 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.
     Fenters et  al.  (1973)  found that monkeys  exposed to  1,880  ug/m  (1 ppm)  NO,  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)  N02  for 90 days were stressed at a temperature of 31°C versus 24°C for controls.
At  the  higher concentration, NO,  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
lungs;  NO, alone did not.   No synergistic effect was seen at NOg concentrations of 9,400 pg/ai
(5 ppm) with heat.
     Freeman and  Juhos  (1976)  exposed pregnant monkeys to NO, continuously  and raised their
offspring  in   similar  environments.   Adult and juvenile  monkeys were  exposed  to  3,800 and
16,900 pg/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 Hyperplasia—Chronic NO^ 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 H0~.   (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 pg/m  (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 NO, did not enhance the tumor production (i.e., N0»  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  (1974)  exposed  rats to  9,400 pg/m  (5  ppm) NO.  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

-------
                                                           WBIE  14-11.  STUOIES OF POTEHT1AI HWEWIASIA
*•
I
Pollutant
Concentration
Pollutant
N02


CO
Synthetic
Smog
N02
coz
o.
s32
N02


N02

N9/»'
940 to
1,500
*
58,000


1,500
5,750
760
5,700
2,360


9,400

PP»
O.S to
0.8
*
50


0,8
5
0.38
2.2
1.26


5

Exposure
Continuous,
30 days


23 to 24
hr/ctay,
8 to 12 mo



12 hr/day.
3 mo

Continuous,
to 11 wk
Species Effect
Mouse Increased hyperplasfa terminal bronchioles
to alveolus. No.dl f f erence fro* NO. alone.
CO (IIS, 000 M9/" ; 100 ppn) alone fOr 30 days
failed to induce hyperplasia.
House By 20 days exposure, increased thickened
bronchial iwnbranes.
By 60 days, very thick aembranes appear to
have villus-Hke hyperplasttc folds.
4 months post-exposure, hyperplasia
regressed towards normal".
Rat, prior No effect on fertility.
to breeding Decrease in litter size and neonatal weight.
Ho teratogenic effects.
Rat Appearance of hyperplaitfc foci in the
shape of 2 to 4 layer pyramids by 3 wk.
Reference
NakajiM et *1.,
1972


LoosH et al..
1972




Sha1*nb«rldze
and
Tsereteli, 1971
Rejthar and
Rejthar, 1974
                                                                            Decreased ciliated cells.
                                                                            Extensive hyperplasia (3 to 4 layers of
                                                                            epitheliun), cuboidal metaplasia in ad-
                                                                            jacent alveoli by S wk.
                                                                            Hyperplasia in all bronchioles,
                                                                            decreased bronchiolar lumina, polymorphous
                                                                            epithelium extensive by 7 wk.  Terminal
                                                                            bronchiolar epitheliun 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.

-------
TABLE 14-11.   STUDIES OF POTENTIAL KYPERPLASIA
Pollutant
NO,


CO
Synthetic
Siaoa
NO,,
coz
°3
s32
NO,


N02

Pollutant
Concentration
MsT"3 ppa
940 to
1.500
+
58,000


1,500
5,750
760
5,700
2,360


9,400

0,5 to
0.8
*
SO


0.8
5
0.38
2.2
1.26


S

Exposure
Continuous,
30 days


23 to 24
hr/day.
8 to 12 BO



12 hr/day.
3 mo

Continuous,
to 11 wk
Species Effect
House Increased hyperplasta teminal bronchioles
to alveolus. No-difference fron NO. alone.
CO (115,000 pg/« ; 100 pp») alone for 30 days
failed to Induce hyperplasla.
House By 20 days exposure, Increased thickened
bronchial »e«branes.
By 60 days, very thick ntnbrims appear to
have vlllus-lfke hyperplastlc folds.
4 months post-exposure, hyperplasla
regressed towards normal.
Rat, prior No effect on fertility.
to breeding Decrease in litter size and neonatal wight.
No teratogenic effects.
Rat Appearance of hyperplastlc foci in the
shape of 2 to 4 layer pyramids by 3 wk.
Reference
MikaJlM tt •!.,
1972


Loosli et •!.,
1972




Shal amber Idze
and
Tseretell, 1971
Rejthar and
Rtjthar, 1974
                  Decreased ciliated cells.
                  Extensive hyperplasla (3 to 4 layers of
                  epithelium), cuboldal metaplasia in ad-
                  jacent alveoli by 5 wk.
                  Hyperplasla In all bronchioles,
                  decreased bronchtolar tuilna, polymorphous
                  cpI theIIu« extensive by 7 wk.  Terminal
                  bronchiotar 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.

-------
found in adjacent alveoli.   By 7 weeks, hyperplasia was apparent in all bronchioles, thus nar-
rowing the bronchiolar luraina.  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/m  (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 NO. with CO (58,000 MS/"1 » 50 ppm) for 30 days revealed the same
                                                                                             3
hyperplastic foci in the terminal bronchioles.  At exposure concentrations up to 115,000 \ig/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),  C02  (0.07  and  0.37  percent),  along with
aldehydes  (0.1  and 2  ppm).   No  effects  were observed  at  0.2 ppm NO .   At 23 ppm NO , more
                                                                      X                X
spontaneous tumors  and cutaneous  abscesses as well  as bilateral  renal  sclerosis were seen.
14.2.3.6   Edeaagenesis and Tolerance—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)  N02 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.
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  NOg-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 EOEHA BY NO.
Pollutant
Concentration
(jg?m3 pp'm Duration
750 0.4 Continuous,
1 wk
940 0.5 5 days/wk,
3 or 6 wk
7,500 to 4 to Continuous,
13,000 7 14 days
£ 56,400 30 Continuous,
i, to 30 days
ca
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
Kleinernan 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 NO. 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 NO. 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 NO,,  in young and  old  animals.  (See  Table  14-13)   Mice were
                                              3                                          3
made tolerant to  an  LC50 dose of 113,000  ug/m   (60 ppm) by prior  exposure  to 9,400 ug/m  (5
ppm)  NO-   for   7  weeks  (hours/day  not  specified).   Tolerance  disappeared  after  3  months
following removal  from the NO, exposure.  Rats also were made tolerant.
14.2.4.  Extrapu 1 monary Ef f ec t s
14.2.4.1     Nitrogen  Dioxide-inducedChanges 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).
     Shalamberidze (1969)  exposed rats continuously to  100 ug/m  (0.05 ppm)  NO.  for 90 days
with no change in blood hemoglobin or erythrocyte levels.
     A 7-day exposure to 940 ug/m   (0.5 ppm) NO.  resulted in 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 pg/m  (0.5
ppm) NO. with 1,000 pg/m3 (0.39 ppm) SO. or 940 ug/m3 (0.5 ppm) NO. with 1,000 [ig/rn3 (0.39 ppm)
       ^3                       *                          '
SQy and 70 ug/m  (0.1 ppm) ammonia.   Animals exposed to NO, and SO., with and without ammonia,
displayed an increase in white blood cells  (WBC)  and  a decrease in RBC and hemoglobin.  Fol-
lowing 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  pg/m  (0.36 ppm) NO. 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)  NO.  did not change  the  carboxyheraoglobin
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) NO. 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/m
(2 ppm) S02 2 hours/day for 15 and 17 weeks.  Exposure to NO. alone produced a significant rise

                                             14-59

-------
                                         TABLE  14-13.
                                               TOLERANCE TO H02 EXPOSURES
Concentration
           ppm
                                Duration
Species
                                                                Effects
                                                                           Reference
ft,
I
          9,400
 9,400 +      5 +
47,000       25
         47,000       25
         18,800       10
         47,000       25
                      7 wk
13 mo
+ 6 wk
                      7 wk
                      5 hr/day,
                      5 days/wk,
                      5 hr/day,
                      1 day/wk,
                      3 wk

                      6 hr/day,
                       2 days
                  Mouse
                                                 Rat
                  Mouse
                  Hamster
                  Rat
                                                  Challenge with LC50 dose (113,000 pg/m       Wagner et  al.,
                                                  (60  ppm)  N0? for 5  hr,  24 hr post-exposure)   1965
                                                  caused 28%  less mortality than in naive mice.

                                                  Challenge with NO,  (132,000 \tg/m  (70 ppm)
                                                  for  5 hr, 3 days post-exposure) caused 0%
                                                  mortality compared  to 67% in pre-exposed
                                                  controls.

                                                  Challenge with NO,  (132,000 jjg/m  (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.

                                                  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
                                                  (jg/m  (10 ppm) as measured by increased DNA
                                                  synthesis.

                                                  Tolerance to normally lethal 131,600 ug/m
                                                  (70  ppm)  NOj.   Protection against further
                                                  cytological injury.
            Increased tolerance to 141,050 ug/m  (75
            ppm) HOy.  Increased G-6-PD, catalase, 41%
            increase cytochrome oxidase.  No effect
            on superoxide dismutase.
                                                                                                Crapo  et al.,
                                                                                                1978

-------
TABLE 14-14.   NITROGEN 01 OX IDE-INDUCED CHANGES IN HEKATQLOGY
Pollutant
Concentration
Pollutant pgTiP pp«
NO

H02

H02



NO,
so|


HO,
SO*
NH
NO-

CO
NO,

N02





100

680

940



940 *
1,000


940 »
1,0*1 +
70
940 to
1,500 »
58,000
1,500

1,880





0.05

0.36

0.5



0.5 *
0.39


0.5 +
0.39 *
0.1
0.5 to
0.8 »
SO
0.8

1





Exposure
Continuous,
90 days
Continuous,
7 days
8 hr/day.
7 days
8 hr/day,
4 BO
8 hr/day.
120 days





Continuous,
1 to 15 m

Continuous,
S days
Continuous,
493 days
followed by
Influenza
A/PR/8/34
virus
Species Effects
Rat No effect on blood hemoglobin or
erythrocytes.
Guinea pig Increased red blood cell 0-2,3-diphOi-
phoglycerate.
Guinea pig Decrease in RBC GSH peroxldase
(p < 0.001).
No change In RBC GSH peroxldate.

Guinea pig Sane effects In both exposures.
Increased WBC and lymphocytes. Decreased
RBC, hemoglobin, neutrophits and
eosinophUs.



House Addition of CO to NO. failed to affect
carboxyhenog 1 ob i n.

House Ho effect on met hemoglobin.

Squirrel No effect on hematocrit, hemoglobin, or
nonkcy clinical biochemical parameters.
following viral challenge increased
leukocyte count.


Reference
ShalambeHdze,
1969
Hersch et *1. ,
197J
Donovan et al. ,
1976
Kenzel et al. ,
1977
Kosnlder et al.
1975





Nakajim and
Kusumto, 1970

NakaJlM and
Kusunoto 1966
f enters et at. ,
1973





-------
                                                      lAUlt  14-14,
Pol luUnt
Concentration
Pollutant
1(0
WO,
NOZ
NOj
NO,
4

502

NO.
sof
NO,
NaCl
MU/-3
940
1,880
1,840 »
2,450
2,400 to
5.C40

5,240

2,400 •
5,000
3,760 »
330
ppa
0.8
I
1.5 *
1.3
1.3 In
3

1.9

1.3 »
1.9
2 +
0.14
Exposure Species
16 hr/tlay, Doj
7 «lays/nk.
4 yr

2 hr/day. Rabbit
15 S. 17 wk

2 hr/day,
15 wk
1 hrAtay,
15 wk
Continuous, Konkey,
14 mo rat
effects
No effects on hewitocrit viscosity,
Cfir&nxyheiioglQb!nt or netheMogl^ln,


Increased leukocytes followed by
decreased phagocytic activity.
Decreased RBC.
Decreased phagocytic activity leukocyte.
No effect on ROC.
No effect on RDC.

Monkey: with or without NaCl, hypertrophy
of respiratory bronchiolar epitheliua.
Reference
Block et al..
19/3


Kitina, 1962






Furiosl et al. ,
1973
NO,
NO,
NO,
               9,400
              18.800

              45,100
              48,900
              73,000 to
             310,000
  5
 10
                             24
39 to
 164
Continuous,
90 days

4 hr
                                        191  days
                                     5 to 60 min
Cynonolgus
monkey, male

Uibit
                                                            Dog
               Dog
Rat:  with or without Nad, polycylheula
with reduced mean corpuscular volume and
normal mean corpuscular hemoglobin concen-
tration.  NeutrophiI/lymphocyte ratio
tendency to shift upwards in both animal
species tested.

No effect on hematological paraceters.
                                               Increased  nitrite 4  nitrate  in blood.
                                               Thought  to react with hemoglobin producing
                                               raethemoglobin.

                                               Increased  WBC disappeared  following cessa-
                                               tion of  NO..  Decreased  heffiatocrit and
                                               hemoglobin;  increased mean corpuscular
                                               volume and mean corpuscular  hemoglobin.

                                               No  effect  on hematocrit  or platelet counts.
Coate and Badger,
1974

Svorcova and
Kaut, 1971
                                                                                Lewis  et  ah,
                                                                                1973
                                                            Carson el al,,
                                                            1962

-------
in leukocytes followed by a decrease in their phagocytlc activity.   Exposure to NO* alone also
reduced the number of RBC, while a mixture of NO- and SO. or SO, alone had no effect.
     Fenters et al.  (1973)  showed that exposing male  squirrel  monkeys  to 1,880 MS/"1  (1 PP")
N0? continuously for  493  days  had no significant effect on hematocrit,  hemoglobin, total pro-
tein, globulins, chloride, sodium, calcium, potassium, glucose, blood urea, nitrogen,  glutaraic-
pyruvic transaminase, lactate  dehydrogenase,  and lactate dehydrogenise isoenzymes.  Challenge
with influenza A/PR/8/34 increased leukocytes in NOo-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) N02 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 NO- 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.
     Block et al.  (1973) conducted several hematological studies on dogs exposed 16 hours/day,
7 days/week, for 4 years  to 940 ug/m3 (0.76 ppra) NO, 1,880 ug/m3 (1 ppm) NO,, or 1,840 ug/m3
                            3
(1.5 ppm) NO plus  2,450 ug/m  (1.3 ppm) NOp.   No changes in hematocrit, viscosity, carboxyhemo-
globin, 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.
     Tusl et al. (1973) exposed rats to 9,400 ug/m  (5 ppm) N0_ for 8 weeks.  The influence of
NO,,  on swimming  of   rats  was  measured.   By  the  5th and  6th weeks  of  exposure,  swimming
performance had decreased 25 percent.  In rats exposed to 1,880 pg/m  (l ppm) NO,, performance
was maintained with a slight tendency toward deterioration.
     Yakimchuk  and Chelikanov  (1968)  reported  that rats exposed to  600  ug/m  (0.32  ppm) N0_
for 3 months developed a delay in their conditioned reflexes to sound and  light.  Shalamberidze
(1969) exposed  rats  to  100 ug/m  (0.05 ppin) N02 for 3 months with no demonstrated effects on
the central nervous system.
     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  S'-nucleotidase.   Increases  were seen in 1,6-diphosphofructose  aldolase, isocitrate
dehydrogenase,  a-hydroxybutyrate dehydrogenase,  phosphocreatine  kinase,  and cholinesterase,
14.2.4.3   Biochemical Markersof 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-IS.   CEKffMl HERVOUS SYSTEM AKO BEHAVIORAL EFFECTS
-0
cn
Pollutant
IK>2

NO.,






NO,
£
N02






N02


NO
£
Auto Exhaust
CO
NO
CO* (0,0?
a»a 0.37%
Aldehydes
Pollutant
Concentration
iKjTiF ppa
100 O.US

1,0(10 O.S3






600 0.32

1,880 1

9,400 5

37,600 JO
6,580 3,5

14 ,000 7. J


?i,000 40
37,600 20
IS 040 3

58,000 SO
(0.2 and 23)


(O.I and 2.0)
Exposure
Continuous,
3 no
8 hr/day.
180 days





Continuous,
3 no
20 min/day,
to 6 fflQ



6 hr/day.
8 wk
6 hr


5 hr
1 day
19 days

6 hr/d»y.
5 days/wit,
2. 5 fflo to
2 yi-

Species Effect
R*t Ho el feet on CHS.

Guinea pig Oecreastd dilate, sorbltol, lactate
dehydrogenise; alanine antnotransferase;
Alfase and 5'-nucteat!dase. Increased
l^'ciipnosiihofnictose aldolast;
fsocltrate, and alpha-hydroxybutyrate
dehydrogcnase; phosphocreatine klnase
and chollnesterase.
Rat Decreased conditioned reflexes to sound
and light.
Rat More or less constant swimming performance
only slight tendency to deterioration.
Swinging performance decreased 25X by 5th and
6th wk of exposure
Swindling velocity declined from 1st no.
Decreased swiimiing performance.

Mouse, nate Decreased voluntary running activity.
: Return to normal within 24 hr post
exposure.
Rat 20% decrease swimming endurance.
10X decrease swimming endurance.

Rat, flale Decreased sound avoidance reflexes,
learning rate lowered.



Reference
Snaliutberldie,
US'!
Drotdz et al,,
19»





YaMncM and
Chelikanov, 1968
lusl et al. , 1973






Murphy et al. ,
1964

Campbell,
1976

Slupfel, 1973





-------
                                             TABLE 14-16.   BIOCHEHIML MARKERS Of ORGAN  EFFECTS
c-
I


Concentration
pg/m3 ppffl *
470 0.25
Exposure
3 hr
to 9,400 to 5








1




1

f


940 0.5




940 0. 5

.000 (HO ;
mainly NO.)



,880 1

,000 1.05


8 hr/day.
7 days

8 hr/day,
4 no.
Continuous,
7-14 days
8 hr/day.
180 days



Continuous,
6 no
B hr/day,
180 days
' Species Effect
House Increase In pentobarbltal- Induced sleep time
In feaale nice only. Repeated dally exposures
caused no effect.
Guinea pig Serun lactic dehydrogenase, total
creatlntne phosphoktnase, SCOT, and SGPT,
chollnesterase and lysozyne elevated.
Lysozyne and chollnesterase depressed.

Guinea pig Albuiiin and globulins found in urine.

Guinea pig Nitrates and nitrites excreted in urine.
Serun cholesterol slightly elevated; total
llplds depressed. Urinary Hg Increased while
liver and brain Hg decreased. Hepatic edema
reported.
Guinea pig Protein synthesis inhibited. Body weight, total
serum proteins, and limunoglobullns decreased.
Guinea pig Plasma changes:
Decreased albuoln, seroimicoid, choltnesterase.
Reference
Miller et at., 1980


Henzel et al..
1977



Sherwfn and
Layffeld, 1974
Kosmider, 1975




Kosnfder et al. ,
1973a
Orozdz et al .
1976
                                                            alanln, and aspartate  transnfnases.
                                                            Increased alpha, and beta]  tn-munoglobul 1ns.
                                                            tntracellular edema of liver.
                                                            Hepatic changes similar to  plasma.

-------
                                               TABLE  14-16.   (continued)

N02
Concentration
|jg/m3
11,660
47,000 to
179,000
ppm
6.2
25 to
95

Exposure
Continuous,
4 days
2
hr
Species
Rat
Rat


Effect
Reference
No effect on serum lysozyme.
Plasma
No? coi
eortfcosterotie
icentration from
increased
47 to 179
propoctional to
mg/m ; at 85
Chow
1974
Tusl
1975
et
et
al.,
al.,
                                                19 days;  at 56  mg/m
                                                to normal in 5  days.
                     x 5 hr/day levels returned
56,400     30        Continuous,   Hamster
                     30 days
Serum antiprotease levels increased
Kleinerman and
Rynbrandt, 1976
Rynbrandt and
Kleinerman, 1977

-------
lysozyme into the  blood  from pulmonary damage was  cited  above (Chow et a!., 1974; Donovan et
al, 1976;  Menzel  et al., 1977).  The  CPK  isoenzyme patterns seen 1n  NO^-exposed  guinea pigs
are difficult  to  differentiate from  CPK  patterns  caused  by myocardial  damage and  are  not
particularly useful (Donovan  et al.,  1976).   Plasma chollnesterase (CHE) was significantly (p
< 0.001) elevated after a 7-day exposure to 940 ug/m  (0.5 ppm) NO, 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.   Host  likely,  the
alterations in  SGOT,  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 yg/m  (0.5 ppm) NO, 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  (l.OS 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 f32-immunoglobins.  Electron micrographs of
the liver suggested intracellular edema.   Kosmider (1975) reported decreased serum cholesterol,
total   lipids,  and  beta   and  gamma lipoproteins in  guinea  pigs  exposed  to 1,000 pg/m  NO
(mainly NO-),  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 displaced.
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
                                                                     3                       *
and added  ammonia.  Nitrogen oxides reacted with ammonia (1,000 pg/m ; 1.4 ppm), reducing the
lipid and  electrolyte  disturbances seen with NO  exposure alone.   Blood  serum  lipids,  lipo-
proteins,  and  cholesterol were  not significantly  altered  from those of  control  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  sodium  and
potassium were lowered,  while magnesium and calcium were  higher  than controls.   No effect on
serum calcium levels was seen with NOX 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) NO-  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  pg/ra  (0.5 ppm) NO, continuously for 7 to 14 days.  Proteinurla was detected in
                                                                   3
another group  of animals exposed for 4  hours  per day to 750 pg/m  (0.4 ppm) NO- (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 pg/m  (0.25 ppm) NO,
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)
exposure  to 235  pg/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)  NOg 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 pg/m  (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 pg/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 NO^ caused more effect than a single exposure to 0-.
14.2.4.4  Teratogenesis and Hutagenesis—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 pg/m  (1.3 ppm) NO,., 12 hours/day for 3 months at which
time exposure  ceased  and the  animals  were bred.   Long-term  NO- exposure  had no effect  on
fertility.  There  was  a statistically significant decrease  in  litter size and neonate weight
(p < 0.001).   In  utero death  due  to NO,  exposure resulted in smaller  litter sizes,  but no
               __  ______                 ^
direct  teratogenic effects  were  observed in  the offspring.   In  fact,  after  several  weeks,
NOg-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 pg/m3 (0.1, 1,
5, and  10 pptn) NO, for 6 hours.   Blood samples were obtained at 0 time,  and  1 week and 2 weeks
post-exposure.    Mouse  leukocyte chromosomal  analysis  revealed  that  NO.  did not  increase
chromatid-  or  chromosome-type alterations.    The  analysis  of primary spermatocytes  showed no
direct  effect  of  N0_  exposure  on  their chromosomes.  Therefore,  in these experiments,  NOg
exposure did not induce mutagenesis.  (See Table 14-17.)

                                        14-68  •

-------
                                            TMLI M-17.  STUDIES OF POTENTIAL MUTAGENISIS, TERATOGENESIS
Pollutant
Concentration
Pollutant
NO.



MS/13
190
1,680
9,400
18,800
ppn Exposure
0.1 6 hr
1
&
10
Species Effect
House 2 wk pott-exposure no increase IB chroutid
or chronosome- type alterations In leukocytes or
primary spermatocytes. Ho nutagenlc effects
noted.
Reference
Gooch et al. ,
1977


NO,
HO,
NO.
 9,400
HO,           9,400 to        5  to
  '          18,800           10
18.800
             18,800
                               10
                               10
Continuous,
to 11 Mk
2 hr/day,
5 day/wk,
  SO wk

2 hr/day,
5 day/Mk,
  SO wk
Rat          Appearance of hypcrplastic foci In the
             shape of 2 to 4 layer pyramids by 3 wk.
             Decreased ciliated cells.
             Extensive hyperplasia (3 to 4 layers of
             epithelium), cuboldal metaplasia )n ad-
             jacent alveoli by S wk.
             Hyperplasia In all bronchioles,
             decreased bronchlolar luain*, polynorphous
             tpithellini extensive by ? wit.  Terminal
             brohchiolar epithelium contained only
             2 or 3 irregular layers, increased number of
             ciliated cells by 9 Mk.   By 11 wk return to
             1 layer epithelium.  Lungs at indefinite state
             of repair from week 7 on.

Mouse        Mice given 4-nitrequlnollne-l-oxide and
                          Continuous fro*
                          pregnancy to
                          3 mo after delivery
                                                        House
                                                        Rat
                                                                                                                      flejthar and
                                                                                                                      Rejthar, 197<
                                                                     NO,
                                                             NO, had no effect on tunor production.
                                                                                                         Ide and Otsu,
                                                                                                         1973
             Mice given 4-nitroquinoline-l-oxlde              Otsu and Ide,
             (carcinogenic agent) * NO, decreased             1975
             Incidence of lung tumors.

             Decreased litter size and increased nor-         Freeman et al.
             tallty of neonates up to IS days post            19746
             delivery.
             Ho teratogentc effects noted.

-------
TABLE 14-17.  (continued)
Pollutant
Concentration
Pollutant iigTa? pp» Exposure Species
Auto Exhaust
CO 58,000
""x

•- CO, (0.07 and
f 0.37%)
•"•4
0 Aldehydes


50 6 hr/day, Rat
5 days/t*.
2.5 m to
(0.2 2 yr
and
23)

(0,1
and
2.0)
Effect Reference

Auto exhaust had no biological effects when Stupfel et til,,
NO was 0.2 ppn. 1973
Exposure to NO (23 pp>) increased nuiber of
spontaneous tuflors, cutaneous abscesses,
and bilateral renal sclerosis.
No tumors or abscesses in lungs.




-------
14.2.4.5  Effects of NOg on Body Weights—Dogs, rabbits, guinea pigs, rats, hamsters, and mice
have been exposed to 100 to 47,000 ug/m  NO- (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
air containing 135 ug/m  (0.07 pprn) NO, 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  NO.  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
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
     a
ug/m   (0.02  ppm)  NO-  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
hours/day for 8 to 12 months.   The smog was composed of 1,500 pg/m  (0.8 ppm) NO,,  5,750 ug/m
                    •5                              3
(5  ppm)  CO, 760 ug/m  (0.38 ppm) 0,, and 5,700 ug/n  (2.2 ppm) SO^.  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

NOZ







Concentration
ug/m3
100
135


1,300 to
1,500
1,900 to
ppm
0.05
0.072


0.7 to
0.8
1 to
Exposure
90 days
Continuous,
100 days

30 days

18 mo
Species
Rat
Rat


House

Dog, rabbit,

No effect.
Ambient air
0.042 ppn SO
rag/ra dust)
No effect.

No effect
Effect

exposure (6.3 opm CO, 0.206 ppn NO,
_, 0.0048 mg/fi) acid mist and 0.88
Decreased body weight.



Reference
Shalamberidze,

1969
Oda et al., 1973


Nakajima et al.

Wagner et al. ,


. , 1972

1965
              guinea pig,
              rat, hamster,
              mouse
18,800     10


18,800     10


24,000     12.5
From birth    Rat
to 62 days
                           Decreased body weight and length of pups.
Freeman et al., 1974b
Continuous,   Cynolmogus   In combination with heat stress decreased body    Coate and Badger,
90 days       monkey       weight.                                            1974
Continuous,   Rat
213 days
                           Decreased body weight.
Freeman and
Haydon, 1964

-------
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 MQ/i"  (4-6 and  5.2 ppra)
for  the irradiated  and non-irradiated  samples,   respectively.   For exhausts with  catalytic
conversion, NO^ concentrations were 5,640 and 3,380 n9/">   (3 and 1.8 ppn) 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/ffl ; 500 ppm) did not significantly alter body weight.  Animals exposed only to raw exhaust
or  575  mg/ffl   (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  NO ,  0.07 or 0.37 percent CO,,  58 mg/m  (50
                                                   X                          £
ppm)  CO  and 0.1 or 2 ppm aldehydes.  With  low concentrations of  NO  ,  no biological effects
                                                                     A
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, NO,  levels were  564, 752,
and  9,588  pg/m3  (0.3,  0.4,  and 5.1  ppm);  nitric  oxide (NO)  levels were  8,733,  13,284, and
10,209 ug/m   (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 NO, 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 Mfl/w  (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 pg/rn
(0.79 to 2.17 ppm) NO-, 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
a!.,  1974;  Vaughan et  a!.,  1969).  The  animals were allowed to recover  for approximately 2
years (Billespie  et al.,  1975) 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  (Stera  et al.,  eds.,  1980).   The high NO, group was exposed to 1,210 ug/m  (0.64 ppm)
                  3              •                                              3
NO, plus 310  ug/m  (0.25 ppm) NO.  The  low NO, group was exposed to 270 ug/m  (0.14 ppm) NO,
                3                                 168
plus  2,050  pg/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  NO, 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 NO- 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 NO- 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., 1975).   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  NO- with low  NO,  there was a rise (p
<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.
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 NO-  group,  there were increases
(p 
-------
mortalities were  evident after  five  daily exposures.   At 196 ug/m  (0.1 ppm) 03  plus 2,800
ug/ra3 (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
              3                                 2                           2
mice were exposed to a combination of 6,580 yg/m  (3.5 ppm) N02 and 980 |jg/m  (0.5 ppm) 03 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
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.
     Ihrlich et  al.  (1979) used another exposure  regimen of  N0«-0,  combinations to evaluate
effects with the  streptococcal  infectivlty model.   For  1,  2,  3,  and 6 months, mice were ex-
posed continuously to 188 pg/m  (0.1 ppm) NO,  on  which were superimposed peaks  (3 hr/day,  5
                           33                            3
days/wk) of either 940 ug/m  (0.5 ppm) NO, or 940 MS/1"  (0.5 ppm) NO- plus  196 ug/m  (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 N02 + 0, mixture.  After 3 mo., the peak exposures to NO,
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 * °3*   However» mortality increased (p <0.05)  after 6 mo exposure to  NOv-Qg peaks, with
or without the baseline of N0_.   In another set of experiments using identical exposure regimens,
the nice  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 + 03
peak, and there  was an  increased response as exposure length increased.  When the peak of N02
+ 03 was superimposed on a baseline of NO., the response was reduced, although it did increase
with time.  The effects in the peak of NO, group were roughly equivalent to those in the group
receiving  a baseline  of  NO,  with an  NO,  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_ + N02<   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 NO, or  air on  which were
superimposed peaks of N02 + 03>  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 N0« 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
                      33                                     3
exposure to 7,520 ug/m  (4 ppm) NO, plus  600 \tg/m  (0.36 ppm) 0,, and after 12,860 ug/m  (6.84
                       3
ppm) NO- plus  760  ug/m  (0.39 ppm) 03 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
gg/m  (2.3 ppm)  NO,  plus 390 ug/ra • (0.2  ppm) 0, 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.
     Furiosi et  al.  (1973)  exposed  monkeys and  rats to aerosols  containing  330  pg/fli  (0.14
ppm) NaCl  and 3,760 ug/m   (2 ppm) NO,  continuously  for 14 months in order  to  delineate  the
                                                                                             3
effect of particulate  aerosols  on NO, toxicity.  Of  the total  NaCl aerosolized, only 5 pg/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
NO- or NOg  in the  presence of NaCl.   With  only half the  concentration  of NaCl  and NOg, 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-like conditions were noted  in the lungs of NO -exposed
animals.    Emik et al.  (1971) reported  that alkaline  phosphatase  activity decreased  in  the
lungs of rats  exposed  2.5 years to ambient  air containing approximately 36 pg/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
10,000 pg/m   (3.8 ppm)  SO-, 10,000 ug/m  (5.3 ppm)  NO,,  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 SO-
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 pg/ra  (1.3 ppm) NO-; (2)
5,000 ug/m3 (1.9 ppm) SO,; (3) 160  »g/m3  (0.06 ppm) SO,  ;  (4)  130 ug/m3 (0.07 ppm) NO,; (5)
          33
2,500 ug/m  (0.95  ppm)  SO, and 1,130 u§/m   (0.6 ppm) N0_.  Low concentrations of SO, and NO,
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 pg/ra  (10.6  ppm) NO containing  1,500 ug/m   (0.8 ppm) NO,.  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 jjj 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.)
     Azoulay et  al.  (1977) exposed rats continuously for 6 weeks to  2,460 iig/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 count.    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
52,890  ug/in   (43  ppm)   NO and  6,768  ufl/n   (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
jt\ vitro  to 25 to 250 pi  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

-------
TABIE 14-19.   NHKIC OXIDE
Pollutant
NO








NO



NO *
NO.
£



NO




NO

NOt

Pollutant
Concentration
|ig/m'* ppm Exposure
2,460 2.0 Continuous,
6 wk







9,470 7.7 8 hr/day.
120 days


13,040 « 10.6 » 1 hr
1,500 0.8




14,800 12 5 hr




19,700 to 16 to 4 hr
61,500 50
52,890 « 43 • Continuous,
6,768 3.6 6 days
Species Effect
Rat Cellular infiltration of alveolar walls and
areas of intra-atveolar edema observed after
2 wk. After 3-wk exposure, emphysema- like
changes observed until 6 wk. Hethemoglobin
undetected. No differences in blood oxygen
saturation, pH. oxygen combining capacity,
AfP, 2,3~d»phosphoglycerate, glucose, lactate,
hemoglobin concentration, hematocrit, or
RBC count.
Guinea pig Decreased blood sodium, magnesium, and chloride;
decreased In and Hg in brain and liver.
Increased blood calcium and urinary
excretion Hg.
Hice, female; Mice and rats showed increased nitrosy) henoglo-
Rat, male; bin (NOHb); NOHb related to concentration of NO.
Rabbit, male By 20 minutes equilibrated, 0. 13X total hemo-
globin. NOHb half-life 10 minutes. No NOHb
produced in rabbits exposed to NO until sodium
rilthionale added to blood.
House Edema and dilation of vessels in submucosal
tissue of trachea. Congested alveoli.
24 hr later proliferation of trachea!
nucosal epithelium.
Anomalies in CNS, heart and cell metabolism.
Guinea pig No significant alteration In
respiratory rate or tidal volume.
Rabbit No effect on lung morphology.

Reference
Aroulay
et al., 1977







Kosmider and
Chorazy, 1975


Oda et al. ,
1975a
Oda et al. ,
1975b


Udai et at.,
1973



Hurphy et al.
1964
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  \i1  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/ra   (7.7  ppin)  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 HO. generated  from  nitric acid  (HNO-).
(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 NO^ and HNQ- effects.   Concentrations of 17,000 and 26,000 vg/m  (9 and
14 ppm)  NO,  administered 4 hours/day, 5 days/week  for  6 weeks produced lung pathology.  When
                                                3
exposure concentration was reduced to 9,400 yg/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 £-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 ug/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 14-70.  NITRIC ACID AND NITRATES

Pollutant
NO.
generated
from HNO,
HNO,
a






Sodfuffl
nitrate

Amraon f un
nitrate

Pb(w )
Ca(NO,)f
NaNO,
KNO,
NH.nO,
' Pollutant
concentration
9,400, 17,000 or
26,000 iig/a
(S, 9 or 14 pp«)
IX solution
(0.15 ml)



'-


0.1 and l.OX at
740 and ,
4,000 pg/«T
100 iN


2,000 ug/m?
2,800 uq/m.
3,100 us/Hi'
4,300 pg/».
4,500 ua/aT
Exposure Species
4 hr/day. Rat, nouse,
S days/uk, guinea pig
6 wk
Intra- Rat
tracheal
injection





7.5 «in Dog


30 nln Guinea pig


3 hr Mouse




Effect
No lesions at 9,400 pg/m3 (S ppm).
Higher concentrations, increased lung pathology.

24 hr post- injection Increased Inflammation of
bronchioles; epithelium lost normal scalloped
appearance. Increased cytoplasm in epitneliun.
Inflamed alveolar septae.
Ho difference In lung wet and dry weight.
Enhanced pulmonary absorption rates of
p-anlnohippuric acid, procaineamide ethobronide,
procaineamlde and nannitol.
No effect on pulmonary function.


Accounted for 58X of total
histamlne release.
Ammonium sulfate released.
After 14 days of observation, no effect on
mortality following cl lenge with S. pyogenes .
(


Reference
Gray et al . ,
1952

Gardiner and
Schanker, 1976






Sackner et al . ,
1976

Charles and
Menzel, 1975

Ehrlich, 1979




ZnNO,
1.250
Increased mortality.

-------
     Charles  and  Henzel (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  ug/»3  Ca(N03)2>  3,100  ug/m3 NaNOg, 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 pg/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
nitrosaroines have  appeared  recently.   (Magee et a!.,  1977;  Hontesano 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 NO,.  Mice were exposed  intermittently  to 75,200
    3
ug/m  (40 ppm)  N02 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  jji y 1yo,  whereas  they were  found  jm vitro when
lung homogenates were exposed to high concentrations of nitrogen oxides (15 percent).
     The nitrosaraines  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/m  (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.   Oimethylnitrosamine 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 chondrosarcornas of the lower vertebrae in rats
(Pelfrene et al., 1967).
     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., 1956),
     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 rn 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 jjj  vivo biosynthesis  of N-nitroso-
raorpholine from mice  exposed to NO,  and  morpholine.   This is the first and  only report of a
direct  link  between  NO,  exposure and  nitrosamine  formation  in vivo.  N-nitrosomorpholine was
                       '
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) N02, 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  NO-  and  concomitant biosynthesis  of  nitrosamines  indicates  a
potential health hazard.  This area  of  investigation  requires  additional  work  in  oj*der 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 (NO,).   A  summary of the
                                         3
research  results observed at 18,800 ug/m  (10.0 ppm) NO, or less is set forth in Table 14-21.
                                                                                  3
While  mechanisms  of  action  can be studied  by  exposures at or-above 18,800  jig/m  (10..0 ppm)
NO,, 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 NO-.
     An unusual  aspect of the toxicity of NO,  is a delay between exposure  and  effect.  This
temporal  sequence is  inherent in understanding the toxicity of NO-  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 thes«
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  14-21.  SUMMARY OF EFFECTS OF N02 IN ANIMALS AT CONCENTRATIONS OF 10 ppm OR LESS
i
O3
tn
Concentration of N02
(jg/m3 ppm
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
Time of
exposure Species
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
Summary of effects
No effect on S. pyogenes infectivity

Emphysematous alterations
Inhibition of conversion of PGE- to
its metabolite. No effect on
PGE2 uptake or efflux
Swollen collagen fibers in lung
Increased* pentobarbital
sleeping time in female mice after
References
Gardner, et al. ,
1981
Port, et al.,
1977
Meniel, 1980
Buell, 1970
Miller, et al.,
1980
        560-940    0.3-0.5
Continuous   Mouse
  3 mo
1 day.  No effects after 2 or 3
days.

NO. + influenza virus caused a high
incidence of adenomatous prolifera-
tion of peripheral and bronchial
epithelial cells
Motomiya, et al.,
1973

-------
TABLE 14-21.  (continued)
Concentration of N02
[i(]/B^ ppM
600

680

740

740

740


£ 940
i
o>
O)
940




940

0.32

0.36

0.4

0.4

0.4


0.5


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 no
8 hr/day
7 days



Continuous
14 days
Species
Rat

Guinea Pig

Guinea Pig

Guinea Pig

Guinea Pig


House


Guinea Pig




Guinea Pig

Summary of effects
Decreased conditioned reflexes

Increased erythrocyte D-2, 3-
diphosphoglycerate
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
animals.
Morphological effects in alveoli


Increase -in serum LOH, CPK, SCOT,
SGPT and cholinesterase, and lung
and plasma lysozyme. Decrease in
erythrocyte GSH peroxidase. No
change in lung GSH peroxidase.
Albumin and globulins in urine

References
Yakimchuk and
Chelikanov, 1958
Hersch, et al. ,
1973
Sherwin, et al. ,
1974
Sherwin and
Carlson, 1973
Belgrade, et al. ,
1981

Blair, et al. .
1969

Donovan, et al. ,
1976; Menzel,
et al., 1977


Sherwin and
Layfield, 1974

-------
                                     TABLE 14-21,  (continued)
Concentration of  N02   Time of
   (jg/m3   ppm
                      exposure    Species
Summary of effects
                                            References
1,000 NO              8  hr/day   Guinea Pig
(mostly x             180  days
 940        0.5      Continuous   House
                     30-45 days
 940        0.5        5 days/wk  House
                       7 wk

 940        0.5      Continuous   Guinea Pig
                       8 hr/day
                       4 mo
 940  or      0.5 or 2 Continuous   House
 3,760                with 1 hr
                     peaks of
                     2 ppm 5
                     days/wk

 940         0.5      Continuous   House
                       12 mo
Nitrates and nitrites in urine; slight
increase in serum cholesterol; decrease
in total serum lipids; hepatic edema;
increase in urinary Hg and decrease
in liver and brain Mg

Morphological alterations of trachea)
nucosa and cilia
                                                  Increase of injected horseradish per-
                                                  oxidase in lung

                                                  Decrease in plasma chollnesterase;
                                                  erythrocyte or lung GSH peroxidase
                                                  unchanged.   Increase in lung acid
                                                  phosphatase and plasma and lung
                                                  lysoiyme

                                                  Horphological  alterations of alveolar
                                                  macrophages;  decreased serum neutraliz-
                                                  ing antibody to influenza virus immuni-
                                                  zation; changes in serum inmunoglobulins
                                                  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
                                                  hyperplas-ia
                                                                                               Kosmider, 1975
                                       Hattori, et a!.,
                                       1972; (Nakajima),
                                       et al., 1969

                                       Sherwin, et al.,
                                       1977

                                       Donovan, et al.,
                                       1976; Henzel,
                                       et al., 1977
                                       Aranyi,  et al.,
                                       1976;  Ehrlich,
                                       et al.,  1975
                                       Hattori,  1973;
                                       Hattori and
                                       Takemura,  1974

-------
                                            TAOLE 14-21.  (continutd)
8
Concentration of N02 Time of
jig/in^ ppm exposure Species
940 or
1,880
940 or
1,880
940
1,000
1,030 -
3,000
1,500
0.5 or 1
0.5 or 1
0.5
0.53
0.55 -
1.6
0,8
Continuous House
1 yr, 5 mo
Continuous House
1 yr, 6 mo
Continuous House
or inter-
mittent
(7-8 hr/day)
180 days Guinea Pig
8 hr/day
Continuous House
5 wk
Continuous Rat
2.75 yr
Summary of effects
No increase in lipofusctn 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
Droidz, et al. ,
1975
Hiyoshi, et al. ,
1973
Haydon, et al. ,
1956; Freeman,
et al., 1966
       1,880    1
       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 narked depression
after 2 wk
Selgrade, et al.,
1981
Seto, et al., 1975

-------
                                     TABLE 14-21.   (continued)
Concentration of  N02   Time of
           ppm        exposure    Species
                                             Summary of effects
                                                                          References
  1,880     1-1.5     Continuous
  2,820                  I mo
 1,880
 1,880
 2,000
1.1
           Continuous
             6 mo
           Continuous
           493 days
8 hr/day
180 days
940 + 2 x 0.5 + 2 x  Continuous
daily     daily      15 days
spikes    spikes
of 1880   of 1
House            Hypertrophy of bronchiolar epithelium
                 after 1-3 mo.   After recovery frow
                 exposure, lymphocyte infiltration

Guinea Pig       Inhibition of  protein synthesis;
                 decrease in body weight, total serum
                 proteins, and  immunoglobulins

Monkey           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

Guinea Pig       Plasma and liver changes:   decrease in
                 albumin,  .seromucoid,  cholinesterase,
                 alanine and aspartate transaminases;
                 increase in alpha and beta, immuno-
                 globulins

House            Increase in mortality due to
                 S.  pyogenes
                                                                                     Chen,  et  al.,  1972
                                                                          Kosnider,  et al.,
                                                                          1973a
                                                                          Fenters,  et al.,
                                                                          1973
Drozdz, et al.,
1976
                                                                                    Gardner, et al.,
                                                                                    1981

-------
TABLE 14-21.   (continued)
Concentration of N02
ug/m3 ppm
2,300 +
2 x
daily
spikes
of 4,700
2,360
2,400-
5,200
2,800
-C.
1
UD
O
2,800 +
8,100
spike
2,800 +
8,100
spike
5,600
3,760
1.2 + 2 x
daily
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
aerosol
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
111 ing et al.. 1980
Ehrlich et al. ,
1977

-------
TABLE 14-21.   (continued)
Concentration of N02 Time of
|ig/m3 ppm exposure
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
Continuous
1-3 wk

Continuous
3 wk
Continuous
43 days
Continuous
14 mo.
Continuous
2yr.
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 11 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 Mad. 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
Fur IDS f, et al.»
1973
Freeman, et al.,
1968c
Goldstein, et al. ,
1973b
Kaut, et al., 1966
Heniel, et al., 19;

-------
                                            TABLE 14-21.  (continued)
       Concentration of N02   Time of
                  ppa        exposure    Species
                                            Summary of effects
                                                                          References
        5,450
2.9
-to
to
        5,640      3


        5,640      3



        6,600      3.5
        .7,500-     4-7
         1,3000
         8,100
         9,400
4.5
24 hr/day    Rat
5 days/wk
  9 no.
         4 hr/day
         4 days
             Monkey
         Continuous   Guinea Pig
         3  days
Continuous   Mouse
or Inter-"
mittent
(7 hr/day,
7 days/wk)

Continuous   Mouse
 14 days

1, 3.5 or    Mouse
7 hrs
           3 hr
             Guinea Pig
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

Increased susceptibility to S. pyogenes
aerosol proportional to duration of
exposure.   No effect when bacterial
challenge was delayed IB hrs.

Increase protein and lipid content of
lavage fluid in vitamin C-depleted but
not normal after 18 hrs
Arner and Rhoades,
1973
Bils, 1976
                                                                          Selgrade, et al.,
                                                                          1981
                                                                                   Gardner, et al.,
                                                                                   1979
Sherwin and Richters,
1971

Gardner, et al.,
1981
Selgrade, et al.,
1981

-------
                                             TABLE 14-21.  (continued)
«£>
U)
Concentration of N02
Hfl/in3 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
3 hr
4 hr
4 hr/day
5 days/wk
2 mo.
7.5 hr/day
5 days/wk
5.5 mo.
14-72 hr
3 days
Continuous
1 wk
Continuous
Species
Rabbit
Guinea Pig
Guinea Pig
Guinea Pig
House
Guinea Pig
Rat
Monkey
Summary of effects
No measurable effect on benzo(a)pyrene
hydroxylase activity of trachea 1
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; Mstological 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
Balchun, et al. ,
1965
Murphy, et al. ,
1964
Csallany, 1975
Selgrade, et al. ,
1981
Rejthar and Rejtha
1974
Henry, et al., 1971
                               2 no.
K. pneumoniae

-------
                                     TABLE  14-21.   (continued)
Concentration of NOj    Time of
           ppm         exposure    Species
                                                       Summary of effects
                                                                                              References
9,400-     5-10      Continuous    Honkey
18,800                 90 days
9,400-     i-10      Continuous   Honkey
18,800                 90 days
9,400
18,800     10
190        0.1
                     Continuous    Honkey
                      133 days
                        6 hr     House
                                                    Infiltration of aacrophages,  lymphocytes
                                                    and some polymorphonuclear  leukocytes;
                                                    hyperplasia of bronchiolar  epithelium
                                                    and Type II cells

                                                    No significant hematological  effects
                                                                                              Busey, et al, ,
                                                                                              1974
                                                                                              Coate and Badger,
                                                                                              1974
                                                    Immunization with mouse-adapted  influenza   Hatsumura, 1970
                                                    virus.  Initial depression  in seru* neutra-
                                                    lization lilers wilh relurn lo normal by
                                                    133 days.  No change in hemagglutination
                                                    inhibition tilers or amnestic response

                                                    No chromosomal alterations  in leukocytes    Gooch, et al., 1977
                                                    or primary spermatocytes

-------
.EXPOSURE
. CHEMICAL REACTION
                                •— SUSCEPTIBILITY TO
                                     MICROORGANISMS

                                — CELL DEATH (mix. «t 24 hr.l
                                     BIOCHEMICAL INDICATORS
                                     OF INJURY (mix. «t IB hr.l  "

                                     REPLACEMENT Of DEAD
                                     AND INJURED CELLS
                                     AND BIOCHEMICAL
                                     INDICATORS Of REPAIR
                                     lm«, »t 48 hr.l
 (log lt)  4     10

   I        hourt
            24   48

            i
                                dtyt
30

 I
                                                2  3
 6   12

tNt    f
Figure 14-4,  Tnmporal sequence of injury and repair hypoth-
esised from short-term single exposures of less than 8 hours.

-------
same  for all  mammalian species exposed  under similar  conditions.   These reactions  will  be
obtained  predominately  with  low  concentrations  of  NO,.   As  the concentration  of N02  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 toxlcity 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
usad  in  regulating  emissions are those more closely aligned to ambient concentrations of NO^.
     Studies of  the reaction  of NO. 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.   Host
investigators  believe  that the chemical reactions of NO, are dominantly with lipid components
of the cell  (Henzel,  1976).   The  reaction of  NO, with  the  unsaturated lipids  of  cellular
nembranes 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 NO..
The protective role of vitamin E in  the  prevention of NOy toxicity at high concentrations is
also supportive of this hypothesis (Menzel, 1976).
     Alternatively, NOg  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 NO, exposures (Selgrade 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   NO, (Goldstein et al., 1977b).  A very
significant  fraction  of  NO,   is  retained  in  the  lung.   The fraction retained  probably
represents  that  NOp  which  is  chemically  reactive  with pulmonary  tissue  via addition  to
unsaturated fatty acids.
     NOg 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 NO,, but HNO-,  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 NO, by water vapor, a significant fraction of NO, is not removed
in the  upper airways  and penetrates deep within the  lung to produce its toxic effects.   As a
strong oxidant, NO, may also oxidize small molecular  weight  reducing  substances and proteins
                                             14-96

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within seconds to  minutes.   Reaction with unsaturated fatty  acids  to produce peroxidation is
essentially instantaneous (Roehm  et  a"!.,  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
animalSNexposed to  NO-  (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  NOg 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-
barbital, by  the  liver  is   inhibited  by  exposure  of  mice  to 470  Mfl/m  (0.25  ppm)  NO- for 3
hours  (Miller   et al.,  1980).   Repeated  exposure  to  NO. 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  N02 inhalation  on other organ  systems  deserve continued surveil-
lance.
     The major pulmonary effect of NO, is cellular  injury among specific cell types within the
lung  (Freeman  et  al.,  1968b).   If the NO- injury is severe, cell death results.  These events
occur within 24 hours  after inhalation.   The  magnitude  and site of the injury resulting from
NO- will  depend  upon  the  concentration of  NO- which  was inhaled;  therefore, the absolute
degree of  response will  depend upon  both  the rate and magnitude of  respiration  and the NO,
concentration.    The moderate  solubility  of  NO-  in  water and the  inability  of  the upper
respiratory tract  to remove all  of  the  NO-  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 ug/m  (1 ppm)  NO- (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 N0_,  that is
                                             14-97

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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 NO,  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  al.,  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) NO-  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 NO- (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 NO, alone (Donovan et
al., 1976).
     Biochemical  indicators  of lung  injury can  provide early evidence  of  toxicity.   The rat
lung prostaglandin  dehydrogenase  is sensitive to exposures of  as little as 3 hr to 376 pg/nr
(0.2 ppm) NO,  (Menzel, 1980).   In this series of experiments, rats were exposed to 376, 3,760
              3
or 35,720 pg/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  E,  (PGE?),  a natural vasoactive  hormone  secreted by the lung and
other organs.   NO,  exposure  inhibited  the  metabolism of  PGE-  to  its  inactive metabolite
13,14~dehydro-15-keto  PGE,,   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).
No alteration of the uptake or release of either  H-PGE, 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

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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  NO,.   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 pg/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
caused  a  50 percent mortality in the animals  exposed  to  9,400  ug/m  (5  ppai)  NO-,  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 NO- by the use of
a silicon drip technique  and monitored the NO, concentrations  with a Mast Meter and intermit-
tent Saltzman determinations.
     Considerable  improvement has  been made in the methods of analysis for NO, 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 NO,.  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 NO,  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

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ascorbate  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 NO,
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 NO, 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  pg/m  (4-7 ppm) N02  (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 pg/m  (4-7 ppm) or to variable recovery of the
radiolabeled protein in tissue extracts.   Since the time of exposure to discrete levels of NO-
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 pg/m  (4-7 ppm) NO, does not produce
pulmonary edema in normal mice.
     The effect  of NO- 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
of the tracheobronchial region of rabbits exposed  to 9,400 pg/m  (5 ppm) NO,  and greater,   taw
                                                                                         3
et al. (1975)  found  no effect of short-term exposures at even higher levels  (75,200 Mg/m ; 40
ppra  for  2 hours) on rat lung microsomal  faenzo(a)pyrene metabolism.  NO-  exposure appears to
have no effect on these cytochrome P.g,j-dependent  enzyme systems.
     There is  no  reason to suppose that all enzymes are equally sensitive to NO, exposure, so
lack of  an effect on some enzymes is not indicative of an  absence  of  a toxic effect at that
NO- 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 NO- at low concentrations
and  short  times  of exposure  (Coffin et  al.,  1976;  Gardner  and Graham,  1976; Ehrlich,  1975).
                                             14-100

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Mortality from exogenous  Infectious  agents 1s Influenced more in proportion to the concentra-
tion of NO,  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 NO- 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 PGE- to its metabolites (Henzel, 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.   NO,  concentrations  as low as 4,700  Mg/"1  {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 (Belgrade 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 NO™  are  illustrated  in  this  figure  on the z  axis.   Thus,  as the
concentration of NO- 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 NO, which has been inhaled.  Increasing the total amount of
NO-  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 NO- 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 pg/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  NO,.   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 NO^.
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 NO-.  Likewise, all  of the other indicators of NO, damage so far examined are
                                             14-101

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•
aw
1
    Figure 14-5.  Pioportionality b«tw»«n Affect (cell death) »nd
    eoncantratton of NOj during a constant exposure period,
    The maximum in cell death I* reached — 18 houri after •*
    poiure and the extent li proportional to tha doii (concan-
    tration x time).
                          14-102

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I
t
2
                             T    I     r    •
                            CHEMICAL REACTION
                        CELL DEATH
                                                    PULMONARY
                                                      FUNCTION
                                                      CHANGES
REPLACEMENT OF DEAD
AND INJURED CELLS
AND BIOCHEMICAL
INDICATORS OF REPAIR
                                        INCREASED
                               SUSCEPTIBILITY TO
                             MICROORGANISM?
    1  -
    Figure 14-6. Temporal sequence of injury and repair hypoth-
    esized from continuous exposure to NC>2 as observed in exper-
    imental animals.
                         14-103

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dose  dependent.   The  biochemical and  physiological functional  Indicators of  damage  change
rapidly wfth  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
detected which are  indicative of cellular injury at concentrations of NO, as low as 376 pg/m
                                     3
(0.2 ppm) (Menzel,  1980)  or 940 pg/m   (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 NO-  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 NO,  exposure  at concentrations  within
the range of 940-2,820 Mg/m3 (0.5-1.5 ppm) N02 (Gardner et al., 1979; Ehrlich and Henry, 1968;
Freeman et al., 1972; Stephens et al., 1971).
     Long-term exposures  to NO-  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 N0_ 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 NO-  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 NOg  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).
These effects have been observed in rats that have been exposed continuously to 3,760 pg/m  (2
ppm) N02 or greater.
     The fatty acid composition of the lung membranes has also been noted to change during the
exposure to NO, (Menzel  et al., 1972).   The mortality from continuous exposure to high concen-
                                             14-104

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trations of  NO, 1s  influenced  by the  level  of  vitamin  E and other  free  radical  scavengers
which  are  included  In  the  diet  (Menzel,  et  a!.,  1972).   These  observations  support  the
hypothesis  that  membrane damage by chemical  oxidation  of unsaturated fatty acids  is  a major
mechanism  of toxicity  of NO,.   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 NO- inhalation (Chow et al.,  1374;  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 NOg.   It should be
noted, however, that certain segments of the population may be unusually sensitive to NO. 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 NO. 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
NO.  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 NO. 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 NO.  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,
the  guinea pig,  when exposed to 940 ug/ra  (0.5 ppm) NO. 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 NO, is highly  toxic.   It  is most
likely  that  all  cells  are  sensitive  to relatively  low concentrations of  NO.  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

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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 NO, which  are  easily  attainable in inhaled air, when rats
                                3
have been exposed  to 3,760 ug/m  (2 ppm) NO, for long periods of time and then are exposed to
an  abrupt  increase  in  concentration  of  NO,,  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  NOg  exposure.   This concern cones about due to the morphology  of  the  lungs of
animals which  have  been  exposed to N0_.  Because NO, 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 NO,  with  an increased
incidence of cancer at the present time.
     As was  noted  in the  discussion of  the effects  of  short-term exposure  to  NO.,  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
model   in mice  which  were  exposed continuously  or intermittently  (7  hr/day) to 2,820 ug/m
(1.5 ppm) NO, (Gardner et al., 1979).  Intermittent exposures of mice to 2,820 ug/m  (1.5 ppm)
NO, 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 NO,.   The intervening
                                                   3
17 hours between each 7 hour exposure to 2,820 pg/m  (1.5 ppm) NO, 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 vg/m  (1-5 PPm), however, or even to 940 ug/m  (0.5 ppm).
     Considerable differences occur  in  the response  to N0_ when animal  species and infectious
agents other than mice and S. pyoqenes are used (Purvis and Ehrlich, 1963; Henry et al., 1970;
Fenters et al.,  1973; Matsumura,  1970a).   Resistance  to K. pneumom'ae  (Purvis  and  Ehrlich,
1963}   is  less  affected  by  NO, 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

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     The recent work of Gardner et al.  (1981) on the effects of short-term exposures to spikes
of NO, similar to those occurring in the urban atmosphere is particularly important in assessing
                                                                                             3
the interaction of  N0_  and pulmonary infections.  Mice  were  exposed to spikes of 8,100 vg/m
(4.5 ppm) NO,  for  1,  3.5, or 7  hours,  and increased mortality due to exposure to S.  gyogengs
was proportional to the  duration of the exposure.   The mice recovered from the exposure by 18
hours.   To mimic the urban environment,  these same spikes were superimposed on a background of
2,800 ug/m   (1-5 ppm) NO-, 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  NQ_  exposure.   These results are consistent with the long-term studies of this
group using the  sane  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 incidence 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 ug/w3 (0.25 to 0.6 ppm) NO, 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,  ML inhalation affects almost all
of the cell types  within the lung.  Depending, then, upon the concentration of NO,, 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 NO- 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 NO,  inhalation.   Bio-
chemical  studies  indicate that  lung  injury occurs on  inhalation  of NO, 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  wg/m   (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;
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
macrophages, decreased serum antibody and immunoglobins (Ehrlich et al., 1975); as 1,000 ug/m
                                             14-107

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(0.53 ppm)  for 8  br/day  for 180  days in  guinea  pigs as  evidenced by  alterations  in serum
enzymes (Drozdz et  al.,  1975);  and as 1,880 ug/»  (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  gg/m   (0.4  ppm)  NO,  have  no
                                                                       3
alteration in  lung  permeability to serum proteins but do at 1,830 \ig/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  NO..   In most cases,  following the simultaneous
inhalation of  NO- and other  air pollutants,  additive, rather than  synergistic,  effects have
been found.  Tobacco smoking  and occupational  exposure add very significantly to the toxicity
of NO-.   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 NO,  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 Mg/m  (0.05 ppm) with spikes  of 200 ug/m  (0.1 ppm)  (Gardner et al.,
1981).   At 940 ug/m  (0.5 ppm) NO, with  1,880  ug/m  (1 ppm) spikes combined with 0.05 ppm 0,
with  0.1  ppm spikes  or  higher, synergism  between  CU  and  NO-  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 NO, 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 NOg  (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 NO-, studies so far conducted in
animals indicate that  the biological  effects of NO-  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
txposura  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 NO, concentra-
                                             14-108

-------
tions  in  the  atmosphere.   It  is  clear  that  the  lowest concentration  at  which NO,,  in
particular, produces biological effects of a reproducible magnitude so far detected in animals
Is 376  ug/ro  (0.2 ppm).   Repeated exposures to  940  pg/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  NCL  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 NQ^ 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

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14.8  REFERENCES

Acton, J.  D.,  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  SO,  and NO-.
     Ann. Occup.  Hyg. 17:13-16, 1976.                                                *        *

Antweiller, H, K. H. Kompch, and A. Brockhaus.  Investigations on  the  influence of NO- and SO-
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     guinea pigs.  Zb. Bakt. Hyg.  I. Abt. Orig. B  160:212-224, 1975.   (in German)

Aranyi, C., J. Renters,  R. Ehrlich, and D. Gardner.  Scanning electron microscopy of  alveolar
     macrophages  after  exposure  to  0_,  NO-  and 0,.   Environ.   Health  Persp. 16:180,  1976.

Arner, E. C.,  and R. 0.  Rhoades.   Long-tern nitrogen  dioxide  exposure.   Effects on lung lipids
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Arnold,  W.  P.,  R.  Aldred,  and F.  Murad.    Cigarette  smoke activates  guanylate  cyclase  and
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Arnold,  W.  P.,  C.  K.  Mittal,  S.   Katsuki,  and F.  Murad.   Nitric  oxide activates guanylate
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Ayaz, K.  L.,  and A. S.  Csallany.  The effect  of continuous  low level  NO. exposure and dietary
     vitamin E upon lipofuscin pigment concentrations  and glutathione peroxidase  activity in
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Ayaz, K.  L.,  and A. S.  Csallany.   Long  term  NO-  exposure of mice in  the presence and absence
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     1978.                                                                          ~~

Azoulay, E., P. Soler, H. C. Blayo, and F. Basset.  Nitric oxide  effects on  lung structure and
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Balchum,  0. J. ,  R. 0. Buckley,  R.  Sherwin,  and M.  Gardner.   Nitrogen dioxide  inhalation and
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Barnes, J.  H.,  and P. N. Magee.   Some toxic  properties of dimethylnitrosamine.  Brit.  J.  Ind.
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Bils,  R.  F.  The  connective tissues and  alveolar walls  in  the  lungs of normal  and  oxidant-
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Blair, W.  H.,  M. C. Henry, and R. Ehrlich.   Chronic  toxicity of  nitrogen dioxide.   II.  Effect
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Blank,  H.   L., W.  Dalbey,  P.  Nettesheim, J.  Price, D.  Creasia, and  F. Snyder.    Sequential
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Block, W.  N. ,  S. Lassiter, J.  F.  Stara,  and  T. R.  Lewis.   Blood  rheology of dogs chronically
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Braughler, J.  M.,  C.  K.  Mittal,  and  F. Hurad.   Effects of  Thiols,  Sugars, and Proteins  on
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Buell, G.  C.   Biochemical  parameters in  inhalation  carcinogenesis.   In:  Inhalation  Carcino-
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Burch, H.  Methods  for Detecting and Evaluating  Ascorbic Acid Deficiency in Han and  Animals.
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Busey, W.  M., W.  B.  Coate, and D. W.  Badger.   Histopathologic  effects of nitrogen  dioxide
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Cabral-Anderson, L. J,, M.  J. Evans, and G. Freeman.  Effects  of NO- on  the  lungs of rats.   I.
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Campbell,  K.  I.   Effect of Nitrogen dioxide  on swimming endurance  in rats.  Clin.  Toxicol.
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Carson, T. R.,  H.  S.  Rosenholtz,  R. T.  Wilinski, and M.  H.  Weeks.   The responses of animals
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Challis,  B.  C.   Rapid formation of carcinogenic  N-nitrosamines in aqueous alkaline solutions.
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Charles,   J.  H., and  D.  B. Menzel.  Ammonium  and sulfate ion release  of histamine from lung
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Chen, C.,  S.  Kusumoto, and T.  Nakajima.   The  recovery processes of histopathological  changes
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Chow, C.   K.,  C.  J. Dillard, and A.  L.  Tappel.    Glutathione peroxidase  system  and lysozyme  in
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Chow, C.   K.,  and A.  L. Tappel.  An enzymatic protective  mechanism against  lipid peroxidation
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Chow, Y.   L.   Nitrosamine  photochemistry:   reactions of  ammonium  radicals.    Accounts  of  Chem.
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Coate, W.  B.,  and  D.  W. Badger.   Physiological  effects  of nitrogen dioxide exposure  and heat
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Coffin, 0.  L.,  and E. J.  Blommer.   Acute toxicity of irradiated auto exhaust.  Arch.  Environ.
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Coffin,  D.  L.,  and D.  E.  Gardner.   Interaction  of  biological  agents  and chemical air pollu-
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Coffin,  D.  L., D.   E.  Gardner,  and E.   J.  Blommer.   Time-dose  response for nitrogen  dioxide
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Coffin, D. L., D. E. Gardner, G. I. Sidorenko, and H. A.  Pinigin.  Role  of time as a factor  in
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     Effects of intermittent exposure.   J.  Toxicol,  Environ. Health 3:821-828,  1977.


                                             14-111

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Coffin,  D.  L., and  H.  E.  Stokinger.   Chapter 5,   In:   Air Pollution, Vol.  2.   A.  C. Stern
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Committee  on  the Challenges  of  Modern  Society,  North Atlantic  Treaty  Organization.   Air
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Cooper,  G.  P.,   J.   P.   Lewkowski,  L.  Hastings,  and  M.  Malanchuk.   Catalytically  and
     noncatalytically treated  automobile exhaust.   Biological  effects  in rats.   J.  Toxicol.
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Craddock, V. M.   Liver  carcinomas induced  in  rats  by single administration of dimethyInitro-
     samine after partial hepatectomy.  J. Natl. Cancer Inst. 47:899-907,  1971.

Crapo, J. D.,  K.  Sjostrom, and R. T.  Drew.   Tolerance and  cross-tolerance using NO, and 09.
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Craven, P. A.,  and F.  R.  DeRubertis.  Restoration of the Responsiveness of Purified Guanylate
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Creasia,  D.  A.   Stimulation  of DMA  synthesis  in  lungs  of  hamsters  tolerant  to  nitrogen
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Crosby, N.  T.,  and R. Sawyer.  N-Nitrosamines:  a review of chemical and biological properties
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Csallany, A.  S.  The effect of nitrogen dioxide on the growth of vitamin E, deficient,  vitamin
     E supplemented and DPPD supplemented mice.  Fed. Proc. 34:913, 1975.   (Abstr.)

Csallany, A.  S.,  and K.  L. Ayaz.  Long  term NO- exposure of mice  in the  presence and  absence
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Csallany, A. S.,  and K.  L, Ayaz.   The effects of  intermittent  nitrogen  dioxide exposure on
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Dalhamn, T., and  J.  Sjoholm.   Studies on  SO-, NQ^  and NH,:  effect  on  ciliary activity in
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Davidson, J.  T., G. A. Lillington, G. B. Haydon, and K. Wasserman.  Physiologic changes in the
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Donovan, D.  H., M.  B.  Abou-Donia, D.  E.  Gardner,  D. L. Coffin, C. Roe, R. Ehrlich, and D. B.
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Drozdz, M.,  E.  Kucharz,  K. Rudyga,  and T.  Holska-Drozdz.   Studies on the effect of long-term
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Drozdz, M.,  M.  Luciak,  D. Kosmider,  T, Mo1 ska-Drozdz,  K.  Ludyga,  and J.  Pasiwicz.  Enzymatic
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Druckrey, H. ,  R.  Preussnann, G. Blum, S.  Ivankovic,  and J.  Afkharo.  Erseugung van Karzionmen
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Druckrey, H., R.  Preussmann,  S.  Ivankovic, 0.  SchmShl,  J.  Afkhan, 6.  Blum,  H.  D. Mennel, M,
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Ehrlich,  R.   Effects  of  air pollutants  on  respiratory  infection.   Arch.   Environ.   Health
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Ehrlich, R.   Effect of nitrogen dioxide on resistance to  respiratory infection.  Bact.  Reviews
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Ehrlich, R.   Interaction between  NO, exposure  and  respiratory  infections.   In:   Scientific
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Ehrlich, R.   Interaction  between environmental  pollutants and  respiratory  infections.   In:
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Ehrlich, R.,  and J. D.  Fenters.   Influence of nitrogen  dioxide  on experimental  influenza in
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Ehrlich, R., J.   C.  Findlay, J. D. Fenters,  and D. E. Gardner.   Health effects of short-term
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Ehrlich,  R.,  J.  C.  Findlay, and D.  E.   Gardner.   Effects  of  Repeated  Exposures  to  Peak
  "   Concentrations  of NO,  and   0,  on Resistance to  Streptococcus  Pneumonia.   J,  Toxicol.
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Ehrlich, R., and M.  C.  Henry.   Chronic toxicity of nitrogen dioxide.   I.  Effect on resistance
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Ehrlich, R.,  and S. Miller.   Effect of  NO,  on  airborne Venezuelan equine encephalomyelitis
     virus.   Appl. Microbiology 23:481-484, 1972.

Ehrlich, R.,  E.  Silverstein,  R.  Maigetter,  J.  D. Fenters,  and  D.  E. Gardner.  Immunologic
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     ppm) exposure.  Arch. Environ. Health 22:178-188, 1971.

Zorn, H.   Alveolar-arterial  oxygen pressure difference and  the  partial  pressure of oxygen in
     tissues  in  relation to nitrogen dioxide.  Staub-Reinhalt.  Luft.  35:170-175, 1975a.  (In
     German)

Zorn, H.  The alveolar-arterial oxygen-tension differential and tissue oxygen partial pressure
     during exposure to N02-  VIO Bericht 247:50-51, 197Sb,  (in German)
                                             14-126

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                   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  (NO.)  as the  NO   compound  currently  of
greatest concern from a public health perspective.  Human health effects  associated with expo-
sure to  nitrogen  dioxide  (NO,) 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 NO,  are,  within limits, reversible such that  the extent of recovery seems to be a
function of  the degree of exposure,  the  length o   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  NO,,  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/n   (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 NO, concentra-
tions, should include:  increased airway resistance, increased sensitivity to bronchoconstric-
tors, and enhanced susceptibility to respiratory infections (World Health Organiiation,  1977).
This group selected  940 ug/m  (0.5 ppm) as  their estimate of the lowest concentration  of N0_
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 roan  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
NOo  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  NO- exposure  in the  etiology  of this
disease as another  potential  occupationally  related NO  hazard.  That hazard,  first noted in
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
htgh levels of  NO  compounds (especially NO,) 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 NO- 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  NO,  was described by Milne (1969), as determined fron  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  NO,  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
witfi P(A-a)Q2 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.
     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 NO- and other NO  compounds encountered with
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 roost 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 -
induced pulmonary  function  changes discussed below.
15.2.1  Studies of Sensory  Effects
15.2.1.1    Effects of Nitrogen Dioxideon 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 NO, 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 pg/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
NO- varying  from  150 to 500 yg/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 pg/m  (0.16 ppm) had no effect on dark adaptation, time for adaptation increased
significantly as  a  result of exposure  to 500  pg/m  (0.26 ppm).   Repeated daily  exposures to
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
NO, was  used alone  or in combination  with  nitric  oxide  (NO), the higher value reported to be
the minimum effective concentration mav 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  N02  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  NO, to
obtain information  on the lowest concentrations at  which the odor would be  detected immedi-
ately.  The odor  of  NO,  was perceived by thr;ee  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  NO,  in the exposure  chamber was 790 pg/m
(0.42 ppm).

                                            15-4

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TABLE 15-1.   EFFECTS OF EXPOSURE  TO  NITROGEN DIOXIDE ON  SENSORY  RECEPTORS  IN  CONTROLLED HUMAN STUDIES

NO, Concen-
trations
M9/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 NO™
Perception of odor of NO,
Perception of odor of NO,
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 (jg/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 i-ig/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 amber idze,
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 NO-.  At concentrations of up to 20,000 M9/w  (10.6
ppm), perception of  the odor of NO. 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
NO, concentrations as low as 230 \ig/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  NO- 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 jig/m  (27 ppm).  When subjects were exposed to an atmosphere containing 2,260
jjg/m  NO, (1.2 ppra)  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
lig/m  (0.11 ppm) was the lowest concentration at which the odor of NO, 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
reported at levels as low as 140 to 200 \jg/m  (0.08 to  0.1 ppm) and occurred almost immediately
upon exposure.
15.2.1.2  Sensory EffectsDue toExposure to Combinations of Nitrogen Dioxide and Other
 Pollutants—Studies   of the effects  of NO, 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 NO, and sulfur dioxide (SO,).  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
adaptation for  single pollutants  to be 600  ug/m (0.23  ppm)  for SO, and 140 pg/m  (0.07 ppm)
for NO,.  The  thresholds for alteration of  odor perception for subjects  exposed  to a single
                  3                                  "?
gas were  230 pg/m   (0.12 ppm)   for N02  and 1,600 pg/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

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         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 gases
           15 healthy
           subjects
                                   The
5 or 21
rain; oral   adaptation was:   NO,, 140 ug/m
or nasal    SO,, 600 >ig/m  (0.2§ ppm).   Whi
inhalation
    lowest effective concentration for dark
                                (0.07 ppm) and
                            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 jig/m  (0.12 ppm) and S02,
1,600 |jg/(ti  (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
Various Not
mixtures reported
of NO
so2> R2so4
aerosol
and NH,
•3
Not
reported




Lowest effective concentrations for odor per-
ception of a combination of gases were reported
to be: NO 20 ug/m (0.01 ppm); SQ? 170 ug/m
(0.06 ppm)* H?S04,aerosol , 110 g/m (0.03 ppm),
and NH,, 300 pg/1 (0.43 ppm). When inhaled
together the odor was perceived whenever the
fractional threshold totaled 1.0 or more.
Kornienko,
1972




Mixture    Four          Not       Threshold  for  changes  in  the  amplitude of alpha
of NO ,                reported    rhythms occurred when  the sum of the .fractional
S02, NH.,                          concentrations of  the  individual gases equaled
H.,50.                              1.0  or more.
                                                                                    Kornienko,
                                                                                    1972

-------
lowest  NO,  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,,  SO-,  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 theEffect of Nitrogen Dioxide on Pulmonary Function in Healthy
Subjects—Controlled experimental  studies in  the laboratory situation  have  been mostly con-
cerned with  exposure to NOj 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 NO, are summarized in Table 15-3.
     Nakamura (1964) determined the effect of exposure to combinations of NO, and sodium chlo-
ride aerosol  (mean diameter 0.95 pm)  on airway resistance (R,..) measured by an interruption
                                                              3W
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 ng/m  sodium chloride aerosol alone.  After resting for 10
to 15  minutes,  individual subjects were exposed for 5 minutes to different NO, concentrations
                        3
ranging from 5,600 pg/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
exposure to  the  NO,  alone, but the  sodium  chloride aerosol alone exerted ho effect on airway
                                                                                3
resistance.   Nitrogen  dioxide alone at concentrations of  5,600 and 11,300 pg/m  (3.0 ,and 6.0
ppm) caused  increases  in R... of 16 and 34 percent, respectively, in the one subject tested at
                           aw
each concentration.
      Von Nieding  et al.  (1970) reported, at the Second International Clean Air Congress, the
results of exposures of 13 healthy  subjects  to  an NO, 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 (PaO,) was induced,
but  the end expiratory  oxygen  partial  pressure (PaO,) 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 NO.
may  have  interfered with  the transfer  of  oxygen from alveolar air  to arterial  blood.   This
                                            15-8

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TABLE 15-3.   EFFECTS OF  EXPOSURE  TO  NITROGEN  DIOXIDE ON PULMONARY FUNCTION
                 IN CONTROLLED STUDIES  OF  HEALTHY  HUMANS**

Concentration Pollu-
ug/m
13,000
9,400
9,400
9,400
7,500
to
9,400
5,600
11,300
ppm tant
7.0 N02
5.0 N02
5. 0 K02
5.0 N02
4.0 NO,
to i
5.0
3.0 N02
6.0 N02
No. of
Healthy Exposure
Subjects Time Effects
Several 10-120 Increased R * in some subjects. Others
rain. tolerated 30,000 yg/m (16 ppm) with no
increase in R_. .
9W
11 2 hrs. Increase in R * and a decrease in AaDO,*
with intermittent light exercise. No,en-
hancement of the effect when,200 ug/m
(0.1 ppm) 0, and 13,000 ug/m (5.0 ppm)
SO- were combined with NO, but recovery
time apparently extended.
16 15 min. Significant decrease in OL-.,*
13 15 min. Significant decrease in PaQ,* but end ex-
piratory Op * unchanged with significant
increase in systolic pressure in the
pulmonary artery.
5 10 mfn. 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.
Reference
Yokoyama ,
1972
Von Nieding
et al.,
1977
Von Nieding
et al., 1973
Von Nieding
et al. ,
1970
Abe, 1967
Nakamura,
1964
                               (continued)

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                                               TABLE  15-3.   (continued)
         Concentration   Pollu-
          ug/m     ppm    tant
 No.  of
 Healthy  Exposure
Subjects    Time
Effects
Reference
tn
i—»
o
         14,000    7.5    N02



          9,400    5.0    N02





          4,700    2.5    N02
  16       2 hrs.    Increased sensitivity to a bronchocon-
                    strictor (acetylcholine) at this concen-
                    tration but not at lower concentrations.

   8      14 hrs.    Increase 1n R   during first 30 rain,  that   Beil and
                    was reduced through second hour followed    Ulmer, 1976
                    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 1n
                    arterial P02* pressure or PC02 pressure.
1,880
1,880
1,300
to
3,800
1,150
1,880
to
3,760
1.0 N02
1.0 N02
0.7 NO,
to i
2.0
0.6 N02
1.0 NO,
to i
2.0
8 2 hrs. No increase in R .
aw
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 2^ hrs. Alternating exercise and rest produced
statistically significant decreases for
hemoglobin hematocrit, and enythrocyte
acetylcholinesterase.
Bell and
Ulmer, 1976
Hackney, et al
1978
Suzuki and
Ishikawa,
1965
Folinsbee
et al., 1978
Posin et al. ,
1978
                                                      (continued)

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TABLE 15-3.   (continued)


Concen
Mfl/m
1,000
1,000
with
560
1,000
with
560
and
45,000
500
500
with
560

500
with
560
and
45,000

t rat ion
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

Pollu-
tant
03
°3
v)
N02
°3
•3
NO,
£
CO
03
°3
.3
NO-

0,
3
NO,
C
CO
No. of
Heal thy Exposure
Subjects Time Effects Reference
4 4 hrs. With each group minimal alterations in Hackney
pulmonary 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.
(~ tm





7 2 hrs. Little or no change in pulmonary function Hackney
found with 0, alone. Addition of NO, or et al.,
of NO™ 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)
01
I


ISJ
No. of
Concentration Pollu- Healthy Exposure
ug/m ppro tant Subjects Time
100 0.05 N0? 11 2 hrs.
with
50 0.025 0,
and
300 0.11 S02
Effects
No effect on R * or AaDO,*; exposed sub-
jects showed increased sensitivity of
bronchial tree to a bronchoconstrictor
(acetylcholine) over controls not exposed
to pollutants.
Reference
Von Nieding
et al . , 1977

* R airway resistance
AaDO- difference between alveolar and
DLCO diffusion capacity of the lung

arterial blood partial pressure of oxygen
for carbon monoxide



PaO. arterial partial pressure of oxygen
P0» partial pressure of oxygen


PC09 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   (AaDO-)
was  accompanied by  a  significant  increase  in  systolic  pressure in  the... pulmonary  artery,
However, the significance of the changes in  A-aPO»  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 NO- 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 pg/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».
                   31W            £.
     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
pg/m3  (5.0  ppm) NO, (Table  15-3).    Abe  (1967)  found  that concentrations  of  7,500  to 9,400
    3
pg/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-
jects  exposed to  NO- concentrations ranging from 1,300 to 3,800 pg/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  pg/m  (5.0 ppm) was not increased by the addition of ozone XO,) to the
                                                        3                                    3
experimental atmosphere  at a concentration of 200  pg/«  (0.1 ppm) or  by adding 13,000 pg/m
(5.0 ppm)  SO-  to  the  N02/0- combination.   When 0, 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 NOg 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 NO, 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  SO- but
not  of  NO,,  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)  NOp monitored by  a continuous  chemiluminescence technique
(Table 15-3).  Pulmonary  measurements included;   ventilatory volume (V^);  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 (0^) 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^g) and closing volume, with slow vital  capacity (VC).
     Hackney et al.  (1978)  found no  statisically   significant  changes  in  pulmonary function
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.
                            3W
     8e11 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 NO- at concentrations of 4,700 ug/m
(2.5 ppm)  or above,  these investigators measured significant increases in R   compared to the
                                                                            3W
controls,  but  no  decrease  in  PaO-   or  increase  in   PaC02-    Airway  resistance was  not
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
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

-------
exposure to 4,700 or 9,400 ug/m  (2.5 or 5.0 ppm).  When the duration of exposure was increased
from 2  to 14 hours,  9,400  ug/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 S, 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  N0_.   The subjects  alternated  15  minutes of exercise
(double resting ventilation) and 15 minutes of rest.   The ambient NO, levels were 1880 or 3760
    3                                                               *
pg/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 vg/m  (2 ppm).  These investigators concluded that
significant blood biochemical  changes resulted from  NO.  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)  itn  a study on eight subjects  exposed to 340
|jg/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 yg/m
(0.5 ppm)  NO-.   One subject experienced the very mild symptom of slight rhinorrhea.  Although
the authors suggest that the changes reported in quasistatic compliance may be due to chance
alone,  there is  uncertainty  whether these changes were due to daily variation or to NO- 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
                   •33                                  o
of NO,  at  100  vg/m  (0.05 ppm), 0,  at 50 ug/m   (0.025 ppm),  and SO, at 300 gg/m  (0.11 ppm)
for 2 hours, no effect on R   or AaDO- was reported (Table 15-3).  Exposure to this combination
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  Rflw.  Constriction  of the
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
pg/m ;  0.5 ppm)  and subsequently to mixtures of 0, and NO- (560 pg/m ; 0.3 ppm) or 0^, NOg and
                                            15-15

-------
CO  (45,900  pg/m ; 30  pprn)  (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
           etW                                                                  w
alterations were  not  increased  by the additions of NO-  or of NOg and CO.   Another group of
seven male  volunteers,  including some believed to  be  unusually reactive  to respiratory irri-
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 ug/m ; 0.3 ppm) or of NO, plus CO (45,900 yg/m  ; 30 ppm).
     Schlipkoter and  Brockhaus  (1963)  determined,  in three  subjects,  the  effects of exposure
to  NO,, 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 MS/1"  (4.8
ppm) NO,, 55,000  ug/m  (50 ppm) CO,  or 13,000 pg/m  (5.0 ppm) SO, 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  SO,  exposure,  50  percent  of   the  dust was
retained.    Retention  increased  to approximately 76 percent  when  the dust was administered in
an  atmosphere containing  9,000  ug/m   (4.8 ppm) NO,.  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 NO, exposures  of short duration.
The study suggests that,  as NO,  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 NO, and sodium chloride aerosol indicated
that sodium chloride  aerosol  had no influence on R  .  When the sodium chloride aerosol (mean
diameter 0.95 urn)  was added to the exposure  atmospheres,  the increases in R   for the group
                                                                              clVr
were approximately 40  percent,  about twice that produced by the gas alone,   A sodium chloride
aerosol comprised of  smaller  particles (mean diameter 0.22 urn) at 1,400 pg/m  , in combination
with the  same  concentrations  of NOg, produced  no increase in R   over that caused by the gas
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 Nad  aerosol  particles averaged  95 urn  in diameter but  did not
                3W
Increase R   when they averaged 22 pm in diameter indicates that when used in the same sequence
          aw
the larger  particles  of NaCl  enhanced the  effect of NO, 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 NO,  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
                                                                              ctw
breathing using a  body  plethysmograph with a temperature  compensation  mechanism.   Most Amer-
ican  investigators have  used constant-volume  body plethysmographs and measure R    during
                                                                                    clW
panting (DuBois,  1956).   Investigators  in this  country also measure arterial partial  pressure
of  oxygen  (PaO,)  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 PaO™.
     Horvath and  Folinsbee (1979) exposed eight young  adults to either filtered air or 980
jjg/m  (0.5 ppm) 0, plus 940 yg/m  (0.5 ppm) N0_ 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 fninutes.   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 NO, on pulmonary  functions  in  healthy volunteers
(Table 15-3)  indicate  that  exposure  of 2  hours  or less  to concentrations  of less  than 4700
pg/m  (2.5  ppm) can induce increases in R   (Beil and Ulmer, 1976).  The lowest concentration
                                                                                             3
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 NO-, 0,,  and SO- 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 NO. at a concentration of 9,400 pg/ffl  (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  0_, 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

-------
TABLE 15-4.  EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON PULHONARY FUNCTION
                 IN CONTROLLED STUDIES OF SENSITIVE HUMANS

Concentration
pg/ra ppm
9,400 5.0
3,800 2.0
to to
9,400 5.0
940 0.5
to to
9,400 5.0
940 0.5
190 0. 1
No. of Exposure
Subjects Time
14 chronic 60 mins.
bronchitics
25 chronic lOmins.
bronchitics
63 chronic 30
bronchitics inhala-
tions
10 healthy 2 hrs.
7 chronic
bronchitics
13 asthmatics
20 asthmatics 1 hr.
Effects
No change in mean PAD.*, during or after expo-
sure compared with prB-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
Aa002* at 7,500 pg/m (4.0 ppn) and above; no
significant change at 3,800 pg/m (2.0 ppn).
Significant increase in R * above 3,000 ugm/
(1.63pp«); no significant effect below 2,800
(jg/m (1.5 ppm).
1 healthy and 1 bronchi tic 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 quasi static compliance when
analyzed as a single group. See pp. 15-28.
Significant increase in SR *. Effect of bron-
choconstriction enhanced after exposure in 13
of 20 subjects. Neither effect observed in 7
of 20 subjects.
Reference
Von Nieding
et al, 1973
Von Nieding
et al . , 1971
Von Nieding
et al., 1971
Kerr, et al. ,
1978
Orehek, et al. ,
1976

*PAO_ : alveolar partial pressure of
R : airway resistance
3w
SR : specific airway resistance
oxygen AaOO-: difference between alveolar and arterial
blood partial pressure of oxygen
PaO« : arterial partial pressure of oxygen

-------
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 pg/m  NO,
                                                                   3w                        c.
(0.5  to 5.0  ppm)  and 25 for PaO~,  PAO~,  AaDO-,  similar measurements for CO-, and other para-
meters at 3700, 7500 and 9400 pg/m  (2,0, 4.0 and 5.0 ppm).   Significant elevations in R   (p
                                                                    3
< 0.1) were  seen  after  exposure to N0~ concentrations of 3,000 pg/m  (1.6 ppm) and higher for
30 inhalations  or approximately 3  minutes  (Von  Nieding et al., 1971).  This increase became
more  pronounced at  concentrations above  3,800  pg/m   (2.0  ppm),  and  disappeared  completely
                                   •3                                             3
below concentrations of  2,800  pg/nr (1.5 ppm).   At levels of 7,500 to 9,400 pg/m  (4.0 to 5.0
ppm), subjects  showed a  significant decrease in PaO, and an increase in AaDQ,; no significant
                             •»                      *                        *
effect was found at 3800 pg/m  (2.0 ppm).
     Kerr et al.  (1978)  studied the effects of  2  hours of exposure to NO, at a concentration
           3
of 940 pg/m   (0.5  ppm)  on 7 chronic bronchi tic 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 NO..  Seven of 13 asthmatics reported sdme 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, plethysraography,  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 NO,
              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 NO- 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  pg/m  (7.5 ppm)   NO,  but not  after 2-hr
                                3
exposures to  4700 or 9400 pg/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 pg/m  (5.0 ppm) NO,.
     Orehek et  al.  (1976)  studied  the effects of  low levels of N0~ 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
                                                                            9W
the subjects  inhaling carbachol after  a 1-hour exposure 10 clean air and, on other  occassions,
after  a  1-hour exposure to  190 ug/m  NO.  (0.1 ppm).  Following NO- exposure alone, slight or
marked increases  in SR   were  observed  in  only  3 of 20 asthmatic test subjects; however, NO.
                       aw                                                                    c
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-
                                                                   3W
jects  was  significantly decreased from 0.66 mg to 0.36 mg as  a result of NO. exposure.  Seven
of the asthmatic subjects showed neither an increase in R    in response to the exposure to NO.
                                                         3W                                  t
alone  nor an  enhanced effect of NO.  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-
                                                   oW
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
                                                                                    oW
responders before  and  after the NO.  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
                              *                                9W
after  NO.  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-
•choconstn'ctive responses being produced in some asthmatics by very low concentrations of NO..
These  results,  however, do  not provide conclusive  evidence  of adverse responses attributable
to  NO.  exposure,   especially   in  view  of  some  of the  reported statistically   significant
NO.-induced  changes not  being markedly  different  in average  magnitude  to  changes  in R
  £                                                                                         ow
apparently due to  individual variations in lung  function  in  the absence of NO..    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 N02 alone.  However,  the mean of measurements
of  R ., in 13 responders to the  carbachol  treatment  was  significantly  higher  after  the NO,
    oW                                                                                      ^
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  NO-  exposure, but
                     oW                                                       £-
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 NO.,  clouding  interpretation of  how  the  observed
effects might relate to  asthma  attacks  under ambient conditions.  The  study  may have health
                                            15-20

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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 NO,.  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  SO, but not NO- and, for this reason, concluded that NO- did not
act by stimulating  the  vagus nerve.   It thus  remains  to be determined as  to  what concentra-
tions of NQ_  may  produce  significant broncoconstriction or other pulmonary mechanical effects
in asthmatics under ambient exposure conditions.
     Another  suggestion  that measurably greater  impact of  exposure to NO- 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, », 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 NO-, although this seems to be a good possibility.
It also is  not known how these  study  results  relate to ambient NO-  exposures of individuals
who are highly reactive to methacholine.
     Thomas  et  al.   (1972)  showed  no effect  of exposure  to NO, at concentrations  of 940 to
          3
6,580 pg/m   (0.5  to 3.5 ppm) on histamine concentrations in sputum or on total sputum weight,
in  five  healthy  subjects,   or  four  patients  reported  to  have chronic  respiratory disease.
     In summary, studies of NO- 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  PaQ-  and  increases in AaDO,, whereas  exposures to concentra-
                              3
tions of NO,  above 2,800  yg/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
individuals differ  very little.   In contrast, in  one  study, exposures to 190 \ig/m  (0.1 ppm)
NO-  for  1 hour were reported  to  have increased mean R    in  3 of 20  asthmatics  and to have
  IL.                                                      OW
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 pg/m   (0.5 ppm)  NO-.   Thus, whereas
NO, exposures  sufficient  to produce increased R    in  healthy  individuals  or those with symp-
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  NO, exposure levels below  those affecting normal,  healthy adults.
                                            15-21

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15.3  EPIDEHIOLOGICAL STUDIES
     Epidemiological 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 NO. 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 NO^-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
NO,.  Still  other  study  results can be questioned on the basis of how representative reported
aerotnetric results are of  actual N0» exposures  of  study  populations.   For these reasons, the
contributions of pre-1970 community air pollution studies to knowledge concerning NO. 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 NO-  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 NO, and  respiratory  diseases in  children.
15.3.1  Effects of NO,, on Pulmonary Function
     Among the  better known  studies evaluating N0--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 N0_ concentrations than for children living
in areas with  lower  NO- concentrations.  However, measurements  of NO, 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

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be unreliable  and not  acceptable  for deriving  quantitative  estimates of NO-  levels  present
in the 1968-69  Chattanooga  study areas,   in view of  some  overlap between NO- levels reported
for  certain  monitoring  sites in  the "high"  NO, pollution  study areas  and NO,  levels  for
some  monitoring  sites  in  the  lower  NO,  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 epidenriologicaT studies in various geographic  areas  have
attempted to provide quantitative assessments of pulmonary  function changes in relationship to
ambient air NO, levels.  These studies, using a more acceptable NO, 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 N0_ concentrations determined from 1-hour
                                                                 2
sampling data, measured  by  the Saltzman technique,  were 100 pg/m  (0.055  ppm) in the downtown
urban area, and 75 pg/m  (0.04 ppm) in the suburban area (Speizer and Ferris, 1973a).   Sulfur
                               3                                    3
dioxide levels averaged 92 pg/m  (0.035 ppm) in the city and 36 pg/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 NOj  concentration  in the  Los Angeles  basin was  96  pg/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 pg/m  (0.1 ppm).  In San Diego, the average and
ninetieth percentile were, respectively,  43 and 113 pg/m  (0.02 and 0.06 ppm) based on Saltzman
method measurements.
     Linn et al.  (1976) performed  a variety of pulmonary function tes'ts 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 N0_ was provided as well.  Most results of FEV, single
breath N» 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 0^) 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
concentrations based on the Saltzman method were 130. and 65 pg/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 pg/m   (0.13 and 0.06 ppm) for Los Angeles and San Francisco, respectively.

                                            15-23

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                      TABLE 15-5.  QUANTITATIVE COMMUNITY HEALTH EPIDEHIOL06ICAL STUDIES OH EFFECTS
                                  OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION
IN5
-pi


Measure
High exposure group:
Annual mean
24-hr concentrations

90th percenti le
Estimated 1-hr
maximum

Low exposure group:
Annual mean
24-hr concentrations
90th percent! le
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


NO
Cone
pg/

96


188
480
to
960

43

113
205
to
430
103
92


75
36

260
to
560
110
to
170
2 Exposure
entrations
m ppra

0.051


0.01
0.26
to
0.51

0.01

0.06
0.12
to
0.23
+ 0.055 <
S0_ 0.035
so
£»
+ 0.04 +
SO, 0.014
SO,
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)




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



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                                               TABLE 15-5.  (continued)



Measure
Los Angeles:
Median hourly NO,
£.
90th percent!" le NO,
L.
Median hourly 0
90th percent! le QX
San Francisco:
Hedian hourly NO,
f-
90th percent! le N02
Median hourly 0
90th percent!" le 0
1-hr concentration
at time of testing
(1:00 p.m.)

N0?
Conce
pg/m

130

250



65

110


40
to
360

Exposure
gtrations
ppm

0.07

0.13
0.15
0.15

0.35

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
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 wanner part of the year
(April -October) NO,, S02 and
TSP* significantly correlated
with V * at 25% and 50% FVC*


Reference

Linn, et
al., 1976









Kagawa and
Toyama ,
1975

                                                         and wifn^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 cl?l? delineation of specific
                                                         pollutant concentrations at which
                                                         effects occur.
bEstimated at 5 to 10 times  annual mean 24-hour averages
 Mean "annual" concentrations  derived  from 1-hour measurements using Saltzman technique
*|EVp j^:   Forced expiratory volume, 0.75 seconds
  max   :   Maximum expiratory  flow rate

 FVC    :   Forced vital  capacity

 TSP    :   Total  suspended particulates

-------
     In a Japanese investigation, relationships of ambient temperature and air pollutants (NQ_,
NO, 0,,  hydrocarbons,  SO,,  and participate matter) to weekly variations in pulmonary function
1n 20  school  children, 11 years of age, were studied in Tokyo by Kagawa and Toyama (1975) and
Kagawa  et  a~l. (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 ($_,„} at 25 and 50 percent of FVC.  in children believed by the investigators to be sen-
       ntax
sitive  to  air pollution,  a significant negative correlation was  observed between exposure to
0, and specific airway  conductance;  other  negative  correlations were found between NO- (as
measured by the  Saltzman  technique),  NO, SO,, and particulate matter, with V_,v at 25 percent
                                            £                                FOaX
or 50 percent FVC.   At high outdoor temperatures NO,, SO,, and particulate matter were signifi-
cantly  correlated  (negatively)  with both V    at  25  percent or 50 percent  FVC,  and specific
                                           fiioX
airway conductance (p < 0.05).
     In the ambient  situation,  however, the above effects were not associated with NO, alone,
but with the combinations of air pollutants, including SO-, particulate matter, and 0,.  During
the period of high outdoor temperatures, correlations between lung function and NO, concentra-
tions  were calculated using  the pollutant  level  in the  ambient air at  the time of testing
(1:00  p.m.).  These  hourly  NO- values ranged from 40 to 360 ug/m  (0.02 to 0.19 ppm), but the
data reported afforded no quantitative estimation of specific NO, levels that might have been
associated with  the  occurrence  of pulmonary function decrements.   The authors (Kagawa et a!.,
1976)  noted that:   "From  the relationship between NO,  and V  „ at 50% FVC in subject No. 16,
                                                      £,       l1i9X
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 NO, 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
NO, concentrations, measured  by the Saltzraan method, ranged  from 300 to 1,130 ug/m  (0.16 to
                                                                           '    3
0.60 ppm).   Highest  measured NO- concentrations ranged  from 340  to 3,000 M9/m  (0.18 to 1.60
ppm).   Test results [VC, FEV-, «, maximal flow rate (MFR) and mid-maximal flow rate (MHFR)] 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
NO, concentrations in their work areas.
     Results  of  epidemiological studies on  the  effects of outdoor ambient  air  NO- exposures
provide no consistent  indication that the mean concentrations of NO- or of NO, in combination
with other pollutants listed in Table 15-5 had any significant effects on lung function in the
                                            15-26

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exposed populations.  One  study  did show some apparent  associations  between V    or specific
                                                                               m2X
airway conductance  and  concentrations  of NO* 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 NQ0 on Acute Respiratory Illness
15.3.2.1   Effects Associated With Ambient Exposures—Only  a  few  community  epidemiological
studies  of outdoor  NOX exposures  have  been  reported  as  demonstrating  associations  between
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 NO,  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-NQ,  exposure neighborhood  than in the  intermediate-  and 1ow-NO, areas.  However,
in this study,  N0_ concentrations were  determined by the Jacobs-Hochheiser method and, as indi-
cated earlier, this method has since been shown  to  be unreliable (Hauser  and Shy,  1972; See
Chapter  7  for  a  more complete discussion).   Meaningful quantitative  estimates  of population
NO, exposures were therefore not available for the study areas;  also, overlaps in reported NO-
levels between  "high" N02 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 NO- 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 NO, 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 sane  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

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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  NO-  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 NO, 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 NO, 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
NO,  exposure  gradient (presumably based on  use of the Jacobs-Hochheiser NO-  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 reside/its 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  ug/m  (0.31  to 0.64 ppm); SO-,
        3                                         3
225 ug/m   (0.09 ppm);  and sulfuric acid, 400 \ig/m  (0.1 ppm).   The report also indicated that
a NOj  concentration  of 1,600 ug/m   (0.85  ppm),  combined with high  concentrations  of  SO-  and
sulfuric acid,  occurred  1 kilometer from the plant.   However,  no information was provided on
the methods used  to  measure NO-  or  by which to assess the relative contribution of NO- 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 NO- 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 NO-,  100  ug/m   or 0.053 ppin 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 N0_ levels associ-
ated with reported health effects.

                                            15-28

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     Petr and  Schmidt  (1967)  studied acute respiratory illness  among  Czechoslovakian 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 NCL  and  SCL-   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 NO, individually were not presented.   Nor was information provided
on the sampling frequency or methology for NO or NO- 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 NO,.  Norman and Keith (1965) demonstrated that the
                                               3               fi     3
concentration  of  NO may vary between  492 x 10  and  1.23 x  10  ug/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 NO, could not be measured in the cigarette smoke but,  in other instances,  concentrations
                       3
as high  as  47,000  ug/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  NO, in cigarette  smoke,  the increases in
some  adverse health  parameters point  strongly in  this  direction.    Specific  health effects
possibly  related  to exposure  to  NO,  in  cigarette  smoke include  increased  acute  respiratory
illnesses or prevalence of chronic respiratory disease.
                                            15-29

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15.2.2.2.2   Epidemi'ologi'cal  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 NO, 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  NO-  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  1s 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  NO-  levels  than
those with  electric stoves.   For  example, Wade  et al. (1975)  reported  that, over a  2-week
period,  the  average  concentration  of NO,  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)  NO, for 2 hours were  measured  in the kitchen.   Other studies of NOg concen-
trations in  homes during the  preparation  of meals have demonstrated  that gas stoves produce
N0» 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 NO, 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

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  lABLt 15-6,   IFfECIS Of  EXPOSURE  10  NHRQGEN DIOXIDE  IN  lilt  HOME  OH LUNG FUNCTION AND
THE INCIDENCE  OF  ACUTE RESPIRATORY  DISEASE  IN EPIDEMIOLOGY  STUDIES  OF HOMES HUH CAS SIOVES
Pollutant*
NO*
Concentration
ug/rn3 ppm
Study
Population
Effects
Reference
Studies of Children
NO. plus
other gas stave
combustion products
NO, plus other gas
stove combustion
products
NO, plys other
gas stove
combustion
products
NO, plus other
gal stove
combustion
products
NO- concentration
not measured at
time of study
NO, concentration
not measured in
sane hones 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 percent! le of 24 hr
avg in activity roorn
39 - 116 ug/«T (.02 -
.06 ppia) (gas) vs.
17.6 - 95.2 ug/B
(.01 - .05 ppin)
(electric). Frequent
peaks ~ 1100 ug/ai (0,6
ppmj-jmax peak - I860
M9/m (1.0 ppi»I 24 - hr
by modified sodium
arsenite; peaks by
chemi luminescence
2bb4 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 yi's 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 ;Q. 10;
boys not sig.) after controlling
for confounding (actors.
Higher incidence of respiratory
sy»pto»s 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 NO. 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 aye 2 and use of
gas stoves (p <.01) and, also,
between lower ftV, FVC levels
and use of gas stoves (p <.01)
Helia et al., 1977
Helia et al. , 1979
florey et al, , 1979
Companion paper to
Kelia et al., 1979;
Goldstein el al. ,
1979
Speuer et al., 1980
Spengler cl al. , 1979

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TMIE 15-6 (continued)
Pollutant*
HO, plus other
gat Steve
combustion
products
NO. plus other
gas stove
combustion
products
NO,
Concentration
Vg/m* ppn
Sample of households
24 hr avg: go. (.005 *
.11 Pfw); electric
(0 - .06 pprn); outdoors
(.015 - ,05 ppn);,several
peaks > 1880 ug/«r (1.0
pp«). Monitoring location
not reported. 24-hr avgs
by sodium arsenite; peaks
by chemi luminescence
Sample of sane
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 reporttd respiratory See also Keller et al.,
illness between homes with gas 1979a
and electric stoves In children
fron birth to 12 years
No evidence that cooking mode Keller et al.. 19?9b
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
ga! stove
combustion
products
NO, plus other
gas stove
combustion
products
Preliminary measure-
Bents peak hourly
470 - 940 ug/«J
max 1880 jjg/m
(1.0 ppn)
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 vith
gas stoves, compared to
those cooking with electric
stoves. 146 households
Members of 441 households
Members of 120 households
(subsaiaple 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 yj electric 1979*
cooking homes
No significant difference among Keller et al,, 1979b
adulU in acute respiratory
disease incidence in gas vs
electric cooking homes

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     Two independent sets of epidemiological studies, ifrom 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 Helia 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 Helia  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

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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 1n 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 NCU  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
stove.  The average hourly concentration of NO, in gas kitchens was 135 ug/m  (0.072 ppm), and
                                    3
in electric kitchens  it was 17 (jg/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 NCL in the home.   However, because
NO, 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

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     Possible  interrelationships  between  NO.  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  N0_  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.   NO, 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,
                                       3                                              3
in kitchens ranged  from 10 to 596  pg/m   (0.005  to 0.317 ppm)  with a mean of 211 pg/m  (0.112
ppm), and levels in bedrooms ranged from 8 to 318 pg/m  (0.004 to 0.169 ppm) with a mean of 56
pg/m  (0.031 ppm).  In homes with electric stoves, levels of NO, in kitchens ranged from 11 to
        3                                            1
353 pg/m  (0.006 to 0.188 ppm) with a mean of 34 pg/m  (0.018 ppm), and in bedrooms NO, levels
                         3                                             3                   -
ranged  from 6 to 70 pg/m   (0,003  to  0.37  ppm)  with a mean  of  26  pg/m  (0.014 ppm).  Outdoor
levels  of  NO,  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 M).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 (FEV,, ,,-> 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 NOo generated by  the use  of gas.  The  authors  note, however, that the  NO,  levels wight
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

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with gas  facilities  had higher levels of NO,  than  were present in the  outdoor air,  reaching
double  the  outdoor concentration  in some  instances.   Indoor annual average  values  in these
houses were  as  high  as 80 pg/m   (0.04 ppm).   Short-term  peak levels in excess of 1,100 pg/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 Helia et  al.  (1977),  but have more importantly removed
the  primary  objection  to  the  earlier Helia  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 NO, 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. _,.  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 NO,  concentrations in homes
with gas  stoves were  as much as  8  times higher than the 24-hour mean and sometimes exceeded
1,880 pg/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
NO,  concentrations  reported, it  can  be determined  that peak  (15-min)  NO,  concentrations in
                                                           3
most homes with gas stoves ranged between 75 and 1,650 ug/in  (0,04 and 0.88 ppm).   The average
peak value would  have  been approximately 750 pg/m  (0.4 ppm).   In homes with electric stoves,
the mean NQ~ 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

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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 NO- 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  NOj,  NO;  and  SO-,  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 NO,
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 NO, 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 vith that of 140 suburban patrol car officers.
The  exposure  of each group to NO, 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 smokers but
not among ex-smokers.   Estimates of annual mean pollution levels,  based on approximately 1,000
hourly samples  (Burgess et al.,  1973),  were,  for  the  urban area, 103 pg/m   (0.055  ppm)  NO,
                                              3                       •
together with  SO,  concentrations  of  90  ug/m    (0.05  ppm); the  NO, concentrations  for  the
                                3                                                      3
suburban area  averaged  75  pg/m  (0.04 ppm)  and SO,  concentrations  averaged   26  pg/m  (0.01
ppm).
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     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 NO, concentrations of approximately 40 to 4i 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  ug/m   (0.13 ppm),  over  that occurring in San  Francisco women  where the
median hourly concentration  of NO, 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 NO- 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  (SHSAs) during  1959 to 1961 and  from  1961 to  1964.
Included  in the  analyses were  NO-,  SO-,  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.
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     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, NOX),  but no association in sunner.  In contrast,  the winter mortality of persons 45
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 Oxidants.  (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 0,  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 NO-  or other
oxides  of nitrogen.   Data  from  such  exposures  or  other  accidental  exposures,  as  those
encountered with  certain fires,  provide some  indications  of NO   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  NO,.
Lowry  and Schuinan  (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.
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Concentrations of NO,  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 NO, poisoning from silage gas estimated at
                        3
560,000 to  940,000  ug/m  (300 to 500 ppm) NO-.  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 ug/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 ug/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,  NO-, 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 conditions, 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  HQ~ 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,
policemen,  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  ug/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 NO-.  They reported that lipid metabolism was impaired subsequent to the
original NO,  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 NO-  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 NQX-QERIVED  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.
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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  water  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 ug.  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
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 NO ,  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

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     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 aer*sol  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
                                                                            aw
carbachol.   Subjects  were  exposed  for  16 minutes  in a double-blind manner  to either sodium
nitrate (NaNO,) or sodium chloride (aerodynamic diameters 0.49 ym, og = 1,7, and 0.46 urn,  og =
                                                    3
1.7, respectively) at a concentration  of 7,000 ug/m .  Following exposure, subjects inhaled a
predetermined  quantity  of  carbachol sufficient  to  increase R   20 to  30 percent.   Prior to
                                                               oW
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,
                                                                                      aw
FEV, „, 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  asthirtatic  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  m'ild  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 NaNO,, (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 jjg/m  .  Eleven previously
healthy adults with uncomplicated influenza A (H,N,) 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
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for exposed  individuals  depends  ypon 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  NO- (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
(Oanke  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 pneutnonitis
(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 pg/kg  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-, dlethyl-, 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 i_n vivo nitrosatlon of secondary amines, contained in the diet, to
                                      15-44

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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  in  vivo formation of nitrosamines in humans or that inhaled nitrosamines repre-
sent significant health hazards.  Questions have been raised as to j_n vivo nitrosation by NO,,
Iqbal et al.  (1980)  have reported that,  indeed,  i_n  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 NC^ (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, N02 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
eta!., 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,
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15.6  SUMMARY AND CONCLUSIONS
     Critical  NO   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, NQ« 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  NO,  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 NO, 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 NO. 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  NO,  exposure in  controlled human  studies (usually at
concentrations higher  than  ambient) include  increases in airway resistance  (R,..) and changes
                                                                               «W
in susceptibility to  the effects of bronchoconstricting agents.  Functional response of human
subjects to NO, 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

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     Increased  airway  resistance  (R   )  and other  physiological  changes suggesting  impaired
                                    aw
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  aVso
indicate that significant  effects  occur  in healthy subjects with shorter (5-15 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
             3                                                                 '
to 3760 ug/m (0.7 to  2.0 ppa) for 10 minutes.   Their data however,  preclude a clear associa-
tion of observed effects with any particular concentration in the range of  1300 to 3760 pg/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 ppn) NO-  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) NO,, respectively;  and in a similar  study,  where Kerr et al. (1979) exposed 10 healthy
                  3
adults  to 940 ug/m   (0.5 ppm) NO- 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 NO,
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 p'pm 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-
choconstrictor  (acetylcholine)  observed  by von  Nieding et al. (1977) at 94  ug/m  (0.05 ppm)
                                 3                                  3
NO-  in  the  presence of 49 ug/m  (0.025 ppro) ozone and  290  ug/m  (0.11 ppm)  SO-.  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  NO,
                      3
levels below 1880 yg/m   (1.0 ppm) for healthy adult subjects.
                                      15-47

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     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 NO, below 2.0 ppra;  nor
                      aw                                                   £.
have controlled  exposure studies  investigated  long-term effects  of repeated  NO-  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 POp gradient, or as  a
reduction  in arterial POp  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  NO- 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 NO- 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
                   aw
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 NOp  levels at or below those associated with significant increases
in R   can increase susceptibility to respiratory infections.
    3W
     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 NOp concentration  that  would cause
                                      15-48

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any  increase  in  R    in  healthy  or  in  susceptible  individuals  after a  single,  short-term
                   aW
exposure.   Obviously,  a barely  detectable  functional response has  less  serious implications
than one associated with disability or djstress.
     An assessment of  the  importance  of studies showing  associations  between exposure to NO.
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 NO.  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 ug 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 arterial  partial  pressure of oxygen.  Expo-
sures to concentrations of NO. 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  diffar  little  and provide  no  particular
support for  the hypothesis that  chronic  bronchitics  are  more sensitive to  NO.  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)
NO. 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)  NO.  for 1 hour were
reported by Orehek et al., (1976) to increase mean airway resistance (R  ) in 13 of 20 asthma-
                                                                       3W
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 NO..

                                      15-49

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     The above clinical 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,  membars 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 NO-  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 NO- 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 NO- 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  NOg  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 NO- 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^
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 NO- levels.
     Only  a  few  American   community  air  pollution  studies  on  the effects  of NO^  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 KO^.
     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 NO- exposures.
                                      15-50

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     Certain other epidemiologies! 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  N0,-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 NO-.  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 (ps.10) were found for some subgroups of children but not others.  Also,  NO,
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  N0_  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
N0«  levels and  pulmonary function measures  in the 6 to 7 year old children.   Only  some weak
associations  (p=  .10) were found between increased  respiratory illness  in  the  same children
and NO, levels in their bedrooms.  The authors suggest, however, that the apparent association
may  be  due  to  NO- 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 NO,,  -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 NO- 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

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facilities where  N0?  levels were monitored (Spengler et a!., 1979), N0? was present in higher
concentrations than was  present in the outside air.  Indoor values monitored in one gas stove
home averaged  as  high as 54 pg/m   (0.03  ppm)  over a two-week period; and short-term (lasting
minutes to hours)  NO, levels in excess of  500 ug/m  (.25 ppm) and even 1,000 ug/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 NO, 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-schoo!  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 apparent 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 sjjp_ra).
     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 N0_  exposure levels and  durations might  be associated  with  the induction of such
                                      15-52

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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 NO- 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 NO, 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 NO, 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 NO- 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 NO-  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  NO, 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

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TABLE 15-?.   HtTROGIN DIOXIDE LEVELS RETORTED IH CAS AND ELECTRIC STOVE HOK£S
Site an
-------
                                                                       IABIE  15-?.  (continued)
tn
 i
in
01
Site and conditions

Kitchen with a gas oven on for
1-hr at 3508F
0.25 ich (no stove vent)
1.0 K<\ (hood vent
above stove)
2.5 ach (hood vent with fan
at 50 CfH)
1,0 Kh (hood vent with fan
at 140 CfH)
Outside during test
83 gas stove hones
50 electric stove hones
53 outdoor samples in
vicinity
46 gas stove



Activity room (gas stove
homes )
Activity room (electric
stave hones)
Outdoors

Kitchen, 3-ft from gas
stove hone



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 neasurenent
over 3 day periods


95lh percent! le of 24-hr
averages measured over a
1 year period



continuous




NO, concentration
(pp«)


1.20
0.80

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
S 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
Cheml luminescent
Analyzer








Modified Jacobs-
Hochheiser
(arsenite modified)

Chenl luminescent
Analyzer


Modified Sodium
Arsenite




Cheni luminescent
Analyzer



Reference

Hollowel et al. .
1978
Test kitchen (27«3J







Keller et al., 1379
Gas and electric
stove homes in
Columbus, Ohio




Speizer et al, , 1980
Activity roon 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.



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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  NOp
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 NOp  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 NOp  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 nitrosation Jm vivo of an exogenous amine,
morpholine,  by  inhaled N0_ has recently been  demonstrated in mice, there  is  no evidence, to
date,  that  nitrogenous atmospheric  pollutants contribute to the j_n vivo formation of nitrosa-
mines in humans or that nitrosamines inhaled from the ambient air represent significant health
hazards.
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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.
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Speizer,  F.  E., B.  G.  Fern's,  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.                                          i

Spengler, J.  D.,  B.  6.  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.  Twis's,  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
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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, H. 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.   Physio!.:
     Respirat. Environ.  Exercise Physio!. 46: 189-196, 1979.

Von  Nieding,  G. , H.  Krekeler,  R.  Fuchs, H. M.  Wagner,  and  K.  Koppenhagen.   Studies of  the
     acute  effect  of NO,, 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  funcn'on  and
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     D.C. , 1970.

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Von Neiding, G.,  H.  M.  Wagner,  H.  Lollgen,  and  K.  Krekeler.  Acute effects of ozone  on lung
     function of men.  VDI-Ber.  270:123-129, 1977.
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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.

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     1969.                                                                          •  ~~

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Yokoyama,  E.   The  respiratory  effects of  exposure  to SO?rN07  mixtures  on healthy subjects.
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Zaldivar,  R. ,  and  W.   H.  Wetterstand.   Further evidence  of  a positive correlation between
     exposure  to  nitrate  fertilizers  (NaNO, and  KNQ»)  and  gastric  cancer  death  rates:
     nitrites and nitrosamines.  Experientia 31: 1354-1355, 1975.
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                           APPENDIX A;  GLOSSARY
AaDCL:  Alveolar-arterial difference or gradient of jthe partial pressure ot
     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:  CBLCHO; 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 C0_.
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Aerolein;  CH_=CHCHO; a volatile, flammable, oily liquid, giving off
     irritant vapor.  Strong irritant of skin and mueuous 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.
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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  ):  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
                                                           H
Aldehyde:  An organic compound characterized by the group -C-H.

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.
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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 (00/C00) 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 (NHL) 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 antithyroid activity; also called
     amitrole,

Ammonification:  Decomposition with production of ammonia or ammonium
     compounds, esp. by the action of bacteria on nitrogenous organic
     matter.

Ammonium:  Anion (NH,) or radical (NH,) derived from ammonia by combination
     with hydrogen.  Present in rainwater, soils and many commercial ferti-
     lizers.

Amnestic;  Pertains to immunologic memory:  upon receiving a second
     dose of antigen, the host "remembers" the first dose and responds
     faster to the challenge.
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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.

          °              -8
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 JHLO?, 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.
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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 (Pa09):   Portion of total pressure of
     dissolved gases in arterial blood as measured directly from arterial
     blood.

Arterialized 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 aminotransferase
     (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.
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Atomic absorption spectrometry:  A measurement method based oa 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, CL-H^NO,,, 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.
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Beta (b)-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 KL-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.
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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.

Brqnchodilator:  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,H_QH, also known as
     butyl alcohol.

Butylated 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.,.ClN202) that
     produces a constriction of the  bronchi; a parasympathetic stimulant
     used in veterinary medicine and topically in glaucoma.
                                      A-9

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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:  En2ymes which have the ability to hydrolyze certain proteins
     and peptides; occur in cellular structures known as lysosomes.

Cation:  A positively charged ion.
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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.
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Chamber study:  Research conducted using a closed vessel in which pollutants
     are reacted or substances exposed to pollutants.

Chemiluiainescence:  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 C_7H,C-OH; 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.
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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 (C?):  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 (COH):  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.                                              "
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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 eopolymer.

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 (C_H,0_) 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 NCL.

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.
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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 N_.  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.
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Desorb;  To release a substance which has been taken into another substance
     or held on its surface; the opposite of absorption or adsorption.

Desquatnation:  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 ArN2Cl , where Ar refers to an aromatic group.

Biazotizer:  A chemical which, when reacted with amines (RHH_,  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 pr
     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 glyeeraldehyde-
     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 0? from HbO .  Also a postulated intermediate in the bio-
     chemical pathway 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.
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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.

DLCQ:  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"hyphosis:  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.

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 trie pressure of pulmonary resistance during airflow.

Dynel:  A trademark for a modacrylic staple fiber spun from a copolyraer
     of acrylonitrile 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.
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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 partieu-
     late matter, bacteria, viruses, and DNA.

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.
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          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.
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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 NCK, 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.
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IFxber-react-ive dye:  A water-soluble dyestuff which reacts chemically
     with tbe 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.
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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).

Gloraular 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.
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Glutamic-oxaloacetic transaminase (SCOT):  An enzyme (EC 2.6.1.1) whose
     serum level increases in rayocardial infarction and in diseases in-
     volving destruction of liver cells.  Also known as aspartate
     aminotransferase.

Glutamic-pyruvie 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.

Glycolytie 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 3f:5'-cyclic phosphate.

H-Thyrnidine:  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.
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Hemagglutination:  The agglutination of red blood cells.  Can be used as
     as a measurement of antibody concentration.

Hematocrit:  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.

Hemochroraatosis:  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-
     heraoglobin (KbC- ) 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 terra referring to donor and recipient cellular elements
     from different organisms, such as red blood cells from sheep and
     alveolar raacrophage 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 rate of 2,000 m /24 hr (1.38 m /min), or as high as 2,880
     in /24 hr (2 in /rain).

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.
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Homogetxatet  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.
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Immunoglobulin (Igr):  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.
     Subtractions of IgG are fractions GI , 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,

Itnpaction:  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 embolij 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 10  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.
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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.
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Isopleth:  A line on a map or chart connecting points of equal value,

Jacobs-Hochheiser method:  The original Federal Reference Method for NC> ,
     currently unacceptable for air pollution work.

Klebsiella pneuinoniae:  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.

tactic 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.
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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.
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Malaise:  A feeling of general discomfort or uneasiness, often the first
     indication of an infection or disease.

Malate 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 CO  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 (HMD):   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.
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Meteorology:  The science that deals with, the atmosphere and its phenomena,

Methemoglobin:  A form of hemoglobin in which 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 spectrophotoroetric technique which
     is used to identify unknown absorbing materials and measure their
     concentrations by using preset wavelengths.

Molecular weight:  The weight of one m'olecule of a substance obtained
     by adding the gram-atomic weights of each of the individual atoms
     in the substance.
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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.

Marine:  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.
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Jfeonate:  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
     (NH/+) 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.
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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 (JLPO.) 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 and 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 .
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Oxidation:  An ion or molecule undergoes oxidation by donating electrons.

Oxidative deamination:  Removal of the SffiL group from an amino 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.

Oxyheraoglobin:  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
     MO, 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
     nex^ton 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.
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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 (PAH):  Pollutant created by action of sunlight on
     hydrocarbons and NO  in the air; an ingredient of photochemical smog.
                        x
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, CJKLNLS, 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 (E.G. 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.
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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 (II) 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.
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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 example's.

Polyamides:  Polymerization products of chemical compounds which contain
     amino (-NH,j) 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.
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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, C^H^NO-, 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.
                                      A-39

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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 KNA.  Cytosine and
     thymine occur in DNA and cytosine and uracil are found in UNA.

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 0
     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 N05, an EPA-approved gas-phase c'hemiluminescent
     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 repellency.

Ribosomal RNA:  The most abundant RNA in a cell and an integral constituent
     of ribosomes.
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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
     corrosiort 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_AsO«, used with sodium hydroxide in the absorbing solu-
     tion of a 24-hour integrated manual method for NO-.

Sodium dithionite:  A strong reducing agent (a supplier of electrons).

Sodium metabisulfite:  Na-S-O., used in absorbing solutions of N0» analysis
     methods.

Sorb:  To take up and hold by absorption or adsorption.
                                      A-41

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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 vaisious 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.
                                      A-42

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Static lung compliance (CL    ):  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.

Stoichiometrie factor:  Used to express the conversion efficiency of a non-
     quantitative reaction, such as the reaction of NO- 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.

Streptococcuspyogenes:  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 (C.-HnN-O^S) , the amide of sulfanilic
     acid and parent compound of most sulfa drugs.
                                      A-43

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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 (S0_):  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.

Teratogenies  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-,KLO_) that is composed of thymine and
     deoxyribose; occurs as a structural part of DNA.

Tidal volume (V_):  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.
                                      A-44

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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.

Transmissivity (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^)^, used in the absorbing solution
     of one analytical method for NCL.

Troposphere:  That portion of the atmosphere in which temperature decreases
     rapidly with altitude, clouds form, and mixing of air masse's 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 invisible0to the human eye of wavelengths between 4x10
     and 5x10   m (4000 to 50A).

Urea-formaldehyde resin:  A compound composed of urea and formaldehyde in
     an arrangement that conveys thermosetting properties.
                                      A-45

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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 (Vp):  The volume of gas exchanged between the  lungs and
     the atmosphere tnat 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.
                                                            o
Visible region:  Light between the wavelengths of 4000-8000 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.
                                      A-46

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   Vitamin Et  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 spectroraetry;  A nondestructive technique which utilizes
        the principle that every  element emits characteristic x-ray emissions .•
        when excited by high-energy radiation.
                                                                  k
   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,
                                          A-47
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