United States
Environmental Protection
Agency
Environmental Criteria and
A-ssessrrent Office
Research Triangle Park NC 27711
EPA-600/8-82-02(
December 1982
Final Report
Research and Development
?/EPA
Air Quality
Criteria for
Oxides of Nitrogen
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EPA-600/8-82-026F
December 1982
AIR QUALITY CRITERIA
FOR
OXIDES OF NITROGEN
FINAL REPORT
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, IM.C. 27711
-------
NOTICE
Mention of trade names or commercial products
does not constitute endorsement or recommenda-
tion for use.
n
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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 (NCL), and the related compounds, nitrites,
nitrates, nitrogenous acids, and nitrosami'nes. Although the emphasis is on
presentation of health and welfare effects data, other scientific data are
presented in order to provide a better understanding of these pollutants in
the environment. To this end, separate chapters are included which discuss
the nitrogen cycle, sources and emissions, atmospheric chemical processes
which transform emissions of nitrogen oxides into related airborne com-
pounds, transport and removal processes, measurement methods, and atmo-
spheric concentrations of nitrogenous pollutants.
Of the oxides of nitrogen which occur in the atmosphere, NO- is the
compound of most concern for human health. Controlled human exposure
studies indicate that in some subjects increases in airway resistance of
the pulmonary system are produced by short exposure to NOo concentrations
in the range of 1300 to 3760 ug/m (0.7 to 2.0 ppm). Studies of population
exposure have demonstrated increased incidences of acute respiratory ill-
ness in young children associated with combustion products from gas stoves
of which N02 is a significant component, but the exact effective concentra-
tions and exposure times are difficult to determine.
Although animal studies do provide support for the mechanism of in-
creased susceptibility to some respiratory pathogens as a consequence of
NO exposure, they cannot provide quantitative data. Increases in animal
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susceptibility due to repeated short-term exposures eventually are as large
as those produced by continuous exposure to the same concentration.
Many other effects have been shown to occur in animals at exposure
concentrations comparable to those causing increases in susceptibility to
respiratory infections. Usually, these have not been demonstrated iYi
humans, but the potential for their occurrence cannot be ignored.
Air pollution degrades the appearance of distant objects and reduces
the range at which they can be distinguished from the background. Nitrogen
dioxide does not significantly reduce visual range but can be responsible
for a portion of the brownish coloration observed in polluted air. NCL
acts as a blue-minus filter for transmitted light. The strength of this
filter effect is theoretically determined by the integral of NOo concen-
tration along the sight path. An NO* concentration-times-distance product
of less than 0.1 ppm-km NO* is sufficient to produce a color shift which
is distinguishable in carefully controlled laboratory tests. However,
empirical observations under a variety of conditions are needed to deter-
mine the perceptibility of NOp in ambient air.
Nitrogen dioxide and particulate nitrates may also contribute to
pollutant haze. The discoloration of the horizon sky due to N(L absorption
is determined by the relative concentrations of NO- and light-scattering
particles. At a visual range of 100 km, typical of the rural great plains
area .of the United States, as little as 0.003 ppm (6 ug/m ) N02 can color
the horizon noticeably. At a visual range of 10 km, typical of urban haze,
at least .0.03 ppm (60 pg/m ) N02 would be required to produce the same
effect. Estimates of the possible ro.Te played by particulate nitrates are
currently hampered by the lack of high-quality data on their concentrations
in ambient air.
iv .
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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 Takes has been successful in a limited
number of cases.
Oxides of nitrogen have also been shown to affect vegetation adversely.
When crops are exposed to nitrogen dioxide alone in controlled studies, the
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ambient concentrations producing measurable injury are above those normally
occurring in this country. Exceptions to this generality have been ob-
served: the growth of Kentucky bluegrass was reduced about 25 percent by
exposures to 210 |jg/m (0.11 ppm) N02 for 103.5 hours per week for 20 weeks
during the winter months. A number of controlled studies on mixtures of
' nitrogen dioxide with sulfur dioxide, show effects greater, in some casesy
much greater, than those effects caused by the individual pollutants alone.
Some leaf injury to pinto bean, radish, soybean, tomato, oat and tobacco
occurred after 4-hour exposure to 280 |jg/m (0.15 ppm) N02 in combination
with 260 [jg/m (0.1 ppm) S02- Similar results were observed in green peas
and Swiss chard. Kentucky bluegrass showed reductions in yield parameters
2
ranging from 30 to 90 percent upon exposure for 20 weeks to 210 (jg/m (0.11
3
ppm) N02 in combination with 290 (jg/m (0.11 ppm) S02 for 103.5 hours per
week.
Nitrogen dioxide has been found to cause deleterious effects to a wide
variety of textile dyes and fabrics, plastics, and rubber. Significant
fading of certain dyes on cotton and rayon has been shown after 12 weeks of
o
exposure to 94 pg/m (0.05 ppm) N02 at high humidity and temperature .(90
percent, 90°F). Similar effects were obtained under similar conditions for
2
• various dyes on nylon, at 188 ug/m (0.1 ppm). Yellowing of several white
fabrics has been shown in exposure to 376 ug/m (0.2 ppm) for 8 hours.
Nitrates and nitrogenous acids have been implicated as possible causative
and/or accelerating agents in the wet corrosion of metals and deterioration
of electrical contracts.
VI
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ABSTRACT
o
This document is an evaluation and assessment of scientific informa-
tion relative to determining the health and welfare effects associated with
exposure to various concentrations of nitrogen oxides in ambient air. The
document is not intended as a complete, detailed literature review. It
does not cite every published article relating to oxides-of nitrogen and
their effects in the environment. The literature through 1978 has been
reviewed thoroughly for information relative to criteria. The major gaps
in our current knowledge, relative to criteria, have been identified.
Though the emphasis is on the presentation of data on health and
welfare effects, other scientific data are presented and evaluated in order
to provide a better understanding of the pollutants in the environment. To
this end, separate chapters concerning the properties and principles of
formation, emissions, analytical methods of measurement, observed ambient
concentrations, the global cycle, effects on vegetation and microorganisms,
mammalian metabolism, effects on experimental animals, and effects on
humans are included.
vn
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TABLE OF CONTENTS
Page
PREFACE . . . . . iii
ABSTRACT vii
LIST OF FIGURES xvi
LIST OF TABLES xx
LIST OF ABBREVIATIONS, ACRONYMS AND SYMBOLS xxy
CONTRIBUTORS AND REVIEWERS xxxrv
SCIENCE ADVISORY BOARD COMMITTEE xlii
1. SUMMARY OF EFFECTS OF OXIDES OF NITROGEN AND RELATED COMPOUNDS
ON HUMAN HEALTH AND WELFARE 1-1
1.1 INTRODUCTION 1-1
1.2 SOURCES, TRANSFORMATIONS AND AMBIENT LEVELS OF NITROGEN
OXIDES i 1-2
1.3 EFFECTS OF NITROGEN OXIDES ON HUMAN HEALTH . 1-3
1.3.1 Nitrogen Dioxide Respiratory System Effects . . . 1-4
1.3.1.1 Controlled Human Exposure Studies .... 1-5
1.3.1.2 Human Epidemiology Studies 1-12
1.3.1.3 Animal Tox.icology Studies 1-20
-. 1.3.2 N02 Sensory System Effects 1-21
1.3.3 Summary of Major Health Effects Conclusions. . . . 1-26
1.4 WELFARE EFFECTS OF NITROGEN OXIDES 1-27
1.4.1 Nitrogen Oxides, Acidic Deposition Processes,
. • • - and Effects 1-28
1.4.2 Effects of NO on Ecosystems and Vegetation . . . 1-35
1.4.3 Effects of Nitrogen Oxides on Materials ..... 1-37
1.4.4 Effects of Nitrogen on Visibility 1-39
2. INTRODUCTION 2-1
3. GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NO AND NO -
DERIVED POLLUTANTS x. ....... 3-1
3.1 INTRODUCTION AND OVERVIEW 3-1
3.2 NITROGEN OXIDES 3-2
3.2.1 Nitric Oxide (NO) 3-2
3.2.2 Nitrogen Dioxide (N0?) 3-9
3.2.3 Nitrous Oxide (N?0) * 3-9
3.2.4 Unsymmetrical Nitrogen Trioxide (OONO) 3-10
3.2.5 Symmetrical Nitrogen Trioxide (NO,) 3-10
3.2.6 Dinitrogen Trioxide (Np03) ... 3-11
3.2.7 Dinitrogen Tetroxide (N90d) 3-11
3.3 NITRATES, NITRITES, AND NITROGEN^ACIDS . 3-11
3.4 AMMONIA (NhU) 3-13
3.5 N-NITROSO COMPOUNDS 3-13
3.6 SUMMARY 3-14
3.6.1 Nitrogen Oxides 3-15
3.6.2 Nitrates, Nitrites and Nitrogen Acids ....... 3-15
3.6.3 N-Nitroso Compounds 3-16
3.7 REFERENCES FOR CHAPTER 3 . . . . 3-17
v i i i
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Page
4. THE NITROGEN CYCLE 4-1
4.1 INTRODUCTION : 4-1
4.2 THE NITROGEN CYCLE 4-1
4.3 THE GLOBAL CIRCULATION OF NITROGEN 4-4
4.3.1 Important Nitrogen Fluxes 4-4
4.3.1.1 Biological Nitrogen Fixation 4-5
4.3.1.2 Industrial Nitrogen Fixation 4-8
4.3.1.3 Nitrogen Fixation by Other Processes . . 4-8
4.3.1.4 Nitrates, Nitrites and the Nitrogen Cycle 4-8
4.3.1.5 Nitrates as Fertilizers 4-8
4.4 AMMONIFICATION AND NITRIFICATION 4-9
4.5 NITRIC OXIDE, NITROGEN DIOXIDE AND THE NITROGEN CYCLE . . 4-9
4.6 NITROUS OXIDE AND THE NITROGEN CYCLE 4-11
4.7 ORGANIC NITROGEN AND THE NITROGEN CYCLE 4-12
4.8 AMMONIA AND THE NITROGEN CYCLE 4-14
4.9 DENITRIFICATION 4-14
4.10 ACIDIC PRECIPITATION 4-15
4.11 SUMMARY 4-15
4.12 REFERENCES FOR CHAPTER 4 4-19
5. SOURCES AND EMISSIONS 5-1
5.1 INTRODUCTION 5-1
5.2 ANTHROPOGENIC EMISSIONS OF NO 5-1
5.2.1 Global Sources of NO x 5-2
5.2.2 Sources of NO in thl United States * 5-2
5.3 EMISSIONS OF AMMONIAX 5-14
5.4 AGRICULTURAL USAGE OF NITROGENOUS COMPOUNDS 5-16
5.5 SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS. . 5-16
5.5.1 Anthropogenic Sources of N-Nitroso Compounds . . . 5-16
: 5.5.2 Volatilization from Other Media 5-19
5.5.3 Atmospheric Formation: N-Nitroso Precursors . . . 5-19
5.5.4 N-Nitrosamines in Food, Water and Tobacco
Products 5-20
5.6 SUMMARY 5-21
5.6.1 Sources and Emissions of NO 5-21
5.6.2 Sources and Emissions of Otner Nitrogenous
Compounds ' 5-22
5.7 REFERENCES FOR CHAPTER 5 5-23
6. ENVIRONMENTAL TRANSPORT AND TRANSFORMATION .6-1
6.1 CHEMISTRY OF THE OXIDES OF NITROGEN IN THE LOWER
ATMOSPHERE 6-1
6.1.1 Reactions Involving Oxides of Nitrogen ...... 6-2
6.1.2 Laboratory Evidence of the NO~-to-Precursor
Relationship 6-12
6.1.3 NO Chemistry in Plumes 6-15
6.1.4 Computer Simulation of Atmospheric Chemistry . . . 6-16
6.2 NITRITE AND NITRATE FORMATION 6-18
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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-?7
6.3.2.3 Wet Deposition 6-2
6.3.3 Source-Receptor Relationships . 6-2b
6.4 MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION 6-30
6.4.1 Non-Photochemical Reaction of Gaseous Amines li
with Oxides of Nitrogen and Nitrous Acid 6-30
6.4.2 Photochemical Reactions of Amines 6-32
6.4.3 Formation of Nitrosamine in Atmospheric
Aerosols 6-37
6.4.4 Environmental Implications 6-37.
6.5 SUMMARY 6-38
6.5.1 Chemistry of Oxides of Nitrogen in the Lower
Atmosphere 6-38
6.5.2 Nitrate and Nitrite Formation 6-39
6.5.3 Transport and Removal of Nitrogenous Species ... 6-40
6.5.4 Mechanisms of Atmospheric Nitrosamine Formation . 6-40
6.5.5 Source-Receptor Relationships . 6-41
6.6 REFERENCES FOR CHAPTER 6 ,6-42
7. SAMPLING AND ANALYSIS FOR AMBIENT NO AND
NO -DERIVED POLLUTANTS x 7-1
7.1 INTRODUCTION 7-1
7.2 ANALYTICAL METHODS FOR NO 7-5
7.2.1 The Reference Meth6d for N02:
Gas-Phase Chemiluminescence 7-5
7.2.2 Other Analytical Methods for NO? 7-6
7.2.2.1 Griess-Saltzman Method 7-6
7.2.2.1.1 General description of method. 7-6
7.2.2.1.2 Continuous Saltzman procedures 7-7
7.2.2.1.3 Manual Saltzman procedure. . . 7-8
7.2.2.2 Jacobs-Hochheiser Method 7-9
7.2.2.3 Triethanolamine Method . 7-10
1.2.2A Sodium Arsenite Method 7-10
7.2.2.5 TGS-ANSA Method 7-'ll
7.2.2.6 Other Methods 7-12
7.2.2.7 Summary of Accuracy and Precision
of N0? Measuring Methods 7-12
7.2.3 Analytical Methods for NO 7-14
7.2.4 Sampling for'NO 7-14
7.2.5 Calibration of NO and N02 Monitoring
Instruments 7-16
7.3 ANALYTICAL METHODS AND SAMPLING FOR NITRIC ACID 7-18
7.4 ANALYTICAL METHODS AND SAMPLING FOR NITRATE 7-19
7.4.1 Sampling for Nitrate from Airborne Particulate
Matter 7-19
7.4.2 Analysis of Nitrate from Airborne Particulate
Matter 7-23
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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 NOV AND OTHER
NITROGENOUS COMPOUNDS x 8-1
8.1 ATMOSPHERIC CONCENTRATIONS OF'WT 8-1
8.1.1 Background Concentrations of NO 8-2
8.1.2 Ambient Concentrations of NO 8-3
8.1.2.1 Monitoring for NO x 8-3
8.1.2.2 Sources of Data . 8-5
8.1.3 Historical Measurements of NO Concentrations . . 8-5
8.1.4 Recent Trends in NO- Concentrations 8-14
8.1.5 Seasonal Variations in N0? Concentrations .... 8-14
8.1.6 Recently Observed Atmospheric Concentrations
of N02 8-14
8.1.7 Spatial and Temporal Variations of NO^
Concentrations as Related to Estimation of
Human Exposures 8-50
8.1.7.1 Spatial and Temporal Variations of
Local N02 Concentrations 8-50
8.1.7.2 Estimating Human Exposure 8-64
8.2 ATMOSPHERIC CONCENTRATIONS OF NITRATES 8-73
8.3 ATMOSPHERIC CONCENTRATIONS OF N-NITROSO COMPOUNDS .... 8-74
8.4 SUMMARY 8-74
8.4.1 Atmospheric Concentrations of NO,, 8-74
8.4.2 Atmospheric Concentrations of Nitrates 8-76
8.4.3 Atmospheric Concentrations of N-Nitroso
Compounds 8-76
8.5 REFERENCES FOR CHAPTER 8 8-77
9. PERTURBATIONS OF THE STRATOSPHERIC OZONE LAYER 9-1
9.1 INTRODUCTION 9-1
9.2 DIRECT ROLE OF NITROGEN OXIDES IN THE OZONE
BALANCE OF THE ATMOSPHERE 9-2
9.3 INDIRECT ROLE OF NITROGEN OXIDES IN THE OZONE
BALANCE OF THE ATMOSPHERE 9-3
9.4 OTHER ATMOSPHERIC EFFECTS OF NITROGENOUS COMPOUNDS ... 9-4
9.5 SUMMARY 9-6
9.6 REFERENCES FOR CHAPTER 9 9-7
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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-H
\
11. ACIDIC DEPOSITION 11-1
11.1 INTRODUCTION ' 11-1
11.1.1 Overview of the Problem 11-1
11.1.2 Ecosystem Dynamics 11-6
11.2 CAUSES OF ACIDIC PRECIPITATION 11-L
11.2.1 Emissions of Nitrogen and Sulfur Oxides ll-i;
11.2.2 Transport of Nitrogen and Sulfur Oxides 11-L
11.2.3 Formation 11-2:
11.2.3.1 Composition and pH of Precipitation 11-21
11.2.3.2 Seasonal Variations in Nitrates and Sulfates. 11-2!
11.2.3.3 Geographic Extent of Acidic Precipitation . . 11-3!
11.2.4 Acidic Deposition . 11-3!
11.3 EFFECTS OF ACIDIC DEPOSITION 11-3!
11.3.1 Aquatic Ecosystems 11-3'
11.3.1.1 Acidification of Lakes and Streams 11-3
11.3.1.2 Effects on Decomposition 11-4
11.3.1.3 Effect on Primary Producers and Primary
Productivity 11-4!
11.3.1.4 Effects on Invertebrates 11-5!
11.3.1.5 Effects on Fish 11-5!
11.3.1.6 Effects on Vertebrates Other Than Fish ... 11-6'
11.3.2 Terrestrial Ecosystems 11-61
11.3.2.1 Effects on Soils 11-6!
11.3.2.2 Effects on Vegetation 11-7!
11.3.2.2.1 Direct Effects on Vegetation . . 11-7'
11.3.2.3 Effects on Human Health 11-8'
11.3.2.4 Effects of Acidic Precipitation on Materials. 11-8'
11.4 ASSESSMENT OF SENSITIVE AREAS 11-91
11.4.1 Aquatic Ecosystems ' 11-9!
11.4.2 'Terrestrial Ecosystems 11-91
11.5 SUMMARY . ll-H
11.6 REFERENCES. 11-H
12. EFFECTS OF NITROGEN OXIDES ON NATURAL ECOSYSTEMS,
VEGETATION AND MICROORGANISMS 12-1
12.1 INTRODUCTION 12-1
12.2 EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS 12-2
12.2.1 Effects of Nitrates 12-5
XII
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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 N0? Injury 12-28
12.3.4 Dose Response . . . 12-29
12.3.4.1 Foliar Injury 12-29!
12.3.4.2 Growth 12~34:
12.3.5 Effects of Gas Mixtures on Plants 12-40
12.3.5.1 Nitrogen Dioxide and Sulfur Dioxide 12-40
12.3.5.2 Nitrogen Dioxide With Other Pollutants. . . . 12-44
12.4 SUMMARY 12-45
12.4.1 Effects on Ecosystems 12-45
12.4.2 Effects on Vegetation 12-46
12.5 REFERENCES FOR CHAPTER 12 12-47
13. EFFECTS OF NITROGEN OXIDES ON MATERIALS 13-1
13.1 EFFECTS OF NITROGEN DIOXIDE ON TEXTILES 13-1
13.1.1 Fading of Dyes by NO 13-1
13.1.1.1 Fading of Dyes on Cellulose Acetate 13-1
13.1.1.2 Fading of Dyes on Cotton and Viscose
Rayon (Cellulosics) 13-2
13.1.1.3 Fading of Dyes on Nylon 13-13
13.1.1.4 Fading of Dyes on Polyester 13-13
13.1.1.5 Economic Costs of NO -Induced Dye
Fading 13-15
13.1.2 Yellowing of White Fibers by NO . 13-15
13.1.3 Degradation of Textile Fibers b$ NO 13-19
13.2 EFFECTS OF NITROGEN DIOXIDE ON PLASTICS ANDX
ELASTOMERS 13-19
13.3 CORROSION OF METALS BY NITROGEN DIOXIDE 13-20
13.3.1 Pitting Corrosion 13-21
13.3.2 Stress Corrosion 13-21
13.3.3 Selective Leaching 13-21
13.3.4 Correlation of Corrosion Rate with Pollution 13-21
13.4 REFERENCES FOR CHAPTER 13 13-26
XTM
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14. STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS 14-1
15.
14.1
14.2
14.3
14.4
14.5
14.6
14.7
14.8
INTRODUCTION
NITROGEN DIOXIDE
14.2.1 Respiratory Tract Transport and Absorption . . . .
14.2.2 Mortality
14.2.3 Pulmonary Effects
14.2.3.1 Host defense mechanisms
14.2.3.1.1 Interaction with
infectious agents
14.2.3.1.2 Mucociliary transport . . .
14.2.3.1.3 Alveolar macrophage . . . .
14.2.3.1.4 Immune system
14.2.3.2 Lung Biochemistry
14.2.3.2.1 Introduction
14.2.3.2.2 Lipid and diet effects . . .
14.2.3.2.3 Sulfhydryl compounds and
pyridine nucleotides ....
14.2.3.2.4 Effects on lung amino
acids, proteins, and
enzymes
14.2.3.2.5 Potential defense
mechanisms
14.2.3.3 Morphology Studies
14.2.3.4 Pulmonary Function . . .
14.2.3.5 Studies of Hyperplasia ...
14.2.3.6 Edemagenesis and Tolerance
14.2.4 Extrapulmonary Effects
14.2.4.1 Nitrogen Dioxide-induced Changes in
Hematology and Blood Chemistry
14.2.4.2 Central Nervous System and
Behavioral Effects
14.2.4.3 Biochemical Markers of Organ Effects . .
14.2.4.4 Teratogenesis and Mutagenesis
14.2.4.5 Effects of NO,, on Body Weights
DIRECT EFFECT OF COMPLEX MIXTURES
NITRIC OXIDE
NITRIC ACID AND NITRATES
N-NITROSO COMPOUNDS
SUMMARY
REFERENCES FOR CHAPTER 14
EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN
15.1
15.2
INTRODUCTION
CONTROLLED HUMAN EXPOSURE STUDIES
15.2.1 Studies of Sensory Effects
15.2.1.1 Effects of Nitrogen Dioxide on
Sensory Systems
15.2.1.2 Sensory Effects Due to Exposure to
. . . 14-1
.- . . 14-1
. . . 14-1
. . . 14-3
. . . T4-3
. . . 1-3
i 14-3
. . . /• J-t o
. . . '14-18
. . . 14-18
. . . 14-24
. . . 14-28
. . . 14-28
. . . 14-28
. . . 14-38
. . . 14-38
. . . 14-40
. . . 14-41
. . . 14-49
. . . 14-54
. . . 14-57
. . . 14-59
. . . 14-59
. . . 14-63
. . . 14-63
. . . 14-68
. . . 14-71
. . . 14-71
. . . 14-78
. . . , 14-80
. . . 'i 14-82
. . . 14-84
. . . 14- 11C
. . . 15-1
. . . 15-1
. . . 15-3
. . . 15-3
. . . 15-3
Combinations of Nitrogen Dioxide and
Other Pollutants 15-6
15.2.2 Pulmonary Function 15-8
15.2.2.1 Controlled Studies of the Effect of
Nitrogen Dioxide on Pulmonary Function
in Healthy Subjects 15-8
xiv
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15.2.2.2 The Effects of Nitrogen Dioxide
Exposure on Pulmonary Function in
Sensitive Subjects 15-17
15.3 EPIDEMIOLOGICAL STUDIES 15-22
15.3.1 Effects of N0? on Pulmonary Function :{,. . 15-22
15.3.2 Effects of NO^ on Acute Respiratory Illness 15-27
15.3.2.1 Effects Associated with Ambient
Exposures 15-27
15.3.2.2 Effects Associated with Indoor
Exposures 15-29
15.3.2.2.1 Tobacco smoking studies 15-29
15.3.2.2.2 Community studies of gas
combustion products 15-30
15.3.3 Effects of NCL Pollution on Prevalence of
Chronic Respiratory Disease 15-38
15.3.4 Extrapulmonary Effects of Exposure to NCL 15-39
15.4 ACCIDENTAL AND OCCUPATIONAL EXPOSURES * 15-40
15.5 EFFECTS OF NO -DERIVED COMPOUNDS . 15-41
15.5.1 Nitrates, Nitrites and Nitric Acid 15-42
15.5.2 Nitrosamines 15-44
15.5.3 Other Compounds 15-45
15.6 SUMMARY AND CONCLUSIONS 15-46
15.6.1 N02 Effects 15-46
15.6.1.1 Pulmonary function effects 15-46
15.6.1.2 Acute respiratory disease effects 15-50
15.6.1.3 Chronic respiratory disease effects . . .,; . . 15-53
15.6.1.4 Sensory system effects 15-56
15.6.2 Effects of NO -Derived Compounds 15-56
15.7 REFERENCES ........... 15-57
GLOSSARY G-l
xv
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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" '..... 1-3^
4 3-1. Absorption Spectrum of Nitric Oxide . 3-5
4-1. Simplified Global Nitrogen Cycle (Terrestrial Systems) . . . 4-2
5-1. Historic NO Emissions by Source Groups 5-4
5-2. Recent NO Emissions by Source Groups 5-7
5-3. Distribution of 1972 Nationwide NO Emissions by Degree of
Urbanization 5-8
5-4. Total NO Emissions by U.S. County 5-10
5-5. Total NO* Emission Density by U.S. County 5-11
5-6. Percent NO Emissions Contributed by Major Point Sources . . 5-12
5-7. Trends in U.S. Usage of Nitrogenous Materials Applied as
Fertilizer 5-17
6-1. Paths of Nitrate Formation in the Atmosphere 6-21
6-2. Schematic Illustration of Scales of Motion in the Atmosphere. 6-25
6-3. Formation and Decay of Diethylnitrosamine, in the Dark and in
Sunlight, from Diethylamine and from Triethylamine 6-36
7-1. Absolute Error in N09, AN09, for 10 Seconds in Dark Sampling
Line . . 7-17
8-1. Trend Lines for Nitric Oxide Annual Averages in Five
CAMP Cities 8-8
.8-2. Trend Lines for Nitrogen Dioxide Annual Averages in Five
CAMP Cities 8-11
8-3. Trends in N02 Air Quality, Los Angeles Basin, 1965-1974 . . . 8-13
8-4. Annual Air Quality Statistics and Three-Year Moving
Averages at Camden, New Jersey 8-,15
8-5. Annual Air Quality Statistics and Three-Year Moving
Averages at Downtown Los Angeles, California 8-16
8-6. Annual Air Quality Statistics and Three-Year Moving
Averages at Azusa, California 8-17
.8-7. Annual Air Quality Statistics and Three-Year Moving
Averages at Newark, New Jersey 8-18
8-8. Annual Air Quality Statistics and Three-Year Moving
Averages at Portland, Oregon 8-19
8-9. Annual Average of Daily Maximum 1-Hour N0? (4-Year Running
Mean) in the Los Angeles Basin 8-20
8-10. Seasonal N02 Concentration Patterns of Three U.S. Urban
Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations). 8-22
8-11. Seasonal NOp Concentration Patterns of Four U.S. Urban
Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations). 8-23
8-12. Distribution of Maximum/Mean N0? Ratios for 120 Urban
Locations Averaged Over the Yeafs 1972, 1973, and 1974 . . . 8-41
xv i
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• Page
8-13. Trends in the Maximum Mean N02 Ratio for Two Groups of Sites. . 8-42
8-14. Average Diurnal Pattern for tne Month During Which the
Highest 1-Hour N02 Concentrations were Reported 8-44
8-15. One-Hr Average Concentration Profiles on Day of Peak NCL
Concentration for Three U.S. Cities 8-45
8-16. One-Hour NO,, Concentrations During Three Days of High
Pollution in Three U.S. Cities 8-46
8-17. Nitric Oxide and Nitrogen Dioxide Concentrations at an Urban
and a Rural Site in St. Louis, Missouri, on January 27-28,
1976 8-47
8-18. Pollutant Concentrations in Central City St. Louis,
October 1, 1976 8-51
8-19. St. Louis RAMS Station Locations 8-59
8-20. Location and Elevation of Clinch River Power Plant
Monitoring Stations 8-65
8-21. Population Exposed to N0« Daily Maximum Hourly Concentration
Above the California One-Hour Standard at Various Frequencies . 8-69
8-22. Population Exposed to N02 Hourly Average Concentration Above
the California One-Hour Standard at Various Frequencies .... 8-71
10-1. Transmittance of N0? Plumes for Selected Values of the
Concentration - Distance Product 10-3
10-2. Relative Horizon Brightness for Selected Values of the
Concentration - Visual Range Product 10-5
10-3. Normalized Light Scattering by Aerosols as a Function of
Particle Diameter .... 10-7
11-1. The sulfur cycle 11-9
11-2. Law of tolerance 11-11
11-3. Historical patterns of fossil fuel consumption in the United
States (adapted from Hubbert (1976)). . 11-14
11-4. Forms of local coal usage in the United States. Electric power
generation is currently the primary user of coal 11-15
11-5A. Trends in emissions of sulfur dioxides 11-16
11-5B. Trends in emissions of nitrogen oxides (1978) 11-16
11-6. Characterization of U.S. sulfur oxide emissions density by
state 11-17
11-7. Characterization of U.S. nitrogen oxide emissions density by
state 11-18
11-8. The transport and deposition of atmospheric pollutants,
particularly oxides of sulfur and nitrogen, that contribute
to acidic precipitation 11-20
11-9. Trends in mean annual concentrations of sulfate, ammonium and
nitrate in precipitation 11-23
11-10. Comparison of weighted mean monthly concentrations of sulfate
in incident precipitation collected in Walker Branch Watershed,
TN, (WBW) and four MAP35 precipitation chemistry monitoring
stations in New York, Pennsylvania, and Virginia . 11-26
xvii
-------
Figure Page
11-11. Seasonal variations in pH(A) and ammonium and nitrate concen-
. trations (B) in wet-only precipitation at Gainesville, Florida . 11-28
11-12. Seasonal variation of precipitation pH in the New York
Metropolitan Area 11-30
11-13. History of acidic precipitation at various sites in and adjacent
to the State of New York 11-32
11-14. pH of rain sample as measured .in the laboratory and used in
combination with the reported amount of precipitation ...... 11-34
tll-15. Annual mas's transfer rates of sulfate expressed as a percentage *
of the estimated total annual flux of the element to the forest
floor beneath a representative chestnut oak stand ........ 11-36
11-16. Schematic representation of the hydrogen ion cycle 11-39
11-17. pH and calcium concentrations in lakes in northern and north-
• western Norway sampled as part of the regional survey of 1975 . 11-42
11-18. The pH values and sulfur loads in lake waters with extremely
sensitive surroundings 11-43
11-19. Total dissolved Al as a function of pH level in lakes in
acidified areas in Europe and North America 11-45
11-20. pH levels in Little Moose Lake, Adirondack region of New York
State, at a depth of 3 meters and at the lake outlet. ...... 11-46
11-21. Numbers of phytoplankton species in 60 lakes having different
pH values on the Swedish West Coast, August 1976 -.. 11-50
11-22. Percentage distribution of phytoplankton species and their
biomasses 11-51
11-23. The number of species of crustacean zooplankton observed in 57
lakes during a synoptic survey of lakes in Southern Norway. . . 11-56
11-24. Frequency distribution of pH and fish population status in
Adirondack Mountain lakes greater than 610 meters evaluation.
Fish population status determined by survey gill netting
during the summer of 1975 (Schofield, 1976b) .... 11-59
11-25. Frequency distribution of pH and fish population status in 40
Adirondack lakes greater than 610 meters elevation, surveyed
during the period 1929-1937 and again in 1975 (Schofield,
1976b) 11-60
11-26. Norwegian salmon fishery statistics for 68 unacidified and 7
acidified rivers 11-62
11-27. Showing the exchangeable ions of a soil with pH+7, the_ soil
solution composition, and the replacement of Na by H from
acid rain 11-67
11-28. Regions in North America with lakes that are sensitive to
acidification by acid precipitation 11-92
.'11-29. Equivalent percent composition of major ions in Adirondack lake
surface waters (215 lakes) sampled in June 1975 11-94
11-30. Percent frequency distribution of sulfate concentrations in
surface water from lakes in sensitive regions (Schofield,
1979) 11-95
11-31. Soils of the Eastern United States sensitive to acid rain-
fall (McFee, 1980). 11-97
xv i i i
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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 NCL Concentrations Prior
to Challenge with Bacteria .... 7 14-12
14-2. Percent Mortality of Mice Versus the Length of Either
Continuous or Intermittent Exposure to 6,600 (jg/m (3.5
ppm) NO- Prior to Challenge with Streptococci .......... 14-13
14-3. Percent Mortality of Mice Versus Length of Either Continuous -
or Intermittent Exposure to 2,800 (jg/m (1.5 ppm) N02
Prior to Challenge with Streptococci 14-14
14-4. Temporal Sequence of Injury and Repair Hypothesized from
Short-Term Single Exposure of Less Than 8 Hours 14-95
14-5. Proportionality Between Effect (Cell Death) and
Concentration of N02 During a Constant Exposure Period .... 14-102
14-6. Temporal Sequence of Jjijury and Repair Hypothesized from
Continuous Exposure to N09 as Observed in Experimental
Animals / 14-103
-\
xix
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LIST OF TABLES
Table
1-1. Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
in Controlled Studies of Healthy Humans Adults
1-2. Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
in Controlled Studies of Sensitive Humans Adults
1-3. Quantitative Community Health Epidemiological Studies on
Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
1-4.; Effects of Exposure to Nitrogen Dioxide in the Home on
Lung Function and the Incidence of Acute Respiratory Disease
in Epidemiology Studies of Homes with Gas Stoves
1-5. Summary of Studies Demonstrating Health Effects in Animals at
Low (< 2.0 ppm) N02 Exposure Levels
1-6. Effects of Exposure to Nitrogen Dioxide on Sensory Receptors
in Controlled Human Studies
3-1. Theoretical Concentrations of Nitrogen Oxides and Nitrogen
Acids Which Would be Present at Equilibrium with Molecular
Nitrogen, Molecular Oxygen, and Water in Air at 25 C, 1 ATM,
50 Percent Relative Humdiity
3-2. Some Physical and Thermodynamic Properties of the Nitrogen
Oxides
3-3. .Theoretical Equilibrium Concentrations of Nitric Oxide and
Nitrogen Dioxide in'Air (50 Percent Relative Humidity) at
Various Temperatures
3-4. Theoretical Concentrations of Dinitrogen Trioxide and
Dinitrogen Tetroxide in Equilibrium with Various Levels of
Gaseous Nitric Oxide and Nitrogen Dioxide in Air at 25°C. . .
4-1. Distribution of Nitrogen in Major Compartments
4-2. Estimates of Global Nitrogen Fixation in the Biosphere . . .
4-3. Estimates of Global Emissions and Fluxes of Oxides of
Nitrogen and Related Compounds
4-4. Estimates of the Global Flux of Nitrates and Nitrites ....
4-5. Estimates of Global Flux of NO
4-6. Estimates of the Global Flux or Nitrous Oxide
4-7. Estimates of the Global Flux of Ammonia and Ammonia Compounds.
4-8. Estimates of Global Denitrification
5-1. Estimated Annual Global Emissions of Nitrogen Dioxide
(Anthropogenic)
5-2. Historic Nationwide NO Emission Estimates 1940-1970 ....
5-3. Recent Nationwide NO Emission Estimates 1970-1976
5-4. NO/NO Ratios in Emissions from Various Source Types ....
5-5. Estimated Ammonia Emission from Fertilizer Application and
Industrial Chemical Production in U.S. (1975)
Page
1-6
1-11
1-14
1-17
1-22
1-25
3-3
3-4
3-8
3-12
4-5
4-6
4-7
4-9
4-10
4-13
4-16
4-17
5-2
5-3
5-5
5-13
5-15
xx
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Table Page
5-6. Nitrogenous Compounds Applied as Fertilizer in the U.S.
1955-1976 5-18
6-1. Reactions of Alkoxyl, Alkylperoxyl and Acylperoxyl
Radicals with NO and NO, . 6-9
6-2. Summary of Conclusions from Smog Chamber Experiments . . . . 6-14
6-3. Predicted Nitrite and Nitrate Concentrations in Simulation
of Experiment EC-237 of the Statewide Air Pollution Research
Center of University of California, Riverside, Using the
Chemical Mechanism of Falls and Seinfeld 6-19
6-4. Maximum Concentrations and Yields of the Products of
Diethylamine and Triethylamine 6-38
7-1. Performance Specifications for Nitrogen Dioxide Automated
Methods 7-3
7-2. Consistent Relationship Test Specifications for Nitrogen
Dioxide 7-3
7-3. Statistical Analysis of NO, Measuring Method Differences . . 7-13
7-4. Summary of Reliability of NO,, Analytical Methods in Common
Use as Obtained by Collaborative Testing 7-15
7-5. Results of 1977 Formal Audit on In-service Chemiluminescent
Analyzers in St. Louis ^. 7-16
7-6. Summary of Nitric Acid Detection Techniques 7-20
7-7. Comparison of Nitrate Collected on Various Filter Types . . . 7-22
7-8. Analytical Methods for Nitrate in Water 7-26
7-9. Methods for Determination of Nitrate in Soils 7-28
8-1. Background NO Measurements. . 8-3
8-2. Yearly Average and Maximum Concentrations of Nitric Oxide
at Camp Stations, Measured by the Continuous Saltzman ;
Colorimetric Method 8-6
8-3.. Five-Yr Averages of Nitric Oxide Concentrations at Camp
Stations, Measured by Continuous Saltzman Colorimetric
Method 8-9
8-4. Yearly Average and Maximum Concentrations of Nitrogen
Dioxide at Camp Stations, Measured by the Continuous
Saltzman Colorimetric Method 8-10
8-5. Five-Year Averages of Nitrogen Dioxide Concentrations at Camp
Stations,, Measured by the Continuous Saltzman Colorimetric
Method 8-12
8-6. Five-Year Changes in Ambient NO,, Concentrations 8-21
8-7. Ratio of Maximum Observed Hourly Nitrogen Dioxide Concen-
trations to Annual Means During 1975 for Selected Locations . 8-25
8-8. Frequency Distribution of 1975 Hourly NO,, Concentrations at
Various Sites in U.S. Urban Areas ... 7 8-27
xxi
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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
NO, Concentrations at Various Sites in U.S. Urban Areas .... 8-32
8-11. Distribution by Time of Day of One-hour Maximum NO,,
Concentrations for One Month in 1975 for Selected Drban !
Sites 8-49
8-12. Mean and Top Five Nitrogen Dioxide Concentrations Reported
From 18 Individual RAMS Stations in St. Louis During 1976 . . . 8-52
8-13. Geographical Variation of Hourly ML Concentrations
During a Period of High N02 Concentrations 8-56
8-14. High Concentrations of Nitrogen Oxides, St. Louis,
Missouri, 1976 8-60
8-15. Monthly Trends in Hourly NO and N0« Concentrations,
Massey Building, Fairfax County, Virginia, 1977 8-61
8-16. Monthly Trends in Hourly NO and NO,, Concentrations,
Lewinsville Station, Fairfax County, Virginia, 1977 8-62
8-17. Monthly Trends in Hourly NO and N0? Concentrations,
Seven Corners Station, Fairfax County, Virginia, 1977 8-63
8-18. Mean NO Concentrations from Isolated Point Source in
Complex Terrain (Clinch River Power Plant) 8-66
8-19. Ten Highest Hourly Average NO Concentrations
Observed at Each Monitoring Site for Isolated Source
(Clinch River Power Plant) . 8-67
8-20. Regionwide Impact of Weekday-Weekend Phenomena on
Population Exposure to Nitrogen Dioxide 8-70
8-21. U.S. Population at Risk to Various 1974 N02 Hourly
Ambient Concentrations 8-72
11-1. Composition of Ecosystems 11-7
11-2. Mean pH Values in the New York Metropolitan Area (1975-1977). . 11-29
11-3. Storm Type Classification 11-29
11-4. Chemical Composition (Mean ± Standard Deviation) of Acid Lakes
(pH <5) in Regions Receiving Highly Acidic Precipitation
(pH <4.5), and of Soft-Water Lakes in Areas Not Subject to
Highly Acidic Precipitation (pH >4.8) ... 11-41
11-5. pH levels Identified in Field Surveys as Critical to Long-Term
Survival of Fish Populations 11-63
11-6. Potential Effects of Acid Precipitation on Soils 11-68
11-7. Types of Direct, Visible Injury Reported in Response to Acidic
Wet Disposition 11-78
11-8. Thresholds for Visible Injury and Growth Effects Associated
with Experimental Studies of Wet Deposition of Acidic
Substances (Alter Jacobson, 1980a,b) 11-81
11-9. Lead and Cooper Concentration and pH of Water from Pipes
Carrying Outflow from Hinckley Basin and Hanns and Steele
Creek Basin, Near Amsterdam, New York 11-88
11-10. Composition of Rain and Hoarfrost at Headingley, Leeds 11-90
11-11. The Sensitivity to Acid Precipitation Based, on Buffer
Capacity Against pH-Change, Retention of H , and Adverse
Effects on Soils 11-98
xx ii
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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 N0? Exposures for 5 Percent Injury Levels on
Selected Vegetation 12-35
12-8. Effect of Chronic N02 Exposures on Plant Growth and Yield . . 12-36
12-9. Plant Response to Suffur Dioxide and Nitrogen Dioxide
Mixtures 12-42
12-10. The Effects of NOp and SO,, Singularly and in Combination on the
Growth of Several Grasses: 12-43
13-1. Fading of Dyes on Cellulose Acetate and Cellulosics
{Cotton and Rayon) 13-3
13-2. Color Changes on Dyed Fabric—Exposed Without Sunlight
in. Pollution and Rural Areas 13-5
13-3. Typical Concentrations of Atmospheric Contaminants in
Exposure Areas 13-7
13-4. Exposure Sites 13-9
13-5. Average Fading of 20 Dye-Fabric Combinations After 12
Weeks Exposure to Nitrogen Dioxide 13-11
13-6. Effect of Nitrogen Dioxide on Fading of Dyes on Nylon
and .Polyester 13-14.
13-7. Estimated Costs of Dye Fading in Textiles 13-16
13-8. Yellowing of Whites by Nitrogen Dioxide 13-18
13-9. Corrosion of Metals by Nitrogen Dioxide . 13-24
14-1. Respiratory Tract Transport and Absorption 14-2
14-2. Mortality from N02 Exposure for 1 to 8 hours 14-4
14-3. Interaction with Infectious Agents 14-6
14-4. The Influence of Concentration and Time on Enhancement
of Mortality Resulting From Various NO- Concentrations .... 14-11
14-5. Mucociliary Transport 14-19
14-6. Alveolar Macrophages 14-21
14-7. Immunological Effects 14-25
14-8. Effects of NCL on Lung Biochemistry 14-29
14-9. Effect of N0? on Lung Morphology 14-42
14-10.. Pulmonary Functions 14-50
14-11. Studies of Potential Hyperplasia 14-55
14-12. Production of Lung Edema by N0? 14-58
14-13. Tolerance to N09 Exposures . 14-60
c.
xxm
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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 N0?: Body Weight -14-72
14-19. Nitric Oxide 14-79
14-20. Nitric Acid and Nitrates 14-81
14-21. Summary of Effects in Animals at Concentrations of
10 ppm or Less 14-85
15-1. Effects of Exposure to Nitrogen Dioxide on Sensory
Receptors in Controlled Human Studies 15-5
15-2. Effects of Exposure to Combinations of Pollutants on
Sensory Receptors in Controlled Human Studies 15-7
15-3. Effects of Exposure to Nitrogen Dioxide on Pulmonary
Function in Controlled Studies of Healthy Humans 15-9
15-4. Effects of Exposure to Nitrogen Dioxide on Pulmonary
Function in Controlled Studies of Sensitive Humans 15-18
15-5. Quantitative Community Health Epidemiological Studies on
Effects of Exposure to Nitrogen Dioxide on Pulmonary Function 15-24
15-6. Effects of Exposure to Nitrogen Dioxide in the Home on
the Incidence of Acute Respiratory Disease in Epidemiology
Studies Involving Gas Stoves 15-31
15-7. Nitrogen Dioxide Levels Reported in Gas and Electric Stove
Homes 15-54
xxiv
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ABBREVIATIONS, ACRONYMS, AND SYMBOLS
O O _TQ
A Angstrom (10 meter)
"A" strain A particular type of influenza virus
AaDOp Difference between alveolar and arterialized partial
pressure of oxygen
AAS Atomic absorption spectroscopy
AATCC American Association of Textile Chemists and Colorists
Ad A particular strain of laboratory mouse
AICHE American Institute of Chemical Engineers
AM Alveolar macrophage
AMP Adenosine monophosphate; adenosine 5' phosphate
ANSA 8-anilino-l-naphthalene-sulfonic acid
APCD Air Pollution Control District
APHA American Public Health Association
A/PR/8 A particular strain of influenza virus
A/PR/8/34 A particular strain of influenza virus
AQCR Air Quality Control Region
AQSM Air Quality Simulation Model
ASTM American Society for Testing and Materials
atm One atmosphere, a unit of pressure
ATP Adenosine triphosphate
avg Average
BAKI Potassium iodide solution acidified with boric acid
BHA Butylated hydroxyanisole
BHT Butylated hydroxytoluene
BP Blood pressure
xxv
-------
scat
C3H
C57BL
C57BL/6
cAMP
GAMP
CD-I
cGMP
°C
14C
CHE
CL;
CLdyn
CLstat
cm
CNS
CO
co2
CoA
C.OH
CPK
CR-1
CRD
CV
C x T
Extinction coefficient due to scatter by aerosols
A particular strain of laboratory mouse
A particular strain of laboratory mouse
A particular strain of laboratory mouse
Cyclic adenosine monophosphate; adenosine 5'-phosphate
Community Air Monitoring Program
A particular strain of laboratory mouse
Cyclic guanosine monophosphate; guanosine 5'-phosphate
Degrees Celsius (Centigrade)
A radioactive form of carbon
Cholinesterase
Lung compliance
Dynamic lung compliance
Static lung compliance
Centimeter
Central nervous system; the brain and spinal cord
Carbon monoxide
Carbon dioxide
Coenzyme A
Coefficient of haze
Creatine phosphokinase
A particular strain of laboratory mouse
Chronic respiratory disease
Closing volume
Exposure concentration in ppm multiplied by time of
exposure in hours or other time measurement
Day
xxvi
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DEN Diethylnitrosamine (also DENA)
DIFKIN Diffusion Kinetics Model
DL-Q Diffusion capacity of the lung for carbon monoxide
DMN Dimethylnitrosamine
DMA Deoxyribonucleic acid
D = CT Dose equals concentration multiplied by time
DPPD N,N diphenylphenylenediamine
EC Prefix of International Commission on Enzymes' identification
numbers
EKG Electrocardiogram
EPA U.S. Environmental Protection Agency
°F Degrees Fahrenheit
FEF: Forced expiratory flow
FET First-edge time
FEV Forced expiratory volume
FEV-, Q One-second forced expiratory volume
FEVg 7r 0.75-second forced expiratory volume
FRM Federal Reference Method for air quality measurement
ft Foot
FT Fourier transform spectroscopy (also FS)
FVC Forced vital capacity
g . Gram
G6P Glucose-6-phosphate
GC Guanylate cyclase
GL Gas chromatography
GC-MS Gas chromatograph in combination with mass spectrometry
GM General Motors Corporation
xxvn
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GMP Guanosine 5'-phosphate; guanosine monophosphate
GSH A tripeptide, glutathione (reduced form)
GSSG The disulfide (oxidized) form of GSH
H' Hydrogen (free radical)
H Tritium; a radioactive form of hydrogen
ha Hectare
HbCL Oxyhemoglobin
HN02 Nitrous acid (also HONO)
HNO, Nitric acid (also HOMO,)
•3 . £
HO1 Hydroxyl free radical (also OH)
H0«' Hydroperoxyl free radical
HQ?NO Pernitrous acid
H02N02 Pernitric acid (also HOON02)
hr Hour
HR Heart rate
hv Planck's constant (h) times the frequency of radiated
energy (v) = Quanta of energy (E)
H202 Hydrogen peroxide
H?S Hydrogen sulfide
H2SO. Sulfuric acid
IARC International Agency for Research on Cancer
Ig Immunoglobulins
IgA Immunoglobulin A fraction
IgG Immunoglobulin G fraction
IgG-, Immunoglobulin G-, fraction
IgGp Immunoglobulin G2 fraction
IgM Immunoglobulin M fraction
xxviii
-------
in Inch
IR Infrared
k Rate constant or dissociation constants
kg Kilograms
km Kilometer
1 Liter (also £)
LC50 Lethal concentration 50%; that concentration which is
lethal to 50 percent of test subjects
LD50 Lethal dose 50%; dose which is lethal to 50 percent of
the subjects
LT50 The time required for 50 percent of the test animals
to die when given a lethal dose
LDH Lactic acid (lactate) dehydrogenase
LPS Bacterial lipopolysaccharide
m Meter
M Molar
M Third body (in a reaction)
MAK 'Maximum permissible concentration (in Germany)
max Maximum
MFR Maximal flow rate
|jg/m Micrograms per cubic meter
mg/m Milligrams per cubic meter
Mg Magnesium
ml Milliliter
mM Millimoles
MMD Mass median diameter
MMFR Mid-maximal flow rate
mo Month
xxix
-------
MPC Maximum permissible concentration (in the U.S.S.R.)
MT Metric Ton
N Nitrogen
N Normal
13
N A radioactive form of nitrogen
N-6-MI N-nitrosoheptamethyleneimine
NA Not applicable
NAAQS National Ambient Air Quality Standard
NaCl Sodium chloride; common table salt
NAD+ Nicotinamide-adenine dinucleotide (+ indicates oxidized
form)
NADB National Air Data Bank
NADH Nicotinamide-adenine dinucleotide (reduced form)
NADPH Nicotinamide-adenine dinucleotide phosphate (reduced
form)
NaOH Sodium hydroxide
NAS National Academy of Sciences
NASN National Air Surveillance Network
NDIR Nondispersive infrared
NEDA N-(l-Naphthyl)-ethylenediamine dihydrochloride
NEDS National Emissions Data System
NEIC National Enforcement Investigations Center
ng Nanogram
NH» Ammonium ion or radial
nm Nanometer
NO Nitric oxide
NOHb Nitrosylhemoglobin
xxx
-------
NO Nitrogen oxides
/V
N?0 Nitrous oxide
NO,, Nitrogen dioxide
N203 Dinitrogen trioxide
NpO. Dinitrogen tetroxide
NSF National Science Foundation
0 Atomic oxygen
0( D) Excited atomic oxygen
0 Ozone
OH Hydroxyl group
0(
32
0( P..) Ground state^ atomic oxygen
P A radioactive form of phosphorus
Alveolar partial pressure of carbon dioxide
Arterial partial pressure of carbon dioxide
PAH p-Ammiohippuric acid
PAN Peroxyacetyl nitrate
PaOv, Arterial partial pressure of oxygen
PAO,, Alveolar partial pressure of oxygen
pH Log of the reciprocal of the hydrogen ion concentration
PHA Phytohemagglutinin
P0? Partial oxygen pressure
ppb Parts per billion
pphm Parts per hundred million
ppm Parts per million
ppt Parts per trillion
Q Cardiac output
QRS A complex of three distinct electrocardiogram waves which
represent the beginning of ventricular contraction
xxx i
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RAMS Regional Air Monitoring System
RAPS Regional Air Pollution Study
R Airway resistance
!RBC Red blood cell; erythrocyte
RM Reference method for air quality measurement
RNA Ribonuclei-c acid
RV Residual volume
SAI Science Applications, Inc.
SD Standard deviation
SCOT Serum glutamic-oxaloacetic transaminase
SGPT Serum glutamic-pyruvic transaminase
SH- Sulfhydryl group
SMSA Standard Metropolitan Statistical Area
SN Suspended nitrates
S02 Sulfur dioxide
SPF Specific pathogen free
SR Specific airway resistance
aw
SRM Standard reference material
SS Suspended sulfates
STP Standard temperature and pressure
TEA Triethanolamine
r -i p
Tg Terragram; 10 metric tons or 10 grams
TGS-ANSA A 24-hour method for the detection of analysis of NO-
in ambient air
tiC Total lung capacity
TPTT 20 percent transport time
TSP Total suspended particulate
xxxi i
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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
maX
V.-p Total volume
V/V Volume per volume
WBC White blood cells
wk Week
yr Year
Zn Zinc
ug Microgram
ul Microliter
urn Micrometer
> Greater than
< Less than
•^ Approximately
xxxm
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CONTRIBUTORS AND REVIEWERS
Principal authors:
Dr. Charles E. Anderson, Department of Botany, North Carolina State Univer-
sity, Raleigh, North Carolina.
Dr. Paul J. Crutzen, National Center for Atmospheric Research, Boulder,
Colorado.
Dr. Sandor J. Freedman, System Sciences, Inc., Chapel Hill, North Carolina.
Dr. J. H. B. Garner, Environmental Criteria and Assessment Office, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Judith A. Graham, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina.
Dr. Daniel Grosjean, Statewide Air Pollution Research Center, University
of California, Riverside, California.
Dr. Steven M. Horvath, Institute of Environmental Stress, University of
California at Santa Barbara, Santa Barbara, California.
Dr. Gory J. Love, Consultant, System Sciences, Inc., Chapel Hill, North
Carolina.
Dr. Daniel B. Menzel, Department of Pharmacology, Duke University, Durham,
North Carolina.
iDr. Joseph Roycroft, Jr., Health Effects Research Laboratory, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina.
Dr. Victor S. Salvin, University of North Carolina, Greensboro, North
Carolina.
I Dr. John H. Seinfeld, Department of Chemical Engineering, California
Institute of Technology, Pasadena, California.
Dr. John C. Trijonis, Technology Service Corporation,, Santa Fe, New Mexico.
Dr. Warren H. White, Technology Service Corporation, Pasadena, California.
Contributing authors and reviewers:
Dr. Martin Alexander, Department of Agronomy,- Cornell University, Ithaca,
New York.
Dr. Patrick L. Brezonik, Department of Environmental Engineering Sciences,
University of Florida, Gainesville, Florida.
xxxiv
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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 Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. George M. Duggan, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. Richard Ehrlich, Illinois Institute of Technology Research Institute,
Chicago, Illinois.
Mr. Robert B. Faoro, Monitoring and Data Analysis Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. C. Eugene Feigley, Department of Environmental Health, University of
South Carolina, Columbia, South Carolina.
Dr. Jack Fishman, National Center for Atmospheric Research, Boulder,
Colorado.
Dr. Robert Frank, Department of Environmental Health, University of Washing-
ton, Seattle, Washington.
Dr. Elliot Goldstein, Department of Internal Medicine, University of
California, Davis, California.
.Dr. Lester D. Grant, Environmental Criteria and Assessment Office, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Mark M. Greenberg, Environmental Criteria and Assessment Office, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Jack D. Hackney, Rancho Los Amigos Hospital Campus, University of
Southern California, Downey, California.
Mr. Albert V. Hardy, System Sciences, Inc., Chapel Hill, North Carolina.
Dr. Steven M. Horvath, Institute of Environmental Stress, University of
California, Santa Barbara, California.
Dr. Harvey E. Jeffries, Department of Environmental Sciences and Engineering,
University of North Carolina, Chapel Hill, North Carolina.
Dr. Evaldo Kothny, California State Department of Health, Berkeley, California.
xxxv
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Mr. William S. Lanier, Industrial Environmental Research Laboratory, U.S. ,
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. David J. McKep, Environmental Criteria and Assessment Office, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina.
Dr. Sidney S. Mirvish, Eppley Institute for Research in Cancer, University
of Nebraska, Omaha, Nebraska.
Mr. Larry J. Purdue, Environmental Monitoring and Support Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Carl M. Shy, Institute of Environmental Health, University of North
Carolina, Chapel Hill, North Carolina.
Mr. Herschel H. Slater, PEDCo Environmental, Inc., Durham, North Carolina.
Mr. Mark G. Smith, System Sciences, Inc., Chapel Hill, North Carolina.
Dr. Edward P. Stahel, Department of Chemical Engineering, North Carolina
State University, Raleigh, North Carolina.
Dr. David T. Tingey, Corvallis Environmental Research Laboratory, U.S.
EnvironmentalProtection Agency, Corvallis, Oregon.
Reviewers:
Mr. Gerald G. Akland, Environmental Monitoring and Support Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Aubrey P. Altschuller, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Mark R. Antell, Division of Stationary Source Enforcement, U.S. Environ-
mental Protection Agency, Washington, D.C.
Mr. John D. Bachmann, Strategies and Air Standards Division, Office of Air
Quality Planning, and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. Ronald L. Baron, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina.
Mr. Norman J. Beloin, Surveillance and Analysis Division, Region I, U.S.
Environmental Protection Agency, Boston, Massachusetts.
Mr. Michael A. Berry, Environmental Criteria and Assessment Office, U.S.:.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Frank M. Black, Environmental Sciences Research Laboratory, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina.
xxxvi
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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.
i
Mr. Angelo P. Capparella, Environmental Criteria and Assessment Office,
U.S. Environmental Protection Agency, Research Triangle Park,
North Carolina.
Capt. Harvey J. Clewell, III, Civil and Environmental Engineering Develop-
ment Office, Tyndall Air Force Base, Florida.
Mr. Stanton Coerr, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. David L. Coffin, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina.
.Dr. Henry S. Cole, Monitoring and Data Analysis Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. Ellis B. Cowling, Department of Plant Pathology, North Carolina State
University, Raleigh, North Carolina.
Mr. Swep T. Davis, Deputy Assistant Administrator for Water Planning and
. Standards, Office of Water and Waste Management, U.S. Environmental
Protection Agency, Washington, D.C.
Dr. Kenneth L. Demerjian, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Marcia C. Dodge, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Thomas G. Dzubay, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Thomas G. Ellestad, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Douglas Fennel!, Environmental Criteria and Assessment Office, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Neil H. Frank, Monitoring and Data Analysis Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. Gustave Freeman, Stanford Research Institute, Menlo Park, California.
xxxvi i
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Dr. Donald E. Gardner, Health Effects Research Laboratory, U.S. Environ-
mental Protection Agency, Research Triangle Park, N.C.
Dr. Philip L. Hanst, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Fred H. Haynie, Environmental Sciences Research Laboratory, U.S. Envi-
ronmental Protection Agency, Research Triangle Park, North Carolina.
Dr. Walter W. Heck, Department of Botany, North Carolina State University,
Raleigh, North Carolina.
Mr. George C. Holzworth, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Allen Hoyt, Environmental Criteria and Assessment Office, U.S. Envi-
ronmental Protection Agency, Research Triangle Park, North Carolina.
Dr. F. Gordon Hueter, Health Effects Research Laboratory, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina.
Mr. Michael H. Jones, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. John H. Knelson, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina.
Dr. Kenneth T. Krost, Environmental Sciences Research Laboratory, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Ms. Pamela A. Mealer, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Mr. Thomas R. McCurdy, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office, U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina.
Mr. M. Rodney Midgett, Environmental Monitoring and Support Laboratory,
U.S. Environmental Protection Agency, Research Triangle Park, North
Carolina.
Mr. Edwin L. Meyer, Monitoring and Data Analysis Division, Office of Air
Quality Planning,and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Mr. William Nelson, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research .Triangle Park, North Carolina.
'xxxviii
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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.
Env.ironmental Protection Agency, Research Triangle Park, North Carolina.
Mr. Orin W. Stopinski, Health Effects Research Laboratory, U.S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina.
Mr. Joseph Suggs, Health Effects Research Laboratory, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina.
Mr. Matthew Van Hook, Air, Noise and Radiation Division, U.S. Environmental
Protection Agency, Washington, D.C.
xxx ix
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Dr. David E. Weber, Corvallis Environmental Research Laboratory, U.S. Envi-
ronmental Protection Agency, Corvallis, Oregon.
Mr. Albert H. Wehe, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina.
Dr. Jerome Weslowski, California State Department of Health, Berkeley, California.
Mr. Larry Zaragoza, Strategies and Air Standards Division, Office of Air
Quality Planning and Standards, U.S. Enviornmental Protection Agency,
Research Triangle Park, North Carolina.
xl
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J
f •
• I
Project management, editing, production, and word processing at System
Sciences, Inc., Chapel Hill, North Carolina, under contract to the Environ-
mental Criteria and Assessment Office, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina:
Dr. Edgar A. Parsons
Ms. Gayla Benignus
Dr. Sandor J. Freedman
Ms. Doris M. Lange
Ms. Elsa M. Lewis-Heise
Ms. Jeannine A. McFarland
Ms. Trudy E. Oakes
Ms. Diane Robinson
Ms. E. L. Rusten
Mr. Mark G. Smith
Mr. Robert E. Wenzel
Word processing and other assistance at the Environmental Criteria and
Assistance Office, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina:
Ms. Del a Bates "
Ms. Diane ChappeTijtS?:
1 Ms. Constance Van^OoJsten
Ms. Evelynne Rash ^n
Ms. Donna Wicker
xli
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CLEAN AIR SCIENCE ADVISORY COMMITTEE
SUBCOMMITTEE ON AIR QUALITY
CRITERIA FOR OXIDES OF NITROGEN
CHAIRMAN:
Dr. Sheldon K. Friedlander, Vice Chairman of Chemical Engineering, Department
of Chemical, Nuclear, and Thermal Engineering, School of Engineering and
Applied Science, University of California, Los Angeles, California 90024
MEMBERS:
Dr. Mary 0. Amdur, Department of Nutrition and Food Science, Room 16-339,
Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Dr. Domingo M. Aviado, Allied Chemical, P.O. Box 1021 R, Morristown, New
Jersey 07960
Dr. Judy A. Bean, College of Medicine, Department of Preventive Medicine and
Environmental Health, University of Iowa, Iowa City, Iowa 52242
Dr. Robert Dorfman, Department of Economics, Harvard University, 325 Lattauer,
Cambridge, Massachusetts 02138
Mr. Harry H. Hovey, Jr., New York Department of Environmental Conservation, 50
Wolf Road, Albany, New York 12233
Dr. Donald H. Pack, 1826 Opalocka Drive, McLean, Virginia 22101
STAFF OFFICER:
Dr. Terry F. Yosie, Science Advisory Board, U.S. Environmental Protection
Agency, Washington, D.C. 20460
xlii
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1. SUMMARY OF EFFECTS OF OXIDES OF NITROGEN AND RELATED
COMPOUNDS ON HUMAN HEALTH AND WELFARE
1.1 INTRODUCTION
This criteria document critically evaluates scientific information on both short- and
long-term health and welfare effects of nitrogen oxides as well as other nitrogenous com-
pounds, such as nitric and nitrous acids, nitrites, nitrates, and nitrosamines. Pursuant to
Sections 108 and 109 of the Clean Air Act, as amended in 1977, it is to serve as a basis for
evaluating the need to promulgate National Ambient Air Quality Standards for any or all of
these compounds. The scientific evidence reviewed includes significant new research published
since the first edition of Air Quality Criteria for Nitrogen Oxides in 1971.
Major questions addressed in this document include the following:
(1) What are identifiable health effects associated with exposure to
airborne nitrogenous compounds?
(2) At what level(s) of exposure do such health effects occur in humans?
(3) Are there population subgroups especially susceptible to the effects
of exposure to airborne nitrogenous compounds?
(4) What are the major welfare effects on visibility, vegetation, and
materials associated with airborne nitrogenous compounds?
(5) At what concentration levels do effects on visibility, vegetation
and materials occur?
(6) To what degree do airborne nitrogenous compounds contribute to
large-scale environmental effects such as acidic precipitation?
(7) Are presently available techniques for measuring atmospheric levels
of nitrogenous compounds adequate?
(8) What are the major sources of airborne nitrogenous compounds?
(9) What concentrations of nitrogenous compounds of concern occur in
ambient air?
This present chapter summarizes available data on the effects on human health and welfare
of nitrogen oxides (NO ), consisting principally of nitrogen dioxide (NOp) and nitric oxide
(NO), and other nitrogenous compounds which may be derived from NO through atmospheric trans-
formations. Since N02 has been most conclusively demonstrated to exert deleterious effects,
the emphasis here has been placed on the interpretation of data bearing on N02 effects in
order to estimate ambient air concentration levels at which such effects on human health and
welfare occur. Information on natural and man-made sources, atmospheric chemical and physical
transformations, techniques of sampling and analysis, and additional data on ambient concen-
trations are also summarized in the present chapter. The reader is referred to the subsequent
document chapters for more detailed information on all of the above topics.
1-1
-------
1.2 SOURCES, TRANSFORMATIONS AND AMBIENT LEVELS OF NITROGEN OXIDES
Oxides of nitrogen have their origin in a number of natural and man-made processes
(Chapters 4 and 5). In terms of sources giving rise to significant human exposure, however,
the most important emissions occur as a result of man's burning of fossil fuels such as coal,
oil or gasoline. Emissions from motor vehicles (mobile combustion) and from installations
burning fossil fuels (stationary combustion) are the two largest sources, constituting about
44 percent and 51 percent of the nationwide NO emissions, respectively, in 1976, In the
stationary combustion category, electric utilities were responsible for approximately 56 per-
cent of the NO emissions and industrial combustion accounted for another 38 percent. In the
mobile combustion category, highway vehicle emissions constituted about 77 percent, with the
rest attributable to non-highway vehicles.
In most ambient situations, NOp is not emitted directly into the atmosphere in significant
amounts (typically less than 10 percent of NO emissions). It is important to note, however,
that NOp forms upwards of 30 to 50 percent of the total NO emissions from certain diesel and
jet turbine engines under specific load conditions. Diesel emissions of NOp may become of
concern in local situations if there is a widespread increase in the use of diesel-powered
vehicles. NO- is formed, generally, from the oxidation of the more commonly emitted compound
nitric oxide (NO). The chemical pathways by which NO is transformed to NO^are complex and
involve other atmospheric constituents such as hydrocarbons and ozone. Also, NOp is not the
final product of atmospheric reactions. It may decompose in the presence of sunLight or it
may undergo further transformation into gaseous nitric acid (HNO,) and/or nitrate aerosols,
small particles suspended in ambient air (Chapter 6). For these and other reasons, the
relationship between NO emissions and resulting ambient N09 concentrations is neither direct
A £ ,
nor constant.
Oxides of nitrogen and their atmospheric transformation products may be transported in
ambient air over distances ranging up to hundreds of kilometers from the emissions source and
over times ranging up to several days. Ultimate removal from the air occurs by a variety of
processes including uptake by vegetation, deposition on surfaces and precipitation by rain or
snow. The times and distances involved in the' transformation, transport, and removal of
atmospheric nitrogenous compounds indicate that these pollutants not only exert an impact in
proximity to primary sources, but are also of concern in relation to deleterious effects
exerted at considerable distances from points of initial emission or transformation. The con-
tribution of nitric acid to the phenomenon of acidic precipitation, which may occur hundreds
of kilometers from a source or sources of NO , is an example of such a non-local impact
(Chapter 11).
It has been suggested that oxides of nitrogen may react in the atmosphere with amines
emitted by certain sources to produce nitrosamines. However, there is little evidence to date
to indicate that this reaction takes place in ambient situations or that the atmospheric route
for human exposure to this class of compounds is a cause for concern.
1-2
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In general, adequate methodology now exists for sampling and analysis of NCL concentra-
tiohs in ambient air (Chapter 7). Techniques for routine determination of atmospheric concen-
trations of nitric acid and nitrate aerosols, however, are currently only in the developmental
stage.
Various government agencies have routinely monitored NCL for some time. The following
summary of recent ambient levels of N0~ occurring nationwide is given to place in perspective
the concentration levels associated with the health and welfare effects discussed later in
this chapter. Chapter 8 contains a more thorough survey of available monitoring data. The
reader should note that not all persons living or working in the areas mentioned will actually
experience the NO- concentrations cited. Moreover, considering the likelihood that fixed
monitoring sites may not intercept the maximum N0~ concentration, there is a possibility that
the concentrations reported underestimate the exposure experienced by at least some portion of
the population in the areas cited.
Examination of selected nationwide monitoring data for 1975 to 1980 reveals that during
at least one of these years, peak 1-hour N0? concentrations equalling or exceeding 750 ug/m
(0.4 ppm) were experienced in Los Angeles and several other California sites; Ashland,
Kentucky; and Port Huron, Michigan. Additional sites reporting at least one peak hourly con-
centration equalling or exceeding 500 ug/m (0.27 ppm) include: Phoenix, Arizona; St. Louis,
Missouri; New York City, New York; 14 additional California sites; Springfield, Illinois;
Cincinnati, Ohio; and Saginaw and Southfield, Michigan. Other scattered sites, distributed
nationwide, reported maxima close to this value. Recurrent NO, hourly concentrations in
3
excess of 250 ug/ m (0.14 ppm) were quite common nationwide in 1975 to 1980.
Annual arithmetic means for NO- concentrations in 1976 exceeded 100 ug/m (0.053 ppm) at
Anaheim, El Cajon, Riverside, San Diego, and Temple City, California. Other sites reporting
yearly arithmetic means for 1976 equalling or exceeding 100 ug/m (0.053 ppm) included
Chicago, Illinois, and Southfield, Michigan. However, virtually none of the same monitoring
sites still operating in 1980 reported values above 100 ug/m in that year (except for one in
2
San Diego; 114 ug/m ).
1.3 EFFECTS OF NITROGEN OXIDES ON HUMAN HEALTH
As summarized above, nitric oxide (NO) is the most prevalent oxide of nitrogen directly
emitted into the ambient air as the result of anthropogenic activities such as fossil fuel
combustion. In addition, other compounds, such as nitrogen dioxide (NO-), gaseous nitric acid
(HN03), nitrites and nitrate aerosols, have been clearly established as being formed in the
ambient air as the result of atmospheric chemical reactions of NO and other nitrogen oxides
with non-nitrogenous substances. The formation of nitrosamines in the ambient air has been
suggested, but not convincingly demonstrated.
Concern has been expressed about possible harmful health effects of virtually all of the
above types of nitrogen oxide compounds. Despite such concern and considerable scientific
inquiry on the subject, there now exist relatively little hard data linking specific health
effects to the majority of the above nitrogen oxide compounds. The one notable exception is
nitrogen dioxide.
1-3
-------
The literature reviewed in detail in Chapter 15 of this document indicates that nitric
oxide (NO) is not of direct concern for human health effects at typical ambient air concentra-
tion levels recorded over U.S. cities. Similarly, there is presently no evidence that nitrites
at levels ordinarily found in the atmosphere are of concern for human health. In addition,
although it has been suggested that atmospheric nitrates may be associated with increased
numbers of asthmatic attacks, no data are presently available that are sufficient upon which
to base firm conclusions regarding the subject.
The lack of strong evidence, or even conclusive pertinent studies, associating health
effects with most nitrogen oxide compounds is in striking contrast to the more extensive and
convincing data base which links a number of specific health effects to nitrogen dioxide (N0~).
Information on NO^ formation and its effects is, therefore, most heavily emphasized both
in the present summary chapter and elsewhere in this document. In regard to the types of
health effects of NO^ most definitively characterized to date, the effects of NCL on the
respiratory system have been most extensively delineated and appear to be of most concern in
terms of both acute and long-term health implications. Major attention is accorded here to
the summary and interpretation of key studies and the overall pattern of results bearing on
respiratory system effects of NCk.
1.3.1 Nitrogen Dioxide Respiratory System Effects
Nitrogen dioxide's effects on human and animal respiratory systems span a broad spectrum
both in terms of initial severity and ultimate long-term health impact. The continuum of '
observed N02 effects ranges from (1) death or irreversible pulmonary damage seen with
accidental high exposures to NO^ primarily in occupational settings; through (2) less severe,
but significant short-term and chronic tissue damage, functional impairment, and exacerbation
of other disease processes observed at lower exposure levels; to (3) comparatively mild
transient effects, such as impaired olfactory reception, which commence at still lower NO-
levels.
Acute high level exposures to N09 that have occurred accidentally or in occupational
3
settings demonstrate that concentrations in the range of 560,000 ug/m (300 ppm) or higher are
3
likely to result in rapid death. Concentrations in the range of 280,000 to 380,000 ug/m
(150-200 ppm) are not likely to cause immediate death, but severe respiratory distress and
death occur after a period of 2 to 3 weeks. In such cases, the cause is almost always bronchi-
olitis fibrosa obliterans. Non-fatal acute exposures to 94,000 to 190,000 ug/m (50 to 100
ppm) N09 are associated with reversible bronchiolitis, whereas acute exposures to 47,000 to
3
140,000 ug/m (25 to 75 ppm) are associated with bronchitis or bronchial pneumonia and are
usually but not always followed by essentially complete recovery. It should be noted that
exposures to such high levels of N0« only typically occur in connection with certain occupa-
tional or accidental (e.g. fires) circumstances, and are not of concern in relation to ambient
air exposures of the general public.
In addition to the above health effects induced by acute high level N02 exposures, how-
ever, a variety of respiratory system effects have been reported to be associated with expo-
sures to lower concentrations of NO-. Extensive literature characterizing such effects has
1-4
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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 ^-induced
respiratory effects characterized by these different approaches include: (1) increased airway
resistance (Ra.,) and other indications of altered pulmonary function as observed in controlled
aW
clinical studies; (2) increased incidence of human respiratory illnesses, as determined by cer-
tain epidemiological studies; and (3) lung tissue damage and increased susceptibility to
respiratory infection, as demonstrated in animal toxicology studies.
Collectively, these studies provide evidence indicating that certain human health effects
may occur as the result of exposures to NOp concentrations approaching or falling within the
range of recorded ambient air NCL levels. Key studies providing evidence for such effects are
summarized and interpreted below in relation to several critical health issues. Those issues
include: (1) consideration of lowest effective single N0~ exposure level(s) inducing partic-
ular respiratory effects in healthy and sensitive human subjects; (2) assessment of lowest
effective exposure levels at which repeated or intermittent N02 exposures produce effects in
human populations; and (3) consideration ,of the relative significance of observed effects in
terms of understanding the likely impact of ambient N02 exposures on human health.
1.3.1.1 Controlled Human Exposure Studies—Controlled human exposure (clinical) studies have
generated extensive information on the lowest effective dose levels for the induction of
respiratory effects by single short-term N02 exposures. Some studies have focussed on such
effects in healthy adults; other studies have assessed respiratory effects in "sensitive"
members of the population, e.g., individuals with chronic respiratory problems. Summarized in
Table 1--1 are the most important controlled human exposure studies of short-term NO- exposure
effects on pulmonary functions in healthy adult subjects.
The studies summarized in Table 1-1 indicate that increased airway resistance (R,..) and
> , 3W
other physiological changes suggesting impaired pulmonary function have been clearly demon-
strated to occur in healthy adults with single 2-hr NO- exposures ranging from 3760 to 13,200
3
ug/m (2.5 to 7.0 ppm). Certain studies also indicate that significant effects occur in
healthy subjects with shorter (3-15 min) exposures to the same or possibly lower levels of NO-
administered either alone or in combination with NaCl aerosol.
More specifically, in regard to the latter point, Suzuki and Ishikawa (1965) observed
altered respiratory function after exposure of healthy subjects to NO, levels of 1300 to 3760
3
ug/m (0.7 to 2.0 ppm) for 10 minutes. Their data however, preclude a clear association of
observed effects with any particular concentration in the range of 1300 to 3760 ug/m (0.7 to
2.0 ppm) N02 exposure.
Hackney et al. (1978) reported no statistically significant changes in any of the pulmo-
nary functions tested with the exception of a marginal loss in forced vital capacity after
exposure to 1880 ug/m (1.0 ppm) NO- for 2 hours on two successive days (1.5% mean decrease, P
<0.05). The authors question the health significance of this small, but statistically signifi-
cant change in forced vital capacity in healthy subjects and suggest that the changes found
may be due to random variation.
1-5
-------
TABLE 1-1. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON
PULMONARY FUNCTION IN CONTROLLED STUDIES OF HEALTHY HUMAN ADULTS**
Concentration Pollu-
ug/mj
13,000
ppm tant
7.0 N02
No. of
Healthy
Subjects
Several
Exposure
Time
10-120
min.
Effects
Increased
tolerated
increase
R * in some
30W000 ug/ni
in Raw
subjects. Others
(16 ppm) with no
Reference***
Yokoyama,
1972
9,400 5.0 NO,
1977
11 2 hrs. Increase in R * and a decrease in AaDO?* von Nieding
with intermittent light exercise. No3en- et al.,
hancement of the effect when 200 ug/m
(0.1 ppm) 03 and 13,000 u/m (5.0 ppm)
SOp were combined with NO- but recovery
time apparently extended.
9,400
9,400
7,500
to
9,400
5,600
11,300
5.0 N02
5.0 N02
4.0 NO,
to ^
5.0
3.0 N02
6.0 N02
16 15 min. Significant decrease in DLrr)*
13 15 min. Significant decrease in PaO?* but end ex-
piratory POp* unchanged witn significant
increase in systolic pressure in the
pulmonary artery.
5 10 min. 40% decrease in lung compliance 30 min.
after exposure and increase in expiratory
and inspiratory flow resistance that
reached maximum 30 min. after exposure.
1 5 min. Increase in R * compared to pre-exposure
values (enhanced by NaCl aerosol).
1 5 min. More subjects were tested at higher
exposures.
von Nieding
et al. , 1973
von Nieding
et al. ,
1970
Abe, 1967
Nakamura,
1964
-------
TABLE 1-1. (continued)
Concentration Pollu-
|jg/ma ppin tant
No. of
Healthy Exposure
Subjects Time Effects
Reference
1
4
,880
,700
1.
2.
0
5
N09
2
N09
8
8
2
2
hrs.
hrs.
No increase
Increased R.
in R .
aw
with no further impairn
Beil
Ulmer
nent
and
, 1976
14,000 7.5 N02
9,400 5.0 N02
at higher concentrations. No change in
arterial P02 pressure or PCO- pressure.
16 2 hrs. Increased sensitivity to a bronchocon-
strictor (acetylcholine) at this concen-
tration but not at lower concentrations.
8 14 hrs. Increase in R during first 30 min. that
was reduced though second hour followed by
greater increases measured at 6, 8 and 14
hrs. Also increased susceptibility to a
bronchoconstrictor (acetylcholine).
1,300 0.7 N0?
to to
3,800 2.0
10 10 mins. Increased inspiratory and expiratory flow Suzuki and
resistance of approximately 50% and 10% of Ishikawa,
control values measured 10 rnins. after 1965
exposure.
1,880 1.0 N02
16 2 hrs. No statistically significant changes
in pulmonary function tests with
exception of small changes in FVC.
(See page 1-9 and 15-17).)
Hackney et al.
1978
1,150 0.6 N02
15 2 hrs. No physiologically significant changes
in cardiovascular, metabolic, or
pulmonary functions after 15, 30
or 60 mins. of exercise.
Folinsbee
et al., 1978
-------
TABLE 1-1. (continued)
00
Concentration
ug/mj
1,000
1,000
with
560
1,000
with
560
and
45,000
500
500
with
560
500
with
560
and
45,000
1,880
to
3,760
ppm
0.50
0.50
0.29
0.50
0.29
30.0
0.25
0.25
0.29
0.25
0.29
30.0
1.0
to
2.0
Pollu-
tant
°3
3
°3
J
N02
°3
•J
NO,
L.
CO
°3
o
°3
tj
NO,
L.
°3
O
NO,
L.
CO
NO,
L.
No. of
Healthy Exposure
Subjects Time Effects Reference
4 4 hrs. With each group minimal alterations in pul- Hackney
monary function caused by 0., exposure. et al . ,
Effects were not increased By addition of 1975
NO, or NO, and CO to test atmospheres.
L. L.
1 2 hrs. Little or no change in pulmonary function Hackney
found with 03 alone. Addition of NO, or et al. ,
of NO, and CO did not noticeably increase 1975
the effect. Seven subjects included some
believed to be unusually reactive to
respiratory irritants.
10 2 1/2 hrs Alternating exercise and rest produced Posin et al.,
significant decrease for hemoglobin, 1978
hematocrit, and erythrocyte acetyl-
chol inesterase.
-------
TABLE 1-1. (continued)
No. of
Concentration Pollu- Healthy Exposure
(jg/m-1
100
with
50
and
300
*R
aw
ppm tant Subjects
0.05 N02 11 2
0.025 0Q
3
0.11 so2
airway resistance
Time Effects
Reference
hrs. No effect on R or AaDO?; exposed sub- von Nieding
jects showed increased sensitivity of et al., 1977
bronchial tree
(acetylchol ine)
to pollutants.
to a bronchoconstrictor
over controls not exposed
AaD02: difference between alveolar and arterial blood partial pressure of oxygen
DL_0 : diffusion capacity of the lung for carbon monoxide
Pa02 : arterial partial pressure of oxygen
P0? : partial pressure of oxygen
PCO? : partial pressure of carbon dioxide
**By descending order of lowest concentration evoking a significant effect.
***Reference citations are for studies listed in the bibliography for Chapter 15.
-------
In a similar study, Kerr et al. (1979) exposed 10 normal healthy adults and 20 subjects
with asthma and chronic bronchitis to 940 ug/m (0.5 ppm) N0? for 2 hours. Although the
authors suggest that the changes reported in quasistatic compliance for normal healthy adults
may be due to chance alone, there is uncertainty whether these changes were due to normal
daily variation or to N02 exposure. No other pulmonary function tests showed significant
changes for the healthy adult group. Only one of the healthy adult group reported mild
symptomatic effects associated with exposure to N0?. The results of the Kerr study concerning
asthmatics and chronic bronchitics are discussed later.
Beil and Ulmer (1976) and Folinsbee et al. (1978) concluded that there were no physio-
logically significant pulmonary effects at exposure levels of 1880 and 1100 ug/m (1.0 and 0.6
ppm) NO,, respectively. Hackney et al. (1975a,b,c) and von Nieding et al. (1977) also con-
3
eluded that there were no physiologically significant effects at NOp levels below 560 ug/m
(0.3 ppm) in the presence of various other air pollutants, with the exception of increased
sensitivity to a bronchoconstrictor (acetylcholine) observed by von Nieding et al. (1977) at
3 3 3
94 ug/m (0.05 ppm) NO,, in the presence of,49 ug/m (0.025 ppm) ozone and 290 ug/m (0.11 ppm)
so2.
The latter von Nieding et al. (1977) finding, however, is difficult to interpret in view
of: (1) controversy over the health significance of altered sensitivity to bronchoconstrictors
in healthy subjects; (2) some uncertainties due to methodological differences between his
techniques and other investigators'; and (3) no confirmation of the von Nieding et al. (1977)
findings by other investigators. Though the von Nieding et al. (1977) findings are interest-
ing, they cannot be accepted at this time as providing conclusive evidence for respiratory
effects occurring at N02 concentrations substantially below 1880 ug/m (1.0 ppm) for healthy
adult subjects.
Several controlled clinical studies have also addressed the issue of whether detectable
respiratory effects can be induced by N0~ in sensitive human subjects at exposure levels below
those affecting healthy human adults. Key clinical studies of the effects of exposure to N0£
on pulmonary function in potentially susceptible groups of the population are presented in
Table 1-2.
The studies by von Nieding et al. (1971; 1973) show that, in persons with chronic bron-
3
chitis, concentrations of 7,500 and 9,400 ug/m (4.0 and 5.0 ppm) produced decreases in
arterial partial pressure of oxygen and increases in the difference between alveolar and
2
arterial partial pressure of oxygen. Exposures to concentrations of N0~ above 2,800 ug/m
(1.5 ppm), for periods considerably less than 1 hour, also produced significant increases in
airway resistance. Thus, results for bronchitic individuals and healthy individuals appear to
differ little.
2
In contrast to the above results for bronchitics, exposures to 190 ug/m (0.1 ppm) N02
for 1 hour were reported by Orehek (1976) to increase mean airway resistance (R...) in 3 of 20
uW
asthmatics and to increase the sensitivity to a bronchoconstrictor (carbachol) in 13 of 20 of
the same individuals. In another study (Kerr et al., 1979), however, measurements of pulmonary
1-10
-------
TABLE 1-2. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON
PULMONARY FUNCTION IN CONTROLLED STUDIES OF SENSITIVE HUMAN ADULTS
Concentration
pg/m3
9,400
3,800
to
9,400
940
to
9,400
940
ppm
5.0
2.0
to
5.0
0.5
to
5.0
0.5
No. of
Subjects
14 chronic
bronchitics
25 chronic
bronchitics
63 chronic
bronchitics
10 healthy
7 chronic
Exposure
Time
60 mins.
10 mins.
30
inhal-
ations
2 hrs.
Effects*
No change in mean PAO?, during or after expo-
sure compared with pre-exposure values, but
PaO? decreased significantly in the first 15
mins. Continued exposure for 60 mins. produced
no enhancement of effect.
Significant decrease in PaO? and increase in
AaDO, at 7,500 pg/m (4.0 ppm) and above; no
significant change at 3,800 pg/m (2.0 ppm).
Significant increase in R above 3,000 pgm/
(1.6~ppm); no significant effect below 2,800
pg/m (1.5 ppm).
1 healthy and 1 bronchitic subject reported
slight nasal discharge. 7 asthmatics reported
Reference
von Nieding
et al , 1973
von Nieding
et al. , 1971
von Nieding
et al. , 1971
Kerr, et al . ,
1979
bronchitics
13 asthmatics
slight discomfort. Bronchitics and asthmatics
showed no statistically significant changes in
any pulmonary functions tested when analyzed
as separate groups but showed small,
statistically significant changes in quasistatic
compliance when analyzed as a single group.
190
0.1 20 asthmatics 1 hr.
Significant increase in SR in 3 of 20
asthmatics. Effect of bronchoconstriction
due to carbachol enhanced after exposure in
13 of 20 asthmatic subjects. Neither effect
observed in 7 of 20 subjects.
Orehek, 1976
*PAO? : alveolar partial pressure of oxygen
SR
aw
airway resistance
specific airway resistance
AaDO?: difference between alveolar and arterial
blood partial pressure of oxygen
PaO,
arterial partial pressure of oxygen
-------
function were not altered in 13 asthmatics or 7 bronchitics as a result of 2 hours of exposure
to 940 ug/m (0.5 ppm) N02 when the groups were analyzed separately. When the data for the
two groups were analyzed together, small but statistically significant changes in quasistatic
compliance and functional residual capacity were reported. However, the authors state that
the changes reported may be due to chance alone. Seven asthmatics and one bronchitic reported
some chest discomfort, dyspnea, headache, and/or slight nasal discharge.
It should be noted that considerable controversy exists regarding interpretation of the
Orehek (1976) study and the health significance of the increased response to a bronchocon-
strictor observed in the study. Conclusive statements regarding the possible unique status of
asthmatics therefore, cannot be made at this time. If the Orehek and Kerr studies are further
corroborated, however, then it is suggested that impairment of lung function in asthmatics may
3
be affected at NO,, levels of 940 ug/m (0.5 ppm) or below.
The above controlled human exposure studies provide important data concerning the effects
of single short-term NO^ exposures on healthy young adults and certain groups defined a priori
as "sensitive", i.e., bronchitics and asthmatics. However, members of other presumed sensitive
populations, e.g., children, the elderly, and individuals with chronic cardiovascular disease,
have not been tested in controlled exposure studies and are not likely to be tested in the
future. Because of constraints on the study of such sensitive polulation groups in controlled
exposure experiments, the question of whether such individuals are at greater risk than healthy
young adults for experiencing respiratory effects with single or repeated short-term NO- expo-
sures cannot be conclusively answered, although existing epidemiological data suggest that this
may be the case for young children.
Other critical health effects issues cannot be adequately addressed by controlled clinical
studies. These include the issues of: (1) assessment of pulmonary impairments induced by
repeated short-term peak exposures or continuous low-level exposures to NO,,; (2) assessment of
possible exacerbation of other disease processes by such NO,, exposures; and (3) evaluation of
morphological or structural tissue damage associated with NO^ exposures, whether of a short-
term, repeated or continuous nature. Some information bearing on the above issues has been
obtained by human epidemiological and animal toxicological studies summarized below.
1.3.1.2 Human Epidemiological Studies—Epidemiological studies of the effects of community
air pollution are complicated because there are usually complex mixtures of pollutants in the
air. Thus, the most that can typically be obtained from such studies is the demonstration of
close associations between health effects and ambient concentrations of a given mixture of
pollutants or subfractions of the mixtures. Furthermore, the association must remain consis-
tent throughout a variety of conditions for likely causality to be ascribed to such observa-
tions and only if other possible confounding or covarying factors have been adequately taken
into account. Epidemiological studies of air pollution effects are also often hampered by
difficulty in defining actual exposures of study populations.
1-12
-------
It is important to note that community epidemic "logical studies prior to 1973 on the
effects of N02 exposure are of questionable validity due to the use of the Jacobs-Hochheiser
technique in measuring atmospheric concentrations of NCL.* For this reason, the contributions
of those community studies to knowledge concerning the effects of NCL are very limited.
Certain other community exposure studies, however, provide better aerometric data as bases for
attempting to quantify ambient air NO- exposure effects and are the central focus of the
present analysis.
Community exposure studies investigating NCL effects on pulmonary function and providing
quantitative data on associated ambient air levels of NCL are summarized in Table 1-3. Most
of these studies consistently tend to indicate that reported daily mean concentrations of peak
levels of NCL, or NCL in combination with other pollutants (all less than 1.0 ppm NCL)
typically had no significant effects on lung function in the exposed study populations.
An exception is the Kagawa and Toyama (1975) study which showed some correlations in 20
Japanese schoolchildren, 11 years of age, between decrements in maximum expiratory flow rate
(Vm^) or specific airway conductance and concentrations of NCL or other specific pollutant
max £
levels at the time of testing. One-hr. NCL concentrations during testing ranged from 40 to
3
360 ug/m (0.02 to 0.19 ppm), but the data were such as not to allow for quantitative estima-
tion of specific NCL levels that might have been associated with the occurrence of pulmonary
function decrements. Also in the ambient situation the effects observed in this study were
generally not associated with NCL alone, but rather with various combinations of air
pollutants, including SCL, particulate matter, and 0,. In addition, weekly variations in
specific airway conductance and in V at 25 percent FVC were most closely correlated with
msx
outdoor temperature levels. These results emphasize that the observed respiratory effects
resulted from a complex interaction of pollutants including NCL and do not allow for clear
attribution of an association of decreased lung function with any specific ambient air concen-
tration of NCL.
Linn et al. (1976), Cohen et al. (1972), Burgess et al. (1973), and Speizer and Ferris
(1973a,b) found no differences in pulmonary function tests in separate epidemiological studies
which also involved complex pollutant mixtures in ambient air.
Several of the above community epidemiological studies also evaluated relationships
between ambient air exposures to N02 at levels reported in Table 1-3 and the occurence of
chronic respiratory diseases, but found no significant associations between the ambient NOp
exposures and the health endpoints measured. A few other community epidemiology studies have
been published which report quantitative associations between ambient N0? exposures and
increased acute respiratory disease incidence, but the methods employed in those studies (e.g.
use of the Jacobs-Hochheiser method for monitoring NCL levels) were such so as to preclude
acceptance of the reported quantitative findings.
*The Jacobs-Hochheiser technique has been withdrawn by EPA and replaced by a new Federal
Reference Method (chemiluminescence) and other equivalent methods (Chapter 7).
1-13
-------
TABLE 1-3. QUANTITATIVE COMMUNITY HEALTH EPIDEMIOLOGICAL STUDIES ON EFFECTS
OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION
N02
Exposure
Concentrations
Measure
High exposure group:
Annual mean
24-hr concentrations
90th percent! le
Estimated 1-hr
a
maximum
Low exposure group:
Annual mean
24-hr concentrations
90th percentile
Estimated 1-hr
maximum
Mean "annual "b 24-hr
concentrations: high
exposure area
low exposure
area
1-hr mean:
high exposure
area
low exposure area
ug/m
96
188
480
to
960
43
113
205
to
430
103
92
75
36
260
to
560
110
to
170
3 ppm
0.051
0.1
0.26
to
0.51
0.01
0.06
0.12
to
0.23
+ 0.055 +
S09 0.035
2 SO
C.
+ 0.04 +
SO. 0.014
* S02
0.14
to
0.30
0.06
to
0.09
Study
Population Effect Reference
Nonsmokers No differences in several ventil- Cohen et al.,
Los Angeles atory measurements including spi- 1972
(adult) rometry and flow volume curves
Nonsmokers
San Diego (adult)
Pulmonary No difference in various pul- Speizer and
function monary function tests. Ferris,
tests admin- 1973a,b
istered to
128 traffic Burgess et al.,
policemen in 1973
urban Boston
and to 140
patrol officers
in nearby sub-
urban areas.
-------
TABLE 1-3. (continued)
Measure
Los Angeles:
Median hourly N09
L,
90th percentile NO-
£.
Median hourly 0
90th percentile DX
San Francisco:
Median hourly N09
C-
90th percentile N02
Median hourly 0
90th percentile 0
1-hr concentration
at time of testing
(1:00 p.m. )
N02 Exposure
Concentrations
ug/m3 ppm
130 0.07
250 0.13
0.07
0.15
65 0.035
110 0.06
0.02
0.03
40 0.02
to to
360 0.19
Study
Population
205 office
workers in
Los Angeles
439 office
workers in
San Francisco
20 school
children
11 years of
age
Effect
No differences in most tests.
Smokers in both cities showed
greater changes in pulmonary
function than non-smokers.
During warmer part of the year
(April-October) N02> SO and
TSP* significantly correlated
with V * at 25% and 50% FVC*
Reference
Linn, et
al. , 1976
Kagawa and
Toyama,
1975
and witn1 specific airway con-
ductance. Temperature was
the factor most clearly correlated
with weekly variations in specific
airway conductance with V at
25% and 50% FVC. Significant
correlation between each of four
pollutants (NO,,, NO, S0? and TSP)
and V at 25% and 50% FVC; but
no clear delineation of specific
pollutant concentrations at which
effects occur.
.Estimated at 5 to 10 times annual mean 24-hour averages
Mean "annual" concentrations derived from 1-hour measur
*FFV
V 0.75'
max :
FVC
TSP
Forced expiratory volume, 0.75 seconds
Maximum expiratory flow rate
Forced vital capacity
Total suspended particulates
measurements using Saltzman technique
-------
As for the results of other epidemiological studies, some support for accepting the hypo-
thesis that children are at special risk for NCL-induced increases in acute respiratory ill-
nesses is derived from certain British and United States studies on indoor pollution effects
as summarized in Table 1-4.
These studies investigated possible decrements in lung function and/or increased respi-
ratory symptom and illness rates among children living in homes using gas stoves for cooking
in comparison to children from homes with electric ranges. Such studies are pertinent for
present purposes because high temperature gas combustion is a source of NO,,.
Several studies substantiate that higher N0? levels accumulate in homes using gas stoves
in comparison to NO,, levels found in homes with electric stoves. Melia et al. (1978) reported
that average N09 concentrations in 2 homes over a 96-hour test period, during which stoves were
3 3
in use for 8.5 to 10 hours, were 136 ug/m (0.072 ppm) when gas was burned and 18 (jg/m (0.01
ppm) in 2 other homes where electricity was used. In this study the N02 concentrations were
monitored at 1.2 meters (4 ft) above floor level and 0.6 and 2.2 meters (2 and 7.5 feet) from
either gas or electric stoves. Other studies, including Goldstein et al. (1979) and Spengler
et al. (1979), confirm that the levels of NO,, in gas stove homes are higher than those in
homes using electric stoves, and studies by Wade et al. (1975) and Mitchell et al. (1974)
also provide additional estimates of indoor N0~ levels resulting from gas stove usage. For
3
example, Wade et al. (1975) reported recurrent daily levels which averaged 280 ug/m (0.15
ppm) in the kitchen for two hours around the time when peak concentrations were generated. In
addition to variations in cooking routine, it should be noted that a variety of factors would
be expected to influence short-term peak averages including interior house design, type and
adjustment of range burners, and presence or absence of positive ventilation. An instantaneous
0
peak of 1,880 ug/m (1.0 ppm) was also measured on one occasion. Long-term average NO, con-
3
centrations, over observation periods of up to 2 weeks ranged from 103 to 145 ug/m (0.055 to
0.077 ppm).
In an initial publication regarding the British studies on health effects associated with
gas stove usage, Melia et al. (1977) reported a weak association between increased respiratory
illness in school children and residence in homes using gas stoves versus electric stoves,
after a number of demographic and other potentially confounding variables were taken into
account. However, Melia et al. (1977) failed to adjust for tobacco smoking in the home in
their first analysis. In other later publications (Melia et al., 1979; Goldstein et al.,
1979; Florey et al., 1979) corrections were made for the number of smokers in the home and,
again, weak associations between gas cooking and respiratory illness in children were found
(independent of smoking and other factors) in urban areas but not in rural ones. There
appeared, however, to be an association in rural areas for girls under the age of eight.
Additionally, four cohorts of children followed longitudinally from 1973 to 1977 initially
1-16
-------
TABLE 1-4. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE IN THE HOME ON LUNG FUNCTION AND
THE INCIDENCE OF ACUTE RESPIRATORY DISEASE IN EPIDEMIOLOGY STUDIES OF HOMES WITH GAS STOVES
i
i—•
•-j
Pollutant3
Studies of Children
NO- plus
otner gas stove
combustion products
NO- plus other gas
stove combustion
products
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
NO;,
Concentration
jjg/m3 ppm
NO- concentration
not measured at
time of study
NO, concentration
not measured in
same homes studied
Kitchens:
9-596 (gas) 0.005-0.317
11-353 (elec) 0.006-0.188
Bedrooms:
7.5-318 (gas) 0.004-0.169
6-70 (elec) 0.003-0.037
(by triethanolamine
diffusion samplers)
95 percentile of 24 hr
avg in activity room
39 - 116 ug/oi (.02 -
.06 ppm) (gas) vs.
17.6 - 95.2 ug/mj
(.01 - .05 ppm)
Study
Population
2554 children from homes
using gas to cook compared
to 3204 children from homes
using electricity. Ages 6-11
4827 children
ages 5-10
808 6- and 7-year-old
chi Idren
8,120 children 6-10 yrs old in
6 different communities with
data collected on lung function
and history of illness before
the age of 2
Effects
Proportion of children with one
or more respiratory symptoms
or disease (bronchitis, day or
night cough, morning cough,
cold going to chest, wheeze,
asthma) increased in homes
with gas stoves vs. electric
stove homes (for girls p -0.10;
boys not sig. ) after controlling
for confounding factors.
Higher incidence of respiratory
symptoms and disease associated
with gas stoves (for boys p -0.02;
girls p -0.15) after controlling
for confounding factors
Higher incidence of respiratory
illness in gas-stove homes
(p -0.10). Prevalence not
related to kitchen N0? levels,
but increased with N0? levels
in bed rooms of children in
gas-stove homes. Lung function
not related to NO., levels in
kitchen or bedroom
Significant association between
history of serious respiratory
illness before age 2 and use of
gas stoves (p <.01) and, also,
between lower FEV, FVC levels
and use of gas stoves (p <.01)
Reference
Melia et
Melia et
Florey et
Companion
Melia et
Goldstein
1979
al. , 1977
al. . 1979
al. , 1979
paper to
al. , 1979;
et al. ,
Speizer et al. . 1980
Spengler et al. . 1979
(electric). Frequent
peaks - 1100 ug/m (0.6
ppm),max peak - 1880
ug/m (1.0 ppmT 24 - hr
by modi fied sodium
arsenite; peaks by
chemiluminescence
-------
TABLE 1-4 (continued)
oo
Pollutant3
NO. plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
N02
Concentration
ug/mj ppra
Sample of households
24 hr avg: gas (.005 -
. 11 ppm); electric
(0 - .06 ppm); outdoors
(.015 - .05 ppm); -.several
peaks > 1880 ug/aT (1.0
ppm). Monitoring location
not reported. 24-hr avgs
by sodium arsenite; peaks
by chemi luminescence
Sample of same
households as reported
above but no new
monitoring reported
Study
Population
128 children 0-5
346 children 6-10
421 children 11-15
174 children under 12
Effects Reference
No significant difference Mitchell et al . , 1974
in reported respiratory See also Keller et al.,
illness between homes with gas 1979a
and electric stoves in children
from birth to 12 years
No evidence that cooking mode Keller et al., 1979b
is associated with the incidence
of acute respiratory illness
Studies of Adults
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
NO- plus other
gas stove
combustion
products
Preliminary measure-
ments peak hourly
470 - 940 ug/BJ
max 1880 ug/m
(1-0 ppm)
See table above
for monitoring
See table above
for monitoring
See table above
for monitoring
Housewives cooking with
gas stoves, compared to
those cooking with
electric stoves
Housewives cooking with
gas stoves, compared to
those cooking with electric
stoves. 146 households
Members of 441 households
Members of 120 households
(subsample of 441 households
above)
No consistent statistically
significant increases in
respiratory illness associated
with gas stove usage
No evidence that cooking with
gas associated with an increase
in respiratory disease
No significant difference in
reported respiratory illness
among adults in gas vs electric
cooking homes
No significant difference among
adults in acute respiratory
disease incidence in gas vs
electric cooking homes
USEPA, 1976
Keller et al. , 1979a
Mitchell et al. . 1974
See also Kel ler et al . ,
1979a
Keller et al. , 1979b
-------
showed greater risk of having one or more respiratory symptoms or diseases in homes with gas
stoves, but the strength of the association varied greatly over the four year study period and
was non-significant for some subgroups. In reviewing their overall results, the British
authors expressed concern that other, potentially confounding factors, such as temperature and
humidity, may have contributed to the apparent relationship between gas stove usage and
increased respiratory illness in school children. The same investigators found no relation-
ship between gas stove usage and lung function levels in subsets of the same children.
Based on initial results from a continuing prospective epidemiological study in the
United States, Speizer et al. (1980) reported that children from households with gas stoves
had a greater history of serious respiratory illness before age 2. In this study, adjustment
of rates of illness before age 2 for parental smoking, socioeconomic status, and other factors
led to a clear association between increased respiratory illness and the presence of gas-
cooking devices. Also found were small but statistically significant lower levels of two
measures of pulmonary function (corrected for height) in school age children from houses with
gas stoves. Monitoring of a subset of the homes with gas facilities revealed that NO- was
present in much higher concentrations than in the outside air, as reported by Spengler et al.
(1979). Continuous NO, measurements in a residence with gas stoves showed that levels exceed-
33
ing 500 |jg/m and even 1000 ug/m can occur during cooking, with such high levels lasting from
minutes to hours. Kitchen annual means may exceed 100 ug/m (0.6 ppm) if one extrapolates
from other studies, as noted by Spengler et al. (1979). Further, short-term hourly N0?
kitchen levels during cooking were noted as possibly being 5 to 10 times higher than measured
mean values. This is in contrast to annual average NOp levels of about 0.02 ppm (and no
marked peaks) in homes with electric stoves.
These findings were interpreted as suggesting that repeated peak short-term exposures to
NCK may be associated with increased incidence of respiratory illness in young preschool-age
children and small decrements in lung function in school age children. Hypothesizing of such
effects being associated with repeated short-term peak NO- exposures is based on annual
average levels of NO, not being very different in the gas stove homes versus electric stove
homes studied by Spengler et al. (1979) and Speizer et al. (1980). However, more definitive
documentation of such respiratory system effects being associated with short-term NO- peak
exposures remains to be provided based on further data collected beyond those included in the
initial analyses discussed by Speizer et al. (1980) and Spengler et al. (1979) from their
continuing prospective epidemiological study. This includes confirmation of the basic find-
ings reported, confirmation of the exclusion of socioeconomic status and other confounding
factors as important contributors to the observed relationships, and more detailed monitoring
of indoor NO, levels in homes of children in the study populations.
Further complicating interpretation of the above findings and determination of the
strength and reliability of the apparent relationships suggested by them are other studies
which failed to find any associations between gas stove usage and increased respiratory ill-
ness or decrements in lung function. In a series of three related studies, Mitchell et al.
1-19
-------
(1974) and Keller et al. (1979a,b) report negative findings with respect to an association
between the use of gas stoves in the home and an increased incidence of respiratory disease in
both adults and children. Initially 441 households in a middle-class suburb in Ohio were
studied. A follow-up study on a subsample of 120 of the original 441 households was also con-
ducted to verify the methodology used previously to collect health data. In addition, these
investigators studied a group of 146 housewives in a community on Long Island, N.Y., confirm-
ing the negative results reported earlier by the U.S. EPA (1976). However, the sample sizes
for children used in these studies were approximately a factor of 10 smaller than those used
in both the British and American studies reporting an association between increased respira-
tory disease and gas cooking. Also, it is not clear that the households sampled in Ohio
constituted a representative sample of the community studied.
1.3.1.3 Animal Toxicology Studies—In addition to epidemiological studies, animal toxicology
studies provide valuable information regarding induction of respiratory system effects by NO-.
Although it is recognized that exposure/effect relationships demonstrated by animal studies
are generally not quantitatively directly extrapolatable as indicators of human health effects
thresholds, they are, nevertheless, highly instructive regarding probable mechanisms by which
NOp may affect human pulmonary function and damage the pulmonary defense system, possibly
causing increased human susceptibility to bacterial infections. Rather than attempt an
exhaustive summary here of the animal toxicology literature assessed in Chapter 14, the
present section concisely highlights key points from that literature as they relate to effects
observed in human studies.
The lowest concentration of N09 that has been shown to produce measurable responses in
3
animals is 376 ug/m (0.2 ppm). At this concentration, rats exposed for 3 hours had an inhi-
bition of the lung metabolic conversion of prostaglandin E~ (a mediator which acts on smooth
muscle) to its inactive 15-keto metabolite 18 hours after exposure ceased. This could
possibly lead to an alteration of vascular or airway smooth muscle tone and, therefore, may
ultimately contribute to the mediation of pulmonary function changes, e.g., increased airway
resistance, observed with human exposure to higher levels (>1.0 ppm) of HOy- Since the
prostaglandin system is intimately involved in the local regulation of blood flow in the lung,
alterations in prostaglandin metabolism may also have profound effects on the perfusion of the
lung and, subsequently, on the gas exchange of the affected lung.
Morphological alterations in animal lung tissue, ranging from very small changes in
collagen to emphysema-like changes have also been observed following NO, exposure. Very small
3
changes occurred in rabbits after 24 or 36 days of exposure (4 hr/day, 5 days/wk) to 470 ug/m
(0.25 ppm). The health significance of the small collagen changes at low exposure levels are
unknown, but it should be noted that collagen metabolism is disrupted in man and animals
during fibrosis. Thus the initial small collagen effects seen after low-level N02 exposure
may be indicative of the initiation of processes of increasingly greater health significance
as they intensify at high NO,, exposure levels. Emphysema-like changes were found in several
1-20
-------
species, most often after chronic exposure, to high concentrations (18,800 ug/m . 10 PP"1)
above ambient air NO,, levels.
Systemic effects have also been observed after NO, exposure. Female mice receiving 470
3
ug/m (0.25 ppm) for 3 hours exhibited an increase in pentobarbital-induced sleeping time.
Such a response implies a potential effect on some aspect(s) of liver xenobiotic metabolism.
Hematological effects have also been observed in guinea pigs after 7 days of exposure to both
690 ug/m (0.36 ppm) and 940 ug/m (0.5 ppm). There is no evidence available establishing that
the same NCL exposure concentrations may produce similar systemic effects in human beings, and
the potential significance of such effects for human health is unclear at this time.
Of more obvious importance are the results of other extensive animal studies that appear
to be consistent with emerging conclusions from human epidemiological studies on gas stove
usage discussed earlier. The latter studies appear to suggest that increased incidence of
acute respiratory illness in humans may occur as a result of repeated short-term exposures to
NOp. Pertinent animal studies summarized in Table 1-5 have demonstrated that repeated short-
term exposures increase susceptibility to some respiratory pathogens as much as does contin-
uous exposure to the same concentration of N0? (see Section 14.2.3.1.1). N0? exposures caus-
ing increased infectivity in animals have been observed across a wide range, beginning at 940
ug/m (0.5 ppm) for repeated exposures during a 90-day period and 3760 ug/m (2.0 ppm) for
single (3 hr) exposures. The results are interpreted here as providing evidence supportive of
tentative conclusions emerging from the above "gas stove" studies, i.e., that repeated expo-
sure to daily peak concentrations of NO- may be effective in impairing the health of exposed
young children by increasing vulnerability to infectious respiratory diseases. The latter
conclusions from the gas stove studies, however, still must be viewed with caution until more
definitive results are obtained. From the mouse studies, it is also apparent that concentra-
tion of NOp has more importance than time of exposure in producing increased susceptibility to
bacterial infection. Of interest, the lowest NO- concentrations (0.5 to 1.5 ppm) found to
induce such effects in animals with repeated or intermittent continuous exposures, do not
greatly exceed to the upper range of repeated NO- peak levels found in gas stove usage homes
hypothesized to be associated with increased respiratory illnesses in children.
1.3.2 NOp Sensory System Effects
In addition to the effects of N0? on pulmonary functions and its possible association
with increased acute respiratory disease in young children, NOp also exerts discernible
effects on sensory receptors (Table 1-6). This includes the detection of N09 as a noxious
3
pungent odor starting at concentration levels as low as 210 ug/m (0.11 ppm) of N02 and
occurring immediately upon exposure. Under some exposure conditions, however, impairment of
odor detection occurs. For example, impaired detection of N02 concentrations of 18,800 ug/m
(10 ppm) or more has been reported. In general, the former sensory effect, odor detection, is
not viewed as a significant health effect of concern (although it could be construed as
affecting human welfare); and the latter olfactory deficit effect, impairment of odor detec-
tion, is of likely negligible health concern in view of its temporary, reversible nature.
1-21
-------
TABLE 1-5. SUMMARY OF STUDIES DEMONSTRATING HEALTH EFFECTS IN ANIMALS
AT LOW (<2.0 ppm)
N02 EXPOSURE LEVELS
N02
Concentrations
ug/md
ppm
Effects
N02 measurement method Reference
3,760 2.0
A single 3-hr exposure caused
increased mortality following
challenge with an infectious
agent in mice.
Chemiluminescence
Ehrlich et al., 1977
2,800 1.5
After 1 wk continuous expo-
sure, mice had a significant-
ly greater increase in suscep-
tibility to infectious pulmon-
ary disease compared to inter-
mittent exposure.
After 2 wks, no differences
between continuous and inter-
mittent exposure modes occurred.
Saltzman and Chemilu- Gardner et al., 1979
minescence procedures
1,880 1.0
(daily 2 hr spike)
188. 0.1
(continuous)
Emphysematous alterations in
mice after 6 mo exposure.
Saltzmanc
Port et al., 1977
940
0.5
In mice challenged with bac-
teria, there was increased
mortality following a 90-day
continuous exposure or a 180
day intermittent exposure.
Saltzmanc
Ehrlich and
Henry, 1968
-------
TABLE 1-5. (continued)
N02
Concentrations
ug/m3ppm
Effects
N0? measurement method Reference
940
940
0.5
0.5
A 7-day intermittent exposure
caused enzymatic alterations
in lungs and blood of guinea
pigs.
Intermittent exposure for 6
hr/day for up to 12 mo caused
morphological changes in lung
alveoli of mice.
Saltzman
Donovan et al., 1976
Blair et al., 1969
940
0.5
Increased susceptibility to
influenza infection in mice.
Saltzman
Ito, 1971
750
0.4
Continuous exposure for one
wk caused increase of protein
in lavage fluid in vitamin C
deficient guinea pigs.
Sherwin and Carlson, 1973.
470
0.25
Swollen collagen fibers
after an intermittent 24
or 36 day exposure of
rabbits
Buell, 1970
667
to
94
0.36
to
0.05
Hematological effects
observed in guinea pigs
after 7 days of.,exposure to
690 or 940 ug/m (0.36 or
0.5 ppm).
Donovan et al., 1976
Menzel et al., 1977
Mersch et al., 1973
-------
TABLE 1-5. (continued)
N02
Concentrations
(jg/m3
ppm
Effects
N0~ measurement method Reference
470
0.25
Increased pentobarbital-
induced sleeping time in
female mice after a 3 hr
exposure. No effects after
2 or 3 days.
Miller et al., 1980
376
0.2
Inhibition of meta-
bolism of prostaglandin
E- in rats to its inactive
15-keto metabolite.
Menzel, 1980
Saltzman, 1954 (See Chapter 7.)
I
ro
-------
TABLE 1-6. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY RECEPTORS IN CONTROLLED HUMAN STUDIES
N02 Concen-
trations
ug/m3
790
410
230
230
200
0
to
51,000
2,260
140
150
to
500
ppm
0.42
0.22
0.12
0.12
0.11
0
to
27
1.2
0.07
0.08
to
0.26
No. of
Subjects
8
13
9
14
28
6
6
4
5
Time
until
effect
Immediate
Immediate
Immediate
Immediate
Immediate
54 minutes
Immediate
5 and 25
minutes
Initial
Repeated
over 3
months
No. of
Subjects
Effects Responding
Perception of odor of N02
Perception of odor of N02
Perception of odor of N0?
Perception of odor of NO-
Perception of odor of NO-
No perception of odor of NO- when
concentration was raised slowly from
0 to 51,000 ug/nT
Perception of odor improved when
relative humidity was increased from
55% to 78%
Impairment of dark adaptation
Increased time for dark adaptation
at 500 ug/nT (0.26 ppm)
Initial effect reversed
8/8
8/13
3/9
most
26/28
0/6
6/6
4/4
Not
Reported
Reference
Henschler et al . ,
1960
Ibid.
Ibid.
Shalamberidze,
Feldman, 1974
Henschler et al . ,
1960
Ibid.
Shalamberidze,
Bondareva, 1963
-------
NC^ exposures also exert effects on other sensory perception functions. Probably most
significant is the NO- effect on dark adaptation. Two different studies (Shalamberidze, 1976,
and Bondareva, 1973) report data indicating that impairment of dark adaptation can occur in
human subjects at NCK exposure levels as low as 130 to 150 ug/m (.07 to .08 ppm). It is
difficult to fully appraise the health significance of such an effect, but it appears to be of
generally negligible concern except, perhaps, for certain occupational or public safety situ-
ations where rapid dark adaptation may be important.
1.3.3 Summary of Major Health Effects Conclusions
Major conclusions regarding NO -associated health effects of most importance for conside-
A
ration in decision-making regarding primary National Ambient Air Quality Standards for NO
A
compounds can be summarized as follows:
(1) At concentrations of 9,400 ug/m (5.0 ppm) or above, exposure to
N02 for as little as 15 minutes will both increase airway resistance
in healthy human adults and impair the normal transport of gases
between the blood and the lungs.
(2) In healthy adult individuals, concentrations of 4,700 ug/m (2.5
ppm) NOp for 2 hours have been reported to increase airway resistance
significantly without altering arterialized oxygen pressure.
Single exposures for 15 minutes to NO, at concentrations of 3,000
3
ug/m (1.6 ppm) are also likely to increase airway resistance in
healthy adults and individuals with chronic bronchitis but not to
interfere with the transport of gases between blood and lungs.
(3) Single exposures for times ranging from 15 minutes to 2 hours to
NO- at concentrations of 2,800 ug/m (1.5 ppm) or below have not
been shown to affect respiratory function in healthy individuals
or in those with bronchitis.
(4) Whether asthmatic subjects are more sensitive than healthy adults
in experiencing NO-'induced pulmonary function changes remains to
be definitively resolved. The results of one controlled human
exposure study suggest that some asthmatics may experience chest
discomfort, dyspnea, headache, and/or slight nasal discharge
following 2 hr exposures to 0.5 ppm NO- but did not provide
convincing evidence of pulmonary function changes in asthmatics
at that N02 concentration.
(5) Certain animal studies demonstrate various mechanisms of action
by which pulmonary function changes of the above type may be
induced in humans at relatively low NO- exposure levels and by
which increasing by more serious histopathological changes leading
to severe emphysematous effects are manifested at increasingly
higher (generally greater than ambient) NO- exposure levels.
1-26
-------
(6) Prospective studies of the effects of indoor air pollution suggest
that, in some instances, an increased incidence of respiratory
illness in young children may be associated with the use of gas
stoves and possibly with NCL produced by these appliances. Much
caution must be applied, however, in fully accepting or using
these study findings for risk assessment purposes until: they
are confirmed by further analyses of data subsequently gathered
in the prospective studies; potential confounding factors are
more definitively ruled out; and clearer exposure/effect relation-
ships are defined via more intensive NO- monitoring in gas stove
homes.
(7) No definitive estimates can yet be provided for peak 1-2 hr, 24
hr, weekly, or annual average N0? exposure levels that may be
associated with any increased respiratory illness in young children
residing in homes using gas stoves, although some basis exists
for suggesting that repeated exposures to peak levels are most
likely to be importantly involved. Peak 1-2 hr NO- levels ranging
up to 0.5-1.0 ppm have been observed in gas stove homes; longer-term
weekly average NO^ levels of 0.05 to 0.07 ppm and annual average
levels of 0.01 to 0.06 ppm were also found in such homes.
(8) Estimates of repeated short-term peak concentrations of ^
possibly associated with increased respiratory illness in homes
with gas stoves are not markedly below the general range of the
lowest (0.5 to 1.0 ppm) intermittent exposure concentrations
found to cause increased susceptibility to respiratory infections
in animal infectivity model studies.
Placing the above conclusions in perspective, it should be noted that ambient air NO^
monitoring results in the United States indicate that peak 1-hr N0~ concentrations rarely
exceed 0.4 to 0.5 ppm. Such peaks occurred during 1975 to 1980 in only a few scattered
locations in the United States, e.g., Los Angeles and several other California sites. Also,
during that period, annual average N0? concentrations exceeding 0.05 ppm were only found in a
relatively few scattered locations, including population centers such as Chicago and Southern
California.
1.4 WELFARE EFFECTS OF NITROGEN OXIDES
In addition to human health effects associated with exposures to nitrogen dioxide
discussed above, considerable attention has been accorded to the investigation of possible
effects of NO- and other NO compounds on aquatic and terrestial ecosystems, vegetation,
t A
visibility, climate, and man-made materials--effects which may impact negatively on public
1-27
-------
welfare in the United States. Concisely summarized below are key points derived from more
detailed discussions in Chapters 10-13 of the relationship of NO compounds to the induction
A
of such welfare effects.
1.4.1 Nitrogen Oxides, Acidic Deposition Processes, and Effects
The occurrence of acidic deposition, especially in the form of acidic precipitation, has
become a matter of concern in many regions of the United States, Canada, northern Europe,
Taiwan and Japan. Acidic precipitation in the Adirondack Mountains of New York State, in
Maine, in eastern Canada, in southern Norway and in southwest Sweden has been reported to be
associated with acidification of waters in ponds, lakes and streams with a resultant disappear-
ance of animal and plant life. Acidic precipitation (rain and snow) is also believed to have
the potential to: (1) leach nutrient elements from sensitive soils, (2) cause direct and
indirect injury to forests, (3) damage monuments and buildings made of stone, and (4) corrode
metals.
Chapter 11 of this document discusses acidic deposition processes and the effects of wet
deposition of sulfur and nitrogen oxides and their products on aquatic and terrestrial eco-
systems. Dry deposition also plays an important role, but contributions by this process have
not been well quantified. Because sulfur and nitrogen oxides are so closely linked in the
formation of acidic precipitation, no attempt has been made to limit the present discussion
solely to nitrogen oxides. A more thorough general review of acidic deposition processes and
associated environmental problems will be presented in a future EPA document.
Sulfur and nitrogen oxides are considered to be the main precursors in the formation of
acidic precipitation. Emissions of such compounds involved in acidification are attributed
chiefly to the combustion of fossil fuels such as coal and oil. Emissions may occur at ground
level, as from automobile exhausts, or from 300 meters (1000 feet) or more in height.
Emissions from natural sources are also involved; however, in highly industrialized areas,
emissions from manmade sources markedly exceed those from natural sources. In the eastern
United States the highest emissions of sulfur oxides derive from electric power generators
burning coal. However, emissions of nitrogen oxides, mainly from automotive sources, tend to
predominate in the West. (Information regarding 'sources and emissions of NO compounds is
discussed in Chapter 5 of this document.)
The fate of sulfur and nitrogen oxides, as well as other pollutants emitted intO'the
atmosphere, depends on their dispersion, transport, transformation and deposition. Sulfur and
nitrogen oxides or their transformation products may be deposited locally or transported long
distances from the emission sources (Altshuller and McBean, 1979; Pack, 1978; Cogbill and
Likens, 1974). Residence time in the atmosphere, therefore, can be brief if the emissions are
deposited locally or may extend to days or even weeks if long range transport occurs. The
chemical form in which emissions ultimately reach the receptor, the biological organism or
material affected, is determined by complex chemical transformations that take place between
the emission sources and the receptor. Long range transport over distances of hundreds or
thousands of miles allows time for many chemical transformations to occur.
1-28
-------
Sulfates and nitrates are among the products of the chemical transformations of sulfur
oxides (especially SCL) and nitrogen oxides. Ozone and other photochemical oxidants are
believed to be involved in the chemical processes that form sulfates and nitrates. When sul-
fates and nitrates combine with atmospheric water, dissociated forms of sulfuric (HLSCL) and
nitric (HNOj) acids result; and when these acids are brought to earth in rain and snow, acidic
precipitation occurs. Because of long range transport, acidic precipitation in a particular
state or region can be the result of emissions from sources in states or regions many miles
away, rather than from local sources. To date, however, the complex nature of the chemical
transformation processes has not made it possible to demonstrate a direct cause and effect
relationship between emissions of sulfur and nitrogen oxides and the acidity of precipitation.
(Transport, transformation, and deposition of nitrogen compounds are discussed in Chapter 6 of
this document; analogous information on sulfur oxides is discussed in a separate document, Air
Quality Criteria for Particulate Matter and Sulfur Oxides, U.S. EPA, 1981).
Acidic precipitation has been arbitrarily defined as precipitation with a pH less than
5.6, because precipitation formed in a geochemically clean environment would have a pH of
approximately 5.6 due to the combining of carbon dioxide with moisture in the air to form car-
bonic acid. Currently the acidity of precipitation in the northeastern United States usually
ranges from pH 3.9 to 5.0; in other regions of the United States precipitation episodes with a
pH as low as 3.9 have also been reported in areas with average pH levels above 5.0 (see Figure
1-D-
The pH of precipitation can vary from event to event, from season to season and from geo-
graphical area to geographical area. Other substances in the atmosphere besides sulfur and
nitrogen oxides can cause the pH to shift by making it more acidic or more basic. For example,
dust and debris swept up in small amounts from the ground into the atmosphere may become com-
ponents of precipitation. In the West and Midwest soil particles tend to be more basic, but
in the eastern United States they tend to be acidic. Also, in coastal areas sea spray
strongly influences precipitation chemistry by contributing calcium, potassium, chlorine and
sulfates. In the final analysis, the pH of precipitation is a measure of the relative contri-
butions of all of these components (Whelpdale, 1979).
It is not presently clear as to when precipitation in the U.S. began to become markedly
more acidic than the 5.6 pH level expected for a geochemically clean environment. Some
scientists argue that it began with the industrial revolution and the burning of large amounts
of coal and others estimate that it began in the United States with the introduction of tall
stacks in power plants in the 1950's. However, other scientists disagree completely and argue
that rain has always been acidic. In other words, no definitive answer to the question exists
at the present time. Also, insufficient data presently exist to characterize with confidence
long-term temporal trends in changes in the pH of precipitation in the United States, mainly
due to the pH of rain not having been continuously monitored over extended periods of time.
1-29
-------
I
CO
o
Chart Ptottlno. Legend
1.0
• Naltauul Atmo»phw*c OeposMon flagrant (NAOP)
D Department of Energy (DOE)
B EmtranmantdProlectbn Agency (EPA/NOAA/WMOI
-e- Uniyenll) ol Cnlllomia
-O- CoUIOfnte Imlflule ol Tachnoloay
& WulU-Slnle Abnospheiic Poraef
' Production PoUutlon Study (MAP1S)
A Electric Power Rauweh Intttuls (EPRI)
© Odi Rtdge Natlonel Laboratory
O CtnHttanJUtnoBfltar* Envfcomnenl Sarvtoi (CAMSAP)
^ UftfYOrsHyolArtrara
0 UnhonHyol FtorUa
Figure 1-1., Average pH isopleths as determined from laboratory analyses of precipitation
sample, weighted by the reported quantity of precipitation.
Source: Wisniewski and Keitz (1981).
-------
Although acidic precipitation (wet deposition) is usually emphasized, it is not the only
process by which acids or acidifying substances are added to bodies of water or to the land.
Dry deposition also occurs. Dry deposition processes include gravitational sedimentation of
particles, impaction of aerosols and the adsorption and absorption of gases by objects at the
earth's surface or by the soil or water. Dew, fog, and frost are also involved in the depo-
sition processes but do not strictly fall into the category of wet or dry deposition (Galloway
and Whelpdale, 1980; Sehmel, 1980; Hicks and Wesley, 1980). Dry deposition processes are not
as well understood as wet deposition at the present time; however, all of the deposition pro-
cesses contribute to the gradual accumulation of acidic or acidifying substances in the
environment.
The most visible changes associated with acidic deposition, that is both wet and dry pro-
cesses, are those observed in the lakes and streams of the Adirondack Mountains in New York
State, in Maine, in the Pre-cambrian Shield areas of Canada, in Scotland, and in the Scandi-
navian countries. In these regions, the pH of the fresh water bodies appears to have
decreased, causing changes in animal and plant populations.
The chemistry of fresh waters is determined primarily by the geological structure (soil
system and bedrock) of the lake or stream catchment basin, by the ground cover and by land
use. Near coastal areas (up to 100 miles inland) marine salts also may be important in deter-
mining the chemical composition of the stream, river or lake. Sensitivity of a lake to acidi-
fication depends on the acidity of both wet and dry deposition plus the same factors — the soil
system of the drainage basin, the canopy effects of the ground cover and the composition of
the waterbed bedrock. The capability, however, of a lake and its drainage basin to neutralize
incoming acidic substances is determined largely by the composition of the bedrocks (Wright
and Gjessing, 1976; Galloway and Cowling, 1978; Hendrey et al. , 1980b). Soft water lakes,
those most sensitive to additions of acidic substances, are usually found in areas with
igneous bedrock which contributes few soluble solids to the surface waters, whereas hard
waters contain large concentrations of alkaline earths (chiefly bicarbonates of calcium and
sometimes magnesium) derived from limestones and calcareous sandstones in the drainage basin.
Alkalinity is associated with the increased capacity of lakes to neutralize or buffer the in-
coming acids. The extent to which acidic precipitation contributes to the acidification pro-
cess has yet to be determined.
The survival of natural living ecosystems in response to marked environmental changes or
perturbations depends upon the ability of constituent organisms of which they are composed to
cope with the perturbations and to continue reproduction of their species. Those species of
organisms most sensitive to particular environmental changes are first removed. However, the
capacity of an ecosystem to maintain internal stability is determined by the ability of all
individual organisms to adjust and survive, and other species or components may subsequently
be impacted in response to the loss of the most susceptible species.
1-31
-------
The capacity of organisms to withstand injury from weather extremes, pesticides, acidic
deposition or polluted air follows the principle of limiting factors (Billings, 1978; Odum,
1971; Moran et al., 1980; Smith, 1980). According to this principle, for each physical factor
in the environment there exists for each organism a minimum and a maximum limit beyond which
no members of a particular species can survive. Either too much or too little of a factor
such as heat, light, water, or minerals (even though they are necessary for life) can jeopar-
dize the survival of an individual and in extreme cases a species. The range of tolerance
(see Figure 1-2) of an organism may be broad for one factor and narrow for another. The
tolerance limit for each species is determined by its genetic makeup and varies from species
to species for the same reason. The range of tolerance also varies depending on the age,
stage of growth or growth form of an organism. Limiting factors are, therefore, factors
which, when scarce or overabundant, limit the growth, reproduction and/or distribution of an
organism.
ZONE OF
INTOLERANCE
LOWER LIMITS
OFTOLtHAJICE
ZONE OF
PHYSIOLOGICAL
STRESS
TOLERANCE RANGE
RANGE OF OPTIMUM
UP9ER UKITS
OF TOLERANCE
ZONE OF
PHYSIOLOGICAL
STRESS
ZONE OF
INTOLERANCE
ORGANISMS
INFREQUENT
ORGANISMS
ABSENT
GREATEST
ABUNDANCE
ORGANISMS
INFREQUENT
ORGANISMS
ABSENT
LOWO-
-GRAOiEMT-
->HIGH
Figure 1-2. idealized conceptual framework illustrating the "law of tolerance," which
postulates a limited tolerance range for various environmental factors within which
species can survive (adapted from Smith, 1980).
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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 Mountains of New York State, in eastern Canada, and parts of Scandinavia the
original aquatic ecosystems have been and are continuing to be replaced by ecosystems differ-
ent from the original due to acidification of the aquatic habitat. Forest ecosystems, how-
ever, appear thus far to have been resistant to changes due to perturbation or stress from
acidifying substances.
The impact of acidic precipitation on aquatic and terrestrial ecosystems is typically not
the result of a single or several individual precipitation events, but rather the result of
continued additions of acids or acidifying substances over time. Wet deposition of acidic
substances on freshwater lakes, streams, and natural land areas is only part of the problem.
Acidic substances exist in gases, aerosols, and particulate matter transferred into the lakes,
streams, and land areas by dry deposition as well. Therefore, all the observed biological
effects should not be attributed to acidic precipitation alone.
The disappearance of fish populations from freshwater lakes and streams is usually one of
the most readily observable signs of lake acidification. Death of fish in acidified waters has
been attributed to the modification of a number of physiological processes by a change in pH.
Two patterns related to pH change have been observed. The first involves a sudden short-term
drop in pH and the second, a gradual decrease in pH with time. Sudden short-term drops in pH
may result from a winter thaw or the melting of the snow pack in early spring and the release
of the acidic constituents of the snow into the water.
Long-term gradual increases in acidity, particularly below pH 5, interfere with reproduc-
tion and spawning, producing a decrease in population density and a shift in size and age of
the population to one consisting primarily of larger and older fish. Effects on yield often
are not recognizable until the population is close to extinction; this is particularly true
for late-maturing species with long lives. Even relatively small increases (5 to 50 percent)
in mortality of fish eggs and fry can decrease yield and bring about extinction.
In some lakes, concentrations of aluminum may be as crucial or more important than pH
levels as factors causing a decline in fish populations in acidified lakes. Mobilization of
certain aluminum compounds in the water due to lowered pH, upsets the osmoregulatory function
of blood in fish. Aluminum toxicity to aquatic biota other than fish has not been assessed.
Although the disappearance of and/or reductions in fish populations are usually
emphasized as significant results of lake and stream acidification, also important are the
effects on other aquatic organisms ranging from waterfowl to bacteria. Organisms at all
trophic (feeding) levels in the food web appear to be affected. Species reduction in number
and diversity may occur, biomass (total mass of living organisms in a given volume of water)
may be altered and processes such as primary production and decomposition impaired.
Significant changes that have occurred in aquatic ecosystems with increasing acidity
include the following:
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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.
5. Biomass and total productivity of benthic macrophytes and algae may increase
due in part to increased lake transparency.
6. Numbers and biomass of herbivorous invertebrates decline. Tolerant inverte-
brate species, e.g., air-breathing insects may become abundant primarily due
to reduced fish predation.
7. Changes in community structure occur at all trophic levels.
An indirect effect of acidification potentially of concern to human health is the possi-
ble contamination of edible fish and of water supplies. Studies in Canada and Sweden reveal
high mercury concentrations in fish from acidified regions. Lead has been found in plumbing
systems with acidified water, and persons drinking the water could be affected by the lead.
However, no examples have yet been documented of such human effects having actually occurred
in response to acidic precipitation processes.
Soils may become gradually acidified from an influx of hydrogen (H ) ions. Leaching of
the mobilizable forms of mineral nutrients may occur. The rate of leaching is determined by
the buffering capacity of the soil and the amount and composition of precipitation. Unless
the buffering capacity of the soil is strong and/or the salt content of precipitation is high,
leaching will in time result in acidification. Anion mobility is also an important factor in
the leaching of soil nutrients. Cations cannot leach without the associated anions also leach-
ing. The capacity of soils to adsorb and retain anions increases as the pH decreases, when
hydrated oxides of iron and aluminum are present (Wiklander, 1980).
Sulfur and nitrogen are essential for optimal plant growth. Plants usually obtain nitro-
gen in the form of nitrate from organic matter during microbial decomposition. Wet and dry
deposition of atmospheric nitrates is also a major source. In soils where sulfur and nitrogen
are limiting nutrients, such deposition may increase growth of some plant species. The amounts
of nitrogen entering the soil system from atmospheric sources is dependent on proximity to
industrial areas, the sea coast, and marshlands. The prevailing winds and the amount of
precipitation in a given region are also important (Halstead and Rennie, 1977).
At present there are no documented observations or measurements of changes in natural
terrestrial ecosystems or agricultural productivity directly attributable to acidic precipita-
tion. The information available regarding vegetational effects concerns the results of a
variety of controlled research studies, mainly using some form of "simulated" acidic rain,
frequently dilute sulfuric acid. The simulated "acid rains" have deposited hydrogen (H ),
sulfate (SO,") and nitrate (N03) ions on vegetation and have caused necrotic lesions in a wide
1-34
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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 seasonal ity of their
A A 0
contributions; (7) the existence and significance of anthropogenic, non-combustion sources of
S0x, NO and HC1; (8) the dry deposition rates for SO , NO , sulfate, nitrate and HC1 over
various terrains and seasons of the year; (9) the existence and reliability of long-term pH
measurements of lakes and headwater streams; (10) the acceptability of current models for
predicting long range transport of SO and NO and for acid tolerance of lakes; (11) the
*. A A
feasibility of using liming or other corrective procedures to prevent or reverse acid damage
and the costs of such procedures; (12) the effects of SO and NOX and hydrogen ion deposition
on ecosystem dynamics in both aquatic and terrestrial ecosystems; (13) the effectiveness of
fertilization resulting from sulfate and nitrate deposition on soils; (14) the effects, if
any, of acidic deposition on agricultural crops, forests and other native plants; and (15) the
x,
effects of acidic deposition on soil microbial processes and nutrient cycling. A more compre-
hensive evaluation of scientific evidence bearing on these issues is being prepared as part of
a forthcoming EPA document on acidic deposition.
1.4.2 Effects of NO on Ecosystems and Vegetation
Chapter 12 discusses NO effects on ecosystems and vegetation. Ecosystems represent the
A
natural order by which living organisms are bound to each other and to their environment.
They are, therefore, essential to the existence of any species on earth, including man, and as
life support systems their value cannot be fully quantified in economic terms.
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Ecosystems are important in the production of food, in the regeneration of essential
nutrients as well as atmospheric components, in the assimilation or breakdown of many pollu-
tants from the air, water, and soil, and in energy flow. They also give aesthetic pleasure
and improve the quality of life.
The nitrogen cycle, an ecosystem function, is essential for all life because nitrogen is
necessary in the formation of all living matter. Man has influenced the cycling of nitrogen
by injecting fixed nitrogen into the environment or contributing other nitrogenous compounds
which perturb the cycle.
Human activities have unquestionably increased the amounts of nitrates and related com-
pounds in some compartments of the environment. The effects of such increased concentrations
of nitrogen compounds may be beneficial or adverse, or both. Effects of both kinds may occur
simultaneously, and may be felt in media or in ecological compartments quite removed from
those that initially receive anthropogenic nitrogenous inputs.
Assessment of the influence of nitrogen oxides on ecosystems is complicated by several
factors. Nitrogen oxides: (1) react with abiotic components of the natural environment as
well as with individual organisms; (2) react with varying numbers of dissimilar populations
within ecosystems; and (3) may suppress individual populations and thus affect ecosystem
functioning.
One function of ecosystems is the cycling of nutrients such as nitrogen. Any effect,
environmental or biological, which interferes with the recycling process could have a
deleterious effect on the total ecosystem.
At the present time there are insufficient data to determine the impact of nitrogen
oxides as well as other nitrogen compounds on terrestrial plant, animal or microbial
communities. It is possible, however, to estimate the approximate magnitude of anthropogenic
nitrogen fluxes to ecosystems, using the limited amount of monitoring data available or mass
balance calculations. Such estimates, and quantitative information about the nitrogen cycle
at specific sites in the system under study, make it possible to reach some conclusions about
the possible ecological significance of the added nitrogen. In addition, where the data base
is more extensive, as it is for a number of lakes in various stages of eutrophication, more
quantitative dose-response relationships can be estimated.
A reduction in diversity within a plant community results in a reduction in the amount of
nutrients present so that the growth of remaining individuals decreases.
Pollutants also act as predisposing agents so that disease, insect pests and abiotic
forces can more readily injure the individual members of ecosystems. The loss of these indi-
viduals result in reduction in diversity and simplification of an ecosystem.
Sensitivity of plants to nitrogen oxides depends on a variety of factors including
species, time of day, light, stage of maturity, type of injury examined, soil moisture,
nitrogen nutrition and the presence or absence of other air pollutants such as sulfur dioxide
and ozone.
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When exposures to N0? alone are considered, the ambient concentrations that produce
measurable injury are higher than those that normally occur in the United States (Chapter 8).
3
Tomato (Lycopersicon esculentum) plants exposed continuously to 470 ug/m (0.25 ppm) for 128
days exhibited a decreased growth and a yield reduction of 12 percent. Leaf drop and reduced
yield occurred in orange trees exposed to 470 ug/m (0.25 ppm) continuously for 8 months.
Pinto bean ( Phaseolus vulgaris), endive (Cicorium endivia) and cotton (Gossypium hirsutum)
exhibited slight leaf spotting after 48 hours of exposure to 1,880 ug/m (1.0 ppm). Other
reports cited no injury in beans (Phaseolus vulgaris), tobacco (Nicotiana tabacum), or petunia
(Petunia multiflora) with a 2-hour exposure to the same concentration.
Exceptions to this generality, however, have been observed. For example, the growth of
Kentucky bluegrass was significantly reduced (approximately 25 percent) by exposures to 210
ug/m (0.11 ppm) N09 for 103.5 hours per week for 20 weeks during the winter months. Similar
exposures to other grass species generally had no deletrious effect on plant growth.
Nitrogen dioxide concentrations ranging from 188 to 1,880 ug/m (0.1 to 1.0 ppm)
increased chlorophyll content in pea (Pisum sativum) seedlings from 5 to 10 percent. The
significance of the increased chlorophyll is not known. Some species of lichens exposed to
3,760 ug/m (2.0 ppm) for 6 hours showed reduced chlorophyll content.
In contrast to studies cited on the effects of N0~ alone, a number of studies on mixtures
of N02 and SO- showed that the N0? injury threshold was significantly decreased and that the
effects of the two gases in combination were at least additive and usually more than additive.
Concentrations at which observable injury occurred were well within the ambient concentrations
of N09 and SO, occurring in some areas of the U.S. A combination of 188 ug/m (0.1 ppm) N09
3
and 262 ug/m (0.1 ppm) S02 for 4 hours caused moderate leaf injury in pinto bean (Phaseolus
vulgaris), radish (Raphanus sativus), soybean (Glycine max), tomato (Lycopersicon esculentum),
oat (Avena sativa), and tobacco (Nicotiana tabacum). Exposure to 282 ug/m (0.15 ppm) N09 in
3 3
combination with 262 ug/m (0.1 ppm) S09 for 4 hours caused more injury. Neither 3,760 ug/m
3
(2.0 ppm) NO-, nor 1,310 ug/m (0.5 ppm) SO, alone caused injury. Research data from grass
3 3
species exposed for 20 weeks to concentrations of 210 ug/m (0.11 ppm) N02 and 290 ug/m (0.11
ppm) SOp for 103.5 hours per week showed significant reductions in yield parameters ranging
from 30 to 90 percent indicating that concentrations of these two gases occurring simultane-
ously can have major deletrious effects on plant growth.
1.4.3 Effects of Nitrogen Oxides on Materials
The damaging effects of atmospheric oxides of nitrogen have been established for a
variety of materials including dyes, fibers, plastics, rubber, and metals as discussed in
Chapter 13 of this document.
Field exposures of cotton, viscose rayon, cellulose acetate, and nylon fabrics colored
with representative dyes demonstrate that fading occurs for specific dyes in air containing
NCL, 03, and SOp. These exposures were carried out in ambient air and protected against sun-
light. Chamber studies using individual pollutants N02, 0.,, and S02 have shown that some
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individual dye-fiber combinations exhibit color fading only in response to NO- exposure,
whereas others are susceptible to 03, as well as combinations of N02 and 03_ S02 introduced
an accelerant effect. Disperse dyes used for cellulose acetate and rayon include vulnerable
anthraquinone blues and reds. The cellulosic fibers cotton and viscose rayon, dyed with
certain widely used direct dyes, vat dyes, and fiber reactive dyes, suffer severe fading on
chamber exposures to 940 ug/m (0.5 ppm) N02 under high humidity (90 percent) and high
temperature (90°F) conditions. Significant fading is observed on 12 weeks exposure to 94
ug/m (0.05 ppm) N09 under high humidity and temperature conditions (90 percent, 90°F).
3
Acid dyes on nylon fade on exposure to N02 at.levels as low as 188 ug/m (0.1 ppm), under
similar conditions. Dyed polyester fabrics are highly resistant to NOp-induced fading. How-
ever, permanent press fabrics of polyester cotton and textured polyester exhibited unexpected
fading when first marketed. The fading was in the disperse dye which migrated under high heat
conditions of curing or heat setting to the reactive medium of resins and other surface addi-
tives.
The yellowing of white fabrics is documented for polyurethane segmented fibers (Lycra and
Spandex), rubberized cotton, optically brightened acetate, and nylon. Yellowing is also re-
ported on fabrics which were finished with softeners or anti-static agents. Nitrogen dioxide
was demonstrated to be the pollutant responsible for color change, with 0, and S02 showing no
effect. Chamber studies using NO- concentrations of 376 ug/m (0.2 ppm) for 8 hours showed
yellowing equivalent to that on garments returned to manufacturers.
The tensile strength of fabrics may be adversely affected by the hydrolytic action of
acid aerosols. Nitrogen dioxide has been demonstrated to oxidize the terminal amine group
(-NH9) of nylon to the degree that the fiber has less affinity for acid-type dyes. Nylon 66
3
may suffer chain scission when exposed to 1,880 to 9,400 ug/m (1.0 to 5.0 ppm) NO^. Field
exposures of fibers emphasize the action of acids derived from $62, although N02 may also be
present in high concentrations in urban sites. Information on the contribution of N02 to
degradation is incomplete.
Although a survey of the market for plastics predicts the use of 1.78 billion pounds in
1982, there is very little information on the effects of N02 on polyethylene, polypropylene,
polystyrene, polyvinylchloride, polyacrylonitrile, polyamides and polyurethanes. Aging tests
involve sunlight exposure as well as exposure to ambient air. Chamber exposure of the above
plastics to combinations of SO,,, N02, and 03 has resulted in deterioration. Nitrogen dioxide
alone has caused chain scission in nylon and polyurethane at concentrations of 1,880 and 9,400
ug/m (1.0 to 5.0 ppm).
The extensive data on corrosion of metals in polluted areas relate the corrosion effects
to the S02 concentrations. The presence of N02 and its contribution is not evaluated despite
its presence as acid aerosol in appreciable concentrations.
Ammonium nitrates were implicated as a factor in the stress corrosion cracking of wires
made of nickel brass alloy used in telephone equipment. Since nitrate salts have been shown
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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
A
degrades the appearance of distant objects and reduces the range at which they can be distin-
guished from the background. These effects are manifest not only in visible plumes, but also
in large-scale, hazy air masses. Haze and plumes can result in the discoloration, deteriora-
tion, and loss of scenic vistas, particularly in areas of the southwestern United States where
visibility is generally good. Under extreme conditions reduced visual range and contrast due
to haze and plumes may impede air traffic. NO- does not significantly reduce visual range;
however, NOp can be responsible for a portion of the brownish coloration observed in polluted
air. It should be noted that non-nitrate particulate matter has also been implicated in the
production of a significant portion of brownish coloration. Under certain circumstances,
brown plumes may be distinguished tens of kilometers downwind of their sources.
Nitrogen dioxide in the atmosphere acts as a blue-minus filter for transmitted light. It
tends to impart a brownish color to targets, including the sky viewed through the plume. The
strength of this filter effect is determined by the amount of NOp concentration along the
sight path; i.e., theoretically, similar effects are exerted by a 1 kilometer-wide plume con-
taining 0.1 ppm (190 ug/m ) of N09 or a 0.1 kilometer-wide plume containing 1.0 ppm (1,900
3
ug/m ) of NOp. Less than 0.1 ppm-km NOp is sufficient to produce a color shift which is
distinguishable in carefully controlled, color-matching tests. Reports from one laboratory
using NOp-containing sighting tubes indicate a visible color threshold of 0.06 ppm-km for the
typical observer. This value was supported by a few field observations of NOp plumes from
nitric acid manufacturing plants under varying operating conditions. The value cited refers
to the effect of NOp in the absence of atmospheric aerosol. Empirical observations under a
variety of conditions are needed to determine the perceptibility of NOp in ambient air.
Plume coloration due to NOp is modified by particulate matter and depends on a number of
factors such as sun angle, surrounding scenery,'sky cover, viewing angle, human perception
parameters, and pollutant loading. Suspended particles generally scatter in the forward
direction and can thus cause a haze layer or a plume to appear bright in forward scatter (sun
in front of the observer) and dark in back scatter (sun in back of the observer) because of
the angular variation in scattered airlight. This effect can vary with background, sky, and
objects. Aerosol optical effects alone are capable of imparting a reddish brown color to a
haze layer when viewed in backward scatter, NOp would increase the degree of coloration in
such a situation. When the sun is in front of the observer, however, light scattered toward
him by the plume tends to washout the brownish light transmitted from beyond. Under these
conditions, light scattering by particles diminishes the plume coloration caused by NOp.
Estimates of the magnitude of this effect attributable to particulate nitrates are currently
hampered by the lack of data on particulate nitrate concentrations in ambient air.
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The discoloration of the horizon sky in an urban, or more extensive regional area, due to
NCk' absorption, is determined by the relative concentrations of N0~ and light-scattering par-
ticles, other environmental conditions, and the physiological response of the observer. A
concentration-visual range product of 0.3 ppm-km NO,, corresponds to color shift which should
be detectable in a polluted layer viewed against relatively clean sky. However, this has not
been tested in a variety of circumstances. At a visual range of 100 km, typical of the
northern Great Plains area of the U.S., 0.003 ppm (6 ug/m ) NO-, would be expected to color the
3
horizon noticeably. At a visual range of 10 km, typical of urban haze, 0.03 ppm (60 ug/m )
NOp would be required to produce the same effect. However, quantitative theoretical calcula-
tions of human perception of NO-, are not fully developed and experimental observations are
needed to evaluate the effect.
Independent of absorption of NO-, wavelength-dependent scattering by small particles can
also produce a noticeable brown coloration in polluted air masses. A significant contribution
to this phenomenon by particulate nitrates is not expected in most urban areas. However, an
assessment of the role of nitrate aerosols in the discoloration and degradation of visual
range must await the availability of a sufficient data base on ambient particulate nitrate
concentrations.
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2. INTRODUCTION
Molecular nitrogen (N,,) and oxygen (02) are normal constituents of the air we breathe.
Together they comprise well over 90 percent of the earth's atmosphere, and both are essential
to life. As a gas in the atmosphere, 0, is vital to the respiration of all life forms except
the anaerobes. N? is essentially inert in all but the nitrogen-fixing organisms. Through the
action of natural or man-made processes, however, the two elements can combine with each other
or with other elements to form toxic compounds. This air quality criteria document compiles
in a single source document available information about the formation and occurrence of such
compounds in the atmosphere, and evidence of their effects on man and the biosphere.
The initial Air Quality Criteria for Nitrogen Oxides (EPA Publication No. AP-84) was
published by the U.S. Environmental Protection Agency (USEPA) in 1971. The information
presented provided the basis for the present annual air quality standard for nitrogen dioxide
(NOp), an arithmetic average not to exceed 100 ug/m (0.05 ppm). At the time, insufficient
information was available to support promulgation of a short-term standard. However, since
the annual standard does not preclude short-term peak N0~ concentrations which may be harmful,
the Congress, in the 1977 amendments to the Clean Air Act, required that the air quality
criteria document for nitrogen oxides (NO ) be revised. In addition to the question of short-
J\
term exposure, this document is required to address nitric and nitrous acids, nitrates,
nitrites, nitrosamines and other derivatives of oxides of nitrogen. N0? is the principal
subject of this document, since available evidence indicates it is the nitrogenous compound of
most concern for human health and welfare. However, the health and welfare effects of other
airborne nitrogen compounds including other nitrogen oxides, nitrogen acids, nitrates, nitrites,
nitrosamines and other derivative compounds are also presented. Also included are descriptions
of the complex chemical reactions occurring in po"nuted atmospheres that link, to some extent,
the atmospheric concentrations of nitrogen oxides with the presence of photochemical oxidants
such as ozone. The ozone/NO relationship is discussed in greater detail in the Air Quality
Criteria for Ozone and Other Photochemical Oxidants, EPA-600/8-78-004.
Nitrogen oxides are produced when fossil fuels are burned, both by the oxidation of
nitrogen in the fuel and by the high-temperature oxidation of atmospheric nitrogen. Most NO
emissions occur as nitric oxide (NO). Available evidence indicates that nitric oxide in the
ambient air is not of direct concern for human health and welfare. NO is, however, further
oxidized in the amosphere to a variety of other nitrogenous compounds. Of these, N02 is the
compound of most concern.
Increases in the U.S. consumption of energy will stimulate increasing combustion of
fossil fuels which can result in an increase in NO emissions. Atmospheric concentrations of
A
NOp and other nitrogenous compounds are, therefore, likely to become higher in the future,
especially if NO emissions control actions do not keep pace with energy production.
A
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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 NCu and various aspects of pulmonary function, particularly
those types of physiological or pathological changes that may lead to the development of
chronic respiratory disease. Other studies have been concerned with the effect of NCL exposure
on susceptibility to acute respiratory disease. Adverse effects of nitrogen compounds on
plants and inanimate materials have also been reported.
The determination of the effects of exposure to airborne nitrogen compounds on human
health encounters four major difficulties. The first is that nitrogen compounds comprise only
a portion of a complex of pollutants in the ambient air. Adverse effects found in epidemio-
logical studies may result from exposure to individual compounds or a combination of multiple
compounds. Epidemiologists, evaluating community studies, have not been able to assess
unequivocally the effects of exposure to individual compounds. Consequently, it is useful to
use the combined results of epidemiological and animal studies to assess potential harmful
effects. Animal studies reported in this document show the effects of exposure to individual
compounds as well as certain effects of the compounds in combination. In some cases, these
studies also show, for individual animal species, the maximum dose of the pollutant tolerated,
target organs, mechanisms of action, and lowest effective dose. In addition, the studies can
show whether there is a consistency of effects across a variety of animal species.
The second problem is the difficulty of assessing, with a high degree of accuracy, the
actual day-to-day exposure to NO of individuals or populations in ambient situations. Because
A
there are a limited number of monitoring stations, air measurement data are not completely
representative of actual human exposure. This difficulty is compounded by the mobility of the
population, the portion of each day spent inside buildings, and the variability of atmospheric
concentrations of pollutants over short distances.
The third problem encountered in determining the effects of exposure to nitrogen compounds
is that dose/response data derived from animal'studies cannot readily be extrapolated to
humans. Indications of probable effects on humans can be obtained from the animal studies,
and a consistent effect among animal species, especially when primates are included, increases
confidence that a similar effect may occur in humans.
The fourth problem is the determination of effective exposure time. NO community studies
usually use data on annual or daily mean levels of exposure. Only occasionally are hourly
values provided. Based on animal studies, however, it may be inferred that repeated inter-
mittent exposure to daily peak values may be more significant in the production of adverse
health effects than is an equivalent or even greater total dose delivered by continuous
exposure to the observed long-term averages. If this is true, the protection of human health
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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.
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3. GENERAL CHEMICAL AND PHYSICAL PROPERTTIES OF N0v
AND NOX-DERIVED POLLUTANTS x
3.1 INTRODUCTION AND OVERVIEW
In this chapter some general chemical and physical properties of NO * and NO -derived
A A
pollutants are discussed by way of introduction to the complex chemical and physical interac-
tions which may occur in the atmosphere and other media. The discussion will be significantly
augmented throughout the document as particular topics are discussed in depth.
There are eight oxides of nitrogen (NO ) that may be present in the ambient air: nitric
oxide (NO), nitrogen dioxide (NO,,), nitrous oxide. (NpO), unsymmetrical nitrogen trioxide
(OONO), symmetrical nitrogen trioxide (ON(O)O), dinitrogen trioxide (N^j), dinitrogen
tetroxide (N204), and dinitrogen pentoxide (NpOr).
Of these, NO and NOp are generally considered the most important in the lower troposphere
because they may be present in significant concentrations (Chapter 8). Their interconverti-
bility in photochemical smog reactions (Chapter 6) has frequently resulted in their being
grouped together under the designation NO , although analytic techniques can distinguish
clearly between them (Chapter 7). Of the two, NO,, is the more toxic and irritating compound
(Chapter 14 and 15).
Nitrous oxide is ubiquitous even in the absence of anthropogenic sources, since it is a
product of natural biologic processes in soil (Chapters 4 and 12). It is not known, however,
to be involved in any photochemical smog reactions. Although N?0 is not generally considered
to be an air pollutant, it participates in upper atmospheric reactions involving the ozone
layer (Chapter 9).
While OONO, ON(0)0, N^O,, N-O,, and NpOr may play a role in atmospheric chemical reactions
leading to the transformation, transport, and ultimate removal of nitrogen compounds from
ambient air (Chapter 6), they are present only in very low concentrations, even in polluted
environments.
Ammonia (NH.,) is generated, on a global scale, during the decomposition of nitrogenous
matter in natural ecosystems and it may also be produced locally in larger concentrations by
human activities such as the maintenance of dense animal populations (Chapter 4). It is
discussed briefly in this document to facilitate understanding of the nitrogen cycle and also
because some researchers have suggested that NH3 is converted to NO in the atmosphere.
Other NO -derived compounds which may be found in polluted air include nitrites, nitrates,
nitrogen acids, N-nitroso compounds, and organic compounds such as the peroxyacyl nitrates
*For all practical purposes, N0y is the sum of nitrogen dioxide (N02) and nitric oxide (NO).
3-1
-------
(RC(0)OON02, where R represents any one of a large variety of possible organic groups)
(Chapter 8).
The peroxyacyl nitrates, of which peroxyacetyl nitrate (CH3C(0)OON02, or PAN) is of most
concern in terms of atmospheric concentrations, have been thoroughly reviewed in the recent
EPA document, Air Quality Criteria for Ozone and Other Photochemical Oxidants (1978) and will
be given only the briefest discussion in this chapter and elsewhere in this document.
Recent discovery of N-nitroso compounds in air, water, and food has led to concern about
possible human exposure to this family of compounds, some of which have been shown to be
carcinogenic in animals. Health concerns also have been expressed about nitrates, which occur
as a component of particulate matter in the respirable size range, suspended in ambient air
(Chapter 15). Some of this particulate nitrate is produced in atmospheric reactions (Chapter
6). Nitrates may also occur in significant concentrations in drinking water supplies but this
occurrence is not believed to be the result of atmospheric production.
Photochemical models predict that up to one-half of the original nitrogen oxides emitted
may be converted on a daily basis to nitrates and nitric acid (HNO~). This atmospheric produc-
tion of nitric acid is an important component of acid rain (Chapter 11).
Table 3-1 summarizes current theoretical estimates of the concentrations of the various
nitrogen oxides and acids that would be present in an equilibrium state assuming initially
only molecules of nitrogen and oxygen at 1 atm pressure, 25°C and 50 percent relative humidity.
The low concentrations of many of the oxides and acids preclude- direct measurement of most of
them in the ambient air. Consequently, most studies leading to predictions of concentrations
rely on theoretical estimates derived from small-scale laboratory studies.
In fact, the thermodynamic equilibrium state is not achieved in polluted, sunlight-
irradiated atmospheres. Rather, expected concentrations of pollutants are influenced by
emissions and subsequent reactions and tend to be much greater than those at equilibrium.
Table 3-1 lists one set of estimated concentrations of nitrogen oxides and acids expected
under more realistic .conditions, derived from computer simulations of photochemical smog
reactions which might occur in more or less typical urban environments.
3.2 NITROGEN OXIDES
Table 3-2 summarizes some important physical properties of nitrogen oxides under standard
temperature and pressure (STP) conditions of 25°C and 1 atm, respectively. The remainder of
this section describes chemical and physical properties of individual nitrogen oxide species.
3.2.1 Nitric Oxide (NO)
Nitric oxide is an odorless gas. It is also colorless since its absorption bands are all
at wavelengths less than 230 nm, well below the visible wavelengths (Figure 3-1). Nitric
oxide is only slightly soluble in water (0.006 g/100 g of water at 24°C and 1 atm pressure).
3-2
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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)
Compound
Concentrations in Hypothetical Atmosphere, ppm
In Typical Sunlight-irragi-
At Equilibrium ated, Smoggy Atmosphere
°2
N2
H20
N02
NO
N03
N2°3
N2°4
N2°5
HONO (cis)
HONO (trans)
HON02
2.06 x 105
7.69 x 105
1.56 x 104
1.91 x 10"4
2.69 x 10"10
3.88 x 10"16
2.96 x 10"20
2.48 x 10"13
3.16 x 10"17
7.02 x 10"9
1.60 x 10"8
1.33 x 10"3
2.06 x 105
7.69 x 105
1.56 x 104
10'1
10'1
io"8-io"9
io"8-io"9
io"7-io"8
io"3-io"5
ID'3
lO'3
io"2-io"3
aTheoretical estimates made using computer simulations of the chemical
reactions rates in a synthetic smog mixture.
3-3
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TABLE 3-2. SOME PHYSICAL AND THERMODYNAMIC PROPERTIES OF THE NITROGEN OXIDES
Molecular Melting Boiling
Weight, Point Point
Oxide g/mol °Ca'b °Ca'b
NO 30.01 -163.6 -151.7
N02 46.01 Liquid, solid
forms largely
as N204
N204 92.02 -11.3 21.2
N20 44.02 -102.4 -89.5
N203 76.02 -102 3.5
(decomposes)
N20B 108.01 30 32.4
(decomposes)
Thermodynamic Functions
(Ideal Gas, 1 atm, 25°C)C
Solubility in Enthalpy of
H20(0 C), Formation,
cm3 (STP)XIOO ga kcal/mol
7.34 21.58
Reacts with H90 7.91
forming HON09 and
HONO
Reacts with H?0 2.17
forming HONO, and
HONO i
130.52 19.61
Reacts with H90 19.80
forming HONO
Reacts with H?0 2.7
forming HON02
Entropy,
cal/mol-deg
50.347
57.34
72.72
52.55
73.91
82.8
uMatheson Gas Data Book (Matheson Company, 1966).
Handbook of Chemistry and Physics (Chemical Rubber Company, 1969-1970).
JANAF Thermochemical Tables (National Bureau of Standards, 1971).
-------
50
I 40
z
UJ
o 30
HI
O
O
z
o
CO
CD
20
10
1500
1700
1900
2100
2300
WAVELENGTH, A
Figure 3-1. Absorption spectrum of nitric oxide (McNesby and Okabe,
1964).
3-5
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It has an uneven number of valence electrons, but, unlike NO-, it does not dimerize in the gas
phase.
Nitric oxide is a principal byproduct of combustion processes, arising from the oxidation
of molecular nitrogen in the combustion air and of organically bound nitrogen present in
certain fuels such as coal and heavy oil. The oxidation of nitrogen in combustion air occurs
primarily through a set of reactions known as the extended Zeldovitch mechanism (Zeldoritch,
1946):
N2 + 0 •* NO + N
N + 02 -> NO + 0
with the additional equation (extended mechanism)
N + OH •* NO + H
The high activation energy of the first reaction above (75 kcal/mol) coupled with its essential
function of breaking the strong N~ triple bond make this the rate limiting step of the
Zeldovitch mechanism. Due to the high activation energy, this mechanism for NO production
proceeds at a somewhat slower rate than the reactions of fuel constituents and is extremely
temperature sensitive (Bowman, 1973). Moreover, the production of atomic oxygen required for
the first step is also highly temperature sensitive. NO formed via this mechanism is often
referred to as "thermal N0x."
In addition to the strong temperature dependence of the rate of the first step of the
Zeldovich mechanism, the temperature also influences the amount of atomic oxygen (0) available
for the reaction. In the immediate vicinity of a flame, the high temperatures coupled with
the kinetics of the hydrocarbons in the fuel can drive the oxygen concentration to several
times its equilibrium level. The local ratio of fuel to air also has a first order effect on
the concentration of atomic oxygen (Bowman, 1973).
The reaction kinetics of thermal NO formation is further complicated by the fact that
certain hydrocarbon radicals can be effective in splitting the N2 bond through reactions such
as (Fenimore, 1976):
CH + N2 -> CHN + N
The rate of oxidation of the fuel (and intermediate hydrocarbon radical fragments) is usually
sufficiently rapid that only negligible quantities of the fuel radicals are available to
attack the molecular nitrogen. However, under fuel-rich conditions, this can become the
dominant mode of breaking the N2 bond and, in turn, can be responsible for significant NO
formation (Engleman et al., 1976). Such reactions appear to have a relatively low activation
energy and can proceed at a rate comparable to oxidation of the fuel. Because of the early
formation of NO by this mechanism, relative to that formed by the Zeldovitch mechanism, NO
thus formed is often referred to as "prompt NO." The importance of this mechanism has not
been quantified for practical systems.
3-6
-------
In fuels such as coal and residual fuel oil, nitrogen compounds are bound within the fuel
matrix. Typically, Number 6 residual oil contains 0.2 to 0.8 percent by weight bound nitrogen
and coal typically contains 1 to 2 percent. If this 1 percent nitrogen were converted quanti-
tatively to NO , it would account for about 2,000 ppm NO in the exhaust of a coal-fired unit.
A A
In practice, only a portion of these nitrogen compounds is converted to NO , with the remainder
being converted to molecular nitrogen (N2). Tests designed to determine the percent of the
NO emissions due to oxidation of bound nitrogen (Pershing and Wendt, 1976) show that upward
of 80 percent of the NO from a coal-fired boiler originate from this source. Details of the
kinetic mechanisms involved in fuel nitrogen oxidation are uncertain due in part to the
variability of molecular composition among the many types (and sources) of coal and heavy oils
and to the complex nature of the heterogeneous processes occurring. Experimental evidence
does, however, lend some insight into the processes involved. A number of fuel-bound nitrogen
compounds have been cited (Axworthy and Schuman, 1973; Martin et a!., 1971; Turner and
Siegmund, 1972), but the degree of conversion to NO does not seem to be significantly
affected by the compound type. NO conversions arising from fuel sources seem also to be
relatively insensitive to temperature in diffusion flames. The most important parameters in
determining fuel-bound nitrogen conversion appear to be the local conditions prevailing when
the nitrogen is evolved from the fuel. Under fuel-rich conditions this nitrogen tends to form
Np, whereas under fuel-lean conditions significant amounts of NO are formed.
Nitric oxide formation kinetics in typical furnaces are not fast enough to reach
equilibrium levels in the high temperature flame zone, while the NO destruction mechanisms are
far too slow to allow the NO, once formed, to reach equilibrium at typical stack temperatures.
This is to say that the NO formation process is kinetically controlled.
Nitric oxide and nitrogen dioxide produced in relatively large concentrations at high
temperatures in combustion processes would revert to lower concentrations characteristic
approximately of the equilibrium values shown in Table 3-3 were it not for the fact that
combustion equipment rapidly converts a large fraction of the thermal energy available to
useful work. This results in a rapid cooling of the combustion gases and a "freezing-in" of
the produced NO and NO,, near concentrations characteristic of the high temperature phase of
the process.
A major implication of the fact that N0x emissions are defined by the kinetics of the
process rather than being an equilibrium phenomenon is that NO emissions can be effectively
modified by changes in the details of the combustion process. For clean fuels such as natural
gas or Number 2 distillate oil with no bound nitrogen, the NO formation is dominated by the
Zeldovitch mechanism. Thus, combustion modifications which reduce peak flame temperature,
limit the gas residence time at peak temperatures and/or reduce the amount of atomic oxygen
available at high temperatures will reduce the NO emissions. Examples of such modifications
3-7
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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 (CALVERT, 1977)
Concentration, |jg/m (ppm)
Temperature, °K (°C) NO N02
-in -A
298 (24.85) 3.29 x 10 |~ 3-53 x 10 4
(2.63 x 10"iU) (1.88 x 10 *)
500 (226.85) 8.18 x 10"J 7.26 x 10~?
' (6.54 x 10~4) (3.86 x 10 *)
1,000 (726.85) 43 3.38
(34.4) (1.80)
1,500 (1,226.85) 1,620 12.35
(1,296) (6.57)
2,000 (1,726.85) 9,946.25 23.88
(7,957) (12.70)
3-8
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are flue gas recirculation, reduced load, reduced combustion air preheat temperature, water
injection and reduced excess air (Bowen and Hall, 1976a, 1976b, 1976c; Bowen and Hall, 1977a,
1977b, 1977c, 1977d, 1977e).
In furnaces fired with coal or heavy oil, the major portion of the NO emissions is from
fuel-bound nitrogen conversion. Thus, combustion modifications which reduce the availability
of oxygen when the nitrogen compounds are evolved will reduce the NO produced. Examples of
such modifications are reduction of the amount of excess air during firing, establishing
fuel-rich conditions during the early stages of combustion (staged combustion), or new burner
designs that tailor the rate of mixing between the fuel and air streams (Bowen and Hall,
1976a, 1976b, 1976c).
3.2.2 Nitrogen Dioxide (NO,,)
Nitrogen dioxide is a reddish-orange-brown gas with a characteristic pungent odor.
Although its boiling point is 21.1°C, the low partial pressure of N02 in the atmosphere pre-
vents condensation. Nitrogen dioxide is corrosive and highly oxidizing. It has an uneven
number of valence electrons and forms the dimer Np04 at higher concentrations and lower
temperatures, but the dimer is not important at ambient concentrations. In the atmosphere NO
can be oxidized to N02 by the thermal reaction:
2 NO + 02 •* 2 N02
However, this reaction is of minor importance in most urban ambient situations, since other
chemical processes are faster. The above reaction is mainly responsible for the NO,, present
in combustion exhaust gases. About 5 to 10 percent by volume of the total emissions of N0x
from combustion sources is in the form of N02, although substantial variations from one source
to another have been observed. Under more dilute ambient conditions, photochemical smog
reactions involving hydrocarbons convert NO to N02 (Chapter 6).
Nitrogen dioxide's principal involvement in photochemical smog stems from its absorption
of sunlight and subsequent decomposition (photolysis) to NO and atomic oxygen (0). Nitrogen
dioxide is an efficient absorber of light over a broad range of ultraviolet and visible wave-
lengths. Only quanta with wavelengths less than about 430 nm, however, have sufficient energy
to cause photolysis. It should also be noted that photons having wavelengths less than about
290 nm are largely absorbed in the upper atmosphere. The effective range of wavelengths
responsible for photolysis of N02 at ground level is, therefore, 290 nm to 430 nm. Because of
its absorption properties, N02 produces discoloration and reduces visibility in the polluted
lower troposphere.
3.2.3 Nitrous Oxide (NpO)
Nitrous oxide is a colorless gas with a slight odor at high concentrations. Nitrous
oxide in the atmosphere arises as one product of the reduction of nitrate by a ubiquitous
3-9
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group of bacteria that use nitrate as their terminal electron acceptor in the absence of
oxygen (denitrification) (Brezonik, 1972; Delwiche, 1970; Focht and Verstraete, 1977; Keeney,
1973).
Although N20 does not play a significant role in atmospheric reactions in the lower
troposphere, it participates in a mechanism for ozone decomposition in the stratosphere.
Nitrous oxide transported to the stratosphere undergoes photolysis by absorbing
ultraviolet (UV) radiation at wavelengths below 300 nm to produce N2 and singlet oxygen
(Johnston and Selwyn, 1975):
NpO + hv -» N2 + 0('D) where hv is a unit of radiant
energy
Singlet oxygen, which also is produced by ozone photolysis, reacts with more nitrous
oxide to produce two sets of products:
N20 + 0('D) -» N2 + 02
and
-» NO + NO
The NO produced enters a catalytic cycle, the net result of which is the regeneration of
NO and the destruction of ozone:
03 + hv -* 02 + 0
N02 + 0 -> NO + 02
These reactions are of concern because of the possibility that increased N~0 resulting
from denitrification of excess fertilizer may lead to a decrease of stratospheric ozone (Cast,
1976; Crutzen, 1976) with consequent potential for adverse human health effects.
3.2.4 Unsymmetrical Nitrogen Trioxide (OONO)
Unsymmetrical nitrogen trioxide is thought to be an intermediate in the reaction of NO
with 02:
NO + 02 j 0-0-N-O
0-0-N-O + NO •* 2N02
There is, however, no direct evidence for the existence of this species. If it does
exist, it is, nevertheless, of little importance in the chemistry of polluted atmospheres,
since the N0/02 reaction accounts for very little of the NO oxidized.
3.2.5 Symmetrical Nitrogen Trioxide (NO.,)
Symmetrical nitrogen trioxide has been identified in laboratory systems containing Nt^/Og,
N09/0, and N90r as an important reactive transient (Johnston, 1966). It is likely to be
L. £. O
present in photochemical smog. This compound can be formed as follows:
0 + N02 (+ M) -> N03 (+ M)
N205 (+ M) -> N03 + N02 (+ M)
3-10
-------
(where M represents any third molecule available to remove a fraction of the energy involved
in the reaction.)
Symmetrical nitrogen trioxide is highly reactive towards both nitric oxide and nitrogen
dioxide.
N03 + NO -»• 2N02
NO, + N09 (+ M) -» N-0, (+ M)
-6 3 -9
Its expected concentration in polluted air is very low (about 10 (jg/m or 10 ppm).
3.2.6 Dinitrogen Trioxide (N.,0,)_ (Also Known as Nitrogen Sesquioxide)
In the atmosphere, hLO, is in equilibrium with NO and N02 according to the following
equation:
NO + NO, j N,0,
t- * £• 3 _4
The equilibrium concentrations at typical urban levels of NO and N09 range from about 10
3-7 -6 3 • ~9
'ug/m (~10 ppm) to 10 ug/m (~10 ppm) (Table 3-4). N90, is the anhydride of nitrous acid
£. O
and reacts with liquid water to form the acid:
N203 + H20 -» 2HONO
3.2.7 Dinitrogen Tetroxide (NpO.) (Also Known as Nitrogen Tetroxide)
Dinitrogen tetroxide is the dimer of N02 formed by the association of N02 molecules. It
also readily dissociates to establish the equilibrium:
2N02 \ N204
Table 3-4 presents theoretical predictions of concentrations of N,,03 and N20^ in equilibrium
with various NO and N02 concentrations.
3.3 NITRATES, NITRITES, AND NITROGEN ACIDS
Nitric acid in the gaseous state- is colorless and photochemically stable. The major
pathway for atmospheric formation of nitric acid is given by:
•OH + N02 -» HN03 where -OH is a hydroxyl free radical
It is a volatile acid, so that at ambient concentrations in the atmosphere, the vapor would
not be expected to coalesce into aerosol and be retained unless the aerosol contains reactants
such as ammonia (NHL) to neutralize the acid, producing particulate nitrates (Chapter 6).
The nitrate ion (NOO is the most oxidized form of nitrogen. Since nitrate is chemically
unreactive in dilute aqueous solution, nearly all of the transformations involving nitrate in
natural waters result from biochemical pathways. The nitrate salts of all common metals are
quite soluble.
Nitrates can be reduced to nitrites by microbial action. Many of the deleterious effects
of nitrate result from its conversion to nitrite. The nitrite ion represents an intermediate
and relatively unstable oxidation state (+3) for nitrogen. Both chemical and biological
processes can result in its further reduction to various products, or its oxidation to nitrate.
Nitrite salts are also quite soluble.
3-11
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TABLE 3-4. THEORETICAL CONCENTRATIONS OF DINITROGEN TRIOXIDE AND
DINITROGEN TETROXIDE IN EQUILIBRIUM WITH VARIOUS LEVELS
OF CASEOUS NITRIC OXIDE AND NITROGEN DIOXIDE IN AIR
AT 25°C (CALVERT, 1977)
Concentration, ppm
NO N0
0.05 0.05 1.3 x 10~9 1.7 x 10"8
0.10 0.10 5.2 x 10"9 6.8 x 10~8
0.50 0.50 1.3 x 10"7 1.7 x 10"6
1.00 1.00 5.2 x 10"7 6.8 x 10"6
3-12
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The nitrite ion is the Lewis base of the weak acid, nitrous acid (HNCL). When NO and NO-
are present in the atmosphere, HN02 will be formed as a result of the reaction:
NO + N02 + H20 -> 2HN02
However, in sunlight-irradiated atmospheres, the dominant pathway for nitrous acid formation
is:
•OH + NO •* HONO
Atmospheric concentrations of HONO are limited by the reverse reaction:
HONO + hv •* -OH + NO
Nitrous acid is a weak reducing agent and is oxidized to nitrate only by strong chemical
oxidants and by nitrifying bacteria. Nitrous acid reacts with amino acids (the Van Slyke
reactions) to yield N«. The reaction of nitrous acid with secondary amines to form N-nitros-
amines is discussed in Section 3.5.
3.4 AMMONIA (NH3)
Ammonia is a colorless gas with a pungent odor. It is extremely soluble in water, forming
the ammonium (NH^ ) and hydroxy (OH ) ions. In the atmosphere, ammonia has been reported
(Soderlund and Svensson, 1976) to be converted into oxides of nitrogen when it reacts with
hydroxyl free radicals (-OH). Burns and Hardy (1975) report that ammonia is oxidized into
nitrates and nitrites in the atmosphere, and in geothermal wells. In the stratosphere, ammonia
can be dissociated by irradiation with sunlight at wavelengths below 230 nm (McConnell, 1973).
3.5 N-NITROSO COMPOUNDS
Organic nitroso compounds contain a nitroso group (-N=0) attached to a nitrogen or carbon
atom. According to Magee (1971), N-nitroso compounds generally can be divided into two
groups—one group includes the dialkyl, alkylaryl, and diaryl nitrosamines, and the other,
alkyl and aryl nitrosamides.
The principal chemical reaction involved in the formation of N-nitrosamines is that of
the secondary amines with nitrous acid. Nitrosation is effected by agents having the structure
ONX, where X = 0-alkoxyl, N0?, N03, halogen, tetrafluoroborate, hydrogen sulfate or OhL . The
equilibrium reaction of nitrosonium ion (ON ), nitrous acid and nitrite ion:
ON+ + OH" * HN02 J H+ + N0~
is shifted to the right at pH > 7. The simplest form of nitrosation of amines involves
electrophilic attack by the nitrosonium ion and subsequent deprotonation.
Mirvish (1970) studied the kinetics of dimethylnitrosamine (DMN) nitrosation and pointed
out that the chief nitrosating agent at pH 1 is dinitrogen trioxide, the anhydride of nitrous
acid, which forms reversibly from two HNO- molecules. The formation of nitrosamines is
dependent on the pK of the amine.
3-13
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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 urn. Nuclear magnetic resonance (NMR), infrared (IR),
ultraviolet (UV), and mass spectrometry (MS) spectra have been reviewed by Magee et al. (1976).
Atmospheric reactions involving nitrosamines are discussed in Chapter 6.
3.6 SUMMARY
There are eight nitrogen oxides which may be present in the ambient air: nitric oxide
(NO), nitrogen dioxide (NO,,), nitrous oxide (N20), unsymmetrical nitrogen trioxide (OONO),
symmetrical nitrogen trioxide (O-N(O)-O), dinitrogen trioxide (N^OO, dinitrogen tetroxide
(NpO,), and dinitrogen pentoxide (N?0r).
Of these, NO and N02 are generally considered the most important in the lower troposphere
because they may be present in significant concentrations in polluted atmospheres. Their
interconvertibility in photochemical smog reactions has frequently resulted in their being
grouped together under the designation NO , although analytic techniques can distinguish
A
clearly between them. Of the two, N02 is the more toxic and irritating compound.
Nitrous oxide is ubiquitous even in the absence of anthropogenic sources since it is a
product of natural biologic processes in soil. It is not known, however, to be involved in
any photochemical smog reactions. Although N~0 is not generally considered to be an air
pollutant, it is a principal reactant in upper atmospheric reactions involving the ozone
layer.
While OONO, ON(0)0, N203> N,,04, and N^Or may play a role in atmospheric chemical reactions
leading to the transformation, transport, and ultimate removal of nitrogen compounds from
ambient air, they are present only in very low concentrations, even in polluted environments.
Ammonia (NH3) originates on a global scale during the decomposition of nitrogenous matter
in natural ecosystems but it may also be produced locally by human activities such as the
maintenance of dense animal populations. Some researchers have suggested conversion of NH, to
NO in the atmosphere.
Compounds derived from NO including nitrites, nitrates, nitrogen acids, N-nitroso com-
pounds, and organic compounds such as the peroxyacyl nitrates [RC(0)OONOp], where R represents
any one of a large variety of possible organic groups, may also be found in polluted air.
The peroxyacyl nitrates, of which peroxyacetyl nitrate [CH3C(0)OON02] or PAN is of most
concern in terms of atmospheric concentrations, have been thoroughly reviewed in the recent
EPA document, Air Quality Criteria for Ozone and Other Photochemical Oxidants.
3-14
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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 (N0~) is produced in minor quantities in the combustion process (5 to 10
percent of the total oxides of nitrogen). In terms of significant atmospheric loading in
populated areas, N0? arises mainly from the conversion of NO to N0? by a variety of chemical
processes in the atmosphere. Nitrogen dioxide is corrosive and highly oxidizing. Its reddish-
orange-brown color arises from its absorption of light over a broad range of visible wavelengths.
Because of its strong absorption in this range (and also in the ultraviolet spectrum), NOp can
cause visibility reduction and affect the spectral distribution of solar radiation in the
polluted, lower atmosphere.
3.6.2 Nitrates, Nitrites, and Nitrogen Acids
Other compounds derived from oxides of nitrogen (NO ) by means of atmospheric chemical
processes include nitrites, nitrates, nitrogen acids, organic compounds such as the peroxyacyl
nitrates, and, possibly, the N-nitroso compounds.
Nitric acid, a strong acid and powerful oxidizing agent, is colorless and photochemically
stable in the gaseous state. Its high volatility prevents condensation into droplets in the
atmosphere unless the droplets contain reactants such as ammonia which neutralize the acid.
Atmospheric reactions such as this may result in the formation of particulate nitrates
suspended in ambient air.
3-15
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3.6.3 N-Nitroso Compounds
The N-nitroso family comprises a wide variety of compounds all containing a nitroso group
(~N=0) attached to a nitrogen or carbon atom. Their formation in the atmosphere has been
postulated to proceed through chemical reaction of amines with NO and N0v-derivatives in gas
A A
phase reactions and/or through atmospheric reactions involving aerosols. Nitroso compounds
are characteristically photosensitive and the nitroso group is split by the ultraviolet radia-
tion in sunlight. Gaseous nitrosamines may also be denitrosated by visible light.
3-16
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3.7 REFERENCES
Axworthy, A. E. , and M. Schuman. Investigation of the mechanism and chemistry of fuel
nitrogen conversion to nitrogen oxides in combustion. Jjr. Proceedings, Coal Combustion
Seminar, U. S. Environmental Protection Agency, Research Triangle Park, North Carolina,
June 19-20, 1973. EPA-650/2-73-021, U. S. Environmental Protection Agency, Research
Triangle Park, NC, September 1973. pp. 9-41.
Bowen, J. S. , and R. E. Hall, Chairmen. Proceedings of the Stationary Source Combustion
Symposium, Volume I—Fundamental Research, U. S. Environmental Protection Agency,
Atlanta, Georgia, September 24-26, 1975. EPA-600/2-76-152a, U. S. Environmental
Protection Agency, Research Triangle Park, NC, June 1976a.
Bowen, J. S. , and R. E. Hall, Chairmen. Proceedings of the Stationary Source Combustion
Symposium, Volume II--Fuels and Process Research and Development, U. S. Environmental
Protection Agency, Atlanta, Georgia, September 24-26, 1975. EPA-600/2-76-152b, U. S.
Environmental Protection Agency, Research Triangle Park, NC, June 1976b.
Bowen, J. S. , and R. E. Hall, Chairmen. Proceedings of the Stationary Source Combustion
Symposium, Volume Ill—Field Testing and Surveys, U. S. Environmental Protection Agency,
Atlanta, Georgia, September 24-26, 1975. EPA-600/2-76-152c, U.S. Environmental Pro-
tection Agency, Research Triangle Park, NC, June 1976c.
Bowen, J. S. , and R. E. Hall, Chairmen. Proceedings of the Second Stationary Source Com-
bustion Symposium, Volume I: Small Industrial, Commercial, and Residential Systems, U.S.
Environmental Protection Agency, New Orleans, Louisiana, August 29-September 1, 1977.
EPA-600/7-77-073a, U.S. Environmental Protection Agency, Research Triangle Park, NC, July
1977a.
Bowen, J. S., and R. E. Hall, Chairmen. Proceedings of the Second Stationary Source Com-
bustion Symposium, Volume II: Utility and Large Industrial Boilers, U. S. Environmental
Protection Agency, New Orleans, Louisiana, August 27-September 1, 1977. EPA-600/7-77-
073b, U. S. Environmental Protection Agency, Research Triangle Park, NC, July 1977b.
Bowen, J. S., and R. E. Hall, Chairmen. Proceedings of the Second Stationary Source Com-
bustion Symposium, Volume III: Stationary Engine, Industrial Process Combustion Systems,
and Advanced Processes, U. S. Environmental Protection Agency, New Orleans, Louisiana,
August 27-September 1, 1977. EPA-600/7-77-073c, U. S. Environmental Protection Agency,
Research Triangle Park, NC, July 1977c.
Bowen, J. S. , and R. E. Hall, Chairmen. Proceedings of the Second Stationary Source Com-
bustion Symposium, Volume IV: Fundamental Combustion Research, U.S. Environmental Pro-
tection Agency, New Orleans, Louisiana, August 27-September 1,^ 1977. EPA-600/7-77-073d,
U. S. Environmental Protection Agency, Research Triangle Park, NC, July 1977d.
Bowen, J. S., and R. E. Hall, Chairmen. Proceedings of the Second Stationary Source Com-
bustion Symposium, Volume V: Addendum, U. S. Environmental Protection Agency, New
Orleans, Louisiana, August 27-September 1, 1977. EPA-600/7-77-073e, U. S. Environmental
Protection Agency, Research Triangle Park, NC, July 1977e.
Bowman, C. T. Kinetics of nitric acid formation in combustion processes. lr\: Fourteenth
Symposium (International) on Combustion, The Combustion Institute, University Park,
Pennsylvania, August 20-25, 1972. The Combustion Institute, Pittsburgh, PA, 1973.
pp.729-738.
3-17
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Brezonik, P. L. Nitrogen: sources and tranformation in natural waters, I_n: Nutrients in
Natural Waters. H. E. Allen and J. R. Kramer, eds. , Wiley-Interscience, New York, NY,
1972. pp. 1-50.
Burns, R. C. , and R. W. F. Hardy. Nitrogen Fixation in Bacteria and Higher Plants.
Springer-Verlag, New York, NY, 1975.
Calvert, J. G. Nitrogen oxides—their properties and effects on atmospheric light trans-
mission. In: Nitrogen Oxides. National Academy of Sciences, Washington, DC, 1977. pp.
4-19. ~~
Chemical Rubber Company. Handbook of Chemistry and Physics. Fiftieth edition. R. C. Weast,
ed. Cleveland, Ohio, 1969-1970.
Council for Agricultural Science and Technology. Effect of Increased Nitrogen Fixation on
Stratospheric Ozone. CAST Report No. 53, Council for Agricultural Science and Tech-
nology, Iowa State University, Ames, IA, January 1976.
Crutzen, P. J. Upper limits on atmospheric ozone reductions following increased application
of fixed nitrogen to the soil. Geophys. Res. Lett. 3:169-172, 1976.
Delwiche, C. C. The nitrogen cycle. Sci. Am. 223:137-146, 1970.
Demerjian, K. L. , J. A. Kerr, and J. G. Calvert. The mechanism of photochemical smog forma-
tion. Adv. Environ. Sci. Technol. 4:1-262, 1974.
Engleman, V. S., V. J. Siminski, and W. Bartok. Mechanism and Kinetics of the Formation of
NO and Other Combustion Pollutants; Phase II. Modified Combustion. EPA-600/7-76-009b,
U. S. Environmental Protection Agency, Research Triangle Park, NC, August 1976.
Fenimore, C. P. Formation of nitric oxide in premixed hydrocarbon flames. I_n: Thirteenth
Symposium (International) on Combustion, Combustion Institute, Salt Lake City, Utah,
August 23-29, 1970. Combustion Institute, Pittsburgh, PA, 1971. pp. 373-380.
Focht, D. D. , and W. Verstraete. Biochemical ecology of nitrification and denitrification.
Adv. Microb. Ecol. 1:135-214, 1977.
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Johnston, H. S,. and G. S. Selwyn. New cross sections for the absorption of near ultraviolet
radiation by nitrous oxide (N20). Geophys. Res. Lett. 2:549-551, 1975.
Keeney, D. R. The nitrogen cycle in sediment water systems. J. Environ. Qual. 2:15-29, 1973.
Magee, P. N. Toxicity of nitrosamines: their possible human health hazards. Food Cosmet.
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In: Chemical Carcinogens. C. E. Searle, ed., ACS Monograph 173, American Chemical
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Emissions from Distillate-Oil-Fired Furnaces. AP-87, U. S. Environmental Protection
Agency, Research Triangle Park, NC, June 1971.
Matheson Company. Matheson Gas Data Book. Fourth Edition. Matheson Co. , Inc., East
Rutherford, NJ, 1966. pp. 367-391.
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McNesby, J. R. , and H. Okabe. Vacuum ultraviolet photochemistry. Adv. Photochem. 3:157-240,
1964.
Mirvish, S. S. Kinetics of dimethylamine nitrosation in relation to nitrosamine carcino-
genesis. J. Natl. Cancer Inst. (U.S.) 44:633-639, 1970.
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U.S. Department of Commerce, Washington, DC, June 1971.
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(International) on Combustion, The Combustion Institute, Cambridge, Massachusetts, August
15-20, 1976. The Combustion Institute, Pittsburgh, PA 1976. pp. 389-399.
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the Nitro and Nitroso Groups. Part 1. H. Feuer, ed. , Interscience Publishers, New
York, NY, 1969. pp. 137-163.
Soderlund, R., and B. H. Svensson. The global nitrogen cycle. In: Nitrogen, Phosphorus, and
Sulfur - Global Cycles: SCOPE Report No. 7. Ecol. Bull. (|?):23-73, 1976.
Turner, D. W. , and C. W. Siegmund. Staged combustion and flue gas recycle: potential for
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21:577-628, 1946.
3-19
-------
-------
4. THE NITROGEN CYCLE
4.1 INTRODUCTION
This chapter presents a discussion of the nitrogen cycle, pointing out the principal
pathways, sources and sinks of nitrogen compounds in the environment on a global scale. This
discussion is intended to provide background and perspective for the discussions relating to
nitrogen and nitrogen oxides as presented in the other chapters of this document. One of the
concerns relating to the effects of nitrogen oxide emissions into the atmosphere is the extent
to which these emissions impinge on the natural cycling of this important nutrient element.
In addition to the nitrogen cycle, this chapter discusses estimates of the flow of
nitrogen through the various biogeochemical compartments or pools in the global cycling of
nitrogen.
The impact of man's intervention into the nitrogen cycle is discussed in Chapters 5 and 6
which describe the sources and the environmental transport of nitrogen oxides. Atmospheric
concentrations are discussed in Chapter 8, the possible effects on the ozone layer in Chapter
9, Chapter 11 is concerned with acidic precipitation, and perturbations of the nitrogen cycle
as evidenced in escosystem effects are specifically discussed in Chapter 12.
4.2 THE NITROGEN CYCLE
The major source of nitrogen is the earth's atmosphere where, in molecular form, it is a
major constituent (79 percent). The flow of nitrogen from the atmosphere and its transforma-
tions in the biosphere are regulated almost entirely by terrestrial and aquatic microorganisms
(Alexander, 1977; Bolin and Arrhenius, 1977; Delwiche, 1970, 1977).
In general outline, the nitrogen cycle is identical in terrestrial, fresh water, and
oceanic habitats; only the microorganisms which mediate the various transformations are
different (Alexander, 1977; Chen et al., 1972; Keeney, 1973) (Figure 4-1). A discussion of
the step-by-step cycling of nitrogen follows.
1. Biological Nitrogen Fixation - Atmospheric nitrogen gas (N^) is transformed into
ammonia (NH., or NHt) or nitrates (NO- ) in which form it enters the food chain. The transfor-
mation is carried out by a wide variety of microorganisms. The microorganisms may be either
symbiotic (living in the roots of leguminous plants) or nonsymbiotic (living independently in
the soil) and the process may be accomplished under aerobic or anaerobic conditions.
2. Organic Nitrogen Formation (assimilation) -- Fixed nitrogen as either nitrates or
ammonia is assimilated by plants and converted into organic molecules such as amino acids,
proteins, nucleic acids and vitamins. Plants are eaten by animals and plant proteins are
converted to animal proteins. In addition, carnivores consume other animals as a protein
source. Nitrogen is bound in plant or animal protein until the organisms die, or as in the
case of animals, certain products are excreted.
3. Deamination or Ammonification -- This is a two-step process, also termed mineraliza-
tion, in which the excretion products of animals and the proteins in dead plants and animals
4-1
-------
i
ro
(f
N2
MOLECULAR
NITROGEN
IN
ATMOSPHERE
BIOLOGICAL FIXATION ®
"OF MOLECULAR NITROGEN &
ELECTRICAL
AND
PHOTOCHEMICAL
FIXATION
NITROGEN
OXIDES:
NO, IMO2
VOLCANIC
ERUPTION
WEATHERING
OF ROCKS
FOREST & GRASSLAND FIRES
STORAGE OF
NITROGENOUS
COMPOUNDS IN
SEDIMENTS. SOILS,
AND SEDIMENTARY
ROCKS
ANIMALS IN GRAZING
FOOD CHAIN
'::'":"'""'"""""'"" DE ATH 'ft WASTES ?&::;%!
AUTOTROPHS
DETRITUS FOOD CHAIN
AMINO
NITROGEN
NH2
3 NIJRIFICAT ON
l-j^VAV-l.-.^W:^:":":^:^ xo::::
NITRITE A—_ AMMONIA A— — i
V— J
V— NH3
DENITRIFICATION
DENITRIFICATION
Figure 4-1. The nitrogen cycle. Organic phase shaded.
-------
are broken down through proteolysis to amino acids. The amino acids in turn are converted
into ammonia (MM,). The ammonia may be assimilated by aquatic or terrestrial plants and
microorganisms may be bound by clay particles in the soil, or it may be converted by micro-
organisms to form nitrates in the process termed nitrification. It may also escape into the
atmosphere.
4. Nitrification -- Nitrates are formed through the conversion by certain specific
bacteria of ammonia first to nitrite (NCL ) and then to nitrate (NCL ). Nitrates may be
assimilated by plants, washed downward through the soil into groundwater or through surface
runoff into streams, rivers, and oceans, and may be transformed into atmospheric nitrogen or
reduced to ammonia.
The organic phase of the nitrogen cycle is complete at this point where plants and
microorganisms are able to assimilate the nitrates produced. Under certain circumstances
nitrate reduction occurs; microorganisms may convert nitrates back to ammonia via the nitrate
step. These processes are the converse of the previous transformations.
Nitrogen, as indicated above, once it is in the nitrate form may be lost from the soil in
several ways. It may be assimilated by plants or microorganisms, or due to its solubility
enter the soil solution and be carried off into the groundwater, lakes and streams, or through
the process of denitrification converted into atmospheric nitrogen (N2).
5. Denitrification -- Nitrates, through bacterial action, are converted into atmospheric
nitrogen. Denitrification is an anaerobic process. Nitrates (NO., ) are converted into
nitrites (N02 ), to nitrous oxide (N20) and finally into nitrogen gas (N2) which goes off into
the atmosphere. In the soil, nitrites rarely accumulate under acidic conditions, nitrites
decompose spontaneously to nitric oxide (NO), and under alpine conditions, they are biologi-
cally converted to N20 and N? (Alexander, 1977). It must be emphasized that this process is
anaerobic and that conversion of nitrates to nitrites is extremely sensitive to the presence
of atmospheric oxygen. If atmospheric oxygen is present, the conversion does not occur.
Denitrification is the greatest biological leak in the otherwise closed soil cycle
(Alexander, 1977; Chapham, 1973). Through denitrification, nitrogen becomes unavailable to
most plants and microorganisms and, therefore, also to animals. Nitrogen gas enters the large
atmospheric reservoir wherein its residence time may be as great as 10 years (Delwiche,
1970). Nitrous oxide has a much shorter residence time. It may be converted to nitrogen gas
in the stratosphere or returned by chemical or biological processes to the soil nitrogen pool.
Were it not for biological nitrogen fixation, the molecular nitrogen released through denitri-
fication would be lost to the organisms on earth.
Another pathway in the atmospheric phase of the nitrogen cycle is the oxidation of
nitrogen by lightening to form nitrogen oxides. Nitrogen oxides in turn may react with water
to form nitrates (Chapham, 1973).
4-3
-------
4.3 THE GLOBAL CIRCULATION OF NITROGEN
The transformation and movement of nitrogen as explained in the foregoing pages related
to the biogeochemical circulation of nitrogen. The circulation of nitrogen is a long term
process. Global nitrogen resides in a number of different compartments or pools, the principal
ones being primary rocks, sedimentary rocks, deep-sea sediments, the atmosphere, and the
soil-water pool. The largest of these pools is the atmosphere composed of 79 percent molecular
nitrogen (Bolin and Arrhenius, 1977; Delwiche, 1970, 1977). The atmosphere is not only an
important reservoir for nitrogenous compounds but also serves as a principal conduit through
which emissions of gaseous and particulate forms of the oxides of nitrogen (NO ) are trans-
formed and conveyed between terrestrial and aquatic systems. Sb'derlund and Svensson (1976)
have hypothesized that a net flow of NO prevails from terrestrial to aquatic systems; losses
of NO from aquatic system to the atmosphere were considered insignificant. Nitrogenous
A
compounds occurring in the atmosphere can be returned to terrestrial or aquatic areas princi-
pally via wet (rainfall) or dry (particulate and gaseous) deposition (Chapter 6).
The distribution of nitrogen in the major compartments as estimated by Delwiche (1977) is
listed in Table 4-1. Delwiche's figures are at variance with those of Soderlund and Svensson
(1976) because of differences in compartment description; for example, "organic sea" as used
by Delwiche includes an "active" 10 cm layer of the ocean bottom whereas Sdderland and Svensson
5 5
give 5.3 x 10 Tg for dissolved organic nitrogen. "Organic soil" is total whereas 3.0 x 10
Tg cited by the other authors is to a depth of one meter. In any case the figures are
estimates and subject to change as new data are obtained.
Q
Turnover times for the three largest "pools" of nitrogen are: 3 x 10 years for atmos-
pheric nitrogen, 2,500 years for nitrogen in the seas when nitrates and organic compounds are
counted together and less than one year for nitrates and nitrites in the soil (Whittaker,
1975). Delwiche (1970, 1977) has pointed out that the transfer rates can be estimated only
within broad limits. The only two quantities of nitrogen known with any degree of accuracy
are the amount of nitrogen in the atmosphere and the rate of industrial fixation (Delwiche,
1970). The amount and the length of time nitrogen is in the atmosphere indicates why the
atmosphere is the greatest source of nitrogen, while the short period of time nitrogen is in
the soil emphasizes why nitrogen is often in short supply as a nutrient element.
4.3.1 Important Nitrogen Fluxes
Various authors have estimated the global flow of nitrogen as it moves through the
nitrogen cycle. The estimates of these authors are presented in Tables 4-2 and 4-3 for ease
of comparison. Most of the estimates are based on extrapolation of experimentally-determined
small-scale emission factors to the global scale, but some are crude estimates, arrived at by
balancing mass flows to account for unknown sources. Particular reference will be made to
those portions of the nitrogen cycle which are most influenced by human activities as it is in
this context that the global flow of nitrogen becomes important.
4-4
-------
TABLE 4-1. DISTRIBUTION OF NITROGEN IN MAJOR COMPARTMENTS
Compartment Tg* N Reference
Atmosphere 3.9 x 109 Garrels et al. , 1975
Plants and animals 1.0 x 104 Delwiche, 1970
Organic, soil 1.7 x 105 Delwiche, 1970
Organic, sea 8.9 x 10 Delwiche, 1970
Inorganic, soil 1.6 x 10 Delwiche, 1970
Inorganic, sea 9.9 x 104 Delwiche, 1970
Sediments 2.0 x 108 Garrels et al. , 1975
Delwiche, 1977
*Tg = 1012 grams
4.3.1.1 Biological Nitrogen Fixation—Biological nitrogen fixation involves the reduction of
atmospheric N, to ammonia (NH,), a form of fixed nitrogen which can be incorporated directly
into the organic substances essential for life. Nitrogen fixation is important in the main-
-tenance of soil fertility in terrestrial, aquatic, and agricultural ecosystems. It is
indirectly responsible for the production of nitrates. Fixed forms of nitrogen serve as
-nutrient sources and, in certain circumstances involving high concentrations, are a source of
environmental pollution.
It has been estimated by Burns and Hardy that, on a global basis, nitrogen fixation in
12
terrestrial ecosystems accounts for 139 Tg (1 Tg = 10 g) of fixed nitrogen produced each
year; leguminous plants account for 35 Tg of this total with the remainder being produced in
forests and grasslands (Burns and Hardy, 1975). Estimates of other investigators differ
considerably and are shown in Tables 4-2 and 4-3.
Nitrogen fixation proceeds slowly in the presence of high levels of ammonia and other
nitrogen-containing compounds, such as chemical fertilizer. Nitrous oxide (N20), a product of
catabolic soil processes, has been shown in laboratory situations to have the potential for
altering the rates of nitrogen fixation through inhibition of nitrogenase (Hardy and Knight,
1966).
In natural waters, the blue-green algae are the principal agents of nitrogen fixation.
Fixation of nitrogen in aquatic regions of the world have been estimated by Soderlund and
4-5
-------
TABLE 4-2. ESTIMATES OF GLOBAL NITROGEN FIXATION
IN THE BIOSPHERE
TgN/yr
1
N?- fixation (total)
terrestrial (biological)...
land and sea (biological)..
aquatic
combustion
other industrial
lightning (atmospheric) ...
Delwiche
(1970)
92
44
N/A
10
18
12
7.6
Burns and
Hardy
(1975)
245
135
175
40
20
30
10
Sdderlund
and Svensson
(1976)
224-324
139
169-269
30-130
19
36
N/A
Robinson
and Robbins
(1975)
166
118
N/A
N/A
16
N/A
N/A
Liu et al
(1977)
227
180
N/A
37
18
36
9
CAST
(1976)
N/A
140
N/A
0.36-3.6
21
N/A
N/A
-------
TABLE 4-3. ESTIMATES OF GLOBAL EMISSIONS AND FLUXES OF
OXIDES OF NITROGEN AND RELATED COMPOUNDS
TgN/yr
Biological N.-fixation
( 1 and and sea) . .
Biological denitrif ication
( land and sea)
NO emissions from land
to atmosphere
NO emissions from land
and sea
NO formed by combustion. . .
NO formed by industrial
processes
Atmospheric NH, trans-
formation to NO
NH, emissions to atmosphere
Atmospheric production of
NO bv liahtnina
Delwiche
(1970)
54
83
(N2,N20)
NA
NA
NA
30
NA
NA
NA
Burns Soderlund Robinson
and Hardy and Svensson and Bobbins Liu et al.
(1975) (1976) (1975) (1977)
175
190(N )
20(N20)
NA
NA
15
30
30
165(land
and sea)
10
169-269
96-191(N,)
36-149(N20)
40-108
NA
19
36
3-8
113-244
(land)
NA
117
338
(N20)
NA
210(NO)
15
NA
NA
870(1 and
and sea)
NA
240
270
(N2.N20)
NA
NA
NA
40
NA
NA
NA
Sze
and Rice
(1976)
260
260
(N2,N20)
NA
NA
NA
NA
NA
NA
NA
CAST
(1976)
NA
171-200
(N2,N20)
NA
NA
NA
NA
NA
NA
NA
Chameides
et al.
(1977)
NA
NA
NA
NA
NA
NA
NA
NA
30-40
-------
Svensson (1976) to be in the range of 20 to 120 Tg N per year. The abundance of the blue-green
algae, Oscillatoria thelbautii, throughout oceanic areas, has been reported to account for a
large percentage of the global nitrogen budget (Carpenter and Price, 1976).
4.3.1.2 Industrial Nitrogen Fixation—The need for fertilizers to be used in the growing of
crops has resulted in the development of the Haber-Bosch process by which inorganically-based
chemical fertilizers are produced. Soderlund and Svensson (1976) estimate that industrial
fixation processes accounted for 36 Tg of fixed nitrogen produced in 1970, nearly 30 percent
of the amount estimated from natural processes. These authors also estimate that combustion
processes account for 19 Tg of NO -derived N emitted into the atmosphere in 1970. These
A
processes release primarily NO.
4.3.1.3 Nitrogen Fixation by Other Processes—Minor amounts of nitrogen can be fixed in the
atmosphere through chemical reactions. Molecular nitrogen can react with ozone (0,) in
stratospheric reactions to produce N?0.
Lightning flashes in the troposphere can convert N? to NO via reaction with monatomic
oxygen. Junge (1958) concluded from analysis of precipitation data that lightning can contri-
bute only 10 to 20 percent of the amounts of nitrate found in rain. However, there are no
direct experimental determinations of this estimate. Crutzen and Ehhalt (1977) estimated that
from 8 to 40 Tg N are fixed each year by lightning.
4.3.1.4 Nitrates, Nitrites, and the Nitrogen Cycle—The microbial oxidation of NH., to nitrates
(NO.,) and nitrites (N0?) is the sole natural source of nitrate in the biosphere (Focht and
Verstraete, 1977) other than atmospheric transformations of NO to nitrates (Chapter 6).
A
Because nitrates are readily leached from soil and are susceptible to denitrification, nitri-
fication can result in large losses of nitrogen from ammonium-based fertilizers applied to
soils.
Nitrates are the fixed nitrogen forms predominant in stream and river effluents. In the
atmosphere, transformation reactions involving NO, NO^, NH3 and acidic aerosols yield particu-
late nitrates, such as ammonium nitrate.
Nitrate is the predominant nitrogenous anion in atmospheric precipitation. Nitrite
content is generally low (Georgii, 1963). The flux of NO.,-N from wet deposition into ter-
restrial systems was estimated by Soderlund and Svensson (1976) to be in a range of 13 to 30
Tg NO,-N per year. Deposition in gaseous form was estimated by these authors to be in a range
of 19 to 50 Tg NO^-N per year and 0.2 to 2.8 Tg NO^-N per year as particulates. By comparison,
global river discharge of nitrate nitrogen (excluding polar and desert areas) was calculated
at 8.1 Tg per year (Soderlund and Svensson, 1976). These estimates of nitrates and nitrite
fluxes are summarized in Table 4-4.
4.3.1.5 Nitrates as Fertilizers—Man's greatest intervention into natural cycles has occurred
because of the shortage of nitrogen as an available nutrient element in the soil (Delwiche,
1970). (It has been estimated that the amount of ammonia nitrogen (NH4~N) that is converted
4-8
-------
TABLE 4-4. ESTIMATES OF THE GLOBAL FLUX OF NITRATES AND NITRITES
TgN/yr
Atmospheric production from N09.
Atmospheric production from NH.,
Total deposition (land and sea)
Total dry deposition (land and sea)...
Total wet deposition (land and sea)...
Burns
and Hardy
(1975)
20
30
60
N/A
N/A
Sbderlund
and Svensson
(1976)
N/A
N/A
18-51
0.3-2.8
18-46
Robinson
and Robbins
(1975)
95
N/A
95
75
20
by microorganisms to nitrate nitrogen (NO,-N) is equivalent to the net nitrogen assimilation
2
(0.017 kg/m ) by plants each year.) (Bowen, 1966; Delwiche, 1977) To alleviate this shortage,
the limiting factor in plant growth, industrial fixation of nitrogen was developed. At the
present time the amount of nitrogen fixed industrially for the production of fertilizer equals
the amount that was fixed by all terrestrial ecosystems before the advent of modern agriculture
(Delwiche, 1970). The world's annual, output of industrially fixed nitrogen was 30 million
:tons in 1968 and it has been estimated it will reach or exceed 100 million tons by the year
2000 (Parr, 1973). Consumption of fertilizer nitrogen in the U.S.A. will probably reach 11
imillion tons in 1980 (Parr, 1973). The impact of this environmental loading has not, until
very recently, been considered.
4.4 AMMONIFICATION AND NITRIFICATION
Nitrogen fixation and denitrification processes in natural systems result in increased
concentrations of ammonium ions (NH.) in the soil or in aquatic systems as a result of ammonia
(NH3) hydration. These ions may be utilized by plants and bacteria to produce protein.
Ammonification is an important process in the renewal of the limited supply of inorganic
nitrogen. Organic compounds, such as amino acids resulting from decay processes, are converted
into NH., and ammonium ions. Volatilization of ammonia from soils may increase the atmospheric
burden of NO as NH, undergoes atmospheric transformation (Chameides et al. , 1977; National
A O
Research Council, 1978).
4.5 NITRIC OXIDE, NITROGEN DIOXIDE AND THE NITROGEN CYCLE
Total N0y emissions to the atmosphere from terrestrial sources were reported by Soderlund
and Svensson (1976) to be in the range of 8 to 25 Tg N per year. Estimates of other authors
regarding NO emissions are presented in Tables 4-3 and 4-5.
4-9
-------
TABLE 4-5. ESTIMATES OF THE GLOBAL FLUX OF NO
(NO AND N0?) >
TgN/yr *
Natural emissions from land to
atmosphere
Natural emissions from land and sea
to atmosphere
Tropospheric production by lightning
Stratospheric production from N?0...
Atmospheric production from NH,
Production during combustion. ...
Other industrial production
Total land deposition
Total aquatic deposition
Total wet deposition (as nitrates;
land and sea)
Total dry deposition (land and sea).
Burns
and Hardy
(1975)
N/A
N/A
10
5
N/A
15
30
31
18
49
11
Soderlund and
Svensson
(1976)
21-89
N/A
N/A
0.3
3-8
19
36
32-83
11-33
18-46
25-70
Robinson
and Robbins
(1975)
N/A
210
N/A
2
N/A
15
N/A
N/A
N/A
75
151
Crutzen
and Ehhalt
(1977)
N/A
N/A
8-40
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
Chameides
et al.
(1977)
N/A
N/A
30-40
N/A
N/A
N/A
N/A
N/A
N/A
N/A
N/A
-------
While 40 to 108 Tg NO -N per year have been estimated to be released from terrestrial
sources to the atmosphere, the bulk is reabsorbed and only 8 to 25 Tg NO -N escapes to the
A
troposphere (Sb'derlund and Svensson, 1976). Hill (1971) has reported that NO and NOp are
absorbed from the atmosphere by plants. Using data obtained from the experiments of Makarov
(1969) and those of Kim (1973), Soderlund and Svensson (1976) estimate that soil contributes
to the atmosphere between 1 to 14 Tg N in the form of NO and NO-; losses from aquatic eco-
systems to the atmosphere were considered by these authors to be minor. The principal source
of gaseous NOX in terrestrial systems is believed to be the chemical decomposition of nitrates
(Soderlund and Svensson, 1976).
In the stratosphere, NO and N02 can be produced through photolysi-s and transformation
reactions involving N20 and 03- Small amounts of these products (about 0.3 Tg annually) are
expected to reenter the troposphere, mainly as N0? and HNO-.
Tropospheric ammonia may be converted to NO, and indirectly to NOp, via reaction with
hydroxyl free radicals (-OH). Soderlund and Svensson (1976) estimate that this reaction
accounts for 3 to 8 Tg NO -N produced annually. A higher estimate (20 to 40 Tg NO -N) was
X X
reported by Chameides and co-workers (1977).
Tropospheric production of NO during lightning discharges has been estimated to account
for 8 to 40 Tg NO -N per year (Chameides et al., 1977; Griffing, 1977; Noxon, 1976).
X
The work of Chameides et al. (1977) suggests that lightning is a significant source of
NO , producing about 30 to 40 Tg NO -N per year. If this estimate is correct, lightning could
X X
account for as much as 50 percent of the total atmospheric production of NO on a global basis
X
(Chameides et al., 1977), or a level comparable to one estimate of the global average of
man-made NO emissions (Crutzen et al., 1978; Noxon, 1978).
Direct observations by Noxon (1976) during a lightning storm indicate that ambient concen-
trations of NOp may be enhanced by a factor of 500 over the normal level. The enhanced levels
decayed rapidly after passage of the storm. Liu et al. (1977) estimated NO production by
lightning at 9 Tg N per year.
Recent studies of the global carbon cycle indicate that burning of wood and other biomass,
largely in tropical land-clearing, may release significant quantities of NO (National Research
A
Council, 1978).
Atmospheric NO returns to earth by two principal mechanisms: wet deposition (rain) and
dry deposition (gaseous and particulate). Dry deposition has been estimated to be twice that
of wet deposition over the same areas (Soderlund and Svensson, 1976).
Tropospheric reactions and transport considerations are discussed in more detail in
Chapter 6.
4.6 NITROUS OXIDE AND THE NITROGEN CYCLE
Nitrous oxide is released from denitrification and nitrification processes in soils and
aquatic environments and is transformed in stratospheric chemical reactions. It is not known
to be involved in tropospheric reactions. After release from soil or water, NpO diffuses to
4-11
-------
the stratosphere and may be converted to oxygen, nitrogen, and oxides of nitrogen (Junge,
1972). The stratosphere represents the only known atmospheric sink for NpO.
From a review of the literature, Soderlund and Svensson (1976) estimated the N?0 flux
from soils to the atmosphere in the range of 16 to 69 Tg N^O-N per year. These authors also
estimate that N^O derived from denitrification processes account for at least 10 percent of
the total amount of nitrogen denitrified. The authors caution, however, that the data avail-
able are too limited to draw more precise estimates. CAST (1976) estimated ^0 production in
soils at 7 Tg N per year.
Total annual marine production and release to the atmosphere of N^O was recently estimated
at 4 to 10 Tg-N by Cohen and Gordon (1979). This estimate was based on new information which
indicates major deficiencies in divergent earlier estimates by Hahn (1974) and Hahn and Junge
(1977), who proposed a net source of 16 to 160 Tg-N/yr, and McElroy et al. (1976), who argued
that the ocean could be a sink for 40 Tg-N/yr of atmospheric NLO.
Soderlund and Svensson (1976), using data obtained by Junge (1972), estimate that 18 Tg
NpO-N per year is conveyed from the troposphere to the stratosphere and converted to N^, 0.,,
and NOX. These estimates are summarized in Table 4-6.
Nitrous oxide is important in the regulation of the amount of ozone in the stratosphere.
Crutzen (1974) has suggested that an increase of 1 percent of the emission rate of nitrous
oxide may cause a 0.2 percent decrease in stratospheric ozone, thus increasing the amount of
ultraviolet radiation reaching the earth. The potential effect of coal- and gas-burning
processes (Pierotti and Rasmussen, 1976) and the increased use of fertilizer nitrogen (Bremner
and Blackner, 1978) on increasing N~0 levels has been suggested to be a cause of concern
regarding 0.> destruction. Pierroti and Rasmussen (1976) report that coal-burning and gas-
burning industrial processes may account for approximately 2 Tg N-O-N produced each year. Liu
and co-workers (1977) suggest that other land-based sources of N^O could include sewage and
nitrogen waste treatment plants.
Nitrous oxide has been reported to be released from soils during nitrification of added
ammonium- or urea-based fertilizers under aerobic conditions (Bremner and Blackmer, 1978).
Urea is rapidly hydrolyzed by a soil enzyme, urease, to form ammonium carbonate. Of the added
nitrogen, approximately 0.04 percent was released as N20. Nitrous oxide also is discussed in
relation to denitrification in Section 4.9.
4.7 ORGANIC NITROGEN AND THE NITROGEN CYCLE
Large transfers of organic nitrogen compounds are found within aquatic and terrestrial
systems (Soderlund and Svensson, 1976). The nitrogen flow between these systems and the
atmosphere is much less than the internal circulations.
Man's agricultural activities have been reported to be a cause of depletion of organic
matter in soils (Paul, 1977; Stanford et al., 1975). Soderlund and Svensson (1976) have
4-12
-------
TABLE 4-6. ESTIMATES OF THE GLOBAL FLUX OF NITROUS OXIDE
TgN/yr
Natural emissions from land
to atmosphere
Natural emissions from land
and sea to atmosphere
Natural emissions from aquatic
areas to atmosphere
Produced during atmospheric
reaction of N? with ozone
Burns
and Hardy
(1975)
13
20
7
15
Soderlund
and Svensson
(1976)
16-69
N/A
20-80
N/A
Robinson
and Robbins
(1975)
N/A
342
N/A
N/A
Crutzen
and Ehhalt
(1977)
12-80
N/A
40-90
N/A
CAST
(1976)
7
N/A
N/A
N/A
-------
estimated that 6 to 13 x 10 Tg-N are lost each year on a global basis (an order-of-magnitude-
type estimate for agricultural lands only). Losses due to forest cutting were not taken into
consideration.
Annual wet deposition of organic nitrogen has been estimated to be in a range of 10 to
100 Tg (Sdderlund and Svensson, 1976). An average organic nitrogen content of 0.1 to 1.0 mg N
per liter of terrestrial precipitation was used as the basis for the calculation. Organic
nitrogen in river discharge was estimated at 9.9 Tg per year (Sbderlund and Svensson, 1976).
4.8 AMMONIA AND THE NITROGEN CYCLE
There is considerable uncertainty as to the sources of atmospheric NhU. A global source
strength of 113 to 224 Tg-N per year has been estimated (Sb'derlund and Svensson, 1976), based
on balancing of estimated total deposition. Sources such as excreta from wild and domestic
animals and humans (Denmead et al., 1974; Healey et al., 1970; Luebs et al., 1973; Stanford et
al., 1975) and coal combustion (Burns and Hardy, 1975; Georgii, 1963; Sb'derlund and Svensson,
1976) may account for a quarter of this total. Other likely major sources of NH3 include
decomposition of organic matter other than excreta, forest fires, and other wild fires, losses
from manufacture, handling and application of ammonia-based fertilizers (Sbderlund and
Svensson, 1976) volatilization from oceans (Bouldin et al., 1974), and possibly from the
senescing leaves of living plants (Farquhar et al. , 1979). Estimation of atmospheric release
from natural and agricultural areas is complicated by the observation that plant cover can
reabsorb substantial amounts of the NH., released at ground level in these areas (Denmead
et al., 1976).
It has been proposed that atmospheric NH., may be converted to NOX by reaction with -OH
radicals (McConnell, 1973; McConnell and McElroy, 1973). A recent estimate of the annual
magnitude of this source is 20 to 40 Tg NOX~N (Chameides et al., 1977). McConnell (1973)
concluded that this reaction and heterogeneous losses are the dominant tropospheric NH3 removal
mechanisms. Atmospheric NH3 returns to terrestrial and aquatic systems via precipitation (as
ammonium salts), by dry deposition of gaseous NH-, and particulate ammonium compounds (Sbderlund
and Svensson, 1976), and by direct gaseous uptake by plants (Denmead et al., 1976). Estimates
of global flux of ammonia are summarized in Table 4-7.
4.9 DENAZIFICATION
In contrast to nitrogen fixation, denitrification results in the release of fixed forms
of nitrogen, principally N?0 and N~ with small amounts of NO, into the atmosphere. Ammonia
production also has been reported (Payne, 1973; Stanford et al., 1975). As plants decay, a
ubiquitous group of specialized microorganisms (e.g., Pseudomonas denitrificans) in soils and
in aquatic systems reduce nitrates and nitrites to nitrogenous gases. Without these bacteria,
most of the atmospheric nitrogen would be in the oceans or in sediments (Delwiche, 1970). On
a time scale of millions of years, losses of these gases to the atmosphere are believed to be
roughly balanced by the amounts of N fixed by natural processes (Sbderlund and Svensson,
4-14
-------
1976). The ratio of N2 to N20 produced is an area of current interest because of the role of
HJy in the destruction of stratospheric ozone (Chapter 9).
Delwiche (1970) estimated that 83 Tg of N^O-N is produced annually from terrestrial and
oceanic sources. Estimates of other investigators of the extent of global denitrification are
considerably higher than those of Delwiche. These estimates, as well as other estimates of
the global budget for nitrogenous compounds, are presented in Tables 4-3 and 4-8. Soil factors
such as acidity (Focht, 1974; Nommik, 1956), moisture content (Soderlund and Svensson, 1976),
temperature (Nommik, 1956; Stanford et al., 1975), and oxygen content (Cady and Bartholomew,
1960; Nommik, 1956) determine proportions of NO, N20 or N~ produced. Major factors affecting
the extent of denitrification losses in soils include availability of an organic carbon sub-
.strate (Focht, 1974; National Research Council, 1978), moisture content, presence or absence
of a cover crop (Burford and Stefanson, 1973), and the type of fertilizer applied (Broadbent
and Clark, 1965; Rolston et al. , 1976).
Conditions favoring release of N^O from nitrates include high soil acidity (low pH),
presence of Q~, limited amounts of easily metabolizable organic compounds, low temperatures
and high initial concentrations of nitrates. Acidity and temperature factors which increase
N20 production also tend to decrease the absolute rate of denitrification (Stanford et al.,
1975). Molecular nitrogen is the principal end product under true anaerobic conditions
(National Research Council, 1978). Nommik (1956) reported that NO production is favored in
acidic anaerobic systems exposed to large amounts of nitrite. However, such conditions are
not likely to occur in natural systems. Anaerobic conditions are promoted when soil moisture
content increases, reducing the diffusion of oxygen through the soil pore spaces (Soderlund
and Svensson, 1976). The production of N?0 by denitrification processes has been reviewed by
CAST (1976), Hahn and Junge (1977), and Crutzen and Ehhalt (1977).
Denitrification also occurs in aquatic ecosystems, and the limited data available suggest
that oceanic systems contribute greater amounts of N~ and N?0 to the atmosphere than ter-
restrial systems (Soderlund and Svensson, 1976). Lake sediments are believed to provide ideal
conditions for denitrifying organisms (Keeney et al., 1971; National Research Council, 1978).
4.10 ACIDIC PRECIPITATION
Increased amounts of NO released to the atmosphere is of concern due to their contribu-
tion to the acidification of precipitation (Likens, 1976). A full discussion pertaining to
acidic precipitation appears in Chapter 11.
4.11 SUMMARY
Nitrogen is an element necessary for all life. The maintenance of an adequate balance
among nitrogen-containing compounds is essential to the integrity of all ecosystems on earth.
Nitrogen resides in five major reservoirs: primary rocks, sedimentary rocks, the deep-sea
sediment, the atmosphere, and the soil-water pool. The web of pathways and fluxes by which
oxides of nitrogen and associated nitrogenous compounds are produced, transformed, transported,
4-15
-------
TABLE 4-7. ESTIMATES OF GLOBAL FLUX OF AMMONIA AND AMMONIUM COMPOUNDS
TgN/yr
Burns
and Hardy
(1975)
Sdderlund
and Svensson
(1976)
Robinson
and Robbins
(1975)
Volatilized from land and sea.
Volatilized from land
Produced from burning of coal.
Terrestrial wet deposition....
Wet deposition over oceans....
Terrestrial dry deposition
(gaseous)
Dry deposition over oceans
(gaseous)
Precipitation as NH. (land
and sea)
Dry deposition as NHt (land
and sea)
Converted to NO in atmosphere
165
N/A
5
N/A
N/A
N/A
N/A
140
N/A
N/A
N/A
113-244
4-12
30-60
8-25
57-114
10-20
38-85
3-8
5-17
860
N/A
N/A
N/A
N/A
679
N/A
150
N/A
40
and stored in the principal nitrogen reservoirs, are commonly referred to as the nitrogen
cycle.
An understanding of the nitrogen cycle is important in placing in perspective man's
intervention as discussed in other chapters of this document.
The atmosphere, composed of 79 percent molecular nitrogen (N,,), is not only an important
reservoir for nitrogenous compounds but also serves as a principal conduit through which
emissions of gaseous and particulate forms of the oxides of nitrogen (NO ) are transformed and
conveyed between terrestrial and aquatic systems. Nitrogenous compounds occurring in the
atmosphere can be returned to terrestrial or aquatic areas principally via wet (rainfall) or
dry (particulate and gaseous) deposition.
Most estimates of the global flows of nitrogen compounds are based on extrapolation of
experimentally-determined small-scale emission factors to the global scale; some are crude
estimates, arrived at by balancing mass flows to account for unknown sources. Since published
estimates differ greatly, it is difficult to assess with any certainty the fraction of N0x
4-16
-------
TABLE 4-8. ESTIMATES OF GLOBAL DENITRIFICATION
TgN/yr
Biological denitrification
(total)
terrestrial
aquatic
Delwiche
(1970)
83
43
40
Burns and
Hardy
(1975)
210
140
70
Soderlund
and Svensson
(1976)
132-340
107-161
25-179
Sze and
Rice
(1976)
260
135
125
Liu et al.
(1977)
245
127
118
CAST
(1976)
171-200
71-100
100
-------
emissions globally which arise from man's activities. In terms of their contribution to NO
A
concentrations in polluted urban airsheds, however, it seems clear that natural ,processes are
generally negligible (see Chapter 8).
The extent to which the use of industrially fixed nitrogen in agriculture has influenced
the nitrogen cycle, the role of nitrous oxide in the nitrogen cycle, and the significance of
increased amount of ammonia due to human activities are all matters of concern.
4-18
-------
4.12 REFERENCES
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York, NY, 1977.
Bolin, B., and E. Arrhenius, Eds. Nitrogen - an essential life factor and a growing environ-
mental hazard: Report from Nobel Symposium No. 38. Ambio 6:96-105, 1977.
Bouldin, D. R. , R. L. Johnson, C. Burda, and C.-W. Kao. Losses of inorganic nitrogen from
aquatic systems. J. Environ. Qual. 3:107-114, 1974.
Bowen, H. J. M. Trace Elements in Biochemistry. Academic Press, Inc., Ltd., London, England,
1966.
Bremner, J. M. , and A. M. Blackmer. Nitrous oxide: emission from soils during nitrification
of fertilizer nitrogen. Science (Washington, D.C.) 199:295-296, 1978.
Broadbent, F. E. , and F. Clark. Denitrification. In: Soil Nitrogen. W. V. Bartholomew and
F. E. Clark, eds., American Society of Agronomy, Inc., Madison, WI, 1965. pp. 344-359.
Burford, J. R. , and R. C. Stefanson. Measurements of gaseous losses of nitrogen from soils.
Soil Biol. Biochem. 5:133-141, 1973.
Burns, R. C., and R. W. F. Hardy. Nitrogen Fixation in Bacteria and Higher Plants. Springer-
Verlag, New York, NY, 1975.
Cady, F. B. , and W. V. Bartholomew. Sequential products of anaerobic denitrification in
Norfolk soil material. Soil Sci. Soc. Am. Proc. 24:477-482, 1960.
Carpenter, E. J. , and C. C. Price, IV. Marine Oscillatoria (Trichodesmium): explanation for
aerobic nitrogen fixation without heterocysts"!Science (Washington, D.C.) 191:1278-1280,
1976.
Chameides, W. L., D. H. Stedman, R. R. Dickerson, D. W. Rusch, and R. J. Cicerone. NO produc-
tion in lightning. J. Atmos. Sci. 34:143-149, 1977.
Chapham, W. B. , Jr. Natural Ecosystems. The MacMillan Co., New York, NY, 1973. pp. 40-42.
Chen, R. L. , D. R. Keeney, and J. A. Konrad. Nitrification in sediments of selected Wisconsin
lakes. J. Environ. Qual. 1:151-154, 1972.
Cohen, Y. , and L. I. Gordon. Nitrous oxide production in the ocean. JGR J. Geophys. Res.
84:347-353, 1979.
Council for Agricultural Science and Technology. Effect of Increased Nitrogen Fixation on
Stratospheric Ozone. CAST Report No. 53, Council for Agricultural Science and Technology,
Iowa State University, Ames, IA, January 1976.
Crutzen, P. J. Estimation of possible variations in total ozone due to natural causes and
human activities. Ambio 3:201-210, 1974.
Crutzen, P. J. , and D. H. Ehhalt. Effects of nitrogen fertilizers and combustion in the
stratospheric ozone layer. Ambio 6:112-117, 1977.
4-19
-------
Crutzen, P. J. , I. S. A. Isaksen, and J. R. McAfee. The impact of the chlorocarbon industry
on the ozone layer. JGR J. Geophys. Res. 83:345-363, 1978.
Delwiche, C. C. The nitrogen cycle. Sci. Am. 223:137-146, 1970.
Delwiche, C. C. Energy relations in the global nitrogen cycle. Ambio 6:106-111, 1977.
Denmead, 0. T. , J. R. Freney, and J. R. Simpson. A closed ammonia cycle within a plant canopy.
Soil Biol. Biochem. 8:161-164, 1976.
Denmead, 0. T. , J. R. Simpson, and J. R. Freney. Ammonia flux into the atmosphere from a
grazed pasture. Science (Washington, D.C.) 185:609-610, 1974.
Farquhar, G. D. , R. Wetselaar, and P. M. Firth. Ammonia volatilization from senescing leaves
of maize. Science (Washington, D.C.) 203:1257-1258, 1979.
Focht, D. D. The effect of temperature, pH and aeration on the production of nitrous oxide
and gaseous nitrogen—a zero-order kinetic model. Soil Sci. 118:173-179, 1974.
Focht, D. D. , and W. Verstraete. Biochemical ecology of nitrification and denitrification.
-Adv. Microb. Ecol. 1:135-214, 1977.
Garrels, R. M. , F. T. Mackenzie, and C. Hunt. Chemical Cycles and the Global Environment:
Assessing Human Influences, William Kaufman, Inc., Los Angeles, CA, 1975.
Georgii, H.-W. Oxides of nitrogen and ammonia in the atmosphere. J. Geophys. Res. 68:3963-
3970, 1963. ~~
Griffing, G. W. Ozone and oxides of nitrogen production during thunderstorms. JGR J. Geophy.
Res. 82:943-950, 1977.
Hahn, J. The North Atlantic Ocean as a source of atmospheric N20. Tellus 26:160-168, 1974.
Hahn, J., and C. E. Junge. Atmospheric nitrous oxide: a critical review. Z. Naturforsch. A.
32A:190-214, 1977.
Hardy, R. W. F. , and E. Knight, Jr. Reduction of N20 by biological N?-fixing systems.
Biochem. Biophys. Res. Commun. 23:409-414, 1966.
Healy, T. V., H. A. C. McKay, A. Pilbeam, and D. Scargill. Ammonia and ammonium sulfate in
the troposphere over the United Kingdom. J. Geophys. Res. 75:2317-2321, 1970.
Hill, A. C. Vegetation: a sink for atmospheric pollutants. J. Air Pollut. Control Assoc.
21:341-346, 1972.
Junge, C. E. The distribution of ammonia and nitrate in rainwater over the United States.
Trans. Am. Geophys. Union. 39:241-248, 1958.
Junge, C. E. The cycle of atmospheric gases - natural and manmade. Q. J. R. Meteorol. Soc.
98:711-728, 1972.
Keeney, D. R. The nitrogen cycle in sediment-water systems. J. Environ. Qual. 2:15-29,
1973.
4-20
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Keeney, D. R., R. L. Chen, and D. A. Graetz. Importance of devitrification and nitrate reduc-
tion in sediments to the nitrogen budgets of lakes. Nature (London) ^3:66-67, 1971.
Kim, C. M. Influence of vegetation types on the intensity of ammonia and nitrogen dioxide
liberation from soil. Soil Biol. Biochem. 5:163-166, 1973.
Likens, G. E. Acid precipitation. Chem. Eng. News 54:29-43, 1976.
Liu, S. C. , R. J. Cicerone, T. M. Donahue, and W. L. Chameides. Sources and sinks of
atmospheric N20 and the possible ozone reduction due to industrial fixed nitrogen
fertilizers. Tellus 29:251-263, 1977.
Luebs, R. E. , K. R. Davis, and A. E. Laag. Enrichment of the atmosphere with nitrogen
compounds volatilized from a large diary area. J. Environ. Qual. 2:137-141, 1973.
Makarov, B. N. Liberation of nitrogen dioxide from soil. Sov. Soil Sci. (Engl. Transl.)
1:49-53, 1969.
McConnell, J. C. Atmospheric ammonia. J. Geophys. Res. 78:7812-7820, 1973.
McConnell, J. C. , and M. B. McElroy. Odd nitrogen in the atmosphere. J. Atmos. Sci. 3_0:1465-
1480, 1973.
McElroy, M. B. , J. W. Elkins, S. C. Wofsy, and Y. L. Yung. Sources and sinks for atmospheric
N20. Rev. Geophys. Space Phys. 14:143-150, 1976.
National Research Council. Nitrates: An Environment Assessment. National Academy of
Sciences, Washington, DC, 1978.
Nommik, H. Investigations on denitrification in soil. Acta Agric. Scand. 6:195-228, 1956.
Noxon, J. F. Atmospheric nitrogen fixation by lightning. Geophys. Res. Lett. 3:463-465,
1976.
Noxon, J. F. Tropospheric N02> JGR J. Geophys. Res. 83:3051-3057, 1978.
Parr, J. F. Chemical and biochemical considerations for maximizing the efficiency of ferti-
lizer nitrogen. J. Environ. Qual. 2:75-84, 1973.
Paul, E. A. Nitrogen cycling in terrestrial ecosystems. In: Environmental Biogeochemistry,
Volume I: Carbon, Nitrogen, Phosphorus, Sulfur and Selenium Cycles, Proceedings of the
2nd International Symposium, Canada Centre for Inland Waters and Others, Hamilton,
Ontario, Canada, April 8-12, 1975. J. 0. Nriagu, ed. , Ann Arbor Science Publishers,
Inc., Ann Arbor, MI, 1977. pp. 225-243.
Payne, W. J. Reduction of nitrogenous oxides by microorganisms. Bacteriol. Rev. 37:409-452,
1973.
Pierotti, D., and R. A. Rasmussen. Combustion as a source of nitrous oxide in the atmosphere.
Geophys. Res. Lett. 3:265-267, 1976.
Robinson, E. , and R. C. Robbins. Gaseous atmospheric pollutants from urban and natural
sources. Jn: The Changing Global Environment. S. F. Singer, ed., D. Reidel Publ. Co.,
Boston, MA, 1975. pp. 111-123.
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Rolston, D. E. , M. Fried, and D. A. Goldhamer. Denitn'fication measured directly from
nitrogen and nitrous oxide gas fluxes. Soil Sci. Soc. Am. J. 40:259-266, 1976.
Soderlund, R. , and B. H. Svensson. The global nitrogen cycle. In: Nitrogen, Phosphorus, and
Sulfur-Global Cycles: SCOPE Report 7. Ecol. Bull. (22):23-73, 1976.
Stanford, G. Nitrogen in soils. Plant Food Rev. 1:2-4, 7, 1969.
Stanford, G., J. 0. Legg, S. Dzienia, and E. C. Simpson, Jr. Denitn'fication and associated
nitrogen transformation in soils. Soil Sci. 120:147-152, 1975.
Sze, N. D. , and H. Rice. Nitrogen cycle factors contributing to N~0 production from ferti-
lizers. Geophy. Res. Lett. 3:343-346, 1976. ^
Whittaker, Robert H. Communities and Ecosystems. 2nd Edition. MacMillan Publishing Co., New
York, NY, 1975.
4-22
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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) N09 is a pollutant of major concern for human health (Chapter 15)
A £
and (2) atmospheric transformation products of NO such as nitric acid (HNO,) and particulate
A O
nitrates are of concern both for their effects on human health and their role in the acidifi-
cation of precipitation (Chapter 11). Emissions of nitrates, nitrites and nitrogenous acids
are not discussed because, except in a few special situations (such as in the vicinity of
nitric acid plants for HN03 or certain agricultural operations for particulate nitrates), they
do not result in significant ambient concentrations. Atmospheric production and ambient con-
centrations of these compounds are discussed in Chapters 6 and 8, respectively. Agricultural
usage of nitrogenous compounds is reviewed because of recent discussion of possible pertur-
bations of the stratospheric ozone layer by nitrous oxide (NpO) (Chapter 9), which is produced
in part from fertilizer not utilized by plants. Sources of N-nitroso compounds and their
possible precursors are reviewed as background material for a discussion of atmospheric burdens
of these pollutants actually observed in ambient air (Chapter 8). Sources of ammonia are dis-
cussed because some researchers have suggested that it is converted to NO in the atmosphere.
5.2 ANTHROPOGENIC EMISSIONS OF NOX
Global estimates of natural emissions of nitrogenous compounds including NO have been
discussed in detail in Chapter 4. Since various authors differ greatly in their estimates of
natural emissions, it is difficult to assess with any certainty the fraction of NO emitted
globally from human activities.
In highly industrialized or populous localities, anthropogenic emissions of NO and/or N02
assume primary importance. Mobile combustion and fossil-fuel power generators are the two
largest source categories. In addition, industrial processes and agricultural operations pro-
duce minor quantities. Although certain industrial processes, such as nitric acid plants, and
certain agricultural activities, such as the application of fertilizer or the operation of
animal feedlots, may result in localized emissions of other nitrogenous compounds, which have
potential as NO sources through atmospheric transformation only NO and NOp are, in general,
considered to be the primary pollutants; the other nitrogen oxides are mainly products of atmo-
spheric reactions (Chapter 6).
In interpreting the emissions inventories to be presented throughout this chapter, it is
important to note that NO emissions are generally calculated as though the compound being
emitted were N0?. This method of presentation serves the purpose of allowing ready comparison
of different sources. Because of the interconvertibility of NO and N0? in photochemical smog
reactions, such an approach has some merit and avoids the difficulty in interpretation asso-
ciated with different ratios of N0/N02 being emitted by different sources. Two points, however,
5-1
-------
should be noted: (1) although NO is the dominant NO compound emitted by most sources, NO,
A £
fractions from sources do vary somewhat with source type and (2) conversion of NO emissions
A
to N02 takes place over spatial and temporal scales which vary with the particular local cir-
cumstances of atmospheric pollutant mix, climatology and topography. For these reasons, NO
emission inventories do not necessarily accurately reflect the potential of various sources
for producing ambient N02 concentrations.
5,2.1 Global Sources of NO
Table 5-1 presents historical estimates of the man-made global production of NO (Robinson
and Robbins, 1972,1975). These estimates are based on 1966 fuel consumption figures (U.S.
Bureau of the Census, 1967) and emission factors available in 1965 (Mayer, 1965). From these
data, Robinson and Robbins (1975) estimated global NO emissions from anthropogenic sources to
6
be 48 x 10 metric tons per year (expressed as N02). These authors also estimated the ratio
of natural emissions of NO from terrestrial and aquatic sources to those from anthropogenic
A
sources to be about 7 to 1. An earlier estimate by Robinson and Robbins (1972) had set the
ratio of natural emissions to anthropogenic emissions at 15 to I. The downward revision was
based on a 55 percent lower estimate of the amount of N02 emitted by natural sources.
TABLE 5-1. ESTIMATED ANNUAL GLOBAL EMISSIONS OF NITROGEN DIOXIDE (ANTHROPOGENIC)
(106 metric tons per year, expressed as N07)
Source
Total combustion and refining
Coal combustion
Petroleum refining
Gasoline combustion
Other oil combustion
Natural gas combustion
Other combustion
Emissions Emissions as N
48.0
24.4
0.6
6.8
12.8
1.9
1.5
14.6
7.4
0.2
2.1
3.9
0.5
0.5
% Total
100
51
1
14
27
4
3
Source: Robinson and Robbins, 1975.
A different estimate was provided by Soderlund and Svensson (1976), who concluded that
the ratio of NO emissions from natural sources to emissions from anthropogenic sources could
range from roughly 1:1 to 4 or 5:1. It is clear that there are considerable uncertainties
associated with global estimates of natural NO emissions (Chapter 4). In particular, esti-
mates of different authors on the magnitude of NO emissions from soils vary greatly. Defini-
tive experiments have yet to be performed.
5.2.2 Sources of N0x in the United States
Table 5-2 and Figure 5-1 provide historical data on estimated emissions of N0x in the
United States for the years 1940 through 1970. A significant upward trend in the two major
5-2
-------
TABLE 5-2. HISTORIC NATIONWIDE NOV EMISSION
6 ESTIMATES 1940-1970 X
(10 metric tons per year, expressed as N0)
Source Category
TRANSPORTATION
Motor vehicles
Aircraft
Railroads
Marine use
Nonhighway use
STATIONARY FUEL COMBUSTION
Electric utilities
Industrial combustion
Commercial
Residential
INDUSTRIAL PROCESS LOSSES
SOLID WASTE DISPOSAL
AGRICULTURAL BURNING
MISCELLANEOUS
Total
1940
2.9
2.7
0
0
0.1
0.2
3.2
0.5
1.8
0.1
0.9
0
0.1
0.2
0.7
7.1
1950
4.7
4.1
0
0.2
0.1
0.3
3.9
1.1
1.8
0.1
0.9
0.1
0.2
0.2
0.4
9.4
1960
7.2
6.6
0
0.1
0.1
0.4
4.7
2.1
1.6
0.2
0.8
0.1
0.2
0.2
0.2
12.7
1970
10.6
8.3
0.3
0.1
0.2
1.8
9.1
4.3
4.1
0.2
0.5
0.2
0.4
0.3
0.1
20.6
NOTE: A zero in this table indicates emissions of less than 50,000 metric
tons/yr. Some totals do not agree due to rounding off.
Source: Cavender et al., 1973.
source categories, transportation and stationary fuel combustion, is discernible over this
30-year period. Total NO emissions almost tripled. Recent emissions estimates, by year, for
1970 through 1976 are presented in Table 5-3 and.Figure 5-2. Emissions from transportation
sources increased by about 20 percent but emissions from stationary fuel combustion sources
and total emissions did not exhibit monotonic behavior.
Minor discrepancies between Tables 5-2 and 5-3 for the year 1970 may be due to rounding
errors and/or to changes in estimation methods used for producing the two tables. It is
believed, however, that trends assessment is reliable within each table. The change in source
category nomenclature is also to be noted.
Figure 5-3 shows the distribution of NO emissions by type of Air Quality Control Region
(AQCR) for 1972. Large urban AQCR's, i.e. those having a Standard Metropolitan Statistical
Area (SMSA) population exceeding 1,000,000, accounted for more than half (53 percent) of the
NO emissions. The population in these same SMSA's was only 38.5 percent of the total U.S.
1\
population in 1970 (U.S. Bureau of the Census, 1973).
5-3
-------
co
o
CO
CO
CO
o
25
20
S. .16
10
ALL OTHER SOURCES
(INDUSTRIAL, SOLID WASTE)
STATIONARY FUEL
COMBUSTION
TRANSPORTATION SOURCES
1940
1950
1960
1970
YEAR
Figure 5-1. Historic NOX emissions by source groups. (Values
shown for each year are cumulative over source groups.)
Source: Cavender et al. (1973).
5-4
-------
TABLE 5-3.6 RECENT NATIONWIDE N0x EMISSION ESTIMATES
(10 metric tons/yr, expressed as N09)
Source Category
TRANSPORTATION
Highway vehicles
Nonhighway vehicles
STATIONARY FUEL COMBUSTION
Electric utilities
Industrial
Residential, commercial
and institutional
INDUSTRIAL PROCESSES
Chemicals
Petroleum refining
Metals
Mineral products
Oil and gas production
and marketing
Industrial organic
solvent use
Other processes
1970
8.4
6.3
2.1
10.9
5.1
5.1
0.7
0.6
0.2
0.3
0
0.1
0
0
0
1971
8.9
6.7
2.2
11.2
5.4
5.1
0.7
0.6
0.2
0.3
0
0.1
0
0
0
1972
9.4
7.1
2.3
11.7
5.9
5.1
0.7
0.7
0.3
0.3
0
0.1
0
0
0
1973
9.7
7.3
2.4
12.1
6.3
5.1
0.7
0.7
0.3
0.3
0
0.1
0
0
0
1974
9.6
7.3
2.3
11.9
6.2
5.0
0.7
0.7
0.3
0.3
0
0.1
0
0
0
1975
9.9
7.6
2.3
11.2
6.1
4.5
0.6
0.7
0.3
0.3
0
0.1
0
0
0
1976
10.1
7.8
2.3
11.8
6.6
4.5
0.7
0.6
0.3
0.3
0
0.1
0
0
0
(continued)
-------
TABLE 5-3. (continued)
Source Category
SOLID WASTE DISPOSAL
MISCELLANEOUS
Forest wildfires and
managed burning
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic
solvent use
Totals
1970
0.3
0.2
0.1
0
0.1
0
0
20.4
1971
0.3
0.3
0.2
0
0.1
0
0
21.3
1972
0.2
0.2
0.1
0
0.1
0
0
22.2
1973
0.2
0.2
0.1
0
0.1
0
0
22.9
1974
0.2
0.2
0.1
0
0.1
0
0
22.6
1975
0.2
0.2
0.1
0
0.1
0
0
22.2
1976
0.1
0.3
0.2
0
0.1
0
0
23.0
NOTE: A zero in this table indicates emissions of less than 50,000 metric tons/yr.
Source: U.S. EPA, 1977a.
-------
I
(O
o
GO
O
00
V)
O
z
25
20
15
10
ALL OTHER SOURCES (INDUSTRIAL, SOLID WASTE)
STATIONARY FUEL COMBUSTION
I
I
TRANSPORTATION SOURCES
I
1970 11971
1972 1973
YEAR
1974 1975 1976
Figure 5-2. Recent I\IOX emissions by source groups. (Values
shown for each year are cumulative over source groups.)
Source: Sparks (1976).
5-7
-------
/MEDIUM SIZED
URBAN A OCR'S
24%
SMALL URBAN/*
AQCR'S >^
\10% S
LARGE
URBAN
53%
AQCR Urbanization3
Large Urban
Medium-sized Urban
Small Urban
Rural
Total
Emissions,
106 tons/yr
11.71
5.30
2.36
2.88
22.25
a. Urbanization is based on largest SMS A population
in an AQCR:
Large Urban = SMS A population 1,000,000
Medium-sized Urban = SMSA population
250,000-1,000,000
Small Urban = SMSA population 50,000-250,000
Rural = AQCR containing no SMSA
b. Miscellaneous sources accounting for 160,000
tons/yr are not included.
Figure 5-3. Distribution of 1972 nationwide NOX emissions by
degree of urbanization (National Research Council, 1975).
5-8
-------
A clear picture of the nationwide distribution of NO emissions can be obtained from the
A
U.S'. maps reproduced in Figures 5-4 through 5-6. Figure 5-4 shows total NO emissions by U.S.
counties as compiled in the National Emissions Data System (NEDS) file of February 1978 (U.S.
EPA, 1978). Regions of high source concentrations are evident near populous and industrial
areas. When the total NO emissions per unit area (emission density) is plotted (Figure 5-5),
the nationwide distribution tends to be more uniform than when emission totals alone are con-
sidered. Areas of relatively high emission densities are still evident throughout the eastern
states and the midwest and on the west coast. The percent contribution of major point sources
to total NO emissions is plotted by U.S. county in Figure 5-6. Comparison of this figure and
A - ., -
Figure 5-4 reveals that, in general, major point sources make a significant contribution to
total NO emissions in those areas where NO emissions are high. (In this discussion, a major
A X
point source is defined as one for which the yearly NO emissions exceed 100 tons.)
Table 5-4 documents NO/NO ratios in emissions from a variety of source types. Examina-
tion of the table reveals that NO is the dominant oxide of nitrogen emitted by most sources
with NO- generally comprising less than 10 percent of the total NO emissions. It is inter-
esting to note, however, that NO,, forms upwards of 30 to 50 percent of the total NO emissions
from certain diesel and jet turbine engines under specific load conditions. Tail gas from
nitric acid plants, if uncontrolled, may contain about 50 percent N02- The variations in
NO/NO ratios by source type reported in the table are possibly of some, significance in local
situations. An example might be in the immediate vicinity of a high-volume roadway carrying a
significant number of diesel-powered vehicles. Situations of this type may assume increasing
importance in the future because of the increasing interest in diesel-powered vehicles which
generally have greater fuel economy than those with gasoline engines.
The national trends shown in Figures 5-1 and 5-2 do not reflect considerable local or
regional differences in the relative amounts of NO emitted by the major source categories.
For example, motor vehicles have been estimated to contribute approximately 90 percent of the
NO emissions in Sacramento, California (California Department of Public Health, 1966). In
San Francisco, California, they are estimated to contribute about 56 percent (California
Department of Public Health, 1966), while in northwestern Indiana the estimate is 8 percent
(Ozolins and Rehmann, 1968). Motor vehicle emissions in Los Angeles County, California, in-
creased 6-fold from 1940 to 1970 (County of Los Angeles, 1971), compared to a 3-fold national
increase.
While industrial process losses (NO emissions from noncombustion industrial sources) are
minor on a national level, these emissions can be important near individual sources. Manu-
facturing of nitric acid, explosives and fertilizers, and petroleum refining are the principal
activities 'in these source categories.
Aircraft are not considered a major source of NO on the national scale. Their impact in
A
the immediate vicinity of major airports has been discussed recently (George et al., 1972;
Jordan and Broderick, 1979). Although the total NO emissions associated with landing and
takeoff operations at a large airport can be several thousand tons per year, most NO emissions
5-9
-------
ONS / YERR
3.000 -
10.000 -
30.000
< 3.000
10.000
30.000
- 100.000
> 100.000
Figure 5-4. Total NOX emissions by U.S. county(U.S. EPA, 1978).
-------
en
i
TONS/SO MI
Figure 5-5. Total NO
x emission density by U S. county (U.S. EPA. t978,.
-------
Ul
I—'
r-o
PERCENT
Figure 5-6. Percent NOX emissions contributed by major point sources, by county (over 100 tons/yr)
(U.S. EPA, 1978).
-------
TABLE 5-4. NO/NO,, RATIOS IN EMISSIONS FROM VARIOUS SOURCE TYPES
Source Type
NO/NO
Reference
Uncontrolled tail-gas from nitric
acid plants
Petroleum refinery heaters--
using natural gas
Linear ceramic tunnel kiln
Rotary cement kilns
Steel soaking pit—natural gas
Wood/bark boiler
Black liquor recovery boiler
Carbon monoxide boiler
Large 2-cycle internal combustion
engine—natural gas
Combined cycle gas turbine
Gas turbine electrical generator—
#2 fuel oil
Gerstle and
Peterson, 1966
Hunter et al.,
1979
* 0.50
0.93-1.00
0.90-1.00
0.94-1.00
0.97-0.99
0.84-0.97
0.91-1.00
0.98-1.00
0.80-1.00
0.83-0.99
0.55-1.00 Wasser, 1976
(no load)-(full load)
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
Industrial boi
#6 fuel oil
Industrial boi
refinery gas
Diesel-powered
lers--natural gas
lers--#2 fuel oil
lers—PS 300 fuel
lers--#6 fuel oil
lers—coal
lers--refinery gas
lers--natural gas and
lers--natural gas and
passenger car--Nissan'
Diesel-powered passenger car--
Peugeot 204d
Diesel-powered passenger car--
various Mercedes
Diesel-powered truck and bus--
various engines
Mobile vehicles internal gasoline
combustion engine
Aircraft turbines (JT3D, TF30)
0.90-1.00
0.95-0.99
* 0.96
0.96-1.00
0.95-1.00
* 0.95
* 1.00
* 1.00
0.77-0.91
(idle)-(SOmph)
0.46-0.99
(idle)-(50mph)
0.88-1.00
0.73-0.98
0.99-1.00
Cato et al.
1976
Braddock and
Bradow, 1975
Springer and
Stahman, 1977a
Springer and
Stahman, 1977b
Wimmer and
Reynolds, 1962
Campau and
Neerman, 1966
0.13-0.28(idle)dSouza and
0.73-0.92 Daley, 1978
(takeoff & cruise)
Earlier studies (Lozano et al., 1968; Chase and Hum, 1970) did not report
such high idle concentrations of NO,,.
5-13
-------
occur during approach, takeoff and climb out, distributing these emissions up to 3,000 feet
above ground level and up to 10 miles from the airport. Even though high NO^/NO ratios occur
during idle of some aircraft turbines (Table 5-4), total emissions at idle are low. It is
currently estimated that high-altitude emissions from existing and projected aircraft fleets
do not represent a significant source of NO with respect to possible effects on stratospheric
ozone, although substantial uncertainties remain (Broderick, 1978).
Factors influencing seasonal variabilities in mobile source NO emissions include tempera-
ture dependences of emissions per vehicle mile (about a 35 percent decrease in emissions for
an ambient temperature increase from 20 to 90°F) (Ashby et al., 1974), and changes in vehicle
miles travelled seasonally (about 18 percent higher in summer than in winter, nationwide)
(Federal Highway Administration, 1978). Further differences exist between vehicle miles
travelled in urban and rural areas and among states in different parts of the country (Federal
Highway Administration, 1978). Variations in NO emissions are also expected due to seasonal
variation in power production from fossil fuel generating plants, which is estimated at 15 per-
cent on a nationwide basis (U.S. Department of Energy, 1978). Production is greatest in the
summer and least in the spring. Greater variations and different seasonal patterns have been
reported for different areas of the country (California Department of Public Health, 1966).
Diurnal variations, notably those associated with motor vehicle traffic, are also important in
their potential impact upon ambient air quality.
It should also be noted that the influence of the source categories considered in this
section upon ambient concentrations at a given location depends upon factors such as land use,
weather and climate, and topography. Emission estimates have other limitations as well.
Aside from possible errors in establishing the emissions from each source, the spatial distri-
bution of sources is usually not well known, since the inventories usually cover large areas.
There is very little temporal resolution, which can often lead to poor understanding of the
expected exposure. Many sources are intermittent. Representing such a source by annual
emission data, therefore, underestimates the potential for short-term exposures. Also,
meteorological parameters exhibit both seasonal and diurnal variability, which can greatly
affect the impact of particular sources on ambient pollution levels.
5.3 EMISSIONS OF AMMONIA
On a global basis, abiotic emissions of ammonia (NH.,) represent only a small fraction of
the total emissions of NH., (National Research Council, 1978; Robinson and Robbins, 1972;
Soderlund and Svensson, 1976). Soderlund and Svensson (1976) calculated that anthropogenic
c- c.
emissions (from coal combustion) accounted for between 4 x 10 to 12 x 10 metric tons per
year. A global loss of 7 x 10 metric tons NH3-N per year from inefficiencies in handling and
applying ammonia-based fertilizers was reported by the Council for Agricultural Science and
Technology (CAST) (1976). A recent report (National Research Council, 1978) indicated that
the United States accounts for about 25 percent of the global use of ammonia-based fertilizer.
Another source (National Research Council, 1979) has reported estimated NH3 emissions for the
5-14
-------
United States at a much lower level, as shown in Table 5-5. Discrepancies in these estimates
by various authors preclude any firm judgements at this time as to NHL emissions resulting
from fertilizer usage.
TABLE 5-5. ESTIMATED AMMONIA EMISSION FROM FERTILIZER APPLICATION
AND INDUSTRIAL CHEMICAL PRODUCTION IN U.S. (1975)
Source of Emission
Ammonia Production
Direct application of
anhydrous ammonia
Ammonium nitrate
Petroleum refineries
Sodium carbonate
(Solvay process)
Di ammonium phosphate
Ammoni ator-granul ators
Urea
Miscellaneous emission from
fertilizer production
Beehive coke ovens
Total
Ammonia Emission
tons/yr
, 19,000
168,000
59,000
32,000
14,000
10,000
10,000
4,000
2,000
1,000
319,000
Rate
tons N/yr
15,600
138,400
48,600
26,400
11,500
8,200
8,200
3,300
1,600 _
800
262,600
a"Direct application" is the term used in agriculture when a chemical
fertilizer is applied to the soil without combining or mixing it with
any other chemical. Direct application of anhydrous ammonia involves
transportation of ammonia to a storage area and to nurse tanks, metering,
and injection into soil.
Source: (National Research Council, 1979).
In addition to volatilization of NH~ from use of fertilizers, emissions from feedlots may
represent a significant local and regional source of ammonia. A National Research Council
report on ammonia indicated that 50 to 100 percent of the urea-nitrogen in urine generated in
feedlots may volatilize as ammonia (National Research Council, 1979). As urea is rapidly
hydrolyzed into NH, and C00, atmospheric contributions of NH,, from feedlot-generated urine of
6
an estimated cattle population of 132 million in the United States could amount to 2 x 10 to
4 x 10 metric tons NhL-N per year. This amount is between one-fourth and one-half of the
rate of anthropogenic emissions of nitrogenous compounds (excluding N«0) to the atmosphere in
the United States (National Research Council, 1978).
5-15
-------
5.4 AGRICULTURAL USAGE OF NITROGENOUS COMPOUNDS
Nitrogenous material applied as fertilizer participates in the nitrogen cycle via a
variety of pathways (Chapters 4 and 12). Emissions of ammonia from agricultural sources have
been discussed above in Section 5.3. Excess fertilizer may be of concern also: (a) by con-
tributing an anthropogenically produced burden to stratospheric concentrations of N^O with
consequent potential for attenuation of the ozone layer (see Chapter 9) and (b) by contribut-
ing, through run-off from agricultural lands, to both nitrate pollution of drinking water and
to changes in natural aquatic ecosystems. The data presented in Figure 5-7 and Table 5-6 are
intended to place usage of nitrogenous materials applied as fertilizer in the U.S. in his-
torical perspective. Examination of Table 5-6 reveals that the total nitrogen applied as fer-
tilizer has increased more than a factor of 5 from 1955 to 1976. Applications of anhydrous
ammonia have increased more than 14-fold and applications of nitrogen solutions have increased
more than fifty times in the same period.
5.5 SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS
N-nitroso compounds may be emitted to the atmosphere during their production or use, and
have been postulated to occur by atmospheric formation or volatilization from water or soil.
Additional routes of human exposure to N-nitroso compounds may include drinking water, foods
and tobacco products.
5.5.1 Anthropogenic Sources of N-Nitroso Compounds
Possible direct anthropogenic sources of N-nitroso compounds include industrial processes
in which these compounds are intermediate or final products, reactants or additives; or in
which they may occur incidentally as impurities. While over 20 N-nitroso compounds are listed
as products in recent commercial directories (Chem Sources, 1975,1977; Stanford Research
Institute, 1977), only four of these were either sold in quantities over 1000 pounds yearly or
resulted in annual sales over $1,000. Although the patent literature on N-nitroso compounds
is sizeable, many are currently synthesized only for research purposes. The well-known toxic
and carcinogenic effects of some N-nitroso compounds and related regulatory actions (U.S.
Department of Labor, 1974) have apparently discouraged their general use.
The two N-nitroso compounds produced in greatest quantity, diphenylnitrosamine and dini-
trosopentamethylenetetramine, are used in the rubber industry as a vulcanizing retarder and a
blowing agent, respectively (Magee, 1972). Neither has been found carcinogenic in laboratory
tests on male rats (Boyland et al., 1968).
Several less direct sources of ambient N-nitroso compounds have been postulated. Some
samples of cured meats, fish and fish meal, soya bean oil and tobacco have been shown to con-
tain N-nitroso concentrations rarely exceeding 1.0 ppm (Fiddler, 1975; Ender et al., 1964;
Hedler, 1971; Hedler et al., 1972; Hoffman et al., 1974). Release of small quantities of N-
nitroso compounds may occur in the processing of such products. Emissions occurring as a re-
sult of certain combustion processes have also been suspected. Analysis for emissions of nitro-
samines (usually only N-nitrosodimethylamine) has been carried out as part of research programs
5-16
-------
o
ID
O
a
<
GO
D
AMMONIUM NITRATE
NITROGEN SOLUTIONS
ANHYDROUS AMMONIA
UREA
1955
1960
1965
YEAR
1970
1975
Figure 5-7. Trends in U.S. usage of nitrogenous material applied
fertilizer (Gerstle and Peterson, 1966).
as
5-17
-------
CJl
TABLE 5-6. NITROGENOUS COMPOUNDS APPLIED AS FERTILIZER IN THE U.S. 1955-1976
(usage in 10 tons of material )
Material Applied
Total N
Ammonium Nitrate
Anhydrous Ammonia
Aqua Ammonia
Nitrogen Solutions
Urea
Ammonium Sulfate
Sodium Nitrate
1955
1.96
1.12
.34
.23
.11
.07
.52
.62
1960
2.74
1.23
.71
.43
.65
.14
.53
.45
1965
4.64
1.63
1.56
.82
1.92
.43
.77
.30
1970
7.46
2.84
3.47
.70
3.24
.53
.78
.09
1973
8.30
3.28
3.41
.66
3.41
.96
.95
.06
1974
9.16
3.17
4.18
.72
4.05
1.03
.93
.05
1975
8.61
2.81
4.02
.70
4.11
1.15
.82
.08
1976
10.34
2.94
4.91
.68
5.55
1.62
1.04
.06
aNumbers are rounded to two decimal places.
Source: Hargett, 1977.
CO
-------
involving automobiles, diesel engines, emission control systems, and fuels and fuel additives.
Tests by five different groups using different techniques all produced negative results (U.S.
EPA, 1977d), although Fine et al. (1976a, 1976b, 1976c) reported the presence of several un-
identified N-nitroso compounds in the exhaust of a truck diesel engine and an automobile in-
ternal combustion engine. No firm explanation of these different results can be given at
present. . '
5.5.2 Volatilization from Other Media
Some N-nitroso compounds, particularly those with low molecular weights, may reach the
atmosphere through volatilization from soil and water. These compounds may be present in soil
or water as deposits or effluents from industrial or agricultural sources, or may be formed d_e
novo from appropriate precursors in water or soil. Nitrosamines have been found in several
commercial herbicides (Fine and Ross, 1976) which, upon application, could be volatilized from
surface water or soil. Volatilization may also occur from N-nitroso compounds formed jm situ.
Formation of N-nitroso compounds in soil and water samples has been demonstrated under labo-
ratory, conditions (Ayanaba and Alexander, 1974; Ayanabe et al. , 1973; Elespuru and Lijinsky,
1973; Tate and Alexander, 1974; Wolfe et al., 1976). Most of these experiments involve pesti-
cides or pesticide ingredients and nitrites, nitrates or nitrous acid, at levels which may
reasonably be expected to occur in some farming or feedlot operations. Direct evidence is
lacking, however, for the volatilization of N-nitroso compounds.
5.5.3 Atmospheric Formation: N-Nitroso Precursors
Possible mechanisms for atmospheric formation of N-nitroso compounds are reviewed in
Chapter 6. In addition to the considerations presented in Chapter 6, it has been postulated
that nitrosamines may be formed and emitted from industrial processes using amines to modify
fly-ash resistivity (U.S. EPA, 1977d; Cavanaugh et al., 1975). A study, however, reported no
detection of nitrosamines in emissions from a power plant using such amine additives (Sparks,
1976).
In general, preliminary considerations of the atmospheric mechanisms suggested that
ambient concentrations of nitrosamines should be investigated in the vicinity of emitters of
two classes of airborne precursors: (1) oxides of nitrogen, nitrites, and/or nitrates and (2)
amines, amides, or other related compounds (U.S. EPA, 1977d). Sources leading to ambient con-
centrations of the nitrogen compounds have been discussed above in Section 5.2. With regard
to the second group, the only suspected N-nitroso precursors for which sources have been
extensively documented are the amines. As of 1975, at least 32 companies were producing
various amines (Chem Sources, 1975). Amines may be emitted directly from these production
facilities, and also may be emitted during subsequent use in many manufacturing processes and
products. Amines have been identified in emissions from decomposition of livestock and poul-
try manure, air sampled over cattle feedlots, and exhaust from rendering of animal matter
(Peters and Blackwood, 1977; Shuval and Gruenar, 1972; U.S. EPA, 1977d). Volatility and
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water-solubility of various amines results in extensive dispersal of these compounds in the
atmosphere, water and soil (Walker et al., 1976). Results of investigations of ambient concen-
trations of N-nitroso compounds in the vicinity of suspected sources are discussed in Section
8.3. These investigations have failed to detect evidence of atmospheric N-nitroso formation.
5.5.4 N-Nitrosamines in Food, Water and Tobacco Products
This section reviews briefly the major non-atmospheric" routes of human exposure to N-
nitroso compounds in order to place possible exposure via the atmospheric route in perspec-
tive.
A variety of raw and processed foods have been tested for N-nitroso compounds. A review
of earlier qualitative studies was published by Sebranek and Cassens (1973). Scanlan (1975)
has summarized a number of the studies reported since 1970. These recent studies concentrate
on processed meats and fish, in which m'trosamines, nitrosopiperidine and nitrosopyrrolidine
have been identified at levels usually considerably less than 1 ppm. Raw and cooked bacon
samples were found by several investigators to contain 1.5 to 139 ppb nitrosopyrrolidine (NPY)
and 1.0 to 30 ppb dimethylnitrosamine (DMN) (Allison et al., 1972; Crosby et al., 1972; Fazio
et al., 1973; Fiddler et al., 1974; Havery et al. , 1976; Pensabene et al., 1974; Sen et al.,
1973a,1974). Other meat products (including luncheon meat, frankfurters and other sausages)
were found to contain 3 to 105 ppb NPY, 1 to 94 ppb DMN, 2 to 25 ppb diethylnitrosaroine (DEN)
and 50 to 60 ppb nitrosopiperidine (NPi) (Allison et al., 1972; Fazio et al., 1972; Panalaks
et al., 1973,1974; Sen, 1972; Sen et al., 1973b; Wasserman et al., 1972). Raw and processed
fish products have shown 1 to 26 ppb DMN and 1 to 6 ppb NPY (Allison et al., 1972; Crosby et
al., 1972; Fazio et al., 1971), with some fish meal samples containing as much as 450 ppb DMN
(Sen et al., 1972). Cheese samples were found to contain up to 4 ppb DMN, 1.5 ppb DEN and 1.0
ppb NPY (Allison et al. , 1972; Crosby et al., 1972). Negative results have been obtained in
other tests for nitrosamines on many food samples, including bacon, ham and other pork products,
fats and oils, cheeses, and total diet samples (Havery et al., 1976).
Contamination of drinking water with N-nitroso coumpounds may occur through water-borne
emissions from the industrial sources discussed in Section 5.5.1 or by nitrosation of pre-
cursors found in natural bodies of water or water supply and treatment systems (U.S. EPA,
1977b,1977c,1977d). N-nitroso compounds have been found in industrial wastewater, and in
samples taken from water near industrial facilities. Nitrosation in lake water samples has
been demonstrated in the laboratory (Ayanaba and Alexander, 1974). Analyses of drinking water
have either failed to detect N-nitroso compounds or have shown concentrations in the 0.1 ppb
range (Fine et al., 1976b,1976c).
There may be significant exposure to N-nitroso compounds in use of cigarettes and other
tobacco products. Mainstream smoke of blended unfiltered U.S. cigarettes was found to contain
the following N-nitroso compounds (amounts in nanograms per cigarette): nitrosodimethylamine
(84), nitrosoethylmethylamine (30), nitrosonornicotine (137), and nitrosodiethylamine (<5)
(Hoffman et al., 1975). N'-nitrosonornicotine found in a variety of chewing tobacco products
5-20
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indicates that such unsmoked products may also be sources of exposure to N-nitroso compounds
(Hoffman et al., 1974).
5.6 SUMMARY
5.6.1 Sources and Emissions of NQ^
, A
Oxides of nitrogen have their origin in a number of natural (Chapter 4) and anthropogenic
processes. Since various authors differ greatly in their estimates of natural emissions, it
is difficult to assess with any certainty the fraction of total global NO emissions origi-
nating from human activities. In terms of sources giving rise to significant human exposure,
however, the most important emissions occur as a result of man's burning of fossil fuels such
as coal, oil or gasoline. Mobile combustion and fossil-fuel stationary combustion are the two
largest source categories, comprising about 44 percent and 51 percent of the nationwide anthro-
pogenic NO emissions, respectively, 1976. In the stationary combustion category, electric
utilities were responsible for approximately 56 percent of the anthropogenic NO emissions,
A
and industrial combustion accounted for another 38 percent. In the mobile combustion category,
highway vehicle emissions comprised about 77 percent, with the rest attributable to
non-highway vehicles. In addition, non-combustion industrial processes such as petroleum
refining and manufacture of nitric acid, explosives and fertilizers may produce quantities of
NO which, while minor on a national basis, may be significant near individual sources.
A
In most ambient situations nitrogen dioxide (NO,), the NO compound of most concern for
human health and welfare, is not emitted directly into the atmosphere in significant amounts
(typically less than 5 percent of NO emissions occur as N02). It arises mainly from the oxi-
dation in the atmosphere of the more commonly emitted compound nitric oxide (NO). However,
some minor source types, notably a number of diesel and jet turbine engines do, under certain
load conditions, emit a significant fraction of their NO emissions as NOp.
In general, the relationship between the magnitude of NO emissions and resulting ambient
NOo concentrations is neither direct nor constant. The influence of sources upon ambient con-
centrations at a given location depends not only on details of the emissions from the source
but also upon such factors as the presence or absence of other atmospheric constituents such
as hydrocarbons and ozone, as well as land use, weather and climate, and topography.
Estimates of historical emissions for the years 1940 through 1970 indicate that total
anthropogenic emissions of NO almost tripled during that period. More recently, emissions
from transportation sources increased by about 20 percent from 1970 to 1976, but emissions from
stationary combustion sources and total emissions did not exhibit a monotonic upward trend.
Examination of NO emissions inventories by U.S. county reveals that, in general, both point
A
and area sources contribute significantly in those places where total NO emissions are high.
A
There are, however, considerable local or regional differences in the relative amounts of NO
emitted by the major source categories. For example, motor vehicles have been estimated to
contribute approximately 90 percent of the NO emissions in Sacramento, California, while the
A
corresponding statistic in northwestern Indiana is only 8 percent. Emissions may also exhibit
5-21
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a significant diurnal and/or seasonal variability. The seasonal variation in power production
from fossil fuel generating plants, e.g., is about 15 percent on a nationwide basis. Diurnal
variations in traffic volume usually lead to marked daily emission profiles for mobile sources.
Representing such sources by annual emissions data only may underestimate their potential for
producing high short-term concentrations. Meteorological variables also exhibit both seasonal
and diurnal variability, which can greatly affect the impact of particular sources on ambient
pollution levels.
5.6.2 Sources and Emissions of Other Nitrogenous Compounds
Principal anthropogenic sources of ammonia (which some researchers have suggested is con-
verted to NO in the atmosphere) include coal combustion, inefficiencies in handling and apply-
A.
ing ammonia-based fertilizers, and volatilization of the urea-nitrogen in animal urine gener-
ated in feedlots. The last source has been estimated to contribute between one-fourth and
one-half of all the anthropogenically produced nitrogenous compounds emitted yearly to the
atmosphere in the United States (N?0 is not included in this estimate).
The use of nitrogen-based fertilizer (which some researchers have implicated in increased
N?0 emissions leading to possible depletion of the stratospheric ozone layer) has risen
markedly in the last two decades in the United States. The total nitrogen applied as ferti-
lizer has increased by more than a factor of 5 from 1955 to 1976. Applications of anhydrous
ammonia have increased more than 14-fold and applications of nitrogen solutions have increased
more than 50 times during the same period. However, recent estimates of the effects of
increased N?0 on stratospheric ozone indicate a much smaller effect than previously suspected
(Chapter 9).
Possible direct atmospheric sources of N-nitroso compounds (some of which are known car-
cinogens) include industrial processes in which these compounds are intermediate or final pro-
ducts, reactants or additives, or may occur incidentally as impurities. Other than NO , the
only proposed N-nitroso precursors for which sources have been extensively documented are the
amines. Amines have been identified in emissions from decomposition of livestock and poultry
manure, air sampled over cattle feedlots, and exhaust from rendering of animal matter. There
is, however, little or no evidence to date to indicate that the atmospheric route for human
exposure to nitrosamines is a cause for concern (Chapter 8).
5-22
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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 nitrosamine formation.
6.1 CHEMISTRY OF THE OXIDES OF NITROGEN IN THE LOWER ATMOSPHERE
Solar radiation triggers a series of reactions in the atmosphere between gaseous organic
molecules and nitrogen oxides, producing a wide variety of secondary pollutants. The totality
of primary and secondary pollutants involved in these photochemical reactions is known as phot
chemical smog. To understand the chemistry of the oxides of nitrogen in the lower atmosphere,
it is necessary to consider the interactions that take place between the oxides of nitrogen
and organic constituents. Several reviews of atmospheric chemistry are available (Heiklen,
1976; Seinfeld, 1975; Stern, 1976), as are detailed discussions of reaction mechanisms (Baldwi
et al., 1977; Carter et at. , 1979; Demerjian et al., 1974; Falls and Seinfeld, 1978; Whitten
and Hogo, 1977) and rate constants (Hampson and Garvin, 1978). In this section the chemistry
of the oxides of nitrogen in the lower atmosphere is briefly reviewed. The above-cited refer-
ences should be consulted for more detail.
Most of the chemistry that occurs in a sunlight-irradiated urban atmosphere involves the
interaction of a variety of unstable, excited molecules and molecular fragments that have only
a transitory existence. These species include: the unexcited and first excited electronic
3 1
states of the oxygen atom, triplet-P oxygen atoms [0( P)], and singlet-D oxygen atoms [0( D)];
ozone (On); symmetrical nitrogen trioxide (NO.,); dinitrogen pentoxide (N205); hydroxyl radical
6-1
-------
(HO); alkylperoxyl radicals (RO^); acylperoxyl radicals RCfO^; and other less important
species. In the formulas, R represents a methyl (CH3), ethyl (C^H^), or another, more complex
hydrocarbon radical. The paths by which these intermediates are formed and destroyed are
important keys in explaining the chemical changes that occur in the polluted atmosphere.
6.1.1. Reactions Involving Oxides of Nitrogen
The major portion of the total oxides of nitrogen emitted by combustion sources is nitric
oxide (NO). The rate at which NO is converted to nitrogen dioxide (ML) through oxidation by
the oxygen in air:
2NO + 02 -» 2N02 (6-1)
is proportional to the square of the nitric oxide concentration since two molecules of NO are
required for the oxidation; it is, therefore, very sensitive to changes in nitric oxide concen-
tration. Reaction 6-1 can be important in the vicinity of sources in generating up to 25 per-
cent of total NO during the initial state of dilution with air when the concentration of NO
A
is still quite high. Reaction 6-1 is much too slow, however, to account for any significant
fraction of the nitric oxide to nitrogen dioxide conversion in the atmosphere for typical
ambient levels of nitric oxide.
Since sunlight triggers the phenomenon of photochemical smog formation, it is important
to recognize those constituents that will absorb light energy. In some cases, these constit-
uents decompose or become activated for reaction. A dominant sunlight absorber in the urban
atmosphere is the brown gas, nitrogen dioxide. Light absorption at wavelengths <430 nm can
cause the rupture of one of the nitrogen-oxygen (N-0) bonds in the nitrogen dioxide (0-N-O)
molecule and generate the reactive ground state oxygen atom, the triplet-P oxygen atom, and a
nitric oxide molecule. The efficiency of this process is wavelength-dependent:
N02 + sunlight (290-430 nm) -> 0(3P) + NO (6-2)
The highly reactive triplet-P oxygen atom formed in air collides frequently with oxygen mole-
cules. During such encounters ozone may be formed:
0(3P) + 02 + M -» 03 + M (6-3)
M in this equation represents a nitrogen, oxygen, or other third molecule that absorbs the
excess vibrational energy released, thereby stabilizing the ozone produced. For most concen-
tration conditions common in polluted atmospheres, the very reactive ozone molecules regenerate
nitrogen dioxide by reaction with nitric oxide:
03 + NO -» N02 + 02 (6-4)
Alternatively, ozone may react with nitrogen dioxide to create a new transient species, sym-
metrical nitrogen trioxide:
03 + N02 -» N03 + 02 (6-5)
The nitrate species forms dinitrogen pentoxide, the reactive anhydride of nitric acid, by
reaction with nitrogen dioxide:
N03 +,.N02 -> N205 (6-6)
6-2
-------
Dinitrogen pentoxide may redissociate to form symmetrical nitrogen trioxide and nitrogen diox-
ide or possibly react with water to form nitric acid (HON05):
N90, •» NO, + NO, * (6-7)
or * D J i
N205 + H20 -» 2HON02 (6-8)
The following reactions may take place between oxygen atoms and N0? and NO:
N0? + 0(3P) •* NO + 0- (6-9)
or 3
NO, + DTP) + M -» NO, + M (610)
or 3
NO + 0(JP) + M •* N02 + M (6-11)
Also, NO and NO, may react to regenerate N0?:
N03 + NO -» 2N02 (6-12)
Nitrous acid is produced by:
NO + N02 + H20 -» 2HONO (6-13)
and may react bimolecularly to regenerate the original reactants:
MONO + HONO -»• NO + N02 + H20 (6-14)
The unexcited and first excited electronic state of the oxygen atom are
produced by ozone photolysis in sunlight:
290-350 nm -» 0? +0(1D) or 0(3P) (6-15)
0, + sunlight ,
6 450-700 nm •* 02 + 0(JP) (6-15b)
The singlet-D oxygen [0( D)] atom is much more reactive than the
•3
ground state triplet-P oxygen [0( P)] atom. For example, it reacts effici-
ently during collision with a water molecule to form an important transient
species in the atmosphere, the hydroxyl radical:
0(1D) + H20 -» 2HO (6-16)
This radical is also formed through the photodecomposition of nitrous acid
(HONO):
HONO + sunlight (290-400 nm) ^ HO + NO (6-17)
The hydroxyl radical can reassociate with nitrogen dioxide to produce nitric
acid:
HO + N02 + M -> HON02 + M (6-18)
or form nitrous acid by reacting with nitric oxide:
HO + NO + M •* HONO + M (6-19)
6-3
-------
A careful review of the net results of reactions 6-1 through 6-19 reveals that these
reactions alone cannot explain the rapid conversion of NO to NCL observed in the ambient atmos-
phere. In fact, if these reactions alone occurred, the original supply of nitrogen dioxide in
our atmosphere would be slightly depleted under irradiation with sunlight, and a small and near
constant level of ozone would be created in a few minutes. The key to the observed nitric
oxide to nitrogen dioxide conversion lies in a sequence of reactions between the transient
species present and other reactive molecules such as the hydrocarbons and aldehydes present in
the polluted atmosphere.
In the presence of hydrocarbons the number of reactions greatly increases. Thus, the hy-
droxyl radicals produced by reactions 6-16 and 6-17 can react with a hydrocarbon (paraffin,
olefin, aromatic, or any compound having C-H bonds):
OH + Hydrocarbon -» R- + H20 (6-20)
Reaction 6-20 produces an alkyl radical (R-) which contains a free electron. This
radical quickly picks up an oxygen molecule from the air to form a peroxyl radical ROp-:
R- + 02 8 R02- (6-21)
Typically, the next reaction in the series converts NO to N0? and produces an oxyl radical,
RO-:
R02- + NO -> RO- + N02 (6-22)
A hydrogen abstraction by molecular oxygen may then produce a hydroperoxyl radical, H02-. The
rest of such an RO- radical typically forms a carbonyl compound, OHC:
RO- + 02 •* OHC + H02- (6-23)
Finally, the hydroperoxyl radical (H0?) can react with a second NO to form N0? to complete the
cycle:
H02- + NO •* OH- + N02 (6-24)
Although this description is very simplified, these series of reactions contain the essential
features of NO to N0? oxidation and subsequent ozone formation.
The initial source of radicals is very important; although the rate and yield of oxidant
formation depend on many other factors, the length of the induction period before accumulation
of oxidant depends strongly on the initial concentration of radicals. (The length of the in-
duction period is important primarily in constant light intensity smog chambers. Diurnally
varying radiation tends to lessen the importance considerably.) In smog chambers and possibly
in the ambient atmosphere, the photolysis of nitrous acid, reaction 6-17, may be the most
important initial source of radicals. Nitrous acid has been detected in smog chambers in con-
centrations sufficient to explain the observed induction time for smog chemistry, but the con-
centrations necessary to initiate smog chemistry in the atmosphere are below the limits mea-
sured by most modern instruments.
Another possible source of radicals in the atmosphere is the photolysis of aldehydes:
RCHO + hv •* HCO + R- (6-25)
Aldehydes are emitted from many sources, including automobiles. They are also formed in smog.
6-4
-------
During the course of the overall smog formation process, the free radical pool is main-
tained by several sources, but the dominant one appears to be photolysis of the aldehydes
formed from the initial hydrocarbons. Since the reactions of free radicals with NO form a
cyclic process, any additional source of radicals will add to the pool and increase the cycle
rate. Conversely, any reaction that removes free radicals will slow the cycle rate. For exam
pie, a primary radical sink and a primary sink for oxides of nitrogen is reaction 6-18 to form
nitric acid.
The hydrocarbon classes important in the chemistry of the polluted troposphere are alkane
olefins, and aromatics. In addition, the oxygenated hydrocarbons, such as aldehydes, ketones,
esters, ethers, and alcohol are also important. A great variety of chemical reactions take
place among these organic species and the free radicals cited above. The reactions of typical
hydrocarbon species are now discussed briefly. Throughout the discussion references to more
extensive coverages are given.
The most important atmospheric reaction involving alkanes is with the OH radical. For
n-butane, for example, the reaction is
CH.,CH<,CH9CH,+ OH- -»• CH,CH9CH9CH0- + H00 (6-26a)
J ^ i J and 6 L * * *
-> CH3CH2CHCH3 + H20 (6-26b)
The alkyl radicals will rapidly add 0^ to form the corresponding peroxyalkyl radicals, e.g.
CH3CH2CH2CH2- + 02 + M -»• CH3CH2CH2CH202- + M (6-27)
(subsequently the third body M will not be indicated). A reaction of substantially lesser
importance is with oxygen atoms,
, Qy
CH.CH-CH-CH, + OrP) ^OH- + CH-,CH,CH,CH909- (6-28a)
j^^j and *
-------
In each case the free radical product will quickly react with 02 to produce a peroxyalkyl
radical that is capable of converting NO to NCk.
Ozone-olefin reactions are a source of free radicals and stable products in air pollution
chemistry. The initial attack of Q^ on an olefin produces an unstable intermediate, which may
decompose by several pathways (Niki, 1979; O'Neal and Blumstein, 1973). For propylene, for
example, the initial step in the reaction with 03 is believed to be:
A
A CH.CH-CH,
0 0 S* 6 d
CH3CH = CH2 + 03 + CH3CH-CH2 -0 (6-30)
^^^ .0 \
CH3CH-CH2
Subsequent decomposition of the products leads to a variety of free radicals and stable
products (Herron and Huie, 1977; Niki et al., 1977). The mechanisms of ozone-olefin reactions
are still under considerable study, although most of the potential paths have been delineated.
The reaction of olefins with atomic oxygen plays a minor role in olefin consumption and
radical and product formation. Again, for propylene the reaction is:
3
CH3CH = CH2 4 0( P) -> CH3CH2- + HCO (6-31a)
or
-» CH-.CO + CH- (6-31b)
or J J
•» CH3CH2CHO (6-31c)
The mechanism of photooxidation of aromatic species in the atmosphere is perhaps the area
of greatest uncertainty in atmospheric hydrocarbon chemistry. The principal reaction of aro-
matics is with the hydroxyl radical (Hendry, 1979; Perry et al., 1977). For aromatic-OH reac-
tions, the initial step can be either addition to or abstraction from the aromatic ring
(Kenley et al., 1978). The free radical addition products may then react, most likely with
either 02 or N02, leading to the cresols or nitrotoluenes, respectively. The abstraction
route probably leads to benzaldehyde. The mechanism of aromatic-OH reactions is yet to be
clarified.
Aldehydes, both aliphatic and aromatic, occur as primary and secondary pollutants and are
direct precursors of free radicals in the atmosphere (Lloyd, 1979). Consequently, aldehyde
chemistry represents an important subject area in atmospheric chemistry. Although aldehydes
are the main oxygenated hydrocarbons generally considered with respect to their role in atmos-
pheric chemistry, other classes of oxygenated hydrocarbons, such as ketones, esters, ethers
and alcohols, are present and participate to a somewhat lesser extent. Major secondary sources
of aldehydes include the reactions of ozone and OH radicals with hydrocarbons, and radical de-
composition products. In addition, aromatic aldehydes can be formed as an ultimate consequence
of the reaction of OH with aromatics, e.g. benzaldehyde. The aldehydic hydrogen-carbon bond
6-6
-------
in aldehydes is relatively weak (CH bond strength is 86 kcal/mol ). Consequently, this hydro-
gen atom will be susceptible under atmospheric conditions to attack by radical species, such
as 0(3P), 0(1D), OH, and H02. Of these OH is by far the most dominant. Hydroxyl radicals are
generally thought to abstract a H-atom from aldehydes—chiefly the aldehydic H-atoms, i.e.
OH + RCHO -» H90 + RCO (6-32)
6 -3
If one assumes an atmospheric concentration of 10 radicals cm , the rates of decay of HCHO
and CH3CHO by reaction with OH are approximately 4.2 percent and 5.8 percent per hour, respec-
tively (Lloyd, 1979).
The photodissociation of aldehydes is an important radical generation mechanism in the
formation of photochemical air pollution. The reactions that are most significant can be
generalized in terms of a radical and a molecular route:
RCHO + hv •* R + HCO (6-33a)
and
•* RH + CO (6-33b)
(Reaction 6-33a was previously given as reaction 6-25.) The radical route is the more impor-
tant one from the point of view of atmospheric chemistry.
As hydrocarbons are oxidized in photochemical smog, they generally produce formaldehyde,
HCHO, at some point. Considerable attention has been given to formaldehyde photolysis in
recent years. There appears to be general agreement that the primary paths are:
HCHO + hv •* H- + HCO (6-34a)
and
•* H2 + CO (6-34b)
Moortgat and Warneck (1979) recently measured the quantum yield for the photolysis of
formaldehyde. Their results imply that the radical pathway (reaction 6-34a) and the nonradical
pathway (reaction 6-34b) occur at approximately equal rates under typical atmospheric conditions
Another primary reaction path of formaldehyde in photochemical smog is the reaction with
OH-:
HCHO + OH- HpO + HCO (A)
In order to compare the rates of photolysis with the depletion of formaldehyde by OH
reaction, one can calculate a photolysis rate of approximately 13 percent per hour for a solar
zenith angle of 20° using the value of the photodissociation rate given by Horowitz and Calvert
(1978).
Formaldehyde photolysis represents an important source of radicals in smog chemistry
through reaction of the products with 02 yielding the hydroperoxyl radical, HO,,-. Thus:
H- + 02 + M H02- + M (B)
HCO- + 02 H02- + CO (C)
Since reactions B and C are very fast in normal atmospheres, reactions 6-34a and 6-34b
are frequently written as:
HCHO + hv 202 2 H02- + CO (0)
and HCHO + OH-0^ H20 + HOj- + CO (E)
6-7
-------
A rate constant for reaction E was recently recommended by the NASA Panel for Data Eval-
uation (National Aeronautics and Space Administration, 1979).
Acetaldehyde, ChLCHO, also appears to play a significant role in smog chemistry. In this
case, photolysis proceeds mainly by the radical pathway: (Calvert and Pitts, 1966).
CH3CHO + hv - CH^ + HCO- (F)
Another primary reaction is the abstraction of hydrogen by the OH radical:
CH3CHO + OH- - ' CH3 C(O)- + H20 (G)
Subsequent reactions of the product radicals of reactions F and G with atmospheric 0? are
very fast so that one may write:
CH3CHO + hv 202 CH30^ + HO^ + CO (H)
and CH3CHO +~OTTr~ 02 CH3C(0)02« + H20 (I)
Acetaldehyde chemistry thus introduces the chemistry of alkylperoxy radicals (ROp via
the methylperoxy radical, CH,OA; and the chemistry of peroxyacyl nitrates [RCCOjOpNO,,] via the
formation of peroxyacetyl nitrate (PAN) from the acetylperoxy radical, CH3(CO)Oi (see reactions
6-42 ff below).
In addition to aldehydes, the ketones, methyethylketone and acetone are known to play a
role in photochemical smog (Demerjian et al., 1974).
The interaction with NO and N0? of the organic free radicals produced by hydrocarbon oxi-
dation represents an extremely important aspect of the chemistry of the oxides of nitrogen in
the polluted atmosphere. The radicals can be classed according to:
acyl
acyl ate
peroxyacyl
In air it can be assumed that combination with 02 is the sole fate of alkyl (R-) and acyl
(RCO-) radicals and that the reaction is essentially instantaneous. Consequently, in reactions
with alkyl or acyl radicals as products, these products are often written as the corresponding
peroxy radicals. Also, acylate radicals will decompose rapidly to give an alkyl radical and
COp. Therefore, only alkoxyl, peroxyalkyl, and peroxyacyl radicals need to be considered
explicitly in terms of NO chemistry. Table 6-1 shows the various reaction combinations that
are important between these radicals and NO and N02-
The reactions of OH with N02 and NO are reasonably well understood and have been previ-
ously listed as reactions 6-18 and 6-19. Rate constants for these two reactions are available
(Hampson and Garvin, 1978).
The rate constant for the reaction of H02 and NO has recently been determined by direct
means and is substantially larger than previously calculated indirectly (Howard and Evenson,
6-8
R-
RO-
ROO-
alkyl
alkoxyl
peroxyalkyl
0
RC-
0
n
RCO-
0
RCOO
-------
TABLE 6-1. REACTIONS OF ALKOXYL, ALKYLPEROXYL AND ACYLPEROXYL RADICALS WITH NO AND NO,
NO N02
Free Radical Reaction Reference
OH OH + NO -> HONO Hampson and
Garvin, 1978
H0~ H09 + NO -> N0? + OH Howard and
* * L Evenson, 1977
RO RO + NO •> RONO Batt et al . ,
(RONO + hv -» RO + NO) 1975
R02 R02 + NO -> N02 + RO
•* RON02
RCO~ RGO, + NO -»• N09 .+ RC09 Cox and Roffey,
j 6 ^ t ig?7
Hendry and
Kenley, 1977
Reaction
OH +
H02
(H02
RO +
(R02
RC03
(RCO
N02 -» HON02
+ NO, -* HONO + 0,
^ ^ H02N02
N02 •* H02 + N02)
NO, -> RON09
^ ^ RCHO'i+ HONO
4- MO -* on Kin
' MUn ~ l\\J n\V\J r\
N02 •* R02 -•- N02)
,NO, -» RCO, + NO,)
-J ^ -J ^
Reference
Tsang et al . ,
1977
Howard, 1977
Graham et al . ,
1977
Wiebe et al . ,
1973
Cox and Roffey,
1977
Hendry and
Kenley, 1977
-------
1977). The HCL-NO reaction, as noted earlier, is a key reaction in the atmospheric conversion
of NO to N02.
The reaction of H02 and NCL has the following two possible mechanisms (Howard, 1977).
Reaction 6-35b is not considered to be important in atmospheric chemistry:
HO, + NO, -» H09N09 (6-35a)
H02 + N02 -» MONO + 02 (6-35b)
In addition, the peroxynitric acid formed in reaction 6-35a thermally decomposes as follows
(Graham et al. , 1977):
H02N02 -> H02 + N02 (6-36)
At the present time it appears that, at the temperatures prevalent in summer smog episodes
(>20°C), peroxynitric acid does not represent an appreciable sink for NO- because of the rapid
thermal decomposition reaction 6-36. At lower temperatures H02N02 will achieve higher concen-
trations and its importance as a sink for N02 increases.
The reactions of RO, R02 and RCO., with NO and N02 represent key reactions in the conver-
sion of NO to N02 and the formation of organic nitrites and nitrates.
The main alkoxyl radical reactions with NO and NO- are:
RO- + NO -» RONO (6-37a)
or
-» RCHO + HNO (6-37b)
and
RO- + N02 -» RON02 (6-38c)
or
-> RCHO + HONO (6-38b)
The reaction of alkylperoxyl radicals with NO is generally assumed to proceed by the oxi-
dation of NO to NO- with formation of an alkoxyl radical:
' R02- + NO -> N02 + RO- (6-22)
Reaction 6-22 is believed to be an important route for the oxidation of NO to N02 in the atmos-
phere (the alkoxyl radical may react further to produce H02, which also converts NO to N02).
It has been postulated that longer chain peroxyalkyl radicals (n>4) from alkane photooxi-
dation will add to NO to form an excited complex that can be stabilized to produce an alkyl
nitrate (Darnall et al., 1976):
R02- + NO + RON02 (6-39)
The peroxyalkyl-N02 reaction proceeds principally by
R02- + N02 -» R02N02 (6-40)
The peroxynitrate may thermally decompose according to
RO^N02 •* R02- + N02 (6-41)
Measured rate constants for the R02-N02 reaction and the R02N02 decomposition are not cur-
rently available.
6-10
-------
Peroxyacyl nitrates have long been recognized as important components of photochemical
air pollution (U.S. EPA, 1978). Peroxyacetyl nitrate (PAN) exists in equilibrium with the
peroxyacyl radical and NO,,:
00
CH3COO- + N02 + CH3COON02 (6-42)
There exists a competition between NO and N02 for the peroxyacyl radical
through:
0 0
CH3COO- + NO •* CH-jCO- + N02 (6-43)
The acetyl radical will rapidly decompose as follows:
0
CH3CO- •* CH3- + C02 (6-44)
followed by:
CH3- + 02 -» CH302- (6-21)
CH302- + NO -> CH30- + N02 (6-22)
CH30- + 02 -» HCHO + H02- (6-23)
HO^ + NO •* OH- + N02 (6-24)
Thus, PAN chemistry is intimately interwoven in the NO to N0? conversion process. Rate con-
stants for reactions 6-42 and 6-43 have recently been reported by two groups of investigators
(Cox and Roffey, 1977; Hendry and Kenley, 1977).
The chemistry of the oxides of nitrogen in a hydrocarbon-containing atmosphere can be sum-
marized as follows: the major observed phenomenon in the system is conversion of NO to N02
and formation of a variety of nitrogen-containing species, such as nitrites and nitrates. The
conversion of NO to N02 is accompanied by accumulation of 0.,. N02 serves as both an initiator
and terminator of the chain reactions that result in conversion of NO to N02 and buildup of
0.,. Termination of the chain reactions leads to nitric acid and organic nitrates. The nature
of the system can be explained by considering its behavior as a function of the initial concen-
trations of NO and hydrocarbon in the irradiation of a static system, as well as the ratio of
two reactants, i.e, the [HC]/[NO ] ratio.
At low [HC]/[NO ] ratios (usually ratios of less than about 1 to 2/1) the rate at which
X
NO is converted to NO,, is influenced by the availability of organic compounds. Therefore, the
effects of reducing organic compounds are to slow the conversion of NO to N02, thereby lowering
the N02/N0 ratio. When this occurs, a larger proportion of the NO that is converted to N02
occurs through the destruction of ozone. This then has to the overall effect of reducing the
rate of ozone formation. If the oxidation of NO by organics is delayed sufficiently so that
the sun has passed its zenith before significant amounts of N0« are created, photodissociation
of NO,, will be diminished and less ozone will accumulate on that day. At moderately high
6-11
-------
[HC]/[NOX] ratios (usually greater than about 5 to 8/1), the greater availability of organic
radicals means that all of these radicals are not consumed as rapidly in reactions with NO,
and more reactions between the radicals and NO- are able to occur. Thus, the amount of ozone
formed and accumulated begins to become limited by the availability of NO , and becomes less
sensitive to additional organic precursors. At very high [HC]/[NO ] ratios (greater than about
20 to 30/1), ozone cannot accumulate because either the ozone is consumed by reaction with
hydrocarbons or radical-radical termination reactions occur which reduce oxygen atom and, hence,
ultimate ozone concentration.
Identification of the nitrogen-containing products in atmospheric reactions has been under
investigation for a number of years (Gay and Bufalini, 1971; Pitts, 1977; Spicer and Miller,
1976). In general, the most important gaseous nitrogen-containing products in the NO -organic
system are nitric acid and PAN. As noted, reactions of NO and N0? with free radicals produce,
in addition to nitrous, nitric, and peroxynitric acids, a variety of organic nitrogen-contain-
ing species (Table 6-1). There currently exist important areas of uncertainty with regard to
the formation of nitrogen-containing products in atmospheric reactions. The extent of for-
mation and decomposition of peroxynitrates, I^NOp, is unknown, and rate constants for the key
reactions in the series, R0~ + NO, are yet to be determined.
6.1.2 Laboratory Evidence of the NO,-to-Precursor Relationship
In the previous section, the nature of chemical reactions involving oxides of nitrogen
and hydrocarbons in the atmosphere was discussed. These reactions have traditionally been
studied experimentally in laboratory vessels called smog chambers. These chambers character-
istically employ radiation sources that closely approximate the UV portion of the solar spec-
trum as observed at the earth's surface and clean, chemically inert interior surfaces. It is
believed that the chemical processes that take place in smog chambers are similar to those that
take place in the atmosphere.
The presence of surfaces in a smog chamber may, however, be a source of difficulty in
interpreting chamber results because of possible surface-catalyzed reactions or absorption of
species on the walls. In addition, most chamber experiments have been conducted by initially
injecting fixed amounts of reactants rather than simulating the continuous time-varying injec-
tion and dilution of reactants that characterize the ambient situation. Nevertheless, the
behavior of irradiated mixtures of oxides of nitrogen and hydrocarbons in smog chambers has
served as the foundation for our understanding of atmospheric chemical mechanisms.
Considerable effort has been devoted to the development of chemical reaction mechanisms
that are capable of describing the processes observed in smog chambers (Baldwin et al., 1977;
Carter et al., 1979; Demerjian et al., 1974; Falls and Seinfeld, 1978; Whitten and Hogo, 1977).
Smog chambers have been used extensively to determine how concentrations of NO and other photo-
A
chemical products respond to changes in the initial composition of nitrogen oxides and organics.
A previous Criteria Document (U.S. EPA, 1978) discusses smog chamber evidence concerning the
relationship between'ozone/oxidant and the photochemical precursors. This section focuses on
how NO- concentrations respond to changes in the input levels of organics and nitrogen oxides.
6-12
-------
Several researchers have used smog chambers to investigate the dependence of nitrogen
dioxide concentrations on the levels of precursor inputs:
• The University of North Carolina (UNC) study, using an 11,000 cubic-foot (311 m ) outdoor
Teflon chamber, a simulated urban hydrocarbon mix, and twelve-hour irradiations (Jeffries
et al., 1975)
• The Bureau of Mines study, using a 100 cubic-foot (2.8 m ) aluminum-glass chamber, auto-
exhaust hydrocarbons, and six-hour irradiations (Dimitriades, 1972,1977)
• The General Motors study, using a 300 cubic-foot (8.5 m ) stainless steel-glass chamber,
a simulated Los Angeles hydrocarbon mix, and six-hour irradiations (Huess, 1975)
o
• The University of California at Riverside study, using a 225 cubic-foot (6.4 m ) glass
chamber, a simulated Los Angeles hydrocarbon mix, and six-hour irradiations (Pitts et al.,
1976)
• The Health, Education and Welfare (HEW) study, using a 335 cubic-foot (9.5 m ) chamber,
auto-exhaust hydrocarbons, and up to ten-hour irradiation time (Korth et al., 1964) and
3
• The HEW study, using a 335 cubic-foot (9.5 m ) chamber, toluene and m-xylene, and 6-hour
irradiations (Altshuller et al., 1970).
Trijonis (1978,1980) has recently reviewed the results of these studies, as summarized in
Table 6-2. As indicated in Table 6-2, the various chamber studies basically agree concerning
the dependence of maximum N0? and average N0? on NO input. With other factors held constant,
maximum NCL and average NO,, tend to be proportional to initial NO . The minor deviations away
from proportionality that sometimes occur tend to be in the direction of a slightly less than
proportional relationship, i.e., a 50 percent reduction in NO input sometimes produces
slightly less than a 50 percent reduction in N0?.
There is less agreement among the chamber studies concerning the dependence of NO, on
initial hydrocarbon concentrations. With respect to maximum NOp, the Bureau of Mines study
indicates essentially no dependence on hydrocarbons. However, three other studies suggest that
hydrocarbon reductions decrease maximum NOp concentrations. The UNC, General Motors, and UC
Riverside studies indicate that 50 percent hydrocarbon control tends to decrease maximal N0~
by 10-20 percent, 25 percent, and 10-15 percent, respectively.
With respect to average N0?, the Bureau of Mines study indicates that hydrocarbon reduc-
tions would tend to increase N0? dosage. This result is consistent with the theoretical argu-
ment of Stephens (1973), who hypothesized that hydrocarbon reduction would increase average
NOp because these reductions would delay and suppress the chemical reactions that consume N02
after it reaches a peak. However, the General Motors chamber study, the UC Riverside study,
and the two HEW studies indicate that hydrocarbons produce no consistent effect on average NOp
concentrations. The UNC experiments imply that a 50 percent reduction in hydrocarbons produces
about a 20 percent decrease in average NOp. There is some question about the UNC conclusion,
however, because the UNC chamber runs were of a 10-hour duration and the NOp levels at the end
of the experiments were greater when hydrocarbons were reduced. The extra NOp remaining after
6-13
-------
TABLE 6-2. SUMMARY OF CONCLUSIONS FROM SMOG CHAMBER EXPERIMENTS
CHAMBER STUDY
University of North
Carolina (Jeffries
et al. , 1975)
MAXIMAL N
Dependence
on NOV
.A
Proportional
or slightly
less than
proportional
Dependence
on HC
50% HC reduc-
tion reduces
maximal NO,
by 10% to 20%
AVERAGE N(
Dependence
on NOX
Proportional
or slightly
less than
proportional
Dependence
on HC
Uncertain, 50% HC
reduction may de-
crease average
N02 by 20% or may
increase average
en
i
Bureau of Mines
(Dimitriades,
1972,1977)
General Motors
(Huess, 1975)
UC Riverside
(Pitts et al.,
1976)
HEW, Auto Exhaust
(Korth et al.,
1964)
HEW, Toluene
(Altshuller et
al., 1970)
Proportional
Slightly less
than propor-
tional
Proportional
No effect
50% HC reduc-
tion reduces
maximal NO,
by 25% <•
50% HC control
reduces maximal
NO. by 10% to
I1V7 ry
15%
Proportional
Proportional
to slightly
less than
proportional
Proportional
Proportional
Proportional
50% HC reduction
increases average
N02 by 10% to 30%
No effect
No effect
No consistent
effect
No effect
-------
the 10-hour period could cause an increase in 24-hour average NOp, even though average NO, was
reduced during the first 10 hours.
Considering the results of all the chamber studies, Trijonis suggested a consensus based
on existing chamber results which would appear to be as follows: fifty percent hydrocarbon
reduction would have little effect on average NOp concentrations (a change of + 10 percent)
but would yield moderate decreases in maximal NOp (a reduction of about 10 to 20 percent). It
should be noted that these conclusions are meant to apply to one basic type of ambient
situation—the situation of well-mixed urban air.
Some additional support for these conclusions was provided recently by studies of actual
ambient data on NO and hydrocarbon levels from a number of cities in the U.S. Using empirical
modelling and historical trend analysis, Trijonis (1978,1980) concluded that the ambient data
were generally consistent with the consensus of chamber results. The exact form of the
NOp/precursor relationship, however, was found to vary somewhat from one location to another,
presumably depending on local hydrocarbon/NO ratios, on the details of the hydrocarbon mix,
A
and on specific meteorological conditions.
Reference is made also to another body of data due to Pitts et al. (1977) (collected for a
different purpose) which also contains potential information on the relationship between NO
and its precursors. However, the data have not been analyzed to date for its pertinence to
the NO precursor question.
6.1.3 NOX Chemistry in Plumes
The atmospheric chemistry involving oxides of nitrogen in plumes from major fuel burning
installations is essentially that described earlier. However, the relatively high concen-
trations of NO and NO^ in such plumes compared with those in the ambient urban atmosphere leads
to certain chemical phenomena particularly characteristic of plumes. For e^dinpl?, within or a
few exit diameters downwind of a source such as the stack of a power plant or the exhaust
system of a motor vfijn'cte, the relatively high NO concentrations which may be present can pro-
duce NO.- in significant amounts through reaction 6-1 given sufficient Op. As another example,
ambient ozone may be quickly scavenged in the plume by the large quantities of NO through
reaction 6-4. Because the rate of the NO-0., reaction is fast relative to that of dilution of
the plume, the rate of conversion of NO to NO- is controlled by the rate at which ambient 0,^
is entrained into the plume by turbulent mixing (Hegg et al., 1977; Kewley, 1978; Shu et al.,
1978; White, 1977). There is some nitric acid produced in power plant plumes during the day-
light hours through the oxidation of nitric oxide (reaction 6-1) and the subsequent photodisso-
ciation of NO- (reaction 6-2), then followed by the combination of N02 with NO^ and H^O
(reactions 6-10 and 6-8). The generation of nitrous acid is also probable since the stack
gases will contain NO, NOp, and HpO (reaction 6-13). Since nitrous acid will photodissociate
to give hydroxyl radicals (reaction 6-17), more nitric acid can be produced by reaction 6-18.
Thus, although the free radical concentration is expected to b* low in power plant plumes, some
NO will be converted to nitric acid. In addition, after sufficiently long travel times during
6-15
-------
which ambient hydrocarbons have been mixed with the plume constituents, the usual free radical
reactions described earlier occur, possibly leading to 0, production.
There are several studies in which measurements have been made of the concentrations of
pollutants in power plant plumes (Davis et al., 1974; Hegg et al., 1977; White et al., 1976).
The most difficult current problem is predicting the rate at which NO is converted to NOp in
such a plume.
6.1.4 Computer Simulation of Atmospheric Chemistry
A key problem underlying the development and evaluation of kinetic mechanisms for atmos-
pheric chemistry is determining the sensitivity of the concentration predictions to those.un-
certain aspects of the reaction scheme. Such a determination can serve as a valuable guide
for future experimental studies and for identifying those parameters that, when varied within
accepted bounds, will be most influential on the predictions of the mechanism.
Although the qualitative aspects of the chemistry of the polluted troposphere appear to
be reasonably well understood, there are many important details that still need to be investi-
gated before a complete quantitative understanding of the photochemical smog system is possible.
Several groups (Baldwin et al., 1977; Carter et al., 1979; Demerjian et al., 1974; Falls and
Seinfeld, 1978; Whitten and Hogo, 1977) have formulated chemical reaction mechanisms for pol-
luted tropospheric chemistry. Some of these are based on specific surrogate hydrocarbon chem-
istries; in others, attempts have been made to simulate the complex ambient atmospheric system
by representing the general features of the hydrocarbon chemistry. All mechanisms contain
.aspects of uncertainty, whether in unknown rate constants, in the importance of competing re-
action paths, or in the manner of representing the reaction of a generalized species. The
measure of the accuracy of a mechanism is usually based on the extent of agreement between pre-
dicted concentration profiles and those generated experimentally in smog chambers.
With the recent elucidation of the chemistry of the reactions of OH and HOp with NO and
NO-, the inorganic portion of the photochemical smog mechanism is now, by and large, well
understood. Uncertainties remaining include
• photolysis rates
• alkane-OH product distributions
• olefin-OH and olefin-0, product distributions
• aromatic chemistry
• alkoxyl radical reactions
• ROX/NOX reactions
A major uncertainty in the predictions lies in the specification of values of the photo-
lysis rate constants. For analyzing smog chamber data, photolysis rate constants relative to
the reported value for NO- are frequently used. Photolysis rate constants as a function of
wavelength can be calculated from:
co
K, = 2 a.(A)<|>.(\)I(\) d\ (6-45)
J J J
6-16
-------
K- = photolysis rate constant for species j
J
a- (A) = absorption cross section of species j
where
. = quantum yield for the photolysis of species j
I (A.) = actinic irradiance
Data applicable to some atmospheric systems have been compiled by Schere and Demerjian (1977).
For species such as NO-, MONO, and (k, extensive experimental determinations of absorption
cross sections are thought to be fairly reliable. However, since cross section and quantum
yield data for formaldehyde, higher aldehydes, and alkyl nitrites are much less well character-
ized, many photolysis rate constants are subject to a large uncertainty. Of course, even if
absorption cross sections and quantum yields could be determined accurately for all photo-
sensitive species, uncertainties in atmospheric photolysis rate constants would still exist,
as meteorological conditions, clouds, dust, and aerosols cause unknown variances in actinic
irradiance.
Whereas rate constants in the inorganic portion of the mechanism are known fairly well,
many more uncertainties, both in reaction rate constants and products, are associated with the
organic reaction steps. Still to be determined are product distributions and reaction rate
constants for the initial steps of the reactions of OH and hydrocarbon species, the largest
uncertainties lying in the routes of the various radical species produced. For example,
although rate constants for alkane-OH reactions are well established, the ratio of internal to
external abstraction for all alkanes is not known. Addition to Op to form peroxyalkyl (RC^)
radicals can be considered as the sole fate of the alkyl radicals first produced in alkane-OH
reactions, but after the formation of alkoxyl radicals through the conversion of NO to NOp,
the reaction mechanism becomes uncertain. Alkoxyl radicals can decompose, react with Op,
isqmerize, or react with NO or NOp, with the importance and rate of each reaction path depend-
ing on the nature of the alkoxyl group. Even for the most studied of the alkane-OH reactions,
the relative rates between decomposition, isomerization, and reaction with Op, NO, and NOp for
alkoxyl radicals have not been measured, but must be estimated (Baldwin et al . , 1977).
Less well understood than alkane reaction mechanisms are olefin oxidation processes,
primarily by OH. Olefin-OH reactions may proceed by addition or abstraction. For smaller ole-
fins, the addition path predominates. However, the abstraction fraction increases with the
size of the olefin. Along the addition path for terminally bonded olefins, there is uncer-
tainty as to the ratio of internal to external addition. Similar to alkyl radicals, the
hydroxy-alkyl radicals formed in the initial OH addition to olefins are thought to immediately
add Op to form hydroxy- peroxyalkyl radicals and thereafter react with NO to give NOg and
hydroxy-alkoxyl species. The fate of the hydroxy-alkoxyl radicals is subject to speculation,
although the analogous alkoxyl reaction paths of decomposition, isomerization, and reaction
with NO, NO- and Op are most likely possibilities.
The inherent uncertainty of the decomposition, reaction with Op, and isomerization of the
alkoxyl and hydroxy-alkoxyl radicals class can be represented by the generalized reaction step:
RO -» aH02 + (l-cr)R02 + pHCHO + yRCHO (6-46)
6-17
-------
From the earlier discussions of alkoxyl radical behavior, RO always gives rise to either H02
or R02 in any of the decomposition, isomerization, or Op reaction pathways. Hence, the stoi-
chiometric coefficients representing the fraction of HOp and ROp found in the lumped RO reac-
tion should sum to one. Since the RO lumped species represents a large class of different-sized
radicals and because splits between reaction paths for even specific radicals are unknown, a
can have a value in the range 0 to 1. Many RO reaction routes produce aldehydes. Thus, 0 < 0
< 1 and 0 < Y £ 1- Since the composition of the RO radical pool is continually changing during
the course of a photooxidation, the actual values of a, p, and y are functions of time. Thus,
the selection of constant values of these coefficients introduces uncertainty.
A comprehensive sensitivity/uncertainty analysis of photochemical smog mechanisms has been
carried out by Falls et al. (1979). In this study the effects of rate constant and mechanistic un<
tainties on predicted concentrations are illustrated.
6.2 NITRITE AND NITRATE FORMATION
The oxides of nitrogen are converted eventually to nitrites and nitrates by the reactions
given in Section 6.1. In particular, the following gaseous nitrites and nitrates have been
identified:
MONO nitrous acid
HON02 nitric acid
HOpNOp peroxynitric acid
RONO alkyl nitrite
RON02 alkyl nitrate
0
ii
RCOON02 peroxyacylnitrate (PAN)
ROpNOp peroxyalkyl nitrate
In addition to these gaseous species, particulate nitrites and nitrates may be formed. The
object of this section is to present estimates of the importance of the various nitrites and
nitrates. In most cases, estimates are necessary'because ambient measurements of the concen-
tration level of all but a very few of the species are lacking.
Typical ambient concentration levels of the gaseous nitrogen-containing species listed
above can be estimated from simulations of smog chamber experiments using chemical mechanisms
representing the hydrocarbon-NO chemistry. Table 6-3 lists calculated, concentrations of MONO,
HON02, H02N02, RONO, RON02, RC.(0)OON02, and R02N02 for smog chamber experiment EC-237 carried
out at the Statewide Air Pollution Research Center of the University of California, Riverside,
using the chemical mechanism of Falls and Seinfeld (1978). The conditions of the experiment
are given in the footnote of Table 6-3. The simulated and predicted concentrations of the
major measured species, such as NO, NO, 0,., PAN, and hydrocarbons, agreed well.
6-18
-------
TABLE 6-3. PREDICTED NITRITE AND NITRATE CONCENTRATIONS IN SIMULATION OF
EXPERIMENT EC-237 OF THE STATEWIDE AIR POLLUTION RESEARCH CENTER OF
UNIVERSITY OF CALIFORNIA, RIVERSIDE, USING THE
CHEMICAL MECHANISM OF FALLS AND SEINFELD (1978)
HONO
HON02
H02N02
RONO
RON02
0
RCOON02
on MO
i\U rtliU f\
60 min.
0.0061
0.067
0.00083
0.0030
0.0041
0.025
0.034
Concentration
180 min.
0.00040
0.22
0.0019
0.00054
0.0070
0.089
0.075
, ppm
300 min.
0.00036
0.29
0.0025
0.000080
0.0072
0.13
0.098
Conditions of the experiment: T = 3Q3°K, k, = 0.3
[NO] = 0.377, [H«0] = 2.4 x 10*. [C0]^= 0.96
[Alkanes] = 1.488, [Non-ethylene Olefins] =
[Aromatic?] = 0.177, [HONO] (assumed}-^ 8.1
ppm). Dilution rate = 2.93 8 10 min .
min , [NO,] = 0.106,
, [Aldehydes]0 = 0.0012,
0.15, [C2HJ° = 0.875,
(All concentrations in
The concentrations of HONO, H02N02, and RONO are predicted to be small relative to those
of NO and N0?. Each of these species has decomposition reactions,
HONO + hv -» OH- + NO (6-17)
H02N02 •+ H02- + N02 (6-36)
RONO + hv -> RO- + NO (6-47)
that, at the temperatures and solar intensities prevalent in the experiment and in the summer
atmosphere, are fast enough to insure that the concentrations of each of the three species are
low. At lower solar intensities than those in the experiment, HONO and RONO can be expected
to reach higher concentrations, and at lower temperatures, such as those in the stratosphere,
H02N02 may accumulate.
Under daytime conditions the reactions that govern the concentration of HONO are 6-17 and
6-19. At night, however, the only apparent destruction route for HONO is reaction 6-14.
Depending on the relative importance of reactions 6-19, 6-13, and 6-14, HONO may reach sub-
stantial concentrations under nighttime conditions. A lower limit on the nighttime concen-
tration of HONO can be estimated from the equilibrium HONO concentration based on reactions
6-13 and 6-14.
6-19
-------
K13[NO][N02][H20]
[MONO] = ; k^ (6-48)
At [NO] = [NO,] =0.1 ppm, [H,0] = 2.4 x 104 ppm (50 percent relative humidity), the equili-
-?
brium MONO concentration calculated from equation 6-48 is 1.9 x 10 ppm.
Like MONO, H02N02 and RONO, PAN undergoes both formation and decomposition steps (reac-
tions 6-42a,b). Unlike these former species, however, the balance between the formation and
decomposition reactions is such that PAN may achieve appreciable concentration levels relative
to those of NO and NO,,. Because the decomposition reaction for PAN is strongly temperature
dependent, the steady state PAN concentration is highly dependent on the temperature. As
temperature increases the role of PAN as an N02 sink decreases markedly; at low temperatures,
on the other hand, steady state PAN concentrations can reach rather substantial levels.
Little is known about the existence and importance of peroxynitrates other than HO^NO-,
and PAN. It was presumed in the mechanism on which the results of Table 6-3 are based that
R02N02 thermally decomposes at a rate between those for HO?NO? and PAN. Assessment of the
importance of R02N02 as a sink for NO will depend on measurement of the rates of reactions
6-40 and 6-41.
In contrast to the other species of Table 6-3, nitric acid and alkyl nitrates apparently
do not undergo appreciable decomposition reactions. Thus, these two species potentially serve
as important atmospheric sinks for N02. Both nitric acid and alkyl nitrates may remain in the
gas phase or react with other atmospheric constituents, such as ammonia, to produce low vapor
pressure species that have a tendency to condense on existing particles or homogeneously
nude ate to form particles.
Figure 6-1 depicts the potential paths by which particulate nitrate species may be formed
from NO and N0?. Path 1 involves the formation of gaseous nitric acid by reactions 6-8 and
6-18. Nitric acid concentrations resulting from these two reactions for the simulated smog
chamber experiment have been given in Table 6-3. Comparisons of the individual rates of reac-
tions 6-8 and 6-18 indicate that reaction 6-18 is the predominant route for gas-phase nitric
acid formation under typical daytime conditions. Nitric acid vapor, once formed, may then
react with NH,, a ubiquitous atmospheric constituent with both natural and anthropogenic
sources, to produce ammonium nitrate, NH.NO, (path 2), which at standard temperature and pres-
sure, exists as a solid. Alternatively, the nitric acid vapor may tie absorbed directly into a
particle (path 3), although thermodynamic and kinetic considerations favor reaction with NH^
to form NH.N03 as the path of conversion of gaseous nitric acid to nitrate in particulate form
(Brandner et al., 1962; Morris and Niki, 1971; Stelson et al., 1979). Path 4 involves the
direct absorption of NO and N02 into an atmospheric particle, a route that is likely for
certain aqueous particles, particularly when accompanied by the absorption of ammonia (path 5)
(Orel and Seinfeld, 1977). Path 6 depicts the formation of organic nitrates through reactions
6-20
-------
|OH,,HO2, H2OJ
Figure 6-1. Paths of nitrate formation in the atmosphere
(Orel and Seinfeld, 1977).
6-21
-------
such as 6-38a, followed by absorption of these nitrates into particles. At present little is
known about the existence or importance of mechanisms such as that depicted by path 6.
There have been a number of measurements of nitric acid and particulate nitrate concen-
trations in ambient air, and several of these are summarized in Chapter 8. Many of the measure-
ments have identified the particulate nitrate as NH.NO,, suggesting that the aerosol may consist
+
of solid NH^NOg or NH4 and N0"3 in solution in approximate stoichiometric balance. It is diffi-
cult to estimate the relative importance of the paths in Figure 6-1 for several reasons. First,
the rate of reaction of nitric acid and ammonia is not well known, although the forward reac-
tion is probably rapid and, in fact, can be presumed to be in equilibrium with the dissociation
of solid ammonium nitrate (Brandner et al., 1962; Morris and Niki, 1971; Stelson et al . , 1979).
NH3(g), + HON02(g) JNH4N0 (6-49)
Second, the rate of absorption of NO and NO- into existing particles depends on the composition
and size of each particle and cannot generally be predicted a priori. In either case it is
apparent that the presence pf NH3 is required, either to form NH.NO, or to neutralize the
acidity of a liquid droplet in which NO and N0? dissolve.
The current state of understanding of atmospheric inorganic nitrate formation can be sum-
marized as follows. The principal gas-phase nitrate forming reaction is reaction 6-18. The
nitric acid vapor formed in reaction 6-18 probably reacts rapidly with ammonia to form small
particles of solid ammonium nitrate such that the equilibrium of reaction 6-49 is established.
In competition with the nitric acid/ammonium nitrate path is the path consisting of direct
absorption of NO and N0~ into aqueous droplets. The relative rates of these two paths cannot
be determined in general. Although measurements of particulate organic nitrate levels have
been reported (Grosjean and Friedlander, 1980), the mechanisms of formation of organic aerosol
nitrates have not been fully identified.
6.3 TRANSPORT AND REMOVAL OF NITROGENOUS SPECIES
The general behavior of nitrogenous species in the atmosphere can be described as follows.
Nitric oxide emissions are converted partially to nitrogen dioxide within the urban atmosphere
as a result of gas-phase reactions. Simultaneously, NO,, is converted to nitric acid vapor and
NO and NO- may also be absorbed into existing particles. The mixture of gases and particles
is transported downwind of the source region, accompanied by continuous conversion of more of
the NO gases to particulate nitrates. Also occurring simultaneously is surface absorption of
NO and NO- as well as of particles containing nitrate. Eventually, rainout and washout serve
to remove more of the remaining gases and particles.
The object of studying the transport and removal processes of nitrogenous species is to
develop the capability to predict the atmospheric residence time of nitrogenous species as they
are transported downwind from a source-rich area. Several recent studies have been reported
in which measurements (usually airborne) have been carried out downwind of large urban com-
plexes in order to obtain material balances on gaseous and particulate pollutants (Breeding et
6-22
-------
al., 1976; Stampfer and Anderson, 1975). A goal of these studies is to determine the relative
roles of transport, removal and conversion of gaseous to particulate pollutants on the overall
pollutant material balance downwind of a major urban source. On the basis of the previous dis-
cussion in this section it is possible to make rough estimates of the relative roles of these
processes in determining the ultimate fate of nitrogenous species.
In the quantitative analysis of urban plume data, it is necessary to have a mathematical
model capable of describing the behavior of both gaseous and particulate pollutants and their
interrelations. Such a model would, in principle, include both gaseous and particulate phases
with detailed treatments of gas-phase and particulate-phase chemistry, as well as size distri-
butions of the particles.
There currently exist a number of mathematical models capable of relating emissions of
primary gaseous species to airborne concentration levels of both primary and secondary gaseous
pollutants. The models include details of atmospheric chemistry and meteorology and have been
exercised in a variety of situations. Models that relate emissions of primary and secondary
gaseous and particulate pollutants, including description of particle size distribution and
chemical composition, are currently under development and not yet available for general use.
In view of this, a "first-order" model that contains all the major mechanisms influencing the
airborne concentrations of gaseous and particulate pollutants can be formulated, one that does
not include details of atmospheric chemistry and particle size distribution, but treats the
competing processes of advection, turbulent diffusion, conversion of gaseous species to partic-
ulate material, settling, deposition, washout and rainout. Such a "first-order" model is in
essence a material balance, designed to provide estimates of the fraction of pollutants that
still remains airborne at a certain distance downwind of the source and the fraction that has
been removed by deposition and gas-to-particle conversion. A model of this type has been
developed by Peterson and Seinfeld (1977) and applied to the prediction of airborne concen-
trations of gaseous and particulate pollutants in the case in which gases are converted to
secondary particulate matter. Although the model of Peterson and Seinfeld is a quantitative
framework within which to evaluate each of these effects, at this time only qualitative esti-
mates for nitrogen-containing species are possible because of lack of knowledge of the relevant
rates and coefficients for such a model. The execution of experimental measurements in urban
plumes and correlation with physical and chemical rate data to predict fractions of nitrogenous
species that are removed by various paths has yet to be performed. See Section 6.3.3 for
further discussion.
In this section the general nature of the transport and removal of nitrogeneous species
is briefly discussed.
6.3.1 Transport and Diffusion
Some atmospheric processes play an important role in the dispersion of air pollutants on
large spatial scales, and others are important on small spatial scales. The interactions amonc
these processes, and their overlapping influences on eventual pollutant distributions, are very
6-23
-------
complex. A classical example, shown in Figure 6-2, is the effect of atmospheric turbulence of
different scales on pollutant transport and dispersion.
The spatial and temporal scales of interest to the long-range transport of nitrogenous
and other pollutant species are on the order of several hundred kilometers and several days.
As shown in Figure 6-2, the atmospheric motions important on these scales range from mesoscale
convection to synoptic-scale cyclonic waves.
Changes of wind speed and direction in the lowest layer of the atmosphere are the result
of many competing physical processes. The interaction between the synoptic-scale air motion
and the surface boundary layer usually produces complex flow patterns. These patterns change
hourly, daily and seasonally. They also vary spatially, especially where terrain is nonuni-
form and the heating or cooling of the surface is inhomogeneous. Vertical air motions result
from divergence in synoptic and mesoscale wind flow. They are also produced by viscous and
frictional forces in the boundary layer and can be particularly large and highly variable in
regions of complex terrain. Although vertical velocities generated by these processes have a
magnitude of only 1-10 centimeters per second, which is 1-2 orders of magnitude less than
generally observed horizontal wind speeds near the surface, they have significant effects on
the net transport and dispersion of air pollutants. Accurate estimates of the vertical com-
ponents of the wind vectors are extremely difficult to obtain on a routine basis, particularly
in the first few hundred meters of the surface. Further, they vary drastically with horizontal
wind speed and the radiation balance of the surface. While vertical diffusion is dominant
generally in the first 10 to 30 km away from the source, lateral (or horizontal) diffusion
becomes important in pollutant transport over large distances. Vertical diffusion in the tro-
posphere is limited to about 10 km in mid-latitudes while the lateral transport eventually
varies through 360 degrees.
6.3.2 Removal Processes
The atmospheric residence times of nitrogenous species (lifetimes) are of the order of
days to weeks, while their inter-specie lifetimes (chemical transformation) might only be as
short as fractions of a second.
Atmospheric residence times are governed by the efficiency with which species are removed
from the atmosphere. The removal (or cleansing) efficiency depends considerably on the
specific physical and chemical nature of the species. For example, NO, N02, and HN03 are
removed within clouds and/or by rain with different efficiencies due to the different solu-
bility and vapor pressure characteristics of the three gases.
There are two types of removal processes that occur in the atmosphere:
• dry deposition
• precipitations scavenging (wet deposition)
Mathematical models capable of describing the behavior of both gaseous and particulate pollu-
tants must include removal terms, particularly for the important nitrogenous species, such as
nitric acid and nitrate aerosol.
6-24
-------
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Figure 6-2. Schematic illustration of scales of motion in the atmosphere.
6-25
-------
6.3.2.1 Dry Deposition of Gases—Gaseous nitrogeneous species are removed from the atmosphere
by surface absorption, so-called deposition. The rate at which an airborne species of concen-
tration c.j (micrograms per cubic meter) is removed across a horizontal surface of unit area at
an elevation z is often expressed as c.^. where v^ is the so-called "deposition velocity,"
which depends on the value of z .
Vegetation has been shown capable of removing significant amounts of N0~ and NO from the
atmosphere. Tingey (1968) showed that alfalfa and oats absorbed NO, from the air in excess of
~12
100 x 10 moles per square meter per second when exposed to an atmosphere containing 460
ug/m NOp (or 1 x 10 moles per cubic meter). More recent work by Rogers et al. (1977), using
a continuous reactor technique, indicated that the N0« uptake in both corn (Zea mays 1.) and
soybean (Glycine max. L.) could be well represented by a chemical kinetic model having two
reactants, the pollutant and the leaf surface. The second order rate constant for N02 uptake
was independent of NO^ concentrations and leaf surface area, but directly dependent upon
inverse total diffusion resistance. Tingey (1968) extrapolated his data to estimate the
removal of NO, from the Salt Lake Valley in Utah. On an annual basis, removal of NO, from the
3
valley with an ambient NO, concentration of 9.6 ug/m (0.005 ppm), which is about 3-4 times
£ c
greater than background NO, levels, would total about 3 x 10 kg NO,. This may be compared
9
with an estimated total global anthropogenic annual N02 emissions of 53 x 10 kg (Robinson and
Robbins, 1970).
Hill (1971) found in his experiments on the uptake rate of gases by an alfalfa canopy that
NO was absorbed with a deposition velocity of 0.1 cm/sec and NO, was absorbed at a velocity of
3
2 cm/sec when present in the air of the chamber at a concentration of 96 ug/m (0.05 ppm).
Using ambient NO,, concentrations found in those areas of Southern California from August to
October of 1968, and assuming a continuous alfalfa cover, Hill estimated that NO, could be .
2
removed at a rate of 0.1 gram/m /day.
Nitrogen oxides (especially N?0) have long been known to be produced by biological action
in soils. Recently, however, Abeles et al. (1971) found that soils could absorb N02 from the
atmosphere as well. They found that when air containing NO, was passed over soil in a test
3
chamber, the concentration of NO, in the air was reduced from an initial value of 190 x 10
3 33
ug/m (100 ppm) to 5.7 x 10 ug/m (3.0 ppm) over a 24-hour period. When soil was autoclaved,
3 3
the total NO, present over the same time period was reduced from 186 x 10 ug/m (97 ppm) to
4 -
only 25 x 10 pg/m (13 ppm). This result would point to a biological sink for NOp in soils.
Ghiorse and Alexander (1976), however, report finding essentially no difference in N02 removal
by soil from air in a closed system when their soil (Lima loam) was either nonsterile, auto-
claved or y-irradiated. The authors point out that autoclaving may drastically alter the phy-
sical and chemical properties of soil and thus introduce artifacts in such studies. They con-
clude that the role of microorganisms in the fate of N0~ in soils is not so much in sorption
but in conversion of nitrite (resulting from such sorption) into nitrate.
Nitric oxide may be absorbed by soils, but is then oxidized almost immediately to NOp.
Mortland (1965) has noted that transition metal ions in the soil promote NO absorption. If
6-26
-------
the soil is saturated with alkaline earth cations though, absorption of NO is halted.
Sundareson et al. (1967) found that alkaline-earth zeolites readily absorb NO and release it
as NO and HMO, when heated. To date, the role of organic matter in the absorption of nitroge
X
-------
The capture of gases and particles by falling raindrops is called washout. Typically,
the duration of washout is relatively short compared with that of rainout. However, pollutant
concentrations at the cloud level are frequently much lower than those near the ground where
washout occurs. Thus, rainout and washout can be of similar importance. The uptake of NO by
1 A
rain depends on physical parameters such as rainfall intensities and raindrop size distri
butions, and on the chemical composition of the raindrops. Models of washout generally reduce
to two limiting cases, mass-transfer-limited and chemical-reaction limited. In the former,
the rate controlling step for absorption is the diffusion of the gases to the falling drop; in
the latter, chemical equilibrium in the drop controls the quantity absorbed. The study of Dana
et al. (1975) suggests that for SCL under typical atmospheric conditions washout is often mass-
transfer-limited. Similar studies for washout of NO have yet to be performed.
6.3.3 Source-Receptor Relationships
The previous sections of this chapter have addressed the scientific basis for our current
understanding of the atmospheric chemical processes describing the transformation of NO, which
is the dominant N0x compound emitted by most sources, into the more toxic N02> and its subse-
quent further transformation, transport and removal. This section addresses the question of
predicting the N02 concentration experienced by a receptor, such as a human being, due to given
emissions of NO (see Chapter 5). Methodology for estimating human exposure using ambient con
centration data derived from fixed monitoring sites is discussed in Chapter 8.
Until very recently, the problem of predicting N0? concentrations has received little
attention in the literature. However, relationships among ambient nitrogen oxides, hydrocar-
bons (HC) and ozone/oxidant (0 ) have been considered in connection with the question of pre-
dicting ambient ozone concentrations (U.S. EPA, 1978). Some of the methodology applicable to
the ozone problem has potential usefulness in the case of NO source-receptor relationships.
A
In this regard two very recent reviews are available (Cole and Summerhays, 1979; Anderson et
al., 1978). In addition, a critical review of atmospheric modeling has also been published
(Turner, 1979).
Relationships between emissions and 0 /NO -related air quality have been pursued following
three distinct approaches that differ mainly in degree of empiricism. In order of decreasing
empiricism, these approaches are as follows:
(1) Empirical Approach. This approach entails statistically or
nonstatistically associating ambient air quality data either with
ambient concentrations of precursors or with precursor emission
rates. These associations are clearly not cause-effect in nature,
and their intended use is not to predict absolute air quality;
rather, it is to estimate changes in air quality resulting from
changes in emission rates.
(2) Mechanistic Models of 0 /HC/NO . This approach entails deriving
cause-effect relationships between oxidant and precursors through
laboratory testing and chemical mechanistic simulations. As in
the preceding case, this approach is intended to predict only
changes in air quality resulting from changes in emission rates.
6-28
-------
(3) Air Quality Simulation Model (AQSM) Approach. This approach
entails deriving the requisite air quality-emission relationships
through mathematical representation of the transport, dispersion,
transformation, and deposition processes. Its intended use is to
predict absolute levels of air quality from given emission rates
and meteorological data.
The air quality-emissions relationships or "models" developed to date through all these
approaches are applicable only to the urban problem, or to situations in which the geographi-
cal dimension of the source-receptor relationship is comparable to that of the urban area.
Techniques for estimating short-term N02 concentrations arising from point sources alone have
been discussed by Cole and Summerhays (1979).
Since the first two approaches predict only changes in air quality resulting from changes
in emission rates rather than absolute levels of air quality, their utility lies mostly in the
technical area of air quality management. The third approach is most pertinent to the dis-
cussion in this section.
If predictions from AQSM models could be made reliably and with a reasonable effort, it
would be possible, e.g., to:
• Determine the impact of different source types and/or individual
sources upon absolute air quality.
• Augment ambient monitoring data with calculated data at points
intermediate to the limited number of monitoring sites practically
available. Such new data would be useful in a number of appli-
cations including the location of "hot spots" and the estimation
of human exposure to NCL concentrations.
Assessment of the specific impacts on air quality of the various source types in the NOp
problem requires consideration of such parameters as local pollutant sources and/or concen-
trations, meteorology, and topography, all of which vary from area to area. Development and
validation of AQSM models applicable to the N02 problem, currently underway at U.S. EPA and
elsewhere, have reached a stage where it is now becoming possible to evaluate their usefulness
and accuracy. At the present time, however, the literature contains little documentation of
specific applications of AQSMs. For this reason, a meaningful discussion of source impacts on
air quality could not be included in this document.
In general, the utility of model types for the above purposes depends not only on the com-
pleteness with which they describe the chemical and physical processes characterizing the NO^
problem, but also on the type of situation to be modelled. For example, prediction of N02 con-
centrations very close to a highway in the absence of all other NO sources except lines of
mobile vehicles might, for practical purposes, be made using a model which did not take into
account the free radical chemistry described previously since these reactions would probably
not have time to occur. On the other hand, prediction of N0? concentrations on an urban scale
resulting from a combination of point and area sources would probably require consideration of
the complex chemistry reviewed in this chapter.
6-29
-------
In summary, it may be stated that the prospects for estimating NOp concentrations at local
receptor points are quite promising but it is not possible to estimate reliably their accuracy
or usefulness based on currently reported applications.
6.4 MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION
This section is limited to a discussion of specific reactions possibly leading to the for-
mation of nitrosamines and related compounds in the atmosphere.
Three mechanisms will be discussed in this section:
• Non-photochemical reactions of gaseous amines with oxides of nitrogen and nitrous
acid
• Photochemical reactions of amines with oxides of nitrogen in the gas phase
• Heterogenous nitrosamine formation processes in atmospheric aerosols
The first two processes have been the object of recent experimental studies, including simu-
lation experiments in environmental chambers, and will be examined in some detail. The third
process involving aerosol particles is purely speculative at this time and will be briefly dis-
cussed in terms of the corresponding evidence in the bulk (liquid) phase.
6.4.1 Non-Photochemical Reaction of Gaseous Amines with Oxides of Nitrogen and Nitrous Acid
Bretschneider and Matz (1973,1976) reported the fast formation of diethylnitrosamine
(DENA) when reacting 50-100 ppm of diethylamine and nitrogen dioxide. DENA formed within
seconds and was reportedly stable for weeks in the dark in the glass reaction vessel. Dimethyl-
nitrosamine was formed in the same way from dimethylamine and N02. The authors also report
that nitrosamine formation can be catalyzed by S02.
A fast reaction between diethylamine and N02 was also reported by Gehlert and Rolle (1977),
who achieved in a few minutes a 90 percent conversion to diethylnitrosamine at 25°C. They pro-
posed the following rate equation:
-d(N09)/dt - k (dimethylamine) (NO,)2 (6-51)
82-21
with a rate constant k^-, = 6.5 x 10 S, Mol s . Initial reactant concentrations ranged
-6 5 -I
from 4 x 10 to 6 x 10 Mol £ . The other major product of the reaction was the amine
nitrate (aerosol), corresponding to the overall equation:
2 N02 + 2(C2H5)2NH -» (C2H5)2NNO + (C2H5)2NH2N03 (6-52)
Neurath and co-workers (1965,1976) investigated the effect of adding several amines on
the thermal oxidation of nitric oxide to nitrogen dioxide in the presence of 10 percent oxygen.
Addition of secondary amines (dimethyl, diethyl, methyl -n-butyl, and pyrrolidine) doubled the
rate of NO oxidation, presumably due to nitrosamine formation:
NO + N02 -> N203 (6-53)
N203 + 2 R2NH -> 2 R2NNO + H20 (6-54)
where R = alkyl group. Addition of tertiary amines (trimethyl, diethyl-methyl, and N-methyl
pyrrolidine) also increased the NO oxidation rate, thus indicating that tertiary amine also
reacted with the oxides of nitrogen under these conditions. The reactions of dimethylamine
6-30
-------
and d i ethyl ami ne with NO in the presence of 10 percent oxygen were also followed by directly
measuring the (decreasing) amine concentration. No reaction was observed between diethylamine
and NO in nitrogen.
Dushumin and Sopach (1976) also report a rapid reaction between dimethylamine, N^O^ (in
equilibrium with NOp) and ozone to form dimethylnitrosamine with a 50 percent conversion
achieved in less than 10 minutes. Since other reaction products included formaldehyde (HCHO)
and dimethylnitramine [(CHO-NNO^], it is suspected that photochemical reactions took place as
well, as is discussed in the next sub-section (6.4.2). Field measurements were performed near
a chemical complex, and dimethylnitrosamine was found in the frost near the complex as well as
in the air up to 30 kilometers from the complex.
In complete contrast with the above studies, low yields of nitrosamines were obtained by
Hanst et al. (1977), Grosjean et al. (1978), and Pitts et al. (1978) in experiments involving
dark reactions of ppm levels of alkylamines and nitrogen oxides in humid air.
Hanst et al. (1977), using long path infrared spectroscopy, followed the reaction of 1
ppm dimethyl amine with 0.5 ppm HOMO (in equilibrium with 2 ppm NO, 2 ppm N0~ and 13,000 ppm
water vapor) in air in a 9 x 0.3 m diameter cylindrical glass cell. Dimethylnitrosamine was
formed in yields of 10 to 30 percent, and the rate of amine disappearance was ~4 percent min .
Grosjean et al. (1978) and Pitts et al. (1978) also report low yields of nitrosamine in
the dark reaction of ~0.5 ppm amine with 0.8 ppm NO and 0.16 ppm NO, in air at 30 percent
3
relative humidity in 50 m Teflon chambers. Nitrosamine yields were 2.8 percent from diethyla-
mine and ^1 percent from dimethylamine. The tertiary amine triethylamine also yielded diethyl-
nitrosamine (0.8 percent yield), while trimethylamine yielded traces of dimethylnitrosamine.
For all four amines the nitrosamines were the only gas phase products found after 2 hours of
reaction in the dark. Light-scattering aerosols were also formed.
Assuming a bimolecular reaction between the amine and nitrous acid, and using the nitrous
acid equilibrium constant of Chan et al. (1976), Hanst et al. (1977) estimated an amine dis-
appearance rate of 0.8 ppm min . This would constitute an upper limit for nitrosamine forma-
tion since (a) the nitrosamine yield is not necessarily 100 percent of the reacted amine, (b)
some of the amine may be lost on the walls of the reaction vessel rather than by chemical reac-
tion, and (c) nitrous acid formation may be controlled by heterogeneous rather than homo-
geneous processes.
With respect to the latter, Cox and Derwent (1976) reported decomposition of 150 ppm
HONO at a rate of 10 to 15 ppm hr , i.e., "*• 200 times slower than the rate predicted using
the data of Chan, et al. More recently, Kaiser and Wu (1977) reinvestigated the kinetics of
formation and decomposition of nitrous acid:
NO + N02 + H20 -» 2 HONO (6-55)
2 HONO •* NO + N02 + H20 (6-56)
6-31
-------
They found the reactions to be heterogeneous under all surface conditions tested. They also
estimated upper limits for the homogeneous rate constants:
kx < 4.4 x 10"40 cm6 molecule"2 s"1
k2 < 1 x 10"20 cm3 molecule"1 s"1
which are more than 100 times slower than those of Chan et al. (1976). Thus, homogeneous (gas
phase) formation of nitrous acid seems too slow to account for HONO formation in the studies
of Hanst at al. (1977) and Grosjean et al. (1978), and heterogeneous formation (being itself
very slow) may account for the low nitrosamine yields reported by these authors. Pitts et al.
(1978) also note that the observed formation of nitrosamines from tertiary amines, for which
no gas phase mechanism could be proposed, may be entirely heterogeneous. Such processes for
the formation of nitrosamines from tertiary amines have been well documented in the bulk
(liquid) phase (Ohshima and Kawabata, 1978; Smith and Loeppky, 1967).
Finally, it should be noted that the accepted mechanism for the liquid phase nitrosation
of secondary amines involves N203 (Mirvish, 1975; Ridd, 1961; Scanlan, 1975) according to the
reactions:
2 HONO j N203 + H20 (6-57)
N203 + R2NH -» R2NNO + HONO (6-58)
and that the corresponding rate of nitrosation, r = k (amine) (HONO) , may apply to the studies
of Hanst and of Pitts and Grosjean in which HONO formation seems to be controlled by hetero-
geneous processes. The mechanisms of Gehlert and Rolle (1977) and Neurath et al. (1976) for
the gas phase reaction also involve N,,03 (or NO and NO-). Furthermore, Hanst et al. (1977)
reported that the amine disappearance rate in a mixture containing 1 ppm dimethylamine, 4 ppm
NO, and 1 ppm N02 in dry nitrogen (i.e., under conditions notjconducive to the formation of
nitrous acid) was comparable to that measured in the amine-HONO-NO -water mixture in air (1
-1 -1
percent min and 4 percent min , respectively). Thus, the conflicting evidence currently
available does not permit firm conclusions regarding the rates, yields and mechanisms of nitro-
samine formation from amines and oxides of nitrogen in the dark.
6.4.2 Photochemical Reactions of Amines
In the smog chamber experiments described in the previous section (Grosjean et al., 1978;
Pitts et al. , 1978), amine-NO -air mixtures were also exposed to sunlight for -\-2 hours.
Diethyl-and triethylamine reacted rapidly to form ozone, peroxyacetylnitrate (PAN) and acetal-
dehyde as the major gas phase products, as well as light scattering aerosols consisting
essentially of the amine nitrates. Several other products were formed in the gas phase includ-
ing diethylnitramine [(CjHrJ-NNO^] and several ethyl substituted amides. These products and
the corresponding yields are listed in Table 6-4.
Irradiation of dimethylamine and trimethylamine under the same conditions yielded ozone,
formaldehyde, dimethylnitramine [(CH-O^NNO-J and several methyl substituted amides in the gas
phase as well as aerosol products (Pitts et al., 1978). Reaction products of dimethylamine
that have also been identified by other investigators include formaldehyde (Dushumin and
6-32
-------
TABLE 6-4. MAXIMUM CONCENTRATIONS AND YIELDS OF THE PRODUCTS OF
DIETHYLAMINE AND TRIETHYLAMINE (GROSJEAN ET AL., 1978; PITTS ET AL. , 1978)
cr>
i
co
CO
Product
GAS PHASE
Ozone
Acetaldehyde
PAN
GAS PHASE (by GC-MS)
Dark
Diethyl ni trosami ne
Sunl ight
Die.thylni trosami nec
Diethyl ni trami ne
Diethyl formamide
Diethylacetamide
Ethylacetamide
Unidentified, MW=87d
Diacetamide
From (C0H5)0NH
Molar
Maximum Conversion
Concentration Yield,
Formula ug/m3 ppb %
03 290
CH^CHO 300 30b
h
CH3CO-OON02 41 4
(C2H5)2NNO 59 14 2.8
(C?Hr)?NNO (destroyed)
(C2H5)2NN02 780 162 32
(C2H5)2NCHO 29 7.0 1.4
(C2H5) NCOCH 3.6 0.8 0.2
C2H5NHCOCH3 42 12 2.4
--
(CH3CO)2NH
Maximum
From
Concentration
ug/m3
17
38
177
178
15
48
41
trace
ppb
260
700
72
4.1
9.1
37
43
3.2
13
12
(C0H ) N
Mol ar
Conversion
Yield,
%a
47b
5b
0.8
1.8
7.4
8.6
0.6
2.6
2.4
(continued)
-------
TABLE 6-4. (continued)
Product
AEROSOL PHASE6
Sunlight
b . (maximum value)
sea L
TSP
Acetamide
Di ethyl hydroxyl ami ne
Nitrates
Fv^rvm t C 9 R ' 9
Maximum
Concentration
Formula ug/m ppb
4 x 10'V1
60
CH3CONH2 3
(C9H,-),NOH
L. -J L.
NO^ 42
NH From
Molar
Conversion Maximum
Yield, Concentration
% ug/m ppb
46 x 10'V1
370
0.2 8.7
7.6
158
(C0H,)0N
Molar
Conversion
Yield,
%d
0.7
0.4
Initial amine concentrations =0.5 ppm (calculated from amount injected).
Taking into account the number of ethyl groups in DEA and TEA.
GNot corrected for artifact formation (maximum ~ 10% of the observed concentration).
Assuming same mass spectrometer response as diethylacetamide.
"Based on volumes sampled:
27.9 m3 (DEA) and 30.8 m3 (TEA).
-------
Sopach, 1976; Hanst et al., 1977), dimethylnitramine (Dushumin and Sopach, 1976; Tuazon et al.,
1978), and the amine nitrate aerosol (Dushumin and Sopach, 1976; Gehlert and Rolle, 1977).
In the experiments conducted with secondary amines (diethyl and dimethyl), the nitrosamine
formed in the dark was progressively destroyed in sunlight, as was reported before for dimethyl-
nitrosamine (Bretschneider and Matz, 1973,1976; Hanst et al., 1977) and diethylnitrosamine
(Bretschneider and Matz, 1973,1976). In contrast, the concentration of diethylnitrosamine
formed in the dark from the tertiary amine, triethylamine, increased upon irradiation for ^ 60
minutes, reaching a level about 3 times its average concentration in the dark prior to being
destroyed upon further exposure to sunlight (Figure 6-3).
The mechanism proposed by the authors (Grosjean et al., 1978; Pitts et al., 1978) involves
hydroxyl radical (OH) abstraction on a secondary C-H bond to produce an alkyl radical, as shown
here for triethylamine:
(C2H5)3N + OH -» (C2H5)2NCHCH3 , (6-59)
followed by the well-known sequence R + 0 ^ RO , RO + NO •* NO + RO (Demerjian et al., 1974.
The alkoxy radical RO then decomposes to give two of the major products, acetaldehyde and
di ethylacetami de:
0
(C-H,.)., NCHCH, -» CH,CHO (C.HjJl (6-60)
c b 1. J a e. b i
-> (C H ^ NPHO + f*H ffi-fi"l^
Further reactions of acetaldehyde lead to PAN, another major product. The diethylamino
radical, (C2Hr)2N, reacts with NO and N02 to form diethylnitrosamine and diethylnitramine,
respectively:
(C2H5)2N NO •* (C2H5)2NNO (6-62)
(C2H5)2N N02 -»• (C2H5)2NN02 (6-63)
It is assumed, by analogy with the simplest dialkylamino radical, NH2, that reaction of
(C2Hc)2N with oxygen is very slow [this has received confirmation very recently in the case of
NH2 (Lesclaux and Demissy, 1978)].
A recent study by Calvert et al. (1978) of the photolysis of dimethylnitrosamine has shown
that the dimethylamine radical, (CH.,)0N, can react with NO almost 10 times faster than with
7
02 and with N02 approximately 10 times faster than with 0?. Nitrous acid and CH3N=CH2 were
also identified as major products. These results suggest that dimethylamine radicals formed
in a NO-N02-polluted atmosphere have a good chance of forming nitrosamines and nitramines even
though the concentrations of NO and N02 are very small when compared to the amount of molecular
oxygen present.
In the case of the secondary amine, diethylamine, the larger nitramine yield indicates
that the diethylamine radical is also produced by other reactions, including OH abstraction on
the N-H bond:
(C2H5)2NH + OH -> (C2H5)2N + H20 (6-64)
Rate constants for the OH-amine reaction have been measured recently (Atkinson et al. ,
1977,1978) and are consistent with both N-H and C-H abstraction. Alkylamines react quite
6-35
-------
5
<
CO
O.
LU
E
TIME, hours
DARK
SUNLIGHT
Figure 6-3. Formation and decay of diethylnitrosamine, in the dark
and in sunlight, from diethylnitrosamine (open squares) and from
triethylamine (open circles)(Pitts et al, 1978).
6-36
-------
rapidly with OH, with atmospheric half-lives of 2-3 hours at typical OH concentrations in the
lower troposphere (Atkinson et al., 1978).
The efficient formation and accumulation of nitramines (reaction 6-63) is due to their
stability in sunlight (Grosjean et al., 1978; Pitts et al., 1978). In contrast, nitrosamines
photodecompose readily:
hv
R2NNO -» R2N + NO (6-65)
and their concentration in sunlight is dicated by the competing reactions 6-62 and 6-65.
Results shown in Figure 6-3 for triethylamine indicate that photochemical formation (reaction
6-62) may prevail upon photodecomposition during daytime under certain conditions, in contra-
diction with the generally accepted idea that any nitrosamine present at night in the atmosphere
should be rapidly destroyed after sunrise (U.S. EPA, 1977; Hanst et al., 1977). Processes
other than photodecomposition, such as direct oxidation of nitrosamines to nitramines by ozone
or other oxidizing species, have not been investigated.
6.4.3 Formation of Nitrosamine in Atmospheric Aerosols
Heterogeneous formation in acid aerosols has been suggested (U.S. EPA, 1976) as a pos-
sible mechanism for nitrosamine production in the atmosphere. The absorption of basic amines
by acidic aerosol droplets (containing sulfuric acid and/or ammonium bisulfate), followed by
reaction with nitrite, nitrous acid, or other species, could theoretically lead to the for-
mation of nitrosamines. The acid media would favor nitrosamine formation (Mirvish, 1975;
Ridd, 1961; Scanlan, 1975) and would prevent rapid photodecomposition during daylight hours
since the absorption of nitrosamines is greatly attenuated in acid solutions (Chow et al.,
1972).
This hypothetical mechanism, which is intuitively plausible, warrants several comments.
First, basic species, such as ammonia, which are present in ambient air at higher concen-
trations than amines, may compete effectively for absorption in acidic aerosol droplets.
Second, nitrosamines photolyze readily in aqueous solutions (Chow et al. , 1972; Polo and Chow,
1976) and atmospheric aerosols seldom achieve the high acidity (pH ^ 1) necessary to prevent
photodecomposition. It should be pointed out, however, that acidic aerosols are not neces-
sarily required, since several studies have shown that nitrosation proceeds quite effectively
at neutral and/or alkaline pH by free radical processes (Challis and Kyrtopoulos, 1977) or due
to catalysis by carbonyl compounds or metal ions (Keefer, 1976; Keefer and Roller, 1973).
Finally, irrespective of the aerosol acidity, reactions of nitrosamine with oxidizing species
in aqueous aerosol droplets may lead to the formation of, for example, nitramines.
6.4.4 Environmental Implications
Of the three mechanisms discussed above, nitrosation in atmospheric aerosols is purely
speculative at this time. The two other processes involve photochemical and non-photochemical
reactions of amines with oxides of nitrogen and related species and may be relevant to the
formation of nitrosamines in the atmosphere.
6-37
-------
Nighttime production of nitrosamines: Conflicting results are presented in the literature
concerning nitrosamine formation rates and yields from secondary and tertiary amines. Several
investigators report low yields (a few percent), essentially controlled by the slow rate of
nitrous acid formation through heterogeneous processes, while others report high yields
achieved within minutes.
Nitrosamines have been shown to form from secondary (Grosjean et al., 1978; Hanst et al.,
1977; Pitts et al., 1978) and tertiary amines (Grosjean et al., 1978; Pitts et al. , 1978) under
simulated atmospheric conditions. Primary amines have not been investigated but should receive
some attention since they have been shown to produce nitrosamines, albeit in low yields, in
the liquid phase (Wartheson et al., 1975).
If one accepts the low yields of Hanst et al. (1977), Grosjean et al. (1978), and Pitts
et al. (1978), nighttime concentrations of nitrosamines in typical urban atmospheric conditions
should be quite low. However, caution should be exercised when extrapolating these laboratory
and smog chamber data to the ambient atmosphere.
Photochemical reactions of amines: Secondary and tertiary amines react readily with the
hydroxyl radical to form aldehydes, PAN, ozone, nitramines, several amides, and the amine
nitrate aerosol. Nitrosamines are also formed but photodecompose rapidly. Little is known
about ambient levels of amines, but they are presumably low (£ 10 ppb), and daytime nitrosamine
levels should be quite low due to their rapid photodecomposition. However, photochemical for-
mation of diethylnitrosamine from the tertiary amine, triethylamine, has been shown to prevail
over photodecomposition for ~ 1 hour in full sunlight (maximum yield ^ 2 percent).
Products other than nitrosamines, i.e., nitramines and amides, may represent health
hazards and may warrant further investigation. In industrial environments where, for example,
50-500 ppb of amine might be released into polluted urban air, nitramines (10-30 percent yield,
or 5 to 150 ppb) and amides (5-15 percent, or 0.5 to 75 ppb) may form in sunlight. Dimethyl-
nitramine (Druckery et al., 1961; Goodall and Kennedy, 1976) and acetamide (Jackson and Dessau,
1961; Weisburger et al. , 1969) are carcinogenic, while dimethylformamide has been identified
in urban air (Pellizzari, 1977) and has been shown to undergo nitrosation (Lijinsky et al.,
1972; Walker et al., 1976). Another amide, N,N-'dimethyl-acetamide, has been identified in
diesel crankcase emissions (Hare and Montalvo, 1977).
6.5 SUMMARY
6.5.1 Chemistry of Oxides of Nitrogen in the Lower Atmosphere
Nitrogen oxides undergo many reactions in the lower atmosphere. Triggered by solar radi-
ation, photochemical reactions involving nitrogen oxides and other compounds, principally gase-
ous organic molecules, result in formation of reactive species capable of initiating a large
number of subsequent reactions. In particular, although anthropogenic emissions of N0x occur
principally as NO, atmospheric reactions may produce the more toxic and irritating compound
NO, which is of direct concern to human health.
6-38
-------
The reactive species, which include a variety of unstable, excited molecules and molecular
fragments having only transitory existence and/or occurring only in extremely low concen-
trations, are the principal agents through which chemical changes occur in the polluted urban
atmosphere. Many of the reaction sequences involving these unstable or short-lived intermedi-
ates are complex in nature, leading inevitably to short-term variations in nitrogen dioxide
concentrations, depending upon a variety of factors such as radiant energy input, temperature,
and the presence or absence of a variety of hydrocarbons. The dependence of NO- concentrations
on hydrocarbons results in a coupling between the chemistry of the oxides of nitrogen and the
photochemical oxidants, causing atmospheric concentrations of either type of pollutant to
depend, to some extent, on atmospheric concentrations of the other. There is considerable
current research on the precise relationships among ambient concentrations of NO and the
A
photochemical oxidants.
Most of the current knowledge both of atmospheric chemical pathways and of the end pro-
ducts of these reactions rests on controlled experiments conducted in small-scale laboratory
smog chambers. It is believed that the chemical processes that take place in these chambers
are similar to those that take place in the atmosphere. It is important to note, however, that
our current understanding of nitrogen chemistry is not complete and that reaction details and
rate constants may be subject to change or new reactions of substantial importance may remain
to be discovered.
A number of smog chamber studies using simulated urban atmospheres have been conducted in
order to define the relationship between levels of NO and hydrocarbon inputs and resulting
NCL concentrations. The results show that, with other factors held constant, both average and
maximum N0~ concentrations tend to be proportional to initial NO inputs. While some disagree-
1 L- A
ment is reported from different chamber studies on the precise effect of hydrocarbon reduction
on NO- concentrations, a consensus would seem to be as follows: Fifty percent hydrocarbon
reduction would have little effect on average N0~ concentrations (a change of + 10 percent)
but would yield moderate decreases in maximal NO, (a reduction of about 10 to 20 percent). It
should be noted that these conclusions are meant to apply to one basic type of ambient
situation—the situation of well-mixed urban air.
6.5.2 Nitrate and Nitrite Formation
In experimental simulations of a daily cycle of polluted atmospheres, peroxyacetyl nitrate
(PAN), known to be very toxic to plants, may be the conversion product of up to one-half of
the oxides of nitrogen. PAN, however, is not the final product of these gas-phase reactions,
since it may decompose. The most likely final gaseous product is nitric acid, a strong acid
and a powerful oxidizing agent. Photochemical models of diurnal atmospheric reactions predict
that up to one-half of the original oxides of nitrogen is converted to nitric acid and nitrates.
It is believed that nitrates are formed when nitric acid vapor reacts rapidly with ambient
ammonia to form small solid particles of ammonium nitrate. Another possible mechanism
resulting in aerosol formation consists of the direct absorption of NO into aqueous droplets
X
6-39
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in the presence of ambient ammonia. The relative importance of these two mechanisms is not
presently known.
Nitric acid produced in the atmosphere is an important component of acidic rain. Particu-
late nitrates may be of concern as a component of respirable participate matter. Both nitric
acid and participate nitrates are of concern for adverse effects on human health.
6.5.3 Transport and Removal of Nitrogenous Species
Over travel distances measured in hundreds of kilometers, more than half the total mass
of most pollutants, including nitrogenous species, may be removed from the atmosphere by a
variety of processes. These processes are usually grouped into the two generic classes, dry
and wet deposition. Gaseous nitrogenous species may be removed by surface absorption (dry depo-
sition). Vegetation and soil are capable of removing significant amounts of NO and N0? from
the atmosphere by this mechanism. Dry deposition of particulate nitrogenous species may occur
through sedimentation, Brownian diffusion, and impaction. The rate or removal by these
mechanisms is strongly dependent on wind speed and the detailed properties of the deposition
surface. Rainout and washout are two wet deposition mechanisms by which nitrogenous gases and
particulates may be removed from the atmosphere. Rainout refers to removal processes taking
place within a cloud; washout refers to removal of aerosols and gases below the cloud layer by
precipitation. The uptake of NO by rain depends upon such parameters as rainfall intensity,
raindrop size, and the chemical composition of the droplets. To date, the detailed processes
of NO removal have not been thoroughly studied.
A
6.5.4 Mechanisms of Atmospheric Nitrosamine Formation
Three mechanisms possibly leading to the atmospheric formation of nitrosamines and related
compounds are as follows:
• Non-photochemical reactions of gaseous amines with oxides of nitrogen and nitrous
acid
• Photochemical reactions of amines with oxides of nitrogen in the gas phase
• Heterogeneous nitrosamine formation processes in atmospheric aerosols.
The first two processes have been the object of recent experimental studies, including simu-
lation experiments in environmental chambers. The third process involving aerosol particles
is purely speculative at this time.
Conflicting results are presented in the literature concerning nitrosamine formation rates
and yields from secondary and tertiary amines. Several investigators report low yields (a few
percent) essentially controlled by the slow rate of nitrous acid formation through hetero-
geneous processes, while others report high yields achieved within minutes.
Nitrosamines have been shown to form from secondary and tertiary amines under simulated
atmospheric conditions. Primary amines have not been investiaged. If one accepts the lowest
yields reported, nighttime concentrations of nitrosamines under typical urban conditions would
not be significant. However, caution should be exercised when extrapolating these laboratory
and smog chamber data to the ambient atmosphere, especially in view of the lack of consensus
on formation rates.
6-40
-------
In sunlight-irradiated atmospheres, secondary and tertiary amines react readily with the
hydroxyl radical to form aldehydes, PAN, ozone, nitramines, several amides, and amine nitrate
aerosol. Nitrosamines are also formed but photodecompose rapidly. Little is known about
ambient levels of amines, but they are presumably low (< 10 ppb), and daytime nitrosamine
levels should be quite low due to their rapid photodecomposition. However, photochemical for-
mation of diethylnitrosamine from the tertiary amine, triethylamine, has been shown to prevail
over photodecomposition for ~ 1 hour in full sunlight (maximum yield ^ 2 percent).
Products other than nitrosamines, i.e., nitramines and amides, may represent health
hazards and may warrant further investigation. Near certain industrial environments where,
for example, 50-500 ppb of amine might be released into polluted urban air, nitramines (10-30
percent yield or 5 to 150 ppb) and amides (5-15 percent, or 0.5 to 75 ppb) may form in sun-
light.
6.5.5 Source-Receptor Relationships
The question of predicting the N02 concentration experienced by a receptor, such as a
human being, due to given emissions of NO has received little attention in the literature
until very recently. Relationships among ambient NO , hydrocarbons, and ozone which make use
of the complex chemistry described above have been considered in connection with the question
of predicting ambient ozone concentrations. Some of the methodology (which includes a variety
of air quality simulation models) applicable to the ozone problem has potential application to
the case of NO source-receptor relationships. However, neither development nor validation of
these models for the N02 problem has reached a stage where it is possible to evaluate with any
certainty either their usefulness or accuracy. For this reason, no general statements can
prudently be made at this time concerning the specific impacts on air quality of various NOX
source types. Such considerations must await documentation of adequate modelling procedures.
6-41
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Spicer, C. W. , and D. F. Miller. Nitrogen balance in smog chamber studies. J. Air Pollut.
Control Assoc. 26:45-50, 1976.
Stampfer, J. F., Jr., and J. A. Anderson. Locating the St. Louis urban plume at 80 and 120 km
and some of its characteristics. Atmos. Environ. 9:301-313, 1975.
Stelson, A. W. , S. K. Friedlander, and J. H. Seinfeld. Note on the equilibrium relationship
between gaseous nitric acid and ammonia and particulate ammonium nitrate. Atmos.
Environ. 13:369-371, 1979.
Stephens, E. R. Photochemical formation of oxidants. In: Proceedings of the Conference on
Health Effects of Air Pollutants, National Academy of Sciences—National Research
Council, Washington, D.C., October 3-5, 1973. Serial No. 93-15, U.S. Senate, Committee
on Public Works, Washington, DC, November.1973. pp. 465-487.
Stern, A. C. , Ed. Air Pollution. 3rd Edition. Volume III. Measuring, Monitoring, and
Surveillance of Air Pollution. Academic Press, Inc., New York, NY, 1976.
Sundareson, B. B. , C. I. Harding, F. P. May, and E. R. Hendrickson. Adsorption of nitrogen
oxides from waste gas. Environ. Sci. Technol. 1:151-156, 1967.
Tingey, D. T. Foliar Absorption of Nitrogen Dioxide. M. A. Thesis, University of Utah, Salt
Lake City, UT, June 1968.
Trijonis, J. Empirical Relationships Between Atmospheric Nitrogen Dioxide and Its Precursors.
EPA-600/3-78-018, U.S. Environmental Protection Agency, Research Triangle Park, NC,
February 1978.
Trijonis, J. Dependence of ambient N02 on precursor control. In: Implications of the Clean
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AIChE Symp. Ser. 76(196):240-248, 1980.
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Tsang, W. , D. Garvin, and R. L. Brown. NBS Chemical Kinetics Data Survey—The Formation of
Nitric Acid from Hydroxyl and Nitrogen Dioxide, 1977.
Tuazon, E. C. , A. M. Winer, R. A. Graham, J. P. Schmid, and J. N. Pitts, Jr. Fourier trans-
form infrared detection of nitramines in irradiated amine-NO systems. Environ. Sci.
Technol. 12:954-958, 1978. x
Turner, D. B. Atmospheric dispersion modeling: a critical review. J. Air Pollut. Control
Assoc. 29:502-519, 1979.
U. S. Environmental Protection Agency. Assessment of Scientific Information on Nitrosamines,
Report of an ad hoc Study Group of the USEPA Science Advisory Board Executive Committee,
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U. S. Environmental Protection Agency. Scientific and Technical Assessment Report on Nitro-
samines. EPA-600/6-77-001, U.S. Environmental Protection Agency, Research Triangle Park,
NC, June 1977.
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Oxidants. EPA-600/8-78-004, U.S. Environmental Protection Agency, Washington, DC, April
1978.
Walker, P., J. Gordon, L. Thomas, and R. Oullette. Environmental Assessment of Atmospheric
Nitrosamines. EPA Contract No. 68-02-1495, The Mitre Corporation, McLean, VA, February
1976.
Wartheson, J. J. , R. A. Scanlan, D. P. Bills, and L. M. Libbey. Formation of heterocyclic
n-nitrosamines from reaction of nitrite and selected primary diamines and amino acids.
J. Agric. Food Chem. 23:898-902, 1975.
Weibe, H. A., A. Villa, T. M. Hellman, and J. Heicklen. Photolysis of methyl nitrite in the
presence of nitric oxide, nitrogen dioxide and oxygen. J. Am. Chem. Soc. 95:7-13, 1973.
Weisburger, J. H. , R. S. Yamamoto, R. M. Glass, and H. H. Frankel. Prevention by arginine
glutamate of the carcinogenicity of acetamide in rats. Toxicol. Appl. Pharmacol. 14:
163-175, 1969.
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tion. Environ. Sci. Technol. 11:995-1000, 1977.
White, W. H. , J. A. Anderson, D. L. Blumenthal, R. B. Husar, N. V. Gillani, J. D. Husar, and
W. E. Wilson, Jr. Formation and transport of secondary air pollutants: ozone and
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3-77-011, U.S. Environmental Protection Agency, Research Triangle Park, NC, January 1977.
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7. SAMPLING AND ANALYSIS FOR AMBIENT N0v AND NO -DERIVED POLLUTANTS
i " "
7.1 INTRODUCTION
This chapter summarizes a variety of methods used for measuring oxides of nitrogen (NO )
A
and other pollutants which may be derived from NO through atmospheric transformations (Chapter
s\
6). Emphasis is placed upon describing methodology currently available or in general use
for routine monitoring of ambient pollutant concentrations.
An appreciation of some of the errors involved in present monitoring techniques is
important in evaluating the quality of ambient pollution data. Three types of errors are
discussed in this section: interferences, systematic errors and random errors.
The measurement of individual pollutants in ambient air is complicated by the presence of
other airborne chemicals which may produce responses in the measuring apparatus generally
indistinguishable from those produced by the pollutant being monitored. These spurious
responses are known as "interferences." Extensive tests are conducted by the U.S. Environmenta
Protection Agency (U.S. EPA) and/or other laboratories on potential interferences in proposed
measurement techniques before they are considered suitable for routine monitoring. This
chapter describes reported interferences for the methods listed. It should be noted, however,
that not all potential interferences have equal significance. Their magnitude will, in
general, depend on the ambient concentrations of the interfering species, the inherent sen-
sitivity of a given procedure to spurious responses, and, in some cases, on details of the
measuring apparatus which may vary from instrument to instrument. An analytic technique
sensitive to interference may still be useful if the interfering species occurs only in low
concentrations in ambient air or may otherwise be accounted for.
In addition to errors introduced by interferences, a given analytic technique may be
subject to systematic over- or underestimation of the pollutant concentration which affects
the accuracy with which these concentrations are known. Such errors are known as "biases."
The assessment of the magnitude of such biases for a given analytical method generally requires
extensive testing by a number of laboratories sampling the same pollutant concentration in
ambient air (collaborative testing).
Random errors introduced by unknown factors such as variability in detailed procedures
used by different operators or sensitivity of the method to small uncontrollable variations in
operational parameters are generally known collectively as an imprecision in the method. A
measure of this type of error often used is the standard deviation of a set of measurements.
Once the standard deviation is known, it may be expected on statistical grounds that about 95
percent of measurements made on the same ambient air sample will yield values for the N0~
concentration which differ from the average by at most + 2 standard deviations. The precision
of a method is also often assessed in collaborative testing procedures. The results of testing
for these two error types are described in this chapter where available.
7-1
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A critical analysis of techniques for measuring nitrogen oxides in ambient air has been
repbrted very recently by Saltzman (1980). In addition, a historical review of USEPA N02
monitoring methodology requirements has been given by Purdue and Mauser (1980).
In considering the analytic techniques described below it must be noted that the state-
of-the-art of measurement technology is constantly changing. For this reason, techniques
currently in use or recommended for use may be replaced by better methods at some future time,
techniques which are presently in the development stage may become routine in the future, or
entirely new techniques may be developed.
Since the publication in 1971 of the original document Air Quality Criteria for Nitrogen
Oxides, there have been significant changes in the technology associated with measurement of
ambient concentrations of both NO and N02- In addition, concern about the potential adverse
human health implications of ambient concentrations of other NO -derived compounds such as
suspended nitrates, nitric-acid, and N-nitroso compounds has led both to development of new
analytic techniques, and to a reexamination of existing methodology for their measurement.
With regard to the measurement of N02, the original Federal Reference Method, the Jacobs-
Hochheiser technique, was discovered to have unresolvable technical difficulties. The USEPA
published the following brief summary of these difficulties on June 8, 1973 when it withdrew
the method (U.S. EPA, 1973):
". . . EPA's analysis indicates that the reference method
is deficient in two aspects. First, the method over-
estimates nitrogen dioxide concentrations at low levels
and underestimates them at high levels because the col-
lection efficiency of the absorbing reagent is dependent
upon nitrogen dioxide concentration being measured.
Second, the method is subject to positive interference
by nitric oxide. Since the variable collection effici-
ency problem cannot be resolved, this method can no
longer serve as the reference method."
After extensive testing, the USEPA promulgated, on December 1, 1976, the chemiluminescence
measurement principle and associated calibration .procedures (U.S. EPA, 1976b) upon which a
number of chemiluminescent analytical instruments are based, These analyzers, once approved
by the U.S. EPA (1975) are referred to as Reference Methods. For purpose of simplicity in
the descriptions to follow, however, the term Reference Method is meant to apply both to the
measurement principle and to the instruments based thereupon. The required performance
specifications which acceptable continuous chemiluminescence analyzers must meet are shown in
Table 7-1.
Equivalent methods are methods based on measurement principles different from the
reference method. Two kinds of equivalent methods are possible—manual and automated
(continuous monitoring analyzers). Candidate automated methods may be designated as equivalent
methods if they meet the performance specifications listed in Table 7-1 and demonstrate a
7-2
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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, Maximum Discrepancy
ppm HO 2 Specification, ppm
Low 0.02 to 0.08 0.02
Medium 0.10 to 0.20 0.02
High 0.25 to 0.35 0.03
7-3
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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-
modified Griess-Saltzman method, the triethanolamine method, the sodium arsenite method, and
the TGS-ANSA method have also been extensively tested and are currently in widespread use
and/or have been extensively tested, and are available for routine measurement of ambient N0?
concentrations. .Both the sodium arsenite method and the TGS-ANSA method were designated as
equivalent methods as of December 14, 1977. This means data obtained by these two methods are
accepted by EPA as equivalent to chemiluminescence data (Reference Method) for the purpose of
establishing attainment status with respect to the National Ambient Air Quality Standard
(NAAQS) for NO . The manual Griess-Saltzman method, although not usually used in ambient
monitoring, is discussed because a number of studies pertinent to an assessment of the health
effects have used this method in laboratory situations (Chapters 14 and 15).
Although adequate chemical techniques exist for the determination of the nitrate fraction
of suspended particulate matter in ambient air, a number of very recent reports have pointed
to significant nitrate artifact formation on the glass fiber filters in widespread use for
collecting the particulate matter. At this time, therefore, most of the existing data base on
urban ambient nitrate concentrations must be considered to be of doubtful validity. Since
consistent relationship to the reference method during side-by-side ambient monitoring.
Candidate manual methods need only demonstrate a consistent relationship to the reference
method to be designated as equivalent methods. Table 7-2 shows the test specifications which
must be met to demonstrate a consistent relationship with the reference method.
positive artifact formation has been shown to be associated with conversion of ambient NCL
and/or nitric acid (HNCO to nitrates and since sulfuric acid aerosol has been implicated in
removal of nitrate, data from certain background sites may be validated in special cases where
it can be shown that the concentrations of these species were sufficiently low during the
monitoring period of interest.
Recent discovery of N-nitroso compounds in food, water, and ambient air has prompted the
development of a variety of new instrumental techniques in the last few years. Measurement
technology is still developing and insufficient time has elapsed for careful evaluation of
existing techniques. In particular, some difficulties have been reported to be associated
with artifact formation under certain sampling conditions.
Development of long-pathlength infrared absorption techniques has recently made possible
the observation of nitric acid in ambient air. However, the technique is presently too elabo-
rate for routine monitoring applications. Other techniques for quantitative analysis of
nitric acid vapor have been reported but have not yet been carefully evaluated.
The sections in this chapter describing briefly the analysis of nitrate in media other
than air (e.g., water, soil, and plant and animal tissue) are included for two reasons: (1)
the basic methodology is similar to that used for analyzing aqueous extracts of nitrate partic-
ulate matter drawn from the ambient air and (2).it is believed appropriate to make some
7-4
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estimate of human exposure from different media with a view towards placing exposure via the
atmospheric route in perspective. Similar considerations prompted the inclusion of material
on techniques for measuring N-nitroso compounds in food and water.
7.2 ANALYTICAL METHODS FOR NO
X
Many methods have been used to measure NO concentrations in air. Some of these methods
directly measure the species of interest; others require that the species be oxidized or
reduced, or separated from interferences before the measurement is made. Of particular
importance in this regard is the new Reference Method, the continuous chemiluminescence method.
The method is specific for NO but may easily be modified for measurement of N0? by first
quantitatively reducing the NO,, to NO. The regulatory specifications relating to the Reference
Method (RM) are prescribed in Title 40 of the Code of Federal Regulations, Part 50, Appendix F.
7.2.1 The Reference Method for NO,,: Gas-Phase Chemi luminescence
Atmospheric concentrations are measured indirectly by first reducing the N02 quantita-
tively to NO, then reacting the resultant NO with 03 and measuring the light intensity from
the reaction.
The use of the gas-phase chemiluminescent reaction of NO and 0, for quantitative measure-
ment of NO was reported initially by Fontijn et al. (1970) and some improvements were described
by Stedman et al. (1972). The sample air stream is mixed with air containing a high 0, concen-
tration (approximately 1 percent). The reaction of NO and 0, forms excited N09 molecules, the
•J L.
number of which is proportional to the NO concentration. Some of the excited N02 molecules
emit electromagnetic radiation with wavelengths between 600 and 2000 nm, with a maximum at
1200 nm (Clough and Thrush, 1967). The reaction chamber is held at reduced pressures to
decrease the collisional deactivation, and the emitted radiation is measured with a photo-
multiplier tube and associated electronics. To reduce interferences of the chemiluminescent
reactions of ozone with other species, optical filters can be employed (Stevens and Hodgeson,
1973). Typical commercial chemiluminescence instruments can detect concentrations as low as
9.5 ug/m3 (0.005 ppm) (Katz, 1976).
Since the detection of N02 by the RM is directly dependent on the analyzer's capability
to reduce N02 to NO, it is important that the conversion be essentially quantitative over a
wide range of N02 concentrations.
Catalytic reduction of N09 to NO is commonly employed in chemiluminescence NO-NO instru-
L. X
ments. These instruments measure NO alone by passing the sample directly to the detector.
The total concentration of NO and N02 (NO ) is measured by drawing the sample through a cataly-
tic reduction unit prior to entering the detector. NO- concentrations are obtained by subtrac-
tion.
Winer et al. (1974) studied the reactions of various nitrogen compounds over carbon and
molybdenum converters. It was found that not only N02 but peroxyacetyl nitrate (PAN) and a
7-5
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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 (NH3) to NO (U.S. EPA, 1973). This can be of importance in measuring NO- exposures
in animal studies, where elevated levels of NHg may be present as a result of biologic pro-
cesses. It is not expected to be of importance in ambient situations using EPA approved
analyzers.
While care must be exercised in the use of chemiluminescence instruments because of
potential interferences, in most ambient situations NO plus NO^ are present in much higher
concentrations than interfering species.
Results of the USEPA's collaborative quality assurance testing of the method (Constant et
al., 1975a) showed that, for one-hour instrumental averaging times for N09 concentrations
3
ranging from 50 to 300 |jg/m (0.027 to 0.16 ppm), the method has an average negative bias of
five percent with a standard deviation of about 14 percent for equivalent samples measured by
different laboratories.
One collaborator had very large biases, and another collaborator had unstable biases.
EPA concluded that for most collaborators (8 out of 10), however, the bias is small and well-
balanced. The method is satisfactory for averaging times of one hour or more.
7.2.2 Other Analytical Methods for NO,
7.2.2.1 Griess-Saltzman Method
7.2.2.1.1 General description of method. This chemical method for collection and analysis of
N02 was originally proposed by Ilosvay (Threadwell and Hall, 1935). Many variations of this
method exist, including both manual and automated versions.
The principle of the reaction is thought to be the formation of nitrous acid by the
reaction of NO- with water. This in turn is reacted with an aromatic amine to form a diazonium
salt. In a further step, addition of an organic coupling agent forms a deeply-colored azo
dye. The amount of NO- collected is related to the light absorbance of the solution.
Many variations of the Griess-Ilosvay reaction have been explored; the variation developed
by Saltzman (1954) is one of the most widely used. A manual version of this method has been
designated as a Tentative Method by the Intersociety Committee on Methods for Ambient Air
Sampling and Analysis (1977c), and was adopted as a standard method by the American Society
for Testing and Materials (ASTM, 1974a). It has been shown that many different reagent formu-
lations are possible so long as they all contain a diazotizer, a coupler, a buffer, and a
surfactant (Kothny and Mueller, 1966).
7-6
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If an extended sampling time is required in the manual version, the azo dye may suffer
bleaching by SCL. Saltzman (1954) recommended addition of acetone to prevent this. In addi-
tion, if the sample is collected in an evacuated bottle or syringe, a long waiting period such
as might occur in a manual procedure may cause some NO to be oxidized to N02 (ASTM, 1974a).
Since the conversion of NC^ to azo dye is not quantitative, a factor is introduced to
represent the conversion efficiency under a given set of experimental conditions. This is
often termed the "stoichiometric factor." If the experimental conditions are the same as
Saltzman1s original formulation (1954) or his modified version (1960) the stoichiometric
factor has been reported to be 0.72 (Saltzman, 1954, 1960; Saltzman and Wartburg, 1965;
Shaw, 1967). Scaringelli et al. (1970) obtained a value of 0.764. However, recent, unpubli-
shed work by two California groups, the California Air Resources Board (CARB) and the Califor-
nia Department of Health Services' Air and Industrial Hygiene Laboratory (AIHL), has shown that
measurements performed by the manual Saltzman technique are sensitive to the exact concentra-
tion of the coupling compound NEDA used in the reagent (Horrocks et al., 1981). Careful evalu-
ation showed that values obtained using either the original Saltzman reagent (1954) (0.5
percent sulfanilic acid, 14 percent acetic acid, and .002 percent NEDA) or the modified
Saltzman reagent (1960) (0.5 percent sulfanilic acid, 5 percent acetic acid, and .005 percent
NEDA) are biased approximately 13 percent too high. The stoichiometric factor is less sensi-
tive to variations in the concentrations of acetic and sulfanilic acids and is independent of
relative humidity, temperature of the absorbing agent, and nitrogen dioxide concentration.
7.2.2.1.2 Continuous Saltzman Procedures. In this procedure, N0? in ambient air is continu-
ously absorbed in a solution of diazotizing-coupling reagents to form an azo-dye which absorbs
light, with a maximum absorbance at approximately 540 nm. The transmittance, which is a
function of the N02 concentration, is measured continuously in a colorimeter and the output
read on a recorder or a digital voltmeter.
The continuous Saltzman procedure currently used in ambient air monitoring has recently
been evaluated by Margeson and Fuerst (1975). The results show that static calibration (with
solutions prepared to contain known quantities of the nitrite ion) is not uniformly reliable,
due to variable collection efficiency of the absorption system. Dynamic calibration pro-
cedures by means of a reliable NOp permeation device, such as the National Bureau of Standards
Standard Reference Material 1629, are recommended since collection efficiency errors and the
use of stoichiometric factors are eliminated by virtue of the fact that errors, if they exist,
cancel out. Ozone has been reported to be a negative interferent in the continuous version
of the method (Baumgardner et al., 1975).
Recently however, Adema (1979) could not confirm the interference in one experimental
arrangement of a modified manual method. Two specific variants of the continuous method
have been used widely for ambient air monitoring. Although both are continuous colorimetric
techniques suitable for averaging times of one hour or more, they differ in the use of two
distinct absorbing solutions, in which azo dyes are formed. The first, sometimes known as the
7-7
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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 alkyl
nitrites, ethyl, n-butyl, and isoamyl have been reported in a manual procedure using this
solution (Thomas et al., 1956). The second method, sometimes known as the Lyshkow-modified
Griess-Saltzman method, uses an absorbing solution consisting of 0.15 percent sulfanilamide,
1.5 percent tartaric acid, 0.005 percent N-(l-naphthyl)-ethylenediamine dihydrochloride (NEDA),
and 0.005 percent 2-naphthol-3, 6-disulfonic acid disodium salt. Both variants are useful in
the range of ambient concentrations from 19 to 9,400 pg/m (0.01 to 5.0 ppm). Results of the
•3
USEPA's quality assurance testing over the range 90 to 370 ug/m (0.05 to 0.2 ppm) indicate an
average bias of six percent with a 13 percent standard deviation among different laboratories
testing equivalent samples (Constant et al., 1975b). Estimates of bias for different labora-
tories, however, varied considerably.
EPA concluded that the overall average results are reasonably accurate but that the
method may produce extremely inaccurate readings in an unpredictable fashion. About half the
collaborators did achieve fairly stable results for the experiment, leading EPA to offer the
subjective judgment that although the method is difficult to use, it will produce reliable
results in some hands.
7.2.2.1.3 Manual Saltzman Procedure. In this method, N0? in ambient air is drawn at a known
rate through an absorbing solution (Saltzman, 1954) in a fritted-glass bubbler for a specified
time period, producing an azo-dye. The absorbance of the solution is subsequently measured
manually with a spectrophotometer. The NO,, concentrations present in ambient air may be
related to the absorbance of the azo-dye solution by calibration with other solutions contain-
ing known quantities of the nitrite ion.
The manual Saltzman procedure is described in this section because a number of studies
bearing on the effects of NO^ on human health have reported using this procedure (see Chapters
14 and 15). When fritted bubblers are employed, the method has been reported to have a usable
range of 10 to 9,400 (jg/m (0.005 to 5.0 ppm). A precision of 1 percent of the mean concentra-
tion is obtainable (Intersociety Committee for Ambient Air Sampling and Analysis, 1977c).
ASTM has evaluated the precision and accuracy of the measurement in ambient situations
(1974b). A fritted bubbler, cleaned with dichromate solution, was used exclusively in the
evaluation. The nominal flow rate for sampling was 0.4 liter/minute. Ten feet of TFE fluoro-
carbon tubing having a nominal inside diameter of 8 mm was used as a sample probe prior to the
fritted bubbler. The technique used to evaluate the accuracy of the method was to spike
ambient air, containing t\0y> with additional, accurately known, concentrations of NOp and then
to attempt to measure the spiking concentrations. The :NO- used for spiking was obtained from
a permeation tube. Results showed an overall positive bias of 18 percent in measuring the
7-8
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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 N0~ concen-
tration.
It should be noted that this evaluation technique subjects the method to possible inter-
ferences from other pollutants in ambient air. As such, it may be taken to, represent the
accuracy of results, in the same N09 concentration range, expected in health-related studies
3
which use ambient air. Maximum ambient N0? concentrations were about 250 pg/m during the
test and maximum total N00 (ambient plus spike) concentrations used in the test were about 400
3
ug/m . Extrapolation of the test results to situations where high N0? levels were measured
without dilution must be viewed as speculative.
In the case of studies which are carefully controlled with regard to the occurrence of
pollutants other than N02, it may be expected that the accuracy of the method would be
significantly improved, although a similar interlaboratory test under interference-free condi-
tions is lacking in the literature.
As discussed in Section 7.2.2.1.1, recent measurements have resulted in a redetermination
of the stoichiometric factor for the Saltzman technique. These results have possible important
implications for the numerical values of effects levels reported both in animal (Chapter 14)
and human (Chapter 15) studies. They strongly suggest that results obtained by the manual
Saltzman technique and referred to Saltzman1s original stoichiometric factor are, in fact,
about 14 percent too high, i.e., effects probably occurred at lower levels than those reported.
7.2.2.2 Jacobs-Hochheiser Method—The Jacobs-Hochheiser technique was formerly the Federal
Reference Method, but is currently unacceptable for air pollution work for reasons cited
above. This technique is discussed here mainly because the method was frequently employed in
past years in obtaining data for use in epidemiological studies.
The method was developed by Jacobs and Hochheiser (1958) to avoid the bleaching of the
azo dye by SO^ that occurs in the Griess-Saltzman method. Nitrogen dioxide is absorbed in a
solution of sodium hydroxide (NaOH) with butanol added as a surfactant to improve gas transfer
when using a fritted bubbler. After sampling, any sulfite from absorbed SOp is oxidized with
hydrogen peroxide. The nitrite in solution, is not affected. The solution may then be stored
for 48 hours or more before analysis. To quantitate the nitrite in solution, the solution is
first acidified with phosphoric acid. A diazotizer and a coupling agent are then added to
produce an azo dye. Solution absorbance is then measured spectrophotometrically. The original
method was designed for intermittent 40-minute sampling but was later modified for composite
sampling over 24 hours. This method, modified again, was employed by the National Air Sampling
Network (NASN) (Morgan et al., 1967a, 1967b) and was adopted as the Federal Reference Method
in 1971 (U.S. EPA, 1971).
The National Academy of Sciences document, on nitrogen oxides (Kothny, 1977) cites an
extensive list of references documenting that the sampling efficiency of the Jacobs-Hochheiser
method is affected by sampling flow rate, porosity of bubbler frits, liquid level, sampling-
7-9
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container material, incoming pollutant concentration, and contaminants present in the sample.
Sampling efficiencies, in the work reviewed, ranged from 15 to 78 percent when 0.1N NaOH alone
was used as an absorbant. In addition to the varying efficiency with which NO- is removed from
the gas sample, the measurement also is affected by the stoichiometric factor. This factor is
also variable and may be affected by the presence of hydrogen donors (Christie et al., 1970;
Huygen and Steerman, 1971; Morgan et al., 1967a, 1967b; Nash, 1970). A composite of 11 sites
sampled in the NASN network gave an average stoichiometric factor of 62 + 7 percent (Morgan et
al., 1967a). The range of measurable concentrations is related to the percent transmission of
azo dye solutions measurable with a spectrophotometer. With 50 ml of absorbing reagent and a
sample flow rate of 200 ml/min for 24 hours, the range of the method is 20 to 740 ug/m (0.01
to 0.4 ppm) NO, (Katz, 1976). Katz (1976) reported relative standard deviations of 14.4 and
3
21.5 percent at NO,, concentrations of 140 and 200 ug/m (0.07 and 0.11 ppm), respectively.
Because the sampling efficiency and stoichiometric factor are significantly affected by
the details of the method employed, by N0? concentration, and by constituents of the sample
other than NO^, the use of many modifications of the Jacobs-Hochheiser method in air quality
and epidemiological studies has led to data of questionable quality, or even questionable
relative comparability.
7.2.2.3 Triethanolamine Method—The method described by Levaggi et al. (1973) utilizes an
absorbing solution of triethanolamine and n-butanol surfactant. After collection, the
analysis for nitrite is performed with Griess-Saltzman reagent to produce the azo dye for
spectrophotometric measurements. Sampling efficiencies up to 95 to 99 percent have been
reported (Intersociety Committee for Ambient Air Sampling and Analysis, 1977c; Levaggi et al . ,
1973). The U.S. EPA has recently reported (Ellis and Margeson, 1974) a laboratory evaluation
of the method for each of three absorbing solutions (0.1N TEA with n-butanol added at the
concentration levels 3 ml/1, 0.5 ml/1 and 0.0 ml/1). The results indicate the collection
efficiency to be constant, at approximately 80 percent for the first two solutions (78.8
3
percent for the last solution), over the range of 30 to 700 ug/m (0.01 to 0.37 ppm) if glass
frits are used. If restricted orifices, which are less fragile and cheaper than glass frits,
are used, the collection efficiency falls to about 50 percent. For this reason, the U.S. EPA
did not subject the method to collaborative testing so that no reliable measure of accuracy
and precision is presently available. No interference is expected from S02, 03, or NO at
ambient levels and the sample solutions are stable for three weeks after sampling. The accu-
racy is considered to be comparable to that of the Griess-Saltzman method (Katz, 1976) with
bias errors less than two percent at a stoichiometric factor of 0.764 (Scaringelli et al.,
1970). This method is presently considered to be a 24-hour method.
7.2.2.4 Sodium-Arsenite Method—The use of an alkaline solution of sodium arsenite
to absorb N02 was described by Christie et al. (1970) and Merryman et al. (1973). Christie
7-10
-------
et al. reported a collection efficiency of 95 percent using an orifice bubbler. The U.S. EPA
recently has evaluated the sodium-arsenite procedure (Beard and Margeson, 1974) and has desig-
nated it an equivalent method as of December 14, 1977. The method is presently considered to
be a 24-hour method. The results showed that the procedure has a constant collection effici-
3
ency for NO^ of 82 percent over the recommended useful concentration range, 20 to 750 ug/m
(0.01 to 0.4 ppm). Results of the USEPA's collaborative quality assurance testing of the
method indicate a negative bias of three percent with an interlaboratory standard deviation of
11 ug/m independent of concentration (Constant et al. , 1974b). EPA concluded that the
measurement errors were essentially uniform for all collaborators, although some dependence on
N02 level was noted. Eight of ten collaborators exhibited a uniform percent bias over all N02
levels tested.
Following absorption, any sulfite is oxidized with peroxide and the solution is then
acidified with phosphoric acid. The azo dye is formed by addition of sulfanilamide and N-(l-
naphthyl) ethylenediamine dihydrochloride. According to Katz (1976), NO in the air sample can
produce a positive interference by increasing the N0? response in the sample by 5 to 15 per-
cent of the NOp actually present. Carbon dioxide, in excess of typical ambient concentra-
tions, can lead to a negative interference and the method response is affected by sample flow
rates in excess of 300 ml/min. The samples are stable for six weeks. Recently, the USEPA
also has conducted an evaluation of potential NO and C0« interferences (Beard et al., 1975).
Results show that, in the range 50 to 310 |jg/m3 (0.04 to 0.25 ppm) NO and 360,000 to 900,000
3
ug/m (200 to 500 ppm) C09, the average effect of these interferents is to increase the in-
3 3
dicated N02 response by 10 ug/m over the range 50 to 250 ug/m N0? (0.03 to 0.13 ppm).
7.2.2.5 TGS-ANSA Method—A 24-hour manual method for the detection and analysis of N02 in
ambient air, the TGS-ANSA method was first reported by Mulik et al. (1974). It has been
designated an equivalent method to the RM as of December 17, 1977. Ambient air is bubbled,
via a restricted orifice, through a solution containing triethanolamine, o-methoxyphenol, and
sodium metabisulfite. The NO^ gas in the ambient sample is converted to nitrite ion (NOp)
which is then analyzed by diazotization and coupling using sulfanilamide and the ammonium salt
of 8-anilino-l-naphthalene-sulfonic acid (ANSA). • The absorbance is read at 550 nm. The
function of the triethanolamine is to provide a basic collecting medium (Levaggi et al.,
1973). The addition of o-methoxyphenol raises the collection efficiency to 93 percent when
using a restricted orifice (Nash, 1970). The sodium metabisulfite inhibits free-radical
formation and, hence, the formation of quinones from the o-methoxyphenol as the solution ages.
The collection efficiency for NO- is constant at concentrations between 20 and 700 ug/m
(0.01 and 0.37 ppm), which is the range of the method with 50 ml of absorbing reagent and a
sampling rate of 200 cm /min for 24 hours. No interferences were reported at an NO, concentra-
3
tion of 100 ug/m (0.05 ppm) for the "following pollutants at the levels shown in parentheses:
7-11
-------
ammonia (205 ug/m3 or 0.29 ppm); CO (154,000 |jg/m3 or 134 ppm); formaldehyde (750 ug/m3 or
0.61 ppm); NO (734 ug/m3 or 0.59 ppm), phenol (150 |jg/m3 or 0.04 ppm); 0, (400 |jg/m3 or 0.2
3
ppm); and 502 ^3^ ^m or ®'^ PP"1)' ^he absorbing reagent is stable for three weeks before
sampling and the collected samples are stable for three weeks after sampling (Fuerst and
Margeson, 1974; Mulik et al., 1974).
Results of U.S. EPA's collaborative quality assurance testing (Constant et al., 1974a)
indicate a lower detectable limit < 15 ug/m (0.008 ppm), an average bias of 9.5 ug/m (0.005
ppm) over the range of 50-300 ug/m (0.03 to 0.16 ppm), and an interlaboratory standard devia-
3
tion of 8.8 ug/m (0.005 ppm). EPA concluded that the errors were essentially uniform for all
collaborators. The biases shown were nearly independent of the NO, level.
7.2.2.6 Other Methods—In addition to the standard wet chemical methods for NO^ measurement,
many other techniques have been explored. Molecular correlation spectrometry compares a
molecular absorption band of a sample or plume with the corresponding absorption band of N02
stored in the spectrometer (Williams and Kolitz, 1968). Spectrometers processing the second
derivative of sample transmissivity with respect to wavelength have been employed to measure
N02 as well as NO (Hager and Anderson, 1970). Infrared lasers and infrared spectrometry have
been applied by Hanst (1970), Hinkley and Kelley (1971) and Kreuzer and Patel (1971).
7.2.2.7 Summary of Accuracy and Precision of NO,, Measuring Methods—Purdue et al. (1975)
reported an extensive comparison of both intra- and intermethod accuracy and precision of the
chemiluminescent, sodium arsenite, TGS-ANSA and continuous colorimetric (Lyshkow modification)
procedures for NO^ measurement. The study was conducted under carefully controlled laboratory
conditions using skilled technicians. Ambient air spiked with N02 was sampled by two identical
instruments for each method tested. In the case of manual methods four samples were taken.
The N09 spikes were varied randomly from day to day over a 20-day sampling schedule. Spikes
3
ranging from 0 to 800 ug/m were used. The sampling period was of 22 hours duration. Table
7-3 gives the results of a statistical analysis of the intra- and intermethod differences.
Examination of the table reveals that the average difference between any of the methods
was never greater than 7.5 ug/m N09. The worst case of intramethod differences occurred with
3
the continuous colorimetric method where there was a small bias of 7.5 ug/m NOp between the
data from the two analyzers. The correlation coefficients for the intermethod comparisons
were greater than 0.985 in all cases. In another phase of the study, no intermethod differ-
ences could be attributed to concentrations of nitric oxide, carbon dioxide, ozone, total
sulfur, or total suspended particulate matter in the ambient air samples. Significant negative
interference in the continuous colorimetric method was found at N09 concentrations of 75 and
3 3
100 ug/m in the presence of ozone at concentrations of 353 and 667 ug/m . At an ozone concen-
tration of 100 pg/m , no interference was detected. At NO concentrations as high as 302 pg/m
no interference was found in the sodium arsenite procedure, although NO has been cited as a
positive interferent in the method.
7-12
-------
TABLE 7-3.
STATISTICAL ANALYSIS OF N02 MEASURING METHOD DIFFERENCE'
Sampling Spiked Ambient
Comparison
Intramethod
Chemil/Chemil
Color/Color
ARS/ARS (A)
ARS/ARS (B)
TGS/TGS (A)
TGS/TGS (B)
ARS (AVARS (B)
RGS (A)/TGS (B)
Intermethod
Chemil/Color
Chemil/ARS
Chemil/TGS
Color/ARS
Color/TGS
ARS/TGS
Pairs
22
20
22
22
20
22
22
20
20
22
20
20
18
20
Meanb
(|jg/niJ)
1.
7.
0.
0.
-0.
0.
-2.
0.
3.
-1.
5.
-3.
3.
7.
3
5
6
2
9
2
6
6
8
9
6
8
8
5
Air
95%,
Standard C.I.
Dev. Lower Upper
5.
7.
5.
5.
3.
9.
5.
7.
7.
9.
9.
11.
11.
7.
6
5
6
6
8
4
6
6
5
4
4
3
3
5
-1.
3.
-1.
-1.
-1.
-3.
-5.
-3.
0.
-5.
+0.
-9.
-1.
+3.
1
8
9
9
9
8
6
8
0
6
9
4
9
8
3.
11.
+3.
1.
0.
+3.
+0.
+3.
+7.
+1.
9.
1.
9.
11.
3
3
8
9
8
8
1
8
5
9
4
5
4
3
Corr.
Coeff.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
999
995
997
996
999
992
997
996
994
991
990
989
985
994
Extracted from Purdue et al. (1975).
Signed difference.
cStandard deviation.
95 percent confidence interval of mean difference.
Correlation coefficient between paired values in calculating mean
difference.
7-13
-------
A summary of available reliability estimates derived from collaborative testing studies
is given in Table 7-4 for four ambient air monitoring procedures: Chemiluminescence,
Griess-Saltzman (continuous colorimetric using dynamic calibration), TGS-ANSA, and sodium
arsenite. Measures of accuracy (bias) and precision (standard deviation) listed in the table
are derived from collaborative testing experiments conducted recently by EPA (Constant et al.,
1974a, 1974b, 1975a, 1975b,). In this type of testing, a number of collaborators, following
analytical procedures according to specified guidelines, sample the same ambient air spiked
with known N0~ concentrations. The collaborators are generally skilled in ambient air monitor-
ing so that the results reported may reasonably be taken to represent an upper limit on the
accuracy and precision obtainable in routine monitoring. The reader should note that the
values for accuracy and precision presented in the table represent averages of data reported
by all collaborators over the entire concentration ranges tested. Since the accuracy and
precision obtained may depend upon the NOp concentrations sampled and, moreover, in the case
of the Griess-Saltzmann procedure, upon the individual collaborator performing the test, the
reader is referred to the original reports for a detailed statistical discussion of the test
results.
Recently, a formal audit was performed on continuous chemiluminescent analyzers (Monitor
Labs 8440) in service in the St. Louis Regional Air Pollution Study (Smith and Strong, 1977)
(see Chapter 8). Table 7-5 summarizes the results of the audit. Three audit levels were
used: 0, 150 and 355 |jg/m NO-. "Acceptable" limits for the difference between measured NC^
values and known audit NO, concentrations were established for the purposes of the study at
3
+19, +30, and +71 (jg/m respectively. At the 0 audit level all 23 analyzers were within
limits; at an audit level of 150 fjg/m , three analyzers were found to "very narrowly" exceed
o
specified limits; at 355 pg/m one different analyzer "very narrowly" exceeded specified
limits. Statistics for the entire network showed average differences of less than 10 percent
at both the 150 and 355 ug/m audit NO- concentrations. Standard deviations were equal to or
less than 10 percent for both non-zero audit levels.
7.2.3 Analytical Methods for NO
Numerous methods, other than the chemiluminescence procedure (discussed in Section 7.2.1),
can be used for direct measurement of NO; however, none are widely used presently for air
quality monitoring. These methods include: ferrous sulfate (FeSo,) absorption and spectro-
photometric measurement of the resulting colored complexion, (Norwitz, 1966), and ultraviolet
(Sweeney et al., 1964) and infrared (Lord et al., 1974) spectroscopy. The spectroscopic tech-
niques require long pathlengths when used to measure concentrations in typical ambient air.
Mass spectrometry and gas chromatography also may be employed, but these methods are rather
elaborate and expensive.
7.2.4 Sampling for N0x
Sampling technique is a particularly important consideration for the measurement of NO
and NO-. Nitric oxide and NOp in the atmosphere during the day are involved in very rapid
7-14
-------
TABLE 7-4. SUMMARY OF RELIABILITY OF NO ANALYTICAL METHODS IN COMMON USE AS OBIA1NED BY COLLABORATIVE TESIING
(CONSTANT ET AL., 1974a, 19?4b, 1975a, 1975b)
I
I—>
en
Range of NO.
Concentrations
Used in Test
Method (ug/m3)
Chemi luminescence 80-300
(Reference Method)
Sodium Arsenite 50-300
(Equivalent Method)
TGS-ANSA 50-300
(Equivalent Method)
Griess-Sal tzman 90-370
(Continuous Colorimetric
with dynamic calibration;
both variants cited in
7.2.2.T)
Bias
(Average
for all
Tests)
-8 ug/m
or
-5%
6. 2 ug/m
or
•v3%
9.5 ug/m3
or
•v. -5%
16.1 ug/n3b
or
•v 6%
Standard Practical
Deviation Lower
(Average Detection
for all Limi t
Tests) (pg/m1) Comments (Reference)
14% <22 One collaborator had very large biases,
and another had unstable biases. For most
collaborators (8 out of 10), however, the
bias was small and well balanced. (Constant
et al. , 1975a)
11 ug/m < 9 Measurement errors were essentially uniform
for all collaborators, although some depen-
dence on NO, level was noted. 8 of 10 col-
laborators exhibited a uniform percent bias
over all NO, levels tested. (Constant et. al.,
1974b)
11.6 (jg/m <15 Errors were essentially uniform for all col-
laborators. The biases shown were nearly
independent of NO, level for range tested.
(Constant et al. , 1974a)
32.7 |jg/m <19 Although overall results are reasonably accu-
rate, method may produce quite inaccurate
readings in an unpredictable fashion. About
half of the collaborators did achieve fairly
stable results. Subjectively, then, the
method will produce reliable results in some
hands. (Constant et al., 1975b)
Depends in detail upon NO, concentration.
Depends significantly on laboratory performing test.
-------
TABLE 7-5. RESULTS OF 1977 FORMAL AUDIT ON IN-SERVICE
CHEMILUMINESCENT ANALYZERS IN ST. LOUIS
(SMITH AND STRONG, 1977)
Number
Audited
23
Number
Found
Opera-
tional
23
Audit
Level
(pg/m3)
0
150
355
"Acceptable"
Limits for
Difference
(ug/m3)
+19
+30
+71
Number
Outside
Limits
0
3
1
Average
Difference
for Network
(ug/m3)
+2
-11
-28
Standard
Deviation
for Network
(|jg/m3)
6
15
26
reactions which keep 03 in a photostat!onary state. The rate of photolysis of N02 (forming NO
and 0 and thus 0,) is nearly equal to the reaction of the NO and 0-, to form N0?. When a
sample is drawn into a dark sampling line, photolysis ceases while NO continues to react with
0, to form NOp. Thus, long residence times in sampling lines must be avoided to obtain a
representative sample. Sampling technique requirements for a given error in tolerance were
discussed by Butcher and Ruff (1971). For example, Figure 7-1, adapted from these authors,
shows the absolute error in N02 introduced in 10 seconds in a dark sampling line due to the
presence of 0, and/or NO in the line in varying concentrations. In general, due to the reac-
tive properties of NO , only glass or Teflon materials should be used in sampling trains.
If NO and N02 are to be measured separately by a method specific for N02, it is necessary
to remove N02 from the sample, then oxidize NO to N02 and measure the N02 concentration.
Several selective absorbers for N02 have been employed, but some of the N02 is converted to NO
in all the absorbers tested. Absorbents include Griess-Saltzman reagent (Huygen, 1970) and
granules impregnated with triethanolamine (Intersociety Committee for Ambient Air Sampling and
Analysis, 1977c; Levaggi et al. , 1972). The triethanolamine is reported to be the best ab-
sorbent, with only two to four percent of the incoming N0? converted to NO.
When NO is to be measured by a method specific to N02, either with or without removal of
N0~ from the sample, it is necessary to oxidize NO to NQ2 in the gas phase. The most fre-
quently used oxidizer is chromic oxide on a fire brick granule support (Intersociety Committee
for Ambient Air Sampling and Analysis, 1977c; Levaggi et al., 1974). This material gives over
99 percent oxidation when the relative humidity in the sample is between 20 and 80 percent.
The chromic oxide also removes S0~.
Considerations relating to the reduction of N02 to NO have been discussed in Section
7.2.1.
7.2.5 Calibration of NO and N00 Monitoring Instruments
Calibration of monitoring instruments or methods may be accomplished either by measuring
a gas of known concentration or by comparing measurements of a stable source with measurements
of the same source made by a primary reference method.
7-16
-------
a.
a.
OC
I-
Z
LU
O
O
o
n
O
0.01 =
0.005 -
0.002 -
0.001
0.001
0.01 0.10
NO CONCENTRATION, ppm
1.0
Figure 7-1. Absolute error in INIO2 and ANOoforlO
seconds in dark sampling line (Butcher and Run, 1971).
7-17
-------
Standard gas sources are the principal means by which NO and NCL measurement instruments
are calibrated. The preparation of standard mixtures of NO in nitrogen was studied by the
National Bureau of Standards (Hughes, 1975). The initial accuracy with which standards may be
prepared, based on either pressure or mass measurements, is quite good. The stability of
mixtures at concentrations above about 50 ppm is satisfactory with only 0 to 1 percent average
change in concentrations over a seven-month period. Other sources which have been employed
occasionally include permeation of compressed NO through membranes to produce dilute NO
streams (Hughes, 1975), electrolytic generation (Hersch and Deuringer, 1963), catalytic
reduction of a known concentration of NO,, (Breitenbach and Shelef, 1973), Qr Dno^0ivsl-s Of
known N02 concentrations and rapid dilution (Guicherit, 1972).
The permeation tube is the only direct source of dilute N0? mixtures in widespread use
(O'Keefe and Ortman, 1966; Scaringelli et al., 1970; Shy, 1970; Shy et al. , 1970). It may be
calibrated by weighing or by rarely used micromanometric measurements. The other common
procedure used to calibrate NO, measurement instruments is gas-phase titration. Stable sources
of known concentrations of both NO and 0, are required. A dilute stream of NO is measured by
NO methods. The 0., is added to the stream at a constant rate. The decrease in NO by reaction
with the added ozone is equal to the N02 formed. Thus, a known NO,, concentration is created.
The U.S. EPA (1976a) recommends the combined use of permeation tubes and gas-phase titration,
using one technique to check the other.
7.3 ANALYTICAL METHODS AND SAMPLING FOR NITRIC ACID
Monitoring for ambient nitric acid is complicated both by the low concentrations present
and by the fact that nitric acid in the atmosphere is in the gaseous state. Collection of a
representative sample without artifact formation presents some technical difficulties. In
general, also, sampling of nitric acid from ambient air is made difficult by its tendency to
adhere to the walls of the sampling lines. It may be necessary to heat sampling lines to
prevent condensation of water, which would result in removal of HNO,.
A microcoulometric method designed to measure nitric acid was developed by Miller and
Spicer (1975; Spicer and Miller, 1976). A Mast microcoulomb detection cell was adapted for
sensing acid gases in samples pretreated with ethylene to remove ozone.
Readings from samples introduced directly into the cell indicate total acid content.
Another sample of the test mixture is passed through loosely-packed nylon fiber which removes
the nitric acid. The cell reading of this sample is representative of total acid content
except nitric acid. Thus, nitric acid concentrations are obtained by subtraction.
The sensitivity of this method at a signal-to-noise ratio of two to one is approximately
2 ppb. No detectable interferences have been reported from S02, NO,,, PAN, H,,S041 and formalde-
hyde (CH20). It should, however, be noted that Spicer et al. (1978a) report significant
artifact nitrate formation on nylon filters under conditions of very high N07 concentrations
3
(56,400 ug/m ; 30 ppm) and high humidity. Although concentrations of this magnitude would not
7-18
-------
be expected to occur in ambient situations, the possible implications of these reported inter-
ferences for measurements obtained by the microcoulometric method have yet to be evaluated.
Using air streams passing through a cellulose filter impregnated with sodium chloride,
Okita et al. (1976) report collection efficiencies for nitric acid ranging from 93 to 100
percent. Interferences from N09 were reported over a range of N09 concentrations up to 15,000
3 3
ug/m (8.0 ppm). The equivalent of about 1 ug NO,,-N/m of artifact gaseous nitrate corre-
3
sponded to 188 ug/m (0.1 ppm) N09 being passed through the filter at relative humidities of
3
55 to 72 percent. Ozone did not enhance artifact formation at a concentra tion of 980 ug/m
(0.73 ppm) in the presence of 1,372 ug/m (0.73 ppm) NCL. Interferences from PAN and n-propyl
nitrate were cited as negligible or very small. Nitrate formation from N02 increased with
increasing relative humidity.
Recently, Tuazon et al. (1978) have reported measurements of nitric acid under ambient
conditions with a detection limit of 2 ppb. The system achieves this sensitivity by means of
a folded-path optical system which results in pathlengths of up to 2 km in the sample cell.
Fringes produced in a high-resolution infrared Michelson interferometer, coupled to the sample
cell, are scanned optically. The resultant variations in signal are related to the Fourier
transform of the spectrum which is recovered automatically by appropriate data processing.
A summary of the current status of methods to measure atmospheric nitric acid has been
published very recently (Stevens and McClenny, 1979). Table 7-6 summarizes the techniques
considered.
Methodology for measuring nitric acid is still in the development stage. Studies
conducted to date are not sufficient to assess with any degree of confidence the suitability
of the methods described in this section for routine ambient monitoring.
7.4 ANALYTICAL METHODS AND SAMPLING FOR NITRATE
Nitrate analyses have been performed routinely for many years and a large number of
chemical methods have been reported. Since analytical methods for inorganic nitrate generally
proceed by aqueous extraction, the final chemical quantitative determination of ion concentra-
tions is similar for samples drawn from air, water, and soil.
7.4.1 Sampling for Nitrate From Airborne Particulate Matter
Particulate nitrate as a fraction of total suspended particulates has been sampled in
this country largely by standardized sampling techniques using high volume (HIVOL) samplers.
USEPA minimum specifications for the HIVOL are well documented (U.S. EPA, 1971). A
continuous 24-hour sample of ambient air, typically at flow rates of approximately 1 to 2
standard cubic meters per minute, is drawn through a glass fiber filter which traps the partic-
ulate matter. The upper size limit of particulate matter collected depends on the geometry of
the sampler housing but is generally above about 30 urn in aerodynamic diameter, well above the
respirable size range. The sampler thus collects all of the respirable material and some
7-19
-------
TABLE 7-6. SUMMARY OF NITRIC ACID DETECTION TECHNIQUES"
Technique
Procedure
Minimum
Detectable
Level (ppbv)
Interferences
Tested
For, To Date
Reference
Cheroiluminescence
Simple modification of chemilumin-
escence procedure used for NO
5.0 NO, NO., PAN, organic
nitrates
Joseph and Spicer, 1978
Chemiluminescence Adaptation of sensitive chemilumin-
escence NO monitor described by
Ritter et al., 1978
0.3 NO, N02, PAN, organic
nitrates
Kelly and Stedman, 1979
Likens, 1976
i
r\3
O
Fourier Transform
Spectrometer
Long path infrared spectrometry
5.0 Most gaseous species in Tuazon et al.,
normal ambient air 1979, 1978
Microcoulometry
Coloriraetry
Sample conditioning with ethylene to 5.0
remove ozone interference; differ-
ence method using direct reading
and reading after nylon trap which
removes HN03
Reduction to NH. of fixed organic <0.1
nitrogen collected on nylon filter,
followed by indophenol ammonia
test. Teflon prefilter.
0 NO SO., H2SO,,
nth, HCHO, PAN/HCOOH,
HN02
Nht, particulate
nitrate
Miller and
Spicer et
Lazrus et
1968, 1979
Spicer, 1975
al. , 1978a, 1978b
al.,
Colorimetry
Collection of HNO, on NaCl impreg-
nated filters, followed by extrac-
tion and hydrazine reduction-
diazotization analysis of nitrate
0.1 N0?, particulate
nitrate
Okita et al., 1976
Forrest et al., 1979
Electron Capture
Gas Chromatography
Collection of HNO^ on nylon or cot-
ton, extraction, Conversion to
nitrobenzene analysis by gas
Chromatography
0.1 NOp, particulate
nitrate
Hare et al., 1979
Tesch and Sievers, 1979
Ross et al., 1975
Adapted from Stevens and McClenny, 1979
-------
fraction of the non-respirable material suspended in ambient air. In typical nitrate monitor-
ing, a portion of the HIVOL filter is subjected to aqueous extraction and the water-soluble
nitrate analyzed as described below in Section 7.4.2.
Recent reports point to serious difficulties associated with the routine use of glass
fiber filters. In a study of nitrate in auto exhaust, Pierson et al. (1974) report that glass
fiber filters collected about twice the amount of nitrate when compared to quartz fiber filters.
Nitrate also was found on glass fiber filters which were inserted downstream of either quartz
or glass fiber primary filters, providing additional evidence of artifact formation from
gaseous constituents. Spicer (1976) reported that glass fiber filters completely removed
gaseous nitric acid when in low concentration in gas streams, while Teflon and quartz filters
showed no corresponding effect. O'Brien et al. (1974) describe very unusual results of parti-
cle size distribution determinations of photochemical aerosol collected in the Los Angeles
basin using a cascade impactor where all particle size fractions were collected on glass fiber
filters. The authors speculated that conversion of gaseous nitrate precursors on the filter
masked the true nitrate size distribution.
Okita et al. (1976) report that untreated glass fiber filters collect nitric acid vapor
with a highly variable collection efficiency (0-56 percent), suggesting erratic nitrate arti-
fact formation in urban atmospheres containing nitric acid.
In an intensive laboratory investigation of interferences in atmospheric particulate
nitrate sampling, Spicer, Schumacher and co-workers (1978a) concluded that all five types of
glass filters investigated exhibited serious artifact formation due to collection of gaseous
nitric acid and, to some extent, NOp as nitrate. Cellulose acetate and nylon filters were
also reported to exhibit severe interferences from nitric acid. Negligible interferences were
reported for polycarbonate and Teflon filters. Interferences on quartz fiber filters varied
with the filter type, with ADL Microquartz showing the least effect at N09 concentrations of
3
592 ug/m (0.315 ppm). When a variety of quartz filter types were tested, the greatest quan-
tity of artifact nitrate was formed on the Gelman AE filter. Artifact nitrate formed on this
filter was calculated to be less than 2 ug/m (0.001 ppm) during a standard 24-hour HIVOL
measurement. The estimate was derived from drawing air samples of about 1 m containing 4,512
0
ug/m (2.4 ppm) NO, through the filters. The relative humidity was 30 + 10 percent.
Most recently, Spicer and Schumacher (1977) reported the' results of a comparison of
nitrate concentrations in samples collected on various filter types in Upland, California
during October and November, 1976 (Table 7-7). During the experiment, meteorological condi-
tions varied from warm, hazy weather to hot, dry, very clean desert wind conditions. Nitrate
analyses were performed by ion exchange chromatography. All filter types used had comparable
particle collection efficiencies according to the manufacturer's specifications. The ratio of
nitrate collected on Glass 1 to that collected simultaneously with identical HIVOL samplers on
Quartz 2 ranged from 4.8 to 36.6 and averaged 18.9. The ratio of nitrate collected on Glass 2
to Quartz 2 ranged from 2.8 to 49 and averaged 10.9.
7-21
-------
TABLE 7-7. COMPARISON OF NITRATE COLLECTED ON VARIOUS TILTERd TYPES
(SPICER AND SCHUMACHER, 1977; SPICER ET AL., 1978a)
ro
ro
DaLe
Oct. 15
Oct. 18
Oct. 19
Oct. 20
Oct. 21
Oct. 22
Oct. 25
Filter
Quartz 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 1
Quartz 2
Glass 2
Quartz 2
NO"
ug/m
1.6
1.6
14.1
0.39
17.0
1.2
28.7
2.3
18.8
0.82
11.2
0.49
38.4
0.78
Date Filter
Oct. 26 Quartz 1
Quartz 2
Oct. 27 Glass 2
Quartz 2
Oct. 28 Glass 1
Quartz 2
Oct. 29 Quartz 1
Quartz 2
Nov. 1 Quartz 2
Quartz 2
New. 2 Glass 2
Quartz 2
Nov. 3 Quartz 1
Quartz 2
NO" 3
(jg/m Date
1.3 Nov. 4
2.1
3.9 Nov. 5
0.52
9.1 Nov. 9
1.9
1.8 Nov. 10
2.9
1.7 Nov. 11
1.7
9.1 Nov. 12
1.6
0.68 Nov. 15
1.1
Fi Her
Glass 2
Quartz 2
Glass 2
Quartz 2
Glass 2
Quartz 2
Quartz 1
Quartz 2
Quartz 2
Quartz 2
Glass 2
Quartz 2
Glass 2
Quartz 2
NO'
l>g/m
3.0
1. 1
6.1
0.98
18.4
3.1
1.9
2.3
2.0
1.9
6.0
1.3
14.3
3.0
Glass 1 - "EPA Type" Gelman AA.
Glass 2 - Gelman A.
Quartz 1 - High purity quartz filter developed by Arthur D. Little under contract to EPA.
Quartz 2 - Pal If lex QAST.
-------
Recently, Marker et al. (1977) have reported laboratory observations of loss of particu-
late nitrate from collecting filters through chemical reaction with sulfuric acid aerosol,
formed from the photochemical oxidation of SO-. Most recently, Appel and coworkers (1979,
1980) have conducted several studies bearing on both positive artifact formation and loss of
nitrate from a variety of filter media. They concluded that gaseous HNO, is the principal
source of artifact nitrate formation, NCL collection only became substantial at high ozone
levels. Ambient particulate nitrate values (at San Jose and Los Alamitos, California) dif-
fered by up to a factor of 2.4 depending upon filter medium and sampling rate, in contrast to
the much larger sampling errors reported by Spicer and Schumacher (1977). Fluoropore (Teflon)
filters in low volume samplers were subject to small error although, under laboratory condi-
tions, passage of NhU- and HNO^-free air through the filter could result in the loss of up to
50 percent of the particulate nitrate. This is consistent with the relatively high vapor pres-
sure of ammonium nitrate (see page 6-49). They also reported that at low HMO, levels nitrate,
on glass fiber filters, indicated (within about 3 percent) total nitrate, i.e., particulate
nitrate plus HNO-> rather than particulate nitrate alone. They concluded that the degree of
error associated with glass fiber filter media could be expected to vary with location, time
of year and day, paralleling changes in nitric acid levels.
These results point to the conclusion that most of the existing data on urban ambient
nitrate concentrations must be considered to be of doubtful validity. It is, furthermore,
doubtful that any of these data can be corrected even if mechanisms for artifact formation are
clarified in the future since nitric acid, which presently appears to play a significant role
in positive artifact formation, is not routinely monitored.
It is, however, possible that data from certain monitoring sites may be validated in
special cases where it can be shown that the species responsible for the artifact processes
were all sufficiently low during the monitoring period of interest.
7.4.2 Analysis of Nitrate from Airborne Particulate Matter
Although most of the nitrate analysis methods described in this section found application
originally in analyzing nitrate in samples of natural waters, they have also been used to
analyze nitrate in aqueous extracts of particulate matter (Hermance et al., 1971) and in
solutions obtained through absorption of nitrogen oxides contained in streams of air
(Kieselbach, 1944b; Kothny, 1974).
The oldest procedures for analyzing nitrate used brucine ^-^^O^) (Intersociety
Committee for Ambient Air Sampling and Analysis, 1977a, Jenkins and Medsker, 1964; Lunge and
Lwoff, 1894; Robinson et al., 1959) or phenoldisulfonic acid (ASTM, 1968; Beatty et al., 1943;
Eastoe and Pollard, 1950; Intersociety Committee for Ambient Air Sampling and Analysis, 1977d;
Taras, 1950). Newer procedures extensively used to analyze nitrate in atmospheric particulate
matter extracts involve the nitration of xylenols [(CH3)2C6H3OH] and separation of the nitro-
derivative by extraction or distillation (Andrews, 1964; Buckett et al. , 1955; Hartley and
Asai, 1960; Holler and Huch, 1949; Intersociety Committee for Ambient Air Sampling and Analysis,
7-23
-------
1977b; Swain, 1957; Yagoda and Goldman, 1943). Recent comparison of a 2,4-xylenol procedure
(Intersociety Committee for Ambient Air Sampling and Analysis, 1977b) with the automated
copper-cadmium reduction and diazotization method (Technicon, 1978) in samples collected near
high density vehicular traffic, demonstrated a negative interference in the former up to a
factor of 3 (Appel et al., 1977).
Nitration of chromotropic acid [C,0H4(OH)2(SCLH)2] (West and Ramachandran, 1966) and
coumarin (CgHgCL) analogs (Laby and Morton, 1966; Skujins, 1964) also have been reported.
Small amounts of nitrate can be assayed by the quenching of the fluorescence after nitration
of fluorescein (C^nH-jpOc) (Axelrod et al., 1970). Nitrate analysis can also be accomplished
through reduction with Devarda alloy to ammonia (NhL) (Kieselbach, 1944a; Richardson, 1938) or
reduction of nitrate to nitrite by zinc (Chow and Johnstone, 1962), cadmium (Morris and Riley,
1963; Strickland and Parsons, 1972; Wood et al., 1967) or hydrazine (NH-NH-) (Mullin and
Riley, 1955). Automation instituted by the NASN improved the hydrazine reduction process by
curtailing the unwanted effects resulting from its sensitivity to motion (Morgan et al.,
1967b). The addition of antimony sulfate [Sb^SO^),] eliminates the chloride interferences
found in most nitration methods (West and Ramachandran, 1966). One brucine procedure circum-
vents the effect of chlorides by adding an excess of sodium chloride before nitration (Inter-
society Committee for Ambient Air Sampling and Analysis, 1977a).
Nitrate analysis by ion-selective electrodes has been used but has several disadvantages:
potential drifts caused by agitation speed, necessity of frequent re-standardization, inter-
ferences caused by nonspecificity of electrodes which respond to other ions in the aqueous
extracts, and non-stoichiometric absorption of the gases in the collecting reagent (DiMartini,
1970; Driscoll et al., 1972; Gordievski et al., 1972). In atmospheric analysis, the electrode
procedure has no advantage over direct UV determination of either nitrite formed in an alka-
line absorbent (Altshuller and Wartburg, 1960) or nitrate (Cawse, 1967) obtained after oxida-
tion and absorption of nitrogen oxides in alkaline permanganate (Kieselbach, 1944b; Kothny,
1974). Microscopic techniques also allow analysis of individual nitrate particles (Bigg et
al., 1974).
Small et al (1975) report an application of 'ion exchange chromatography to the measure-
ment of a wide variety of cations and anions including the nitrate and nitrite ion. The novel
feature of the method is the use of a second ion exchange "stripper" column (after a conven-
tional separating column) which effectively eliminates or neutralizes the eluting ions. Since
only the species of interest in a background of deionized water leaves the stripper column,
concentration determinations may be made by a simple and sensitive conductometric technique.
Mulik et al (1976) report the application of this technique to measurement of water-soluble
nitrate on HIVOL filters. The separator column, containing a strong basic resin, separates
anions in a background of carbonate eluant. The stripper column, containing a strong acid
resin, converts the sample ion and the carbonate eluant to nitric and carbonic acid, respec-
tively. Since carbonic acid has low conductivity, the nitrate ion alone is effectively
measured in a conductivity detector. Under the experimental conditions, sensitivity of 0.1
7-24
-------
pg/m£ was reported. The related standard deviation was 1 percent (95 percent confidence
level) for ten replicate injections at the 5 ug/ml level. At this concentration level, no
interferences were found from fluoride, chloride, nitrite, sulfite, sulfate, silicate, or
carbonate. Positive interferences were found for bromide and phosphate but the authors suggest
techniques for eliminating these.
In other recent work, Glover and Hoffsommer (1974) and Ross et al (1975) report a tech-
nique for assay of aqueous nitrate and nitrite extractions by conversion to nitrobenzene.
Both techniques involve the nitration of benzene in the presence of sulfuric acid to form
nitrobenzene, a relatively stable compound, followed by gas chromatographic analysis. Careful
calibration is required in both procedures, since a significant fraction of the nitrobenzene
formed may be lost to the acid layer. Ross et al. recommend a calibration procedure whereby a
standard is subject to the same reaction procedures as the unknown, while Glover and Hoffsommer
use internal calibration with added nitrotoluene. The lower detection limits reported by Ross
-12
et al. are in the range of 10 g nitrobenzene in a 1 u£ sample. Conversion efficiences for
KN03, KN02 and HN03 were reported as 90.3 + 7.9, 100.4 + 4.2 and 99.9 + 5.2 percent, respec-
tively. Glover and Hoffsommer report, similar recovery rates for KN03 and KN02.
Several methods in current use for analysis of nitrate in water and soil are applicable
also to analysis of nitrate derived from ambient air samples (Sections 7.4.3 and 7.4.4).
7.4.3 Nitrate in Water
Current methodology for determination of nitrate in water is summarized in Table 7-8. No
single method is satisfactory over the broad range of concentrations and water matrices to be
found in environmental samples. Since nitrate species are highly labile, a variety of tech-
niques have been used to preserve them during storage, including refrigeration, freezing, and
addition of sulfuric acid and of mercuric chloride. Simple refrigeration is adequate for
periods up to a day; freezing is effective for longer preservation (Brezonik and Lee, 1966).
Mercuric chloride is effective, especially when coupled with refrigeration or freezing, but
the mercuric ion slowly degrades columns used in various reduction methods (Table 7-8) and
also is toxic (Howe and Holley, 1969; U.S. EPA, 1974).
The strong absorption of the nitrate ion in the range 210-220 nm allows direct spectro-
photometric measurement (Altshuller and Wartburg, 1960; Bastian et al., 1957; Mertens and
Massart, 1973). Iron and nitrite are significant interferants. Absorbance of nitrate is also
influenced by changes in acidity. At 210 nm, a variation of 20 percent in perchloric acid
concentration causes an error of approximately 5 parts per thousand in nitrate measurement.
One author's report indicates that the spectrophotometric method is three times more sensitive
than the brucine method (Noll, 1945).
Nitrate ion selective electrodes have also been used for measurement of nitrate in water
(Keeney et al. , 1970; Langmuir and Jacobson, 1970). The method, however, is not currently in
widespread use.
7-25
-------
TABLE 7-8. ANALYTICAL METHODS FOR NITRATE IN WATER
Method
Range
(mg/£
nitrate-nitrogen)
Interferences
Reference
1. UV absorbance
2. Ion selective
electrode
0.1-10
0.2 - 1400
Nitration and Oxidation Reactions
3. Phenoldisulfonic
acid
4. Brucine
5. Chromotropic
6. Automated
fluorimetric
with substituted
benzophenone
7. Szechrome
Reduction Methods
8. Zinc
9. Amalgamated
cadmium
10. Copperized
cadmium
0.1 - 2.0
0.1 - 5.0
0.05- 4.0
0.05- 1.0
0.02- 1.0
<0.01- 1.0
<0.01- 1.0
11. Hydrazine-copper <0.01- 1.0
Organic matter
Chloride, ionic
strength
Chloride
Many, but all
readily removed
APHA, 1976
APHA, 1976
APHA, 1976
APHA, 1976
APHA, 1976
Organic color, Afghan and
chloride, sulfide, Ryan, 1975
but readily removed
Unknown
Sensitivity
varies with age
of column
Sensitivity
varies with age
of column
Sensitivity
varies with age
of column
Reduction is pH
sensitive
12. Devarda's alloy
2 ->200
Szekely, 1975
O'Brien and
Fiore, 1962
APHA, 1976
Technicon, 1978
U.S. EPA, 1974
APHA, 1976
Strickland and
Parsons, 1972
Kamphake,
1976
APHA, 1976
7-26
-------
Wet chemical methods for nitrate analysis are colorimetric and fall generally into two
major reaction categories: (1) nitration reactions which involve the substitution of a hydro-
gen in an aromatic compound by the NCL moiety, and (2) reduction of nitrate to nitrite.
Nitration and oxidation reactions generally require a strong acid medium as well as
heating. Since it is desirable that only one extraction be used for all forms of mineral
nitrogen, methods of analysis not subject to chloride interference are preferred because many
air samples may contain chloride derived from suspended sea salts. Some nitration methods are
subject to serious chloride interferences. While chloride interferences can be eliminated
from the brucine method (Intersociety Committee for Ambient Air Sampling and Analysis, 1977a),
experience has shown that results obtained using this method are difficult to reproduce.
Interferences from nitrite and chlorine can be eliminated in the chromotropic acid method
(APHA, 1976).
Procedures which involve reduction of nitrate to nitrite are widely used because there is
a simple, sensitive and well-tested analytical procedure for determination of the nitrite
(NCO ion (Section 7.2.1). Although nitrate is readily reduced by a variety of agents includ-
ing hydrazine, metallic zinc or cadmium, difficulties with quantitative recovery have been
reported (Henriksen, 1965; Mullin and Riley, 1955; Nydahl, 1976; O'Brien and Fiore, 1962;
Strickland and Parsons, 1972; Technicon, 1978; U.S. EPA, 1974). Techniques presently recom-
mended to avoid these difficulties have been documented by the American Public Health Associa-
tion (Stainton, 1974). Columns using copperized cadmium (Strickland and Parsons, 1972; U.S.
EPA, 1974) or amalgamated cadmium granules (National Research Council, 1978) or copperized
cadmium wire (Bremner 1965) give stoichiometric or near stoichiometric reductions. These
methods are widely used and are regarded as accurate, sensitive and acceptable procedures
(APHA, 1976; National Research Council, 1978; U.S. EPA, 1974). Nitrate can be reduced quanti-
tatively to ammonia by Devarda's alloy and subsequently analyzed by titration or colorimetric-
ally.
7.4.4 Nitrate in Soil
As in the case of certain techniques for measurement of nitrate in water, some techniques
used in analysis for nitrate in soil can be adapted for atmospheric work.
Nitrate levels in soil samples can change rapidly through nitrification, denitrification
and flushing of nitrate. Biocides have been used to prevent microbial activity but they are
often ineffective (Bremner, 1965). Cold storage (Allen and Grimshaw, 1962) and rapid air or
oven drying have also been used. Most extraction methods employ a salt solution such as
CaSO,, KpSO, or KC1 (Bremner, 1965). Methods of removing turbidity include flocculation with
aluminum hydroxide (Cawse, 1967) or calcium salts as well as the use of activated charcoal,
ion exchange resins or hydrogen peroxide, but the last three techniques may cause changes in
nitrate content (Bremner, 1965). Ultraviolet methods used in analysis of atmospheric nitrate
samples require similar flocculation techniques to remove turbidity, color and other inter-
ferences.
Analytical methods are summarized in Table 7-9.
7-27
-------
TABLE 7-9. METHODS FOR DETERMINATION OF NITRATE IN SOILS
Method
Range, mg/£c
Interferences
References
ro
CD
1. Ion electrode
2. Phenoldisulfonic
acid
3. Brucine
4. Reduction of NO,
by Cd Griess- i
Illosvay method
2 -1400
0.1 - 2
0.1 - 2
0.02-0.1
5. Reduction to NH3 by 1 -1000
Devarda alloy, steam
distillation of NH,
6. UV absorbance
Chloride, bromide, nitrite, iodide, Carlson and
sulfide, ionic strength Keeney, 1971
Chloride, organic matter, nitrite Bremner, 1965
None
Bremner, 1965; Bremner
and Keeney, 1965,
APHA, 1976
Bremner, 1965; Bremner
and Keeney, 1965
APHA, 1976
Labile amide, phosphate, nitrite Bremner, 1965
Cawse, 1967
Range on soil basis varies widely depending on soil:solution ratio of extractant.
-------
7.4.5 Nitrate in Plant and Animal Tissue
Methods analogous to those described above have been applied to measurement of nitrate in
plant and animal tissue. Nitrate ion concentrations have been measured in tobacco extracts
using a spectrophotometric procedure (Barkemeyer, 1966). Wegner (1972) has described a proce-
dure for determining both nitrate and nitrite in biological fluids. Fudge and Truman (1973)
described the analysis of nitrate and nitrite in meat products. Methods of analysis for plant
tissue have been recently described by Carlson and Keeney (1971).
7.5 SAMPLING AND ANALYTICAL METHODS FOR NITROSAMINES
The sampling and analytical techniques for nitrosamines depend on the medium in which the
nitrosamine to be sampled and analyzed is found.
Since it is of some importance to place human exposure via the atmospheric medium in
perspective with regard to other media such as food and potable water, the discussion of
analytical techniques in this section includes methodology appropriate to the three most
important media: air, food and water.
7.5.1 Nitrosamines in Air
Because of the low nitrosamine concentrations in air, sample concentration methods are
necessary. One suitable concentration procedure is the adsorption of nitrosamines on a solid
substance. Bretschneider and Matz (1976) report using chemically pure active carbon. Another
effective technique is the use of chemically bonded stationary phases (Pellizzari et al.,
1975). In this method, nitrosamines are collected by passing air through a cartridge packed
with a solidsorbent. Samples are desorbed by flash heating the cartridge contents into a gas
chromatographic column. The chromatograph may then be interfaced to a mass spectrometer for
component identification and measurement. The sorbents Tenax and Chromosorb have been
evaluated at sampling rates up to 9 £/min. Results showed that they maintained efficiencies
of > 90 percent. Carbowax 600 and 400, and oxypropionitrile, coated or chemically bonded to a
support, were also highly efficient (> 90 percent).
EPA's National Enforcement Investigations Center (U.S. EPA, 1977a, 1977b) reports the use
of a basic collecting medium (IN KOH) shielded by foil to preclude irradiation by light. The
KOH solutions are subsequently extracted with dichloromethane. Before evaporative concentra-
tion, 2,2,4 ' trimethylpentate was added as a keeper. It is important in using either solid
sorbents or liquid KOH traps, that the procedure be carefully checked to ensure that the
measurement is free of artifacts.
Fine et al. (1974) have developed a method for detecting N-nitroso compounds based on
catalytic cleavage of the N-NO bond and the subsequent infrared detection of chemiluminescence.
The technique, called thermal energy analysis (TEA), is coupled with gas chromatography and,
sometimes, with high-pressure liquid chromatography (Fine and Rounbehler, 1975). The technique
is highly sensitive with a detection limit of about 1 ng/m£. The TEA detector operates by
splitting the nitrosyl radical off N-nitroso compounds coming from a chromatographic column.
7-29
-------
The nitrosyl radical is then reacted with ozone, yielding excited nitrogen dioxide which
subsequently decays to the ground state by emission of near-infrared radiation. The intensity
of this radiation is proportional to the number of nitrosyl radicals present. Artifact forma-
tion has not been reported to be a significant problem in the method (Pellizzari, 1977). TEA
responses have also been reported for some compounds containing the 0-nitroso, 0-nitro,
C-nitroso, and N-nitroso groups and two recent papers describe approaches for distinguishing
N-nitroso responses (Hansen et al., 1979; Krull et al., 1979).
7.5.2 Nitrosamines in Water
The usual precautions employed in the collection of samples for organic analysis should
be followed when sampling water for nitrosamine analysis. Stabilization to pH 8 may be needed
and samples should be protected from light and kept cold because of the photosensitivity of
nitrosamines.
Several analytical procedures for the determination of N-nitroso compounds in water have
been reported. Fine et al (1975) reported two concentration and extraction procedures—one
based on a liquid-liquid extraction, and the other based on the adsorption of the organic
fraction and its subsequent extraction with chloroform. Gas chromatography and high-pressure
liquid, chromatography, each combined with detection by TEA, have been used by Fine and
co-workers (1975) to measure part per trillion concentrations of volatile and non-volatile
non-ionic nitroso compounds, respectively, in water supplies.
Older techniques for the detection and estimation of N-nitrosamines in water are polaro-
graphy (Walters, 1971) and colorimetry (Mohler and Mayrhofer, 1968), but neither method has
the sensitivity required for environmental samples. Furthermore, the colorimetric method has
exacting experimental conditions and cannot be used for complicated mixtures.
7.5.3 Nitrosamines in Food
Determination of nitrosamines in foodstuffs is made difficult by the complexity of food,
many components of which contain nitrogen and react chemically in a manner similar to nitros-
amines. Many methods have been used to detect nitrosamines in food, including polarography,
UV absorption, thin layer chromatography, and gas chromatography, but these methods generally
have been plagued with contamination and artifact problems. Gas chromatography-mass spectro-
metry (GC-MS) is presently the most acceptable procedure for the measurement of nitrosamines
in food. Wassermann (1972) and Eisenbrand (1975) have published surveys of analytical tech-
niques used in the isolation and detection of nitrosamines.
GC-MS also appears to be the most acceptable method for analysis of nitrosamines in
tobacco smoke, but nitrogen-specific GC detectors have also been used (Spincer and Westcott,
1976).
7.6 SUMMARY
Since the publication in 1971 of the original document Air Quality Criteria for Nitrogen
Oxides, there have been significant changes in the technology associated with measurement of
ambient concentrations of NO and NO -derived pollutants.
A X
7-30
-------
With regard to the measurement of NCL, the original Reference Method, the Jacobs-Hochheiser
technique, was discovered to have unresolvable technical difficulties and was withdrawn by the
U.S. Environmental Protection Agency on June 8, 1973. Since that time, adequate methodology
has been validated for measuring both NO and NO- in concentrations encountered in ambient air.
Accurate techniques utilizing standardized gas sources, permeation tubes, or a gas-phase
titration have commonly been used for calibration. The chemiluminescence technique is specific
for NO. Nitrogen dioxide concentrations can be determined also with appropriate modifications
of this method. Such a modification was adopted on December 1, 1976, as the Reference Method
for NO- measurements. As of December 14, 1977, the sodium-arsenite procedure and the TGS-ANSA
method were designated equivalent methods, suitable for 24-hour instrumental averaging times.
The chemiluminescence method must be used with care when modified for measurement of N0~ since
a number of compounds which may be present in the atmosphere may interfere with the instru-
ment's accuracy. Variations of the Griess-Saltzman method are specific for N0?. Under certain
circumstances, ozone can be a significant negative interferent in the method. Dynamic calibra-
tion of the Griess-Saltzman methods in current use is considered necessary for reliable
measurement.
Although adequate chemical techniques exist-for the determination of the nitrate fraction
of suspended particulate matter in ambient air, a number of very recent reports have pointed
to significant positive nitrate artifact formation on the glass fiber filters in widespread
use for collecting the particulate. In addition, negative artifacts result from the volatili-
zation of the ammonium nitrate. At this time, therefore, almost the entire urban data base on
ambient nitrate concentrations must be considered to be of doubtful validity.
Recent discovery of N-nitroso compounds in food, water, tobacco products, and ambient air
has prompted the development of a variety of new instrumental techniques in the last few
years. Measurement technology is still developing and insufficient time has elapsed for
careful evaluation of existing techniques, particularly in the area of sampling.
Development of long pathlength infrared absorption techniques has recently made possible
the observation of nitric acid in ambient air, but the procedure is expensive and does not
currently lend itself to routine atmospheric measurement. Other analytical methods are avail-
able for routine monitoring but have yet to be carefully evaluated.
7-31
-------
7.7 REFERENCES
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Saltzman method. Anal. Chem. 51:1002-1005, 1979.
Afghan, B. K. , and J. F. Ryan. Substituted benzophenone as a fluorometric reagent in auto-
mated determination of nitrate. Anal. Chem. 47:2347-2353, 1975.
Allen, S. E. , and H. M. Grimshaw. Effect of low-temperature storage on the extractable
nutrient ions in soils. J. Sci. Food Agric. 13:525-529, 1962.
Altshuller, A. P., and A. F. Wartburg. Ultraviolet determination of nitrogen dioxide as
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American Public Health Association. Standard Methods for the Examination of Water and Waste-
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(Griess-Saltzman reaction) ASTM Designation: D1607-69. I_n: 1974 Annual Book of ASTM
Standards, Part 26. Gaseous fuels; Coal and Coke; Atmospheric Analyses. American
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American Society for Testing and Materials. Interlaboratory Cooperative Study of the Pre-
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and Materials, Philadelphia, PA, 1974b.
Andrews, D. W. W. A sensitive method for determining nitrate in water with 2,6-xylenol.
Analyst (London) 89:730-734, 1964.
Appel, B. R. , E. M. Hoffer, E. L. Kothny, and S. M. Wall. Interference in 2,4-xylenol pro-
cedure for nitrate determination in atmospheric aerosols. Environ. Sci. Technol. 11:
189-190, 1977.
Appel, B. R. , S. M. Wall, Y. Tokiwa, and M. Haik. Interference effects in sampling particu-
late nitrate in ambient air. Atmos. Environ. 13:319-325, 1979.
Appel, B. R. , S. M. Wall, Y. Tokiwa, and M. Haik. Simultaneous nitric acid, particulate
nitrate and acidity measurements in ambient air. Atmos. Environ. 14:549-554, 1980.
Axelrod, H. D. , J. E. Bonelli, and J. P. Lodge, Jr. Fluorimetric determination of trace
nitrates. Anal. Chim. Acta 51:21-24, 1970.
Barkemeyer, V. H. The determination of nitrate in tobacco by UV-spectrometry. Beitr.
Tabakforsch. 3:455-459, 1966.
7-32
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Bastian, R. , R. Weberling, and F. Pal ill a. Ultraviolet spectrophotometric determination of
nitrate. Application to analysis of alkaline earth carbonates. Anal. Chem. 29:1795-
1797, 1957. ~
Baumgardner, R. E., T. A. Clark, J. A. Hodgeson and R. K. Stevens. Determination of an ozone
interference in the continuous Saltzman nitrogen dioxide procedure. Anal. Chem. £7:515-
521, 1975.
Beard, M. E. , and J. H. Margeson. An Evaluation of Arsenite Procedure for Determination of
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ment of air pollutants. Anal. Chem. 45:443A-449A, 1973.
Stevens, R. K. and W. A. McClenny. Introduction. In: Current Methods to Measure Atmospheric
Nitric Acid and Nitrate Artifacts, Presentations at a Workshop, U.S. Environmental
Protection Agency, Southern Pines, North Carolina, October 3-4, 1978. R. K. Stevens,
ed:, EPA-600/2-79-051, U.S. Environmental Protection Agency, Research Triangle Park, NC,
March 1979. pp. 1-7.
7-41
-------
Strickland, J. D. H. , and T. R. Parsons. A Practical Handbook of Seawater Analysis, Second
Edition. Bulletin 167, Fisheries Research Board, Ottawa, Ontario, Canada, 1972. pp.
71-76.
Swain, J. S. Determination of nitrates in boiler water by 1:3 xylen-4-ol (2:4-xylenol).
Chem. Ind. (London): 479-480, April 20, 1957.
Sweeney, M. P. , D. J. Swartz, G. A. Rost, R. MacPhee, and J. Chao. Continuous measurement of
oxides of nitrogen in auto exhaust. J. Air Pollut. Control Assoc. 14:249-254, 1964.
Szekely, E. Szechrome analytical reagents. Research Department Authority, Ben-Gurion
University, Negev, Israel, 1975.
Taras, M. J. Phenoldisulfonic acid method of determining nitrate in water. Photometric
study. Anal. Chem. 22:1020-1022, 1950.
Technicon Industrial Systems. Technicon Auto Analyzer II. Nitrate and Nitrite in Water and
Waste Water (Range: 0.04-2.0 mg N/I). Industrial Method No. 100-70W/B, Technicon Instru-
ments Corp., Tarrytown, NY, January 1978.
Tesch, J. , and R. Sievers. Selective collection and measurement of particulate nitrate and
gaseous HN03 in ambient air. I_n: Current Methods to Measure Atmospheric Nitric Acid and
Nitrate Artifacts, Presentations at a Workshop, U.S. Environmental Protection Agency,
Southern Pines, North Carolina, October 3-4, 1978. R. K. Stevens, ed., EPA-600/2-79-051,
U.S. Environmental Protection Agency, Research Triangle Park, NC, March 1979. pp. 67-77.
Thomas, M. D. , J. A. MacLeod, R. C. Robbins, R. C. Goettelman, R. W. Eldridge, and L. H.
Rogers. Automatic apparatus for determination of nitric oxide and nitrogen dioxide in
the atmosphere. Anal. Chem. 28:1810-1816, 1956.
Treadwell, F. P., and W. T. Hall. Analytical chemistry. I_n: Quantitative Analysis, Volume
II, 8th ed. John Wiley and Sons, Inc., New York, 1935. p. 318.
Tuazon, E. C. , A. M. Winer, R. A. Graham, and J. N. Pitts, Jr. Measurements of ambient HN03
in the California south coast air basin by kilometer pathlength Fourier transform in-
frared spectrometry. I_n: Current Methods to Measure Atmospheric Nitric Acid and Nitrate
Artifacts, Presentations at a Workshop, U.S. Environmental Protection Agency, Southern
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Environmental Protection Agency, Research Triangle Park, NC, March 1979. pp. 9-26.
Tuazon, E. C. , R. A. Graham, A. M. Winer, R. R. Easton, J. N. Pitts, Jr., and P. L. Hanst. A
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dioxide (chemiluminescent). Fed. Regist. 38:15177-15180, June 8, 1973.
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7-42
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U.S. Environmental Protection Agency. Ambient air monitoring reference and equivalent methods.
Fed. Regist. 40:7042-7070, February 18, 1975.
U. S. Environmental Protection Agency. Ambient air monitoring references and equivalent
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procedure. Fed. Regist. 4J:52686-52695, December 1, 1976b.
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in the Central United States. EPA-330/1-77-001, U.S. Environmental Protection Agency,
Denver, CO, February 1977a.
U. S. Environmental Protection Agency. Reconnaissance of Environmental Levels of Nitrosamines
in the Southeastern United States. EPA-330/1-77-009, U.S. Environmental Protection
Agency, Denver, CO, August 1977b.
Walters, C. L. The detection and estimation of trace amounts of N-nitrosamines in a food
matrix. Lab. Pract. 20:574-578, 1971.
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pounds Analysis and Formation, Proceedings of a Working Conference, International Agency
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Preussmann, E. A. Walker, and W. Davis, eds. , IARC Scientific Publication No. 3, Inter-
national Agency for Research on Cancer, Lyon, France, 1972. pp. 10-15.
Wegner, T. N. Simple and sensitive procedure for determining nitrate and nitrite in mixtures
in biological fluids. J. Dairy Sci. 55:642-644, 1972.
West, P. W. , and T. P. Ramachandran. Spectrophotometric determination of nitrate using chro-
motropic acid. Anal. Chim. Acta 35:317-324, 1966.
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7-43
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8. OBSERVED ATMOSPHERIC CONCENTRATIONS OF NO
AND OTHER NITROGENOUS COMPOUNDS x
8.1 ATMOSPHERIC CONCENTRATIONS OF NOV
A
In this section, selected examples of ambient concentrations of NO are presented in
A
order to place possible human exposure in nationwide perspective. N02 is given particular
emphasis since it is the oxide of nitrogen of most concern to human health. The data presentei
are not intended to be a compendium of ambient monitoring activities. They have been
summarized to give a representative picture of N0? concentrations in the United States and, in
particular, to provide a rational basis for deciding whether or not existing ambient N02
levels are a cause for concern when viewed in the context of the health and welfare effects
reviewed elsewhere in this document.
The relationship, nationwide, between short-term peaks and annual average concentrations
is reviewed to estimate the variability in peak-to-mean ratios of NOp concentrations. If the
variability is small, then a rational basis for protecting human health and welfare might be
derived from either considerations of the lowest peak concentrations or of the lowest annual
means considered tolerable. If the variability is large, then this fact would point to the
necessity of considering separately the effects of peak and long-term NO,, concentrations.
The question of whether or not any "typical" diurnal .pattern of N02 concentrations exists
nationwide is discussed. This question has bearing on the problem of estimating human exposure
to ambient NOp concentrations. Other considerations bearing on human exposure are also
illustrated with recent data on the temporal and spatial variability of N02 concentrations in
a single airshed. Data are also presented to illustrate certain general types of atmospheric
mechanisms potentially leading to high short-term N02 concentrations. An example is given of
late morning NOp peaks which typify photochemical pollution processes such as occur frequently
in the Los Angeles area and elsewhere. Also illustrated is another, less familiar, mechanism,
ozone titration, in which NO is rapidly oxidized to N02 by ambient ozone. This mechanism is
of interest because of its potential for producing high NOp concentrations both in urban areas
and in plumes from point sources. Peak concentrations so produced generally occur later in
the day than those produced by photochemical processes.
Where examples of atmospheric mechanisms leading to high N02 concentrations are described.
the examples are to be viewed as illustrative only. Detailed evaluations of the relative
importance of different mechanisms as well as the relative impacts of various source types and
appropriate ameliorative actions are outside the scope of this document and are best con-
sidered in the State Implementation Plans on a case-by-case, area-by-area basis.
It is important to note that although a careful attempt has been made to include only
high quality monitoring data in this chapter, the data cited have not usually been derived
from monitoring activities subject to a formal quality assurance program. Identification of
the analytic procedures used to obtain the data cited in this section is generally available
8-1
-------
in the tables accompanying the text. Reference is made to Chapter 7 of this document for a
discussion of the reliability of these procedures. In the absence of a formal program of
audit for the wide variety of laboratories conducting ambient monitoring, the estimates of
reliability given in Chapter 7 are best considered as upper bounds. Specifically, the
California Air Resources Board's (CARB) Air Monitoring Technical Advisory Committee (AMTAC)
composed of the CARB, the Air Industrial Hygiene Laboratory, EPA Region IX, and the local air
pollution control districts, have reported NO , NO, and N09 concentrations to be on the
J\ £
average biased about 14 percent higher than the true value. The bias was independently
determined by three agencies participating in AMTAC and applies to any analyzer calibrated by
the manual Saltzman procedure. This affects virtually all California sites. A joint report
is being prepared by the Air Industrial Hygiene Laboratory Section of the Department of Health
Services and the CARB regarding factors affecting the Saltzman reagent. The formulation of
the reagent used in the calibration procedure contained 0.5 percent sulfanilic acid, 5.0
percent acetic acid, and 0.005 percent NEDA (see Chapter 7). The bias reported applies to
both static and dynamic calibration procedures. All the California data cited in this chapter
are to be considered subject to biases of the reported magnitude.
8.1.1 Background Concentrations of NO
Data on background concentrations of nitrogen oxides are extremely limited. Robinson and
Robbins (1972) summarized measurements of NO and N02 concentrations from various locations,
such as Panama, the mid-Pacific, Florida, Hawaii, Ireland, North Carolina, Pike's Peak, and
Antarctica. From these data, they estimated that the mean background NO and N0~ concentra-
tions for land areas between 65°N and 65°S are 3.8 ug/m3 (0.002 ppm) and 7.5 |jg/m3 (0.004
ppm), respectively. The measurements cited for North Carolina and Pike's Peak indicate that
background concentrations of NO and N0? combined can range from 0.001 to 0.005 ppm in remote
areas of the United States (Robinson and Robbins, 1972).
More recent measurements using modern methods have yielded results pointing to lower
values. Noxon (1975) reports lower tropospheric N09 concentrations at a remote site in
3
Colorado mountains of up to 0.20 ug/m (0.0001 ppm) measured by ground-based absorption
spectroscopy. In a more extensive study, Noxon (1978) reports detailed background measure-
ments at the Colorado site and at a number of other widely dispersed locations using methodo-
logy with a sensitivity of 0.03 ug/m (0.015 ppb) at sea level. The author concludes that in
the truly unpolluted troposphere the column abundance of N09 is less than 5 x 10 molecules/
2
cm . Assuming an effective length for the NO, column of about 2 km (Chameides, 1975; Crutzen
3
et al., 1978), this implies a ground level N0? background concentration of less than 0.3 ug/m
(0.15 ppb). If the length of the column is 0.5 km (Ritter et al., 1979), background NO, con-
3
centrations of 0.94 ug/m (0.5 ppb) would be implied. In addition, Noxon reports that the
ground level N0~ concentration produced at distances greater than 50 km from urban centers
seldom exceeds that for truly unpolluted air by more than a factor of 2. Measurements by
8-2
-------
Ritter et al. (1979) using chemiluminescence analyzers at a site in Michigan showed NO long-
. A
term average concentrations in presumably clean air coming from Canada to be in the range of
0.56 to 0.94 |jg/m (0.3 to 0.5 ppb). Measurements made at the Colorado site led Ritter et al.
to conclude that tropospheric NO is confined to the lower 0.5 km of the troposphere. Table
8-1, taken directly from Ritter et al., summarizes background NO measurements.
TABLE 8-1. BACKGROUND N0x MEASUREMENTS (RITTER ET AL., 1979)
Author
Junge (1956)
Lodge and Pate (1966)
Breeding et al . (1973)
Moore (1974)
Drummond (1976)
Cox (1977)
Galbally (1977)
Ritter et al. (1979)
Location
Florida
Panama
Central U.S.
Boulder, CO
Wyoming
Ireland
S. Australia
Rural MI
Fritz Peak, CO
Date
1956
1966
1973
1974
1976
1977
1977
1977
1977
NO Concentration
Observed, ppb
1.0-2.0
0.5
1.0-3.0
0.1-0.3
0.1-0.4
0.2-2.0
0.1-0.5
0.3-0.5
0.2 and up
8.1.2 Ambient Concentrations of NO
8.1.2.1 Monitoring for NO --Data from stationary monitoring sites may be used to estimate the
exposure experienced by nearby receptors. The air arriving at a fixed observation point at
any time has a unique history. The aspects of this history which determine the ambient concen-
trations and relative amounts of nitrogen oxides are the sources encountered along the trajec-
tory and a variety of meteorological variables. Atmospheric reactions, such as those that
oxidize NO to N0?, are functions of the concentrations of pollutants emitted to the atmosphere,
temperature, sunlight, and time. Other meteorological factors, such as wind speed, vertical
temperature structure, and the region's topography, affect the dispersion and dilution of both
the directly emitted pollutants and the products of atmospheric reactions.
Given the complex nature of the processes which give rise to potential human exposures,
one practical means of estimating these exposures is by monitoring atmospheric concentrations.
Air monitoring data relevant to assessing ambient levels of NO or NO -derived pollutants are
collected to meet a variety of specific objectives including:
8-3
-------
• Determination of current air quality and trend analysis
• Determination of the state of attainment of National
Ambient Air Quality Standards
• Preparation of environmental impact statements
• Development of effective control strategies and
evaluation of their effectiveness
• Development and validation of mathematical models
which relate the strength of source emissions to
predicted concentrations for a variety of meteorological
and topographic conditions
• Research, such as studies of the effects of ambient air
pollution on human health and welfare.
In general, each specific objective requires special consideration as to site location,
frequency and techniques of sampling, and the total amount of data collected. For example,
several years of N0? data from a number of strategically located sites distributed nationwide
might be required for national pollutant trends analysis. A greater number of sites, also
collecting data on a regular basis throughout the year, might be necessary for determining
compliance with the National Ambient Air Quality Standards. In contrast, only a few carefully
chosen days of detailed measurements of various pollutant concentrations and emissions, and
meteorological parameters as well, might suffice for validation of mathematical air quality
models. The ambient air quality data reported in this chapter are mainly related to the first
of the above objectives.
Once an air monitoring station's location is chosen, additional practical considerations
arise relating to the actual placement of probes for sampling ambient air. Building surfaces
and other obstacles may possibly scavenge N0~ from ambient air. For this reason, probes must
be located a certain minimum distance away from such obstacles. It is important, also, that
the oxides of nitrogen in the parcel of air sampled have had sufficient time to undergo
atmospheric chemical reactions (such as conversion of NO emissions to NO-) characteristic of
the polluted atmosphere. For this reason, and to avoid sampling air dominated by any one
source, probes must also be located some minimum distance from primary sources. Siting
considerations have been reviewed in more detail by Ludwig and Shelar (1978); and EPA has
proposed guidelines for air quality surveillance and data reporting which include more
detailed discussion of considerations noted briefly in this section (U.S. Environmental
Protection Agency, 1978).
8-4
-------
8.1.2.2 Sources of Data—The emphasis in monitoring NO has been primarily on NCk, since it
is the only nitrogen oxide for which a National Ambient Air Quality Standard has been set.
The most complete collection of monitoring data for the United States is EPA's National
Aerometric Data Bank (NADB), which receives data from a variety of Federal, state, and local
air monitoring programs. The analytical methods with sufficient temporal resolution to assess
short-term exposures are continuous versions of the Griess-Saltzman method (e.g., the Lyshkow-
modified Griess-Saltzman) and chemiluminescence. These data are reported as 1-hr average
concentrations and are archived in SAROAD (Storage and Retrieval of Aerometric Data) a
computer-assisted storage and retrieval system of EPA's NADB. Other data, using 24-hr
instrumental averaging, are also available in SAROAD. Most of these data were obtained using
the sodium arsenite method. Most frequently, these data are not collected every day but on a
regular schedule yielding 24-hr measurements, typically once every 6 days.
Another important source of data in recent years, albeit only from the greater St. Louis
area, is the intensive monitoring activity carried out as part of the Regional Air Pollution
Study (RAPS). Nitrogen dioxide data from this study are routinely available on an hourly
basis (minute-by-minute data are also available) as obtained with chemiluminescence monitors
at 25 Regional Air Monitoring Sites (RAMS). These data are archived in a special RAPS data
base maintained at EPA's Research Triangle Park Environmental Research Center.
8.1.3 Historical Measurements of NO Concentrations
In past years, the EPA Continuous Air Monitoring Program (CAMP) provided the data set
covering the longest period of time on both NO and N02 concentrations available in this
country. Caution is necessary in using these data because collection and reporting proce-
dures were not subject to detailed quality assurance checks and more than one operation and
maintenance procedure may have been used over the years at a given site. However, the data
base presented here does not include data taken by the Jacobs-Hochheiser method, because this
method has been withdrawn by EPA (Chapter 7). The data collected provide a useful historical
perspective on trends of NO concentrations. Table 8-2 presents 12 years of measurements of
A
nitrogen oxide (NO) at 6 CAMP stations for the time period 1962-1973. The annual average NO
concentrations are plotted in Figure 8-1. Trends in concentrations during 1962-1973 were
generally upward for all sites monitored. When the annual means are grouped by 5-year periods,
1962-1966 and 1967-1971 (Table 8-3), both the second highest value and the annual means
averaged over all CAMP cities showed an increase of about 15 percent from the earlier to later
time period. Similar, though more geographically variable, results obtained for nitrogen
dioxide (N02) concentrations at most CAMP sites (Table 8-4, 8-5; Figure 8-2). St. Louis data
showed a marked decrease, however, in both annual average concentrations and average of second
highest value between the two 5-year periods (Table 8-5). Upward trends in annual average N02
concentrations were observed in 3 of the 5 CAMP cities over the 9-year period, 1963 to 1971.
Figure 8-3 is a graphical presentation of changes in N02 air quality in the Los Angeles basin
between the years 1965 and 1974. The average increase in annual means for 11 stations in the
basin was about 20 percent, but individual area results varied widely, as seen in Figure 8-3.
8-5
-------
TABLE 8-2. YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITRIC OXIDE AT CAMP STATIONS,
MEASURED BY THE CONTINUOUS SALTZMAN COLORIMETRIC METHOD (U.S. EPA. 1975a)
00
Concentration,
Denver
Year
1962
1963
1964
1965
1966
1967
1968
1969
Mean
--
--
--
37
(30)
49
(39)
49
(39)
49
(39)
49
(39)
Max
--
--
--
652
(522)
627
(502)
590
(472)
738
(590)
677
(542)
Washington
Mean
37
(30)
49
(39)
49
(39)
37
(30)
49
(39)
62
(50)
49
(39)
49
(39)
Max
788
(630)
1,060
(848)
1.070
(856)
751
(600)
1,240
(1,000)
1,390
(1,112)
837
(670)
959
(767)
, pg/m3 (ppb), 25°C
Chicago
Mean
123
(98)
123
(98)
123
(98)
123
(98)
123
(98)
98
(78)
86
(")
135
(108)
Max
739
(704)
615
(492)
1,105
(884)
750
(600)
775
(620)
763
(610)
739
(591)
1,920
(1,536)
St. Louis
Mean
--
--
49
(39)
37
(30)
37
(30)
49
(39)
37
(30)
37
(30)
Max
--
--
923
(738)
443
(354)
688
(550)
393
(314)
492
(394)
873
(698)
Cincinnati
Mean
37
(30)
37
(30)
49
(39)
37
(30)
49
(39)
37
(30)
74
(60)
49
(39)
Max
702
(562)
615
(492)
787
(630)
750
(600)
1,230
(984)
1,685
(1,348)
1,242
(994)
861
(689)
Phi ladelphia
Mean Max
25 431
(20) (345)
62 1.845
(50) (1,476)
62 1,400
(50) (1,120)
62 1,083
(50) (866)
74 2.290
(60) (1.832)
74 1,820
(60) (1,456)
62 1,735
(50) (1,388)
49 1,083
(39) (866)
(continued)
-------
TABLE 8-2. (continued)
Concentration, ug/m (ppb).
Denver
Year Mean
1970 62
(50)
1971 62
(50)
1972 74
(60)
1973 74
(60)
-j ,
Max
750
(600)
677
(542)
788
(630)
652
(522)
Washington
Mean
62
(50)
49
(39)
86
(69)
123
(98)
Max
1,430
(1,144)
775
(620)
825
(660)
640
(512)
Chicago
Mean
172
(137)
135
(108)
160
(128)
221
(177)
Max
2,240
(1.792)
824
(659)
787
(630)
775
(620)
25°C
St. Louis
Mean
62
(50)
62
(50)
62
(50)
74
(60)
Max
689
(551)
615
(492)
714
(571)
750
(600)
Cincinnati
Mean
49
(39)
62
(50)
49
(39)
49
(39)
Max
960
(768)
750
(600)
763
(610)
689
(551)
Phi lade) phi a
Mean
74
(60)
49
(39)
62
(50)
--
Max
1.672
(1,338)
935
(748)
800
(640)
--
-------
&MICA6O C8MP'
<€
1
9EWVER CAMP
S
•800
" so
J I
PHILADELPHIA CAW
t a e !
T
ST. S.OUIS CAM?
°S2 "O '©« °®5 *S6 °®y °®8 'S3 TO 71
YEAR
Figure 8-1. Trend lines for nitric oxide annual averages in five
CAMP cities. —D— :data satisfying NADB minimum sampling
criteria; —o— : invalid average (based on incomplete data).
*!Mote change in ordinate scale for these data (U.S. EPA, 1973).
8-8
-------
TABLE 8-3. FIVE-YEAR AVERAGES OF NITRIC OXIDE CONCENTRATIONS AT CAMP STATIONS,
MEASURED BY CONTINUOUS SALTZMAN COLORIMETRIC METHOD (U.S. EPA, (1973)
Station
Average-Concentration,
(ppb), 25°C
Average of Annual
2nd Highest Value
(ppb), 25°C
1962-1966
1967-1971
Change, %
1962-1966
1967-1971
Change, %
Chicago
Cincinnati
Denver 44.9 (35.9)
Philadelphia 55.2 (44.2)
St. Louis 39.8 (31.8)
CAMP average 61.2 (49.0)
122.6 (98.1) 125.4 (100.3) + 2
43.8 (35.0) 53.6 (42.9) +22
54.4 (43.52) +21
65.4 (52.3) +18
47.6 (38.1) +19
69.3 (55.4) +13
731 (584.8)
782 (625.6)
633 (506.4)
969 (775.2)
1,067 (853.6)
620 (496.0)
1,331 (1,064.8) 1,395 (1,116.0)
541 (287.8) 578 (462.4)
804 (643.2) 926 (740.8)
+32
+36
- 2
+ 5
+ 7
+15
-------
TABLE 8-4. YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITROGEN DIOXIDE AT CAMP STATIONS.
MEASURED BY THE CONINUOUS SALTZMAN COLORIMETRIC METHOD (U.S. EPA, 1975a)
Concentration, pg/m , at 25°C
Denver
00
i
i — •
o
Year
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
Mean
—
—
--
75
56
75
75
56
75
75
75
94
Max
--
--
--
507
602
583
488
620
639
676
583
846
Washington
Mean
56
56
75
56
75
75
94
75
94
75
113
--
Max
545
394
413
770
319
376
432
432
545
413
1,202
--
Chicago
Mean
75
75
94
75
113
94
94
94
113
113
94
132
Max
394
376
865
319
564
470
319
358
395
1,090
413
676
St. Louis
Mean
--
—
56
56
56
38
38
56
56
56
94
56
Max
-
--
394
226
357
282
319
714
244
244
376
508
Cincinnati
Mean
56
56
56
56
75
56
56
56
75
56
75
75
Max
470
377
620
301
432
432
1,036
394
433
301
319
207
Philadelphia
Mean
38
75
75
75
75
75
75
75
94
75
75
--
Max
226
584
471
358
413
413
358
245
377
770
545
--
-------
to
LU
cc
LU
CM
O
200
100
0
100
50
0
100
50
0
100
50
0
100
50
CHICAGO CAMP
I I I
i r
CINCINNATI CAMP
I I I
n
•CD-
DENVER CAMP
PHILADELPHIA CAMP
I I I I I I
n o n
I I I
T I
u u
n
ST. LOUIS CAMP
I I I
'62 '63 '64 '65 '66 '67 '68 '69 '70 '71 '72
YEAR
Figure 8-2. Trend lines for nitrogen dioxide annual averages in five
CAMP cities. -D— : data satisfying IMADB minimum sampling cri-
teria;-O- : invalid average (based on incomplete data). *Mote change
in ordinate scale for these data (U.S. EPA, 1973).
8-11
-------
TABLE 8-5. FIVE-YEAR AVERAGES OF NITROGEN DIOXIDE CONCENTRATIONS AT CAMP STATIONS,
MEASURED BY THE CONTINUOUS SALTZMAN COLORIHETRIC METHOD (U.S. EPA. 1973)
CO
I
Average, Concentration ,
pg/ni (ppb), 25°C
Station
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
CAMP average
1962-1966
86.1 (45.8)
62.0 (33.0)
66.0 (35.1)
67.7 (36.0)
58.5 (31.1)
68.1 (36.2)
1967-1971
101.2 (53.8)
60.0 (31.9)
67.9 (36.1)
77.6 (41.3)
54.2 (28.8)
72.2 (38.4)
Change, %
+18
- 3
+ 3
+15
- 7
+ 6
Average of Annual
2nd Highest Value.
ug/m (ppb), 25 C
1962-1966
444 (236.2)
391 (208.0)
498 (264.9)
361 (192.0)
320 (170.2)
403 (214.4)
1967-1971
499 (265.4)
367 (195.2)
493 (262.2)
414 (220.2)
267 (142.0)
408 (217.0)
Change, %
+12
- 6
- 1
+15
-16
+ 1
-------
+3%
0%< +50%
™ . _
+ 1 7% .y J" ~— •- r-J
lk \
1
'<
+7%J +36% '-.
"
>
AVERAGE N02 CONCENTRATION CHANGE (11 STATIONS): +20%
Figure 8-3. Trends in IMO2 air quality, Los Angeles Basin, 1965-1974
(Trijonis et al., 1976).
8-13
-------
8.1.4 Recent Trends in NO., Concentrations
Examination of data on trends in NCL concentrations during more recent years presents a
variable picture at selected sites across the nation (Figures 8-4 through 8-9). Since
measured concentrations, particularly those dealing with short-term peak excursions, may be
expected to depend upon specific site considerations as well as varying meteorological para-
meters, the only data presented are those from the same site over the years plotted. Consis-
tent downward trends are observed at Camden, New Jersey, for all statistics presented (Figure
8-4). A generally downward trend for peak one-hour levels is also discernible at a site in
downtown Los Angeles (Figure 8-5), accompanied by a relatively level pattern for other statis-
tics plotted; and in Azusa, California (Figure 8-6), similar generally level trends are
apparent for all statistics plotted for 1971-1980. Nitrogen dioxide air quality seems to have
steadily improved in Newark, New Jersey (Figure 8-7) from 1971 to 1977, the last year of
available N02 data at the Newark site plotted. No clearcut trend is discernible in Portland,
Oregon (Figure 8-8), although an unusually high one-hour peak level was recorded in 1979
during a day on which several other air pollutants (such as CO) were also markedly elevated
over usual levels. Figure 8-9 shows trends in a 4-year running average of annual averages
(during 1970-1975) of daily maximum 1-hr N02 concentrations in the Los Angeles basin. A
marked decrease in both the highest annual average and in the mean of 5 sites is apparent,
although the lowest annual average increased over the same period. By comparison (Table 8-6),
N02 concentrations spanning the years 1969 to 1974 generally increased for nearby sites in
rapid growth areas of Orange County, California, whereas other California sites listed in TabTe
8-6 generally experienced declines in N0~ levels.
8.1.5 Seasonal Variations in NO,, Concentrations
In this section, a few examples of seasonal variations in N02 concentrations are
presented which demonstrate that no single nationwide pattern exists for the monthly averages
of daily maximum 1-hr data. The month-to-month variations in average N02 concentrations may
be the combined result of high photochemical activity in the summer months, time-varying
emissions of NO (with high emissions of NO during the winter in some areas), time-varying
emissions of hydrocarbons, and area-specific meteorological conditions throughout the year.
The data presented are, for the most part, averaged over several years of monitoring, a
procedure which may be expected to yield representative patterns for the regions reported.
Examination of Figures 8-10 and 8-11 reveals that Chicago, Illinois, experiences a marked peak
in N02 concentrations during the summer months while concentrations in Denver, Colorado,
appear to peak in the winter. In contrast to the above patterns, certain sites in southern
California (Los Angeles, Azusa, and Pomona) do not exhibit a marked seasonality. (The pattern
for Lennox, as published in Trijonis, 1978, was discovered to be a duplicate of the Denver
pattern and is corrected here).
8.1.6 Recently Observed Atmospheric Concentrations of NO.,
In this section, representative examples of observed concentrations of N02 in recent
years are presented. In summary, the data cited illustrate the following points:
8-14
-------
1100
1000 —
ANNUAL STATISTICS
J-YEAR MOVING AVERAGES
— X — INCOMPLETE DATA
MAXIMUM ONE-HOUR OBSERVATION
99th PERCENTILE
90lh PERCENTILE
ARITHMETIC MEAN
COLORIMETRIC - GRIESS SALTZMAN
•68 '69 70 71 72 73 74 75 76 77 78 79 "80
Figure 8-4. Annual air quality and 3-year moving averages at Camden, New Jersey. [Data adapted from Trijomi
[1978], augmented with data from SAROAD.j
8-15
-------
I
en
O
P
4
cc
2
HI
0
O
U
LU
O
X
g
o
in
o
o
cc
z
ANNUAL STATISTICS
3-YEAR MOVING AVERAGES
MAXIMUM ONE-HOUR OBSERVATIONS
COLORIM£TRIC - LYSHKOW [14-; POSITIVE BIAS,
O
111
z
p
o
u
in
5
g
'63 '64 '65 '66 '67 '68 '69 70 71 72 73 74 75 76 77 78 79 '80
YEAR
Figure 8-5. Annual air qualtiy statistics and 3-year moving averages at downtown Los Angeles.
California. [Data adapted from Trijonis [1978], augmented with data from SAROAD.j
8-16
-------
5
z
o
u
z
o
o
LLJ
o
X
O
LU
O
O
cc
900
800
700
600
500
400
300
200
I
100
O
MAXIMUM ONE-HOUR OBSERVATIONS
\ ,*.:•
x
99lh PERCENTILE
ANNUAL STATISTICS
• • • • 3-YEAR MOVING AVERAGES '
-X- INCOMPLETE DATA
90th PERCENTILE
COLORIMETRIC - LYSHKOW [14°= POSITIVE BIAS
63 '64 '65 '66 '67 '68 '69 70 '71 '72 73 74 75 76 77 78 79 '80
Figure 8-6. Annual air quality statistics and 3-year moving averages at Azusa, California. [Data
adapted from Trijonis [1978], augmented with data from SAROAD.]
8-17
-------
700
600 -r
z
o
p
tr
Z
LU
u
z
o
u
LU
D
x
UJ
O
O
a
1
ANNUAL STATISTICS
3-YEAR MOVING AVERAGES
— X — INCOMPLETE DATA
MAXIMUM ONE-HOUR OBSERVATION I
V
99th PEHCENTILE
90lh PERCENTILE
ARITHMETIC MEAN
COLOHIMETRIC - GRIESS SALTZMAN
79 '80
Figure 8-7. Annual air quality statistics and 3-year moving averages at Newark, New Jersey. [Data
adapted from Trijonis [1978], augmented with data from SAROAD.]
8-18
-------
I
"tt
Z
g
LU
u
Z
o
o
LU
o
X
O
5
z
UJ
o
o
ANNUAL STATISTICS
> • • • • 3-YEAR MOVING AVERAGES
— X — INCOMPLETE DATA
MAXIMUM ONE-HOUR OBSERVATIONS
99th PERCENTILE
90th PERCENTILE
COLORIMETRIC LYSHKOW
I I
CHEMILUMINESCENCE
I
70
71
Figure 8-8. Annual air quality statistics and 3-year moving averages at Portland, Oregon. [Data
adapted from Trijonis [1978], augmented with data from SAROAD.]
8-19
-------
340
320
300
280
O 260
Z 240
O
u
rvi
O
220
200
180
HIGHEST AVERAGE
BASINWIDE MEAN (5 SITES)
LOWEST AVERAGE
1970
1971
1972
YEAR
1973
1974
1975
Figure 8-9. Annual average of daily maximum 1-hour IM02 (4-year
running mean) in the Los Angeles Basin (U.S. EPA, 1976a).
8-20
-------
TABLE 8-6. FIVE-YEAR CHANGES IN AMBIENT N02 CONCENTRATIONS'
NET PERCENTAGE CHANGE IN NO, CONCEN
TRATIONS FROM 1969 TO 1974
STATIONS
LOS ANGELES BASIN SITES
Orange County: Anaheim
(rapid growth) La Habra
Average for Orange County
Los .Angeles County: Azusa
(slow growth) Lennox
Los Angeles
L.A. (Westwood)
L.A. (Reseda)
Average for Los Angeles County
OTHER CALIFORNIA SITES
Oakland
Pittsburg
Redwood City
Sal inas
San Rafael
Santa Cruz
Stockton
Average for Other California Sites
NEW JERSEY SITES
Bayonne
Camden
Newark
Average for .New Jersey Sites
OTHER SITES
Chicago, IL
Portland, OR
Annual
Mean
+ 9%
+99%
+54%
+17%
- 7%
- 5%
+ 8%
- 4%
+ 3%
- 7%
- 8%
-24%
- 1%
+ 5%
+15%
- 3%
- 3%
-27%
- 9%
+ 2%
-14%
+32%
-.7%
90th
Percenti le
+ 5%
+60%
+33%
+ 7%
-11%
- 2%
+113
-10%
- 1%
- 9%
- 4%
-25%
- 1%
0%
-24%
-44%
-15%
-18%
- 7%
0%
- 8%
+51%
+44%
Yearly
Maximum
+13%
+72%
+43%
+ 6%
+ 1%
-28%
+32%
-13%
- 1%
-14%
-12%
- 9%
+27%
0%
-27%
-21%
- 8%
-36%
-52%
0%
-24%
+94%
- 3%
Adapted from Trijonis (1978).
8-21
-------
10
D.
a
2
O
DC
H
Z
LU
U
O
O
I
I
z'
g
cc
t-
u
U
O
O
a
a
O
z
HI
O
O
O
15
10
15
10
HOUSTON/MAE 1975-1976
I I I I
I
6 7
MONTH
I I
DENVER 1967-1973
I I
6 7
MONTH
T
CHICAGO 1969 1973
III I
67
MONTH
NO-
10 11
10 11 12
9 10 11 12
12
Figure 8-10. Seasonal NC>2 concentration patterns of three U.S.
urban sites (monthly averages of daily maximum 1-hr concentra-
tions). Adapted from Trijonis (1978).
8-22
-------
CO
ro
OJ
25
I 20
CL
a
z"
9. 15
z
LU
u
z
o
u
10
E
I
o
u
o
u
AZUSA 1969-1974
567
MONTH
8 9 10 11 12
20
15
10
POMONA 1969-1974
1 2 3 4 5 6 7 8 9 10 11 12
MONTH
Q.
a
z
iu
U
O
u
20
15
10
a
a i
Z
o
z
UJ
y
z
o
o
LOS ANGELES 1969-1974
I I I I I
2345678
MONTH
15
10
LENNOX 1969-1974 (SEE TEXT)
9 10 11 12
NO-
1 I I I I I I I I I
1 2 3 4 5 6 7 8 9 10 11 12
MONTH
Figure 8-11. Seasonal NO2 concentration patterns of four U.S. urban sites (monthly averages of daily maximum 1-hr concentrations).
Adapted from Trijonis (1978).
-------
• Annual average concentrations of NOp are not a reliable index of short-term (3-hr or
less) human exposure.
• Although a distinct recurrent diurnal pattern is discernible in some areas of the
country, in many areas peak diurnal values occur at almost any time of day.
• Nitrogen dioxide levels of concern on a short-term basis may occur not only in urban
areas, but also in certain small cities and suburban areas.
Reference is made to Tables 8-7, 8-8, and 8-9 for the identification of analytic proce-
dures used to obtain data on ambient NCL concentrations cited in this section.
Examination of Tables 8-7 and 8-8 for 1975, and Table 8-9 for 1976-1980, reveals that
during at least one of these years, peak 1-hr N09 concentrations equalling or exceeding 750
3
ug/m (0.4 ppm) were experienced in: Los Angeles and several other California sites; Ashland,
Kentucky; and Port Huron, Michigan. Additional sites reporting at least one peak hourly con-
centration equalling or exceeding 500 pg/m (0.27 ppm) during those years include: Phoenix,
Arizona; St. Louis, Missouri; New York City, New York; 14 additional California sites;
Springfield, Illinois; Cincinnati, Ohio; and Saginaw and Southfield, Michigan. Other
scattered sites, distributed nationwide, reported maxima close to this value, including some
approaching 500 (jg/m in 1980. As shown in Tables 8-7 to 8-9 recurrent NO, hourly concentra-
3
tions in excess of 250 pg/m (0.14 ppm) were quite common nationwide in both 1975 and subse-
quent years, but very few exceeded 750 pg/m (0.4 ppm). Table 8-10 presents data for 24-hr
average N02 concentrations at various sites in 1976 to 1980. It is important to note that
only data from monitoring stations meeting EPA National Air Data Branch (NADB) sampling
criteria* were chosen for listing in this section. The number of stations meeting these
criteria varies from year to year, so that many of the areas reported in Tables 8-9 and 8-10
are not identical with those listed in Tables 8-7 and 8-8 for 1975. The data for the wide
range of areas represented in these four tables do show, however, that occasional peak NO^
concentrations of possible concern for human health (see Chapter 15) occurred in the nation in
the mid-1970s. More recently available data for 1976-1980 from the SAROAD system suggest that
basically the same patterns of occasional peak N0~ levels approaching or exceeding 0.4 to 0.5
ppm still occur from time to time in scattered areas of the United States.
* NADB sampling criteria are as follows:
1) For continuous observations with sampling intervals of less than 24 hours:
a) Data representing quarterly periods must reflect a minimum of 75 percent of the total
number of possible observations for the applicable quarter.
b) Data representing annual periods must reflect a minimum of 75 percent of the total
number of possible observations for the applicable year.
2) For noncontinuous observations with sampling intervals of 24 hours or greater:
a) Data representing quarterly periods must reflect a minimum of five observations for
the applicable quarter. Should there be no measurements in 1 of the 3 months of the
quarter, each remaining month must have no less than 2 observations reported for the
applicable period.
b) Data representing annual periods must reflect four quarters of observation that have
satisfied the quarterly criteria.
8-24
-------
TABLE 8-7. RATIO OF MAXIMUM OBSERVED HOURLY NITROGEN DIOXIDE
CONCENTRATIONS TO ANNUAL MEANS DURING 1975 FOR SELECTED LOCATIONS (U.S. EPA, 1977a)*
State
00
ro
Kentucky
3
[jg/m
Maximum hourly concentration - yearly arithmetic mean
Location
Method Au
Paducah
Louisville
Ashland
714/66 =10.8
895/85 =10.5
Method Bl
California
Colorado
Georgia
Illinois
Anaheim
Azusa
Costa Mesa
Los Angeles
Lynwood
San Bernadino
Napa
San Francisco
Barstow
Fontana
Chula Vista
Visalia
Denver3
Atlanta
Chicago3
East St. Louis
940/101= 9.3
696/112= 6.2
658/58 =11.3
1053/126= 8.4
1128/129= 8.7
602/97 =6.2
470/76 =6.2
188/49 =3.8
432/62 =7.0
432/39 =11.1
-
-
-
-
-
.
-
-
-
_
-
-
-
-
-
-
'
-
-
489/78 =6.3
451/64 =7.1
226/48 =4.7
555/96 =5.8
489/76 =6.4
395/104= 3.8
395/109= 3.6
244/41 =6.0
293/65 =4.5
348/84 4.1
(continued)
-------
TABLE 8-7. (continued)
State
Ma i ne
Maryland
Michigan
Oregon
Texas
Location
Bangor
Essex
Grand Rapids
Detroit
Portland
Dallas
ug/m
Maximum hourly concentration -
Method Ab
270/49 =5.5
-
279/67 =4.2
207/50 =4.1
-
yearly arithmetic mean
Method BC
-
282/53 =5.3
338/58 =5.8
-
432/32 =13.5
CD
I
ro
en
More than one station reporting.
Method A: Instrumental Colorimetric-Lyshkow (MOD) method, a variation of
the continuous Greiss-Saltzman Method.
Method B: Instrumental Chemiluminescence Method. ..
*For comparison purposes, pote that: 1.0 ppm N0_ = 1880 ug/m ; 0.5 ppm ~ 940
ug/m ; 0.1 ppm = 188 ug/m ; 0.05 ppm = 94 ug/m ; and 0.01 ppm =? 18.8 ug/m .
-------
TABLE 8-8. FREQUENCY DISTRIBUTION OF 1975 HOURLY NO, CONCENTRATIONS
AT VARIOUS SITES IN U.S. URBAN AREAS (U.S. EPR, 1977a)*
Concentrations (ug/m ) Maximum
equalled or exceeded by observed
stated percent of observations concentration
Location
Arizona
Phoenix
Cal ifornia
Los Angeles
Redlandsj:
Redlands
Riverside,
Riverside
San Diego,
San Diego
Colorado
Denver,
Denver
Kentucky
Ashland3
Michigan,
Detroit
Missouri
St. Louis3
New Jersey
Newark,
Newark
New York .
n
New York City
Ohio b
Cincinnati
Pennsylvania ,
Philadelphia
Texas ,
Dallas0
W
271
526
282
226
301
395
226
395
282
265
297
150
338
273
226
226
282
301
132
5%
188
301
169
150
226
282
150
282
188
177
209
113
244
169
169
169
150
226
94
10%
152
226
132
132
188
226
113
226
150
149
173
94
207
150
132
132
103
207
75
50%
69
94
56
56
94
113
38
113
94
90
68
56
75
81
75
56
47
113
19
(ug/m3)
660
1053
545
357
564
658
508
865
432
483
895
338
658
494
376
526
395
451
432
Obtained by Instrumental Colorimetric-Lyshkow (Mod) method, a variation
of the Griess-Saltzman method.
Obtained by Chemiluminescence Method.
Obtained by Instrumental Colorimetric-Griess-Saltzman method.
*For comparison purposes, note tbat: 1.0 ppm NOp = 1880 ug/m ; 0.5 ppm
= 940 ug/m ; 0.1 ppm = 188 ug/m ; 0.05 ppm = 94 ug/m ; and 0.01 ppm
= 18.8 ug/in .
8-27
-------
TABLE 8-9. FREQUENCY DISTRIBUTION OF 1976, 1978. AND 1980 HOURLY NITROGEN
DIOXIDE CONCENTRATIONS AT VARIOUS U.S. SITES (U.S. EPA. 1976c, 1979, 1981)*
Location SAROAD Site ID Method
Arizona
Phoenix 030600002G01
Tucson 030860002G01
CD
1
ro
00 California
Anaheim 050230001101
Chino 051300001101
Costa Mesa 051740002101
El Cajon 055300002101
Fontana 052680001101
Fremont 052780001101
La Habra 053620001101
Instrumental
Chemi luminescence
Instrumental
Chemi 1 umi nescence
Griess-Sal tzman
(Lyshkow)
Instrumental
Chemi luminescence
Griess-Saltzman3
(Lyshkow)
Instrumental
Chemi luminescence
Instrumental
Chemi luminescence
Griess-Sal tzman
(Lyshkow)
Griess-Sal tzman
(Lyshkow)
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Concentrations equalled or
exceeded by stated percent
of observations (ug/m )
1% 10% SOX
226
150
91
132
150
301
395
338
226
414
226
-
301
263
263
320
301
244
244
-
207
301
207
~
320
-
-
150
75
38
94
100
150
188
150
132
132
150
-
132
113
113
188
169
169
132
-
132
150
113
""
169
-
"
56
38
5
56
56
56
94
75
56
19
94
-
19
38
38
94
94
94
56
-
56
56
56
- "
75
-
"
Maximum
observed
concentration
(pg/m )
451
226
132
451
432
414
865
564
470
602
301
-
639
564
583
545
508
338
564
-
470
526
320
526
-
2nd Highest Yearly
observed arithmetic
concentration mean.
(pg/m ) (ug/m )
432
207
132
357
301
414
752
545
395
583
282
-
639
545
526
489
432
282
508
-
432
526
282
508
-
60
44h
17b
51b
61°
69
103
90b
7l"
54b
94
-
53b
53b
50
108
1Mb
95°
63
K
73°
80
66
91
~
-------
TABLE 8-9. (continued)
00
I
ro
to
Concentrations equalled or
exceeded by stated percent
of observations (ug/m )
Location
California (cont. )
Oakland
Oceanside
Redlands
Riverside
San Diego
San Diego
San Jose
San Jose
SAROAD Site ID Method
055300004F01 Instrumental
Chemi luminescence
055320003101 Instrumental
Chemi luminescence
056200001101 Instrumental
Chemi 1 umi nescence
056400005F01 Instrumental
Chemi 1 umi nescence
056800006101 Instrumental
Chemi luminescence
056800004101 Instrumental
Chemi luminescence
056980004A05 Instrumental
Chemi luminescence
056980004101 Griess-Sal tzmana
(Lyshkow)
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1%
301
-
-
263
244
207
169
-
-
338
301
282
244
226
226
357
376
320
301
-
-
320
244
207
10%
150
-
-
113
113
75
75
-
-
207
169
150
113
132
113
188
207
207
169
-
-
169
13Z
132
50%
56
-
-
38
56
38
38
-
-
94
94
75
56
56
38
94
94
94
66
-
-
75
75
75
Maximum
observed
concentration
(ug/mJ)
545
-
-
620
602
357
470
-
-
564
564
414
451
432
357
585
940
470
479
-
-
526
414
301
2nd highest
observed
concentration
(ug/mj)
489
-
-
620
545
338
451
-
-
526
489
395
451
395
357
564
846
451
461
-
-
507
414
282
Yearly
arithmetic
mean.
77
-
-
57b
58b
40b
47
-
-
113b
101b
90
63b
7"b
55P
105
112b
114°
86
-
~
86
78.
D
79
-------
TABLE 8-9. (continued)
CD
i
to
O
Concentrations equalled 01
exceeded by stated percent
of observations (ug/m )
Location
Georgia
Atlanta
Illinois
Chicago
Chicago
Springfield
Kentucky
Ashland
Michigan
Port Huron
Saginaw
Southfield
SAROAD Site ID Method
110200001F01 Instrumental
Chemi luminescence
141122001P10 Instrumental
Chemi luminescence
141122002A05 Instrumental
Chemi luminescence
147280003F01 Instrumental
Chemi 1 umi nescence
180080008F01 Griess-Saltzman3
(Lyshkow)
234340003F01 Griess-Saltzman3
(Lyshkow)
234760002F01 Griess-Saltzman3
(Lyshkow)
234880002F01 Griess-Saltzman*
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1%
160
160
160
273
-
-
263
-
-
90
113
-
209
141
-
222
188
-
291
312
120
363
292
-
10%
103
113
104
179
-
-
169
-
-
55
70
-
113
75
-
121
145
-
154
169
89
181
163
-
50%
66
66
56
113
-r
-
94
-
-
19
36
-
55
34
-
65
71
-
76
86
45
83
102
-
• Maximum
: observed
concentration
(ug/m )
244
348
301
461
-
-
461
-
-
519
239
-
572
306
-
832
450
-
643
649
189
645
365
-
2nd highest
observed
concentration
(ug/mj)
216
292
273
442
-
-
442
-
-
293
205
-
464
275
-
815
438
-
622
629
180
585
361
-
Yearly
arithmetic
mean,
(ug/ni )
67b
72b
61b
116
-
-
108
-
-
"b
40b
-
63h
41b
-
73h
79b
~
86b
94b
48°
100
106
-
-------
TABLE 8-9. (continued)
Concentrations equalled or
exceeded by stated percent
of observations (uq/m )
Location
New Jersey
Newark
Ohio
Q-, Cincinnati
i
CJ
t->
Pennsylvania
Philadelphia
Utah
Salt Lake City
Salt Lake City
SAROAD Site ID Method
313480002A05 Instrumental
Chemi 1 umi nescence
361220019A05 Instrumental
Chemi luminescence
397140023H01 Grei ss-Saltzmana
(Lyshkow)
460920001F01 Instrumental
Chemi luminescence
460920001A05 Instrumental
Chemi 1 umi nescence
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1%
226
-
167
147
150
103
188
-
-
244
188
207
226
-
10%
122
-
117
94
98
70
113
-
-
132
113
113
132
-
50*
75
-
66
56
47
38
75
-
-
75
56
56
75
-
• Maximum
. observed
concentration
(ug/mj)
338
-
196
677
254
150
451
-
-
470
263
357
470
-
2nd highest
observed
concentration
(ug/ni )
320
-
192
508
235
145
451
-
-
451
263
357
432
-
Yearly
arithmetic
mean,
(ug/m )
80
h
70
60
55
41
74
-
-
8°b
65b
61D
75
-
Data obtained using dynamic calibration procedures.
Data not satisfying NADB minimum sampling criteria.
*For comparison ourposes. note that: 1.0 ppm NO ~ 1880 ug/m ; 0.5 ppm ? ppm940 ug/m 0.1 ppm ~ 188 ug/m ; 0.05 ppm ~ 94 ug/m ; and 0.01
ppm = 18.8 ug/m .
-------
TABLE 8-10. FREQUENCY DISTRIBUTION OF 1976, 1978, AND 1980 24-HOUR AVERAGE NO, CONCENTRATIONS AT VARIOUS SITES
IN U.S. URBAN AREAS (ALL DATA OBTAINED BY SODIUM ARSENITE METHOD) (U.S. EPA, 1976c. 1979, 1981)a
Concentrations
Second or exceeded by
Location
Alabama
Birmingham
Alaska
Fairbanks
Arizona
Tucson
Arkansas
oo Little Rock
i
CO
PO
California
Fresno
Long Beach
San Bernadino
Colorado
Denver
Site Code
010380003P01
II
II
020160001P01
ii
11
030860001F01
11
11
041440003F01
11
11
052800002F01
II
II
054100001F01
"
11
056680001F01
"
11
060580001P01
11
"
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
fug/nO
127
" -
-
110
-
-
127
-
-
105
93
79
147
-
-
339
-
-
156
-
-
163
-
-
highest
(ug/m )
117
-
-
103
-
-
96
-
-
100
72
76
133
-
-
285
-
-
154
-
-
140
-
-
(ug/m ) equalled
stated percent
of observations
10%
107
-
-
85
-
-
69
-
-
65
58
53
118
-
-
215
-
-
124
-
. -
102
-
-
50%
66
-
-
59
-
-
45
-
-
32
28
27
49
-
-
101
-
-
78
-
-
46
-
-
Annual
arithmetic
mean..
(ug/m )
69
-
-
59
-
-
47
-
-
37
31
30
58
-
-
119
-
-
85
-
-
55
-
-
-------
TABLE 8-10. (continued)
CD
co
to
Location
Connecticut
Bridgeport
Greenwich
Florida
Jacksonvi 1 le
Orlando
Georgia
Atlanta
Hacon
Site Code
070060123F01
"
11
070330008F01
070060004F01
070330004F01
101960033H01
11
"
101960002P01
"
11
101960032H01
II
11
103280004F01
11
11
110200038G02
II
110200001P01
II
II
110200039G01
11
11
110200041G01
11
n
113440008F01
113440007F02
113440007F02
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
I960
Maximum
143
134
207
101
93
123
138
-
-
100
-
-
93
50
-
91
71
74
133
60
106
123
73
-
120
99
98
100
74
-
109
84
92
C
Second
highest
(ug/m )
139
130
196
80
80
101
91
-
-
89
-
-
81
47
-
76
57
72
81
52
73
95
69
-
115
88
93
92
60
-
85
58
86
Concentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10*
123
108
114
54
65
82
90
-
-
79
-
-
67
47
-
50
47
64
72
52
64
94
69
-
92
88
72
83
60
-
71
53
58
50%
66
62
69
33
38
47
55
-
-
59
-
-
50
34
-
32
34
40
48
44
42
56
44
-
64
54
42
45
32
-
36
30
32
Annii.i 1
arithmetic
mean
(ug/ni )
70
66
78
36
39
52
59
-
-
58
-
-
53.
33b
-
32h
34b
41
52.
41b
41
61.
45b
-
59h
59b
39
51h
33b
-
40
33b
36
-------
TABLE 8-10. (continued)
Location
Idaho
Boise City
11 1 inois
Chicago
Peoria
Indiana
Indianapolis
CD
i
cx> Iowa
Bellevue
Kentucky
Ashland
Paducah
Site Code
130220007F01
II
"
141220002P01
n
"
141220001P01
n
"
146080001P01
11
"
152040025H01
11
11
152040015H01
n
n
280180002F01
II
II
180080003F01
11
11
180080008F01
"
"
183180020F01
11
n
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/mj)
96
-
-
172
-
-
117
-
-
94
-
-
308
-
-
128
-
92
126
-
-
94
173
92
93
84
-
90
-
-
C
Second
highest
(ug/m )
83
-
-
140
-
-
113
-
-
72
-
-
132
-
,-
122
-
90
97
-
-
93
123
87
89
79
-
82
-
-
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10*
66
-
-
130
-
-
99
-
-
68
-
-
86
-
-
89
-
90
87
-
-
79
72
65
76
76
-
71
-
-
50%
47
-
-
91
-
-
70
-
'
52
-
-
50
-
-
53
-
51
41
-
-
46
30
42
43
38
-
40
-
-
Annual
arithmetic
mean..
(ugV)
50
-
-
91
-
-
73
-
^
51
-
-
56
-
-
54
-
55b
46
-
-
48
35b
41
47
41
-
44
-
-
-------
TABLE 8-10. (continued)
CO
Location
Louisiana
Baton Rouge
Maine
Bangor
Maryland
Baltimore
Silver Spring
Michigan
Detroit
Minnesota
St. Paul
Site Code
190280002F01
11
11
200100001F01
11
"
S
210120018F01
11
"
210120007H01
11
11
2U480005G01
"
"
231180001P01
11
H
231180018F01
H
ii
2311B0016F01
11
"
243300031P01
11
11
rear
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
102
89
119
126
80
-
137
-
-
90
103
-
98
-
-
138
-
-
123
-
-
99
-
-
91
126
103
C
Second
highest
(ug/m )
88
88
93
103
70
-
134
-
-
88
94
-
82
-
-
122
-
-
115
-
-
86
-
-
83
113
86
loncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%
75
68
71
80
61
-
95
-
-
80
93
-
66
-
-
91
-
-
105
-
-
67
-
-
71
86
68
50*
48
47
52
50
42
-
60
-
-
57
60
-
38
-
-
62
-
-
62
-
•
45
-
-
52
56
49
Annual
arithmetic
mean.
51
49
54
51b
46b
-
63
-
-
57.
62b
-
39
-
-
66
-
-
68
-
-
48
-
-
54
58
47
-------
TABLE 8-10. (continued)
00
i
to
01
Location
Missouri
Kansas City
St. Louis
Nebraska
Lincoln
New Hampshire
Nashua
North Carolina
Beloont
Charlotte
Wins ton- Sal em
Site Code
171800012P01
11
11
264280072P01
11
11
264280001P01
"
"
281560004G01
11
281560012G01
300480005F01
11
"
340300001F02
11
340300003F02
340700001G01
-'"vv
11
344460002G02
11
11
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/m )
147
-
-
136
-
-
Ill
-
-
112
120
86
151
-
-
107
-
84
84
112
154
80
95
148
C
Second
highest
(ug/m-5)
147
-
-
127
-
-
105
-
-
91
59
86
116
-
-
103
-
57
80
103
132
68
91
94
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%
69
-
• -
109
-
-
94
-
-
70
21
69
76
-
-
96
-
57
67
88
91
65
76
55
50*
49
-
-
71
-
-
64
-
-
45
11
48
46
-
-
67
-
28
46
54
54
43
39
24
Annual
arithmetic
mean,
(ug/mj)
50
-
-
73
"
-
59
-
-
46
14
47
54
-
-
73
h
31°
48
57
58
45
43
33
-------
TABLE 8-10. (continued)
oo
OJ
Location
Ohio
Akron
Campbell
Cincinnati
Cleveland
Moraine
Toledo
Oklahoma
Tulsa
Oregon
Portland
Site Code
360060006H01
11
11
360060004H01
II
11
360960001101
11
11
361220018H01
"
361220019P01
"
H
361300033H01
H
11
361300012H01
11
"
364550001G01
ii
"
366600007H01
II
"
373000112F01
11
11
381460001P01
" •
ii
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
19SO
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/m )
96
139
93
100
135
86
128
110
103
158
105
-
121
-
-
193
259
136
189
222
132
126
-
-
117
162
102
193
-
-
102
-
-
C
Second
highest
(ug/m )
91
109
93
91
126
83
125
100
90
139
100
-
98
-
-
181
247
126
175
207
121
91
-
-
115
116
101
157
-
-
98
-
-
oncentrat ions (ug/m ) equalled
or exceeded by stated percent
of observations
10*
70
87
75
82
82
76
92
79
84
106
105
-
89
-
-
127
197
112
127
135
115
84
-
-
80
92
90
119
-
-
90
-
-
50%
45
52
53
48
47
52
60
51
45
61
95
-
61
-
-
83
92
71
87
92
79
52
-
-
53
58
59
68
-
-
53
-
-
Annua 1
ari thmetic
mean3
(ug/m )
46
57
54
53
53
52
63
54
51
70.
93b
-
62
-
-
88.
109b
68
87
99
78
53
-
-
56
64
59
74
-
-
57
-
-
-------
TABLE 8-10. (continued)
CD
Co
00
Location
South Carolina
Mount Pleasant
Spartanburg
Tennessee
Chattanooga
Eastridge
Knoxville
Nashville
Texas
Austin
Dallas
Site Code
42170000 1F01
ii
"
422040001F01
11
"
440380025G01
"
ii
44C900001G01
"
"
441740005G01
"
•i
442540002G01
••
11
450220004F01
"
"
450220012F01
"
11
451310023H01
11
11
451310002F01
"
11
451310002H01
11
"
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
I960
1976
1978
1980
1976
1978
1980
Maximum
(ug/mj)
118
43
63
121
105
119
94
-
-
124
-
-
119
-
-
145
125
156
117
94
75
93
106
-
91
231
-
97
238
265
108
. 133
-
(
Second
highest
(ug/ni )
74
34
40
90
99
45
92
-
-
95
-
-
114
-
-
115
124
140
71
86
70
79
77
-
88
190
-
96
165
202
105
131
-
loncentrdtions (ug/m ) equalled
or exceeded by stated percent
of observations
10%
37
29
32
74
83
43
74
-
"
64
-
-
101
-
-
97
106
113
47
86
55
58
57
-
77
112
-
83
127
183
eo
104
-
50%
16
14
9
38
28
3
48
-
-
46
-
-
70
-
-
64
56
54
27
44
32
20
17
-
50
54
-
52
74
84
57
62
-
Annual
arithmetic
mean,
(pg/m )
20
16..
15b
42
33..
18b
51
-
-
47
-
-
70
-
-
69
65n
60b
30.
46b
35
24
22
-
51
63
-
52
77.
98b
57
63
-
-------
TABLE 8-10. (continued)
CD
i
to
10
Location
Fort Worth
Houston
Utah
Salt Lake City
Washington
Seattle
Wisconsin
Hi Iwaukee
Site Code
451880021H02
"
11
451880022H02
11
11
452560009H01
"
it
460920001POX
11
11
491840001P01
"
11
512200045F01
"
Year
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
1976
1978
1980
Maximum
(ug/m )
153
94
-
138
91
-
162
170
128
364
-
-
119
139
-
148
133
81
C
Second
highest
(ug/ni )
143
94
-
124
66
-
137
116
101
182
-
-
114
113
-
115
125
76
oncentrations (ug/m ) equalled
or exceeded by stated percent
of observations
10%
102
94
-
95
91
-
127
102
99
120
-
-
91
113
-
88
95
76
50%
74
65
-
63
61
-
56
66
30
57
-
-
66
90
-
62
65
54
Annual
arithmetic
mean.,
(ug/m )
71.
74b
-
61b
59b
-
64
Mb
46
70
-
-
66h
93b
-
60
67b
57b
aFor comparison purposes, note that: 1.0 ppm N0? = 1880 ug/m3; 0.5 ppm
= 94 ug/n> : and 0.01 ppro = 18.8 ug/m .
Data do not satisfy NAOB minimum sampling criteria.
940 ug/m3; 0.1 ppm = 188 ug/m3; 0.05 ppm
-------
Since the National Ambient Air Quality Standard for N02 is stated in terms of the annual
arithmetic mean, much attention has focused on long-term averages. One question which arises,
then, is whether observed annual averages are an adequate index of the frequency and levels of
short-term exposures. The data in Table 8-7, taken from SAROAD, show the ratios of the maximum
hourly N02 concentrations to the annual means ov various cities for 1975. These ratios ranged
from about 3.6 in Chicago, Illinois, to 13.5 in Dallas, Texas. Thus, it may be seen that
these ratios, between the highest 1-hr NCL value during 1975 and the annual arithmetic mean
for 1975, were quite different in various parts of the nation. To further illustrate this
point, Figure 8-12 shows the distribution of maximum-to-mean NCL ratios averaged over the
years 1972, 1973, and 1974 for 120 urban sites (Trijonis, 1978). Over 70 percent of the sites
have maximum-to-mean ratios in the range of 5 to 8; about 8 percent of the sites have ratios
exceeding 10. Figure 8-13 shows long-term trends in the maximum-to-mean NOp ratios for groups
of sites in New Jersey and in the Los Angeles basin (Trijonis, 1978). (No Jacobs-Hochheiser
data were used.) It is important to note that although the averaging procedure might be
expected to smooth out fluctuations in the data, there is, nevertheless, no consistent value
over the years for the ratio in either area. Looking back on Figures 8-4 to 8-8, marked
variations in peak to mean ratios over many years at the same or different sites are apparent.
It may be concluded, therefore, that the annual mean is not a good indicator of the highest
short-term exposure level in the geographic areas considered.
Table 8-8 shows the frequency distribution of 1-hr N0~ measurements at various sites in
1975 (U.S. EPA, 1977a). It may be seen here that there was great variability across the
nation for all the percentile values presented. Also, it is obvious that the median value is
not always indicative of the potential for short-term exposure. For instance, Los Angeles,
Riverside, and San Diego, California, had high median values of 94 (0.05 ppm), 113 (0.06 ppm),
3
and 113 ug/m (0.06 ppm) respectively. St. Louis, Missouri, on the other hand, had the
moderate median value of 75 ug/m (0.040 ppm), but exceeded more than half the California
sites reported for the one-percentile level. It may also be seen from this table that some
small cities may experience peak concentrations of NOp even higher than those observed in
center-city locations in major metropolitan areas.' Ashland, Kentucky, reported a maximum of
895 ug/m (0.48 ppm), which exceeded the maximum reported in most major metropolitan areas
across the country. A similar conclusion may be drawn from Table 8-9, in that Port Huron,
Michigan, reported a peak value of 832 ug/m (0.44 ppm), which is exceeded in the listing only
by Anaheim, California.
Two major factors that affect NOp concentrations, mobile source emissions and photo-
chemical oxidation, have fairly consistent diurnal patterns in most urban areas. These usually
contribute, to the observed diurnal variation in NO concentrations. Such a variation is
typified by a rapid increase in N0~ in the morning as the result of NO emissions and photo-
chemical conversion to N0~. This is followed by a decrease of NO^ in the midmorning hours due
to advection and increasing vertical dispersion and also loss of NO^ in various atmospheric
8-40
-------
s
o
I
u.
O
15
B
c
468
MAXIMUM/MEAN RATIO
Figure 8-12. Distribution of maximum/mean IM02 ratios for 120
urban locations averaged over the years 1972, 1973, and 1974
(adapted from Trijonis, 1978).
8-41
-------
cc
(M
o
z
<
UJ
5
O
5
i
x
I
I I I I
I I
T
I
V
I
T
I
b
I I
l
'64 '65 '66 '67 '68 '69 '70 '71 '72 '73 '74
YEAR
'64 '65 '66 '67 '68 '69 '70 '71 '72 '73 74
YEAR
Figure 8-13. Trends in the maximum mean NOo ratio for two
groups of sites: (a) average of five locations within the Los
Angeles Basin (Anaheim, La Habra, Azusa, Pomona, San Ber-
nadino); (b) average of two New Jersey sites (Bayonne and
Newark).
Source: Adapted from Trijonis (1978).
8-42
-------
transformation reactions. Peaks in the NOp concentration are often observed corresponding to
emissions occurring during the late afternoon rush hour. In some areas, small lunchtime
maxima occur. At many sites evening peaks occur. Ground-level NO concentrations usually
build up slowly during the night.
To illustrate variations of NOp, concentration data from the month of the highest observed
1-hr NOp concentration in three cities are presented in Figure 8-14 (U.S. EPA, 1975b). The
monthly average 1-hr measurements were computed separately for each hour of the day. This
gives the composite diurnal pattern as shown in Figure 8-14 for the month containing that
year's highest reported short-term (1-hr) concentration. The data from Los Angeles during
January 1975, and Denver during April 1975, followed the "typical" urban pattern described
above, although the average NOp levels in Los Angeles were considerably higher. The pattern
for Chicago during June 1975, was quite different. The extremely broad peak with the maximum
between 2:00 and 3:00 p.m. was the result of individual daily maxima which did not occur at
the same time of day during the month of June. This is one illustration of the fact that no
standard diurnal pattern exists nationwide.
To further illustrate the diurnal trends in the same three cities, data from the day of
the highest 1-hr N02 concentration in 1975 are plotted (U.S. EPA, 1975b) (Figure 8-15). In
all three cities the diurnal patterns are similar to the average patterns. The extremely
sharp, high peak in the Los Angeles data exemplifies the combined effects of poor atmospheric
dispersion, high emissions, and photochemical activity which are quite common in this region.
In Figure 8-16, 1-hr average NOp concentration data are plotted versus time for periods
of 3 days during which high NOp levels were observed (U.S. EPA, 1975b). The Los Angeles data
showed a diurnal profile typical for the area on the afternoon on January 15, during which the
NOp concentration climbed steadily after a small morning peak. This situation was probably
the result of low wind speeds and a strong elevated inversion restricting both advection and
dilution. The data for Ashland, Kentucky, show the same basic diurnal trend seen in Los
Angeles on the first two days and much lower levels on the third day. The data from McLean,
Virginia, at much lower overall concentration values, had quite a different pattern. The
major increase in N0? concentration did not take place until 5:00 or 6:00 p.m.
Figure 8-17 shows the NOp and NO concentration profiles obtained from a center-city
station in St. Louis, Missouri, and the NOp concentration from a rural site, 45 km north of
the center-city location (U.S. EPA, 1976b). The center-city site showed a rapid buildup of NO
during the morning with a slower rise in the NO, concentration. The rural site, at this time,
reported NO- concentrations at or near the instrumental limits of detection. During the
morning and early afternoon, the winds experienced at both sites were light and from the north-
west. Between 1:00 and 2:00 p.m. the wind direction at the center-city site shifted and began
coming from the south and south-east over the next several hours. A similar change occurred
between 5:00 and 6:00 p.m. at the rural site. After the shift in direction, the wind speed
increased somewhat at the rural site, and more gradually increased in the downtown area. Since
8-43
-------
OO
LOS ANGELES. JANUARY 1975
DENVER. APRIL 1975
CHICAGO JUNE 1975
24
Figure 8-14. Average diurnal pattern for the month during which the highest 1-hoiir NO2 concentrations were reported (U.S. EPA. 1975b).
-------
CD
I
LOS ANGELES, CALIFORNIA. JANUARY 17. 1975
DENVER. COLORADO. APRIL 5. 1975
CHICAGO. ILLINOIS. June 21, 1975
Figure 815. One hour average concentration profiles on day of peak NC>2 concentration for three U.S. cities (U.S. EPA, 1975b).
-------
ASHLAND. KENTUCKY, NOVEMBER 1920. 1975
LOS ANGELES. CALIFORNIA. JANUARY 15 17. 1975
MclEAN. VIRGINIA. AUGUST 27 ?9. 1975
-p.
en
MIDNIGHT
NOON
MIDNIGHT
NOON
TIMEOFDAV
MIDNIGHT
NOON
Figure 816. One-hour NC>2 concentrations during three day! of high pollution in three U.S. citiel (U.S. EPA. 1975b).
-------
0.10
(188.0)
NO2 AT RAMS STATION 5 (CENTER CITVI
NO2 AT RAMS STATION 22 (45 km NORTH OF CENTER CITV)
12
15
TIME, hours
18
21
0.22
(271)
0.20
(246)
Figure 8-17. Nitric oxide and nitrogen dioxide concentrations at an urban and a rural site in St. Louis, Missouri, on January 27-28, 1976
(U.S. EPA, 1976b).
-------
other monitoring sites in and around St. Louis did not show a consistent, concomitant varia-
tion of N02 concentrations, the most likely explanation for the data presented is dispersion
or plume impaction from a variety of industrial sources, located roughly to the south of the
sites reported herein.
The above discussion indicates that short-term excursions of N02 concentrations to levels
well above the average can occur at night and are not necessarily associated directly with
traffic emission and photochemical oxidation, even though the levels shown in Figure 8-17 are
considerably lower than those associated with the morning peaks shown in Figures 8-15 and
8-16. To further illustrate this phenomenon, the monthly maximum concentrations observed at
each hour of the day are listed for selected individual months from six geographically-
dispersed urban locations in Table 8-11 (U.S. EPA, 1975b).
The data from Newark, New Jersey, show peak concentrations in the late hours before
midnight, and only a mild diurnal variation for the rest of the day. Portland, Oregon,
experienced consistently elevated maxima for all hours between 2:00 and 11:00 p.m.
Los Angeles, California, as expected from the previous data, experienced the highest
short-term NO- levels in the mid-morning hours and a marked diurnal pattern. Chicago,
Illinois, exhibited only a mild diurnal pattern in monthly maximum concentration for the month
illustrated. In Denver, Colorado, elevated N02 levels are apparent from 9:00 a.m. to 7:00
p.m. In El Paso, Texas, both morning and early evening elevations in N02 concentrations are
apparent. It also can ,be seen that, for all hours on at least one day during the month, N02
concentrations exceeded the monthly mean.
To summarize, the above data indicate that very high N02 concentrations, of a few hours
duration, can occur in urban areas associated with the Los Angeles-type diurnal pattern of
photochemical air pollution. In some cities, the diurnal N02 peak can be lower but may last
longer. In other areas, relatively high concentrations may occur almost any time of day.
Some qualitative insight into possible causes for the different diurnal patterns observed
may be gleaned from examination of Figure 8-18. This figure presents data from RAPS on NO,
N02, and 0, concentrations for part of one day in St. Louis, Missouri. It is presented for
illustrative purposes only.
On the day in question, October 1, 1976, the winds were sufficiently calm so that the
pollutant profiles and patterns were the result of local processes rather than pollutant
transport. In the early morning hours before sunrise, Figure 8-18 shows a significant and
constant NO- concentration, presumably carried over from the previous day. During these
hours, the 0, concentration is quite low, near the instrumental detection limits. Nitric oxide
concentrations are high, most probably the result of continuous emissions during the night and
early morning hours. There is no discernible N02 formation. After sunrise, the N02 concentra-
tion increased sharply as a result of photochemical reactions. Photochemical generation of
N02 is followed by a concomitant rapid increase in 03 concentrations, which depresses the NO
concentrations until the later afternoon hours when decreasing radiant energy and increasing
8-48
-------
TABLE 8-11. DISTRIBUTION BY TIME OF DAY OF ONE-HOUR MAXIMUM N0? CONCENTRATIONS'
FOR ONE MONTH IN 1975 FOR SELECTED URBAN SITES (U.S. EPA, 1976b)
(pg/m3)
12 am
1 am
2 am
3 am
4 am
5 am
6 am
7 am
8 am
9 am
10 am
11 am
12 am
1 pm
2 pm
3 pm
4 pm
5 pm
6 pm
7 pm
8 pm
9 pm
10 pm
11 pm
Monthly
average
of all
hours
Newark
New Jersey
(July)
160
160
160
160
140
140
160
180
200
210
230
200
200
180
200
200
200
230
200
160
180
230
350
330
96
Los Angeles
Cal ifornia
(September)
320
280
240
210
240
240
260
430
850
1100
660
260
240
230
190
170
170
230
240
260
260
280
300
300
130
Denver
Colorado
(November)
__.b
130
130
110
160
190
230
240
170
300
300
320
330
250
210
300
230
250
240
300
270
220
180
140
98
Portland
Oregon
(May)
110
94
94
94
94
75
75
94
110
110
110
130
110
110
170
170
150
150
150
150
150
150
150
130
51
Chicago
111 inois
(September)
180
160
160
150
150
160
220
260
210
220
, 240
300
340
260
260
260
250
230
210
210
200
200
180
200
110
El Paso
Texas
(October)
94
75
75
75
75
170
75
150
150
150
130
110
56
94
94
75
170
150
230
210
170
130
110
110
51
Data presented to two significant figures only.
"'NO data available.
8-49
-------
NO emissions overwhelm the ozone generating mechanism. From about 4:00 to 6:00 p.m. there is
still sufficient ozone present to oxidize NO to N02 rapidly in a simple titration reaction
apparently not involving hydrocarbons. This ozone scavenging mechanism would seem to be
identical to that observed in plumes from power plants (Section 6.1.3). Significant quantities
of NO are oxidized leading to high nighttime N02 concentrations. It may be postulated that
this mechanism is operative also in other localities exhibiting elevated N0? levels after
photochemical activity, including N02 photodissociation, decreases in the evening. Rapid
reaction of NO and 03 leading to increased NO,, concentrations has also been observed across a
high-traffic-volume freeway in Los Angeles (Fankhauser, 1977).
Although the data presented in Figure 8-18 were carefully chosen as an unusually good
example of ozone scavenging, Table 8-12 shows that elevated N02 levels in the late evening
hours are a fairly common phenomenon in the Greater St. Louis area. Fifty-three of the 89
high N02 values reported in Table 8-12 occurred between the hours of 7:00 p.m. and 6:00 a.m.
Variations in the values for peak concentrations and annual means from station to station
for the densely-monitored St. Louis area documented in Table 8-12 are also an indication of
the possible importance of local sources and small-scale meteorological and topographical
features in determining ambient pollutant concentrations.
8.1.7 Spatial and Temporal Variations of N00 Concentrations as Related to
Estimation of Human Exposure
Currently, if a single monitoring station in an Air Quality Control Region (AQCR) reports
ambient concentrations in excess of that safe for human health and welfare, this fact is
considered cause for concern. While this assumption appears reasonable if human health and •
welfare are to be protected, particularly if the monitoring station has been located in urban
or other population centers specifically to monitor population exposure (SAROAD purpose
designation 01, population-oriented), it may be of interest for some purposes to consider
methods for estimating human exposures in more detail. Some considerations involved in making
such exposure estimates are discussed in this section.
8.1.7.1 Spatial and temporal variations of local NO,, concentrations—Table 8-13 gives the N02
hourly concentrations measured at all 25 RAMS sites in St. Louis during a period of high
pollution for this area from 7 a.m. on October 1, 1976 to 2 a.m. on the following day. It is
presented as one illustration of the geographic and temporal variability of maximum N0? concen-
trations which may be experienced in a single airshed. It should be noted that few areas in
this country are as densely monitored as St. Louis was during 1975-76.
Sources of NO in the St. Louis area include mobile vehicles, other area sources, and a
wide variety of industrial point sources. The data presented are not necessarily to be taken
as typical of urban areas since the impact of a number of factors including source emission
strengths, their diurnal emission patterns, meteorological factors, topography and the presence
of other photochemical pollutants and their precursors may vary from area to area. In general,
a meaningful survey of the phenomenology or possible causes of the variability of high N02
concentrations on a nationwide basis is lacking in the literature.
8-50
-------
CD
cn
a 0.20
Z~
o
<
en
i-
z
ui
U
Z
o
o
2 o.io
3
NO
NO FORMATION
OF NO,
. PHOTOCHEMICAL FORMATION OF NO-
OZONE SCAVENGING
FORMATION OF NO,
NIGHTTIME NO2 CARRYOVER
L—L
\
/
AFTERNOON NO., CARRYOVER
SUNRISE
10 12 14
TIME OF DAY (CST)
16
18
20
Figure 8-18. Pollutant concentrations in Central City St. Louis, October 1, 1976, average of RAMS sites 101, 102, 106, and 107. Illustra
tion of photochemical and ozone scavenging formation of NO2 (U.S. EPA, 1976b).
-------
TABLE 8-12. MEAN AND TOP FIVE HOURLY NITROGEN DIOXIDE CONCENTRATIONS REPORTED FROM
18 INDIVIDUAL RAMS STATIONS IN ST. LOUIS DURING 1976 (U.S. EPA, 1976b)
00
(J1
Site Number
101
(Center-city)
104
105
107
108
Date of
Measurement
Nov.
Nov.
Nov.
Nov.
Nov.
May
Oct.
May
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Aug.
Oct.
Sept
Aug.
July
Aug.
Oct.
19
19
19
19
19
1
1
1
1
2
1
1
1
1
1
1
2
25
2
. 1
30
26
30
2
Time of
Measurement
10
9
8
7
11
7
6
8
5
6
_ _. f ^
1"
7
10
8
9
6
7
7
9
8
7
8
11
9
8
pm
pm
pm
pm
pm
am
pm
am
pm
pm
irst value
pm
pm
pm
pm
pm
pm
pm .
am
am
am
am
am
am
am
Cone
ug/m
481
454
443
434
411
293
291
287
284
284
inval
350
337
334
332
358
353
271
266
263
636
566
321
312
291
Distance from
§ntration Arithmetic Mean Site 101
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
idate
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
ppm ug/m"' ppm
2556 53 0.0282
2415
2358
2310
2187
1559 48 0.0253
1549
1526
1512
1509
!U
1864 44 0.0235
1795
1776
1768
1907 57 0.0305
1880
1441
1413
1400
3383 33 0.0174
3010
1707
1659
1548
(km)
0
<4
<4
<4
<20
(continued)
-------
TABLE 8-12. (continued)
CO
in
u>
Date of
Site Number Measurement
109 Apr. 30
Oct. 1
Oct. 1
Oct. 1
Apr. 7
114 Oct. 2
Oct. 2
Oct. 2
Oct. 1
Oct. 2
115 Dec. 4
Oct. 2
May 10
Sept. 22
July 6
116 May 7
May 7
Oct. 2
Oct. 1
Oct. 1
102 Oct. 1
Oct. 2
Oct. 2
Oct. 1
Oct. 1
Time of
Measurement
8 am
6 pm
7 pm
8 pm
12 am
8 am
12 am
3 am
9 pm
9 am
10 am
8 am
10 am
9 am
11 pm
11 pm
10 pm
7 pm
8 pm
7 pm
7 pm
8 am
9 am
6 pm
8 pm
Concgr
ug/m
289
216
197
186
173
305
281
276
275
273
286
170
152
145
128
457
326
228
206
206
374
365
363
354
331
itration Arithmetic Mean
ppm ug/m ppm
0.1537 26 0.0138
0.1147
0.1049
0.0991
0.0922
0.1524 32 0.0172
0.1495
0.1466
0.1462
0.1452
0.1520 22 0.0116
0.0903
0.0809
0.0771
0.0682
0.2430 23 0.0120
0.1734
0.1214
0.1098
0.1094
0.1990 62 0.0329
0.1940
0.1929
0.1882
0.1762
Distance from
Site 101
(km)
<20
<20
<20
<20
<10
(continued)
-------
TABLE 8-12. (continued)
00
in
Site Number
106
110
111
112
117
Date of
Measurement
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Feb. 24
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Oct. 1
Aug. 23
Oct. 1
Oct. 1
May 19
May 19
May 19
May 19
May 19
Time of
Measurement
10 pm
9 pm
11 pm
7 pm
8 pm
7 am
7 pm
6 pm
10 pm
11 pm
8 pm
7 pm
9 pm
6 pm
10 pm
11 pm
10 pm
8 am
7 pm
9 pm
2 am
6 am
4 am
3 am
5 am
Concei
ug/m
460
446
442
408
405
405
263
257
201
200
419
406
399
387
368
318
317
315
308
308
676
566
544
461
360
ntration Arithmetic Mean
ppm ug/m ppm
0.2449 56 0.0298
0.2375
0.2352
0.2169
0.2156
0.2155 34 0.0182
0.1398
0.1366
0.1069
0.1067
0.2230 45 0.0241
0.2161
0.2121
0.2060
0.1956
0.1689 52 0.0275
'0.1686
0.1677
0.1637
0.1636
0.3594 21 0.0110
0.3008
0.2891
0.2450
0.1914
Distance from
Site 101
(km)
<10
<10
<10
<10
<20
(continued)
-------
TABLE 8-12. (continued)
oo
I
en
en
Date of
Site Number Measurement
118 Sept. 17
Sept. 15
Nov. 6
Nov. 6
Nov. 6
119 Feb. 3
Feb. 3
Feb. 3
Feb. 3
Feb. 3
120 Oct. 11
Sept. 3
Oct. 11
Oct. 11
Aug. 23
Time of
Measurement
8 am
10 am
9 pm
8 pm
7 pm
11 pm
10 pm
8 pm
9 pm
7 pm
6 pm
7 am
8 am
7 pm
8 am
Concer
|jg/m
149
136
134
132
127
360
343
336
336
316
360
296
258
248
236
itration Arithmetic Mean
ppm pg/m ppm
0.0791 21 0.0111
0.0722
0.0715
0.0705
0.0677
0.1917 35 0.0184
0.1825
0.1787
0.1786
0.1681
0.1916 37 0.0198
0.1430
0.1372
0.1322
0.1254
Distance from
Site 101
(km)
<20
y20
<20
-------
Table 8-13. GEOGRAPHICAL VARIATION OF HOURLY NO. CONCENTRATIONS DURING A PERIOD Of HIGH NO., CONCENTRATIONS (U.S. EPA, 1976b)
[St. Couis, October 1 and 2. 1976 (ppm)]
CD
en
cr>
RAMS
Stat
101
102
103
104
105
106
Hour of Day
ion 789
0.07 0.12 0.12 0.18
0 07 0 12 0.17 0 11
0.05 0.10 0.15 0 12
0.05 0.07 0.12 0.14
0.07 0.11 0.10 0.08
10 11 12
0.14 0.08 0.09
0 12 0 10 0 08
0 10 0.07 0 06
0.07 0.04 0.05
0.08 0.06 0.06
13
0.09
0 06
0 04
0.07
0.07
0.05
14
0.10
0 05
0 02
0.07
0.10
0.06
15
0.06
0 07
0.03
0.08
0.06
0.10
16
0.12
0 13
0.06
0.15
0.08
0.11
17
0.19
0 19
0 15
0.15
0.17
0.17
18
0.20
0 20
0.16
0.15
0.19
0.22
19
0.19
0 18
0.13
0.15
0.18
0.22
20
0 17
0.14
0.13
0.18
0.24
21
0.18
A
0.15
0.13
0.18
0.24
22
0.16
0.13
0.13
0.11
0.13
0.24
23
0.17
ft
0.12
0.09
0.11
0.20
24 1 2
A «
* *
0.09 0.08
0.08 0.07
0.08 0.08
0.17 0.15
* n 1 *»
108 0.06 0.10 0.09 0.08 0.05 0.05 0.02 0.03 0.02 0.02 0.04 0.10 0.04 0.09 0.11 0.12 0.11 0.11 0.09 0.10
109 * * * * 0.02 0.01 0.02 0.03 0.02 0.02 0.04 0.11 0.10 0.10 0.08 0.08 0.07 0.05 0.04 0.04
110 0.03 0.04 0.08 0.07 0.04 0.01 0.02 0.04 0.06 0.05 0.08 0.14 0.14 0.10 0.10 0.11 0.11 0.09 0.07 0.07
111 0.05 0.07 0.08 0.06 0.04 0.04 0.03 0.03 0.04 0.06 0.11 0.21 0.22 0.22 0.21 0.20 0.17 0.13 0.12 0.08
112 0.05 0.06 0.05 0.06 0.08 0.05 0.04 0.02 0.03 0.06 0.16 0.15 0.16 0.16 0.16 0.17 0.17 0.15 0.15 0.13
113************** 0.21 0.20 0.21 0.21 0.18 0.17
(continued)
-------
TABLE 8-13. (continued)
Hour of Day
RAMS
Station 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 1
114 * * * * 0.04 0.03 0.03 0.03 0.01 0.01 0-04 0.07 0.07 0.09 0.15 0.13 0.13 0.15 0.14 0.14
115 0.04 0.07 0.07 0.05 0.03 0.02 0.02 0.03 0.03 0.03 0.04 0.05 0.05 0.03 0.03 0.03 0.06 0.05 0.04 0.03
116 0.04 0.06 0.04 0.03 0.02 0.01 0.01 0.01 0.02 0.02 0.03 0.05 0.11 0.11 0.10 0.07 0.05 0.04 0.04 0.05
117 0.03 0.02 0.02 0.01 0.01 0.01 0.00 0.01 0.02 0.02 0.02 0.02 0.02 0.04 0.07 0.07 0.06 0.04 0.07 0.05
118 0.02 0.02 0.02 0.02 0.01 0.01 0.01 0.02 0.02 0.03 0.04 0.03 0.03 0.03 0.05 0.06 0.04 0.03 0.06 0.05
CD
^ 119 0.04 0.04 0.04 0.03 0.03 0.02 0.02 0.02 0.02 0.03 0.04 0.07 0.10 0.12 0.11 0.10 0.10 0.10 0.09 0.07
--si
^20 * * * * * * * 0 01 * * * * * * * * * * * *
121 0.05 0.04 0.02 0.01 0.03 0.02 0.01 0.00 0.00 0.01 0.01 0.02 0.08 0.14 0.16 0.13 0.12 0.17 0.14 0.09
122 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.01 0.01 0.01 0.01 0.01 0.02 * * *
123 0.00 * * 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 ********
124 0.03 0.02 0.01 0.01 0.01 0.01 0.00 0.00 0.02 0.03 0.04 0.03 0.02 0.01 0.01 0.01 0.01 0.02 0.02 0.01
125 0.01 0.01 0.01 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.01 0.00 0.00 0.00 0.00 0.00 0.01 0.01 0.01
*Data missing.
-------
Figure 8-19 shows the locations of the 25 RAMS sites. The concentric circles locate
these stations within distances of 4, 10, 20 and 40 km of "center-city" Station 101. Compari-
son of Table 8-14 and Figure 8-19 reveals that with a 4 km radius the peak hourly N0~ concen-
trations varied from 0.15 to. 0.20 ppm; within a 10 km radius values ranged from 0.15 to 0.24
ppm; within a 20 km radius a four-fold variation from 0.06 to 0.24 was experienced; and within
a 40 km radius values ranging from 0.01 to 0.24 ppm were reported. The major peak occurred
after sundown at almost all sites, presumably due to the ozone titration mechanism. A
subsidiary photochemical peak is discernible in the late morning at central sites. Significant
N02 carry-over is evident at the start of the period reported. Both the duration and time of
occurrence of peak hourly values is variable from station to station as indicated by the
underlined portions in Table 8-13.
Another way of viewing the extent of the variability of NO concentrations in the St.
Louis area is presented in Table 8-14. This table is intended to illustrate the occurrence of
high NO- concentrations shown by monitoring throughout an airshed even though the events may
not take place at the same times and may not be associated with the same air mass. The sites
represented in the tables are located in a center-city location subject to nearby automobile
and truck traffic (101); in an outlying city location within a few kilometers of an electric
power plant and a number of heavy industrial sites (104); and in a high-density single family
residential community (111). It can be seen from these tables that both the highest NO hourly
readings and the corresponding NO/NO- ratios are quite different for Station 111 than for
Stations 101 and 104. Some evidence of spatial smoothing in both the highest and second
highest hourly NO^ concentrations by month is apparent in the data.
A somewhat different scenario is presented by the same type of data (Fairfax County;
Keyes et al.) (Tables 8-15 through 8-17) from three monitoring stations in Fairfax County,
Virginia, near Washington, D.C. These stations are located in an urban complex dominated by
area sources (70 percent of N0x emissions from area sources). Locations for the monitoring
stations cited in the table include an office complex, a high-volume transportation intersec-
tion, and a suburban commercial center. The maximum separation between stations is approxi-
mately 15 km.
The data reported show a considerable variation in the ratio of the highest hourly NO to
the corresponding hourly N02, suggesting a considerable variation in local NO area emissions
or in monitor siting. Nevertheless, it is important to note that the highest hourly N02
concentrations reported by month are quite similar at all stations. Presently, an insufficient
number of analyses have been conducted on a nationwide basis to determine whether or not this
observation is typical of area-source-dominated urban airsheds.
In a final scenario, very recent ground level NO measurements from a large isolated
source in complex terrain are presented (Pickering et al., 1980). (Individual N02 values were
not reported.) Measurements of this type are extremely rare in the literature. Exhaust gases
from the 712 MW Clinch River power plant, burning low sulfur coal, are emitted through two
8-58
-------
00
I
(Jl
CRYSTAL CITY
NOTE: Site* are aligned in approximate concentric circles of 4, 10. 20. and 40 km. respectively; adapted from Nelson (1979).
Figure 8-19. St. Louis RAMS station locations.
-------
TABLE 8-14. HIGH CONCENTRATIONS OF NITROGEN OXIDES,
ST. LOUIS, MISSOURI, 1976 (U.S. EPA, 1976b)
Month
RAMS STATION 101
January
February
March
April
May
June
RAMS STATION 104
January
February
March
April
May
June
RAMS STATION 111
January
February
March
April
May
June
Highest-NO
(Mg/m >
329
475
260
500
179
303
362
474
303
406
276
228
644
617
456
434
267
226
Corresponding
126
59
147
199
*
190
111
103
99
91
*
99
76
*
134
128
*
152
Highest3N02
162
146
147
247
175
225
111
194
121
293
155
151
109
124
136
182
143
181
2nd Highest
N02 (ug/m )
152
140
140
207
163
211
96
173
120
293
152
126
101
116
134
180
130 "
176
8-60
-------
TABLE 8-15. MONTHLY TRENDS IN HOURLY NO AND NO- CONCENTRATIONS,
MASSEY BUILDING STATION, FAIRFAX COUNTY, VIRGINIA, I977a (KEYES ET AL.)
Month
January
February
March
April
May
June
July
August
September
October
November
December
Highest NO
(ug/nT)
655
650
350
230
40
80
20
70
125
420
680
645
Corresponding
N02 (jjg/m )
140
105
105
120
20
85
65
95
75
43
120
Highest.,
N02 (|jg/m )
160
190
140
160
180
170
85
95
115
225
115
120
2nd Highest
N02 (ug/m )
150
170
130
130
160
75
75
105
130
105
115
3
Annual Average NO,,: 40 ug/m
Second Highest N02: 190 ug/m
Peak/mean =4.8
Data from Fairfax County (Va.) Air Pollution Control Agency.
8-61
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TABLE 8-16. MONTHLY TRENDS IN HOURLY NO AND NO, CONCENTRATIONS,
LEWINSVILLE STATION, FAIRFAX COUNTY, VIRGINIA, 1977 (KEYES ET AL.)
Month
January
February
March
April
May
June
July
August
September
October
November
December
Highesjj NO
680
630
615
380
290
290
650
515
580
700
680
Corresponding
65
65
95
120
180
75
10
75
40
45
75
Highest3
130
290
190
290
225
170
280
280
160
140
130
2nd Highest
125
225
180
255
205
140
265
235
150
130
120
Annual Average NO,: 56 ug/m
Second Highest NO-: 280 ^g/m
Peak/mean =5.0
aData from Fairfax County (Va.) Air Pollution Control Agency.
8-62
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TABLE 8-17. MONTHLY TRENDS IN HOURLY NO AND N0? CONCENTRATIONS,
SEVEN CORNERS STATION, FAIRFAX COUNTY, VIRGINIA, 1977a (KEYES ET AL.)
Month
January
February
March
April
May
June
July
August
September
October
Highes| NO
630
620
540
665
240
170
185
320
505
420
Corresponding
N02 (M9/m )
10
50
0
0
40
20
55
105
105
85
Highest.
N02 (ug/m )
150
205
120
265
190
140
170
235
205
160
2nd Highest
N02 (ug/nv )
120
145
110
195
170
130
150
150
170
150
Annual Average NO-: 46
Second Highest N02: 235
Peak/mean =5.1
aData from Fairfax County (Va.) Air Pollution Control Agency.
8-63
-------
stacks, 42 m apart, each 138 m high. The surrounding terrain has ridges exceeding 1.5 times
stack height within 3 to 5 km of the plant in all quadrants of the compass. Figure 8-20 shows
the location and elevation of the monitoring sites. Table 8-18 gives the mean of one-hour NO
A
concentrations over an extended monitoring period from November 20, 1976 to September 30,
1977. It is important to note that the average values reported are subject to large error
since many readings were near the detection limit of the analytical instruments. The data do,
however, indicate the magnitude of the average values. Much greater confidence can be placed
in the individual 10 highest NO readings recorded at each site (Table 8-19). Perhaps the
most significant point to note for this discussion are the extremely high peak to mean ratios
for NO observed at all sites (compare Tables 8-18 and 8-19). Although detailed analysis of
the frequency distribution of high NO concentrations has yet to be made, it seems appropriate
to state that the probability is small for detecting the maximum impact of a plume with fixed
monitoring stations. This observation may be expected to hold true also in regions subject to
a variety of point and area sources. In terms of estimating human exposure due to large point
sources, therefore, fixed monitoring sites may be expected to provide data mainly on the
long-term average impact of such sources.
8.1.7.2 Estimating human exposure—The examples of local variability of significant NO-
concentrations just presented have some bearing on the question of estimating human exposure
to this pollutant. Such an estimation might include a study of the spatial variation of N0?
concentrations for time periods during which human health and/or welfare are or may be
adversely affected and might take into account the mobility of the population at risk. In an
area like Fairfax County, it is possible that the relatively small spatial variation in high
NO- concentrations which is evident from the data presented in Table 8-14 might enable esti-
mates of exposure to high NO- concentrations to be made from data gathered at a single monitor-
ing station. In an area like St. Louis, more detailed monitoring might be required due to the
greater variation in ambient levels across this urban area. In addition, the occurrence of
high NOp concentrations during the late evening hours when most of the population is presumably
indoors would point to the desirability of considering relationships between indoor and outdoor
pollutant concentrations. These are only a few examples of the methodological difficulties
associated with detailed estimates of actual human exposure.
Few attempts to perform such exposure estimates have been reported in the literature.
Recently, an exposure model has been reported for the Los Angeles area (Horie et al., 1977).
The main thrust of this work was to estimate population exposure to NO- concentrations as a
percentage of time the population was potentially exposed to NO, concentrations exceeding the
T
California Ambient Air Quality Standard (CAAQS) (470 ug/m or 0.25 ppm for 1-hr averages).
Presentation of this model is in no sense intended to reflect on consideration of a National
Ambient Air Quality Standard but is included only to illustrate an existing exposure
methodology.
8-64
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CD
15 KM
10 KM NASH'SFORD
5 KM
CARBO ^J-
^ CLEVELAN
Figure 8-20. Location and elevation of Clinch River Power Plant monitoring stations (Pickering et al., 1980).
-------
TABLE 8-18. MEAN NOV CONCENTRATIONS FOR ISOLATED POINT SOURCE
IN COMPLEX TERRAIN (CLINCH RIVER POWER PLANT) (ppb) (PICKERING et al., 1980)
Station NO N09 NO
A. £
Tower 29 15 15
Munsey 75 1
Hockey 53 2
Lambert -
Johnson -
Castle 25 11 13
Kents 11 7 3
Nashs 15 9 6
8-66
-------
TABLE 8-19. TEN HIGHEST HOURLY AVERAGE NOV CONCENTRATIONS OBSERVED AT EACH
MONITORING SITE FOR ISOLATED SOURCE (CLINCH RIVER POWER PLANT) (PICKERING ET AL., 1980)
i
CTl
Rank
1
2
3
4
5
6
7
8
9
10
Rank
1
2
3
4
5
6
7
8
9
10
NO
Cone.
(ppb)
619
549
482
467
457
448
430
420
414
397
NO
Cone?
(ppb)
834
601
553
262
235
229
228
226
211
207
Tower
Date
1/28/77
12/30/76
3/15/77
12/30/76
7/7/77
1/26/77
1/28/77
12/23/76
12/30/76
12/23/76
Nashs
Date
8/10/77
Will
8/10/77
2/10/77
7/8/77
2/10/77
7/12/77
2/11/77
Will
5/6/77
Hour
10
14
11
20
8
20
13
10
16
9
Hour
16
12
15
12
10
11
10
12
13
10
NO
Cone.
(ppb)
568
399
329
255
219
205
170
164
146
130
NO
Con?.
(ppb)
816
589
464
435
410
394
375
365
350
290
Hockey
Date
6/30/77
7/5/77
8/15/77
6/30/77
7/6/77
7/2/77
4/20/77
3/21/77
5/14/77
7/20/77
Castle
Date
2/15/77
2/8/77
2/8/77
2/11/77
2/11/77
2/11/77
2/8/77
2/11/77
2/10/77
2/11/77
Hour
5
3
9
4
8
6
4
11
10
3
Hour
15
11
10
9
10
11
12
12
10
8
NO
Cone.
(ppb)
353
103
101
92
89
83
80
79
79
78
NO
Con?.
(ppb)
419
408
297
280
276
252
206
186
173
170
Kents
Date
8/13/77
2/19/77
8/8/77
12/14/76
11/24/76
12/14/76
8/8/77
8/6/77
12/19/76
1/13/77
Munsey
Date
3/9/77
3/9/77
7/6/77
7/6/77
3/9/77
3/9/77
6/16/77
3/21/77
3/9/77
7/2/77
Hour
22
4
7
11
24
12
3
15
6
17
Hour
9
8
9
8
7
10
8
11
11
6
-------
In the model, NOp data for 1973 from 26 monitoring stations were combined with population
data from Regional Statistical Areas (RSAs) developed by the Southern California Association
of Governments and employment data, computed for each RSA from 1970 Census data. A number of
receptor points were assigned to each RSA according to the size of the population and the land
area. The number of people associated with each receptor point was then computed. For the
non-working population, exposure estimates were made by assuming this sub-population to be
stationary. In the case of workers, the population was stratified by the residence location
and by the working location. Air quality data in the latter case was classified into two time
categories: (1) non-working time and (2) working time (weekdays 7 am to 6 pm). Additionally,
weekday-weekend differences in exposure were assessed from data on weekday-weekend differences
in air quality.
Using the static population assumption, the distribution of the population exposed at
various frequencies of standard violations (population-at-risk distribution) were determined
for both N02 hourly average concentrations and NCk daily maximum hourly concentrations.
Figure 8-21 shows the distributions of the population exposed at various percentages of days
exceeded during three time periods; all the time, weekdays and weekends. It can be seen that
the entire population was exposed for a smaller percentage of days during weekends than week-
days. An average person in the Los Angeles AQCR was exposed to NO- air pollution above the
CAAQS 4.4 percent of the days during weekdays, and only 2.1 percent of the days during the
weekends (Table 8-20).
The distribution of the population exposed at various percentages of hours exceeded is
shown in Figure 8-22. Again, the entire population was exposed for a smaller percentage of
hours above the CAAQS during weekends than weekdays. Therefore, it can be concluded that
people in the Los Angeles AQCR were less frequently exposed to a concentration above the CAAQS
during weekends than weekdays because of the markedly better N0? air quality over weekends.
The regionwide impacts of weekday-weekend phenomena on population exposure to NO- are
summarized in Table 8-20. The regional averages of daily risk frequency and hourly risk
frequency were, respectively, 3.7 percent of the days and 0.46 percent of the hours. In other
words, an average person in the Los Angeles Basin was exposed in 1973 to a concentration above
the CAAQS 14 days per year or 40 hours per year. The regional averages of daily risk frequency
are 4.4 percent of the days during weekdays and 2.1 percent of the days during weekends. The
regional averages of hourly risk frequency are 0.57 percent of the hours during weekdays and
0.18 percent of the hours during weekends. Therefore, it can be said that in 1973 an average
person in the Los Angeles Basin received a less frequent exposure above the CAAQS during
weekends than weekdays by 2.3 percent of the days or by 0.39 percent of the hours.
Table 8-20 also presents the regional averages of risk frequency, which were computed by
considering diurnal population movement between residence and workplace (values in
parentheses). The refined estimates of regional average risk frequency are close to but a
8-68
-------
I I I I I I II I I I I 1 I I I I I I I I I I j I !_
u
z
LU
o
LLJ
CC
U.
Q
01
ALL TIME
WEEKDAY
WEEKEND
Z
LU
cc
o
5
O
LLJ
O
a.
X
UJ
Z
O
D
a
O
a
u.
O
O
P
O
<
cc
u.
0.01
I I I I I I I I I I I \ I I I \ I I I \ I I I
5 10
PERCENT OF DAYS ABOVE THE CALIFORNIA STANDARD
Figure 8-21. Population exposed to IMC>2 daily maximum hourly
concentration above the California one-hour standard at various
frequencies (Horie et al., 1977).
15
8-69
-------
TABLE 8-20. REGIONWIDE IMPACT OF WEEKDAY-WEEKEND PHENOMENA ON POPULATION
EXPOSURE TO NITROGEN DIOXIDE: DAYS AND HOURS EXCEEDING
THE CALIFORNIA AMBIENT AIR QUALITY STANDARD (FAIRFAX COUNTY)
Time Period
All time
Weekday
Weekend
Weekday /Weekend
Difference
Percent of Days Exceeded3
3.7 (3.8)
4.4 (4.5)
2.1 (2.1)
+2.3 (+2.4)
Percent of Hours Exceeded
0.46 (0.50)
0.57 (0.63)
0.18 (0.18)
+0.39 (+0.45)
Percentages in parentheses computed based on the mobile population assumption.
8-70
-------
o
UJ
o
O
u
<
I
Z
Ul
CC
O
Q
UJ
1/7
O
o.
X
UJ
z
o
CL
o
Q.
LL
O
z
o
\-
o
<
cc
0.1
0.01
I I I I I I I I I I I I I I I I ! I I II I I I L_
ALL TIME
\ WEEKDAY
\
WEEKEND
Mill I I I I I I I I \\ I I h^ I I I IM I I I I
0.5 1 1.5
PERCENT OF HOURS ABOVE THE CALIFORNIA STANDARD
Figure 8-22. Population exposed to NO? hourly average concentration
above the California one-hour standard (470 ^g/m^; 0.25 ppm) at vari-
ous frequencies.
Source: Horie et al., 1977.
8-71
-------
little greater than those based on the static population assumption. According to the refined
estimates, an average person in the Los Angeles Basin received less frequent exposure above
the CAAQS during weekends than weekdays by 2.4 percent of the days or by 0.45 percent of the
hours.
A rough nationwide estimate of the population at risk to various levels of NCL air
pollution can be obtained from a data base recently described (Freedman et al. , 1978). The
data base includes data on monitoring for all counties in the contiguous United States (taken
directly from 1974 SAROAD file) along with 1970 Census data. For the purposes of this
analysis, the assumption is made that the entire county population is potentially at risk to
the second highest one-hour N02 concentration reported in the county, provided that the moni-
toring site reporting was located specifically to monitor population exposure (SAROAD purpose
code 01). In 1974, 121 U.S. counties having total population of 65,009,289 persons had at
least one monitor reporting such hourly NO,, data. Of these counties 112 were selected as
having data which warranted inclusion in this analysis. The results of the population-at-risk
computation is presented in Table 8-21. Fifty-seven percent of the U.S. population in counties
reporting one-hour N09 data in 1974 were potentially at risk to one-hour NO, concentrations
3
which exceeded 250 ug/m at least twice during the year; 29 percent to one-hour N00 concentra-
3
tions which exceeded 500 ug/m at least twice during the year; and 14 percent to one-hour N09
3
concentrations which exceeded 750 ug/m at least twice during the year. The population at
risk comprised at least 41, 21, and 10 million people for the corresponding N02 concentration
levels. More sophisticated and/or more recent exposure estimates on a nationwide level are
lacking in the literature.
TABLE 8-21. U.S. POPULATION AT RISK TO
VARIOUS 1974 N02 HOURLY AMBIENT CONCENTRATIONS3
County
Count
68
24
6
1974 Second Highest % Monitored
1-hour N02 3 Total 1970 Population Population Potentially
Concentration (ug/m ) Potentially at Risk at Risk
250
500
750
41,837,864 57
21,341,617 29
10,106,698 14
Computed from data in Freedman et al. (1978).
8-72
-------
8.2 ATMOSPHERIC CONCENTRATIONS OF NITRATES
Although extensive monitoring has been carried out for nitrates suspended in ambient air,
recent reports (Section 7.4.1) document serious and apparently unresolvable difficulties
associated with nitrate artifact formation on the filter media routinely used to collect
samples. At present, therefore, it seems most prudent to report data only for those few
recent measurements which were collected using Teflon filters not believed to be subject to
the positive artifact formation reported.
It should be noted, however, that Marker et al. (1977) report that nitrate could be
removed from glass fiber filters when aerosols containing sulfate passed through the filters.
Since the same mechanism may operate when Teflon filters are used, the data reported below
must be considered as preliminary.
A 24-hr sample from Philadelphia, Pennsylvania, on February 24, 1977, indicated an ambient
nitrate concentration of 0.18 M9/m in "the fine particle fraction (<2.4(j) of a sample collected
by a dichotomous sampler using Teflon filters (Dzubay and Stevens, 1975; Stevens et al.,
1978b). Data from Glendora, California, obtained with a dichotomous sampler during 10 days in
early March, 1978, show nitrate concentration ranging from 0.17 to 0.47 |jg/m in the fine
fraction with a mean of 0.28 ug/m (Stevens et al. , 1978a). Concentrations from the coarse
fraction (particles with aerodynamic diameter between 2.4 u and 16 u) range from 0.06 to 0.83
ug/m with a mean of 0.22 ug/m . Measurements at a number of sites near freeways in Los
o
Angeles gave fine fraction nitrate concentrations up to 2.0 ug/m and similar readings up to
2.1 ug/m at nearby background sites (Dzubay et al., 1979). Nitrate did not increase signifi-
cantly in the roadway (Trijonis, 1978). Other data from California obtained using quartz
filters are summarized in Table 7-7 and in Spicer et al. (1978).
Few measurements of ambient nitric acid vapor concentrations have been carried out.
Sampling from aircraft in non-urban areas at altitudes ranging from 0.2 to 8 km was conducted
by Huebert and Lazrus (1978) during August and September of 1977. Those areas not influenced
by urban plumes evidenced concentrations ranging from 0.05 to 0.75 ug/m (0.02 to 0.3 ppb),
with most values below 0.4 ug/m (0.15 ppb).
Miller and Spicer (1974), using a modified microcoulometric method, report up to 25 ug/m
(10 ppb) HN03 in Los Angeles, California. In a more extensive report, Spicer (1977) cites
measurements in St. Louis, Missouri, for 26 days during July and August 1973, yielding maximum
3 3
23-hr average HNOj concentrations of 30 ug/m (12 ppb) and a 1-hr maximum of 200 ug/m (80
ppb). In West Corvina, California, 29 sampling days during August and September 1973, gave
3 3
23-hr average values up to 65 ug/m (26 ppb) and a 1-hr maximum of 78 ug/m (31 ppb). Hanst
et al. (1975), in failing to detect HNO-, in Pasadena, California, set an upper limit of 25
3
ug/m (10 ppb) on its concentration in this area. Recently, Tuazon et al. (1978) report
observing up to 15 ug/m (6 ppb) in Riverside, California, during approximately one day of
monitoring in October 1976.
8-73
-------
The data available are not sufficient to place human exposure to suspended nitrates or
nitric acid vapor in nationwide perspective. Furthermore, extreme caution must be exercised
in interpreting any health studies making use of ambient nitrate data derived using filter
media that are subject to artifact formation.
8.3 ATMOSPHERIC CONCENTRATIONS OF N-NITROSO COMPOUNDS
Although ambient atmospheric data on N-nitroso compounds are sparse when viewed from a
nationwide perspective, a number of measurements from scattered locations, mostly near
suspected sources, have been reported. Some of these data are presented in this section in
order to indicate the possible magnitude of the existing atmospheric burden of this class of
compounds.
Fine (1976a,b) first reported dimethylnitrosamine (DMN) in ambient air in 1975. Levels
3 3
ranged up to 0.95 ug/m in Baltimore, Maryland, and up to 0.051 ug/m in Belle, West Virginia.
Later, Fine (1976) reported concentrations up to 15 ug/m near the same site in Baltimore and,
independently, Pellizzari (1977) reported values up to 32 ug/m from the same area using a
different analytical method. Fine (1976) reported a level of 0.8 ug/m for a 3-minute sample
taken in New York City, New York. Fine (1976a,b) failed to detect DMN in Philadelphia,
Pennsylvania; Waltham, Massachusetts; and at a site near Wilmington, Delaware. Sampling by
EPA's National Enforcement Investigations Center (NEIC) (U.S. EPA, 1977b) showed little indi-
cation of N-nitroso compounds in the vicinity of suspected sources at 32 locations in Kansas,
Missouri, Illinois, Indiana, Iowa, and Nebraska when contamination problems were resolved. No
evidence was found by NEIC to substantiate secondary production in the vicinity of amine
sources. In other monitoring by NEIC (U.S. EPA, 1977c) near suspected sources in Mclntosh,
Alabama; Charlotte and Salisbury, North Carolina; and Chattanooga, Tennessee, only one sample
near the Alabama site showed evidence of N-nitroso compounds (0.040 ug/m DMN) in the atmos-
phere. Fine (1976) reported monitoring for atmospheric DMN at several sites in New York,
New Jersey, and Massachusetts under a variety of meteorological conditions. DMN was not found
in any of 25 samples taken throughout northern New Jersey; nor in any of 15 samples in the
Boston, Massachusetts, area. Only one of 18 samples in New York City showed a measurable DMN
concentration (0.016 ug/m ). Since a cryogenic trap was used in the sampling procedure for
this measurement, the possibility of artifact formation cannot be ruled out.
In summary, these measurements point to the conclusion that the atmospheric route for
N-nitroso compounds is not a significant pathway for possible human exposure. In addition, no
evidence has been found to date for the nitrosation of amines in ambient air.
8.4 SUMMARY
8.4.1 Atmospheric Concentrations of NO,,
Examination of both historical data and for the years 1975 to 1980 allows some general
conclusions to be drawn about the nationwide experience with respect to ambient NOp concentra-
tions. In summary, the data cited illustrate the following points.
8-74
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• Annual average concentrations of NCL are not reliable index of short-term (3 hour or
less) human exposure, and vice versa.
• Although a distinct recurrent diurnal pattern is discernible in some areas of the
country, in many areas peak diurnal values may occur at almost any time of day.
• Just as there is no standard diurnal pattern nationwide for peak N0? concentrations,
there is also no standard nationwide pattern for the month-by-month variations in
monthly averages of daily maximum 1-hr concentrations. Peak monthly averages occur
at different times of year in different locations.
• The direction and magnitude of recent trends in N02 concentrations also tend to be
area-specific.
• The oxidation of NO to NCk by ozone scavenging (chemical reaction with ambient 0,,
which is generated photochemically during daylight hours) may at some times be an
important mechanism in some areas of the country for producing high NO^ levels after
photochemical activity has ceased. In other areas photochemical reactions involving
ambient hydrocarbons may be the dominant mechanism.
The following summary of recent ambient levels of NCL occurring nationwide is given to
provide perspective on the concentration levels associated with the health and welfare effects
discussed elsewhere in this document.
Examination of selected nationwide monitoring data for 1975 to 1980 reveals that during
at least one of these years, peak 1-hr NO^ concentrations equalling or exceeding 750 ug/m
(0.4 ppm) were experienced in Los Angeles and several other California sites; Ashland,
Kentucky; and Port Huron, Michigan. Additional sites reporting at least one peak hourly con-
centration equalling or exceeding 500 ug/m (0.27 ppm) include: Phoenix, Arizona; St. Louis,
Missouri; New York City, New York; 14 additional California sites; Springfield, Illinois;
Cincinnati, Ohio; and Saginaw and Southfield, Michigan. Other sites, distributed nationwide,
reported maxima close to this value. Recurrent NO, hourly concentrations in excess of 250
3
ug/m (0.14 ppm) were quite common nationwide in 1975 to 1980.
The data also show that Long Beach, California; Indianapolis, Indiana; and Salt Lake
City, Utah, all experienced at least one day when the 24-hr average N09 concentration exceeded
3
300 ug/m (0.16 ppm) during 1975 to 1980. In addition, San Bernadino, California; Denver,
Colorado; Chicago, Illinois; Nashua, New Hampshire; Cincinnati and Cleveland, Ohio; Tulsa,
Oklahoma; and Fort Worth and Houston, Texas, all reported at least one 24-hr period where
average N00 concentrations exceeded 150 ug/m (0.08 ppm).
3
Annual arithmetic means for N02 concentrations in 1976 exceeded 100 ug/m (0.053 ppm) at
Anaheim, El Cajon, Riverside, San Diego, and Temple City, California. Other sites reporting
3
yearly arithmetic means for 1976 equalling or exceeding 100 ug/m (0.053 ppm) included Chicago,
Illinois, and Southfield, Michigan. However, by 1980 virtually none of the still operating
monitoring sites reported annual average levels over 100 ug/m (except one in San Diego;
114 ug/m3).
8-75
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8.4.2 Atmospheric Concentrations of Nitrates
Few high quality data exist on concentrations of nitrates suspended in ambient air. Very
recent data, taken by sampling techniques not subject to positive artifact formation, range
3 3
from 0.18 ug/m in Philadelphia, Pennsylvania, to 2.1 ug/m at sites in Los Angeles. The data
available are not sufficient to place human exposure in nationwide perspective.
8.4.3 Atmospheric Concentrations of N-Nitroso Compounds
N-nitroso compounds have recently been observed in ambient air, mostly at locations near
known or suspected sources. The data reported to date are indicators only of atmospheric
burdens at a few special locations. No evidence has been reported to substantiate secondary
production in the vicinity of amine sources.
Observed concentrations of dimethylnitrosamine (DMN) ranged up to 32 pg/m at a site in
Baltimore, Maryland, near a known emission source. An extensive monitoring survey by EPA's
National Enforcement Investigation Center showed no indication of N-nitrosamines in the
vicinity of 32 suspected sources throughout the Midwest. Similar monitoring at four sites in
the Southeast yielded a trace of DMN in only one sample from one site. Similar results were
obtained in sampling by other researchers in the greater New York-New Jersey area and near
Boston, Massachusetts. Considering the small and infrequently observed atmospheric burdens of
nitrosamines reported, in conjunction with the potential human exposure from certain foodstuffs
and tobacco, the atmospheric route for human exposure does not, at this time, seem to be a
significant one.
8-76
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8.5 REFERENCES
Breeding, R. J. , J. P. Lodge, Jr., J. B. Pate, D. C. Sheesley, H. B. Klonis, B. Fogle, J. A.
Anderson, T. R. Englert, P. L. Haagenson, R. B. McBeth, A. L. Morris, R. Pogue, and A. F.
Wartburg. Background trace gas concentrations in the central United States. J. Geophys.
Res. 78:7057-7064, 1973.
Chameides, W. L. Tropospheric odd nitrogen and the atmospheric water vapor cycle. JGR J.
Geophys. Res. 80:4989-4996, 1975.
Cox, R. A. Some measurements of ground level NO, N0g and 0, concentrations at an unpolluted
maritime site. Tellus 29:356-362, 1977. ^ d
Crutzen, P. J. , I. S. A. Isaksen, and J. R. McAfee. The impact of the chlorocarbon industry
on the ozone layer. JGR J. Geophys. Res. 83:345-363, 1978.
Drummond, J. W. Atmospheric Measurements of Nitric Oxide Using a Chemiluminescent Detector.
Ph.D. thesis, University of Wyoming, Laramie, WY, 1976.
Dzubay, T. G. , and R. K. Stevens. Ambient air analysis with dichotomous sampler and x-ray
fluorescence spectrometer. Environmental" Science and Technology 9:663-668, 1975.
Dzubay, T. G. , R. K. Stevens, and L. W. Richards. Composition of aerosols over Los Angeles
freeways. Atmos. Environ. 13:653-659, 1979.
Fairfax County. Hourly monitoring data available from Air Pollution Control Division, Health
Department, 4080 Chain Bridge Road, Fairfax, Virginia 22030.
Fankhauser, R. K. Nitric oxide, nitrogen dioxide, ozone interrelationships across the free-
way. In: Symposium for Discussion of the Los Angeles Catalyst Study, U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina, April 12-13, 1977.
EPA-600/4-77-036, U.S. Environmental Protection Agency, Research Triangle Park, NC, June
1977. pp. 343-357.
Fine, D. H. Final Report of Monitoring for N-nitroso Compounds in the States of West
Virginia., New York, New Jersey, and Massachusetts. EPA Contract No. 68-02-2363. U.S.
Environmental Protection Agency, Research Triangle Park, North Carolina, November 1976.
Fine, D. H. , D. P. Rounbehler, N. M. Belcher, and S. S. Epstein. N-/iitroso compounds in the
environment. In: International Conference on Environmental Sensing and Assessment,
Volume 2, A Joint Conference Comprising the International Symposium on Environmental
Monitoring and Third Joint Conference on Sensing Environmental Pollutants, World Health
Organization and Others, Las Vegas, Nevada, September 14-19, 1975. Institute of
Electrical & Electronics Engineers, Inc., New York, NY, 1976a. session 30-7.
Fine, D. H. , D. P. Rounbehler, N. M. Belcher, and S. S. Epstein. N-nitroso compounds in air
and water. In: Environmental N-nitroso Compounds Analysis and Formation, Proceedings of
a Working CorfFerence, International Agency for Research on Cancer, Tallinn, Estonian SSR,
October 1-3, 1975. E. A. Walker, P. Bogovski, L-. Griciute, and W. Davis, ed. , IARC
Scientific Publications No. 14, International Agency for Research on Cancer, Lyon,
France, 1976b. pp. 401-408.
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Freedman, S. J. , E. Lewis-Heise, J. D. Wilson, and A. V. Hardy, Jr. Population at Risk to
Various Air Pollution Exposures: Data Base "POPATRISK." EPA-600/1-78-051, U.S. Environ-
mental Protection Agency, Research Triangle Park, NC, June 1978.
Galbally, I. E. Measurement of nitrogen oxides in the background atmosphere. J_n: Air Pollu-
tion Measurement Techniques, Parts I and II, Report and Lectures of the World Meteoro-
logical Organization Air Pollution Measurement Techniques Conference, Gothenburg, Sweden,
October 11-15, 1976. WMO No. 460, Special Environmental Report No. 10, World Meteoro-
logical Organization, Geneva, Switzerland, 1977. pp. 179-185.
Hanst, P. L. , E. W. Wilson, R. K. Patterson, 8. W. Gay, Jr., L. W. Chaney, and C. S. Burton.
A Spectroscopic Study of California Smog. EPA-650/4-75-006, U.S. Environmental Protec-
tion Agency, Research Triangle Park, NC, February 1975.
Marker, A. B. , L. W. Richards, and W. E. Clark. The effect of atmospheric S02 photochemistry
upon observed nitrate concentrations in aerosols. Atmos. Environ. 11:87-91, 1977.
Horie, Y. , A. S. Chaplin, and E. D. Helfenbein. Population Exposure to Oxidants and Nitrogen
Dioxide in Los Angeles. Volume II: Weekday/Weekend and Population Mobility Effects.
EPA-450/3-77-004b, U.S. Environmental Protection Agency, Research Triangle Park, NC,
January 1977.
Huebert, B. J. , and A. L. Lazrus. Global tropospheric measurements of nitric acid vapor and
particulate matter. Geophys. Res. Lett. 5:577-580, 1978.
Junge, C. E. Recent investigations in air chemistry. Tellus 8:127-139, 1956.
Keyes, D. L. , B. Kumar, R. D. Coleman, and R. 0. Reid. The material presented on the
Washington, D.C. area is largely due to Energy and Environmental Analysis, Inc., 1111
North 19th Street, Arlington, Virginia 22209.
Lodge, J. P. , Jr. , and J. B. Pate. Atmospheric gases and particulates in Panama. Science
(Washington, D.C.) 153:3734, 408-410, 1966.
Ludwig, F. L. , and E. Shelar. Site Selection for the Monitoring of Photochemical Air Pollut-
ants. EPA-450/3-78-013, U.S. Environmental Protection Agency, Research Triangle Park,
NC, April 1978.
Miller, D. F. , and C. W. Spicer. A continuous analyzer for detecting nitric acid. Presented
at the 67th Annual Meeting, Air Pollution Control Association, Denver, CO, June 9-13,
1974. paper no. 74-17.
Moore, H. Isotopic measurement of atmospheric nitrogen compounds. Tellus 26:169-174, 1974.
Nelson, E. Regional Air Pollution Study. High Volume Filter Measurements of Suspended Par-
ticulate Matter. EPA-600/4-79-003, U.S. Environmental Protection Agency, Research
Triangle Park, NC, January 1979.
Noxon, J. F. Nitrogen dioxide in the stratosphere and troposphere measured by ground-based
absorption spectroscopy. Science (Washington, D.C.) 189:547-549, 1975.
Noxon, J. F. Tropospheric N02- JGR J. Geophys. Res. 83:3051-3057, 1978.
Pellizzari, E. D. The Measurement of Carcinogenic Vapors in Ambient Atmospheres. EPA-600/7-
77-055, U.S. Environmental Protection Agency, Research Triangle Park, NC, June 1977.
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Pickering, K. E. , R. H. Woodward, and R. C. Koch. Power Plant Stack Plumes in Complex Terrain:
Data Analysis and Characterization of Plume Behavior. EPA-600/7-80-008, U.S. Environ-
mental Protection Agency, Research Triangle Park, NC, January 1980.
Ritter, R. A., D. H. Stedman, and T. J. Kelly. Ground level measurements of nitric oxide,
nitrogen dioxide and ozone in rural air. In: Nitrogenous Air Pollutants, Proceedings of
.a Symposium, 175th National Meeting, American Chemical Society, Anaheim, California,
March 12-17, 1978. D. Grosjean, ed., Ann Arbor Science Publishers, Inc., Ann Arbor, MI,
1979. pp. 325-343.
Robinson, E. , and R. C. Robbins. Emissions, concentrations, and fate of gaseous atmospheric
pollutants, jjr. Air Pollution Control. Part II. W. Strauss, ed. , Wiley-Interscience,
New York, NY, 1972. pp. 1-93.
Spicer, C. W. The fate of nitrogen oxides in the atmosphere.
7:163-261, 1977.
Adv. Environmental Sci. Technol,
Spicer, C. W., P. M. Schumacher, J. A. Kouyoumjian, and D. W. Joseph. Sampling and Analytical
Methodology for Atmospheric Particulate Nitrates. Final Report. EPA-600/ 2-78-067, U.S.
Environmental Protection Agency, Research Triangle Park, NC, April 1978.
Stevens, R. K. , T. G. Dzubay, G. Russwurm, and D. Rickel. Sampling and analysis of atmos-
pheric sulfates and related species. In: Sulfur in the Atmosphere, Proceedings of the
International Symposium, United Nations Environmental Program and Others, Dubrovnik,
Yugoslavia, September 7-14, 1977. Atmos. Environ. 12:55-68, 1978b.
Stevens, R. K. , T. G. Dzubay, D. T. Mage, R. Burton, G. Russwurm, and E. Tew. Comparison of
nitrates and sulfates collected by Hi-yol and dichotomous samplers. Presented to
American Chemical Society, Division of Environmental Chemistry, Miami, Florida, September
1978a.
.Trijonis, J. Empirical Relationships Between Atmospheric Nitrogen Dioxide and Its
Precursors. EPA-600/3-78-018, U.S. Environmental Protection Agency, Research Triangle
Park, NC, February 1978.
Trijonis, J. , et al. The Relationship of Ambient N02 to Hydrocarbon and NO Emissions.
Draft report from Technology Service Corporation to EPA under Contract No. 68-02-2299.
U.S. Environmental Protection Agency, Office of Research and Development, Research
Triangle Park, NC.
Tuazon, E. C. , R. A. Graham, A. M. Winer, R. R. Easton, J. N. Pitts, Jr., and P. L. Hanst. A
kilometer pathlength Fourier-transform infrared system for the study of trace pollutants
in ambient and synthetic atmospheres. Atmos. Environ. 12:865-875, 1978.
U. S. Environmental Protection Agency. Air quality and emissions trends. I_n: The National
Air Monitoring Program: Air Quality and Emissions Trends—Annual Report. Volume 1.
EPA-450/l-73-001a, U.S. Environmental Protection Agency, Research Triangle Park, NC,
August 1973. pp. 4-1-4-41.
U. S. Environmental Protection Agency. National Aerometric Data Bank, 1975a.
U. S. Environmental Agency. SAROAD. Data reported were abstracted from the 1975 SAROAD raw
data file maintained at the National Air Data Branch, Durham, NC, 1975b.
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U. S. Environmental Protection Agency. National Air Quality and Emissions Trends Report,
1975. EPA-450/1-76-002, U.S. Environmental Protection Agency, Research Triangle Park,
NC, November 1976a.
U. S. Environmental Protection Agency. RAPS. Data reported are abstracted from the 1976 data
file for the Regional Air Pollution Study program maintained at the Environmental
Research Center, Research Triangle Park, NC, 1976b.
U. S. Environmental Protection Agency. SAROAD. Data reported were abstracted from the 1976
SAROAD raw data file maintained at the National Air Data Branch, Durham, NC, 1976c.
U. S. Environmental Protection Agency. Air Quality Data - 1975 Annual Statistics Including
Summaries with Reference to Standards. EPA-450/2-77-002, U.S. Environmental Protection
Agency, Research Triangle Park, NC, May 1977a.
U. S. Environmental Protection Agency. Reconnaissance of Environmental Levels of Nitrosamines
in the Central United States. EPA-330/1-77-001, U.S. Environmental Protection Agency,
Denver, CO, February 1977b.
U. S. Environmental Protection Agency. Reconnaissance of Environmental Levels of Nitrosamines
in the Southeastern United States. EPA-330/1-77-009, U.S. Environmental Protection
Agency, Denver, CO, August 1977c.
U.S. Environmental Protection Agency. Air Quality Data - 1978 Annual Statistics including
Summaries with Reference to Standards. EPA-450/4-79-037, U.S. Environmental Protection
Agency, Research Triangle Park, NC, November 1979.
U.S. Environmental Protection Agency. Air Quality Data - 1980 Annual Statistics Including
Summaries with Reference to Standards. EPA-450/4-81-027, U.S. Environmental Protection
Agency, Research Triangle Park, NC, August 1981.
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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 NO (NO + N02) could catalyze the destruction of ozone and control its
stratospheric abundance by the set of photochemical reactions:
03 + hv -» 0 + 02 (9-1)
(wavelengths shorter than 1140 nm)
0 + N02 •* NO + 02 (9-2)
NO + 03 •* N02 + 02 (9-3)
2 03 -> 3 02 net
The main sdurce of NO in the stratosphere is probably the oxidation of nitrous oxide
(N20) via the reactions (Crutzen, 1971; Nicolet and Vergison, 1971; McElroy and McConnell,
1971):
0, + hv -» 0(ln.) + 0, (9-4)
J £
(wavelengths shorter than 310 nm)
O^D) + N20 •* 2 NO (9-5)
Because of its relatively low solubility and low reactivity in water, nitrous oxide is not
removed in clouds and through precipitation in the troposphere. In contrast, direct transport
of NO and N0« into the stratosphere from the earth's surface is strongly prohibited by wet
removal of N0? and especially its oxidation product HNO,, which is formed by the reaction:
OH + NO, (+M) -» HNO, (+M) (9-6)
1
The hydroxyl radical (OH) is primarily formed by the attack of 0( D) on water vapor,
following reaction 9-4, above:
O^D) + H20 -» 2 OH (9-7)
This radical, and therefore also ozone, plays an extremely important role in the photo-
chemistry of the atmosphere. In the troposphere (0-10 km in middle and high latitudes, or 0-lf
km in the tropics) it attacks a host of gases which otherwise would be inert, such as CO, H2,
hydrocarbons and chlorinated hydrocarbons. This ensures that only a small portion (~10% or
less) of the ground level emissions of such gases can reach the stratosphere. As a result,
photochemical activity in the stratosphere is strongly limited and ozone is protected from
9-1
-------
otherwise larger destruction. Nitrous oxide, however, is nearly inert to attack by all known
tropospheric gases, including OH (Biermann et al., 1976).
9.2 DIRECT ROLE OF NITROGEN OXIDES IN THE OZONE BALANCE OF THE ATMOSPHERE
The oxides of nitrogen, NOX, play a remarkable catalytic role in the ozone balance of the
atmosphere. Above about 24 km, the net effect of N0x additions to the stratosphere is ozone
destruction by the set of reactions already discussed (reactions 9-1, 9-2, 9-3). At lower
altitudes the opposite is true. The essential reason for this is the following set of
reactions.
R02 + NO -» RO + N02 (9-8)
N02 + hv •* NO + 0 (9-9)
0 + 02 + M + 03 + M (9-10)
R02 + 02 •* RO + 03 net
This is the same set of reactions which is at the core of ozone production under photo-
chemical smog conditions, when reactions 9-8 through 9-10 are preceded by reactions of the type
R + 02 +. M -> R02 + M (9-11)
with the net result: R + 2 0^ •» RO + 0,. The radical R can here stand for such radicals as
CHoCO and H. In the non-urban troposphere, ozone production may, however, still take place
from the oxidation of hydrocarbons emitted by vegetation and of carbon monoxide, provided
sufficient NO is present. In the case of carbon monoxide the sequence of reactions starts
with
CO + OH (+M) -» H + C02 (+M) (9-12)
followed by reaction 9-11 (with R = H) and reactions 9-8 through 9-10, leading to the net
result: CO + 2 02 -» C02 + 0^. Because it is conceivable that both carbon monoxide and nitric
oxide concentrations have been increasing due to human activities, there is a discrete possibi-
lity of worldwide ozone increases, especially in the Northern Hemisphere's troposphere (Fishman
and Crutzen, 1978).
It should be added that the origin of tropospheric ozone is currently not well known.
Traditional thinking in the meteorological community explained the presence of ozone in the
troposphere by its formation in the stratosphere (Chapman, 1930) via the reaction
02 + hv -» 2 0 (\ < 240 nm) (9-13)
0 + 02 + M -> 03 + M (x2) (9-14)
3 02 -» 2 03 net
and its downward transport into the troposphere in the vicinity of frontal zones or tropopause
breaks (Danielsen and Mohnen, 1977). The tropospheric ozone production taking place near urban
9-2
-------
centers was thought to be only of minor global importance. However, it seems now that ozone
production can also take place in the "clean" troposphere as long as NOV volume mixing ratios
-11
are not too small (> 10 ), because of the fast rate of reaction 9-8.
In the Tower stratosphere (~1O24 km) the chain of reactions 9-8 through 9-10 (with R =
H) tends to counteract the effect of the reactions
OH + 03 •* H02 + 02 (9-15)
H02 + 03 -» OH + 2 02 (9-16)
2 03 -» 3 02 net
by deferring it into the sequence
OH + 03 •* H02 + 02
H02 + NO •* OH + N02
N02 + hv •* NO + 0
no net chemical effect
Additions of NO to the lower stratosphere, therefore, tend to increase local ozone concen-
trations by causing smaller ozone losses. The importance of the ozone-producing aspects of
NO catalysis below about 24 km is dramatically emphasized by the recent discovery of Howard
and Evenson (1977), who found reaction 9-8 to be at least an order of magnitude faster than
previously determined through indirect measurements of the rate constant. This finding has
resulted in substantial downward revisions of estimated total ozone column reductions due to
stratospheric NO additions from high-flying aircraft. As a result of the peculiar photochem-
ical action of N0x, we notice also a decrease in altitude of the center of gravity of strato-
spheric ozone by transfer of mass from above 24 km to below 24 km. As NO is produced by the
oxidation of NJ) via reactions 9-4 and 9-5, the same conclusions are valid regarding the
possible effects of a future rise in the atmospheric content of nitrous oxide. Such an
increase may be caused by man's intervention in the nitrogen cycle through an increasing use
of nitrogen fertilizer and other agricultural activities.
9.3 INDIRECT ROLE OF NITROUS OXIDE IN THE OZONE BALANCE OF THE ATMOSPHERE
In addition to the direct effects to the stratospheric ozone layer caused by the catalytic
cycle involving the nitrogen oxides, the existence of NO also has an important influence on
the impact of catalytic ozone destruction initiated by other atmospheric constituents. In
particular, catalytic destruction of stratospheric ozone via reactive chlorine species proceeds
as follows:
03 + hv •* 0 + 02 (9-17)
0 + CIO -»• Cl + 02 (9-18)
03 + Cl -» CIO + 02 (9-19)
2 03 •* 3 02 net
9-3
-------
The initial release of Cl (and subsequent formation of CIO) to the stratosphere occurs when
degradation of chlorinated compounds such as chlorofluoromethanes (e.g., fluorocarbon-11 and
fluorocarbon-12), methyl chloroform, and methyl chloride takes place by either direct photo-
lysis or attack by reactive species which prevail in the stratosphere (Molina and Rowland,
1974). However, the ozone-destroying frequencies of these catalytic cycles are not additive
since the presence of both reactive chlorine and reactive nitrogen compounds may result in a
short-circuit of either catalytic cycle. For example, the formation of chlorine nitrate in
the stratosphere through the reaction
CIO + N02 + M -> C10N02 + M (9-20)
removes both reactive chlorine and nitrogen from the atmosphere which would have otherwise been
able to take part in catalytic ozone-destroying cycles. As a result, the inclusion of C10NCL
in stratospheric models of ozone depletion predictions lowered the depletion estimates by about
a factor of two (Crutzen et al., 1978).
Lastly, it should be pointed out that new measurements of reaction rates which involve
only reactive nitrogen species can likewise influence other catalytic cycles of ozone destruc-
tion. A good example of such an occurrence is the recently reported rate constant for the
reaction
H02 + NO -> OH + N02 (9-8)
by Howard and Evenson (1977), which was shown to proceed much faster than had been
previously believed (Hampson and Garvin, 1975). An increase in this rate constant
OH
increases the ^ ratio in the model calculations. Because more OH is calculated
by the numerical models, smaller concentrations of HC1 are computed to exist. Since HC1 is
one of the primary reservoirs of reactive chlorine species, the increased OH concentrations
which have been brought about by the reaction of NO with HO,,, result in the release of more
chlorine atoms into the atmospheric system via
HC1 + OH -» H20 + Cl (9-21)
Thus, it is important to point out that the nitrogen cycle in the stratosphere has a direct
bearing on the catalyzing power of other stratospheric cycles involving the ozone layer. This
interaction may be interfering or enhancing depending on which region of the ozone layer is
being examined or at which altitudes certain reactions dominate the overall chemistry.
9.4 OTHER ATMOSPHERIC EFFECTS OF NITROGENOUS COMPOUNDS
The environmental effects of ozone changes in the stratosphere are, however, not solely
related to the function of ozone as a shield against the penetration of solar ultraviolet
radiation to ground level. Ozone is also an important gas for the heat budget of the atmo-
sphere. An effective lowering of the center of gravity of the ozone layer, which would be the
result of NO additions to the stratosphere, may have significant climatic implications
(Ramanathan, 1974), as it may cause a warming of the lower stratosphere and the earth's surface
9-4
-------
by the increased absorption of ultraviolet solar radiation and enhanced trapping of thermal
9.6 urn radiation emitted from the warm surface of the earth.
The significance of nitrous oxide is also not restricted to its importance as a source of
stratospheric NO via reactions 9-4 and 9-5. Because of its absorption bands at about 7.8 urn
A
and 17.0 |jm, nitrous oxide (N20) likewise contributes significantly to the atmospheric "green-
house" effect by trapping outgoing terrestrial radiation. It has, therefore, been estimated
that a doubling of the atmospheric NpO content could cause an increase in surface temperatures
by as much as 0.7°K (Wang et al., 1976). Several recent studies have been designed to esti-
mate the possible extent of future atmospheric NpO build-up due to increased use of nitrogen
fertilizer (Council for Agricultural Science and Technology, 1976; Crutzen, 1976; Crutzen and
Ehhalt, 1977; Liu et al., 1976; McElroy, 1974; McElroy et al., 1977; Rice and Sze, 1976; Sze
and Rice, 1976). It is difficult, however, to estimate the doubling time with any certainty.
Three important but poorly understood factors determining the release of NpO from soil and
water to the atmosphere are the following:
I. The release of N/,0 in the denitrification process. This microbiological process,
which is currently considered to be the main source of atmospheric NpO, takes place
in anaerobic microenvironments, and involves the reduction of nitrate to NpO and
molecular nitrogen (Np). It is this process which presumably balances nitrogen
fixation, i.e., the conversion of Np to fixed nitrogen. A growing amount of obser-
vational evidence is now accumulating, which indicates that the yield of NpO versus
Np in agricultural and water environments is less than 20 percent (Delwiche, 1977;
Rolston, 1977). It remains, however, important to gather additional information
from field studies to improve the data base for this important environmental factor.
2. The pathway of fertilizer nitrogen in the environment. This involves knowledge of
such factors as the actual amount of denitrification in agricultural fields, leach-
ing of nitrate to groundwater, volatilization of ammonia and its transport and con-
versions in the atmosphere, the cycling and decomposition of animal manures in the
environment, and the extent of transfer of agricultural fixed nitrogen to the
natural ecosystems, which may be expected to have much longer turnover times than
those systems which are directly affected by agriculture. Studies of these matters
have been conducted by Liu et al. (1976), McElroy et al. (1977), and Crutzen and
Ehhalt (1977).
3. The role of the oceans in the worldwide NpO budget. While initial studies indicated
a large source of NpO in the oceans (National Research Council, 1978), recent in-
vestigations point towards a much smaller role of oceans in the global NpO budget
(Hahn, 1974; Weiss, 1977).
The scientific problems connected with possible future increases in atmospheric NpO con-
centrations are being investigated by several research groups and the issue has been reviewed
in a recently published report by an ad hoc committee of the National Research Council,
(1978). The issue is further complicated by the fact that the nitrogen cycle is coupled to
9-5
-------
other cycles, such as those of carbon and phosphorus (Simpson et al., 1977). It is, therefore,
fair to say that many years of active research are needed to assess reliably this potentially
important global environmental issue.
9.5 SUMMARY
Stratospheric ozone protects life at the earth's surface from potentially harmful ultra-
violet radiation from the sun. The main source of NO in the stratosphere is the oxidation of
A
nitrous oxide (N~0). Nitrous oxide is ubiquitous, even in the absence of human activities,
since it is a product of natural biologic processes in soil, but significant quantities may
also arise from the denitrification of the increased quantities of fixed nitrogen, which are
introduced into the nitrogen cycle by the growing use of nitrogen fertilizers. Recent reports
indicate that somewhat less than 20 percent of the "excess" nitrogen eventually escapes as
N20, with most of the rest returned to the atmosphere as Np. Since N~0 is not believed to
take part in any atmospheric chemical reactions below the stratosphere, all the N-O produced
terrestrially is available for stratospheric reactions. The concern expressed by some authors
in the recent past, that N20 arising from excess fertilizer might decrease the total strato-
spheric ozone by as much as 20 percent for a 100 percent increase in total N20, has recently
been reevaluated in the light of new information on rate constants for certain stratospheric
chemical reaction pathways. These new considerations point to the likelihood of a much
smaller dependence of total stratospheric ozone on N?0 abundance.
Ozone is also an important gas for the heat budget of the atmosphere. An effective low-
ering of the "center of gravity" of the ozone layer, which would be the result of NO addi-
tions to the stratosphere, may have significant climatic implications. Nitrous oxide likewise
contributes to the atmospheric "greenhouse" effect by trapping outgoing terrestrial radiation.
One author recently estimated that a doubling of the atmospheric burden of N~0 could'increase
surface temperatures by as much as 0.7°C. It is difficult, however, to estimate the doubling
time with any certainty. Since global estimates of the end effects of excess fertilizer rest
on a number of poorly known parameters, and since the issues are further complicated by the
fact that the nitrogen cycle is coupled to other cycles, such as the carbon cycle, no defini-
tive conclusions can prudently be drawn.
9-6
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9.6 REFERENCES
Biermann, H. W. , C. Zetzch, and F. Stuhl. Rate constant for the reaction of OH with N«0 at
298k. Ber. Bunsenges. Phys. Chem. 80:909-911, 1976. ^
Chapman, S. A theory of upper atmospheric ozone. Mem. R. Meteorol. Soc. 3:103-125, 1930.
Cohen, Y. , and L. I. Gordon. Nitrous oxide production in the ocean. JGR J. Geophys. Res. 84:
347-353, 1979.
Council for Agricultural Science and Technology. Effect of Increased Nitrogen Fixation on
Atmospheric Ozone. CAST Report No. 53, Council for Agricultural Science and Technology,
Iowa State University, Ames, IA, January 1976.
Crutzen, P. J. The influence of nitrogen oxides on the atmospheric ozone content. Q. J. Roy.
Met. Soc. 96:320-325, 1970.
Crutzen, P. J. Ozone production rates in an oxygen-hydrogen-nitrogen oxide atmosphere. J.
Geophys. Res. 76:7311-7328, 1971.
Crutzen, P. J. Upper limits on atmospheric ozone reductions following increased applications
of fixed nitrogen to the soil. Geophys. Res. Letter 3:169-172, 1976.
Crutzen, P. J. , and D. H. Ehhalt. Effects of nitrogen fertilizers and combustion on the
stratospheric ozone layers. Ambio 6:112-117, 1977.
Crutzen, P. J. , I. S. A. , Isaksen, and J. R. McAfee. The impact of the chlorocarbon industry
on the ozone layer. JGR J. Geophys. Res. 83:345-363, 1978.
Danielsen, E. F., and V. A. Mohnen. Project dustorm report: ozone transport, j_n situ measure-
ments and meteorological anlyses of tropopause folding. JGR J. Geophys. Res. 82: 5867-
5877, 1977.
Delwiche, C. C. Nitrous oxide and denitrification. In: Denitrification Seminar, The Ferti-
lizer Institute, San Francisco, California, October 25-27, 1977. The Fertilizer Insti-
tute, Washington, DC, 1977. 8 pp.
Fishman, J. , and P. J. Crutzen. The origin of ozone in the troposphere. Nature (London)
274:855-858, 1978.
Hahn, J. The North Atlantic Ocean as a source of atmospheric NpO. Tellus 26:160, 1974.
Hampson, R. F. , Jr., and D. Garvin, Eds. Chemical Kinetics and Photochemical Data for Model-
ing Atmospheric Chemistry. NBS Technical Note 866, U.S. Department of Commerce, National
Bureau of Standards, Washington, DC, June 1975.
Howard, C. J. , and K. M. Evenson. Kinetics of the reaction of H0? with NO. Geophys. Res.
Letters 4:437-440, 1977.
Johnston, H. S. Reduction of stratospheric ozone by nitrogen oxide catalysts from supersonic
transport exhaust. Science (Washington, D.C.) 173:517-522, 1971.
9-7
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Liu, S. C. , R. J. Cicernone, T. M. Donahue, and W. L. Chameides. Limitation of fertilizer
induced ozone reduction by the long lifetime of the reservoir of fixed nitrogen. Geophys.
Res. Letter 3:157-160, 1976.
McElroy, M. B. Statement of Michael B. McElroy. In: Fluorocarbons--Impact on Health and the
Environment: Hearings" before the Subcommvttee on Public Health and Environment,
Committee on Interstate and Foreign Commerce. Serial No. 93-110, U.S. Congress, House of
Representatives, Washington, DC, December 11-12, 1974. pp. 336-346.
McElroy, M. B. , and J. C. McConnell. Nitrous oxide: a natural source of stratospheric NO.
J. Atmos. Sci. 28:1095-1098, 1971.
McElroy, M. B. , S. C. Wofsy, and Y. 1. Yung. The nitrogen cycle: perturbations due to man
and their impact on atmospheric N90 and 07. Phil. Trans. R. Soc. London B: Biol. Sci.
277:159-181, 1977. L 6
Molina, M. J., and F. S. Rowland. Stratospheric sink for chlorofluoromethanes: chlorine
atom-catalysed destruction of ozone. Nature (London) 249:810-812, 1974.
National Research Council. Nitrates: An Environmental Assessment. National Academy of
Science, Washington, DC, 1978.
Nicolet, M. , and E. Vergison. Nitrous oxide in the stratosphere. Aeron. Acta A(90):l-16,
1971.
Ramanathan, V. A simplified stratospheric radiative transfer model: theoretical estimates of
the thermal structure of the basic and perturbed stratosphere. Paper given at AIAA/AMS
2nd Int. Conf. Environmental Impact Aerospace Operations in High Atmosphere, San Diego,
July 8-10, 1974.
Rice, H., and N. D. Sze. The Analysis of Fertilizer Impacts on the Ozone Layer—Final Report.
Document P-2123, Environmental Research and Technology, Inc., Washington, DC, September
1976.
Rolston, D. E. Field-measured flux of nitrous oxide from soil. I_n: Denitrification Seminar,
The Fertilizer Institute, San Francisco, California, October 25-27, 1977. The Fertilizer
Institute, Washington, DC, 1977. 6 pp.
Simpson, H. J., W. S. Broecker, R. M. Garrels, S.' P. Gessel, H. D. Holland, W. T. Holser, C.
Junge, I. R. Kaplan, M. B. McElroy, W. Michaelis, K. Mopper, M. Schidlowski, W. Seiler,
J. H. Steele, S. C. Wofsy, and R. F. Wollast. Man and the global nitrogen cycle: group
report. I_n: Global Chemical Cycles and Their Alterations by Man, Report of the Dahlem
Workshop, Dahlem Konferenzen, Berlin, Germany, November 15-19, 1976. W. Stumm, ed. ,
Dahlem Konferenzen, Berlin, Germany, 1977. pp. 253-274.
Sze, N. D., and H. Rice. Nitrogen cycle factors contributing to N?0 production from ferti-
lizers. Geophys. Res. Letter 3:343-346, 1976.
Wang, W. C., Y. L. Yung, A. A. Lacis, T. Mo, and J. E. Hansen. Greenhouse effects due to
man-made perturbations of trace gases. Science (Washington, D.C.) 194:685-690, 1976.
Weiss, R. F. Nitrous oxide in the atmosphere and the sea. Jji: Denitrification Seminar, The
Fertilizer Institute, San Francisco, California, October 25-27, 1977. The Fertilizer
Institute, Washington, DC, 1977. 3 pp.
9-8
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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 respon-
sible for a portion of the brownish coloration often observed in polluted air (Hodkinson,
1966; Husar and White, 1976). However, it should also be noted that non-nitrate particulate
matter has been implicated in the production of a significant fraction of brownish coloration
(Husar and White, 1976). In addition, where nitrates occur as fine particles, they may con-
tribute to the reduction of visual range (White and Roberts, 1977; Trijonis et al., 1978b).
(See Chapter 6 for a discussion of atmospheric processes resulting in ambient burdens of NOp
and particulate nitrate.)
10.1 NITROGEN OXIDES AND LIGHT SCATTERING AND ABSORPTION
Deterioration in visibility is due to the absorption and scattering of light by gaseous
molecules and suspended solid or liquid particles (Middleton, 1952). Absorbed light is trans-
formed into other forms of energy, such as heat, while scattered light is re-radiated in all
directions with no change in wavelength. The importance of each process is determined by the
absorption and scattering coefficients, b and b . These coefficients specify the rate at
3 5
which a beam of light is attenuated in passing through the atmosphere:
dl /I = -b dx, and dl/I = -bdx,
da So
where I is the intensity of the beam, and dl and dl are the changes in I due to absorption
a s
and scattering over the incremental distance dx. The sum of the absorption and scattering co-
efficients is the total extinction coefficient, b = b + b..
a s
The absorption and scattering coefficients of particulate matter and the different gases
are additive. It is, therefore, meaningful to speak of the impact of an individual species on
visibility. The effects of gases and particulate matter can be distinguished as follows (the
subscripts g and p denote the respective contributions from gases and particulates):
b = ba + bs
= b +b + b + b
ag ap sg sp
In polluted atmospheres, the term bao is dominated, at visible wavelengths, by the contribu-
ag
tion from NO,,, which absorbs strongly in the blue region of the spectrum. The scattering due
to trace gases is negligible, so that b can be regarded as the constant background due to
Rayleigh scattering by clean air. Absorption and scattering by particles depend on their size
and composition (National Air Pollution Control Administration, 1969). Nitrate compounds
may constitute a significant fraction in the optically important particle size range, but
current information on ambient nitrate concentrations is insufficient to make any conclusive
assessment.
10-1
-------
10.2 EFFECT OF NITROGEN DIOXIDE ON COLOR
Under typical ambient conditions, light scattering dominates total extinction,
which is related to reduction of contrast and visual range. The most significant optical
effect of N02, however, involves discoloration. The absorption coefficient for N0? can be
used to calculate the visual impact of N02 in the atmosphere (Dixon, 1940).
10.2.1 Nitrogen Dioxide and Plumes
Under certain circumstances, brown plumes may be distinguished tens of kilometers down-
wind of their sources. Nitrogen dioxide in a plume acts as a blue-minus filter for trans-
mitted light. It tends to impart a brownish color to targets, including the sky, viewed
through the plume. The strength of this filter effect is determined by the integral of N02
concentration along the sight path; e.g., theoretically similar effects would be produced by a
1 kilometer-wide plume containing 0.1 ppm (190 ng/m ) NO, or a 0.1 kilometer-wide plume con-
q t-
taining 1.0 ppm (1,900 [jg/m ) N02.
Figure 10-1 shows the calculated transmittance of particle-free N02 plumes for several
values of the concentration-distance product. Less than 0.1 ppm-km N02 is sufficient to pro-
duce a color shift which is distinguishable in carefully-controlled, color-matching tests
(MacAdam, 1942). Reports from one laboratory using NO^-containing sighting tubes indicate a
visible color threshold of 0.06 ppm-km for the typical observer. This value was supported by
a few field observations of N0~ plumes from nitric acid manufacturing plants under varying
operating conditions (Hardison, 1970). The value cited refers to the effect of N0? in the
absence of atmospheric aerosol. Empirical observations under a variety of conditions are
needed to determine the perceptibility of N02 in ambient air.
Discoloration of plumes and haze layers by N02 is modified by particulate matter and also
depends on a number of factors such as sun angle, surrounding scenery, sky cover, viewing
angle, human perception parameters, and pollutant loading. The relative importance of aerosol
or N02 in determining the color and appearance of a plume or haze layer can be addressed, in
part, in terms of the relative extinction as a function of wavelength. Suspended particles
generally scatter much more in the forward direction than in any other direction. This fact
means a plume or haze layer can appear bright in forward scatter (sun in front of the obser-
ver) and dark in back scatter (sun in back of the observer) because of the angular variation
in scattered air light. This effect can vary with background sky and objects. Aerosol opti-
cal effects alone are capable of imparting a reddish brown color to a haze layer when viewed
in backward scatter. N02 would increase the degree of coloration in such a situation
(Ahlquist and Charlson, 1969; Charlson et al., 1978). When the sun is in front of the obser-
ver, however, light scattered toward him by particles in the plume tends to wash out the
brownish light transmitted from beyond. Under these conditions, particle scattering dimin-
ishes the plume coloration. Specific circumstances of brown layers must be observed on a
case-by-case basis.
10.2.2 Nitrogen Dioxide and Haze
A common feature of pollutant haze is its brown color. The discoloration of the horizon
sky due to N02 absorption is determined by the relative concentrations of N02 and light-
10-2
-------
u
z
<
a:
4000
BLUE
5000 6000
WAVELENGTH, 2,
7000
RED
Figure 10-1. Transmittance exp(-b|\JC)2x) °' ^"^2 P'umes f°r
selected values of the concentration-distance product (Adapted
from Hodkinson, 1966.)
10-3
-------
scattering particles. In a uniform atmosphere, the effect of NO- at any given wavelength is
described by the following relationship (Robinson, 1968):
Bhorizon/Bhorizon"N02^ = °> = ~ = " + ^'*
where Bhorizon and Bhorizon^N02-' = °^ are the bri9ntness of the horizon sky, with and without
N02.
The ratio bNCL/b is more easily related to experience when expressed in terms of concen-
tration, [NOp], and visual range, VR. As discussed in Section 10.3, visual range under certain
simplifying assumptions is inversely proportional to extinction, which is typically dominated
by scattering. Samuels et al. (1973) compared human observations with instrumental measure-
ments and found indications that VR and b are related by the formula, VR = (3 + l)/b .
Since, in addition, b^ is proportional to [NO-], it follows that the ratio bN02/b is pro-
portional to the product [NO,,] VR. Figure 10-2 shows, for several values of this product, the
calculated alteration contributed by N02 to horizon brightness which is in turn a function of
aerosol scattering. It should be noted that this calculation neglects the wavelength depend-
ence of the scattering, which can be substantial in relatively clean air and mitigates the
discoloring effects of NO-.
The interpretation of Figure 10-2 is similar to that of Figure 10-1. A concentration-
visual range product of 0.3 ppm-km N0~ corresponds to a color shift which should be detect-
able in a polluted layer viewed against relatively clean sky. At a visual range of 100
kilometers, typical of the rural northern great plains area of the United States, 0.003 ppm (6
3
ug/m ) NO, might suffice to color the horizon noticeably. At a visual range of 10 kilometers,
3
typical of urban haze, 0.03 ppm (60 ug/m ) NOp might be required to produce the same effect.
However, quantitative theoretical calculations of human perception of NO^ are not fully devel-
oped and experimental observations are needed to evaluate the actual effect.
Independent of absorption by NO^, wavelength-dependent scattering by small particles can
also produce a noticeable brown coloration in polluted air masses (Husar and White, 1976).
Unlike the coloration due to absorption, which is independent of sun angle, the brown colora-
tion contributed by scattering is most intense when the sun is in back of the observer.
10.3 EFFECT OF PARTICULATE NITRATES ON VISUAL RANGE
The visual range in a uniform atmosphere is inversely proportional to the extinction co-
efficient. For a "standard" observer, the Koschmeider formula expressing this relationship
is:
VR = 3.9/b
where b is the extinction coefficient. Taking account of the response as a function of wave-
length of the light-adapted eye of a "standard observer" and of the wavelength dependence of
10-4
-------
1.0
0.9
o.e
0.7
e
• 0.6
o"
1 O.S
I
5
I...
B
0.3
0.2
0.'
4000
BLUE
6000 6000
WAVELENGTH.A
7000
RED
Figure 10-2. Relative horizon brightness, bs/(bs + b^o-?'. for
selected values of the concentration-visual product, assuriiing
bj = 3/{visual range). (Adapted from Hodkinson, 196G.)
10-5
-------
Rayleigh scattering, it is possible to compute a mean extinction coefficient in a pure atmo-
sphere containing no aerosols and no light absorbing gases under standard temperature and
o
pressure conditions (0 C, 1.013 bars). The value of b so obtained (Penndorf, 1957) is about
4-1 S9 .
0.12 (10 m) , corresponding to a visual range of about 320 km.
Recently, Malm (1979) has examined critically the concept of visual range as a measure of
visibility. The simple Koschmeider formula, which generally works reasonably well in urban
areas (Horvath and Noll, 1969), is shown to depend upon a number of simplifying assumptions
such as: a homogeneous atmosphere, a flat earth, a horizontal viewing aspect, a black target,
and a sky radiance which is the same at the object as at the viewing point. Depending upon
particular circumstances, these assumptions may have a marked effect upon the relation between
the visual range calculated from the Koschmeider formula and the real visual range defined as
the distance from a target at which a given (threshold) contrast is achieved. Malm suggests
that visibility may be better characterized by apparent target contrast or by color changes of
selected vistas rather than by visual range.
A definitive assessment of the contribution made by nitrate aerosols to total extinction
(and therefore to degradation of visibility) is not possible because sufficient high-quality
data are not available for particulate nitrates. However, to the extent that particulate
nitrates are secondary aerosols formed in the 0.1 to 1 micron size range (Lee and Patterson,
1969), it would be expected, on theoretical grounds, that they would be efficient scatterers
of light. As shown in Figure 10-3, light scattering per unit mass of aerosol exhibits a pro-
nounced resonance at a particle size of 0.5 microns, which is approximately equal to the wave-
length of the center of the spectrum of visible light.
Theoretical calculations based on the Mie theory of light scattering from aerosols indi-
cate that particles found in the 0.1 to 1 micron size range (such as in secondary aerosols)
should exhibit extinction coefficients per unit mass on the order of 0.06 + 0.03, where the
units are (104m)"1/(Mg/m3) (Latimer et al. , 1978a, 1978b, 1978c; Ursenback et al., 1978; White
and Roberts, 1977). Similar calculations indicate that particles occurring in the coarse size
range above 2 microns, such as dust or sea spray (Bradway and Record, 1978; Whitby and
Sverdrup 1980), should exhibit much lower extinction coefficients per unit mass, on the order
of 0.006 + 0.003 where the units are (104m)~V(ug/m3) (Latimer et al., 1978a, 1978b, 1978c;
Ursenback et al., 1978; White and Roberts, 1977). These results are confirmed by empirical
studies (Cass, 1976; Trijonis et al., 1978a,1978b; Waggoner et al., 1976; White and Roberts,
1977), which typically find extinction coefficients per unit mass of sulfates (a prevalent
secondary aerosol) to be 0.04 to 0.10 (10 m) /((jg/m ). For the remainder of TSP (mostly
coarse particles), the extinction coefficient per unit mass is 0.004 to 0.01 (10 m) /(ug/m ).
Because nitrate aerosols tend to be hygroscopic, light-scattering per unit mass of
nitrate can rise significantly with increasing relative humidity (Covert, 1974; Hidy et al.,
1974). As relative humidity increases, the mass of water attached to nitrate particles
increases and corresponding shifts in the particle size distribution occur. These effects are
10-6
-------
I o.io
(-
z
KPT 008
w E
Z _- 0.06
2?
< — 0.04
in
t-
I
U 0.02
I I T
I I I I
,
0.030,050.070.10 0.2 0.3 0.50.7 1.0 2.0 3.0 5.07.010.0
PARTICLE DIAMETER, microns
Figure 10-3. Normalized light scattering by aerosols as a function of
particle diameter. Computed for unit density spherical particles of
refractive index 1.5 (White and Roberts, 1977).
10-7
-------
especially pronounced at relative humidities above 70%; at very high relative humidities
(90-100%), rather small shifts in relative humidity may produce pronounced changes in the
amounts of light-scattering from a fixed amount of nitrate aerosol.
Even though nitrate aerosols are suspected of occurring in the optically critical 0.1 to
1 micron size range, and even though light-scattering by nitrates may be significantly
augmented by relative humidity effects, the actual contributions of nitrate to haze levels may
not be significant because ambient nitrate levels may be very low (see data in Chapter 8). A
complete characterization of the role nitrates play in visibility degradation must wait until
high-quality data bases on nitrates are generated.
10.4 SUMMARY
Air pollution degrades the appearance of distant objects and reduces the range at which
they can be distinguished from the background. These effects are manifest not only in visible
plumes, but also in large-scale, hazy air masses. Haze and plumes can result in the deterio-
ration and loss of scenic vistas, particularly in areas of the southwestern United States
where visibility is generally good. Under extreme conditions reduced visual range and con-
trast due to haze and plumes may impede air traffic. NO- can be responsible for a portion of
the brownish coloration observed in polluted air. However, it should be noted that non-
nitrate particulate matter has also been implicated in the production of a significant portion
of brownish coloration. Under certain circumstances, brown plumes may be distinguished tens
of kilometers downwind of their sources.
Nitrogen dioxide in a plume acts as a blue-minus filter for transmitted light. It tends
to impart a brownish color to targets, including the sky viewed through the plume. The
strength of this filter effect is determined by the amount of NO^ concentration along the
sight path; i.e., theoretically similar effects would be produced by a 1 kilometer-wide plume
containing 0.1 ppm (190 ug/m) of NO, or a 0.1 kilometer-wide plume containing 1.0 ppm (1,900
3
ug/m ) of NOp. Based on laboratory tests plus very limited supporting observations in the
field, the visible threshold for coloration produced by NO- in the atmosphere might be a con-
centration-distance product of about 0.06 ppm-km. Empirical observations under a variety of
conditions are needed to determine the perceptibility of N0? in ambient air.
Plume coloration due to N0? is modified by particulate matter, and depends on a number of
factors such as sun angle, surrounding scenery, sky cover, viewing angle, human perception
parameters, and pollutant loading. Suspended particles generally scatter in the forward
direction, and can thus cause a haze layer or a plume to appear bright in forward scatter (sun
in front of the observer) and dark in back scatter (sun in back of the observer) because of
the angular variation in scattered air light. This effect can vary with background sky and
objects. Aerosol optical effects alone are capable of imparting a reddish brown color to a
haze layer when viewed in backward scatter. N0? would increase the degree of coloration in
such a situation. When the sun is in front of the observer, however, light scattered toward
him by particles in the plume tends to wash out the brownish light transmitted from beyond.
10-8
-------
Under these conditions, particle scattering diminishes the plume coloration. Estimates of the
magnitude of this effect attributable to particulate nitrates are currently hampered by the
lack of data on particulate nitrate concentrations in ambient air.
Nitrogen dioxide and particulate nitrates may also contribute to pollutant haze. The
discoloration of the horizon sky due to NCL absorption is determined by the relative concen-
trations of NCL and light-scattering particles. A concentration-visual range product of 0.3
ppm-km N0? corresponds to a color shift which should be detectable in a polluted layer viewed
against a relatively clean sky. At a visual range of 100 km, typical of the rural U.S. great
3
plains, 0.003 ppm (6 (j/m ) N09 might suffice to color the horizon noticeably. At a visual
3
range of 10 km, typical of urban haze, 0.03 ppm (60 ug/m ) NOp might be required to produce
the same effect. For the reason cited above, no reasonable estimate of particulate nitrate
contribution to this phenomenon can currently be made. Similarly, an assessment of the role
of nitrate aerosols in the degradation of visual range must await the availability of a suffi-
cient data base on ambient particulate nitrate concentrations.
10-9
-------
10.5 REFERENCES
Ahlquist, N. C. , and R. J. Charlson. Measurement of the wavelength dependence of atmospheric
extinction due to scatter. Atmos. Environ. 3:551-564, 1969.
Bradway, R. M., and F. A. Record. National Assessment of the Urban Particulate Problem.
Volume II. Particle Characterization. EPA-450/3-76-025, U.S. Environmental Protection
Agency, Research Triangle Park, NC, July 1978.
Cass, G. R. The Relationship between Sulfate Air Quality and Visibility at Los Angeles. EQL
Memorandum No. 18, California Institute of Technology, Pasadena, CA, August 1976.
Charlson, R. J. , A. P. Waggoner, and J. F. Thielke. Visibility protection for Class I Areas:
The Technical Basis. CEQ517714498, Council of Environmental Quality, Washington, DC,
August 1978.
Covert, D. S. A Study of the Relationship of Chemical Composition and Humidity to Light
Scattering by Aerosols. Ph.D. Thesis, University of Washington, Seattle, WA, 1974.
Dixon, J. K. Absorption coefficient of nitrogen dioxide in the visible spectrum. J. Chem.
Phys. 8:157-160, 1940.
Hardison, L. C. Techniques for controlling the oxides of nitrogen. J. Air Pollut. Control
Assoc. 20:377-382, 1970.
Hidy, G. M. , B. Appel, R. J. Charlson, W. E. Clark, D. Covert, S. K. Friedlander, R. Giaugue,
S. Heisler, W. W. Ho, J. J. Huntzicker, T. Novakov, L. W. Richards, R. Ragaini, T. B.
Smith, G. Sverdrup, S. Twiss, A. Waggoner, H. H. Wang, J. J. Wesolowski, K. T. Whitby,
and W. White. Characterization of Aerosols in California (ACHEX). Final Report. Volume
IV. Analysis and Interpretation of Data. ARB-R-358-74-37, State of California, Air
Resources Board, Sacramento, CA, September 1974.
Hodkinson, J. R. Calculations of colour and visibility in urban atmospheres polluted by
gaseous N02- Air Water Pollut. 10:137-144, 1966.
Horvath, H. , and K. E. Noll. The relationship between atmospheric light scattering co-
efficient and visibility. Atmos. Environ. 3:543-552 1969.
Husar, R. B. , N. V. Gillani, J. D. Husar, and D. E. Patterson. A study of long range trans-
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ing on Air Pollution Modeling and Its Application, North Atlantic Treaty Organization,
Airlie House, Virginia, September 7-10, 1976. N.51, North Atlantic Treaty Organization,
Committee on the Challenges to Modern Society, Berlin, Germany, 1976. pp. 469-486.
Husar, R. B. , and W. H. White. On the color of the Los Angeles smog. Atmos. Environ. 10:
199-204, 1976.
Latimer, D. A., R. W. Bergstrom, S. R. Hayes, M.-K. Liu, J. H. Seinfeld, G. Z. Whitten, M. A.
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Latimer, D. A., R. W. Bergstrom, S. R. Hayes, M.-K. Liu, J. H. Seinfeld, G. Z. Whitten, M. A.
Wojcik, and M. J. Hillyer. The Development of Mathematical Models for the Prediction of
Anthropogenic Visibility Impairment. Volume II: Appendices. EPA-450/3-78-110b, U.S.
Environmental Protection Agency, Washington, DC, September 1978b.
Latimer, D. A., R. W. Bergstrom, S. R. Hayes, M.-K. Liu, J. H. Seinfeld, G. Z. Whitten, M. A.
Wojcik, and M. J. Hillyer. The Development of Mathematical Models for the Prediction of
Anthropogenic Visibility Impairment. Volume III: Case Studies for Selected Scenarios.
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1978c.
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chloride, and ammonium particulate in several urban areas. Atmos. Environ. 3:249-255,
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Malm, W. Considerations in the measurement of visibility. J. Air Pollut. Control Assoc.
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Sulfate-light scattering ratio as an index of the role of sulphur in tropospheric optics.
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White, W. H., and P. T. Roberts. On the nature and origins of visibility-reducing aerosols in
the Los Angeles Air Basin. Atmos. Environ. 11:803-812, 1977.
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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 ele-
ments from sensitive soils, causing direct and indirect injury to forests. It also has the
potential for damaging monuments and buildings made of stone, for corroding metals and for
deteriorating paint.
The story of acidic precipitation is an ever-changing one. New information concerning
the phenomenon is forthcoming nearly every day. The sections that follow emphasize the
effects of wet deposition of sulfur and nitrogen oxides and their products on aquatic and
terrestrial ecosystems. Dry deposition also plays an important role, but contributions by
this process have not been quantified. Because sulfur and nitrogen oxides are so closely
linked in the formation of acidic precipitation, no attempt has been made to limit the dis-
cussion which follows to the main topic of this document, nitrogen oxides.
Chapter 12 emphasizes the effects of the dry deposition of nitrogen oxides on vegetation
and ecosystems. The sources and emissions of nitrogen oxides are discussed in Chapter 5 and
those of sulfur oxides in Air Quality Criteria for Particulate Matter and Sulfur Oxides.
Chapter 6 discusses the transformation and transport of nitrogen oxides. Ambient air concen-
trations are discussed in Chapter 8, and the nitrogen cycle in Chapter 4.
11.1.1 Overview of the Problem
The generally held hypothesis is that sulfur and nitrogen compounds are largely respon-
sible for the acidity of precipitation. The emissions of the sulfur and nitrogen compounds
involved in acidification are attributed chiefly to the combustion of fossil fuels. Emissions
may occur at ground level, as from automobile exhausts, or from stacks of 1000 feet or more in
height. Emissions from natural sources are also involved; however, in highly industrialized
areas, emissions from man-made sources well exceed those from natural sources. In the eastern
United States the highest emissions of sulfur oxides are from electric power generators using
coal, while in the West, emissions of nitrogen oxides,"chiefly from automotive sources, pre-
dominate.
The fate of sulfur and nitrogen oxides, as well as other pollutants emitted into the
atmosphere, depends on their dispersion, transport, transformation and deposition. Sulfur and
nitrogen oxides may be deposited locally or transported long distances from the emission
sources. Therefore, residence time in the atmosphere will be brief if the emissions are
deposited locally or may extend to days or even weeks if long range transport occurs. The
-------
chemical form in which emissions ultimately reach the receptor is determined by the complex
chemical transformations that take place between the emission sources and the receptor. Long
range transport over distances of hundreds or even thousands of miles allows time for a
greater number of chemical transformations to occur.
Sulfates and nitrates are among the products of the chemical transformations of sulfur
and nitrogen oxides. Ozone and other photochemical oxidants are believed to be involved in
the chemical processes that form them. When sulfates and nitrates combine with atmospheric
water, dissociated forms of sulfuric (HLSO.) and nitric (HNO.) acids result. When these acids
are brought to earth in rain and snow, acidic precipitation occurs. Because of long range
transport, acidic precipitation in a particular state or region can be the result of emissions
from sources in states or regions many miles away, rather than from local sources. To date,
however, the complex nature of the chemical transformation processes has not made it possible
to demonstrate a direct cause and effect relationship between emissions of sulfur and nitrogen
oxides and the acidity of precipitation.
Acidic precipitation is arbitrarily defined as precipitation with a pH less than 5.6.
This value has been selected because precipitation formed in a geochemically clean environment
would have a pH of approximately 5.6 due to the combining of carbon dioxide in the air with
water to form carbonic acid. Acidity of solutions is determined by the concentration of
hydrogen ions (H ) present and is expressed in terms of pH units—the negative logarithm of
the concentration of hydrogen ions. The pH scale ranges from 0 to 14, with a value of 7
representing a neutral solution. Solutions with values less than 7 are acidic, while values
greater than 7 are basic. Because pH is a logarithmic scale, a change of one unit represents
a tenfold change in acidity, hence pH 3 is ten times as acidic as pH 4. Currently the acidity
of precipitation in the northeastern United States normally ranges from pH 3.0 to 5.0; in
other regions of the United States precipitation episodes with a pH as low as 3.0 have been
reported. For comparison, the pH of some familiar substances are: cow's milk, 6.6; tomato
juice, 4.3; cola (soft drink) 2.8, and lemon juice, 2.3.
The pH of precipitation can vary from event to event, from season to season and from
geographical area to geographical area. Substances in the atmosphere can cause the pH to
shift by making it more acidic or more basic. Dust and debris swept up in small amounts from
the ground into the atmosphere may become components of precipitation. In the West and
Midwest soil particles tend to be more basic, but in the eastern United States they tend to be
acidic. Gaseous ammonia from decaying organic matter makes precipitation more acidic, so in
areas where there are large stockyards or other sources of organic matter, acidic
precipitation would be more likely to occur.
In the eastern United States sulfur oxide emissions are greater than nitrogen oxides,
therefore, sulfates are greater contributors to the formation of acids in precipitation in
11-2
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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 bed-
rocks.
Soft water lakes, those most sensitive to additions of acidic substances, are usually
found in areas with igneous bedrock which contributes few solids to the surface waters,
whereas hard waters contain large concentrations of alkaline earths (chiefly bicarbonates of
calcium and sometimes magnesium) derived from limestones and calcareous sandstones in the
drainage basin. Alkalinity is associated with the increased capacity of lakes to neutralize
or buffer the incoming acids. The extent to which acidic precipitation contributes to the
acidification process has yet to be determined.
The disappearance of fish populations from freshwater lakes and streams is usually one of
the most readily observable signs of lake acidification. Death of fish in acidified waters has
been attributed to the modification of a number of physiological processes by a change in pH.
Two patterns of pH change have been observed. The first involves a sudden short-term drop in
pH and the second, a gradual decrease in pH with time. Sudden short-term drops in pH often
result from a winter thaw or the melting of the snow pack in early spring and the release of
the acidic constituents of the snow into the water. Fish may be killed at pH levels above
those normally causing death.
A gradual decrease in pH, particularly below 5, can interfere with reproduction and
spawning of fish until elimination of the population occurs. In some lakes, aluminum mobili-
zation in fresh waters at a pH below 5 has resulted in fish mortality and appears to be as
important as pH.
Although the disappearance of and/or reductions in fish populations are usually empha-
sized as significant results of lake and stream acidification, changes of equal or greater
importance are the effects on other aquatic organisms ranging from waterfowl to bacteria.
Organisms at all tropic (feeding) levels in the food web appear to be affected. Species re-
duction in number and diversity may occur, biomass (total number of living organisms in a
given volume of water) may be altered and processes such as primary production and decomposi-
tion impaired.
Primary production and decomposition are the bases of the two major food webs (grazing
and detrital) within an ecosystem by which energy is passed along from one organism to another
through a series of steps of eating and being eaten. Green plants, through the process of
photosynthesis, are the primary energy producers in the grazing web, while bacteria initiate
the detrital food web by feeding on dead organic matter. Disruption of either of these two
food webs results in a decrease in the supply of minerals and nutrients, interferes with their
11-4
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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 (SO^") and nitrate (NO^) ions on vegetation and have caused nicrotic lesions in
a wide variety of plants species under greenhouse and laboratory conditions. Such results
must be interpreted with caution, however, because the growth and morphology of leaves under
greenhouse conditions are often not typical of field conditions. Based on laboratory studies,
the sensitivity of plants to acidic deposition seems to be associated with the wettability of
leaf surfaces. The shorter the time of contact, the lower the resulting dose and the less
likelihood of injury.
Soils may become gradually acidified from an influx of hydrogen (H ) ions. Leaching of
the mobilizable forms of mineral nutrients may occur. The rate of leaching is determined by
the buffering capacity of the soil and the amount and composition of precipitation. Unless
the buffering capacity of the soil is strong and/or the salt content of precipitation is high,
leaching will in time result in acidification. At present there are no studies showing this
process has occurred because of acidic precipitation.
Damage to monuments and buildings made of stone, and corrosion of metals can result from
:acidic precipitation. Because sulfur compounds are a dominant component of acidic precipi -
tation and are deposited during dry deposition also, the effects resulting from the two pro-
cesses cannot be distinguished. In addition, the deposition of sulfur compounds on stone
surfaces provides a medium for microbial growth that can result in deterioration.
Human health effects due to the acidification of lakes and rivers have been postulated.
Fish in acidified water may contain toxic metals mobilized due to the acidity of the water.
Drinking water may contain toxic metals or leach lead from the pipes bringing water into the
homes. Humans eating contaminated fish or drinking contaminated water could become ill. No
instances of these effects having occurred have been documented.
Several aspects of the acidic precipitation problem remain subject to debate because
existing data are ambiguous or inadequate. Important issues include: (1) the rate at which
rainfall is becoming more acidic and the rate at which the problem is becoming geographically
more widespread; (2) the quantitative contributions of various acids to the overall acidity
of rainfall; (3) the relative extent to which the acidity of rainfall in a region depends
on local emissions of nitrogen and sulfur oxides versus emissions transported from distant
11-5
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sources; (4) the relative importance of changes in total mass emission rates compared to
changes in the nature of the emission patterns (ground level versus tall stacks) in contribu-
ting to regional acidification of precipitation; and (5) the relative contribution of wet and
dry deposition to the acidification of lakes and streams.
11.1.2 Ecosystem Dynamics
The emission of sulfur and nitrogen oxides into the atmosphere, their transformation,
transport and deposition, either as acidic precipitation or in dry form, as well as the re-
sponses of aquatic and terrestrial ecosystems to acidic deposition are all natural phenomena
that have been in existence as long as humans can remember. Environmental problems arise be-
cause the natural systems are being overloaded by emissions from the combustion of fossil
fuels from anthropogenic sources.
Life on the planet Earth depends on the movement of energy and minerals through the bio-
sphere, that thin layer of life surrounding the earth. The living systems (forest, grass-
lands, cultivated fields, lakes, rivers, estuaries and oceans) within the biosphere obtain
energy from the sun, nutrients from the earth's crust, the lithosphere, gases from the atmos-
phere and water from the hydrosphere. All of the living systems are interdependent. Energy
and nutrients move from one to another. The living systems together with their physical en-
vironment, the lithosphere, hydrosphere and atmosphere, make up the ecosystem that is the
planet Earth (Billings, 1978; Boughey, 1971; Odum, 1971; Smith, 1980).
Ecosystems are basically energy processing systems "whose components have evolved to-
gether over a long period of time. The boundaries of the system are determined by the en-
vironment, that is, by what forms of life can be sustained by the environmental conditions of
a particular region. Plant and animal populations within the system represent the objects
through which the system functions" (Smith, 1980).
Ecosystems are composed of biotic (living) and abiotic (non-living) components. The
biotic component consists of: (a) producers, green plants that capture the energy of the sun;
(b) consumers that utilize the food stored by the producers for their energy; and (c) the
decomposers who break down dead organic matter and convert it into inorganic compounds again.
(See Table 11-1). The abiotic components are the soil matrix, sediment, particulate matter,
dissolved organic matter and nutrients in aquatic systems, and dead or inactive organic matter
in terrestrial systems (See Table 11-1) (Billings, 1978; Boughey, 1971; Smith, 1980).
Ecosystems are open systems. They both receive from and contribute to the environment
that surrounds them. The environment contributes gases, nutrients, and energy. Ecosystems
utilize these substances and, in turn, make their own contributions to the environment. En-
ergy flows through the system unidirectionally while water, gases and nutrients are usually
recycled and fed back into the system. The functioning of ecosystems is greatly influenced by
the extent to which the gases and nutrients are fed back into the system. When materials are
not returned to an ecosystem through recycling, they must be obtained in another way. The
organismal populations are the structural elements of the ecosystem through which energy flows
and nutrients are cycled (Smith, 1980; Billings, 1978; Odum, 1971).
11-6
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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)
''Adapted from: Billings (1978)
11-7
-------
Energy from the sun is the driving force in ecosystems. If the sun's energy were cut off
all ecosystems would cease to function. The energy of the sun is captured by green plants
through the process of photosynthesis and stored in plant tissues. This stored energy is
passed along through ecosystems by a series of feeding steps, known as food chains, in which
organisms eat and are eaten. Energy flows through ecosystems in two major food chains, the
grazing food chain and the detrital food chain. The amount of energy that passes through the
two food chains varies from community to community. The detrital food chain is dominant in
most terrestrial and shallow-water ecosystems. The grazing food chain may be dominant in
deep-water aquatic ecosystems (Smith, 1980). The fundamental processes involved in these two
food chains are photosynthesis, the capture of energy from the sun by green plants, and
decomposition, the final dissipation of energy and the reduction of organic matter into
inorganic nutrients.
In addition to the flow of energy, the existence of the living world depends upon the
circulation of nutrients through the ecosystems. Both energy and nutrients move through the
ecosystem as organic matter. It is not possible to separate one from the other. Both influ-
ence the abundance of organisms, the metabolic rate at which they live and the complexity and
structure of the ecosystem (Smith, 1980). Nutrients, unlike energy, after moving from the
living to the nonliving return to the living components of the ecosystem in a perpetual cycle.
It is through the cycling of nutrients that plants and animals obtain the minerals necessary
for their existence.
The gaseous and sedimentary cycles are the two basic types of nutrient or biogeochemical
cycles. The gaseous cycles involve carbon, oxygen and nitrogen. Water, also, is sometimes
considered as belonging to the gaseous cycle. In the gaseous cycles, the main nutrient reser-
voirs are the atmosphere and the ocean. In the sedimentary cycle, to which phosphorus
belongs, the soil and rocks of the earth's crust are the reservoir. The sulfur cycle is a
combination of the two cycles because it has reservoirs in both the atmosphere and the earth's
crust.
Nitrogen, sulfur and water cycles are involved in acidic deposition. Nitrogen, through
the agency of plants (chiefly legumes and blue green algae), moves from the atmosphere to the
soil and back (see Figure 4-1, Chapter 4). Human intrusion into the nitrogen cycles include
the addition of nitrogen oxides to the atmosphere and nitrates to aquatic ecosystems. Sulfur
enters the atmosphere from volcanic eruptions, from the surface of the ocean, from gases
released in the decomposition processes and from the combustion of fossil fuels (see Figure
11-1). Both the nitrogen and sulfur cycles have been overloaded by the combustion of fossil
fuels by man. For these cycles to function, an ecosystem must possess a number of structured
relationships among its components. By changing the amounts of nitrogen and sulfur moving
through the cycles, humans have perturbed or upset the structured relationships that have
existed for thousands of years and altered the movement of the elements through the
ecosystems. The pathways the elements take through the system depend upon the interaction of
the populations and their relationships to each other in terms of eating and being eaten.
11-8
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Photochemical
Oxidation
Direct Utilization
of Atmospheric SO?
by Plants
Animals in the
Grazing Food Chain
Inorganic
Sulfate V
SO4
A
Weathering
of Rocks
Death & Wastes
O <>
Detritus Food Chain
— Oxi
^
Bacterial . Sulfh
cation Heduction( Su
ydryl
fur
toH2S N R-SH
1 — - s
-fc-
\
jlfideX^ oxidation
L_\
^ 1
I
1
1
V
Er
Forest &
Grassland
Fires
SO,
Spontaneous
Oxidation
in
Atmosphere
Volcanic
-H7S
Sulfur Compounds in
Sediments, Fuels, Soils,
and Sedimentary Rocks
Combustion
of
Sulfur-Containing
Fuels
Figure 11-1. The sulfur cycle (organic phase bounded by dashed line).
Source: Chapham (1973).
11-9
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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;
Moran et al., 1980; Odum, 1971; Smith, 1980). The range of tolerance (see Figure 11-2) of an
organism may be broad for one factor and narrow for another. The tolerance limit for each
species is determined by its genetic makeup and varies from species to species for the same
reason. The range of tolerance also varies depending on the age, stage of growth or growth
form of an organism. Limiting factors are, therefore, factors which, when scarce or over-
abundant, limit the growth, reproduction and/or distribution of an organism (Billings, 1978;
Boughey, 1971; Moran et al., 1980; Odum, 1971; Smith, 1980). The increasing acidity of water
in lakes and streams is such a factor.
11-10
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ZONE OF
INTOLERANCE
IOWER LIMITS
OF TOLERANCt
ZONE OF
PHYSIOLOGICAL
STRESS
TOLERANCE RANGE
RANGE OF OPTIMUM
UWEH LIMITS
OFTOLER«»C[
ZONE OF
PHYSIOLOGICAL
STRESS
ZONE OF
INTOLERANCE
ORGANISMS
INFREQUENT
ORGANISMS
ABSENT
GREATEST
ABUNDANCE
ORGANISMS
INFREQUENT
ORGANISMS
ABSENT
LOW«-
-GRADIENT-
->HIGH
Figure 11-2. Law of tolerance.
Source: Adapted from Smith (1980).
11-11
-------
Organisms can exist only within their range of tolerance. Some populations of organisms,
annual plants, insects, and mice, for example, respond rapidly. They increase in numbers
under favorable conditions and decline rapidly when conditions are unfavorable. Populations
of other organisms, such as trees and wolves, fluctuate less in response to favorable or
unfavorable conditions. Ecosystems that contain both types of populations are more stable
bacause they are able to absorb changes and still persist because the structure of the eco-
system permits it to persist even though populations within it fluctuate widely in response to
environmental changes (Moiling, 1973; Smith, 1980). Other ecosystems are resistant; their
structure enables them to resist changes. Typically, most resistant ecosystems have large
living components, trees for example, and store nutrients and energy in the standing biomass.
Such resistant systems, such as forests, once highly disturbed are very slow in returning to
their original state (Smith, 1980).
Aquatic ecosystems which lack components in which energy and nutrients may be stored for
long periods of time usually are not very resistant to environmental changes (Smith, 1980).
For example, an influx of pollutants such as effluents from sewage disrupts the system because
more nutrients enter the system than it can handle. However, since the nutrients are not re-
tained or recycled within the system it returns to its original state in a relatively short
time after the perturbation is removed.
No barriers exist between the various environmental factors or between an organism or
biotic community and its environment. Because an ecosystem is a complex of interacting com-
ponents, if one factor is changed, almost all will change eventually. "The ecosystem reacts
as a whole. It is practically impossible to wall off a single factor or organism in nature
and control it at will without affecting the rest of the ecosystem. Any change no matter how
small is reflected in some way throughout the ecosystem: no 'walls' have yet been discovered
that prevent these interactions from taking place" (Billings, 1978).
Continued or severe perturbation of an ecosystem can overcome its resistance or prevent
its recovery with the result that the original ecosystem will be replaced by a new system. In
the Adirondack Mountains of New York State, in eastern Canada and parts of Scandinavia the
original aquatic ecosystems have been and are continuing to be replaced by ecosystems dif-
ferent from the original due to acidification of the aquatic habitat. Forest ecosystems
appear to be more resistant because, thus far, changes due to stress from acidifying
substances have not been detected. The sections that follow discuss the response of aquatic
and terrestrial ecosystems to stressing or perturbation by acidic deposition. Sulfur and
nitrogen oxide emissions, their transformation, transport and deposition in acidic form is
elucidated in the context of the ecosystem processes that were discussed above.
11.2 CAUSES OF ACIDIC PRECIPITATION
11.2.1 Emissions of Nitrogen and Sulfur Oxides
The generally held hypothesis is that nitrogen and sulfur compounds are largely responsi-
ble for the acidity of precipitation (Bolin et al., 1972; Likens and Borman, 1974; Likens,
11-12
-------
1976; Smith, 1872). The emissions of the nitrogen and sulfur compounds involved in the
acidification are attributed chiefly to the combustion of fossil fuels. Natural sources can
also be involved; however, in highly industrialized areas emissions from manmade sources
usually exceed those from natural sources (see Chapter 5).
Since 1900 there has been a nearly exponential increase in the consumption of gas, and
oil in the United States (see Figure 11-3). Although the total consumption of coal has not
increased greatly since about 1925, the consumption of oil and gas has continued to rise pre-
cipitously, thus overshadowing coal as the dominant fuel source during the past 50 years
(Hubbert, 1976). Within this overall increase in fossil-fuel use, however, there have been
shifts in the pattern of consumption. Whereas a considerable proportion of coal was used for
transportation and heating, oil and gas have since taken over these functions, and now coal is
predominantly devoted to electric power generation (Figure 11-4). In fact, electric power
generation is the primary factor accounting for an absolute increase in coal consumption over
the past two decades. (The decline in coal use in the 1930s was due to the general economic
depression, and the decline in the 1950s was due to the availability of relatively inexpensive
oil and gas.) Approximately 550 MM tons (Robinson, 1978) were used annually during
1918-1928 compared to 672 MM tons during 1979 (Hamilton, 1980). There was, however, a sea-
sonal shift in the pattern of coal consumption. Summer coal consumption has increased since
I960, while winter consumption has decreased due to increased summer usage by the electric
utilities.
These changes in the pattern of fuel use have been accompanied by changes in the pattern
of pollutant emissions. Figure 11-5A and 11-5B illustrate the rise since 1940 in emissions of
sulfur and nitrogen oxides, the primary gaseous pollutants resulting from the combustion of
fossil fuels. Although there has been a net increase in both categories, the more consistent
rise has been in emissions of nitrogen oxides. Almost all (93 percent) emissions of sulfur
oxides in the United States arise from stationary point sources, principally industrial and
power plant stacks. Nitrogen oxide pollutants, on the other hand, originate about equally
from transportation (mobile) sources and from stationary sources, which include not only
industrial and power plants, but residential and institutional heating equipment as well
(Office of Air Quality Planning and Standards, 1978). (see Tables 5-2 and 5-3, Chapter 5.)
The geographic distributions of sources of the gaseous precursors of acidic precipitation
are depicted in Figures 11-6 and 11-7. Clearly, the dominant sources of sulfur oxides in the
United States are in the eastern half of the country, particularly the northeastern quadrant.
Major nitrogen oxide sources also show a tendency to be concentrated somewhat in the north-
eastern quadrant of the country.
Chapter 5, Section 5.2.2 should be consulted for a more detailed account of the sources
and emissions of nitrogen oxides.
11.2.2 Transport of Nitrogen and Sulfur Oxides
Among the factors influencing the formation as well as the location where acidic deposi-
tion occurs is the long-range transport of nitrogen and sulfur oxides. Neither the gases nor
11-13
-------
2050
Figure 11-3. Historical patterns of fossil fuel consumption in the
United States (adapted from Hubbert, 1976).
11-14
-------
z
o
I-
o.
5
D
O
o
o
CJ
>
_l
DC
LU
800
700
600
500
400
300
200
100
0
I I
I I
TOTAL
- OTHER _
-OVENCOKE
ELECTRIC
UTILITIES
RES. &COMM.
HEATING
RAILROADS
1900 10 20 30 40 50
YEAR
60
70 80 90 2000
Figure 11-4. Forms of coal usage in the United States. Electric
power generation is currently the primary user of coal. (Data
from U.S. Bureau of Mines, Minerals Yearbooks 1933-1974)
11-15
-------
V)
in
t/i
i
IU
in
O
UJ
x
O
35
30
20
15
2 io
1940
35
30
4A
c
O
.S 25
*-
S 20
15
10
0
1940
TRANSPORTATION
1950
1960
YEAR
1970
1980
T
TOTAL
TRANSPORTATION
I I
1950
1960
YEAR
1970
1980
Figure 11-5a. Trends in emissions of sulfur dioxides.
Figure 11-5b. Trends in emissions of nitrogen oxides.
Source: Office of Air Quality Planning and Standards
(1978).
11-16
-------
KEY
EMISSION DENSITY, tons/mi"2
D«
5~10
20-50
>50
r?l 10-20
Figure 11-6. Characterization of U.S. SOX emissions density by state (U.S. Dept. of Energy, 1981).
(Roman numerals indicate EPA Regions.)
-------
oo
EMISSION DENSITY, tons/mi'
20-50
>30
Figure 11-7. Characterization of U.S. NOX emissions density by state (U.S. Dept. of Energy, 1981).
(Roman numerals indicate EPA Regions.)
-------
their transformation products always remain near the sources from which they have been emitted.
They may be transported for long distances downwind (Altshuller and McBean, 1979; CogbilT and
Likens, 1974; Pack et: al. , 1978).
The geographic picture of the problem of acidic precipitation in North America can be
better understood in the light of some information on prevailing wind patterns. Winds trans-
port the precursors of acidic precipitation from their points of origin to areas where the
acidified rain and snow eventually fall. Prevailing winds in the eastern United States tend
to be from the west and southwest. Atmospheric pollutants, therefore, are carried in a gener-
ally northeasterly direction. Thus, pollution originating in the Ohio River valley can be
carried toward the New England states. Seasonal meteorological patterns, however, can modify
the direction of windflow, particularly in the summer. The Maritime Tropical air masses from
the Gulf of Mexico that occur in late summer have the greatest potential for the formation and
transport of high concentrations of sulfate into the northeastern United States and into
eastern Canada (Altshuller and McBean, 1969).
Cogbill and Likens (1974) associated acidic rainfall in central New York during 1972-73
with high altitude air masses transported into the region from the Midwest. They stated that
the NO and S02 that is involved in acidic rain formation may be transported distances of 300
to 1500 km. Reports by Miller et al., (1978) Wolff et al. , (1979) and Galvin et al. (1978)
all support the concept that the trajectories of the air masses which come from the Midwest
carry sulfur and nitrogen compounds which acidify precipitation in New York State.
A significant though disputed factor in this transport picture is the height at which the
pollutants are emitted. Industrial and power plant smokestacks emit their effluents into the
atmosphere at higher elevations than do motor vehicles or most space heating equipment. In
fact, there has been a trend since the 1960s toward building higher stacks as a means of dis-
persing pollutants and thereby reducing pollutant concentrations in the vicinity of power
plants, smelters, and similar sources (Grennard and Ross, 1974). The result has been that
sulfur and nitrogen oxides are carried by prevailing winds for long distances and allowed to
diffuse over greater areas through the atmosphere (See Figure 11-8.). Concomitantly,
long-range transport allows greater time for chemical reactions to convert these pollutant
gases into particulate forms which are more easily removed by wet processes (Eliassen and
Saltbones, 1975; Prahm et al., 1976; Smith and Jeffrey, 1975). Chapter 6 discusses the
chemical transformations and wet and dry deposition as well as transport and diffusion of
nitrogen oxides in the atmosphere. Sulfates and nitrates combine with atmospheric water to
form dissociated forms of nitric (HN03) and sulfuric (H2S04) acids. These acids are con-
sidered to be the main components of acidic precipitation.
The mechanisms of these chemical reactions are quite complex and depend on a host of
variables ranging from physical properties of the pollutants to weather conditions and the
presence of catalytic or interacting agents (Fisher, 1978). Although these processes of at-
mospheric chemistry are not well understood, it does appear that the long-range transport of
11-19
-------
PREVAILING WINDS
ro
o
DRY DEPOSITION
(ATMOSPHERIC CHEMICAL REACTIONS
iAND TRANSFORMATIONS^
Figure 11-8. The transport and deposition of atmospheric pollutants, particularly oxides of sulfur and
nitrogen, that contribute to acidic precipitation.
Source: Modified from U.S. EPA (1979).
-------
sulfur compounds can cover 1000 to 2000 km over three to five days (Pack et al. , 1978). Thus,
the impact of sulfur pollutants in the form of acidic precipitation may be far removed from
their points of origin. It is not yet clear whether the atmospheric transport of nitrogen
oxide pollutants is comparable to that of sulfur compounds, (Pack, 1978) but in the northeast
nitrates are currently thought to contribute 15 to 30 percent of the acidity of polluted pre-
cipitation. This figure has increased over the past few years and is expected to increase
still further in the future (National Research Council, 1978).
11.2.3 Formation
Precipitation is that portion of the global water cycle by which water vapor from the at-
mosphere is converted to rain or snow and then is deposited on the earth surfaces (Smith,
1980). Water moves into the atmosphere by evaporation and transpiration (water vapor lost by
vegetation). Once it reaches the atmosphere, the water vapor is cooled, then condenses on
solid particles and soon reaches equilibrium with atmospheric gases. One of the gases is car-
bon dioxide. As carbon dioxode dissolves in water, carbonic acid (hLCO,) is formed. Carbonic
acid is a weak acid and in distilled water only dissociates slightly, yielding hydrogen ions
and bicarbonate ions (HC03 ). When in equilibrium with normal atmospheric concentrations and
pressures of carbon dioxide, the pH of rain and snow is approximately (Likens et al., 1979).
The pH of precipitation may vary and become more basic or more acidic depending on sub-
stances in the atmosphere. Dust and debris may be swept from the ground in small amounts and
into the atmosphere where it can become a component of rain. Soil particles are usually
2+
slightly basic in distilled water and release positive ions, such as calcium (Ca ), magnesium
2+ + +
(Mg ), potassium (K ), and sodium (Na ) into solution. Bicarbonate usually is the corre-
sponding negative ion. Decaying organic matter adds gaseous ammonia to the atmosphere. Am-
monia gas in rain or snow forms ammonium ions (NH. ) and tends to increase the pH. In coastal
iareas sea spray plays a strong role in the chemistry of precipitation. The important ions
entering into precipitation—sodium, magnesium, calcium, potassium, and the anions chloride
_ o-
(Cl ) and sulfate (S04 )--are also those most abundant in ocean water (Likens, 1976; Likens
et al., 1979).
Gases, in addition to C02, which enter precipitation, are sulfur dioxide ($02) and the
nitrogen oxides (NO ). Some sulfur gases originate from natural sources, e.g. volcanoes and
swamps. Others originate from industrial emissions. In the wet atmosphere, both SOp and hLS
can be oxidized to sulfuric acid. Nitrogen oxides in the atmosphere are converted to nitric
acid (Likens, 1976; Likens et al. , 1979). Strong acids dissociate completely in dilute aque-
ous solutions and lower the pH to less than 5.6. Acidic precipitation has been considered by
many scientists to be rain or snow with a pH below 5.6. (Galloway and Cowling, 1978; Likens et
al., 1979; Wood, 1975).
Additional acidic or potentially acidifying substances present in both wet and dry depo-
sition are sulfur trioxide (S0,~), sulfate S0.~), nitric oxide (NO), nitrogen dioxide (NO,),
- *
nitrite (NOp ), nitrate (NO, ), ammonium (NH. ), chlorine (Cl ) hydrochloric acid (HC1), and
Brdnsted acids [e.g., dissolved iron (Fe) and ammonium (NH^ )] (Whelpdale, 1979).
11-21
-------
The amounts of the various substances in the atmosphere originating from seawater, desert
sands, volcanic islands, or vegetated land influence the chemistry of natural precipitation.
In regions with calcareous soils, calcium and bicarbonate may enter precipitation as dust,
subsequently increasing the pH of rain or snow to 6.0 or above (Likens et al., 1979).
11.2.3.1 Composition and pH of Precipitation—Sulfur and nitrogen compounds are chiefly re-
sponsible for the acidity of precipitation. Continuous measurement of pH in rain by Likens et
al., (1972) for the Hubbard Brook Experimental Forest in Hew Hampshire from 1964 to 1971
indicated the precipitation was acid with an annual weighted average pH range of 4.03 to 4.19.
(A weighted average takes into account the amount of rain as well as its composition.) Cog-
bill and Likens (1974) using precipitation from the Ithaca area, and Hubbard Brook reported
that their analysis of precipitation which consistently had a pH of less than 4.4 showed that
65 percent of the acidity was due to H-SO,, 30 percent to HMO,, and less than 5 percent was
due to HC1. Hendry (1977) found that sulfate contributed 69 percent, nitrate 23 percent, and
chloride 8 percent of the free acidity in rainfall at Gainesville, Florida, during 1976.
In 1976, Likens (1976) reported that the continued monitoring of precipitation at the
Hubbard Brook Forest through 1974 indicated the mean annual pH for the years 1964-1974 ranged
from 4.03 to 4.21. No statistically significant trend was noted; however, pH values of 2.1
and 3.0 were observed for individual storms at various locations. The increased deposition of
hydrogen ion was due to an increase in nitric acid in the precipitation (rain and snow) fall-
ing there. This change in the composition of acidic precipitation suggests that the sources
of nitrogen oxide emissions increased while those for sulfur oxides remained constant.
The acidity of precipitation is a reflection of the free hydrogen ions in precipitation.
The contribution of sulfate and nitrate anions has changed with time, and analysis indicates
that the nitrate anion makes up an ever-increasing fraction of the total negative ion equiva-
lents. Following the reasoning of Granat (1972), Likens et al. (1976) found [assuming 2H per
2- + 2-
SO. ion as in H?SO. or one H ion per SO. as in (NH.-..SO.] that the contribution of sulfate
to acidity declined from 83 to 66 percent of the total acidity between 1964 to 1974 at Hubbard
Brook, and the contribution of nitrate increased from 15 to 30 percent of the total during the
same period. Furthermore, increased annual input' of H was closely correlated with increased
input of nitrate, but there was little correlation between H input and sulfate input.
Data for nitrate, ammonium, and sulfate in rain at Ithaca and Geneva, New York, consti-
tute the longest record of precipitation chemistry in the United States (Likens, 1972). Data
are available from 1915 to the present, but long gaps exist in the measurements, especially at
the Geneva site. Figures 11-9 (A) to (C) show that marked changes in composition have oc-
curred at Ithaca: a gradual decline in ammonium, an increase in nitrate beginning around 1945,
and a marked decrease in sulfate starting between 1945 and 1950. Early data for Ithaca showed
higher concentrations of sulfate in winter than in summer, presumably because of greater local
burning of coal in winter. Data for 1971 showed the reverse trend, however, with nearly half
the annual sulfate input occurring during the months of June to August. Likens (1972) con-
cluded that, despite deficiencies in the historical data and questions
11-22
-------
Z
01
UJ
K
<
t-
i
I
I I I I I I I
1920 1930 1940 1950 1960
YEAR
1970
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0
J I
I I I I
I I I
1920 1930 1940 1950 1960 1970
YEAR
4
Z
—
=
Z
1920 1930 1940 1950 1960 1970
YEAR
0.6
0.5
0.4
0.3
0.2
0.1
0
I
J I
J I
1968 1970 1972 1974
YEAR
SOURCE: (A), (B), and (C) modified from Likens (1972); (D) modified from Likens (1976).
Figure 11-9. Trends in mean annual concentrations of sulfate, ammonia, and nitrate in precipitation.
(A), (B), and (C) present long-term data for Ithaca, New York; (D) presents data for eight years averaged
over eight sites in New York and one in Pennsylvania. One point in (A), for 1946-47, is believed to be an
anomaly (see Likens, 1972, for discussion).
11-23
-------
concerning their reliability, the trends are real and can be explained by changes in fuel
consumption patterns, i.e., natural gas began to replace coal for home heating near the time
of the shifts in precipitation chemistry. On the basis of United States Geological Survey
data for nine stations, Likens (1976) reported a sharp increase in nitrate concentrations in
New York state during the past decade [Figure 11-9 (D)].
Galvin and Cline (1978) sampled the snow in a wilderness area of northern New York State.
Analysis of the samples by ion chromatography indicated that only nitrate and sulfate were
present in appreciable quantities with the concentration of nitrate being larger than sulfate.
The absence of chloride in the samples suggests that the source of the nitrate and sulfate was
inland.
Data for eastern North America indicate a roughly three-fold increase in nitrate in rain-
fall since 1955, whereas sulfate in rain has roughly doubled in this period. According to
Nisbet (1975), sulfate/nitrate ratios in rainfall averaged about 4 in the eastern United
States in 1955-1956, but the average ratio had fallen to about 3 in 1972-1973. Nisbet calcu-
lated that the fraction of H deposition attributable to nitrate rose from 19 percent in 1955-
1956 to 24 percent in 1972-1973, while the deposition attributable to H2S04 decreased from 80
to 73 percent.
2- +
Lindberg et al. (1979) noted that SO, and H were by far the dominant constituents of
precipitation at the Walker Branch Watershed, Tennessee. Comparison with the annual average
concentration of major elements in rain at the Walker Branch Watershed on an equivalent basis
indicated that H constitutes approximately 50 percent of the cationic strength and trace ele-
ments account for only 0.2 percent. Sulfate constituted approximately 65 percent of the ani-
onic strength and on an equivalent basis was 3.5 times more concentrated than NO,, the next
most abundant anion. The incident precipitation for the 2-year (1976-1977) period was
described as "a dilute mineral acid solution", primarily H-SO,, at a pH approximating 4.2 and
containing relatively minor amounts of various trace salts (Lindberg et al., 1979). In
Florida, Hendry (1977) and Hendry and Brezonik (1980) found that sulfate contributed 69 per-
cent, nitrate 23 percent, and chloride 8 percent of the free acidity in rainfall at
Gainesville, Florida, during 1976.
2-
Based on most reports, sulfate (SO, ) appears to be the predominant anion in acidic pre-
cipitation in the Eastern United States. In the west in California, however, nitrate (NO,)
seems to predominate. Liljestrand and Morgan (1978) reported that their analyses of acidic
rainfall collected from February 1976 to September 1977 in the Pasedena, CA, area showed that
the volume-weighted mean pH was 4.0, with nitric acid being 32 percent more important as a
source of acidity than sulfuric acid. The major cations present were H , NH., K , Ca and
2+ - - 2-
Mg while the major anions were Cl , NO, and SO. . McColl and Bush (1978) also noted the
strong influence of nitrate on rain in the Berkeley, CA, region. However, they note that in
2-
bulk precipitation (wet plus dry fall-out) that sulfate (SO. ) constituted 50 percent of the
total anions.
11-24
-------
Nearly all of the nitrate in rainfall is formed in the atmosphere from NO . Little is
derived from wind erosion of nitrate salts in soils. Similarly, nearly all of the sulfate in
rainfall is formed in the atmosphere from S02 (National Research Council, 1978). Thus, all
atmospherically derived nitrate and sulfate contribute to the acidification of precipitation,
since H is associated stoichiometrically with the formation of each. A second stoichiometric
process that affects the acidity of rain is the reaction of nitric and sulfuric acids with
ammonia or other alkaline substances (e.g., dust particles) in the atmosphere to form neutral
nitrate and sulfate aerosols. To the extent that such neutralization occurs, the acidity of
precipitation will be reduced (National Research Council, 1978). However, since much of the
ammonium ion reaching soil is converted to nitrate, these neutral salts still have an acidi-
fying effect on the soil.
11.2.3.2 Seasonal Variations in Nitrates and Sulfates—Seasonal fluctuations in composition
as well as pH of rainfall have been reported by many workers. In addition, the composition of
rainfall and pH fluctuates from event to event, from locality to locality, and from storm to
storm.
2- +
In general SO. and H concentrations in precipitation in the eastern United States are
higher in the summer than in the winter. Wolff et al. (1979) found this to be true for the
New York Metropolitan Area. Hornbeck et al. (1977) and Miller et al. (1978) both stated that
a summer maximum for sulfate was associated with an increase in hydrogen ion concentration in
upstate New York, the Hubbard Brook Experimental Forest in New Hampshire, and in portions of
Pennsylvania. Pack (1978) using data (1977) from the four original MAP3S (Multistate Atmos-
pheric Power Production Pollution Study) precipitation chemistry networks, plotted the
weighted monthly sulfate ion concentrations (Figure 11-10). Maximum sulfate concentrations
occurred from June through August. Lindberg et al. (1979) studying wetfall deposition of
2- +
sulfate in the Walker Branch Watershed, also noted summer maxima for SO. and H . Using the
same MAP3S data as did Pack, they plotted weighted mean concentrations of sulfate in rain
collected from November 1976 through November 1977. The concentrations at Walker Branch
Watershed, Tennessee, are lower than all of the stations except remote Whiteface Mountain, New
York. The regional nature of the wet deposition of sulfate is apparent. Reasons for the
existence of the high summer maxima of sulfate for the eastern United States are discussed in
some detail in Chapter 5, Section 5.3.4.
Seasonal variations of nitrogen compounds and of pH in precipitation have been reported
by several workers, but no simple trends are apparent (see U.S. Environmental Protection
Agency Air Quality Criteria for Particulate Matter and Sulfur Oxides, 1981). Hoeft et al.
(1972) found relatively constant levels of nitrate in rain and snow collected in Wisconsin
throughout the year, but deposition of ammonia and organic nitrogen was lowest in winter and
highest in spring, perhaps because of the thawing of frozen animal wastes. Haines (1976)
reported large random variations, but relatively small seasonal variations, for nitrogen forms
in wet-only precipitation at Sapelo Island, Georgia; nitrogen concentrations were lowest dur-
ing the rainy months of July and September. The highest nitrogen loadings occurred during
11-25
-------
Figure 11-10. Comparison of weighted mean monthly concentrations of sulfate
in incident precipitation collected in Walker Branch Watershed, Tenn. (WBW)
and four MAP3S precipitation chemistry monitoring stations in New York,
Pennsylvania, and Virginia (Lindberg et al., 1979).
11-26
-------
July and were associated with the lowest range in pH, 4.2-4.8. Hendry (1977) and Hendry and
Brezonik (1980) found relatively smooth seasonal trends in ammonia and nitrate concentrations
in both wet-only and bulk collections (wet- and dryfall) at Gainesville, Florida, with lowest
concentrations in winter (Figure 11-11). In addition, the pH of the bulk precipitation showed
no seasonal trend. Wet-only collections, however, showed the lowest pH value (4.0) during the
spring and summer. This historical record suggests there has been an increase in the concen-
tration of inorganic nitrogen in Florida over the past 20 years.
Scavenging by rainfall produces large changes in atmospheric contaminant concentrations
during a given rainfall event. The decline in constituent levels is usually rapid, at least
in localized convective showers, and low, steady-state concentrations are usually reached
within the first half hour of a rain event.
Major ions [chloride (Cl ) and sulfate (SO.")], inorganic forms of nitrogen [nitrate
(N03 ) and ammonium (NH. )], total phosphorus and pH were measured in rain collected in
5-minute segments within three individual rainstorms. Initially, rapid decreases were ob-
served for nitrate and ammonium and total phosphorus. There was also a decrease in pH from
4.65 to 4.4. Steady state concentrations were reached in 10 minutes. Two other storms
sampled in the same manner showed similar but less defined patterns (Hendrey and Brezonik,
1980).
Wolff et al. (1979) examined spatial meteorological and seasonal factors associated with
the pH of precipitation in the New York Metropolitan Area. Seventy-two events were studied
rom 1975 through 1977. There was some site-to-site variability among the eight sites they
studied in the Manhattan area (Table 11-2). They also noted that the pH varied according to
storm type (Table 11-3). Storms with a continental origin have a lower pH than storms origi-
nating over the ocean. The storms with trajectories from the south and southwest had the
lowest pH's, while those from the north and east had the highest pH's (Wolff et al., 1979).
The mean pH of precipitation falling on the New York Metropolitan Area during a 2-year
(1975 to 1977) study was 4.28; however, a pronounced seasonal variation was observed (Figure
11-12). The minimum pH at all sites except Manhattan occurred during July to September, while
the maximum occurred during October to December, the minimum pH in Manhattan, however, occur-
red January to March and then gradually increased through the year. The lowest pH of 4.12 for
the New York Metropolitan area occurred during the summer months (Wolff et al., 1979). In
general, the pH of rain is usually lower in the summer than in the winter and is associated
with the high summertime sulfate concentrations. In addition, the lowest pH's were associated
with cold fronts and air mass type precipitation events. These events occur more frequently
during the summer months. The lower pH's also occurred on westerly or southwesterly winds
(Wolff et al., 1979).
Seasonal variations in pH measured at several sites in New York State 70 km (45 mi.)
apart demonstrated a significant difference between seasons (Winter had an average pH of 4.2;
summer, 3.9.) but no significant difference between sites. In New Hampshire, however, six
11-27
-------
4.80
4.60
1. 4.40
4.20
0.40
I I
J I
I I
MAM
O
0.30
cc £
u
O
u
0.20
0.10
JASONDJFMAM.J
1976 *4+ 1977
MONTH
Figure 11-11. Seasonal variations in pH (A) and ammonium and
nitrate concentrations (B) in wet-only precipitation at Gainesville,
Florida. Values are monthly volume-weighted averages of levels
in rain from individual storms (Hendry, 1977).
11-28
-------
TABLE 11-2. MEAN pH VALUES IN THE NEW YORK METROPOLITAN
AREA (1975-1977)
Site Mean pH SD No. obsd Range
Caldwell, N.J.
Piscataway, N.J.
Cranford, N.J.
Bronx, N.Y.
Manhattan, N.Y.
High Point, N.J.
Queens, N.Y.
Port Chester, N.Y.
All sites
4.32
4.25
4.34
4.31
4.29
4.25
4.63
4.60
4.28
0.26
0.36
0.34
0.37
0.25
0.30
0.35
0.19
0.32
50
64
48
57
39
25
20
21
72
3.35-5.60
3.57-5.50
3.44-5.95
3.42-5.75
3.80-5.50
3.74-4.90
3.98-5.28
4.00-5.10
3.50-5.16
From Wolff et al. (1979).
TABLE 11-3. STORM TYPE CLASSIFICATION
Type
Description of dominant storm
system
No.
obsd
Mean
pH
1
2
3
4
5
6
7
8
Closed low-pressure system which formed
over continental N. Amer.
Closed low-pressure system which formed in
Gulf of Mexico or over Atlantic Ocean
Closed low which passed to W or N of N.Y.C.
Closed low which passed to S or E of N.Y.C.
Cold front in absence of closed low
Air mass thunderstorm
Hurricane Belle
Unclassified
22
21
26
17
16
5
1
6
4.35
4.43
4.39
4.39
4.17
3.91
5.16
4.31
From Wolff et al. (1979).
11-29
-------
4.3
4.3
4.4
a 4.3
4.2
4.0 JFM AMJ JAS ONO
MONTHS OF THE YEAR (ISTi through 1977)
Figure 11-12. Seasonal variation of precipitation pH in the
New York Metropolitan Area (Wolff et al, 1979).
11-30
-------
summer storms sampled at 4 sites less than 3 km (2 mi.) apart showed a significant difference
(3.8 to 4.2) indicating considerable variation in pH may occur in the same storm.
Stensland (1978, 1980) compared the precipitation chemistry for 1954 and 1977 at a site
in central Illinois. The pH for the 1954 samples had not been measured, but were calculated
and compared with those measured in 1977. The corrected pH for 1954 was 6.05; the pH for 1977
was 4.1. The more basic pH in 1954, according to the author, could have resulted from low
levels of acidic ions (e.g. sulfate or nitrate) or from high amounts of basic ions (e.g.
calcium and magnesium). Stensland suggests that the higher pH in 1954 was due to calcium (Ca )
and magnesium (Mg ) ions from the soil.
11.2.3.3 Geographic Extent of Acidic Precipitation—Acidic precipitation has been a reality
in New York State for an undetermined period of time. Data collected by the United States
Geological Survey (Harr and Coffey, 1975) over a ten-year period are presented in Figure 11-13.
These curves represent the pH of precipitation at eight different locations in New York State
and one location in Pennsylvania. Each of these locations represents an area within a given
watershed. The pH of precipitation has remained nearly at the same general average during the
entire ten-year period; therefore, since data for the years prior to 1965 are lacking, it is
difficult to determine when the pH in precipitation first began to decrease (Harr and Coffey,
1975).
That precipitation is acidic in parts of the country other than the northeastern United
States is apparent (see Figure 11-14). Average pH values around 4.5 have been reported as far
south as northern Florida (Hendry and Brezonik, 1980; Likens, 1976), from Illinois (Irving,
1978), the Denver area of Colorado (Lewis and Grant, 1980) the San Francisco Bay area of
California (McColl and Bush, 1978; Williams, 1978), Pasadena, California (Liljestrand and
Morgan, 1978), the Puget Sound area of Washington (Larsen et al., 1975), and from eastern
Canada (Dillon et al., 1978; Glass et al., 1979). Data from the San Francisco Bay area in-
dicate that precipitation has be come more acidic in that region since 1957-1958 (McColl and
Bush, 1978). The pH decreased from 5.9 during 1957-1958 to 4.0 in 1974, and seems to be re-
lated to an increase in the NCs concentration (McColl and Bush, 1978). Another report, using
data from the California Air Resources Board (CARB) (Williams, 1978), states that acidic pre-
cipitation has been reported from such widespread areas as Pasadena, Palo Alto, Davis, and
Lake Tahoe.
Studies in the Great Smoky Mountain National Park (Herrmann and Baron, 1980) indicate a
downward trend in pH has occurred there over the past twenty years. Over a period of 20 years,
there has been a drop in pH from a range of 5.3-5.6 to 4.3 in 1979.
The absence of a precipitation monitoring network throughout the United States in the
past makes determination of trends in pH extremely difficult and controversial. This short-
coming has been rectified recently through the establishment of the National Atmospheric Depo-
sition Program funded by State, Federal and private agencies and headquartered at North
Carolina State University, Raleigh, N.C. Under the program, monitoring stations collect
11-31
-------
7.0
6.0
S.O
40
3.0
0.0*
7.0
6.0
S.O
4.0
3.0
o.o'i
6.0
S.O
4.0
3.0
o.o"
6.0
S.O
4:0
0.0*
ALBANY. NEW YORK
ALLEGHENY STATE PARK. NEW YORK
ATHENS. PENNSYLVANIA
CANTON, NEW YORK
1965
1366
1967
196B
1969
YEAR
1970
1971
1972
1973
Figure 11-13. History of acidic precipitation at various sites in and adjacent
(Harr and Coffey, 1975).
to State of New York
11-32
-------
7.0
6.0
50
40
0.0*
7.0
60
* SO
4.0
0.0*
HINCKLEY.NEWVORK
MAYS POINT, NEW YORK
70
6.0
5,0
4.0
MINEOLA. NEW YORK
6.0
5,0
4 0
00
ROCK HILL. NEW YORK
UPTON, NEW YORK
5.0 I
1965
1972
1973
Figure 11-13 (cont'd). History of acidic precipitation at various sites in and adjacent to State
of New York (Harr and Coffey, 1975).
11-33
-------
Ched Plotting Legend
• I
NattoMl Almmptoric Depo«lnoo PIDO/MII (NADP)
OctMrlmenl ol Energy (DOE)
Envfronmenlti Prolwlkm Aoawy (EPA/NOAA/WHO)
V of CtlHomt*
Intiilut* ol Technology
io Almotptwrtc Power
Production Poirutton Sludy (14AP3S)
Etocirtc Po«w RM«VC*I Imlllut* (EPHI»
O*fe Rtdg* NiiKmtl Laboratory
oiifimil S*rvtca (CANSAP)
Figure 11-14. pH of rain samples as measured in the laboratory and used in combination with the
reported amount of precipitation.
Source: Wisniewski and Keitz (1981).
-------
precipitation samples, determine their pH and then send the samples to a Central Analytical
Laboratory in Illinois to be analyzed. This long-term network plans to have 75 to 100 collec-
tion sites throughout the United States; 74 are already operational.
11.2.4 Acidic Deposition
The previous sections of this chapter have discussed the formation, composition and geo-
graphic distribution of acidic precipitation. Usually when the effects of acidic deposition
are discussed, emphasis is placed on the effects resulting from the scavenging of sulfur and
nitrogen compounds by precipitation. Dry deposition of gaseous and particulate and aerosol
forms of these compounds also occurs and is beginning to receive more emphasis in research
(Chamberlain, 1980; Galloway and Wheledale, 1980; Schlesinger and Hasey, 1980; Schmel, 1980;
Stensland, 1980). Gaseous compounds reach the surface of the earth by turbulent transfer
while particulate sulfates and nitrates reach the earth's surface by gravitational sedimenta-
tion, turbulent transfer and impaction (Galloway and Whelpdale, 1980; Hicks and Wesely, 1980;
Schmel, 1980). A comparison of the relative significance of wet and dry deposition is diffi-
cult. Dry deposition, however, is always removing pollutants from the atmosphere, while
removal by wet deposition is intermittent (Schmel, 1980). Marenco and Fontan (1976) suggest
that dry deposition is more important than wet in removing air pollutants from manmade
sources.
Lindberg et al. (1979) have calculated the annual mass transfer rates of sulfates to the
forest floor in Tennessee (Figure 11-15). Their calculations for SO. suggest wet deposition
by incident precipitation to be 27 percent compared with a total dry deposition of 13 percent.
The dry deposition and foliar absorption of S(L, a very important component, is missing from
this calculation. The wet and dry deposition percentages are only an indication of the rela-
tive magnitude of the two processes. The percentages do, however, point out that the effects
of acidic deposition usually attributed to precipitation scavenging alone are probably a
result of both wet and dry deposition. At the present time the accuracy with which dry depo-
sition can be measured is still under question.
The studies of McColl and Bush (1978), Hendry and Brezonik (1980), and Schlesinger and
Hasey (1980) also point out that both wet and dry deposition are important when considering
+ 2- -
the effects of H , SO. , and NO, ions on aquatic and terrestrial receptors.
The effects of the dry deposition of SCL and particulate matter on vegetation and terres-
trial ecosystems is discussed in Chapter 8. The processes of wet and dry deposition of sulfur
oxides are discussed in Chapter 6 of Air Quality Criteria for Particulate Matter and Sulfur
Oxides. The nitrogen cycle is discussed in Chapter 4, transformation and transport of nitro-
gen oxides in Chapter 6 and the effects of nitrogen oxides on vegetation in Chapter 12 of this
document.
11.3 EFFECTS OF ACIDIC DEPOSITION
Acidic precipitation has been implicated in the degradation of aquatic ecosystems, the
disintegration of stone buildings and monuments and as a potential source of harm to forests
and other terrestrial ecosystems. The sections that follow discuss these effects.
11-35
-------
IN CLOUD
PRECIPITATION
SCAVENGING
25%
TOTAL DRY
DEPOSITION
BELOW CLOUD
PRECIPITATION
SCAVENGING
M
i '• •
4 V 'ill
TO LEAFY
CANOPY
TO GROUND
(DORMANT PERIOD)
2%,
i i 'u ,i
I ',"1 i i a" Ml'i •
INCIDENT PRECIPITATION
TO BRANCHES
(DORMANT PERIOD
1%
WASH-OFF 0
DRY DEPOSITION
EXTERNAL
FLUX
100%
Figure 11-15. Annual mass transfer rates of sulfate expressed as a percentage of the estimated
total annual flux of the element to the forest floor beneath a representative chestnut oak stand
(Lindbergetal., 1979).
11-36
-------
11.3.1 Aquatic Ecosystems
Acidification of surface waters is a major problem in regions of southern Scandinavia
(Aimer et al. , 1974; Gjessing et al., 1976; Oden, 1968), Scotland (Wright et al. , 1980a),
eastern Canada (Beamish and Harvey, 1972; Dillon et al., 1978), and the eastern United
States - in the Adirondack Region of New York State (Pfeiffer and Festa, 1980; Schofield,
1976a,b,c,d), in Maine (Davis et al. , 1978), and in northern Florida (Crisman et al. , 1980).
Damage to fisheries is the most obvious affect of acidification on freshwater lite. The d.is-
appearance of fish populations from acidified freshwater lakes and streams was first noted in
southern Norway in the 1920's. In 1959, Dannevig (1959) proposed that acidic deposition was
the probable cause for acidification and thus far the loss of fish populations (Leivestad et
al., 1976). Subsequent studies have verified this postulate. Declines in fish populations
have been related to acidification of surface waters in southern Norway (Jensen and Snekvik,
1972; Wright and Snekvik, 1978), southwestern Sweden (Aimer et al., 1974) southwestern Scot-
land (Wright et al., 1980a), the Adirondack Region of New York State (Schofield, 1976a,b,c,d),
and the LaCloche Mountain Region in southern Ontario (Beamish and Harvey, 1972). Acidifica-
tion may also have serious repercussions on other aquatic biota inhabiting these systems.
Changes in the acidity and chemistry of freshwater affect the communities of organisms living
there. Pertinent details of these effects are described in the following sections.
11.3.1.1 Acidification of Lakes and Streams—Precipitation enters lakes directly as rain or
snow or indirectly as runoff of seepage water from the surrounding watershed. The relative
magnitude of the influents from these two sources is dependent on the surface area and volume
of the lake, and the size of the watershed and its soil volume and type. In general, the
watershed plays a dominant role in determining the composition of water entering the lake. As
a result, the water will be strongly influenced by processes in the edaphic environment of the
watershed, such as weathering, ion exchange, uptake and release of ions by plants, carbon
dioxide production by vegetation, microbial respiration, and reduction and oxidation reactions
of sulfur and nitrogen compounds (Seip, 1980). Precipitation as a direct source of water to
the lake plays a relatively greater role when lake areas are large in comparison to the size
of the watershed.
Acidification of surface waters results when the sources of hydrogen ion exceed the
ability of an ecosystem to neutralize the hydrogen ion. In general, the soils and crust of
the earth are composed principally of basic materials with large capacities to buffer acids.
However, areas where bedrock is particularly resistant to weathering and soils are thin and
poorly developed have much less neutralizing ability. This inability to neutralize hydrogen
ion does not arise from a limited soil or mineral buffering capacity. Instead low cation
exchange capacity and slow mineral dissolution rates in relation to the relatively short re-
tention time of water within the soil system may result in incomplete neutralization of soil
waters and acidification of surface waters (Driscoll, 1980). Characteristics of regions sen-
sitive to surface water acidification are discussed in more detail in Section 11.4.1.
11-37
-------
Sources of hydrogen ion to the edaphic-aquatic system include, besides acidic deposition,
mechanisms for internal generation of hydrogen ion - oxidation reactions (e.g., pyrite oxida-
tion, nutrification), cation uptake by vegetation (e.g., uptake of NH. or Ca ), or genera-
tion of organic acids from incomplete organic litter decomposition (Figure 11-16). The rela-
tive importance of the hydrogen ion content in acidic deposition to the overall hydrogen ion
budget of an ecosystem has been discussed by many researchers (Rosenquist, 1976; SNSF Project,
1977).
The consensus is that changes in internal hydrogen ion generation related to land use or
other changes (e.g., Drablos and Sevaldrud, 1980) can not consistently account for the wide-
spread acidification of surface waters occurring in .southern Scandinavia, the Adirondack
Region of New York, the LaCloche Mountain Area of Ontario, and elsewhere. Driscoll (1980)
developed a hydrogen ion budget for the Hubbard Brook Area in New Hampshire. Based on these
calculations, atmospheric hydrogen ion sources represent 48 percent of the total Hubbard Brook
ecosystem hydrogen ion sources.
As noted above, freshwater ecosystem sensitive to inputs of acids are generally in areas
of poor soil development and underlain by highly siliceous types of bedrock resistant to dis-
solution through weathering (Likens et al, 1979). As a result, surface waters in such areas
typically contain very low concentrations of ions derived from weathering. The waters are
diluted .with low levels of dissolved salts and inorganic carbon, and low in acid neutralizing
capacity. The chemical composition of acid lakes is summarized in Table 11-4 for lakes in
southern Norway (Gjessing et al., 1976), the west coast (Hornstrbm et al. , 1973), and west-
central regions of Sweden (Grahn, 1977), the LaCloche Mountains of southeastern Ontario
(Beamish, 1976), and the vicinity of Sudbury, Ontario (Scheider et al., 1975), as well as for
lakes not yet affected by acidification but in regions of similar geological substrata in
west-central Norway (Gjessing et al. , 1976) and the experimental lakes area of northwestern
Ontario (Armstrong and Schindler, 1971). Basic cation concentrations (Ca, Mg, Na, K) are low
(e.g., calcium levels of 18-450 ueq/liter or 0.4 - 9 mg/liter) relative to world-wide averages
[15 mg/liter calcium (Livingstone, 1963)]. Bicarbonate is the predominant anion in most
freshwaters (Stumm and Morgan, 1970). However, in acid lakes in regions affected by acidic
deposition, sulfate replaces bicarbonate as the dominant anion (Beamish, 1976; Wright and
Gjessing, 1976). With a decreasing pH level in acid lakes, the importance of the hydrogen ion
to the total cation content increases.
Surveys to determine the extent of effects of acidic deposition on the chemistry of lakes
have been conducted in Norway (Wright and Snekvik, 1978; Wright and Henriksen, 1978), Sweden
(Aimer et al., 1974; Dickson, 1975), Scotland (Wright et al. , 1980a), the LaCloche Mountain
area of Ontario (Beamish and Harvey, 1972), the Muskoka-Haliburton Area of south-central
Ontario (Dillon et al., 1978), and the Adirondack Region of New York State (Schofield, 1976b),
Maine (Davis et al. , 1978), and Pennsylvania (Arnold et al. , 1980). In regions of similar
geological substrata not receiving acidic deposition, lake pH levels average 5.6-6.7 (Arm-
strong and Schindler, 1971). Of 155 lakes systematically surveyed in southern Norway in
11-38
-------
ALLOCHTHONOUS SOURCES OF HYDROGEN ION
PRECIPITATION,
DRY DEPOSITION,
X DRAINAGE WATER
p- ECOSYSTEM BOUNDARY
HYDROGEN ION
SOURCES
OXIDATION RXN
CATION UPTAKE
PYRITE
OXIDATION
NH+ UPTAKE
HYDROGEN ION
SINKS
REDUCTION RXN
ANION UPTAKE
OXIDE
WEATHERING
STREAM EXPORTS
H+,HC03~, OH-LIGANDS,
ORGANIC ANIONS
Figure 11-16. Schematic representation of the hydrogen ion
cycle (Driscoll, 1980).
11-39
-------
October 1974, over 70 percent had pH levels below 6.0, 56 percent below 5.5, and 24 percent
below 5.0 (Wright and Henriksen, 1978). Of 700 lakes in the SjJrlandet Region of southern
Norway surveyed in 1974 to 1975 (May-November), 65 percent had pH levels below 5.0 (Wright and
Snekvik, 1978). On the west coast of Sweden, of 321 lakes investigated during 1968-1970, 93
percent had a pH level 5.5 or lower. Fifty-three percent had pH levels between 4.0 and 4.5
(Dickson, 1975). In the LaCloche Mountain Region of Ontario, 47 percent of 150 lakes sampled
in 1971 had pH levels less than 5.5, and 22 percent had pH levels below 4.5 (Beamish and
Harvey, 1972). In the Adirondacks, 52 percent of the high elevation (> 610 m) lakes had pH
values below 5.0 (Schofield, 1976b). In each of these studies, the pH level of an individual
lake could be related to, in most cases, the intensity of the acidic deposition and the geo-
logic environment of the watershed. Atmospheric contributions of sea salts are also important
in coastal regions.
Several methods have been developed to assess the degree of acidification in a lake and
relate it to inputs of hydrogen ion or sulfate. Henriksen (1979) utilized alkalinity-calcium
and pH-calcium relationships in lakes to estimate the degree of acidification experienced by a
surface water. This technique is based on the premise that when carbonic acid weathering
occurs one equivalent of alkalinity (acid neutralizing capacity) is released to the aquatic
environment for every equivalent of basic cation (Ca, Mg, K, or Na) dissolved. On the other
hand, if mineral acid weathering is occurring, for example as a result of acidic deposition,
one equivalent of hydrogen ion is comsumed for every equivalent of cation solubilized. There-
fore, for a given basic cation level, there is less aqueous acid neutralizing capacity in
lakes in systems experiencing strong acid weathering than in systems experiencing carbonic
acid weathering. When comparing alkalinity plots from two watersheds, one experiencing strong
acid contributions and the other undergoing largely carbonic acid weathering (assuming both
watersheds have similar edaphic environments), the difference in alkalinity between the two
plots for a given calcium level (the dominant basic cation) should be indicative of the amount
of strong acid the watershed receives and the degree of acidification of the surface water.
For waters with pH levels below 5.6, alkalinity is approximately equal to the negative of the
hydrogen ion concentration. Therefore, pH level can be substituted for alkalinity, and
pH-calcium plots developed (Figure 11-17). Data of this type for Norway indicate that sig-
nificant acidification of lakes has occurred in areas receiving precipitation with volume-
weighted average concentrations of H above 20-25 |jeq/liter (pH 4.7-4.6) and sulfate concen-
trations above 1 mg/liter (20 ueq/liter) (Henriksen, 1979).
Henriksen (1979) also utilized the concentration of excess sulfate in lake water (sulfate
in excess of that of marine origin) to estimate acidification. This suggests that bicarbonate
anions lost in acidified lakes have been replaced by an equivalent amount of sulfate. Aimer
et al. (1978) plot pH levels in Swedish lakes as a function of excess sulfur load (excess
sulfur in lake water multiplied by the yearly runoff) (Figure 11-18). Based on this relation-
ship, they estimate that the most sensitive lakes in Sweden may resist a load of only about
11-40
-------
TABLE 11-4. CHEMICAL COMPOSITION (MEAN ± STANDARD DEVIATION) OF ACID LAKES (pH •*>) 1N REGIONS RECEIVING HIGHLY
ACIDIC PRECIPIIAFION (pH <4.b), AND OF SOFT-WATER LAKES IN AREAS NOT SUBJECT TO HI GHLV ACIDIC PRECIPITATION
(pH >4.8)
Region
I. LAKES IN ACID AREAS
Southernmost
Norway
Sweden
West-centra 1
Sweden
North America
La Cloche Mtns,
Ontario
Sudbury ,
Ontario
11. LAKES IN UNAFFECTED
Scandinav ia
West-central
Norway
North America
Exper i mental
Lakes Area,
Ontario
No. of
lakes
Measured: 26
Less s w*:
Less s w*:
Measured: 6
Less s w*:
Measured: 4
Less s w*:
Measured: 4
Less s w*:
AREAS
Measured: 23
Less s w*;
Measured: 40
Less s w*.
Speci fie
tomJuclancetl H (pH)
27*10 18*11 (4.76)
18
«*»
47+23 22+15 (4.66)
22
38+8 20+9 (4.7)
20
120+40 36+5 (4.5)
36
13+3 6±2 (5.2)
6
19 0.2-2 (5.6-6.7)
0.2-2
Na
70+40
9
-50
165+120
20
26+4
9
100±30
50
50+20
9
40
4
K
5+3
4
13
15+8
12
10±3
10
40+10
40
3±1
3
10
10
Ca
56+35
50
-
75+10
70
150+25
150
450±180
450
ia+9
16
80
80
Mg
41+16
25
80+40
50
75±B
65
310+120
300
16+5
7
75
65
~ M-q/1
HCOn
11+26
11
0
0
-
"
0
0
8+2
8
13+8
13
60
60
HCl
71+ 45
0
440
0
170+90
0
22+6
0
50+20*
0
46*21
0
40
0
SO,, N03
100*33 4+2
92 4
200 8
155 8
200+70 19+4
180 19
290+40
290
800+290
800
33+8 5+2
30 5
60 r( ncf!
fiji-i'. inq
el al. . 19/6
el al. , 19/6
Grdhn, 19//
Beamish,
Armstrong,
1971
Gjessing
el al. . 1976
Armstrong,
1971
"Less s w = Concentrations after subtracting the seauater contribution according to the procedure explained by
Wri(|ht and Cjessing (1976).
"Dala (or 112 lakes
IMeasured after past liming of the lakes
t^iS/cm al 20T
-------
a
7.0
7.5
[Cal
Figure 11-17. pH and calcium concentrations in lakes in northern and northwestern Norway
sampled as part of the regional survey of 1975, in lakes in northwestern Norway sampled in
1977 (o) and in lakes in southernmost and southeastern Norway sampled in 1974 («).
Southern Norway receives highly acid precipitation (pH 4.2-4.5} and a large number of lakes
have lost their fish populations due to high acidity. Inset shows areas in which these lakes
are located. Areas south of isoline receive precipitation more acid than pH 4.6 (Henriksen, 1979).
! 11-42
-------
I
a
CURVE 2
0123
EXCESS S IN LAKE WATER. g/m2/vear
Figure 11-18, The pH value and sulfur loads in lake waters with extremely sensitive surroundings
(curve 1) and with slightly less sensitive surroundings (curve 2). (Load = concentration of
"excess" sulfur multiplied by the yearly runoff.) (Aimer et al., 1978).
11-43
-------
2 ?
0.3 g/m of sulfur in lake water each year. At 1 g/m of sulfur, the pH level of the lake
will probably decrease below 5.0.
Elevated metal concentrations (e.g., aluminum, zinc, manganese, and/or iron) in surface
waters are often associated with acidification (Beamish, 1976; Hutchinson et al., 1978; Scho-
field and Trojnar, 1980; Wright and Gjessing, 1976). Mobility of all these metals is in-
creased at low pH values (Stumm and Morgan, 1970). For example, an inverse correlation be-
tween aluminum concentration and pH level has been identified for lakes in the Adirondack
Region of New York State, southern Norway, the west coast of Sweden, and Scotland (Wright et
al. , 1980b). (Figure 11-19). Aluminum appears to be the primary element mobilized by strong
acid inputs in precipitation and dry deposition (Cronan, 1978).
Aluminum is the third most abundant element by weight in the earth's crust (Foster,
1971). In general, aluminum is extremely insoluble and retained within the edaphic environ-
ment. However, with increased hydrogen ion inputs (via acidic deposition or other sources)
into the edaphic environment, aluminum is rapidly mobilized. Cronan and Schofield (1979)
suggest that input of strong acids may inhibit the historical trend of aluminum accumulation
in the B soil horizon. Consequently, aluminum tends to be transported through the soil pro-
file and into streams and lakes. Evidence from field data (Schofield and Trojnar, 1980) and
laboratory experiments (Driscoll et al., 1979; Muniz and Leivestad, 1980) suggest that these
elevated aluminum levels may be toxic to fish. Concentration of aluminum may be as or more
important than pH levels as a factor leading to declining fish populations in acidified lakes.
Aluminum toxicity to aquatic biota other than fish has not been assessed.
Surface water chemistry, particularly in streams and rivers, may be highly variable with
time. Since many of the neutralization reactions in soils are kinetically slow, the quality
of the leachate from the edaphic system into the aquatic system varies with the retention time
of water in the soil (Johnson et al., 1969). The longer the contact period of water with
lower soil strata, the greater the neutralization of acid contribution from precipitation and
dry deposition. Therefore, during periods of heavy rainfall or snowmelt, and rapid water dis-
charge, pH levels in receiving waters may be relatively depressed.
Many of the regions currently affected by acidification experience freezing temperatures
during the winter and accumulation of a snowpack. In the Adirondack Region of New York ap-
proximately 55 percent of the annual precipitation occurs during the winter months (Schofield,
1976b). Much of the acid load deposited in winter accumulates in the snowpack, and may be
released during a relatively short time period during snowmelt in the spring. In addition, on
melting, 50 to 80 percent of the pollutant load (including hydrogen ion and sulfate) may be
released in the first 30 percent of the meltwater (Johannessen and Henriksen, 1978). As a
result, melting of the snowpack and ice cover can result in a large influx of acidic pollu-
tants into lakes and streams (Figure 11-20) (Gjessing et al., 1976; Hultberg, 1977; Schofield
and Trojnar, 1980). The rapid flux of this meltwater through the edaphic environment, and its
interaction with only upper soil horizons, limits neutralization of the acid content. As a
result, surface waters only moderately acidic during most of the year may experience extreme
11-44
-------
1000
~oi
=1 100
<
10
t
- I
\
SOUTH NORWAY 1974
^^~
ft
^~ • ft* •
— •* • *•« • •
«_«_ 9 ft
1
154 LAKES
•
ft •
•
.' *f "•*
•
9
I
1000
en
5 100
10
— | | _
SCOTLAND
72 LAKES
*.'."••
"': ' • " '• '.
V
9
1 1 '
1567845678
pH
1000
1 100
<
10
4
_ [
1 — "
WEST COAST SWEDEN
ft *
— ft
0
• ' 7
«
1
37 LAKES
—
^^^
1
5671
1000
5 100
10
t i
PH
' .- ' '
" ° ADIRONDACKS USA
134 LAKES
~~ %'*r{:;'*'. * •
• ..^.v
^^ *A*' • • " • ~~~
' " ..** . * • *
. • * •'•'' '
• ft • •
« •
• •
I .
15678
pH pH
Figure 11-19. Total dissolved Al as a function of pH level in lakes in acidified areas in Europe and
North America (Wright et al., 1980b).
11-45
-------
a
F
1976/77
M
Figure 11-20. pH levels in Little Moose Lake, Adirondack region of New York State, at a depth of 3
meters and at the lake outlet (adapted from Schofield and Trojnar, 1980).
11-46
-------
drops in pH level during the spring thaw. Basic cation concentrations (Ca, Mg, Na, K) may
also be lower during this time period (Johannessen et al., 1980). Similar but usually less
drastic pH drops in surface waters (particularly streams) may occur during extended periods of
heavy rainfall (Driscoll, 1980). These short term changes in water chemistry may have sig-
nificant impacts on aquatic biota.
11.3.1.2 Effects on Decomposition—The processing of dead organic matter (detritus) plays a
central role in the energetics of lake and stream ecosystems (Wetzel, 1975). The organic
matter may have been generated either internally (autochthonous) via photosynthesis within the
aquatic ecosystem or produced outside the lake or stream (allochthonous) and later exported to
the aquatic system. Detritus is an important food source for bacteria, fungi, some protozoa,
and other animals. These organisms through the utilization of detritus release energy, min-
erals and other compounds stored in the organic matter back into the environment. Initial
processing of coarse particulate detritus is often accomplished by benthic invertebrate fauna.
Among other things, the particles are physically broken down into smaller units, increasing
their surface area. Biochemical transformations of particulate and dissolved organic matter
occur via microbial metabolism and are fundamental to the dynamics of nutrient cycling and
energy flux within the aquatic ecosystem.
In general, the growth and reproduction of microorganisms is greatly affected by hydrogen
ion concentration (Rheinheimer, 1971). Many bacteria can grow only within the range pH 4-9
and the optimum for most aquatic bacteria is between pH 6.5 and 8.5. There are more acidi-
philic fungi than bacteria; consequently in acid waters and sediments the proportion of fungi
in the microflora is greater than in waters or sediments with neutral or slightly alkaline pH
levels. Most aquatic fungi require free oxygen for growth (Rheinheimer, 1971).
Numerous studies have indicated that acidification of surface waters results in a shift
in microbial species and a reduction in microbial activity and decomposition rates. It should
be noted, however, that microorganisms in general are highly adaptive. Given sufficient time,
a given species may adapt to acid conditions or an acid-tolerant species may invade and colo-
nize acidified surface waters. Therefore, some caution is necessary in interpreting short-
term experiments on the effects of acidification 'on microbial activity and decomposition. On
the other hand, increased accumulations of dead organic matter (as a result of decreased de-
composition rates) are commonly noted in acidic lakes and streams.
Abnormal accumulations of coarse organic matter have been observed on the bottoms of six
Swedish lakes. The pH levels in these lakes in July 1973 were approximately 4.4 to 5.4. Over
the last three to four decades, pH levels appear to have decreased 1.4 to 1.7 pH units (Grahn
et al., 1974). In both Sweden and Canada, acidified lakes have been treated with alkaline
substances to raise pH levels. One result of this treatment has been an acceleration of
organic decomposition processes and elimination of excess accumulations of detritus (Andersson
et al., 1975; Scheider et al. , 1975). Litterbags containing coarse particulate detrital
matter have been used to monitor decomposition rates in acidified lakes and streams. In
general, the rates of weight loss were reduced in acidic waters when compared with more
11-47
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neutral waters (Leivestad et al. , 1976; Traaen, 1980; Peterson, 1980). Traaen (1980) found
that after 12 months of incubation dried birch leaves or aspen sticks showed a weight loss of
50-80 percent in waters with pH levels 6 to 7 as compared to only a 30-50 percent weight loss
in waters with pH 4 to 5. Petersen (1980) likewise found reduced weight loss of leaf packs
incubated in an acidic stream when compared to leaf packs in either a stream not affected by
acidification or a stream neutralized with addition of lime. Petersen, however, found no
evidence of differences in microbial respiration between the streams. The acidic stream did
show a reduction in the invertebrate functional group that specializes in processing large
particles (shredders). Gahnstrb'm et al. (1980) found no significant differences in oxygen
consumption by sediments from acidified and non-acidified lakes. Rates of glucose decompo-
sition were also studied in lake sediment-water systems adapted to pH values from 3 to 9.
Glucose transformation increased at pH levels above 6. Lime treatment of acidic Lake Hb'gsjb'n
in Sweden also increased rates of glucose processing. However in a humic lake, the maximum
rate of glucose transformation occurred at the i_n situ value pH 5 (Gahnstrom et al., 1980).
Laboratory and field experiments involving decomposition rates have fairly consistently
found decreasing microbial activity with increasing acidity. Traaen (1980) found that litter
decomposition at pH level 5.2 was only 50 percent of that at pH 7.0 and at pH 3.5, only 30
percent that at pH 7.0. In addition, increasing acidity (pH 7.0 to 3.5) led to a shift from
bacterial to fungal dominance. Incubations of profundal lake sediments at pH 4, 5, and 6
indicated a significant reduction in community respiration with increasing acidity, as well as
a possible inhibition of nitrification and a lowering of sediment redox potentials. Bick and
Drews (1973) studied the decomposition of peptone in the laboratory. With decreasing pH,
total bacterial cell counts and numbers of species of ciliated protozoans decreased, decompo-
sition and nitrification were reduced and oxidation of ammonia ceased below pH 5. At pH 4 and
lower, the number of fungi increased.
Disruption of the detrital trophic structure and the resultant interference with nutrient
and energy cycling within the aquatic ecosystem may be one of the major consequences of acidi-
fication. Investigations into the effects of acidification on decomposition have, apparently,
produced somewhat inconsistent results. However, many of these apparent inconsistencies arise
only from a lack of complete understanding of the mechanisms relating acidity and rates of
decomposition. It is fairly clear that in acidic lakes and streams unusually large accumula-
tions of detritus occur, and these accumulations are related, directly or indirectly, to the
low pH level. The processing of organic matter has been reduced. In addition, this accumula-
tion of organic debris plus the development of extensive mats of filamentous algae on lake
bottoms (discussed in Section 11.3.1.3) may effectively seal off the mineral sediments from
interactions with the overlying water. As a result, regeneration of nutrient supplies to the
water column is reduced both by reduced processing and mineralization of dead organic matter
and by limiting sediment-water interactions. Primary productivity within the aquatic system
may be substantially reduced as a result of this process (Section 11.3.1.3). These ideas have
11-48
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been formulated into the hypothesis of "self-accelerating oligotrophication" by Grahn et al.
(1974).
11.3.1.3 Effect on Primary Producers and Primary Productivity—Organisms obtain their food
(energy) directly or indirectly from solar energy. Sunlight, carbon dioxide, and water are
used by primary producers (phytoplankton, other algae, mosses, and macrophytes) in the process
of photosynthesis to form sugars which are used by" the plants or stored as starch. The stored
energy may be used by the plants or pass through the food chain or web. Energy in any food
chain or web passes through several trophic levels. Each link in the food chain is termed a
trophic level. The major trophic levels are the primary producers, herbivores, carnivores,
and the decomposers. Energy in an ecosystem moves primarily along two main pathways: the
grazing food chain (primary producers-herbivores-carnivores) and the detrital food chain
(Billings, 1978; Odum, 1971; Smith, 1980). Interactions between these two food chains are,
however, extensive. Green plants convert solar energy to organic matter and, as such, are the
base for both food chains. The grazing food chain involves primarily living organic matter;
the detrital food chain, dead organic matter. Any changes as a result of acidification in the
green plants and primary production within the aquatic ecosystem may therefore have a profound
effect on all other organisms in the aquatic food web. As noted in Section 11.3.1.2, a por-
tion of the detrital food chain is supported by dead organic matter imported into the aquatic
system from external sources.
Extensive surveys of acidic lakes in Norway and Sweden (Aimer et al. , 1978; Leivestad
et al., 1976) have observed changes in species composition and reduced diversity of
phytoplankton correlated with decreasing lake pH level (Figure 11-21). Generally at normal pH
values of 6 to 8, lakes in the west coast region of Sweden contain 30 to 80 species of phy-
toplankton per 100-ml sample in mid-August. Lakes with pH below 5 were found to have only
about a dozen species. In some very acid lakes (pH<4), only three species were noted. The
greatest changes in species composition occurred in the pH interval 5-6. The most striking
change was the disappearance of many diatoms and blue-green algae. The families Chlorophyceae
(green algae) and Chrysophyceae (golden-brown algae) also had greatly reduced numbers of
species in acidic lakes (Figure 11-22). Dinofla'gellates constituted the bulk of the phyto-
plankton biomass in the most acidic lakes (Aimer et al., 1978). Similar phenomena were
observed in a regional survey of 55 lakes in southern Norway (Leivestad et al., 1976) and in a
study of nine lakes in Ontario (Stokes, 1980). Changes in species composition and reduced
diversity have also been noted in communities of attached algae (periphyton) (Aimer et al.,
1978; Leivestad et al. , 1976). Mougeotia, a green algae, often proliferates on substrates in
acidic streams and lakes.
Shifts in the types and numbers of species present may or may not affect the total levels
of primary productivity and algal biomass in acidic lakes. Species favored by acidic condi-
tions may or may not have comparable photosynthetic efficiencies or desirability as a prey
item for herbivores. On the other hand, decreased availability of nutrients in acidic
water as a result of reduced rates of decomposition (Section 11.3.1.2) may decrease primary
11-49
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80
70
M 60
UJ
O
a 50
00
u.
40
00
I I I I I I I
I I I I I I I
PHYTOPLANKTON SPECIES IN 60 LAKES
ON THE SWEDISH WEST COAST
AUGUST 1976
30
z
20
10
0
pH 4.1 4.3 4.5 4.7 4.9 5.1 5.3 5.5 5,7 5.9 6.1 6.3 6.5 6.7 6.9 7.1
NUMBER 11043243312103310020350541231011
OF LAKES
Figure 11-21. Numbers of phytoplankton species in 60 lakes having different pH values on the Swedish
West Coast, August 1976 (adapted from Aimer et al., 1978).
11-50
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pH 4.60-5.45
pH 6.25-7.70
BIOMASS
SPECIES
DIATOMEAE
\ CHLOROPHYCEAE
^t
CHRYSOPHYCEAE
CYANOPHYCEAE
PYRROPHYTA
SEPTEMBER 1972
Figure 11-22. Percentage distribution of phytoplankton species and their biomasses.
September 1972, west coast of Sweden. Biomass = living weight per unit area
(adapted from Aimer et al., 1978).
11-51
-------
productivity regardless of algal species involved. In field surveys and experiments, rela-
tionships between pH level and total algal biomass and/or productivity were not as consistent
as the relationship between pH and species diversity.
Kwiatkowski and Roff (1976) identified a significant linear relationship of decreasing
chlorophyll a concentrations (indicative of algal biomass) with declining pH level in six
lakes near Sudbury, Ontario, with a pH range of 4.05 to 7.15. In addition, primary productiv-
ity was reduced .in the two most acid lakes (pH 4-4.6). Stokes (1980) also reports a decrease
in total phytoplankton biomass with decreasing pH level for nine lakes in the same region of
Ontario. Crisman et al. (1980) reported a linear decrease in functional chlorophyll a
measurements with declining pH for 11 lakes in northern Florida, pH range 4.5 to 6.9. On the
other hand, Aimer et al. (1978) note that in 58 nutrient-poor lakes in the Swedish west coast
region, the largest mean phytoplankton biomass occurred in the most acid lakes (pH <4.5). Van
and Stokes (1978) concluded that they have no evidence that the phytoplankton biomass in Car-
lyle Lake, with a summer pH level about 5.1, is below that observed in circumneutral lakes in
the same region. In a continuing whole-lake acidification project (Schindler et al., 1980), a
lowering of the epilimnion pH level from 6.7-7.0 in 1976 to 5.7-5.9 in 1978 resulted in no
significant change in the chlorophyll concentration or primary production. Both j_n situ and
experimental acidification have resulted in large increases in periphyton populations (Hall et
al., 1980; Hendrey, 1976; Muller, 1980). Hendrey (1976) and Muller (1980) observed carbon,
uptake by periphyton incubated ui vitro. They found that, although the total rate of photo-
synthesis increased with decreasing pH level due to the larger biomass at the lower pH, the
photosynthesis per unit biomass decreased with pH.
From the above discussion it is obvious that not only is there no clear correlation be-
tween pH level and algal biomass or productivity, but the effects of acidification appear
inconsistent between systems. Again, these apparent inconsistencies probably reflect a lack
of knowledge about exact mechanisms relating acidification and lake metabolism, and also the
complexity of these mechanisms and interactions. Changes in the algal community biomass and
productivity probably reflect the balance between a number of potentially opposing factors;
those that tend to decrease productivity and biomass versus those that tend to increase pro-
ductivity and/or biomass when acidity increases. Factors working to decrease productivity and
biomass with declining pH levels may include: (1) a shift in pH level below that optimal for
algal growth, (2) decreased nutrient availability as a result of decreased decomposition rates
and a sealing-off of the mineral sediments from the lake water; and (3) decreased nutrient
availability as a result of changes in aquatic chemistry with acidification. For example,
despite the fact that the optional pH range for growth of label 1 aria flocculosa is between 5.0
to 5.3 (Cholonsky, 1968) or higher (Kallqvist et al. , 1975), this species dominated experi-
mentally acidified stream communities at pH level 4 in three out of five replicates (Hendrey
et al., 1980a). As noted in Section 11.3.1.1, aluminum concentrations increase with decreas-
ing pH level in acidified lakes and streams. Aluminum is also a very effective precipitator
of phosphorus, particularly in the pH range 5 to 6 (Dickson, 1978; Stumm and Morgan, 1970).
11-52
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In oligotrophic lakes, phosphorus is most commonly the limiting nutrient for primary pro-
ductivity (Schindler, 1975; Wetzel, 1975). Therefore, chemical interactions between aluminum
and phosphorus may result in a decreasing availability of phosphorus with decreasing pH level,
and, as a result, decreased primary production.
Factors working to increase productivity and/or biomass with acidification of a lake or
stream may include: (1) decreased loss of algal biomass to herbivores; (2) increased lake
transparency; and (3) increased nutrient availability resulting from nutrient enrichment of
precipitation. Decreased population of invertebrates (as discussed in Section 7.3.1.4),
particularly herbivorous invertebrates, may decrease grazing pressure on algae and result in
unusual accumulations of biomass. Hendrey (1976) and Hall et al. (1980) include this
mechanism as one hypothesis to explain their observation of increased biomass of periphyton at
pH level 4 despite a decreased production rate per unit biomass.
Increases in lake transparency over time have been correlated with lake acidification in
Sweden (Aimer et al., 1978) and the Adirondack Region of New York (Schofield, 1976c). In
addition, after the second year of experimental lake acidification (pH 6.7-7.0 to 5.7-5.9) in
northwestern Ontario (Schindler et al., 1980), lake transparency increased by 1-2 m. These
increases in transparency have not been correlated with decreases in phytoplankton biomass.
Two mechanisms have been proposed. Aluminum acts as a very efficient precipitator for humic
substances. Dickson (1978) found that humic substances are readily precipitated in the pH
range 4.0 to 5.0. Dickson (1978) and Aimer et al. (1978) suggest that increases in aluminum
levels with lake acidification (Section 11.3.1.1) have resulted in increased precipitation of
humics from the water column and therefore increased lake transparency. Aimer et al. (1978)
provide data for one lake on the west coast of Sweden. The pH level declined from above 6 to
about 4.5 between 1940 and 1975. The secchi disc reading increased from about 3m to about 10m
over the same period. Organic matter in the water (as estimated by KMnO. demand) decreased
from 24 to 8 mg/liter from 1958 to 1973. Schindler et al. (1980) on the other hand, found no
change in levels of dissolved organic carbon with acidification. Instead, changes in hydro-
lysis of organic matter with declining pH level may affect the light absorbancy characteris-
tics of the molecules. Levels of particulate organic carbon, and changes with pH level, were
not reported by Schindler et al. (1980). >
Acidification of precipitation (and dry deposition) has been accompanied by increases in
levels of sulfate and nitrate. Both of these are nutrients required by plants. However, as
noted above, the primary nutrient limiting primary productivity in most oligotrophic lakes is
phosphorus. Aimer et al. (1978) report that atmospheric deposition rates of phosphorus have
also increased in recent years. The world-wide extent of the correlation between acidic
deposition and increased atmospheric phosphorus loading, however, is not known. It is expect-
ed that changes in atmospheric phosphorus loading would be much more localized than changes in
acidic deposition. It is possible that in some areas increased atmospheric loading of phos-
phorus has occurred in recent years coincidently with increased acidic deposition. Increased
phosphorus nutrient loading into lakes may then increase primary production rates.
11-53
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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 (1977) reported that
in five to six lakes studies in the last three to five decades the macrophyte communities
dominated by Lobelia and Isoetes have regressed, whereas communities dominated by Sphagnum
mosses have expanded. Acidity levels in these lakes apparently have increased approximately
1.3 to 1.7 pH units since the 1930-40's. In acid lakes where conditions are suitable the
Sphagnum peat moss may cover more than 50 percent of the bottom above the 4-m depth, and may
also grow at much lower depths (Aimer et al., 1978). The Sphagnum invasion may start at lake
pH levels just below 6 (Aimer et al., 1978). Similar growths of Sphagnum occur in Norwegian
lakes (Galloway, 1978). Increases in Sphagnum as a benthic macrophyte have been documented
from one lake in the Adirondack Region of New York (Hendrey and Vertucci, 1980).
Under acid conditions the Sphagnum moss appears to simply outgrow flowering plant aquatic
macrophytes. In laboratory tests, the growth and productivity of the rooted macrophyte
Lobelia was reduced by 75 percent at a pH of 4, compared with the control (pH 4.3-5.5). The
period of flowering was delayed by ten days at the low pH (Laake, 1976). At low pH levels
(pH<5), essentially all the available inorganic carbon is in the form of carbon dioxide or
carbonic acid (Stumm and Morgan, 1970). As a result, conditions may be more favorable for
Sphagnum, an acidophile that is not able to utilize the carbonate ion.
Besides the shift in macrophyte species, the invasion of Sphagnum into acid lakes may
have four other impacts on the aquatic ecosystem. Sphagnum has a very high ion-exchange
capacity, withdrawing basic cations such as Ca from solution and releasing H (Aimer et al.,
1978; Anschutz and Gessner, 1954). As a result, the presence of Sphagnum may intensify the
acidification of the system and decrease the availability of basic cations from other biota.
Second, dense growths of Sphagnum form a biotype that is an unsuitable substratum for many
benthic invertebrates (Grahn, 1977). Growths of Sphagnum in acidic lakes are also often
associated with felts of white mosses (benthic filamentous algae) and accumulations of
non-decomposed organic matter. In combination, these organisms and organic matter may form a
very effective seal. Interactions between the water column and the mineral sediments, and the
potential for recycling of nutrients from the sediments back into the water body, may be
reduced (Grahn, 1977; Grahn et al., 1974). These soft bottoms may also be colonized by other
macrophytes. In Sweden, Aimer et al. (1978) report that growths of Juncus, Sparaganium,
Utricularia, Nuphar, and/or Nymphaea, in addition to Sphagnum, may be extensive in acidic
lakes. Thus primary production by macrophytes in lakes with suitable bottoms may be very
11-54
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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 zoo-
plankton) as a result of fish predation or other reasons often results in the prevalence of
small-bodied species (Lynch, 1979). . Surveys of acidic lake waters often have shown the domi-
nance of small-bodied herbivores in the zooplankton community (Hendrey et al. , 1980a). Fish
also often are absent at these pH levels (Section 11.3.1.5). Different zooplankton species
may have different physiological tolerances to depressed pH levels (e.g., Potts and Frye,
1979). Food supplies, feeding habits, and grazing of zooplankton may also be altered with
acidification as a consequence of changes in phytoplankton species composition and/or de-
creases in biomass or productivity of phytoplankton. Zooplankton also rely on bacteria and
detrital organic matter for part of their food supply. Thus an inhibition of the microbiota
or a reduction in microbial decomposition (Section 11.3.1.2) may also affect zooplankton
populations. "These alternate mechanisms postulate for changes in community structure and/or
production of/zooplankton communities probably play an important role in zooplankton responses
to acidification.
Synoptic and intensive studies of lakes and streams have also demonstrated that numbers
of species of benthic invertebrates are reduced along a gradient of decreasing pH level (Aimer
et al., 1978; Conroy et al. , 1976; Leivestad et al. , 1976; Roff and Kwiatkowski, 1977;
Sutcliffe and Carrick, 1973). In 1500 freshwater localities in Norway studied from 1953-73,
snails were generally present only in lakes with pH levels above 6 (0kland, 1980). Likewise
Gammarus Lacustris, a freshwater shrimp and an important element in the diet of fish in
Scandinavia, was not found at pH levels below 6.0 (0kland, 1980). Experimental investigations
11-55
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C/J
LLJ
0.
" -,
LL 3
O
cc
Ul
00
D
Z _
4.0-4.49 4.5-4.99 5.0-5.49 5.5-5.99 6.0-6.49
2 ' 9 16 7 11
>6.5 pH INTERVAL
12 NUMBER OF LAKES
Figure 11-23. The number of species of crustacean zooplankton observed in 57 lakes during a
synoptic survey of lakes in southern Norway (Leivestad et al., 1976).
11-56
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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
particularly sensitive to low pH levels and their populations were reduced in headwater
streams of the Hubbard Brook watershed in New Hampshire. In laboratory studies, Bell (1971),
Bell and Nebecker (1969), and Raddum (1978) measured the tolerance of some stream macroinver-
tebrates to low pH levels. Tolerance seems to be in the order caddisflies > stoneflies > may-
flies (Hendrey et al., 1980a).
2 2
Leivestad et al. (1976) reported on decreased standing crops (numbers/m and g/m ) of
benthic invertebrates in two lakes with pH levels near 4.5 as compared to five lakes with pH
near 6.0. Chironamids were the dominant group in all lakes. No fish were found in the acid
lakes. Lack of predation by fish should favor increases in benthic biomass, the opposite of
that observed. Hendrey et al. (1980a), on the other hand, from data from eight Ontario lakes
(pH 4.3 - < 5.7) reported no reduction in abundance of benthos related to pH level.
Air-breathing aquatic insects (e.g., backswimmers, water boatmen, water striders) appear
very tolerant of acidic environments. Population densities are often greater in acidic lakes
and in the most acid lakes than in circumneutral lakes. Abundance of these large inverte-
brates may be related to reduced fish predation (Hendrey et al. , 1980a).
Hall et al. (1980) experimentally acidified a stream to pH 4 and monitored reactions of
macroinvertebrate populations. Initially following acidification there was a 13-fold increase
in downstream drift of insect larvae. Organisms in the collector and scraper functional
groups were affected more than predators. Benthic samples from the acidified zone of Norris
Brook contained 75 percent fewer individuals than those for reference areas. There was also a
37 percent reduction in insect emergence; members of the collector group were most affected.
Insects seem to be particularly sensitive at emergence (Bell, 1971). Many species of aquatic
insects emerge early in the spring through cracks in the ice and snow cover. These
early-emerging insects are therefore exposed in m'any cases to the extremely acidic conditions
associated with snowmelt (Hagen and Langeland, 1973).
Low pH also appeared to prevent permanent colonization by a number of invertebrate
species, primarily herbivores, in acidified reaches of River Dudden, England (Sutcliffe and
Carrick, 1973). Ephemeroptera, trichoptera, Ancylus (Gastropoda) and Gammarus were absent in
these reaches.
Damage to invertebrate communities may influence other components of the food chain.
Observations that herbivorous invertebrates are especially reduced in acidic streams, as
reported in Norris Brook and River Dudden, support the hypothesis (Hall et al., 1980; Hendrey,
1976) that changes in invertebrate populations may be responsible for increased periphytic
11-57
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algal accumulations in acidic streams and benthic regions of acidic lakes (Hendrey et al.,
196iOa). Benthic invertebrates also assist with the essential function of processing dead
organic matter. Petersen (1980) noted that decomposition of coarse particulate organic matter
in leaf packs was lower in an acidic stream than in two streams with circumneutral pH levels.
The invertebrate community also showed a reduction in the invertebrate functional group that
specializes in processing large particles (shredders). In unstressed aquatic ecosystems, a
continuous emergence of different insect species is available to predators from spring to
autumn. In acid-stressed lakes or streams, the variety and numbers of prey may be reduced.
Periods may be expected to occur in which the amount of prey available to fish (or other
predators) is diminished.
11.3.1.5 Effects on Fish—Acidification of surface waters has had its most obvious, and per-
haps the most severe, impact on fish populations. Increasing acidity has resulted not just in
changes in species composition or decreases in biomass but in many cases in total elimination
of populations of fish from a given lake or stream. Extensive depletion of fish stocks has
occurred in large regions of Norway, Sweden, and parts of eastern North America. Both commer-
cial and sport fisheries have been affected in these areas. However, precise assessments of
losses—in terms of population extinctions, reductions in yields, or economic and social
impacts—either have not been attempted or are still in the process of evaluation. Potential
damage to fish populations inhabiting other acid-sensitive aquatic ecosystems in New England,
the Appalachians, and parts of southeastern, north central, and northwestern United States
have not yet been assessed (Galloway, 1978).
Declines in fish populations have been related to acidification of surface waters in the
Adirondack Region of New York State (Schofield, 1976a), southern Norway (Jensen and Snekvik,
1972; Wright and Snekvik, 1978), southwestern Sweden (Aimer et al., 1974), the LaCloche Moun-
tain Region in southern Ontario (Beamish and Harvey, 1972), and southwestern Scotland (Wright
et al., 1980a). Schofield (1976a, 1976d) estimated that in 1975 fish populations in 75 per-
cent of Adirondack lakes at high elevation (<610 m) had been adversely affected by acidifica-
tion. Fifty-one percent of the lakes had pH values less than 5, and 90 percent of these lakes
were devoid of fish life (Figure 11-24). Comparable data for the period 1929 to 1937 indi-
cated that during that time only about 4 percent of these lakes had pH values below 5 and were
devoid of fish (Figure 11-25). Therefore, entire fish communities consisting of brook trout
( Salvelinus fontinalis), lake trout (Salvelinus namaycush), white sucker ( Catostomus
commersoni), brown bullhead (Icaturus nebulosus) and several cyprinid species were apparently
eliminated over a period of 40 years. This decrease in fish populations was associated with a
decline in lake pH level. A survey of more than 2000 lakes in southern Norway, begun in 1971,
found that about one third of these lakes had lost their fish population (primarily brown
trout, Sal mo trutta L.) since the 1940's (Wright and Snekvik, 1978). Fish population status
was inversely related to lake pH level (Leivestad et al., 1976). Declines in salmon popula-
tions in southern Norwegian rivers were reported as early as the 1920's. Catch of Atlantic
11-58
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20
e/5
O
cc
m 10
NO FISH PRESENT
FISH PRESENT
PH
Figure 11-24. Frequency distribution of pH and fish population status in Adirondack Mountain
lakes greater than 610 meters elevation. Fish population status determined by survey gill netting
during the summer of 1975.
Source: Schofield (1976a).
11-59
-------
20
10
o
CC
UJ
m
2
D
Z
10
1975
NO FISH PRESENT
FISH PRESENT
1930s
i-n
6
PH
Figure 11-25. Frequency distribution of pH and fish pop-
ulation status in 40 Adirondack lakes greater than 610 meters
elevation, surveyed during the period 1929-1937 and again in
1975.
Source: Schofield (1976a).
11-60
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salmon (Sal mo salar, L.) in nine acidified southern Norwegian rivers is now virtually zero
(Figure 11-26). In northern and western rivers not affected by acidification, no distinct
downward trend in catch has occurred (Jensen and Snekvik, 1972; Leivestad et al. , 1976; Wright
et al., 1976). Similar changes have been observed in Sweden (Aimer et al., 1974) where it is
estimated that 10,000 lakes have been acidified to a pH less than 6.0 and 5,000 below a pH of
5.0 (Dickson, 1975). Populations of lake trout, lake herring (Coregonus artedii), white
suckers, and other species disappeared rapidly during the 1960's from a group of remote lakes
in the LaCloche Mountain Region of Ontario (Beamish et al., 1975).
It is difficult to determine at what pH level fish species disappear from lakes. Disap-
pearance of the fish is usually not due to massive fish kills, but is the result of a gradual
depletion of the population following reproductive failures (Leivestad et al. , 1976). Field
surveys in Scandinav.ia and eastern North America (Aimer et al., 1974; Schofield, 1976a, 1976b,
1976c; Wright and Snekvik, 1978) suggest that many species do not occur in lakes with pH
values below 5.0.
c-jp •
,«.,;'However, large spatial and temporal functions in pH, and the possibility for "refuge
areas" from acidic conditions during critical periods make it extremely difficult to general-
ize about effects of acidification on fish populations based on grab samples or annual mean pH
levels. The pH levels identified in the literature as critical for reproduction of a species
or correlated with the absence of a species in lake surveys are summarized in Table 11-5.
Values range from pH 4.4 to over 6.0, and are highly species dependent.
Recent field and laboratory studies (Baker and Schofield, 1980; Dickson, 1978; Driscoll
et al., 1979; Muniz and Leivestad, 1980; Schofield and Trojnar, 1980) .have indicated that
aluminum levels in acidic surface waters (Section 11.3.1.1, Figure 11-19) may be highly toxic
to fish (and perhaps other biota). Schofield and"Trojnar (1980) analyzed survival of brook
trout stocked into 53 Adirondack lakes as a function of 12 water quality parameters. Levels
of pH, calcium, magnesium, and aluminum were significantly different between the two groups of
lakes, with and without trout survival. However, after accounting for the effects of aluminum
concentrations on differences between the two groups of lakes, differences in calcium, magne-
sium, and pH levels were no longer significant. Aluminum, therefore, appears to be the
primary chemical factor controlling survival of trout in these lakes. Likewise, in laboratory
experiments with natural Adirondack waters and synthetic acidified aluminum solutions, levels
of aluminum, and not the pH level per ^e_, determined survival and growth of fry of brook trout
and white suckers (Baker and Schofield, 1980). In addition, speciation of aluminum had a sub-
stantial effect on aluminum toxicity. Complexation of aluminum with organic chelates elimin-
ated aluminum toxicity to fry (Baker and Schofield, 1980; Driscoll et al., 1979). As a
result, waters high in organic carbon, e.g., acidic bog lakes, may be less toxic to fish than
surface waters at similar pH levels but with lower levels of dissolved organic carbon.
11-61
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STAVANGER
RIVER TOVDAL
RIVER OALALVEN
'«.
300
250
v>
O 1 200
150
I I 1
1900
1920
1940
1960
1980
v>
30
20
10
1900
i I r
7 ACID RIVERS
1920
1940
1960
1980
Figure 11-26. Norwegian salmon fishery statistics for 68 unacidified and 7 acidified
rivers (adapted from Aimer et al., 1978).
11-62
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TABLE 11-5. pH LEVELS IDENTIFIED IN FIELD SURVEYS AS
CRITICAL TO LONG-TERM SURVIVAL OF FISH POPULATIONS
Family
Salmom'dae
Species
Brook trout (Salvelinus
fontinalis)
Lake trout (Salvelinus
namaycush)
Critical pH
5.0
5.1
5.2-5.5
Reference
Schofield, 1976c
Schofield, 1976c
Beamish, 1976
Brown trout (Salmo trutta)
Arctic char (Salvel inus alpinus)
5.0
5.2
Aimer et al., 1978
Aimer et al., 1978
Percidae
Catostomidae
Ictaluridae
Cyprinidae
Centrarchidae
Esocidae
Perch (Perca fluviatilis)
Yellow perch (Perca flayescens)
Walleye (Stigostedion vitreum)
White sucker (Catostomus
commersoni)
Brown bullhead (Icaturus
nebulosus)
Minnow (Phoxinus phoxinus)
Roach (Rutilus Rutilus)
Lake chub (Couesius plumbeus)
Creekchub (Semotilus atromaculatus)
Commonshi ner (Notfopis cornutas)
Goldenshiner (Notemigonus
crysoleucas)
Smallmouth bass (Micropterus
dolomieui)
Rock bass (Ambloplites rupestris)
Pike (Esox lucius)
4.4-4.9
4.5-4.7
5.5-6.0+
4.7-5.2
5.1
4.7-5.2
5.0
5.5
5.5
4.5-4.7
5.0
5.5
4.9
5.5-6.0+
4.7-5.2
4.4-4.9
Aimer et al . , 1978
Beamish, 1976
Beamish, 1976
Beamish, 1976
Schofield, 1976c
Beamish, 1976
Schofield, 1976c
Aimer et al. , 1978
Aimer et al . , 1978
Beamish, 1976
Schofield, 1976c
Schofield, 1976c
Schofield, 1976c
Beamish, 1976
Beamish, 1976
Aimer et al. , 1978
Inorganic aluminum levels, and not low pH levels, may therefore be a primary factor
leading to declining fish populations in acidified lakes and streams. However, many labora-
tory or i_n situ field experiments have been conducted on the effects of pH on fish without
taking into account aluminum or other metal concentrations in naturally acidic waters. As a
result, many of the conclusions based on these experiments regarding pH levels critical for
fish survival are suspect. Therefore these experiments will not be reviewed here.
Sensitivity of fish and other biota to low pH levels has also been shown to depend on
aqueous calcium levels (Bua and Snekvik, 1972; Trojnar, 1977; Wright and Snekvik, 1978). In
southern Norway, the mean calcium level in lakes studied was approximately 1.1 mg/liter, as
compared to about 3 mg/liter in the LaCloche Mountain Region (Table 11-4) or 2.1 mg/liter in
11-63
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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 al. , 1980; Wright
and Snekvik, 1978). Field observations (Aimer et al., 1974; Beamish, 1974; Jensen and
Snekvik, 1972; Schofield, 1976a) indicate changes in population structure over time with
acidification. Declining fish populations consist primarily of older and larger fish with a
decrease in total population density. Recruitment failure may result from inhibition of adult
fish spawning and/or increased mortality of eggs and larvae. Effects on spawning and de-
creased egg deposition may be associated with disrupted spawning behavior and/or effects of
acidification on reproductive physiology in maturing adults (Lockhart and Lutz, 1977). Field
observations by Beamish et al., (1975) related reproductive failure in white suckers to an
inability of females to release their eggs. On the other hand, Amundsen and Lunder (1974)
observed total mortality of naturally spawned trout eggs in an acid brook a few weeks after
spawning. A summary of Norwegian studies (Leivestad et al., 1976) concluded that egg and fry
mortality is the main cause of fish reproduction failure. Spawning periods and occurrence of
early life history stages for many fish species coincide with periods of extreme acidity,
particularly during and immediately after snowmelt in the spring.
In some lakes, fish population decreases are associated with a lack of older fish
(Rosseland et al. , 1980). In Lake Tveitvatn on the Tovdal River in southern Norway, brown
trout mortality apparently occurs primarily after the first spawning. Since 1976, no fish
past spawning age have been found and population density has decreased steadily (Rosseland
et al., 1980). Fish kills of adult salmon in rivers in southern Norway have been recorded as
early as 1911 (Leivestad et al., 1976).
When evaluating the potential effects of acidification on fish, or other biotic, popula-
tions, it is very important to keep in mind the highly diversified nature of aquatic systems
spatially, seasonally, and year-to-year. As a result of this diversity, it is necessary to
evaluate each system independently in assessing the reaction of the population to acidifica-
tion. Survival of a fish population may depend more on the availability of refuge areas from
acid conditions during spring melt or of one tributary predominantly fed by baseflow and
supplying an adequate area for spawning than on mean annual pH, calcium, or inorganic aluminum
levels.
11.3.1.6 Effects on Vertebrates Other Than Fish—Certain species of amphibians may be the
vertebrate animals, other than fish, most immediately and directly affected by acidic deposi-
tion (Rough and Wilson, 1977). Their vulnerability is due to their reproductive habits. In
temperate regions, most species of frogs and toads, and approximately half of the terrestrial
salamanders, lay eggs in ponds. Many of these species breed in temporary pools formed each
year by accumulation of rain and melted snow. Approximately 50 percent of the species of toads
11-64
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and frogs in the United States regularly breed in ephemeral pools; about one-third of the sal-
amander species that have aquatic eggs and larvae and terrestrial adults breed in temporary
pools. Most of these pools are small and collect drainage from a limited area. As a result,
the acidity of the eater in these pools is strongly influenced by the pH of the precipitation
that fills them. Ephemeral pools are usually more acidic than adjacent permanent bodies of
water. Rough and Wilson (1977) report that in 1975, in the vicinity of Ithaca, N.Y. , the
average pH of 12 temporary ponds was 4.5 (range 3.5 to 7.0), while the average pH of six per-
manent ponds was 6.1 (range 5.5 to 7.0). Amphibian eggs and larvae in temporary pools are ex-
posed to these acidic conditions.
Rough and Wilson (1977) and Rough (1976) studied the effect of pH level on embryonic de-
velopment of two common species of salamanders: the spotted salamander (Ambystoma maculatum)
and the Jefferson salamander (A. jeffersonianum). In laboratory experiments, embryos of the
spotted salamander tolerated pH levels from 6 to 10 but had greatest hatching success at pH 7
to 9. The Jefferson salamander tolerated pH levels 4 to 8 and was most successful at 5 to 6.
Mortality of embryos rose abruptly beyond the tolerance limits. In a four-year study of a
large breeding pond (pH 5.0-6.5) 938 adult spotted salamanders produced 486 metamorphosed
juveniles (0.52 juveniles/adult), while 686 adult Jefferson salamanders produced 2157 juvenile
(3.14 juveniles/adult). Based on these findings, Rough and Wilson (1977) predict that con-
tinued acidic deposition may result in substantial shift in salamander and other amphibian
populations.
Gosner and Black (1957) report that only acid-tolerant species of amphibians can breed in
the acid (pH 3.6 to 5.2) sphagnoceous bogs in the New Jersey Pine Barrens.
Frog populations in Tranevatten, a lake near Gothenberg, Sweden, acidified by acidic pre-
cipitation, have also been investigated (Hagstrom, 1977; Hendrey, 1978). The lake has pH
levels ranging from 4.0 to 4.5. All fish have disappeared, and frogs belonging to the species
Rana temporaria and Bufo bufo are being elimated. At the time of the study (1977) only adult
frogs eight to ten years old were found. Many egg masses of Rana temporaria were observed in
1974, but few were found in 1977, and the few larvae (tadpoles) observed at that time died.
Frogs and salamanders are important predators on invertebrates, such as mosquitoes and
other pest species, in pools, puddles, and lakes. They also are themselves important prey for
higher tropic levels in an ecosystem. In many habitats salamanders are the most abundant ver-
tebrates. In a New Hampshire forest, for example, salamanders were found to exceed birds and
mammals in both numbers and biomass (Hanken et al., 1980).
The elimination of fish and vegetation from lakes by acidification may have an indirect
effect on a variety of vertebrates: species of fish-eating birds (e.g., the bald eagle, loon,
and osprey), fish-eating mammals (e.g., mink and otter), and dabbling ducks which feed on
aquatic vegetation. In fact, any animal that depends on aquatic organisms (plant or animal)
for a portion of its food may be affected.
11-65
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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. C02 produced by plant roots and micro-organisms;
3. oxidation of NH4+ and S, FeS2> and H2$ to HN03 and H2S04;
4. very acid litter in coniferous forests, the main acidifying
source for the A and B horizons;
5. atmospheric deposition of H-SO, and some HNO,, N0x, HC1 and
NH4+ (after nitrification to HN03).
In addition to the acidifying factors listed above, the use of ammonium fertilizers on culti-
vated lands increases the hydrogen cations in the water solution. Ammonium fertilizers are
oxidized by bacteria to form nitrate (NO^ ) and hydrogen ions (H ) (Donahue et al., 1977).
Increased leaching causes soils to become lower in basic Ca , Mg , Na , and K cations
(Donahue et al., 1977). Sensitivity to leaching is according to the following sequence: Na
» K+ > Mg2+ > Ca2+ (Wiklander, 1979).
Norton (1977) cited the potential effects of acidic deposition on soils that are listed
in Table 11-6. Of those listed, only the increased mobility of cations and their accelerated
loss has been observed in field experiments. Overrein (1972) observed an increase in calcium
leaching under simulated acid rain conditions and increased loss by leaching of Ca , Mg ,
11-66
-------
SOIL PARTICLES
ACID RAIN
SOIL SOLUTION
~
-
WEATHERING— ».
-
•*•
*
+
Ca24
K*
Na*— T
NH;
SO2"
H3por
Ca24
Mg24
"H* K4
Na*
NOJ
so,2-
fc
V J
CAN BE LEACHE
Figure 11-27. Showing the exchangeable ions
of a soil with pH 7, the soil solution com-
position, and the replacement of Na+ by H+
from acid rain (Wiklander, 1979).
11-67
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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.
2~
Acidic precipitation increases the amounts of S04 and N03 entering the soils. Nitrate
is easily leached from soil; however, because it is usually deficient in the soil for both
plants and soil microorganisms, it is rapidly taken up and retained within the soil-plant
system (Abrahamsen et al., 1976; Abrahamsen and Dollard, 1979; Gjessing et al. , 1976). The
fate of sulfate is determined by its mobility. Retention of sulfate in soils appears to depend
on the amount of hydrous oxides of iron and aluminum present. The amounts of these compounds
present varies with the soil type. Insignificant amounts of the hydrated oxides of iron (Fe)
and aluminum (Al) are found in organic soils; therefore, sulfate retention is low (Abrahamsen
and Dollard, 1979). The presence of hydrated oxides of iron and aluminum, however, is only
11-68
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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
leaching was in the following order: Cl~ ~ N03" < S042 < H2P04" (Wiklander, 1980). Additions
of sulfuric acid to a soil will have no effect on cation leaching unless the sulfate is
mobile, as cations cannot leach without associated anions (Johnson et al., 1980; Johnson,
1980; Johnson and Cole, 1980).
Leaching of soil nutrients is efficiently inhibited by vegetation growing on it. Plant
roots take up the nutrients frequently in larger amounts than required by the plants. Large
amounts of these nutrients will later be deposited on the soil surface as litter or as leach-
ate from the vegetation canopy (Abrahamsen and Dollard, 1979).
In lysimeter experiments in Norway, plots with vegetation cover were used. One plot had
a dense layer of the grass, Deschampsia flexuosa (L.) Trin. and the other a less dense cover.
The soil retained 50 percent of the SO. added to it. The greatest amount was retained in
the lysimeters covered with grass; the relative retention increased with increasing additions
of sulfate (Abrahamsen and Dollard, 1979). Leaching of cations from the soil was reduced by
2- 2+ 2+
the retention of the SO, ; however, leaching of Ca and Mg increased significantly as the
acidity of the simulated rain increased. In the most acid treatment leaching of Al was highly
significant. The behavior of K , NO., , and NH. was different in the two lysimeter series.
These ions were retained in the grass-covered lysimeters whereas there was a net leaching of
K and NO, in the other series. Statistically significant effects were obtained only when
the pH of the simulated rain was 3.0 or lower (Abrahamsen and Dollard, 1979).
The Scandinavian lysimeter experiments appear to demonstrate that the relative rate of
adsorption of sulphate increases as the amounts applied are increased. In the control
lysimeters the output/input ratio was approximately one. These1 results are in agreement with
results of watershed studies which frequently appear to demonstrate that, on an annual basis,
sulfate outflow is equal to or greater than the amounts being added (Abrahamsen and Dollard,
1979; Gjessing et al. , 1976). Increased outflow'may be attributed to dry deposition and the
weathering of sulfur-bearing rocks. The increased deposition of sulfate via acidic precipita-
tion appears to have increased the leaching of sulfate from the soil. Together with the
retention of hydrogen ions in the soil this results in an increased leaching of the nutrient
cations K+, Ca +, Mg +, Mn (Abrahamsen and Dollard, 1979). Shriner and Henderson, (1978)
however, in their study of sulfur distribution and cycling in the Walker Branch Watershed in
eastern Tennessee noted the additions of sulfate sulfur by precipitation were greater than the
amount lost in stream flow. Analysis of the biomass and soil concentrations of sulfur indi-
cated that sulfur was being retained in the mineral soil horizon. It is suggested that leach-
ing from organic soil horizons may be the mechanism by which sulfur is transferred to the
mineral horizon. Indirect evidence suggests that vegetation scavenging of atmospheric sulfate
11-69
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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).
McFee et al. (1977) calculated that 1000 cm of rainfall at pH 4.0 could reduce the base
saturation of the upper 6 cm of a midwestern United States forest soil by 15 percent and lower
the pH of the A-l horizon (the surface layer in most agricultural soils) by 0.5 units if no
countering forces are operating in the soil. They note, however, that many counteracting
forces could reduce the final effect of acidic precipitation, including the release of new
cations to exchange sites by weathering and nutrient recycling by vegetation.
Lowered soil pH also influences the availability and toxicity of metals to plants. In
general, potentially toxic metals become more available as pH decreases. Ulrich (1975)
reported that aluminum released by acidified soils could be phytotoxic if acid rain continued
for a long period. The degree of ion leaching increased with decreases in pH, but the amount
of cations leached was far less than the amount of acid added (Malmer, 1976). Baker et al.
(1977) found that sulfur dioxide in precipitation increased the extractable acidity and alumi-
num, and decreased the exchangeable bases, especially calcium and magnesium. Although dilute
sulfuric acid in sandy podsolic soils caused a significantly decreased pH of the leached
material, the amount of acid applied (not more than twice the yearly airborne supply over
southern Scandinavia) did not acidify soil as much as did nitrate fertilizer (Tamm et al.,
1977). Highly acidic rainfall, frequently with a pH less than 3.0, in combination with heavy
metal particulate fallout from smelters, has caused soils to become toxic to seedling survival
and establishment according to observations by Hutchinson and Whitby (1977). Very low soil
pH's are associated with mobility of toxic aluminum compounds in the soils. High acidity,
high sulfur, and heavy metals in the rainfall have caused fundamental changes in the structure
of soil organic matter. The sulfate and heavy metals were borne by air from the smelters in
the Sudbury area of Ontario and brought to earth by dry and wet deposition. Among the metals
11-70
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deposited in rainfall and dustfall were nickel, copper, cobalt, iron, zinc, and lead. Most of
these metals are retained in the upper layers of soil, except in very acid or sandy soils.
The accumulation of metals is mainly an exchange phenomenon. Organic components of
litter, humus, and soil may bind heavy metals as stable complexes (Tyler, 1972). The heavy
metals when bound may interfere with litter decay and nutrient cycling, and in this manner
interfere with ecosystem functioning (Tyler, 1972). Acidic precipitation, by altering the
equilibria of the metal complexes through mobilization, may have a negative effect upon the
residence time of the heavy metals in soil and litter (Tyler, 1972, 1977).
Biological processes in the soil necessary for plant growth can be affected by soil
acidification. Nitrogen fixation, decomposition of organic material, and mineralization,
especially of nitrogen, phosphorus and sulfur, might be affected (Abrahamsen and Dollard,
1979; Alexander, 1980; Malmer, 1976; Tamm et al. , 1977). Nearly all of the nitrogen, most of
the phosphorus and sulfur as well as other nutrient elements in the soil are bound in organic
combination. In this form, the elements are largely or entirely unavailable for utilization by
higher plants (Alexander, 1980). It is principally through the activity of heterotrophic
microorganisms that nitrogen, phosphorus, and sulfur are made available to the autotrophic
higher plants. Thus, the microbial processes that -lead to the conversion of the organic forms
of these elements to the inorganic state are crucial for maintaining plant life in natural or
agricultural ecosystems. The key role of these degradative processes is the fact that
nitrogen is limiting for food production in much of the world and governs primary productivity
in many terrestrial habitats (Alexander, 1980).
Many, and probably most, microbial transformations in soil may be brought about by
several species. Therefore, the reduction or elimination of one population is not necessarily
detrimental since a second population, not affected by the stress, may fill the partially or
totally vacated niche. For example, the conversion of organic nitrogen compounds to inorganic
forms is characteristically catalyzed by a number of species, often quite dissimilar, and a
physical or chemical perturbation affecting one of the species may not seriously alter the
rate of the conversion. On the other hand, there are a few processes that are in fact carried
out, so far as it is now known, by only a single species, and elimination of that species
could have serious consequences. Examples of this are the nitrification process, in which
ammonium is converted to nitrate, and the nodulation of leguminous plants, for which the
bacteria are reasonably specific according to the leguminous host (Alexander, 1980).
The nitrification process is one of the best indicators of pH stress because the respon-
sible organisms, presumably largely autotrophic bacteria, are sensitive both in culture and in
nature to increasing acidity (Dancer et al., 1973). Although nitrification will sometimes
occur at pH values below 5.0, characteristically the rate decreases with increasing acidity
and often is undetectable much below pH 4.5. Limited data suggest that the process of sulfate
reduction to sulfide in soil is markedly inhibited below a pH of 6.0 (Connell and Patrick,
11-71
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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
11-72
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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
11-73
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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 Laflen (1976) found that
SO.-S deposition in Iowa was greatest in fall and winter when precipitation was low. They
also estimated that the additions of sulfur by precipitation were the same for Ames, Iowa in
1976 as were reported for 1923, approximately 15 Ibs/acre. The average annual additions of
sulfur by precipitation were similar to that reported for rural Wisconsin by Hoeft et al.
(1972)
Experimental data have shown that even though plants are supplied with adequate soil sul-
fate they can absorb 25 to 35 percent of their sulfur from the atmosphere (Brady, 1974). Par-
ticularly if the soil sulfur is low and atmosphere sulfur high, most of the sulfur required by
the plant can come from the atmosphere (Brady, 1974). Atmospheric sulfur would be of benefit
chiefly to plants growing on lands with a low sulfur content (Brezonik, 1976).
Tree species vary in their ability to utilize sulfur. Nitrogen and sulfur are'biochem-
ically associated in plant proteins, therefore, a close relationship exists between the two in
plants. Apparently, nitrogen is only taken up at the rate at which sulfur is available. Pro-
tein formation is, therefore, limited by the amount of sulfur available (Turner and Lambert,
1980). Conifers accumulate as sulfate any sulfur beyond the amount required to balance the
available nitrogen. Protein formation proceeds at the rate at which nitrogen becomes avail-
able. Trees are not injured when sulfur is applied as sulfate rather than SQy (Turner and
Lambert, 1980).
. When discussing the effects of acidic precipitation, or the effects of sulfates or
nitrates on soils, a distinction should be made between managed and unmanaged soils. There
appears to be general agreement that managed agricultural soils are less susceptible to the
influences of acidic precipitation than are unmanaged forest or rangeland soils. On managed
soils more than adequate amounts of lime are used to counteract the acidifying effects of fer-
tilizers in agricultural soils. Ammonium fertilizers, usually as ammonium sulfate [(NH.USO.]
or ammonium nitrate, (NH.NO,) are oxidized by bacteria to form sulfate (SO. ) and/or nitrate
(NO.,) and hydrogen ions (H ) (Brady, 1974; Donahue et al., 1977). The release of hydrogen
ions into the soil causes the soil to become acidified. Hydrogen ions are also released into
the soil when plants take up mineral nutrients. Hence, substances (notably various complexes
of ammonium and sulfate ions), although of neutral pH, or nearly so, are acidifying in their
effects when they are taken up by plants or animals. Thus, the concept of "acidifying precip-
itation" must be added to the concept of "acid precipitation."
The acidifying effects of fertilization or acidic precipitation is countered in managed
soils through the use of lime. Liming tends to raise the pH and thereby eliminate most major
problems associated with acidic soils (Donahue et al., 1977; Likens et al., 1977). Costs of
liming all natural soils would be prohibitive as well as extremely difficult to carry out.
11-74
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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, 1976; Hutchinson and
Whitby, 1977) mercury, (Brezonik, 1976) and cobalt (Hutchinson and Whitby, 1977). Rain over
Britain and the Netherlands, according to Gorham, (1976) contained the following elements in
addition to those reported for North American precipitation: aluminum, arsenic, beryllium,
cerium, chromium, cesium, antimony, scandium, selenium, thorium, and vanadium. Again it is
obvious that many of these elements will be found in precipitation in highly industrialized
areas and will not be of biological importance until they enter an ecosystem where they may
come into contact with some form of life, as in the case of heavy metals in the waters and
soils near Sudbury, Ontario. Of chemical elements found in precipitation, magnesium, iron,
copper, zinc, arid manganese are essential in small amounts for the growth of plants; however,
at high concentrations these elements, as well as the other heavy metals, can be toxic to
plants and animals. Furthermore, the acidity of precipitation can affect the solubility,
mobility, and toxicity of these elements to the foliage or roots of plants and to animals or
microorganisms that may ingest or decompose these plants.
Wiklander (1979) has pointed out that based on the ion exchange theory, ion exchange
experiments, and the leaching of soil samples, the following conclusions can be drawn about
the acidifying effect on soils through the atmospheric deposition of mineral acids.
1. At a soil pH > 6.0 acids are fully neutralized by decomposition of CaGO, and other
unstable minerals and by cation exchange.
2. At soil pH F 5.5 the efficiency of the proton to decompose minerals and to replace
2+ 2+ + +
exchangeable Ca , Mg , K , and Na decreases with the soil pH. Consequently, the
acidifying effect of mineral acids on soils decreases, but the effect on the runoff
water increases in the very acid soils.
2+ 2+ + +
3. Salts of CA , Mg , K , and NH. in the precipitation counteract the absorption of
protons and, in that way, the decrease of the base saturation. A proportion of the
acids percolate through the soil and acidify the runoff.
The sensitivity of various soils to acidic precipitation depends on the soil buffer
capacity and on the soil pH. Noncalcareous sandy soils with pH J 5 are the most sensitive to
acidification; however, acidic soils would be most likely to release aluminum.
Very acid soils are less sensitive to further acidification because they are already
adjusted by soil formation to acidity and are therefore more stable. In these soils easily
weatherable minerals have disappeared, base saturation is low, and the pH of the soil may be
less than that of precipitation. The low nutrient level is a crucial factor which limits
11-75
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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
11-76
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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, de-
composition, reproduction, tree growth, and the-structure of forest systems.
The additions of hydrogen, sulfate and nitrate ions to soil and plant systems have both
positive and negative effects. It has generally been assumed that the free hydrogen ion con-
centration in acidic precipitation is the component that is most likely to cause direct, harm-
ful effects on vegetation (Jacobson, 1980a). Experimental studies support this assumption;
however, to date, there are no confirmed reports of exposure to ambient acidic precipitation
causing foliar symptoms on field grown vegetation in the continental United States (Jacobson,
1980a) and Canada (Linzon, personal communication, 1980).
11.3.2.2.1 Direct effects on vegetation. Hydrogen ion concentrations equivalent to that
measured in more acidic rain events (< pH 3.0) have been observed experimentally to cause
tissue injury in the form of necrotic lesions to a wide variety of plant species under green-
house and laboratory conditions. This visible injury has been reported as occurring between pH
3.0 and 3.6 (Shriner, 1980). The various types of direct effects which have been reported are
shown in Table 11-7. Such effects must be interpreted with caution because the growth and
morphology of leaves on plants grown in greenhouses frequently are atypical of field condi -
tions (Shriner, 1980).
Small necrotic lesions, the most common form of direct injury, appear to be the result of
the collection and retention of water on plant surfaces and the subsequent evaporation of
these water droplets once a lesion occurs. The depression formed by the lesion further
enhances the collection of water. A large percentage of the leaf area may exhibit lesions
after repeated exposures to simulated acid rain at pH concentrations of 3.1, 2.7, 2.5 and 2.3
(Evans et al., 1977a, 1977b). In leaves injured by simulated acidic rain, collapse and dis-
tortion of epidermal cells on the upper surface is frequently followed by injury to the
palisade cells and ultimately both leaf surfaces are affected (Evans et al. , 1977b). Evans et
al. (1978) using six clones of Populus spp. hybrids found that leaves that had just reached
full expansion were more sensitive to simulated acid rain at pH 3.4, 3.1, 2.9, and 2.7 than
were unexpended or those which were fully expanded. On two of the clones, gall formation due
to abnormal cell proliferation and enlargement occurred. Other effects attributed to simu-
lated acid rain include the modification of the leaf surface, e.g. epicuticular waxes, and
alteration of physiological processes such as carbon fixation and allocation.
Lee et al. (1980) studied the effects of simulated acidic precipitation on crops.
Depending on the crop studied, they reported positive, negative or no effects on crop yield
when exposed to sulfuric acid rain at pH values of 3.0, 3.5 and 4.0 when compared to crops
exposed to a control rain of pH 5.6. The yield of tomatoes, green peppers, strawberries,
alfalfa, orchard grass and timothy were stimulated. Yields of radishes, carrots, mustard
greens and broccoli were inhibited. Potatoes were ambiguously affected except at pH 3.0 where
11-77
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TABLE 11-7. TYPES OF DIRECT, VISIBLE INJURY REPORTED IN RESPONSE TO ACIDIC WET DISPOSITION
I
~--J
00
Injury Type
Pitting, curl
shortening, death
1-mm necrotic lesions,
premature abscission
Cuticular erosion
Chlorosis
(A) small , shallow
circular depressions:
slight chlorosis
(B) larger lesions,
chlorosis always present
palisade collapse
(C) 1-mm necrotic lesions
general distortion
(D) 2-mm bifacial necrosis
due to coalescence of
smaller lesions, total
tissue collapse.
Wrinkled leaves, excessive
adventitious budding, pre-
Species pH Range
Yellow birch 2.3-4.7
Kidney bean, 3.2
soybean,
loblolly pine,
E. white pine,
willow oak
Willow oak 3.2
Sunflower, 2.3-5.7
bean
Sunflower, 2. 7
bean
Sunflower, 2.7
bean
Sunflower, 2.7
bean
Sunflower, 2.7
bean
Bean 1.5-3.0
Reference Remarks
Wood and Bormann (1974)
Shriner et al . (1974)
Shriner (1978a)
Lang, et al . (1978)
Evans et al .
(1977b)
Evans et al. More frequent near
(1977b) veins. (A) - (D)
represent sequential
stages of lesion
Evans et al. development, through
(1977b) time, up to 72 h (one
6-min rain event daily
for 3 d)
Evans et al .
(1977b)
Evans et al .
(1977b)
Ferenbaugh
(1976)
mature abscission
-------
TABLE 11-7 (Continued).
Injury Type
Incipient bronzed spot
Bifacial necrotic pitting
Necrotic lesions,
premature abscission
Marginal and tip necrosis
Galls, hypertrophy,
hyperplasia
Dead leaf cells
Species
Bean
Bean
E. white pine,
scotch pine,
spinach,
sunflower,
bean
Bean, poplar,
soybean, ash
birch, corn,
wheat
Hybrid poplar
Soybean
pH Range
2.0-3.0
2.0-3.0
2.6-3.4
Submicron
H2S04
aerosol
2.7-3.4
3.1
Reference
Hindawi et al .
(1980)
Hindawi et al .
(1980)
Jacobsen and
van Leuken
(1977)
Lang et al .
(1978)
Evans et al.
(1978)
Irving (1979)
Remarks
After first few hours
After 24 h (reported
pool ing of drops =
more injury)
Injury associated with
droplet location
within 24-48 h.
Shriner (1980).
-------
their yield as well as that of beets was inhibited. Visible injury of tomatoes could possibly
have decreased their market value. In sweet corn, stem and leaf production was stimulated,
but no statistically significant effects on yield were observed for 15 other crops. Results
suggest that the possibility of yield's being affected by acid rain depends on the portion of
the plant being utilized as well as the species. Plants were regularly examined for foliar
injury associated with acid rain. Of the 35 cultivars examined, the foliage of 31 was injured
at pH 3.0; 28 at pH 3.5; and 5 at pH 4.0. Foliar injury was not generally related to effects
on yield. However, foliar injury of swiss chard, mustard greens, and spinach was severe
enough to adversely affect marketability. These results are from a single growing season and
therefore considered to be preliminary.
Studies indicate that wet deposition of acidic or acidifying substances may result in a
range of direct or indirect effects on vegetation. Environmental conditions before, during
and after a precipitation event affect the responses of vegetation. Nutrient status of the
soil, plant nutrient requirements, plant sensitivity and growth stage and the total loading or
+ -
deposition of critical ions e.g. H , N03 and SO^ all play a role in determining vegetational
response to acidic precipitation.
Wettability of leaves appears to be an important factor in the response of plants to acid
deposition. This has been demonstrated in the work of Evans et al. (1977b), Jacobson and Van
Leuken (1977), and Shriner (1978a), who variously report a threshold of between pH 3.1 and 3.5
for development of foliar lesions on beans. The cultivars of Phaseolus vulgaris L. used in
the above studies are all relatively non-waxy and therefore fairly easily wettable. Waxy
leaves apparently minimize the contact time for the acid solutions, thus accounting for the
<400X increase in H ion concentration required to induce visible injury. Table 11-8
summarizes the thresholds, including range, species sensitivity, concentration, and time, for
visible injury associated with experimental studies of wet deposition of acidic substances.
Leaching of chemical elements from exposed plant surfaces is an important effect rain,
fog, mist, and dew have on vegetation. Substances leached include a great diversity of
materials. All of the essential minerals, amino acids, carbohydrate growth regulators, free
sugars, pectic substances, organic acids, vitamins, alkaloids, and alleopathic substances are
among the materials which have been detected in plant leachates (Tukey, 1970). Many factors
influence the quantity and quality of the substances leached from foliage. They include fac-
tors associated directly with the plant as well as those associated with the environment. Not
only are there differences among species with respect to leaching, but individual differences
also exist among individual leaves of the same crop and even the same plant, depending on the
physiological age of the leaf. Young, actively growing tissues are relatively immune to
leaching of mineral nutrients and carbohydrates, while mature tissue which is approaching
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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)
00
Effect
Foliar lesions, decrease
in growth
Foliar aberrations,
decrease in growth
Foliar lesions
Foliar lesions
Foliar lesions
Foliar lesions
Foliar symptons, no
reduced growth
Increased growth,
i ncreased/decreased
nutrient content
Reduced growth
Reduced yield
Reduced growth
Reduced yield
Species
Yel low birch
Bean
Bean, sunflower
Bean
Hybrid poplar
Sunflower
Soybean
Lettuce
Pinto bean
Pinto bean
Soybean
Soybean
Threshold
pH 3.1
pH 2.5
pH 3.1
pH 3.2
pH 3.4
pH 3.4
pH 3.0
pH 3.0, 3.2
pH 3.1
pH 2.7
pH 3.1
pH 2.5
Reference
Wood and
Bormann (1974)
Ferenbaugh
(1976)
Evans et al .
(1977b)
Shriner (1978a)
Evans et al .
(1978)
Jocobson and
Van Leuken (1977)
Jacobson (1980b)
Jacobson (1980b)
X
Jacobson (1980b)
Remarks
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse
greenhouse (varied
with S04~ & N03")
greenhouse
-------
TABLE 11-8 (Continued).
Effect
Increased yield
Foliar symptoms
Reduced growth
Reduced yield
Reduced quality
No foliar symptoms, or
effects on growth
No foliar symptoms, but
a) decreased growth, yield
b) increased yield
No effect on growth, yield
Reduced quality
Species
Soybean
Tomato
Tomato
Tomato
Tomato
Soybean
Soybean
Soybean
Soybean
Tomato
Tomato
Threshold Reference Remarks
pH 3.1
pH 3.0 Jacobson (1980b) greenhouse
pH 3.0
pH 3.0
pH 3.0
pH 3.1 Irving (1979) field
pH 2.8 Jacobsen (1980b) field, low ozone
pH 2.8 field, high ozone
pH 2.8 field, low ozone
pH 3.0 Jacobson (1980b) field
pH 3.0 field
Highest pH to elicit a negative response, or lowest pH to elicit a positive response
Shriner (1980).
-------
senescence is very susceptible. The stage of plant development, temperature, and rainwater
falling on foliage and running down plant stems or tree bark influences leaching. Rainwater,
which naturally has a pH of about 5.6, washing over vegetation may become enriched with
substances leached from the tissues (Nihlgard, 1970).
Leaching of organic and inorganic materials from vegetation to the soil is part of the
normal functioning of terrestrial ecosystems. The nutrient flow from one component of the
ecosystem to another is an important phase of nutrient cycling (Comerford and White, 1977;
Eaton et al. , 1973). Plant leachates have an effect upon soil texture, aeration, permea-
bility, and exchange capacity. Leachates, by influencing the number and behavior of soil
microorganisms, affect soil-forming processes, soil fertility, and susceptibility or immunity
of plants to soil pests and plant-chemical interactions (Tukey, 1970).
It has been demonstrated under experimental conditions that precipitation of increased
acidity can increase the leaching of various cations and organic carbon from the tree canopy
(Abrahamsen et al., 1976; Wood and Bormann, 1975). Foliar losses of potassium, magnesium, and
calcium from bean plants and maple seedlings were found to increase as the acidity of an arti-
ficial mist was increased. Below a pH of 3.0 tissue damage occurred; however, significant
increases in leaching were measured at pH 3.3 and 4.0 with no observable tissue damage (Wood
and Bormann, 1975). Hindawi et al. (1980) also noted that as the acidity of acid mist
increased so did the foliar leaching of nitrogen, calcium, phosphorous, and magnesium.
Potassium concentrations were not affected, while the concentration of sulfur increased.
Abrahamsen and Dollard (1979), in experiments using Norway spruce (Picea abies L. Karst),
observed that despite increased leaching under the most acid treatment, there was no evidence
of change in the foliar cation content. Wood and Bormann (1977), using Eastern white pine
(Pinus strobus L.), also noted no significant changes in calcium, magnesium or potassium con-
tent of needles. Tukey (1970) states that increased leaching of nutrients from foliage can
accelerate nutrient uptake by plants. No injury will occur to the plants as long as roots can
absorb nutrients to replace those being leached; however, injury could occur if nutrients are
in short supply. To date, the effects, if any, of the increased leaching of substances from
vegetation by acidic precipitation remain unclear.
Some experimental evidence suggests that acidic solutions affect the chlorophyll content
of leaves and the rate of photosynthesis. Sheridan and Rosenstreter (1973) reported marked
reduction of photosynthesis in a moss exposed to increasing H ion concentrations. Sheridan
and Rosenstreter (1973), Ferenbaugh (1976), and Hindawi et al. (1980) reported reduced chloro-
phyll content as a result of tissue exposure to acid solutions. In the case of Ferenbaugh
(1976), however, the significant reductions in chlorophyll in the leaves of Phaseolus vulgaris
at pH 2.0 were associated with large areas of necrosis. A significant aspect of this study
was the loss of capacity by the plant to produce carbohydrates. The rate of respiration in
these plants showed only a slight but significant increase while the rate of photosynthesis at
11-83
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pH 2.0 increased nearly fourfold as determined by oxygen evolution. Ferenbaugh concluded that
due to a reduction in biomass accumulation and sugar and starch concentrations, photophos-
phorylation in the treated plants was in some way being uncoupled by the acidic solutions.
Irving (1979) reported a higher chlorophyll content and an increase in the rate of photo-
synthesis in field-grown soybeans exposed to simulated rain at pH 3.1. She attributed the
increases to improved nutrition due to the sulfur and nitrogen components of the simulated
acid rain overcoming any negative effects.
Vegetation is commonly exposed to gaseous phytotoxicants such as ozone and sulfur dioxide
at the same time as acidic precipitation. Little information is available upon which to eval-
uate the potential for determining the effects of the interaction of wet-and dry-deposited
pollutants on vegetation. Preliminary studies by Shriner (1978b), Irving (1979), and Jacobson
et al. (1980) suggest that interactions may occur. Irving (1979) found that simulated acid
precipitation at pH of 3.1 tended to limit the decrease in photosynthesis observed when field
-grown soybeans were exposed 17 times during the growing season to 0.19 ppm of SO,,. Shriner
(1978b), however, reported no significant interaction between multiple exposure to simulated
rain at p 4.0 and four S02 exposures (3 ppm peak for 1 hr.) upon the growth of bush beans.
Shriner (1978b) also exposed plants to 0.15 ppm ozone (4 3-hour exposures) in between 4 weekly
exposures to rainfall of pH 4.0, and observed a significant growth reduction at the time of
harvest. Jacobson et al. (1980), using open-top exposure chambers with field-grown soybeans,
compared growth and yield between three pH levels of simulated rain (pH 2.8, 3.4, and 4.0) and
two levels of ozone (<0.03 and <0.12 ppm). Results demonstrated that ozone depressed both
growth and yield of soybeans with all three rain treatments, but that the depression was
greatest with the most acidic rain. Ozone concentrations equal to or greater than those used
in the studies are common in most areas of the northeastern United States where acidic deposi-
tion is a problem (Jacobson et al. , 1980); therefore, the potential for ozone-acidic deposi-
tion interaction is great.
Shriner (1978a) studied the effect of acidic precipitation on host-parasite interactions.
Simulated acid rain with a pH of 3.2 inhibited the development of bean rust and production of
telia (a stage in the rust life cycle) by the oak-leaf rust fungus Cronartium fusiforme. It
also inhibited reproduction of root-knot nematodes and inhibited or stimulated development of
halo blight of bean seedlings depending on the time in the disease cycle during which the
simulated acid rain was applied. The effects which inhibited disease development could result
in a net benefit to plant health. Shriner (1977, 1980) also observed that root nodulation by
Rhizobium on common beans and soybeans was inhibited by the simulated acid rain, suggesting a
potential for reduced nitrogen fixation by legumes so effected.
Plants such as mosses and lichens are particularly sensitive to changes in precipitation
chemistry because many of their nutrient requirements are obtained directly through precipita-
tion. These plant forms are typically absent from regions with high chronic SO^ air pollution
11-84
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and acidic precipitation (Denison et al. , 1977; Sheridan and Rosenstreter, 1973). Gorham
(1976) and Giddings and Galloway (1976) have written reviews concerning this problem. Most
investigations on the effects of air pollution on epiphytes have dealt with gaseous pollu-
tants. Very few studies have considered acidic precipitation. Denison et al. (1977),
however, did observe that the nitrogen-fixing ability of the epiphytic lichen Lobaria oregana
was reduced when treated with simulated rainfall with a pH of 4.0 and below. Investigations
concerning the effects of acidic precipitation on epiphytic microbial populations are very few
(Abrahamsen and Dollard, 1979).
Limited fertilization could occur in the bracken fern Pteridium aquilinum under condi-
tions of acidic precipitation (pH and sulfate concentrations) that prevail in the northeastern
United States. Evans and Bozzone (1977), using buffered solutions to simulate acidic precipi-
tation, observed that flagellar movement of sperm was reduced at pH levels below 5.8.
Fertilization was reduced after exposure to pH's below 4.2. Sporophyte production was also
reduced by 50 percent at pH levels below 4.2 when compared to 5.8. Addition of sulfate (86
mM) decreased fertilization at least 50 percent at all pH values observed. In another study,
Evans and Bozzone (1978) observed that both sperm motility and fertilization in gametopnytes
of Pteridium aquilinum were reduced when anions of sulfate, nitrate, and chloride were added
to buffered solutions.
Sulfur and nitrogen in precipitation have been shown to play an important role in vegeta-
tional response to acidic deposition. Jacobson et al. (1980) investigated the impact of simu-
lated acidic rain on the growth of lettuce at acidities of pH 5.7 and 3.2. At pH 3.2, solu-
tions were compared with N03:S04 mass ratios of 20:1, 2:1, and 1:7.5. The high nitrate at pH
3.2 showed no difference from the treatments controls at pH 5.7 for those growth parameters
(root dry weight, apical leaf dry weight) that responded to treatment; however, the results
were significantly less than those from the low nitrogen, high sulfur, treatment. These
observations suggest that sulfur was possibly a limiting factor in the nutrition of these
plants, with the result that the plant response to sulfur overwhelmed the hydrogen ion effect.
Other studies also have cited the beneficial effects of simulated acidic precipitation.
Irving and Miller (1978) observed that an acidic simulant had a positive effect on producti-
vity of field-grown soybeans as reflected by seed weight. Increased growth was attributed to
a fertilizing effect from sulfur and nitrogen delaying senescence. Irving and Miller (1978),
in the same study, also exposed soybeans to S0~ and acidic precipitation. No visible injury
was apparent in any of the plots; however, a histological study revealed significant increases
in the number of dead mesophyll cells in all plots when compared to the control. The propor-
tion of dead mesophyll cells of plants exposed to acid rain and S02 combined was more than
additive when compared to the effects of each taken singly. Wood and Bormann (1977) reported
an increase in needle length and the weight of seedlings of Eastern white pine with increasing
acidity of simulated precipitation where sulfuric and nitric acid were used to acidify the
11-85
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mist. Increased growth was attributed to increased N(L application. Abrahamson and Dollard
(1979) also presented data suggesting positive growth responses in forest tree species result-
ing from nitrogen and sulfur in simulated rain. Simulated acidic precipitation was observed
to increase the growth of Scots pine saplings in experiments conducted in Norway. Saplings in
plots watered with acid rain of pH 3.0, 2.5, and 2.0 grew more than the control plots. The
application of acid rain increased the nitrogen and sulfur content of the needles. As the
acidity of the artificial rain was adjusted using sulfuric acid only, the increased growth was
probably due to increased nitrogen mineralization and uptake. Turner and Lambert (1980)
reported evidence indicating a positive growth response in Monterey pine from the deposition
of sulfur in ambient precipitation in Australia.
Acidifying forest soils that are already acid by acidic precipitation or air pollutants
is a slow process. Growth effects probably could not be detected for a long time. To iden-
tify the possible effects of acidification on poor pine forests, Tamm et al. (1977) conducted
experiments using 50 kg and 100 kg of sulfur per hectare as dilute sulfuric acid (0.4 percent)
applied annually with and without NPK (nitrogen, phosphorous, potassium) fertilizer. Nitrogen
was found to be the limiting factor at both experimental sites. Acidification produced no
observable influence on tree growth. Lysimeter and soil incubation experiments conducted at
the same time as the experiments described above suggest that even moderate additions of sul-
furic acid or sulfur to soil affect soil biological processes, particularly nitrogen turnover.
The soil incubation studies indicated that additions of sulfuric acid increased the amount of
mineral nitrogen but lowered the amount of nitrate.
Soil fertility may increase as a result of acidic precipitation as nitrate and sulfate
ions, common components of chemical fertilizers, are deposited; however, the advantages of
such additions are possibly short-lived as depletion of nutrient cations through accelerated
leaching could eventually retard growth (Wood, 1975). Laboratory investigations by Overrein
(1972) have demonstrated that leaching of potassium, magnesium, and calcium, all important
plant nutrients, is accelerated by increased acidity of rain. Field studies in Sweden corre-
late decreases in soil pH with increased additions of acid (Oden et al., 1972).
Major uncertainty in estimating effects of acid rain on forest productivity is the capac-
ity of forest soils to buffer against leaching by hydrogen ions. Forest canopies have been
found to filter 90 percent of the hydrogen ions from rain (pH 4.0) falling on the landscape
during the growing season (Eaton et al., 1973). As a result, solutions reaching the forest
floor are less acidic (pH 5.0). Mayer and Ulrich (1977), however, point out that their
studies suggest that for most elements the addition by precipitation (wetfall plus dryfall) to
the soil beneath the tree canopy is considerably larger than that by precipitation to the
canopy surface as measured by rain gauges on a non-forested area. The leaching of meta-
bolites, mainly from leaf surfaces, and the washing out from leaves, branches, and stems of
airborne particles and atmospheric aerosols intercepted by trees from the atmosphere, are
suggested as the reason for the mineral increase.
11-86
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Forest ecosystems are complicated biological organizations. Acidic precipitation will
cause some components within the ecosystem to respond even though it is not possible at pre-
sent to evaluate the changes that occur. The impact of the changes on the ecosystem can only
be determined with certainty after the passage of a long period of time.
11.3.2.3 Effects on Human Health—One effect of acidification that is potentially of concern
to human health is the possible contamination by toxic metals of edible fish and of water sup-
plies. Studies in Sweden (Landner and Larsson, 1972; Turk and Peters, 1977), Canada
(Tomlinson, 1979; Brouzes et al., 1977), and the United States (Tomlinson, 1979) have revealed
high mercury concentrations in fish from acidified regions. Methylation of mercury to mono-
methyl mercury occurs at low pH while dimethyl mercury forms at higher pH (Fagestrom and
Jerneldv, 1972). Monomethyl mercury in the water passing through the gills of fish reacts
with thiol groups in the hemoglobin of the blood and is then transferred to the muscle.
Methyl mercury is eliminated very slowly from fish; therefore, it accumulates with age.
Tomlinson (1979) reports that in the Bell River area of Canada precipitation is the
source of mercury. Both methyl mercury and inorganic mercury were found in precipitation.
The source of mercury in snow and rain was not known at the time of the study.
Zinc, manganese, and aluminum concentrations also increase as the acidity of lakes
increases (Schofield, 1976b). The ingestion of fish contaminated by these metals is a
distinct possibility.
Another human health aspect is the possibility that, as drinking-water reservoirs
acidify, owing to acidic precipitation, the increased concentrations of metals may exceed the
public-health limits. The increased metal concentrations in drinking water are caused by
increased watershed weathering and, more important, increased leaching of metals from house-
hold plumbing. Indeed, in New York State, water from the Hinckley Reservoir has acidified to
such an extent that "lead concentrations in water in contact with household plumbing systems
exceed the maximum levels for human use recommended by the New York State Department of
Health" (Turk and Peters, 1977). The lead and copper concentrations in pipes which have stood
over night (U) and those in which the water was used (F) are depicted in Table 11-9.
11.3.2.4 Effects of Acidic Precipitation on Materials—Acidic precipitation can damage the
abiotic as well as the biotic components of an ecosystem. Of particular concern in this sec-
tion are the deteriorative effects of acidic precipitation on materials and cultural artifacts
of manmade ecosystems. At present in most areas, the dominant factor in the formation of
acidic precipitation is sulfur, usually as sulfur dioxide (Cowling and Dochinger, 1978;
Likens, 1976). Because of this fact, it is difficult to isolate the effect of acidic precipi
tation from changes induced by sulfur pollution in general. (The effects of sulfur oxides on
materials are discussed in Chapter 10.) High acidity promotes corrosion because the hydrogen
ions act as a sink for the electrons liberated during the critical corrosion process (Nriagu,
1978). Precipitation as rain affects corrosion by forming a layer of moisture on the surface
11-87
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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
(ug/1)
66
2
40
6
52
5
88
2
240
3
PH
—
7.4
6.3
6.3
6.8
7.1
6.3
6.3
4.5
5.0
U, unflushed, (water stands in pipes all night); F, flushed
From Turk and Peters (1977).
+ 2"
of the material and by adding hydrogen (H ) and sulfate (S02 ) ions as corrosion stimulators.
Rain also washes out the sulfates deposited during dry deposition and thus serves a useful
function by removing the sulfate and stopping corrosion (Kucera, 1976). Rain plays a critical
role in the corrosive process because in areas where dry deposition predominates the washing
effect is greatest, while in areas where the dry and wet deposition processes are roughly
equal, the corrosive effect is greater (Kucera, 1976). The corrosion effect, particularly of
certain metals, in areas where the pH of precipitation is very low may be greatly enhanced by
that precipitation (Kucera, 1976). In a Swedish study the sulfur content of precipitation,
2
expressed as meq/m per year, was found to correlate closely with the corrosion rate of steel.
The metals most likely to be corroded by precipitation with a low pH are those whose corrosion
resistance may be ascribed to a protective layer of basic carbonates, sulfates, or oxides, as
used on zinc or copper. The decrease in pH of rainwater to 4.0 or lower may accelerate the
dissolution of the protective coatings (Kucera, 1976).
Materials reported to be affected by acidic precipitation, in addition to steel, are:
copper materials, linseed oil, alkyd paints on wood, antirust paints on steel, limestone,
sandstone, concrete, and both cement-lime and lime plaster (Cowling and Dochinger, 1978).
11-88
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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 hair--are readily discernable. In pictures taken in
1969 after 267 years, no features are visible (Cowling and Dochinger, 1978).
It is not certain in what form sulfur is absorbed into stone, as a gas (SCO forming sul-
furous or sulfuric acid or whether it is deposited in rain. Rain and hoarfrost both contain
sulfur compounds. Schaffer (1932) compared the sulfate ion in both rain and hoarfrost at
Heachingley, Leeds, England in 1932 (Table 11-10) and showed that the content of hoarfrost was
approximately 7 times greater than rain. Wet stone surfaces unquestionably increase the con-
densation or absorption of sulfates. Stonework kept dry and shielded from rain, condensing
dew, or hoarfrost will be damaged less by SCL pollution than stone surfaces which are exposed
(Sereda, 1977).
Acid rain may leach ions from stonework just as acidic runoff and ground water leaches
ions from soils or bedrock; however, at the present time it is not possible to attribute the
deleterious effects of atmospheric sulfur pollution to specific compounds.
Microbial action can also contribute to the deterioration of stone surfaces. Tiano et
al. (1975) isolated large numbers (250 to 20,000 cells per gram) of sulfate-reducing bacteria
from the stones of two historical buildings of Florence, Italy. The majority of the bacteria
belonged to the genus Thiobacillus. This genus of chemosynthetic aerobic microorganisms
oxidizes sulfide, elemental sulfur, and thiosulphate to sulfate to obtain energy (Andersson,
1975). Limestone buildings and particularly mortar used in the construction of brick and
stone buildings are particularly susceptible to when Thiobacillus can convert reduced forms of
sulfur to sulfuric acid. Sulfate in acidic precipitation as well as other sulfur compounds
11-89
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TABLE 11-10. COMPOSITION OF RAIN AND HOARFROST AT HEADINGLEY, LEEDS
Average rain Hoarfrost
parts per million parts per million
Suspended matter
Tar
Ash
Acidity
Sulphur as SO,
Sulphur as SO-
Total sulphur
Chlorine
Nitrogen as NH^
Nitrogen as N-Oc
Nitrogen as albuminoid
115
15
28
1.9
22
5.7
27.7
7.3
1.98
0.196
0.434
4620
158
67
102.9
148
41.0
189.0
94.6
8.57
0.0
1.618
Schaffer (1932).
deposited in dry deposition could permit the formation of sulfur compounds utilizable by
microorganisms. (For more information concerning the effects of sulfur oxides on materials,
please consult Chapter 10).
11.4 ASSESSMENT OF SENSITIVE AREAS
11.4.1 Aquatic Ecosystems
Why do some lakes become acidified by acidic precipitation and others not? What deter-
mines susceptibility? Are terrestrial ecosystems likely to be susceptible; if so, which ones?
The sensitivity of lakes to acidification is determined by: (1) the acidity of both wet
deposition (precipitation) and dry deposition, (2) the hydrology of the lake, (3) the soil
system, geology, and canopy effects, (4) the surface water. Given acidic precipitation, the
soil system and associated canopy effects are most important. The hydrology of lakes includes
the sources, amounts, and pathways of water entering and leaving a lake. The capability of a
lake and its drainage basin to neutralize acidic contributions as well as the mineral content
of its surface water is largely governed by the composition of the bedrock of the watershed.
The chemical weathering of the watershed strongly influences the salinity (ionic composition)
11-90
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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, 1979b;
Wright and Henriksen, 1978).
Wright and Henriksen (1978) point out that the chemistry of Norwegian lakes could be
accounted for primarily on the basis of bedrock geology. They examined 155 lakes and observed
that 59 of them lay in granite or felsic gneiss basins. Water in these lakes was low in most
major ions and had low electrical conductivity. [The fewer the minerals in water the lower
its conductivity (Wetzel, 1975).] The waters in the lakes surveyed were "among the softest
waters in the world" (Wright and Henriksen, 1978). Sedimentary rocks generally weather
readily, whereas igneous rocks are highly resistant. The Adirondacks, as pointed out by Scho-
field (1979a), have granite bedrock with much of the area covered with a mantle of mixed
-gneisses. Shallow soils predominate in the area. Thus, areas are susceptible to acidifica-
tion.
Limestone terrains, on the other hand, are capable of buffering intense concentrations of
acids. Glacially derived sediment has been found to be more important than bedrock in assimi-
lating acidic precipitation in the Canadian Shield area (Kramer, 1976). Generally, however,
bedrock geology is the best predictor of the sensitivity of aquatic ecosystems to acidic
precipitation (Hendrey et al., 1980b).
Areas with aquatic ecosystems that have the potential for being sensitive to acidic
precipitation are shown in Figure 11-28. In Figure 11-27, the shaded areas on the map indi-
cate that the bedrock is composed of igneous or metamorphic rock while in the unshaded areas
it is of calcareous or sedimentary rock. Metamorphic and igneous bedrock weathers slowly;
therefore, lakes in areas with this type of bedrock would be expected to be dilute and of low
alkalinity [<0.5 meq HCOj/liter (Galloway and Cowling, 1978)]. Galloway and Cowling (1978)
verified this hypothesis by compiling alkalinity data. The lakes having low alkalinity
existed in regions having igneous and metamorphic rock (Galloway and Cowling, 1978). Hendrey
et al. (1980b) have developed new bedrock geology maps of the eastern United States for
predicting areas which might be impacted by acidic precipitation. The new maps permit much
greater resolution for detecting sensitivity than has been previously available for the
region. '
Henriksen (1979) has developed a lake acidification "indicator model" using pH-calcium
and calcium-alkalinity relationships as an indicator for determining decreased surface water
11-91
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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
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acidification. The indicator is based on the observation that in pristine lake environments
(e.g., Northwest Norway or the Experimental Lakes Area in Northwest Ontario, Canada) calcium
is accompanied by a proportional amount of bicarbonate because carbonic acid is the primary
chemical weathering agent. The pH-calcium relationship found for such regions is thus defined
as the reference level for unacidified lakes. Acidified lakes (e.g., Southeast Norway and the
Adirondack region) will exhibit lower pH or lower alkalinity than the reference lakes, at com-
parable calcium levels, due to the replacement of bicarbonate by strong acid anions.
Schofield (1979b) has illustrated the use of Henriksen's model with data from Norway, the
Adirondacks, and the Experimental Lakes Area of Ontario, Canada. In the acidified lakes sul-
fate replaces bicarbonate as the major anion present (Figures 11-29 and 11-30) and is derived
primarily from precipitation. Since the bicarbonate lost in acidified lakes has been replaced
by an equivalent amount of sulfate, the concentration of excess sulfate serves as an index of
the amount of acidification that has taken place. Henriksen (1979) compared estimated acidi-
fication in Norwegian lakes to the pH and sulfate concentrations in the prevailing precipita-
tion and concluded that significant lake acidification had occurred in areas receiving preci-
pitation with an annual average (volume weighted) pH below 4.6 to 4.7 and sulfate concentra-
tions above 1 mg/1. This approximate threshold of precipitation acidity may be applicable to
sensitive lake districts in other regions as well. For reference, the estimated annual bulk
deposition sulfate for the acidified lake districts in the Adirondacks and southern Norway are
approximately 30 to 60 kg SO./ha, as compared with only 5 to 10 kg SO./ha in the reference
areas of northern Norway and the Experimental Lakes Area in Ontario. A comparison of lake pH
with regional sulfate loading levels in Sweden suggests that critical loading levels for sensi-
tive lakes are in the range of 15 to 20 kg SO./ha/yr. The amount of precipitation must also
be considered since it affects total sulfate additions.
The report by Hendrey et al. (1980b) compared pre-1970 data with post-1975 data. A marked
decline in both alkalinity and pH of sensitive waters of North Carolina and New Hampshire were
tested. In the former, pH and alkalinity have decreased in 80 percent of the streams and in
the latter pH has decreased 90 percent since 1949. These areas are predicted to be sensitive
by the geological map on the basis of their earlier alkalinity values. Detailed county by
county maps of other states in the eastern United States suggest the sensitivity of these
regions to acidic precipitation.
Though bedrock geology generally is a good predictor of the susceptibility of an area to
acidification due to acidic precipitation, other factors also have an influence. Florida, for
example, is underlaid by highly calcareous and phosphate rock, suggesting that acidification
of lakes and streams is highly unlikely. Many of the soils, however, (particularly in
northern Florida) are very mature, have been highly leached of calcium carbonate, and, as a
result, some lakes in which groundwater infilow is minimal have become acidified (Hendry and
Brezonik, 1980). Conversely, there are areas in Maine with granitic bedrock where lakes have
11-93
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o
Z
LU
O
40 60
EQUIVALENT PERCENT
eo
Figure 11-29. Equivalent percent composition of major ions in Adirondack lake
surface waters (215 lakes) sampled in June 1975.
Source: Schofield (1979b).
11-94
-------
30
10
NW Norway
(58)
to
CJ 0
-------
not become acidified, despite receiving precipitation with an average pH of approximately 4.3,
because the drainage basins contain lime-bearing till and marine clay (Davis et al., 1978).
Small amounts of limestone in a drainage basin exert a strong influence on water quality in
terrain which would otherwise be vulnerable to acidification. Soils in Maine in the areas
where the pH of lakes has decreased due to acidic precipitation are immature, coarse, and
shallow and are derived largely from granitic material and commonly have a low capacity for
assimilating hydrogen ions from leachate and surface runoff in lake watersheds (Davis et al.,
1978). The occurrence of limestone outcroppings in the Adirondack Mountains of New York state
are highly correlated with lake pH levels. The occurrence of limestone apparently counteracts
any effects of acidic precipitation. Consequently, when predicting vulnerability of a parti-
cular region to acidification, a careful classification of rock mixtures should be made. Rock
formations should be classified according to their potential buffering capacity, and the type
of soil overlying the formations should be noted. Local variations in bedrock and soils are
very important in explaining variations in acidification between lakes within an area.
11.4.2 Terrestrial Ecosystems
Predicting the sensitivity of terrestrial ecosystems to acidic precipitation is much more
difficult than for aquatic ecosystems. With aquatic ecosystems it is possible to compare
affected ecosystems with unaffected ones and note where the changes have occurred. With ter-
restrial ecosystems, comparisons are difficult to make because the effects of acidic precipi-
tation have been difficult to detect. Therefore, predictions regarding the sensitivity of
terrestrial ecosystems must, as much as possible, use the data which link the two ecosystems,
i.e., data on bedrock geology. Since, in most regions of the world, bedrock is not exposed
but is covered with soil, it is the sensitivity of different types of soil which must be
assessed. Therefore, the first step is to define "sensitivity" as it is used here in relation
to soils and acidic precipitation. Sensitivity of soils to acidification alone, though it may
be the most important long-term effect, is too narrow a concept. Soils influence the quality
of waters in associated streams and lakes and may be changed in ways other than simple pH-base
saturation relationships, e.g., microbiological populations of the surface layers, accelerated
loss of aluminum by leaching. Therefore, criteria need to be used that would relate soil
"sensitivity" to any important change brought about in the local ecosystem by acid precipita-
tion (McFee, 1980).
All soils are not equally susceptible to acidification. Sensitivity to leaching and to
loss of buffering capacity varies according to the type of parent material from which a soil
is derived. Buffering capacity is greatest in soils derived from sedimentary rocks, especi-
ally those containing carbonates, and least in soils derived from hard crystalline rocks such
as granites and quartzites (Gorham, 1958). Soil buffering capacity varies widely in different
regions of the country (Figure 11-31). Unfortunately, many of the areas now receiving the
most acidic precipitation also are those with relatively low natural buffering capacities.
11-96
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REGIONS WITH SIGNIFICANT
AREAS OF SOILS THAT ARE
NON SENSITIVE
SLIGHTLY SENSITIVE
SENSITIVE
WITHIN THE EASTERN U.S.
Figure 11-31. Soils of the eastern United States sensitive to acid rainfall (McFee, 1980).
11-97
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The buffering capacity of soil depends on mineralogy, texture, structure, organic matter,
pH, base saturation, salt content, and soil permeability. Above a pH of 5.5 virtually all of
the H ions, irrespective of source, are retained by ion exchange and chemical weathering.
Below pH 5.5, the retention of the H ion decreases with the soil pH in a manner determined by
the composition of the soil (Donahue et al., 1977). With a successive drop in the soil pH
below 5.0, an increasing proportion of hydrogen ions (H ) and deposited sulfuric acid will
pass through the soil and acidify runoff water (Donahue et al., 1977). The sensitivity of
different soils based on pH, texture, and calcite content is summarized in Table 11-11.
TABLE 11-11. THE SENSITIVITY TO ACID PRECIPITATION BASED ON: BUFFER
CAPACITY AGAINST pH-CHANGE, RETENTION OF H , AND ADVERSE EFFECTS ON SOILS
Noncalcareous
Buffering
H retention
Adverse
effects
Calcareous
soils
Very high
Maximal
None
clays
pH > 6
High
Great
Moderate
sandy soils
pH > 6
Low
Great
Considerable
Cultivated
soils
pH > 5
High
Great
None -
slight
Acid
soils
pH < 5
Moderate
Slight
Slight
Reference: Wiklander (1979).
Soils are the most stable component of a terrestrial ecosystem. Any changes which occur
in this component would probably have far-reaching effects. McFee (1980) has listed four
parameters which are of importance in estimating the sensitivity of soils to acidic precipita-
tion. They are:
1. The total buffering or cation exchange capacity which is provided
primarily by clay and soil organic matter.
2. The base saturation of that exchange capacity which can be estimated
from the pH of the soil.
3. The management system imposed on the soil; is it cultivated and
amended with fertilizers or lime or renewed by flooding or by other
additions?
4. The presence or absence of carbonates in the soil profile.
In order that the factors listed above could be used in broad scale mapping of soils,
McFee evaluated them for wide applicability and ready availability. In natural soils the most
serious effects would be caused by changes in pH by leaching of soil minerals. Susceptibility
of soils to changes in either of these categories is most closely associated with the cation
exchange capacity (CEC). Soil with a low CEC and a circumneutral pH is likely to have the pH
rapidly reduced by an influx of acid. Soils with a high CEC, however, are strongly buffered
against pH changes or changes in the composition of the leachate. Acidic soils with a pH near
that of acidic precipitation will not rapidly change pH due to acidic precipitation, but will
11-98
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probably release Al ions into the leachate (McFee, 1980). Soils having a low CEC are
usually low in plant nutrients; therefore, significant changes in their productivity could
occur with only a slight loss of nutrients (McFee, 1980).
Even though CEC or buffering capacity does not completely define soil sensitivity to pos-
sible influents of acid, for the reasons given above it was the primary criterion used by
McFee for the regional mapping of soil sensitivity to acidic precipitation in the eastern
United States. Further, though it is frequently stated in much of the literature that soils
with low CEC or sandy soils having low organic matter are likely to be most susceptible to
effects of acidic precipitation, the "low CEC" values are not quantified? To develop a
working set of classes, it was necessary to make certain assumptions and "worst case" calcu-
lations. Since soils in general are rather resistant to change due to additions of acid, a
fairly high addition of acid was assumed and the question asked, "What is the maximum effect
that it can have on soil, and how high would the CEC have to be to resist that effect?"
(McFee, 1980)
To determine sensitivity of a soil, McFee arbitrarily chose a span of 25 years. It was
hypothesized that a significant effect could occur if the maximum influx of acid (100 cm of
precipitation at pH 3.7 per annum) during that period equaled 10 to 25 percent of the cation
exchange capacity in the top 25 cm of soil. Soils are considered slightly sensitive if the
top 25 cm of soil has an average CEC of 6.2 to 15.4 meq/100 g (assuming a bulk density of 1.3
g/cc). If the same influx of acid exceeds 25 percent of the CEC in the top 25 cm, i.e., when
the CEC is less than 6.2 meq/100 g, the soils are considered sensitive.
Based on the above concepts, the soils of the eastern United States including effects of
cultivation were mapped (Figure 11-30) by McFee. The areas containing most of the soils
potentially sensitive to acidic precipitation are in the upper Coastal Plain and Piedmont
regions of the southeast, along the Appalachian Highlands, through the east central and north-
eastern areas, and in the Adirondack Mountains of New York (McFee, 1980). The present limited
state of knowledge regarding the effects of acidic precipitation on soils makes a more
definitive judgment of the location of areas with the most sensitive soils difficult at the
present time.
The capacity of soils to absorb and retain anions also important in determining whether
soils will become acidified was not discussed by McFee (1980). The capacity for anion absor-
ption is great in soils rich in hydrated oxides of aluminum (Al) and iron (Fe). Reduced
leaching of salt cations is of great significance not only in helping to prevent soil acidifi-
cation but in geochemical circulation of nutrients, fertilization in agriculture and prevent-
ing water pollution (Johnson et al., 1980; Johnson, 1980; Wiklander, 1980). (See Section
11.3.2.1) This parameter, as well as those listed by McFee (1980) should be used in
determining the sensitivity of soils to acidification by both wet and dry deposition.
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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 perturbations only through the
response of the populations of organisms of which they are composed. Species of organisms
sensitive to environmental changes are removed. Therefore, the capacity of an ecosystem to
maintain internal stability is determined by the ability of individual organisms to adjust
their physiology or behavior. The success with which an organism copes with environmental
changes is determined by its ability to yield reproducing offspring. The size and success of
a population depends upon the collective ability of organisms to reproduce and maintain their
numbers in a particular environment. Those organisms that adjust best contribute most to
future generations because they have the greatest number of progeny in the population.
The capacity of organisms to withstand injury from weather extremes, pesticides, acidic
deposition or polluted air follows the principle of limiting factors. According to this
principle, for each physical factor in the environment there exists for each organism a
minimum and a maximum limit beyond which no members of a particular species can survive.
Either too much or too little of a factor such as heat, light, water, or minerals (even though
they are necessary for life) can jeopardize the survival of an individual and in extreme cases
a species. When one limiting factor is removed another takes its place. The range of toler-
ance of an organism may be broad for one factor, narrow for another. The tolerance limit for
each species is determined by its genetic makeup and varies from species to species for the
same reason. The range of tolerance also varies depending on the age, stage of growth or
growth form of an organism. Limiting factors are, therefore, factors which, when scarce or
overabundant, limit the growth, reproduction and/or distribution of an organism. The
increasing acidity of water in lakes and streams appears to be such a factor. Significant
changes that have occurred in aquatic ecosystems with increasing acidity include the
following:
1. Fish populations are reduced or eliminated.
2. Bacterial decomposition is reduced and fungi may dominate saprotrophic communi-
ties. Organic debris accumulates rapidly, tying up nutrients, and limiting
nutrient mineralization and cycling. .
3. Species diversity and total numbers of species of aquatic plants and animals are
reduced. Acid-tolerant species dominate.
4. Phytoplankton productivity may be reduced due to changes in nutrient cycling and
nutrient limitations.
5. Biomass and total productivity of benthic macrophytes and algae may increase due
partially to increased lake transparency.
6. Numbers and biomass of herbivorous invertebrates decline. Tolerant invertebrate
species, e.g., air-breathing bugs (water-boatmen, back-swimmers, water striders)
may become abundant primarily due to reduced fish predation.
7. Changes in community structure occur at all trophic levels.
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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 (SO* ) and nitrate (NO,) 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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12. EFFECTS OF NITROGEN OXIDES ON NATURAL ECOSYSTEMS, VEGETATION AND MICROORGANISMS
12.1 INTRODUCTION
Ecosystems are complex self-sustaining natural systems and are composed of living organ-
isms and the several nonliving components of the environment within which the organisms exist.
Within an ecosystem are included all of the interactions that bind the living and nonliving
components together into a stable system, i.e., the interactions between organisms or communi-
ties of organisms, the relationships between organisms and the physical environment and the
interactions of the various aspects of the nonliving environment (Boughey, 1971; Odum, 1971;
Smith, 1974; Whittaker, 1975). After centuries of relatively stable annual climatic and geo-
chemical conditions, they may become self-perpetuating (Boughey, 1971, Odum, 1971; Smith, 1974;
Whittaker, 1975).
Evaluating the contribution of functioning natural ecosystems to human welfare is a very
complex task and involves weighing both economic and human social values; however, it is clear
that this natural order by which living organisms are bound to each other and to their envir-
onment is essential to the existence of any species on earth, including man (Boughey, 1971;
Odum, 1971; Smith, 1974; Whittaker, 1975). As life support systems, the value of ecosystems
cannot be quantified in economic terms.
This chapter discusses the effects in general of nitrogen oxides on natural ecosystems
and, more specifically, their effects on certain species of plants and microorganisms.
12.2 EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS
Climatic, physiochemical, or biological changes, regardless of their source of nature,
will affect the functioning of an ecosystem. Some ecosystems are durable and relatively
stable when subjected to a given environmental change; others become unstable given the same
change.
It is difficult to assess the complex cause and effect relationships of any pollutant,
even when it is studied using only a single organism. When attempting to assess such relation-
ships within populations, communities and ecosystems, the problems become even greater. Addi-
tional complications in determining the effects of a single pollutant on natural communities
are created by the presence of multiple contaminants that may promote synergistic or antago-
nistic effects.
The response of ecosystems to environmental changes or perturbations is determined by the
response of their constituent organisms. The factors which determine the response of organ-
isms and changes which may occur within ecosystems are discussed in Section 11.1.2 Ecosystem
Dynamics in Chapter 11.
Terrestrial, marine, and freshwater ecosystems are functionally important to the inte-
grity of the biosphere. They are important: (1) in the production of food; (2) the mainte-
nance of forests; (3) as global support systems for the regeneration of essential nutrients
and atomspheric components; (4) for their aesthetic value in maintaining natural vegetative
communties; and (5) in the assimilation or destruction of many pollutants from the air, water,
and soil.
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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 entire-
ly by terrestrial and aquatic microorganisms through a complicated series of reactions that
are collectively termed the "nitrogen cycle." These transformations are more accurately
described as a "nitrogen web" because the image of a simple loop of compounds through which
nitrogen successively passes bears little resemblance to reality.
The nitrogen cycle or web has been greatly modified by man, both locally and on a global
scale, through agricultural activity, industrial production, fuel burning and waste disposal.
The nitrogen cycle in the biosphere and the modifications caused by man's activities are
discussed in Chapter 4.
In terrestrial and aquatic systems, the major nonbiological processes of the nitrogen
cycle involve phase transformations rather than chemical reactions. These transport processes
include volatilization of ammonia and other gaseous forms of nitrogen; sedimentation of par-
ticulate forms of organic nitrogen; and sorption (e.g., of ammonium ions by clays). Under-
standing of the biospheric nitrogen cycle and of the factors that control the cycle depends
primarily on an understanding of biological principles, especially those of microbial ecology.
The biological transformations shown in Figure 4-1 (Chapter 4) involve only six major
processes (Figure 12-1). These processes are discussed here in outline only. For details see
Chapter 4.
These processes are:
1. Assimilation of inorganic forms of nitrogen (primarily ammonia or nitrates) by plants and
microorganisms to form organic nitrogen, e.g., amino acids, proteins, purines, pyrimidines,
and nucleic acids. In this report the term ammonia is used for gaseous NH, and collectively
for NH.+ plus NH3, when there, is no need or intention to distinguish between these forms.
Ammonium (ion) is used specifically to indicate the cationic form NH.+.
2. Heterotrophic conversion of organic nitrogen from one organisms (food and prey) to another
organism (consumer or predator). Nitrogen is bound in plant or animal protein until the
organisms die or as the case of animals certain products are excreted.
3. Ammonification, the decomposition of organic nitrogen to ammonia. (The ammonia may be
assimilated by aquatic or terrestrial plants and microorganisms, may be bound by clay particles
12-2
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(4)
(1,5)
NO,
(2)
Figure 12-1. Simplified biological nitrogen cycle, showing major
molecular transformations. Numbers in parentheses correspond
to numbered processes discussed in text: (1) assimilation;
(2) heterotrophic conversion; (3) ammonification; (4) nitrifica-
tion; (5) denitrification; (6) nitrogen fixation (National
Research Council, 1978).
12-3
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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 may be transformed into atmospheric
nitrogen or reduced to ammonia.
5. Denitrification, implies the gaseous loss of nitrogen, usually as molecular nitrogen (N~),
nitrous oxide (N20) or nitric oxide (NO), to the atmosphere as a result of microbial reduction
of nitrate. Nitrate is reduced to nitrous oxide (N^O) and molecular nitrogen (N2) under
anaerobic conditions. Nitrates (N03 ) are converted into nitrites (NO- ), to nitrous oxide (a
gas) (N20) and finally into nitrogen gas (N^) which goes off into the atmosphere. In the soil,
nitrites rarely accumulate under acidic conditions but are decomposed spontaneously to nitric
oxide (NO), and under alkaline conditions they are biologically converted to N~0 and N2
(Alexander, 1977a; Brock, 1970). It must be emphasized that this process is anaerobic and
that conversion of nitrates to nitrites is extremely sensitive to the presence of atmospheric
oxygen. If atmospheric oxygen is present, the conversion does not occur. Some evidence
exists for the nonbiological chemical production of nitrogen gas or nitrogen oxides (Delwiche
and Bryan, 1976).
6. Biological Nitrogen Fixation is the transformation of atmospheric nitrogen gas into
ammonia, nitrates and other nitrogen-containing compounds. The transformation is carried out
by a variety of microorganisms. The microorganisms may be either symbiotic (living in the
roots of leguminous plants) or nonsymbiotic (living independently in the soil) and the process
may be accomplished under aerobic or anaerobic conditions.
The predominant agents of assimilation in water are autotrophic algae and on land, higher
plants. In soils, bacteria are important agents of assimilation of inorganic nitrogen.
Heterotrophic conversions (e.g., of organic nitrogen in plants to animal protein) are highly
complicated processes involving numerous steps, but are not treated in any detail here.
Ammom'fication and nitrification together constitute the process of mineralization.
Bacteria and fungi are the principal agents of ammonification in soils; autolysis of cells and
excretion of ammonia by zooplankton and fish are important processes in aquatic systems.
Ammonification is important in renewing the limited supply of inorganic nitrogen for futher
assimilation and growth by plants. Nitrification is mediated primarily by aerobic bacteria
that obtain their energy by oxidizing ammonia to nitrite and nitrate. Nitrification converts
ammonia, which is volatile but readily absorbable, into nitrate, a nonvolatile but easily
leached form.
On an ecosystem scale, denitrification is considered sink since the products (N2 and N20)
are readily lost to the atmosphere and most organisms cannot use nitrogen in these gaseous
forms. Denitrification is carried out by a ubiquitous group of bacteria that use nitrate as
their terminal electron acceptor in the absence of oxygen.
12-4
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Nitrogen fixation is important as a souce of available nitrogen for plant growth in both
natural and managed agricultural ecosystems. On a global scale and over millions of years,
nitrogen fixation balances the losses by denitrification; on time scales of decades to
thousands of years, the two processes may be out of phase without significantly affecting the
nitrogen content of the global atmosphere.
Nitrogen fixation is only an indirect source of nitrate in the biosphere, but this pro-
cess is important in global nitrogen balances, and in the current controversy over the deple-
tion of stratospheric ozone by N?0. (See Chapter 9).
Numerous texts, monographs, and papers review the nitrogen cycle, (Alexander, 1977a;
Bartholomew and Clark, 1965; Brezonik, 1972, Brock, 1970; Delwiche, 1970; Delwiche and Bryan,
1976; Delwiche, 1977, Hutchinson, 1944; Hutchinson, 1954; Hutchinson, 1957; Keeney, 1973;
Sb'derlund and Svensson, 1976) and other reviews cover specific aspects of the cycle in detail.
This discussion emphasizes the processes of the nitrogen cycle that are important to an under-
standing of the accumulation of nitrate and its transformation in the biosphere. Because the
literature dealing with nitrate and the nitrogen cycle is so extensive, no attempt has been
made to provide exhaustive documentation here.
As indicated above, of the many functions occurring within ecosystems, the recycling of
nutrients is one of the most important. The nitrogen cycle is one example of the cycling of a
cycling process could be detrimental to the lives of plants and animals.
12.2.1 Effects of Nitrates
Ecological effects of increased nitrates can be beneficial or detrimental or both.
Effects of both kinds may occur simultaneously, may cause effects in media or in ecological
compartments quite removed from those that initially receive the manmade nitrogenous injec-
.tions. In some natural ecosystems, such as lakes and estuaries, the addition of nitrogen can
"contribute to eutrophic conditions that are considered undesirable. Nitrate as nitric acid
contributes to the acidity of rainfall (Chapter 11) and some nitrates and related compounds
are toxic to plants, animals and microorganisms.
In most nonagricultural terrestrial ecosystems, the major processes that provide nitrogen
for plant growth are mineralization (ammonification and nitrification) of soil organic nitro-
gen and biological fixation of atmospheric nitrogen. When fluxes of nitrogen enter such
systems as a result of human activities, the added inputs in many cases represent a signifi-
cant fraction of total nitrogen inputs. On the basis of such mass-balance considerations, it
seems likely that such fluxes are important nutrient sources that could support increased
biotic productivity (National Research Council, 1978).
Except in ecosystems that receive fertilizer or nitrogenous wastes, the most important
manmade contributions are likely to be from atmospheric pathways, total (inorganic plus
organic) nitrogen loadings in wet and dry precipitation may be equivalent to from 8 to 25
percent of the nitrogen used by plants in different natural ecosystems. Even in heavily
managed ecosystems, annual atmospheric fluxes may be substantial; for instance, the calculated
12-5
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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 terre-
strial systems, where the major influxes are from atmospheric deposition. Second, far less is
known of the responses of nonagricultural plant communities to increased supplies of fixed
nitrogen than is known for cultivated crops. It is possible, however, to estimate the appro-
ximate magnitude of anthropogenic nitrogen fluxes to ecosystems, using the limited amount of
monitoring data available or mass-balance calculations (see Appendix A of the National Academy
of Sciences: Nitrates; an Environmental Assessment) (National Research Council, 1978). Such
estimates, and quantitative information about the nitrogen cycle at specific sites in the
system under study, make it possible to reach some conclusions about the possible ecological
significance of the added nitrogen. In addition, where the data base is more extensive, as it
is for a number of lakes in various stages of eutrophication, more quantitative dose-response
relationships can be estimated.
Living organisms are exposed to nitrates and related compounds through air, water, soil,
and food webs. The rate of exposure depends on proximity to sources and on a great many envi-
ronmental transport and transformation processes (illustrated in Figure 12-2). Biological
productivity can be increased deliberately by fertilization, as in agricultural crops, or
accidentally through run off to terrestrial or lake systems.
12.2.2 Terrestrial Ecosystems
Additions of nitrate and other forms of nitrogen from the atmosphere to ecosystems is an
integral function of the terrestrial nitrogen cycle. Higher plants and microorganisms can
assimilate the inorganic forms rapidly. The contribution of inorganic nitrogen in wet preci-
pitation (rain plus snow) is usually equivalent to only a few percent of the total nitrogen
assimilated annually by plants in terrestrial ecosystems; however total nitrogen contributions,
including organic nitrogen, in bulk precipitation (rainfall plus dry fallout) can be signifi-
cant, especially in unfertilized natural systems.
In absolute terms, atmospheric contributions of nitrate can range from less than 0.1 kg
N/ha-yr in the Northwest (e.g., Fredericksen, 1972) to 4.9 kg N/ha-yr in the eastern United
States (Henderson and Harris, 1975; Likens et al., 1970). Inorganic nitrogen (ammonia-N plus
nitrate-N) loadings in wet precipitation ranged from less than 0.5 kg/ha-yr to more than 3.5
kg/ha-yr in Junge's (1958) study of rainfall over the United States. On the other hand, total
nitrogen loads in bulk precipitation range from less than 5 kg/ha-yr in desert regions of the
West to more than 30 kg/ha-yr near barnyards in the Midwest. Total contributions of nitrogen
from the atmosphere commonly range from about 10 to 20 kg N/ha-yr for most of the United
States (National Research Council, 1978).
12-6
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AIR
NO
PANS. NO"
AEROSOLS
COMBUSTION
. N2O.
OZONE
DEPLETION
INCREASED.
UV
CLIMATE
MODIFICATION
FERTILIZER
NOj, NH4+
LAND
RUNOFF
NO,
VOLATILIZATION
NH,
^ [ INCREASED
PRODUCTIVITY
FOOD
PRODUCTION
DENITRIFICATION
NO,
-NH.
1
NO-
1 3
WASTE
DISPOSAL
1
T
.UPTAKE BY
VEGETATION
VEGETATION,
LITTER BUFFERING
JSOIL
BUFFERING
TOXICITY
SOIL
NO3 BUFFERING
NITRIFICATION
NO,
ACCUMULATION
IN SOIL AND
GHOUNDWATER
NH,
ACID
SOIL
(SOIL
(BUFFERING
NO-
LEACHING
H+ LEACHING
I
BIOLOGICAL
EFFECTS
T
WATER
•NO,
-B*
INCREASING
N:P
IMBALANCE
LOWpH.
TOXICITY
BIOLOGICAL
EFFECTS
Figure 12-2. Schematic presentation of environmental effects of manipulation of the nitrogen cycle. Human-caused perturbations are shown
at left, culminating in ecological and climatic effects, at right. Processes that buffer against the effects are indicated with the symbol( [X] )
on the arrows representing the appropriate pathways (National Research Council, 1978);
-------
In comparison, rates of annual uptake by plants range from 11 to 125 kg N/ha-yr in
selected ecosystems from several bioclimatic zones (National Research Council, 1978). Since
the lowest additions are generally associated with desert areas, where rates of uptake by
plants are low, and the highest additions usually occur in moist areas where plant uptake is
high, the contributions of ammonia and nitrate from rainfall to terrestrial ecosystems are
equivalent to about 1 to 10 percent of annual plant uptake. The typical fluxes (additions) of
total nitrogen in bulk precipitation, on the other hand, represent from about 8 to 25 percent
of the annual plant needs in eastern deciduous and western coniferous forest ecosystems.
Although these comparisons suggest that plant growth in terrestrial ecosystems depends to .a
significant extent on atmospheric loadings, it is not yet possible to estimate the importance
of these contributions when compared to biological nitrogen fixation and mineralization of
nitrogen in the soil. In nutrient-impoverished ecosystems, such as badly eroded abandoned
croplands or soils subjected to prolonged leaching by acid precipitation, nitrogen additions
from atmospheric fluxes are certainly important to biological productivity. Such sites, how-
ever, are relatively limited in extent. In largely unperturbed forests, recycled nitrogen
from the soil organic pool is the chief source of nitrogen for plants, but new nitrogen to
support increased production must come either from biological fixation or from atmospheric
influxes. It seems possible, therefore, that man generated contributions could play a signi-
ficant ecological role in a relatively large portion of the forested areas near industrialized
regions.
12.2.3 Effects of Nitrogen Oxides
12.2.3.1 Terrestrial Plant Communities—Studies of plant communities suggest that individual
species differ appreciably in their sensitivity to chemical stress, and that such differences
are reflected in the changes occurring within plant communities. A common alteration in a com-
munity under stress is the elimination of the more sensitive populations and an increasing
abundance of species that tolerate or are favored by the stress (Woodwell, 1970). The response
of plant populations or species to an environmental perturbation will depend upon life cycles
of the plants, microhabitats in which they are growing, and their genetic constitution (geno-
type). Abundant evidence exists to show that in plant communities undergoing structural
changes that reduce environmental or biological variability new species become dominant
(Botkin, 1976; Daniel, 1963; Jordan, 1969,; Keever, 1953; McCormick, 1963; McCormick, 1969;
Miller, 1973; Miller and Yoshiyama, 1973; Smith, 1974; Treshow, 1968; Woodwell, 1962; Woodwell,
1963; Woodwell, 1970). Furthermore, the specific pollutant to which a community is exposed
for prolonged periods of time will govern the capacity of the community to recover. In turn,
an alteration in the community composition, size of the community, or its rate of energy fixa-
tion will influence the animal populations in the vicinity and microorganisms in the under-
lying soil. These changes, in their turn, will modify the behavioral patterns or alter compe-
tion among the prevalent organisms.
Investigations of the influence of nitrogen oxides on economically important plant species
have revealed differential susceptibility of plant species, differential effects due to diurnal
conditions and age, and difficulties in predicting synergistic effects when a plant population
12-8
-------
is exposed to more than one pollutant simultaneously. Little information is known about the
specific effect of nitrogen oxides on plants in natural communities. Evidence of visible
injury to plant communities has seldom been demonstrated. In fact, visible injury may repre-
sent only a fraction of the actual harm done to terrestrial communities. Evidence exists, how-
ever, that the vigor and survival rate of plants have been affected deleteriously by air pol-
lution (Hepting, 1964). Many instances of injury to higher plants that have been ascribed to
pathogens or unknown factors may, in fact, reflect a toxicity associated with nitrogen oxides.
Nevertheless, since plants respond simultaneously to many environmental factors, it is fre-
quently difficult to determine which of the potential environmental stresses are responsible
for damage to the major species or to the community composition. Thus, it is likely that the
response to modest nitrogen oxide stresses would not be recognized because the vigor and
visual appearance of plants would be influenced by temperature, soil type and moisture,
drainage, interspecific competition, and other factors. Only severe injury could likely be
ascribed to a particular pollutional episode (Hepting, 1964).
The agent of stress may have ecological importance inasmuch as the species tolerance to
such environmental factors as moisture, temperature, and light, its capacity to compete, and
its ability to withstand attack by parasitic organisms, may be affected as well. Moreover,
physiological aspects of plant development, including growth, photosynthetic and respiratory
rate, and flowering may be influenced by the pollutant. These alterations in the environment
and in the plant community will influence energy flow through the ecosystem, its productivity,
and the succession of indigenous species.
Studies have been conducted on the effect of air pollutants on ecosystems and plant com-
munities (Parmeter and Cobb, 1972; Wenger et al., 1971). It is the general conclusion of
these investigations that further research on the influence of nitrogen oxides on plant commu-
nities is required. The available information clearly is too small to warrant meaningful
generalizations at this time; however, there is information detailing the effects on indivi-
dual plant species. These effects are discussed in Section 12.3.
12.2.3.2 Effects on Animal Communities—Surprisingly little attention has been given to the
effect of nitrogen oxides on animal populations or communities. Although laboratory studies
of a few individual species have been carried out, it is difficult to extrapolate from these
laboratory tests on animals maintained under careful conditions, to populations in the field.
The interaction of the various stresses in nature and the uncertainty of cause and effect
relationships make any conclusions from laboratory studies quite tenuous. Because species
differ enormously in their susceptibility to air pollutants, extrapolation from laboratory
tests on one species to potential effects on another is fraught with problems.
One of the few studies conducted on animal populations is that of McArn et al. (1974) who
reported that granule-rich microphages appeared in the lung tissues of English sparrows nesting
in urban areas with high pollution levels. The microphages were not reported to be present in
the lungs of sparrows inhabiting windswept, unpolluted areas. In this study, potential
chronic effects could not be determined owing to the relatively short life-span of these birds.
12-9
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Beyond this limited amount of knowledge, the literature concerning the effects of nitro-
gen oxides on natural animal populations or communities is extremely sparse. No conclusions
can be drawn about whether ambient levels of nitrogen oxides in the atmosphere have an effect
on the composition or functioning of animal communities or populations.
12.2.3.3 Effects of Nitrogen Oxides on Microbial Processes in Nature—Microorganisms are
essential for the functioning of key processes in terrestrial, marine, and freshwater communi-
ties. They are the chief agents for decomposing organic materials in soils and waters.
Microfloras are the major agents for destruction of synthetic chemicals introduced into soils
and waters. Marine algae are essential for the generation of the oxygen required to sustain
life in all higher animals. In soil, the bacteria, fungi, and actinomycetes convert compounds
of nitrogen, sulfur, and phosphorus to the inorganic state, thereby providing plants with the
required inorganic nutrients. Biologic nitrogen fixation and nitrification are affected sole-
ly by these microscopic organisms, which also maintain soil structure and form the humus
important to abundant plant growth. In addition, many of the pathogens that are constantly
discharged into soils and waterways are eliminated by microbial actions.
Since microorganisms are critical to the balance of ecosystems, any disturbance in their
activities could have serious consequences on a local, regional, or global scale. The poten-
tial impact on microorganisms by substances as widespread and pervasive as the nitrogen oxides
must therefore be assessed. Surprisingly, this subject has been neglected to date. The few
data are based on NO concentrations in excess of those found in the atmosphere.
Therefore, the knowledge concerning the potential impact of nitrogen oxides on microbial
processes in soils and waters is sparse. Although ambient concentrations probably do not sig-
nificantly affect biologic processes in natural ecosystems, it is not possible to support this
view with experimental data (Alexander, 1977b).
12.2.4 Aquatic Ecosystems, Nitrogen and Eutrophication
The overenrichment of surface waters, usually lakes, with nutrients is termed eutrophi-
cation. This process results in an array of water quality changes that are generally regarded
as undersirable. Phosphorus and nitrogen are the most important nutrients that stimulate
eutrophication, and in most lakes phosphorus is considered the more critical of the two. In
coastal and estuarine ecosystems, however, nitrogen is more often the limiting nutrient and
nitrogen inputs may control eutrophication. Furthermore, in many already-eutrophic lakes,
biotic productivity is controlled by nitrogen, because the N/P ratios of pollutants from many
cultural sources (e.g., domestic sewage) are far below the ratios needed for plant growth.
The role of nitrogen in cultural eutrophication therefore appears to be important, although it
is complex and poorly quantified relative to the role of phosphorus.
The sources of manmade nitrogen reaching surface waters include sewage, industrial wastes,
animal manures, surface runoff and sub-surface transport of nutrients from urban and agricul-
tural lands, and atmospheric fluxes. It has been estimated (National Research Council, 1978)
12-10
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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 nitro-
gen inputs, rather than nitrate per se, must be considered.
The average atmospheric input of 10 to 20 kg N/ha-yr that is typical for most of the
United States is also a sufficient nutrient loading to support a moderate increase in biotic
productivity in some lakes, especially shallow, oligotrophic lakes that may be nitrogen-limited.
Atmospheric nitrogen fluxes may contribute to slight eutrophication in such cases; however, it
is unlikely that these inputs alone would induce serious water quality problems.
12.2.4.1 Eutrophication of Lakes—Cultural or man-induced eutrophication has been one of the
most intensively studied water quality problems in the past ten to fifteen years. Although
many lakes become naturally more productive and nutrient-rich as they fill in and age, natural
eutrophication is a slow process, and its effects are unlikely to be perceived within a single
human lifetime. However, addition of excessive amounts of nutrients from sewage effluents,
agricultural runoff, urban runoff and other anthropogenic sources can greatly modify the
characteristics of lake in a matter of a few years; the literature is replete with examples of
this phenomenon.
The over-enrichment or eutrophication of surface waters, usually lakes, with nutrients
results in an array of water quality changes that are generally considered undesirable. These
changes most commonly include the proliferation or "blooms" of algae and aquatic macrophytes,
the depletion of dissolved oxygen in bottom water, a decrease in water clarity, the loss of
cold water fisheries, shortened food chains, and takeover by rough fish. Table 12-1 summa-
rizes changes in common trophic state indicators that occur when lakes become eutrophic, and
Table 12-2 lists some common water use problems that may result from eutrophication.
Eutrophication is usually considered undesirable. This somewhat narrow viewpoint, how-
ever, ignores the fact that nutrient-rich waters are more productive not only of algae, but
also of fish. Lakes are not now a significant source of protein in the United States, but
lake fish may be an important food resource in a food-hungry world. Many sports fishermen
prefer moderately eutrophic lakes, unless they are seeking coldwater fish, which cannot sur-
vive in such lakes because of oxygen depletion in the cold bottom waters. A conflict thus
exists between the desires of some fishermen and the preferences of swimmers and other recrea-
tional users of lakes, who generally favor the clearest and most oligotrophic situation. On
the other hand, continued nutrient enrichment eventually is undesirable to sport fishermen
also, since game fish disappear, rough fish predominate, and excessive aquatic weed growths
may hinder or prevent boating in highly eutrophic lakes.
For some functions of some oligotrophic lakes, where nitrogen may be the limiting
nutrient, the contribution from runoff or atmosphere fluxes may be essential to maintaining
biological productivity. The point at which the effects on productivity of nitrate input to
12-11
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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)
2
Biological Indicators
Algal bloom frequency (I)
Algal species diversity (D)
Chlorophyll a (I)
Proportion of blue green algae in plankton (I)
Primary production (I)
Littoral vegetation (I)
Zooplankton (I)
Fish (I)
Bottom fauna (I)
Bottom fauna diversity (D)
(I) after parameter signifies that value increases with eutrophication;
. (D) signifies that value decreases with eutrophication.
2
Biological parameters have important qualitative changes, i.e., species
changes as well as quantitative (biomass) changes as eutrophication proceeds.
SOURCE: (Brezonick, 1969).
12-12
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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
Transmissibility of water in canals impaired by extensive macrophyte
growths
Toxicity of algal blooms to cattle and wildlife
Increases in water loss in arid regions caused by evapotranspiration
from floating vegetation
SOURCE: (Brezonick, 1969).
12-13
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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 bioshphere com-
pared to nitrogen, and because the phosphorus in minerals and soils is relatively immobile,
whereas nitrogen compounds are quite mobile. Lake Tahoe (California, Nevada) is a well-known
example of a nitrogen-limited oligotrophic lake. In highly eutrophic lakes nitrogen is fre-
quently the limiting nutrient, most often because domestic sewage, the chief nutrient source
for many eutrophic lakes, is imbalanced with respect to nitrogen and phosphorus. The total
N/P ration (by weight) in sewage is about 3:1 to 4:1, largely because of the widespread use of
phosphate detergents. By comparison, the annual N/P ratio of healthy plants is about 7:1 to
8:1 (by weight).
Miller et al. (1974) conducted algal nutrient bioassays on waters from 49 lakes through-
out the United States and found that phosphorus limited growth in 35 lakes; nitrogen was limit-
ing in eight lakes; and some other nutrient was limiting in six. The incidence of phosphorus
noted in National Eutrophication Survey data on Florida lakes (National Research Council, 1978).
12.2.4.2 Eutrophication in Coastal Waters—Studies of estuarine waters at several locations
along the east coast of United States have indicated that low concentrations of dissolved
nitrogen limit primary production (Goldman et al., 1973; Goldman, 1976; Ryther and Dunstan,
1971; Thayer, 1971).
Additions of nitrate to such estuarine systems stimulate primary production and can pro-
duce changes in the dominant species of plants, leading to cultural eutorphication and ulti-
mately to deterioration of water quality. However, the significance of nitrogen as a limiting
nutrient varies in different estuaries and even on a spatial and temporal basis within a sin-
gle estuarine system [e.g., Thayer (1971), Estabrook (1973), Goldman (1976)]. Furthermore,
not all estuaries are nitrogen-limited; Myers (1977) found that phosphate was the primary
limiting nutrient in near-shore waters off the Gulf of Mexico near Appalachicola, Florida.
The high degree of heterogeneity in the role of nitrogen as a control of productivity in
coastal areas makes it difficult to establish quantitative relationships between nitrate
loading and water quality.
The reasons that nitrogen is more important as a limiting nutrient in marine coastal
waters than in fresh waters are uncertain. A higher rate of phosphorus exchange between sedi-
ment and water in saline waters is one possibility. It has also been suggested that denitri-
fication of the nitrate that diffuses into anoxic sediments limits the amount of available
nitrogen in estuarine areas, but this hypothesis needs further study.
A number of symposia have treated the causes and consequences of eutrophication in con-
siderable detail (Allen and Kramer, 1971; Likens, 1971; Middlebrooks et al., 1973; National
12-14
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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 (1974) was the first to determine critical nutrient levels associated with water
quality degradation in lakes. He concluded from a study of 17 lakes in southeastern Wisconsin
that lakes with spring maximum concentrations of more than 300 mg/1 of inorganic nitrogen and
more than 10 to 15 mg/1 of orthophosphate-P could be expected to have algal nuisances in the
summer. These numbers have been widely quoted and used as water quality guidelines in many
areas of the United States, in spite of the narrow data base from which they were developed.
Vollenweider (1968, in a classic study, developed the concept of nutrient loading rates
and presented graphs of critical areas nutrient loading (grams of nitrogen or phosphorus per
square meter of lake surface per year) versus mean depth, as management guidelines. Figure
12-3 presents Vollenweiger1s loading graph for nitrogen. Vollenweider (1968) presented a semi-
theoretical mass balance nutrient model as the basis for his loading graphs.
Simple nutrient input-output models have provided insights into the dynamics of nutrients
in lakes, and they offer a rational basis for the development of critical nutrient loading
rates and lake management guidelines (e.g., Dillon and Rigler, 1975). Such models to date,
however, have been oriented primarily toward phosphorus, under the assumption that it is the
key limiting nutrient in lakes. Further studies are needed to develop more accurate loading
guidelines for nitrogen and to obtain quantitative data to apply the input-output models to
nitrogen-limited systems.
12.2.4.3 Nitrogen Cycling in Eutrophic Lakes—Eutrophication leads not only to increased rates
of nitrogen cycling in lakes; it also provides conditions for some reactions in the nitrogen
cycle that normally do not occur in oligotrophic lakes. For example, nitrogen fixation by
blue-green algae is essentially limited to eutrophic lakes (Home, 1977; Stewart et al., 1971).
Although blue-green algae are cosmopolitan, they are seldom the dominant phylum in oligotrophic
lakes, and nitrogen-fixing species (e.g., Anabaena spp., Aphanizomenon flos-aquae) are rare in
non-eutrophic lakes. This fact is ironic in view of the well-known inhibition of fixation by
high concentrations of inorganic nitrogen. However, fixation in eutrophic lakes is generally
associated with nitrogen depauperate periods, such as late summer in temperate surface waters.
Maximum bloom development by nitrogen-fixing blue-green algae requires an adequate supply of
phosphorus, and dissolved phosphorus is usually growth-limiting in oligotrophic waters. For
example, Vanderhoef et al. (1974) studied nitrogen fixation in Green Bay (Lake Michigan) and
found that the nonfixing blue-green Microcystis predominated in areas where all nutrients were
high. Nitrogen-fixing Aphanizomenon increased with declining combined nitrogen concentrations
and showed increased efficiency of fixation as inorganic nitrogen levels decreased. The stand-
ing crop of this species decreased with decreasing phosphate concentrations. Finally, diatoms
12-15
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10.0
5.0
2 .
5
3
z
LU
O
O
CC
UJ
cc
2.0
1.0
0.5
0.2
EUTROPHIC LAKES
OLIGOTROPHIC LAKES
I
I
10 20
MEAN DEPTH, meters
50
100
Figure 12-3. Areal loading rates for nitrogen plotted against mean
depth of lakes (Volienweider, 1968).
12-16
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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 where fixation supplies up to 50 percent of the annual nitrogen
input have been reported. Even in the typical case where fixation makes only a small contri-
bution to the total loading, however, the process is still significant in maintaining nuisance
blue-green algal blooms in lake surface waters.
Denitrification occurs in the anoxic hypolimnia of stratified eutrophic lakes, and can
represent a significant term in lacustrine nitrogen balances (see National Research Council,
1978). Denitrification also occurs in the anoxic sediments of lakes. The sources of nitrate
for sediment denitrification may be upward seepage of groundwater, downward diffusion of
nitrate from the lake water column, or nitrification in the oxygenated surface layer of
sediment. Sediment denitrification can occur in oligotrophic lakes, since their sediments are
also anoxic. However, Chen et al. (1972) reported much higher rates in sediments from a hard
water eutrophic lake than in those from a soft water oligotrophic lake.
12.2.4.4 Form of Nitrogen Entering Lakes—It is difficult to generalize about the percentage
of the total nitrogen loading to lakes that is contributed as nitrate. Nutrient budgets are
generally presented by source (streams, rainfall, sewage effluents, etc.) rather than by
nitrogen form. Lake Wingra, Wisconsin (National Research Council, 1978) represents one of the
few cases where nitrogen loading rates have been broken down according to form. Table 12-3
indicates that 47 percent of the total nitrogen loading to Lake Wingra was in the form of
nitrate.
TABLE 12-3. NITRATE-N LOADINGS TO LAKE WINGRA
Source
Precipitation on
lake surface
Dry fallout
Spring flow
Urban runoff
Average
TOTAL
Kilograms
N03~-N/yr
440
480
4,140
600
_ _ _
5,660
Percent
N as NO
40
22
96
13
" ~
47
Total
3~'N
SOURCt: (National Research Council, 1978).
12-17
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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 composition,
making generalizations tenuous. Kluesener and Lee (Kluesener, 1972; Kluesener and Lee, 1974)
summarized average nitrogen component concentrations from several urban runoff studies. The
grand means of the data they collected are: NH,-N, 0.44 mg/liter; NO, -N, 0.51 mg/liter;
organic nitrogen, 2.0 mg/liter.
In summary, the contribution of nitrate to eutrophication is uncertain, because of a lack
of data dealing with nitrate per se, and due to the ease with which various forms of nitrogen
are interconverted. Nitrogen contributions from human activities can promote increased bio-
logical productivity in aquatic systems, but the role of nitrogen in eutrophication is under-
stood much less quantitatively than the role of phosphorus. The effects that nitrogen
additions may have on productivity, phytoplankton sucession, and 'other processes within
aquatic ecosystems are certain to be influenced by other variables, such as light and tempera-
ture; however, there is little quantitative information available regarding the raltionships
among these factors.
12.2.5 The Value of a Natural Ecosystem
Ecosystems are usually evaluated by modern man solely on the basis of their economic
value to him, i.e., dollars and cents value to man. This economic value, in turn, is depen-
dent on the extent to which man can manipulate the ecosystem for his own purpose. This single-
purpose point of view makes it difficult to explain the many benefits of a natural ecosystem
to man's welfare in terms of the conventional cost-benefit analysis. Natural forests are
among the most efficient in the fixation of solar energy. Most agriculture, by comparison, is
inefficient in total energy fixed; however, in transforming solar energy into food for man it
may be highly efficient, so agriculture is emphasized (Woodwell, 1978).
Many functions of natural ecosystems and their benefits to man are unknown to the deci-
sion makers. Gosselink et al. (1974) have, however, placed a value on a tidal marsh by
assigning monetary values to the multiple contributions to man's welfare such as fish nur-
series, food suppliers, and waste-treatment fucntions of the marsh. They estimate the total
social values to range from $50,000 to $80,000 per acre.
Using four different categories, Gosselink et al. (1974) developed a step-wise means of
assessing the true value of natural tidal marshes to society as a whole. The value was based
on commercial usage, social usage and the monetary value of natural ("undeveloped") estuarine
environments.
The categories or levels of marshlands to which monetary values were assigned are: (1)
commercial and recreational use, e.g., shell fish production and sport fishing; (2) potential
for development, e.g., aquaculture, draining for industrial use; (3) waste assimilation or
12-18
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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. $50,000; and (4) a. $4,100; b. $82,000.
The foregoing estimates for category (1) were based on identifiable 1974 commercial and
recreational uses for which monetary values could be determined rather well. For category (2)
the income-capitalization approach was used to estimate the values for development potential
and for aquaculture. The estimates for tertiary sewage treatment (3) and life support (4)
represent estimates of what man would have to pay for this useful work that is now performed
by an acre of estuary were it not available to do this work.
Shortcomings exist in evaluating the environment solely in terms of direct uses or pro-
ducts. "Such cost-accounting ignores the extremely valuable life-support work that natural
areas carry on without any development or direct use by man. It is this 'free work of nature'
that is grossly, undervalued, simply because it has always been taken for granted or assumed to
be unlimited in capacity" (Gosselink et al. , 1974). Development by man of a salt marsh may
adversely affect its functioning in tertiary sewage treatment or as a life support system,
therefore, it is important to evaluate it before deciding what kind of development, if any, is
in the long-term best interest of both the environment and the economy (Gosselink et al.,
1974).
Westman (1977) also evaluated the benefits of natural ecosystems by estimating the mone-
tary costs associated with the loss of the free services (absorption or air pollution, pro-
vided by the ecosystems. Westman estimated that the oxidant damage to the San Bernardino
National Forest could result in a cost of $27 million per year (1973 dollars) for sediment
removal alone due to erosion as long as the forest remained in the early stages of succession.
Estimates of the cost in currency of the values of items and qualities such as clean air
and water, untamed wildlife, and wilderness, once regarded as priceless, are an attempt to
rationalize the activities of civilization (Westman, 1977). When estimating the monetary cost
in currency of the values lost through the damaging of ecosystems, the assumption is usually
made that the decision makers will choose the alternative which is most socially beneficial as
indicated by costs compared to benefits. As Westman (1977) points out, the assumption "that
decisions that maximize benefits cost ratios simultaneously optimize social equity and utility"
are based on certain inherent corollaries. These are:
"(1) The human species has the exclusive right to use and manipulate
nature for its own purposes. (2) Monetary units are socially acceptable
as means to equate the value of natural resources destroyed and those
developed. (3) The value of services lost during the interval before
the replacement or substitution of the usurped resource has occurred
is included in the cost of the damaged resource. (4) The amount of
, compensation in monetary units accurately reflects the full value of
the loss to each loser in the transaction. (5) The value of the item
to future generations has been judged and included in an accurate way
in the total value. (6) The benefits of development accrue to the
12-19
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same sectors of society, and in the same proportions, as the
sectors on whom the costs are levied, or acceptable compensation
has been transferred. Each of these assumptions, and others not
listed, can and have been challenged" (Westman, 1977).
In the case of (4) above, for example, the losses incurred when the development of natural
ecosystems are involved, include species other than man. These losses are seldom, if ever,
compensated. The public at large also is usually not consulted to determine whether the dol-
lar compensation is adequate and acceptable. Frequently, there is no direct compensation.
Corollary (5) can never be fulfilled because it is impossible to determine accurately the
value to future generations.
It should be remembered that ecosystems are life support systems and therefore their
worth, in the final analysis, cannot be valued in dollars and cents.
12.3 EFFECTS OF NITROGEN OXIDES ON VEGETATION
Of the various nitrogen oxides (NO ) in the ambient air (Chapter 8) only nitric oxide (NO)
and nitrogen dioxide (NO,,) are considered important phytotoxicants. The direct effect of NO
on vegetation are usually associated with and confined to areas near specific industrial
sources. For example, vegetation injury from exposure to NO- has been observed near nitric
acid factories and arsenals, but there are no published reports on vegetation injury in the
field due to NO or other oxides of nitrogen.
The direct effects of NO on vegetation are reviewed in this chapter with emphasis on
studies relating NO effects to known exposure concentrations and durations. Since most avail-
A
able data pertained to NOp, this pollutant receives the most attention. Also, when NO- was
experimentally combined with other pollutants such as S02, injury occurred at much lower doses
than had been found in earlier studies with NOp alone. This suggests that, in certain circum-
stances NOp in conjuction with other gases in the ambient air may behave synergistically.
The contribution of NO to the increased acidity of precipitation and its effects on eco-
systems is discussed in Chapter 11.
12.2.1 Factors Affecting Sensitivity of Vegetation to Oxides of Nitrogen
A notable feature of the response of vegetation to NOp stress is the varied degrees of
NOp-induced injury. This variation ranges from overt leaf chlorosis and necrosis to alter-
ations of leaf metabolism. These differing responses can be explained by the physiological
processes affecting NOp uptake into the leaf, pollutant toxicity at target sites and cellular
repair capacity. Since plants develop as a consequence of environmental-genotypic inter-
actions, each plant possesses a unique set o structural and functional properties which change
continuously in response to genetic and environmental stimuli. These interactions between
environmental and genetic factors underlie and explain the dissimilar plant responses to N0?
exposures.
Information on relative sensitivity (differential response) to NOp is summarized in Table
12-4. The three classes - susceptible, intermediate, and tolerant - are approximate because
12-20
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TABLE 12-4. RELATIVE SENSITIVITY OF SEVERAL PLANT SPECIES TO NITROGEN DIOXIDE (HECK AND TINGEY, 1979;
MACLEAN, 1977; TAYLOR AND MACLEAN, 1970; TAYLOR ET AL., 1975, U.S. ENVIRONMENTAL PROTECTION AGENCY, 1971)
Plant Type
Susceptible
Intermediate
Tolerant
Coniferous Trees
I
N)
Field Crops & Grasses
Fruit Trees
Larix decidua Mill.
(European Larch)
Larix leptolepis Gord.
(Japanese larch)
Avena sativa L. (Oats)
cv. Clintland 64
cv. 329-80
cv. Pendek
Bromus inermis, L.
(Bromegrass)
cv. Sac Smooth
Hordeum distichon L.
(Barleyl
Medicago sativa, L. (Alfalfa)
Nicotians glutinosa L. (Tobacco)
Nicotiana tobacum L. (Tobacco)
Scorzonera hispanica L.
(Viper1s grass)
T._ incarnatum L. (Crimson or
Italian Clover)
Trifolum pratense L. (Red clover)
Triticum vulgare. Vill. (Wheat)
cv. Wells
Vicia sativa L. (Spring vetch)
Hal us sj>. (Showy apple)
Abies alba Mill. (White Fir)
Abies homolepis Sieb. & Zucc.
(Nikko or Japanese fir)
Abies pectinata DC (Common
Silver Fir)
Chamaecyparis Lawsoniana [Murr. ]
Parl (Lawson's cypress)
Picea glauca [Moench] Voss
fwhite Spruce)
Picea pungens glauca. Regel
(Colorado Blue Spruce)
Gossypium hirsutum, L. (Cotton)
cv. Acala 4-42
cv. Paymaster
Nicotiana tabcacum, L. (Tobacco)
cv7White Gold
cv. Bel-B
cv. Bel W3
Poa annua, L. (Annual bluegrass)
Secale cereale L. (Rye)
Triticum aestivum L. (Wheat)
Zea Mays L. (Sweet Corn)
Citrus sg. (Orange, grapefruit,
tangelo)
Pinus Hugo Turra (Knee pine or
dwarf mountain pine)
Pinus nigra Arnold (Austrian pine)
Taxus baccata L. (English yew)
Nicotiana tabacum, L. (Tobacco)
cv. Burley 21
Poa pratensis L. (Kentucky bluegrass)
Sorghum sp.fSorghum)
cv. Martin
Zea Hays L. (Corn)
cv. Pioneer 509-W
cv. Golden Cross
Hosta plantaginea (Lam.) Aschers
(Fragrant plantian lily)
-------
TABLE 12-4 (continued)
Plant Type
Susceptible
Intermediate
Tolerant
Mains sylvestris Hill.
fApple)
Pyrus communis L. (Wild Pear)
Garden Crops
Ornamental Shrubs
and Flowers
I
hJ
r-o
(Leek)
ium qraveolens L. (Celery)
Brassica oleracea botrytis. L.
rBroccoli) cv. Calabrese
Caucus carota L. (Carrot)
Lactuca sativa. L. (Lettuce)
Petroselinum hortense Nym.
(Parsley)
Phaseolus vulgaris, L. (Bean)
cv. Pinto
Pi sum sativum L. (Pea)
Raphaims sativus L. (Radish)
cv. Cherry Belle
Rheum rhaponticum L. (Rhubarb)
Sinapis alba (White mustard)
Antirrhinum majus L.
(Giant Snapdragon)
Begonia multiflora (Tuberous-
rooted begonia)
Begonia rex, Putz. (Begonia)
cv. Thousand Wonders White
Bougainvillea spectabilis
Willd. (Bougainvillea)
Callistcphus chinensis ! L.1
Nees (China aster)
Chrysanthemum sg. (Chrysan-
santhemum)
cv. Oreyon
Hibiscus Rosa-sinensis L.
(Chinese^ hibiscus)
Impatiens sultani, Hook.
(Sultana) cv. White Imp
Citrus sinensis (L.) Osbeck
fNavel Orange)
Apium graveolens rapaceum
(Celery)
Cichorium Endivia, L. (Endive)
Ruffee
Fragaria chiloensis
grandiflora (Pine strawberry)
Lycopersicon esculentum, Mill
(Tomato)
cv. Roma
Phaseolus uulgaris humi1 is
Alef. (Bush bean)
Solanum tuberosurc L. (Potato)
Dahlia variabilis Willd.
(DahlTal
Fuchsia hybrida Voss (Fuchsia)
Gardenia jasminpides Ellis
(Cape Jasmine)
Gardenia radicans Thunb.
(GardenTal
Ixora coccinea L. (Ixora)
Ligustrum licidum Ait.
(Ligustrum)
Petunia X hybrida Hort.
Volm.-Andr. (Coiranon
Garden Petunia)
Pi ttosporum tobi ra Ait.
(Japanese pittosporum)
Rhododendron catawbiense Michx.
(Catawaba rhododendron)
Allium cepa L. (Onion)
Asparagus officinal is L. (Asparagus)
Brassica oaulorapa Pasq. (Kohlrabi)
Brassica oleracea acephala DC (Kale)
Brassica oleracea capitata L.
(Cabbagu)
Brassica oleiacea capitiata rubra L.
(Red cahbaye)
Cucumis salivus, L. (Cucumber)
cv. Long HarkeLeer
PhaseoI in vulgjris, L. (Bush Bean)
Carissa carandas L. (Cariisa)
Codiaeum varieq.jlum Blume (Croton)
Chrysanthemum le^canthemum L. (Daisy)
Convallari majajis L. (Lily-of-the-valley)
Erica carnea L. (Spring heath)
Gladiolus communis L. (Gladiolus)
Erica ^£. (HeatTT)
Hosta s£. (PUntain lily)
Juniperus coi.ferta Parl. (Shore juniper)
Rhodudendron 6j>. (Alaska)
-------
TABLE 1Z-4 (continued)
Plant Type
Susceptible
Intermediate
Tolerant
Trees & Shrubs
K>
I
Weeds
Lathyrus odoratus L. (Sweet pea)
Lupinus augustifolius L. (Lupine)
Nerium oleander L. (Oleander)
Pyracantha coccinea Roem.
(Fire thorn1)
Rhododendron canescens (Michx.)
Sweet (Hoary Azalea)
Rosa sjg. (Rose)
Vinca minor L. (Periwinkle)
cv. Bright Eyes
Betula pendula Roth. (European
white birch)
Helaleuca leucadendra (L.) L.
(Brittlewood)
Brassica sp. (Mustard)
Helianthus annuus L.
(Common Sunflower)
Acer platanoides L. (Norway
maplei
Acer palmatum Thunb.
(Japanese maple)
Tilia grandiflora (Summer)
Ti lia cordata Mill. (Small-
leaved European linden)
Halva parviflora L.
(Cheeseweed)
Stellaria media [L.] Cyrill
(Chickweed)
Taraxacum officinale Weuer
(Dandelion)
Carpiniii. betulus L. (European horrih**Mn)
Fagus by Ivatica L. (Beech)
Fagus byl v/atica atropurpurea Kirchr>
(Purp IK- leaved beech)
Ginyko bi loba L. (Gingko)
Quercus r^bur L. (English oak)
Robinia pbgudoacacia L. (Black looj"5'-)
Sambucus nigra L. (European elder)
Huds. (Scotch elm)
Ulmus monuna With. (Mountain ela)
Amaranthus retroflexus L. (Pigweed;
Cheii'jpodium album L. (Lamb1 s-quart<»*rs)
Chenopodiug] sp. (Neetle-leaved goo'>*^ oot)
-------
they are based on subjective criteria obtained from several sources. Most of the classifi-
cations are developed from experimental fumigations conducted at various locations, at
different times of the year, under different environmental conditions using different N02
exposure concentrations. Methods for assessing injury, such as percentage of leaves injured,
amount of leaf surface affected, defoliation, etc. also varied. Therefore, a plant species
considered tolerant by one investigator may be considered susceptible by another. Also, the
interaction between genetic and environmental factors that control plant sensitivity is such,
that given different sets of environmental parameters or other variables, the relative N0_
sensitivity of species or cultivars within species can change.
A given plant and its individual leaves, will vary in sensitivity to NCL, depending on
the stage of development. In tobacco (Nicotiana sj>.) the oldest leaves became chlorotic,
middle age leaves became chlorotic with necrotic lesions, and injury to the younger leaves
was limited to necrosis (Van Haut and Stratmann, 1967). In Ixora (Ixora coccinea) (Maclean et
al., 1968) mustard (Brassica, ^p_.), (Benedict and Breen, 1955) and tobacco (Nicotiana glutinosa)
(Benedict and Breen, 1955) the older leaves were more sensitive. In other species such as
chickweed (Stellaria media), dandelion (Taraxacum officinale), and pigweed (Amaranthus
retroflexus) the middle age leaves were more sensitive. However, in sunflower (Helianthus
annuus) middle age and older leaves respond similarly (Benedict and Breen, 1955). In citrus
(Citrus s£.) necrosis was most severe on the youngest leaves (Maclean et al., 1968). Emerging
or elongating needles of conifers were more susceptible than mature needles (Van Haut and
Stratmann, 1967).
Only a few studies have reported the influence of edaphic factors on plant sensitivity to
NC^. Increasing soil moisture increased sensitivity in several weed and vegetable species
(Benedict and Breen, 1955; Kato et al., 1974a).
Because of a possible relationship between atmospheric NCL and nitrogen metabolism, the
influence of soil nitrogen on the plant response to NCL has been studied. Rogers et al. (1979)
was unable to show differences in NCL uptake in corn (Zea mays) or soybean (Glycine max)
plants that were grown in soil with varying levels of nitrogen. In contrast, Srivastava et al.
(1975c) reported that N02 uptake in bean (Phaseolus vulgaris) decreased with increasing levels
of soil nitrogen. They also reported that NCL-induced foliar injury decreased with increasing
levels of soil nitrogen. Similar results were found in studies of other vegetables (Kato et
al., 1974a; Kato et al. , 1974b). Zahn (1975) reported that increasing the available soil
nitrogen reduced NCL-induced foliar injury. However, Troiano and Leone (1974) found that
tobacco (Nicotiana glutinosa) grown on a low level of soil nitrogen was more resistant than
when grown on a higher level of soil nitrogen. Kato et al. (1974a, 1974b) reported that plants
grown on NH.-N source were more sensitive to NCL-induced injury and contained higher levels
of foliar nitrite after NCL exposure than plants grown on a NO,-N source. Kidney beans
(Phaseolus vulgaris) and sunflower (Helianthus annuus) were grown on either ammonium, nitrate,
nitrite or minus nitrogen sources. The plants that received either nitrate or nitrite through
12-24
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the nutrient solution contained less nitrite in the foliage following a 3-hour exposure to
7.52 mg/m3 (4 ppm) N02 than plants grown on minus nitrogen or ammonium (Yoneyama et al.,
1979). Similarly, tomato (Lycopersicon esculentum) and sunflower (Helianthus annuus) were
grown at three levels of nitrogen nutrition ranging from 26 to 260 ppm N (Matsumaru et al. ,
1979). The plants were exposed to 0.56 mg/m3 (0.3 ppm) NOp for 2 weeks. Plant growth was
depressed between 0 and approximately 21% with no clear trend between the nitrogen concentra-
tion in the growth media and growth reductions.
Nitrogen nutrition can influence the effects of NO on tomatoes (Anderson and Mansfield,
1979). The plants were grown on either low, medium, or high levels of soil nitrogen and ex-
posed to a concentration range 0 to 0.98 mg/m3 (0.8 ppm) NO for 50 days. At a low level of
soil nitrogen, plant growth increased with increasing levels of NO. At the medium level of
soil nitrogen, the 0.49 and 0.08 mg/m3 (0.4 and 0.8 ppm) levels of NO significantly reduced
growth. At the high level of soil nitrogen, all levels of NO reduced plant growth compared to
the controls.
Several researchers have studied the effect of light and time of day on plant sensitivity
to NOp. Zahn (1975) noted that alfalfa (Medicago sativa) exposed to N02 during the night were
injured more extensively than plants exposed during the day. These findings were supported by
Czech and Nothdurft (1952) who discovered that the toxic dose for 1-hour exposures of sugar
beets (Beta vulgaris) was 10 times greater in the day time, 188 mg/m3 (100 ppm) than at night,
18.8 mg/m3 (10 ppm). Van Haut and Stratmann (1967) found leaf injury in oats (Avena sativa)
was greater at night, but they also reported that once injury was initiated, the development
of necrotic lesions was more rapid on warm sunny days. Kato et al. (1974a,b) determined that
vegetable plants were severely injured from N0« exposures in the dark and contained higher
foliar levels of nitrite than plants exposed in the light. Taylor (1968) reported that bean
(Phaseolus vulgaris) plants were injured by 5.6 mg/m3 (3 ppm) NOp in the darkness and that
this dose caused as much damage as 11.3 mg/m3 (6 ppm) N0_ in the light. Zeevaart (1076) ex-
posed 9 plant species to N02 in both light and dark. Eight species exhibited more damage when
exposed in the dark. Injury was associated with an increase in nitrite and a decrease in ex-
pressed cell sap pH; fumigation of the plants with NH, + N0~ reduced injury. However, with
o c.
tobacco (Nicotiana glutinosa) light was required for injury to develop and there was no asso-
ciation between injury and either nitrite or cell sap pH. In studies with several vegetable
plants, Inden (1975) showed that plants were most sensitive when exposed to N02 in the dark.
Also leaves treated with the photosynthetic inhibitor DCMU were very sensitive to N02 expo-
sures in the light. Plant susceptibility also varies at different times during the day. In a
series of 2-hr exposures beginning at 0800-1000 hours and ending at 2000-2200 hours, injury to
rye (Secale cereale) plants was greatest at mid-day (Van Haut and Stratmann, 1967).
12.3.2 Mode of Action
Since NO-'induced perturbations occur at cellular sites within mesophyll tissue, N02 up-
take into the leaf is requred. Absorption is governed by factors regulating gaseous exchange
12-25
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between the atmosphere and the leaf (Nobel, 1974). The N0? diffuses from the boundary layer--
bulk air interface and terminates with extraction onto mesophyll cell surfaces. The driving
force for NCL uptake is a concentration gradient and net movement along this gradient is
impeded by several leaf resistances: boundary layer, stomatal and mesophyll (residual)
resistance.
Rodgers et.al. (1979) suggested that N02 uptake in corn (Zea mays) and soybean (Glycine
max) was directly related to stomatal resistance in the NO- concentration range of 0 to 1.09
mg/m3 (0.58 ppm). Also, NO- uptake increased with light intensity through the action of light
on stomatal resistance. In studies with beans (Phaseolus vulgaris) and higher NOo concentra-
tions over the range of 0 to 13.16 mg/m3 (7 ppm), NOo uptake was controlled more by internal
leaf factors (mesophyll resistance) than stomatal resistance (Srivastava et al., 1975a,
1975b); N02 uptake was also reported to increase with concentration and decline with increas-
ing exposure time. The N0? uptake rate in the dark was approximately one-half the rate in the
light. Sunflower (Helianthus annuus) leaves absorbed approximately 14 percent as much NO- in
the dark as in the light (Yoneyama et al. , 1979). Even though NO- uptake in the dark is
lower, N02 exposures in the dark cause greater injury (see 12.2.1).
Nitrogen dioxide reacts in water to produce nitrate, NO, , and nitrite N09 in dilute
•J £.
solutions. Similar reactions would be expected when NO- dissolves in the aqueous layer sur-
rounding leaf mesophyll cells. Plants contain the enzymes, nitrate reductase that reduces
nitrate to nitrite, and nitrite reductase that reduces nitrite to ammonia which can then be
metabolized into organic nitrogen compounds. The nitrate reductase is induced in plants by
the presence of its substrate, nitrate. Zeevaart (1974) grew plants with ammonia as the sole
nitrogen source and showed that f^ exposures induced nitrate reductase activity and enzyme
activity increased with NO- concentration and duration of exposure. Yoneyama et al. (1979)
showed that exposure to 7.52 mg/m3 (4 ppm) NO- for 6 hours increased nitrite reductase
activity from 2- to 3-fold.
Faller (1972) grew sunflowers (Helianthus annuus) on a nitrogen free media and exposed the
plants to N02 for three weeks at NO- concentrations ranging from 0 to 6 mg/m3 (3.2 ppm). The
control plants showed severe signs of nitrogen deficiency and restricted growth. However, the
sypmtoms of nitrogen deficiency decreased and plant growth increased as the NO- concentration
increased up to 29 percent more than the control levels. Also the nitrogen content of the
plants was significantly increased by the exposure. Results of this study show that plants
can use atmospheric sources of nitrogen (i.e., NO-) as their sole nitrogen source. Tomato
(Lycopersicon esculentum), sunflower (He!ianthus annuus), and corn (Zea mays) derived approx-
imately 16, 22 and 14% of their nitrogen, respectively, from NO- when the plants were exposed
to 0.56 mg/m3 (0.3 ppm) for 2 weeks (Matsumaru et al., 1979). The absorption rate of NO,,,
based on plant dry weight, showed little change with soil nutrition and ranged around approx-
imately 0.8 mg/g dry weight/day for tomato and sunflower to 0.3 mg/g dry weight/day for corn.
Zeevaart (1976) grew peas (Pisum sativum) with ammonia as the only nitrogen source. When
exposed to NO-, nitrate and nitrite accumulated in the leaves. At the beginning of the
12-26
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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). Expo-
sures also increased the soluble amino (NHj) groups in several plants and the protein content
increased by 10-20 percent. Troiano and Leone (1977) reported that N02 exposures increased
the organic nitrogen content of tomato plants (Lycopersicon esculentum).
Matsushima (1972) found that exposure to 75.2 mg/m3 (40 ppm) N09 for 16 hours stimulated
14
amino acid synthesis (indicated by C labeling) although there was little change in organic
acid synthesis. Using very high concentrations of NOo (0.01-5 percent by volume) Durmi-
shidze and Nutzsubidze (1976) showed that 10 species of decidious trees, 5 species of grasses
and 5 species of coniferous trees readily assimilated isotopically-labeled N02 and incorpo-
rated it into amino acids. Spinach (Spinacia oleracea) was exposed to 7.52 mg/m3 (4 ppm)
N02 for 2.5 hours to determine the metabolic fate of the nitrogen from the N0? (Yoneyama and
Sasakawa, 1979). Isotopically labeled nitrogen was incorporated into both amino acids and
amides in a pattern suggesting that the nitrogen was assimilated through the glutamine
sythethase/glutamate synthase pathway. Rogers et al. (1979) reported that the plants accumu-
lated isotopically labeled nitrogen proportional to the ambient NOp concentration over at
range of 0.19 to 0.75 mg/m3 (0.1 to 0.4 ppm). Following a 3-hour exposure to 0.60 mg/m3 (0.32
ppm) N02, over 97% of the absorbed N02 was incorporated into reduced nitrogen compounds.
However, the majority of this nitrogen remained in foliage, with only 3-5% being exported to
the roots.
When plants are exposed to high levels of NOp the injured leaves frequently exhibit a
waxy or water-soaked appearance prior to necrosis. This suggests that cell membranes were
disrupted, possibly beyond repair. Berge (1963) suggested that N0« may cause cellular plas-
molysis implying damage to cellular membranes. He also noted a decline in starch grains.
Felmeister and colleagues (1970) discussed the propensity of NO- to attach to lipid mono-
layers, especially those monolayers containing unsaturated lipids. These lipids have been
proposed to be components of biological membranes. The work of Estefan et al. (1970) sug-
gested that the products of NO* action on lipid m'onolayers included both transient and stable
free radicals. Because of the high concentrations used in their experiments, it is not
apparent that a similar response would occur at ambient concentrations.
Well burn et al. (1972) studied the effects of NOg exposures on the ultrastructure of
chloroplasts i_n vivo. Broad bean (Vicia faba) plants were exposed for 1 hour to 1.9, 3.8, or
5.6 mg/m3 (1.0, 2.0, or 3.0 ppm). The leaves were harvested immediately after exposure and
prepared for electron microscopy. Examination of the chloroplasts showed that N0? caused a
swelling of the thylakoids associated with the stroma. These swellings appeared to be rever-
sible since thylakoid swelling was not observed in chloroplasts of leaves exposed to unpol-
luted air immediately following NO 2 fumigation.
Kandler and Ullrich (1964) demonstrated that there was a reduced amount of carotene and
chlorophyll in leaves after actue NO^ exposure. Some species of lichens exposed to 3.76 mg/m3
12-27
-------
(2.0 ppm) N02 for 6 hours had reduced chlorophyll content; a dose of 7.52 mg/m3 (4.0 ppm) N02
for 6 hours reduced chlorophyll content even further (Nash, 1976).. In contrast, Taylor and
Eaton (1966) found that chlorophyll content increased following chronic exposures to NO-.
Similarly, Horsman and Wellburn (1975) found that 0.188 to 1.88 mg/m3 (0.1 to 1.0 ppm) N02
applied to pea (Pisum sativum) seedlings increased their chlorophyll content 5 to 10 percent.
They also noted the deeper green color and downward curving of the leaves observed by Taylor
and Eaton (1966).
hi vivo experiments performed by Hill and Bennett (1970) showed that both NO and NO- in-
hibited apparent photosynthesis of oat (Avena sativa) and alfalfa (Medicago sativa) plants at
concentrations below those that cause foliar lesions. The threshold dose for this inhibition
was 0.74 mg/m3 (0.6 ppm) for NO and 1.13 mg/m3 (0.6 ppm) for N02 in 90 minute fumigations, but
the inhibition occurred faster for NO than N09. The NO -induced inhibition of photosynthesis
C. A
was not permanent. The rate of recovery for a given NOinduced inhibition level was faster
than for NO,,. Recovery from NO-inhibited photosynthesis was generally complete within 1 hour.
Full recovery from NO,,-induced inhibition of more than 25 percent required more than 4 hours.
However, complete recovery of non-foliar injured plants was noted consistently within 1 day
following fumigation. In fumigations introducing both NO and N02 (1:1) simultaneously, the
degree of inhibition of apparent photosynthesis was the same as the sum of that induced by
each pollutant when introduced separately.
Capron and Mansfield (1976) found a reduction in the photosynthetic rate of tomato
(Lycopersicon esculentum) plants exposed to 0.47 mg/m3 (0.25 ppm) N02, 0.31 mg/m3 (0.25 ppm)
NO or higher concentrations over a 20-hour period. The effect of the two gases in combination
was an additive inhibition of photosynthesis. Srivastava et al. (1975a) studied the effects
of N02 on the gas exchange of the primary leaves of bean (Phaseolus vulgaris). Apparent pho-
tosynthesis and dark respiration were both inhibited by N02 concentrations between 1.88 and
13.5 mg/m3 (1 and 7 ppm). The degree of inhibition increased with increasing N0? concentra-
tion and exposure time. In exposures to N02, transpiration rate was effected less than photo-
synthesis or respiration. Hence, it was proposed that the principal effects of N02 on leaf
gas exchange occurred in the leaf mesophyll cells and not on the stomata (Hill and Bennett,
1970; Srivastava et al., 1975a).
12.3.3 Visible Symptoms of NO, Injury
No one visual symptom or set of symptoms reliably indicates plant exposure to N02> The
diagnosis of injury resulting from N02 is often difficult (Applied Science Associates, Inc.,
1976; Taylor and Maclean, 1970). The injury pattern may vary within a species, cultivar, age
of leaf, season of year, and/or pollutant dose.
Acute foliar marking produced by high concentrations of nitrogen dioxide exposures are
characterized by water-soaked lesions which appear first on the upper leaf surface, followed
by rapid tissue collapse. With time these lesions extend through the leaf and produce small,
irregular necrotic patches. Necrotic areas are usually white to tan or brown and resemble S0?-
induced symptoms. Lesions occur between the veins of all sensitive plants, and may be
12-28
-------
located anywhere on a leaf surface, but they are most prominent at the apex along the margins.
In monocots, acute N0« exposures most often result in yellow to ivory to white necrosis that
begins at or just below the tips of the leaf blades. Necrotic margins and striped necrotic
lesions between the veins also occur. In most grains and grasses, injury from acute exposures
affects the entire width of the leaf blade.
In conifers, acute N0? injury usually begins at the needle tips and progresses towards
the base. The boundary between healthy and injured tissues is sharply delineated by a brown
or red-brown band. Young emerging needles show N0_ injury at the tips, whereas older needles
may develop necrosis in the central or basal portions of the needles. Injured needles may
drop prematurely.
Chlorosis is one symptom of chronic NC^ exposure but is nonspecific and can be a symptom
of injury caused by other pollutants. For many chronic exposures, chlorosis precedes the ap-
pearance of chronic lesions. Cereal, grains, and corn leaves often develop longitudinal chlo-
rotic bands before necrosis develops. In monocots, chlorosis may occur as transition zones be-
tween healthy tissue and the necrotic tips. In some broad leaf plants, chlorosis from chronic
N02 exposures begins with many small yellow-green areas on the leaf surface which may merge as
exposure continues. In some species, chlorosis may be concentrated near the leaf margins.
12.3.4 Dose Response
Exposures to most pollutants, including NO , are usually classified arbitrarily as acute
or chronic. In experimental fumigations, acute exposures are of short duration at high pol-
lutant concentrations. Chronic exposures are for longer periods (usually intermittent, occa-
sionally continuous) at low concentrations. The ranges of concentrations and durations of ex-
posure (doses) for acute and chronic exposures have not been defined. Most botanic investi-
gators would designate NO^ exposures of 3 to 5 mg/m3 (1.6 to 2.66 ppm) or greater for up to 48
hours as acute and those for longer periods at lower concentrations as chronic. However,
these definitions do not apply in the field near sources of NO emissions. There, an acute
exposure is any single exposure causing plant injury. The term "chronic" is applied to a
series of exposures that result in injury where no single exposure has an effect by itself.
12.3.4.1 Foliar Injury-Thomas (1952) observed that leaves of plants growing near nitric acid
factories often had brown and black spots near the leaf margins. This was an early indication
that oxides of nitrogen may be phototoxic. Haagen-Smit (1951) was one of the first to recog-
nize the importance of N02 in causing photochemical smog effects on vegetation. He found that
N02 added to experimental fumigation mixtures caused plant injury similar to that caused by
ozone, but he provided no information on the direct effects on plants. Subsequently, Haagen-
Smit et al. (1952) tested N0~ at 0.75 mg/m3 (0.4 ppm) on 5 species but observed no injury.
Middleton (1958), Middleton et al. (1958) and Thomas (1961) all recognized that N02 appeared
in photochemically polluted atmospheres as a by-product of combustion, but they postulated
that levels were and would continue to be too low to cause vegetation injury.
Korth et al. (1964) found that beans (Phaselous vulgaris), tobacco (Nicotiana tobacum),
and petunia (Petunia multiflora) were not injured by 1.88 mg/m3 (1.0 ppm) N02 for 2 hours.
12-29
-------
Middleton et al. (1958) suggested that 5.64-7.52 mg/m3 (3-4 ppm) for 8 hours was a threshold
concentration that could cause visible injury on pinto bean (Phaseolus vulgaris) leaves.
Czech and Nothdurft (1952) fumigated agricultural and horticultural crops with N02 in the
laboratory and in small greenhouses. Rape (Brassica napus), wheat (Triticum satuvim), oats
(Avena sativa), peas (Pisum sp_.), potatoes (Solanum tuberosum), and beans (Phaseolus vulgaris)
showed little or.no injury from 56.4 mg/m3 (30 ppm) NCL for 1 hour. Alfalfa (Medicago sativa),
sugar beets (Beta vulgaris), winter rye (Secale cereale), and lettuce (Lactuca sativa) showed
some effects. Fujiwara (1973) reported that 37.6-94 mg/m3 (20-50 ppm) NO for 30 to 60
minutes injured most plants studied.
Heck (1964) fumigated cotton (Gossypium hirsutum), pinto beans (Phaseolus vulgaris) and
endive (Cicorium endivia) under controlled conditions with 1.88 mg/m3 (1.0 ppm) N02 for 48
hours and observed slight but definite spotting of leaves. There was no injury produced at
1.88 mg/m3 (1.0 ppm) N02 for 12 hours. In another study, the same species were fumigated with
0.94, 3.76 and 6.58 mg/m3 (0.5, 2.0, and 3.5 ppm) N02 for 21 hours. At exposures of 6.58
mg/m3 (3.5 ppm) N02 mild necrotic spots appeared on cotton (Gossypium hirsutum) and bean
(Phaseolus vulgaris) leaves and the endive leaves (Cicorium endivia) were completely necrotic.
Taylor and Cardiff (unpublished data, cited in Taylor et al., 1975) exposed field crops
to N02 in sunlight chambers. They found that several field crops exposed to 18.88 mg/m3 (10
ppm) N02 for 90 minutes suffered little or no injury; but in tomato, a 90-rninute exposure to
28.20 mg/m3 (15 ppm) increased the extent of injury by 90 percent. They concluded that the
injury threshold for several field crops would be 18.80 to 28.20 mg/m3 (10 to 15 ppm) N02 for
90 minutes.
Maclean et al. (1968) exposed 14 ornamental and 6 citrus species to N02 concentrations
ranging from 18.8 to 470 mg/m3 (10 to 250 ppm) for 0.2 to 8 hours. Necrosis occurred in the
citrus species when the leaves were exposed to 376 mg/m3 (200 ppm) for 4 to 8 hours or 470
mg/m3 (250 ppm) for 1 hour. Nonspecific marginal and intercostal necrosis developed within 1
hour after exposure. Young citrus leaves wilted and abscised at some lower doses.
Heck and Tingey (1979) conducted a series of short term fumigations which exposed field
and vegetable crops to various N02 concentrations. In one experiment 10 field and vegetable
species were exposed to 15.04, 30.08, or 60.16 mg/m3 (8, 16, or 32 ppm) N02 for 1 hour (Table
12-5). At 60.16 mg/m3 (32 ppm) levels of NO,,, all species showed visual injury. However, at
15.04 mg/m3 (8 ppm) N02 exposure, only brome grass (Bromus inermis) and tomato (Lycopersicon
esculentum) exhibited foliar injury. In a second experiment, 22 crop species were given 9
different time and concentrations treatments. Exposure durations varied from 0.5 to 7 hours
and N02 concentrations ranged from 3.76 to 37.6 mg/m3 (2-20 ppm) (Table 12-6). An important
conclusion from these experiments was that the extent of injury was greatest when the N02
levels were high, even for short time periods. . For example, cotton exposed 28.2 mg/m3 (15
ppm) for 1-hour had an injury rate of 27 percent for the three most sensitive leaves. When
cotton was exposed to 18.8 mg/m3 (10 ppm) N02 for 2-hours the comparable injury rate was 2
percent. Therefore dose is not always a good predictor of injury.
12-30
-------
TABLE 12-5. ACUTE INJURY TO SELECTED CROPS AFTER A
1-HOUR EXPOSURE TO NITROGEN DIOXIDE (HECK AND TINGEY, 1979)
Plants .
(Common, Cultivar, Scientific)
Tomato, Roma
(Lycopersicon esculentum)
Wheat, Wellsc
(Triticum durum)
Soybean, Scott
(Glycine max)
Tobacco, Bel W,5
(Nicotiana tabacum)
Bromegrass, Sac Smooth
(Bromus inermis)
Swiss Chard, Fordhook Giant0
(Beta vulgaris cicla)
Tobacco, White Goldb
(Nicotiana tabacum)
Cotton, Acala 4-42c
(Gossypium hirsutum)
Beet, Perfected Detroit0
(Beta vulgaris)
Orchard Grass, Potomac0
(Dactylis glomerata)
Tobacco, Bel W3°
8 ppm
1
0
0
0
2
0
0
0
0
0
0
Injury Index
16 ppm
48
47
26
23
17
11
1
0
0
1
0
32 ppm
100
90
100
97
97
62
70
54
36
18
5
aPlants were exposed in Cincinnati, Ohio.
Plants were exposed in August with light intensity at 2200 ft-c,
temperature 28°C, humidity 75 percent.
its were exposed in January with light
temperature 21°C, humidity 70 percent.
°Plants were exposed in January with light intensity at 1400 ft-c,
Scientific name is given only when plant is first listed.
12-31
-------
TABLE 12-6. PERCENT LEAF AREA INJURED BY DESIGNATED DOSAGE OF NITROGEN DIOXIDE (HECK AND TINGEY, 1979)
K>
U>
Plants
(Common, Cultivar, Scientific)
Oats, Clintland 64
(Avena sativa)
Radish, Cherry Belle
(Raphanus sativus)
Bromegrass, Sac Smooth
Begonia- Thousand Wonders*
White , (Begonia Rex)
Chrysanthemum, Oregon *
(Chrysanthemum sp.)
Sultana, White Imp *
(Impatiens sultani)
Oats, 329-80b
(Avena sativa)
Cotton, Paymaster
(Gossypium hirsutum)
Wheat, Wells
Cotton, Acala 4-42
Periwinkle, Bright Eyes *
(Vinca minor)
Dosage (ppm x hr) 2. 5
(ppm) 5
(hr) 0.5
0
0
0
0
1
0
2
0
3
0
0
4
4
1
0
0
0
1
1
0
2
0
2
0
0
6
3
2
0
0
0
0
1
0
1
6
1
0
0
10
20
0.5
80
95
69
26
34
51
32
50
31
28
13
14
7
2
2
0
0
0
0
0
1
0
3
0
0
15
15
1
84
90
50
35
41
26
18
27
34
28
20
20
5
4
0
1
1
4
4
0
9
2
3
0
1
20
10
2
39
31
26
49
25
24
14
2
2
1
23
35
5
7
21
2
0
5
1
0
14
1
1
I
I
Oats, Pendekc
(Avena sativa)
0 39
-------
TABLE 12-6 (continued)
I
OJ
u>
Plants
(Common, Cultivar, Scientific)
Broccoli, Calabreese
(Brassica oleracea botrytis)
Tobacco, Bel B
(Nicotiana tabacum)
Tobacco, White Gold
Tobacco, Bel VL
Tobacco, Burley 21
(Nicotiana tabacum)
Corn, Pioneer 509-W
(Zea mays)
Corn, Golden Cross
(Zea mays)
Azalea, Alaska * .
(Rhododendron, sp.)
Sorghum, Martin
(Sorghum, sp. )
Cucumber, Long Marketer
(Cucumis sativus)
Dosage (ppm x hr) 2.5
(ppm) 5
(hr) 0.5
0
0
0
0
0
1
0
0
0
0
4
4
1
0
0
0
0
0
0
0
0
0
0
6
3
2
0
3
I
6
0
0
0
0
0
0
10
20
0.5
19
18
18
15
8
1
0
0
0
0
14
7
2
0
0
0
0
0
0
0
0
0
0
15
15
1
21
17
6
2
0
1
0
1
0
0
20
5
4
0
0
0
0
0
0
0
0
0
0
20
10
2
0
0
0
0
0
0
0
0
0
0
35
5
7
0
0
0
0
0
0
2
0
0
0
Plants were exposed in Cincinnati, Ohio. Each value is the average of 4 replicate plants
except as noted. Plants are listed in general order of sensitivity.
Injury estimates based on the average of the three most sensitive leaves except for plants
indicated (*) when the estimate was based on the total leaves per plant.
-------
Heck and Tingey (1979) summarized the foliar injury data from their acute NCL exposures
using the following model:
C = AQ + A1I + A2/T
C = Concentration ppm
A , A-,, Ap = constants (partial regression coefficients specific
for pollutant, plant species and environmental conditions.
I = percent injury
T = Time hours
The model recognizes the separate influence of time and concentration and permits the develop-
ment of three-dimensional injury response surfaces. The model was used to estimate the N02
exposure durations and concentrations necessary to produce injury on susceptible, intermedi-
ate, and tolerant plants at the threshold injury level (Table 12-7).
12.3.4.2 Growth—Czech and Nothdruft (1952) using 1-hour exposures to 1,880 mg/m4 (1000 ppm)
N02 reported that the fresh weight of sugar beet (Beta vulgaris) roots were one-third less
than that of the control plants. Zahn (1975) summarized the results of chronic exposures of
10 plant species to 2-4 mg/m3 (1.06-2.12 ppm) N02 for 213 to 1900 hours (Table 12-8). The
effects ranged from a 37 percent yield reduction in endive to no effect in roses. Exposures
to 1.13 mg/m3 (0.6 ppm) N02 for 30 days reduced the growth of buckwheat (Fagopyrum esculentum)
and eggplant (Solanum melongana) (Fujiwara, 1973). The same concentration for 51 days in-
creased the yield of rice (Oryza sativa). Stratmann (personal communication, cited in Taylor
et al., (1975) showed that bush bean (Phaseolus vulgaris) growth was slowed by exposure to
1.88 mg/m3 (1.0 ppm) N02 for 14 days. He suggested that a likely threshold dose for injury
would be 0.752 mg/m3 (0.4 ppm) N02 over a prolonged time period.
Taylor and Eaton (1966) found reduced fresh and dry weights of unifoliar leaves of pinto
bean (Phaseolus vulgaris) plants exposed to N02 at 0.62 mg/m3 (0.33 ppm) for 10 and 19 days.
Also, leaves from tomato plants (Lycopersicon esculentum) exposed for 10 and 22 days to 0.21
to 1.17 mg/m3 (0.11 to 0.62 ppm) were usually significantly smaller than corresponding leaves
from non-fumigated plants. One of the most comprehensive reports on the effects of N02 on
growth and yield is that of Spierings (1971). Continuous exposures of tomato plants (Lycoper-
sicon esculentum) to 0.47 mg/m3 (0.25 ppm) during the entire growth period (128 days) reduced
growth of leaves, petioles and stems. The crop matured slightly earlier and there were sub-
stantial decreases in fresh weight yield (22 percent), average fruit weight (12 percent), and
the number of fruit (11 percent). After exposures to 0.94 mg/m3 (0.5 ppm) for 10 days or 0.47
mg/m3 (0.25 ppm) for 29 days, fumigated tomato plants were taller than the controls, but stems
were smaller in diameter, leaves were not as large, and the fresh weights of the plants were
less.
12-34
-------
TABLE 12-7. PROJECTED N09 EXPOSURES THAT MAY INDUCE 5 PERCENT
FOLIAR INJURY LEVELS ON SELECTED VEGETATION (HECK AND TINGEY, 1979)
Concentrations Producing Injury
Time (hr)
0.5
1.0
2.0
4.0
8.0
Susceptible
ppm
6-10
4-8
3-7
2-6
2-5
m3/m3
11.28-18.80
7.52-15.04
5.64-13.16
3.76-11.28
3.76- 9.40
Intermediate
ppm
9-17
7-14
6-12
5-10
4-9
m3/m3
16.92-31.96
13.16-26.32
11.18-22.56
9.40-18.80
7.52-16.92
Tolerant
ppm
> 16
> 13
> 11.
> 9
> 8
m3/m3
> 30.08
> 24.44
> 20.68
> 16.92
> 15.04
UJ
Ln
Plant type.
-------
TABLE 12-8. EFFECT OF CHRONIC N02 EXPOSURES ON PLANT BROWTH AND YIELD (ZAHN, 1975)
Plant Type
Concentration
Duration
of Exposure
(hours)
Effect
Wheat
Bush Bean
334
639
No effect on grain yield,
but the straw yield was
reduced 12%.
Yield reduced 27%;
Some chlorosis
Endive
Carrot
Radish
Currant
Roses
European Larch
Spruce
2
4
4
2
4
2
2-3
620
357
278
213
357
537
1900
Yield reduced 37%
Yield reduced 30%;
Some chlorosis
Yield reduced 13%
Yield reduced 12%
No injury
No injury
7% decrease in linear
growth. Growth was de-
creased 17% in the year
following the exposure.
Necrosis did not occur on any plants.
12-36
-------
Thompson et al. (1970) exposed navel orange trees to N0? continuously for 290 days. When
compared to trees exposed to filtered air, those fumigated with N02 concentrations ranging
from 0.12 to 0.47 mg/m3 (0.06 and 0.25 ppm) showed a significant increase in fruit drop
throughout the exposure period and a significant reduction both in number and weight of fruit
at harvest. At Upland, California, ambient and twice ambient levels of^ NO^ were added to
carbon filtered air supplied to navel oranges (Citrus sinensis) with no effects on leaf drop
or yield (Thompson et al. , 1971). Recent studies suggested that 0.47 mg/m3 (0.25 ppm) or less
of N0_ supplied continuously for 8 months will increase leaf drop and reduce the yield of
navel oranges (Citrus sinensis) Taylor et al., 1975).
To determine the effects of NO on the growth of tomatoes (Lycopersicon esculentum), four
different tomato cultivars were exposed to 0.49 mg/m3 (0.4 ppm) NO for 35 days (Anderson and
Mansfield, 1979). In two cultivars, total weight, shoot weight and leaf areas was reduced,
however, in the other cultivars, NO stimulated plant growth. Exposure of another tomato cul-
tivar to 0.75 mg/m3 (0.4 ppm) NO for 19 days reduced leaf area, leaf weight and stem weight
(Capron and Mansfield, 1977). In the same study, 0.19 mg/m3 (0.1 ppm) N02 had no effect on
plant growth and the mixture of 0.19 mg/m3 (0.1 ppm) N02 and 0.49 mg/m3 (0.4 ppm) NO reduced
growth to the same extent as the NO alone (Capron and Mansfield, 1977). Tomatoes grown at
three levels of soil nitrogen and were exposed to a concentration range of 0 to 0.98 mg/m3
(0.8 ppm) NO. At harvest (50 days), total weight, shoot weight, and leaf area were measured
(Anderson and Mansfield, 1979). At a low level of soil nitrogen, NO stimulated plant growth
as reflected in all growth parameters. At a medium level of soil nitrogen, plant growth was
decreased at a concentration of 0.49 mg/m3 (0.4 ppm) NO. At the high level of soil nitrogen,
all levels of NO depressed plant growth.
Because of the inter-relationship between concentration and time, there is no single
threshold dose for an effect. Maclean (1975) summarized the literature to illustrate the re-
lationship between NO,, concentration and duration of exposure (dose) for various effects
(Figure 12-4). Three threshold curves are shown in Figure 12-5. These are approximate esti-
mates, as reported in the literature, based on various responses of many plant species, to
acute and chronic N02 doses. The threshold curve for N02 doses that result in the death of
plants is short because it is based on limited information. N0? doses approaching this thresh-
old result in complete defoliation of some species but are not lethal. The threshold curve
for leaf injury is based on observations at many NOp doses. The shift in leaf injury from
necrosis to chlorosis for N02 doses along this curve generally occurred between 10 and 100
hours. Because no measurable effects have been reported for NOo doses below the lower curve,
it can be considered as the threshold for metabolic and growth effects. N02 doses in the area
between this curve and the threshold curve for leaf injury are those that do not injure leaves
but often result in growth suppression or effects on photosynthesis or other plant processes.
These thresholds (Figure 12-5), assuming that they are reasonable estimates for vegeta-
tion in general, can serve as points of reference to evaluate air quality standards for N02 in
12-37
-------
1000
100
O'
ID
•o
IT
V)
O
Q.
X
o' o'
10
1.0
Fo
_l
1.0 10
NO-, ppm
H
o
o1
c.O
100
Figure 12-4. Summary of effects of NC>2 on vegetation. The points
describe a dosage line above which injury was detected (Jordan, 1969).
individual points were taken from the following references: (A) Mid-
dleton et al., 1958; (B) Hill et al.r 1974; (C) Czech and Northdurft,
1952; (D) H. Strattman (in Taylor et al., 1975); (E) Heck, 1964;
(F) Taylor and Eaton, 1966; (G) Thompson et al., 1970; and (H)
Matsushima, 1971.
l?-38
-------
Q.
a
z"
u
z
o
o
DAYS
,0.01 0.1 1.0 10 100
1000
100
10
1.0
0.1
DEATH
METABOLI
II
THRESHOLD FOR
FOLIAR LESIONS
0.1 1.0 10 100 1000
DURATION OF EXPOSURE, hours
1000
100
10
1.0
10,000
"o>
z"
o
o
z
o
o
CNI
O
Figure 12-5. Threshold curves for the death of plants, foliar lesions,
and metabolic or growth effects as related to the nitrogen dioxide
concentration and the duration of exposure (MacLean, 1975).
12-39
-------
the atmosphere in the absence of other gases and they can be viewed with respect to N02 con-
centrations that occur in the atmosphere.
12.3.5 Effects of Gas Mixtures on Plants
Mixtures of dissimilar pollutants often occur in nature. A typical combination includes
NOp with sulfur dioxide (SOp) and/or ozone (03). Reinert et al. (1975) reviewed information
on these types of pollutant combinations. Earlier the assumption was made that NO at normal
atmospheric concentrations was important only on the basis of its participation in the photo-
chemical oxidant reactions. However, based on studies in which plants were exposed to combi-
nations of pollutants including NOp it now appears that ambient concentrations of NQ2 in con-
junction with other pollutants may have a direct effect on plants. The results of these
studies are described.
12.3.5.1 Nitrogen Dioxide and Sulfur Dioxide—To determine the impact of ambient air pollu-
tion on vegetation, NCL and SOp have been evaluated for their combined effects.
Tingey et al. (1971) found that neither 3.76 mg/m3 (2.0 ppm) NOp nor 1.31 .mg/m3 (0.5 ppm)
SOp alone caused foliar injury. However, a mixture of 0.188 mg/m3 (0.10 ppm) NOp and 0.262
mg/m3 (0.10 ppm) SOp administered for 4 hours caused foliar injury to pinto bean (Phaseolus
vulgaris), radish (Raphanus sativus), soybean (Glycine max), tomato (Lycopersicon esculentum),
oat (Avena sativa) and tobacco (Nicotiana tabacum). Exposure to 0.282 mg/m3 (0.15 ppm) NOp"in
combination with 0.262 mg/m3 (0.1 ppm) SOp for 4-hours caused greater foliar injury. Traces
of foliar injury were observed at 0.094 mg/m3 (0.05 ppm) NOp and 0.131 mg/m3 (0.05 ppm) SOp.
Matsushima (1971) observed more leaf injury on several plant species from a mixture of
NOp and SOp than that caused by each pollutant alone. He also tested different sequences of
exposure. When NOp exposure preceded SOp, the degree of injury was similar to that resulting
from individual exposures to either gas. But when SOp exposure was followed by NOp the degree
of leaf injury increase as would be typical of simultaneous exposures to both pollutants.
Fujiwara et al. (1973) found greater-than-additive effects when peas (Pisum sativum) were ex-
posed to 0.188 mg/m3 (0.1 ppm) N02 in combination with 0.262 mg/m3 (0.1 ppm) S02- When 0.376
mg/m3 NOp and 0.524 mg/m3 SOp (0.2 ppm of each gas) were used, the effect was only additive.
When a large number of desert species were exposed to either SOp or combinations of SOp
and NOp (ratio approximately 4:1) injury from SOp and mixtures of SOp + NOp was similar (Hill
et al., 1974). N02 decreased the foliar injury threshold of S02 on tomatoes (Lycopersicon
esculentum), geranium (Pelargonium S£.), and petunia (Petunia s^.) (de Cormis and Luttringer,
1976). Exposure to 0.79 mg/m3 (0.3 ppm) S02 caused no foliar injury but the same concentra-
tion of S02 in conjunction with 0.94 mg/m3 (0.5 ppm) N02 caused foliar injury. Injury from
the gas mixture increased with increasing humidity.
Observations in the vicinity of an arsenal emitting low concentrations of both N02 and
SOp found foliar injury on several conifer species which was attributed to the interaction of
the 2 gases (Skelly et al., 1972). The maximum observed 1-hour concentration of NO was 0.585
12-40
-------
ppm and 2-hour maximum for SQp was 0.670 ppm. Effects on growth rate of two tree species was
correlated with production activities at the arsenal over a 30-year period suggesting that
mixtures of NOp and SOp may reduce plant growth (Stone and Skelly, 1974).
Bennett et al. (1975) studied the effects of NOp and SOp mixtures on radish (Raphanus
sativus), swiss chard (Beta vulgaris). oats (Avena sativa) and peas (Pisum sativum). Treat-
ments consisted of 1- and 3-hour fumigations with the pollutants separately and with SOp and
N02 (1:1) mixtures in concentrations ranging from 0.33-2.62 mg/m3 S02 and 0.23-1.88 mg/m3 N02
(0.125 to 1.0 ppm). No visible injury occurred on experimental plants treated with NO- alone
or from exposures to S02 concentrations of less than or equal to 1.31 mg/m3 (0.5 ppm). The
minimum exposure doses which caused visible injury to radish leaves were 1-hour exposures to a
mixture of 0.94 mg/m3 N02 and 1.31 mg/m3 S02 (0.5 ppm of each gas) or to 1.95 mg/m3 (0.75 ppm)
SOp alone. The data indicated that S0? and NOp in combination may enhance the phytotoxicity
of these pollutants, but relatively high doses were required to cause injury.
Reinert et al. (1975) summarized the effects of gas mixtures on foliar injuries to a
number of crops (Table 12-9). The data indicate that ambient concentrations of NOp and SO,,
may interact to injure vegetation.
A study was conducted to determine the effects of low concentrations of N02 and S02
singly and in combination on the growth of four grass species (Ashenden, 1979a; Ashenden and
Mansfield, 1978; Ashenden and Williams, 1980). Plants were grown and exposed in four small
greenhouses which received either charcoal filtered air, 0.21 mg/m3 (0.11 ppm) N02, 0.29 mg/m3
(0.11 ppm) SOp or a mixture of both gases at these'same concentrations. The plants were ex-
posed for 103.5 hours per week, which resulted in weekly mean concentrations of 0.13 mg/m3
..; (0.068 ppm) N02 and 0.18 mg/m3 (0.068 ppm) S02. The plants were harvested, monthly and various
•growth parameters were measured. The results of the experiments are summarized in Table
,.. 12-10. Nitrogen dioxide significantly reduced growth parameters of orchard grass and Kentucky
bluegrass, but had no effect or slightly stimulatory effect on the growth of Italian ryegrass
and timothy. However, growth parameters of all the species were reduced by S02- The combina-
tion of N02 and S02 significantly reduced the growth parameters of all species tested and many
of the effects were determined to be synergistic. These data were collected during the winter
when the plants were in a period of slow growth which may have increased the pollutant's toxi-
city. However, the data clearly show that intermittent exposures to ambient concentrations of
NOp and SOp singly and in combination can significantly depress yield parameters of important
forage grasses.
Alfalfa (Medicago sativa) exhibited a greater-than-additive response, i.e., a greater in-
hibition of apparent photosynthesis (COp uptake) when NOp and SOp were applied together for 2
hours at 0.47 mg/m3 (0.25 ppm) and 0.655 mg/m3 (0.25 ppm) S02 (White et al., 1974). A mixture
of 0.282 mg/m3 (0.15 ppm) N02 and 0.393 mg/m3 (0.15 ppm) S02 for 2-hours decreased apparent
photosynthesis 7 percent more than when the total of the two gases was applied independently.
At higher concentrations, 0.5 ppm of each gas, the effects were not greater-than-additive.
12-41
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TABLE 12-9. PLANT RESPONSE TO SULFUR DIOXIDE AND NITROGEN DIOXIDE MIXTURES
(TINGEY ET AL., 1971; MATSUSHIMA, 1971; BENNETT ET AL., 1975; HILL ET AL., 1974)
i
j>
NJ
Plant Species
Avena sativa L.
Beta vulgaris var. cicla L.
Lathyrus odoratus L.
Raphanus sativus L.
A. sativa
R. sativus
Phaseolus vulgaris L.
R sativus
Nicotiana tabacum L.
Orzopsis hymendoides (R&S) Ricker
Populus tremuloides Michx.
Sphaeralcea munroana Spach.
P. vulgaris
Lycopersicon esculentum Mill.
Cucumis sativus L.
A. sativa
Capsicum frutescens L.
P. vulgaris Pinto
A. sativa
R. sativus
Glycine max (L. ) Merr.
N. tabacum
L. esculentum
Exposure
Chamber '
CE
CE
CE
CE
CE
CE
CE
CE
GH
F
F
F
GH
GH
GH
GH
GH
GH
S0,/N0,
(fom)
0.75/0.75
0.75/0.75
0.75/0.75
0.75/0.75
0.15-0.25/0.1-0.2
0.15-0.25/0.1-0.2
0.15-0.25/0.1-0.2
0.5/0.5
0.1/0.1
0.5-0.7/0.15-0.21
0.5-0.7/0.15-0.21
0.5-0.7/0.15-0.21
1.5/15
2.3/13
2.3/12
2.4/13
2.4/15
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
0.05-0.25/0.05-0.25
Exposure
duration
(hours)
1 or 3
1 or 3 .
1 or 3
1 or 3
4
4
4
1 or 3
4
2
2
2
1.17
1 -
0.67
1
1
4
4
4
4
4
4
Plant
Response
(% injury)
0-5
0-5
0-5
5-8
0
0
0
0-5
0-10
16
1
31
70-75
35-85
50-100
40-75
10-58
0-24
0-27
0-27
0-35
0-18
0-17
Mixture.
Response '
-t-
+
+
+
*
*
*
+
+
0
0
0
+
+
+
-
+
+
+
+
+
+
+
Plant
Age
(weeks)
4-5
1-5
4-5
4-5
2-3
2-3
2-3
4-5
7-8
A
A
A
3-4
3-5
3-4
3-4
5-6
3-4
3-4
3-4
3-4
7-8
5-6
aCE, Control environment; GH, greenhouse; F, field.
+, Greater than additive; 0, additive; -, less than additive.
c* Not defined.
-------
TABLE 12-10. THE EFFECTS OF NO- AND S02 -SINGULARLY AND IN COMBINATION ON THE GROWTH OF SEVERAL GRASSES1
(Ashenden, 1979a; Ashenden and Mansfield, 1978; Ashenden and Williams, 1980)
to
I
Response
Leaf Area
Number of Tillers
Dry Weight
green leaves
Dry Weight
dead leaves
and stubble
Dry Weight
roots
2
Species
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Orchard grass
Kentucky bluegrass
Italian ryegrass
Timothy
Pollutant3
N02
21
17
1+
30+
1
9
17
6
7
29*
10
14+
46*
27*
5
12
11
47*
35+
1+
so2
5
28*
22
11
10
27*
23*
33*
28*
39*
28*
25*
52*
37*
3+
47*
37*
54*
7+
58*
N02 + S02
72*
84*
43*
82*
32*
61*
32*
55*
83*
88*
65*
84*
67*
57*
28*
64*
85*
91*
58*
92*
Effect Synergistic
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
Data are expressed as percent reductions from the control and are derived from references 127a and 127b.
The exposures were for 20 weeks (140 days). Plants were exposed for 103.5 hr/week. The concentrations
of NO- and SO- during exposure were 0.11 ppm which resulted in a weekly average concentration of 0.068
ppm.
f\
The scientific names are: Orchard grass, Dactyl is glomerata; Kentucky bludgrass, Poa pratensis; Italian
ryegrass, Lolium multiforum; Timothy, Phleum pratense.
Numbers followed by + indicate increase above the control and * indicates significant reductions of the
5% significance level or greater.
-------
Exposures of alfalfa (Medicago sativa) to 0.62 mg/m3 (0.33 ppm) N02 and 2.62 mg/m3 (1 ppm) S02
at an ambient C0? concentration for 1 to 3 hours reduced the photosynthetic rate approximately
50 percent (Hou et al., 1977). When the ambient carbon dioxide concentration was increased
645 ppm, the inhibitory effect of N02 and S02 on photosynthesis was only 50 percent as large
as at ambient C02 levels. In studies with pea (Pisum sativum) Bull and Mansfield (1974)
reported that over the concentration range of 0-0.47 mg/m3 (0.25 ppm) NOp and 0-0.655 mg/m3
(0.025 ppm) S02, photosynthesis was inhibited. The duration of exposure was not given. The
effect of the two gases was additive in inhibiting of photosynthesis. In bean (Phaseolus
vulgaris) when 0.188 mg/m3 (0.10 ppm) N02 and 0.262 mg/m3 (0.10 ppm) S02 were applied indivi-
dually the pollutants stimulated short-term increases in transpiration, but the combination of
N02 and S02 decreased the transpiration rate (Ashenden, 1979b).
Horsman and Wellburn (1975) studied the effects of NO,, and S0? mixtures on several enzyme
systems in peas (Pisum sativum). Peroxidase activity was enhanced somewhat by S02 alone but
not by N02> However, 0.188 mg/m3 (0.1 ppm) N02 plus 0.524 mg/m3 (0.2 ppm) S02 for 6 days in-
creased the activity by 24 percent. A 100 percent increase occurred when 0.188 mg/m3 (0.1
ppm) N0? plus 5.24 mg/m3 (2.0 ppm) S0? was used for 6 days. The effect was much greater-than-
additive. The increase in peroxidase activity was considered a typical stress response of the
plant. Similar studies have shown that glutamate dehydrogenase activity is stimulated as a
greaterh-than-additive response by mixtures of N02 and S02 (Wellburn et al., 1976).
12.3.5.2 Nitrogen Dioxide with Other PoUutants—Matsushima (1971) reported that combinations.
of N02 and 0, were less injurious to pepper (Capsicum furtesceans) and tomato (Lycopersicon
esculentum) than similar concentrations of either gas alone. Loblolly pine and American syca-
more (Platanus occidental is) were exposed to either 0.10 mg/m3 (0.05 ppm) ozone and/or 0.19
mg/m3 (0.10 ppm) N02 for 6 hours per day for 25 days and effects on injury and growth were
determined. At this concentration N02 had no deletrious effects on plant growth or injury.
The combination of 0., plus N0? yielded the same results as the effects of ozone alone.
Reinert and Gray (1977) obtained different results using different pollutant combinations with
radish (Raphanus sativus), pepper (Capsicum protescerus) and tomato (Lycopersicon esculentum).
They found that N02> S02 or 0, were less injurious when used individually than when in combi-
nations of N02 + S02, NO^ + 03, or S02 + 03- de Cormis and Luttringer (1976) found that a
mixture of 0.31 mg/m3 (0.12 ppm) S02> 0.56 mg/m3 N02 (0.3 ppm) and 0.2 mg/m3 (0.1 ppm) 03
caused extensive leaf necrosis in tomato (Lycopersicon esculentum) within 2 hours.
It is clear from these limited data that levels of N02 generally considered below the
injury threshold may interact with other common air pollutants to induce vegetation injury.
Extensive research is needed to verify this phenomenon under field conditions. It appears
that concentrations of N02 between 0.188 mg/m3 (0.1 ppm) to 0.47 mg/m3 (0.25 ppm) can cause
direct effects on vegetation in combination with certain other pollutants.
12-44
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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 pollu-
tants from the air, water, and soil, and in energy flow. They also give aesthetic pleasure
and improve the quality of life.
The nitrogen cycle, an ecocystem function, is essential for all life because nitrogen is
necessary in the formation of all living matter. Man has influenced the cycling of nitrogen
by injecting fixed nitrogen into the environment or contributing other nitrogenous compounds
which perturb the cycle.
Human activities have unquestionably increased the amounts of nitrates and related com-
pounds in some compartments of the environment. The effects of such increased concentrations
of nitrogen compounds may be beneficial or adverse, or both. Effects of both kinds may occur
simultaneously, and may be felt in media or in ecological compartments quite removed from
those that initially receive anthropogenic nitrogenous inputs.
Assessment of the influence of nitrogen oxides on ecosystems is complicated by several
factors. Nitrogen oxides: (1) react with abiotic components of the natural environment as
well as with individual organisms; (2) react with varying numbers of dissimilar populations
within ecosystems; and (3) may suppress individual populations and thus affect ecosystem func-
tioning.
One function of ecosystems is the cycling of nutrients such as nitrogen. Any effect, en-
vironmental or biological, which interferes with the recycling process could have a deleter-
ious effect on the total ecosystem.
At the present time there are insufficient data to determine the impact of nitrogen
oxides as well as other nitrogen compounds on terrestrial plant, animal or microbial communi-
ties. It is possible, however, to estimate the approximate magnitude of anthropogenic
nitrogen fluxes to ecosystems, using the limited amount of monitoring data available or mass
balance calculations. Such estimates, and quantitative information about the nitrogen cycle
at specific sites in the system under study, make it possible to reach some conclusions about
the possible ecological significance of the added nitrogen. In addition, where the data base
is more extensive, as it is for a number of lakes in various stages of eutrophication, more
quantitative dose-response relationships can be estimated.
A reduction in diversity within a plant community results in a reduction in the amount of
nutrients present so that growth of remaining individuals decreases.
12-45
-------
Pollutants act as predisposing agents so that disease, insect pests and abiotic forces
can more readily injure the individual members of ecosystems. The loss of these individuals
results in reduction in diversity and simplification of an ecosystem.
12.4.2 Effects on Vegetation
Sensitivity of plants to N02 varies with species, time of day, light, stage of maturity,
type of injury assayed, soil moisture, and nitrogen nutrition.
When exposures to N02 alone are considered, the ambient concentrations that produce
measurable injury are higher than those that normally occur in the United States (Chapter 8).
Tomato (Lycopersicon esculentum) plants exposed continuously to 0.47 mg/m3 (0.25 ppm) for 128
days were reduced in growth and suffered a decreased yield of 12 percent. Leaf drop and
reduced yield occurred in naval oranges exposed to 0.47 mg/m3 (0.25 ppm) continuously for 8
months. Pinto beans (Phaseolus vulgaris), endive (Cicorium endivia) and cotton (Gossypium
hirsutum) exhibited slight leaf spotting after 48 hours of exposure to 1.88 mg/m3 (1.0 ppm).
Reduced growth in bush beans (Phaseolus vulgaris) was reported after a 14-day exposure to 1.88
mg/m3 (1.0 ppm). Other reports cited no injury in beans (Phaseolus vulgaris), tobacco (Nico-
tiana tabacum), or petunia (Petunia multiflora) after a 2-hour exposure of the same concentra-
tion.
Exceptions to this generality, however, have been observed. For example, the growth of
Kentucky bluegrass was significantly reduced (approximately 25 percent) by exposures to 0.21
mg/m3 (0.11 ppm) N02 for 103.5 hours per week for 20 weeks during the winter months. Similar
exposures to other grass species generally had no deletrious effect on plant growth.
Nitrogen dioxide concentrations ranging from 0.188 to 1.88 mg/m3 (0.1 to 1.0 ppm) in-
creased chlorophyll content in pea (Pisum sativum) seedlings from 5 to 10 percent. The sig-
nificance of the increased chlorophyll is unknown. Some species of lichens, a plant sometimes
used as an indicator of the presence of phytotoxic gases, exposed to 3.96 mg/m3 (2.0 ppm) for
6 hours showed a reduced chlorophyll content.
In contrast to the studies cited on the effects of N02 alone, a number of studies on mix-
tures of NO,, with S02 showed that the N02 injury threshold was significantly decreased and
that the effects of the two gases in combination were at least additive and usually greater-
than-additive. Concentrations at which observable injury occurred were well within the
ambient concentrations of N02 and SO- occurring in some areas of the United States. Neither
3.96 mg/m3 (2.0 ppm) N0? nor 1.21 mg/m3 (0.5 ppm) S02 alone caused foliar injury. Research
data from grass species exposed for 20 weeks to concentrations of 0.21 mg/m3 (0.11 ppm) NO-
and 0.29 mg/m3 (0.11 ppm) S02 for 103.5 hours per week showed significant reductions in yield
parameters ranging from 30 to 90 percent indicating that concentrations of these two gases
occurring simultaneously can have major deletrious effects on plant growth.
12-46
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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 (NOp). This chapter presents an evaluation of the effects of oxides of nitrogen on
textile dyes, man-made and natural fibers, plastics, elastomers and metals.
It should be pointed out that some exposure situations described in this chapter, which
lead to an economic loss (mostly involving textiles), characteristically take place indoors.
Although indoor and outdoor pollutant concentrations are not always directly related or
proportional, it is reasonable to expect that much of the pollution in indoor environments
comes from ambient air. Indoor sources such as gas appliances in homes or combustion-powered
fork lifts in warehouses may also contribute to indoor pollutant levels.
13.1 EFFECTS OF NITROGEN OXIDES ON TEXTILES
The types of damage to textiles attributed to NO action include:
Fading of dyes on cellulose acetate (also known as acetate and cellulose acetate
rayon), cotton, viscose rayon (Upham and Salvin, 1975), and nylon.
Color changes on permanent press garments containing polyesters.
Yellowing of white fabrics.
13.1.1 Fading of Dyes by Nitrogen Oxides
13.1.1.1 Fading of Dyes on Cellulose Acetate—The NO fading of acetate, dyed blue, or in
X
shades in which blue is a component, results in pronounced reddening. Rowe and Chamberlain
(1937) demonstrated that the causative factors were nitrogen oxides in combustion gases. The
blue dyes which were and are still in widespread use are derivatives of anthraquinone.
Blue dyes, such as Disperse Blue 3, a dye commonly used to test for the presence of NO ,
contain amino groups which are susceptible to nitrosation and oxidation by NO . The fading of
Disperse Blue 3 as a result of NO action is caused by the formation of a nitrosamine at the
vulnerable alkylamine site(s), or the production of a phenolic group (-OH) at the amine
site(s), through oxidation (Couper, 1951). Both of these reaction products have a red color,
which is seen when certain fabric-dye combinations are exposed to NO^.
Salvin et al. (1952) found that cellulose acetate.is an excellent absorber of NO^.
Absorption characteristics of fibers also are believed to play an important role in dye-fading
mechanisms. Polyester and polyacrylic fibers have low NO^ absorption rates while nylon,
cotton, viscose rayon and wool have intermediate rates. While cellulose acetate and cellulose
triacetate have high NO- absorption rates, the NO- is released upon heating. Nylon and wool,
13-1
-------
materials which contain reactive amino groups, hold the NO- in chemical combination and
release it upon hydrolysis. The oxides of nitrogen are retained by cotton and viscose rayon,
fabrics collectively referred to as cellulosics.
Both blue and red dyes having the anthraquinone structure are susceptible to NO action.
A
These dyes include Disperse Blue 7, Disperse Blue 3, Disperse Red 11 and Disperse Red 55. The
fading of these dyes is recognized and noted in shade books published by dye suppliers.
Asquith and Campbell (1963) have noted that fading also occurs with certain yellow dyes
of the diphenylamine class.
Dye fading associated with NO- exposure of cellulose acetate and cellulosics is sum-
marized in Table 13-1. Testing methods predictive of dye fading have been summarized in the
literature (American Association of Textile Chemists and Colorists, 1972; Hemphill et al.,
1976; Salvin, 1974a; Seibert, 1940). Selected anthraquinone-b and blue dyes exhibit high
resistance to fading by NO (Salvin and Walker, 1959; Seymour and Salvin, 1949).
Chemical changes such as those cited in consumer complaints of dye fading on cellulose
acetate, cotton and rayon, can take place within three months at NO- concentrations of 380
3
ug/m (0.2 ppm) (Hemphill, et al., 1976). Also, the additional acid introduced by SO-, fre-
quently present in significant concentrations in ambient air, appears to accelerate the fading
by NO- even though SO-, by itself, produces no change. (See Table 13-1.)
13.1.1.2 Fading of Dyes on Cotton and Viscose Rayon (Cellulosicsj—Although the effects of
NO on dyed acetate are well documented, the effects on dyes used for the cellulosic fibers
X
have received much less attention. Anomalous cases of fading were reported by McLendon and
Richardson (1965) in their study of color changes of dyed cotton placed in gas-heated clothes
dryers. Additional effects reported by other investigators are summarized in Table 13-1.
The American Association of Textile Chemists and Colorists (AATCC) conducted service
exposure trials to determine whether air contaminants could be one of the variables in light-
fastness tests (Salvin, 1964; Schmitt, 1960). Urban and rural sites were chosen in areas of
high and low atmospheric contaminant concentrations: Phoenix, Arizona (low), Sarasota,
Florida (low), Los Angeles, California (high), and Chicago, Illinois (high). Sulfur dioxide,
oxides of nitrogen and 0, were monitored in each exposure area. A wide range of fibers*was
dyed with a range of dyes in common use on the fibers (Table 13-2). The fabric samples were
exposed to ambient air for 30 and 120 days in covered cabinets which excluded the action of
light. Fading was demonstrated on a range of fabrics, including cotton and rayon, for which
the cause could be NO , 03 or SO-. The dyes applicable to cellulosics which exhibited appre-
ciable color change represented four major classes: direct, vat, sulfur and fiber-reactive
dyes.
Table 13-3 presents typical atmospheric pollutant concentrations in Los Angeles, Chicago
and the rural exposure sites. Chicago's high SO- concentration was principally due to burn-
ing of coal; ozone concentrations were low. The concentrations of NO are high in both Los
13-2
-------
TABLE 13-1. FADING OF DYES ON CELLULOSE ACETATE AND CELLULOSICS
(COTTON AND RAYON)
OJ
I
Concentration
of Pollutant
Dyed Fiber
Acetate
Acetate
Acetate
Acetate
Cotton-Rayon
Acetate-
Cotton, Rayon
Exposure Pollutant
Gas heated N02
rooms
Chamber N02
Pittsburgh- N09-0.
Urban, ^ J
Ames-Rural
Chamber N02
Clothes dryer N0~
Los Angeles3 NO-
+ °3
*so2
Chicago3 , N02
°3
+ so2
MQ/m
3,760
3,760
N/A
3,760
1,128-
3,760
489
412
131
414
10
655
ppm
2.0
2.0
2.0
0.6-
2.0
0.26
0.21
0.05
0.22
0.005
0.25
Time Effect
N/A Fading
16 hr Fading
6 mo Fading
16 hr Fading
1 hr Fading
cycle
30 to Fading
120
days
Reference
Rowe and
Chamberlain, 1937
Seibert, 1940
Salvin and
Walker, 1955
Salvin,
et al., 1952
McLendon and
Richardson, 1965
Salvin, 1964
(continued)
-------
TABLE 13-1 (continued)
co
Dyed Fiber
Cotton-Rayon
Cotton- Rayon
Range of
Fibers
Range of
Fibers
Range of
Fibers
Acetate-
Cotton, Rayon
Acetate-
Cotton, Rayon
Exposure
Chamber
Chamber
Field-Urban,
Rural
Chamber
Chamber
Chamber
Survey
Pollutant
S02-N0£
S02-N02
and 03
S02-N02+03
N02
N02 + Xenon
arc radiation
N02
NO
cn^ H C
bU2, l-l-ji
Concentration
of Pollutant
/ 3
|jg/m ppm
3,760 2.0
N/A
N/A
94 to 0.05 to
940 0.5
940 0.5
94 to 0.05 to
940 0.5
Service
Complaints
Time
16 hr
54 hr
24 mo
12 wk
20 to
80 hr
N/A
N/A
Effect
Fading
Fading
Fading
Fading
Fading
Fading
Fading
Reference
Salvin,
Ajax et
Beloin,
Beloin,
Hemphil
et al. ,
Upham
et al. ,
1969
al. , 1967
1972
1973
1
1976
1976
Upham and
Salvin, 1975
Concentrations also shown in Table 13-3
-------
TABLE 13-2. COLOR CHANGES ON DYED FABRIC-EXPOSED WITHOUT
SUNLIGHT IN POLLUTION AND RURAL AREAS
International Grey Scale;3 5 = no change; Y = yellow; W = weaker;
G = greener; R = redder; and B = bluer
Code Index No.
ACETATE
Disperse Red 35
Disperse Blue 27
Oxides of nitrogen
fading control
Disperse Blue 3
Ozone control--grey
dyed with:
Disperse Blue 27
Disperse Red 35
Phoenix
4.5Y
3.0W
3.5
3.0
Los Angeles
4.0Y
2.0W
1.5R
1.5
Chicago
4.5Y
2.5W
2. OR
3.5
Sarasota
4.5Y
2.0W
3.5
2.5
Disperse Yellow 37
Disperse Blue 27
Disperse Red 60
WOOL
Acid Black 26A
Acid Red 89
Acid Violet 1
Acid Blue 92
Acid Red 18
COTTON
Direct Dyes
Direct Red 1
Congo Red B
Direct Red 10
Direct Blue 76
Direct Blue 71
Direct Blue 86
Vats
Vat Yellow 2
Vat Blue 29
Vat Blue 6
Vat Red 10
4.5
4.5
5.0
5.0
5.0
4.5
4.5
5.0
4.0
4.0
4.5
4.0
4.0
4.0
5.0
3G
4.0
5.0
5.0
4.0
5.0
4.5
3.5
4.0
4.0
4.0
1.5
2.5
3.5
2 grey
2.5R
1G
4.0
3G
3.5R
4.5
.4.0
3.5
4.0
3.5
3.5
3.0
2.5
3.5
1.5
2.5
3B
1R
2R
1G
3G
2.5G
3.0
3.5
4.0
4.5
4.5
4.5
2.5Y
4.0
4.0
4.5
3.0
2Y
4.0
4.0
3R
2.5G
5.0
1.5G
4R
5.0
(continued)
SOURCE: Salvin, 1964.
13-5
-------
TABLE 13-2 (continued)
Code Index No.
Fiber Reactives
Reactive Yellow 4
Reactive Red 11
Reactive Blue 9
Reactive Yellow 16
Reactive Yellow 13
Reactive Red 23
Reactive Red 21
Reactive Blue 19
Reactive Blue 21
Reactive Yellow 12
Reactive Red 19
Reactive Red 20
Reactive Blue 17
COTTON
Sulfur Dyes
Sulfur Yellow 2
Sulfur Brown 37
Sulfur Green 2
Sulfur Blue 8
Sulfur Black 1
NYLON
Acid Red 85
Acid Orange 49
Disperse Blue 3
Disperse Red 55
Disperse Red 1
Alizarine Light Blue C
ORLON
Basic Yellow 11
Basic Red 14
Basic Blue 21
Disperse Yellow 3
Disperse Red 59
Disperse Blue 3
Phoenix
5.0
5.0
4.5
5.0
5.0
5.0
5.0
4.5
4G
5.0
5.0
5.0
4.5
3.5R
5.0
3B
4.0
4.5
5.0
5.0
5.0
5.0
5.0
5.0
5.0
5.0
4.5
4.0
5.0
5.0
Los Angeles
5.0
5.0
4R
, 5.0
.5.0
5.0
5.0
3.0
1.5G
4.5
5.0
4.0
3.0
3R
4.5
2. OB
3.5G
4.5
4.5
4.5
4.0
4.5
4.5
4.5
4.0
5.0
4.5
5.0
5.0
5.0
Chicago
4.5
4.5
3. OR
4.0
4.0
4.5
4.0
1R
1.5G
3.5
3.5B
4.0
1 grey
2. OR
4.5
2. OB
3G
4.5
3.0
3.0
3.5
4.0
3.0
3.5
4.0
4.5
• 4.0
4.5
4.5
4.0
Sarasota
4.5
5.0
4.5
5.0
5.0
5.0
5.0
4.0
3G
4.5
4.5
4.5
4.0
2.5R
4.0
2B
4.0
4.5
5.0
4.5
3.0W
3.5
4.5
4.5
4.5
4.5
5.0
4.5
4.5
4.5
The International Grey Scale is a numerical method of showing the degree
of shade change. It is geometric rather than arithmetic. Essentially,
a shade change of 4 shows a change which is slight and is not too easily
recognized. A shade change of 3 is appreciable and is easily recognized.
A shade change of 2 is severe. A shade change of 1 is disastrous. These
numbers are indicative of the shade change with 4 being passable and 3.5
a matter of judgement.
13-6
-------
TABLE 13-3. TYPICAL CONCENTRATIONS3 OF ATMOSPHERIC CONTAMINANTS IN EXPOSURE AREAS
Oxides of Nitrogen
Sulfur Dioxide
Carbon Monoxide
Ozone
Aldehydes
(Phoenixu-raSarasota) Los An9eles
(ppm) (jjg/m ) (ppm) (|jg/m )
0.01 0.26
0.03 80 0.05 130
23.00 26,000
0.06-0.11 120-220 0.21 410
0.3
Chicago
(ppm) (pg/m )
0.22
0.25 650
16.00 18,000
0.005 10
Concentrations shown are average concentrations measured over a two-month period, relative humidity
data not available.
SOURCE: Salvin, 1964.
-------
Angeles and Chicago, and are of similar magnitude. These differences in pollutant concentra-
tions correlate with the fact that the Disperse Blue 3, which characteristically reacts to
NO , showed pronounced reddening changes in both Los Angeles and Chicago while being almost
unchanged (in the International Grey Scale ratings) in the rural exposure areas of Phoenix and
Sarasota (Table 13-2). It should be noted that humidity differences are present between
Phoenix, which is dry, and coastal Florida, which is humid. Humidity was not measured in Los
Angeles and Chicago.
In a laboratory experiment (Salvin, 1969) designed to produce changes similar to those
shown on service exposure, the AATCC NO test with Disperse Blue 3 was not used. Instead, the
German Fastness Commission test was used, which has shown changes in dyes on cellulose. In
this method, discussed by Rabe and Dietrich (1956) oxides of nitrogen are generated by the
addition of phosphoric acid to a dilute sodium nitrite solution. The dyed fabric is exposed
to the nitrogen oxides in a closed system under high humidity conditions, in contrast to the
AATCC test procedure, in which the nitrogen oxides are generated by combustion of natural gas
or butane under conditions of low humidity. The dyed fabrics which showed fading changes in
the service exposures in Los Angeles and Chicago showed similar changes upon laboratory expo-
sure under the high humidity conditions of the German Fastness Commission test procedure
(Salvin, 1969).
The effect of NO on fiber reactive dyes has been reported by Imperial Chemical Industries
X
in its shade card of Procion Dyes. The vulnerability of certain reactive dyes on cotton to
N0x also has been reported by Hertig (1968) in his critical study of the International Stand-
ards Organization test procedure (Rabe and Dietrich, 1956) for color fastness to NO . This
method employs high humidity conditions.
The effects of air pollutants were examined by the U.S. Environmental Protection Agency
(USEPA) in laboratory trials (Ajax et al., 1967) using the same dye-fabric combinations
employed in the AATCC (Salvin, 1964) study (Table 13-2). The dye-fabric combinations were
exposed to air to which diluted auto exhaust and S0? were added over a 54-hour period.
Neither the auto exhaust nor S0? produced significant fading. However, irradiation of the
auto exhaust, which contains both hydrocarbons and oxides of nitrogen, gave products which
3
caused significant fading. The addition of SO- at a concentration of 2,620 pg/m (1.0 ppm)
produced additional fading. The synergistic effect of SO- is suggested as being responsible
for the observed results.
Beloin (1972) carried out a USEPA field exposure study of the fading of 67 dye-fabric
combinations (using 56 dyes) representative of the AATCC service exposure described in Table
13-2. The exposures were carried out in eleven nationwide urban and rural sites for consecu-
tive three-month periods over a period of two years.
The exposure sites are listed in Table 13-4. Rural areas were selected to serve as
controls with the same climatic conditions as the urban areas but with low levels of pollution.
Phoenix, Arizona and Sarasota, Florida were chosen as low pollution areas with extremes in
13-8
-------
TABLE 13-4. EXPOSURE SITES
City
Washington, DC
Poolesville, MD
Tacoma, WA
Purdy, WA
Los Angeles, CA
Santa Paula, CA
Chicago, IL
Argonne, IL
Phoenix, AZ
Sarasota, FL
Cincinnati, OH
Location
Municipal Building
Poolesville High School
Franklin Gault School
PHS Shellfish Laboratory
LA County Air Pollution Control
District Building
Federal Post Office
Central Office Building
Argonne National Laboratory
Desert Sunshine Exposure Tests
Sun Test Unlimited
Taft High School
Type
Urban
Rural
Urban
Rural
Urban
Rural
Urban
Rural
Suburban
Rural
Urban
Average
Fade, NBS
Units3
5.0
4.3
4.3
2.9
5.7
4.0
7.2
4.0
2.7
3.1
4.8
On the NBS scale, a change of three units is noticeable; three to six
units are considered appreciable; changes above six units are
classified as severe.
SOURCE: Beloin, 1972.
13-9
-------
relative humidity and high temperatures. The exposures were carried out in louvered covered
cabinets to avoid exposure to light. The dye production sales for 28 of the 56 different dyes
tested totalled over 30 million dollars (U.S. Tariff Commision, 1967). Of the 67 dye-fabric
combinations, 25 were cellulosics.
The sites were monitored for CL, N02 and SO^. The gas fading control (Disperse Blue 3 on
cellulose acetate) showed high correlation with NO concentration. Fadings on the 0, test
A. *J
ribbon were demonstrated in the rural areas as well as the urban sites.
It can be concluded from the data that appreciable fading takes place in the absence of
light. Of the 67 dye-fabric combinations tested, 64 percent showed appreciable fading. Urban
sites produce significantly higher fading than corresponding rural sites. In the presence of
high temperature and high humidity, air pollution increases fading rate. Fading changes were
severe in those fabrics dyed with direct and reactive dyes.
The data did not isolate the action of SOp, 03, or N02, but a statistical analysis
identified N02 as a significant variable (at 99 percent level) causing fading in some samples.
Chicago samples incurred highest average fading. However, Chicago had high concentrations of
S02, as well as N02-
Beloin (1973) also conducted laboratory studies designed to determine the effects of the
individual air pollutants on dyed fabrics. Exposure was made of 20 dyed fabrics chosen on the
basis of their appreciable change in the field study noted above. Cotton and viscose rayon
were 9 of the 20 dyed fabrics (Table 13-5) used in the trials. Reactive dyes and one type of
vat dye were used. The pollutants were SO,, NO, N0~, and 0,. Two concentration levels were
used for nitrogen dioxide: 940 and 94 ug/m (0.5 ppm and 0.05 ppm). Temperature and humidity
were varied: 32°C and 13°C, and 90 and 50 percent relative humidity, respectively. The
fabrics were exposed for 12 weeks.
Under the higher humidity/temperature conditions, N02 at a concentration of 940 ug/m
(0.5 ppm), caused severe changes on 8 of the 9 samples. Significant fading also occurred at
3
high humidity with an NO- concentration of 94 |jg/m (0.05 ppm) (Beloin, 1973). Color changes
were reported as Hunter Color Units, which approximate the NBS units.
The AATCC Committee on Color Fastness to Light carried out light-fastness tests with
added contaminants using Xenon arc irradiation (Hemphill et al., 1976). The objective was to
establish a relationship between light-fastness tests made in natural daylight in Florida and
Xenon arc exposure in the laboratory Weatherometer. The contaminants included separate addi-
tions of 940 |jg/m3 (0.5 ppm) N02, 294 ug/m3 (0.15 ppm) 03 and 786 |jg/m (0.3 ppm) S02. In one
trial, all three contaminants were added to the exposure cycle under Xenon arc irradiation.
Of the 29 dyed fabric combinations exposed, 14 were cellulosic (cotton or rayon). The addi-
tion of NOp alone caused increased fading compared to the control in over half of dyed
cellulosic fabrics examined.
Upham and co-workers (1976) carried out a chamber study of the effect of atmospheric
pollutants on selected drapery fabrics. Fabrics were exposed to 0.05 and 0.5 ppm each of S02
13-10
-------
TABLE 13-5. AVERAGE FADING OF 20 DYE-FADRIC COMBINATIONS3 AFTER 12 WEEKS EXPOSURE TO NITROGEN DIOXIDE
Hunter Color Units
94 pg/m3 NO,
Material
Cotton
Rayon
Wool
Cotton
Acrylic
Cotton
Nylon
Wool
Acrylic
Cotton
Wool
Dye
Direct
Direct
Acid
Reactive
Basic
Azoicc
Acid
Acid
Basic
Sulfur
Acid
Color Index No.
Red 1
Red 1
Red 151
Red 2
Red 14
Red
Orange 45
Yellow 65
Yellow 11
Green 2
Violet 1
Low Temp.
Average
12.78eC
7.2
3.4
T
T
T
T
5.6
T
T
T
T
High Temp.
Average
32.22°C
8.0
T
T
T
T
T
17.0
T
T
3.3
T
Low
Humidity
Average
(50% RH)
7.4
T
T
T
T
T
10.1
T
T
T
T
High
Humidity
Average
(90% RH)
7.8
T
T
T
T
T
9.5
T
T
T
T
Low Temp.
Average
12.78 C
18.0
13.4
T
10.4
T
T
21.5
T
T
6.5
T
940 pg/m
High Temp.
Average
32.22°C
20.4
16.3
T
6.9
T
T
27.9
T
T
6.6
T
3 NO,
Low
Humidity
Average
(50% RH)
16.1
12.6
T
9.7
T
T
24.3
T
T
6.1
T
High
Humidity
Average
(90% RH)
22.3
17.0
T
7.6
T
T
25.1
T
T
7.1
4.1
SOURCE: Be loin, 1973.
(continued)
-------
TABLE 13-5. (continued)
CO
I
ro
94 pg/m3 NO,
Material
Cotton
Cellulose
Acetate
Nylon
Cellulose
Acetate
Polyester
Cotton
Cotton
Cotton
Acetate
Dye
Direct
Disperse
Disperse
Disperse
Disperse
Reactive
Reactive
Vat
—
-------
(131 and 1310 MS/™3), 03 (98 and 980 ug/m3), and N02 (94 and 940 ug/m3) under Xenon arc irra-
diation, at various humidities. The effect of N09 was pronounced, especially on a vat-dyed
3
drapery fabric. The most noticeable color changes were at 940 ug/m (0.5 ppm) and 90 percent
relative humidity.
In summary, the investigations by Beloin both in the field study (Beloin, 1972) and the
chamber study (Beloin, 1973) show that, at concentrations of N0? present in urban atmospheres,
representative dyes for cotton and rayon will suffer serious fading. NCk resistant dyes are
available; however, limitations of brightness of shade and difficulty of application introduce
production problems and the need for greater quality control resulting, generally, in in-
creased costs. The AATCC work confirms the vulnerability to NO,, of several dyes widely used
on cellulosic fibers, especially certain blue dyes.
13.1.1.3 Fading of Dyes on Nylon—The fading of dyed nylon in polluted atmospheres has been
noted in exposure trials carried out by the AATCC (Salvin, 1964) and by the U.S. Environmental
Protection Agency (Beloin, 1972). However, consumer complaints have been few and have been
blamed on light-produced color changes in garments, draperies, or in home furnishings for the
nylon fiber normally used in these products. The standard AATCC test procedure for N0?, which
demonstrated the vulnerability of the disperse dyes used on acetate, showed little change when
the same dyes were used on nylon (Table 13-6). The problem of fading on nylon became of
considerable interest as nylon found use in carpets. The quality of nylon for this end use is
estimated at over 500 million pounds, distributed between Nylon 66 and Nylon 6.
Field exposures of a range of dyes on nylon, in areas of high air pollution (N02, S02 and
03), resulted in unexpected failures of these dyes (Beloin, 1972; Salvin, 1964). In contrast,
the same dyes on polyester showed no changes (Table 13-6). The fading of disperse blue dyes
on nylon carpets was shown to be due to 03 in the presence of high humidity (Salvin, 1974b).
Acid dyes, which are more resistant to On, were substituted as a remedial measure. However,
the remedy presented additional problems. The vulnerability of acid dyes on nylon to NO^ was
the basis of a bulletin issued by Imperial Chemical Industries (1973) on a range of acid dyes
marketed as Nylomines. The fading effect of NOp, derived from combustion gases, was deter-
mined at 65 and at 95 percent relative humidity on three cycles of exposure in their tests.
Certain violet and blue dyes are rated as exhibiting significant change. The dye manufac-
turers point out the importance of dye selection in carpets and in home furnishings which are
likely to be exposed for long periods in air contaminated with NOo from gas burner fumes.
Acid dyes on nylon were included in the range of dyes exposed to visible light radiation
and NO, by Hemphill in the AATCC study (Hemphill et al. , 1976). Under high humidity condi-
3
tions and at an N02 concentration of 940 ug/m (0.5 ppm), for 30 to 100 hours, fading was
found to be greater for certain dyes in those exposures where Xenon arc irradiation and N02
were present than in the control exposure with Xenon arc irradiation and NO^-free air
(Table 13-6).
13.1.1.4 Fading of Dyes on Polyester—Polyester dyed with disperse dyes did not show N02~
induced fading changes in AATCC field exposures in urban atmospheres of Chicago and Los
Angeles (Table 13-6) (Salvin, 1964). The same fabrics in various urban sites (Beloin, 1972)
13-13
-------
TABLE 13-6. EFFECT OF NITROGEN DIOXIDE ON FADING OF DYES ON NYLON AND POLYESTER
I
I—I
-p>
Dyed Fibers
Nylon
Polyester
Nylon
Polyester
Nylon
Polyester
Nylon
Nylon
Polyester
Permanent
Press
Polyester
Textured
Double Knit
Concentration
of Pqllutant
Exposure Pollutant
Chicago NO,,
Los Angeles
Chicago NOp
Los Angeles
Urban Sites N02
Urban Sites N02
Chamber N02
High Humidity
Chamber NOp
High Humidity
Chamber N02
High Humidity
Chamber N02
High Humidity
Xenon Arc
Chamber N0?
Chamber N02
ug/m"
188
282
376
282
376
376
188 to
1,880
188 to
1,880
376
940
940
940
ppm
0.1
0.15
0.2
0.15
0.2
0.2
0.1
to 1
0.1
to 1
0.2
0.5
0.5
0.5
Time
30 to 120 days
30 to 120 days
30 to 120 days
30 to 120 days
3 to 24 months
3 to 24 months
12 weeks
12 weeks
48 hours
30 to 120 hours
16 hours
16 hours
Effect
Fading
Unchanged
Fading
Unchanged
Fading
Unchanged
Fading
More
fading than
without N02
Fading
Fading
Reference
Salvin, 1964
Salvin, 1964
Beloin, 1972
Beloin, 1972
Beloin, 1973
Beloin, 1973
Imperial Chemical
Industries, 1973
Hemphill et al . , 1976
Salvin, 1966
Urbanik, 1974
-------
also showed no changes; high or low humidity had no effect. However, a large number of com-
plaints regarding fading of permanent press garments (65 percent polyester--35 percent cotton)
were recorded in 1965, when this product first was marketed.
Investigation of the anomalous fading of polyester dyes in permanent press fabrics by
Salvin (1966) indicated that fading did not take place on dye contained within the polyester
fiber matrix. Fading was found to take place on the surface of the fiber as a result of dye
migration from the fiber subsurface to the modified urea-formaldehyde resin used on the blend
to stabilize the cotton. When exposed to NCL or 03, the components of the resin finish absorb
the contaminants and fading occurs. The measures which can be used to eliminate the problem
are (a) selection of dyes with lower rate of migration, (b) substitution of the magnesium
chloride catalyst with zinc nitrate and, (c) reduction in quantity of non-ionic surfactant
which acts as an acceptor for the dye and an absorber for either NO^ or :03. Urbanik (1974)
suggests changes in the magnesium chloride catalyst formulation, used in the resin finish, in
order to suppress dye migration.
The introduction, in 1966, of double-knit garments made from textured polyester also was
accompanied by cases of fading of the garments attributed to either NCL or On. The fading
attributed to N0~ was noted in those dyes of level dyeing properties. Dye migrates in the
final heat-setting step to lubricant oils or residual surfactant on the surface of the fabric,
where fading takes place.
13.1.1.5 Economic Costs of N0x -induced Dye Fading—Barrett and Waddell (1973), in a 1973
status report to the U.S. Environmental Protection Agency, reported'preliminary estimates that
annual economic costs of NO -induced dye fading in textiles amounted to $122.1 million. These
estimates were based on figures reported by Upham and Salvin (1975).
The economic costs to the nation as a result of 0, damage to textiles is approximately 70
percent of the costs attributed to NO damage. These costs of NO and 0, action are tabulated
in Table 13-7.
The basis for the estimates included not only the reduced wear life of textiles of
moderate fastness to NO but also the costs of research and quality control. The major share
A
of the costs is the extra expense involved in using dyes of higher NO resistance and in the
use of inhibitors. Additional costs also are incurred in dye application and in increased
labor expenditures.
The factors relating to higher costs in the textile industry as a result of N0x action
are discussed in Chapter 8, "The Effects of Nitrogen Oxides on Materials," in the National
Academy of Sciences report on nitrogen oxides (Salvin et al., 1977).
13.1.2 Yellowing of White Fabrics by NO,
The survey of the effects of air pollutants on textiles (Upham and Salvin, 1975) reported
a number of instances in which white fabrics yellowed. This discoloration occurred in areas
protected from light. Causes of yellowing were not established, except for the observation
that contact with ambient air currents seemed to be a causative factor.
13-15
-------
TABLE 13-7. ESTIMATED COSTS OF DYE FADING IN TEXTILES
Pollutant
NO Fading on
Fading on
Fading on
Yel lowing
Subtotal
OT Fading on
Fading on
Fading on
Subtotal
Effect $
acetate and triacetate
viscose rayon
cotton
of white acetate-nylon-Spandex
acetate and triacetate
nylon carpets
permanent-press garments
million3
73
22
22
6
122
25
42
17
84
Total
206
aAll costs rounded to nearest million, therefore some totals do not agree.
SOURCE: Barrett and Waddell, 1973.
13-16
-------
Using 18 fabric samples which were the subjects of manufacturers' complaints, Salvin
(1974c) investigated the effects of specific air pollutants or combinations and the effects of
humidity and temperature. The products tested include polyurethane segmented fiber, rubberized
cotton, optically-brightened acetate, nylon, nylon treated with permanent antistatics, and
resin-treated cotton containing softeners (Table 13-8).
Nitrogen dioxide was established as the pollutant responsible for yellowing of white
fabrics in the complaint fabrics tested. Yellowing was not demonstrated when fabrics were
exposed to 0,, S0~, or hydrogen sulfide (HUS).
The standard AATCC test procedure (conducted in low humidity) for effects of N02 does not
always result in the yellowing effect observed on service exposure in areas shielded from
light. This is especially true of cotton and nylon fabrics. Whereas the standard test
procedure for NO showed change on cellulose acetate fabrics, high humidity test procedures
A
demonstrated yellowing in nylon.
Although fibers without additives do not show yellowing following exposure to NO^, the
polyurethane-segmented fibers (e.g., Lycra and Spandex) are exceptions. These fibers contain
urethane groups which react directly with N0~ to form yellow-colored nitroso compounds.
Yellowing of Spandex and Lycra fibers occurred in the standard AATCC test for NO- fading
(Salvin, 1974c). In the tests carried out, less yellowing was shown on certain samples
submitted which contained inhibitors.
Garments containing rubberized cotton did show yellowing on exposure to N02 in the AATCC
standard test procedure. With increase in temperature of the test, yellowing was more
pronounced in those areas of the garment where rubber is present (Burr and Lannefeld, 1974).
The antioxidant in rubber employed against ozone action is diphenyl ethylene diamine. On
storage, this product vaporizes from the rubber to the surface of the cotton fabric. This
material already is well known as the inhibitor used on cellulose acetates to suppress fading
of dyes by N02- It forms a yellow nitroso compound.
Optical brighteners, compounds widely used to improve the whiteness of fabrics, are of
various structures and are specific to particular fibers. They function by transforming UV
radiation to visible light in the purple-blue range. Brighteners may react with NO^ and
result in yellow-colored compounds.
The American Association of Textile Chemists and Colorists (1957) has conducted a study
of the yellowing of a range of softeners. In the range of fabrics examined for yellowing of
the softeners, variable degrees of yellowing were demonstrated upon exposure to NOp. The
yellowing was especially noted on those softeners of a cationic nature. Softeners have been
synthesized which are resistant to yellowing by oxides of nitrogen (Dexter Chemical Company).
The unexpected yellowing of nylon treated with an antistatic agent has been reported
(Salvin, 1974c). The treated nylon showed no yellowing on exposure in the standard N02 AATCC
test method. Under high humidity and with an increase in temperature during testing, however,
yellowing similar to that obtained in service testing was observed.
13-17
-------
TABLE 13-8. YELLOWING OF WHITES BY NITROGEN DIOXIDE
00
Fiber
Survey
Rubberized
Cotton
Rubberized
Cotton
Spandex
Acetate
Optical
brightener
Nylon
Optical
brightener
Nylon
Anti-stat
finish
Cotton
Cationic
softener
Exposure Pollutant
Service N/A
Complaints
Chamber N0?
Chamber N02
Chamber N02
Chamber N02
Chamber N02
High Humidity
Chamber N02
High Humidity
Chamber N02
Concentration
of Pollutant
ug/m ppm Time Effect
N/A Yellowing
376 0.2 16 hr Yellowing
376 0.2 16 hr Yellowing of
anti-oxidant
376 0.2 8 hr Action on
fiber
376 0.2 8 hr Yellowing
376 0.2 16 hr Yellowing
376 0.2 16 hr Yellowing
376 0.2 16 hr Yellowing
Reference
Upham and
Salvin, 1975
Burr and
Lannefeld,
1974
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
Salvin, 1974c
-------
13.1.3 Degradation of Textile Fibers by Nitrogen Oxides
Cotton and nylon are the two fibers whose strength is reduced by the hydrolytic action of
acid aerosols. This problem assumes economic importance because industrial fabrics comprise
the end use for 18 percent of all fibers, many of which are used in the production of cordage,
belts, tarpaulins and awnings. These products are exposed to air pollutants over long periods
of time. Premature losses of strength are costly and create safety hazards.
A chamber study of the combined action of N02 and light on cotton did demonstrate that
N02 contributed to strength loss (Morris, 1966). Cotton yarns were exposed to sunlight. In
one cabinet, air was filtered through carbon to remove oxides of nitrogen. The second cabinet
contained fibers exposed to sunlight and air containing monitored levels of 03 and NO-.
Exposure was carried out for a total of 72 days. Since the test area (Berkeley, California)
was low in SO^, this service exposure would emphasize the effects of nitrogen oxides. The
degradation (strength loss) of the cotton fiber was greater in the presence of the unfiltered
ambient air. The results of this study show that the combined effects of sunlight and NO
A
gave increased deterioration over sunlight alone. The contributions of Oo and other oxidants
was not determined.
It is not possible to isolate the effects of nitrogen oxides from that of sulfur oxides
in field studies which have shown strength loss in cotton (Brysson et al., 1967; Brysson et
a!., 1968; Morris, 1966; Travnicek, 1966). The effect of N0,> on fiber degradation of cotton
requires further investigation.
Inconclusive results were shown by Zeronian et al. (1971) in a study of the effect of
N02, combined with Xenon arc radiation, on a range of man-made fibers, including acrylics,
nylons and polyester. These workers exposed modacrylic-acrylic, nylon, and polyester fibers
to the combined action of Xenon arc radiation and air containing 376 pg/m (0.2 ppm) N02 at 30
percent relative humidity at 48°C, and at 43 percent relative humidity at 43 C. The fabrics
were exposed for 108 hours to Xenon arc irradiation in a Weatherometer and intermittently were
sprayed with water. The same series of fabrics was subjected to identical weathering condi-
tions but without N02. Modacrylic (Dynel), acrylic (Orion), and polyester showed only slight
differences in degradation in exposures with and without N0~. These materials are considered
resistant to the action of acids. The results for nylon were not conclusive, although signif-
icantly greater degradation (loss of tensile strength, increased viscosity) at 48°C occurred
in the presence of NO^, under irradiation. Further experimentation would be suggested to test
N0~ effects in the absence of irradiation and under higher humidity conditions.
13.2 EFFECTS OF NITROGEN DIOXIDE ON PLASTICS AND ELASTOMERS
The maintenance of strength of plastics and elastomers upon exposure of these materials
to light, air and atmospheric contaminants is a matter of importance.
A 1977 survey (Chemical and Engineering News, 1977) predicts a market for these materials
in 1982 of 1.78 billion pounds. Under the generic term of plastics are included polyethylene,
propylene, polystyrene, polyvinyl chloride, polyacrylonitrile and polyamides.
13-19
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Aging is the term used to denote deterioration of chemical and physical properties which
can' occur upon weathering. This degradation has been blamed on the known effects of sunlight.
The comparative resistance to sunlight can be shown upon exposure in the laboratory to carbon
or Xenon arc irradiation. The substitution of plastics for metals, particularly in automo-
biles, where long periods of outside exposure are involved, brings this problem into focus.
The effects of air pollutants, such as N02, have been assessed in laboratory trials.
The polymers which represent the structures in plastics, as well as textiles, were
subjected by Jellinek et al. (1969) to the action of SCL, N0?, and ozone obtained by action of
UV radiation on the oxygen-containing mixture. These combinations of SCL, NCL, and ozone
represent the components of smog. The polymers include polyethylene, polypropylene, poly-
styrene, polyvinyl chloride, polyacrylonitrile, butyl rubber and nylon. All polymers suffered
deterioration in strength. The elastomer, butyl rubber, was more susceptible to SCL and NCL
than other polymers. However, the effect of CL on the rubber was more pronounced than that of
the S02 or the N02-
Jellinek (1970) examined the reaction of linear polymers, including nylon and polypropy-
lene, to N02 at concentrations of 1,880 to 9,400 (jg/m3 (1.0 to 5.0 ppm). Nylon 66 suffered
chain scission. (Chain scission results in polymers having lower molecular weights and lower
strength.) Polypropylene tended to crosslink. Chain scission of polymers caused by small
concentrations of S02 and N02 took place in the presence of air and UV radiation.
The action of NCL and 0^ on polyurethane also was investigated by Jellinek (1974). The
tensile strength of linear polyurethane was reduced by N02 alone and also by N02 pl.us 0^.
Chain scission resulting in lower molecular weights and formation of nitro- and nitroso-groups
along the polymer backbone occurred upon exposure to NO,,.
13.3 CORROSION OF METALS BY NITROGEN DIOXIDE
The corrosion of metals by air pollutants is due to the presence of acids or salts on the
metal which enter into electrochemical reactions. Numerous small electrochemical cells form
on the ferrous metal surfaces which are in contact with the contaminated air. Localized
anodes and cathodes form and the electrical conductivity is increased where the surface of the
metal is wet; the moisture contains increasing quantities of acid aerosols or anions therefrom.
The normal rusting process is the formation of an iron-oxide which acts as a protective
film. However, the presence of an acid aerosol such as sulfuric acid, as derived from S02,
can break down this protective oxide layer, exposing new surfaces to electrolytic corrosion.
An analysis of the contributing effects of air pollutants was offered in the examination
of the contributions of N02 to corrosion in the review by the National Research Council
(Salvin et al., 1977).
The forms of metal corrosion include new corrosion (uniform and general attack), galvanic
corrosion, crevice corrosion, pitting, selective leaching, and stress corrosion. A liquid
film or the presence of a hydrated salt plays a role in most of these corrosion types. In
attempting to assess the contribution of nitric acid aerosols derived from N02 and nitrate
13-20
-------
salts, the various mechanisms of corrosion must be understood to attenuate the problem and to
predict the effect of a variable change.
Thus the mechanisms of galvanic, pitting, crevice, and selective leaching corrosion
require the presence of an electrolyte or solvent. Hydrated salt solutions can serve as the
electrolyte in galvanic corrosion.
The general approach taken by investigators to the effects of air pollutants on corrosion
has been to establish the extent of the damage with the goal of obtaining data which could be
used in economic analyses of corrosion due to air pollutants. Waddell (1974)in his estimates
of the economic damages of air pollution includes a section on costs of metal corrosion.
Using data supplied by the Rustoleum Corporation, Barrett and Waddell (1973) estimated costs
at $7.5 billion in 1958.
Material damage due to air pollutants emphasizes S02 as the major causative agent in the
corrosion of metals (Fink et al., 1971; Gillette, 1975). Fink and co-workers (1971) estimated
corrosion damage of metals caused by air pollution at approximately $1.5 billion.
When consideration is given to the mechanisms of corrosion which are due to electrolytic
action rather than oxidation, the importance of NCL in the corrosion process emerges. The
presence of nitrates on surfaces, to give both the requisite hygroscopic film and the electro-
lyte for galvanic corrosion, becomes important. The potential of nitrates in upsetting the
homogeneity of the protective oxide film becomes a factor.
Haynie et al. (1976) investigated the separate or combined effects of 502, NO- and 0,
under controlled conditions of pollutant, humidity and temperature. The materials tested
included: weathering steel, galvanized steel, aluminum alloys, paints, drapery fabrics, vinyl
house siding, marble, and white sidewall tire rubber. Sulfur dioxide and relative humidity
appeared the most important factors for producing corrosion. A similar conclusion was
reported by Yocum and Grappore (1976)in a review of the effect of air pollutants emanating
from power plants.
The premature failure of nickel brass springs in telephone equipment primarily in the Los
Angeles area has been investigated by Hermance and co-workers (1971). Although most failures
occurred in California, springs did show occasional failure in other parts of the country.
This report reviewed the earlier findings that the springs had a fogged appearance and were
covered with a hygroscopic dust rich in nitrates. The failure was attributed to stress
corrosion. A survey of nitrate accumulation was made in California and other locations.
Nitrate deposition correlated with relay failure.
Previous laboratory studies by Hermance (1966) and McKinney and Hermance (1967) confirmed
that hygroscopic nitrates such as zinc or ammonium cause stress corrosion cracking of the
anodic nickel brass wires. Salts of other anions under the same conditions did not cause
2
cracking at the nitrate concentration levels found in Los Angeles. Up to about 15 ng/cm of
surface area, an applied positive potential was necessary. Cracking was found to be low when
the relative humidity was less than 50 percent.
13-21
-------
A field study (Hermance et al., 1971) was made of the incidence of breakage as related to
the' nitrate accumulation. The nitrate accumulations were measured in New York City, Bayonne,
New Jersey, Philadelphia, Baltimore, and Washington, D.C. Although the accumulations were
high, breakage in these areas was lower than anticipated.
The important finding illustrated in this work is that the nitrates salts are more hygro-
scopic than the chloride and sulfate salts. As such, they may lower the threshold humidity
requirements for the formation of an aqueous medium, which can serve as the electrolyte or
solvent for wet corrosion.
Hermance (1966) also reported on the failure of other telephone equipment, which did not
involve nickel brass alloys, that took place in Los Angeles, New York, Detroit and Cleveland.
The nickel base of palladium-capped contacts of cross box switches corroded in the presence of
nitrates, forming bright greenish corrosion products which gradually crept over the palladium
o
cap of the contacts. The heavy nitrate deposits were greater than 15.5 ug/cm . Stress corro-
sion occurred in the absence of anodic electrical current.
The function of NCL in changing the defect structure of many oxides, thereby increasing
or decreasing the rate of oxidation of metals and alloys, was suggested by Lazareva et al.
(1973) in the study of the oxidation of tungsten alloys.
A field study of the effect of air pollutants on electrical contact materials was carried
out by Chiaranzelli and Joba (1966), in which the formation of corrosion films in various
areas of pollution was correlated with the concentration of pollutants present. Nitrogen
dioxide, SCL, H~S and dust were monitored. This study did not isolate the specific contribu-
tion of NO-2 to the problem of electrical contacts although it did point out that areas of high
humidity showed greater corrosion.
It is in the study of catastrophic failure of materials exposed to air pollutants that
investigators seek to establish the specific causative agent. The long-term exposures by the
ASTM of various metals in different locations sought to establish which metal or alloy was
most resistant. The case of the telephone equipment failure as investigated by Hermance et
al. (1971) did show that nitrates were a contributory factor, although no relation to the
concentration of NCL in the air was established.
Gerhard and Haynie (1974) examined the cases of catastrophic failure of metals in which
structures failed unexpectedly, leading to loss of life as well as well as collapse of the
metal structure. Their conclusion was that air pollutants were a probable contribution to the
corrosion that was the cause of failure. However, there is no finding that determined the
relationship between levels of particular pollutants and the occurrence of the failure.
Nitrogenous compounds, however, were implicated in a situation in which steel cables on a
bridge in Portsmouth, Ohio failed after 12 years of service. The cause of failure was traced
to river water contaminated with ammonium nitrate that had concentrated at natural crevices
(Romans, 1965). Nitrogen dioxide was not considered a factor.
13-22
-------
A review of the voluminous literature on corrosion has produced no further references to
investigations of NCL action, in the absence of SOp. The above studies are summarized in
Table 13-9.
13.4 SUMMARY
The damaging effects of atmospheric oxides of nitrogen have been established for a
variety of materials including dyes, fibers, plastics, rubber and metals. Field exposures of
cotton, viscose rayon, cellulose acetate, and nylon fabrics colored with representative dyes
demonstrate that fading occurs for specific dyes in air containing NOp, 03, and SO-. These
exposures were carried out in ambient air and protected against sunlight. Chamber studies
using individual pollutants NOp, CU, and SOp have shown that some individual dye-fiber
combinations exhibit color fading only in response to N0? exposure, whereas others are suscep-
tible to 0,, as well as combinations of NCL and 0,. S0? introduced an accelerant effect.
Disperse dyes used for cellulose acetate and rayon include vulnerable anthraquinone blues and
reds. The cellulosic fibers cotton and viscose rayon, dyed with certain widely used direct
dyes, vat dyes, and fiber reactive dyes, suffer severe fading on chamber exposures to 940
ug/m (0.5 ppm) NO, under high humidity (90 percent) and high temperature (90°F) conditions.
3
Significant fading is observed on 12 weeks exposure to 94 (jg/m (0.05 ppm) N02 under high
humidity and temperature conditions (90 percent, 90°F).
Acid dyes on nylon fade on exposure to NO,, at levels as low as 188 ug/m (0.1 ppm), under
similar conditions. Dyed polyester fabrics are highly resistant to NOp-induced fading.
However, permanent .press fabrics of polyester cotton and textured polyester exhibited
unexpected fading when first marketed. The fading was in the disperse dye which migrated
under high heat conditions of curing or heat setting to the reactive medium of resins and
other surface additives.
The yellowing of white fabrics is documented for polyurethane segmented fibers (Lycra and
Spandex), rubberized cotton, optically brightened acetate, and nylon. Yellowing is also
reported on fabrics which were finished with softeners or anti-static agents. Nitrogen
dioxide was demonstrated to be the pollutant responsible for color change, with 03 and SO,,
showing no effect. Chamber studies using N0? concentrations of 376 ug/m (0.2 ppm) for 8
hours showed yellowing equivalent to that on garments returned to manufacturers.
The tensile strength of fabrics may be adversely affected by the hydrolytic action of
acid aerosols. Nitrogen dioxide has been demonstrated to oxidize the terminal amine group
(-NH2) of nylon to the degree that the fiber has less affinity for acid-type dyes. Nylon 66
may suffer chain scission when exposed to 1,880 to 9,400 ug/m (1.0 to 5.0 ppm) NO,,. Field
exposures of fibers emphasize the action of acids derived from S02, although NOg may also be
present in high concentrations in urban sites. Information on the contribution of NO,, to
degradation is incomplete.
13-23
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TABLE 13-9. CORROSION OF METALS BY NITROGEN DIOXIDE
co
i
tSi
•fa.
Metal
Mechanics of
Nickel Brass
Nickel Brass
Nickel
Tungsten
Electronic
contacts
Metal parts
Exposure
Corrosion - Function
Los Angeles
Los Angeles
Los Angeles
New York
Chamber
Field
Field
Pollutant
of Nitrates
Nitrates
Nitrates
Nitrates
N02
K02-S02-H2S
N02-S02-03
Effect
Strength
Loss
Strength
Loss
Corrosion
Change oxide
surface
Corrosion
film
Failure
Reference
Salvin et al. , 1977
Hermance et al . , 1971
McKinney and
Hermance, 1967
Hermance, 1966
Lazareva et al . , 1973
Chiaranzelli and
Joba, 1966
Gerhard and Haynie,
1974
Economic Costs of Corrosion
Fink et al., 1971
-------
Although a survey of the market for plastics predicts the use of 1.78 billion pounds in
1982, there is essentially no information on the effects of NO^ on polyethylene, polypropy-
lene, polystyrene, polyvinyl chloride, polyacrylonitrile, polyamides and polyurethanes. Aging
tests involve sunlight exposure as well as exposure to ambient air. Chamber exposure of the
above plastics to combinations of SO^, NO^, and 0, has resulted in deterioration. Nitrogen
dioxide alone has caused chain scission in nylon and polyurethane at concentrations of 1,880
and 9,400 |jg/m3' (1.0 to 5.0 ppm).
The extensive data on corrosion of metals in polluted areas relate the corrosion effects
to the 502 concentrati°ns- The presence of NO^ and its contribution is not evaluated despite
its presence as acid aerosol in appreciable concentrations.
Ammonium nitrates were implicated as a factor in the stress corrosion cracking of wires
made of nickel brass alloy used in telephone equipment. Since nitrate salts have been shown
to be more hygroscopic than either chloride or sulfate salts, the presence of nitrates may
lower the humidity requirements for the formation of an aqueous electrolyte system in the wet
corrosion of metals.
13-25
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13.5 REFERENCES
Ajax, R. L. , C. J. Cohlee, and J. B. Upham. The effects of air pollution on the fading of
dyed fabrics. J. Air Pollut. Control Assoc. 17:220-224, 1967.
American Association of Textile Chemists and Colorists. Cationic softeners—their secondary
effects on textile fabrics. Intersectional contest paper. Philadelphia, Pennsylvania.
Amer. Dyestuff Reporter 46:41, 1957.
American Association of Textile Chemists and Colorists. AATCC Technical Manual. Volume 48.
Research Triangle Park, North Carolina. 1972, 370 pp.
Asquith, R. S. , and B. Campbell. Relation between chemical structure and fastness to light
and gas fumes of nitrophenylamine dyes. J. Soc. Dyers Colour. 79:678-686, 1963.
Barrett, L. B. , and t. E. Waddell. Cost of Air Pollution Damage: A Status Report. AP-85,
U.S. Environmental Protection Agency, Research Triangle Park, NC, February 1973.
Beloin, N. J. A field study-fading of dyed fabrics by air pollution. Text. Chem. Color.
4:43-48, 1972.
Beloin, N. J. A chamber study-fading of dyed fabrics exposed to air pollutants. Text.
Chem. Color. 5:128-133, 1973.
Brysson, R. J. , B. J. Trask, and A. S. Cooper, Jr. The durability of cotton textiles: the
effects of exposure in contaminated atmospheres. Am. Dyest. Rep. £7:15-20, 1968.
Brysson, R. J. , B. J. Trask, J. B. Upham, and S. G. Booras. The effects of air pollution on
exposed cotton fabrics. J. Air Pollut. Control Assoc. 17:294-298, 1967.
Burr, F. K. , and T. E. Lannefeld. Yellowing of white fabrics by gas fume fading. Asian
Textile J. 2:27, 1974.
Chemical and Engineering News. Reinforced plastics continue heady growth. Chem. Eng. News
55:22, November 7, 1977.
Chiaranzelli, R. V., and E. L. Joba. The effect of air pollution on electrical contact
materials: a field study. J. Air Pollut. Control Assoc. 16:123-127, 1966.
Couper, M. Fading of a dye on cellulose acetate by light and by gas fumes: 1,4-bis
(methylamino)-anthraquinone. Text. Res. J. 21:720-725, 1951.
Dexter Chemical Company. Dextrol softeners resistant to oxides of nitrogen. Technical
bulletin.
Fink, F. W. , F. H. Buttner, and W. K. Boyd. Technical-Economic Evaluation of Air-Pollution
Corrosion Costs on Metals in the U.S. APTD 0654, U.S. Environmental Protection Agency,
Research Triangle Park, NC, February 1971.
Gerhard, J. , and F. H. Haynie. Air Pollution Effects on Catastrophic Failure of Metals.
EPA-650/3-74-009, U.S. Environmental Protection Agency, Research Triangle Park, NC,
November 1974.
Gillette, D. G. Sulfur dioxide and material damage. J. Air Pollut. Control Assoc. 25:1238-
1243, 1975.
13-26
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Haynie, F. H. , J. W. Spence, and J. B. Upham. Effect of Gaseous Pollutants on Materials—a
Chamber Study. EPA-600/3-76-015, U.S. Environmental Protection Agency, Research
Triangle Park, NC, February 1976.
Hemphill, J. E. , J. E. Norton, 0. S. Ofjord, and R. L. Stone. Color fastness to light and
atmospheric contaminants. Text. Chem. Color. 8:25-27, 1976.
Hermance, H. W. Combatting the effects of smog on wire-sprung relays. Bell Lab. Rec:
48-52, 1966.
Hermance, H. W. , C. A. Russell, E. J. Bauer, T. F. Egan, and H. V. Wadlow. Relation of
air-borne nitrate to telephone equipment damage. Environ. Sci. Technol. 5:781-785,
1971.
Hertig, J. Testing nitric oxide fastness-experience and recommendations. Textilveredlung
3:180-190, 1968.
Imperial Chemical Industries. Nylomine Dyes: Effect of Burnt Gas Fumes. ICI Bulletin
D1322, Imperial Chemical Industries Ltd, Manchester, England, 1973.
Jellinek, H. H. G. Chain scission of polymers by small concentrations (1 to 5 ppm) of sulfur
dioxide and nitrogen dioxide, respectively, in the presence of air and near ultraviolet
radiation. J. Air Pollut. Control Assoc. 20:672-674, 1970.
Jellinek, H. H. G. Degradation of polymers at low temperatures by N02, 03, and near-ultra-
violet light radiation. Cold Regions Res. Eng. Lab., Hanover, New Hampshire. USN TIS
AD 782950/OGA, 1974. 31 pp.
Jellinek, H. H. G. , F. Flajsman, and F. J. Kryman. Reaction of S09 and N09 with polymers.
J. Appl. Polym. Sci. 13:107-116, 1969. * L
Lazareva, I. Y. , D. A. Prokoshkin, E. V. Vasil'eva, and S. A. Skotnikov. Reactional diffu-
sion during oxidation of tungsten alloys in an atmosphere with a high concentration of
nitrogen. Prot. Coat. Met. (Engl. Transl.) 5:57-60, 1973.
McKinney, N. , and H. W. Hermance. Stress corrosion cracking rates of a nickel-brass alloy
under applied potential. In: Stress Corrosion Testing, A Symposium, 69th Annual Meet-
ing, American Society forTesting and Materials, Atlantic City, New Jersey, June .26 -
July 1, 1966. ASTM Special Technical Publication No. 425, American Society for Testing
and Materials, Philadelphia, PA, December 1967. pp. 274-291.
McLendon, V., and F. Richardson. Oxides of nitrogen as a factor in color changes of used and
laundered cotton articles. Am. Dyest. Rep. 54:15-21, 1965.
Morris, M. A. Effect of weathering on cotton fabrics. Bull. Calif. Agric. Exp. Stn.
(823):l-29, 1966.
Rabe, P., and R. Dietrich. A comparison of methods for testing the fastness to gas fading of
dyes on acetate. Am. Dyest. Rep. 45:737-740, 1956.
Romans, H. B. Stress Corrosion Test.' Environments and Test Periods Report of ASTM Task
Group B. January 1965. p. 58.
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Rowe, F. M., and K. A. J. Chamberlain. The "fading" of dyeings on cellulose acetate rayon.
The action of "burnt gas fumes" (oxides of nitrogen, etc. in the atmosphere) on
cellulose acetate rayon dyes. J. Soc. Dyers Colour. 52:268-278, 1937.
Salvin, V. S. Relation of atmospheric contaminants and ozone to lightfastness. Am. Dyest.
Rep. 53:33-41, 1964.
Salvin, V. S. The effect of dry heat on disperse dyes. Am. Dyest. Rep. 55:490-501, 1966.
Salvin, V. S. Testing atmospheric fading of dyed cotton and rayon. Am. Dyest. Rep. 5:28-29,
1969.
Salvin, V. S. Color fastness to atmospheric contaminants. Textile Chem. and Color.
6(7):164-166, 1974a.
Salvin, V. S. Color fastness to atmospheric contaminants—ozone. Textile Chem. and Color.
6:41-45, 1974b.
Salvin, V. S. Yellowing of white fabrics due to air pollutants. Collected papers of the
American Association of Textile Chemists and Colorists. National Technical Conference,
New Orleans, 1974c. pp. 40-51.
Salvin, V. S., and R. A. Walker. Service fading of disperse dyestuffs by chemical agents
other than the oxides of nitrogen. Text. Res. J. 25:571-582, 1955.
Salvin, V. S. , and R. A. Walker. Relation of dye structure to properties of disperse dyes.
Am. Dyest. Rep. 48:35-43, 1959.
Salvin, V. S. , N. Bornstein, and C. T. Bowman. Effects of N02 on materials. In: Nitrogen
Oxides. National Academy of Sciences, Washington, DC, 1977. pp. 159-196.
Salvin, V. S., W. D. Paist, and W. J. Myles. Advances in theoretical and practical studies
of gas fading. Am. Dyest. Rep. 41:297-302, 1952.
Schmitt, C. H. A. Lightfastness of dyestuffs on textiles. A. Getting best results through
optimum dyeing methods. B. Accurate evaluation through proper light test procedures.
Am. Dyest. Rep. 49:974-980, 1960.
Seibert, C. A. Atmospheric (gas) fading of colored cellulose acetate. Am. Dyest. Rep.
29:366-374, 1940.
Seymour, G. W. , and V. S. Salvin. Process of Reacting a Nitro-Hydroxy-Anthraquinone with a
Primary Amine and a Product Thereof. Patent No. 2,480,269, U.S. Patent Office, August
30, 1949.
Travnic'ek, Z. Effects of air pollution on textiles, especially synthetic fibers. In:
Proceedings of the 1st International Clean Air Congress, Part I, International Union of
Air Pollution Prevention Associations, London, England, October 4-7, 1966. National
Society for Clean Air, London, England, 1966. pp. 224-226.
Upham, J. B., and V. S. Salvin. Effects of Air Pollutants on Textile Fibers and Dyes.
EPA-650/3-74-008, U.S. Environmental Protection Agency, Research Triangle Park, NC,
February, 1975.
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Upham, J. B. , F. H. Haynie, and J. W. Spence. Fading of selected drapery fabrics by air
pollutants. J. Air Pollut. Control Assoc. 26:790-792, 1976.
Urbanik, A. Reduction in blooming of disperse dyes on durable press fabrics. Textile Chem.
and Color. 6:78-80, 1974.
U.S. Tariff Commission. U.S. production of dyes and synthetic chemicals. Washington, D.C.,
1967.
•i
Waddell, T. E. The Economic Damages of Air Pollution. EPA-600/5-74-012, U.S. Environmental
Protection Agency, Washington, DC, May 1974.
Yocum, J. E. , and N. Grappone. Effects of Power Plant Emissions on Materials. EPRI EC-139,
Electric Power Research Institute, Palo Alto, CA, July 1976.
Zeronian, S. H. , K. W. Alger, and S. T. Omaye. Reaction of fabrics made from synthetic
fibers to air contaminated with nitrogen oxide, ozone, or sulfur dioxide. J_ri: Pro-
ceedings of the Second International Clean Air Congress, International Union of Air
Pollution Prevention Associations, Washington, D.C., December 6-11, 1970. H. M. Englund
and W. T. Beery, eds. , Academic Press, Inc., New York, NY, 1971. 'pp. 468-476.
13-29
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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
(Crocker et al. , 1977), the North Atlantic Treaty Organization document (Committee on the
Challenges of Modern Society, 1973) and the USEPA document concerning short-term effects of
N02 (U.S. Environmental Protection Agency, 1978). A World Health Organization monograph has
been recently published (World Health Organization, 1977), as have two excellent interpretive
reviews by Coffin and Stokinger (1977) and by Morrow (1975). The reader is referred to these
publications for a general background on the toxicity of the oxides of nitrogen (NO ).
Most of the data presented in this chapter relate to nitrogen dioxide (N0~) because it
appears to be the most toxic oxide of nitrogen and most widely distributed in a manner affect-
ing human health. The data presented are confined to animal studies as they may relate to
human health.
The focus of this chapter is to present information relating to effects on animals as a
result of exposures to nitrogen oxides and other nitrogen-containing compounds at concentra-
tions below 9,400 (jg/m (5 ppm). Data derived from exposures to higher concentrations of
these compounds have been presented in concise form. Except for a few instances, these data
are presented in the tables only.
14.2 NITROGEN DIOXIDE
14.2.1 Respiratory Tract Transport and Absorption
Nitrogen dioxide is soluble and can be absorbed in the mucous lining of the
nasopharyngeal cavity where it converts to nitrous and nitric acid. However, few data
examining respiratory tract uptake and transformation have been published. (See Table 14-1.)
Yokoyama (1968) used isolated upper airways of the dog and rabbit to measure N02 removal,
which amounted to 42.1 percent of the incoming NO;, concentration. Dalhamn and Sjbholm (1963)
measured the concentration of N0~ in a stream of water-saturated air before and after it had
been passed through the nose and out a tracheal cannula inserted in an anesthetized rabbit.
Considerable variation occurred between animals, but about 50 percent of the incoming NOp was
removed on a single passage through the nasopharyngeal cavity.
Goldstein et al. (1977b) exposed monkeys for 9 minutes to 560 to 1,710 pg/m (0.3 to 0.91
-] o
ppm) NO- plus NOp. During quiet respiration, 50 to 60 percent of the inspired pollutant was
retained by the animal; radioactivity was distributed throughout the lungs. Once absorbed,
NCL or chemical intermediates derived from NO, remained within the lung for prolonged periods
-IT f-
following exposure. N-radioactivity was detectable in extrapulmonary sites as well. The
authors postulated that N02 reacted with water in the nasopharynx and lungs to form nitric and
nitrous acids which then react with pulmonary and extrapulmonary tissues.
14-1
-------
TABLE 14-1. RESPIRATORY TRACT TRANSPORT AND ABSORPTION
N02
Concentration Duration
ug/m3
Not
Reported
560 to
1,710
188,000
ppm (min)
Not Not
Reported Reported
0.3 to 9
0.91
100 < 45
Species Effect
Dog and Removal of 42.1% by isolated upper airways.
rabbit Concentration and flow rates not given.
13
Monkey Concurrent exposure to N0? demonstrated that
N0? was evenly distributed fn the lungs and
absorbed into the blood.
Rabbit Absorption of approximately 50% N0? in the
nasopharyngeal cavity.
Reference
Yokoyama, 1968
Goldstein et
al. , 1977b
Dalhamn and
Sjohblm, 1963
i—1
-p*
ro
-------
Observed effects of exposure to much higher concentrations of N0~ include cessation of
cilia beating (Dalhamn and Sjoholm, 1963) and detection of nitrates and nitrites in urine of
^
animals (Svorcova and Kaut, 1971).
14.2.2 Mortality
In a survey of the acute toxicity of NO, to mice, rats, guinea pigs, rabbits, and dogs,
3
Mine et al. (1970) found that concentrations below 94,000 |jg/m (50 ppm) rarely produced mor-
tality at exposures up to 8 hours. The effects varied from species to species. (See Table
14-2.) Dogs and rabbits appear to be relatively resistant to acute toxicity. In rats,
factors associated with increased mortality at high concentrations of NOp include cold stress
and adrenalectomy.
Dietary supplementation of Vitamin E (45 to 100 mg d, 1-crtocopherol) has been shown to
protect against mortality and increase mean survival of animals exposed, for long periods of
•3
time, to high concentrations of NO- (37,600 to 62,000 ug/m ; 20 to 33 ppm) (Fletcher and
Tappel, 1973; Menzel et al., 1972). The influence of dietary components on NO- toxicity is
discussed more fully in Section 14.2.3.2.1.
14.2.3 Pulmonary Effects
14.2.3.1 Host Defense Mechanisms—In the past, environmental toxicologists have been con-
cerned with measurement and description of effects of single toxic agents such as S0~
(Fairchild et al., 1972), N02 (Coffin et al., 1976; Ehrlich, 1963; Purvis and Ehrlich, 1963),
and 0, (Coffin and Gardner, 1972) on host defense mechanisms. Accumulation of considerable
information indicates a pathophysiological interrelationship between exposure to atmospheric
pollutants and enhanced respiratory susceptibility to bacterial .and viral infections.
Due to practical difficulties associated with the study of the effects of air pollutants
on the susceptibility of the human respiratory system to microbial infection, animal exposures
have been undertaken and several models used.
Normally, the lungs are protected from viral and bacterial infection by the combined
activities of the mucociliary, phagocytic (alveolar macrophage), and immune systems. The muco-
ciliary system, which extends from the nares to the terminal bronchioles, removes 50 to 90
percent of deposited particles within hours after' they enter the lung (Cooper et al. , 1977;
Murphy, 1964). It is important to emphasize that the discontinuous nature of the mucous
blanket precludes complete cleansing of microbes and particles from the bronchial tree.
Surviving microbes and residual particles are phagocytized, killed, and/or removed by macro-
phages that are attracted to the foreign bodies by chemotactic factors. Microorganisms, upon
entrance to the lung, also stimulate the formation of various humoral defense mechanisms.
Interference, by N0?) with any of the interdependent steps in this complex sequence of humoral
and phagocytic reactions or with components of the mucociliary transport system increases host
susceptibility to infection.
14.2.3.1.1 Interaction with infectious agents. Extensive studies using the infectivity model
to examine the effect of NO on susceptibility to airborne infection are reviewed by Ehrlich
14-3
-------
TABLE 14-2. MORTALITY FROM N02 EXPOSURE FOR 1 TO 8 HOURS
N02
Concentration
ug/mj
94,000
to
141,000
141,000
141,000
141,000
141,000
141,000
173,000
ppm
50
to
75
75
75
75
75
75
92
Duration
(hr)
4 or 8
1 to 8
1 to 8
1 to 8
1 to 8
1 to 8
< 8
Species
Rat
Rat
Guinea pig
Rabbit
Dog
Mouse
Mouse
Effect
Increased mortality with cold stress,
adrenal ectomy, and exercise.
No increase with heat or prior N0?
Estimated LT50* 3.7 hr
Estimated LT50 4.0 hr
Estimated LT50 2.7 hr
Estimated LT50 >8 hr
Estimated LT50 2.3 hr
Genetic effects on mortality of inbred
mouse strains. LT50 for CF1, 3.33 hr;
C57BL/6, 6.53 hr
Reference
Hine et al . ,
Hi ne et al . ,
Hine et al . ,
Hine et al . ,
Hine et al . ,
Hine et al . ,
Goldstein et
1973a
1970
1970
1970
1970
1970
1970
al.,
*LT50 = Time at which 50% of the animals would die during continuous exposure to the indicated concentration.
-------
(1975), Coffin et al. (1976) and Gardner and Graham (1976). (See Table 14-3.) The infecti-
vity model system has been employed successfully with hamsters (Ehrlich, 1966), mice (Coffin
and Gardner, 1972; Coffin et al., 1976; Ehrlich, 1963; Fairchild et al., 1972; Purvis and
Ehrlich, 1963), and squirrel monkeys (Henry et al., 1970). Animals are randomly selected for
exposure to either a test substance in air (in this case NOp) or filtered air. After
exposure, control and exposed animals are placed in another chamber and exposed for a brief
period (approximately 15 minutes) to aerosols of a specific infectious agent, such as
Streptoccoccus pyogenes (S. pyogenes), Klebsiella pneumoniae (K^_ pneumom'ae), Diploccoccus
pneumoniae (th_ pneumoniae), influenza A^/Taiwan virus, or A/PR/8 influenza virus. The animals
are then returned to clean air for a 15-day holding period and the mortality rates in the NO,,-
exposed and control groups are compared. The mortality of the control group is usually 15 to
20 percent. Death is due to pneumonia and its consequences (Gardner and Graham, 1976).
In a series of investigations, the relationships of concentration and time to suscepti-
bility to respiratory infection and to subsequent mortality in infections with S. pyogenes
were examined (Gardner et al., 1977b; Gardner et al., 1977a, Coffin et al., 1977). The con-
0
centrations of NCL were varied from 1,880 to 26,320 ug/m (1 to 14 ppm), and the duration of
exposure ranged from 0.5 to 7 hours so that the product of concentration and time equalled a
value of 7. Exposure to high concentrations of N02 for brief periods of time resulted in more
severe infections and in greater mortality than did prolonged exposures to lower concentra-
tions of NO,,. This indicated that susceptibility to infection was influenced more by concen-
tration of NOp than by duration of exposure. (See Table 14-4.)
As depicted in Figure 14-1, Gardner et al. (Gardner et al., 1977b), using the same model,
examined the effect of varying durations of continuous exposure on the mortality of mice ex-
posed to 6 constant concentrations of NO, (940 (jg/m to 52,670 ug/m ; 0.5 to 28 ppm). S.
3
pyogenes was used for all concentrations, except 940 ug/m (0.5 ppm), in which case K.
pneumom'ae was used. A linear dose-response (p < 0.05) indicated that mortality increases
with increasing length of exposure to a given concentration of NOp. Mortality also increased
with increasing concentration of NO,,. When C x T was held constant, the relationship between
concentration and time produced significantly different mortality responses. At a constant C
o
x T of approximately 21 (ppm x hour), a 14-hour exposure at 2,800 ug/m (1.5 ppm) N09
3
increased mortality by 12.5 percent whereas a 1.5-hour exposure at 27,300 ug/m (14 ppm) NO^
enhanced mortality by 58.5 percent. These studies confirmed the previous conclusion that
concentration is more important than time in determining the degree of injury induced by NO,,
in this model. According to Larsen et al. (1979), N02 modeling studies have shown that the
concentration (c) of N02 expected to cause a certain mortality level (z) as a function of the
hours of exposure (t) can be expressed as c = 9.55 (2.42)zt ' .
Gardner et al. (1979) also compared the effect of continuous versus intermittent exposure
to NOp followed by bacterial challenge with S. pyogenes (Figures 14-2, 14-3). Mice were
exposed either continuously or intermittently (7 hours/day, 7 days/week) to 2,800 ug/m or
6,600 pg/m3 (1-5 or 3.5 ppm) N02> Figure 14-2 illustrates the results of continuous and
14-5
-------
TABLE 14-3. INTERACTION WITH INFECTIOUS AGENTS
N02
Concentration
ug/m3
560
to
940
940
940
to
1,880
18,800
ppm
0.3
to
0.5
0.5
0.5
to
1
10
Exposure Species
Continuous, Mouse
3 mo
Continued
3 mo more
Intermit- Mouse
ent 6 or 18
hr/day, to 12 mo
Continuous,
90 days
Continuous Mouse,
39 days female
2 hr/day,
1, 3, 5
days
Infective
Agent Effect Reference
A/PR/8 virus High incidence of adenomatous Motomiya et al.,
proliferation of peripheral 1973
and bronchial epithelial cells.
NOp alone & virus alone caused
less severe alterations.
No enhancement of effect of N0?
and virus.
K. pneumoniae Increased mortality after Ehrlich and
6 mo intermittent exposure Henry, 1968
or after 3, 6, 9, or 12 mo
continuous exposure. Following
12 mo exposure, increased
mortality was significant only
in continuously exposed mice.
A/PR/8 virus Significantly increased suscep- Ito, 1971
tibility to infection.
1,880 1 17 hr Mouse S. aureus
after N0£
4,320 2.3
12,400 6.6
2820 to 1.5 to (See Figure 14-1) Mouse S. pyogenes
52,670 28
Bactericidal activity unchanged.
6% decrease in bactericidal
activity (p<0.05).
35% decrease in bactericidal
activity (p<0.01).
Increased mortality with in-
creased time and concentration.
Goldstein et al.,
1973b
Gardner et al.,
1979
-------
TABLE 14-3. (continued)
N02
Concentration
ug/ms ppm
1,880 1
5,600 3
2,820 1.5
6,600 3.5
8,100 4.5
2,800 1.5
(8,100 4.5)
spike
Exposure Species
3 hr Mouse
Continuous Mouse
or inter-
mittent
7 hr/day,
7 days/wk
Continuous
or inter-
mittent
7 hr/day,
7 days/wk,
to 15 days
1, 3. 5 or Mouse
7 hrs
Cont. 62 hrs. Mouse
then spike for
1, 3.5 or 7 hr. ,
then cont. 18
hrs.
Infective
Agent Effect Reference
S. pyogenes Exercise on continuously moving 11 ling et al . ,
wheels during exposure increased 1980
mortality at 5,600 ug/m (3 ppm)
N02.
S. pyogenes After 1 wk, mortality with con- Gardner et al.,
tinuous exposure greater (p < 1979
0.05) than that for intermit-
tent. After 2 wk, no signif-
icant difference between con-
tinuous and intermittent expo-
sure.
Increased mortality with in-
creased duration of exposure.
No significant difference
between continuous and intermit-
tent exposure. With data adjusted
for total difference in C X T,
mortality essentially the same.
S. pyogenes Mortality proportional to dura- Gardner et al.,
tion when bacterial challenge (1982)
was immediately, but not 18
hrs post exposure
S. pyogenes Mortality increased with 3.5 Gardner et al. ,
and 7 hr. single spike when (1982)
bacterial challenge was
immediately or 18 hrs post
exposure
-------
TABLE 14-3. (continued)
I
oo
N02
Concentration
ug/mj ppm
2,800 1.5
(8,100 4.5)
continuous:
100 0.05+
100 0.05 03
with spikes 2x per
200 0.1+
200 03 0.1 03
continuous:
940 0.5
100 0, 0.05 07
Exposure Species
Cont. for 14 d Mouse
spike 2x1 hr/d
5 days/wk x 2 wk
Cont. Mouse
day:
15 days
(spikes-1 hr,
twice/day, 5
days/wk)
Mouse
Infective
Agent Effect
S. pyogenes 1 wk or 2 wk needed for in-
creased mortality depending
on time of infection (See
text for details)
S. pyogenes No effect
S. pyogenes Increased mortality with N00
alone; no effect 0, alone;
Reference
Gardner et al. ,
(1982)
Gardner et al . ,
(1982)
Gardner et al. ,
(1982)
with spikes 2 x per day:
1,880 1.0+
synergistic effect 0., + N09
200 0,
0.1 0-
continuous:
2,300 1.2+
200 0.1 0-
with spikes 2 x per day:
4,700 2.5
Cont. 15 days
(spikes-1 hr,
twice/day, 5
days/wk)
600 03 0.3 03
2,800
1.5
Cont.
Mouse
Mouse
>. pyogenes Increased mortality with NO,
alone and 0., alone; additiv^
effect of 03 + N02
S. pyogenes Elevated temp. (32° C) in-
creased mortality
Gardner et al.,
(1982)
Gardner et al.,
(1982)
-------
TABLE 14-3. (continued)
N02
Concentration
ug/m-1
3,570
7,140
13,160
17,200
27,800
3,760
4,700
47,000
9,400
18,800
28,200
6,580
65,830
ppm Exposure
1.9 4 hr
3.8
7
9.2
14.8
2 3 hr
2.5 2 hr
25
5
10
15
3.5 2 hr
35 2 hr
Infective
Species Agent
Mouse Infected with
S. aureus
prior to NO-
exposure
Mouse S. pyogenes
Mouse Challenge
with K.
pneumoniae
before and
after ex-
posure
Mouse K. pneumoniae
challenge
Hamster after
Effect Reference
Physical removal of bacteria Goldstein et al . ,
unchanged at 3,570 and 7,140 1973b
ug/mj (1.9 and 3.8 ppm).
7% lower bactericidal activity
(p<0.05).
14% lower bactericidal activity
50% lower bactericidal activity
Increased mortality (p<0.05) Ehrlich et al.,
1977
No effect og mortality. At Purvis and
47,000 ug/m (25 ppm) effect Ehrlich, 1963
when bacterial challenge was
up to 72 hrs. but not later,
after N02 exposure ceased.
Significant increase in
mortality on K. pneumoniae
challenge 1 and 6 hr post NO-.
When K. pneumoniae challenge
27 hr post WO, effect only at
28,200 ug/m fl5 ppm).
NO, toxic to all species and in- Ehrlich, 1975
creased mortality. Each species
had decreased resistance to NO.
-------
TABLE 14-3. (continued)
N02
Concentration
|jg/m3
94,050
9,400
ppm Exposure
50 2 hr
5 Continuous,
2 mo
Species
Squirrel
monkey
Squirrel
monkey
Infective
Agent Effect
K. pneumonias One-third died after infection.
and A/PR/8
Reference
Henry et al . ,
1970
19,000 10 Continuous
1 mo
9,400 5 2 mo
19,000 10 1 mo
virus
Death within 2-3 days after in-
fection. Increased susceptibil-
ity to infection. Decreased lung
clearance of viable bacteria.
Squirrel K. pneumoniae Mortality 2/7. Bacteria present
monkey in lung of survivors upon
autopsy.
Mortality 1/4. Bacteria present
in lungs of survivors at
autopsy.
Henry et al.,
1969
94,000 50 2 hr
Mortality 3/3.
-------
TABLE 14-4. THE INFLUENCE OF CONCENTRATION AND TIME ON EHNANCEMENT
OF MORTALITY RESULTING FROM VARIOUS N02 CONCENTRATIONS3
Concentration x time
Concentration
pg/rn3
2,820
6,580
13,160
26,320
52,640
ppm
1.5
3.5
7
14
28
Time
(hrs)
4.7
2.0
1.0
.5
.25
7
%
Mortality
6.4
18.7
30.2
21.7
55.5
Time
(hrs)
9.3
4.0
2.0
1.0
.5
14
%
Mortal ity
10.2
27.0
41.8
44.9
67.2
Time
(hrs)
14.00
6.00
3.00
1.50
.75
21
%
Mortality
12.5
31.9
48.6
58.5
74.0
aThese are predicted values obtained from Figure 1 of Gardner et al., 1979.
14-11
-------
o
2
01
DC
Q
>
QC
O
o
U
CM
O
U
cc
90
80
70
60
50
40
30
20
10
0
-10
1 1 II II II I II III
15 253035
minutes
1
•-W-
2357 14 24 48
hours
96
1416 30 23 6 9 12
days e»~f-«a months "H
TIME
Figure 14-1. Regression lines of percent mortality of mice versus length of continuous exposure to various NC>2 concentrations prior to
challenge with hacterin (Gardner et al., 1977h).
-------
a:
O
OJ 01
O
a:
90
80
70
60
50
40
30
20
10
—a
cr
D
O
n
o
a
O CONTINUOUS
D INTERMITTENT
o—
CONTINUOUS NO2 EXPOSUHEXA
INTERMITTENT NC»2 EXPOSURE
ffV
0 7
127
151
175
199
223
247
271
295
343
TIME, hours
Figure 14-2. Percent mortality of mice versus the length of either continuous or intermittent exposure to 6,600 ug/m^ (3.5 ppmj IMO2 pnor
to challenge with streptococci (Gardner et al., 1977b; Gardner et al.r 1977a; Coffin et al., 1977).
-------
O
CE
o
(J
I
fM
O
UJ
tr
UJ
30
20
t 10
_J
<
tr
O
o
oc
0 7
O* CONTINUOUS
O
D
D INTERMITTENT
D
D
a
'CONTINUOUS AND INTERMITTENT
TREATMENT MEANS ARE SIGNIFICANTLY
DIFFERENT ATp<0.05
CONTINUOUS N07 EXPOSURE
'/ INTERMITTENT NOzEXPOSURE
79
151
319
TIME, hours
487
Figure 14 3. Percent mortality of mice versus length of either continuous or intermittent exposure to 2.800
challenge with streptococci (Gardner etal., 1977b; Gardner et al.. 1977a; Coffin et al., 1977).
(1.5 ppm) NO2 prior to
-------
intermittent exposure to 6,600 ug/m (3.5 ppm) NO^ for periods up to 15 days. There was a
significant increase in mortality for each of the experimental groups with increasing duration
of exposure. When the data were adjusted for the difference in C x T, the mortality was
essentially the same for the continuous and intermittent groups. The continuous exposure of
3
mice to 2,800 ug/m (1.5 ppm) N0~ increased mortality after 24 hours of exposure. During the
first week of exposure, the mortality was significantly higher in mice exposed continuously to
NOp than in those exposed intermittently. By the 14th day of exposure, the difference between
intermittent and continuous exposure became indistinguishable (Figure 14-3).
Mice were exposed continuously or intermittently (6 or 18 hours/day) to 940 ug/m (0.5
ppm) NOp for up to 12 months (Ehrlich and Henry, 1968). Neither exposure regimen affected
murine resistance to K^_ pneumoniae infection during the first month. Those exposed con-
tinuously exhibited decreased resistance to the infectious agent as demonstrated by enhanced
(p < 0.05) mortality at 3, 6, 9, and 12 months. In another experiment, an enhancement (p <
0.1) did not occur at 3 months but was observed after 6 months of exposure. After 6 months,
mice exposed intermittently (6 or 18 hours/day) to N0? showed significant (p < 0.1) increases
in mortality over that of controls (18%). After 12 months exposure to NCL, mice in the three
experimental groups showed a reduced capacity to clear viable bacteria from the lung. This
was first observed after 6 months in the continuously exposed mice and after 9 months in the
two intermittently exposed groups. These changes, however, were not statistically tested for
significance. Only the continuously exposed animals showed increased mortality (23%) over
controls following 12 months exposure. Therefore, while it is not possible to directly com-
pare the results of studies using S^_ pyogenes to those using K^ pneumoniae, the data suggest
that as the concentration of N0? is decreased, a longer exposure time is necessary for the
intermittent exposure regimen to produce a level of effect equivalent to that of continuous
exposure.
Gardner et al. (1982) investigated further the effects of intermittent exposures on the
response of mice to airborne infections. The objective of these studies was to investigate
the toxicity of spikes of NOp exposure superimposed on a lower continuous NO^ exposure. Such
a regimen approximates the pattern of exposure which man receives in urban environments. Mice
were exposed to spikes of 8,100 ug/m (4.5 ppm) for 1, 3.5 or 7 hrs and exposed to S. pyogenes
either immediately or 18 hrs afterwards. Mortality was proportional to the duration of the
spike when mice were exposed immediately, but mice recovered from the exposure by 18 hrs.
When these same spikes were superimposed on a continuous background of 2,800 ug/m (1.5 ppm)
for 62 hrs preceding and 18 hours following the spike, mortality was significantly enhanced
(p < 0.05) only by a spike of 3.5 or 7 hrs when the infectious agent was administered 18 hours
after the spike. Possible explanations for these differences in the presence or absence of a
background exposure are that mice continuously exposed are not capable of recovery or that
alveolar macrophages or polymorphonuclear leukocytes recruited to the site of infection are
impaired by the continuous exposure to NOp- The effect of multiple spikes was examined by
14-15
-------
exposing mice for 2 weeks to two daily spikes (morning and afternoon) of 1 hr of 8,100 ug/m
(4.5 ppm) superimposed to a continuous background of 2,800 ug/m (1.5 ppm). Spikes were not
superimposed on the continuous background during weekends. Mice were exposed to the infec-
tious agent either immediately before or after the morning spike. When the infectious agent
was given before the morning spike, the increase in mortality did not approach closely that of
a continuous exposure to 2800 |jg/m (1.5 ppm). However, in mice exposed after the morning
spike, by 2 weeks of exposure, the increased mortality over controls approached that equiva-
2
lent to continuous exposure to 2,800 ug/m (1.5 ppm).
In this same study, Gardner et al. (1982) also examined the effects of exposure to spikes
of 03 and NO,,, and heat stress. At the lowest concentration of 0, and NOp examined, 100 ug/m
(0.05 ppm) with spikes of 200 ug/m (0.1 ppm), no differences in mortality were observed com-
pared to clean air controls. When mice were exposed to intermediate (0.5 ppm NOp with 1.0 ppm
spikes and 0.05 ppm 03 with 0.1 ppm spikes) or high (1.2 ppm N0~ with 2.5 ppm spikes and
0.1 ppm 0, with 0.3 ppm spikes) doses, mortality was increased synergistically; e.g., mortal-
ity was greater than the arithmetic sum of the mortality due to the single gas exposure. When
mice were stressed by elevated temperature (32°C), 7 daily, but not 4 daily, exposures to
2,800 ug/m (1.5 ppm) enhanced mortality and decreased survival times.
Another stress, exercise, was also evaluated with the infectivity model (Illing et al. ,
1980). Mice running on an activity wheel during exposure were more susceptible to 5,600 ug/m
(3.0 ppm) than those resting.
Gardner et al. (1982) concluded that while a simple log-log relationship exists for the
mortality associated with a given exposure-time product with mice continuously exposed to NCL
$
or given intermittent regular exposures, no such relationship exists for mice continuously
exposed';to a constant concentration of NO- upon which are superimposed spikes of greater con-
centration. The relationship is highly complex depending in part upon the duration of the
spike and the time since the last exposure of the spike.
Mice, hamsters, and monkeys were exposed to NOp for 2 hours followed by a challenge of K.
pneumoniae (Ehrlich, 1975). Nitrogen dioxide enhanced the mortality due to the pathogen in
all species tested. Differing results among species were found. This could be due to differ-
ing sensitivity to either the pathogen or N09, or a combination of both. All three squirrel
3
monkeys -exposed to 94,050 ug/m (50 ppm) NO, died from the pneumonia (Henry et al., 1969).
T
Lower concentrations tested (9,400 to 65,830 ug/m ; 5 to 35 ppm) had no effect in monkeys.
The hamster model, which exhibited enhanced mortality due to N09 at concentrations > 65,830
o 3
ug/m (35 ppm) but not at 9,400 to 47,000 ug/m (5 to 25 ppm), had intermediate sensitivity.
The mouse model was sensitive to NOp exposure as evidenced by enhanced mortality following
exposure to 6,580 ug/m3 (3.5 ppm) but not to 2,820 to 4,700 ug/m3 (1.5 to 2.5 ppm) N02 for 2
hours (Ehrlich, 1975). No effect on mortality was observed in mice exposed for 2 hours to
o
4,700 ug/m (2.5 ppm) (Purvis and Ehrlich, 1963). However, when S. pyogenes was the infec-
tious agent, a 3-hour exposure to 3,760 ug/m (2 ppm) NO., caused an increase (p < 0.05) in
mortality (Ehrlich et al., 1977).
14-16
-------
The persistence of the N02 effect was investigated by Purvis and Ehrlich (1963) who
exposed mice for 2 hours to NOp before or after an aerosol challenge with K. pneumoniae. At
9,400, 18,800, 28,200, and 47,000 (jg/m3 (5, 10, 15, and 25 ppm) N02> there was a significant
enhancement of mortality in mice challenged with bacteria 1 and 6 hours after the N0? ex-
posure. When bacterial challenge was delayed for 27 hours, there was an effect only in the
3 3
group exposed to 28,200 |jg/m (15 ppm). Exposure to 4,700 ug/m (2.5 ppm) caused no effect at
any of the bacterial challenge times tested. Exposure of 47,000 ug/m (25 ppm) N0? for 2 hours
with subsequent K. pneumoniae challenge 6 and 14 days later did not affect mortality. When
the experimental regimen was reversed and mice were exposed for 2 hours to 47,000 ug/m (25
ppm) NO,,, mortality was significantly increased 1, 6, 27, 48 and 72 hours after bacterial
challenge. Dose response studies in which mice were challenged 1 hour after a 2 hour NO,
3
exposure showed that 6,580 ug/m (3.5 ppm) had a significant effect; exposure concentrations
of 2,820 and 4,700 (jg/m3 (1.5 and 2.5 ppm) did not.
Environmental stress has been shown to enhance the toxic effect of NO,. Mice placed on
3
continuously moving exercise wheels during exposure to 5,600 ug/m (3 ppm) N00, but not 1,880
3
ug/m (1 ppm), for 3 hours showed enhanced mortality over nonexercised N0? exposed mice (p <
0.06) using the infectivity model (Illing et al., 1980). The presence of other environmental
factors, ozone (0,) (Ehrlich et al., 1977, Gardner et al., 1982) or tobacco smoke (Henry
et al., 1971), also augments the deleterious effect of NO,, on host resistance to experimental
infection (see Section 14.3).
3 3
Squirrel monkeys exposed continuously to N02 levels of 18,800 ug/m and 9,400 ug/m (10
ppm and 5 ppm) in air for 1 and 2 months, respectively, showed increased susceptibility to a
challenge with K. pneumoniae or influenza A/PR/8 virus and reduced lung clearance of viable
bacteria (Henry et al., 1970). All six animals exposed to 18,800 ug/m (10 ppm) died within 2
to 3 days of infection with the influenza virus. At 9,400 ug/m (5 ppm), one of three monkeys
died. Susceptibility to viral infection also was enhanced when the N09 exposure occurred 24
3
hours after infectious challenge. Exposure to 94,000 ug/m (50 ppm) N02 for 2 hours was not
fatal, whereas the same exposure followed by challenge with K. pneumoniae was fatal to three
out of three monkeys (Henry et al., 1969). After challenge with K. pneumoniae, two of seven
3
monkeys exposed to 9,400 ug/m (5 ppm) for 2 months died and the rest had bacteria in the
lungs on autopsy. After an exposure to 18,800 ug/m (10 ppm) for 1 month, one of four monkeys
died, and the pathogen was present in the lungs of the remainder of the animals at autopsy 19
to 51 days post-exposure.
Mice exposed continuously for 3 months to 560 to 940 ug/m (0-3 to 0.5 ppm) NO,, followed
by challenge with A/PR/8 influenza virus demonstrate significant pulmonary pathological
responses. Motomiya et al. (1973) reported a greater incidence of adenomatous proliferation
of bronchial epithelial cells following combined .exposures; viral exposures or N0~ alone
caused less severe alterations than the combination of N02 plus virus. Continuous N02 expo-
sure for an additional 3 months did not enhance further the effect of N02 or the subsequent
virus challenge.
14-17
-------
Ito (1971) challenged mice with influenza A/PR/8 virus after continuous exposure to 940
to 1,880 ug/m3 (0.5 to 1 ppm) N00 for 39 days and to 18,800 (jg/m3 (10 ppm) NO, for 2 hours
3
daily for 1, 3, and 5 days. Acute and intermittent exposure to 18,800 ug/m (10 ppm) NO, as
3
well as continuous exposure to 940 to 1,880 ug/m (0.5 to 1 ppm) N02 increased the suscepti-
bility of mice to influenza virus as demonstrated by increased mortality.
The enhancement in mortality following exposure to NO^ and a pathogenic organism could be
due to several factors. One could be a decreased ability of the lung to kill bacteria.
Studies by Goldstein et al. (1973b, 1974) illustrated this concept in a series of experiments
which show decreased bactericidal activity following exposure to various pollutants. In the
first experiments, mice breathed aerosols of Staphylococcus aureus (S. aureus) labelled with
32
radioactive phosphorus ( P) and were then exposed to N02 for 4 hours (Goldstein et al.,
1973b). Physical removal of the bacteria was not affected by any of the N02 concentrations
used up to 27,800 ug/m3 (14.8 ppm). Concentrations of 13,200, 17,200, and 27,800 ug/m3 (7,
9.2, and 14.8 ppm) N09 lowered bactericidal activity by 7, 14, and 50 percent, respectively,
3
when compared to controls (p < 0.05). Lower concentrations (3,570 and 7,140 ug/m ; 1.9 and
3.8 ppm) had no significant effect. In another experiment, mice breathed NO,, for 17 hours and
then were exposed to an aerosol of S. aureus. Four hours later the animals were examined for
the amount of bacteria present in their lungs. No difference in the inhalation of bacteria
was found with N0? exposure. Concentrations of 4,320 and 12,400 ug/m (2.3 and 6.6 ppm) NO,,
decreased pulmonary bactericidal activity by 6 and 35 percent, respectively, compared to con-
trol values (p < 0.05). Exposure to 1,880 ug/m (1 ppm) NO,, had no significant effect.
Goldstein et al. hypothesized that the decreased bactericidal activity was due to defects in
alveolar macrophage function. The detailed effects of N02 exposure on the function of
alveolar macrophages are presented in Section 14.2.3.1.3.
14.2.3.1.2 Mucociliary transport. Mucociliary transport is the principal mechanism for
removal of inspired and aspirated particles from the tracheobronchial tree. Concentrations of
N0« greater than 9,400 ug/m (5 ppm) decrease rates of ciliary beating as measured J_n vitro
(Kita and Omichi, 1974) and of mucociliary transport j_n vivo (Giordano and Morrow, 1972). The
effect of lower concentrations of N09 on mucociliary function is unknown. (See Table 14-5)
3
Schiff (1977) exposed hamster tracheal ring cultures to 3,760 ug/m (2 ppm) N02 for 1.5
hours/day, 5 days/week, for 1, 2, and 3 weeks. Tracheal cultures infected with influenza
virus immediately after the initiation of the NO,, exposure were not different from control
infected cultures. However, explants infected after 1 or 2 weeks of N02 exposure showed
decreased ciliary activity and morphological changes compared to controls held in filtered
air. After 14 days exposure to N0? non-infected cultures showed a decrease in ciliary
activity and morphological changes. After 4 weeks exposure of the uninfected cultures, there
was a 63 percent decrease in ciliary activity. In addition, tracheal organ cultures exposed
to N02 exhibited a more rapid production of virus than explants held in filtered air.
14.2.3.1.3 Alveolar macrophage. Exposures of animals to N02 concentrations ranging from
13,160 to 112,800 ug/m (7 to 60 ppm) cause a variety of structural and physiological
14-18
-------
TABLE 14-5. MUCOCILIARY TRANSPORT
N02
Concentration
|jg/m3 ppm Exposure Species
11,280 6 7 days/wk, Rat, female
6 wk
Effect
Increase in TPTT and FET3: decrease in muco-
ciliary velocity, p<0.02. Functional
impairment reversed within 1 wk.
Reference
Giordano and
Morrow, 1972
TPTT = Twenty percent transport time.
FET = First-edge time.
-pa.
I
-------
abnormalities in alveolar macrophages. (See Table 14-6.) Alveolar macrophages (AM) isolated
from animals exposed to these concentrations of NO,, show diminished phagocytic activity,
(Gardner et al., 1969) appearance of intracellular dense bodies, (Katz and Laskin, 1976) in-
creased congregation of AM on epithelial cells, (Sherwin et al., 1968) enhanced wheat germ
lipase-induced binding of autologous and heterologous red blood cells to AM, (Hadley et al.,
1977) increased J_n vitro penetration of AM by virus, (Williams et al., 1972) reduced j_n vitro
production of interferon, (Valand et al., 1970) and increased mitochondrial and decreased
cytoplasmic NAD+/NADH ratios. (Mintz, 1972; Simons et al., 1974) An increased number of
polymorphonuclear leukocytes was observed in lung lavages of animals exposed to high levels of
N02 (Gardner et al., 1969). (Table 14-6.)
Aranyi et al. (1976) used scanning electron microscopy (SEM) to study the effect of
exposure to Ntk on the anatomic integrity of mouse alveolar macrophages which were lavaged
from the lung. No changes in the AM surface were observed after continuous exposure of mice
for 4, 12, and 24 weeks to 940 ug/m (0.5 ppm) without peaks or 188 ug/m3 (0.1 ppm) N09 with
3
3-hour peaks at 1,880 ug/m (1 ppm) for 5 days/week. Macrophages from mice continuously
3 3
exposed to 3,760 ug/m (2 ppm) without peaks or 940 ug/m (0.5 ppm) N09 with 1-hour peaks of
3
3,760 |jg/m (2 ppm) N0~ for 5 days/week, showed distinctive morphological alterations after 21
weeks total exposure. Loss of surface processes, appearance of fenestrae, bleb formation,
denuded surface areas, as well as, occasionally, complete deterioration of the cells were seen.
Structural changes were still observed at the same N09 concentrations after continuous expo-
3 3
sure to a baseline of 940 ug/m (0.5 ppm) with peaks of 3,760 ug/m (2 ppm) NOg for 28 or 33
weeks. These observations appear to correlate well with a reduction in i_n vitro phagocytic
activity and increased susceptibility to infection.
Acton and Myrvik (1972) administered an intratracheal injection of parainfluenza-3 virus
to rabbits prior to 3-hour exposures to 9,400, 28,200, 47,000, or 94,000 ug/m (5, 15, 25, or
50 ppm) N02. Alveolar macrophages harvested from exposed, as well as control animals, were
challenged with rabbitpox virus. Macrophages from control animals infected with influenza had
increased resistance (75 percent) to pox virus. However, there was partial loss of resistance
o
48 hours following exposures to 28,200 ug/m (15 ppm) NO,. No decrease in resistance was
3
observed with 9,400 ug/m (5 ppm) NO,. Phagocytic capabilities were adversely affected in
o
macrophages from animals exposed to 28,200 to 94,000 ug/m (15 to 50 ppm) N09. At a concen-
3
tration of 94,000 ug/m (50 ppm), NO,, stimulated oxygen uptake and hexose monophosphate shunt
activity in the AM.
Nitrogen dioxide-induced alteration of receptor sites of the alveolar macrophages has
been studied by Goldstein et al. (Goldstein et al. , 1977a; Goldstein, 1979). It was found
3
that j_n vitro exposure of rat alveolar macrophages to 4,512 ug/m (2.4 ppm) N0« for 1 hour
resulted in a 64 percent increase in agglutination by concanavalin A (Goldstein et al.,
3
1977a). Alveolar macrophages collected from rats exposed to 22,748 ug/m (12.1 ppm) N02 for 2
hours displayed a 40 percent increased agglutinability to concanavalin A. Following exposure
of alveolar macrophages to 6,768 ug/m (3.6 ppm) NOp for 1 hour, incubation of macrophages
14-20
-------
TABLE 14-6. ALVEOLAR MACROPHAGES
N02
Concentration
ug/m3 ppm
940 0.5
188 0.1
[with 3
hr peaks
of 13880
ug/m
(1 ppm)]
3,760 2
940 0.5
[with 1
hr peaks
of 33760
(jg/m
(2 ppm)]
Exposure Species
Continuous exposure Mouse
for 4, 12, 24 wks
Exposure for 4, 12,
24 wks , 5 days/wk
Continuous exposure Mouse
for 21, 28, 33 wks
Continuous exposure
for 21, 28, 33 wks,
5 days/wk
Effect Reference
Alveolar macrophage (AM) surface Aranyi et al.,
unchanged. 1976
Distinct morphological altera- Aranyi et al.,
tions after 21 wk total exposure. 1976
Loss of surface processes, appear-
ance of fenestrae, bleb formation,
denuded surface areas, and complete
deterioration of cells were noted.
6,768 3.6 1 hr
Rat
22,748 12.1 2 hr
Incubation of macrophages with
3H-concanavalin A revealed no
significant alterations in
binding. At this concentration,
agglutination was enhanced 47%.
40 percent increase in con-
canavalin A agglutination of
macrophages.
Goldstein et al. ,
1977a
-------
TABLE 14-6. (continued)
N02
Concentration
ug/m3
9,400
28,200
ppm Exposure Species
5 3 hr exposure Rabbit
after infection
15 with parainf luenza-3
virus. Challenge
with rabbit pox virus.
Effect Reference
Control AM had increased Acton and Myrvik,
resistance (75%) to pox virus. 1972
Partial loss of resistance,
following 28,200 ug/m (15 ppm)
47,000
94,000
18,800
25
50
i — »
i
ro
no
13,200
15,000
to
112,800
18,800
47,000
7
8
to
60
10
25
24 hr
3 hr
24 hr
10
Rabbit
Rabbit
Rat
7 wk
continuous
Guinea pig
Decreased phagocytic capabilities
at all concentrations except
9,400 ug/m (5 ppm).
Reduction in resistance,
decreased phagocytic
capabilities, stimulation
of 0? uptake plus hexose-
monophospate shunt activity.
Increased rosette formation in AM Hadley et al. ,
treated with wheat germ lipase. 1977
Increased number of poly-
morpho-nuclear leukocytes in
lavage fluid persisted for more
than 72 hr.
Gardner et al.
1969
Phagocytic activity was unchanged. Katz and Laskin,
n ^ u 4- • 1976
Depressed phagocytosis was
seen on 3rd day of culture.
Macrophages apparently recovered
by 7th day of culture.
63% increase in epithelial cells
positive for macrophage congrega-
tion. Presence of 7 or more AM
on a single epithelial cell-2.5
times more frequent.
Sherwin et al.,
1968
-------
TABLE 14-6. (continued)
N02
Concentration
|jg/m3
19,000
43,300
ppm
10
23
Exposure
3 hr
1 hr
Species
Rabbit
Rabbit
Effect
50% inhibition of phagocytic
activity.
Increased mi tochondrial and
Reference
Gardner et al . ,
1969
Mintz, 1972
47,000
47,000
25 3 hr
25
Rabbit
3 hr
Rabbit
decreased cytoplasmic NAD /NADH
were observed.
No development of resistance with
NO-, exposure immediately after
infection with parainfluenza-3
virus or up to 24 hr before viral
inoculation. Increased lung ab-
sorption of virus. No effect
on viral potency.
Viral uptake not affected
when infected with para-
inf luenza-3 virus after N0_
exposure. No inhibition of
viral RNA synthesis. Twice
as many virus attached and
penetrated exposed AM.
Valand et al.
1970
Wi11iams et al. ,
1972
-------
3 3
with H-concanavalin A revealed no significant alterations in binding of H-concanavalin A to
the macrophages. At this concentration of NO,, agglutination was enhanced 47 percent.
3
Green and Schneider (1978) exposed baboons to 3,760 ug/m (2 ppm) NOp for 8 hr/day, 5
days/wk for 6 months and examined the response of their alveolar macrophages to migration
inhibition factor (MIF). MIF is a substance produced by lymphocytes which inhibits migration
of macrophages and thus influences their protective functions. Two of three of the antigen-
sensitized, NOp-exposed animals did not respond to MIF. Macrophages from 3 of the 4 NOp-
exposed baboons had diminished responsiveness to MIF.
Voisin et al. (1976; 1977) exposed guinea pig macrophages, i_n vitro, to 188, 1,880,
3,760, and 9,400 ug/m (0.1, 1, 2, and 5 ppm) NO, for 30 minutes. The surviving cells showed
3
decreased bactericidal activity, especially at the 9,400 ug/m (5 ppm) level, as well as re-
3
duction in ATP content and changes in morphology. Following exposure to 188 ug/m (0.1 ppm)
NO,, the alveolar macrophage membranes appeared to be spread out and to emit cytoplasmic pro-
3
jections. These projections were much more evident upon exposure to 1,880 and 3,760 ug/m (1
3
and 2 ppm) NOp. At 3,760 ug/m (2 ppm) NO,,, the nucleus became hard to identify due to its
washed-out appearance.
Vassallo et al. (1973) found that jjj vitro exposure to N0? for 15 to 20 minutes could
damage the AM. Phagocytosis and bactericidal capability were adversely affected by NOp con-
centrations at 15 mM (690 ppm) (p < 0.05). Both 5 and 10 mM (230 and 460 ppm) NOp increased
CO, production from C-l- and C-6-glucose and from C-1-pyruvate (p < 0.05) in the
14
resting AM, with similar results occurring in phagocytizing cells, except for the C-6-
glucose substrate. Nitrogen dioxide diminished the conversion of formate to COp by approxi-
mately 50 percent. A concentration of 0.5 mM (23 ppm) also prevented the inhibition of AM
catalase activity caused by a subsequent addition of aminotriazale, whereas NOp alone did not
inhibit its activity.
14.2.3.1.4 Immune system. The effects of exposures of animals to NOp on a few parameters of
the immune response have been investigated by a small number of workers (Antweiller et al.,
1975; Balchum et al. , 1965; Ehrlich and Fenters, 1973; Ehrlich et al., 1975; Fenters et al.,
1971; Fenters et al., 1973; Kosmider et al., 1973b; Matsumura, 1970a). (See Table 14-7.) It
should be emphasized that local responses within the lung are critical in regard to anti-
microbial defense and that these responses are, for the most part, unstudied. Ehrlich et al.
3 3
(1975) exposed male SPF Swiss albino mice continuously to 3,760 ug/m (2 ppm) or 940 ug/m
(0.5 ppm) N02 with daily 1-hour peaks of 3,760 ug/m (2 ppm) for 5 days/ week for 3 months.
After exposure, all mice were vaccinated with influenza Ap/Taiwan/1/64. Mean serum neutraliz-
ing antibody titer was four-fold lower with N02 exposure (p < 0.05) than with controls. Con-
trol mice breathing filtered air also showed a depressed serum neutralizing antibody titer 2
weeks after vaccination (p < 0.05). However, 4 to 8 weeks after vaccination there were no
differences between controls and treated. The hemagglutination inhibition titer was not
affected. Non-vaccinated mice exposed to either NO, regimen had decreased serum IgA and
3
increased serum IgG-^ (p < 0.05). Mice breathing 940 ug/m (0.5 ppm) N02 with peaks of 3,760
14-24
-------
TABLE 14-7. IMMUNOLOGICAL EFFECTS
-F=.
I
ro
en
Pollu- Pollutant Concentration
tant ug/m^
N02 3.760
940 with
daily 1 hr
3,760
N02 1,880
N02 1,880
N02 9,400
N02 9,400
9,400
28,200
N02 10,000
NO, 37,600
* 75,200
131,700
ppm
2
0.5 with
daily 1 hr
2
1
1
5
5
5
15
5.3
20
40
70
Exposure Species
24 hr/day, 5 days/wk. Mouse,
3 mo followed by vacci- male
nation with influenza
A2/Tai wan/1/64 virus
Continuous, 493 days; Monkey
challenge 5 times with
monkey adapted influenza
A/PR/8/34 virus during
exposure
6 mo followed by intra- Guinea pig
nasal challenge with
D. pneumoniae
Continuous, to 169 days; Monkey
challenge with mouse
adapted influenza
A/PR/8/34 virus 24 hr
prior to exposure
4 hr/day, 5. days/wk Guinea pig
7.5 hr/day, 5 days/wk
Continuous, 33 days Guinea pig
Gas 30 min, then aerosol Guinea pig
of egg albumin or bovine
serum albumin for 45 min,
Effects
4-fold decrease in serum neutralizing antibody
titer. Hemaggluti nation inhibition titers
unchanged. Before viral challenge, decreased
serum IgA and increased serum IgG... Increased
IgM and IgG. (p < 0.05). Serum IgA unchanged,
IgM increased (p < 0.05) after virus.
Hemaggluti nation inhibition titers unchanged.
Increased mean serum neutralizing antibody
titers after 493 days exposure. Titers
increased 7-fold 21 days post virus. Titers
increased 11-fold 41 days post virus.
Increased respiratory infection. Decreased
hemolytic activity of complement. Decreased
all immunoelectrophoretic fractions. In-
creased mortality following D. pneumoniae.
Hemaggluti nation inhibition titers or amnestic
response unchanged. Initial depression in serum
neutralization titers with return to normal by
133 days.
Lung tissue serum antibodies increased
with intensity and duration of exposure.
No effect on antibody production.
Reference
Ehrlich et al. ,
1975
Fenters et al. ,
1973
Kosmider et al. ,
1973b
Fenters et al. ,
1971
Balchum et al. ,
1965
Antweiler, 1975
Anaphylactic attacks in 50% exposed animals by Matsumura, 1970a
5th aerosol administration at highest concentra-
tion. No effect at lower levels. Hemagglutination
repeated 5-7 times on
different days
tests unchanged. Less antigen needed in active
cutaneous anaphylaxis test at highest levels
(p < 0.05).
-------
TABLE 14-7. (continued)
Pollu- Pollutant Concentration
tant jjg/m3 ppm Exposure Species Effects Reference
i
INi
CTi
N07 56,400 30 Exposure 30 min then Guinea pig Mortality increased at NO. Matsumura et al.,
75,200 40 nebulized acetylcholine. > 94,000 ug/m (50 ppm). 1972
84,600 45
94,000 50
NO. 75,000 40 Sensitized to egg and Guinea pig Mortality: 20% Matsumura, 1970b
150,000 80 bovine serum albumin by 37%
intraperitoneal injection;
3 days later exposure for
30 min to pollutants then
antigen 30 min later.
-------
(jg/m (2 ppm) also had increases in IgM and IgG2 (p < 0.05). A different response was seen
after the mice received the virus. Serum IgA increased (p < 0.05) only when mice were held in
filtered air, vaccinated and exposed to 940 or 3,760 pg/m (0.5 or 2 ppm) NO-. Immunoglobulin
M (IgM) concentrations were elevated in all N09-exposed groups. A significant increase (p <
•>
0.05) took place in only the following groups: (a) continuous exposure to 940 or 3,760 ug/m
3 3
(0.5 or 2 ppm), (b) continuous exposure to 940 or 3,760 ug/m (0.5 or 2 ppm) or to 3,760 ug/m
(2 ppm), pre-vaccination and clean air afterwards, and.(c) 3 months filtered air and 3,760
ug/m (2 ppm) N0? post-vaccination. Similar results were observed for IgG? and IgG-, determi-
nations.
The immune system of monkeys exposed to N02 was studied in an additional series of experi-
ments (Ehrlich and Renters, 1973; Renters et al., 1971; Fenters et al., 1973). Renters et al.
(1971) injected mouse-adapted influenza A/PR/8/34 intratracheally 24 hours prior to continuous
3
exposure to 9,400 ug/m (5 ppm) N02. Hemagglutination inhibition titers to influenza titers
were not changed. Initially serum neutralization titers were depressed by N0~. By 133 days,
the effect had disappeared. The amnestic response was not affected.
Fenters et al. (1973) described the effects of continuous exposures of 1,880 ug/m
(1 ppm) N02 for 493 days on monkeys challenged five times via intratracheal injection to live
monkey-adapted influenza virus A/PR/8/34 during N02 exposure. Again, hemagglutination inhibi-
tion titers were not significantly affected by N0~ exposures. However, the mean serum neutra-
lizing antibody titers were significantly higher in animals exposed to N02 for 493 days.
Twenty-one days post-vaccination, animal titers were increased 7-fold over controls. Forty-
one days post-challenge, N02~treated animals exhibited an 11-fold enhancement. Even after 266
days of N0? exposure, titers were higher when compared to controls. Again, the authors
hypothesized that NO,, enhanced the ability of the monkey-adapted virus to become established
and multiply.
Antweiler et al. (1975) did not find any alteration in guinea pig specific antibody
titers when compared to controls, even after 33 days of exposure to 10,000 ug/m (5.3 ppm) NO,,.
On the basis of experiments in which the continuous exposure of guinea pigs to 1,880
ug/m (1 ppm) NQ? for 6 months resulted in an increased incidence of infection, particularly
within the lung, Kosmider and colleagues postulated an adverse effect of NO,, on immune func-
tion (Kosmider et al. , 1973b). These investigators also claimed that NOp causes decreases in
complement concentrations when measured by a hemolysis assay; reductions in all immunoglobulin
fractions when tested by immunoelectrophoresis; and increased mortality in mice exposed to
1,880 ug/m (1 ppm) of N02 when infected intranasally with D. pneumoniae. Because of the
importance of these observations, they require confirmation.
Balchum et al. (1965) exposed guinea pigs to 9,400 ug/m (5 ppm) N02 for 4 hours/day, 5
days/week and to 9,400 ug/m3 (5 ppm) N02 or to 28,200 ug/m3 (15 ppm) N0? for 7-1/2 hours/day,
5 days/week. There was a noticeable increase in the titer of serum antibodies against Tung
3 3
tissue in all guinea pigs exposed to 9,400 ug/m (5 ppm) or 28,200 pg/m (15 ppm) N02 as early
as 160 hours after N0? inhalation. The antibody titers increased with the intensity and dura-
tion of exposure to NO,,.
14-27
-------
14.2.3.2 Lung biochemistry
14.2.3.2.1 Introduction. Nitrogen dioxide-related studies of lung biochemistry have been
directed to either an investigation of the mechanism of toxic action of NO^ or to the
detection of indicators of early damage by NCL exposure. Two theories of action of NCL on
biological systems have evolved as a result of these studies. The dominant theory is that N02
initiates lipid peroxidation, which subsequently causes cell injury or death and the symptoms
associated with NO^ inhalation. The second theory is that N0~ oxidizes low molecular weight
reducing substances and proteins. This oxidation results in a metabolic dysfunction which
evidences itself as the toxic symptom. Nitrogen dioxide may, in fact, act by both means and,
as a consequence, may affect the intermediary metabolism of animals and thus, their growth and
maturation. Several potential biochemical mechanisms related to detoxification of N02 or to
responses to NCL intoxication have been proposed. The effects of NCL exposure on lung bio-
chemistry will be discussed in this context. (See Table 14-8.)
14.2.3.2.2 Lipid and diet effects. The dietary background of animals affects their response
to all types of toxicants. For the most part, diet effects concerning NCL have been neglected
and are unreported in the literature. A significant body of evidence has evolved, however, to
support the idea that lipids and vitamin E are the most important dietary components in
determining the response of animals to NCL exposure. Roehm et al. (1971) studied the j_n vitro
oxidation of unsaturated fatty acids by CL and NCL. A common mechanism of action was sug-
gested for these two oxidizing air pollutants. Both NO, and CL initiated the oxidation of
£ O
unsaturated fatty acids through free radicals. Typically, an induction period was noted with
either anhydrous thin films or aqueous emulsions of linolenic acid exposed to 2,800 ug/m (1.5
ppm) NCL. The addition of free radical scavenging agents such as vitamin E, butylated hydroxy-
toluene (BHT), or butylated hydroxyanisol (BHA) delayed the onset of oxidation i_n vitro. The
rate of oxidation of linolenic acid in thin films was proportional to concentrations of NCL
3
ranging from 940 to 10,200 pg/m (0.5 to 5.4 ppm). Thin-layer chromatography of the oxidation
products of linolenic acid showed a conversion to polar nitrogen-containing compounds and to
peroxides. A proposed mechanism of formation of these products follows (Menzel, 1976):
00-
C=C + N00 -» -C-C-NO,
00• OOH
-C -C-NO, + RH •* -C -C-NO,
i i 2 i i i
R- + 02 .-> ROO- -» ROOH
Nitrohydroperoxides and fatty acid hydroperoxides are produced from the oxidation of
unsaturated fatty acids by N0?. Phenolic antioxidants prevent the autoxidation of unsaturated
14-28
-------
TABLE 14-8. EFFECTS OF
N02 ON LUNG BIOCHEMISTRY
ro
10
N02
Concentration
|jg/m3
94
940
94
or 940+
equal
amount
ammonia
376
3,760
35,720
ppm
0.05
0.5
0.05 or
0.5+
equal
amount
ammonia
0.2
2
19
Exposure
8 hr/day,
122 days
3 hr
Species
Guinea
Pig
Rat
Effect
No effect on total weight of phosphol ipid.
Significant alterations (p <0.05) in
individual phospholipid classes.
3
At 376 ug/m (0.2 ppm) inhibition of
conversion of prostaglandin E« (PGEO
to its metabolite (15-keto PGE0) 18
Reference
Trzeciak et al . ,
1977
Menzel ,
1980
750
1,880
5,640
9,400
9,400
hr post exposure. No effect on uptake
or efflux of PGE?.
At 3,760 and 35,720 ug/m3 (2 and 19 ppm),
no effect on uptake of PGE?. Efflux
altered 18 hr post-exposure. Conversion
of PGE2 to 15-keto PGE2
60 hr post-exposure.
inhibited 18 and
0.4
1.0
3.0 or
5.0
5.0
72 hr
Guinea Pig
3 hr
Guinea Pig
No effect at 750 ug/m . Increase in lung
lavage protein and lipid content in
vitamin C depleted but not normal
at 1,880 ug/m . (See Edema Section
4.2.3.6)
Increased lung lavage protein and lipid
content in vitamin C depleted guinea pigs
after 18 hr post exposure. (See Edema
Section 4.2.3.6)
Selgrade et al.,
1981
Selgrade et al.,
1981
-------
TABLE 14-8. (continued)
CO
O
N02
Concentration
pg/m3 ppm
750 0.4
750 0.4
750 0.4
Exposure
72 hr or
1 wk
Continuous,
1 wk
4 hr/day,
7 days
Species
Guinea Pig
Guinea
pig
Guinea
pig
Effect
No mortality or effect on lung lavage
fluid composition. (See Edema Section
4.2.3.6)
Increase in lung protein content of guinea
pigs with an unquantified vitamin C defi-
ciency, most likely due to plasma leakage
(see edema section 4.2.3.6). Some may
result from cell death.
Increase in acid phosphatase (EC 3.1.3.2).
Reference
Sel grade et al . ,
1981
Sherwin and
Carlson,
1973
Sherwin et al . ,
1974
750 to 0.4 to Continuous
940 0.5 1.5 yr
1,790 to 0.95 to
1,880 I
940 0.5
8 hr/day,
7 days
8 hr/day,
4 mo
Mouse Growth reduced; vitamin E (30 or 300 mg/kg
diet) improved growth.
Guinea Increase in serum LDH, CPK, SCOT, SGPT,
pig plasma cholinesterase, lung and plasma
lysozyme. Decrease in RBC GSH peroxidase.
Lung GSH peroxidase and acid phosphatase
unchanged.
Decrease in plasma cholinesterase,
plasma and lung lysozyme, and RBC
GSH peroxidase. Lung GSH peroxidase
unchanged. Increase in lung acid
phosphatase.
Csallany,
1975
Menzel et al.,
1977
-------
TABLE 14-8. (continued)
-P.
i
OJ
N02
Concentration
|jg/m3
940
1,880
ppm Exposure
0.5 Continuous,
1 17 mo
Species
Mouse
Effect
Decreased body weight with vitamin E
deficient, vitamin E supplemented (30 and
Reference
Csallany and
Ayaz, 1978a
940
1,880
940
1,880
3,760
0.5
0.5
1
Continuous,
17 mo
Continuous,
17 mo
Mouse
Mouse
1,880
1,880
4,330
11,560
1
1
2.3
6.2
Continuous,
2 wk
Continuous,
4 days
Rabbit
Rat
Continuous Guinea
1 to 3 wk pig
300 ppm) and DPPD supplemented (30 ppm).
No change in tissue weight with exception
of increased kidney weight in 1 ppm exposed
animals with vitamin E deficient diet.
Slightly decreased survival rate.
No change in blood and lung GSH-peroxidase
activity.
Suppression of GSH-peroxidase activity.
No increase in lipofuscin or glutathione
peroxidase. Vitamin E (30 or 300 mg/kg)
prevented lipofuscin accumulation
(EC 1.11.19).
Decrease in lecithin synthesis after 1 wk;
Less marked depression after 2 wk.
Activities of GSH reductase (EC 1.6.4.2)
and glucose-6-phosphate dehydrogenase
(EC 1.1.1.49) increased at 11,560
ug/m (6.2 ppm) level proportional to
duration of exposure. Plasma lysozyme
(EC 3.2.1.16) and GSH peroxidase
(EC 1.11.1.9) not affected. No effects
at 1,880 or 4,330 ug/nr (1 or 2.3 ppm).
Increase in number of lactic acid dehydroge-
nase (EC 1.1.2.3) positive cells with time
exposure. Suggest Type I (LDH negative)
cells decrease as Type II (LDH positive)
cells increase.
Ayaz and
Csallany, 1978
Ayaz and
Csallany,
1977
Seto et al.,
1975
Chow et al.,
1974
Sherwin et al.,
1972
-------
TABLE 14-8. (continued)
N02
Concentration
(jg/m3
ppm
Exposure
Species
Effect
Reference
CO
ro
5,450 2.9 Continuous,
5 days/wk,
9 mo
Rat
5,640 3
18,800 10
18,800 10
28,200 15
Continuous, Rat
17 days
Continuous
4 wk
5,640
5,600
13,200
3
3
7
4 hr/day,
4 days
7 days
4 days
Squirrel
monkey
Rat
4 days
4 days
Increase in lung wet weight (12.7%) and
decrease in total lipid (8.7%). Decrease
in saturated fatty acid content of lung
lavage fluid and tissue. Increase in
surface tension of lung lavage fluid.
Decrease in linoleic and linolenic acid
of lavage fluid.
Decrease in unsaturated fatty acids in
lavage and lung tissue. Vitamin E (as
d,1-a-tocopheryl acetate 100 mg/kg diet)
reduced NO- effect.
Thickening of collagen fibrils.
No effects on parameters tested.
Increase in lung weight, G-6-PD,
glutathione reductase, glutathione
peroxidase.
Increase in lung weight, G-6-PD,
6-P-gluconate dehydrogenase,
glutathione reductase.
Increase in lung weight, DMA
content, G-6-PD, 6-P-gluconate dehydro-
genase, glutathione reductase, disulfide
reductase, glutathione peroxidase,
succinate oxidase, cytochrome oxidase;
no effect on lung protein.
Arner and
Rhoades, 1973
Menzel et al.,
1972
Bils, 1976
Mustafa et al.,
1979a, b
-------
TABLE 14-8. (continued)
to
OJ
N02
Concentration
(jg/nr*
9,400
9,400
9,400
ppm
5
5
5
Exposure
14 to 72 hr
12 hr
0.33, 1, 2
Species
Mouse
Rat
Rat
Effect
Increase in lung protein (14 to 58 hr) by
radio-label .
Incorporation of 14Oproline into
insoluble collagen increased (58%).
Increase in glucose utilization and lactate
Reference
Csallany, 1975
Hackner et al . ,
1976
Ospital et al . ,
9,400 5
37,600 20
94,000 50
11,000 6
15.000
18,800 10
and 4 days
3 hr
4 hr/day,
30 days
Continuous
14 days
production. Lesser increase in pyruvate 1976
production.
Rabbit
Mouse
Mouse
Benzo(a)pyrene hydroxylase (EC 1.14.12.3)
activity or tracheal mucosa not affected.
Increase in GSH reductase (EC 1.6.4.2) and
glucose-6-phosphate dehydrogenase
(EC 1.1.1.49) activities.
Increase in lung protein.
Palmer et al'. ,
1972
Csallany,
1975
Csallany,
1975
5 hr Hamster
once a week (Vitamin
4 to 8 wk A defi-
cient)
Lipid droplets in alveolar walls. Alveolar Kim, 1977; 1978
necrosis and thickening of epithelial base-
ment membrane with calcium deposits on inner
and outer surfaces. Presence of virus par-
ticles within epithelial plasma membrane.
Reduced DNA uptake. Decrease in basal cell
growth. No reversion of Type II from Type I
cell. No LDH isoenzyme III in terminal airway.
Following 8 weeks of exposure, hypertrophy and
hyperplasia of bronchiolar-epithelial cells,
diffuse loss of cilia, membrane damage, and
mitochondrial damage.
-------
TABLE 14-8. (continued)
N02
Concentration
ug/m3
ppm
Exposure Species
Effect
Reference
28,000 15
53,000 28
7 days
Mouse
56,400 30 Continuous Hamster
to 30 days
56,400 30 Continuous Hamster
to 50 days
56,400 30 22 hr/day, Hamster
3 wk
62,040
75,200
33
40
Continuous
to 23 days
5 hr
Rat
Rat
Increase in GSH levels, GSH reductase,
glucose-6-phosphate dehydrogenase, and GSH
peroxidase.
Increase in lung proteolytic activity and
in serum antiprotease at 2 days.
Declined to normal values at 50 days.
Csallany, 1975
Kleinerman and
Rynbrandt,
1976
Increase in lung proteolytic activity at Rynbrandt and
2 and 5 days, but the optimum pH was acidic Kleinerman,
(3.0). Not active at physiological pH of 1977
7.2. Attributed to cathepsins,
C, D, and E.
A, B,, B,
Loss of body weight; increase dry lung
weight; decrease in total lung collagen
within 4 days and total lung elastin with-
in 10 days. Collagen levels return to
normal by day 14 of exposure. 3 wk fol-
lowing exposure, lung elastin levels had
returned to normal.
High level of dietary antioxidants in-
creased the time until 50% mortality
occurred (LT50). LT50 of vitamin E
depleted rats was 11.1 days versus 170
days for vitamin E supplemented rats.
14
Increased incorporation of C-palmitic
acid in lung lecithin. Accumulation of
disaturated lecithin by 6 hr post-NO?
with maximum accumulation by 48 hr.
Kleinerman and Ip,
1979
Menzel et al., 1972
Blank et al.
1978
-------
TABLE 14-8. (continued)
N02
Concentration
5~ ppm
Exposure
Species
Effect
Reference
75,200
132,000
40
70
2 hr
Rat
Benzo(a)pyrene hydroxylase (EC 1.14.12.3),
phenol-0-methyl transferase (EC 2.1.1.25)
and catechol-0-methyl transferase
(EC 2.1.1.6) not affected.
Law et al.
1975
co
ui
-------
fatty acids by N02 by reacting with both fatty acid hydroperoxyl free radicals and
nitrohydroperoxyl free radicals generated by addition of N02 to unsaturated fatty acids:
00- OOH
-C -C-NO, + AOH -» -C -C-NO, + AO-
i i £ i i £
ROD- + AOH -»• ROOH + AO-
where AOH represents a phenolic antioxidant.
Rats evidenced increased mortality (Fletcher and Tappel, 1973; Menzel et al. , 1972) and
decreased content of unsaturated fatty acids in lung lavage fluid (Menzel et al., 1972; Thomas
et al., 1968) when exposed to N02 concentrations ranging from 18,800 to 62,000 ug/m (10 to 33
ppm). The effect was greater in animals fed diets depleted in vitamin E.
The effect of N09 exposure on the metabolism of vasoactive compounds by the rat lung was
, T
studied by Menzel (1980). Rats were exposed for 3 hours to 376 ug/m (0.2 ppm), 3,760 ug/m
3 3
(2 ppm), and 35,720 ug/m (19 ppm) NO, and their lungs were excised and perfused with H-Pro-
3
sta glandin E9 ( H-PGE9), a natural product of the lung that acts on smooth muscles, up to 6
3
days at various times. N09 exposure did not affect the unidirectional uptake of H-PGE,, at 0
3
or 18 hr post-exposure, while efflux of H-PGE, and its metabolites from the lung were altered
3
18 hours post exposure to 3,760 and 35,720 ug/m (2 and 19 ppm) N02- Eighteen hours following
376, 3,760, and 35,720 ug/m3 (0.2, 2, and 19 ppm) N02, the conversion of the perfused PGE2 to
its 15-keto metabolite was inhibited by 37, 41, and 62 percent, respectively. Recovery was
3
not complete until 60 hr following 376 ug/m (0.2 ppm) NO, exposure, and 90 hr following 3,760
3 3
ug/m (2 ppm) exposure. Recovery had not occurred in animals exposed to 35,720 ug/m (19 ppm)
HOy for a period of 160 hours post exposure. No edema was observed following exposure to any
of the three levels of pollutant.
Arner and Rhoades (1973) exposed rats to 5,450 ug/m (2.9 ppm) N02 for 24 hours/day, 5
days/week, for 9 months. The lung wet weight increased by 12.7 percent compared to that of
their control counterparts. The increase (p < 0.05) in lung wet weight was the same as the
increase in lung water content. The lipid content of the lung was depressed (p < 0.05) by 8.7
percent. An analysis of the lungs showed that a decrease occurred in the total saturated
fatty acid content. Unfortunately, values for unsaturated fatty acids of biological impor-
tance, such as the essential fatty acid arachidonic acid, were not reported. The surface
tension of extracts of the lung increased, and the authors suggest that the increased surface
tension corresponded to a decrease in the lung surfactant concentration.
3 3
Trzeciak et al. (1977) exposed guinea pigs to 940 ug/m (0.5 ppm), 94 ug/m (0.05 ppm),
or these same N02 concentrations plus an equal amount of ammonia, for 8 hours/day for a total
of 122 days. Lung phospholipids were analyzed, and no difference was found in the total
weight of phospholipid of exposed versus control lungs. Significant alterations (p < 0.05)
were found in the individual phospholipid classes. Decreases were noted in phosphatidyl
ethanolamine, sphingomyelin, phosphatidyl serine, phosphatidyl glycerol-3-phosphate, and
14-36
-------
phosphatidic acid. Increases were noted in the lysophosphatidyl ethanolamine content, while
the phosphatidyl choline (lecithin) content remained constant or was slightly depressed. Such
changes could be indicative of change in cell type or cell function.
3
Lecithin synthesis appeared to be depressed in the lungs of rabbits exposed to 1,880 |jm
(1 ppm) NO 2 for 2 weeks (Seto et al., 1975). The most marked effect was observed after 1 week
of exposure and appeared to decline after the second week of exposure.
•3
Csallany (1975) exposed mice continuously for 1.5 years to 750 to 940 ug/m (0.4 to 0.5
ppm) or 1,790 to 1,880 ug/m (0.95 to 1 ppm) NO- and fed the animals a basal diet which was
either deficient in or supplemented with vitamin E at 30 or 300 mg/kg of diet. The author
indicated that N0? reduced the growth rate in all four diet groups, but the vitamin E-supple-
mented groups were improved over the non-supplemented groups. High levels of vitamin E in the
diet failed to provide greater improvement in growth rate over that of normal amounts of vita-
min E in the diet. In other studies from this group, (Ayaz and Csallany, 1977; Ayaz and
Csallany, 1978; Csallany and Ayaz, 1978a) female weanling mice were exposed to 940 or 1,880
ug/m (0.5 or 1 ppm) NOp continuously for 17 months. Animals were divided into three groups
receiving the basal diet with either a normal supplement of vitamin E (30 mg/kg) or 300 mg/kg
and a third group supplemented with the synthetic antioxidant N,N'-diphenylphenylenediamine
(DPPD) at 30 mg/kg. After 17 months of exposure, the presence of lipofuscin pigment in the
liver, lungs, spleen, heart, brain, kidney, and uterus was determined. While no effect could
be ascribed to NOp exposure, vitamin E supplementation decreased the concentration of lipo-
fuscin pigment in the liver, but not in other tissues. Lipofuscin pigment is proposed to be
an end product of lipid oxidation accumulated in tissues.
Exposure of vitamin A deficient hamsters to 18,800 ug/m (10 ppm) NOp, 5 hours once a
week for 4 to 8 weeks caused lung damage as compared to NO^-exposed, non-vitamin A deficient
hamsters (Table 14-8) (Kim, 1977; 1978).
A recent series of experiments have investigated the effect of vitamin C deficiency on
NOp toxicity (Selgrade et al., 1981). Normal or vitamin C depleted guinea pigs were exposed
to 752, 1880, 5460, or 9400 ug (0.4, 1.0, 3.0, or 5.0 ppm) N02/m3 for 72 hrs and the lung
lavage protein and lipid content determined. No effect was observed in guinea pigs having
normal vitamin C blood contents, but depleted guinea pigs, having an average of 25% of the
normal blood vitamin C content, had 2-5 times the control lavage fluid and lipid content with
3
the exception of those guinea pigs exposed to 752 ug (0.4 ppm) N09/m . Exposure of normal or
3
vitamin C depleted guinea pigs exposed to 752 ug/m (0.4 ppm) for as long as 1 week had no
effect on the composition of the lavage fluid. At 9400 ug (5 ppm) N02/m for 72 hrs these
changes in lavage fluid composition were correlated with mortality (50%) and alveolar edema as
observed by conventional light microscopic histopathology in vitamin C depleted guinea pigs.
When vitamin C depleted guinea pigs were exposed to 9400 ug (5 ppm) N02/m for 3 hrs, increas-
ed protein and lipid contents were not observed until 15 hrs after exposure. These results
conflict with those of Sherwin and Carlson who found increased protein content of lavage fluid
14-37
-------
from guinea pigs exposed to 752 ug/m (0.4 ppm) for 1 week. Differences may be due to the
reproducibility of exposure, methods of monitoring NCL during exposure, protein measurement in
the lavage fluid and differences in the degree of vitamin C deficiency.
14.2.3.2.3 Sulfhydryl compounds and pyridine nucleotides. Oxidation of sulfhydryl compounds
and pyridine nucleotides in the lung is well-established for 0, exposures, (Evans et al.,
1974) but little evidence has been reported for N09.
3
In experiments involving exposure of mice to very high (>143,000 ug/m , 76 ppm) concen-
trations of NOp, several investigators reported that a wide variety of sulfur-containing
compounds reduced the toxicity of NO,, (Fairchild et al., 1959; Fairchild and Graham, 1963).
For example when mice were first exposed to benzenethiol (14 ppm) for 24 to 72 hours prior to
4 hours of NOp exposure only 1/20 died, whereas 10/20 of the NO^-exposed mice not pretreated
with benzenethiol died. Inferences drawn from the protective effect of these compounds sug-
gest that sulfhydryl compounds within the lung were being oxidized to disulfides (Fairchild
et al., 1959). Included among the compounds observed to exert a protective effect are: (1)
hydrogen sulfide (2) benzenethiol, (3) d.crnapthylurea, (4) phenylthiourea, and (5) a number
of thyroid-blocking agents.
2
Ospital et al. (1976) reported that exposure to 9,400 pg/m (5 ppm) NOp for 8 hours
altered the glucose metabolism of slices made from the lungs of exposed rats. Glucose utili-
zation and lactate production were increased by 28 and 43 percent, respectively, while
o
pyruvate production rose by 6 percent. Exposure of rats to 9,400 (jg/m (5 ppm) NOp for 1, 2,
and 4 days produced similar alterations, but individual values were not reported. Neither in-
creased hexose monophosphate shunt nor citric acid (Krebs) cycle activity could account for
the increased glucose utilization. The authors concluded that NOp exposure increased the
activity of the glycolytic pathway and suggested that this increase may be related to an
increased biosynthesis due to injury.
14.2.3.2.4 Effects on lung amino acids, proteins, and enzymes. Concentrations of NO, >9,400
3
ug/m (5 ppm) produce lung edema with concommitant infiltration of serum protein and enzymes.
Alterations in the cell types of the lung also occur (see Section 14.2.3.3). Thus, some
reports of changes in lung enzymes and proteins may reflect either edema or altered cell popu-
lations rather than direct effects of N09 on lung enzymes.
3
Sherwin et al. (1972) exposed guinea pigs to 3,760 ^ig/m (2 ppm) NOp for 1, 2, or 3
weeks. They examined lung sections histochemically for lactic acid dehydrogenase (LDH). With
this technique, LDH is primarily an indicator of Type II pneumocytes rather than Type I. The
number of Type II pneumocytes per alveolus was determined. In control lung sections, a mean
of 1.9 Type II cells per alveolus was found with a range of 1.5 to 3.4 Type II cells per
alveolus in upper lobes of the lung. A range of 1.6 to 3.1 Type II pneumocytes per alveolus
was found in the lower lobes. Exposure to N0? increased the LDH content of the lower lobes of
the lung by increasing the number of Type II cells per alveolus (p < 0.05). The increase was
progressive over the 1-, 2-, and 3-week exposure period. The authors then contended that the
14-38
-------
increase in lung LDH content was due to the replacement of Type I pneumocytes by Type II
pneumocytes as shown in morphological studies (see Section 14.2.3.3).
Several other biochemical indicators of lung damage have been studied. Sherwin et al.
(1974) exposed guinea pigs with an unquantified vitamin C deficiency to 750 ug/m (0.4 ppm)
N0~ for 4 hours/day for 7 days and found an increase in acid phosphatase activity (p < 0.05).
An increased aldolase activity was reported by Kosmider et al. (1975) in the blood, liver, and
brain of NO^-exposed guinea pigs, but was statistically significant only in liver samples.
Values for the lung and exposure levels were not reported.
The effect of N02 on the important enzyme benzpyrene hydroxylase was studied by Palmer et
al. (1972). Since lung cancer in man is predominantly of bronchial rather than parenchymal
origin, benzpyrene hydroxylase activity of the tracheobronchial region of the lung was studied
in rabbits which had been exposed to 9,400, 37,600, or 94,000 ug/m3 (5, 20, or 50 ppm) N02 for
3 hours. No effect was observed on the benzpyrene hydroxylase activities in NO, exposure, but
3
On exposure of 1,400 to 19,600 ug/m (0.75 to 10 ppm) markedly decreased benzpyrene hydroxy-
lase activity in a dose-related manner. Law et al. (1975) studied the effect of NO- on
benzpyrene hydroxylase, microsomal 0-methyl transferase, catechol 0-methyl transferase, and
supernatant catechol 0-methyl transferase activities of the lungs of rats. While benzpyrene
hydroxylase activity ,of the lung could be induced by treatment with the carcinogen, 3-methyl-
cholanthrene, exposure to 75,200 or 132,000 ug/m (40 or 70 ppm) NO^ for 2 hours had no
effect. Thus, the studies of Palmer et al. and Law et al. agree that N0~ has no effect on
benzpyrene hydroxylase activity of the lung. The 0-methyl transferase activity studied by Law
et al. relates to the ability of the lung to metabolize the important catecholamine hormones.
This metabolism does not appear to be affected by N09 treatment.
3
Menzel et al. (1977) exposed guinea pigs 8 hr/day to 940 ug/m (0.5 ppm) NO- for 4
months. After an initial exposure of 7 days, serum LDH, total creatine phosphokinase (CPK),
glutamic-oxalacetic transaminase (SCOT), and glutamic-pyruvic transaminase (SGPT) were
elevated. Lung GSH peroxidase and acid phosphatase were not affected. In contrast to the
findings of Chow et al., (1974) lung lysozyme levels were elevated as were plasma levels. The
release of isomeric forms of CPK was characteristic of generalized damage to the lung. The
elevation in total CPK was statistically significant (p < 0.05) while the elevations in LDH,
SCOT, and SGPT were not significant because of the large variance in the exposed groups.
A major concern has been the effect of NO- exposure on the structural proteins of the
lung, since elastic recoil is lost following exposure. Bils (1976) reported a thickening of
the collagen fibrils in squirrel monkeys exposed to 5,640 ug/m (3 ppm) N02 for 4 hours/day
for 4 days. Kosmider et al. (1973a) reported that the urinary hydroxyprol ine and acid muco-
polysaccharide contents of guinea pigs exposed to 1,880 ug/m (1 ppm) NO- for 6 months were
increased (p < 0.05). Presumably these increases represented degradation of collagen. Hacker
et al. (1976) measured the incorporation of C-proline into soluble and insoluble collagen
fractions in the lungs of rats exposed to 9,400 ug/m (5 ppm) N0? for 12 hours. Incorporation
14-39
-------
14
of C-proline into insoluble collagen was 58 percent greater in the NCL-exposed animals than
in air-exposed control groups, supporting the biochemical evidence for greater collagen turn-
over in NCL-exposed animals.
Enzymes observed to have increased activity following exposure to high concentrations of
N0~ included aldolase (i_n vitro) (Ramazzotto and Rappaport, 1971) and serum antiprotease (J_n
vivo) (Kleinerman and Rynbrandt, 1976). Plasma lysozyme activity was reported to be unaffect-
ed (KI vivo) (Chow et al. , 1974).
14.2.3.2.5 Potential defense mechanisms. Menzel (1970; 1976) proposed that antioxidants
might protect the lung from damage by N0~ by inhibiting lipid peroxidation. Data related to
this hypothesis have been reported. (Ayaz and Csallany, 1977; Ayaz and Csallany, 1978;
Csallany, 1975; Fletcher and Tappel, 1973; Menzel et al., 1972; Thomas et al., 1968) Chow and
Tappel (1972) proposed an enzymatic mechanism for the protection of the lung against lipid
peroxidation damage by ozone. They proposed the following scheme:
p-oxidation
t
ROM k 4 GSH . NADP Glucose-6-P04
GSH Reductase G-6-P Dehydrogenase
RH ^ ROOH ' v GSSG >-' X NADPH ' \ 6-Phosphogluconate
where R is an aliphatic organic radical
Chow et al. (1974) exposed rats to 1,880, 4,330, or 11,560 ug/m3 (1, 2.3, or 6.2 ppm) N02
continuously for 4 days to determine the effect on the glutathione peroxidase system. They
determined the activity of GSH reductase, glucose-6-phosphate dehydrogenase, and GSH peroxi-
dase in the soluble fraction of exposed rat lungs. Linear regression analysis of the correla-
tion between the N0? concentration and enzymatic activity was found to have a significant
positive correlation coefficient of 0.63 (p < 0.001) for GSH reductase and 0.84 (p < 0.003)
for glucose-6-phosphate dehydrogenase. No correlation was found between the GSH peroxidase
activity and the NO, exposure concentration. The activities of GSH reductase and glucose-6-
3
phosphate dehydrogenase were significantly increased during exposure to 11,560 ug/m (6.2 ppm)
N02.
Ayaz and Csallany (1978) exposed female mice continuously for 17 months to 940 and 1,880
ug/m (0.5 and 1 ppm) N0? and fed the animals a basal diet which was either deficient in vita-
min E or supplemented with 30 or 300 mg/kg of diet. Blood, lung, and liver tissues were
assayed for glutathione peroxidase activity. Exposure to 940 ug/m (0.5 ppm) N09 did not
3
alter blood or lung GSH peroxidase; however, 1,880 ug/m (1 ppm) NO- exposure suppressed
enzyme activity. A combination of vitamin E deficiency and 1,880 ug/m (1 ppm) N02 exposure
resulted in the lowest GSH peroxidase in blood and lung. Liver GSH-peroxidase was unaffected
by either vitamin deficiency or NOp exposure.
14-40
-------
Donovan et al. (1976) and Menzel et al. (1977) exposed guinea pigs continuously to 940
|jg/m (0.5 ppm) NO^ for 4 months. After an initial short-term exposure of 7 days or at the
completion of a long-term exposure at 4 months, animals were killed, and the lung and red
blood cell (RBC) GSH peroxidase levels were determined. Short-term exposure to NOp depressed
RBC GSH peroxidase but did not affect lung levels. Long-term exposure, on the other hand,
affected neither lung nor RBC GSH peroxidase. These studies confirm the results in rats and
indicate a distinct difference in the effect of N0? and 03 on the lung.
Since protection against NO,, occurs with vitamin E, lipid peroxidation most likely
occurs, but the GSH peroxidase defense system does not appear to be induced. Chow et al.
(1974) concluded: "Since exposure of rats to NO- has insignificant effect on lung GSH
peroxidase activity, but had significantly increased the activities of GSH reductase and G-6-P
dehydrogenase, it appears that this oxidant attacks mainly glutathione and NADPH while 03 not
only initiates lipid peroxidation but also directly attacks these reducing substances."
Selgrade et al. (1981) expanded the studies of Sherwin and Carlson (1972) on the effects
of vitamin C deficiency on NO^ toxicity. These studies were aimed at measuring the infiltra-
tion of plasma proteins into the airways as an index of NOp-induced damage. The degree of
vitamin C deficiency produced by Selgrade et al. was mild, being on the average a sufficient
reduction in vitamin C intake to produce a 25% decrease of the vitamin C blood levels. At
0
high levels of NO- exposure, 9400 ug (5.0 ppm) NO-Xm for 72 hrs, 50% of the vitamin C
depleted guinea pigs died, while none of the normally supplemented animals was affected. When
exposed to greater than 752 ug/m (0.4 ppm), lavage fluid protein and lipid content was
increased. Unlike the studies of Sherwin and Carlson (1973), Selgrade et al. found no effect
0
at 752 ug/m (0.4 ppm) for up to 1 week. The vitamin C status of the guinea pigs in the
Sherwin and Carlson study is not documented in sufficient detail to judge if this is the
reason for the discrepancy in the two studies, but taken together these investigations support
a role for dietary vitamin C as well as vitamin E in influencing the susceptibility of animals
to NO-. Since vitamin C is readily oxidized and reduced, it could serve to detoxify oxidative
products formed by NOp or to maintain the intracellular redox potential.
14.2.3.3 Morphology Studies—Nitrogen dioxide produces morphological alterations starting in
the terminal airways and adjacent alveoli. (See Table 14-9.) A comprehensive summary review
has been prepared by Coffin and Stokinger (1977).
The events leading to emphysema from NO,, exposure of the rat have been described by
Freeman and co-workers. (Cabral-Anderson et al., 1977;- Evans et al., 1972; 1973a; 1973b;
1974; 1975; 1976; 1977; Freeman et al. , 1966; 1968c; 1972; Stephens et al., 1971; 1972) The
q
earliest alterations resulting from exposures to concentrations above 22,600 ug/m (12 ppm)
were seen within 24 hours of continuous exposure. These alterations included increased macro-
phage aggregation, desquamation of the Type I pneumocytes and ciliated bronchiolar cells,
and accumulation of fibrin in the small airways. The cuboidal Type II pneumocytes slowly
differentiate into the squamous Type I cells as replacements and alter the appearance of the
14-41
-------
TABLE 14-9. EFFECT OF NC>2 ON LUNG MORPHOLOGY
-t»
ro
N02
Concentration
|jg/m3
188 +
daily 2-hr
spike of
1,880
470
553
940
940
940
1,880
940
to
1,500
1,030 to
3,000
ppm Exposure Species
0.1 + Continuous, Various
daily 6 mo species
spike
of 1
0.25 4 hr/day, Rabbit
5 days/wk,
24 or 36
days
0.34 6 hrs/day, Mice
5 days/wk
6 wk
0.5 Continuous, Mouse
12 mo
0.5 6, 18, or Mouse
24 hr/day,
to 12 mo
0.5 4 hr Rat
1 1 hr
0.5 Continuous, Mouse
to 1 mo
0.8
0.55 Continuous, Mouse
to 1.6 5 wk
Effect
Emphysematous alterations.
Isolated swollen collagen fibers.
Hyperplasia and hypertrophy of alveolar
type II cells. Decrease in body weight,
spleen weight, and area of splenic lymphoid
nodules.
At 10 days:
Clara cell damage
Loss and shortening of cilia
Alveolar edema in interstitial space
and epithelium
At 35 to 40 days:
Bronchial hyperplasia
At 6 mo:
Fibrosi s
At 12 mo:
Bronchial hyperplasia
Alveolar damage. Interstitial pneumonia
may have confused interpretation.
Degranulation of mast cells. Response
seemed reversible.
Damage to tracheal mucosa and cilia.
Damaged cilia, increase in mucus secretion
by nonciliated cells.
Reference
Port et al. ,
1977
Buell, 1970
Sherwin et al . ,
Kuraitis et al .
Hattori , 1973
Hattori and
Takemura, 1974
Blair et al . ,
1969
Thomas et al . ,
Nakajima et al.
1972
Nakajima et al.
1969
Miyoshi , 1973
1979
, 1979
1967
>
1
-------
TABLE 14-9. (continued)
-Pi
OJ
N02
Concentration
ug/m3
1,500
1,880
1,880 to
2,820
3,760
32,000
3,760
3,760
3,800
3,760
32,000
ppm Exposure
0.8 Continuous,
to 33 mo
1 Continuous,
493 days
1 to Continuous,
1.5 1 mo
2 Continuous,
43 days
17
2 Continuous,
3 wk
2 Continuous,
3 wk
2 , Continuous ,
14 mo
2 Continuous,
to 360 days
17 Continuous,
7 days
Species
Rat
Monkey
Mouse
Rat
Guinea
pig
Guinea
pig
Monkey
(Macaca
speciosa)
Rat
Effect
Normal growth. Decreased respiratory rate
(-20%). Tachypnea exaggerated with exposure.
Normal gross and microscopic appearance.
Suggestive evidence of changes in terminal
bronchioles.
Virus-challenged animals had slight emphysema,
thickened bronchial and bronchiolar epithelium
NO, exposure alone produced no effect.
Same morphology as others. Recovery for 1 to
3 mo showed lymphocyte infiltration up to 3 mo
No changes in terminal bronchi. Cilia lost
and altered by 72 hr. Greater cilia loss and
focal hyperplasia by 7 days. Regeneration of
cilia by 14 days. Substantial recovery by 21
Earlier and greater injury of same type
and sequence as at lower level with loss
of Type I cells.
Increased number of LDH positive cells/
alveolus (presumably Type II cells)
Type II cell hypertrophy.
Hypertrophic bronchiolar epithelium, particu-
larly in the area of respiratory bronchiole.
NaCl aerosol had no added effect.
3
At 3,760 ug/m (2 ppm), cell division of Type
II cells peripheral to terminal brochiolar-
alveolar junction seen.
Cell division seen at 24 hr, peak at 2 days,
decreased to preexposure by 5 days.
Reference
Freeman et al . , 1966
Renters et al. , 1973
Chen et al . ,
1972
Stephens et al . ,
1972
days.
Sherwin et al . ,
1972
Sherwin et al . ,
1973
Furiosi et al . ,
1973
Evans et al . ,
1972; 1978a
-------
TABLE 14-9. (continued)
\
N02
Concentration
ug/m3
32,000
5,640
9,400
18,800
18,800
28,200
ppm Exposure Species
17 Continuous,
1 day
3 4 hr/day, Squirrel
4 days with monkey
intermittent
exercise
5 Continuous, Monkey
10 90 days
10 Continuous, Rat
90 days
15 Continuous,
75 days
Effect Reference
Type II cell proliferation.
Thickening of alveolar wall and basal lamina. Bils, 1976
Interstitial collagen.
Infiltration of macrophages, lymphocytes, and Busey et al.,
occasionally polymorphonuclear leukocytes. 1974
Hyperplasia of bronchiolar epithelium and Type
II cells.
Decrease in length and weight of neonates Freeman et al.,
exposed, delivered and reared in NO,,. 1974b
Delayed lung development in progeny exposed
in utero and raised in N00. 75 days required
18,800
10
Continuous, Guinea
6 wk pig
18,800 to 10 to
47,000 25
6 mo
19,100 to 10.2 to 12 mo
21,500 11.4
Dog
Cat
to make up deficit.
Type II cell hypertrophy, 1 to 6 wk exposure
with increased lamellar bodies within Type II
cells.
Emphysema and death.
Intraluminal mucus. Increase in goblet cells.
Thickening of epithelium. Fly ash (9,950 to
10,200 ug/m ) had no effect.
Yuen and Sherwin,
1971
Riddick et al.,
1968
Kleinerman et al. ,
1976
-------
TABLE 14-9. (continued)
N02
Concentration
ppm Exposure Species
Effect
Reference
28,000
14
48 hrs
28,000 to 15 to
32,000 17
28,200 15
24 hr
48 hr
28,200 15 4 days/wk,
5 wk, total
31.5 hr
5 days/wk,
18 wk,
total 93.5
hr
28,000 15 Continuous,
1,4,10,16
and 20 wk
•^28,000 15 Subacute
28,200 15 24 hr
Rat
Rat
Rat
Rat
Rat
Rat
Hamster
Neonate-20 days of age: loss of cilia;
flat luminal surface of epithelium. No
nodules. No significant injury of Type I
cells. Weanling-30 to 35 days of age:
tissue nodules (size increases with exposure),
Type I cell injury. 40 days: hypertrophy
and stratification of nonciliated cells
in terminal bronchioles; polyploid exten-
sions of epithelium in terminal airways.
Division of Clara cells replaced damaged
ciliated cells.
Increased cell division, especially Type II
cells.
No effect on blood methemoglobin.
In lung increased atelectasis and alveolar
thickening. In liver increased granular changes,
karyolysis and karyorhexis. Suppressed by
Vitamin E supplementation. No effect on
tissue lipofuscin pigment by N0~ exposure or
dietary Vitamin E. Lung lipid extract distri-
bution not affected by N0~ exposure.
Hyperplasia of terminal bronchiolar and
alveolar epithelium reversible on discontinu-
ation of exposure; alterations of interstitial
structural features of alveoli not reversible.
Newborn rats up to age 3 wk relatively resis-
tent to exposure compared to mature rats.
3H-thymidine (Tdr) 24 hr post-NO-, 1 and 24 hr
post TdR, label in smallest ciliated airways,
less in trachea. Increase in lung parenchyma
distant from airways. Deep parenchyma 8% Type
II cells of which 11% labelled 24 hr post-NO?.
25% AM labelled. No change in AM population?
Stephens et al.,
1978
Evans et al.,
1976
Evans et al.,
1974
Csallany and Ayaz,
1978a
Freeman et al.
1969
Lunan et al., 1977
Hackett, 1978
-------
TABLE 14-9. (continued)
N02
Concentration
ug/m3
28,200
to
32,000
28,200
to
32,000
28,000
to
31,960
32,000
69,000
150,000
ppm Exposure Species
15 48 hr Rat
to
17
15 Continuous, Rat
to lifetime
17
15 12 and 24 hr Rat
to
17
17 Continuous, Rat
90 days
37.2 4 hr Dog
80 3 hr Cat
Effect
Alveolar macrophage division seen with DMA
synthesis.
Bronchial epithelium hypertrophic and meta-
plastic. Increased mucus. Connective tissue
damage. Fibrosis at junction of respiratory
bronchiole and alveoli. Emphysema.
Loss of cytoplasmic projections of nonciliated
(Clara) cells and exfoliation of ciliated cells.
Collagen damage. Large fibers and thickened
basement membrane.
Interstitial edema.
Some alveolar desquamation.
12 and 24 hr post-NCL, degeneration of Clara
cells, loss of cilia distal portion of terminal
bronchioles. Clara cell hyperplasia evident
48 to 168 hr post-NO?. Loss of pneumonocytes
resulted in substantial centroacinar denudation
of basal lamina in lungs 12 and 24 hr post-NO™.
Serous and serofibrinous edema, neutrophilic
emigration and extravasation of erythrocytes
evident 24-hr post-NO? exposure. Peri-
bronchiolar congestion and edema. 50% proximal
alveolar spaces filled with serous edema fluid.
Increased number of AM and hyperplasia of type
II pneumocytes.
Reference
Evans et al. ,
1973a
Freeman et al . ,
1968c; 1972
Stephens et al. , 1971
Evans et al . ,
1978b
Stephens et al . ,
1971
Guidotti and
Liebow, 1977
Langloss et al . ,
1977
-------
parenchyma into a "gland-like" tissue in the region of the ducts. Incorporation of H-thymi-
dine by Type II cells was observed within 12 hours after initial exposure, the number of
labeled cells becoming maximal in about 48 hours and decreasing to pre-exposure levels by 6
days, despite persistent exposure (Evans et al., 1975). This pattern of incorporation of
3 3
H-thymidine, indicative of cell replication, was documented at 3,760 ug/m (2 ppm) N0~ as
3
well as at 32,000 ug/m (17 ppm) (Evans et al., 1972). On continued exposure, there is a
change in the normally irregular contour formed by the ciliated and nonciliated cuboidal cell
layer of the terminal airways due to a loss of the bud-like cytoplasmic projections of non-
ciliated (Clara) cells and the exfoliation of ciliated cells (Evans et al. , 1978b). Later,
aberrations in ciliogenesis occur and cilia often appear within vacuoles surrounded by cyto-
plasm.
Renters et al. (1973) exposed monkeys to 1880 (jg/m (1 ppm) N0~ continuously for 493
days. Four monkeys were challenged with influenza A/PR/8/34 virus one day before and 41, 83,
146, and 266 days after initiation of NOp exposure. Monkeys exposed to N02 and virus devel-
oped moderate emphysema with thickened bronchial and bronchiolar epithelium. No effect was
observed in monkeys exposed to N0~ alone or controls.
Age is a factor in determining the response of the lungs to NOj. Newborn rats up to the
age of about 3 weeks are relatively resistant to high subacute concentrations (about 28,000
ug/m ; 15 ppm) compared to more mature animals. (Lunan et al., 1977) On the contrary, old
rats about 2 years of age or more have a 24-hour delay in renewing injured or desquamated Type
I pneumocytes, relative to younger animals, and also have a lower threshold for death from
pulmonary edema induced by N02 (Evans et al., 1977).
Sherwin and co-workers (Kuraitis et al. , 1979; Sherwin et al., 1979) exposed mice to 553
0
ug/m (0.34 ppm) NOj 6 hours/day, 5 days/week for 6 weeks. Lactate dehydrogenase positive
type II cells were quantitated and shown to be hyperplastic and hypertrophied. Body weights,
spleen weights, and area of splenic lymphoid nodules were decreased following exposure to N02-
Buell (1970) reported the isolation of swollen, damaged, insoluble collagen fibers from
the lungs of rabbits exposed to 470 ug/m (0.25 ppm) for 4 hours/day, 5 days/week for 24 or 36
days. Modifications of collagenous tissue are evident early and late and may be reflected in
the increased excretion of collagen degradation products in the urine.
While hyperplasia of the terminal bronchiolar and alveolar epithelium is reversible on
2
discontinuation of exposure to 28,000 ug/m (15 ppm) N02, the interstitial structural altera-
tions of alveoli are not (Freeman et al., 1969a). Bronchiolar epithelial alterations are
observed during lifetime exposure to 3,760 ug/m (2 ppm) (Freeman et al., 1968a,c). Similar
changes in rats without enlargement of lungs have been seen after a lifetime exposure to 1,500
ug/m (0.8 ppm) NO- (Freeman et al., 1968c).
3
Embryonic and adult hamster tracheal cells were exposed as cultures to 1,880 ug/m
(1 ppm) NO- for 6 hours (Samuelsen et al., 1978). Cells so treated lost their ability to grow
3
and form colonies. Hamster lung fibroblasts (V-79), when exposed J_n vitro to 216 ug/m (0.12
ppm) NO- for periods up to 6 hours, also failed to divide and form colonies.
14-47
-------
Blair et al. (1969) did microscopic studies of the temporal alterations of lung morpho-
logy in mice exposed to 940 ug/m (0.5 ppm) NO-, for 6, 18, and 24 hours per day. Exposed mice
were found to have expanded alveoli after 3 to 12 months of exposure. However, interstitial
pneumonia may have confused the interpretation. Continuous exposures of mice to 940 to 1,500
ug/m (0.5 to 0.8 ppm) for 1 month induced proliferation of epithelial cells of the mucuous
membranes, degeneration and loss of mucous membranes, edema in alveolar epithelial cells, loss
of cilia, and an influx of monocytes. (Hattori, 1973; Hattori and Takemura, 1974; Nakajima et
al., 1972; Nakajima et al., 1969) Mice exposed continuously for 5 weeks to 1,030 to 3,000
ug/m (0.55 to 1.6 ppm) NOp exhibited damaged cilia and an increase in mucus secretion by
nonciliated cells.
Furiosi et al. (1973) investigated the influence of a 14-month continuous exposure to
3,800 ug/m3 (2 ppm) N02 and 330 ug/m3 (0.1 ppm) NaCl (0.1 to 10.3 urn), alone and in com-
bination, on monkeys (Macaca speciosa). Rats were exposed simultaneously but received
approximately 1,880 ug/m (1 ppm) NO,, due to differences in the .exposure cages. The NaCl
exposure alone caused no effects. In monkeys, the NOp exposure resulted in hypertrophy of the
bronchiolar epithelium, particularly in the area of the respiratory bronchiole which is
confluent with the alveolar duct. Morphological changes were observed also in the more
proximal bronchiolar epithelium. When NaCl was combined with N02, NaCl appeared to have no
influence. Neither were alveolar epithelial changes noted. In rats, the results were similar
to an earlier study with equivocal findings, (Freeman et al., 1966) in which the animals were
exposed to about 1,500 pg/m (0.8 ppm) N0? for over 2 years. In the latter study, (Freeman et
al. 1966) it was reported that rats exposed continuously up to 33 months exhibited an essen-
tially normal gross and microscopic appearance with suggestive evidence of changes in the
terminal bronchioles.
Recovery from exposure to NO, has been reported (Chen et al., 1972; Evans et al., 1978b).
o
In mice sacrificed after exposure to 1,880 to 2,820 ug/m (1 to 1.5 ppm) N02 for 30 days, the
morphological changes were similar to those described above (Chen et al., 1972). Lymphocytes
infiltrated around the bronchioles during the ensuing 1- to 3-month period in clean air. This
was not observed in mice sacrificed either during or immediately after N02 exposure, leading
the authors to speculate that this might have been an autoimmune response.
Bils (1976) observed connective tissue changes in squirrel monkeys that respired 5,640
q
ug/m (3 ppm) N02 for 4 hours/day for 4 days with intermittent exercise during exposure.
Thickening of the alveolar wall between the air and capillary spaces, in the basal lamina, and
in the interstitial areas was seen. Numerous fenestrations were found in the alveolar walls
in the centroacinar area.
Coffin and Stokinger (1977) suggest that fenestrations are related to the pores of Kohn.
Since the frequency of such pores differs among species, attenuation of alveolar septae and
distention of their pores may be recognized, depending on the species. Reduction in .the
elasticity of connective tissue, regardless of species, combined with the loss of Type I
cells, could result in enlargement of the pores. They contend that the process may be largely
14-48
-------
irreversible once the pores are enlarged. Thus, the mechanisms resulting in their appearance,
although fenestration may not be prominent in all species, may be a hallmark of pathogenesis.
Port et al. (1977) investigated the effects of NO, on several species using light and
3
scanning electron microscopy. Exposure to 188 ug/m (0.1 ppm) was continuous for 6 months.
Upon this regimen were superimposed daily 2-hour peaks of 1,880 ug/m (1 ppm) l^. Although
bronchioles and alveolar ducts were not found to be remarkable, occasional foci of distended
alveoli were seen under the pleura. Large variations in pore size (up to 5-fold) and in
number (up to 10 per alveolus) were seen. Alveolar pores were thought to be involved in the
development of emphysema induced by NO- in some species but not in others.
3 3
In exposures to 940 ug/m (0.5 ppm) for 4 hours or 1,880 ug/m (1 ppm) for 1 hour, rats
sustained reversible lung-tissue change (Thomas et al., 1967). In tissues from animals sac-
rificed immediately after exposure, the mast cells were ruptured and disoriented and showed
loss of cytoplasmic granules. The occurrence was primarily in the pleura, bronchi, and sur-
rounding tissues, but most markedly in the mediastinum. This response seemed reversible,
since animals sacrificed 24 to 27 hours after exposure appeared to have only a few ruptured
mast cells. The investigators considered the release of granular material from the lung mast
cells in response to N0~ inhalation to signify the potential onset of an acute inflammatory
reaction.
14.2.3.4 Pulmonary Function—Exposures of animals to 9,400 ug/m (5 ppm) NO^ or lower have
been reported to have produced a variety of effects on pulmonary function. (See Table 14-10.)
Elevated respiratory rates throughout the life-span of rats were observed after the animals
2
were exposed to 1,500 ug/m (0.8 ppm) NOp for periods up to 2.75 years (Freeman et al., 1966;
Haydon et al., 1965).
Rats exposed to 5,400 ug/m (2.9 ppm) N02 for 24 hours/day, 5 days/week, for 9 months
exhibited a 13 percent (p < 0.05) decrease in lung compliance and lowered lung volumes when
compared to controls (Arner and Rhoades, 1973). Freeman et al., (1968c) however, observed
that resistance to airflow and dynamic compliance were not affected when rats were exposed for
o
2 years to 3,800 ug/m (2 ppm) N0?. Tachypnea (rapid breathing) was observed.
Rats and cats exhibited a tendency toward' increased respiratory rates and decreased
arterial 0~ partial pressure when exposed to 940 to 38,000 ug/m (0.5 to 20 ppm) NO^ (Zorn,
1975b). Oxygen uptake in the blood was impaired and remained so several hours after exposure
was terminated (Zorn, 1975a).
Murphy et al. (1964) exposed guinea pigs to various concentrations of NO, between 9,780
, , f.
and 24,440 ug/m (5.2 and 13 ppm). At 9,780 ug/m (5.2 ppm), there were no significant in-
creases in respiratory rate until after 3 hours of exposure. When guinea pigs exposed to this
concentration for 4 hours were returned to clean air, recovery occurred within approximately 1
hour. At higher concentrations, respiratory rates increased earlier. Tidal volume also
decreased during the 4-hour exposure to 9,780 ug/m (5.2 ppm). The net effect was to maintain
minute ventilation at a nearly constant level. No significant alterations in respiratory
2
function in rabbits were observed when animals were exposed to 9,400 |_g/m (5 ppm) NO^ for 6
hours/day over a period of 18 months (Wagner et al. , 1965).
14-49
-------
TABLE 14-10. PULMONARY FUNCTIONS
Pollutant
N02
N02
NO,
N02
NO,
N02
NO,
NO,
N02
Concentration
ug/m3 ppm Exposure
940 to 0.5 to Continuous
38,000 20
1,500 0.8 Continuous,
to 2.75 yr
1,880 1 16.5 mo. NO
alone or with
subsequent in-
fluenza virus
A/PR/8/34
challenge.
3,800 2 2 yr
3,800 2 10 yr
16,900 9 5 yr
5,400 2.9 Continuous,
5 days/wk,
9 mo
9,400 5 6 hr/day,
18 mo
9,400 5 7.5 hr/day,
5 days/wk,
5. 5 mo
Species
Rat. cat
Rat
Squirrel
monkey
Rat
Monkey
(Macaca
speciosa).
Pregnant and
offspring
Rat
Rabbit
Guinea pig
Effect
Increased respiratory rates.
Decreased arterial oxygen pressure.
Impaired 02 uptake in blood.
Increased respiratory rates.
Little change In tidal volume, minute
volume, and respiratory rate.
Resistance or dynamic compliance
unchanged. Tachypnea.
No change in mean respiratory rate
or functional residual capacity of
juveniles.
Decreased (13%, p < 0.05) lung com-
pliance and lowered lung volume.
Respiratory function unchanged.
No increase in total resistance to
airflow.
Reference
Zorn. 1975a;
1975b
Freeman et al . ,
1966
Haydon et al. ,
1956
Fenters et al. , 1973
Freeman et al . ,
1968c
Freeman and Juhos,
1976
Arner and Rhoades,
1973
Wagner et al . ,
1965
Balchum et al . ,
1965
-------
TABLE 14-10. (continued)
Pollutant
NO,
£
NO,
£.
NO,
c
NO,
so|
NO- +
so2
NO,
£
NO, .
Concentration
; ug/m*
9,400
18,800
9,400
18,800
9,780
10,000
10,000
10,000 +
10,000
15,000 to
22,600
ppm
5
10
5
10
5.2
5.3
3.8
5.3 +
3.8
8 to
12
Exposure
Continuous,
90 days
Continuous,
2 mo.
K. pneu-
moniae
challenge
Continuous,
1 mo.
K. pneu-
momae
challenge
4 hr
6 days/wk,
6 mo
continuous,
12 wk
Species
Cynomologus
monkey
Squirrel
monkey
Guinea pig
Guinea pig
Rabbit
Effect
Unchanged with heat stress.
Impaired distribution of ventilation of
the lungs; increased respiratory rates;
decreased tidal volume; addition of heat
stress decreased dynamic compliance of
lungs.
Gradual reduction in tidal volume.
Increased respiratory rate. Minor
changes in minute respiratory volume.
After challenge, minute volumes decreased
and remained depressed.
Elevation in minute respiratory volume
due to increased tidal volume and respira-
tory rate by 2 wk and throughout exposure.
3 days after challenge, marked reduction
in minute volume.
Increased respiratory rate, return to
normal levels in clean air. Decreased
tidal volume.
Respiratory frequency, flow rate, or
minute volume unchanged in all regimens.
Increased nonelastic resistance and
functional residual capacity.
Reference
Coate and Badger,
1974
Henry et al . . 1970
Murphy et al. ,
1964
Antweiler and
Brockhaus, 1976
Davidson et al. ,
1967
Static lung compliance unchanged.
-------
TABLE 14-10. (continued)
I
Ul
N3
N02
Concentration
Pollutant ug/m3 ppm
NO, 18,«00 10
. 28.200 15
65,800 35
94.000 50
94.000 50
Exposure
2 hr, K/
pneumoniae
challenge
2 hr, chal
with K. pneu-
moniae after
24~hr
Species Effect Reference
Squirrel Decreased tidal volume, increased respira- Henry et aV. , 1969
monkey, male tory rate 2 to 4 hr post exposure.
and female No enhancement by K. pneumoniae.
No mortality. Less drastic effects
on respiratory function.
Tidal and minute volume decreased by 4 hr.
Mortality: 2/3 within 5 to 72 hr.
Increased respiratory rate.
Tidal volume decreased.
Respiratory rate increased.
Death within 72 hr.
94.000 50
2 hr
NO, 19,200 to
* 21,400
10.2 to Continuous.
11.4 12 mo
Cat
fly ash 10,000 to
10,200
elutriated 2.100 to
dust of 1,600
fly ash
NO, 28,200 15
Continuous,
lifetime
Rat
Respiratory rate increased 2-fold.
Decreased tidal volumes.
Minute volumes constant.
Respiratory rates high for 72 hr,
•return to normal by 7 days.
Increased total airway resistance and
upstream resistance.
Decrease in static lung compliance.
•Internal surface area unchanged.
No effect due to fly ash.
Increased tidal volumes 50 to 350%.
Minor increased resistance and de-
creased compliance 15 to 20 wk.
Increased emphysema.
Kleinerman et al. ,
1976
Freeman et al.
1972
-------
TABLE 14-10. (continued)
N02
Concentration
Pollutant ug/m3
N02 38,400
ppm Exposure Species
20.4 20 to 22 Hamster
hr/day,
7 days/wk,
12 to 14 mo
Effect Reference
Increased total pulmonary resistance Kleinerraan, 1977
during passive ventilation and maximal
airflow with concurrent decreased flow
values. Return to normal within 3 mo.
Static lung compliance unchanged.
Decreased surface area.
N02 56,000 30
i
Ul
15 min Rabbit
NO- 56,400 to 30 to 7 to 10 days. Hamster
65,800 35 followed by
papain
Redistribution of lung perfusion resulting
in reduced storage activity in peripheral
zones of lung.
NO, + papain increased lung volumes.
Nof + papain increased pulmonary
resistance (p < 0.05). Pulmonary
resistance unchanged by papain.
von Nieding et al.
1973
Niewoehner and
Kleinerman, 1973
-------
Henry et al. (1970) exposed male squirrel monkeys continuously to 18,800 and 9,400 ug/m
(10 and 5 ppm) NO^ for 1 and 2 months, respectively. Elevation in minute respiratory volume
due to increased tidal volume and respiratory rate was apparent by 2 weeks and persisted
q
throughout exposure to 18,800 ug/m (10 ppm) NOp. At the end of the exposure period, monkeys
were challenged with K. pneumoniae; 3 days later minute volume was markedly reduced. Only
minor changes in minute respiratory volumes were noted in monkeys exposed to 9,400 ug/m (5
ppm) NOp for 2 months. The tidal volumes displayed a gradual reduction during the 2 months,
while at the same time respiratory rates increased. After challenge with bacteria, minute
volumes decreased and remained depressed.
Renters et al. (1973) found that monkeys exposed to 1,880 ug/m (1 ppm) N02 for 16.5
months showed little change in tidal volume, minute volume, and respiration rate. Subsequent
challenge with influenza virus A/PR/8/34 produced no subsequent alterations either.
Environmental factors, such as heat stress, in combination with NO, exposure have been
3
examined. (Coate and Badger, 1974) Monkeys continuously exposed to 9,400 and 18,800 ug/m (5
and 10 ppm) NO^ for 90 days were stressed at a temperature of 31°C versus 24°C for controls.
At the higher concentration, N02 impaired the distribution of ventilation of the lungs, in-
creased respiratory rates, and decreased tidal volumes. The addition of heat stress did not
further impair distribution of ventilation, but it did decrease dynamic compliance of the
3
lungs; N02 alone did not. No synergistic effect was seen at N02 concentrations of 9,400 ug/m
(5 ppm) with heat.
Freeman and Juhos (1976) exposed pregnant monkeys to N0? continuously and raised their
offspring in similar environments. Adult and juvenile monkeys were exposed to 3,800 and
16,900 ug/m (2 and 9 ppm) NO, for 10 and 5 years, respectively. No changes due to exposure
*- &•
could be seen in mean respiratory rate or functional residual capacity in the juveniles.
14.2.3.5 Studies of Hyperp1asia--Chronic N02 exposure produces a transient hyperplasia of the
Type II cells of the lung. This hyperplasia has stimulated inquiries into the potential for
neoplasia or tumor formation due to NO^. (See Table 14-11.)
The studies by Ide and Otsu (1973) revealed evidence of some tumor production in mice
exposed to 9,400 to 18,800 ug/m3 (5 to 10 ppm) N02 for 2 hours/day, 5 days/week for 50 weeks
after receiving injections of 0.25 mg 4-nitroquinoline-l-oxide (a lung-tumor-specific carcino-
gen), but N02 did not enhance the tumor production (i.e., N02 had no synergistic or inhibitory
properties with a known carcinogen). No tumors were observed in mice exposed to N0? alone.
These data are of questionable value for predicting potential interactions with the broader
classes of carcinogens.
Rejthar and Rejthar (1975) exposed rats to 9,400 ug/m (5 ppm) N02 continuously for
periods of 3, 5, 7, 9, and 11 weeks. The rats were then killed. Following a 3-week exposure,
the bronchioles contained uniform cuboidal one-layer epithelium composed of nonciliated cells.
The cells showed vacuolization, and hyperplastic foci appeared in the bronchiolar epithelium.
The foci were 2- to 4-layer pyramidal formations. By 5 weeks, extensive hyperplasia composed
of three to four layers of epithelial cells was apparent. Centers of cuboidal metaplasia were
14-54 °
-------
TABLE 14-11. STUDIES OF POTENTIAL HYPERPLAS1A
i
en
en
Pollutant
Concentration
Pollutant
NO.
CO
Synthetic
Smog
N02
CO
03
so2
N02
N02
ug/mj
940 to
1.500
+
58.000
1,500
5,750
760
5,700
2.360
9,400
ppm
0.5 to
0.6
+
50
0.8
b
0.38
2.2
1.26
5
Exposure
Continuous ,
30 days
23 to 24
hr/day ,
8 to 12 mo
12 hr/day.
3 mo
Continuous,
to 11 wk
Species Effect
House Increased hyperplasia terminal bronchioles
to alveolus. No difference from N02 alone.
CO (115,000 ug/m3, 100 ppm) alone for 30 days
failed to induce hyperplasia.
House By 20 days exposure, increased thickened
bronchial membranes.
By 60'days, very thick membranes appear to
have villus-like hyperplastic folds.
4 months post-exposure, hyperplasia
regressed towards normal.
Rat, prior No effect on fertility.
to breeding Decrease in litter size and neonatal weight.
No teratogenic effects.
Rat Appearance of hyperplastic foci in the
shape of 2 to 4 layer pyramids by 3 wk.
Reference
Nakajima et al . ,
1972
Loosl i et al . ,
1972
Shalamberidze
and
Tsereteli. 1971
Rejthar and
Rejthar, 1975
Decreased ciliated cells.
Extensive hyperplasia (3 to 4 layers of
epithelium), cuboidal metaplasia in ad-
jacent alveoli by 5 wk.
Hyperplasia in all bronchioles,
decreased bronchiolar lumina, polymorphous
epithelium extensive by 7 wk. Terminal
bronchiolar epithelium contained only
2 or 3 irregular layers, increased number of
ciliated cells by 9 wk. By 11 wk return to
1 layer epithelium. Lu"9s at indefinite state
of repair from week 7 on.
-------
TABLE 14-11. (continued).
en
O-i
Pollutant
Concentration
Pollutant pg/mj
NO, 9,400 to
* 18,800
NO, 18,800
C.
NO, 18,800
c.
Auto Exhaust
CO 58,000
N0x
A
C02 (0.07 and
0.37%)
Aldehydes
ppm
5 to
10
10
10
50
(0.2
and
23)
(0.1
and
2.0)
Exposure Species
2 hr/day, Mouse
5 day/wk,
50 wk
2 hr/day, Mouse
5 day/wk,
50 wk
Continuous from Rat
pregnancy to
3 mo after
delivery
6 hr/day, Rat
5 days/wk,
2.5 mo to
2 yr
Effect Reference
Mice given 4-nitroquinoline-l-oxide and Ide and Otsu,
NO,; NO, had no effect on tumor production. 1973
L. £.
Mice given 4-nitroquinoline-l-oxide Otsu and Ide,
(carcinogenic agent) + NOp decreased 1975
incidence of lung tumors.
Decreased litter size and increased mor- Freeman et al.,
tality of neonates up to 15 days post 1974
delivery.
No teratogenic effects noted.
Auto exhaust had no biological effects when Stupfel et al.,
NO was 0.2 ppm. 1973
Exposure to NO (23 ppm) increased number of
spontaneous tumors, cutaneous abscesses,
and bilateral renal sclerosis.
No tumors or abscesses in lungs.
-------
found in adjacent alveoli. By 7 weeks, hyperplasia was apparent in all bronchioles, thus, nar-
rowing the bronchiolar lumina. Polymorphous epithelium was extensive with a few ciliated
cells in hyperplastic areas. After 9 weeks, terminal bronchiolar epithelium generally showed
two or three irregular layers. The number of ciliated cells increased, but cilia were often
located atypically in intercellular spaces. A return to a single layer of epithelium without
cilia was observed after 11 weeks. Seven weeks after exposure to NO,,, the lungs appeared to
be in a state of repair moving towards reversal of the lesions.
Nakajima et al. (1972) exposed mice to 940 to 1,500 ug/m3 (0.5 to 0.8 ppm) N02 for 30
days. Examination revealed hyperplasia from the terminal bronchiole to the alveolus. Mice
exposed to the same concentrations of N0? with CO (58,000 ug/m ; 50 ppm) for 30 days revealed
the same hyperplastic foci in the terminal bronchioles. At exposure concentrations up to
115,000 ug/m (100 ppm) for 30 days, CO by itself failed to induce hyperplasia in mice.
Stupfel et al. (1973) exposed rats to automotive exhaust 6 hours/day, 5 days/week for
periods of 2.5 months to 2 years. The exhaust contained 58,000 ug/m (50 ppm) CO, two dif-
ferent concentrations of NO (0.2 and 23 ppm), C09 (0.07 and 0.37 percent), along with
A C.
aldehydes (0.1 and 2 ppm). No effects were observed at 0.2 ppm NO . At 23 ppm NO , more
A A
spontaneous tumors and cutaneous abscesses as well as bilateral renal sclerosis were seen.
14.2.3.6 Edemagenesis and To1erance--Sherwin and Carlson (1973) reported an increase of
protein in the lavage fluid from lungs of guinea pigs with an unquantified vitamin C defi-
ciency exposed continuously to 750 ug/m (0.4 ppm) NO- for 1 week (p < 0.001). (See Table
14-12.) Proteins were identified and measured by disc electrophoresis. No remarkable dif-
ferences were noted in the composition of the filtered proteins obtained by pulmonary lavage.
3 3
Mice injected with H-rabbit albumin accumulated H in their lungs following 14 day, con-
tinuous exposure to 7,500 to 13,000 ug/m (4 to 7 ppm) NO-. (Sherwin and Richters, 1971)
Using injected horseradish peroxidase as a marker, this group of researchers recently reported
increased retention of protein in pulmonary air spaces after exposure to 940 ug/m (0.5 ppm)
NO- for 5 days/week for 3 weeks (Sherwin et al., 1977). Greater retention of horseradish
peroxidase occurred after 6 weeks of exposure.
Selgrade et al. (1981) reexamined this problem focusing on the role of vitamin C
deficiency in promoting of NO^-induced edema. (See "Section 14.2.3.2.2 Lipid and Diet
Effects" for a detailed description of the concentrations, times and effects.) They found
that vitamin C depletion enhanced both edema formation, as measured by protein and lipid
content of the lavage fluid, and increased mortality at 9400 ug/m (5.0 ppm). There are
differences in the two studies, however. Selgrade et al. found no effect of exposure to 752
ug/m (0.4 ppm) for up to 1 week whereas Sherwin and Carlson (1973) did. Selgrade et al. also
found a new protein in the lavage fluid not found in serum and found that the lipid content,
while increased, did not reflect that of the serum. Sherwin and Carlson used disc gel
electrophoresis to measure protein content while Selgrade et al. used the microchemical Lowry
method. The qualitative difference in identification of proteins may also have resulted from
the use of gel scanning by Selgrade et al. and the improvements in gel resolution brought
14-57
-------
TABLE 14-12. PRODUCTION OF LUNG EDEMA BY NO,
en
oo
Pollutant
Concentration
ug/m3 ppm.
750 0.4
940 0.5
7,500 to 4 to
13,000 7
56,400 30
Duration
Continuous ,
1 wk
5 days/wk,
3 or 6 wk
Continuous ,
14 days
Continuous ,
to 30 days
Species Effects
Guinea pig Increased proteins in lung
lavage fluid of exposed animals with
an unquantified vitamin C deficiency
detected by disc gel electrophoresis.
Mouse Horseradish peroxidase used as a
marker for proteins showed greater
sequestering in exposed mice at 3 wk
than 6 wk. Suggests edema.
Mouse H rabbit albumin infiltration
indicates lung edema.
Hamster Lung wet weight elevated at 1
and 30 days.
Reference
Sherwin and
Carlson, 1973
Sherwin et al . ,
1977
Sherwin and
Richters, 1971
Kleinerman and
Rynbrandt, 1976
-------
about in recent developments in this field. The major difference may lie, however, in the
degree of vitamin C depletion of the guinea pigs in the two studies. Those of Sherwin and
Carlson are not documented with blood vitamin C levels. Selgrade et al. found only mild
depletion was necessary. Consequently, future studies will be needed to clarify this point.
Taken together, these two studies and those reported above suggest that NCL damage to the lung
can be modified by the dietary intake and that lavage fluid composition is a sensitive measure
of damage to the lung.
The development of tolerance to lethal concentrations of N02 has been correlated with
lethal edema production. Wagner et al. (1965) examined the question of tolerance along with
several other characteristics. They found that tolerance could be evoked by prior exposure to
low or high concentrations of N00, in young and old animals. (See Table 14-13) Mice were
3 3
made tolerant to an LC50 dose of 113,000 (jg/m (60 ppm) by prior exposure to 9,400 (jg/m
(5 ppm) N02 for 7 weeks (hours/day not specified). Tolerance disappeared after 3 months
following removal from the N02 exposure. Rats also were made tolerant.
14.2.4. Extrapulmonary Effects
14.2.4.1 Nitrogen Dioxide-induced Changes in Hematology and Blood Chemistry-Exposure of
experimental animals and humans to NO,, alone or in combination with other pollutants produces
an array of hematological perturbations (see Table 14-14) with a biological significance which
is not easily interpretable (see Chapter 15 for human studies).
3
Shalamberidze (1969) exposed rats continuously to 100 |jg/m (0.05 ppm) N02 for 90 days
with no change in blood hemoglobin or erythrocyte levels.
A 7-day exposure to 940 ug/m (0.5 ppm) N02 resulted tn a depression in GSH peroxidase
levels of RBC in guinea pigs (p < 0.001) which was not observed after exposure for 4 months
(Donovan et al., 1976; Menzel et al., 1977).
Kosmider et al. (1975) exposed guinea pigs for 8 hours/day for 120 days to 940 ug/m (0.5
ppm) N02 with 1,000 ug/m3 (0.39 ppm) S02 or 940 ug/m3 (0.5 ppm) N02 with 1,000 ug/m3 (0.39
ppm) SO- and 70 ug/m (0.1 ppm) ammonia. Animals exposed to N02 and S02, with and without
ammonia, displayed an increase in white blood cells (WBC) and a decrease in RBC and hemoglobin.
Following exposure, a differential count of white cells revealed a decrease in neutrophils and
eosinophils and an increase in lymphocytes.
Mersch et al. (1973) exposed guinea pigs to 680 ug/m (0.36 ppm) N02 continuously for 1
week. Following exposure, RBC D-2,3-diphosphoglycerate was significantly increased (p < 0.05),
a measure which could reflect tissue deoxygenation.
Studies reported by Nakajima and Kusumoto (1970) showed that addition of 58,000 ug/m (50
ppm) CO to 940 to 1,500 ug/m (0.5 to 0.8 ppm) N02 did not change the carboxyhemoglobin
concentration in the blood of mice exposed 24 hours/day for 1 to 1.5 months to CO alone. They
also exposed mice to 1,500 ug/m (0.8 ppm) N02 for 5 days and found that methemoglobin levels
were not affected (Nakajima and Kusumoto, 1968).
Mitina (1962) exposed rabbits to 2,400 to 5,640 ug/m3 (1.3 to 3 ppm) N02 and/or 5,240 ug/nT
(2 ppm) S02 2 hours/day for 15 and 17 weeks. Exposure to N02 alone produced a significant rise
14-59
-------
TABLE 14-13.
TOLERANCE TO N02 EXPOSURES
N02
Concentration
ug/m3
9,400
9,400 +
47,000
ppm Duration
5 7 wk
5 + 13 mo
25 + 6 wk
Species Effects Reference
Mouse Challenge with LC50 dose (113,000 ug/m3 Wagner et al.,
(60 ppm) NO- for 5 hr, 24 hr post-exposure) 1965
caused 28% less mortality than in naive mice.
Rat Challenge with NO- (132,000 ug/m3 (70 ppm)
for 5 hr, 3 days post-exposure) caused 0%
47,000
en
o
25
18,800 10
47,000 25
7 wk
5 hr/day,
5 days/wk,
5 hr/day,
1 day/wk,
3 wk
6 hr/day,
2 days
mortality compared to 67% in pre-exposed
controls.
Mouse Challenge with NO- (132,000 ug/m3 (70 ppm)
for 5 hr, 3 days post-exposure) caused no
mortality 24 hr post-challenge compared to
29% in naive mice. Tolerance disappeared
in 1 mo.
Hamster Tolerance developed to normally lethal 5 hr Creasia, 1978
18,800 ug/m (10 ppm) NO exposure. Protec-
tion against further cytological injury but
not against the cytotoxic effects of >18,800
ug/m (10 ppm) as measured by increased DMA
synthesis.
3
Tolerance to normally lethal 131,600 ug/m
(70 ppm) N0_. Protection against further
cytological injury.
Rat Increased tolerance to 141,050 ug/m (75 Crapo et al.,
ppm) NO.. Increased G-6-PD, catalase, 4l£ 1978
increase cytochrome oxidase. No effect
on superoxide dismutase.
-------
TABLE 14-14. NITROGEN DIOXIDE-INDUCED CHANGES IN HEHATOLOGY
Pollutant
Concentration
Pollutant
NO,
NO,
N02
NO
S°2
NO
$
CO
NO,
2
ug/m3^
100
680
940
940 +
1.000
940 +
1,021 +
70
940 to
1,500 +
58,000
1.500
1,880
ppm
0.05
0.36
0.5
0.5 +
0.39
0.5 +
0.39 *
0.1
0.5 to
0.8 +
50
0.8
1
Exposure
Continuous,
90 days
Continuous,
7 days
8 hr/day,
7 days
8 hr/day,
4 mo
8 hr/day,
120 days
Continuous,
1 to 1.5 mo
Continuous ,
5 days
Continuous,
493 days
fol lowed by
influenza
A/PR/8/34
virus
Species Effects
Rat No effect on blood henioglobin or
erythrocytes.
Guinea pig Increased red blood cell D-2,3-diphos-
phoglycerate.
Guinea pig Decrease in RBC GSH peroxidase
(p < 0.001).
No change in RBC GSH peroxidase.
Guinea pig Same effects in both exposures.
Increased WBC and lymphocytes. Decreased
RBC, hemoglobin, neutrophils and
eosinophils.
Mouse Addition of CO to N02 failed to affect
carboxyhemoglobin.
Mouse No effect on metnemoglobin.
Squirrel No effect on hematocrit, hemoglobin, or
monkey clinical biochemical parameters.
Following viral challenge increased
leukocyte count.
Reference
Shalamberidze,
1969
Mersch et al. .
1973
Donovan et al. ,
1976
Henzel et al. ,
1977
Kosmider et al.
1975
Nakajima and
Kusumoto, 1970
Nakajima and
Kusumoto 1968
Renters et al. ,
1973
-------
TABLE 14-14. (continued)
I
CT1
Pollutant
Concentration
Pollutant
NO
NO.
NO
N02
NO,
C
so2
£-
NO,
S02
NO,
NaCl
N0?
NO,
L.
NO.
NO,
£
ug/mj
940
1,880
1,840 +
2,450
2,400 to
5,640
5,240
2,400 +
5,000
3,760 +
330
9,400
18,800
45,100
48,900
73,000 to
310,000
ppm
0.8
1
1.5 +
1.3
1.3 to
3
1.9
1.3 +
1.9
2 +
0.14
5
10
24
26
39 to 5
164
Exposure
16 hr/day,
7 days/wk,
4 yr
2 hr/day,
15 & 17 wk
2 hr/day,
15 wk
2 hr/day,
15 wk
Continuous,
14 mo
Continuous,
90 days
4 hr
191 days
to 60 min
Species
Dog
Rabbit
Monkey,
rat
Cynomolgus
monkey, male
Rabbit
Dog
Dog
Effects
No effects on hematocrit viscosity,
carboxyhemoglobin, or methemoglobin.
Increased leukocytes followed by
decreased phagocytic activity.
Decreased RBC.
Decreased phagocytic activity leukocyte.
No effect on RBC.
No effect on RBC.
Monkey: with or without NaCl, hypertrophy
of respiratory bronchiolar epithelium.
Rat: with or without NaCl, polycythemia
with reduced mean corpuscular volume and
normal mean corpuscular hemoglobin concen-
tration. Neutrophil /lymphocyte ratio
tendency to shift upwards in both animal
species tested.
No effect on hematological parameters.
-
Increased nitrite & nitrate in blood.
Thought to react with hemoglobin producing
methemoglobin.
Increased WBC disappeared following cessa-
tion of NOp. Decreased hematocrit and
hemoglobinf increased mean corpuscular
volume and mean corpuscular hemoglobin.
No effect on hematocrit or platelet counts.
Reference
Bloch et al. ,
1973
Mitina, 1962
Furiosi et al. ,
1973
Coate and Badger,
1974
Svorcova and
Kaut, 1971
Lewi s et a 1 . ,
1973
Carson et al . ,
1962
-------
in leukocytes followed by a decrease in their phagocytic activity. Exposure to N02 alone also
reduced the number of RBC, while a mixture of NO, and SO, or SO, alone had no effect.
£.£-£. n
Fenters et al. (1973) showed that exposing male squirrel monkeys to 1,880 ug/m (1 ppm)
N02 continuously for 493 days had no significant effect on hematocrit, hemoglobin, total pro-
tein, globulins, chloride, sodium, calcium, potassium, glucose, blood urea, nitrogen, glutam-
icpyruvic transaminase, lactate dehydrogenase, and lactate dehydrogenase isoenzymes. Challenge
with influenza A/PR/8/34 increased leukocytes in l^-exposed animals above levels in similarly
challenged controls.
Coate and Badger (1974) exposed monkeys to 9,400 and 18,800 ug/m (5 and 10 ppm) N0? for
90 days with no direct effect on hematological parameters. In another study, monkeys and rats
3 3
were exposed to 330 ug/m (0.14 ppm) NaCl and 3,760 ug/m (2 ppm) N02 for 14 months (Furiosi
et al., 1973). Exposure to N02 with or without NaCl produced polycythemia with reduced mean
corpuscular volume and approximately normal mean corpuscular hemoglobin concentration. In
monkeys and rats exposed to NO, with and without NaCl, the ratio of neutrophils to lymphocytes
was greater.
Bloch et al. (1973) conducted several hematological studies on dogs exposed 16 hours/day,
7 days/week, for 4 years to 940 pg/m3 (0.76 ppm) NO, 1,880 (jg/m3 (1 ppm) NO,, or 1,840 ug/m3
3
(1.5 ppm) NO plus 2,450 ug/m (1.3 ppm) N0?. No changes in hematocrit, viscosity, carboxyhe-
moglobin, or methemoglobin were found.
14.2.4.2 Central Nervous System and Behavioral Effects—Information regarding the effects of
NO- on the central nervous system or on animal behavior is limited to a few studies, (see
Table 14-15), most of which have uncertain relationships to humans.
3
.. Tusl et al. (1973) exposed rats to 9,400 ug/m (5 ppm) NO- for 8 weeks. The influence of
N09 on swimming of rats was measured. By the 5th and 6th weeks of exposure, swimming
3
performance had decreased 25 percent. In rats exposed to 1,880 (jg/m (1 ppm) N02, performance
was maintained with a slight tendency toward deterioration.
Yakimchuk and Chelikanov (1972) reported that rats exposed to 600 ug/m (0.32 ppm) N02
for 3 months developed a delay in their conditioned reflexes to sound and light. Shalamberidze
(1969) exposed rats to 100 ug/m (0.05 ppm) NO- for 3 months with no demonstrated effects on
the central nervous system.
o
Exposure of guinea pigs to 1,000 ug/m (0.53 ppm) N02 8 hours/day for 180 days affected
brain enzyme levels (Drozdz et al., 1975). Decreases were seen in brain malate dehydrogenase,
alanine aminotransferase, sorbitol dehydrogenase, lactate dehydrogenase, adenosine triphospha-
tase, and 5'-nucleotidase. Increases were seen in 1,6-diphosphofructose aldolase, isocitrate
dehydrogenase, a-hydroxybutyrate dehydrogenase, phosphocreatine kinase, and cholinesterase.
14.2.4.3 Biochemical Markers of Organ Effects—A major goal has been the detection of early
enzymatic markers of NO- effects. Studies of enzyme levels in different animal species
indicate that the earliest enzymatic changes of nitrogen dioxide effects occur in guinea pigs.
(See Table 14-16) Several such marker enzymes have been determined in blood. Release of
14-63
-------
TABLE 14-15. CENTRAL NERVOUS SYSTEM AND BEHAVIORAL EFFECTS
I
CD
Pollutant
Concentration
Pollutant
NO
NO
NO
2
NO
NO
NO
Auto Exhaust
CO
NO
CO* (0.07
and 0.37%
Aldehydes
ug/m3
100
1,000
600
1,880
9,400
37,600
6.580
14,000
75,000
37,600
15,040
58,000
ppm . Exposure
0.05 Continuous,
3 mo
0.53 8 hr/day,
180 days
0. 32 Conti nuous ,
3 mo
1 20 m in/day.
to 6 mo
5
20
3.5 6 hr/day.
8 wk
7.7 6 hr
40 5 hr
20 1 day
8 19 days
50 6 hr/day,
(0.2 and 23) 5 days/wk,
2.5 mo to
2 yr
(0.1 and 2.0)
Species Effect
Rat No effect un CMS.
Guinea pig Decreased malate, sorbilol, laclate
dehydrogenase; alanine aminotrans ferase ;
AlPase and 5' -nucleotidase. Increased
1 , 6- diphospho fructose aldolase;
isocitraLe, and alpha-hydroxybutyrate
dehydrogenase, phosphocreatine kinase
and chol inesterase.
Rat Decreased conditioned reflexes to sound
and 1 i ght .
Rat More or less constant swimming performance
only slight tendency to deterioration.
Swimming performance decreased 25% by 5th and
6th wk of exposure
Swimming velocity declined from 1st mo.
Decreased swimming performance.
Mouse, male Decreased voluntary running activity.
Return to normal within 24 hr post
exposure.
Rat 20% decrease swimming endurance.
10% decrease swimming endurance.
5% decrease swimming endurance.
Rat, male Decreased sound avoidance reflexes,
learning rate lowered.
Reference
Sha 1 amltpr i
-------
TABLE 14-16. BIOCHEMICAL MARKERS OF ORGAN EFFECTS
N02
Concentration
ug/m3
470
to 9.400
940
940
1.000
1.880
2.000
ppm
0.25
to 5
0.5
0.5
(NO ;
mainly*N02)
1
1.05
Exposure
3 hr
8 hr/day,
7 days
8 hr/day,
4 mo.
Continuous,
7-14 days
8 hr/day,
180 days
Continuous,
6 mo
8 hr/day,
180 days
Species Effect
Mouse Increase in pentobarbital-induced sleep time
in female mice only. Repeated daily exposures
caused no effect.
Guinea pig Serum lactic dehydrogenase, total
creatinine phosphokinase, SCOT, and SGPT.
cholinesterase and lysozyrae elevated.
Lysozyme and cholinesterase depressed.
Guinea pig Albumin and globulins found in urine.
Guinea pig Nitrates and nitrites excreted in urine.
Serum cholesterol slightly elevated; total
lipids depressed. Urinary Mg increased while
liver and brain Mg decreased. Hepatic edema
reported.
Guinea pig Protein synthesis inhibited. Body weight, total
serum proteins, and immunoglobul ins decreased.
Guinea pig Plasma changes:
Decreased albumin, seromucoid, cholinesterase,
Reference
Miller et al. , 1980
Menzel et al . ,
1977
Shervin and
Layfield, 1974
Kosmider, 1975
Kosmider et al . ,
1973a
Drozdz et al. ,
1976
alanin, and aspartate transminases.
Increased alpha, and beta2 immunoglobulIns.
Intracellular edema of liver.
Hepatic changes similar to plasma.
-------
TABLE 14-16. (continued)
N02
Concentration
ug/m3 ppm
11,660 6.2
Exposure
Continuous ,
4 days
Species
Rat
Effect
No effect on serum lysozyme.
Reference
Chow et al . ,
1974
47,000 to 25 to 2 hr
179,000 95
56,400
30
Rat
Continuous, Hamster
30 days
Plasma corticosterone increased proportional to Tusl et al.,
No,, concentration from 47 to 179 mg/m ; at 85 1975
mg7m x 5 hr/day levels returned to normal in
19 days; at 56 mg/m x 5 hr/day levels returned
to normal in 5 days.
Serum antiprotease levels increased
Kleinerman and
Rynbrandt, 1976
Rynbrandt and
Kleinerman, 1977
I
en
en
-------
lysozyme into the blood from pulmonary damage was cited above (Chow et al., 1974; Donovan
et al, 1976; Menzel et al., 1977). The CPK isoenzyme patterns seen in N0--exposed guinea pigs
are difficult to differentiate from CPK patterns caused by myocardial damage and are not par-
ticularly useful (Donovan et al., 1976). Plasma cholinesterase (CHE) was significantly (p <
2
0.001) elevated after a 7-day exposure to 940 ug/m (0.5 ppm) N0? but fell on long-term expo-
sure (4 months)•(p < 0.001). CHE levels are indicators of hepatic and myocardial disease,
being elevated in hemochromatosis, and usually depressed during active hepatocellular disease
(MacQueen and Plant, 1973; Moore et al., 1957). Increased CHE is seen with cardiac surgery,
but values are depressed consistently with myocardial infarction (MacQueen and Plant, 1973).
Aside from metastatic carcinoma from the liver to the lung, pulmonary disease including
pneumonia has not been previously associated with changes in CHE levels. Most likely, the
alterations in SCOT, SGPT, and LDH reported in the guinea pig studies are related to NO^-
induced hepatic damage. (Donovan et al., 1976) The persistent alteration in CHE, albeit
lower activity, after 4 months exposure to 940 ug/m (0.5 ppm) N0? suggests an hepatic lesion.
Another study indicating hepatic damage (Drozdz et al. , 1976) revealed decreased plasma
levels of albumin, seromucoid, alanine and aspartate transaminases when guinea pigs were
exposed to 2,000 ug/m (1.05 ppm) NO,, for 8 hours/day for 180 days. In agreement with Donovan
et al. (1976), Drozdz et al. (1976) reported decreased plasma cholinesterase levels. This
group also found increased serum levels of a,- and p^-immunoglobins. Electron micrographs of
the liver suggested intracellular edema. Kosmider (1975) reported decreased serum choles-
terol, total lipids, and beta and gamma lipoproteins in guinea pigs exposed to 1,000 ug/m NO
(mainly NOp), 8 hours/day for 120 days. At the same time, there was an increase in serum
alpha (a) lipoproteins. Blood serum sodium and magnesium were reduced while liver and brain
were depleted of magnesium and zinc as well. Cell permeabilities were changed and ions dis-
placed. Edema of the liver mitochondria occurred. At the same time, urine had increased
secretions of nitrite, nitrate, and coproporphyrin. Respiratory rate rose significantly with
little or no excitement or aggressiveness. Kosmider also exposed these animals to the same
schedule of NO and added ammonia. Nitrogen oxides reacted with ammonia (1,000 ug/m ; 1.4
ppm), reducing the lipid and electrolyte disturbances seen with NO exposure alone. Blood
serum lipids, lipoproteins, and cholesterol were not significantly altered from those of con-
trol guinea pigs breathing filtered clean air. There was a decrease in the urinary excretion
of nitrites, nitrates, and coproporphyrin from NO -ammonia treated animals. Blood serum
A
sodium and potassium were lowered, while magnesium and calcium were higher than controls. No
effect on serum calcium levels was seen with NO alone. Liver mitochondria contracted, in
contrast to the edematous state seen in NO -exposed groups. Earlier, Kosmider et al. (1973a)
also reported a general decrease in protein synthesis evidenced by decreased serum proteins
and declining body weights of guinea pigs exposed continuously to 1,880 ug/m (1 ppm) N02 for
6 months.
An interesting observation of proteinuria in the guinea pig was reported by Sherwin and
Layfield (1974) who found consistently higher levels of urinary protein (p < 0.01) in animals
14-67
-------
breathing 940 ug/m (0.5 ppm) NO, continuously for 7 to 14 days. Proteinuria was detected in
3
another group of animals exposed for 4 hours per day to 750 |jg/m (0.4 ppm) N0? (p < 0.05).
Disc electrophoresis of the urinary proteins demonstrated the presence of albumin, and alpha,
beta, and gamma globulins. The presence of high molecular weight proteins in urine is charac-
teristic of the nephrotic syndrome. Histopathological studies of the kidney were negative.
The influence of NO, on pentobarbital (PEN)-induced sleeping time was investigated in mice.
3
(Miller et al., 1980) A 3-hour exposure to concentrations as low as 470 ug/m (0.25 ppm) NCL
caused a significant increase in PEN-induced sleeping time in female mice. No significant
effects on PEN-induced sleeping time in females were detected after 1 or 2 days (3 hr/day)
3
exposure to 235 ug/m (0.125 ppm) NO,. None of the exposure regimens affected the time
3
required for the drug to induce sleep. Two or three days (3 hr/day) exposure to 470 ug/m
(0.25 ppm) N02 caused no significant effect in female mice. This trend of a reduction or
disappearance of the effect after repeated exposure was observed at other, higher, con-
centrations also. When the effects of repeated daily exposures (3 hr/day) to 9,400 (jg/ni (5
ppm) NO- were compared in male and female mice, the females had a significantly increased
PEN-induced sleeping time after 1 and 2 days of exposure. However, a significant increase in
PEN-induced sleeping time was not observed in males until the 3rd day of exposure. Since the
duration of PEN-induced sleeping time is primarily determined by hepatic mixed function
oxidase activity, it is possible that NO- may alter some aspects of xenobiotic metabolism.
Ozone (Graham, 1979) also increased PEN-induced sleeping time in female, but not male,
mice. Unlike NO, however, as the concentration was decreased, an increased number of daily
3
3-hr exposures were needed to observe the effect. For example, at 490 ug/m (0.25 ppm) 0,, a
significant effect was observed only after 6 and 7 days (3 hr/day) of exposure. Thus, for
this model system, a single exposure of N02 caused more effect than a single exposure to 0,.
14.2.4.4 Teratogenesis and Mutagenesis—There is little or no evidence in the literature
demonstrating that exposure to NO, is teratogenic or mutagenic in animals. Shalamberidze and
3
Tsereteli (1971) exposed rats to 2,360 ug/m (1.3 ppm) N02, 12 hours/day for 3 months at which
time exposure ceased and the animals were bred.- Long-term N02 exposure had no effect on
fertility. There was a statistically significant decrease in litter size and neonate weight
(p < 0.001). J_n utero death due to N02 exposure resulted in smaller litter sizes, but no
direct teratogenic effects were observed in the offspring. In fact, after several weeks,
N02-exposed litters approached weights similar to controls. (See Table 14-17.)
Gooch et al. (1977) exposed C3H male mice to 190, 1,880, 9,400, and 18,800 ug/m3 (0.1, 1,
5, and 10 ppm) N02 for 6 hours. Blood samples were obtained at 0 time, and 1 week and 2 weeks
post-exposure. Mouse leukocyte chromosomal analysis revealed that N0? did not increase
chromatid- or chromosome-type alterations. The analysis of primary spermatocytes showed no
direct effect of N02 exposure on their chromosomes. Therefore, in these experiments, N02
exposure did not induce mutagenesis. (See Table 14-17.)
14-68
-------
TABLE 14-17. STUDIES OF POILNT1AL MUIAGENES1S, IER/UOGLNLS1S
Pol lutant
Concen tra tion
Pol lutant
NO
NO
1
9
18
9
pg/m •'•
190
,880
,100
,800
,100
ppm
0.1
1
5
10
5
Exposure Species
E
6 hr Mouse 2 wk post-e
or chr
Meet
xposure no
increase-
omosome- type alterat
primary spe
noted.
Continuous, Rat Appearance
to 11 wk shape
of 2
rmatocytes.
No
of hyperplastic
to 4 layer
ions
in
in
chromatid
leukocytes or
Reference
Gooch et a 1 . .
1977
mutagenic effects
loci
pyrami ds
i n
by
the
3 wk.
Rejthar and
Rejthar, J97!>
i
Oi
N0
N0
9,100 to
18.800
18,800
18,800
5 to
10
10
10
2 hr/day,
5 day/wk,
50 wk
2 hr/day,
5 day/wk,
50 wk
Mouse
Mouse
Continuous from Rat
pregnancy to
3 mo after delivery
Decreased ciliated cells.
Extensive hyperplasia (3 to 1 layers of
epithelium), cubciidal metaplasia in ad-
jacent alveoli by 6 wk.
Hyperplasia in all bronchioles,
decreased bronch iolar luinina, polymorphous
epithelium extensive by 7 wk. Terminal
brohchiolar epithelium contained only
2 or 3 irregular layers, increased number of
ciliated cells by 9 wk. By 11 wk return to
1 layer epithelium. Lungs at indefinite state
of repair from week 7 on.
Mice given 1-nitroquinoline-1-oxide and
N0?; N0_ had no effect on tumor production.
Mice given 4-nitrogutnoline-1-oxide
(carcinogenic agent) + NO, decreased
incidence of lung tumors.
Decreased litter size and increased moi—
tality of neonates up to 15 days post
deIivery.
No teratogenic effects noted.
Ide and Otsu,
1973
Otsu and Ide,
1975
Freeman et al .
]971b
-------
TABLE 14-17. (continued)
Pollutant
Auto Exhaust
CO 58
NO
CO. (0.07 and
Aldehydes
Pollutant
Concentration
ug/m3 ppm Exposure
,000 50 6 hr/day.
5 days/wk,
2.5 mo to
(0.2 2 yr
and
23)
(0.1
and
2.0)
Species Effect Reference
Rat Auto exhaust had no biological effects when Stupfel et al.,
NO was 0.2 ppm. 1973
Exposure to NO (23 ppm) increased number of
spontaneous tuffiors, cutaneous abscesses,
and bilateral renal sclerosis.
No tumors or abscesses in lungs.
-------
14..2.4.5 Effects of NO., on Body Weights—Dogs, rabbits, guinea pigs, rats, hamsters, and mice
have been exposed to 100 to 47,000 |jg/m N0? (0.05 to 25 ppm) up to 18 months without reported
body weight loss (Nakajima et al., 1972; Shalamberidze, 1969; Wagner et al., 1965). (See Table
14-18.) Oda et al., (1973) however, observed reduced body weights of rats exposed to ambient
3
air containing 135 ug/m (0.07 ppm) NOp amongst other pollutants over a 100-day period.
14.3 DIRECT EFFECT OF COMPLEX MIXTURES
The oxidation of organic substances contained in solid, liquid, and gaseous fuels, as
well as the reaction of atmospheric oxygen and atmospheric nitrogen at furnace temperatures,
are sources for complex mixtures of nitrogen oxides in the atmosphere. Vehicles and power
plants release large amounts of nitrogen oxides into the atmosphere. The biological and/or
toxicological effects of the combination of these nitrogen oxides with other pollutants is the
scope of this section. Much of the research reported here was conducted with complex pol-
lutant mixtures and had no single-pollutant controls. Thus, the precise contribution of the
given level of N02 to the effects observed is not possible to discern. However, in some of
these studies, NO concentration was varied between groups or NO was present in one group and
A X
absent in another. In these instances, the influence of NO can be elucidated.
Emik et al. (1971) noted that males of the C57B1/6 strain of mice exposed to ambient air
in California died sooner than either C57B1/6 females or males and females of the A and A/J
strains exposed to clean, filtered air. Guinea pigs and other strains of mice demonstrated no
difference in survival when exposed to clean or polluted air. Concentrations of about 40
ug/m (0.02 ppm) N0~ were observed during the study. A number of other pollutants were also
present.
Loosli et al. (1972) exposed specific pathogen-free mice to synthetic smog 23 to 24
3 3
hours/day for 8 to 12 months. The smog was composed of 1,500 ug/m (0.8 ppm) N09, 5,750 ug/m
•D -D t-
(5 ppm) CO, 760 ug/m (0.38 ppm) 03, and 5,700 ug/m (2.2 ppm) S02- The lungs of mice exposed
for 20 days had thickened bronchial membrane due to cell proliferation. By 60 days the
membranes were markedly thickened and appeared to have villus-like hyperplastic folds, whereas
evidence of hyperplasia in control animals was .absent. When mice were removed from smog
exposure after 4 months, the hyperplasia regressed.
Hysell et al. (1975) studied the toxicological effects on animals of automotive
emissions, with or without a catalytic converter and with or without irradiation. Female
lactating rats and their 2-week-old offspring were exposed for 7 days. Infant mortality was
increased following exposure to auto emissions containing 9,400 ug/m (5 ppm) N02 without
catalytic conversion, whereas mortality was not affected in animals exposed to emissions
modified by catalytic conversion. Adult male rats and hamsters were exposed to these regimens
for 6 days. An increase in hemolysis-resistant RBC due to high ambient CO followed exposure
to raw exhaust with no catalyst. Blood eosinophils in rats exposed to converted exhaust were
not affected. Animals developed extensive pulmonary changes when exposed to irradiated,
unconverted auto exhaust. Hamsters developed purulent bronchitis, bronchiolitis, and broncho-
14-71
-------
TABLE 14-18. EXTRAPULMONARY EFFECTS OF N02: BODY WEIGHT
N02
Concentration
pg/m3
100
135
1,300 to
1,500
1,900 to
47,000
E 18,800
ro
18,800
24,000
ppm
0.05
0.072
0.7 to
0.8
1 to
25
10
10
12.5
Exposure
90 days
Continuous,
100 days
30 days
18 mo
From birth
to 62 days
Continuous,
90 days
Continuous,
213 days
Species
Rat
Rat
Mouse
Dog, rabbit,
guinea pig,
rat, hamster
mouse
Rat
Cynolmogus
monkey
Rat
Effect
No effect.
Ambient air exposure (6.3 ppm CO, 0.206 ppm NO,
0.047 ppm S0?, 0.0048 mg/m acid mist and 0.88
mg/m dust) Decreased body weight.
No effect.
No effect
Decreased body weight and length of pups.
In combination with heat stress decreased body
weight.
Decreased body weight.
Reference
Shalamberidze, 1969
Oda et al. , 1973
Nakajima et al. ,
1972
Wagner et al. , 1965
Freeman et al . ,
Coate and Badger
1974
Freeman and
Haydon, 1964
1974b
t
-------
pneumonia when exposed to such exhaust. An initial increase in the number of alveolar
macrophages at the level of the terminal bronchioles, a proliferation of respiratory
epithelium in the ducts, and a thickening of the alveolar septae were observed.
Extramedullary hematopoiesis in rat livers resulted from high CO concentrations. Occasional
degenerative changes in renal and hepatic tissue were also seen in these animals.
Lee et al. (1976) exposed lactating rats 24 hours/day for 7 days to auto emissions with
and without catalytic conversion and with and without irradiation. Nitrogen dioxide
concentrations in the unconverted auto exhaust were 8,650 and 9,780 |jg/m (4.6 and 5.2 ppm)
for the irradiated and non-irradiated samples, respectively. For exhausts with catalytic
3
conversion, N0~ concentrations were 5,640 and 3,380 ug/m (3 and 1.8 ppm) for irradiated and
non-irradiated samples, respectively. Animals exposed to unconverted auto exhaust, whether
irradiated or not, had a significant decrease in body weight by day 7 (p < 0.001). Exposure
to converted and irradiated exhaust also produced a significant loss in weight (p < 0.02), but
the presence of the converter was associated with less weight loss. Exposure to CO (575
mg/m ; 500 ppm) did not significantly alter body weight. Animals exposed only to raw exhaust
or 575 mg/m (500 ppm) CO had hematocrit levels (p < 0.001) significantly elevated above
controls by day 7. Exposure to raw exhaust enhanced serum lactate dehydrogenase activity
(LDH), whereas CO had no such effect. Serum glutamate-oxaloacetate transaminase (SGOT) was
not affected by any exposure regimen. Reduction of effects in converted exhaust-exposed
groups was attributed to the decreased CO levels in the chamber.
Stupfel et al., (1973) in two separate experiments, exposed specific pathogen-free rats
to auto exhaust fumes 6 to 8 hours/day, 5 days/week, for periods of 2.5 months to 2 years.
The exhaust gas contained either 0.2 or 23 ppm N0x, 0.07 or 0.37 percent C02, 58 mg/m (50
ppm) CO and 0.1 or 2 ppm aldehydes. With low concentrations of NOX, no biological effects
were observed. When NO was increased to 23 ppm, body weight was reduced and spontaneous
tumors and emphysema were increased. The heart rate and the QRS wave of the EKG were not
affected. Sound avoidance reflexes were decreased.
Cooper et al. (1977) exposed rats 24 hours/day for 38 to 88 days to automobile exhaust
with and without catalytic converters. During three experiments, N02 levels were 564, 752,
and 9,588 ug/m3 (0.3, 0.4, and 5.1 ppm); nitric oxide (NO) levels were 8,733, 13,284, and
10,209 (jg/m3 (7.1, 10.8, and 8.3 ppm); and total hydrocarbon levels were 16, 14, and 50 ppm
(methane). Spontaneous locomotor activity, as measured by standard running wheels, was 63,
54, and 64 percent of control values, respectively. The authors concluded that the
suppression of activity was primarily related to either hydrocarbon or nitrogen oxide
compounds of the exhaust. However, it should be noted that a 10-fold increase in N02 did not
result in a further reduction in activity levels.
Murphy (1964) investigated the effects of a 4-hour exposure to irradiated or raw auto
exhaust on pulmonary function of guinea pigs. Since irradiated exhaust produced more changes,
14-73
-------
subsequent studies were performed with irradiated exhaust maintained at equilibrium values or
at cyclic values. For the equilibrium group, the following pollutant concentrations were mea-
sured: 2.42 ppm formaldehyde, 0.2 ppm acrolein, 0.8 ppm oxidant, 5,000 ug/m (2.66 ppm) NO,,,
and 300 ppm carbon monoxide (CO). For the "cyclic" exposure, concentrations varied: 1.3 to
1.9 ppm formaldehyde, 0.06 to 0.1 ppm acrolein, 0.56 to 0.95 ppm oxidant, 1,485 to 4,079 ug/m
(0.79 to 2.17 ppm) NOp, and 150 to 250 ppm CO. Flow resistance was increased in both exposure
groups with the equilibrium condition causing a more rapid and greater increase. During the
first 1.5 hours of exposure, breathing frequency decreased, with the greater change occurring
under equilibrium exposure conditions. For equilibrium exposure these values remained de-
pressed, whereas in the cyclic group frequency increased. Increases in tidal volume were
observed in both groups after 1.5 hours of exposure; in the cyclic group tidal volumes had
decreased below control by 2.5 hours.
Beagles were exposed to auto exhaust and pollutant mixtures, 16 hours/ day, for 61
months. Pulmonary function studies were made at 18, 36, and 61 months of exposure (Lewis et
al., 1974; Vaughan et al., 1969). The animals were allowed to recover for approximately 2
years (Gillespie et al. , 1976) and were then examined again. Only those results related to
NO will be described here. The results of this study have been described in full by several
3
authors (Stara et al. , eds. , 1980). The high NO, group was exposed to 1,210 ug/m (0.64 ppm)
T "?
NO, plus 310 ug/m (0.25 ppm) NO. The low N00 group was exposed to 270 ug/m (0.14 ppm) N09
3 168
plus 2,050 ug/m (1.67 ppm) NO. Vaughan et al. reported no alterations in CO diffusing
capacity, dynamic compliance, or total expiratory resistance to air flow after 18 months of
exposure. By 36 months, (Lewis et al., 1974) analysis of variance indicated no significant
changes; however, a significant number of animals exposed to high N0? and low NO had an
abnormally (p < 0.005) low CO diffusing capacity. More changes were observed after 61 months
of exposure (Lewis et al., 1974). In the dogs breathing the low N02 and high NO and raw auto
exhaust, with and without SO , residual volume was increased (p < 0.05) compared to animals
exposed to air or high N0? and low NO (p < 0.05). The common treatment factor causing this
effect appeared to be the higher concentration of NO. Irradiated auto exhaust exposure
increased (p < 0.05) the mean nitrogen washout values. A significant number of beagles
exposed to high NO,, and low NO had a lower mean carbon monoxide diffusing capacity/total lung
capacity and a lower peak flow rate compared to control. A number of alterations in pulmonary
function were found in other exposed groups. The authors attribute the results observed in
the dogs exposed to high NO^-low NO to an alteration of the alveolar capillary membrane.
After the 61-month exposure terminated, the animals were allowed to recover for 2 years
before pulmonary function measurements were made again (Gillespie et al., 1976). In several
instances, alterations occurred during this recovery period. In all pollutant-exposed dogs,
total lung capacity was increased relative to the control group of animals. Those animals
which received the NO- and NO mixtures experienced modest increases in inspiratory volume,
vital capacity, and total lung capacity. Other groups of animals also had a number of
changes.
14-74
-------
Orthoefer et al., (1976) utilizing the same beagles exposed for 68 months, evaluated
biochemical alterations 2.5 to 3 years after the animals had recovered. In groups exposed to
irradiated auto exhaust with and without SO and high N09 with low NO, there was a rise (p
A £.
<0.05) in lung prolyl hydroxylase (the rate-limiting enzyme for collagen synthesis). A high
correlation was seen between lung weights and hydroxyproline content in animals exposed to
NO . No effects were observed in the hydroxyproline/total ninhydrin reactive material.
A
Histological and morphological examinations revealed no significant differences in collagen
content of exposed tissues. No difference was seen in the collagen/protein ratios between
tissues.
Beagle lung morphology was evaluated by Hyde et al. (1978) 32 to 36 months after the
68-month exposure period terminated. Several morphometric parameters were affected, but only
those relating to NO will be described here. In the high N09 group, there were increases
" £.
(p <0.05) in total lung capacity and right lung volume and decreases (p <0.05) in the surface
density of the alveoli and the volumetric density of parenchymal tissue. For the high NO
group, there were no significant changes in the morphometric parameters examined. Alveoli
were enlarged in both the high N0~ and high NO groups. In the high NOp but not the high NO
groups, there was increased ciliary loss without squamous metaplasia and nonciliated
bronchiolar cell hyperplasia. In the high NO group, there were lesions in the interalveolar
pores. In the most severely affected lungs of dogs in the high N02 group, morphological
changes considered to be analogous to human centrilobular emphysema were present. Since these
morphometric/ morphologic measurements were made after a 2.5 to 3 year holding period in clean
air, it is not known whether these disease processes abated or progressed over the clean air
period.
Coffin and Blommer (1967) investigated the effects of a 4-hour exposure to irradiated
auto exhaust containing varying concentrations of N09, NO, CO, and oxidant on mice which were
3
also challenged with S. pyogenes. Those mixtures containing greater than 752 ug/m (0.4 ppm)
N02 and 25 |jg/m3 (0.02 ppm) NO in the presence of 115 ug/m3 (100 ppm) CO and between 0.52 and
0.67 ppm oxidant caused an increase in mortality (p < 0.05). Mixtures of N02 and NO at lower
concentrations were not tested. Other pollutant combinations were also tested. Concentra-
tions between 376 and 1,500 ug/m (0.2 and 0.8 ppm) N09, 0.15 and 0.48 ppm oxidant, and 29 and
3
115 ug/m (25 and 100 ppm) CO were found to increase mortality in the infectivity model.
Using the infectivity model in which the mortality of pollutant-exposed mice challenged
with S. pyogenes is measured, Ehrlich et al. (1977) investigated the effects of combinations
of 03 and NO-. Mice were exposed for 3 hours to various concentrations of the gases alone and
in combination. The lowest concentrations causing a significant enhancement of mortality were
o 3
a mixture of 98 ug/m (0.05 ppm) 0-, and 3,760 ug/m (2 ppm) N09. The effect was additive.
3
This concentration of 0, alone caused no significant change; 3,760 ug/m (2 ppm) NOp, however,
resulted in a significant enhancement of mortality. Multiple 3-hour daily exposures also were
tested. With the mixture of 98 ug/m3 (0.05 ppm) 03 and 3,760 ug/m (2 ppm) N02, excess
14-75
-------
o
mortalities were evident after five daily exposures. At 196 ug/m (0.1 ppm) 0, plus 2,800
3
ug/m (1.5 ppm) N02, there was a significant effect when the mice were examined after 20 daily
exposures, but not after 10. In the latter case, the author attributed the effect to the
presence of 0,; in the former case, the author suggested a synergistic relationship. When
03
mice were exposed to a combination of 6,580 ug/m (3.5 ppm) N02 and 980 ug/m (0.5 ppm) O, for
3 hours, followed 1 hour later by challenge with S. pyogenes, bacterial clearance from the
lung was reduced. Control mice cleared 50 percent bacteria from the lungs in 81 minutes.
Exposed animals took 131 minutes to clear the same amount of bacteria. When the NO., con-
3 e. .,
centration was reduced to 3,760 ug/m (2 ppm) and the initial 0^ concentration was maintained,
no distinguishable effect on bacterial clearance was observed.
Ehrlich et al. (1979) used another exposure regimen of NO^-Og combinations to evaluate
effects with the streptococcal infectivity model. For 1, 2, 3, and 6 months, mice were ex-
3
posed continuously to 188 ug/m (0.1 ppm) N02 on which were superimposed peaks (3 hr/day, 5
days/wk) of either 940 ug/m3 (0.5 ppm) N02 or 940 ug/m3 (0.5 ppm) N02 plus 196 ug/m3 (0.1 ppm)
0.,. Other groups received the peak exposures only. After the indicated exposure period, mice
received S. pyogenes and were observed for mortality over a 14-day period in clean air. For
the 1- or 2-month exposures the only significant (p <0.05) change was a decrease in mortality
after 1 mo. of peak exposure to the N0? + 0-, mixture. After 3 mo., the peak exposures to N0?
only or N02 + 0., increased (p <0.05) mortality. At the same time, there was a decrease
(p <0.05) in mortality in the group exposed to a baseline of N02 with peaks of either N02 or
N02 + On. However, mortality increased (p <0.05) after 6 mo exposure to N02-0., peaks, with
or without the baseline of N02. In another set of experiments using identical exposure regimens,
the mice were returned to their respective pollutant exposures over the 14-day observation
period following bacterial challenge. In these studies, the increased susceptibility to in-
fection occurred earlier compared to those animals held in clean air for the 14 day period.
Generally in these animals, the most changes occurred in the group receiving the N02 + 0^
peak, and there was an increased response as exposure length increased. When the peak of NOp
+ 0., was superimposed on a baseline of N02, the response was reduced, although it did increase
with time. The effects in the peak of N02 group were roughly equivalent to those in the group
receiving a baseline of N02 with an N02 peak superimposed. These exposure regimens also
affected alveolar macrophages. For example, the most extensive effect occurred after a 3 mo.
exposure to the peak of 0, + NO,,. There were decreases (p <0.05) in the number of recoverable
alveolar macrophages, their percent viability and percent phagocytosis. Lung morphological
changes in infected mice were also observed using scanning electron microscopy. Marked
changes were observed after 3. mo. of exposure to a baseline of N02 or air on which were
superimposed peaks of N02 + 0,. Alveolar pores were greatly enlarged in some areas. Adjacent
to these areas, alveolar walls were thickened and fused with smaller pores. Peak exposures to
N02 only caused less extensive effects.
14-76
-------
, Goldstein et al. (1974) found that mixtures of N02 and 0., would decrease bactericidal
activity of the lungs. Mice received S. aureus aerosols before a 4-hour pollutant exposure.
Reductions (p < 0.01) in bactericidal activity of 36.9 and 111 percent were seen after
exposure to 7,520 ug/m3 (4 ppm) NO, plus 600 pg/m (0.36 ppm) 0,, and after 12,860 ug/m (6.84
3
ppm) NO- plus 760 ug/m (0.39 ppm) 0, respectively. Lower gas concentrations had no effect.
The protocol was then changed so that mice were exposed to pollutants for 17 hours before S.
aureus challenge. Bactericidal activity was generally more impaired at higher gas concentra-
tions. The lowest gas concentrations to cause a significant effect (p < 0.05) were 4,320
3 3
ug/m (2.3 ppm) N0~ plus 390 ug/m (0.2 ppm) 03 which decreased bactericidal activity 13 per-
cent. However, decreases in pulmonary bacterial deposition were observed at these concentra-
tions. It is the authors' contention that this latter effect is due to ventilatory defects
induced by 0, alone, whereas the reduction in bactericidal function is equivalent to the
injury that would be expected from each individual gas.
2
Furiosi et al. (1973) exposed monkeys and rats to aerosols containing 330 (jg/m (0.14
ppm) NaCl and 3,760 ug/m (2 ppm) N09 continuously for 14 months in order to delineate the
3
effect of particulate aerosols on NO- toxicity. Of the total NaCl aerosolized, only 5 (jg/m
('< 0.001 ppm) had a particle size between 5 and 10.3 microns, with the remainder being
smaller. NaCl aerosol alone had no effect on the experimental animals. Following 14 months
exposure, the bronchiolar epithelium was hypertrophic to similar degrees in monkeys exposed to
N02 or N02 in the presence of NaCl. With only half the concentration of NaCl and N02, rats
exposed to these agents revealed marginal results. Animals exposed to NO- with and without
NaCl developed polycythemia with reductions in mean corpuscular volumes although mean corpuscu-
lar hemoglobin concentration was normal.
Kosmider et al. (1973a) exposed guinea pigs 8 hours/day for 6 months to 1 ppm oxides of
nitrogen (NO- + N?0.) or 1 ppm oxides of nitrogen (NO- + N-0.) plus a somewhat larger quantity
of ammonia. The oxides of nitrogen alone decreased animal body weight gain over the 6-month
period; 62 grams versus 395 grams for controls and 120 grams for NO plus ammonia. Reduction
in total serum protein was observed with a marked decrease in the levels of albumin, alpha-2
and gamma globulins and with an increase in alpha-1 and beta fractions. Higher incidences of
spontaneous infections also were observed. Disorders in acid-base balance were reported.
Increased appearance of urobilinogen, acid mucopolysaccharides, and hydroxyproline was
observed. Hemorrhage and emphysematous-1ike conditions were noted in the lungs of NO -exposed
animals. Emik et al. (1971) reported that alkaline phosphatase activity decreased in the
2
lungs of rats exposed 2.5 years to ambient air containing approximately 36 ug/m (0.019 ppm)
N02, 0.011 ppm NO, 03, PAN, etc.
Antweiler and Brockhaus (1976) exposed female guinea pigs 6 days/week for 6 months to
o ' o
10,000 ug/m (3.8 ppm) S02, 10,000 M9/m (5-3 ppm) N02, or a combination of the two pollu-
tants. After 6 months of exposure, there were no effects on respiratory frequency, flow rate,
or minute volume, nor were there increases in mortality or difference in weight gain between
treated and control animals.
14-77
-------
, Shalamberidze and Tsereteli (1971) reported on the effects of low concentrations of S0?
and NO, on the estrous cycle and reproductive functions of rats. Female albino rats were
3
exposed 12 hours/day for 3 months to one of the following: (1) 2,360 ug/m (1.3 ppm) N02; (2)
5,000 ug/m3 (1.9 ppm) S09; (3) 160 (jg/m3 (0.06 ppm) S09 ; (4) 130 (jg/m3 (0.07 ppm) NO,; (5)
11
2,500 ug/m (0.95 ppm) S02 and 1,130 ug/m (0.6 ppm) N02> Low concentrations of S02 and N02
did not affect the rats' estrous cycle or induce morphological changes in reproductive organs.
Exposure to high concentrations did alter the estrous cycle. Estrus was less frequent, more
prolonged, and occurred at lengthened intervals. At 7 months after exposure, the estrual
indices returned to normal. Morphologically, changes included a depletion of glandular
epithelium in the uterus as well as a depletion of thyroid connective tissue between follicles
with a mild cellular degeneration of the adrenals, ovaries, and uterus. The number of ovarian
primordial follicles was also decreased. Long-term exposure had no effect on the rats'
ability to conceive, although litter size and average weight of progeny were significantly
reduced (p < 0.001).
Oda et al. (1975a; 1975b) exposed female mice and male rats and rabbits for 1 hour to
13,040 ug/m3 (10.6 ppm) NO containing 1,500 ug/m3 (0.8 ppm) N02- Shortly after NO exposure,
mice and rats had increased nitrosylhemoglobin (NOHb). Production of NOHb was proportional to
the concentration of NO. Within 20 minutes equilibrium was reached, with NOHb being 0.13
percent of total hemoglobin. NOHb levels declined rapidly when mice were placed in clean air
for 1 hour. NOHb had a half-life of 10 minutes. NOHb was not detected in rabbits until
reduced j_n vitro with sodium dithionate.
14.4 NITRIC OXIDE
The toxicological data base of nitric oxide (NO) is not extensive and most of it has been
done in recent years. (See Table 14-19.)
3
Azoulay et al. (1977) exposed rats continuously for 6 weeks to 2,460 ug/m (2 ppm) NO.
Following exposure, no significant differences were seen in blood oxygen saturation, pH,
oxygen combining capacity, 2,3-diphosphoglycerate, ATP, glucose, lactate, hemoglobin
concentration, hematocrit, and red blood cell cpunt. Methemoglobin was not detected. No
striking histological changes were found in the lungs until 2 weeks of exposure. At this
time, 3 of 4 exposed and 1 of 4 controls appeared to show inflammatory changes including
cellular infiltration of alveolar cells. Inflammatory changes, including cellular
infiltration of alveolar walls and areas of intra-alveolar edema, were observed. Following 3
weeks of exposure to NO, animals evidenced some emphysemic-like changes with increased
incidence until 6 weeks of exposure. Hugod (1979) exposed rabbits continuously for 6 days to
•3 O
52,890 ug/m (43 ppm) NO and 6,768 ug/m (3.6 ppm) NO^. No significant effect on lung
morphology was observed following exposure.
Arnold et al. (1977b) and Braughler et al. (1979) exposed various tissues from male rats
iji vitro to 25 to 250 ul NO gas for 10 seconds. The activity of guanylate cyclase (GC) (an
enzyme that forms cyclic GMP, an important biochemical regulator of cells) in various tissues
14-78
-------
TABLE 11-19. NITRIC OXIDE
Pol 1 ulan I
Concentration
Pollutant jig/in1 ppm
NO 2,160 2.0
Exposure Species
Continuous, Rat
6 wk
Effect
Cellular infiltration of alveolar walls and
areas of intra-alveolar edema observed after
Reference
Azoulay
et al. , 1977
NO
9,170
7.7
8 hr/day,
120 days
Guinea pig
2 wk. After 3~wk exposure, emphysema-1 ike
changes observed until 6 wk. Melhemoglobin
undetected. No differences in blood oxygen
saturation, pH, oxygen combining capacity,
ATP, 2,3-diphosphoglycerate, glucose, lactate,
hemoglobin concentration, hematocrit, or
RBC count.
Decreased blood sodium, magnesium, and chloride;
decreased Zn and Mg in brain and liver.
Increased blood calcium and urinary
excretion Mg.
Kosmider and
Chorazy, 1975
-p»
1
to
NO
N00
NO
13,010 + 10.6
1,500 0.8
11,800 12
1 hr
5 hr
Mice, female;
Rat, male;
Rabbit, male
House
NO
NO*
NO.
19,700
61,500
52,890
6,768
to 16 to
50
+ 13 +
3.6
4 hr
Continuous ,
6 days
Guinea pig
Rabbit
Mice and rats showed increased nitrosyl hemoglo- Oda et al.,
bin (NOHb); NOHb related to concentration of NO. 1975a
By 20 minutes eguiIibratcd, 0.13% total nemo- Oda et al. ,
globin. NOHb half-life 10 minutes. No NOHb 1975b
produced in rabbits exposed to NO until sodium
dithionate added to blood.
Edema and dilation of vessels in submucosal Udai et al.,
tissue of trachea. Congested alveoli. 1973
24 hr later proliferation of tracheal
mucosal epithelium.
Anomalies in CNS, heart and cell metabolism.
No significant alteration in Murphy et al.
respiratory rate or tidal volume. 1964
No effect on lung morphology. Hugod,
1979
-------
was, increased in proportion to the dose of NO. The levels of this enzyme were increased 19-
to 33-fold in supernatants of liver, lung, tracheal smooth muscle, heart, kidney, cerebral
cortex, and cerebellum with increases of 5- to 14-fold in supernatant of skeletal muscle,
spleen, intestinal muscle, adrenal, and epididymal fat pads. Following NO activation, GC
activity decreased with a half-life of 3 to 4 hours at 4°C. When tissue was re-exposed, the
GC activity was reactivated. Braughler et al. (1979) also found that exposure of rat liver
fractions to 165 ul NO increased GC activity, but purification of the enzyme resulted in an
apparent loss of enzyme activation by NO. Restoration of this activity could be accomplished
with the addition of dithiothreitol, methemoglobin, BSA, or sucrose. Sodium nitrite increased
GC activity as well. Nitric oxide increased cyclic GMP (cGMP) but had no effect on cyclic AMP
(cAMP). Craven and DeRubertis (1978) exposed rat liver fractions to NO at the rate of 1
ml/min for 2 seconds and found similar increased activity in liver GC. They also found that a
nitrosyl-heme complex was formed during exposure.
Kosmider and Chorazy (1975) reported that following the exposure of guinea pigs to 9,470
ug/m (7.7 ppm) NO 8 hours/day for 120 days, blood sodium, magnesium, and chloride were
reduced with a significant rise in calcium. Liver and brain levels of magnesium and zinc were
reduced while there was an enhanced urinary excretion of magnesium.
14.5 NITRIC ACID AND NITRATES
Gray et al. (1952) conducted some of the earliest experiments investigating inhalation
toxicity for rats, guinea pigs, and mice exposed to N09 generated from nitric acid (HNO,).
£. o
(See Table 14-20.) No measurement of aerosol particle size was made. Results were expressed
as evidence of NO,, toxicity, whereas the experimental method could not adequately distinguish
3
the difference between N02 and HN03 effects. Concentrations of 17,000 and 26,000 ug/m (9 and
14 ppm) N09 administered 4 hours/day, 5 days/week for 6 weeks produced lung pathology. When
3
exposure concentration was reduced to 9,400 ug/m (5 ppm), no lesions were observed.
Gardiner and Schanker (1976) investigated the effects of nitric acid-induced lung damage
on the absorption of drugs from the lungs. Rats were given an intratracheal injection of 1
percent nitric acid solution (0.15 ml), and drug absorption rates from treated versus control
lungs were measured with time. One day following nitric acid exposure, there was significant
bronchiolar inflammation with inflammatory cell infiltration. The bronchiolar epithelium lost
its normal scalloped appearance and tended to have an increase in cellular cytoplasm.
Alveolar septae adjacent to inflamed bronchioles appeared broadened by enlarged or swollen
alveolar cells. Wet and dry weights of the exposed lungs did not differ. Treatment with
nitric acid enhanced the pulmonary absorption rates (20 percent) of p_-aminohippuric acid,
procaineamide ethobromide, procaineamide, and mannitol.
Sackner et al. (1976) exposed dogs for 7.5 minutes to an aerosol, with particles less
than 1 urn in diameter, containing 740 and 4,000 [jg/m (0.1 and 1 percent) of sodium nitrate in
order to observe potential effects on cardiopulmonary function. Sodium nitrate at either
concentration had no effect on functional residual capacity, static lung compliance, or total
respiratory resistance.
14-80
-------
TABLE 14-20. NITRIC ACID AND NITRATES
J>
I
CD
Pollutant
NO
generated
from HN03
HNO,
J
Sodium
nitrate
Pollutant
concentration
9,400, 17.000 or
26.000 ug/ni
(5, 9 or 14 ppra)
1% solution
(0.15 ml)
0.1 and 1.0% at
740 and ,
Exposure
4 hr/day,
5 days/wk.
6 wk
Intra-
tracheal
injection
7.5 min
Species
Rat, mouse.
guinea pig
Rat
Dog
Effect
No lesions at 9,400 ug/m (5 ppm).
Higher concentrations, increased lung pathology.
24 hr post-injection increased inflammation of
bronchioles; epithelium lost normal scalloped
appearance. Increased cytoplasm in epithelium.
Inflamed alveolar septae.
No difference in lung wet and dry weight.
Enhanced pulmonary absorption rates of
p-aminohippuric acid, procaineamide ethobromide,
procaineamide and mannitol.
No effect on pulmonary function.
Reference
Gray et al. ,
1952
Gardiner and
Schanker, 1976
Sackner et al. ,
1976
Sodium
nitrate
Ammonium
nitrate
Pb(N03)2
NaNO,3 2
KNO,
NH jNO-
0.1
and 1.0% at
740 and
4,000 pg/m
100
2,000
2,800
3,100
4,300
4,500
mM
pg/m,
Mg/m3
M9/"13
pg/m
30 min Guinea pig Accounted for 58% of total Charles and
histamine release. Henzel, 1975
Ammonium sulfate released.
3 hr Mouse After 14 days of observation, no effect on Ehrlich, 1979
mortality following challenge with S. pyogenes.
1,250 pg/mj
Increased mortality.
-------
Charles and Menzel (1975) incubated 100 mM ammonium nitrate with guinea pig lung frag-
ments for 30 minutes and measured the release of histamine. Ammonium nitrate released 58.1
percent of the total histamine.
Ehrlich (1979) investigated the effect of nitrates on resistance to respiratory infection
in mice. The animals were exposed to the compounds for 3 hr, after which they were challenged
with a viable aerosol of S. pyogenes, and mortality was determined after a 14-day observation
period. No significant effects were observed at the following maximal concentrations tested:
2,000 ug/m3 Pb(N03)2, 2,800 |jg/m3 Ca(N03)2> 3,100 ug/m3 NaN03, 4,300 ug/m3 KN03, and 4,500
ug/m NH.NO.,. However, zinc nitrate increased mortality in a significant linear concentra-
3
tion-related fashion with about 1,250 ug/m causing a 20 percent increase in mortality. This
result was similar to that of zinc sulfate. Thus, it appeared that the effect was more due to
the cation than the anion.
14.6 N-NITROSO COMPOUNDS
Reviews of the acute toxicity, carcinogenicity, mutagenicity, and detection of
nitrosamines have appeared recently. (Magee et al., 1976; Montesano and Bartsch, 1976; U.S.
Environmental Protection Agency, 1977) These compounds and nitrosamides are highly toxic and
potent carcinogens. N-Nitrosamines require metabolic activation to their mutagenic and carci-
nogenic active intermediates and are most toxic to the liver and kidneys. Nitrosamides, on
the other hand, tend to decompose at physiological pH, probably to active intermediates
similar to those produced from nitrosamines, and thus often act locally.
The detection of nitrosamines in food and water had promoted a broader search for their
presence in the environment. Evidence for the presence of dimethylnitrosamine in air has been
reviewed in the Scientific and Technical Assessment Report on Nitrosamines (U.S. Environmental
Protection Agency, 1977). Henschler and Ross (1966) investigated the possible formation of
nitrosamines from tissue amines exposed to N09. Mice were exposed intermittently to 75,200
3
ug/m (40 ppm) N0? for 38 hours every tenth day for periods up to 1.5 years. No lung tumors
were found in exposed animals. In fact, when compared to controls, there was a slight inhibi-
tion of the formation of lung adenomas and spontaneous skin fibro-adenomas. The formation of
nitrosamines by reaction of amines with nitrogen oxides has been observed in the laboratory
but not in the atmosphere (Challis, 1977; Gehlert and Rolle, 1977). Nitrosamines would not be
expected to accumulate to any great extent in ambient air because they are readily decomposed
by sunlight (Chow, 1973; Polo and Chow, 1976). Kaut (1970) examined the lungs of rats exposed
for 3 hours to mixtures of 10,000 to 500,000 ug/m nitrogen oxides for the presence of nitroso
compounds. None of the compounds were found i_n vivo, whereas they were found J_n vitro when
lung homogenates were exposed to high concentrations of nitrogen oxides (15 percent).
The nitrosamines are acutely toxic with a single oral dose of 27,000 to 41,000 ug/m
being the LD50 for dimethylnitrosamine to the rat. Diethylnitrosamine, another compound
detected in the air, is much less toxic with an LD50 of 216,000 ug/m3 (Heath and Magee, 1962).
Inhalation toxicity has not been reported. Industrial use of nitrosamines as solvents suggest
14-82
-------
that they are rapidly absorbed and exert their toxic action equally well on inhalation and
ingestion. These compounds were acutely toxic to every animal species tested and were also
poisonous to humans (Barnes and Magee, 1954; Freund, 1937).
Nitrosamines have caused hepatotoxicity, including the formation of "blood cysts", which
are the necrotic areas of parenchyma filled with recently extravasated erythrocytes, and
central and sublobular hepatic necrosis. Renal tubule damage is the dominant feature of the
kidney damage. Dimethylnitrosamine produces venous occlusions in the liver (McLean et al.,
1965). Ultrastructural changes in the liver after diethyl- and dimethylnitrosamine include
separations of the fibrillar and granular components of the hepatocyte and the formation of
electron dense plaques at the periphery of the nucleolus (Svoboda and Higginson, 1968).
Lysosomal alterations occurred within 35 minutes of exposure to dimethylnitrosamine and
reached a maximum at 12 hours (Svoboda and Higginson, 1968).
Nitrosamines and nitrosamides (N-nitroso compounds) have induced tumors in a wide variety
of organs of experimental animals, often at organs distant from the site of administration.
Single or repeated inhalation exposures to dimethylnitrosamine resulted in tumors of the nasal
cavities and kidneys (Druckrey et al. , 1967). N-Nitrosoheptamethyleneimine produced squamous
neoplasia of the lung in rats, histologically similar to human lung cancer (Lijinsky et al.,
1969).
Many N-nitroso compounds are mutagenic if assayed by the appropriate system. Bacteria,
in general, are not capable of activating nitrosamines, and such assay systems therefore
require supplementations with animal-derived activating enzymes to detect the mutagenicity of
these compounds. Nitrosamides, which will spontaneously decompose in the bacteriological
medium, do not require enzyme activation. More than 20 N-nitroso compounds have been shown to
be mutagenic in microbial systems (McCann et al., 1975).
N-Nitroso compounds are also teratogens. The nitrosamide, N-nitrosoethylurea, given to
rats on the 12th day of gestation (Napalkov and Alexandrov, 1968) or N-nitrosomethyl-urea
given on the 13th or 14th (von Kreybig, 1965) can cause fetal death and resorption and, for
the progeny which do reach term, a variety of malformations.
The N-Nitroso compounds, therefore, are an important class of chemical carcinogens for
the following reasons:
Most vital tissues are susceptible to the carcinogenic action of this class of compounds.
Bone can be included in this list, based on the recent finding that l-(2-hydroethyl)-l-
nitrosourea induced osteogenic osteosarcomas or chondrosarcomas of the lower vertebrae in rats
(Pelfrene et al., 1976).
In several instances, a single exposure to neonatal animals has induced tumors as the
animals reached adulthood (Druckrey et al., 1963; Magee and Barnes, 1959). Single-exposure
induction of tumors can also occur in adult rats that are pregnant (Druckrey et al., 1967) or
recovering from a partial hepatectomy (Craddock, 1971).
14-83
-------
. N-Nitroso compounds can induce cancers transplacentally. Brain and spinal cord tumors
(Ivankovic and Druckrey, 1968) and renal tumors (Wrba et al., 1967) were found in progeny of
pregnant rats treated with N-nitrosoethylurea. Diethylnitrosamine has transplacentally
induced trachea! papillomas in rats (Mohr et al., 1966).
Small amounts of carcinogenic nitrosamines have been detected in some samples of urban
air (Fine et al., 1976) and in the food supply (Crosby and Sawyer, 1976).
N-Nitroso compounds could present a hazard, not only because people are exposed to these
compounds but also because they can be produced i_n vivo, at least in experimental animals.
Nitrosation reactions are catalyzed by acid and hence should occur preferentially in the
stomach.. Their reactions have been induced in animals by feeding nitrite with amines or
amides (Mirvish, 1972; 1977; Rounbehler et al., 1977). Also, under these situations acute
toxic effects have been observed and N-nitroso compounds have been detected by chemical
analysis (Mirvish, 1975).
A recent report by Iqbal et al. (1980) demonstrates HI vivo biosynthesis of N-nitroso-
morpholine from mice exposed to NCL and morpholine. This is the first and only report of a
direct link between NO, exposure and nitrosamine formation in vivo. N-nitrosomorpholine was
3
detected in animals with as low as 376 ug/m (0.2 ppm) NO, exposure for 4 hours. After 4
3
hours of exposure at 94,000 ug/m (50 ppm) NO,,, a maximum of 2230 ng N-nitrosomorpholine/mouse
was detected. These quantities are extremely small, and it is not known what the biological
significance (in terms of mutation or cancer) is to this exposure. However, the possibility
of low level exposure to N02 and concomitant biosynthesis of nitrosamines indicates a
potential health hazard. This area of investigation requires additional work in order to
quantitate this potential health hazard to man (Iqbal et al., 1980).
14.7 SUMMARY
The biological effects of nitrogen oxides have been examined in a number of animal
species. Thus far, the most toxic among these is nitrogen dioxide (N09). A summary of the
3
research results observed at 18,800 ug/m (10.0 ppm) N00 or less is set forth in Table 14-21.
3
While mechanisms of action can be studied by exposures at or above 18,800 ug/m (10.0 ppm)
N02, this concentration is judged to be the maximum at which animal studies provide relevant
data to estimating the human health effects of ambient or near ambient concentrations of N02.
An unusual aspect of the toxicity of N02 is a delay between exposure and effect. This
temporal sequence is inherent in understanding the toxicity of N02 and has important implica-
tions for the effects of both short-term and long-term exposures to this air pollutant.
Despite the differences in N0~ sensitivity among animal species and the many different
endpoints of toxicity, illustrated in Figure 14-4. A composite has been drawn from these
different studies to illustrate the relationship with time following a single short-term ex-
posure of 4 hours or less. These results are drawn primarily from a single species, the rat.
A similar sequence could be drawn for other species. It is likely that this sequence is the
14-84
-------
TABLE 11-21. SUMMARY OF EFFECTS OF N02 IN ANIMALS AT CONCENTRATIONS OF 10 ppm OR LESS
Concentration of N02 Time of
pjjin exposure Species
Summary of effects
References
00
en
188
188 + 2
hr daily
spike of
1,880
376
470
470
0.1 spike
2 x daily
with 0.05
baseline
0.1 + 2
hr daily
spike
of 1
0.2
0.25
0.25
560-940 0.3-0.5
Continu- Mouse
ous, 15
days
Continuous Mouse
6 mo
3 hrs
Rat
4 hr/day Rabbit
5 days/wk
24 or 36
days
3 hr/day Mouse
up to 3 d
Continuous Mouse
3 mo
No effect on S. pyogenes infectivity
Emphysematous alterations
Inhibition of conversion of PGE? to
its metabolite. No effect on
PGE_ uptake or efflux
Swollen collagen fibers in lung
Increased1 pentobarbital
sleeping time in female mice after
1 day. No effects after 2 or 3
days.
N0« * influenza virus caused a high
incidence of adenomatous prolifera-
tion of peripheral and bronchial
epithelial cells
Gardner, et al.,
1981
Port, et al.,
1977
Men2el, 1980
Buell, 1970
Miller, et al. ,
1980
Motomiya, et al. ,
1973
-------
TABLE 14-21. (continued)
Concentration of N02
|jg/m3 ppm
i — »
-El
1
CD
cn
600
680
740
740
740
940
940
0.32
0.36
0.4
0.4
0.4
0.5
0.5
Time of
exposure
3 mo
7 days
4 hr/day
7 days
Continuous
1 wk
Continuous
2 wk
6,18 or
24 hr/day
12 mo
8 hr/day
7 days
Species
Rat
Guinea Pig
Guinea Pig
Guinea Pig
Guinea Pig
Mouse
Guinea Pig
Summary of effects
Decreased conditioned reflexes
Increased erythrocyte D-2, 3-
diphosphogly cerate
Increase in lung acid phosphatase
Increase in protein of lung lavage
in vitamin C deficient animals
No effect on protein or lipid in
lung lavage in vitamin C deficient
animal s.
Morphological effects in alveoli
Increase in serum LDH, CPK, SCOT,
SGPT and chol inesterase, and lung
and plasma lysozyme. Decrease in
References
Yakimchuk and
Chelikanov, 1972
Mersch et al . ,
1973
Sherwin et al . ,
1974
Sherwin and
Carlson, 1973
Selgrade et al . ,
1981
Blair et al . ,
1969
Donovan et al . ,
1976; Menzel
et al. , 1977
940
0.5
Continuous Guinea Pig
14 days
erythrocyte GSH peroxidase. No
change in lung GSH peroxidase.
Albumin and globulins in urine
Sherwin and
Layfield, 1974
-------
TABLE 14-21. (continued)
Concentration of N02 Time of
ug/m3 ppm exposure
Species
Summary of effects
References
1,000 N0>
(mostly
N00
940
940
940
-p«
CO
940 or
3,760
940
0.5
0.5
0.5
0.5 or 2
0.5
8 hr/day Guinea Pig
180 days
Continuous Mouse
30-45 days
5 days/wk Mouse
7 wk
Continuous Guinea Pig
8 hr/day
4 mo
Continuous Mouse
with 1 hr
peaks of
2 ppm 5
days/wk
Continuous Mouse
12 mo
Nitrates and nitrites in urine; slight
increase in serum cholesterol; decrease
in total serum lipids; hepatic edema;
increase in urinary Mg and decrease
in liver and brain Mg
Morphological alterations of tracheal
mucosa and cilia
Increase of injected horseradish per-
oxidase in lung
Decrease in plasma cholinesterase;
erythrocyte or lung GSH peroxidase
unchanged. Increase in lung acid
phosphatase and plasma and lung
lysozyme
Morphological alterations of alveolar
macrophages; decreased serum neutraliz-
ing antibody to influenza virus immuni-
zation; changes in serum immunoglobulins
At 10 days: damage to clara cells and
cilia and alveolar edema. At 35-40
days: bronchial hyperplasia. At 6
mo: fibrosis. At 12 mo: bronchial
hyperplasia
Kosmider, 1975
Nakajima et al. ,
1972; Nakajima
et al., 1969
Sherwin et al. ,
1977
Donovan et al.,
1976; Menzel
et al., 1977
Aranyi et al.,
1976; Ehrlich
et al., 1975
Hattori, 1973;
Hattori and
Takemura, 1974
-------
TABLE 14-21. (continued)
CD
CO
Concentration of N02
|jg/m3 ppm
940 or 0.5 or 1
1,880
940 or 0.5 or 1
1,880
940 0.5
1,000 0.53
1,030 - 0.55 -
3,000 1.6
1,500 0.8
Time of
exposure Species
Continuous Mouse
1 yr, 5 mo
Continuous Mouse
1 yr, 6 mo
Continuous Mouse
or inter-
mittent
(7-8 hr/day)
180 days Guinea Pig
8 hr/day
Continuous Mouse
5 wk
Continuous Rat
2.75 yr
Summary of effects
No increase in lipofuscin or glutathione
peroxidase
Growth reduced; vitamin E improved
growth
Increased susceptibility to K. pneumoniae
after 90 days continuous or 180 days
intermittent exposure
Alterations in several serum enzymes
Cilia damaged; increased mucus secretion
Increase in respiratory rate
References
Ayaz and Csallany,
1977
Csallany, 1975
Ehrlich and Henry,
1968
Drozdz et al . ,
1975
Miyoshi et al . ,
1973
Haydon et al . ,
1965; Freeman
1,880
1,880
Continuous Guinea Pig
3 days
Continuous Rabbit
2 wk
Increase protein and lipid content of
lavage fluid in vitamin C- depleted
but not normal
Decrease in lung lecithin synthesis
after 1 wk; less marked depression
after 2 wk
et al., 1966
Belgrade et al. ,
1981
Seto et al., 1975
-------
TABLE 14-21. (continued)
Concentration of NO^ Time of
ug/m3 ppm exposure Species
Summary of effects
References
00
10
1,880 1-1.5
2,820
1,880
1,880
2,000
1.1
Continuous Mouse
1 mo
Continuous Guinea Pig
6 mo
Continuous Monkey
493 days
8 hr/day
180 days
.Guinea Pig
940 + 2 x 0.5 + 2 x Continuous Mouse
daily daily 15 days
spikes spikes
of 1880 of 1
Hypertrophy of bronchiolar epithelium
after 1-3 mo. After recovery from
exposure, lymphocyte infiltration
Inhibition of protein synthesis;
decrease in body weight, total serum
proteins, and immunoglobulins
Immunization with monkey-adapted in-
fluenza virus. Increased serum neutra-
lizing antibody titers at 93 days of
exposure. No change in hemagglutina-
tion inhibition titers; no effect on
hematocrit or hemoglobin; increased
leukocytes in blood. Slight emphysema
and thickened bronchial and bronchiolar
epithelium in virus-challenged monkeys
Plasma and liver changes: decrease in
albumin, seromucoid, cholinesterase,
alanine and aspartate transaminases;
increase in alpha and beta? immuno-
globulins
Increase in mortality due to
S. pyogenes
Chen et al., 1972
Kosmider et al.,
1973a
Renters et al.,
1973
Drozdz et al.,
1976
Gardner et al. ,
1981
-------
TABLE 14-21. (continued)
ID
O
Concentration of N02
[jg/m3 ppm
2,300 +
2 x
daily
spikes
of 4,700
2,360
2,400-
5,200
2,800
2,800 +
8,100
spike
2,800 +
8,100
spike
5,600
3,760
1.2 + 2 x
dai ly
spikes
of 2.5
1.26
1.3-3
1.5
1.5 +
4.5
spike
1.5 +
4.5
3
2
Time of
exposure Species
Continuous Mouse
15 days
12 hr/day Rat, prior
3 mo to breeding
2 hr/day Rabbit
15 & 17 wk
Continuous Mouse
or inter-
mittent
(7 hr/day,
7 days/wk)
Continuous Mouse
62 hrs be-
fore & 18 hr
after a spike
for 1,3.5 or 7 hr
14 d; 2 Mouse
daily 1 hr
spike x 5
d/wk x 2 wk
3 hr Mouse
3 hr Mouse
Summary of effects
Increase in mortality due to
S. pyogenes
No effect on fertility; decrease in litter
size and neonatal weight; no teratogenic
effects
Increased leukocytes in blood with
decreased phagocytosis; decreased number
of erythrocytes
After 1 wk, increased susceptibility to
S. pyogenes aerosol greater in continuous
exposure group. After 2 wk, no signifi-
cant difference between modes of ex-
posure
Increased susceptibility to S. pyogenes
aerosol after 3.5 or 7 hr single spike
when bacterial challenge was delayed
18 hrs after spike
Increased susceptibility to S. pyogenes
aerosol
Increased susceptibility to S. pyogenes
aerosol in mice exercising compared to
those not exercising
Increased susceptibility to S. pyogenes
References
Gardner et al . ,
1981
Goldstein et al . ,
1973
Blair et al . ,
1969
Gardner et al. ,
1979
Gardner et al . ,
1981
Gardner et al . ,
1981
11 ling et al. , 198
Ehrl ich et a) . ,
aerosol
1977
-------
TABLE 14-21. (continued)
Concentration of N02
ug/m3 ppm
3,760 2
3,760 2
3,760 2
3,800 2
3,800 2
4,280 2.3
5,000 2.7
5,450 2.9
Time of
exposure
Continuous
1-3 wk
Continuous
3 wk
Continuous
43 days
Continuous
14 mo.
Continuous
2 yr.
17 hr
8 wk
Continuous
20 days
Species
Guinea Pig
Guinea Pig
Rat
Rat
Monkey
Rat
Mouse
Rat
Rat
Summary of effects
Increase in number of lactic acid de-
hydrogenase positive lung cells (pre-
sumably Type II cells) with time of
exposure
Type II cell hypertrophy
Between 72 hr - 7 days increasing loss
of cilia and focal hyperplasia; by
14 days, cilia regenerated and recovery
was evident at 21 days
Polycythemia with or without NaCl. Hyper-
trophy of bronchiolar epithelium
Increase in respiratory rate; no change
in resistance or dynamic compliance
Decreased pulmonary bactericidal activity
(no measurable effect at 1 ppm x 17 hr.
or 3.8 ppm x 4 hr. )
Decreased body weight
Decrease in linoleic and linolenic acid
of lung lavage fluid
References
Sherwin et al. ,
1972
Sherwin et al. ,
1973
Stephens et al . ,
1972
Furiosi et al . ,
1973
Freeman et al . ,
1968c
Goldstein et al. ,
1973b
Kaut et al . , 1966
Menzel et al. , 197
-------
TABLE 14-21. (continued)
Concentration of N02
ug/m3 ppm
5,450 2.9
5,640 3
5,640 3
6,600 3.5
t— >
4=>
10
7,500- 4-7
1,3000
Time of
exposure Species
24 hr/day Rat
5 days/wk
9 mo.
4 hr/day Monkey
4 days
Continuous Guinea Pig
3 days
Continuous Mouse
or Inter-
mittent
(7 hr/day,
7 days/wk)
Continuous Mouse
14 days
Summary of effects
Decrease in lung compliance and volume;
increased lung weight and decreased total
lung lipid; decreased saturated fatty
acid content of lung lavage fluid and
tissue; increased surface tension of
lung lavage fluid
Thickening of basal laminar and alveolar
walls; interstitial collagen
Increased protein and lipid content of
lavage fluid in vitamin C-depleted but
not normal
Increased susceptibility to S. pyogenes
aerosol with increased duration of ex-
posure. No significant difference
between modes of exposure
Increase of injected radio- labeled pro-
tein in lung
References
Arner and Rhoades,
1973
Bils, 1976
Sel grade et al . ,
1981
Gardner et al . ,
1979
Sherwin and Richte
1971
8,100 4.5
9,400
1, 3.5 or Mouse
7 hrs
3 hr
Guinea Pig
Increased susceptibility to S. pyogenes
aerosol proportional to duration of
exposure. No effect when bacterial
challenge was delayed 18 hrs.
Increase protein and lipid content of
lavage fluid in vitamin C-depleted but
not normal after 18 hrs
Gardner et al. ,
1981
Selgrade et al.,
1981
-------
TABLE 14-21. (continued)
VD
OJ
Concentration of N02
|jg/m3 ppm
9,400-
94,000
9,400
9,400
.9,400
9,400
9,400
9,400
9,400
5-50
5
5
5
5
5
5
5
Time of
exposure Species
3 hr Rabbit
4 hr Guinea Pig
4 hr/day Guinea Pig
5 days/wk
2 mo.
7.5 hr/day Guinea Pig
5 days/wk
5.5 mo.
14-72 hr Mouse
3 days Guinea Pig
Continuous Rat
1 wk
Continuous Monkey
Summary of effects
No measurable effect on benzo(a)pyrene
hydroxylase activity of tracheal
mucosa
Increase in respiratory rate and
decrease in tidal volume
Increased lung tissue serum anti-
bodies
No increase in airflow resistance
Increased lung protein by radio-label
method
50% mortality; histological evidence of
edema; increased protein and lipid con-
tent of lavage fluid in vitamin C
depleted but not normal
Hyperplasia began by 3 wks
Increased susceptibility to
References
Palmer et al . ,
1972
Murphy et al . ,
1964
Balchum et al . ,
1965
Murphy et al . ,
1964
Csallany, 1975
Selgrade et al . ,
1981
Rejthar and Rejthc
1975
Henry et al . , 197C
2 mo.
K. pneumoniae
-------
TABLE 14-21. (continued)
Concentration of NO
ug/m^ ppm
9,400-
18,800
5-10
2 Time of
exposure
Continuous
90 days
Species
Monkey
Summary of effects
Infiltration of macrophages, lymphocytes
and some polymorphonuclear leukocytes;
hyperplasia of bronchiolar epithelium
and Type II cells
References
Busey et al . ,
1974
9,400-
18,800
9,400
18,800
190
5-10
5
10
0.1
Continuous Monkey
90 days
Continuous Monkey
133 days
No significant hematological effects
Coate and Badger,
1974
Immunization with mouse-adapted influenza Matsumura, 1970
virus. Initial depression in serum neutra-
lization titers with return to normal by
133 days. No change in hemagglutination
inhibition titers or amnestic response
6 hr
Mouse
No chromosomal alterations in leukocytes
or primary spermatocytes
Gooch et al., 1977
-------
t
2
u
UJ
UJ
Q
UJ
EC
UJ
CO
m
O
I ""I 'I I
» EXPOSURE
CHEMICAL REACTION
iiiIPM
— SUSCEPTIBILITY TO
MICROORGANISMS
—— CELL DEATH (max. at 24 hr.)
-— BIOCHEMICAL INDICATORS
OF INJURY (max. at 1B hr.) .~T
REPLACEMENT OF DEAD
AND INJURED CELLS
AND BIOCHEMICAL
INDICATORS OF REPAIR
(max. at 48 hr.)
I I I
(log scale) 4 10 24 48
I hours I
14
days
30
I
23 6
months
Figure 14-4. Temporal sequence of injury and repair hypoth-
esized from short-term single exposures of less than 8 hours.
12
14-95
-------
same for all mammalian species exposed under similar conditions. These reactions will be
obtained predominately with low concentrations of N02. As the concentration of NCL is
increased more than 100-fold over ambient concentrations, complications arise which tend to
obscure the sequence of events. It is not clear, further, whether or not these higher
concentrations are truly relevant to the toxicity of NO,, to man as it occurs in the atmosphere
of urban areas. In any event, the animal studies most important to determining the standards
used in regulating emissions are those more closely aligned to ambient concentrations of NCL.
Studies of the reaction of N02 with cellular constituents clearly illustrate that the
chemical reactions are essentially instantaneous (Roehm et al., 1971; Menzel, 1976) when
compared with the length of time required for demonstration of a biological effect. Most
investigators believe that the chemical reactions of N0? are dominantly with lipid components
of the cell (Menzel, 1976). The reaction of N02 with the unsaturated lipids of cellular
membranes results in a chemical reaction characterized by the formation of peroxidic products.
This is a devastating event in terms of the organization and properties of the cellular
membrane necessary to maintain the integrity of the cell. Many of the biological effects can
be ascribed to the peroxidation of cellular membranes, the most obvious example of which is
pulmonary edema, a commonly observed phenomenon on exposure to high concentrations of N02.
The protective role of vitamin E in the prevention of N02 toxicity at high concentrations is
also supportive of this hypothesis (Menzel, 1976).
Alternatively, N0? could oxidize a number of small molecular weight compounds such as
glutathione, pyridine nucleotides and ascorbic acid. Thiol oxidation could be coupled to
lipid peroxidation through the glutathione peroxidase-glutathione reductase cycle (Chow et
al., 1974). The increased pulmonary edema found in guinea pigs mildly depleted of vitamin C
(ascorbic acid) suggests that vitamin C also plays an important role in the maintenance of
cellular integrity during N02 exposures (Belgrade et al., 1981).
Inhaled NO,, is rapidly taken up and distributed throughout the lung as has been
13
determined using short lived radiotracer studies with NQ2 (Goldstein et al., 1977b). A very
significant fraction of N0? is retained in the lung. The fraction retained probably
represents that N0? which is chemically reactive with pulmonary tissue via addition to
unsaturated fatty acids.
NOp is an acid anhydride and reacts with water vapor at ambient concentrations in the air
and more so at the increased temperature and humidity existing within the respiratory system.
The exact chemical species which reaches the pulmonary surface to produce the observed lesions
is most likely N02, but HN02, and perhaps NO may be formed in the liquid lining the airways
(Goldstein et al., 1977b). HN02 and HNO., will be rapidly neutralized by the biological sub-
stances dissolved in the liquid layer lining the airways of the lung.
Despite the hydration of N02 by water vapor, a significant fraction of N02 is not removed
in the upper airways and penetrates deep within the lung to produce its toxic effects. As a
strong oxidant, N0? may also oxidize small molecular weight reducing substances and proteins
14-96
-------
within seconds to minutes. Reaction with unsaturated fatty acids to produce peroxidation is
essentially instantaneous (Roehm et al., 1971). It is not likely, so far as is known, that
NO- reaching the respiratory portions of the lung would be able to penetrate the lung cells
and attain a significant concentration within the blood. Nitrate is formed as a consequence
of reactions with cellular constituents and has been detected in the blood and urine of
animals exposed to N02 (Kosmider, 1975). Levels of nitrate attained during NO- exposure are
unlikely to induce biological responses of the nature which have been observed. Because of
the high reactivity of NO^, the predominant response observed on the inhalation of NCL is
direct injury to the tissues of the lung. The effects on organs distal to the lung are likely
to result from the production of secondary toxicants in the lung which are circulated to other
parts of the body. A direct proof of this hypothesis of circulating toxins following
inhalation of NO- has not been found, but effects on organs other than the lung have been
found (Miller et al., 1980). The metabolism of xenobiotic compounds, for example pento-
o
barbital, by the liver is inhibited by exposure of mice to 470 ug/m (0.25 ppm) N02 for 3
hours (Miller et al., 1980). Repeated exposure to N02 resulted in a return to normal
metabolism of pentobarbital. While the implications of these observations are difficult to
understand, decreased drug metabolism represents the inhibition of an important detoxification
pathway in the liver for a variety of compounds to which man is exposed both intentionally
(drugs, pesticides, and food additives) and unintentionally (naturally occurring or adventi-
tious toxicants, mutagens, and carcinogens). Inhibition of drug metabolism is generally
recognized as an adverse effect of a drug, and thus, these effects are also adverse. Future
•studies on the effects of HQy inhalation on other organ systems deserve continued surveil-
lance.
The major pulmonary effect of N02 is cellular injury among specific cell types within the
lung (Freeman et al., 1968b). If the N02 injury is severe, cell death results. These events
occur within 24 hours after inhalation. The magnitude and site of the injury resulting from
N02 will depend upon the concentration of N02 which was inhaled; therefore, the absolute
degree of response will depend upon both the rate and magnitude of respiration and the N02
concentration. The moderate solubility of N02 in water and the inability of the upper
respiratory tract to remove all of the N0? which is inhaled result in injury to specific
regions within the lung. At concentrations near those found in urban environments, the region
of the lung bounded by the terminal and respiratory bronchioles and adjacent alveoli are those
which are most affected (Freeman et al., 1968,b,c; 1969b, 1974a). Emphysematous alterations
have been reported in mice exposed for 6 months to 188 ug/m (0.1 ppm) NO, with a daily 2-hour
3
spike of 1,880 (jg/m (1 ppm) N02 (Donovan et al., 1976). The bronchiolar region represents
the terminal portion of the lung and is intimately involved in the exchange of oxygen and
carbon dioxide. This is the region of the lung which is most essential for the maintenance of
life. Some differences may exist between man and rodents because this region of the lung is
proportionately much shorter in the rat than in man. At high concentrations of Nt^, that is
14-97
-------
above ~9,400 ug/m (~5 ppm), segments of the upper airways, as well as those centering around
the alveoli, may be affected. As cells are exposed to NOp and begin to die, protein and
nucleic acid synthesis is stimulated in the surviving stem cells and a wave of mitosis occurs
which reaches its maximum at about 48 hours during or after exposure. The type I cell of the
lung (a thin, squamous cell across which gases are exchanged) appears to be the most sensitive
and to be injured at lower concentrations than the type II cell (a cuboidal cell that produces
surfactant) (Evans et a!., 1973b). The nature of this injury can be sufficiently severe that
the cell dies, sloughs off, and leaves debris within the alveoli. Other cells in the upper
airway, such as ciliated cells, are similarly sensitive and may be replaced by other stem
cells known as Clara cells. These effects on the lung result in dramatic changes in its
structure and cell composition.
Swollen collagen fibers occur in rabbits exposed to 470 ug/m (0.25 ppm) N02 for 4
hr/day, 5 days/wk for 24 days (Buell, 1970). Presumably, these swollen collagen fibers
represent alterations in the basement membrane or disruptions in collagen synthesis. One can
not speculate on the potential pathological sequelae of collagen dysfunction, except to note
that collagen metabolism is disrupted in man and animals during fibrosis. Some alterations in
collagen metabolism are suggested by the long-term exposures of dogs to auto exhaust
containing NO and N02 (Orthoefer et al., 1976). Increased number and size of interalveolar
pores found in these dogs after near life-time exposures (Hyde et al., 1978) emphasize the
importance of the emphasematous alterations found in mice on exposure to N02 alone (Donovan et
al., 1976).
Biochemical indicators of lung injury can provide early evidence of toxicity. The rat
2
lung prostaglandin dehydrogenase is sensitive to exposures of as little as 3 hr to 376 ug/m
(0.2 ppm) N09 (Menzel, 1980). In this series of experiments, rats were exposed to 376, 3,760
3
or 35,720 ug/m (0.2, 2 or 19 ppm) for 3 hours. The lungs were then removed and used as an
isolated, ventilated and perfused lung preparation to determine the uptake, release and
metabolism of prostaglandin E2 (PGE2), a natural vasoactive hormone secreted by the lung and
other organs. N0? exposure inhibited the metabolism of PGE2 to its inactive metabolite
13,14-dehydro-15-keto PGE0. While there was no difference in the amount of inhibition
3
produced by exposure to 376 and 3,760 ug/m (0.2 and 2 ppm) N00, the time required to return
3
to basal levels of activity was greater for those rats exposed to 3,760 ug/m (2 ppm) than to
376 ug/m (0.2 ppm). Rats exposed to 35,720 ug/m (19 ppm) NO, required the longest time for
3
recovery to basal levels. Recovery required 60 hours following exposure to 376 ug/m (0.2
3 3
ppm), 90 hours following 3,760 ug/m (2 ppm) and 160 hours following 35,720 ug/m (19 ppm).
3
No alteration of the uptake or release of either H-PGE2 or its metabolites by the exposed rat
lungs was found. None of the lungs examined showed any evidence of edema as judged by the wet
weight to dry weight ratio. Since the prostaglandin system is intimately involved in the
local regulation of blood flow in the lung, alterations in the metabolism of these potent
14-98
-------
hormones may have profound effects on the perfusion of the lung and subsequently on the gas
exchange of the affected lung.
As pointed out above, vitamin C appears to play an important role in the maintenance of
the integrity of the airways to macromolecules. Selgrade et al. (1981) repeated in part the
experiments of Sherwin and Carlson (1973) in which guinea pigs were depleted of vitamin C and
exposed to N09. Selgrade et al. failed to find an increase in the lavage fluid protein or
3
lipid content of guinea pigs exposed to 740 |jg/m (0.4 ppm) NO,, even after exposure for 2
3
weeks. Exposure to 1,880, 5,640 or 9,400 ug/m (1, 3 or 5 ppm) NO, for 3 days caused
3
increased protein and lipid content of the lavage fluid. A single exposure to 9,400 ug/m (5
ppm) for 3 hours also produced similar changes in the lavage fluid content after 18 hours in
vitamin C-depleted guinea pigs, but not in normal guinea pigs. Vitamin C depletion also
o
caused a 50 percent mortality in the animals exposed to 9,400 ug/m (5 ppm) NOp, but no
mortality in animals having normal vitamin C levels.
The differences between the Sherwin and Carlson and the Selgrade et al. studies may be
explained by differences in the exposure systems, in the vitamin C status of the guinea pigs,
and in the methods of analysis. Sherwin and Carlson exposed guinea pigs to N0? by the use of
a silicon drip technique and monitored the N02 concentrations with a Mast Meter and intermit-
tent Saltzman determinations.
Considerable improvement has been made in the methods of analysis for NOp and exposure of
animals. Selgrade et al. used a chemiluminescent meter and a Hinners chamber for exposure.
Considerable variation could have occurred in the chamber NO^ concentration using the older
methods. The degree of vitamin C depletion used by Selgrade et al. was quite mild, represent-
ing only a 25 percent reduction of the serum levels of the vitamin. No details are provided
in the Sherwin and Carlson study to allow an assessment of the degree of vitamin C deficiency
of the animals. More completely depleted guinea pigs could have been more susceptible.
Sherwin and Carlson also used disc electrophoresis to estimate the protein concentration of
the lavage fluid, while Selgrade et al. used the direct chemical method of Lowry et al. Addi-
tionally, Selgrade et al. found another protein not detected by Sherwin and Carlson. The new
protein was detectable only on careful photometric scanning of the gels and could have gone
undetected in the earlier study since considerable improvement in technique has been possible
by advances in the field of protein chemistry, especially electrophoresis.
These studies illustrate that vitamin C deficiency may lead to greater susceptibility to
ambient levels of N02. Burch (1961) compared the vitamin C levels reported in guinea pigs and
in human autopsy tissue samples from a number of organs. Guinea pig tissue ascorbate concentra-
tions reach saturation levels on continued intake of ascorbate. Since human leukocytes also
reach saturation levels on high vitamin C intake, a similar saturation curve for human tissues
is likely. Thus, the 25 percent reduction in serum vitamin C levels that resulted in these
major changes in susceptibility to N0? represent conditions likely to occur in man with low
vitamin C intake. Burch found 29 percent of 1,000 subjects in 8 high schools to have serum
14-99
-------
ascbrbate levels below 0.4 percent, an arbitrary biochemical deficiency level, while 48
percent of 150 students from a poor area had values below 0.4 percent. Oral contraceptive use
(Wynn, 1975) and smoking (Hoefel, 1977) also lower the blood ascorbate levels in man. At
present the dose response curve for vitamin C intake and changes in lung permeability by NOp
exposure are not known, so one cannot relate the changes reported by Selgrade et al.
quantitatively to the present levels of vitamin C intake by the U.S. population and the risk
of persons having low vitamin C to adverse effects associated with NOp exposure. The subject
is obviously important and should be reviewed as further information becomes available.
Another sensitive measure of injury is the appearance of proteins in the airways.
Increased protein content of the pulmonary lavage fluid or the appearance of radiolabeled
serum proteins in the airways is taken as an indicator of pulmonary edema. Radiolabeled
albumin or rabbit serum proteins injected into the blood stream of mice were detected in the
airways after exposure to 7,520-13,170 (jg/m (4-7 ppm) N0? (Sherwin and Richters, 1971).
Under normal circumstances, such exudates of serum proteins do not occur and represent a
major, deleterious alteration in the permeability of the airways. While there was a trend
toward increased amounts of radiolabeled protein in the airways of exposed mice, the results
were not statistically supportable, mainly because of the large variation in the values.
These variations could have been due to variations of the NO, concentration during exposure
3
since the exposure ranged from 7,520 to 13,170 ug/m (4-7 ppm) or to variable recovery of the
radiolabeled protein in tissue extracts. Since the time of exposure to discrete levels of N02
is not known and since only trends toward increased levels of proteins within the airways were
3
reported, one must conclude that exposure to 7,520-13,170 |jg/m (4-7 ppm) NOp does not produce
pulmonary edema in normal mice.
The effect of N02 inhalation on the metabolism of the carcinogen benzo(a)pyrene by the
lung has been investigated. Palmer et al. (1972) found no effect on benzo(a)pyrene metabolism
3
of the tracheobronchial region of rabbits exposed to 9,400 ug/m (5 ppm) NO, and greater. Law
3
et al. (1975) found no effect of short-term exposures at even higher levels (75,200 ug/m ; 40
ppm for 2 hours) on rat lung microsomal benzo(a)pyrene metabolism. N02 exposure appears to
have no effect on these cytochrome P.,-Q~dependent enzyme systems.
There is no reason to suppose that all enzymes are equally sensitive to N0? exposure, so
lack of an effect on some enzymes is not indicative of an absence of a toxic effect at that
N02 concentration. Further, some enzymatic changes, such as increased acid phosphatase levels
(Sherwin and Carlson, 1973), may represent changes in the cell population due to death of some
cells and replacement by a new younger cell population.
Pulmonary defenses against infectious agents are affected by short-term exposures to N02-
The infectivity model in which pollutant-exposed animals receive an aerosol of live microbes
has proven to be a particularly sensitive indicator of pulmonary injury and has been respon-
sible for the development of most of the data indicating toxicity of N02 at low concentrations
and short times of exposure (Coffin et al. , 1976; Gardner and Graham, 1976; Ehrlich, 1975).
14-100
-------
Mortality from exogenous infectious agents is influenced more in proportion to the concentra-
tion of NOp than to the duration of exposure. This observation is consistent with the hypo-
thetical temporal sequence of injury. Pulmonary damage occurs rapidly on exposure to NCL but
the functional effects of pulmonary damage may be observed much later, depending upon the
extent of damage and the system which has been used to measure the damage; e.g., pulmonary
conversion of PGE2 to its metabolites (Menzel, 1980) or susceptibility to airborne infections.
(Coffin et al., 1976; Gardner and Graham, 1976; Ehrlich, 1975) The infectivity model tends to
be an integral of many of the defensive mechanisms of the lung and, therefore, to reflect the
overall damage which has occurred. NCL concentrations as low as 4,700 ug/m (2.5 ppm) may
result in excess mortality from a single exposure of only 3 hours (Ehrlich et al., 1977). The.
injury of a 3-hour exposure appears to be repaired within 24 to 36 hours after exposure, but
not by 18 hours (Selgrade et al., 1981).
In Figure 14-5 a short-term exposure of constant duration has been given to an animal and
only one of the properties of intoxication is illustrated, the death of type I cells. In-
creasing concentrations of N02 are illustrated in this figure on the z axis. Thus, as the
concentration of NOp is increased, the magnitude of cellular death increases while the time at
which cell death occurs is constant. The magnitude of cell death is proportional to the
logarithm of the concentration of NCL which has been inhaled. Increasing the total amount of
NOp inhaled by manipulations in the respiratory pattern will likewise increase the magnitude
of cell death, but not influence the time at which cellular death occurs. Mice made to run
and to inhale more and more deeply N0~ are more susceptible to airborne infection than those
resting (Selgrade et al., 1981). Eventually, sufficient cells will be injured to produce
mortality during the peak wave of death of alveolar cells. Death through respiratory insuf-
ficiency and pulmonary edema, however, does not occur at concentrations achievable in the
urban atmosphere. Concentrations greater than 47,000 ug/m (25 ppm) are necessary to achieve
mortality. This is not to say, however, that severe pulmonary damage is not achieved at lower
concentrations near those which occur regularly in urban areas.
The delay between end of exposure and observation of biological effect complicates the
understanding of the effects of long-term exposure to HO*- This is especially so with expo-
sure regimens resembling those that occur in the atmosphere where exposure to relatively high
concentrations of NO- may occur repeatedly over a short time period. Figure 14-6 illustrates
the sequence of events which is hypothesized to occur on continuous long-term exposure to NOg.
The sequence of events is essentially similar to that in short-term exposure. The chemical
reactions between the inhaled NO- and cellular constituents are instantaneous and achieve a
constant level throughout the exposure. During the first 14 days of exposure, cell death and
replacement of pulmonary cells are the dominant features. This is expressed as a wave of
mitosis or cellular division which reaches its maximum about 48 hours after the onset of
exposure. The extent of cell death is illustrated in Figure.14-6 and is proportional to the
concentration of ML. Likewise, all of the other indicators of N02 damage so far examined are
14-101
-------
i
u
it,
e
so ©o
TIME AFTER iEGINNIMG 5SPOSJRE
Figure 14-5. (Proportionality between effect Ccetl death) ami
concentration of NC>2 during a constant exposure period.
The maximum in cell death h reached - 18 hours after sx-
posurs end the extent is proportional to the dote (concen-
tration
14-102
-------
c
s
t
£
I
U
01
01
D
iu
cc
iu
II I •
CHEMICAL REACTION
PULMONARY
FUNCTION
CHANGES
BIOCHEMICAL
REPLACEMENT OF DEAD
AND INJUREDCELLS
AND BIOCHEMICAL
INDICATORS OF REPAIR
INCREASED
SUSCEPTIBILITY TO
MICROORGANISMS
LEVATED
.CELL
TURNOVER
INCIDENCE
OF EMPHYSEMA
LIKE PATHOLOGY
HYPOTHETICA
TOLERANCE
1 -
10
24 48
14
6 12 (log scale)
hours
days
months
Figure 14-6. Temporal sequence of injury and repair hypoth-
esized from continuous exposure to NO2 as observed in exper-
imental animals.
14-103
-------
dose dependent. The biochemical and physiological functional indicators of damage change
rapidly with injury and repair, reaching a relatively steady state after about a week or two
(Menzel et al., 1972; Donovan et al., 1976; Menzel et al., 1977). Several enzymes have been
o
detected which are indicative of cellular injury at concentrations of N0? as low as 376 ug/m
(0.2 ppm) (Menzel, 1980) or 940 ug/m3 (0.5 ppm) (Donovan et al., 1976; Menzel et al. , 1977)
during the injurious phase of continuous exposure, that is greater than 7 days. Pulmonary
macrophages are aggregated within the lung and the degree of aggregation has been estimated by
a number of biochemical techniques (Aranyi et al., 1976; Ehrlich et al., 1975). Again, the
infectivity model is highly sensitive to N02 exposure. The susceptibility to infection as
measured by this technique rises almost linearly during this period. The infectivity model
has been used to illustrate excess mortalities due to N0? exposure at concentrations within
the range of 940-2,820 ug/m3 (0.5-1.5 ppm) N02 (Gardner et al., 1979; Ehrlich and Henry, 1968;
Freeman et a!., 1972; Stephens et al. , 1971).
Long-term exposures to N02 also result in major alterations of lung morphology. These
are very difficult to interpret because of the fine gradation and slow development of response
once the initial phase of replacement of cells susceptible to NCL has passed (Freeman et al. ,
1968c, 1972; Stephens et al., 1971; 1972). The development of an emphysema-like disease in
experimental animals requires considerable time as has been demonstrated in studies of rats
and mice. The development of obstruction to airflow, distension and destruction of the
alveolar tissue in experimental animals requires considerable time (Freeman et al., 1972).
When compared to the life span, the time required for damage in experimental animals is
equivalent to that required for the development of emphysema in man. The process of emphysema
development on N02 exposure is indeed complex, but it is clear that the effects are interpre-
table in terms of the changes in the cell populations and structural alterations concommitant
to that. A major pathologic change is an increase in the distance between the air space and
the capillary in the respirable or alveolar region of the lung (Henry et al., 1970; Evans et
al., 1972, 1974; Buell, 1970). Other effects include the loss of ciliated cells which are
responsible for removing particles from the lung .and narrowing of the airways and alteration
in the morphology of the cells lining the junction between the respiratory segment and the
mucous containing segment (Stephens et al., 1971, 1972). The cell type in the alveoli most
sensitive to NO^, the type I cells, is replaced by type II cells, the type I cell progenitor,
but the appearance of the type I cells maturing in the presence of N02 is significantly
different from those maturing in the absence of N02 (Evans et al., 1974). Other alterations
in the lung include the appearance of collagen in areas which are normally devoid of this
fibrous protein and the aggregation of macrophages (Stephens et al., 1971; Buell, 1970).
2
These effects have been observed in rats that have been exposed continuously to 3,760 ug/m (2
ppm) N02 or greater.
The fatty acid composition of the lung membranes has also been noted to change during the
exposure to N02 (Menzel et al., 1972). The mortality from continuous exposure to high concen-
14-104
-------
trations of NOp is influenced by the level of vitamin E and other free radical scavengers
which are included in the diet (Menzel, et al., 1972). These observations support the
hypothesis that membrane damage by chemical oxidation of unsaturated fatty acids is a major
mechanism of toxicity of NOp. These changes in fatty acid composition of the lung are
accompanied by enzyme changes which in part may be protective and aid in the destruction of
the peroxidic products formed in the lung on N02 inhalation (Chow et al., 1974; Donovan et al.,
1976). It should be emphasized that at no point is it possible to provide adequate levels of
vitamin E or other dietary factors that provide complete protection against NOp. It should be
noted, however, that certain segments of the population may be unusually sensitive to N0? should
their intake of vitamin E and other antioxidants be marginal. A similar conclusion can be
reached with regard to vitamin C intake. Normal levels of vitamin C provide protection when
compared to marginal or deficient levels, but still do not prevent completely NOp toxicity.
The level of vitamin C intake in some populations may also be marginal as discussed above.
The temporal sequence of events suggests that the response of the animal to inhalation of
NOp returns to near normal levels during continuous exposure. These results are misleading,
since it has clearly been observed in long-term studies of rats that the morphology of the
lung has changed from its normal structure to that resembling emphysema (Freeman et al.,
1968c; 1972; Stephens et al, 1972). This raises the question of tolerance to resistance and
recovery during continuous exposure. It is possible that, at some point, the rate of replace-
ment of dead and injured cells resulting from the continuous inhalation of NO- may return to
levels equivalent to that found in clean air (Stephens et al., 1972). Tolerant cells, as
compared to naive cells, may be more resistant to N02 because they are younger or because they
may -have produced a protective mechanism such as specific increases in enzymes capable of
degrading the secondary reaction products formed on NOp inhalation. Some enzymes such as
glutathione peroxidase, glutathione reductase, and glucose-6-phospate dehydrogenase in the rat
may be increased as a protective mechanism (Chow et al., 1974), or they more likely may
reflect a proliferation of young cells within the organ which contain higher enzyme concentra-
tions (Sherwin et al., 1974). These cells are younger because all of the lung cells are dying
and being replaced at a more rapid rate than that which would occur normally in the lung in
pollutant free air. Not all species exhibit this protective increase in enzymes. For example,
3
the guinea pig, when exposed to 940 ug/m (0.5 ppm) NOp for 4 months failed to develop higher
levels of these potentially protective enzymes (Donovan et al., 1976; Menzel et al., 1977).
Importantly, when cultured lung cells are coated with a very thin layer of nutrients to
resemble the condition within the lung, direct exposure to NOp is highly toxic. It is most
likely that all cells are sensitive to relatively low concentrations of NOp and that no
adaptation in the true sense ever occurs. The apparent adaptation that may be seen in pul-
monary function measurements of people living in polluted areas vs. those who live in non-
polluted areas may be artifactual in the sense that large changes in pulmonary tissue may be
necessary before permanent alterations may be detected in pulmonary function. In other words,
14-105
-------
a major pathophysiologic change must occur before it is detected by pulmonary physiology
methods. Biochemical and morphological techniques are more sensitive, but so invasive that
they can only be used on experimental animals. In further support of the idea that all cells
are sensitive to concentrations of N09 which are easily attainable in inhaled air, when rats
3
have been exposed to 3,760 ug/m (2 ppm) N02 for long periods of time and then are exposed to
an abrupt increase in concentration of N02, a second wave of mitosis and subsequent
alterations in biochemical, physiologic, and morphologic indicators of cell damage occur in
exactly the same temporal sequence (Evans et al., 1972). Thus, although "adaptation" may
appear to occur, the ultimate development of an emphysema-like condition occurs in the rats on
long-term exposure, and they remain sensitive to alterations to higher concentrations of NO,,.
An important consideration has been the question of tumor formation or malignant meta-
plasia due to NCL exposure. This concern comes about due to the morphology of the lungs of
animals which have been exposed to NO,,. Because N02 produces a stimulation or rapid turnover
of cells, a transient hyperplasia of the type II lung cell and nonciliated bronchiolar cell is
observed. Such a hyperplasia .represents a part of the natural repair mechanism. There is,
however, no evidence to indicate that such changes represent tumor formation or malignant
metaplasia. Thus, there is no data to connect the inhalation of N02 with an increased
incidence of cancer at the present time.
As was noted in the discussion of the effects of short-term exposure to NCL, the lag
between exposure and biological effect represents a potential situation for accumulation of
biological effects. Such a cumulative effect has been demonstrated using the infectivity
2
model in mice which were exposed continuously or intermittently (7 hr/day) to 2,820 |jg/m
(1.5 ppm) N02 (Gardner et al., 1979). Intermittent exposures of mice to 2,820 ug/m (1.5 ppm)
N02 eventually become equivalent to continuous exposure when the infectivity model is used. A
total of 319 hours of exposure (13.3 days) is required before a 7 hour/day exposure becomes
equivalent to continuous exposure. The time period for equivalence between intermittent and
continuous exposures will be shortened relative to the concentration of N09. The intervening
3
17 hours between each 7 hour exposure to 2,820 ug/m (1.5 ppm) N02 are inadequate for complete
recovery. Excess mortality upon challenge with bacterial pathogens could be observed after 7
3 3
days of continuous exposure to 2,820 ug/m (1.5 ppm), however, or even to 940 |jg/m (0.5 ppm).
Considerable differences occur in the response to N02 when animal species and infectious
agents other than mice and S. pyogenes are used (Purvis and Ehrlich, 1963; Henry et al. , 1970;
Renters et al., 1973; Matsumura, 1970a). Resistance to K. pneumoniae (Purvis and Ehrlich,
1963) is less affected by N02 exposure than resistance to S. pyogenes. Squirrel monkeys
(Henry et al., 1970) were the least sensitive animals tested using this end point, and
hamsters (Ehrlich, 1975) demonstrated intermediate sensitivity when compared to mice. The
quantitative extension of such data to man is difficult because analogous human data are not
available. Even though both infectious agents are human pathogens, the direct extension of
this data to man is difficult, in part, because of differences in anatomical structure of the
lung, and in part, because of differences in native and acquired immunity.
14-106
-------
The recent work of Gardner et al. (1981) on the effects of short-term exposures to spikes
of N02 similar to those occurring in the urban atmosphere is particularly important in asses-
sing the interaction of NO, and pulmonary infections. Mice were exposed to spikes of 8,100
3
|jg/m (4.5 ppm) N02 for 1, 3.5, or 7 hours, and increased mortality due to exposure to S.
pyogenes was proportional to the duration of the exposure. The mice recovered from the expo-
sure by 18 hours. To mimic the urban environment, these same spikes were superimposed on a
background of 2,800 (jg/m (1.5 ppm) N0?, which resulted in a significant (p < 0.05) increase
in mortality with a spike of 3.5 or 7 hours duration, when the bacterial challenge was delayed
for 18 hours after the peak N0? exposure. These results are consistent with the long-term
studies of this group using the same model system where it was found that the magnitude of the
exposure was more important than the product of time and concentration. These data suggest
that the alterations in the lung leading to increased susceptibility to airborne infections
occur with relatively brief exposures approaching those encountered in the urban environment.
These experiments provide an experimental basis for the observations relating increased inci-
dence of respiratory infections with gas stove exposure in man (References ERC/RTP Review,
1976; Melia et al. , 1978; Spengler et al., 1979; Speizer et al., 1980; Goldstein et al., 1979
from Chapter 15). The effect of cooking stoves on respiratory infections is discussed more
fully in Chapter 15 (Section 15.2.2.2.2). Levels of 470 to 1,100 pg/m3 (0.25 to 0.6 ppm) N02
were found in the vicinity of gas stoves for about 2 hours (References ERC/RTP Review, 1976;
Mitchell et al., 1974 from Chapter 15).
In terms of the probable temporal sequence of events, N0? inhalation affects almost all
of the cell types within the lung. Depending, then, upon the concentration of N02, different
cells will be affected in addition to those which are most susceptible at lower concentra-
tions. The mode of exposure, that is the rate and depth of respiration, will also influence
the specific cell types which are damaged. Because the rate of chemical reaction of NO,, with
cell constituents is almost instantaneous when compared to the time required for biological
expression of injury, it may be expected that the concentration of N02 during a given exposure
will have a greater effect on determining the end point used to measure toxicity than would
the duration of exposure. Sensitive biochemical parameters are difficult to interpret because
of the need to correlate biochemical changes with pathological processes. They are viewed,
then, as indicators of death or injury of specific cells following N02 inhalation. Bio-
chemical studies indicate that lung injury occurs on inhalation of N09 at levels as low as
3
376 ug/m (0.2 ppm) for 3 hours in mice, as evidenced by changes in prostaglandin metabolism
(Menzel, 1980); as 470 pg/m3 (0-25 ppm) for 3 hr/day for 1 day as evidenced by increased
pentobarbital metabolism in mice (Miller et al., 1980); as 940 pg/m (0.5 ppm) for 8 hr/day
for 7 days as evidenced by alterations in serum enzymes in guinea pigs (Donovan et al., 1976;
3
Menzel et al., 1977); as 940 ug/m (0.5 ppm) continuous exposure with 1-hour peaks of 3,760
ug/m (2 ppm) for 5 days/wk in mice as evidenced by morphological alterations in alveolar
3
macrophages, decreased serum antibody and immunoglobins (Ehrlich et al., 1975); as 1,000 pg/m
14-107
-------
(0.53 ppm) for 8 hr/day for 180 days in guinea pigs as evidenced by alterations in serum
3
enzymes (Drozdz et al., 1975); and as 1,880 ug/m (1 ppm) continuously for 2 weeks in rabbits
as evidenced by decreased lecithin synthesis (Seto et al., 1975). Not all effects have the
same sensitivity; for example, guinea pigs exposed to 740 ug/m (0.4 ppm) NO, have no
3
alteration in lung permeability to serum proteins but do at 1,880 (jg/m (1 ppm) when rendered
slightly deficient in vitamin C (Selgrade et al., 1981).
Because of the universal toxicity of NO,, to pulmonary cells, it is likely that other air
pollutants such as ozone, sulfuric acid, sulfur dioxide, and particulate matter may injure the
same cells within the lung as are injured by N02. In most cases, following the simultaneous
inhalation of NQ2 and other air pollutants, additive, rather than synergistic, effects have
been found. Tobacco smoking and occupational exposure add very significantly to the toxicity
of N02. At present, the data are not sufficient to provide a detailed evaluation of this
important variable in the response of the human population. Because of the delay between the
exposure to N02 and effect, the sequence of exposures to air pollutants may be particularly
important. No synergism occurs between 0, and NO, at the lowest concentrations examined for
3 3
each pollutant of 100 ug/m (0.05 ppm) with spikes of 200 ug/m (0.1 ppm) (Gardner et al.,
1981). At 940 ug/m3 (0.5 ppm) N02 with 1,880 ug/m3 (1 ppm) spikes combined with 0.05 ppm 03
with 0.1 ppm spikes or higher, synergism between 0, and NQ2 occurs using mice in the
infectivity experiment (Gardner et al., 1981).
Another area of possible toxicity may be the formation of nitroso compounds, because
nitrosamides and nitrosamines are known carcinogens. Nitrosamines and nitrosamides have
recently come into the public view through their formation in foodstuffs containing nitrites.
In this case, nitrite has been added to the foodstuffs to prevent bacterial contamination and
spoilage. Gas phase reactions between NOp and amines to form nitrosamines have been reported,
and inhaled, injected or ingested nitrosamines produce lung tumors in exposed animals. At the
moment, no evidence exists that nitrosamines or nitrosamides are formed in ambient air from
nitrogen oxides. The detection of nitrosamines in the body of mice gavaged morphroline and
breathing N02 (Iqbal et al., 1980) suggests that nitrosamine formation in the lung can occur.
The contribution of inhalation vs. ingestion as sources of nitrosamines remains to be quanti-
fied. Similarly, the role of inhaled nitrites and nitrates found in atmospheric particles is
unknown and should be studied further. A few experiments indicate that inhaled nitrate pro-
duces biological effects through the release of histamine and other intracellular hormones.
-Whether such effects occur in man is not known. Continued surveillance of these important
areas is needed.
While much remains to be learned about the toxicity of N0?, studies so far conducted in
animals indicate that the biological effects of N02 are likely to be displaced from the time
of exposure. As shown in Figures 14-4 through 14-6, this delay between onset of symptoms and
exposure to N02 may explain many of the confounding factors observed in epidemiologic data,
but complicates further the question of effects of transient episodes of high N0~ concentra-
14-108
-------
tions in the atmosphere. It is clear that the lowest concentration at which NOp, in
particular, produces biological effects of a reproducible magnitude so far detected in animals
3 3
is 376 ug/m (0.2 ppm). Repeated exposures to 940 ug/m (0.5 ppm) also produce measurable
adverse effects. The observation of cumulative effects is especially important, suggesting
that under appropriate circumstances intermittent short-term exposure to N0? may eventually
become equivalent to continuous long-term exposure. These observations, when compared to the
data which have been accumulated on the long-term effects of NO^, may be particularly
pertinent to the potential toxicity of this air pollutant to man. There is little doubt that
the inhalation of NO- results in toxicity, regardless of the species which has been exposed.
Thus, animal experiments are truly indicative of the hazard of this air pollutant to man.
14-109
-------
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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 (NCO as the NO compound currently of
greatest concern from a public health perspective. Human health effects associated with expo-
sure to nitrogen dioxide (N0~) have been the subject of three literature reviews since .1970.
Each focussed mainly on the effects of short-term exposures.
In the first review, published in 1971, the Committee on Toxicity of the National Academy
of Sciences-National Research Council issued guides to short-term exposures of the public to
NO (National Academy of Sciences, 1970). A review of the then current literature showed:
(1) that the individuals most susceptible to NO,, action are those predisposed by age,
heredity, and preexisting respiratory disease; (2) that many of these individuals respond most
sensitively at concentrations to which healthy individuals are unresponsive; and (3) that the
effects of NOp are, within limits, reversible such that the extent of recovery seems to be a
function of the degree of exposure, the length of the interval between exposures, and the
health and/or age of the exposed individuals. This committee acknowledged that too much cri-
tical information was missing to permit highly conclusive recommendations about short-term
exposure to N09, but did conclude that the exposure limit for the general public for 10
3
minutes, 30 minutes, or 60 minutes should be established at 1,880 ug/m (1.0 ppm).
A more complete review was published by the National Academy of Sciences in 1977
(National Academy of Sciences, 1977). This document covered the medical, biological, and
physical effects of the nitrogen oxides and made recommendations for future research, but
included no suggestions for legislative exposure limitations.
A task group on environmental health criteria for oxides of nitrogen, representing the
World Health Organization, recommended in 1978 that the effects of pollution designated as
"adverse", in addition to the morphological and other changes produced by high N02 concentra-
tions, should include: increased airway resistance, increased sensitivity to bronchoconstric-
tors, and enhanced susceptibility to respiratory infections (World Health Organization, 1977).
This group selected 940 ug/m (0.5 ppm) as their estimate of the lowest concentration of NOp
at which adverse health effects due to short-term exposure might be expected to occur, but did
not state their rationale explicitly.
The following assessment appraises most of the studies included in these previous reviews
plus additional, more recent, pertinent publications. This assessment includes discussion of
controlled human exposure studies and epidemiological studies of human health effects associ-
ated with indoor and outdoor exposures to NO compounds. In addition, studies on the effects
of accidental and occupational exposures to oxides of nitrogen are concisely reviewed in this
chapter.
15-1
-------
Placing the present assessment in historical perspective, it should be noted that concern
regarding NO effects on human health was originally derived from cases of accidental or occu-
pational exposures to NO compounds. For example, the earliest evidence for potential damage
to man due to NO exposures occurred in the chemical industry where, as early as 1804, the
deaths of a man and his dog after breathing nitric acid fumes were recorded (Raminez, 1974).
Other occupational exposures have since been seen with the use of explosives which generate
NOp during misfires and welding operations which generate substantial quantities of NO .
Burning of plastics, shoe polish, and nitrocellulose also results in potentially excessive
quantities of NO . High concentrations of ambient NO^ were clearly associated with acute .pul-
monary edema and death. Lowry and Schuman (1956) were among the earliest investigators who
demonstrated that exposures to NO- in excess of 200 ppm would induce such effects. Their des-
cription of silo fillers' disease clearly implicated N02 exposure in the etiology of this
disease as another potential occupationally related NO hazard. That hazard, first noted in
A
1914 (Hayhurst and Scott, 1914), when four individuals died suddenly after entering a recently
filled silo, was earlier mistakenly attributed to high concentrations of carbon dioxide.
A fairly typical clinical picture of signs and symptoms associated with exposures to very
high levels of NO compounds (especially N02) has emerged from case studies of accidental and
occupational exposures, as reviewed by Milne (1969) and Horvath et al. (1978). Acute exposure
to high concentrations (> 47,000 ug/m ; 25 ppm) of NOp produces an almost immediate reaction
consisting usually of cough, dyspnea, and tightness of the chest and respiratory tract caused
by acute bronchitis or pulmonary edema. Such exposure may be quickly fatal. If the exposure
has not been overly excessive, exposed individuals may recover without further complications.
However, if the exposure concentration and duration are greater, more intense symptoms may
occur after a latent period of 2 to 3 weeks. These consist of severe respiratory distress
usually occurring quite suddenly and can result in death within a few days. The cause of
these symptoms is always bronchiolitis fibrosa obliterans. When symptoms are not sufficiently
severe to cause death, subjects frequently appear to recover fully. Such a biphasic reaction
to exposure to N0? was described by Milne (1969), as determined from a literature review of
clinical case studies.
Horvath et al. (1978) more recently reviewed data accumulated on 23 patients exposed to
nitrogen dioxide in agriculture or industrial situations. Their review confirmed that, during
the acute phase following severe N02 exposures, varying combinations of restrictive and
obstructive ventilatory defects, impaired diffusion capacity and hypoxemia are found. However,
Horvath et al. (1978) also noted some evidence for pulmonary dysfunction persisting after
follow-up periods of 2.5 to 13.5 years, including diminished exercise tolerances with dyspnea
during exertion. Fleming et al. (1979) recently conducted physiologic studies on a patient
exposed to nitric acid fumes during the acute (immediate) and delayed (13 weeks later) stages.
The acute changes were as anticipated. During the delayed stage, elastic recoil and
resistance to flow were normal. However, dynamic compliance was reduced and dependent upon
15-2
-------
respiratory frequency and, more significantly, oxygen transport was abnormal during exercise
with P(A-a)0,> of 20 mm Hg. Dysfunction of small airways was evident. Many of the individuals
who were discussed in the above case studies detected a pungent odor when initially exposed to
NO compounds in various occupational situations.
X
The above types of effects noted in relation to accidental and occupational exposures (as
discussed in more detail later in Section 15.4) helped to direct attention to possible human
health effects induced by lower concentrations of N09 and other NO compounds encountered with
£ A
indoor or outdoor exposures to ambient air pollutants. Further, the observations made on sub-
jects inadvertantly exposed to clearly toxic levels of NO compounds contributed to the con-
ceptual framework regarding possible functional changes associated with lower level NO expo-
sures, the physiological bases of such changes, and the methodological approaches employed in
attempting to measure such changes in animal toxicology, controlled human exposure, and
epidemiological studies.
15.2 CONTROLLED HUMAN EXPOSURE STUDIES
Controlled exposure studies are useful because they can provide accurate measurements of
the effects of specific exposures to single or simple combinations of pollutants. However,
controlled studies usually do not provide definitive evidence of the effects that might be ex-
pected in ambient situations. In the uncontrolled natural environment, exposures are changing
constantly in regard to both the mixture of pollutants present and the concentrations of each.
The inability to extend controlled exposure studies over several months limits the extent to
which human studies have been useful in determining the effects of repeated, short-term expo-
sures to the highest levels of pollutants occurring in the natural environment.
For these reasons, controlled exposure studies usually are designed to determine the
effects of a short, single exposure to a pollutant at a concentration believed to be high
enough to produce some response. Obviously, in such studies the safety of test subjects is
the overriding factor in determining the concentrations and exposure times that can be used.
Initial estimates of these factors are often first obtained from animal studies. Prudence re-
quires, however, that exposure times be limited to those causing initial responses. When
effects are detected, additional studies are undertaken to collect evidence of the lowest con-
centration at which effects can be measured in both healthy and selected, sensitive volunteers.
As noted above, the methods and physiological basis for most controlled studies are based on
observations made on subjects inadvertently exposed to toxic levels of NO^. These include
controlled human exposure studies on the sensory effects of NO compounds as well as NO -
X X
induced pulmonary function changes discussed below.
15.2.1 Studies of Sensory Effects
15.2.1.1 Effects of Nitrogen Dioxide on Sensory Systems--The significance of effects on
sensory receptors, if any, is unknown. The stimulation of a sensory receptor does invoke
within an individual a specific response resulting from the neural transmission of the
stimulation.
15-3
-------
Changes in the intensity of light to which an individual is exposed initiate such a bio-
chemically transmitted response. An impairment of dark adaptation, then, represents a slowing
of the mechanism by which the eye adjusts to changes in light intensity. Because the response
to the stimulus is delayed, this effect on dark adaptation must be considered to be an impair-
ment. Whether or not it is reversible or whether or not the reversibility persists after each
repeated insult, impairment of dark adaptation is reported at lower concentrations of N0? than
is any other physiologic system tested.
Shalamberidze (1967) reported that impairment of dark adaptation occurred at NO, concen-
3
trations as low as 140 ug/m (0.07 ppm) (Table 15-1). The tests, as reported by the investi-
gator, demonstrated changes in ocular sensitivity to light by determining reflex changes in
the functional state of the cerebral cortex. This study, however, gave results that conflict-
ed with those reported by Bondareva (1963) (Table 15-1). This latter investigator determined
normal dark-adaptation curves for five volunteers and then exposed them to concentrations of
3
NOp varying from 150 to 500 ug/m (0.08 to 0.26 ppm) to determine alterations that might be
related to the changed atmosphere. While her results indicated that exposure to concentra-
tions of 300 ug/m (0.16 ppm) had no effect on dark adaptation, time for adaptation increased
significantly as a result of exposure to 500 ug/m (0.26 ppm). Repeated daily exposures to
3
500 ug/m (0.26 ppm) NO^ over a period of 3 months, however, induced an apparent physiological
adjustment that largely reversed the initial increase in the time for adaptation. It has been
suggested (National Academy of Sciences, 1977) that, since Bondareva did not indicate whether
NOp was used alone or in combination with nitric oxide (NO), the higher value reported to be
the minimum effective concentration may have been due to differences in the test atmospheres.
The perception of odors is a response to chemical stimulation of the olfactory
receptors, but this perception fades with adaptation. The olfactory epithelium contains
neural tissue which directly contacts airborne substances. Thus, interference with normal
olfactory function could possibly reflect either direct or indirect interruption of neuro-
chemical processes. Olfactory insensitivity to NO- could reduce awareness of potentially
hazardous situations arising from increasing levels of the pollutant.
Studies of odor perception show that sensitive individuals can detect the characteristic
pungent odor of NO,, at a concentration of 200 ug/m (0.11 ppm) (Table 15-1). Other studies
have indicated that, by increasing relative humidity in the exposure atmosphere, odor percep-
tion is improved and respiratory irritation also is increased. Increasing the concentration
gradually in the controlled exposure atmosphere results in a raising of the threshold so that
its odor becomes less irritating.
Henschler et al. (1960) exposed groups of 20- to 35-year-old healthy males to N02 to
obtain information on the lowest concentrations at which the odor would be detected immedi-
ately. The odor of NO, was perceived by three of nine volunteers when the concentration was
3 3
230 ug/m (0.12 ppm), by 8 of 13 subjects when the concentration was 410 ug/m (0.22 ppm), and
by all of eight subjects when the concentration of N02 in the exposure chamber was 790 ug/m
(0.42 ppm).
15-4
-------
TABLE 15-1. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY RECEPTORS IN CONTROLLED HUMAN STUDIES
N0? Concen-
trations
ug/m
790
410
230
230
200
0
to
51,000
2,260
140
150
to
500
ppm
0.42
0.22
0.12
0.12
0.11
0
to
27
1.2
0.07
0.08
to
0.26
Time
No. of until
Subjects effect
8 Immediate
13 Immediate
9 Immediate
14 Immediate
28 Immediate
6 54 minutes
6 Immediate
4 5 and 25
minutes
5 Initial
Repeated
over 3
months
No. of
Subjects
Effects Responding
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
Perception of odor of N0?
No perception of odor of N0? when
concentration was raised slowly from
0 to 51,000 ug/m
Perception of odor improved when
relative humidity was increased from
55% to 78%
Impairment of dark adaptation
Increased time for dark adaptation
at 500 ug/m (0.26 ppm)
Initial effect reversed
8/8
8/13
3/9
most
26/28
0/6
6/6
4/4
Not
Reported
Reference
Henschler et al . ,
1960
Ibid.
Ibid.
Shal amberidze,
1967
Feldman, 1974
Henschler et al . ,
1960
Ibid.
Shalamberidze,
1967
Bondareva, 1963
-------
The duration of exposure over which odor could be perceived varied considerably among subjects
and was unrelated to the concentration of NCL. At concentrations of up to 20,000 ug/m (10.6
ppm), perception of the odor of N02 was lost after periods ranging from less than a minute to
13 minutes. However, regardless of the concentration, odor perception sensitivity returned
within 1 to 1.5 minutes after subjects left the exposure chamber. Some subjects exposed to
N02 concentrations as low as 230 ug/m (0.12 ppm) reported a metallic taste, dryness, and con-
striction in the upper respiratory tract. Such symptoms lessened and eventually disappeared
with repeated exposures. When N02 was added gradually to the exposure chamber over a period
of approximately 1 hour, exposed subjects did not perceive the odor even when it reached a
level of 51,000 ug/m (27 ppm). When subjects were exposed to an atmosphere containing 2,260
2
|jg/m NOp (1.2 ppm) at 55 percent relative humidity, after which the humidity was increased
very rapidly to 78 percent, a sharp increase in odor perception occurred along with a corre-
spondingly sharp increase in irritation of the mucous membranes of the respiratory tract. It
is possible that the increased irritation, and perhaps the increased odor perception, is the
result of chemical reactions between nitrogen oxides and water in the controlled atmosphere
that increase the concentrations of nitrogenous acids.
Odor perception studies were also conducted by Feldman (1974), who reported that 200
3
|jg/m (0.11 ppm) was the lowest concentration at which the odor of NOp was detected. At this
concentration, 26 of 28 healthy subjects perceived the odor immediately.
In summary, controlled exposure studies indicate that two types of sensory receptors .may
be involved in the initial response in humans to the presence of NO,,. The sensory effects
involved are the impairment of dark adaptation and the perception of odor. Effects were
3
reported at levels as low as 140 to 200 ug/m (0.08 to 0.1 ppm) and occurred almost immediately
upon exposure.
15.2.1.2 Sensory Effects Due to Exposure to Combinations of Nitrogen Dioxide and Other
Pollutants—Studies of the effects of N02 in combination with other pollutants on sensory
receptors are summarized in Table 15-2. These studies, all from the Soviet Union, report that
the effects of the test gases, when inhaled together, were additive, as they related to the
minimum concentrations causing impairment of dark adaptation, odor perception, and changes in
the amplitude of alpha rhythms in the brain.
Shalamberidze (1967) exposed 15 healthy subjects for periods of 5 or 25 minutes to various
combinations of N02 and sulfur dioxide (SOp). His studies were designed to compare the lowest
concentrations at which dark adaptation is impaired by combinations of pollutants to levels of
the individual gases causing impairment. He reported the minimum levels for impairment of dark
3 3
adaptation for single pollutants to be 600 ug/m (0.23 ppm) for S02 and 140 ug/m (0.07 ppm)
for N00. The thresholds for alteration of odor perception for subjects exposed to a single
3 3
gas were 230 ug/m (0.12 ppm) for N02 and 1,600 ug/m (0.61 ppm) for SO,,. In these studies,
combinations of the gases produced an impairment of dark adaptation or odor perception whenever
the fractional threshold concentrations for the separate gases totaled one or more. The
15-6
-------
TABLE 15-2. EFFECTS OF EXPOSURE TO COMBINATIONS OF POLLUTANTS ON SENSORY RECEPTORS
IN CONTROLLED HUMAN STUDIES
Pollutant Subjects
Exposure
Effects
Reference
Various
Combina-
tions of
N02 and
otner
15 healthy
subjects
5 or 25
min; oral
or nasal
inhalation
gases
The lowest effective concentration for dark
adaptation was: N02, 140 ug/m (0.07 ppm) and
S02, 600 ug/m .(.0.23 ppm). When inhaled to-
gether, the gases acted additively. Dark
adaptation was impaired when the sum of the
fractional threshold concentrations for the
separate gases equaled 1.0 or more.
Lowest effective concentration for odor percep-
tion was: 3N02, 230 ug/m (0.12 ppm) and S02(
1,600 ug/m (6.16 ppm). When inhaled togetner
these gases acted additively. Odor was per-
ceived when the sum of the fractional thresh-
old concentrations equaled 1.0 or more.
Shalamberidze,
1967
en
i
Various
mixtures
of NO
SO fl SO
aerosoT
and NH,
Not
reported
Not
reported
Lowest effective concentrations for odor per-
ception of a combination of gases were reported 1972
to be: NO 20 ug/nT (0.01 ppm); SQ? 170 ug/rn
(0.06 ppm)? H?SO.,.aerosol , 110 g/m (0.03 ppm),
and NH3, 300 flg/m (0.43 ppm). When inhaled
together the odor was perceived whenever the
fractional threshold totaled 1.0 or more.
Kornienko,
Mixture
of NO
SO NH.
Four
Not Threshold for changes in the amplitude of alpha Kornienko,
reported rhythms occurred when the sum of the fractional 1972
concentrations of the individual gases equaled
1.0 or more.
-------
lowest N02 concentration causing impairment of dark adaptation was approximately 60 percent
lower than the minimum concentration needed for odor perception. For SO^, dark-adaptation im-
pairment occurred at a concentration about 38 percent below that at which the odor was detected.
Kornienko (1972) determined odor-perception capabilities in a group of subjects exposed
to individual gases or combinations of NO,,, SCL, sulfuric acid aerosol, and ammonia. He
reported also that the odor of any gas mixture was perceived whenever the sum of the fractional
threshold concentrations of the component gases totaled one or more. Kornienko also investi-
gated the effects of mixtures of these same gases on alpha rhythm in the brain. Again, he
determined that the earliest decreases in amplitude, in response to combinations of the gases,
occurred whenever the fractional threshold concentrations for the individual gases totaled one
or more.
15.2.2 Pulmonary Function
15.2.2.1 Controlled Studies of the Effect of Nitrogen Dioxide on Pulmonary Function in Healthy
Subjects—Controlled experimental studies in the laboratory situation have been mostly con-
cerned with exposure to N02 alone although a few studies have considered effects during expo-
sure to one or two additional air pollutants. These studies have generally been conducted on
young healthy adults and/or on subjects suspected of being sensitive, e.g., individuals who
have chronic respiratory problems. Controlled experimental studies on exposures of normal
subjects to N02 are summarized in Table 15-3.
Nakamura (1964) determined the effect of exposure to combinations of NCL and sodium chlo-
ride aerosol (mean diameter 0.95 urn) on airway resistance (R.,.,.) measured by an interruption
QW
technique (Table 15-3). Two groups of seven and eight healthy subjects, 18 to 27 years old,
were exposed for 5 minutes to 1,400 ug/m sodium chloride aerosol alone. After resting for 10
to 15 minutes, individual subjects were exposed for 5 minutes to different N09 concentrations
3
ranging from 5,600 ug/m (3.0 ppm) to 7,500 (4 ppm). Nitrogen dioxide concentrations were
measured by the Saltzman method. Each individual in each group showed increased R after
aW
exposure to the NO, alone, but the sodium chloride aerosol alone exerted no effect on airway
3
resistance. Nitrogen dioxide alone at concentrations of 5,600 and 11,300 |jg/m (3.0 and 6.0
ppm) caused increases in Rnvi of 16 and 34 percent, respectively, in the one subject tested at
3W
each concentration.
Von Nieding et al. (1970) reported, at the Second International Clean Air Congress, the
3
results of exposures of 13 healthy subjects to an NOp level of 9,400 ug/m (5.0 ppm) for 15
minutes (Table 15-3). Concentrations were measured by the colorimetric Saltzman method. At
this level, a significant decrease in arterialized oxygen partial pressure (Pa02) was induced,
but the end expiratory oxygen partial pressure (Pa02) remained unchanged. A reduced oxygen
pressure in arterial blood would suggest a reduction in the transfer of oxygen from inspired
air to blood in the lungs. The steady oxygen pressure in expired air would indicate that a
constant supply of oxygen was delivered to the lungs. Together, the results suggest that N02
may have interfered with the transfer of oxygen from alveolar air to arterial blood. This
15-8
-------
TABLE 15-3. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION
IN CONTROLLED STUDIES OF HEALTHY HUMANS**
Concentration Pollu-
ug/nT
ppm tant
No. of
Healthy
Subjects
Exposure
Time
Effects
Reference
13,000 7.0 N02 Several
10-120 Increased R * in some subjects. Others Yokoyama,
min. tolerated 3BVOOO ug/m (16 ppm) with no 1972
increase in R
aw
9,400 5.0 N02
11 2 hrs. Increase in R * and a decrease in AaDO * Von Nieding
with intermittent light exercise. No,en- et al.,
hancement of the effect when,200 ug/m 1977
(0.1 ppm) 0., and 13,000 ug/m (5.0 ppm)
S0? were combined with N0? but recovery
time apparently extended.
9,400
9,400
7,500
to
9,400
5,600
11,300
5.0 N02
5.0 N02
4.0 N0?
to ^
5.0
3.0 N02
6.0 N02
16 15 min. Significant decrease in DL *
13 15 min. Significant decrease in Pad * but end ex-
piratory 0? * unchanged with significant
increase in systolic pressure in the
pulmonary artery.
5 10 min. 40% decrease in lung compliance 30 min.
after exposure and increase in expiratory
and inspiratory flow resistance that
reached maximum 30 min. after exposure.
1 5 min. Increase in R * compared to pre-exposure
values (enhanced by NaCl aerosol).
1 5 min. More subjects were tested at higher
exposures.
Von Nieding
et al. , 1973
Von Nieding
et al. ,
1970
Abe, 1967
Nakamura ,
1964
(continued)
-------
TABLE 15-3. (continued)
Concentration Pollu-
ug/m
ppm tant
No. of
Healthy
Subjects
Exposure
Time
Effects
Reference
14,000 7.5
9,400 5.0
4,700 2.5
en
i
16 2 hrs. Increased sensitivity to a bronchocon-
strictor (acetylcholine) at this concen-
tration but not at lower concentrations.
8 14 hrs. Increase in R during first 30 min. that
was reduced tnrough second hour followed
by greater increases measured at 6, 8 and
14 hrs. Also increased susceptibility to
a bronchoconstrictor (acetylcholine).
8 2 hrs. Increased R with no further impairment
at higher concentrations. No change in
arterial P0?* pressure or PCO? pressure.
Beil and
Ulmer, 1976
1,880
1,880
1,300
to
3,800
:1,150
1,880
to
3,760
1.0 N02
1.0 N02
0.7 N0?
to i
2.0
0.6 - N02
1.0 N0?
to
2.0
8 2 hrs. No increase in R
dW
16 2 hrs. No statistically significant changes
in pulmonary function with the exception
of small but statistically significant
changes in FVC; see pp. 15-20.
10 10 mins. Increased inspiratory and expiratory flow
resistance of approximately 50% and 10% of
control values measured 10 mins. after
exposure.
15 2 hrs. No physiologically significant change
in cardiovascular, metabolic, or pulmo-
nary functions after 15, 30 or 60 mins.
or exercise.
10 2h hrs. Alternating exercise and rest produced
statistically significant decreases for
hemoglobin hematocrit, and enythrocyte
acetylchol inesterase.
Beil and
Ulmer, 1976
Hackney, et al
1978
Suzuki and
Ishikawa,
1965
Fol insbee
et al. , 1978
Posin et al . ,
1978
(continued)
-------
TABLE 15-3. (continued)
en
i
Concentration
ug/m ppm
1,000
1,000
with
560
1,000
with
560
and
45,000
500
500
with
560
500
with
560
and
45,000
0.50
0.50
0.29
0.50
0.29
30.0
0.25
0.25
0.29
0.25
0.29
30.0
Pollu-
tant
03
°3
J
N02
°3
J
NO,
/
L.
CO
03
°3
O
NO,
L-
0,
3
NO,
}
C-
CO
No. of
Healthy Exposure
Subjects Time Effects Reference
4 4 hrs. With each group minimal alterations in Hackney
p.ulmonary function caused by 0., exposure. et al . ,
Effects were not increased by addition of 1975a,b,c
NO, or NO, and CO to test atmospheres.
L. c.
7 2 hrs. Little or no change in pulmonary function Hackney
found with 03 alone. Addition of NO- or et al.,
of N02 and CO did not noticeably increase 1975a,b,c
the effect. Seven subjects included some
believed to be unusually reactive to
respiratory irritants.
(continued)
-------
TABLE 15-3. (continued)
Concea
ug/m
100
with
50
and
300
tration
ppm
0.05
0.025
0.11
Pollu-
tant
N02
°3
SO,
No. of
Healthy Exposure
Subjects Time Effects
11 2 hrs. No effect on R w* or AaDO *; exposed sub-
jects showed increased sensitivity of
bronchial tree to a bronchoconstrictor
(acetylchol ine) over controls not exposed
to pollutants.
Reference
Von Nieding
et al. , 1977
aw
**
airway resistance
AaD02: difference between alveolar and arterial blood partial pressure of oxygen
DL_0 : diffusion capacity of the lung for carbon monoxide
Pa02 : arterial partial pressure of oxygen
P0? : partial pressure of oxygen
PCO? : partial pressure of carbon dioxide
By descending order of lowest significant effect shown by each study.
-------
increased difference between the alveolar and arterialized oxygen partial pressures (AaD02)
was' accompanied by a significant increase in systolic pressure in the pulmonary artery.
However, the significance of the changes in A-aP02 are questionable in part due to the tech-
niques employed and there is apparently some question as to the conditions present in their
exposure chambers. Regardless of these questions, the potential of high N0? exposure to modify
the delivery of. oxygen to tissues remains unanswered. As noted later, no evidence for
increased oxygen uptake during light to moderate exercise has been found.
Von Nieding et al. (1977) also exposed 11 healthy subjects, aged 23 to 38 years, to
9,400 |jg/m (5.0 ppm) NO^ for 2 hours. Pulmonary function values, recorded prior to exposure,
when the exposure was terminated, and 1 hour after exposure was terminated, were compared with
similar values from control subjects exposed to clean air for 2 hours. Test subjects who
underwent a regimen of intermittent light exercise during the testing period showed significant
increases both in R and in AaDO^-
Von Nieding and co-workers (1973) observed a significant decrease in the lung's diffusion
capacity for CO (DL~Q) in 16 healthy subjects resulting from a 15-minute inhalation of 9,400
|jg/m3 (5.0 ppm) NO, (Table 15-3). Abe (1967) found that concentrations of 7,500 to 9,400
3
|jg/m (4.0 to 5.0 ppm) for 10 minutes produced increases in both expiratory and inspiratory
flow resistance in five healthy males; these increases reached a maximum 30 minutes after the
end of exposure. Effective compliance (change in lung volume per unit change in air pressure),
observed in this study 30 minutes after cessation of exposure, was decreased by 40 percent when
compared with controls.
Increases in the inspiratory and expiratory flow resistance, observed in 10 healthy sub-
3
jects exposed to N02 concentrations ranging from 1,300 to 3,800 ug/m (0.7 to 2.0 ppm) for 10
minutes, were reported by Suzuki and Ishikawa (1965) (Table 15-3). Ten minutes after the
exposure ceased, inspiratory resistance was increased 53 percent and expiratory resistance 13
percent. Information on variations in the results at different levels of exposure was not
provided in this report. Since the exposure levels were reported by the authors to have varied
during the studies, results are difficult to interpret. It is unlikely that concentrations of
NO- would have varied extensively during a controlled exposure of 10 minutes duration. Results
reported, however, were the averages of the responses of the 10 test subjects and may have
reflected a response averaged across several exposure concentrations. The effect of NO, at a
3
concentration of 9,400 ug/m (5.0 ppm) was not increased by the addition of ozone (0,) to the
3 3
experimental atmosphere at a concentration of 200 ug/m (0.1 ppm) or by adding 13,000 ug/m
(5.0 ppm) S02 to the N02/03 combination. When 03 or the 03 plus the S02 was added to the
experimental atmosphere, the pulmonary function values, measured 1 hour after exposure was
terminated, had not normalized as much as had the values in subjects exposed to N02 alone.
Since subsequent measurements were not made, the only conclusion to be drawn from the study
results is that recovery time following exposure to the multiple pollutants was delayed.
15-13
-------
Yokoyama (1972) measured airway resistance in volunteers exposed to various concentrations
of N00 for periods of 10 to 120 minutes. He measured increases in airway resistance at 13,200
3
ug/m (7.0 ppm) and higher. He also recorded wide variations in individual sensitivity. Some
volunteers tolerated concentrations as high as 30,000 ug/m (16 ppm) with no increase in airway
resistance. Because atropine effectively blocked the bronchoconstrictive effect of S09 but
not of N02, this investigator suggested that the mechanism for the increase in airway
resistance was unrelated to vagal stimulation.
Folinsbee et al. (1978) concluded from studies of three groups of five healthy males,
ranging in age from 19 to 29 years, that no physiologically significant alterations in the
measurements of pulmonary, cardiovascular, or metabolic factors were produced by 2-hour expo-
sures to 1,150 ug/m (0.61 ppm) NO^ monitored by a continuous chemiluminescence technique
(Table 15-3). Pulmonary measurements included: ventilatory volume (VV); tidal volume (V-,-);
forced vital capacity (FVC); forced expiratory volume (FEV) at 1, 2, and 3 seconds, and forced
expiratory flow (FEF) at 50 and 75 percent of vital capacity exhaled. Other measurements
included oxygen (02) and carbon dioxide (CO-) percentages in inspired and expired air, cardiac
output, blood pressure, heart rate, steady state diffusion capacity of the lungs for carbon
monoxide (DL^Q) and closing volume, with slow vital capacity (VC).
Hackney et al. (1978) found no statisically significant changes in pulmonary function
o
in.16 healthy individuals exposed for 2 hours to 1,800 ug/m (1.0 ppm) NO- with the exception
of a marginal loss in forced vital capacity (FVC). The authors question the health signifi-
cance of this latter small, but statistically significant change in FVC. That is, Hackney
et al. (1978) stated:
"As indicated, no changes with exposure were apparent except for a
mean loss of 1.5% in FVC after the second exposure as compared to con-
trol. That this change represents other than a random variation is
doubtful, due to its small size, its marginal statistical significance,
and the relative large number of statistical comparisons being made."
Nitrogen dioxide was monitored by a continuous chemiluminescence analyzer and checked by the
Saltzman method. Pulmonary functions measured included FVC, FEV, peak and maximum expiratory
flow, closing volume (CV), R , and others.
aw
Beil and Ulmer (1976) exposed healthy volunteers (groups of 8 or 16) for 2 hours to 1,880,
4,700, 9,400, and 14,000 ug/m (1.0, 2.5, 5.0, and 7.5 ppm) NO,. Nitrogen dioxide concen-
trations were monitored by the continuous chemiluminescence method. An additional group was
exposed for 2 hours to clean air. Following exposure to l^ at concentrations of 4,700 ug/m
(2.5 ppm) or above, these investigators measured significant increases in R compared to the
aW
controls, but no decrease in Pa09 or increase in PaC09. Airway resistance was not
3
increased at a concentration of 1,880 ug/m (1.0 ppm). Nitrogen dioxide concentrations of
9,400 or 14,000 ug/m (5.0 or 7.5 ppm) did not produce significantly greater increases than
o
did 4,700 ug/m (2.5 ppm). In these healthy subjects, increased sensitivity to a bronchocon-
strictor (0.5 percent acetylcholine for 1 minute inhalation at the rate of 0.12 liter per
second) was observed after exposure for 2 hours to 14,000 ug/m (7.5 ppm) N02 but not after
15-14
-------
2
exposure to 4,700 or 9,400 ug/m (2.5 or 5.0 ppm). When the duration of exposure was increased
3
from 2 to 14 hours, 9,400 |jg/m (5.0 ppm) NO, caused an initial increase in R during the
£. aw
first 30 minutes. Airway resistance tended to return toward normal during the second hour.
This was followed by even larger increases in R measured after 6, 9, and 14 hours of exposure.
The effect of exposure on two consecutive days was reversible, and R measured 24 hours after
aw
initiation of exposure (10 hours after exposure was terminated) had returned to pre-exposure
levels. Exposure of healthy subjects for 14 hours to 9,400 ug/m (5.0 ppm) increased sensi-
tivity to acetylcholine; the effects of longer exposures to lower concentrations were not
tested.
Posin et al. (1978) exposed 10 subjects for 2.5 hours to filtered air on day one and on
two consecutive days (days 2 and 3) to N02. The subjects alternated 15 minutes of exercise
(double resting ventilation) and 15 minutes of rest. The ambient NO, levels were 1880 or 3760
3
ug/m (1 or 2 ppm). Statistically significant decreases were observed for hemoglobin, hemato-
crit, and erythrocyte acetylcholinesterase. Glucose-6-phosphate dehydrogenase was elevated
after the second exposure to 3760 ug/m (2 ppm) NO, and levels of peroxidased red blood cell
3
lipids were elevated after exposure to 3760 ug/m (2 ppm). These investigators concluded that
significant blood biochemical changes resulted from N0? inhalation. However, there are some
questions as to the validity of these conclusions since there is considerable variability in
the measurements that were made,
In contrast, Horvath and Folinsbee (1979) in a study on eight subjects exposed to 940
ug/m (0.50 ppm) under a variety of ambient temperature conditions with one period of 30
minutes of exercise during the two hours failed to observe any changes in pulmonary functions.
Also, Kerr et al. (1979) studied 10 normal healthy subjects exposed for 2 hours to 940 ug/m
(0.5 ppm) NOp. One subject experienced the very mild symptom of slight rhinorrhea. Although
the authors suggest that the changes reported in quasi static compliance may be due to chance
alone, there is uncertainty whether these changes were due to daily variation or to N02 expo-
sure (see also page 15-27). No other significant alteration in pulmonary function resulted
from the exposure.
When von Nieding and co-workers (1977) exposed 11 healthy subjects to a combination
of N02 at 100 ug/m3 (0.05 ppm), 03 at 50 ug/m3 (0.025 ppm), and S02 at 300 ug/m3 (0.11 ppm)
for 2 hours, no effect on R or AaDO, was reported (Table 15-3). Exposure to this combination
aw L.
of pollutants did, however, produce what was interpreted by the investigators as dose-dependent
increases over controls (not exposed to the pollutants) in the sensitivity of the bronchial
tree to administered acetylcholine as measured by increases in R . Constriction of the
aw
bronchi is a physiological alteration similar to that experienced by many individuals as asthma
attacks. The suggestion provided by this study is that exposure to air pollutants may increase
susceptibility to asthma attacks in some individuals.
Hackney et al. (1975a; 1975b; 1975c) exposed four healthy male volunteers to 0, (1,000
•3 3
|jg/m ; 0.5 ppm) and subsequently to mixtures of 03 and NO,, (560 pg/m ; 0.3 ppm) or 03> N02 and
15-15
-------
2
CO (45,900 |jg/m ; 30 ppm) (Table 15-3). Volunteers were exposed for 4 hours plus about 1
additional hour during which several tests of pulmonary function were performed. The exposure
regimen was designed to simulate exposure experienced during severe pollution episodes in Los
Angeles on a summer day. The exposure time, however, was about twice that experienced in the
ambient situation. Under these conditions, minimal alterations in pulmonary functions (FVC,
FEV, CV, R and others) were measured when test subjects were exposed to 0-, alone. These
3w o
alterations were not increased by the additions of N02 or of N02 and CO. Another group of
seven male volunteers, including some believed to be unusually reactive to respiratory irri-
Q
tants, was exposed under a similar protocol with an exposure time of 2 hours and to 500 ug/m
(0.25 ppm) 0-,. Again, little or no change in pulmonary function was found with 0, exposure
3 3
alone, or with addition of NO- (560 ^g/m ; 0.3 ppm) or of N02 plus CO (45,900 ug/m ; 30 ppm).
Schlipkbter and Brockhaus (1963) determined, in three subjects, the effects of exposure
to N09, carbon monoxide (CO), and SO,, on pulmonary deposition of inhaled dusts. A suspension
3
of homogenized soot (particle sizes 0.07 to 1.0 urn) was combined with either 9,000 [jg/m (4.8
ppm) N02, 55,000 ug/m3 (50 ppm) CO, or 13,000 ug/m3 (5.0 ppm) S02 and administered to experi-
mental subjects by inhalation. The individual pollutant concentrations were the maximum
acceptable concentrations in the Federal Republic of Germany. Pulmonary retention was deter-
mined by measuring the differences between the concentrations of dust in the inhaled and exhaled
air. Under control conditions and with CO and S02 exposure, 50 percent of the dust was
retained. Retention increased to approximately 76 percent when the dust was administered in
3
an atmosphere containing 9,000 (jg/m (4.8 ppm) N02. Greater proportions of dust particles in
the range of 0.3 to 0.8 urn were retained than were other size particles. This study is signi-
ficant in that it demonstrates a potential additive or greater than additive mechanism that
could operate in ambient situations involving significant N02 exposures of short duration.
The study suggests that, as N02 concentrations in inhaled air increase, the response induced
may result in respiratory retention of larger proportions of inhaled particles. If the partic-
ulate matter includes toxic materials, the additional impact on health could be significant.
Nakamura's (1964) studies on the interaction of N02 and sodium chloride aerosol indicated
that sodium chloride aerosol had no influence on R, . When the sodium chloride aerosol (mean
aw
diameter 0.95 urn) was added to the exposure atmospheres, the increases in R=l, for the group
aW
were approximately 40 percent, about twice that produced by the gas alone. A sodium chloride
aerosol comprised of smaller particles (mean diameter 0.22 (jm) at 1,400 ug/m , in combination
with the same concentrations of N00, produced no increase in R=ii over that caused by the gas
L. aW
alone. The consistent sequential methodology used in this study tends to reduce the credi-
bility of this study; nevertheless, the fact that the final exposure challenge in the sequence
increased the R when the NaCl aerosol particles averaged 95 |jm in diameter but did not
aw
increase R when they averaged 22 \m in diameter indicates that when used in the same sequence
61W
the larger particles of NaCl enhanced the effect of N02 while the smaller particles did not.
15-16
-------
Von Nieding and his co-workers (1970;1977) ^have conducted a number of studies of the
effects of N02 on pulmonary function in healthy and bronchitic subjects. Some of the methods
used for these studies differ from those employed routinely in the United States, and for this
reason may not be directly comparable. For example, von Nieding measured R during normal
breathing using a body plethysmograph with a temperature compensation mechanism. Most Amer-
ican investigators have used constant-volume body plethysmographs and measure R during
aw
panting (DuBois, 1956). Investigators in this country also measure arterial partial pressure
of oxygen (PaCL) in blood drawn directly from an artery, as opposed to a drop of blood
obtained by pricking the ear lobe. In spite of the differences in technique, and the opinion
offered here that the American methodology may be more accurate over the entire range of
possible values, it is generally agreed that, in the hands of competent technicians, the
methods used by von Nieding provide valid information on directional changes in airway resist-
ance or changes in PaCL.
Horvath and Folinsbee (1979) exposed eight young adults to either filtered air or 980
3 3
ug/m (0.5 ppm) 0., plus 940 |jg/m (0.5 ppm) NO^ in filtered air under four different environ-
mental conditions: (1) 25°C, 45% RH; (2) 30°C, 85% RH; (3) 35°C, 40% RH; and (4) 40°C, 50%
RH. There were a total of eight exposures for each subject with a minimum of 1 week between
exposures. During the exposures, the subject first rested for 60 minutes, then exercised for
30 minutes at 35-40% of his predicted maximum aerobic capacity and then rested for the final
30 minutes. Repeat tests were generally made on each subject at the same time of the day.
The pulmonary responses to ozone alone were as found in previous studies by the same research
group. No additive effect or interaction between ozone and nitrogen dioxide was observed.
In summary, studies on the effects of N0? on pulmonary functions in healthy volunteers
(Table 15-3) indicate that exposure of 2 hours or less to concentrations of less than 4700
ug/m (2.5 ppm) can induce increases in R (Beil and Ulmer, 1976). The lowest concentration
aw o
producing this effect is somewhat uncertain but is likely in the range of 1300 to 3800 ug/m
(0.7 to 2.0 ppm) (Suzuki and Ishikawa, 1965). Other changes in pulmonary function have been
reported at higher concentrations. Exposure to a low-level mixture of N02, 03, and S02 was
also reported to increase sensitivity of healthy subjects to a bronchoconstrictor.
15.2.2.2 The Effects of Nitrogen Dioxide Exposure on Pulmonary Function in Sensitive
Subjects—Subjects such as patients with asthma or chronic bronchitis have been studied by
several investigators, as summarized in Table 15-4. For example, Von Nieding et al. (1973)
exposed 14 patients with chronic bronchitis to N02 at a concentration of 9,400 ug/m (5.0 ppm)
for 15 minutes (Table 15-4). Alveolar partial pressures of oxygen measured before, during,
and after inhalation of NO, were not altered significantly (p > 0.05). The earlobe
2
arterialized blood partial pressure of 00, however, decreased from an average of 102 x 10 to
2
95 x 10 pascals (76.6 to 71.4 torr) during exposure to the pollutant. Accompanying this was
a significant increase in the difference of partial pressure of oxygen in alveoli (PA02) and
15-17
-------
en
i—•
00
TABLE 15-4: EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION
IN CONTROLLED STUDIES OF SENSITIVE HUMANS
Concentration
ug/m ppm
9,400
3,800
to
9,400
940
to
9,400
5.0
2.0
to
5.0
0.5
to
5.0
No. of
Subjects
14 chronic
bronchitics
25 chronic
bronchitics
63 chronic
bronchitics
Exposure
Time Effects
60 mins. No change in mean PAD-*, during or after expo-
sure compared with pre-exposure values, but
PaO * decreased significantly in the first 15
mins. Continued exposure for 60 mins. produced
no .enhancement of effect.
lOmins. Significant decrease-in PaCL and increase in
AaDO * at 7,500 ug/m (4.0 ppm) and above; no
significant change at 3,800 ug/m (2.0 ppm).
30 Significant increase in R * above 3,000 ugm/
inhala- (1.63ppm); no signif icantaeffect below 2,800
tions ug/m (1.5 ppm).
Reference
Von Nieding
et al, 1973
Von Nieding
et al. , 1971
Von Nieding
et al. , 1971
940 0.5 10 healthy
7 chronic
bronchitics
13 asthmatics
2 hrs. 1 healthy and 1 bronchitic subject reported
slight nasal discharge. 7 asthmatics reported
slight discomfort. Bronchitics and asthmatics
showed no statistically significant changes for
all pulmonary functions tested when analyzed as
separate groups but showed small but statistically
significant changes in quasistatic compliance when
analyzed as a single group. See pp. 15-28.
Kerr, et al.,
1978
190
0.1 20 asthmatics 1 hr.
Significant increase in SR *. Effect of bron-
choconstriction enhanced after exposure in 13
of 20 subjects. Neither effect observed in 7
of 20 subjects.
Orehek, et al.,
1976
*PA02
Raw
SR
aw
alveolar partial pressure of oxygen
airway resistance
specific airway resistance
AaDO
2'
PaO,
difference between alveolar and arterial
blood partial pressure of oxygen
arterial partial pressure of oxygen
-------
2 2
in earlobe arterialized blood from an average of 34 x 10 to 43 x 10 pascals (25.5 to 32.3
torr). When exposure was continued for an additional 60 minutes, further significant distur-
bances of respiratory gas exchange were not observed.
Von Nieding et al. (1970;1971) also conducted a set of studies on NO, exposure with 88
3
chronic bronchitics (Table 15-4). Of these, 63 were tested for R at 940 to 9400 ug/m N09
cLW £-
(0.5 to 5.0 ppm) and 25 for Pa02, PA02, AaD02, similar measurements for C0?, and other para-
meters at 3700, 7500 and 9400 ug/m3 (2.0, 4.0 and 5.0 ppm). Significant elevations in R (p
« dW
< 0.1) were seen after exposure to NOp concentrations of 3,000 ug/m (1.6 ppm) and higher for
30 inhalations or approximately 3 minutes (Von Nieding et al., 1971). This increase became
0
more pronounced at concentrations above 3,800 ug/m (2.0 ppm), and disappeared completely
below concentrations of 2,800 ug/m3 (1.5 ppm). At levels of 7,500 to 9,400 ug/m3 (4.0 to 5.0
ppm), subjects showed >a significant decrease in Pa02 and an increase in AaD02; no significant
effect was found at 3800 ug/m3 (2.0 ppm).
Kerr et al. (1978) studied the effects of 2 hours of exposure to N09 at a concentration
3
of 940 ug/m (0.5 ppm) on 7 chronic bronchitic and 13 asthmatic subjects. A 15-minute pro-
gram of light to medium exercise on a bicycle ergometer was included in the exposure protocol.
One of seven chronic bronchitics reported a slight nasal discharge associated with the exposure
to NOp. Seven of 13 asthmatics reported some evidence of slight discomfort, dyspnea, and head-
ache with exercise. No significant changes were found in any of the pulmonary function para-
meters measured by spirometry, plethysmography, or esophageal balloon techniques when the
groups were analyzed separately. When data for the two groups were analyzed together, small
but statistically significant changes in quasistatic compliance were reported. However, the
authors clearly stated:
"The results of this investigation are in general negative, which is
in itself useful. Although exposure to higher concentrations of NOp
have been shown by others to alter function, and very high concen-
trations to result in significant damage to the respiratory system,
it would appear that no significant alteration in pulmonary function
is likely to result from a 2-hr exposure to 0.5 ppm N02 alone in
normal subjects or subjects with chronic obstructive pulmonary
disease. The few significant changes reported here may be due to
chance alone."
Several studies have utilized a challenge with acetylcholine in order to further clarify
the pulmonary responses to nitrogen dioxide. Von Neiding et al. (1977) suggested that there
was an increased sensitivity of the bronchial tree to administered acetycholine in subjects
exposed to a very low level of NO,. Beil and Ulmer (1976) reported an increased sensitivity
3
to acetylcholine after a 2-hour exposure to 14,100 ug/m (7.5 ppm) N09 but not after 2-hr
3
exposures to 4700 or 9400 ug/m (2.5 or 5.0 ppm) NO,. They further found an increased sen-
3
sitivity to acetylcholine in subjects exposed for 14 hours to 9400 ug/m (5.0 ppm) N02>
Orehek et al. (1976) studied the effects of low levels of NOp exposure on the bronchial
sensitivity of asthmatic patients to carbachol, a bronchoconstricting agent. In this study
the carbachol was used to induce a response in asthmatics similar to the response occurring
15-19
-------
when they are exposed to particular natural agents to which they are sensitive. Nitrogen
dioxide concentrations were monitored by the Saltzman method. For 20 asthmatics, dose-
response curves were developed for changes in specific airway resistance (SR ) as a result of
aW
the subjects inhaling carbachol after a 1-hour exposure to clean air and, on other occassions,
o
after a 1-hour exposure to 190 (jg/m NOp (0.1 ppm). Following NOp exposure alone, slight or
marked increases in SR were observed in only 3 of 20 asthmatic test subjects; however, N09
clW £
exposure at 0.1 ppm enhanced the effect of the bronchoconstrictor in 13 of 20 subjects. The
mean dose of carbachol producing a two-fold (100%) increase in SR in the 13 sensitive sub-
jects was significantly decreased from 0.66 mg to 0.36 mg as a result of NOp exposure. Seven
of the asthmatic subjects showed neither an increase in R in response to the exposure to N09
aW L-
alone nor an enhanced effect of NOp on carbachol-induced bronchoconstriction.
Unfortunately, the reported statistical significance of some of the data is rendered
difficult to interpret, likely due to the small sample size. For example, the mean dose of
carbachol producing a 100 percent increase in R was reported to be 0.36 mg for 7 non-
aw
responders and 0.66 mg for 13 responders, a non-statistically significant difference. On the
other hand, the mean doses of carbachol producing a 100 percent increase in R for 13
aw
responders before and after the NOp exposure were 0.66 mg and 0.36 mg, respectively; but,
in this instance, the same absolute difference in means was reported to be statistically
significant. Similarly, a 15 percent difference in mean R for 13 responders before and
dW
after NOp exposure alone was reported to be statistically significant, but a 20 percent
difference in the initial mean R between responders and non-responders was reported to not
aW
be significant.
The results of this study are of interest because they are suggestive of possible bron-
choconstrictive responses being produced in some asthmatics by very low concentrations of NOp.
These results, however, do not provide conclusive evidence of adverse responses attributable
to NOp exposure, especially in view of some of the reported statistically significant
NOp-induced changes not being markedly different in average magnitude to changes in R
apparently due to individual variations in lung function in the absence of NOp. The testing
protocol used in the study was an extremely sensitive one, i.e., employing known sensitive
subjects, a potent pharmacologic agent, and measurements of flow resistance. It is obvious
from the reported responses of the 20 subjects to the test regimen that only three showed
measurable variations as a result of exposure to NOp alone. However, the mean of measurements
of R in 13 responders to the carbachol treatment was significantly higher after the N0?
3W £-
exposure than it had been prior to exposure. The criticism of this reported change was that
the comparisons of R were made in subjects selected not at the time of N0~ exposure, but
3W ^
after the fact, following the carbachol exposure. There was no report of the initiation of
an asthma attack, or even wheezing, or lack of such symptoms in any subject, as a result of
the combined insults of carbachol and NOp, clouding interpretation of how the observed
effects might relate to asthma attacks under ambient conditions. The study may have health
15-20
-------
implications, however, since it suggests that those asthmatics whose illness results from
vagal stimulation might be predisposed to have more severe attacks (once induced by other
agents) as a result of also breathing N0?. However, such a suggestion (that the effects of a
potent vagal stimulus may be increased by the inhalation of low levels of NO- seems to be at
odds with the report of Yokoyama (1972) discussed earlier, who found that atropine blocked the
bronchoconstrictor effect of SOp but not NCL and, for this reason, concluded that NOp did not
act by stimulating the vagus nerve. It thus remains to be determined as to what concentra-
tions of N02 may produce significant broncoconstriction or other pulmonary mechanical effects
in asthmatics under ambient exposure conditions.
Another suggestion that measurably greater impact of exposure to N0? occurs in highly
susceptible individuals is obtained from the studies of Barter and Campbell (1976). These
investigators studied a group of 34 subjects with mild bronchitis and showed that decreases in
FEV, p, over a period of 5 years, were related to the subjects' degree of reactivity to the
bronchoconstrictor, methacholine. Even minimal cigarette smoking, a source of significant
concentrations of nitrogen oxides (Norman and Keith, 1965), led to ventilatory deterioration,
which the investigators believed to be serious when methacholine reactivity was high.
However, heavy smoking had little effect on ventilatory function when reactivity to methacho-
line was slight. It is not certain that the effective material in the cigarette smoke causing
the impairments in ventilatory function was NOp, although this seems to be a good possibility.
It also is not known how these study results relate to ambient NOp exposures of individuals
who are highly reactive to methacholine.
Thomas et al. (1972) showed no effect of exposure to NCL at concentrations of 940 to
3
6,580 ug/m (0.5 to 3.5 ppm) on histamine concentrations in sputum or on total sputum weight,
Jn five healthy subjects, or four patients reported to have chronic respiratory disease.
In summary, studies of N00 effects on pulmonary function in potentially susceptible popu-
3
lation groups show that, in persons with chronic bronchitis, concentrations of 9,400 ug/m
(5.0 ppm) produce decreases in PaOp and increases in AaDOp, whereas exposures to concentra-
tions of NOp above 2,800 ug/m (1.5 ppm), for periods considerably less than 1 hour, produce
significant increases in R (p < 0.1). Thus, results from bronchitic individuals and healthy
aW 3
individuals differ very little. In contrast, in one study, exposures to 190 ug/m (0.1 ppm)
N09 for 1 hour were reported to have increased mean R in 3 of 20 asthmatics and to have
£ uW
enhanced the effects of a bronchoconstrictor in 13 of the same 20 individuals. However,
in another study, no measurements of pulmonary function were significantly altered in 13
asthmatics as a result of 2 hours of exposure to 940 ug/m (0.5 ppm) NOp. Thus, whereas
NO-, exposures sufficient to produce increased R in healthy individuals or those with symp-
£ 3W
toms of chronic respiratory illness may indeed produce much greater and more severe responses
in other highly susceptible segments of the population (e.g., asthmatics), controlled human
exposure studies to date do not convincingly demonstrate pulmonary function changes in suscep-
tible population groups at NOp exposure levels below those affecting normal, healthy adults.
15-21
-------
15.3 EPIDEMIOLOGICAL STUDIES
Epidemiologies! studies of the effects of community air pollution are complicated because
there are complex varieties of pollutants present in the ambient air that exposed populations
breathe. Thus, the most that can usually be demonstrated by such studies is that an associa-
tion exists between observed health effects and a mixture of air pollutants. In order for
inferences to be drawn regarding likely causal relationships between any individual pollutant
present in such mixtures and observed effects, consistent associations must be demonstrated
between variations in exposures to the pollutant and particular types of effects under a
variety of circumstances (of course with potentially covarying or confounding variables having
been adequately controlled for or taken into account in the analysis of study results).
In attempting to demonstrate qualitative or quantitative relationships between N02 and
health effects, presently available epidemiological studies have been notably hampered by dif-
ficulties in defining actual exposure levels or durations for study populations. For example,
many N02-related epidemiological studies conducted prior to 1970 are of questionable validity
due to a number of instrumental and analytical problems inherent in the air monitoring tech-
nique (Jacobs-Hochheiser method) typically employed for measuring atmospheric concentrations of
NCL. Still other study results can be questioned on the basis of how representative reported
aerometric results are of actual N0? exposures of study populations. For these reasons, the
contributions of pre-1970 community air pollution studies to knowledge concerning N02 exposure
effects are highly limited at this time and are, therefore, not discussed in detail here.
Rather, only selected pre-1970 studies and other relevant post-1970 studies are discussed
below, together with notation (as appropriate) of certain major problems affecting interpre-
tation or acceptance of their results. The outdoor pollution studies thusly assessed can be
conveniently divided into the following categories: (1) those evaluating potential associa-
tions between N02 exposures and diminished pulmonary functions; and (2) those evaluating pos-
sible increased risks for acute or chronic respiratory diseases in response to NO,, exposures.
In addition to the outdoor ambient air pollution studies, other epidemiological evalua-
tions of the effects of indoor air pollution are also discussed, with particular emphasis on
possible relationships between indoor exposures to N0? and respiratory diseases in children.
15.3.1 Effects of NOp on Pulmonary Function
Among the better known studies evaluating NO^-related health effects are those conducted
by Shy et al. (1970a,b;1973) on schoolchildren during 1968-69 in Chattanooga, Tennessee. Shy
et al. (1970a) reported that values for 0.75-second forced expiratory volume were lower in
those children living in areas of apparently high N02 concentrations than for children living
in areas with lower NOp concentrations. However, measurements of N02 concentrations used in
this study were done by means of the Jacobs-Hochheiser method*, which was subsequently found to
"The Jacobs-Hochheiser technique has been withdrawn by EPA and replaced by a new Federal Refer-
ence Method (chemiluminescence) and other equivalent methods (see Chapter 7).
15-22
-------
be unreliable and not acceptable for deriving quantitative estimates of NCL levels present
in the 1968-69 Chattanooga study areas. In view of some overlap between NCL levels reported
for certain monitoring sites in the "high" NO^ pollution study areas and NO,, levels for
some monitoring sites in the lower N02 pollution study areas (based on the original
Jacobs-Hochheiser readings), even qualitative comparisons of effects observed between the
study areas are of questionable value. This is especially true given that differential
effects observed with pulmonary function tests were stated to be small (although statistically
significant) and showed inconsistencies during the testing period.
Several other community health epidemiological studies in various geographic areas have
attempted to provide quantitative assessments of pulmonary function changes in relationship to
ambient air NCL levels. These studies, using a more acceptable NCL measurement technique (the
Saltzman method), are summarized in Table 15-5. For example, Speizer and Ferris (1973b)
administered pulmonary function tests to 128 traffic policemen in urban Boston and to 140
patrol officers in nearby suburban areas (Table 15-5) but found no differences in pulmonary
function between the two study groups. Mean 24-hour N09 concentrations determined from 1-hour
3
sampling data, measured by the Saltzman technique, were 100 (jg/m (0.055 ppm) in the downtown
urban area, and 75 (jg/m (0.04 ppm) in the suburban area (Speizer and Ferris, 1973a). Sulfur
dioxide levels averaged 92 ug/m (0.035 ppm) in the city and 36 ug/m (0.014 ppm) in the subur-
ban area.
Cohen et al. (1972) also found no differences in the results of several ventilatory tests,
including spirometry and flow-volume curves, for nonsmoking adults living in the San Gabriel
Valley of the Los Angeles basin and similar nonsmokers from San Diego (Table 15-5). The
average N02 concentration in the Los Angeles basin was 96 ug/m (0.05 ppm) based on the
Saltzman method. The ninetieth percentile of the daily averages in this area, i.e., the level
exceeded only 10 percent of the time, was 188 ug/m (0.1 ppm). In San Diego, the average and
ninetieth percentile were, respectively, 43 and 113 ug/m (0.02 and 0.06 ppm) based on Saltzman
method measurements.
Linn et al. (1976) performed a variety of pulmonary function tests during the summer and
winter seasons on 205 office workers of both sexes in Los Angeles and 439 similar individuals
in San Francisco. Additional information about respiratory symptoms was obtained by means of
personal interviews. This study was undertaken primarily to determine the effects of oxidant
air pollution, but information regarding NO- was provided as well. Most results of FEV, single
breath Np tests, and interviews showed no differences between cities. Los Angeles women did
report nonpersistent cough and phlegm more often than did San Francisco women, and smokers in
both cities showed greater changes in pulmonary function than did nonsmokers. Median hourly
oxidant values (primarily 03) were 0.07 and 0.02 ppm in Los Angeles and San Francisco, respec-
tively. Ninetieth percentile oxidant values were 0.15 and 0.03 ppm. The median hourly NO,
•3 t-
concentrations based on the Saltzman method were 130 and 65 ug/m (0.07 and 0.035 ppm), respec-
tively, for Los Angeles and San Francisco. The 90th percentile hourly NO, concentrations were
•3 '
250 and 110 ug/m (0.13 and 0.06 ppm) for Los Angeles and San Francisco, respectively.
15-23
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TABLE 15-5. QUANTITATIVE COMMUNITY HEALTH EPIDEMIOLOGICAL STUDIES ON EFFECTS
OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY FUNCTION
en
ro
Measure
High exposure group:
Annual mean
24-hr concentrations
90th percentile
Estimated 1-hr
a
maximum
Low exposure group:
Annual mean
24-hr concentrations
90th percentile
Estimated l~hr
maximum3
Mean "annual" 24-hr
concentrations: high
exposure area
low exposure
area
1-hr mean:
high exposure
area
low exposure area
NO
Conce
ug/m
96
188
480
to
960
43
113
205
to
430
103
92
75
36
260
to
560
110
to
170
Exposure
gtrations
ppm
0.051
0.1
0.26
to
0.51
0.01
0.06
0.12
to
0.23
+ 0.055 +
S0? 0.035
so2
+ 0.04 +
SO,, 0.014
S0?
0.14
to
0.30
0.06
to
0.09
Study
Population Effect Reference
Nonsmokers No differences in several ventil- Cohen et al.,
Los Angeles atory measurements including spi- 1972
(adult) rometry and flow volume curves
Nonsmokers
San Diego (adult)
Pulmonary No difference in various pul- Speizer and
function monary function tests. . Ferris,
tests admin- 1973a,b
istered to
128 traffic Burgess et al.,
policemen in 1973
urban Boston
and to 140
patrol officers
in nearby sub-
urban areas.
-------
TABLE 15-5. (continued)
en
i
r-o
en
N09 Exposure
Measure
Los Angeles:
Median hourly N09
^
90th percent! le N0?
t-
Median hourly 0
90th percentile 0
X
San Francisco:
Median hourly N0?
90th percentile N02
Median hourly 0
90th percentile 0
1-hr concentration
at time of testing
(1:00 p.m.)
Concegtrat
ug/m
130
250
65
110
40
to
360
ions
ppm
0.07
0.13
0.07
0.15
0.035
0.06
0.02
0.03
0.02
to
0.19
Study
Population
205 office
workers in
Los Angeles
439 office
workers in
San Francisco
20 school
chi Idren
11 years of
age
Effect
No differences in most tests.
Smokers in both cities showed
greater changes in pulmonary
function than non-smokers.
During warmer part of the year
(April-October) NO SO and
TSP* significantly correlated
with V * at 25% and 50% FVC*
may
Reference
Linn, et
al. , 1976
Kagawa and
Toyama ,
1975
and with specific airway con-
ductance. Temperature was
the factor most clearly correlated
with weekly variations in specific
airway conductance with V at
25% and 50% FVC. Significant
correlation between each of four
pollutants (NO NO, S0? and TSP)
and V at 25% and 50% FVC; but
no clear delineation of specific
pollutant concentrations at which
effects occur.
.Estimated at 5 to 10 times annual mean 24-hour averages
Mean "annual" concentrations derived from 1-hour measurements using Saltzman technique
*VEV0.75:
max
FVC
TSP :
Forced expiratory volume, 0.75 seconds
Maximum expiratory flow rate
Forced vital capacity
Total suspended particulates
-------
In a Japanese investigation, relationships of ambient temperature and air pollutants (NO-,
NO,' 03, hydrocarbons, S02, and participate matter) to weekly variations in pulmonary function
in 20 school children, 11 years of age, were studied in Tokyo by Kagawa and Toyama (1975) and
Kagawa et al. (1976). Of all the factors assessed, temperature was most closely correlated
(p < 0.05) with variations in specific airway conductance, and with maximum expiratory flow
rate (Vmax) at 25 and 50 percent of FVC. In children believed by the investigators to be sen-
sitive to air pollution, a significant negative correlation was observed between exposure to
Og and specific airway conductance; other negative correlations were found between NO- (as
measured by the Saltzman technique), NO, SO,, and particulate matter, with V at 25 percent
c. (TlciX
or 50 percent FVC. At high outdoor temperatures NOp, SOp, and particulate matter were signifi-
cantly correlated (negatively) with both Vm=v at 25 percent or 50 percent FVC, and specific
fTlaX
airway conductance (p < 0.05).
In the ambient situation, however, the above effects were not associated with N0« alone,
but with the combinations of air pollutants, including SOp, particulate matter, and 0.,. During
the period of high outdoor temperatures, correlations between lung function and N02 concentra-
tions were calculated using the pollutant level in the ambient air at the time of testing
(1:00 p.m.). These hourly N02 values ranged from 40 to 360 ug/m3 (0.02 to 0.19 ppm), but the
data reported afforded no quantitative estimation of specific N02 levels that might have been ,
associated with the occurrence of pulmonary function decrements. The authors (Kagawa et al.,
1976) noted that: "From the relationship between NO, and V at 50% FVC in subject No. 16, :
£- max
who showed the highest correlation, it seems that NO, started having a significant effect
above a concentration of 4 pphm." The basis for this statement, however, is not obvious from
the published (Kagawa and Toyama, 1975; Kagawa et al. , 1976) data or statistical analyses,
which do not appear to provide sufficient bases for estimating N0~ air concentrations associ-
ated with pulmonary function decrements.
In other Japanese studies measurements of pulmonary function in employees exposed to
diesel exhausts in railroad tunnels were reported by Mogi et al. (1968) and by Yamazaki et al.
(1969). Results of pulmonary function tests were compared with similar results from employees
in other situations in which exposure was classified as medium, light, or "no-pollution." Mean
3
NO, concentrations, measured by the Saltzman method, ranged from 300 to 1,130 (jg/m (0.16 to
• 3
0.60 ppm). Highest measured N02 concentrations ranged from 340 to 3,000 ug/m (0.18 to 1.60
ppm). Test results [VC, FEV-j^ Q, maximal flow rate (MFR) and mid-maximal flow rate (MMFR)] from
475 employees were highest in those working in "no-pollution" areas. Results obtained on the
remaining subjects showed a decrease in pulmonary function which did not correlate with the
N02 concentrations in their work areas.
Results of epidemiological studies on the effects of outdoor ambient air N0? exposures
provide no consistent indication that the mean concentrations of N02 or of N02 in combination
with other pollutants listed in Table 15-5 had any significant effects on lung function in the
15-26
-------
exposed populations. One study did show some apparent associations between Vm,v or specific
rnaX
airway conductance and concentrations of NOp and other pollutants at the time of testing, but
the contributions of individual air pollutants were difficult to disentangle and appeared to
be less than those attributable to temperature variations.
15.3.2 Effects of NO,, on Acute Respiratory Illness
15.3.2.1 Effects Associated With Ambient Exposures—Only a few community epidemiological
studies of outdoor NO exposures have been reported as demonstrating associations between
A
ambient air levels of NO compounds and measurable health effects. However, methodological
problems with all of the studies preclude acceptance of any of the results as clear evidence
for increases in acute respiratory illness due to NO exposures.
Shy and co-workers (Shy, 1970; Shy et al., 1970b; 1973) studied the effects of community
exposure to N0? in residential areas of Chattanooga on respiratory illness rates in families.
The distances of three study communities from a large point source of N0~ resulted in an
apparent gradient of exposure over which the illness rates were determined. The incidence of
acute respiratory disease was assessed at 2-week intervals during the 1968-69 school year and
the respiratory illness rates adjusted for group differences in family size and composition
were reported to be significantly higher for each family segment (mothers, fathers, children)
in the high-NOp exposure neighborhood than in the intermediate- and low-NO^ areas. However,
in this study, NO- concentrations were determined by the Jacobs-Hochheiser method and, as indi-
cated earlier, this method has since been shown to be unreliable (Mauser and Shy, 1972; See
Chapter 7 for a more complete discussion). Meaningful quantitative estimates of population
N0? exposures were therefore not available for the study areas; also, overlaps in reported N02
levels between "high" N0? area monitoring sites and those for lower NO- study areas make quali-
tative comparisons between the study areas somewhat problematic. In addition, no basis was
provided by which the relative contribution of NOj exposures could be separated from those of
other pollutants present in the study areas.
Additional data on acute respiratory disease rates in the same Chattanooga study areas
were collected in 1972-1973, by which time no differences in N02 levels existed between the
study areas as measured by the Saltzman technique. Preliminary analyses of these data were
reported by Shy and Love (1979), but further (final) analyses of these data remain to be com-
pleted, peer reviewed, and published.
In an earlier retrospective study in the same Chattanooga areas, Pearlman et al. (1971)
investigated the frequency of lower respiratory disease among first- and second-grade school
children and among children born between 1966 and 1968. Responses on 14 percent of the health
status questionnaires were validated against physician and hospital records, with overall
accuracy of parental reporting of illness episodes being 70.5, 67.9, and 90.0 percent for
bronchitis, croup, and pneumonia, respectively. No significant study area differences in ill-
ness rates were found for croup, pneumonia, or a combined "any lower respiratory disease"
category in pre-school infants or schoolchildren; nor did illness rates for these illness
15-27
-------
categories follow the reported pollutant gradient for any age group classified by period (1,2,
or 3 yrs) of residence in the respective study areas. Similarly, illness rates for bronchitis
failed to follow the reported NOp exposure gradient (except for schoolchildren of 3 yr
residence), with intermediate area bronchitis rates otherwise generally exceeding those deter-
mined for the children in the high N02 area. Only bronchitis rates in schoolchildren who had
lived in the area for 3 or more years followed the exposure gradient and were found to be signi-
ficantly higher than for children from the low N02 area. The validity of this reported differ-
ence, however, appears to be questionable in view of: (1) its internal inconsistency with the
other study results reported; (2) the only moderately high accuracy (70.5 percent) of reporting
of bronchitis rates in comparison to the accuracy (90 percent) for pneumonia rates; and (3)
the reported inability of parents to date precisely the occurrence of bronchitis episodes,
making it impossible to separate such illnesses occurring before residence in the exposure
areas from those occurring thereafter. Also, the same difficulties in defining the reported
NOp exposure gradient (presumably based on use of the Jacobs-Hochheiser N0« method) for the
study areas used in this study likely apply as noted above for the Shy et al. 1968-69
Chattanooga studies.
Polyak (1968) reported 44 percent more health clinic visits for respiratory, visual,
nervous symptoms, and skin disorders by residents living within 1 kilometer of a Soviet Union
chemical works than by residents living more than 3 kilometers from the factory complex. The
study subjects, none of whom worked at the chemical plant, were exposed to a combination of
pollutants. Concentrations reported were: NO.,, 580 to 1,200 vq/tn (0.31 to 0.64 ppm); SO,,
3 3
225 (jg/rn (0.09 ppm); and sulfuric acid, 400 ug/m (0.1 ppm). The report also indicated that
a NOp concentration of 1,600 ug/m (0.85 ppm), combined with high concentrations of S02 and
sulfuric acid, occurred 1 kilometer from the plant. However, no information was provided on
the methods used to measure N02 or by which to assess the relative contribution of N02 expo-
sures to the reported health effects.
In another study from the Russian literature, Giguz (1968) studied illness rates and other
factors in 16- to 19-year-old vocational trainees in the Soviet Union. Individuals training
in fertilizer or chemical manufacturing plants (N=145) were compared with 85 individuals of
the same age not exposed to pollutants found in the manufacturing plants. Exposure concentra-
tions of N02 and ammonia, gases expected by the investigators to occur in highest concentrations
in this situation, did not exceed the maximum permissible concentrations (average daily mean:
for N02, 100 |jg/m3 or 0.053 ppm in 1964) in the U.S.S.R. (Nikolaeva, 1964). Subjects were
exposed to the pollutants for 3 hours a day for 150 days during the first year of training,
and for 6 hours a day for 200 days during the second year. During the second year of training,
exposed individuals were reported to have an increased incidence of acute respiratory disease
and increased serum levels of beta-lipoproteins, cholesterol, and albumin. However, this
report lacks important information related to air pollutant sampling frequencies and methods,
making it difficult to evaluate the reliability of quantitative estimates of NO,, levels associ-
ated with reported health effects.
15-28
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Petr and Schmidt (1967) studied acute respiratory illness among Czechoslovak!an school-
children living near a large chemical complex. They found a disease incidence twice that
observed in children of the same age living in a low-exposure community of similar socio-
economic characteristics. A greater number of hypertrophied tonsils and cervical lymph nodes
also were found in children from two towns, each having high pollution but differing with
respect to relative concentrations of NCK and S02. Children from the area having the lower
concentrations of NO had much lower lymphocytogram values and higher indices of proliferation
and differentiation of monocytes. The clinical significance of these differences is not known
and the results of the Petr and Schmidt (1967) study are difficult to interpret because data
on concentrations of NO and N02 individually were not presented. Nor was information provided
on the sampling frequency or methology for NO or N09 measurements or on levels of other pollut-
ants such as acid aerosols, particulate nitrates, sulfates, or total suspended particulate
matter. It is probable that such a variety of pollutants was present around a large chemical
complex, but no basis was provided by which to assess the relative contribution to reported
health effects of NO compounds from among other air pollutants present.
/\
15.3.2.2 Effects Associated With Indoor Exposures
15.3.2.2.1 Tobacco smoking studies. Tobacco smoke is a major source of nitrogen oxides, and
may include significant concentrations of N09. Norman and Keith (1965) demonstrated that the
1 C T
concentration of NO may vary between 492 x 10 and 1.23 x 10 |jg/m (400 and 1,000 ppm) in
cigarette smoke depending on the type of filter included and the extent to which the cigarette
is smoked, i.e., the last puff contained higher concentrations than did the fourth puff.
Often N09 could not be measured in the cigarette smoke but, in other instances, concentrations
3
as high as 47,000 |jg/m (25 ppm) were found. In confined spaces such as meeting rooms, con-
centrations of N0~ might build up to potentially hazardous levels, when several individuals
-are smoking. Smoking then may represent a significant source of exposure for nonsmokers as
well as smokers.
Many adverse health effects have been associated with smoking, particularly cigarette
smoking. It has not been possible, however, to implicate conclusively any single factor in
cigarette smoke as the one primarily responsible for the effects observed. Other major pollu-
tants in cigarette smoke include CO and tars. Each of these materials, in experimental situa-
tions, causes a fairly unique type of effect. Consequently, even though no specific adverse
effects can be attributed conclusively only to the N0? in cigarette smoke, the increases in
some adverse health parameters point strongly in this direction. Specific health effects
possibly related to exposure to N02 in cigarette smoke include increased acute respiratory
illnesses or prevalence of chronic respiratory disease.
15-29
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15.2.2.2.2 Epidemiological Studies of Gas Combustion Products. Combustion of natural or
manufactured gas within confined spaces leads to increases in N0? concentrations. Although
some CO and other pollutants may also be produced by gas-burning appliances, the relative
efficiencies of the combustion process cause the largest quantities of N0? to be produced
when CO production is lowest. This tends to suggest that increased health effects, if
observed in homes with gas stoves, are more likely the result of NOp exposure than CO expo-
sure; however, effects due to exposure to other potentially toxic products of gas combustion
cannot be ruled out.
Social characteristics of family life, as well as the size and type of housing, also
affect exposure parameters for those people living in homes with pollution produced by gas
appliances or other sources. For example, a home with a small kitchen containing a gas stove
may represent a greater hazard for individuals who spend much time in the kitchen, especially
if the social custom is to heat as little of the home as possible, and most or all of the
family spend considerable time in or near the kitchen. In such homes, relatively frequent
(almost continuous) exposure periods to gas stove pollutants may be experienced by family
members. In other homes, however, such as those with central heating, family members may spend
much less time in the kitchen and, therefore, experience less exposure to gas combustion pro-
ducts.
Several studies show that homes with gas stoves typically have higher N0? levels than
those with electric stoves. For example, Wade et al. (1975) reported that, over a 2-week
3
period, the average concentration of NOp in kitchens with gas stoves exceeded 94 ug/m (0.05
ppm) and that in different parts of the house, the concentrations fluctuated with use of the
stoves. Nitrogen dioxide was monitored by a chemiluminescence method. Average levels of 280
ug/m (0.15 ppm) NOp for 2 hours were measured in the kitchen. Other studies of NOp concen-
trations in homes during the preparation of meals have demonstrated that gas stoves produce
NOp concentrations usually within the range of 470 to 1100 ug/m (0.25 to 0.6 ppm) in the im-
mediate vicinity of the stove (Mitchell et al., 1974; U.S. Environmental Protection Agency,
1976). The highest level recorded was 1,880 ug/m (1.0 ppm). The high concentrations are
significantly reduced within 2 hours after the stove is turned off. The specific time for
reduction of peak concentrations by any given percentage after the cessation of stove usage,
however, depends upon such parameters as the presence or absence of ventilation devices and
the details of interior architecture. Other studies also indicate NO- is higher in homes using
gas than those using electricity (Melia et al., 1978; Goldstein et al., 1979; Spengler et al.,
1979).
Observations of elevated NOp and other air pollutant levels in gas stove homes in com-
parison to electric stove homes have prompted epidemiological investigations of possible health
effects associated with the higher levels of indoor air pollutants in homes using gas stoves.
The results of such epidemiological studies are summarized in Table 15-6.
15-30
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1ABLL 15-6. EFFECTS OF EXPOSURE [0 N11KOGEN FJIOXIUE IN MIL HOME ON LUNG FUNCTION AND
THE INCIDENCE OF ACUTE RESPIRA10RY DISEASE IN EPIDEMIOLOGY STLIULES OF HOMES W1III GAS SIOVLS
----- - - ....
Pollutant3
NO;,
Concentration
pg/mj ppm
Study
Population
if feels
Reference
Studies of Children
NO^ plus
other gas stove
combustion products
NO,, plus other gas
stove combustion
products
NO. plus other
gas stove
combustion
products
NO. plus other
gas stove
combustion
products
NO,, concentration
not measured at
time of study
N0« concentration
not measured in
same homes studied
Kitchens:
9-596 (gas) 0.005-0.317
11-353 (elec) 0.006-0.188
Bedrooms:
7.5-318 (gas) 0.004-0. 169
6-70 (elec) 0.003-0.037
(by triethanolamine
diffusion samplers)
95 percentile of 24 hr
avg in activity room
39 - 116 ug/m ( . 02 -
.06 ppm) (gas) vs.
17.6 - 95.2 ug/m
(.01 - .05 ppm)
(electric). Frequent
peaks ~ 1100 ug/m (0.6
ppm)-max peak ~ 1880
ug/m (1.0 ppm) 24 - hr
by modified sodium
arsenite; peaks by
chemi luminescence
2554 children from homes
using gas to cook compared
to 3204 children from homes
using electricity. Ages 6-11
4827 children
ages 5-10
808 6- and 7-year-old
chi Idren
8,120 children 6-10 yrs old in
6 different communities with
data collected on lung function
and history of illness before
the age of 2
Proportion of children with one
or more respiratory symptoms
or disease (bronchitis, day or
night cough, morning cough,
cold going to chest, wheeze,
asthma) increased in homes
with gas stoves vs. electric
stove homes (for girls p -0.10;
boys not sig. ) after controlling
for confounding (actors
Higher incidence of respiratory
symptoms and disease associated
with gas stoves (for boys p -0.02;
girls p -0.15) after controlling
for confounding factors
Higher incidence of respiratory
illness in gas-stove homes
(p ~0.10). Prevalence not
related to kitchen N0? levels,
but increased with NO,, levels
in bed rooms of children in
gas-stove homes. Lung function
not related to NO- levels in
kitchen or bedroom
Significant association between
history of serious respiratory
illness before age 2 and use of
gas stoves (p <.01) and, also,
between lower FEV, FVC levels
and use of gas stoves (p ^.01)
Melia tt al. , 19/7
Melia et al. , 19/9
Florey et al. , 1979
Companion paper to
Melia et dl , 1979,
Goldstein et al . ,
1979
Speizer et al . , 1980
Spengler et al. , 1979
-------
TABLE 15-6 (continued)
CO
rsi
Pollutant3
NO- plus other
gas stove
combustion
products
NO, plus other
gas stove
combustion
products
N02
Concentration
ug/m3 ppm
Sample of households
24 hr avg: gas (.005 -
. 11 ppm); electric
(0 - .06 ppm); outdoors
(.015 - .05 ppm)- several
peaks > 1880 ug/m (1.0
ppm). Monitoring location
not reported. 24-hr avgs
by sodium arsenite; peaks
by chemi luminescence
Saeiple of same
households as reported
above but no new
monitoring reported
Study
Population
128 children 0-5
346 children 6-10
421 children 11-15
174 children under 12
Effects Reference
No significant difference Mitchell et al., 1974
in reported respiratory See also Keller et al..
illness between homes with gas 1979a
and electric stoves in children
from birth to 12 years
No evidence that cooking mode Keller et al. , 1979b
is associated with the incidence
of acute respiratory illness
Studies of Adults
NO. plus other
gas stove
combustion
products
NO- plus other
ga§ stove
combustion
products
NO. plus other
gas stove
combustion
products
NO- plus other
gal stove
combustion
products
Preliminary measure-
ments peak hourly
470 - 940 ug/g
max 1880 ug/m
(1.0 ppm)
See table above
for monitoring
See table above
for monitoring
See table above
for monitoring
Housewives cooking with
gas stoves, compared to
those cooking with
electric stoves
Housewives cooking with
gas stoves, compared to
those cooking with electric
stoves. 146 households
Members of 441 households
Members of 120 households
(subsample of 441 households
above)
No consistent statistically USEPA, 1976
significant increases in
respiratory illness associated
with gas stove usage
No evidence that cooking with Keller et al., 1979a
gas associated with an increase
in respiratory disease
No significant difference in Mitchell et al., 1974
reported respiratory illness See also Keller et al.,
among adults in gas vs electric 1979a
cooking homes
No significant difference among Keller et al., 1979b
adults in acute respiratory
disease incidence in gas vs
electric cooking homes
-------
Two independent sets of epidemiological studies, from Britain and the United States, pro-
vide data suggesting likely associations between respiratory illness symptoms in children and
residence in homes using gas stoves for cooking versus residence in homes using electrical
stoves. Much caution must be employed, however, in interpreting the results of such studies
in terms of specifically implicating NO^ exposures in the etiology of the reported health
effects and in attempting to define pertinent exposure/effect relationships.
Results of the British studies have been reported by Melia et al. (1977; 1978; 1979),
Goldstein et al. (1979), and Florey et al. (1979). The initial study, conducted from 1973 to
1977, investigated the effects of indoor and outdoor air pollution on respiratory illness in a
large cohort of primary school children from randomly selected areas of England and Scotland.
Results for the first year (1973) of the study were reported by Melia et al. (1977). Addi-
tional results from the last year of the study (1977) and from longitudinal analyses (1973 to
1977) were reported by Melia et al. (1979).
The cross-sectional analysis of 1973 results discussed by Melia et al. (1977), involved
2,554 children from homes with gas stoves and 3,204 from homes with electric stoves and
examined the prevalence of bronchitis, cough, colds going to the chest, wheeze, and asthma by
means of questionnaires. Crude prevalences for each condition were higher in children from
homes where gas was used and statistically significant (p <0.05) for bronchitis, cough, and
colds going to the chest in both sexes, and for wheeze in girls. The authors reported that
this "cooking effect" appeared to be independent of the effects of age, social class, lati-
tude, population density, family size, overcrowding, outdoor levels of particulate matter
(smoke) and sulfur dioxide, and types of fuel used for heating. This conclusion was based on
the proportion of children with more than one disease or symptom being higher for homes with
gas cooking when these various factors were taken into account; however, when the factors were
taken into account, the main finding of the proportion of children with one or more respira-
tory symptoms or diseases remaining higher in both boys and girls from gas stove homes only
approached statistical significance for girls (p~ 0.10) but not boys. Furthermore, data for
several of the variables were missing so that only very small numbers remained within necessary
subgroups, prompting the authors to state that the results from these analyses were not con-
clusive and needed to be confirmed by follow-up data then being collected. Nevertheless, the
authors concluded that elevated levels of nitrogen oxides arising from combustion of gas might
be the cause of the increased respiratory illness.
In 1977, another cross-sectional study of similar design was conducted on a different set
of children, 3,017 from homes with an electric stove, and 1,810 from homes with a gas stove
(Melia et al., 1979). Crude prevalences indicated that cough in boys (p ~0.02), and colds
going to the chest in girls (p <0.05) were significantly higher in homes with gas stoves.
15-33
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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 in girls), but not
rural ones. In rural areas there only appeared to be an association for girls under eight
years old. The effect of number of smokers was significant in rural areas (p <0.005).
In addition to results for the 1977 cross-sectional analysis, Melia et al. (1979)
reported that four cohorts of children from the 1973 study who were followed up for 1 to 4
years showed greater risk of having one or more respiratory symptoms or diseases in homes with
gas stoves relative to homes with electric stoves in 1973. In later years, however, as the
cohorts grew older, the relative risk showed considerable variation. In most groups the risk
was greater in gas stove homes, but there were groups with negligible increased risk and
groups for which the risk was greater in homes with electric stoves. The authors report no
consistent change in the size of the relative risk with time except possibly a decline from
1973 to 1977 for the youngest cohort. Comparing the 1973 and 1977 results, the effect of gas
cooking seemed to be smaller in 1977, at least among girls. The prevalences tended to be
higher in 1973 for children of the same age. The authors stated that differences in weather
conditions could not explain this observation, but speculated that past high levels of atmos-
pheric pollution may have contributed to these results. Nevertheless, Melia et al. (1979)
stated, in summary, that they observed an association between respiratory illness and the use
of gas for cooking in two different groups of children seen 4 years apart in their national
survey.
In another study by Melia et al. (1978) concentrations of N0? were determined in the
kitchens of two gas cooking homes and two electric cooking homes. Concentrations of NO- were
determined using TEA diffusion tubes (Palmes, 1976) placed 0.6 m and 2.2 m from the kitchen
0
stove. The average hourly concentration of N09 in gas kitchens was 135 ug/m (0.072 ppm), and
"\
in electric kitchens it was 17 ug/m (0.009 ppm); the difference in these levels was signifi-
cant at p <0.05. This study also established that reproducibility of the diffusion tubes was
± 3 percent.
These studies by Melia et al. provide suggestive evidence of an association between the
use of gas stoves and increased incidence of acute respiratory disease symptoms in children,
and between the use of gas stoves and increased levels of N0« in the home. However, because
NCL concentrations were not directly monitored in the homes used in the health studies, only
these qualitative conclusions may be drawn regarding their study results.
15-34
-------
Possible interrelationships between N02 exposures in gas stove homes and increased
respiratory infection and decreased lung function were investigated in a further British study
reported by Goldstein et al. (1979) and Florey et al. (1979). In these later investigations
levels of NO- were determined in gas and electric cooking homes, and the prevalence of
respiratory symptoms among children in the gas cooking homes was found to be higher than in
the electric stove homes (p -0.10). The sample was 808 children aged 6 to 7 years from 769
different homes in a 4-square-km area in Cleveland, UK. The study was conducted for a two-
week period during February 1978. N02 was measured by TEA diffusion tubes attached to walls
in the kitchen area and in the children's bedrooms. In homes with gas stoves, levels of NO-
in kitchens ranged from 10 to 596 ug/m (0.005 to 0.317 ppm) with a mean of 211 ug/m3 (0.112
ppm), and levels in bedrooms ranged from 8 to 318 \jg/m (0.004 to 0.169 ppm) with a mean of 56
O
ug/m (0.031 ppm). In homes with electric stoves, levels of NO- in kitchens ranged from 11 to
353 pg/m3 (0.006 to 0.188 ppm) with a mean of 34 ug/m3 (0.018 ppm), and in bedrooms NO, levels
o n f.
ranged from 6 to 70 ug/m (0.003 to 0.37 ppm) with a mean of 26 ug/m (0.014 ppm). Outdoor
levels of N09 were determined using diffusion tubes systematically located throughout the
3
area, and the weekly average ranged from 26 to 45 pg/m (0.014 to 0.024 ppm).
Information on the prevalence of respiratory symptoms was collected and grouped as in
previous studies. Cooking fuel was found to be associated with respiratory illness,
independent of social class, age, sex, or presence of a smoker in the house (p = 0.06).
However, when social class was excluded from the regression, the association was weaker (p
~0.11). For the 6- to 7-year-old children living in gas stove homes, there appeared to be an
'increase of respiratory illness with increasing levels of NO- in their bedrooms (p ~0.10), but
no significant relationship was found between respiratory symptoms in those children or their
siblings or parents and levels of NO- in kitchens. Lung function tests (FEVg ^r, PEFR, MMF)
were also performed on the 6- to 7-year-old children, but no significant relationship was
found between lung function and concentrations of NO- in either kitchen or bedroom. These
studies, therefore, at most found a weak association between prevalence of respiratory illness
in 6- to 7-year-old children and gas cooking in their homes which may have been due to levels
of N02 generated by the use of gas. The authors note, however, that the NO- levels might
possibly be a proxy for some other factor more directly related to respiratory disease, such
as temperature or humidity.
Results from United States studies finding associations between gas stove use and
increased respiratory illness in children have also been published (Spengler et al, 1979;
Speizer et al, 1980). Spengler et al. (1979) presented data on annual nitrogen dioxide
concentrations inside and outside electric- and gas-cooking homes in five of six American
communities included in a prospective epidemiological investigation. In all instances, houses
15-35
-------
with gas facilities had higher levels of NCL than were present in the outdoor air, reaching
double the outdoor concentration in some instances. 'Indoor annual average values in these
3 3
houses were as high as 80 ug/m (0.04 ppm). Short-term peak levels in excess of 1,100 ug/m
(0.58 ppm) occurred regularly in kitchens. Houses with electric cooking services had lower
concentrations than were observed in the outdoor environment.
Respiratory disease rates were evaluated in these same six communities by Speizer et al.
(1980). Children from households with gas stoves had a significantly greater history of
serious respiratory illness before age 2 (average difference 32.5/1000 children). In this
study, adjustment of rates of illness before age 2 for parental smoking and socioeconimic
status led to a clear association with presence of gas stoves (p <0.01). These findings
corroborate those reported earlier by Melia et al. (1977), but have more importantly removed
the primary objection to the earlier Melia studies, i.e., the role of parental smoking.
Speizer et al. (1980) also found small but significantly (p <0.01) lower levels of FEV-, and
FVC, corrected for height, in children from houses with gas stoves. Although these reported
pulmonary function changes were statistically significant, the authors noted that the changes
are most likely of relatively minimal immediate physiological importance.
Considerable caution should be exercised at this time before fully accepting findings of
increased incidence of respiratory disease in children living in gas stove homes and attribut-
ing such effects to NO^ exposure. Such caution is warranted in view of the following :
(1) The findings are based on initial data analyses from long-term prospective studies
and assume adequate control for and exclusion of contributions of potential con-
founding factors (e.g., socio-economic status, humidity, temperature) to the
reported associations between gas stove home residence and increased respiratory
illness history in young children. Confidence in such findings would be greatly
enhanced if they were further confirmed by analyses of data subsequently collected
in the studies, analyses that more definitively rule out effects of potentially
confounding factors.
(2) The need to define better quantitative exposure/effect or dose-response relation-
ships between peak, 24-hr, weekly or annual average NOp exposures and any resulting
increases in respiratory disease symptoms in young children residing in homes using
gas cooking stoves.
(3) Results from other studies discussed below, which did not find significant associa-
tions between increased respiratory illness and residence in gas stove homes.
Several studies, all American, have failed to find evidence of associations between gas
stove usage and increased respiratory illnesses. For example, in a U.S. Environmental
Protection Agency study (Table 15-6) the incidence of acute respiratory illness among women
15-36
-------
using gas cook stoves was compared with the incidence among women using electric cook stoves
(U.S. Environmental Protection Agency, 1976). Concentrations of NO, as high as 940 ug/m (0.5
3
ppm) to 1880 ug/m (1.0 ppm) were found for durations of 1/2 to 1 hour each time the gas stove
was used for the preparation of a meal. There was no difference in the incidence of respira-
tory disease in these women.
Keller et al. (1979a) determined the incidence of respiratory disease in 209 suburban
Ohio middle-class families with gas stoves and in 232 similar families with electric stoves.
Health data were obtained through biweekly telephone calls for one year. In addition, pul-
monary function tests (FEV~ 75 and FVC) were conducted on a 42 percent sample of the partici-
pants representative of both sexes and both types of households. No differences in illness
rates or in the results of pulmonary function tests were detected. Nitrogen dioxide and NO
levels were monitored over 24-hour periods in 83 of the homes with gas stoves. For this
monitoring, a sodium arsenite procedure was used and continuous chemiluminescence measurements
were made for 3-day periods in each of 46 homes. Reported peak N0« concentrations in homes
with gas stoves were as much as 8 times higher than the 24-hour mean and sometimes exceeded
0
1,880 ug/m (1.0 ppm). The location of the peak concentrations within the home was not
reported, but probably was within a few feet of the stove. On the basis of the range of mean
N09 concentrations reported, it can be determined that peak (15-min) N09 concentrations in
3
most homes with gas stoves ranged between 75 and 1,650 ug/m (0.04 and 0.88 ppm). The average
peak value would have been approximately 750 ug/m (0.4 ppm). In homes with electric stoves,
"the mean N02 concentration was lower than the mean of 53 outdoor determinations.
Keller et al. (1979b) extended this study of gas versus electric cooking services on 120
of the original households with school age children. Reports of respiratory illness and
symptoms were obtained by telephone interview every 2 weeks for 13 months. When the onset of
respiratory illness occurred within 3 days of a call, a household visit was made to examine
the ill person and to obtain a throat culture. "Well" controls were also examined. The only
significant difference (p <0.05) in the incidence of reported acute respiratory illness
occurred among children 12 to 18 years of age, with a larger percentage occurring in electric-
stove households. Symptoms of "tearing and redness Of eye" and frequency of consulting
physicians were higher in homes with gas stoves. However, overall, no significant differences
were found between the two groups confirming the earlier finding by Keller et al. (1979a) that
there was no evidence that gas or electricity in households was associated with the incidence
of acute respiratory illness. (A more detailed account of these studies is contained in two
reports by Lutz et al., 1974,1977.) Nitrogen dioxide and NO concentrations were monitored
over periods of 24 hours using a sodium arsenite procedure and continuous chemiluminescence.
15-37
-------
15.3.3 Effects of NO., Pollution on Prevalence of Chronic Respiratory Disease
Only a few published epidemiological studies have attempted to investigate possible
associations between ambient air exposures to NOp or other NO compounds and the prevalence of
chronic respiratory diseases. The results of such studies are concisely assessed below.
The prevalence of chronic bronchitis among Japanese post office employees in 1962 and in
1967 was investigated by Fujita et al. (1969). Nearly 7,800 employees in Tokyo, Tsurumi, and
Kawasaki, Japan were categorized on the basis of their work sites being "downtown and
industrial," "intermediate," or "suburban." Chronic bronchitis rates were higher in 1967 than
in 1962 for all age groups, for all smoking categories, and for employees who worked both
indoors and outdoors. Overall bronchitis rates associated with downtown, intermediate, and
suburban areas increased, respectively, from 5.0, 3.7, and 3.7 per 100 employees in 1962 to
8.4, 8.0, and 8.1 per 100 employees in 1967. The investigators speculated that the increases
in chronic bronchitis were caused by concomittant increases in the atmospheric concentrations
of NOp, NO, and SOp, but the aerometric data available for the 1962-67 study period are
insufficient to establish any such hypothesized relationships.
Another study of chronic bronchitis among 400 housewives (30 to 39 years old) living in
six localities in Japan was reported by the Central Council for Control of Environmental
Pollution (1977). This study, conducted during the winter of 1970-71, reportedly found an
association between prevalence rates for chronic bronchitis in areas where annual average NOp
concentrations were in the range of 0.02 to 0.03 ppm. However, insufficient information was
provided by which to evaluate the validity of the reported findings, and population NOp expo-
sure in this study was likely confounded by high atmospheric particle levels also reported to
be present in the same study areas.
In an American study discussed earlier, Speizer and Ferris (1973a) compared the preva-
lence of chronic respiratory disease among 128 policemen who patrolled on foot in congested
business and shopping areas of central Boston witti that of 140 suburban patrol car officers.
The exposure of each group to NOp was determined at several work locations for the central
city officers and in the patrol cars of suburban officers. Nitrogen dioxide was measured by
the Saltzman method. Among urban policemen, small but not statistically significant increases
in the prevalence of chronic respiratory disease were found among nonsmokers and stackers but
not among ex-smokers. Estimates of annual mean pollution levels, based on approximately 1,000
j
hourly samples (Burgess et al. , 1973), were, for the urban area, 103 ug/m (0.055 ppm) NO,
o e-
together with S00 concentrations of 90 ug/m (0.05 ppm); the N00 concentrations for the
3 3
suburban area averaged 75 ug/m (0.04 ppm) and SO- concentrations averaged 26 ug/m (0.01
ppm).
15-38
-------
Cohen et al. (1972) similarly found no differences in the prevalence of chronic respira-
tory disease between a nonsmoking population in the Los Angeles basin and a similar population
in San Diego. The Los Angeles group was exposed to concentrations of NO,, between 90 and 100
3 3
ug/m (0.05 ppm) plus oxidant levels of about 90 ug/m (0.045 ppm); the San Diego group was
exposed to N09 concentrations of approximately 40 to 45 ug/m (0.02 ppm) and concentrations of
3
oxidants of approximately 76 ug/m (0.038 ppm).
Linn et al. (1976) also found no increase in chronic respiratory disease in Los Angeles
women exposed to a median hourly NO,, concentration of 130 ug/m (0.07 ppm) with a 90th percen-
3
tile value of 250 (jg/m (0.13 ppm), over that occurring in San Francisco women where the
3
median hourly concentration of N00 was 65 ug/m (0.035 ppm) and the 90th percentile was 110
3
ug/m (0.06 ppm). Median hourly oxidant values in the two areas were, respectively, 0.07 and
0.02 ppm. These investigators concluded that cigarette smoking was much more significant than
was Los Angeles air pollution in the development of chronic respiratory illness.
In summary, the epidemiology studies assessed above did not establish any credible
association between chronic respiratory disease prevalence in human populations and the con-
centrations of N0£ to which these populations were exposed.
15.3.4 Extrapulmonary Effects of Exposure to NO
Nitrogen oxides, as well as other components of polluted air, have been reported to be
correlates of daily mortality, heart disease, and lung cancer, based on certain epidemiologic
studies reported in the early 1970's.
For example, Hickey et al. (1970) compared air pollution measurements made at National
Air Sampling Network (NASN) stations with geographical differences in mortality rates for
various categories of cancer, cardiovascular disease, and respiratory disease in 38 U.S.
Standard Metropolitan Statistical Areas (SMSAs) during 1959 to 1961 and from 1961 to 1964.
Included in the analyses were NOp, S0?, suspended sulfates, total particulates, calcium,
chromium, copper, iron, lead, manganese, nickel,, tin, titanium, vanadium, zinc, and water
hardness. Mortality rates were analyzed both with and without regard to age, sex, and race
differences. Nitrogen dioxide and SO,, repeatedly were positively associated with age-, race-,
and sex-adjusted, and unadjusted mortality rates for various cancers, and for arteriosclerotic
heart disease. Other pollutants were variably, and often negatively, associated with these
mortality categories. However, the quality of both the monitoring data and the mortality
data, as well as the fact that specific pollutant exposures of individuals dying of these
different diseases could not be evaluated, are such that the findings preclude more than
speculative conclusions regarding possible risk of death or disease due to pollutant exposure.
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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 NO ), but no association in summer. In contrast, the winter mortality of persons 45
A
to 64 years old, 65 years and older, and all ages combined in Los Angeles, California, was
significantly and positively related to daily nitrogen oxide concentrations during the period
of 1962 to 1969 but summer mortality was not. These results, therefore, do not provide con-
vincing evidence of a relation between NO air pollution and daily mortality, given that
winter mortality results for New York City were opposite to those for Los Angeles and the
associations were not consistent across seasons.
Interactions of atmospheric NO pathways with those of photochemical oxidants, discussed
elsewhere in this document and also in the Air Quality Criteria for Ozone and Other
Photochemical Qxidants, (U.S. Environmental Protection Agency, 1978) may lead to increases,in
the incidence of skin cancer in certain population groups. Epidemiological studies have
demonstrated that solar UV radiation is carcinogenic (Douglas and Owen, 1976). Outdoor
workers, such as farmers or fishermen, have a higher incidence of both basal cell and squamous
cell carcinoma of the skin than do less-exposed individuals. Chemical reactions in the
atmosphere involving nitrogenous compounds may lead to a decrease in the stratospheric concen-
tration of 03 and a resultant increase in the amount of UV radiation penetrating to the
earth's surface, but such effects have not yet been conclusively demonstrated.
15.4 ACCIDENTAL AND OCCUPATIONAL EXPOSURES
As noted earlier in this chapter, there are a number of occupational situations in which
workers are intermittently or continuously exposed to high concentrations of NQ~ or other
oxides of nitrogen. Data from such exposures, or other accidental exposures, as those
encountered with certain fires, provide some indications of N0x exposure levels associated
with severe toxic effects in humans.
There have been a few cases of unusually high levels of exposure for short periods of
time which confirm a potential lethal hazard associated with short-term exposure to N02-
Lowry and Schuman (1956) reported the development of illness of four farmers who entered
freshly-filled silos in which high concentrations of NO^ had built up. These men experienced
cough and dyspnea shortly after entering the silos. These symptoms disappeared after several
days, but were followed in about 3 weeks by cough, malaise, weakness, dyspnea, and fever.
Chest X-rays showed multiple discrete nodules scattered in both lungs. Two of the patients
died while the other two improved dramatically after receiving high doses of steroids.
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Concentrations of N02 were estimated to be in the range of 380,000 to 7,500,000 ug/m (200 to
4,000 ppm).
Grayson (1956) reported on two other cases of N02 poisoning from silage gas estimated at
560,000 to 940,000 (jg/m3 (300 to 500 ppm) N02- Indications from this study are that exposure
to concentrations in this range is likely to result in fatal pulmonary edema or asphyxia. The
study further indicated that concentrations in the range of 280,000 to 380,000 yq/m (150 to
200 ppm) are likely to produce bronchiolitis; exposure to 94,000 to 190,000 ug/m (50 to 100
ppm) are associated with reversible bronchiolitis, and exposure to concentrations in the range
of 47,000 to 140,000 (jg/m (25 to 75 ppm) are associated with bronchitis or bronchial
pneumonia with apparent complete recovery probable.
Gregory et al. (1969) studied mortality of survivors of a fire at Cleveland Clinic
(Cleveland, Ohio), in May 1929. At the time of the fire, persons were exposed to high concen-
trations of NO, N02, CO, and hydrogen cyanide resulting from the combustion of X-ray film in
which nitrocellulose was a basic material. Exposure was such that it caused 97 deaths within
2 hours and, over the next 30 days, 26 died. Under such extreme condi-tions, several factors,
including various atmospheric pollutants, may have contributed to the immediate deaths. The
conditions at the time of the fire, however, and the symptoms in many of the individuals who
subsequently died, were most consistent with symptoms expected as a result of inhalation of
very high N0? concentrations. In spite of the significant number of deaths within 30 days of
the fire, the survival rate over the next 30 years for exposed clinic employees, firemen,
pol.icemen, and rescue workers did not differ from that of unexposed similar groups. This
suggested an absence of residual effects (excess mortality) due to the intense acute exposure.
Another study (Lowry and Schuman, 1956), performed on 70 male chemical workers exposed to
750 to 5000 (jg/m (0-4 to 2.7 ppm) NO,, in their work place daily for 4-6 years, compared
various blood lipid concentrations in these subjects to values obtained on a control group of
80 men not exposed to N0?. They reported that lipid metabolism was impaired subsequent to the
original N0? exposure. Adequate information to evaluate the significance of this finding was
not available. However, as discussed earlier, Horvath et al (1978) reviewed case studies for
acute N02 exposure victims which also suggest that certain pulmonary function decrements may
persist for periods up to 13 years after initial exposure.
15.5 EFFECTS OF NOX'DERIVED COMPOUNDS
Many compounds may be derived from various oxides of nitrogen in the atmosphere, with
formation mechanisms and concentrations depending on many factors including the concentration
of various nitrogen and non-nitrogen materials present, temperature, humidity, and sunlight.
The compounds believed to represent the greatest potential risk to health include nitric acid,
nitrates, nitrites, and nitrosamines.
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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 wat«£ per kilogram body weight is higher in the infant than in adults
(Kravitz et al., 1956). Cyanosis may be produced at concentrations of about 10 percent,
methemoglobin; however, symptoms are not likely to become obvious at concentrations less than
20 percent.
The total weekly intake of nitrate in the general populations of the United States
(Ashton, 1970) and in England (Hill et al., 1973) has been estimated to average about
400,000 to 500,000 (jg. Because concentrations in water, in cured meats, and in vegetables vary
greatly, as do the quantities of these materials consumed by individuals, the ingestion
estimates must be applied with caution. However, since the worst case situation would pro-
bably find less than 40 ug/m nitrate in ambient air (Pitts and Loyd, 1973), an adult engaged
o
in heavy exercise, who might inhale 20 m of air per day could be expected to inhale no more
than 5,600 ug of nitrate per week, or less than 1.5 percent of the lowest estimate of total
weekly intake. Thus, it is considered to be unlikely that the concentrations of nitrate in
the ambient air contribute significantly to the production of acute nitrate poisoning.
Nitrate aerosols could be significant from an air pollution standpoint in that they are
the final stage in the atmospheric oxidation of NOX, a process that includes the formation of
various nitrogenous acids. However, the earlier discussion of measurement techniques (Section
7.4.1) suggest that many of the data now available relevant to atmospheric concentrations of
nitrates represent measurements of the atmospheric nitrate plus artifact nitrate formed on the
collection filter by the reaction between the filter substrate and nitrogen compounds includ-
ing nitric acid. No published epidemiological studies on the effects of atmospheric nitrates
are yet available where the ambient air levels of nitrates were measured following collection
of particulate matter glass filters (which substantially avoids artifact formation).
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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 aerosol on pulmonary function
and on the sensitivity of test subjects to the bronchoconstricting effects of carbachol.
Included in these studies were 7 healthy subjects (mean age 28) and 13 mild asthmatics (mean
age 25) selected on the basis of a demonstrated abnormal increase in R after inhaling
i 3W
carbachol. Subjects were exposed for 16 minutes in a double-blind manner to either sodium
nitrate (NaNO,) or sodium chloride (aerodynamic diameters 0.49 urn, ag = 1.7, and 0.46 urn, ag =
3
1.7, respectively) at a concentration of 7,000 |jg/m . Following exposure, subjects inhaled a
predetermined quantity of carbachol sufficient to increase R 20 to 30 percent. Prior to
exposure, after 8 and 16 minutes of exposure, and again after the inhalation of carbachol, the
following pulmonary measurements were made: functional residual capacity (FRC), R , FEV,
FEV-, g, maximum and partial expiratory flow rates at 60 and 40 percent total lung capacity.
None of the tests of pulmonary function were affected by the nitrate exposure although two of
the asthmatic subjects did demonstrate mild potentiation of the response to carbachol after
nitrate exposure. All subjects remained asymptomatic. These results suggested that in
healthy individuals or in mild asthmatics, short-term exposure to NaNO., at concentrations
approximately 100 times the total nitrate in ambient air exposures, does not affect pulmonary
function. These investigators did point out that their study results might have been quite
different had they (1) used an "acidic" nitrate in their exposure atmosphere rather than the
neutral NaN03, (2) had the exposure time been extended beyond the 16 minutes, or (3) had the
'study included symptomatic asthmatics.
Utell et al. (1980) also examined the potential synergy between acute exposure to a
pollutant (sodium nitrate aerosol) and acute respiratory infections. The mass median aerody-
namic diameter of the aerosol was 0.49 pm; the concentration 7,000 ug/m . Eleven previously
healthy adults with uncomplicated influenza A (H,NO were studied at the time of acute illness
and 1, 3, and 6 weeks later. Significant decreases in specific airway conductance and partial
expiratory flows at 40% of total lung capacity were observed at the initial examination and 1
week later. By the third week, inhalation of sodium nitrate no longer produced changes in air
way function. Control studies were made with sodium chloride aerosol. They concluded that
individuals with acute respiratory disease were susceptible to bronchoconstriction from this
air pollutant--one that normally did not influence airway function.
"Nitric acid fumes," a term used to designate the mixture of nitric acid vapor plus the
reaction products of nitric acid and various metals or organic material, has been known to
produce varying degrees of upper respiratory irritation within minutes of exposure. Prognosis
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for exposed individuals depends upon the concentration of the acid plus its products of reac-
tion and the duration of exposure. The clinical picture sometimes is biphasic and similar to
that shown by individuals exposed to high concentrations of N0? (Treiger and Przypyszny,
1947). In other instances, the picture is quite different and may reflect the toxicity of
reaction products, particularly those produced by,the reaction of nitric acid and some metals
(Danke and Warrack, 1958). Extended exposure to lower concentrations of nitric acid vapors
have been postulated as the probable cause of chronic bronchitis or a chemical pneumonitis
(Fairhall, 1957). Neither these effects nor the concentration that might cause them are well
documented.
There are no data available relating to the effects of inhaling nitric acid vapors in
concentrations likely to occur in the ambient atmosphere; however, it does seem likely that
such a highly ionized and strongly corrosive material would be a potent respiratory irritant
even at low concentrations. .
15.5.2 Nitrosamines
A few epidemiological studies have attempted to link environmental nitrates, nitrites,
and nitroso compounds with human cancer. The International Agency for Research on Cancer
(IARC) investigated a possible association between these compounds in the diet and esophageal.
cancer in specific areas of Iran and France, where these tumors occur at a high rate and in
nearby areas where the tumor rates are lower (Bogovski, 1974). Fifteen of 29 samples of cider
contained 1 to 10 M9/k9 of dimethylnitrosamine and two samples also contained diethylnitrosa-
mine (1 ug/kg). Benzo(a)pyrene also occurred in some samples. Correlations between dietary
intake of N-nitroso compounds and esophageal cancer were not established (Bogovski, 1974).
A similar study was conducted in the Anyang region of China, where 20 percent of deaths
from all causes reportedly result from esophageal cancer (Cordination Group for Research on
Etiology of Esophagal Cancer in North China, 1975). Twenty-three percent of the food samples
from, the areas with the highest cancer rates were reported to contain dimethyl-, diethyl-, and
methylbenzyl-nitrosamine. Confirmation of this analysis by gas chromatography and mass spec-
troscopy, however, is required before the finding can be accepted. Dietary nitrite levels
were higher in the areas of high cancer incidence than in low incidence areas. Chickens in
the area associated with high esophageal cancer in humans also had a high incidence of similar
tumors, suggesting an environmental etiology for the disease.
Zaldivar and Wetterstand (1975) and Armijo and Coulson (1975) have shown some correlation
between the per capita use of fertilizer and the incidence of stomach cancer in Chile. It has
been hypothesized that nitrate from fertilizer first enters the diet by way of meat,
vegetables, and drinking water. Nitrates are then reduced to nitrites by microbial action,
and are thus available for j_n vivo nitrosation of secondary amines, contained in the diet, to
15-44
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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 J_n vivo formation of nitrosamines in humans or that inhaled nitrosamines repre-
sent significant health hazards. Questions have been raised as to i_n vivo nitrosation by NCL.
Iqbal et al. (1980) have reported that, indeed, jjn vivo nitrosation of amines does occur in
mice. There are a number of endogenous and exogenous amines available to an organism for
nitrosation. In the preliminary studies of Iqbal et al., they gavaged mice with an exogenous
amine, morpholine, and then exposed mice for 0.5 hour to 50 ppm NO,,. Production of N-nitroso-
morpholine (NMOR) was measured in the mouse. Longer exposures to this concentration of NO^
for up to 4 hours resulted in higher levels of the nitrosamine. They also exposed gavaged
.mice for 4 hours to NO^ (from 0.2 to 50 ppm) and reported increased levels of NMOR. The site
or mechanisms of the NMOR biosynthesis were not identified.
Nitrosation of amines in the stomach has been demonstrated to occur in humans (Sander and
Seif, 1969), in rodents (Sander et al., 1968), and in dogs (Mysliwy et al., 1974). Preformed
nitrosamines have been found in tobacco (Hecht et al., 1974; Hoffman et al., 1974) and in
tobacco smoke (Klus and Kuhn, 1973; Neurath, 1967).
15.5.3 Other Compounds
Recent studies by Pitts et al. (1978) have demonstrated that, in sunlight, very low
concentrations of diethylamine and triethyl amines behaved like hydrocarbons and reacted with
NO, HOy or nitrous acid to form 03, PAN, acetaldehyde plus diethylnitramine and several amides
including acetamide. Peroxyacetyl nitrate (PAN) is a strong eye irritant at a concentration of
4,945 ug/m (1.0 ppm). The effects of this compound are discussed at length in Air Quality
Criteria for Ozone and Other Photochemical Oxidants (U.S. Environmental Protection Agency,
1978). In addition to nitrosamines, diethylnitramine (Goodall and Kennedy, 1976; Druckey
et al., 1961) and acetamide (Jackson and Dessau, 1961; Weisberger, et al. 1969) have been
shown to be carcinogenic in test animals. However, the significance of these materials as
human carcinogens is unknown.
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15.6 SUMMARY AND CONCLUSIONS
Critical N0x human health effects issues include: (1) qualitative characterization of
identifiable health effects associated with exposure to various NO compounds; (2) delineation
of the seriousness of the identified effects in terms of their reversibility/irreversibility
and their impact on normal human functions and activities; (3) quantitative characterization
of exposure/effect or exposure/response relationships for health effects of concern; and (4)
identification of sensitive populations at special risk for manifestation of such effects at
ambient air NO,, levels.
Of the oxides of nitrogen, NOp appears to be the compound of greatest concern in terms of
human health effects documented as likely to occur at exposure levels within the range of or
approaching ambient air concentrations encountered in the United States. Based on this, the
main focus of the present section is on the summarization of key points and conclusions
regarding N02 health effects and their likely significance for protection of public health.
Brief comments are also provided in regard to certain NO -derived compounds hypothesized to be
of public health concern.
15.6.1 N02 Effects
A broad spectrum of human and animal health effects have been reported to be associated
with N0? exposure. These range from (1) death or serious, irreversible lung damage associated
with very high accidental or experimental exposures in the range of 150-300 ppm or higher;
through (2) less severe but clearly significant short-term or chronic lung tissue damage,
functional impairment, or aggravation of other disease processes at exposure levels of 5 to
100 ppm; to (3) impairment of lung defense mechanisms and other, milder, temporary effects,
e.g..changes in pulmonary function and sensory system effects, occurring at N0£ levels below 5
ppm. Of most relevance here is consideration of the effects occurring at levels below 5 ppm.
15.6.1.1 Pulmonary Function Effects—Numerous controlled human exposure studies have examined
the effects of single, short-term NO,, exposures on pulmonary function. The most frequently
observed pulmonary function effects of N0« exposure in controlled human studies (usually at
concentrations higher than ambient) include increases in airway resistance (R ,) and changes
aW
in susceptibility to the effects of bronchoconstricting agents. Functional response of human
subjects to N0? are commonly assessed with measurements of flow resistance (total respiratory,
pulmonary, or airway) and maximum expiratory flow rate (related to lung volume). Both types
of measurements are influenced by changes in diameter of the laryngotracheobronchial system.
Airway narrowing, or bronchoconstriction, increases flow resistance and reduces maximal
expiratory flow rate.
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Increased airway resistance (R,.,) and other physiological changes suggesting impaired
QW
pulmonary function have been clearly demonstrated to occur in healthy adults with single 2-hr
NO- exposures ranging from 3760 to 13,200 ug/m (2.5 to 7.0 ppm). Certain studies also
indicate that significant effects occur in healthy subjects with shorter (5-15 min) exposures
to the same or possibly lower levels of N0« administered either alone or in combination with
NaCl aerosol. More specifically, in regard to the latter point, Suzuki and Ishikawa (1965)
observed altered respiratory function after exposure of healthy subjects to NO,, levels of 1300
3
to 3760 ug/m (0.7 to 2.0 ppm) for 10 minutes. Their data however, preclude a clear associa-
3
tion of observed effects with any particular concentration in the range of 1300 to 3760 ug/m
(0.7 to 2.0 ppm) NO- exposure.
In contrast, Hackney, et al. (1978) reported no statistically significant changes in any
of the pulmonary functions tested with the exception of a marginal loss in forced vital capac-
ity after exposure to 1880 ug/m (1.0 ppm) N02 for 2 hours on two successive days (1.5% mean
decrease, P <0.05). However, the authors question the health significance of this small, but
statistically significant change and suggest that it may simply be due to random variation.
Also, Beil and Ulmer (1976) and Folinsbee et al. (1978) concluded that there were no physio-
logically significant pulmonary effects at exposure levels of 1880 and 1100 ug/m (1.0 and 0.6
ppm) N09, respectively; and in a similar study, where Kerr et al. (1979) exposed 10 healthy
3
adults to 940 ug/m (0.5 ppm) N02 for 2 hours, only small changes were found in quasistatic
compliance. However, the authors again suggested that such results may be due to chance
alone, especially since no other pulmonary function tests showed significant changes for the
healthy adult group and only one subject reported mild symptomatic effects associated with NOp
exposure. In general, then, these studies appear to have found no observed effect levels for
pulmonary function changes in healthy adults across a range of 0.5 to 1.0 ppm NO,,.
Hackney et al. (1975) and von Nieding et al. (1977) also concluded that there were no
physiologically significant effects at NO^ levels below 560 ug/m (0.3 ppm) in the presence of
various other air pollutants, with the possible exception of increased sensitivity to a bron-
3
choconstrictor (acetylcholine) observed by von Nieding et al. (1977) at 94 ug/m (0.05 ppm)
N02 in the presence of 49 ug/m (0.025 ppm) ozone and 290 ug/m (0.11 ppm) S02. The von
Nieding finding, however, is difficult to interpret in view of: (1) controversy over the
health significance of altered sensitivity to bronchoconstrictors in healthy subjects; (2)
uncertainties due to methodological differences between his techniques and other investiga-
tors'; and (3) no confirmation of von Nieding's et al. (1977) findings by other investigators.
Thus, no presently available controlled human exposure study can be accepted at this time as
providing conclusive evidence for meaningful pulmonary function changes occurring at N09
3 *-
levels below 1880 ug/m (1.0 ppm) for healthy adult subjects.
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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 N09 below 2.0 ppm; nor
oW C.
have controlled exposure studies investigated long-term effects of repeated NOo exposures.
Secondary effects of brochoconstriction can add to the biological significance of observed
functional alterations. One such possible secondary effect is the interference with alveolar-
capillary gas exchange (measured as an increase in alveolar-arterial PO- gradient, or as a
reduction in arterial PCL or oxyhemoglobin saturation). The relation, if any, between bron-
choconstriction associated with a single exposure to NO^ and possible development of chronic
respiratory disease during prolonged or intermittent exposure is unknown. It is unlikely,
however, that the slight increases in airway resistance which were observed to occur after a
single exposure to N0? at or below 2.0 ppm represent a significant adverse health effect for
healthy adults.
More difficult to interpret is the health significance of NKL exacerbation of pulmonary
function changes induced by bronchoconstrictors. Monitoring a subject's response to a bron-
choconstrictor is a sensitive experimental approach that utilizes (1) the action of neurotrans-
mitters (e.g., acetylcholine) normally present in the body, (2) pharmacologic products with
similar properties (e.g., carbachol), or (3) nervous system-mediated reflexes. The purpose of
the bronchoconstrictor is to test the response of the individual's airways to a standardized
challenge. This response in individual subjects may be altered by underlying disease such as
asthma, by respiratory infection or by previous exposure to an air pollutant. A reasonable
hypothesis is that the magnitude of response to a particular experimental challenge such as a
synthetic bronchoconstrictor may be used to predict the individual's level of risk when
exposed to ambient pollutants. However, it is also known that increases in bronchial sensi-
tivity can be produced by sudden changes in temperature or even by emotional stress. Thus, it
is believed to be unlikely that the relatively mild and inconsistent bronchoconstriction
produced by a single short exposure to NOp represents a health hazard with or without the
added increase in constrictive potential due to any of these other natural or induced
influences.
Increases in R and increased sensitivity to bronchoconstrictors are both suggestive of
3W
irritation in the .laryngo-tracheo-bronchial system. The consequence of repeated short-term
exposures has not been determined in human volunteers; however, studies with animals suggest
that repeated exposures to N02 levels at or below those associated with significant increases
in R,,, can increase susceptibility to respiratory infections.
aW
For purposes of this review, the intensity of the response in test individuals has been
given little consideration in assessing potential health risk. This approach was taken
because the intent, usually, was to determine the lowest NO- concentration that would cause
15-48
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any increase in Rflw in healthy or in susceptible individuals after a single, short-term
exposure. Obviously, a barely detectable functional response has less serious implications
than one associated with disability or distress.
An assessment of the importance of studies showing associations between exposure to NOp
and increased airway resistance must consider also the known wide variations in susceptibility
within human populations. Thus, an exposure sufficient to produce slightly increased airway
resistance in healthy individuals may produce much greater and more severe responses in, highly
susceptible segments of the population, e.g., in those with symptoms of chronic respiratory
illness or asthmatics.
Several controlled clinical studies have specifically addressed the issue of whether
detectable respiratory effects can be induced by NOp in sensitive human subjects at exposure
levels below those affecting healthy human adults. For example, the studies by von Nieding et
al. (1971; 1973) show that, in persons with chronic bronchitis, concentrations of 7,500 (jg and
9,400 pg/m (4.0 and 5.0 ppm) produced decreases in arterial partial pressure of oxygen and
increases in the difference between alveolar and arterial partial pressure of oxygen. Expo-
sures to concentrations of M^ above 2,800 ug/m (1.5 ppm), for periods considerably less than
1 hour, also produced significant increases in airway resistance. Thus, results for bronchi-
tic individuals and healthy individuals appear to differ little and provide no particular
support for the hypothesis that chronic bronchitics are more sensitive to NOo exposure than
healthy adults.
In another study (Kerr et al., 1979), measurements of pulmonary function were not altered
in 13 asthmatics or 7 bronchitics as a result of 2 hours of exposure to 940 ug/m (0.5 ppm)
NOp when the groups were analyzed separately. When the data for the two groups were analyzed
together, however, small but statistically significant changes in quasistatic compliance and
functional residual capacity were reported. Nevertheless, the authors state that the changes
reported may be due to chance alone. Seven asthmatics and one bronchitic reported some chest
discomfort, dyspnea, headache, and/or slight nasal discharge.
In contrast to the above results, exposures to 190 ug/m (0.1 ppm) NOo for i hour were
reported by Orehek et al., (1976) to increase mean airway resistance (R,..) in 13 of 20 asthma-
dw
tics and to increase the sensitivity to a bronchoconstrictor (carbachol) in these same individ-
uals. However, considerable controversy exists regarding interpretation of the Orehek (1976)
study and the health significance of the increased response to a bronchoconstrictor observed
in the study. Also, its basic findings remain to be independently replicated.
Based on the above results, conclusive statements regarding the possible special risk
status of asthmatics in response to NO^ exposure cannot be made at this time. The Kerr et al.
(1979) study results do suggest, however, that increased occurrence of personal discomfort and
symptoms may occur in asthmatics as the result of short-term (2 hr) exposures to 0.5 ppm Nt^.
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The above clinical studies provide important data concerning the effects of single short-
term NOo exposures on healthy young adults and certain groups defined a priori as "sensitive",
i.e., bronchitics and asthmatics. However, members of other presumed sensitive populations,
e.g., children, the elderly, and individuals with chronic cardiovascular disease, have not
been tested in controlled clinical studies and are not likely to be tested in the future.
because of medical ethics limitations on the use of such subjects in experimental studies.
Therefore, statements on whether such individuals are at greater risk than healthy young
adults for experiencing respiratory effects with single short-term NOp exposures cannot be
made based on controlled human exposure studies.
It is informative to compare the above controlled human exposure study results with
findings from epidemiological studies investigating possible effects of ambient air NOp expo-
sures on pulmonary function parameters in human adults and children. In that regard, no
evidence of pulmonary function decrements was obtained in several epidemiological studies
(Cohen et al., 1972; Speizer and Ferris 1973a,b; Burgess et al., 1973; Linn et al., 1976) of
adults exposed to ambient maximum hourly N(L levels as high as 0.50 ppm or annual average NO-
levels up to 0.06 ppm. These results appear to be consistent with no observed effects for
pulmonary function changes in healthy adults generally obtained in the above controlled human
exposure studies with exposures to NO^ levels of 1.0 ppm or below. None of the presently
available epidemiological studies, however, provide information regarding NOp effects on
pulmonary functions in bronchitis or asthmatics. Also, critical evaluation of other epidemio-
logical studies, on children, reveals that such studies to date do not provide useful quanti-
tative information upon which to base estimates of ambient N02 levels associated with pul-
monary function decrements in children.
15.6.1.2 Acute Respiratory Disease Effects—Epidemiological studies of outdoor and indoor air
pollution have also been employed in an effort to demonstrate an association between NO 2
exposures and the occurrence of acute respiratory disease symptoms and illnesses in both human
adults and children. Such studies only provide relatively limited evidence for such associa-
tions possibly existing at ambient air N(L levels.
Only a few American community air pollution studies on the effects of hK^ on acute
respiratory disease are available, but all were found to be of questionable validity due to
the use of the Jacobs-Hochheiser technique in measuring atmospheric concentrations of ^2-
A few reports on other outdoor air pollution studies on the subject were found in the
foreign literature, but were such as to preclude confident evaluation of the methodology
involved or contained information which precluded reliable attribution of observed health
effects to ambient air N0? exposures.
15-50
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Certain other epidemiclogical studies on indoor air pollution, in contrast to the outdoor
pollution studies, appear to provide useful information regarding associations between N0?
exposures and acute respiratory disease effects. More specifically, some support for accept-
ing the hypothesis that children are at special risk from NCL-induced increases in acute
respiratory illnesses might be derived from certain British and American studies on indoor
pollution effects summarized above in Table 15-6.
The British studies by Melia et al. (1977, 1979) provided initial evidence suggesting
that increased acute respiratory symptoms and illness rates may occur among school children
living in homes using gas stoves for cooking in comparison to children from homes using
electric ranges. High temperature gas combustion is a source of NOo. However, the first
study (Melia, 1977) did not take parental smoking into account, and, when socioeconomic status
was controlled for in the statistical analyses for each of the two studies, only relatively
weak associations (p=.10) were found for some subgroups of children but not others. Also, N0?
levels were not monitored in the study homes. In later British studies, by Florey et al.
(1979) and Goldstein et al. (1979), NO^ levels were measured in the kitchens and bedrooms of
children residing in gas stove homes; but no significant relationships were found between
weekly NCL levels in the kitchen and acute respiratory illness symptoms in 6 to 7 year old
children or their siblings or parents. Nor were any significant associations found between
N02 levels and pulmonary function measures in the 6 to 7 year old children. Only some weak
associations (ps .10) were found between increased respiratory illness in the same children
and N02 levels in their bedrooms. The authors suggest, however, that the apparent association
may be due to NOg serving as a proxy for some other variable (humidity, temperature) more
important in the etiology of acute respiratory infections in the children. The later British
studies,therefore, do not appear to have provided convincing evidence to substantiate the
initial hypothesis of possible NCL -induced increases in acute respiratory disease effects in
children residing in gas-stove homes. Consistent with this, United States studies by Keller
et al. (1979 a,b) failed to find any evidence supporting the existence of the hypothesized
relationship between NOp and acute respiratory illness in school-aged American children living
in gas stove homes.
On the other hand in the United States study recently reported by Speizer et al. (1980),
children from households with gas stoves were reported to have a greater history of serious
respiratory illness before age 2. In this study, adjustment of rates of illness before age 2
for parental smoking and socioeconomic status led to a clearly significant (p <.01) associa-
tion with the presence of gas-cooking devices. Also found were small but statistically
significant lower levels of two measures of pulmonary function, corrected for height, in
children from houses with gas stoves. In all instances in the subset of study homes with gas
15-51
-------
facilities where NO^ levels were monitored (Spengler et al., 1979), NOp was present in higher
concentrations than was present in the outside air. Indoor values monitored in one gas stove
3
home averaged as high as 54 ug/m (0.03 ppm) over a two-week period; and short-term (lasting
o q
minutes to hours) N02 levels in excess of 500 ug/m (.25 ppm) and even 1,000 [jg/m (0.5 ppm)
occurred in the kitchen during cooking.
The Speizer/Spengler findings tend to support the original hypotheses initially advanced
by Melia et al. (1977) regarding associations between exposure to N0? produced by gas combus-
tion and increased acute respiratory disease in children residing in homes using gas stoves.
Also, the small but significant decrements in pulmonary function observed by Speizer et al.
(1980) in the children at age 6 to 7, while not likely of much immediate physiological or
health consequence, may be indicative of persisting residual effects of the early childhood
respiratory infections on lung development and growth. Furthermore, other studies by Colley
et al. (1973), Kiernan et al. (1976), and Tausseg (1977) suggest that increased rates of
respiratory illness in young pre-school children may result in increased susceptability for
respiratory infection lasting into early adulthood. Such considerations regarding possible
long-term health consequences, together with the obvious immediate health significance of
respiratory infections in young children, argue for treating any such effects as being
sufficiently adverse as to be of clear concern in terms of public health protection.
Certain factors as noted earlier (page 15-36), however, should be taken into account
before fully accepting at this time the above findings and their potential implications. This
includes an apparent inconsistency between the Speizer findings and the results of the Keller
studies, which found no association between residence in gas-stove usage homes and respiratory
illness rates in American school children. Several explanations for the apparant discrepancy
can be advanced. For example, the sample sizes for children used in the Keller studies were
approximately 10 times smaller than the sample size employed in the Speizer study, thereby
reducing the likelihood of Keller demonstrating statistically significant associations between
gas stove usage and increased respiratory illness .among children from gas stove homes. Also,
the associations reported by Speizer were for increased respiratory illness rates before the
age of two, whereas the Keller findings apply to older, school-aged children 6 to 7 years old.
If both sets of findings are accurate, however, then they may suggest that the increased
respiratory infections observed before the age of two by Speizer are not associated, after
all, with long-term, persisting consequences of the type hinted at by the Colley and Kiernan
findings (vida supra).
If one does accept the Speizer findings as being indicative of increased respiratory
infections occurring in young children living in gas stove homes, then the question remains as
to what N02 exposure levels and durations might be associated with the induction of such
15-52
-------
effects. Unfortunately, no clear resolution of this issue is presently available. The
authors themselves (Speizer et al., 1980) speculate that repeated exposures to intermittently
high peak levels of NC^ may be most important in contributing to the increased incidence of
respiratory illness. This hypothesis is based primarily on their observations (Spengler et
al., 1979) of long-term NO- annual averages levels in gas stove homes not differing much from
those found in electric homes, and of the latter lacking the occurrence of intermittent marked
1- or 2-hr indoor air NC^ peak concentrations associated with periodic use of the gas stoves
for cooking.
Estimates of specific NO,, levels, either for 1-2 hr peaks or for long-term (24 hr,
weekly, annual) average levels that might be associated with increased respiratory illness in
young children cannot be clearly derived based alone on the limited monitoring data reported
by Spengler et al. (1979). Rather, additional data from other studies of ML levels typically
encountered in American homes using gas stoves may also be of value in attempting to estimate
the effective NO^ exposure parameters. The results of several such studies are summarized in
Table 15-7, along with the Spengler et al. (1979) findings. Collectively, the studies found
daily peak 1-2 hr ^ levels generally to average between 0.04 and 0.50 ppm (depending on room
of house monitored) but some instantaneous peak levels in kitchens were at times as high as
1.0 ppm); whereas 24-hr and annual average levels fell in the range of 0.02 to 0.07 ppm, and
0.02 to 0.06 ppm, respectively. Reported increases in respiratory disease symptoms in young
children residing in gas stove homes could be associated with any of these NO- exposure
levels/durations.
Placing such levels in perspective against reported ambient air levels in the United
States, examination of selected nationwide monitoring data for 1975 to 1980 (discussed in
Chapter 8) reveals that peak 1-hr N02 concentrations only occassionally equalled or exceeded
0.4 ppm in a few locations nationwide (e.g., Los Angeles; several other California sites;
Ashland, Kentucky; and Port Huron, Michigan). Similarly, annual average NO,, levels
during the 1975 to 1980 period exceeded 0.05 ppm in some areas, including such heavily
populated locations as Anaheim and San Diego, California, and Chicago, Illinois.
15.6.1.3 Chronic Respiratory Disease Effects—A number of investigators have failed to find
an association between long-term mean ambient NO/, exposure and the prevalence of chronic
respiratory disease in adults. In contrast, long term NO^ concentrations have been reported
to be associated with mortality, various cancers, and arteriosclerotic heart disease. Such
epidemiologic results, however, are not consistent in their findings; one even showed a
significant negative correlation between N0~ and mortality. In addition, the quality of data
available for such long-term studies is such that the results must be viewed with much skepti-
cism until they can be substantiated by additional research.
15-53
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TABLE 15-7. NITROGEN DIOXIDE LEVELS REPORTED IN GAS AND ELECTRIC STOVE HOMES
ui
-p-
Site and conditions
Parameter
NO, concentration
(ppm)
Home 1: 2000 ft.
split-level with
well ventilated
kitchen.
range (mean)
Kitchen, 1 meter froa stove
Living room
Bedroom
Outdoors
Study simulated typical
gas stove use patterns
Kitchen
Living room
Bedroom
Outdoors
Daily peak
24-hr avg
Dai ly peak
24-hr avg
Daily peak
24-hr avg
Daily peak
24-hr avg
Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
Peak 1-hr
24-hr avg
2-hr avg
2-hr avg
2-hr avg
2-hr avg
avg
avg
avg
avg
.04-.
.01-.
.01-.
.01-
.02-.
.02-.
.02-.
.01-
28
08
.17
Ob
.09
04
.08
.05
(-10)
(.04)
(4)6)
(-03)
(.05)
(-03)
(.04)
(.02)
Measurement Reference
method
Hone 3: 2- story Home 4: 1500 ft2
apartment with ranch style with
small, unventi- kitchen open to
lated kitchen. other rooms.
range (mean) range (mean)
.03-.
.03-.
.01-
.01-
.02-
.03-.
.01-
.02-.
.31
.13
.06
.04
.19
.05
.09
.03
(.
(.
(.
(-
(.
(.
(.
(-
45
.07
40
07
24
.05
07
.04
10) .05-. 41 (.18)
06) .04-. 11 (.06)
04) .04-. 35 (.11)
03) .03-. 07 (.04)
07)
03)
04) .02-. 12 (.05)
02) .01-. 04 (.02)
Chemi luminesent Cote, Wade, and
Analyzer Yocom, 1974
Suburban homes
in Connecticut
Chemi luminesent Hollowel et al.
Analyzer 1980
Energy efficient
research house,
.33-. 44 air changes
per hour (ach).
-------
TABLE 15-7. (continued)
en
in
Site and conditions
Kitchen with a gas oven on for
1-hr at 350°F
0.25 ach (no stove vent)
1.0 ach (hood vent
above stove)
2.5 ach (hood vent with fan
at 50 CFH)
7.0 ach (hood vent with fan
at 140 CFM)
Outside during test
83 gas stove homes
50 electric stove homes
53 outdoor samples in
vicinity
46 gas stove
Activity room (gas stove
homes)
Activity room (electric
stove homes)
Outdoors
Kitchen, 3^ ft from gas
stove home
Parameter
1-hr average
1-hr average
1-hr average
1-hr average
1-hr average
24-hr average
24-hr average
24-hr average
continuous measurement
over 3 day periods
95th percentile of 24-hr
averages measured over a
1 year period
continuous
NO- concentration
(ppm)
1.20
O.BO
0.40
0.10
0.03
range (mean)
.01-. 11 (0.05)
0-.06 (.02)
.02-. 05 (.03)
peak values in some homes
exceeded 1 ppm; peaks during
cooking reached as high as
8 x 24-hr average
.02-. 06
.01-. 05
.01-. 06
peak concentrations
in the range of 0.25-
0.50 were observed for
10-15 minute periods
during oven or stove use.
Measurement
method
Chemi luminescent
Analyzer
Modified Jacobs-
Hochheiser
(arsenite modified)
Chemi luminescent
Analyzer
Modified Sodium
Arsenite
Chemi 1 umi nescent
Analyzer
Reference
Hollowel et al. ,
1978
Test kitchen (27m3)
Kel ler et al. , 1979
Gas and electric
stove homes in
Columbus, Ohio
Speizer et al. , 1980
Activity room in
5-11 gas and
electric stove
homes in each of
six communities.
Also monitored in
1 kitchen of a gas
stove home for 2 wks.
-------
15.6.1.4 Sensory System Effects--In addition to pulmonary function and respiratory disease
effects, NO, exposures have been shown to exert effects on sensory systems. This includes
3
detection of NO- as a pungent odor at concentrations as low as 210 ug/m (0.11 ppm) of N0?
immediately upon exposure. Under higher exposure conditions (10 ppm) impaired odor detection
occurs. Both of these sensory effects, however, appear to be of negligible health concern in
view of their temporary, reversible nature and generally minor impact on normal human func-
tions and activities. Probably of somewhat greater importance are certain other NO- sensory
effects, especially impairment of dark adaption which can occur in human subjects at NO,
3
levels as low as 130 to 150 ug/m (.07 to .08 ppm). It is difficult to appraise fully the
health significance of such an effect, however; but it appears to be of generally negligible
health concern except, perhaps, for certain occupational or public safety situations where
rapid dark adaptation may be important.
15.6.2 Effects of NO -Derived Compounds
Nitrate poisoning (i.e., the formation of sufficient methaemoglobin to produce cyanosis)
occurs not infrequently in the United States, most often in children. It is not believed,
however, that the inhalation of atmospheric nitrates is important in producing symptoms since
the quantity absorbed from the air would represent a relatively small fraction of that
ingested by other routes (e.g., food and water). Even if absorption from the lung was several
times that from the gut, atmospheric nitrates probably would still be unimportant in this
regard.
Nitrate aerosols and nitric acid vapor may represent significant respiratory irritants.
Two studies have suggested that increases in atmospheric nitrate concentrations or combined
nitrate and sulfate concentrations were associated with increases in asthma attacks. A
laboratory study, however, indicated that short-term exposure to sodium nitrate at concentra-
tions at least 100 times the total nitrate in ambient exposures had no effect on pulmonary
function in healthy individuals or in asthmatics. .
Chemical reactions in the atmosphere involving N02 and hydrocarbons can produce peroxy-
acetyl nitrate (PAN), a strong eye irritant. The effects of PAN have been thoroughly reviewed
recently in the document Air Quality Criteria for Ozone and Other Photochemical Oxidants (U.S.
EPA, 1978) and reference is therefore made to this document for further information.
Although the existence of a mechanism for the m'trosation i_n vivo of an exogenous amine,
morpholine, by inhaled NO- has recently been demonstrated in mice, there is no evidence, to
date, that nitrogenous atmospheric pollutants contribute to the i_n vivo formation of nitrosa-
mines in humans or that nitrosamines inhaled from the ambient air represent significant health
hazards.
15-56
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Klus, H. , and H. Kuhn. Determination of nornicotine nitrosamine in the smoke condensate of
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GLOSSARY
AaDOy Alveolar-arterial difference or gradient of the partial pressure of
oxygen. An overall measure of the efficiency of the lung as a gas ex-
changer. In healthy subjects, the gradient is 5 to 15 mm Hg (torr).
A/PR/8 virus: A type of virus capable of causing influenza in laboratory
animals; also, A/PR/8/34.
Abscission: The process whereby leaves, leaflets, fruits, or other plant
parts become detached from the plant.
Absorption coefficient: A quantity which characterizes the attenuation with
distance of a beam of electromagnetic radiation (like light) in a substance.
Absorption spectrum: The spectrum that results after any radiation has
passed through an absorbing substance.
Abstraction: Removal of some constituent of a substance or molecule.
Acetaldehyde: CH3CHO; an intermediate in yeast fermentation of car-
bohydrate ana in alcohol metabolism; also called acetic aldehyde,
ethaldehyde, ethanal.
Acetate rayon: A staple or filament fiber made by extrusion of cellulose
acetate. It is saponified by dilute alkali whereas viscose rayon remains
unchanged.
Acetylcholine: A naturally-occurring substance in the body which can
cause constriction of the bronchi in the lungs.
Acid: A substance that can donate hydrogen ions.
Acid dyes: A large group of synthetic coal tar-derived dyes which
produce bright shades in a wide color range. Low cost and ease
of application are features which make them the most widely used
dyes for wool. Also used on nylon. The term acid dye is derived
from their precipitation in an acid bath.
Acid mucopolysaccharide: A class of compounds composed of protein
and polysaccharide. Mucopolysaccharides comprise much of the
substance of connective tissue.
Acid phosphatase: An enzyme (EC 3.1.3.2) which catalyzes the disassociation
of phosphate (PO.) from a wide range of monoesters of orthophosphoric
acid. Acid phosphatase is active in an acidic pH range.
Acid rain: Rain having a pH less than 5.6, the minimum expected from
atmospheric CO
G-l
-------
Acrolein: ChL=CHCHO; a volatile, flammable, oily liquid, giving off
irritant vapor. Strong irritant of skin and mucuous membranes. Also
called acrylic aldehyde, 2-propenal.
Acrylics (plastics): Plastics which are made from acrylic acid and are
light in weight, have great breakage resistance, and a lack of
odor and taste. Not resistant to scratching, burns, hot water,
alcohol or cleaning fluids. Examples include Lucite and Plexiglass.
Acrylics are thermoplastics and are softened by heat and hardened
into definite shapes by cooling.
Acrylic fiber: The generic name of man-made fibers derived from acrylic
resins (minimum of 85 percent acrylonitrite units).
Actinic: A term applied to wavelengths of light too small to affect
one's sense of sight, such as ultraviolet.
Actinomycetes: Members of the genus Actinomyces; nonmotile, nonspore-
forming, anaerobic bacteria, including both soil-dwelling saprophytes
and disease-producing parasites.
Activation energy: The energy required to bring about a chemical reaction.
Acute respiratory disease: Respiratory infection, usually with rapid
onset and of short duration.
Acute toxicity: Any poisonous effect produced by a single short-term
exposure, that results in severe biological harm or death.
Acyl: Any organic radical or group that remains intact when an organic
acid forms an ester.
Adenoma: An ordinarily benign neoplasm (tumor) of epithelial tissue;
usually well circumscribed, tending to compress adjacent tissue rather
than infiltrating or invading.
Adenosine monophosphate (AMP): A nucleotide found amoung the hydrolysis
products of all nucleic acids; also called adenylic acid.
Adenosine triphosphatase (ATPase): An enzyme (EC 3.6.1.3) in muscle
and elsewhere that catalyzes the release of the high-energy, ter-
minal phosphate group of adenosine triphosphate.
Adrenalectomy: Removal of an adrenal gland. This gland is located near
or upon the kidney and is the site of origin of a number of hormones.
Adsorption: Adhesion of a thin layer of molecules to a liquid or solid sur-
face.
Advection: Horizontal flow of air at the surface or aloft; one of the
means by which heat is transferred from one region of the earth
to another.
G-2
-------
Aerodynamic diameter: Expression of aerodynamic behavior of an irregularly
shaped particle in terms of the diameter of a sphere of unit density
having identical aerodynamic behavior to the particle in question.
Aerosol: Solid particles or liquid droplets which are dispersed or sus-
pended in a gas.
Agglutination: The process by which suspended bacteria, cells or similar
particles adhere and form into clumps.
Airborne pathogen: A disease-causing microorganism which travels in the
air or on particles in the air.
Air pollutant: A substance present in the ambient atmosphere, resulting
from the activity of man or from natural processes, which may cause
damage to human health or welfare, the natural environment, or
materials or objects.
Airway conductance: Inverse of airway resistance.
Airway resistance (R,w): The pressure difference between the alveoli
and the mouth required to produce an air flow of 1 liter per second.
Alanine aminotransferase: An enzyme (EC 2.6.1.2) transferring amino
groups from L-alanine to 2-ketoglutarate. Also known as alanine
transaminase.
Albumin: A type of simple, water-soluble protein widely distributed
throughout animal tissues and fluids, particularly serum.
0
M
Aldehyde: An organic compound characterized by the group -OH.
Aldolase: An enzyme (EC 4.1.2.7) involved in metabolism of fructose
which catalyzes the formation of two 3-carbon intermediates in the
major pathway of carbohydrate metabolism.
Algal bloom: Sudden spurt in growth of algae which can affect water
quality adversely.
Alkali: A salt of sodium or potassium capable of neutralizing acids.
Alkaline phosphatase: A phosphatase (EC 3.1.3.1) with an optimum pH of
8.6, present ubiquitously.
Allergen: A material that, as a result of coming into contact with appro-
priate tissues of an animal body, induces a state of sensitivity result-
ing in various reactions; generally associated with idiosyncratic
hypersensitivities.
Alpha-hydroxybutyrate dehydrogenase: An enzyme (EC 1.1.1.30), present
mainly in mitochondria, which catalyzes the conversion of hydro-
xybutyrate to acetoacetate in intermediate biochemical pathways.
G-3
-------
Alpha rhythm: A rhythmic pulsation obtained in brain waves exhibited
in the sleeping state of an individual.
Alveolar capillary membrane: Finest portion of alveolar capillaries,
where gas transfer to and from blood takes place.
Alveolar macrophages (AM): Large, mononuclear, phagocytic cells found
on the alveolar surface, responsible for the sterility of the lung.
Alveolar oxygen partial pressure (PACL): Partial pressure of oxygen in the
air contained in the air sacs of the lungs.
Alveolar septa: The tissue between two adjacent pulmonary alveoli, con-
sisting of a close-meshed capillary network covered on both surfaces
by thin alveolar epithelial cells.
Alveolus: An air cell; a terminal, sac-like dilation in the lung. Gas
exchange (0?/CO?) occurs here.
Ambient: The atmosphere to which the general population may be exposed.
Construed here not to include atmospheric conditions indoors, or in
the workplace.
Amine: A substance that may be derived from ammonia (NH,) by the re-
placement of one, two or three of the hydrogen (H) atoms by hydro-
carbons or other radicals (primary, secondary or tertiary amines,
respectively).
Amino acids: Molecules consisting of a carboxyl group, a basic amino
group, and a residue group attached to a central carbon atom. Serve
as the building blocks of proteins.
p-Aminohippuric acid (PAH): A compound used to determine renal plasma
flow.
Aminotriazole: A systemic herbicide, C^H.N., used in areas other than
croplands, that also possesses some anlithyroid activity; also called
amitrole.
Ammonification: Decomposition with production of ammonia or ammonium
compounds, esp. by the action of bacteria on nitrogenous organic
matter.
Aminonium
with
lizers.
urn: Anion (NH.) or radical (NH.) derived from ammonia by combination
ith hydrogen. Present in rainwater, soils and many commercial ferti-
Amnestic: Pertains to immunologic memory: upon receiving a second
dose of antigen, the host "remembers" the first dose and responds
faster to the challenge.
G-4
-------
Anaerobic: Living, active or occurring in the absence of free oxygen.
Anaerobic bacteria: A type of microscopic organism which can live in
an environment not containing free oxygen.
Anaphylactic dyspneic attack: Difficulty in breathing associated with
a systemic allergic response.
Anaphylaxis: A term commonly used to denote the immediate, transient
kind of immunological (allergic) reaction characterized by contraction
of smooth muscle and dilation of capillaries due to release of
pharmacologically active substances.
Angiosperm: A plant having seeds enclosed in an ovary; a flowering plant.
Angina pectoris: Severe constricting pain in the chest which may be
caused by depletion of oxygen delivery to the heart muscle; usually
caused by coronary disease.
o _o
Angstrom (A): A unit (10 cm) used in the measurement of the wavelength
of light.
Anhydride: A compound resulting from removal of water from two molecules
of a carboxylic (-COOH) acid. Also, may refer to those substances
(anhydrous) which do not contain water in chemical combination.
Anion: A negatively charged atom or radical.
Anorexia: Diminished appetite; aversion to food.
Anoxic: Without or deprived of oxygen.
Anthraquinone: A yellow crystalline ketone, C-w-HgOp, derived from
anthracene and used in the manufacture of ayes.
Anthropogenic: Of, relating to or influenced by man. An anthropogenic
source of pollution is one caused by man's actions.
Antibody: Any body or substance evoked by the stimulus of an antigen
and which reacts specifically with antigen in some demonstrable way.
Antigen: A material such as a foreign protein that, as a result of
coming in contact with appropriate tissues of an animal, after a
latent period, induces a state of sensitivity and/or the production of
antibody.
Antistatic agent: A chemical compound applied to fabrics to reduce or
eliminate accumulation of static electricity.
Arachidonic acid: Long-chain fatty-acid which serves as a precursor
of prostaglandins.
G-5
-------
Area source: In air pollution, any small individual fuel combustion
or other pollutant source; also, all such sources grouped over a
specific area.
Aromatic: Belonging to that series of carbon-hydrogen compounds in
which the carbon atoms form closed rings containing unsaturated
bonds (as in benzene).
Arterial partial pressure of oxygen (PaO^): Portion of total pressure of
dissolved gases in arterial blood as measured directly from arterial
blood.
Arterial ized partial pressure of oxygen: The portion of total pressure
of dissolved gases in arterial blood attributed to oxygen, as
measured from non-arterial (e.g., ear-prick) blood.
Arteriosclerosis: Commonly called hardening of the arteries. A condition
that exists when the walls of the blood vessels thicken and become
infiltrated with excessive amounts of minerals and fatty materials.
Artifact: A spurious measurement produced by the sampling or analysis
process.
Ascorbic acid: Vitamin C, a strong reducing agent with antioxidant proper-
ties.
Aspartate transaminase: Also known as aspartate ami notransf erase
(EC 2.6.1.1). An enzyme catalyzing the transfer of an amine group
from glutamic acid to oxaloacetic, forming aspartic acid in the
process. Serum level of the enzyme is increased in myocardial in-
farction and in diseases involving destruction of liver cells.
Asphyxia: Impaired exchange of oxygen and carbon dioxide, excess of
carbon dioxide and/or lack of oxygen, usually caused by ventilatory
problems.
Asthma: A term currently used in the context of bronchial asthma in
which there is widespread narrowing of the airways of the lung.
It may be aggravated by inhalation of pollutants and lead to
"wheezing" and shortness of breath.
Asymptomatic: Presenting no subjective evidence of disease.
Atmosphere: The body of air surrounding the earth. Also, a measure of
pressure (atm. ) equal to the pressure of air at sea level, 14.7 pounds
per square inch.
Atmospheric deposition: Removal of pollutants from the atmosphere onto
land, vegetation, water bodies or other objects, by absorption,
sedimentation, Brownian diffusion, impaction, or precipitation in rain.
G-6
-------
Atomic absorption spectrometry: A measurement method based on the
absorption of radiant energy by gaseous ground-state atoms. The
amount of absorption depends on the population of the ground state
which is related to the concentration of the sample being analyzed.
Atropine: A poisonous white crystalline alkaloid, C-^HpoNO.,, from
belladonna and related plants, used to relieve spasms and to dilate
the pupil of the eye.
Autocorrelation: Statistical interdependence of variables being analyzed;
produces problems, for example, when observations may be related
to previous measurements or other conditions.
Autoimmune disease: A condition in which antibodies are produced against
the subject's own tissues.
Autologous: A term referring to cellular elements, such as red blood cells
and alveolar macrophage, from the same organism; also, something
natually and normally ocurring in some part of the body.
Autotrophic: A term applied to those microorganisms which are able to
maintain life without an exogenous organic supply of energy, or which
only need carbon dioxide or carbonates and simple inorganic nitrogen.
Autotrophic bacteria: A class of microorganisms which require only
carbon dioxide or carbonates and a simple inorganic nitrogen com-
pound for carrying on life processes.
Auxin: An organic substance that causes lengthening of the stem when
applied in low concentrations to shoots of growing plants.
Awn: One of the slender bristles that terminate the glumes of the
spikelet in some cereals and other grasses.
Azo dye: Dyes in which the azo group is the chromophore and joins
benzene or napthalene rings.
Background measurement: A measurement of pollutants in ambient air due
to natural sources; usually taken in' remote areas.
Bactericidal activity: The process of killing bacteria.
Barre: Bars or stripes in a fabric, caused by uneven weaving, irregular
yarn or uneven dye distribution.
Basal cell: One of the innermost cells of the deeper epidermis of the
skin.
Benzenethiol: A compound of benzene and a hydrosulfide group.
G-7
-------
Beta (p)-lipoprotein: A biochemical complex or compound containing both
lipid and protein and characterized by having a large molecular
weight, rich in cholesterol. Found in certain fractions of human
plasma.
Bilateral renal sclerosis: A hardening of both kidneys of chronic
inflammatory origin.
Biomass: That part of a given habitat consisting of living matter.
Biosphere: The part of the earth's crust, waters and atmosphere where
living organisms can subsist.
Biphasic: Having two distinct successive stages.
Bleb: A collection of fluid beneath the skin; usually smaller than
bullae or blisters.
Blood urea: The chief end product of nitrogen metabolism in mammals,
excreted in human urine in the amount of about 32 grams (1 oz.)
a day.
Bloom: A greenish-gray appearance imparted to silk and pile fabrics
either by nature of the weave or by the finish; also, the creamy
white color observed on some good cottons.
Blue-green algae: A group of simple plants which are the only N^-fixing
organisms which photosynthesize as do higher plants.
Brightener: A compound such as a dye, which adheres to fabrics in order
to provide better brightness or whiteness by converting ultraviolet
radiation to visible light. Sometimes called optical bleach or
whitening agent. The dyes used are of the florescent type.
Broad bean: The large flat edible seed of an Old World upright vetch
(Vicia faba), or the plant itself, widely grown for its seeds and
for fodder.
Bronchi: The first subdivisions of the trachea which conduct air to
and from the bronchioles of the lungs.
Bronchiole: One of the finer subdivisions of the bronchial (trachea)
tubes, less than 1 mm in diameter, and having no cartilage in
its wall.
Bronchiolitis: Inflammation of the smallest bronchial tubes.
Bronchiolitis fibrosa obliterans syndrome: Obstruction of the bronchioles
by fibrous granulation arising from an ulcerated mucosa; the condition
may follow inhalation of irritant gases.
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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.
Bronchodilator: An agent which causes an increase in the caliber (diameter)
of a bronchus or bronchial tube.
Bronchopneumonia: Acute inflammation of the walls of the smaller bronchial
tubes, with irregular area of consolidation due to spread of the in-
flammation into peribronchiolar alveoli and the alveolar ducts.
Brownian diffusion: Diffusion by random movement of particles suspended
in liquid or gas, resulting from the impact of molecules of the
fluid surrounding the particles.
Buffer: A substance in solution capable of neutralizing both acids
and bases and thereby maintaining the original pH of the solution.
Buffering capacity: Ability of a body of water and its watershed to
neutralize introduced acid.
Butanol: A four-carbon, straight-chain alcohol, C,HqOH, also known as
butyl alcohol. ^ 3
Butyl ated hydroxytoluene (BHT): A crystalline phenolic antioxidant.
Butylated hydroxyanisol (BHA): An antioxidant.
14
C labeling: Use of a radioactive form of carbon as a tracer, often
in metabolic studies.
14
C-proline: An amino acid which has been labeled with radioactive carbon.
Calcareous: Resembling or consisting of calcium carbonate (lime), or
growing on limestone or lime-containing soils.
Calorie: Amount of heat required to raise temperature of 1 gram of
water at 15 C by 1 degree.
Cannula: A tube that is inserted into a body cavity, or other tube
or vessel, usually to remove fluid.
Capillary: The smallest type of vessel; resembles a hair. Usually
in reference to a blood or lymphatic capillary vessel.
Carbachol: A chemical compound (carbamoylcholine chloride, CgH-icClN^Op) that
produces a constriction of the bronchi; a parasympathetic stimulant
used in veterinary medicine and topically in glaucoma.
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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: Enzymes 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.
G-ll
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Chamber study: Research conducted using a closed vessel in which pollutants
are reacted or substances exposed to pollutants.
Chemiluminescence: A measurement technique in which radiation is pro-
duced as a result of chemical reaction.
Chemotactic: Relating to attraction or repulsion of living protoplasm
by chemical stimuli.
Chlorophyll: A group of closely related green photosynthetic pigments
occurring in leaves, bacteria, and organisms.
Chloroplast: A plant cell inclusion body containing chlorophyll.
Chlorosis: Discoloration of normally green plant parts that can be
caused by disease, lack of nutrients, or various air pollutants,
resulting in the failure of chlorophyll to develop.
Cholesterol: A steroid alcohol CpyH.cOH; the most abundant steroid in
animal cells and body fluids.
Cholinesterase (CHE): One (EC 3.1.1.8) of a family of enzymes capable
of catalyzing the hydrolysis of acylcholines.
Chondrosarcoma: A malignant neoplasm derived from cartilage cells,
occurring most frequently near the ends of long bones.
Chromatid: Each of the two strands formed by longitudinal duplication
of a chromosome that becomes visible during an early stage of cell
division.
Chromophore: A chemical group that produces color in a molecule by absorbing
near ultraviolet or visible radiation when bonded to a nonabsorb-
ing, saturated residue which possesses no unshared, nonbonding valence
electrons.
Chromosome: One of the bodies (46 in man) in the cell nucleus that is the
bearer and carrier of genetic information.
Chronic respiratory disease (CRD): A persistent or long-lasting intermittent
disease of the respiratory tract.
Cilia: Motile, often hairlike extensions of a cell surface.
Ciliary action: Movements of cilia in the upper respiratory tract, which
move mucus and foreign material upward.
Ciliogenesis: The formation of cilia.
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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 (CV): The lung volume at which the flow from the lower
parts of the lungs becomes severely reduced or stops during expiration,
presumably because of airway closure.
Codon: A sequence of three nucleotides which encodes information re-
quired to direct the synthesis of one or more amino acids.
Coefficient of haze (COM): A measurement of visibility interference in the
atmosphere.
Cohort: A group of subjects included in a test or experiment; usually
characterized by age, class or other characteristic.
Collagen: The major protein of the white fibers of connective tissue,
cartilage, and bond. Comprises over half the protein of the mammal.
Collisional deactivation: Reduction in energy of excited molecules
caused by collision with other molecules or other objects such
as the walls of a container.
Colorimetric: A chemical analysis method relying on measurement of the
degree of color produced in a solution by reaction with the pollutant
of interest.
Community exposure: A situation in which people in a sizeable area are
subjected to ambient pollutant concentrations.
Compliance: A measure of the change in volume of an internal organ (e.g.
lung, bladder) produced by a unit of pressure.
Complement: Thermolabile substance present in serum that is destructive
to certain bacteria and other cells which have been sensitized by
specific complement-fixing antibody.
Compound: A substance with its own distinct properties, formed by the
chemical combination of two or more elements in fixed proportion.
Concanavalin-A: One of two crystalline globulins occurring in the jack
bean; a potent hemagglutinin.
Conifer: A plant, generally evergreen, needle-leafed, bearing naked seeds
singly or in cones.
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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 copolymer.
Coproporphyrin: One of two porphyrin compounds found normally in feces
as a decomposition product of bilirubin (a bile pigment). Porphyrin
is a widely-distributed pigment consisting of four pyrrole nuclei
joined in a ring.
Cordage: A general term which includes banding, cable, cord, rope, string,
and twine made from fibers. Synthetic fibers used in making cordage
include nylon and dacron.
Corrosion: Destruction or deterioration of a material because of reaction
with its environment.
Corticosterone: A steroid obtained from the adrenal cortex. It induces
some deposition of glycogen in the liver, sodium conservation, and
potassium excretion.
Cosmopolitan: In the biological sciences, a term denoting worldwide
distribution.
Coulometric: Chemical analysis performed by determining the amount of a
substance released in electrolysis by measuring the number of
coulombs used.
Coumarin: A toxic white crystalline lactone (CgHgO-) found in plants.
Coupler: A chemical used to combine two others in a reaction, e.g. to
produce the azo dye in the Griess-Saltzman method for NOp.
Crevice corrosion: Localized corrosion occurring within crevices on metal
surfaces exposed to corrosives.
Crosslink: To connect, by an atom or molecule, parallel chains in a complex
chemical molecule, such as a polymer.
Cryogenic trap: A pollutant sampling method in which a gaseous pollutant
is condensed out of sampled air by cooling (e.g. traps in one method
for nitrosamines are maintained below -79 C, using solvents maintained
at their freezing points).
Cuboidal: Resembling a cube in shape.
Cultivar: An organism produced by parents belonging to different species
or to different strains of the same species, originating and persist-
ing under cultivation.
G-14
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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 Np. It is essentially an anaerobic process; it
can occur in the presence of low levels of oxygen only if the micro-
organisms are metabolizing in an anoxic microzone.
De novo: Over again.
Deoxyribonucleic acid (DNA): A nucleic acid considered to be the carrier
of genetic information coded in the sequence of purine and pyrimidine
bases (organic bases). It has the form of a double-stranded helix
of a linear polymer.
Depauperate: Falling short of natural development or size.
Derivative spectrophotometer: An instrument with an increased capability
for detecting overlapping spectral lines and bands and also for
suppressing instrumentally scattered light.
G-15
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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.
Desquamation: The shedding of the outer layer of any surface.
Detection limit: A level below which an element or chemical compound
cannot be reliably detected by the method or measurement being used for
analysis.
Detritus: Loose material that results directly from disintegration.
DeVarda alloy: An alloy of 50 percent Cu, 45 percent Al, 5 percent Zn.
Diastolic blood pressure: The blood pressure as measured during the period
of filling the cavities of the heart with blood.
Diazonium salt: A+chemical compound (usually colored) of the general
structure ArN?Cl , where Ar refers to an aromatic group.
Diazotizer: A chemical which, when reacted with amines (RNHL, for example),
produces a diazonium salt (usually a colored compound).
Dichotomous sampler: An air-sampling device which separates particulates
into two fractions by particle size.
Differentiation: The process by which a cell, such as a fertilized egg,
divides into specialized cells, such as the embryonic types that
eventually develop into an entire organism.
Diffusion: The process by which molecules or other particles intermingle
as a result of their random thermal motion.
Diffusing capacity: Rate at which gases move to or from the blood.
Dimer: A compound formed by the union of two like radicals or
molecules.
Dimerize: Formation of dimers.
1,6-diphosphofructose aldolase: An enzyme (EC 4.1.1.13) cleaving fructose
1,6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde-
3-phosphate.
D-2,3-diphosphoglycerate: A salt or ester of 2,3-diphosphoglyceric acid,
a major component of certain mammalian erythrocytes involved in the
release of CL from HbO?. Also a postulated intermediate in the bio-
chemical patnway involving the conversion of 3- to 2-phosphoglyceric
acid.
Diplococcus pneumoniae: A species of spherical-shaped bacteria belonging
to the genus Streptococcus. May be a causal agent in pneumonia.
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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.
DL-Q: The diffusing capacity of the lungs for carbon monoxide. The ability
of the lungs to transfer carbon monoxide from the alveolar air into the
pulmonary capillary blood.
Dorsal hypnosis: Abnormal curvative of the spine; hunch-back.
Dose: The quantity of a substance to be taken all at one time or in
fractional amounts within a given period; also the total amount of a
pollutant delivered or concentration per unit time times time.
o
Dose-response curve: A curve on a graph based on responses occurring
in a system as a result of a series of stimuli intensities or doses.
Dry deposition: The processes by which matter is transferred to ground
from the atmosphere, other than precipitation; includes surface ab-
sorption of gases and sedimentation, Brownian diffusion and impaction
of particles.
Dyeing: A process of coloring fibers, yarns, or fabrics with either
natural or synthetic dyes.
Dynamic calibration: Testing of a monitoring system using a continuous
sample stream of known concentration.
Dynamic compliance (C,. ): Volume change per unit of transpulmonary
pressure minus tne^pressure of pulmonary resistance during airflow.
Dynel: A trademark for a modacrylic staple fiber spun from a copolymer
of acrylom'trile and vinyl chloride. It has high strength, quick-
drying properties, and resistance to alkalies and acids.
Dyspepsia: Indigestion, upset stomach.
Dyspnea: Shortness of breath; difficulty or distress in breathing; rapid
breathing.
Ecosystem: The interacting system of a biological community and its
environment.
Eddy: A current of water or air running contrary to the main current.
G-17
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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 particu-
late matter, bacteria, viruses, and DMA.
Electronic excitation energy: Energy associated in the transition of
electrons from their normal low-energy orbitals or orbitals of higher
energy.
Electrophilic: Having an affinity for electrons.
Electrophoresis: A technique by which compounds can be separated from a
complex mixture by their attraction to the positive or negative
pole of an applied electric potential.
Eluant: A liquid used in the process of elution.
Elute: To perform an elution.
Elution: Separation of one material from another by washing or by dissolving
one in a solvent in which the other is not soluble.
Elutriate: To separate a coarse, insoluble powder from a finer one by
suspending them in water and pouring off the finer powder from the
upper part of the fluid.
Emission spectrometry: A rapid analytical.technique based on measurement
of the characteristic radiation emitted by thermally or electrically
excited atoms or ions.
Emphysema: An anatomic alteration of the lung, characterized by abnormal
enlargement of air spaces distal to the terminal bronchioles, due
to dilation or destructive changes in the alveolar walls.
Emphysematous lesions: A wound or injury to the lung as a result of
emphysema.
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Empirical modeling: Characterization and description of a phenomena
based on experience or observation.
Encephalitis: Inflammation of the brain.
Endoplasmic reticulum: An elaborate membrane structure extending from the
nuclear membrane or eucaryotic cells to the cytoplasmic membrane.
Endothelium: A layer of flat cells lining especially blood and lymphatic
vessels.
Entropy: A measure of disorder or randomness in a system. Low entropy
is associated with highly ordered systems.
Enzyme: Any of numerous proteins produced by living cells which catalyze
biological reactions.
Enzyme Commission (EC): The International Commission on Enzymes, established
in 1956, developed a scheme of classification and nomenclature under
which each enzyme is assigned an EC number which identifies it by
function.
Eosinophils: Leukocytes (white blood cells) which stain readily with the
dye, eosin.
Epidemiology: A study of the distribution and determinants of disease
in human population groups.
Epidermis: The outermost living layer of cells of any organism.
Epididymal fat pads: The fatty tissue located near the epididymis. The
epididymis is the first convoluted portion of the excretory duct
of the testis.
Epiphyte: A plant growing on another plant but obtaining food from the
atmosphere.
Epithelial: Relating to epithelium, the membranous cellular layer which
covers free surfaces or lines tubes or cavities of an animal body,
which encloses, protects, secretes, excretes and/or assimilates.
Erosion corrosion: Acceleration or increase in rate of deterioration
or attack on a metal because of relative movement between a corrosive
fluid and the metal surface. Characterized by grooves, gullies, or
waves in the metal surface.
Erythrocyte: A mature red blood cell.
Escherichia coli: A short, gram-negative, rod-shaped bacteria common
to the human intestinal tract. A frequent cause of infections in
the urogenital tract.
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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 NOp, the EPA-approved analyzers based
on the gas-phase chemiluminescent measurement principle and associated
calibration procedures; regulatory specifications prescribed in Title
40, Code of Federal Regulations, Part 50, Appendix F.
Fenestrae: Anatomical aperatures often closed by a membrane.
Fiber: A fine, threadlike piece, as of cotton, jute, or asbestos.
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Fiber-reactive dye: A water-soluble dyestuff which reacts chemically
with the cellulose in fibers under alkaline conditions; the dye
contains two chlorine atoms which combine with the hydroxyl groups of
the cellulose.
Fibrin: A white insoluble elastic filamentous protein derived from fibrino-
gen by the action of thrombin, especially in the clotting of blood.
Fibroadenoma: A benign neoplasm derived from glandular epithelium, in-
volving proliferating fibroblasts, cells found in connective tissue.
Fibroblast: An elongated cell with cytoplasmic processes present in
connective tissue, capable of forming collagen fibers.
Fibrosis: The formation of fibrous tissue, usually as a reparative or
reactive process and not as a normal constituent of an organ or
tissue.
Flocculation: Separation of material from a solution or suspension by
reaction with a flocculant to create fluffy masses containing the
material to be removed.
Fly ash: Fine, solid particles of noncombustible ash carried out of a
bed of solid fuel by a draft.
Folded-path optical system: A long (e.g., 8-22 m) chamber with multiple
mirrors at the ends which can be used to reflect an infrared beam through
an ambient air sample many times; a spectrometer can be used with such
a system to detect trace pollutants at very low levels.
Forced expiratory flow (FEF): The rate at which air can be expelled from
the lungs; see expiratory flow rate.
Forced expiratory volume (FEV): The maximum volume of air that can be
expired in a specific time interval when starting from maximal
inspiration.
Forced vital capacity (FVC): The greatest volume of air that can be
exhaled from the lungs under forced conditions after a maximum
inspiration.
Fractional threshold concentration: The portion of the concentration
at which an event or a response begins to occur, expressed as a
fraction.
Free radical: Any of a variety of highly-reactive atoms or molecules
characterized by having an unpaired electron.
Fritted bubbler: A porous glass device used in air pollutant sampling
systems to introduce small bubbles into solution.
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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).
Glomular nephrotic syndrome: Dysfunction of the kidneys characterized
by excessive protein loss in the urine, accumulation of body fluids
and alteration in albumin/globulin ratio.
Glucose: A sugar which is a principal source of energy for man and other
organisms.
Glucose-6-phosphate dehydrogenase: An enzyme (EC 1.1.1.49) catalyzing
the dehydrogenation of glucose-6-phosphate to 6-phosphogluconolactone.
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Glutamic-oxaloacetic transaminase (SGOT): An enzyme (EC 2.6.1.1) whose
serum level increases in myocardial infarction and in diseases in-
volving destruction of liver cells. Also known as aspartate
aminotransferase.
Glutamic-pyruvic transaminase (SGPT): Now known as alanine aminotransferase
(EC 2.6.1.2), the serum levels of this enzyme are used in liver function
tests.
Glutathione (GSH): A tripeptide composed of glycine, cystine, and glutamic
acid.
Glutathione peroxidase: An enzyme (EC 1.11.1) which catalyzes the destruction
of hydroperoxides formed from fatty acids and other substances.
Protects tissues from oxidative damage. It is a selenium-containing
protein.
Glutathione reductase: The enzyme (EC 1.6.4.2) which reduces the oxidized
form of glutathione.
Glycolytic pathway: The biochemical pathway by which glucose is con-
verted to lactic acid in various tissues, yielding energy as a
result.
Glycoside: A type of chemical compound formed from the condensation of
a sugar with another chemical radical via a hemiacetal linkage.
Goblet cells: Epithelial cells that have been distended with mucin and when
this is discharged as mucus, a goblet-shaped shell remains.
Golgi apparatus: A membrane system involved with secretory functions
and transport in a cell. Also known as a dictyosome.
Grana: The lamellar stacks of chlorophyll-containing material in plant
chloroplasts.
Griege carpet: A carpet in its unfinished state, i.e. before it has
been scoured and dyed. The term also is used for woven fabrics
in the unbleached and unfinished state.
Ground state: The state of minimum electronic energy of 'a molecule or
atom.
Guanylate cyclase (GC): An enzyme (EC 4.6.2.1) catalyzing the trans-
formation of guanosine triphosphate to guanosine 3':5'-cyclic phosphate.
H-Thymidine: Thymine deoxyribonucleoside: One of the four major nucleosides
in DNA. H-thymidine has been uniformly labeled with tritium, a radio-
active form of hydrogen.
Haze: Fine dust, smoke or fine vapor reducing transparency of air.
G-23
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Hemagglutination: The agglutination of red blood cells. Can be used as
as a measurement of antibody concentration.
Heuiatocrit: The percentage of the volume of a blood sample occupied by
cells.
Hematology: The medical specialty that pertains to the blood and blood-
forming tissues.
Hemochromatosis: A disease characterized by pigmentation of the skin
possibly due to inherited excessive absorption of iron.
Hemoglobin (Hb): The red, respiratory protein of the red blood cells,
hemoglobin transports oxygen from the lungs to the tissues as oxy-
hemoglobin (HbO-) and returns carbon dioxide to the lungs as hemoglobin
carbamate, completing the respiratory cycle.
Hemolysis: Alteration or destruction of red blood cells, causing hemoglobin
to be released into the medium in which the cells are suspended.
Hepatectomy: Complete removal of the liver in an experimental animal.
Hepatic: Relating to the liver.
Hepatocyte: A liver cell.
Heterogeneous process: A chemical reaction involving reactants of more
than one phase or state, such as one in which gases are absorbed into
aerosol droplets, where the reaction takes place.
Heterologous: A term referring to donor and recipient cellular elements
from different organisms, such as red blood cells from sheep and
alveolar macrophage from rabbits.
Hexose monophosphate shunt: Also called the phosphogluconate oxidative
pathway of glucose metabolism which affords a total combustion of
glucose independent of the citric acid cycle. It is the important
generator of NADPH necessary for synthesis of fatty acids and the
operation of various enzymes. It serves as a source of ribose and
4- and 7-carbon sugars.
High-volume sampler (Hi-vol): Device for taking a sample of the particulate
content of a large amount of,air, by drawing air through a fiber filter
at a typical cate of 2,000 m /24 hr (1.38 m /min), or as high as 2,880
mV24 hr (2 nT/min).
Histamine: An amine derived from the amino acid, histidine. It is a
powerful stimulant of gastric secretion and a constrictor of bronchial
smooth muscle. It is a vasodilator and causes a fall in blood
pressure.
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Homogenate: Commonly refers to tissue ground into a creamy consistency
in which the cell structure is disintegrated.
Host defense mechanism: Inherent means by which a biologic organism
protects itself against infection, such as antibody formation,
macrophage action, ciliary action, etc.
Host resistance: The resistance exhibited by an organism, such as man,
to an infecting agent, such as a virus or bacteria.
Humoral: Relating to the extracellular fluids of the body, blood and
lymph.
Hybrid: An organism descended from parents belonging to different
varieties or species.
Hydrocarbons: A vast family of compounds containing carbon and hydrogen
in various combinations; found especially in fossil fuels. Some
contribute to photochemical smog.
Hydrolysis: Decomposition involving splitting of a bond and addition
of the H and OH parts of water to the two sides of the split bond.
Hydrometeor: A product of the condensation of atmospheric water vapor (e.g.
fog, rain, hail, snow).
Hydroxyproline: An amino acid found among the hydrolysis products of
collagen.
Hygroscopic: Pertaining to a marked ability to accelerate the condensation
of water vapor.
Hyperplasia: Increase in the number of cells in a tissue or organ ex-
cluding tumor formation.
Hyperplastic: Relating to hyperplasia; an increase in the number of
cells.
Hypertrophy: Increase in the size of a tissue element, excluding tumor
formation.
Hypertension: Abnormally elevated blood pressure.
Hypolimnia: Portions of a lake below the thermocline, in which water
is stagnant and uniform in temperature.
Hypoxia: A lower than normal amount of oxygen in the air, blood or tissues.
G-25
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Immunoglobulin (Ig): A class of structurally related proteins consist-
ing of two pairs of polypeptide chains. Antibodies are Ig's and
all Ig's probably function as antibodies.
Immunoglobulin A (IgA): A type of antibody which comprises approximately
10 to 15 percent of the total amount of antibodies present in normal
serum.
Immunoglobulin G (IgG): A type of antibody which comprises approximately
80 percent of the total amount of antibodies present in normal serum.
Subfractions of IgG are fractions G-,, and G~.
Immunoglobulin M (IgM): A type of antibody which comprises approximately
5 to 10 percent of the total amount of antibodies present in normal
serum.
Impact!on: An impinging or striking of one object against another; also,
the force transmitted by this act.
Impactor: An instrument which collects samples of suspended particulates
by directing a stream of the suspension against a surface, or into a
liquid or a void.
Index of proliferation: Ratio of promonocytes to polymorphic monocytes
in the blood.
Infarction: Sudden insufficiency of arterial or venous blood supply
due to emboli, thrombi, or pressure.
Infectivity model: A testing system in which the susceptibility of
animals to airborne infectious agents with and without exposure to air
pollutants is investigated to produce information related to the
possible effects of the pollutant on man.
Inflorescence: The arrangement and development of flowers on an axis;
also, a flower cluster or a single flower.
Influenza A^/Taiwan Virus: An infectious viral disease, believed to
have originated in Taiwan, characterized by sudden onset, chills,
fevers, headache, and cough.
Infrared: Light invisible to the human eye, bgtween the wavelengths
of 7x10"' and lO'^m (7000 and 10,000,000 A).
Infrared laser: A device that utilizes the natural oscillations of atoms
or molecules to generate coherent electromagnetic radiation in the
infrared region of the spectrum.
Infrared spectrometer: An instrument for measuring the relative amounts
of radiant energy in the infrared region of the spectrum as a function
of wavelength.
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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 N02,
currently unacceptable for air pollution work.
Klebsiella pneumoniae: A species of rod-shaped bacteria found in soil,
water, and in the intestinal tract of man and other animals. Certain
types may be causative agents in pneumonia.
Kyphosis: An abnormal curvature of the spine, with convexity backward.
Lactate: A salt or ester of lactic acid.
Lactic acid (lactate) dehydrogenase (LDH): An enzyme (EC 1.1.1.27) with
many isomeric forms which catalyzes the oxidation of lactate to
pyruvate via transfer of H to NAD. Isomeric forms of LDH in the
blood are indicators of heart damage.
Lamellar bodies: Arranged in plates or scales. One of the characteristics
of Type II alveolar cells.
Lavage fluid: Any fluid used to wash out hollow organs, such as the lung.
Lecithin: Any of several waxy hygroscopic phosphatides that are widely
distributed in animals and plants; they form colloidal solutions in
water and have emulsifying, wetting and hygroscopic properties.
Legume: A plant with root nodules containing nitrogen fixing bacteria.
Lesion: A wound, injury or other more or less circumscribed pathologic
change in the tissues.
Leukocyte: Any of the white blood cells.
Lewis base: A base, defined in the Lewis acid-base concept, is a sub-
stance that can donate an electron pair.
Lichens: Perennial plants which are a combination of two plants, an alga
and a fungus, growing together in an association so intimate that they
appear as one.
Ligand: Those molecules or anions attached to the central atom in a
complex.
Light-fastness: The ability of a dye to maintain its original color under
natural or indoor light.
Linolenic acid: An unsaturated fatty acid essential in nutrition.
Lipase: An enzyme that accelerates the hydrolysis or synthesis of fats
or the breakdown of lipoproteins.
G-28
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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.
Mai ate dehydrogenase: An enzyme (EC 1.1.1.37) with at least six isomeric
forms that catalyze the dehydrogenation of malate to oxaloacetate
or its decarboxylation (removal of a COj group) to pyruvate. Malate,
oxaloacetate, and pyruvate are intermediate components of biochemical
pathways.
Mannitol: An alcohol derived from reduction of the sugar, fructose.
Used in renal function testing to measure glomerular (capillary)
filtration.
Manometer: An instrument for the measurement of pressure of gases or
vapors.
Mass median diameter (MMD): Geometric median size of a distribution of
particles based on weight.
Mass spectrometry (MS): A procedure for identifying the various kinds of
particles present in a given substance, by ionizing the particles
and subjecting a beam of the ionized particles to an electric or
magnetic field such that the field deflects the particles in angles
directly proportional to the masses of the particles.
Maximum flow (V ): Maximum rate or expiration, usually expressed at
50 or 25 percent of vital capacity.
Maximum mid-expiratory flow rate (MMFR): The mean rate of expiratory gas
flow between 25 and 75 percent of the forced expiratory vital capacity.
Mean (arithmetic): The sum of observations divided by sample size.
Median: A value in a collection of data values which is exceeded in
magnitude by one-half the entries in the collection.
Mesoscale: Of or relating to meteorological phenomena from 1 to 100
kilometers in horizontal extent.
Messenger RNA: A type of RNA which conveys genetic information encoded
in the DNA to direct protein synthesis.
Metaplasia: The abnormal transformation of an adult, fully differentiated
tissue of one kind into a differentiated tissue of another kind.
Metaproterenol: A bronchodilator used for the treatment of bronchial
asthma.
Metastases: The shifting of a disease from one part of the body to another;
the appearance of neoplasms in parts of the body remote from the seat
of the primary tumor.
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Meteorology: The science that deals with the atmosphere and its phenomena.
Methemoglobin: A+form of hemoglobin in whiclj! the normal reduced state
of iron (Fe ) has been oxidized to Fe . It contains oxygen in
firm union with ferric (Fe ) iron and is not capable of exchanging
oxygen in normal respiratory processes.
Methimazole: An anti-thyroid drug similar in action to propylthiouracil.
Methyltransferase: Any enzyme transferring methyl groups from one compound
to another.
Microcoulometric: Capable of measuring millionths of coulombs used in
electrolysis of a substance, to determine the amount of a substance
in a sample.
Microflora: A small or strictly localized plant.
Micron: One-millionth of a meter.
Microphage: A small phagocyte; a polymorphonuclear leukocyte that is
phagocytic.
Millimolar: One-thousandth of a molar solution. A solution of one-
thousandth of a mole (in grams) per liter.
Minute volume: The minute volume of breathing; a product of tidal volume
times the respiratory frequency in one minute.
Mitochondria: Organelles of the cell cytoplasm which contain enzymes
active in the conservation of energy obtained in the aerobic part
of the breakdown of carbohydrates and fats, in a process called
respiration.
Mobile sources: Automobiles, trucks and other pollution sources which are
not fixed in one location.
Modacrylic fiber: A manufactured fiber in which the fiber-forming sub-
stance is any long chain synthetic polymer composed of less than 85
percent but at least 35 percent by weight of acrylonitrite units.
Moeity: One of two or more parts into which something is divided.
Mole: The mass, in grams, numerically equal to the molecular weight of
a substance.
Molecular correlation spectrometry: A spectrophotometric technique which
is used to identify unknown absorbing materials and measure their
concentrations by using preset wavelengths.
Molecular weight: The weight of one molecule of a substance obtained
by adding the gram-atomic weights of each of the individual atoms
in the substance.
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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.
Murine: Relating to mice.
Mutagen: A substance capable of causing, within an organism, biological
changes that affect potential offspring through genetic mutation.
Mutagenic: Having the power to cause mutations. A mutation is a change
in the character of a gene (a sequence of base pairs in DNA) that
is perpetuated in subsequent divisions of the cell in which it occurs.
Myocardial infarction: Infarction of any area of the heart muscle usually
as a result of occlusion of a coronary artery.
Nares: The nostrils.
Nasopharyngeal: Relating to the nasal cavity and the pharynx (throat).
National Air Surveillance Network (NASN): Network of monitoring stations
for sampling air to determine extent of air pollution; established
jointly by federal and state governments.
Near ultraviolet: Radiation of the wavelengths 2000-4000 Angstroms.
Necrosis: Death of cells that can discolor areas of a plant or kill
the entire plant.
Necrotic: Pertaining to the pathologic death of one or more cells, or
of a portion of tissue or organ, resulting from irreversible damage.
G-32
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Neonate: A newborn.
Neoplasm: An abnormal tissue that grows more rapidly than normal; synonymous
with tumor.
Neoplasia: The pathologic process that results in the formation and
growth of a tumor.
Neutrophil: A mature white blood cell formed in bone marrow and released
into the circulating blood, where it normally accounts for 54 to 65
percent of the total number of leukocytes.
Ninhydrin: An organic reagent used to identify amino acids.
Nitramine: A compound consisting of a nitrogen attached to the nitrogen
of amine.
Nitrate: A salt or ester of nitric acid (NO/).
Nitrification: The principal natural source of nitrate in which ammonium
(NhL-t-) ions are oxidized to nitrites by specialized microorganisms.
Other organisms oxidize nitrites to nitrates.
Nitrite: A salt or ester of nitrous acid (N0~~).
Nitrocellulose: Any of several esters of nitric acid formed by its action
on cellulose, used in explosives, plastics, varnishes and rayon;
also called cellulose nitrate.
Nitrogen cycle: Refers to the complex pathways by which nitrogen-containing
compounds are moved from the atmosphere into organic life, into the
soil, and back to the atmosphere.
Nitrogen fixation: The metabolic assimilation of atmospheric nitrogen by
soil microorganisms, which becomes available for plant use when the
microorganisms die; also, industrial conversion of free nitrogen into
combined forms used in production of fertilizers and other products.
Nitrogen oxide: A compound composed of only nitrogen and oxygen. Components
of photochemical smog.
Nitrosamine: A compound consisting of a nitrosyl group connected to the
nitrogen of an amine.
Nitrosation: Addition of a nitrosyl group.
N-Nitroso compounds: Compounds carrying the functional nitrosyl group.
Nitrosyl: A group composed of one oxygen and one nitrogen atom (-N=0).
Nitrosylhemoglobin (NOHb): The red, respiratory protein of erythrocytes
to which a nitrosyl group is attached.
G-33
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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 (HjPO,) and nucleosides.
Nucleotide: A compound consisting of a sugar (ribose or deoxyribose),
a base (a purine or a pyrimidine), and a phosphate; a basic structural
unit of RNA and DNA.
Nylon: A generic name chosen by E. I. du Pont de Nemours & Co., Inc.
for a group of protein-like chemical products classed as synthetic
linear polymers; two main types are Nylon 6 and Nylon 66.
Occlusion: A point which an opening is closed or obstructed.
Olefin: An open-chain hydrocarbon having at least one double bond.
Olfactory: Relating to the sense of smell.
Olfactory epithelium: The inner lining of the nose and mouth which contains
neural tissue sensitive to smell.
Oligotrophic: A body of water deficient in plant nutrients; also generally
having abundant dissolved oxygen and no marked stratification.
Oribitals: Areas of high electron density in an atom or molecule.
Orion: An acrylic fiber produced by E. I. du Pont de Nemours and Co., Inc.,
based on a polymer of acrylonitrite;. used extensively for outdoor
uses, it is resistant to chemicals and withstands high temperatures.
Osteogenic osteosarcoma: The most common and malignant of bone sarcomas
(tumors). It arises from bone-forming cells dfid affects chiefly
the ends of long-bones.
Ovarian primordial follicle: A spheroidal cell aggregation in the ovary
in which the primordial oocyte (immature female sex cell) is surrounded
by a single layer of flattened follicular cells.
Oxidant: A chemical compound which has the ability to remove electrons
from another chemical species, thereby oxidizing it; also, a substance
containing oxygen which reacts in air to produce a new substance, or
one formed by the action of sunlight on oxides of nitrogen and hydro-
carbons.
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Oxidation: An ion or molecule undergoes oxidation by donating electrons.
Oxidative deamination: Removal of the NH~ group from an ami no compound
by reaction with oxygen.
Oxidative phosphorylation: The mitochondrial process by which "high-
energy" phosphate bonds form from the energy released as a result of
the oxidation of various substrates. Principally occurs in the tri-
carboxylic acid pathway.
Oxyhemoglobin: Hemoglobin in combination with oxygen. It is the form
of hemoglobin present in arterial blood.
Ozone layer: A layer of the stratosphere from 20 to 50 km above the
earth's surface characterized by high ozone content produced by ultra-
violet radiation.
Ozone scavenging: Removal of 0, from ambient air or plumes by reaction with
NO, producing NO- and 0^-
Paired electrons: Electrons having opposite intrinsic spins about their
own axes.
Parenchyma: The essential and distinctive tissue of an organ or an ab-
normal growth, as distinguished from its supportive framework.
Parenchymal: Referring to the distinguishing or specific cells of a
gland or organ.
Partial pressure: The pressure exerted by a single component in a mixture
of gases.
Particulates: Fine liquid or solid particles such as dust, smoke, mist,
fumes or smog, found in the air or in emissions.
Pascal: A unit of pressure in the International System of Units. One
pascal is equal to 7.4 x 10 torr. The pascal is equivalent to one
newton per square meter.
Pathogen: Any virus, microorganism, or other substance causing disease.
Pathophysiological: Derangement of function seen in disease; alteration
in function as distinguished from structural defects.
Peptide bond: The bond formed when two amino acids react with each other.
Percentiles: The percentage of all observations exceeding or preceding
some point; thus, 90th percentile is a level below which will fall 90
percent of the observations.
Perfusate: A liquid, solution or colloidal suspension that has been passed
over a special surface or through an appropriate structure.
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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 (PAN): Pollutant created by action of sunlight on
hydrocarbons and NO in the air; an ingredient of photochemical smog.
/s.
pH: A measure of the acidity or alkalinity of a material, liquid, or solid.
pH is represented on a scale of 0 to 14 with 7 being a neutral state,
0 most acid, and 14 most alkaline.
Phagocytosis: Ingestion, by cells such as macrophages, of other cells,
bacteria, foreign particles, etc.; the cell membrane engulfs solid or
liquid particles which are drawn into the cytoplasm and digested.
Phenotype: The observable characteristics of an organism, resulting from
the interaction between an individual genetic structure and the
environment in which development takes place.
Phenylthiourea: A crystalline compound, C^HgN^S, that is bitter or tasteless
depending on a single dominant gene in the tester.
Phlegm: Viscid mucus secreted in abnormal quantity in the respiratory passages.
Phosphatase: Any of a group of enzymes that liberate inorganic phosphate
from phosphoric esters (B.C. sub-subclass 3.1.3).
Phosphocreatine kinase: An enzyme (EC 2.7.3.2) catalyzing the formation of
creatine and ATP, its breakdown is a source of energy in the contraction
of muscle; also called creatine phosphate.
Phospholipid: A molecule consisting of lipid and phosphoric acid group(s).
An example is lecithin. Serves as an important structural factor
in biological membranes.
Photochemical oxidants: Primary ozone, NO,,, PAN with lesser amounts of
other compounds formed as products of atmospheric reactions involving
organic pollutants, nitrogen oxides, oxygen, and sunlight.
Photochemical smog: Air pollution caused by chemical reaction of various
airborne chemicals in sunlight.
Photodissociation: The process by which a chemical compound breaks down into
simpler components under the influence of sunlight or other radiant energy.
G-36
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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 (Fl) bonds: Bonds in which electron density is not symmetrical about a
line joining the bonded atoms.
Pinocytotic: Refers to the cellular process (pinocytosis) in which the cyto-
plasmic membrane forms invaginations in the form of narrow channels
leading into the cell. Liquids can flow into these channels and the
membrane pinches off pockets that are incorporated into the cytoplasm
and digested.
Pitting: A form of extremely localized corrosion that results in holes in
the metal. One of the most destructive forms of corrosion.
Pituary: A stalk-like gland near the base of the brain which is attached
to the hypothalmus. The anterior portion is a major repository for
for hormones that control growth, stimulate other glands, and regulate
the reproductive cycle.
Placenta: The organ in the uterus that provides metabolic interchange between
the fetus and mother.
Plasmid: Replicating unit, other than a nucleus gene, that contains
nucleoprotein and is involved in various aspects of metabolism in
organisms; also called paragenes.
Plasmolysis: The dissolution of cellular components, or the shrinking
of plant cells by osmotic loss of cytoplasmic water.
Plastic: A plastic is one of a large group of organic compounds synthesized
from cellulose, hydrocarbons, proteins or resins and capable of being
cast, extruded, or molded into various shapes.
Plasticizer: A chemical added to plastics to soften, increase malleability
or to make more readily deformable.
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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 examples.
Polyamides: Polymerization products of chemical compounds which contain
ami no (-NH2) and carboxyl (-COOH) groups. Condensation reactions
between the groups form amides (-CONH?). Nylon is an example of
a polyamide.
Polycarbonate: Any of various tough transparent thermoplastics characterized
by high impact strength and high softening temperature.
Polycythemia: An increase above the normal in the number of red cells in the
blood.
Polyester fiber: A man-made or manufactured fiber in which the fiber-
forming substance is any long-chain synthetic polymer composed of
at least 85 percent by weight of an ester of a dihydric alcohol and
terephthalic acid. Dacron is an example.
G-38
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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, CrHgNCL, that can be synthesized from glutamate
by animals.
Promonocyte: An immature monocyte not normally seen in the circulating
blood.
Proteinuria: The presence of more than 0.3 gm of urinary protein in a
24-hour urine collection.
Pulmonary: Relating to the lungs.
Pulmonary edema: An accumulation of excessive amounts of fluid in the lungs.
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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 RNA. Cytosine and
thymine occur in DNA and cytosine and uracil are found in RNA.
QRS: Graphical representation on the electrocardiogram of a complex of three
distinct waves which represent the beginning of ventricular contraction.
Quasistatic compliance: Time dependent component of elasticity; compliance
is the reciprocal of elasticity.
Rainout: Removal of particles and/or gases from the atmosphere by their
involvement in cloud formation (particles act as condensation nuclei,
gases are absorbed by cloud droplets), with subsequent precipitation.
Rayleigh scattering: Coherent scattering in which the intensity of the
light of wavelength A., scattered in any direction making an angle
with the incident direction, is.directly proportional to 1 + cos 9
and inversely proportional to A. .
Reactive dyes: Dyes which react chemically with cellulose in fibers under
alkaline conditions. Also called fiber reactive or chemically
reactive dyes.
Reduction: Acceptance of electrons by an ion or molecule.
Reference method (RM): For N02> an EPA-approved gas-phase chemiluminescent
analyzer and associated calibration techniques; regulatory specifications
are described in Title 40, Code of Federal Regulations, Part 50,
Appendix F. Formerly, Federal Reference Method.
Residual capacity: The volume of air remaining in the lungs after a maximum
expiratory effort; same as residual volume.
Residual volume (RV): The volume of air remaining in the lungs after a
maximal expiration. RV = TLC - VC
Resin: Any of various solid or semi-solid amorphous natural organic sub-
stances, usually derived from plant secretions, which are soluble in
organic solvents but not in water; also any of many synthetic substances
with similar properties used in finishing fabrics, for permanent press
shrinkage control or water repel!ency.
Ribosomal RNA: The most abundant RNA in a cell and an integral constituent
of ribosomes.
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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
corrosion processes.
Septa: A thin wall dividing two cavities or masses of softer tissue.
Seromucoid: Pertaining to a mixture of watery and mucinous material such
as that of certain glands.
Serum antiprotease: A substance, present in serum, that inhibits the activity
of proteinases (enzymes which destroy proteins).
Sigma (s) bonds: Bonds in which electron density is symmetrical about a
line joining the bonded atoms.
Silo-filler's disease: Pulmonary lesion produced by oxides of nitrogen
produced by fresh silage.
Single breath nitrogen elimination rate: Percentage rise in nitrogen fraction
per unit of volume expired.
Single breath nitrogen technique: A procedure in which a vital capacity
inspiration.of 100 percent oxygen is followed by examination of nitrogen
in the vital capacity expirate.
Singlet state: The highly-reactive energy state of an atom in which certain
electrons have unpaired spins.
Sink: A reactant with or absorber of a substance.
Sodium arsenite: Na-jAsO.,, used with sodium hydroxide in the absorbing solu-
tion of a 24-hour integrated manual method for N02-
Sodium dithionite: A strong reducing agent (a supplier of electrons).
Sodium metabisulfite: Na9S?Or, used in absorbing solutions of NO-, analysis
methods. 6 * D *
Sorb: To take up and hold by absorption or adsorption.
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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 various radiations.
Spectrophotometry: A technique in which visible, UV, or infrared radiation
is passed through a substance or solution and the intensity of light
transmitted at various wavelengths is measured to determine the spectrum
of light absorbed.
Spectroscopy: Use of the spectrometer to determine concentrations of an
air pollutant.
Spermatocytes: A cell destined to give rise to spermatozoa (sperm).
Sphingomyelins: A group of phospholipids found in brain, spinal cord, kidney
and egg yolk.
Sphygomenometer: An apparatus, consisting of a cuff and a pressure gauge,
which is used to measure blood pressure.
Spirometry: Also called pneometry. Testing the air capacity of the lungs
with a pneometer.
Spleen: A large vascular organ located on the upper left side of the abdominal
cavity. It is a blood-forming organ in early life. It is a storage
organ for red corpuscles and because of the large number of macrophages,
acts as a blood filter.
Sputum: Expectorated matter, especially mucus or mucopurulent matter expec-
torated in diseases of the air passages.
Squamous: Scale-like, scaly.
Standard deviation: Measure of the dispersion of values about a mean
value. It is calculated as the positive square root of the average of
the squares of the individual deviations from the mean.
Standard temperature and pressure: 0°C, 760 mm mercury.
Staphylococcus aureus: A spherically-shaped, infectious species of bacteria
found especially on nasal mucous membrane and skin.
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Static lung compliance (Cistat): Measure of lung's elastic recoil (volume
change resulting from cnange in pressure) with no or insignificant air-
flow.
Steady state exposure: Exposure to air pollutants whose concentration
remains constant for a period of time.
Steroids: A large family of chemical substances comprising many hormones and
vitamins and having large ring structures.
Stilbene: An aromatic hydrocarbon C-./.H-,- used as a phosphor and in making
dyes. I4 u
Stoichiometric factor: Used to express the conversion efficiency of a non-
quantitative reaction, such as the reaction of NCL with azo dyes in air
monitoring methods.
Stoma: A minute opening or pore (plural is stomata).
Stratosphere: That region of the atmosphere extending from 11 km above the
surface of the earth to 50 km. At 50 km above the earth temperature
rises to a maximum of 0 C.
Streptococcus pyogenes: A species of bacteria found in the human mouth,
throat and respiratory tract and in inflammatory exudates, blood stream,
and lesions in human diseases. It causes formation of pus or even fatal
septicemias.
Stress corrosion cracking: Cracking caused by simultaneous presence of
tensile stress and a specific corrosive medium. The metal or alloy is
virtually unattached over most of its surface, while fine cracks progress
through it.
Strong interactions: Forces or bond energies holding molecules together.
Thermal energy will not disrupt the formed bonds.
Sublobular hepatic necrosis: The pathologic death of one or more cells, or
of a portion of the liver, beneath one or more lobes.
Succession: The progressive natural development of vegetation towards
a climax, during which one community is gradually replaced by others.
Succinate: A salt of succinic acid involved in energy production in the
citric acid cycle.
Sulfadiazine: One of a group of sulfa drugs. Highly effective against
pneumococcal, staphlococcal, and streptococcal infections.
Sulfamethazine: An antibacterial agent of the sulfonamide group, active
against homolytic streptococci, staphytococci, pneumococci and meningococci,
Sulfanilimide: A crystalline sulfonamide (CcHgO^S), the amide of sulfanilic
acid and parent compound of most sulfa arugs.
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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 (SQ2): Colorless gas with pungent odor released primarily from
burning of fossil fuels, such as coal, containing sulfur.
Sulfur dyes: Used only on vegetable fibers, such as cottons. They are
insoluble in water and must be converted chemically in order to be
soluble. They are resistant (fast) to alkalies and washing and fairly
fast to sunlight.
Supernatant: The clear or partially clear liquid layer which separates
from the homogenate upon centrifugation or standing.
Surfactant: A substance capable of altering the physiochemical nature of
surfaces, such as one used to reduce surface tension of a liquid.
Symbiotic: A close association between two organisms of different species in
which at least one of the two benefits.
Synergistic: A relationship in which the combined action or effect of two
or more components is greater than that of the components acting separately.
Systolic: Relating to the rhythmical contraction of the heart.
Tachypnea: Very rapid breathing.
12
Terragram (Tg): One million metric tons, 10 grams.
Teratogenesis: The disturbed growth processes resulting in a deformed
fetus.
Teratogenic: Causing or relating to abnormal development of the fetus.
Threshold: The level at which a physiological or psychological effect begins
to be produced.
Thylakoid: A membranous lamella of protein and lipid in plant chloroplasts
where the photochemical reactions of photosynthesis take place.
Thymidine: A nucleoside (C^H^Ot-) that is composed of thymine and
deoxyribose; occurs as a strnctural part of DMA.
Tidal volume (Vj): The volume of air that is inspired or expired in a single
breath during regular breathing.
Titer: The standard of strength of a volumetric test solution. For example,
the titration of a volume of antibody-containing serum with another
volume containing virus.
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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.
Transmissiyity (UV): The percent of ultraviolet radiation passing through a
a medium.
Transmittance: The fraction of the radiant energy entering an absorbing
layer which reaches the layer's further boundary.
Transpiration: The process of the loss of water vapor from plants.
Triethanolamine: An amine, (HOCH?CH?)qN, used in the absorbing solution
of one analytical method for NO^.
Troposphere: That portion of the atmosphere in which temperature decreases
rapidly with altitude, clouds form, and mixing of air masses by convection
takes place. Generally extends to about 7 to 10 miles above the earth's
surface.
Type 1 epithelial cells: Squamous cells which provide a continuous lining
to the alveolar surface.
Type I pneumonocytes: Pulmonary surface epithelial cells.
Type II pneumonocytes: Great alveolar cells.
Ultraviolet: Light invisiblebto the human eye of wavelengths between 4x10
and 5xlO"9 m (4000 to 50A).
Urea- formaldehyde resin: A compound composed of urea and formaldehyde in
an arrangement that conveys thermosetting properties.
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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 (Vr): The volume of gas exchanged between the lungs and
the atmosphere that occurs in breathing.
Villus: A projection from the surface, especially of a mucous membrane.
Vinyl chloride: A gaseous chemical suspected of causing at least one type
of cancer. It is used primarily in the manufacture of polyvinyl
chloride, a plastic.
Viscose rayon: Filaments of regenerated cellulose coagulated from a solution
of cellulose xanthate. Raw materials can be cotton linters or chips
of spruce, pine, or hemlock.
6
Visible region: Light between the wavelengths of 4000-800Q A.
Visual range: The distance at which an object can be distinguished from
background.
Vital capacity: The greatest volume of air that can be exhaled from the
lungs after a maximum inspiration.
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Vitamin E: Any of several fat-soluble vitamins (tocopherols), essential
in nutrition of various vertebrates.
Washout: The capture of gases and particles by falling raindrops.
Weak interactions: Forces, electrostatic in nature, which bind atoms and/or
molecules to each other. Thermal energy will disrupt the interaction.
Also called van der Waal's forces.
Wet deposition: The process by which atmospheric substances are returned
to earth in the form of rain or other precipitation.
Wheat germ lipase: An enzyme, obtained from wheat germ, which is capable
of cleaving a fatty acid from a neutral fat; a lipolytic enzyme.
X-ray fluorescence spectrometry: A nondestructive technique which utilizes
the principle that every element emits characteristic x-ray emissions
when excited by high-energy radiation.
Zeolites: Hydrous silicates analogous to feldspars, occurring in lavas
and various soils.
Zooplankton: Minute animal life floating or swimming weakly in a body of water.
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TECHNICAL REPORT DATA
(Please read Insrructions on the reverse before completing)
EPA- 600/8-82- 026F
4. TITLE AND SUBTITLE
AIR QUALITY CRITERIA FOR
Report
7. AUTHOR(S)
See list of Contributors
2.
OXIDES OF NITROGEN: Final
and Reviewers
9. PERFORMING ORGANIZATION NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Research and Development
Environmental Criteria and Assessment Office (MD-52)
Research Triangle Park, N.C. 27711
12. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
,401 M Street, S.W., Washington, D.C. 20460
3. RECIPIENT'S ACCESSION NO.
PB-83-163337 "
5. REPORT DATE
December 1982
6. PERFORMING ORGANIZATION CODE
8. PERFORMING ORGANIZATION REPOR'
10. PROGRAM ELEMENT NO.
A9DA1A
11. CONTRACT/GRANT NO.
13. TYPE OF REPORT AND PERIOD COVE
Final
14. SPONSORING AGENCY CODE
EPA/600/21
15. SUPPLEMENTARY NOTES
16. ABSTRACT
This criteria document focuses on a review and assessment of the effects on human
health and welfare of the nitrogen oxides, nitric oxide (NO) and nitrogen dioxide
(NOp), and the related compounds, nitrites, nitrates, nitrogenous acids, and
nitrosamines. Although the emphasis is on presentation of health and welfare
effects data, other scientific data are oresented in order to provide a better
understanding of these pollutants in the environment. To this end, separate
chapters are included which discuss the nitrogen cycle, sources and emissions,
atmospheric chemical processes which transform emissions of nitrogen oxides into
related airborne compounds, transport and removal processes, measurement methods,
and atmospheric concentrations of nitrogenous pollutants.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS t. COSATI I Icld/Groi
8. DISTRIBUTION STATEMENT
Release unlimited
19. SECURITY CLASS t'fliis Report)
Uncla s_s_rfie
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