EXTERNAL REVIEW DRAFT
NOVEMBER 1978
DRAFT
Do not cite or quote
AIR QUALITY CRITERIA
FOR
OXIDES OF NITROGEN
DRAFT
Do not cite or quote
NOTICE
This document is an external review draft. It has not
been formally released by EPA and should not at this
stage be construed to represent Agency policy. It is
being circulated for comment on its technical accuracy
and policy implications.
Environmental Criteria and Assessment Office
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
-------
EXTERNAL REVIEW DRAFT
NOVEMBER 1978
DRAFT
Do not cite or quote
AIR QUALITY CRITERIA
FOR
OXIDES OF NITROGEN
DRAFT
Do not cite or quote
NOTICE
This document is an external review draft. It has not
been formally released by EPA and should not at this
stage be construed to represent Agency policy. It is
being circulated for comment on its technical accuracy
and policy implications.
Environmental Criteria and Assessment Office
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
-------
CONTRIBUTORS AND REVIEWERS
Mr. Gerald G. Akland, Environmental Monitoring and Support Laboratory
(EMSL), USEPA
Or. Martin Alexander, Cornell University
Dr. Aubrey P. Altshuller, Environmental Sciences Research Laboratory
(ESRL), USEPA
Dr. Charles E. Anderson, North Carolina State University
Mr. John D. Bachmann, Strategies and Air Standards Division, Office of
Air Quality Planning and Standards (SASD, OAQPS), USEPA
Dr. Ronald L. Baron, Health Effects Research Laboratory (HERL), USEPA
Mr. Norman J. Beloin, Survey and Analysis Division, Region I, USEPA
Mr. Michael A. Berry, ECAO
Dr. Patrick Brezonik, University of Florida
Dr. Robert H. Bruce, ECAO
Dr. Joseph J. Bufalini, ESRL
Mr. Ronald C. Campbell, SASD, OAQPS
Dr. John B. Clements, EMSL
Dr. David L. Coffin, HERL
Dr. Ellis B. Cowling, North Carolina State University
Dr. T. Timothy Crocker, University of California at Irvine
Dr. Paul Crutzen, National Center for Atmospheric Research, Boulder CO
Mr. Swep T. Davis, Deputy Assistant Administrator for Water Planning and
Standards, USEPA
Dr. Basil Dimitriades, ESRL
Mr. George Duggan, SASD, OAQPS
Dr. Thomas G. Dzubay, ESRL
Dr. Richard Ehrlich, IIT Research Institute
Mr. Thomas G. Ellestad, ESRL
Mr. Robert B. Faoro, Monitoring and Data Analysis Division, Office of Air
Quality Planning and Standards, USEPA
Dr. C. Eugene Feigley, University of North Carolina at Chapel Hill
Mr. Douglas Fennel1, ECAO
Dr. Robert Frank, University of Washington
Dr. Sandor J. Freedman, System Sciences, Inc.
Dr. Gustave Freeman, Stanford Research Institute
Dr. Donald E. Gardner, HERL
Dr. J. H. B. Garner, ECAO
Dr. Elliot Goldstein, University of California at Davis
Ms. Judith A. Graham, HERL
Mr. Mark Greenberg, ECAO
Dr. Daniel Grosjean, University^of California at Riverside
Dr. Jack D. Hackney, Rancho Los Amigos Hospital
Dr. Philip L. Hanst, ESRL
Mr. Albert V. Hardy, Jr., System Sciences, Inc.
Mr. Fred H. Haynie, ESRL
Dr. Walter W. Heck, North Carolina State University
m
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Dr. F. Gordon Neuter, HERL
Dr. Steven M. Horvath, University of California at Santa Barbara
Mr. Allen Hoyt, ECAO
Dr. Harvey E. Jeffries, University of North Carolina at Chapel Hill
Mr. Michael Jones, OAQPS
Dr. John H. Knelson, HERL
Dr. Elvado Kothny, California State Department of Health at Berkeley
Dr. Kenneth T. Krost, ESRL
Mr. William S. Lanier, Industrial Environmental Research Laboratory, USEPA
Dr. Gory J. Love, System Sciences, Inc.
Mr. Thomas McMullen, ECAO
Dr. Daniel B. Menzel, Duke University
Mr. M. R. Midget, EMSL
Dr. Sidney S. Mirvish, University of Nebraska
Mr. Edwin L. Meyer, MDAD, OAQPS
Dr. Steven Nesnow, HERL
Mr. Dennis J. Reutter, ESRL
Mr. Harold G. Richter, MDAD, OAQPS
Dr. Joseph Roycroft, Jr., HERL
Dr. Victor S. Salvin, University of North Carolina at Greensboro
Dr. John H. Seinfeld, California Institute of Technology
Dr. Joseph Seitler, Office of Toxic Substances, USEPA
Dr. Carl M. Shy, University of North Carolina at Chapel Hill
Mr. James R. Smith, HERL
Mr. Mark G. Smith, System Sciences, Inc.
Dr. Edward P. Stahel, North Carolina State University
Mr. Robert K. Stevens, ESRL
Mr. Orin Stopinski, HERL
Mr. Joseph Suggs, HERL
Dr. David T. Tingey, Corvallis Environmental Research Laboratory (CERL), USEPA
Dr. John Trijonis, Technology Service Corporation
Dr. David E. Weber, CERL
Dr. Jerome Wesolowski, California State Department of Health at Berkeley
Dr. Warren H. White, Technology Service Corporation
IV
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TABLE OF CONTENTS
LIST OF FIGURES
LIST OF TABLES
LIST OF ABBREVIATIONS AND SYMBOLS
ABSTRACT '
CONTRIBUTORS AND REVIEWERS '. ". ". '.
1. SUMMARY AND CONCLUSIONS
1. 1 INTRODUCTION . . .
1. 2 GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NO AND NO -
DERIVED POLLUTANTS x. . . .x.
1. 2.1 Introduction and Overview
1. 2.2 Nitrogen Oxides ,
1. 2.3 Nitrates, Nitrites, and Nitrogen Acids
1. 2.4 N-Nitroso Compounds
1. 3 ANALYTIC METHODS AND SAMPLING FOR AMBIENT NO and NO -
DERIVED POLLUTANTS X. . . . .
1. 4 SOURCES AND EMISSIONS
1. 4.1 Relative Significance of Natural and
Anthropogenic Sources of NO
1. 4.2 Sources of NO in the UniteQ States
1. 4.3 Emissions of ATnmonia
1. 4.4 Agricultural Usage of Nitrogenous
Compounds
1. 4.5 Sources of N-nitroso Compounds and
Possible Precursors
1. 5 ENVIRONMENTAL TRANSPORT AND TRANSFORMATION
1. 5.1 Chemistry of Oxides of Nitrogen in the Lower
Atmosphere
1. 5.2 Nitrate and Nitrite Formation
1. 5.3 Transport and Removal of Nitrogenous Species . .
1. 5.4 Mechanisms of Atmospheric Nitrosamine Formation .
1. 6 ATMOSPHERIC CONCENTRATIONS OF NOY AND OTHER NITROGENOUS
COMPOUNDS x
1. 6.1 Atmospheric Concentrations of N(X>
1. 6.2 Atmospheric Concentrations of Nitrates
1. 6.3 Atmospheric Concentrations of N-Nitroso Compounds
1. 7 NATURAL ECOSYSTEMS, VEGETATION AND MICROORGANISMAL
STUDIES
1. 7.1 The Nitrogen Cycle
1. 7.2 Effects of N07 on Vegetation
1. 8 GLOBAL EFFECTS . . /
1. 8.1 Perturbations of the Stratospheric Ozone
Layer
1. 8.2 Acidic Precipitation
-------
1. 9 EFFECTS ON MATERIALS OF NO and NO -DERIVED
POLLUTANTS x. . . .x
1.10 EFFECTS OF NITROGEN OXIDES ON VISIBILITY . . . .
1.11 STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON
ANIMALS
1.12 EFFECTS ON HUMANS
1.12.1 Controlled Exposure Studies
1.12.2 Community Exposure Studies
1.12.3 Accidental and Occupational Exposures . .
1.12.4 Effects of NO -Derived Compounds . . . .
1.13 CONCLUSIONS . . . .x
2. INTRODUCTION
3. GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NOY AND NOY-DERIVED
POLLUTANTS .............
3.1 INTRODUCTION AND OVERVIEW
3.2 NITROGEN OXIDES .
3.2.1 Nitric Oxide (NO)
3.2.2 Nitrogen Dioxide (NOJ
3.2.3 Nitrous Oxide (N?0) 7 ,
3.2.4 Unsymmetrical Nitrogen Trioxide (OONO) . .
3.2.5 Symmetrical Nitrogen Trioxide (NO.,) . . . .
3.2.6 Dinitrogen Trioxide (N«03) (Also Known as
Nitrogen Sesquioxide) 7 :
3.2.7 Dinitrogen Tetroxide (NoO.) (Also Known
as Nitrogen Tetroxide)
3.3 NITRATES, NITRITES, AND NITROGEN ACIDS
3.4 AMMONIA (NHJ
3.5 N-NITROSO COMPOUNDS
3.6 REFERENCES FOR CHAPTER 3 ,
4. SAMPLING AND ANALYSIS FOR AMBIENT NO AND
NO -DERIVED POLLUTANTS *
4.f INTRODUCTION
4.2 ANALYTICAL METHODS FOR NO
4.2.1 The Federal Reference Method for N0?:
Gas-Phase Chemiluminescence . . .
4.2.2 Other Analytical Methods for NO, . .
4.2.2.1 Griess-Saltzman HethodS . .
4.2.2.2 Jacobs-Hocheiser Method . .
4.2.2.3 Triethanolamine Method . . .
4.2.2.4 Sodium Arsenite Method . . .
4.2.2.5 TGS-ANSA Method
4.2.2.6 Other Methods
4.2.3 Analytical Methods for NO
4.2.4 Sampling for NO . .
4.2.5 Calibration of NO and N02 Monitoring
Instruments
VI
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4.3 ANALYTICAL METHODS AND SAMPLING FOR NITRIC ACID . . .
4.4 ANALYTICAL METHODS AND SAMPLING FOR NITRATE
4.4.1 Sampling for Nitrate from Airborne Particulate
Matter
4.4.2 Analysis of Nitrate from Airborne Particulate
Matter
4.4.3 Nitrate in Water
4.4.4 Nitrate in Soil
4.4.5 Nitrate in Plant and Animal Tissue ......
4.5 SAMPLING AND ANALYTICAL METHODS FOR NITROSAMINES . . ,
4.5.1 Nitrosamines in Air
4.5.2 Nitrosamines in Water ,
4.5.3 Nitrosamines in Food ,
4.6 REFERENCES FOR CHAPTER 4 ,
5. SOURCES AND EMISSIONS
5.1 INTRODUCTION
5.2 ANTHROPOGENIC EMISSIONS OF NO
5.2.1 Global Sources of NO x
5.2.2 Sources of NO in th£ United States
5.3 EMISSIONS OF AMMONIAX '
5.4 AGRICULTURAL USAGE OF NITROGENOUS COMPOUNDS
5.5 SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS
5.5.1 Anthropogenic Sources of N-Nitroso Compounds .
5.5.2 Volatilization from Other Media
5.5.3 Atmospheric Formation: N-Nitroso Precursors .
5.5.4 N-Nitrosamines in Food, Water and Tobacco
Products
5.6 REFERENCES FOR CHAPTER 5
6. ENVIRONMENTAL TRANSPORT AND TRANSFORMATION .......
6.1 CHEMISTRY OF THE OXIDES OF NITROGEN IN THE LOWER
ATMOSPHERE
6.1.1 Reactions Involving Oxides of Nitrogen . . .
6.1.2 Laboratory Evidence of the N02-to-Precursor
Relationship
6.1.3 NO Chemistry in Plumes
6.2 NITRITE Affo NITRATE FORMATION
6.3 TRANSPORT AND REMOVAL OF NITROGENOUS SPECIES . . . .
6.3.1 Transport and Diffusion ,
6.3.2 Removal Processes ,
6.3.2.1 Dry Deposition of Gases ,
6.3.2.2 Dry Deposition of Particles . . . ,
6.3.2.3 Wet Deposition ,
6.4 MECHANISMS OF ATMOSPHERIC NITROSAMINES FORMATION . ,
6.4.1 Non-Photochemical Reaction of Gaseous Amines
with Oxides of Nitrogen and Nitrous Acid . ,
6.4.2 Photochemical Reactions of Amines
6.4.3 Formation of Nitrosamine in Atmospheric
Aerosols
6.4.4 Environmental Implications
6.5 REFERENCES FOR CHAPTER 6 ,
vii
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7. OBSERVED ATMOSPHERIC CONCENTRATIONS OF NO AND OTHER
NITROGENOUS COMPOUNDS .
7.1 ATMOSPHERIC CONCENTRATIONS OF NO ...
7.1.1 Background Concentrations of NO
7.1.2 Ambient Concentrations of NO . *
7.1.2.1 Monitoring for NO .*. .
7.1.2.2 Sources of Data ....
7.1.3 Historical Measurements of NO Concentration
7.1.4 Recent Trends in N02 Concentrations
7.1.5 Seasonal Variations in N00 Concentrations. .
7.1.6 Recently Observed Atmospheric Concentrations
of NO,
7.2 ATMOSPHERIC CONCENTRATIONS OF NITRATES
7.3 ATMOSPHERIC CONCENTRATIONS OF N-NITROSO COMPOUNDS . .
7.4 REFERENCES FOR CHAPTER 7
8. NATURAL ECOSYSTEMS, VEGETATION, AND MICROORGANISMS ....
8.1 EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS .
8.1.1 Effects of Nitrates
8.1.2 Effects of Nitrogen Oxides
8.1.3 The Value of a Natural Ecosystem
8.2 EFFECTS OF NITROGEN OXIDES ON VEGETATION
8.2.1 Factors Affecting Sensitivity of Vegetation to
Oxides of Nitrogen
8.2.2 Mechanisms of Action
8.2.3 Visual Symptoms
8.2.4 Dose Response
8.2.5 Effects of Mixtures
8.2.6 Summary and Conclusions
8.3 REFERENCES FOR CHAPTER 8
9. GLOBAL EFFECTS
9.1 PERTURBATIONS OF THE STRATOSPHERIC OZONE LAYER
9.2 ACIDIC PRECIPITATION
9.2.1 Formation and Composition
9.2.1.1 Temporal and Spatial Trends in Rainfall
9.2.2 Effects of Freshwater Ecosystems
9.2.2.1 Effects at the Ecosystem Level
9.2.2.2 Summary
9.2.3 Effects on Forest Ecosystems
9.2.3.1 Soil Effects
9.2.3.2 Seed Germination
9.2.3.3 Vegetation Effects . .
9.2.3.4 Microorganismal Effects
9.3 SUMMARY
9.4 REFERENCES FOR CHAPTER 9
vm
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10. EFFECTS OF NITROGEN OXIDES ON MATERIALS
10.1 EFFECTS OF NITROGEN DIOXIDE ON TEXTILES
10.1.1 Fading of Dyes by NO
10.1.1.1 Fading of D$es on Cellulose Acetate
10.1.1.2 Fading of Dyes on Cotton and Viscose
Rayon (Cellulosics)
10.1.1.3 Fading of Dyes on Nylon
10.1.1.4 Fading of Dyes on Polyester ....
10.1.1.5 Economic Costs of NO -Induced Dye
Fading x
10.1.2 Yellowing of White Fibers by NO
10.1.3 Degradation of Textile Fibers bj NO ....
10.2 EFFECTS OF NITROGEN DIOXIDE ON PLASTICS AND
ELASTOMERS
10.3 CORROSION OF METALS BY NITROGEN DIOXIDE
10.3.1 Pitting Corrosion
10.3.2 Stress Corrosion
10.3.3 Selective Leaching
10.3.4 Correlation of Corrosion Rate with Pollution
10.4 REFERENCES FOR CHAPTER 10
11. EFFECTS OF NITROGEN OXIDES ON VISIBILITY
11.1 NITROGEN OXIDES AND LIGHT SCATTERING AND ABSORPTION
11.2 EFFECT OF NITROGEN DIOXIDE ON COLOR ,
11.2.1 Nitrogen Dioxide and Plumes ,
11.2.2 Nitrogen Dioxide and Haze ,
11.3 EFFECT OF PARTICIPATE NITRATES ON VISUAL RANGE . . ,
11.4 REFERENCES FOR CHAPTER 11
12. STUDIES ON THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS . .
12.1 INTRODUCTION
12.2 NITROGEN DIOXIDE
12.2.1 Respiratory Tract Transport and Absorption . .
12.2.2 Mortality
12.2.3 Pulmonary Effects .
12.2.3.1 Host defense mechanisms
12.2.3.1.1 Interaction with
infectious agents
12.2.3.1.2 Mucociliary transport . . .
12.2.3.1.3 Alveolar macrophage ....
12.2.3.1.4 Immune system
12.2.3.2 Lung biochemistry
12.2.3.2.1 Introduction
12.2.3.2.2 Lipid and diet effects . .
12.2.3.2.3 Sulfhydryl compounds and
pyridine nucleotides . . .
12.2.3.2.4 Effects on lung amino acids,
proteins, and enzymes ...
12.2.3.2.5 Potential defense
mechanisms
IX
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12.2.3.3 Morphology studies
12.2.3.4 Pulmonary function
12.2.3.5 Studies of hyperplasia
12.2.3.6 Teratogenesis and mutagenesis . . .
12.2.3.7 Edemogenesis and tolerance
12.2.4 Extrapulmonary Effects
12.2.4.1 Nitrogen dioxide-induced changes in
hematology and blood chemistry . . .
12.2.4.2 Central nervous system and
behavioral effects
12.2.4.3 Biochemical markers of organ effects
12.2.4.4 Effects of N02 on body weights . . .
12.3 DIRECT EFFECT OF COMPLEX MIXTURES
12.4 NITRIC OXIDE
12.5 NITRIC ACID AND NITRATES
12.6 N-NITROSO COMPOUNDS
12.7 SUMMARY
12.8 REFERENCES FOR CHAPTER 12
13. EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN . . .
13.1 CONTROLLED HUMAN EXPOSURE STUDIES
13.1.1 Studies of Sensory Effects
13.1.1.1 Effects of nitrogen dioxide on
sensory systems ...
13.1.1.2 Sensory effects due to exposure to
combinations of nitrogen dioxide
and other pollutants
13.1.2 Pulmonary Function
13.1.2.1 Controlled studies of the effect of
nitrogen dioxide on pulmonary function
in healthy subjects
13.1.2.2 The effects of nitrogen dioxide
exposure on pulmonary function in
sensitive subjects
13.2 COMMUNITY EXPOSURE STUDIES
13.2.1 Effects of NO- on Pulmonary Function
13.2.2 Effects of N0£ on Acute Respiratory Illness . .
13.2.2.1 Effects associated with ambient
exposures
13.2.2.2 Effects associated with indoor
exposures ....
13.2.3 Effects of NO- Pollution on Prevalence of
Chronic Respiratory Disease
13.2.4 Extrapulmonary Effects of Exposure to NO,
13.3 ACCIDENTAL AND OCCUPATIONAL EXPOSURES . . . . ?
13.4 EFFECTS OF NO -DERIVED COMPOUNDS
13.4.1 Nitratls, Nitrites and Nitric Acid ...
13.4.2 Nitrosamines ...
13.4.3 Other Compounds
13.5 SUMMARY OF EFFECTS ON HUMANS
13.6 REFERENCES FOR CHAPTER 13
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LIST OF FIGURES
Figure Page
3-1. Absorption Spectrum of Nitric Oxide
5-1. Historic NO Emissions by Source Groups . . .;
5-2. Recent NO Emissions by Source Groups
5-3. Distribution of 1972 Nationwide NO Emissions by Degree of
Urbanization. x
5-4. Total NO Emissions by U.S. County
5-5. Total NO Emission Density by U.S. County
5-6. Percent ftO Emissions Contributed by Major Point Sources. . . .
5-7. Trends in 6.S. Usage of Nitrogenous Material Applied as
Fertilizer
6-1. Paths of Nitrate Formation in the Atmosphere
6-2. Schematic Illustration of Scales of Motion in the Atmosphere. .
6-3. Formation and Decay of Diethylnitrosamine, in the Dark and in
Sunlight, from Diethyl amine (Filled Circles) and from
Triethylamine (Open Circles)
7-1. Trend Lines for Nitric Oxide Annual Averages in Five
CAMP Cities
7-2. Trend Lines for Nitrogen Dioxide Annual Averages in Five
CAMP Cities
7-3. Trends in N0? Air Quality, Los Angeles Basin, 1965-1974 . . . .
7-4. Annual Air Quality Statistics and Three-Year Moving
Averages at Camden, New Jersey
7-5. Annual Air Quality Statistics and Three-Year Moving
Averages at Downtown Los Angeles, California
7-6. Annual Air Quality Statistics and Three-Year Moving
Averages at Azusa, California
7-7. Annual Air Quality Statistics and Three-Year Moving
Averages at Newark, New Jersey
7-8. Annual Air Quality Statistics and Three-Year Moving
Averages at Portland, Oregon
7-9. Annual Average of Daily Maximum 1-Hour N02 (4-Year Running
Mean) in the Los Angeles Basin
7-10. Seasonal N0? Concentration Patterns of Three U.S. Urban
Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations. ,
7-11. Seasonal NO,, Concentration Patterns of Four U.S. Urban
Sites (Montnly Averages of Daily Maximum 1-Hr Concentrations. ,
7-12. Distribution of Maximum/Mean N0? Ratios for 120 Urban
Locations Averaged Over the Years 1972, 1973, and 1974. . . .
7-13. Trends in the Maximum Mean N0? Ratio for Two Groups of
Sites: (a) Average of Five High Growth Locations Within the
Los Angeles Basin (Anaheim, La Habra, Azusa, Pomona, San
Bernadino); (b) Average of Two New Jersey Sites (Bayonne
and Newark)
7-14. Average Diurnal Pattern for the Month During Which the
Highest 1-Hour N02 Concentrations were Reported: (•) Los
Angeles, California, January 1975; (o) Denver, Colorado, April
1975; (x) Chicago, Illinois, June 1975
XI
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LIST OF FIGURES (continued)
Figure Page
7-15. One-Hr Average Concentration Profiles on Day of Peak NCL
Concentration for Three U.S. Cities: (t) Los Angeles,
California January 17, 1975; (o) Denver, Colorado, April 5,
1975; (x) Chicago, Illinois, June 21, 1975
7-16. One-Hour N02 Concentrations During Three Days of High
Pollution in Three U.S. Cities: (•) Ashland, Kentucky, November
19-20, 1975; (o) Los Angeles, California, January 15-17, 1975;
McLean, Virginia, August 27-29, 1975
7-17. Nitric Oxide and Nitrogen Dioxide Concentrations at an Urban
and a Rural Site in St. Louis, Missouri, on January 27-28,
1976; (•) NO,, at RAMS Station 5 (Center City); (o) N0? at
RAMS Station 22 (45 km north of center city); (x) NO at
Rams Station 5 (Center City)
7-18. Pollutant Concentrations in Central City St. Louis,
October 1, 1976, Average of RAMS Sites 101, 102, 106,
and 107
8-1. Schematic representation of the nitrogen cycle, emphasizing
human activities that affect fluxes of nitrogen
8-2. Estimates of mass flow of nitrogen
8-3. Simplified biological nitrogen cycle
8-4. Schematic presentation of environmental effects of
manipulation of the nitrogen cycle
8-5. Areal loading rates for nitrogen plotted against mean
depth of lakes
8-6. 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 . .
8-7. Summary of effects of N02 on vegetation
9-1. Average pH of Annual Precipitation in the Eastern United States. .
9-2. Cation Inputs in Precipitation at Hubbard Brook, N. H
9-3. Seasonal Variation in pH and Ammonium Nitrate Concentrations in
Wet-Only Precipitation at Gainesville, Florida
9-4. Hydrogen Ion Deposition in Precipitation Plotted Against Nitrate
Deposition and Sulfate Deposition
9-5. Trajectory Map Indicating Source Strengths for SO- Emissions
Affecting the Eastern United States
9-6. Hardness of Surface Waters in the United States
9-7. Calcium Content of Surface Soils in the United States
9-8. Status of Fish Populations in Norwegian Lakes in Relation to pH
of Water
11-1. Transmittance Exp(~bNO,,x) of N0? Plumes for Selected Values
of the Concentration -Distance Product
11-2. Relative Horizon Brightness b /(b + bNn ) for Selected
Values of the Concentration -Visual Range Product,
Assuming b_ = 3/(Visual Range) - - - •
11-3. Normalized Light Scattering by Aerosols as a Function of
Particle Diameter
xii
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LIST OF FIGURES (continued)
12-1. Regression Lines of Percent Mortality of Mice Versus Length of
Continuous Exposure to Various NO- Concentrations Prior to
Challenge with Streptococci
12-2. Percent Mortality of Mice Versus the Length of Either Continuous
or Intermittent Exposure to 6,600 ug/m (3.5 ppm) NO* Prior to
Challenge with Streptococci
12-3. Percent Mortality of Mice Versus Length of Either Continuous or
Intermittent Exposure to 2,800 ug/m (1.5 ppm) N02 prior to
Challenge with Streptoccoci
12-4. Temporal Sequence of Injury and Repair Hypothesized from
Short-Term Single Exposure of Less Than 8 Hours
12-5. Temporal Sequence of Injury and Repair Hypothesized from
Continuous Exposure to N02 as Observed in Experimental Animals .
12-6. Proportionality between Effect (Cell Death) and Concentration of
N02 during a Constant Exposure Period.
xm
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LIST OF TABLES
Table Page
1-1. Summary of Observed Effects on Animals of Short-Duration
Exposures to N0? Concentrations of 1 PPM or Less
1-2. Effects on Humans and Animals of Exposures to N02
3-1. Theoretical Concentrations of Nitrogen Oxides ana Nitrogen
Acids Which Would be Present at Equilibrium with Molecular
Nitrogen, Molecular Oxynen, and Water in Air at 25°C, 1 ATM,
50 Percent Relative Humidity
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. Comparison of Nitrate Collected on Various Filter Types. . . .
4-2. Analytical Methods for Nitrate in Water. . .
4-3. Methods for Determination of Nitrate in Soils
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. Estimated Ammonia Emission from Fertilizer Application
and Industrial Chemical Production in U.S. (1975)
5-5. Nitrogenous Compounds Applied as Fertilizer in the U.S.
1955-1976
6-1. Reactions of Alkoxyl, Alkylperoxyl and Acylperoxyl
Radicals with NO and N02
6-2. Summary of Conclusions from Smog Chamber Experiments
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
6-4. Maximum Concentrations and Yields of the Products of
Diethylamine and Tri ethyl ami ne
7-1. Background NO Measurements
7-2. Yearly AveragI and Maximum Concentrations of Nitric Oxide
at Camp Stations, Measured by the Continuous Saltzman
Colorimetric Method
7-3. Five-Yr Averages of Nitric Oxide Concentrations at Camp
Stations, Measured by Continuous Saltzman Colorimetric
Method
7-4. Yearly Average and Maximum Concentrations of Nitrogen
Dioxide at Camp Stations, Measured by the Continuous
Saltzman Colorimetric Method
xiv
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LIST OF TABLES (continued)
Table Page
7-5. Five-Yr Averages of Nitrogen Dioxide Concentrations at Camp
Stations, Measured by the Continuous Saltzman Colorimetric
Method
7-6. Five-Year Changes in Ambient N0? Concentrations
7-7. Ratio of Maximum Observed Hourly Nitrogen Dioxide Concen-
trations to Annual Means During 1975 for Selected Locations. . .
7-8. Frequency Distribution of 1975 Hourly N02 Concentrations at
Various Sites in U.S. Urban Areas
7-9. Frequency Distribution of 1976 Hourly Nitrogen Dioxide
Concentrations at Various U.S. Sites
7-10. Frequency Distribution of 1976 24-Hr Average N02 Concen-
trations at Various Sites in U.S. Urban Areas (All Data
Obtained by Sodium Arsenite Method)
7-11. Distribution by Time of Day of One-Hour Maximum N02
Concentrations for One Month in 1975 for Selected urban
Sites
7-1?. Mean and Top Five Nitrogen Dioxide Concentrations Reported
From 18 Individual Rams Stations in St. Louis During 1976. . . .
8-1. Common trophic state indicators and their responses to
eutrophi cation
8-2. Water use problems resulting from eutrophication
8-3. Nitrate-M loadings to Lake Wingra
8-4. Relative sensitivity of several plant species to
nitrogen dioxide
8-5. Effects of chronic nitrogen dioxide exposures on several
crop species
8-6. Projected N02 exposures for 5 percent injury levels on
selected vegetation
9-1. Calculated Changes in Stratospheric Ozone due to Hypothetical
Changes in the Global Tropospheric Background Mole Fractions
of N?0
9-2. Deposition of Sulfuric and Nitric Acids in Precipitation in
Eastern North America
9-3. Sulfuric and Nitric Acids are Major Sources of Acidity in
Precipitation
9-4. Hydrochloric, Sulfuric and Nitric Acids are Strongest of
Several Potentially Important Proton Donors in Rain and Snow.
9-5. Summary of Effects of pH Changes on Fish
9-6. Potential Effects of Acid Precipitation on Soils
9-7. Potential Effects of Acid Precipitation on Vegetation . . . .
10-1. Fading of Dyes on Cellulose Acetate and Cellulosics
(Cotton and Rayon) by Nitrogen Dioxide
10-2. Color Changes on Dyed Fabric-Exposed Without Sunlight
in Pollution and Rural Areas
10-3. Typical Concentrations of Atmospheric Contaminants in
Selected Areas
10-4. Exposure Sites
xv
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LIST OF TABLES (continued)
Table Page
10-5. Average Fading of 20 Dye-Fabric Combinations After 12
Weeks Exposure to Nitrogen Dioxide
10-6. Effect of Nitrogen Dioxide on Fading of Dyes on Nylon
and Polyester
10-7. Estimated Costs of Dye Fading in Textiles
10-8. Yellowing of Whites by Nitrogen Dioxide
10-9. Corrosion of Metals by Nitrogen Dioxide
12-1. Summary of Observed Effects on Animals of Exposure to N02
Concentrations below 30 ppm
12-3. Mortality from N02 Exposure for 1 to 8 hours
12-4. Interaction with infectious Agents
12-5. Mucociliary Transport
12-6. Alucolar Nacrophages
12-7. Immunological Effects
12-8. Effects on Lung Biochemistry
12-9. Effect of NO- on Lung Morphology
12-10. Pulmonary Functions
12-11. Studies of Potential Hyperphasia, Mutagenesis, Teratogenesis . . .
12-12. Tolerance to N02 Exposures
12-13. Production of Lung Edema by N0«
12-14. Nitrogen Dioxide-Induced Changes in Hematology
12-15. Central Nervous System and Behavioral Effects
12-16. Biochemical Markers of Organ Effects
12-17. Extrapolmonary Effects of N0p: Body Weight
12-18. Nitric Oxide
12-19. Nitric Acid and Nitrates
13-1. Effects of Exposure to Nitrogen Dioxide on Sensory
Receptors in Controlled Human Studies ,
13-2. Effects of Exposure to Combinations of Pollutants on
Sensory Receptors in Controlled Human Studies
13-3. Effects of Exposure to Nitrogen Dioxide on Pulmonary Function
in Controlled Studies of Healthy Humans
13-4. Effects of Exposure to Nitrogen Dioxide on Pulmonary
Function in Controlled Studies of Sensitive Humans
13-5. Effects of Exposure to Nitrogen Dioxide on Pulmonary
Function in Community Studies
13-6. Effects of Exposure to Nitrogen Dioxide on the Incidence of
Acute Respiratory Disease in Community Studies
13-7. Effects of Exposure to Nitrogen Dioxide on the Prevalence
of Chronic Respiratory Disease in Community Studies
13-8. Effects of Exposure to Nitrogen Dioxide on Extra Pulmonary
Parameters
xvi
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ABSTRACT
Nitrogen oxides resulting from human activities are being emitted
into the atmosphere in significant quantities. Emissions are likely to
increase as energy production grows.
This criteria document focuses on a review and assessment of the
effects on human health and welfare of nitrogen oxides and the related
compounds, nitrites, nitrates, nitrogenous acids, and nitrosamines. Its
primary purpose is to provide a scientific basis to aid regulatory
officials with their decisions concerning possible need for control.
In healthy individuals and in individuals believed to be pre-
disposed to respiratory difficulties, exposures for less than one hour
to N02 at concentrations of 3000 ug/m (1.6 ppm) or above have caused
increases in airway resistance. More severe effects have been produced
by exposures to higher concentrations. Other studies have suggested that,
as a group, asthmatics are particularly sensitive to nitrogen dioxide
and may be affected at levels considerably below 3000 ug/m (1.6 ppm).
However, this suggestion is yet to be confirmed.
Field studies provide indications of increases in the incidence of
acute respiratory diseases in populations exposed with some regularity
for short periods to N0« concentrations of 940 ug/m (0.5 ppm) N02 or
higher, or to long term concentrations over 100 ug/m (0.05 ppm).
However, these studies also have interpretive difficulties: since other
pollutants were present in the atmosphere, the effects cannot be
xv ii
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attributed to NCL alone.
Examination of ambient monitoring data for the years 1975 and 1976
reveals that concentrations of N02 in excess of 940 ug/m (0.5 ppm) for
1-hour duration were experienced in Los Angeles, California. In addi-
tion, a few other sites reported concentrations close to this value.
o
One-hour concentrations exceeding 470 ug/m (0.25 ppm) were fairly
common throughout the nation. Yearly arithmetic means in excess of 100
ug/m (0.05 ppm) were reported in 1976 from several sites in California,
from Chicago, Illinois, and from Southfield, Michigan. Yearly arithmetic
means in excess of 50 ug/m (0.025 ppm) were a quite common occurrence
nationwide.
Atmospheric nitrates may act as repsiratory irritants at concentrations
in excess of 8 ug/m and at such concentration cause increases in asthma
attacks. Nitric acid is a strong caustic irritant and may be at least a
partial cause -of increases in asthma attacks associated with increased
nitrate levels. There is no evidence that nitrites in the atmosphere are
harmful to human health.
Recent discovery has been made of severe and, apparently, unresolvable
difficulties with artifact nitrate formation on the glass fibre filters
routinely used to collect participate nitrate suspended in ambient air.
Preliminary data collected by new techniques are not sufficient to place
human exposure to these pollutants in nationwide perspective, but
point, generally, to lower values than previously reported. Similarly,
ambient measurements of nitric acid vapor are too few to allow estima-
tion of the health impact of this pollutant.
acvlii
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Although a few N-nitroso compounds have been Identified in
low concentrations in the atmosphere near a few suspected sources,
most ambient measurements have yielded negative results. At this
time, therefore, there is no evidence that the concentrations of
nitrosamines in the atmosphere are sufficient to be implicated as
significant causes of human disease.
Of the oxides of nitrogen which occur in the atmosphere nitrogen
dioxide (N02) is by far the most toxic to be discovered. Because of
the high reactivity of N02, the predominant response observed in the
inhalation of N02 is direct injury to the tissues of the lung. An
unusual aspect of the toxicity of N02 is a delay between exposure and
effect. This temporal sequence is important to an understanding of
the toxicity of N02 in both short-term and long-term exposures to
this air'pollutant.
Results of animal experiments in N02 exposure do not directly
model human response, but because the same cell types exist in the
lungs of animals and man, the mechanisms of toxicity revealed are
considered pertinent to man. The majority of animal experiments can
be classed as one of two general types: 1) those causing measurable
alteration in cellular biochemistry and, 2) those inducing suscepti-
bility to pathogenic bacteria - the infectivity model.
Biochemical reactions predominantly affect the lipid components
of cells. The region of the lung bounded by the terminal and
respiratory bronicoles and adjacent alveoli - the region intimately
involved in the essential exchange of oxygen and carbon dioxide -
is most affected. One of the most sensitive biochemical indicators
-------
of Injury to these deep-lung cells is a change in cellular
permeability, which has been detected at a concentration as low as
752 ug/m (0.4 ppm) NOg. Macrophages, resident within the airways,
are particularly senstive to N02 exposure. Biochemical parameters of
injury often return to normal or near normal values within a week or
two of cessation of exposure.
The infectivity model has proven to be a particularly sensitive
indicator of pulmonary injury; the procedure integrates many of the
defense mechanisms of the lung and, therefore, reflects the overall
damage that has occurred. Increased susceptibility to a pathogen
may result in excess animal mortality following a single 3-hour exposure
to an N02 concentration as low as 1880 ug/m (1 ppm).
Long term exposures to N02 induce rapid changes in the biochemical
and physiological function indicators of cell injury and repair of
cell death and replacement; a relatively steady state is reached after
about a week or two.
Because N02 produces a stimulation or rapid turnover of cells, a
transient hyperplasia of specific cell types is observed in animals.
There is at the present time, however, no evidence to connect the
inhalation of N02 with an increased incidence of cancer.
The apparent adaptation responses noted in human pulmonary
function measurements suggest that only major pathophysiologic changes
in human pulmonary tissue may be detectable by this relatively insensitive
method of measurement, in contrast to the measurements which are possible
in experimental animals using biochemical and morphological techniques.
Nitrogen dioxide has been found to cause deletrious effects on a
wide variety of textile dyes and fabrics, plastics, and rubber.
-------
Significant fading of certain dyes on cotton and rayon has been
o
shown after 12 weeks of exposure to 94 ug/m (0.05 ppm) N0? at high
humidity and temperature (90 percent, 90°F). Similar effects were
obtained under similar conditions for various dyes on nylon, at
o
188 ug/m (0.1 ppm). Yellowing of several white fabrics has been
o
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 contacts.
Haze and brown plumes resulting from emissions of nitrogen oxides
may result in the deterioration of visibility and loss of scenic
vistas. At a visual range of 10 kilometers, typical of urban haze,
o
380 ug/m (0.2 ppm) NOg would produce the same effect. Particulate
nitrates may also impair the visual range.
When crops are exposed to nitrogen dioxide alone in controlled
studies, the ambient concentrations producing measurable injury
are above those normally occurring in this country. However, a
number of controlled studies on mixtures of nitrogen dioxide with
sulfur dioxide show effects greater, in some cases much greater,
than those effects caused by the individual pollutants alone.
Some leaf injury to pinto bean, radish, soybean, tomato, oat and
2
tobacco occurred after 4-hour exposure to 280 ug/m (0.15 ppm) NOg
o
in combination with 260 ug/m (0.1 ppm) S02. Similar results
were observed in green peas and swiss chard.
Oxides of nitrogen as a class are major precusor to acidic pre-
cipitation. A number of direct effects of acidic precipitation on both
terrestrial and aquatic biota have been reported. The effects include
xxi
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tissue damage and physiological impairment in plants, lethal effects
on fish, and possible 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, and the extent to
which synergisms may occur between acidic precipitation and other
forms of environmental stress is unknown. The long-term effects
of acidification on aquatic ecosystems have been better documented.
These effects are widespread, regionally and globally, and can include
decimation of fish populations. Little is known about the recovery
of ecosystems from such effects, but liming of soils and lakes has been
successful in a limited number of cases.
xxii
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CHAPTER 1
SUMMARY AND CONCLUSIONS
1.1 INTRODUCTION
The oxides of nitrogen of primary concern in the atmosphere are
nitric oxide and nitrogen dioxide. These pollutants may undergo a variety
of atmospheric chemical transformations leading to other compounds of
possible concern such as nitric acid, suspended particulate nitrates, and
N-nitroso compounds.
Oxides of nitrogen have their origin in a number of natural and man-
made processes. In terms of significant human exposure, however, the most
important emissions occur as a result of the burning of fossil fuels, such
as coal, oil or gasoline.
Increasing energy demands can be met only by the construction of
additional generating facilities, many of which, according to current
plans, will be coal-fired. For this reason, the atmospheric concentra-
tions of the nitrogenous pollutants of concern are likely to become even
higher in the future, especially if control actions do not keep pace with
energy production.
A criteria document is designed to consolidate scientific information
relative to a specific set of pollutants in a manner that will assist
regulatory officials in making the complex decisions concerning possible
control actions. Since publication, in 1971, of the original Air Quality
Criteria for Nitrogen Oxides, there has been published a considerable body
of additional information relating to the effects of nitrogenous compounds
on human health and welfare. In addition, investigations of atmospheric
chemical processes, of the occurrence and distribution of atmospheric
1-1
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burdens of these compounds, and of techniques for their measurement have
also resulted in new material important for understanding the current impact
of nitrogenous pollutants on human populations.
This document reviews the available scientific evidence, new and old,
in the context of society's concern for human health and welfare.
This chapter summarizes the information contained in the document and,
in addition, presents the specific conclusions derived from the totality of
data available.
1.2 GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NOV AND NO -DERIVED
J\ /v
POLLUTANTS
1.2.1 Introduction and Overview
There are eight nitrogen oxides which may be present in the ambient air:
nitric oxide (NO), nitrogen dioxide (NOg), nitrous oxide (N20), unsymmetrical
nitrogen trioxide (OONO), symmetrical nitrogen trioxide (O-N(O)-O), dinitrogen
trioxide (NpO^), dinitrogen tetroxide (N^O.), and dinitrogen pentoxide (NgOg).
Of these, NO and NOg 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 clearly
A
between them. Of the two, N0« 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 NpO is
not generally considered to be an air pollutant, it is a principal reactant
in upper atmospheric reactions involving the ozone layer.
1-2
-------
While OONO, ON(0)0, N203, N204, and N205 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 (NFL) 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.
O X
Compounds derived from NOX including nitrites, nitrates, nitrogen
acids, N-nitroso compounds, and organic compounds such as the peroxyacyl
nitrates [RC(0)OON02], 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 Oxtdahts.
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 concen-
trations in public and private drinking 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
1-3
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oxides emitted may be converted on a daily basis to nitrates and nitric acid.
This atmospheric production of nitric acid may be an important component of
acidic rain.
1.2.2 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, N02 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 wave-
lengths. Because of its strong absorption in this range (and also in the
ultraviolet spectrum), N02 can cause visibility reduction and affect the
spectral distribution of solar radiation in the polluted, lower atmosphere.
1.2.3 Nitrates. Nitrites, and Nitrogen Acids
Other compounds derived from oxides of nitrogen (NOX) by means of atmos-
pheric chemical processes include nitrites, nitrates, nitrogen acids, organic
1-4
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compounds such as the peroxyacl nitrates, and, possibly, the N-nitroso
compounds.
Nitric acid, a strong acid and a 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.
1.2.4 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 NO derivatives in gas phase reactions and/or through
^\ ^\
atmospheric reactions involving aerosols. Nitroso compounds are characteris-
tically photosensitive and the nitroso group is split by the ultraviolet
radiation in sunlight. Gaseous nitrosamines may also be denitrosated by
visible light.
1.3 ANALYTIC METHODS AND SAMPLING FOR AMBIENT NOY AND NO -DERIVED POLLUTANTS
J\ J\
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
/% y\
pollutants.
With regard to the measurement of NOg, the original Federal 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
1-5
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validated for measuring both NO and NOg in concentrations encountered in
ambient air. 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 Federal Reference Method for N02 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 NOg since a number of compounds which may be present in the atmosphere may
interfere with the instrument's accuracy. Variations of the Griess-Saltzman
method are specific for NCL. Dynamic calibration of the Griess-Saltzman
methods in current use is considered necessary for reliable measurement.
Under certain circumstances, ozone can be a significant negative interferent
in the method. Both the chemiluminescence and two variations of the
Griess-Saltzman procedure (one using a modified Saltzman solution and one
using a Lyshkow solution) have been applied to produce satisfactory measurement
with instrumental averaging times of 1 hour or more. Accurate techniques
utilizing standardized gas sources, permeation tubes, or a gas-phase
titration have commonly been used for calibration.
Although adequate chemical assay techniques exist for the determination
of the nitrate fraction of suspended parti oilate 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. 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
1-6
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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 available for
routine monitoring but have yet to be carefully evaluated.
1.4 SOURCES AND EMISSIONS
1.4.1 Relative Significance of Natural and Anthropogenic Sources of NO
™^™"^™"^"—"^^^""™™^^™"™™^ ^•^""^"^•^^^•-^•^^^^^^ ^~—^^^^^^—^—~^^^—f _ _ I ^—^^ —^^^MV^^^ _ .^_^V^_^H_^
Since various authors differ greatly in their estimates of natural
emissions, it is difficult to assess with any certainty the fraction of
total NO emitted globally from human activities. In highly industrialized
/\
or populous localities, however, anthropogenic emissions of NO and/or N0£
assume primary importance. Mobile combustion and fossil-fuel power
generators are the two largest source categories. In addition, industrial
processes and agricultural operations produce minor quantities. Certain
industrial processes, such as nitric acid production, and certain
agricultural activities, such as the use of fertilizer or the operation of
animal feedlots, may result in localized emission? of other nitrogenous
compounds.
1.4.1 Sources of NO., in the United States
X
Estimates of historical emissions spanning the years 1940 through 1970
indicate that total anthropogenic emissions of NO increased almost 3-fold.
/\
More recently, emissions from transportation sources increased by about
1-7
-------
20 percent from 1970 to 1976, but emissions from stationary combustion sources
and total emissions did not exhibit a simple upward trend. Examination of NO
A
emissions inventories by U.S. county reveals that, in general, both point and
area sources contribute significantly in those places where total NO emissions
A
are high. There are, however, considerable local or regional differences in
the relative amounts of NO emitted by the major source categories. For
A
example, motor vehicles have been estimated to contribute approximately 90
percent of the NOX emissions in Sacramento, California, while the corresponding
statistic in norhtwestern Indiana is only 8 percent. Emissions may also exhibit
a significant diurnal and/or seasonal variability. For example, seasonal
variation in NOX emissions from electric generating plants of as much as 60
percent have been reported. 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. In general the influence of sources
upon ambient concentrations at a given location depends upon factors such as
land use, weather and climate, and topography. Meteorological variables
also exhibit both seasonal and diurnal variability, which can greatly affect
the impact of particular sources on ambient pollution levels.
1.4.3 Emissions of Ammonia
Principal anthropogenic sources of ammonia include coal combustion,
inefficiencies in handling and applying ammonia-based fertilizers, and volati-
zatoin of the urea-nitrogen in animal urine generated 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 (N20 is not included in this estimate).
1-8
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1.4.4 Agricultural Usage of Nitrogenous Compounds
The use of nitrogen-based fertilizer has risen markedly in the last two
decades in the United States. The total nitrogen applied as fertilizer 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.
1.4.5 Sources of N-nitroso Compounds and Possible Precursors
Possible direct atmospheric sources of N-nitroso compounds include
industrial processes in which these compounds are intermediate of final products,
reactants or additives, or may occur incidentally as impurities. While over 20
,N-nitroso compounds are listed as products in recent commercial directories, only
4 of these were either sold in quantities over 1000 pounds yearly or resulted
in annual sales over $1,000. The two N-nitroso compounds produced in greatest
quantity, diphenylnitrosamine and dinitrosopenthamethylenetetramine, are used
/
in the rubber industry as a vulcanizing retarder and a blowing agent, respec-
tively. Neither has been found carcinogenic in laboratory tests on male rats.
Preliminary considerations of proposed atmospheric mechanisms for nitro-
samine formation suggested that ambient concentrations 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. With regard to the second class, the only proposed N-nitroso
precursors for which sources have been extensively documented are the amines.
In addition, 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.
1-9
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Non-atmospheric sources of N-nitroso compounds include food, water, and
tobacco products. Raw and cooked bacon samples were found by several investi-
gators to contain 1.5 to 139 ppb nitrosopyrrolidine (NPY) and 1.0 to 3.0 ppb
dimethylnitrosamine (DMN). Other meat products (including luncheon meat
and various sausages) were found to contain 3 to 105 ppb NPY, 1 to 94 ppb
DMN, 2 to 25 ppb diethylnitrosamine (DEN) and 50 to 60 ppb nitrosopiperidine
(NPi). Raw and processed fish products have shown 1 to 26 ppb DMN and 1 to
6 ppb NPY. Cheese samples were found to contain up to 4 ppb DMN, 1.5 ppb
DEN and 1.0 ppb NPY. Analyses of drinking water have either failed to
detect N-nitroso compounds or have shown concentrations in the 0.1 ppb range.
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), nitrosoethylmethyl-
amine (30), nitrosonornicotine (137), and nitrosodiethyl amine (<5). N'-nitro-'
sonornicotine found in a variety of chewing tobacco products indicates that
such unsmoked products may also be sources of exposure to N-nitroso compounds.
1.5 ENVIRONMENTAL TRANSPORT AND TRANSFORMATION
1.5.1 Chemistry of Oxides of Nitrogen in the Lower Atmosphere
Nitrogen oxides undergo many reactions in the lower atmosphere. Trig-
gered by solar radiation, photochemical reactions involving nitrogen oxides
and other compounds, principally gaseous organic molecules, result in forma-
tion of reactive species capable of initiating a large number of subsequent
reactions. In particular, although anthropogenic emissions of NO occur
A
principally as NO, atmospheric reactions may produce the more toxic and
irritating compound NOp, which is of direct concern for human health.
1-10
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The reactive species, which include a variety of unstable, excited
molecules and molecular fragments having only transitory existence and/or
occurring only in extremely low concentrations, 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
intermediates are complex in nature, leading inevitably to short-term varia-
tions 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, such as the olefins, aromatics,
paraffins, and methane and acetylene. The dependence of N02 concentrations
on hydrocarbons results in a coupling between the chemistry of the oxides of
nitrogen and the photochemical oxidants, causing atmospheric concentrations
of either type of pollutant to depend, to some extent, on atmospheric con-
centrations of the other. There is considerable current controversy on the
precise relationships among ambient concentrations of NO and the photo-
A
chemical oxidants.
Most of the current knowledge both of atmospheric chemical pathways and
of the end products of these reactions rests on controlled experiments con-
ducted 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 reac-
tions 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
TV
1-11
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hydrocarbons inputs and resulting N02 concentrations. The results show
that, with other factors held constant, both average and maximum NC^
concentrations tend to be proportional to initial NO inputs. While some
^\
disagreement is reported from different chamber studies on the precise
effect of hydrocarbon reduction on NOg concentrations, a consensus would
seem to be as follows: Fifty percent hydrocarbon reduction would have
little effect on average NOg concentrations (a change of +. 10 percent) but
would yield moderate decreases in maximal NOg (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.
1.5.2 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 in the presence of ambient ammonia.
A
The relative importance of these two mechanisms is not presently known.
Nitric acid produced in the atmosphere may be an important component
1-12
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of acidic rain. Particulate 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.
1.5.3 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
deposition). Vegetation and soil are capable of removing significant amounts
of NO and N02 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 de-
position 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
J\
thoroughly studied.
1.5.4 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
1-13
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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 simulation experiments in environmental chambers. The third
process involving aerosol particles is purely speculative at this time.
Conflicting results are presented in the literature concerning nitro-
samine 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 and tertiary amines
under simulated atmospheric conditions. Primary amines have not been
investigated. If one accepts the lowest yields reported, nighttime concen-
trations 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.
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
formation of diethylnitrosamine from the tertiary amine, triethylamine, has
1-14
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been shown to prevail over photodecompositon 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 sunlight.
1.6 ATMOSPHERIC CONCENTRATIONS OF NOY AND OTHER NITROGENOUS COMPOUNDS
/\
1.6.1 Atmospheric Concentrations of N00
£
Examination of both historical data and of data for the years 1975 and
1976 enables some general conclusions to be drawn about the nationwide ex-
perience with respect to ambient N02 concentrations. In summary, the data
cited illustrate the following points.
o Annual average concentrations of NOp are not a reliable
index of short-term (3 hour or less) human exposure, and
vice versa.
o Although a distinct and fairly recurrent diurnal pattern
is discernible in some areas of the country, in many areas
peak diurnal values may occur almost any time of day.
o Just as there is no standard diurnal pattern nationwide for
peak N0£ concentrations, there is also no standard nation-
wide pattern for the month-by-month variations in monthly
averages of daily maximum 1-hour concentrations. Peak monthly
averages occur at different times of year in different locations.
o The direction and magnitude of recent trends in N0« concentra-
tions also tend to be area-specific.
1-15
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o The oxidation of NO to NOp 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 NOp
levels after photochemical activity has ceased. In other areas
photochemical reactions involving ambient hydrocarbons may
be the dominant mechanism.
Examination of selected nationwide monitoring data in 1975 reveals that
exposures to NOg concentrations of 1,000 yg/m (0.53 ppb) or greater for
1-hour duration, were experienced in Los Angeles, California. Peak 1-hour
o
exposures equalling or exceeding 750 yg/m (0.4 ppm) were reported also at
other sites in California; Ashland, Kentucky; Joliet, Illinois; and
Cincinnati, Ohio. Additional sites reporting at least one peak hourly N02
concentration equalling or exceeding 500 yg/m (0.27 ppm) include: Denver,
Colorado; Phoenix, Arizona; St. Louis, Missouri; New York City, New York; as
well as several more California sites. Other sites, distributed nationwide,
reported maxima close to this value. Recurrent N0« hourly concentrations in
o
excess of 250 yg/m (0.13 ppm) were quite common nationwide in 1975.
Selected nationwide monitoring data in 1976 show that hourly concentrations
equalling or exceeding 750 yg/m (0.4 ppm) were experienced in Anaheim,
California, and Port Huron, Michigan. Sites reporting 1-hour peak concen-
o
trations equalling or exceeding 500 yg/m (0.27 ppm) included 14 sites in
California; Springfield, Illinois; Ashland, Kentucky; Saginaw and South-
field, Michigan; Kansas City, Missouri; Buffalo, New York; and Cincinnati,
Ohio. Data for 1976 show that large segments of the population were quite
commonly exposed to recurrent N0« hourly concentrations in excess of 250
1-16
-------
o
yg/m (0.13 ppm).
The 1976 data also show that Long Beach, California; Indianapolis,
Indiana; and Salt Lake City, Utah, all experienced at least one day when the
24-hour average N02 concentration exceeded 300 yg/m (0.16 ppm). In addi-
tion, 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-hour period
where average N02 concentrations exceeded 150 yg/m (0.08 ppm).
Annual arithmetic means for N0~ concentrations in 1976 exceeded 100
o
pg/m (0.053 ppm) at Anaheim, El Cajon, Riverside, San Diego, and Temple
City, California. Other sites reporting yearly- arithmetic means for 1976
equalling or exceeding 100 yg/m (0.53 ppm) included Chicago, Illinois, and
Southfield, Michigan.
1.6.2 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 from 0.18 yg/m in Philadelphia,
Pennsylvania, to 2.1 yg/m at sites in Los Angeles. The data available
are not sufficient to place human exposure in nationwide perspective.
1.6.3 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
1-17
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32 yg/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.
1.7 NATURAL ECOSYSTEMS, VEGETATION AND MICROORGANISMAL STUDIES
Terrestrial, marine, and freshwater ecosystems are functionally impor-
tant to the integrity of the biosphere. They are important (1) in the
production of food, (2) in the maintenance of forests, (3) as global support
systems for the regeneration of essential nutrients and atmospheric components,
(4) for their aesthetic value in maintaining natural vegetative communities,
and (5) in the assimilation or destruction of many pollutants from the air,
water, and soil.
Many functions of natural ecosystems and their benefits to man are
unknown to the decision makers. Gosselink, Odum, and Pope have, for
example, placed a value on a tidal marsh by assigning monetary values to the
multiple contributions to man's welfare such as fish nurseries, food
suppliers, and waste-treatment function of the marsh. They estimate the
total social values to range from $50,000 to $80,000 per acre.
The relationship between the various components of an ecosystem is a
1-18
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structured rather than a haphazard one. The biotic components are linked
together by functional interdependence, while the abiotic components comprise
the totality of physical factors and chemical substances that interact with
the biotic units. The processes occurring within the biotic and abiotic
units and the interactions between them are subject to environmental influences,
Communities, because of the interactions of their populations and of the
individuals that comprise them, respond to stresses differently from
individuals. Man is an integral part of these communities and, as such, is
directly involved in the complex ecological interactions that occur within
the communities and within the ecosystem of which they are a part.
The stresses placed on the communities and the ecosystems in which
they exist can be far-reaching, inasmuch as the changes that occur may be
irreversible. Responses to stresses may include: (1) Reduction in
standing crop, (2) Inhibition of growth or reduction in productivity,
(3) Differential kill (removal of sensitive organisms at the species and
subspecies level), (4) Food chain disruption, (5) Successional setback,
and (6) Changes in nutrient cycling rates.
1.7.1 The Nitrogen Cycle
The major chemical species of nitrogen in the biosphere are interrelated
through a complicated series of reactions that collectively comprise the
"nitrogen cycle."
The circulation of nitrogen is a long term process with the turnover
times for atmospheric nitrogen estimated at 3 X 108 years, for nitrogen in
the seas 2,500 years and for nitrates and nitrites in the soil less than
one year.
Nitrogen is an essential element to all life. It is necessary in the
1-19
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formation of the cells of which all living matter is composed. The pro-
duction 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.
Man has intervened in the nitrogen cycle in the soil, air and aquatic
habitats. Nitrogen being in short supply as a plant nutrient in the soil
has lead to the addition of large amounts of nitrate fertilizers. The
inability of plants to assimulate these fertilizers in the large amounts
spread on the soil has lead them to be leached into streams, rivers, lakes,
ponds and down to the water table. The resulting high levels of nitrates
in the streams, lakes, and ponds has caused excessive plant and micro-
organismal growth and the eutrophication of these aquatic habitats.
1.7.2 Effects of NO^ on Vegetation
Sensitivity of plants to nitrogen oxides depends on a variety of
factors including species, time of day, stage of maturity, type of injury
examined, soil moisture, and the presence or absence of other air pollutants
such as sulfur dioxide and ozone.
When exposures to N02 alone in controlled studies are considered, the
concentrations producing measurable injury are above those ambient concen-
trations normally occurring in this country. Tomato plants exposed
continuously to 750 to 940 yg/m (0.4-0.5 ppm) for 45 days became etiolated
and suffered a decrease in yield of 22 percent. Leaf drop and reduced yield
o
occurred in orange trees exposed to 470 yg/m (0.25 ppm) continuously for 8
months. Pinto beans, endive and cotton exhibited slight leaf spotting after
48 hours of exposure to 1,880 yg/m (1.0 ppm). Growth depression in bush
o
bean was observed with a 14-day exposure to 1,880 yg/m (1.0 ppm). Other
1-20
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reports cited no injury in beans, tobacco, or petunia with a 2-hour exposure
to the same concentration.
3
Nitrogen dioxide concentrations ranging from 188 to 1,880 yg/m (0.1
to 1.0 ppm) increased chlorophyll content in pea seedlings from 5 to 10
o
percent. Some species of lichens exposed to 3,960 yg/m (2.0 ppm) for 6
hours showed a reduction in chlorophyll content. The significance of these
observations is, however, not clear at present.
A number of controlled studies on mixtures of N02 with sulfur dioxide
(SOg) show effects greater, in some cases much greater, than those effects
2
caused by the individual pollutants alone. Neither 3,960 yg/m (2.0 ppm)
o
N02 nor 1,300 yg/m (0.7 ppm) S02 alone caused injury in Bel W3 tobacco.
However, a combination of 190 yg/m3 (0.1 ppm) N02 and 270 yg/m3 (0.1 ppm)
S02 for 48 hours caused moderate leaf injury. Pinto bean, radish, soybean,
tomato, oat, and tobacco exhibited some leaf injury after a 4-hour exposure
to 280 yg/m3 (0.15 ppm) N02 in combination with 260 yg/m3 (0.1 ppm) S02.
3 o
Separate exposure to 3,960 yg/m (2.0 ppm) N02 and 1,300 yg/m (0.7 ppm) S02
caused no injury. Similar results were observed in green peas and Swiss
chard.
In one report, combinations of ozone and N02 were less injurious to
pepper and tomato than similar concentrations of either gas alone.
Another report cites some increased injury from combinations of
N02+S02+03 and S02+03 in radish, pepper, and tomato compared to exposure to
the individual pollutants. Doses ranged from 0.1 ppm to 0.6 ppm for 3 to 6
hours for each pollutant.
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1.8 GLOBAL EFFECTS
1.8.1 Perturbations of the Stratospheric Ozone Layer
Stratospheric ozone protects life at the earth's surface from poten-
tially harmful ultraviolet radiation from the sun. The main source of NO
r\
in the stratosphere is the oxidation of nitrous oxide (N20). 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 form 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 NgO, with most of the
rest returned to the atmosphere as Ng. Since NgO is not believed to take
part in any atmospheric chemical reactions below the stratosphere, all the
NpO produced terrestrially is available for stratospheric reactions. The
concern expressed by some authors in the recent past, that NgO arising from
excess fertilizer might decrease the total stratospheric ozone by as much as
20 percent for a 100 percent increase in total N£O, has recently been
reevaluated in the light of new information on rate constants for certain
stratospheric chemical reaction pathways. These new considerations point to
the likelihood of a much smaller dependence of total stratospheric ozone on
NpO abundance.
Ozone is also an important gas for the heat budget of the atmosphere.
An effective lowering of the "center of gravity" of the ozone layer, which
would be the result of NO additions to the stratosphere, may have
A
significant climatic implications. Nitrous oxide likewise contributes to
the atmospheric "greenhouse" effect by trapping outgoing terrestrial
1-22
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radiation. One author recently estimated that a doubling of the atmospheric
burden of NgO could increase surface temperatures by as much as 0.7°C.
However, 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 definitive conclusions can prudently be drawn.
1.8.2 Acidic Precipitation
Long term measurements in Northern Europe, especially Scandinavia,
indicate that the pH of precipitation is becoming more acidic. Recent
measurements in the Northeastern U.S. and in California indicate the same
trend is occurring there. The main causes of the increased acidity are
increases in anthropogenic emissions of nitrogen and sulfur oxides over
the last several decades.
The effects of the increasing acidity of precipitation on aquatic
ecosystems in eastern North America and Scandinavia have already been
well documented. The lakes in these areas are extremely vulnerable to
additions of acidic precipitation because they are usually soft water lakes
with a low buffering capacity.
Many changes, most of which involve decreases in biological activity
and important changes in nutrient cycling, result from the acidification
of freshwater ecosystems. Increased accumulations of organic matter
results from decreased decomposer activity. Phytoplankton and zooplankton,
bottom fauna and several other groups of invertebrates decrease in numbers
of species when the pH drops below six, thus affecting the variety of food
available for fish and other animals that depend on aquatic ecosystems.
1-23
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Fish populations are seriously affected by pH's less than 5.5. The
elimination of fish is often a result of chronic reproductive failure in
acid conditions and damage done to the newly hatched larvae and other
sensitive stages. Fishery yields do not indicate such an insidious process
until extinction is imminent. There is strong evidence that the main
cause of extensive losses of salmonid fish stocks as well as other popula-
tions of economic importance both in Scandinavia, the northeastern part
of the United States and parts of southwestern Canada is the increased
acidity of precipitation.
The effects of acidic precipitation on terrestrial ecosystems have
not been as well documented; however, field and laboratory studies suggest
that the following vegetational effects could occur.
Direct Effects:
(1) Damage to protective surface structures such as cuticle.
(2) Interference with guard cell function (potential disruption
of gaseous exchange processes).
(3) Poisoning of plant cells after diffusion through stomata or cuticle.
(4) Disturbance of normal metabolism without tissue necrosis.
(5) Alteration of leaf- and root-exudation processes.
(6) Interference with reproductive processes.
(7) Synergistic interaction with other environmental stress factors.
Indirect Effects:
(1) Accelerated leaching of substances from foliar organs.
(2) Increased susceptibility to drought or other stress factors.
(3) Alteration of symbiotic associations.
(4) Alteration of host-parasite interactions.
1-24
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Other effects include increased leaching of minerals from the soil,
decreased soil respiration (an index of microbial activity) and upset of
ni trogen mi neral i zati on.
1.9 EFFECTS ON MATERIALS OF N0v AND NO -DERIVED POLLUTANTS
X X
The annual economic cost to the nation of dye fading on textiles due to
NOX was estimated at $122.1 million in 1973. The bases for this estimate
includes not only reduced wear life of textiles of moderate fastness to
NO but also the added cost of remedial measures by textile manufacturers in
3\
the use of more expensive dyes, dyeing processes, research and quality
control. Although the average consumer is not aware that air pollutants as
well as light are responsible for fading colors, textile manufacturers are
informed of potential deficiencies which could lead to severe color changes
in warehouses and on retail shelves which make goods unsaleable, with
resulting economic losses.
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 N02, 03, and SOg. The exposures were
carried out in ambient air and protected against sunlight. Chamber studies
using individual pollutants N02, 03, and S0« have shown that some individual
dye-fiber combinations exhibit color fading only to N09 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 ng/m3 (0.5 ppm) N02 under high humidity (90 percent) and high temperature
1-25
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_ A
(90 F) conditions. Significant fading is observed on exposures to 94 yg/m
(0.05 ppm) N02 under high humidity conditions.
Acid dyes on nylon fade on exposure to N0« at levels as low as 188
o
yg/m (0.1 ppm), especially under high humidity conditions. Dyed polyester
fabrics are highly resistant to N02-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 where fabrics were finished with
softeners or anti-static agents. Nitrogen dioxide was demonstrated to be
the pollutant responsible for color change, with 03 and S02 showing no
o
effect. Chamber studies using N02 concentrations of 376 yg/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 (-NHL) of nylon to the degree that the
fiber has less affinity for acid-type dyes. Nylon 66 may suffer chain
o
scission when exposed to 1,880 to 9,400 yg/m (1.0 to 5.0 ppm) N02. Field
exposures of fibers emphasize the action of acids derived from S02, although
N02 may also be present in high concentrations on exposure 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
1-26
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billion pounds in 1982, there is essentially no information on the effects
of N02 on polyethylene, polypropylene, polystyrene, polyvinyl chloride,
polyacrylonitrile, polyamides and polyurethanes. Ageing tests involve
sunlight exposure as well as exposure to ambient air. Chamber exposures of
the above plastics to the combinations of SCLt NCL, and (L has shown deteriora-
o
tion. At concentrations of 1,880 to 9,400 yg/m (1.0 to 5.0 ppm) N02 alone
has caused chain scission for nylon and polyurethane.
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 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.
1.10 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 manifest not only in visible smoke plumes, but also in large-scale, hazy
air masses. In regions of good visibility, such as the southwestern United
States, haze and smoke plumes can result in the deterioration and loss of
scenic vistas. In other areas, reduced visual range due to haze and plumes
may impede air and surface traffic. It has long been known that N02 is
responsible for a significant portion of the brownish coloration observed in
1-27
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polluted air.
The most significant optical effect of NO^ involved discoloration due
to wavelength-dependent absorption. Traversal by natural light of as little
as 1 kilometer of air containing 188 yg/m3 (0.1 ppm) N02 is sufficient to
produce a distinguishable color shift in carefully controlled colormatching
tests. Under usual ambient viewing conditions, a pale color would be
produced in a white target with a 1 kilometer pathlength at a concentration
of 940 yg/m (0.5 ppm) N02. Similar effects would be produced for similar
values of pathlength x concentration.
A common feature of pollutant haze is its disagreeable brown color. At
a visual range of 100 kilometers, typical of the rural southwestern United
States, 38 yg/m (0.02 ppm) NOp would suffice to color the horizon noticeably.
At a visual range of 10 kilometers, typical of urban haze, 380 yg/m (0.2
ppm) N02 would produce the same effect. Brown plumes may be distinguishable
for tens of kilometers downwind of their source.
Independently of wavelength-dependent absorption of light by NOp^
wavelength-dependent scattering by small particles resulting from atmo-
spheric transformation of NOg can also produce a noticeable brown coloration
in air masses. This effect depends upon the line-of-sight of the observer
with respect to the sun and is most apparent to an observer with the sun
at his back.
Particulate nitrates may also impair the visual range. Estimates of
the magnitude of this impairment, however, are made difficult by recently
discovered inaccuracies in the measured atmospheric loadings of suspended
3
nitrates. If it is assumed that nitrate concentrations up to 4 yg/m are
typical of an urban haze with 10 km visibility, then one would conclude that
1-28
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up to 8 percent of the total extinction is due to suspended particulate
nitrates.
1.11 STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS
The biological effects of nitrogen oxides have been examined in a
number of animal species. Thus far, the most toxic among these is N02. A
summary of the biological effects resulting from short-duration exposures
to 1,880 ug/m3 (1.0 ppm) or less is shown in Table 1-1.
Short Term Exposure
Inhaled N02 is taken up rapidly and distributed throughout the lung as
shown by radiotracer studies. A large fraction of N02 is retained in the
lung, probably representing the fraction that has reacted chemically with
pulmonary tissue. While N02 is the probable chemical species producing
lesions of the pulmonary lumen, nitrous, nitric, and perhaps nitric oxide
(NO) may be formed in the liquids overlying the epithelium. Due to the
rapidity of reaction, N02 is not likely to attain a measurable concen-
tration within the blood, as shown by _in vitro experiments. Effects on
organs distal to the lung are likely to result from products formed in the
lung and circulated to other parts of the body. Direct proof of this
hypothesis has not been found.
Cellular injury and death following initial exposure of the lung to
N02 occurs during a period of less than 24 hours. The magnitude and site
of injury depend, in part, upon the concentration of N02 inhaled as well as
the solubility of N02 in water. At concentrations of N02 usually found in
1-29
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urban environments, the region of the terminal and respiratory bronchioles
and adjacent alveoli is most affected. Higher concentrations (above 9,400
ug/m ; 5.0 ppm) may affect segments of the upper airways as well and
penetrate deeper into the alveoli. Type I pneumocytes and Clara cells may
be sloughed off and replaced by cells less sensitive to NOp. The bio-
chemical, physiological, and morphological alterations due to NOp are a
consequence of this injury.
Changes in cell permeability have been reported at concentrations as
3
low as 752 ug/m (0.4 ppm) N02. Pulmonary macrophages are damaged in turn.
Often the biochemical parameters of injury return to normal or near normal
values within 1 to 2 weeks after cessation of exposure.
The infectivity model has proven to be a particularly sensitive
indicator of pulmonary injury. Mortality of mice from exposure to
infectious agents is influenced more in proportion to the concentration of
NOp than to the duration of exposure. These responses are consistent with
a temporal sequence of injury which suggests that pulmonary damage occurs
rapidly upon exposure but that effects, as shown in Figures 12-3, 12-4, and
12-5, may be observed later. Results of infectivity experiments are
measured in terms of mortality in excess of that observed in contrls
exposed to infectious agents but not NOp. Low NOp concentrations (e.g.,
1,880 M9/M ; 1-0 ppm) may result in only a small excess mortality on a
single exposure of 3 hours; high concentrations (47,000 ug/m ; 25 ppm) may
1-30
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Initiate other mechanisms such as edema, which may complicate interpre-
tation of the excess mortality observed.
Long-Term Exposure
The sequence of events upon continuous exposure is similar to that
seen with short-term exposure. During the first 14 days of exposure, cell
death and replacement of pulmonary cells are the dominant features. These
and all other indicators of N02 exposure are dose dependent.
Some enzymes indicative of cellular injury have been found in elevated
o
amounts in the serum of animals exposed to 940 ug/m (0.5 ppm) N02 during
the injurious phase (greater than 7 days). Susceptibility to infection
rises almost linearly during this period. Even though excess mortality is
o
very little at concentrations in the range of 940 to 2,820 ug/m (0.5 to 1.5
ppm) NOp, it is statistically and biologically significant.
The development of an emphysema-like disease in the experimental
animal requires considerable time. Morphological alterations are apparent
in rats exposed continuously to 3,760 ug/m (2.0 ppm) N02 or greater.
The influence of dietary control upon the fatty acid composition of
lung membranes and the reduction in mortality by diet supplementation with
vitamin E (high N0« exposures) support the hypothesis that membrane damage
by chemical oxidation of unsaturated fatty acids is a major mechanism of
toxicity by N0«.
The question of tolerance or resistance and recovery upon continuous
exposure to N0« remains unresolved. Tolerant cells may be more resistant
1-31
-------
to N0? because they are younger or as a result of the Induction of pro-
tective mechanisms. Elevated levels of lung enzymes have been observed in
the rat; induction did not appear to occur in the guinea pig upon exposure
to 940 pg/m (0.5 ppm) for 4 months. Direct MQy exposure of cultured lung
cells coated with a <0.1 mm layer of nutrients was toxic; this supports the
idea that all cells are relatively sensitive to N02.
While N02 stimulates a rapid turnover of cells and transient hyper-
pi asi a of certain cells may be seen, no evidence has been found for an
enhanced rate of tumor formation or malignant metaplasia. Such hyperplasia
represents part of the natural repair mechanism.
Intermittent exposures of mice to 2,820 pg/m (1.5 ppm) NOp eventually
become equivalent to continuous exposure when the infectivity model is
used. Because considerable differences occur in the response to NOp
between animal species and the infectious agents used, extension of such
data to man is difficult. Difficulties in extrapolation also derive from
the differences in anatomical structure of the lung and differences in
native and acquired immunity. The infectivity model, however, may be
viewed as a general indicator of sensitivity.
In summary, the lowest dose at which either biochemical changes or
reduction in resistance to infectivity can be detected in experimental
animals is 940 ug/m3 (0.5 ppm) N02 for 4 hours or more. While the temporal
sequence of N02 toxicity in man is unknown, it is likely to be similar to
that found in animals because cells must be renewed. A delay between
1-32
-------
exposure and effect, as well as additive effects of repeated short-term
exposures, may also occur in man.
Toxicity of Other Oxides of Nitrogen
Of great concern is nitric oxide or NO. To date, NO has been found to
be much less toxic than NOp, but it may have important biochemical effects
which are expressed through the changes in the intracellular concentration
of cyclic nucleotides (cyclic GMP). Because of the potential effects of
such hormonal changes, continued observation and cognizance of the potential
of toxicity of NO to man is highly important.
Another area of potential toxicity may be the formation of nitroso
compounds, because nitrosamides and nitrosamines are suspected carcinogens.
Nitrosamines and nitrosamides have recently come into the public view
through their formation in foodstuffs containing nitrites. At the moment,
there is no evidence that nitrosamines or nitrosamides are formed in
ambient air from n trogen oxides; nor has it been demonstrated that they
are formed jn vivo in the lungs from the inhalation of nitrogen dioxide.
Similarly, the role of inhaled nitrates found in atmospheric particles is
unknown and should be studied further. A few experiments indicate that
inhaled nitrate produces 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.
1-33
-------
1.12 EFFECTS ON HUMANS
Critical human health effect issues include consideration of (1) the
lowest level at which a single exposure will cause adverse health effects,
(2) the lowest levels at which repeated or intermittent exposures may
produce adverse health effects, and (3) the lowest long term mean levels
associated with the occurrence of adverse health effects.
Of the oxides of nitrogen, NOg is the compound of greatest concern. A
number of controlled exposure studies of the effects of N0« provide some
information on the effects of single, short-term exposures (Table 1-2).
Very few human studies provide information on the effects of repeated
controlled exposures, and for this reason heavy reliance must be placed on
animal studies. Although animal data cannot be extrapolated to humans
directly, they do demonstrate mechanisms that might be operative in humans
as well. Since it is very difficult to undertake studies of the effects on
humans of long-term repeated or intermittent exposures in a clinical setting,
it is necessary to review carefully for evidence of long-term or short-term
exposure concentrations the very few community studies that have reported
evidence of adverse human health effects (Table 1-2).
1.12.1 Controlled Exposure Studies
The most frequently observed effects of NOg exposure in controlled
-•%
human studies (usually at concentrations higher than ambient) include
increases in airway resistance (R.,,) and changes in susceptibility to the
aw
effects of bronchoconstricting agents. The functional response of human
subjects to N02 is 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 laryngo-trachsobronchial system. Airway
1-34
-------
narrowing, or bronchoconstriction, increases flow resistance and reduces
maximal expiratory flow rate.
Is is difficult to assess the biological significance of the reduction
in airway diameter associated with a single exposure of the human experi-
mental subject to Nt^. In attempting the assessment, one should consider
the magnitude, persistence, and site of change within the airways, as well
as the degree to which change is perceived by the subjects, and associated
symptoms, and whether the response is typical of the individual. To date
there has been almost no systematic attempt to measure the functional
response of individuals to repeated N02 exposures. Secondary effects of
brochoconstriction can add to the biological significance of the functional
alteration. One such possible secondary effect is the interference with
alveolar-capillary gas exchange (measured as an increase in alveolar-
arterial Pn gradient, or as a reduction in arterial Pn or oxyhemoglobin
U2 °2
saturation). The relation, if any, between bronchoconstriction associated
with a single exposure to N02 and possible development of chronic res-
piratory disease during prolonged or intermittent exposure, is unknown. It
is unlikely, however, that the slight increase in airway resistance which
occurs after a single exposure represents a significant adverse health
effect for healthy persons.
An assessment of the importance of studies showing associations between
exposure to NOg and increased airway resistance must consider also the known
wide variations in susceptibility within human populations. Thus, an
exposure sufficient to produce increased airway resistance in healthy
individuals, or in those with some symptoms of chronic respiratory illness,
may indeed produce much greater and more severe responses in highly
1-35
-------
susceptible segments of the population. Studies to date are inadequate for
determining the effects in the more susceptible groups.
Monitoring a subject's response to a bronchoconstrictor is a sensitive
experimental approach that utilizes (1) the action of hormones (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 may be used to predict the individual's level of
risk when exposed to ambient pollutants. However, it is known that increases
in bronchial sensitivity 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 N02 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 bronchonconstrietors are
aW
both suggestive of 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 expo-
sures to N02 levels at or below those associated with significant increases
in RflW can increase susceptibility to respiratory infections.
For purposes of this review, the intensity of the response in test in-
1-36
-------
dividuals has been given little consideration in assessing potential health
risk. This approach was taken because the intent, usually, was to
determine the lowest N00 concentration that would cause any increase in R.lf
c. aW
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.
Controlled exposure studies have demonstrated increases in airway
resistance in both healthy and selected susceptible groups of the population
resulting from single, short-term exposures, often for 1 hour or less, to
N02 concentrations greater than 2,800 pg/m (1.5 ppm). Effective exposure
concentrations, however, have been higher than those usually found in ambient
situations. The controlled human studies demonstrate the types of effects
that can be produced by single, short-term exposures, but it is difficult to
determine the significance of such study results for populations exposed to
ambient conditions. This is due primarily to the fact that there is currently
no adequate methodology to extrapolate results from a single exposure at a
high concentration to predict effects of multiple intermittent exposures or
to combinations of air pollutants experienced in ambient situations.
Controlled studies are hampered also by the inability to reproduce ambient
exposure conditions, including multiple pollutants, in a controlled
exposure environment.
Study results show that pulmonary function in some healthy subjects
was impaired, as evidenced by increased airway resistance resulting from a
o
5-minute exposure to 5,600 yg/m (3.0 ppm) N02. This impairment was approx-
imately doubled when a sodium chloride aerosol of average particle size
0.95 pro was added to the exposure atmosphere. Another study demonstrated
increased retention of particulate matter in the lung during exposure to
1-37
-------
9,000 ug/m3 (4.8 ppm) N02 as well. At higher concentrations of N02 [9,400
ug/m3 (5.0 ppm) and vabove], exposures of 1 hour or less have been reported
to cause a variety of pulmonary effects including decreases in arterialized
oxygen partial pressure, increased differences between the alveolar and
arterialized oxygen partial pressure and decrease in the diffusion capacity
of the lung for carbon monoxide. These same studies showed no increase in
airway resistance as a result of short-term exposure to N02 at concentrations
3
of 2,800 ug/m (1.5 ppm) or less. Additional studies have reported that
effects on neither pulmonary function nor other measured cardiovascular
factors nor metabolic factors were produced by a 2-hour exposure to 1,160
3 3
ug/m (0.6 ppm) N02 or by a 4-hour exposure to 560 ug/m (0.3 ppm) N02
combined with either 500 ug/m (0.24 ppm) 0* or the same concentration of
0, plus 45,900 ug/m (30 ppm) CO. Study results at N02 concentrations of
2,800 ug/m (1.5 ppm) or lower were negative even when subjects underwent a
period of exercise to increase the total quantity of N02 to which the
airways were exposed.
Bronchitic subjects exposed for less than 1 hour to N02 at concentra-
g
tions of 3,000 to 3,800 ug/m (1.6 to 2.0 ppm) exhibited increased airway
resistance. No significant changes in Rau, were observed in this supposedly
On
o
more sensitive group at concentrations of 2,800 ug/m (1.5 ppm) or less;
considerably higher concentrations were necessary to produce evidence of an
impaired rate of transport of oxygen to arterial blood. In subjects with
symptoms of bronchitis, 15 minutes of exposure to N02 concentrations ranging
o
from 7,500 to 9,400 ug/m (4.0 to 5.0 ppm) were associated with decreases
in the 02 partial pressure in arterialized blood.
Increased sensitivity to the effects of bronchial constricting agents
1-38
-------
(carbachol or acetylcholine) caused by inhalation of NCL at very low levels
has been suggested by the results of certain studies. These studies, which
reported increased sensitivity to the bronchoconstrictors resulting from
exposure for 1 hour to concentrations of N02 as low as 190 yg/m3 (0.1 ppm), do
suggest that asthmatics may represent a group particularly sensitive to the
effects of NOp. However, replication of these studies is necessary.
1.12.2 Community Exposure Studies
Community exposure studies can provide indications of the effects of
ambient pollutant mixtures containing significant concentrations of NOg.
Nevertheless, very few definitive data are available from community studies
due to a lack of means to measure or estimate actual human exposure.
Interpretations of data are impeded also by the knowledge that any effects
observed are produced by a complex, constantly changing combination of
pollutants. However, small but significant decreases in pulmonary function
in children, and increases in the incidence of acute respiratory infections,
were observed after continuous exposure in a area of higher NOp concentra-
tions but in which there were also significant concentrations of other air
pollutants. Consequently, based on the results of these studies, the
indicated health impairments cannot be attributed solely to either the
average N0« nor to the short-term peak NOg concentrations to which the
population was exposed.
A study of children (6 to 11 years of age) in England and Scotland
reported increased illness rates in those living in homes with gas stoves,
compared with children from homes with electric stoves. Data collected for
this study were adjusted for a variety of demographic and climatic factors,
1-39
-------
but not for tobacco smoking. Consequently, although increased illness rates
may have been associated with gas stoves, the potential deleterious concentra-
tions in these homes may have resulted from the combination of the pollutants
produced by a gas stove and that produced by parental smoking. The concen-
trations of N02 occurring in the homes of the children studied were not
monitored. However, other studies in the United States and Great Britain
have monitored maximum N02 concentrations ranging from 470 to 940 yg/m3
(0.25 to 0.5 ppm) in kitchens in which gas stoves were being used. Reports
of these monitoring studies also do not indicate that homes of smokers were
excluded. Therefore, the concentrations monitored may have been the
combined result of burning gas from stoves and parental smoking.
A similar study conducted in a middle class suburban area of the
United States found no increase in respiratory illness associated with gas
stoves. This study did include monitoring for N02 but no considerations of
the smoking habits of the inhabitants are reported. Maximum concentrations
of N02 in the homes were approximately 8 times higher than the 24-hour
mean and sometimes exceeded 1,800 yg/m (1.0 ppm). It can be speculated
that the divergence of results between the British and the American studies
may be related to differing social customs that increase exposure in British
homes; it 1s possible, however, that factors not considered in the study
may have caused the increased illness rates among the British children.
A number of investigators have failed to find an association between
long-term mean ambient N02 exposure and the prevalence of chronic respira-
tory disease in adults. Long term N02 concentrations, however, have been
found to be associated with mortality, various cancers, and arterio-
sclerotic heart disease. The studies are not consistent in their findings,
1-40
-------
however; one even showed a significant negative correlation between N02
and mortality. In addition, the quality of data available for such long-
term studies is such that the results must be viewed with some skepticism
until they can be substantiated by additional research.
1.12.3 Accidential and Occupational Exposures
Very high rates of exposure of N02 that have occurred accidentally or
in occupational settings have demonstrated that concentrations in the range
o
of 560,000 ug/m (300 ppm) or higher are likely to result rapidly in death.
•o
Concentrations in the range of 280,000 to 380,000 vg/m (150-200 ppm) are
not likely to cause immediate death, but severe respiratory distress and
death may occur after a period of 2 to 3 weeks. In such cases the cause is
always bronchiolitis fibrosa obliterans. Exposures to 94,000 to 190,000
3
ug/m (50 to 100 ppm) N02 are associated with reversible bronchiolitis and
3
exposures to 47,000 to 140,000 yg/m (25 to 75 ppm) are associated with
bronchitis or bronchial pheumonia and usually complete recovery. The data
also indicate that following recovery there probably are no residual effects
of the exposure.
1.12.4 Effects of NO -Derived Compounds
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^™^ —^—^^
Nitrate poisoning (i.e., the formation of sufficient methaemoglobia to
produce cyanosis) occurs not infrequently in the United States, most often
in children. It is not believed, however, that the inhalation of atmos-
pheric 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.
1-41
-------
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 concen-
trations were associated with increases in asthma attacks. A laboratory
study, however, indicated that short-term exposure to sodium nitrate at
concentrations 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 peroxyacetyl 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 and reference
is therefore made to this document for further information.
There is no evidence, to date, that nitrogenous atmospheric pollutants
contribute to the in vivo formation of nitrosamines or that nitrosamines
inhaled from the ambient air represent significant health hazards.
1.13 CONCLUSIONS
Conclusions from the review of available data are as follows:
A. Single exposures for times ranging from 15 minutes to 2 hours to
N0£ concentrations of 2,800 yg/m (1.5 ppm) or below have not been shown
to affect respiratory function in healthy individuals or in those with
symptoms of bronchitis.
B. Single exposures for 15 minutes to NOp concentrations of 3,000
2
yg/m (1.6 ppm) are likely to increase airway resistance in individuals
with chronic bronchitis but not to interfere with the transport of gases
between the blood and the lungs. In healthy individuals, exposure to con-
centrations of 4,700 yg/m (2.5 ppm) N02 for 2 hours have been reported
1-42
-------
to increase airway resistance without altering arterialized oxygen pressure.
Asthmatics may represent a particularly sensitive group which is affected
by much lower concentrations but currently available data are inconclusive.
C. At concentrations of 9,400 yg/m (5.0 ppm) or above, exposure to
N0« for as little as 15 minutes will both increase airway resistance in
healthy humans and impair the normal transport of gases between the blood
and the lungs.
D. Animal studies demonstrate several mechanisms for producing damage
that might be important to humans. Of particular interest in this regard
is the animal infectivity model, which indicates that repeated, short-term
exposures increase susceptibility to respiratory infection as much as do
continuous exposures to the same concentrations.
E. Data from one community study show that the incidence of respira-
tory illness was found to be greater in an area of high N0« concentrations.
The increases, however, cannot be attributed conclusively to the long-
or short-term concentration of NOg, since other pollutants also were
present.
F. Studies of the effects of indoor pollution show that, in some
instances, an increased incidence of respiratory illness was associated
with the use of gas stoves and possibly with the NO,, produced by these
appliances.
6. Estimates of the short-term peak concentrations of N0« possibly
associated with increases in respiratory illness in communities, or of
the peak N0« concentrations associated with increased respiratory illness
in homes with gas stoves, fall in the general range of the intermittent
exposure concentrations causing increased susceptibility to respiratory
1-43
-------
infection in the animal infectivity model (940 yg/m ; 0.5 ppm).
H. No additional data are available relative to safe long-term
mean exposure concentrations, that were not available in 1971 when the
initial Air Quality Criteria for Oxides of Nitrogen was published.
I. There is no evidence, to date, that nitrogenpus atmospheric
pollutants contribute to the in vivo formation of nitrosamines or that
nitrosamines inhaled from the ambient air represent significant health
hazards.
J. Atmospheric nitrates may act as respiratory irritants at concen-
trations in excess of 8 yg/m3, and at such concentrations may cause increases
in asthma. Present ambient concentration data, however, are too sparse to
place estimated human exposure in nationwide perspective.
K. Ambient concentrations of N02, reported as recently as 1975 and
1976, may cause damage and/or injury to white fabrics and certain dyed
acetate-cotton and rayon fibers.
L. Ambient concentrations of N02, reported as recently as 1975 and
1976, may cause noticeable atmospheric discoloration in both rural and
urban areas.
M. Ambient concentrations of N02 (in combination with S02), reported
as recently as 1975 and 1976, may cause some leaf damage to pinto bean,
radish, soybean, tomato, oat, tobacco, green pea and Swiss chard.
N. The long term effects of acidic precipitation on aquatic and
terrestrial ecosystems are wide spread, regionally and globally. A number
of the direct effects reported include tissue damage and physiological
impairment in plants, lethal effects on fish, and possible impacts on host-
parasite or pathogenic processes.
1-44
-------
I
-p«
en
1 clul c 1-JL. 3uru1nRl UT Ub
EXPOSURES TO
*
Topic Species
Respiratory Monkey
Tract Trans-
port and
Absorption
Interaction Mouse, female
with Infec- Swiss albino
tious Agents
Mouse
Lung Bio- Guinea Pig
chemistry
Lung Mouse
Morphology
Rabbit
Monkey
SERvtUlFrELlS ur ANiMACS TJf bHU^HTOKKI iUrt
N02 CONCENTRATIONS OF 1 PPM OR LESS
N02
Concentration
yg/m3
560 to
1,710
940
1,880
750
750
940
940
470
5,640
ppm
0.3 to
0.9
0.5
1.0
0.4
0.4
0.5
0.5
0.25
3.0
(continued)
Effect
Exposure to trace amounts of 1JN02 in the presence
of unlabeled N0« demonstrated that N0« was evenly
distributed in the lungs and absorbed into the blood.
Increased mortality after 6 mo intermittent exposure,
6 hr/day, and subsequent exposure to K. pneumom'ae.
Increased mortality following a single 3-hr exposure
to N02 and subsequent exposure to S. pyogenes.
Acid phosphatase increased after 4 hr/day exposure
for 1 wk.
Increase in uptake of labeled protein by the lung;
most likely due to plasma leakage. Some may result
from cell death. Proteinuria noted. Exposure for
4 hr/day, 8 to 10 days.
Increase in serum LDH, CPK, SGOT, SGT and cholin-
esterase, lung and plasma lysozyme. Decrease in RBC
GSH peroxidase. Lung GSH peroxidase unchanged.
Exposure for 8 hr/day, 1 wk.
Alveolar damage. Exposure for 6 hr/day up to 12 mo.
Isolated swollen collagen fibers after exposure
4 hr/day, 5 days/wk, 24 or 36 days.
Thickening of alveolar wall and basal lamina. Inter-
stitial collagen. Exposure for 4 hr/day, 4 days.
-------
Table 1-1. (continued)
-p.
cr>
N02
Concentration
*
Topic
Hyperplasia
Mutagenesls,
Teratogenesis
Lung
Edema
Hematologlcal
Changes
Central Ner-
vous System
and Behavioral
Effects
Species
Mouse, C3H
male
Guinea P1g
Guinea P1g
Guinea P1g
vg/m3
190
1,880
750
940 +
1,000
so2
1,000
ppm
0.1
1.0
0.4
0.5 +
0.39
so2
0.53
Effect
No mutagenlc effects observed. No Increase 1n chomatld
or chromosome- type alterations in leukocytes or pri-
mary spermatocytes 2 wk post-exposure. Exposure for
6 hr.
Increased serum proteins 1n lavage of exposed animals
detected by disc gel electrophoresis. Exposure for
4 hr/day, 1 wk.
Increased WBC, decreased RBC, decreased neutrophils
and eosinophils, increased lymphocytes. Exposure
for 8 hr/day, 10 days.
Various changes in enzyme levels after 8 hr/day, 180
days exposure.
*Topics correspond to table headings in Chapter 12.
-------
Table 1-2. EFFECTS ON HUMANS AND ANIMALS OF EXPOSURES TO NO,
NO.
Concentrations
Human Studies
vg/m
ppm
Community Studies
Controlled
Exposure Studies
Animal Studies*
NO, Measurement Method
5,600
3.0
5 mln exposure produced 19%
Increase 1n R that rose to
41% when NaClaT0.95 pm) was
added to the atmosphere.
Nakamura, 1964 (Section
13.1.2.1, Reference 9))
Saltzman, 1954
3,760
2.0
A single 3 hr exposure
caused Increased mor-
tality following chal-
lenge with an Infectious
agent. Ehrllch et al.,
1977 (Section 12.2.3
Reference 2")
Chemlluminescence
3,000
1.6
Exposure for 15 mln caused
significant Increases 1n
R In patients with chronic
bronchitis, von Nledlng'and
Krekeler, 1971 (Section
13.1.2.2, Reference 24)
Saltzman**
2,800
1.5
No Increase In R 1n healthy
Individuals or 1H patients
with chronic bronchitis pro-
duced by exposure for 15 mln.
von Nledlng and Krekeler,
1971 (Section 13.1.2.2,
Reference 24)
After 1 wk continuous
exposure, mice had a
significantly greater
Increase In suscepti-
bility to Infectious
pulmonary disease com-
pared to Intermittent
exposure.
Saltzman procedure
used 1n human studies.
Saltzman and Cheml-
lumlnescence proce-
dures used In animal
studies.**
(continued)
-------
Table 1-2 (continued)
NO-
Concentrations
3
Human Studies
Community Studies
Controlled
Exposure Studies
Animal Studies
Measurement Method
After 2 wk, no differ-
ences between continu-
ous and Intermittent
exposure modes occurred.
Gardner et al. (1n
press) (Section 12.2.3
Reference 27)
1,880
1.0
Healthy subjects exposed
for 2 hr showed no signif-
icant change In pulmonary
function. Hackney, 1978
(Section 13.1.2.,
Reference 16)
Saltzman**
Chemlluminescence
188 &
dally
2 hr
spike
1,880
0.1 con-
tinuous ft
dally 2 hr
spike
1.0
Emphysematous altera-
tions 1n mice after 6
mo exposure. Port et
al., 1977 (Section
12.2.3 , Reference112)
Saltzman**
1,150
0.6
Exposure for 2 hr caused no
significant change 1n pul-
monary, cardiovascular, or
metabolic factors measured.
Follnsbee et al., 1978
(Section 13.1.2.1,
Reference 15)
Saltzman**
Chemlluminescence
-------
Table 1-2 (continued)
N0n
Concentrations
itg/m ppm
940 0.5
Human Studies
Community Studies
Controlled
Exposure Studies
Animal Studies
In mice challenged with
N00 Measurement Method
Sal tzman**
bacteria, there was In-
creased mortality follow-
ing a 90-day continuous
exposure or a 180 day In-
termittent exposure.
Ehrllch and Henry, 1968
(Section 12.2.3
Reference 28)
940
940
VD
0.5
0.5
A 7-day Intermittent ex-
posure caused enzymatic
alterations In lungs and
blood. Donovan et al.,
1976 (Section 12.2.3
Reference 82)
Intermittent exposure for
6 hr/day for up to 12 mo
caused morphological
changes. Blair et al.,
1969 (Section 12.2.3
Reference 109)
Saltzman**
470
to
940
0.25
to
0.5
This range of concentration
of NO- has been shown to
occur regularly 1n the vi-
cinity of gas stoves during
meal preparation. Highest
recorded value was 1,880
pg/nr (1.0 ppm). A study
of children living In
NO, not measured by
Mefla et al.
Cheml1um1nescence
method used by Wade
et al.
(continued)
-------
Table 1-2 (continued)
NO-
Concentrations
Human Studies
JJEOL
Community Studies
Controlled
Exposure Studies
Animal Studies
NO,, Measurement Method
homes 1n which gas stoves
were used showed higher
rates of respiratory symp-
toms and disease when com-
pared to children living
1n homes In which electric
stoves were used.
Mella et al., 1977, 1978; Wade
et al., 1975 (Section
14.2.2.2, References 53-55)
560
0.3
i
ui
o
Exposure for 4 hr caused
no alteration 1n pulmonary
function 1n addition to,
that caused by 500 v9/m
0, 1n healthy and suscep-
tfble Individuals.-
Hackney et al., 1975
(Section 13.1.2.1,
Reference 22)
Saltzman**
Cheirri luminescence
190
0.1
Exposure for 1 hr reported
to cause Increased R 1n
some asthmatics, who were
also exposed to a broncho-
constrictor which Induces
Increased susceptibility
to N0?. Statistical treatment
of data raises questions as
to validity of results.
Orehek et al., 1976 (Section
13.1.2.2, Reference 26)
Saltzman**
Single exposures for 3 hr or less at an NO- concentration of 940 gg/m (0.5 ppm) or less have usually failed to demonstrate positive effects
1n animals.
**
Saltzman, 1954 (Chapter 4, Reference 11 ).
-------
CHAPTER 2
INTRODUCTION
Nitrogen and oxygen are normal constituents of the air we breathe.
Together they comprise well over 90 percent of the earth's atmosphere.
Both nitrogen and oxygen are essential to life as we know it. In mo-
lecular, atmospheric form, 02 is vital to the respiration of all life forms
except the anaerobes, while Ng is essentially inert in all but the nitrogen
fixing organisms. However, when through the action of natural or man-
made processes the two elements combine, some very toxic compounds can be
formed. This air quality criteria document compiles into a single source
document information relevant to the formation and occurrence of such
atmospheric toxins and evidence of their effects on man and the biosphere.
The initial Air Quality Criteria for Nitrogen Oxides (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, an arithmetic average
not to exceed 100 ug/m3 (0.05 ppm). At the time insufficient information
was available to support promulgation of a short-term standard. Because
the establishment of the annual standard does not preclude short-term
excursions of N02 concentrations to levels which may be harmful, the Congress,
in the 1977 amendments to the Clean Air Act, explicitly required that the
air quality criteria document for nitrogen oxides be revised to include
any new evidence that might indicate whether or not a short-term NO
/%
standard is warranted.
N02 and NO are the principal subjects of this document, however, the
health and welfare effects of other nitrogen compounds such as nitrogen
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acids, nitrates, nitrites, and nitrosamines are also presented since
current knowledge of atmospheric chemistry indicates that they may be
derived from or interact with nitrogen oxides. Also included are. descrip-
tions of the complex chemical reactions occurring in polluted atmospheres
that link, to some extent, the atmospheric burdens of the nitrogen oxides
with photochemical oxidants. These latter relationships have been discussed
in greater detail in the Air Quality Criteria for Ozone and Other Photo-
chemical Oxidants, EPA-600/8-78-004.
Nitrogen oxides (NOX) are produced when fossil fuels are burned, both
as direct products of combustion and by the high-temperature oxidation of
atmospheric nitrogen, usually to nitric oxide (NO). Nitric oxide may be
further oxidized, within the combustion process or in the atmosphere, to a
variety of nitrogen oxides. Of these, N02 is the compound of most concern.
The quantities of fossil fuels burned determine the quantities of NO
emitted into the atmosphere and the amount of N02 produced. Increases in
energy production are expected to continue at a rate which will require
construction of additional and larger facilities, many of which will be
fired with coal. Thus, the anticipated trend is toward increases in
nitrogen oxide emissions.
Considerable information has been developed since publication of the
original Air Quality Criteria for Nitrogen Oxides in 1971. Information
demonstrating the toxic nature 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 have been pursued to demon-
strate relationships between exposure to N02 and various aspects of
pulmonary function, particularly those types of physiological or patho-
2-2
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logical changes that may lead to the development of chronic respiratory
disease. Other studies have been concerned with susceptibility to acute
respiratory disease. The effects of nitrogen compounds on plants or
inanimate materials have also been reported.
Although studies to date have indicated that NO,, is the compound of
most concern, other nitrogen compounds, as mentioned above, may be equally
important with respect to their potential for producing harmful effects.
Because nitrogen oxides are precursors of many of these substances, infor-
mation pertaining to the health effects associated with exposure to NOg-
derived compounds has been included here.
Efforts to determine the effect of exposure to airborne nitrogen
compounds on human health have been impeded by four major difficulties.
The first is that nitrogen compounds comprise only a portion of a complex
of pollutants in the ambient air. Adverse effects may result from exposure
to individual compounds, to multiple compounds, or to the products of
atmospheric interactions between certain compounds. Epidemologists,
evaluating community studies, have not been able to assess the effects of
exposure to individual compounds and consequently, it has been necessary
to rely to a great extent on animal studies to infer potential harmful
effects. Animal studies have been used in an effort to show the effects of
exposure to individual compounds and the relative effects of the compounds
in combination. These studies can 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 the
consistency of effects across a variety of animal species.
The second problem is the inability to assess, with a high degree of
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accuracy, the actual day-to-day exposure profile of individuals in ambient
situations. Since practical considerations limit the amount of monitoring
possible, air measurement data rarely are truly representative of actual,
detailed, individual human exposure. Even when this is the purpose of the
air measurements, the mobility of the population and the portion of each
day spent inside buildings, together with the known variability of air
concentrations of pollutants over short distances, make the measurements
little more than possible indices of actual exposure. They do indicate,
however, with a high degree of probability, that at least some individuals
were exposed at some time to the measured ambient levels. Of course, the
shorter the time period considered, the greater is the chance that the
monitoring is representative of actual human exposure.
The third problem encountered in determining the effect of exposure
to nitrogen compounds is that animal data cannot readily be extrapolated to
humans, particularly with respect to explicit dose-response relationships.
Indications of probable effects 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.
Nevertheless, human studies are necessary to confirm that the suspected
effects are indeed produced.
The fourth problem is the determination of effective exposure time.
Community studies usually provide data on annual or daily mean levels of
exposure. Only occasionally are hourly values provided. Repeated inter-
mittent exposure to daily peak values, however, is quite possibly more
significant in the production of adverse health effects than is an
equivalent or even greater total dose delivered by continuous exposure to
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the observed long-term mean levels. For this reason, the protection of
health might be addressed more effectively by reducing the peak concentra-
tions rather than the long-term means. The subject of effective control
strategies, however, is outside the scope of this document.
Publication of this criteria document has only one purpose: fn response
to the 1977 Clean Air Act Amendments, to provide regulatory officials with
the best possible summarization of available data relevant to the effect
on human health and welfare of exposures to nitrogen oxides or other toxic
materials evolving from nitrogen oxides in the atmosphere.
To this end, 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 of origin, (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
pollution on visibility, ecologic systems, plants, and materials and (6)
the relationship of atmospheric nitrogenous compounds to global phenomena
such as acidic precipitation and perturbations of the stratospheric ozone
layer.
It is not intended that this publication represent a detailed
literature review of the subjects covered. For this reason, not every
published manuscript is cited; however, those major publications relevant
to the topics covered are included.
As in all similar endeavors, a cutoff time for literature review has
been necessary. Consequently, material published after mid-1978 could not
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be Included. In reviewing and summarizing the literature, an attempt has
been made to present both positive and negative data when both have been
available. In some instances, questions concerning the quality of studies
have been included, but the needs for subsequent studies have not, for the
most part, been addressed.
Chapter 1 summarizes all of the data reviewed in detail in Chapter 3
through 13 and in addition addresses risk assessment through interpretation
of study results.
As is appropriate in a criteria document, the discussion is descriptive
of the range of exposure and the attendant effects. The information is
presented, and the evidence is evaluated, but not judgements are made con-
cerning the maximum levels of exposure that should be permitted. Such
judgements would constitute recommendations concerning air quality stan-
dards and management, which are prescriptive in nature and not within the
purview of this effort.
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CHAPTER 3
GENERAL CHEMICAL AND PHYSICAL PROPERTIES OF NOV
AND NO -DERIVED POLLUTANTS x
A
3.1 INTRODUCTION AND OVERVIEW
In this chapter some general chemical and physical properties of NO
/\
and NO -derived pollutants are discussed by way of introduction to the
A
complex chemical and physical interactions 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 that may be present in the ambient
air: nitric oxide (NO), nitrogen dioxide (N02), nitrous oxide (N^O),
unsymmetrical nitrogen trioxide (OONO), symmetrical nitrogen trioxide
(ON(O)O), dinitrogen trioxide (N203), dinitrogen tetroxide (N^), and
dinitrogen pentoxide (N205).
Of these, NO and N02 are generally considered the most important in
the lower troposphere because they may be present in significant concen-
trations. Their interconvertibility in photochemical smog reactions has
frequently resulted in their being grouped together under the designation
NO , although analytic techniques can distinguish clearly between them. Of
y\
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 N20 is not generally considered to be an air pollutant, it parti-
cipates in upper atmospheric reactions involving the ozone layer.
While OONO, ON(0)0, N203, N204, and N205 may play a role in atmos-
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pheric 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 (NHJ is generated, on a global scale, during the decomposi-
tion of nitrogenous matter in natural ecosystems and it may also be pro-
duced locally in larger concentrations by human activities such as the
maintenance of dense animal populations. It is discussed briefly in this
document to facilitate understanding of the nitrogen cycle and also because
some researchers have suggested that NH^ is converted to NOX in the atmospher
Other NO -derived compounds which may be found in polluted air include
A
nitrites, nitrates, nitrogen acids, N-nitroso compounds, and organic
compounds such as the peroxyacyl nitrates (RCfOjOONOg. where R represents
any one of a large variety of possible organic groups).
The peroxyacyl nitrates, of which peroxyacetyl nitrate (CH^COJOOM^,
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 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 com-
ponent of particulate matter in the respirable size range, suspended in
ambient air. Some of this particulate nitrate is produced in atmospheric
reactions. Nitrates may also occur in significant concentrations in
drinking water supplies but this occurrence is not believed to be the
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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 (HN03). This atmospheric production of nitric acid may be an
important component of acid rain.
Table 3-1 summarizes current theoretical estimates of the concentrations
of the various nitrogen oxides and acids that would be present in an equili-
brium 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
i-n 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.
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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). It has an
uneven number of valence electrons, but, unlike N02$ 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
2
a set of reactions known as the extended Zeldovitch mechanism:
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 N2 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
3 : ' '' ' '
sensitive. Moreover, the production of atomic oxygen required for the
,-*•••. ! - - ' -- - "
first step is also highly temperative sensitive. NO formed via this
mechanism is often referred to as "thermal NO ."
;-.'- ..'j''-**.-
In addition to the strong temperature dependence of the rate of the
first step of the Zeldovich mechanism, the temperature also influences the
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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.
The reaction kinetics of thermal NO formation is further complicated
by the fact that certain hydrocarbon radicals can be effective in splitting
4
the N2 bond through reactions such as:
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
5
the Ng bond and, in turn, can be responsible for significant NO formation.
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.
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 quantitatively to NOX,
it would account for about 2,000 ppm NO in the exhaust of a coal-fired
'. X
unit. In practice, only a portion of these nitrogen compounds are converted
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to NO , with the remainder being converted to molecular nitrogen (N2).
Tests designed to determine the percent of the NO emissions due to oxida-
A
tion of bound nitrogen show that upward of 80 percent of the N0x 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
7-9
have been cited, but the degree of conversion to NO does not seem to be
A
significantly affected by the compound type. NO conversions arising from
A
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 N2, whereas under fuel-lean conditions significant amounts of
NOX 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 con-
centrations at high temperatures in combustion processes would revert to
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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 N02 near concentrations characteristic of the
high temperature phase of the process.
A major implication of the fact that NO emissions are defined by the
A
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
A
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 tempera-
ture, 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 are flue gas recirculation,
reduced load, reduced combustion air preheat temperature, water injection
and reduced excess air. '
In furnaces fired with coal or heavy oil, the major portion of the NO,,
emissions is from fuel-bound nitrogen conversion. Thus, combustion modifi-
cations which reduce the availability of oxygen when the nitrogen compounds
are evolved will reduce the NO produced. Examples of such modifications
J\
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.
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3.2.2 Nitrogen Dioxide
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 prevents condensation. Nitrogen dioxide is corrosive
and highly oxidizing. It has an uneven number of valence electrons and
forms the dimer N204 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 N02 present in combustion exhaust gases. About 5 to 10
percent by volume of the total emissions of NO from combustion sources is
n
in the form of N02, although substantial variations from one source to
another have been observes. Under more dilute ambient conditions, photo-
chemical 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 wavelengths. 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,
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lower troposphere.
3.2.3 Nitrous Oxide (M)
Nitrous oxide is a colorless gas with a slight odor at high concen-
trations. Nitrous oxide in the atmosphere arises as one product of the
reduction of nitrate by a ubiquitous group of bacteria that use nitrate as
12 1S
their terminal electron acceptor in the absence of oxygen (denitrification).
Although N20 does not play a significant role in atmospheric reactions
in the lower troposphere, it participates in a mechanism for ozone decom-
position in the stratosphere.
Nitrous oxide transported to the stratosphere undergoes photolysis by
absorbing ultraviolet (UV) radiation at wavelengths below 300 nm to produce
N« and singlet oxygen:
N20 + 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:
A
NO + 03 -> N02 + 02
03 + hv -*• 02 + 0
N02 + 0 •*• NO + 02
These reactions are of concern because of the possibility that increased
N20 resulting from denitrification of excess fertilizer may lead to a
3-9
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17 18
decrease of stratospheric ozone ' with consequent potential for adverse
human health effects.
3.2.4 Unsymmetrical Nitrogen Trioxide (OONQ)
Unsymmetrical nitrogen trioxide is thought to be an intermediate in
the reaction of NO with (L:
NO + 02 + 0-0-N-O
0-0-N-O + NO -> 2N02
There is, however, no direct evidence for the existence of this
species. If it does exist, it is, nevertheless, of little importance in the
chemistry of polluted atmospheres, since the N0/02 reaction accounts for
very little of the NO oxidized.
3.2.5. Symmetrical Nitrogen Trioxide (NOJ
Symmetrical nitrogen trioxide has been identified in laboratory
systems containing N02/03, N02/0, and N20g as an important reactive
19
transient. It is likely to be present in photochemical smog. This
compound can be formed as follows:
03 + N02 + N03 + 02
0 + N02 (+ M) -> N03 (+ M)
N205 (+ M) + N03 + N02 (+ M)
(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 H. 2N02
N03 + N02 (+ M) -». N20 (+ M)
3-10
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Its expected concentration in polluted air is very low (about 10
yg/m or 10 ppm).
3.2.6 Pi nitrogen Trioxide (NpOo) (Also Known as Nitrogen Sesquioxide)
In the atmosphere, N203 is in equilibrium with NO and N02 according to
the following equation:
NO + N02 j N203
The equilibrium concentrations at typical urban levels of NO and N02 range
from about 10"4 yg/m3 (^10~7 ppm) to 10"6 yg/m3 (^10~9 ppm) (Table 3-4).
N203 is the anhydride of nitrous acid and reacts with liquid water to form
the acid:
N203 + H20 -*• 2HONO
3.2.7 Pi nitrogen Tetroxide (N^) (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 equili-
brium:
2N02 + N204
Table 3-4 presents theoretical predictions of concentrations of N203 and
NgO. in equilibrium with various NO and NOp 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 + N09 -»• HNO, where -OH is a hydroxyl free radical
fc v
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
3-11
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the acid, producing particulate nitrates (Chapter 6).
The nitrate ion (NOI) 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 bio-
chemical 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.
The nitrite ion is the Lewis base of the weak acid, nitrous acid
(HN02). When NO and N02 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 ami no acids (the Van Slyke reactions) to yield N2< The reaction
of nitrous acid with secondary amines to form N-nitrosamines is discussed
in Section 3.5.
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3.4 AMMONIA (NH3)
Ammonia is a colorless gas with a pungent odor. It is extremely
soluble in water, forming the ammonium (NH4+) and hydroxy (OH") ions. In
20
the atmosphere, ammonia has been reported to be converted into oxides of
nitrogen when it reacts with hydroxyl free radicals («OH). Burns and Hardy21
report that ammonia is oxidized into nitrates and nitrites in the atmosphere,
and in geothermal wells. In the stratosphere, ammonia can be dissociated
99
by irradiation with sunlight at wavelengths 230 nm.
3.5 N-NITROSO COMPOUNDS
Organic nitroso compounds contain a nitroso group (-N=0) attached to a
23
nitrogen or carbon atom. According to Magee, N-nitroso compounds generally
can be divided into two groups—one group includes the dialkyl, alkylaryl,
and diary! nitrosamines, and the other, alky! 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, NOZ,
NOZ, halogen, tetrafluoroborate, hydrogen sulfate or OFL . The equilibrium
reaction of nitrosonium ion (ON ), nitrous acid and nitrite ion:
ON* + OH" + HN02 j H+ + NO" -
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 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
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HNCL molecules. The formation of nitrosamines is dependent on pH of the
amine.
Nitroso compounds are characteristically photosensitive and the
nitroso group is split by UV radiation. Gaseous nitrosamines may be
denitrosated by visible light. The electron absorption spectra of several
25
nitrosamines are given in the literature; the characteristic spectra show
a low intensity absorption maximum around 360 ym and an intense band around
235 urn. Nitrosamines show three relatively intense bands in the infrared
region of 7.1-7.4, 7.6-8.6, and 9.15-9.55 ym. Nuclear magnetic resonance
(NMR), infrared (IR), ultraviolet (UV), and mass spectrometry (MS) spectra
26
have been reviewed by Magee et al.
Atmospheric reactions involving nitrosamines are discussed in Chapter 6.
3-14
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3.5 REFERENCES FOR CHAPTER 3
1. U. S. Environmental Protection Agency. Air Quality Criteria for
Ozone and Other Photochemical Oxidants. EPA-600/8-78-004. U. S.
Environmental Protection Agency, Office of Research and Develop-
ment, Washington, D.C., April 1978.
2. Zeldovich, Y. B. Acta Physiochem. URSS. 21: 577, 1946.
3. Bowman, Craig Thomas. Kinetics of nitric acid formation in com-
bustion processes. In: Fourteenth Symposium (International) on
Combustion. The Combustion Institute. 1973. p. 729.
4. Fenimore, C. P. Formation of nitric oxide in premixed hydrocarbon
flames. In: Thirteenth Symposium (International) on Combustion.
The Combustion Institute. 1971.
5. 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. Environ-
mental Protection Agency, 1976.
6. Pershing, D. W., and J. 0. L. Wendt. Pulverized coal combustion:
the influence of flame temperature and coal composition on thermal
and fuel NO . Sixteenth Symposium (International) on Combustion.
The Combustton Institute, 1976. p. 389.
7. Martin, G. B., D. W. Pershing and E. E. Berkau. Effects of fuel
additives on air pollutant emissions from distillate oil-fired
furnaces. Publ. No. AP-87; NTIS No. PB 213-630. U. S. Environ-
mental Protection Agency, Research Triangle Park, North Carolina,
1971. 82 pp.
8. Turner, D. W., and C. W. Siegmund. Staged combustion and flue gas
recycle: potential for minimizing NO from fuel oil combustion.
Exxon Research and Engineering Company^ Paper presented at the
First American Flame Days. Chicago, Illinois. September 5-7,
1972. 8 pp.
9. Axworthy, A. E., and M. Schuman. Investigation of the mechanism
and chemistry of fuel nitrogen to nitrogen oxides in combustion.
Rocket-Dyne Corp. Paper presented at the Pulverized Coal Com-
bustion Seminar, Research Triangle Park, North Carolina. June
1973. pp. 9-43.
10. Proceedings of the Second Stationary Source Combustion Symposium.
EPA-600/7-77-073 (a-e). U. S. Environmental Protection Agency,
Research Triangle Park, North Carolina, 1977.
11. Proceedings of the First Stationary Source Combustion Symposium.
EPA-600/2-76-150 (a, b, c). U. S. Environmental Protection Agency,
Research Triangle Park, North Carolina, 1976.
3-15
-------
12. Kenney, D. R. The nitrogen cycle in sediment water systems. J.
Environ. Quality 2: 15-29, 1973.
13. Delwiche, C. C. The nitrogen cycle. Scientific American 223(3):
137-146, 1970.
14. Brezonik, P. L. Nitrogen: sources and tranformation in natural
waters. In: Nutrients in Natural Waters. H. E. Allen and J. R.
Kramer, eds. Wiley-Interscience, New York, 1972.
15. Focht, D., and W. Verstraete. Biochemical ecology of nitrification
and dem'trification. Ann. Rev. Microbial Ecol. (In press).
16. Johnston, H. S,. and 6. Selwyn. New cross sections for the absorp-
tion of near ultraviolet radiation by nitrous oxide (N90). Geophys.
Res. Lett. 2: 549-551, 1975. L
17. Crutzen, P. J. Upper limits on atmospheric ozone reductions follow-
ing increased application of fixed nitrogen to the soil. Geophys.
Res. Lett. 3.(3): 169-172, 1976.
18. Council for Agricultural Science and Technology (CAST). Effect of
increased nitrogen fixation on stratospheric ozone. Report No. 53.
January 1976. 33 pp.
19. Johnston, H. S. Experimental chemical kinetics. In; Gas Phase
Reaction Rate Theory. Ronald Press, New York, 1966. pp. 14-35.
20. Soderlund, R., and B. H. Svensson. The global nitrogen cycle. In:
Nitrogen, Phosphorus, and Sulfur - Global Cycles. SCOPE Report No.
7. B. H. Svensson and R. Soderlund, eds. Ecol. Bull. (Stockholm)
22: 23-73, 1976.
21. Burns, R. C., and R. W. F. Hardy. Nitrogen Fixation in Bacteria
and Higher Plants. Springer-Verlag, Berlin-Heidelberg, Berlin.
J.Z7/D*
22. McConnell, J. C. Atmospheric ammonia. J. Geophys. Res. 78: 7812-
7820, 1973. —
23. Magee, P. N. Toxicity of nitrosamines: their possible human
health hazards. Fd. Cosmetic Toxicol. _9: 207-218, 1971.
24. Mirvish, S. S. Kinetics of dimethylamine nitrosation in relation
to nitrosamine carcinogenesis. J. Nat. Cancer Inst. 44: 633-639,
1970. —
25. Rao, C. N. R., and K. R. Bhaskar. Chapter 3. In: The Chemistry
of the Nitro and Nitroso Groups. Part 1. H. Feuer, ed. Inter-
science, New York, 1969.
26. Magee, P. N., R. Montesano, and R. Preussman. Chapter 11. In:
Chemical Carcinogens. C. E. Searle, ed. American Chemical Society,
Washington, D.C., 1976.
3-16
-------
27. Demerjian, K. L., J. A. Kerr, and J. G. Calvert. The mechanism of
photochemical smog formation. Adv. Environ. Sci. Techno!. 4: 1-
262, 1974.
28. Matheson of Canada, Ltd. Matheson Gas Data Book. Fourth edition.
Whitby, Ontario, 1966. 500 pp.
29. The Chemical Rubber Company. Handbook of Chemistry and Physics.
Fiftieth edition. R. C. Weast, ed. Cleveland, Ohio, 1969-1970.
30. U. S. Department of Commerce, National Bureau of Standards. OANAF
Thermochemical Tables. Second edition. NBS 37. U. S. Government
Printing Office, Washington, D.C., 1971. 1141 pp.
31. Nitrogen Oxides. National Research Council, National Academy of
Sciences. Washington, D.C. 1977.
32. McNesby, J. R., and H. Okabe. Vacuum ultraviolet photochemistry.
Adv. Photochem. 3: 157-240. 1964.
3-17
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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
27
Concentrations In Hypothetical Atmosphere, ppm
Compound At Equilibrium
In Typical Sunlight-irradv
ated, Smoggy Atmosphere
°2
N.
H20
N02
NO
N03
liO»* -5
2 3
N90.
2 4
l*f\\Jr
2 5
HONO (cis)
HONO (trans)
HON02
2.06 x IO5
7.69 x IO5
A
1.56 x 1(T
-4
1.91 x 10 *
2.69 x IO"10
3.88 x IO"16
2.96 x 10"20
2.48 x 10"13
3.16 x IO"17
7.02 x IO"9
1.60 x 10"8
1.33 x 10"3
2.06 x IO5
7.69 x IO5
A
1.56 x HT
i
10"
io-1
io-8-io-9
10"8-10"9
10"7-10"8
io'3-io-5
io-3
io-3
io"2-io-3
theoretical estimates made using computer simulations of the chemical
reactions rates in a synthetic smog mixture.
3-18
-------
Table 3-2. SOME PHYSICAL AND THERMODYNAMIC PROPERTIES OF THE NITROGEN OXIDES
co
UD
Molecular
Weight,
Oxide g/mol
NO 30.01
N02 46.01
N204 92.02
N20 44.02
N203 76.02
N205 108.01
Melting Boiling Solubility in
Point Point H20(0°C), cm3
oca,b oca,b (STP)/100 ga
-163.6 -151.7 7.34
Liquid, solid Reacts with HpO
forms largely forming HONO, and
associated as HONO
-11.3 21.2 Reacts with H?0
forming HON09 and
HONO L
-102.4 -89.5 130.52
-102 3.5 Reacts with H20
(decomposes) forming HONO
30 32.4 Reacts with H20
(decomposes) forming HON02
Themodynamic Functions
Gas, 1 atm, 25°C)C
Enthalpy of
Formation,kcal/mol
21.58
7.91
2.17
19.61
19.80
2.7
(Ideal
Entropy,
cal/mol-deg
50.347
57.34
72.72
52.55.
73.91
82.8
a po
Matheson Gas Data Book
Handbook of Chemistry and Physics
CJANAF Thermochemical Tables30
-------
Table 3-3 THEORETICAL EQUILIBRIUM CONCENTRATIONS OF
NITRIC OXIDE AND NITROGEN DIOXIDE IN AIR
(50 PERCENT RELATIVE HUMIDITY) AT VARIOUS
TEMPERATURES31
—
Concentration, mg/m (ppm)
Temperature, °K (°C) NO N02
298 (24.85) 3.29 x ID'}!!3.53 x 10'J
(2.63 x 10'1U) (1.88 x 10"4)
500 (226.85) 8.18 x 10'J 7.26 x 10'f
(6.54 x 10"^) (3.86 x 10'2)
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)
3-20
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Table 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°C31
Concentration, ppm
NO N02 N203 N204
0.05 0.05 1.3 x 10"9 1.7 x 10"8
0.10 0.10 5.2 x 10"9 6.8 x 10"8
0.50 0.50 1.3 x 10"7 1.7 x 10"6
1.00 1.00 5.2 x 10"7 6.8 x 10"6
3-21
-------
6 50
40
111
5 30
UJ
O
o
g
i-
o.
cc
o
20
10
A i
1500 1700 1900 2100
WAVELENGTH. A
2300
Figure 3-1. Absorption Spectrum of Nitric
32
Oxide. From McNesby and Okabe.
3-22
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CHAPTER 4
SAMPLING AND ANALYSIS FOR AMBIENT
NO AND NO -DERIVED POLLUTANTS
J\ /\
4.1 INTRODUCTION
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 NOp. In addition, concern about the potential adverse human health
implications of ambient concentrations of other NO -derived compounds such
A
as suspended nitrates, nitric acid, and the 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 U. S. Environmental Protection Agency (USEPA)
published the following brief summary of these difficulties on June 8, 1973
when it withdrew the method:
" 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 collection
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 efficiency prob-
lem cannot be resolved, this method can no longer serve
as the reference method."
After extensive testing, the continuous chemiluminescence method
was declared the new Federal Reference Method as of December 1, 1976.
In addition, several other methods, notably the Lyshkow-modified Griess-
Saltzman method, the instrumental colorimetric Griess-Saltzman method,
4-1
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the triethanolamine method, the sodium arsenite method, and the TGS-ANSA
method have also been extensively tested and are in current use for mea-
surement of ambient NCL 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 (Federal
Reference Method) for the purpose of establishing compliance status with
respect to the NAAQS for NO .
A
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 artifact formation has been shown to be associated
with conversion of ambient N02 and/or nitric acid (HN03) to nitrates, data
from certain background sites may be validated where it can be shown that
N02 and HNO^ concentrations 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 deve-
loping 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
4-2
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recently made possible the observation of nitric acid in ambient air.
However, the technique is presently too elaborate 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 particulate
matter drawn from the ambient air and (2) it is believed appropriate to
make some 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.
4.2 ANALYTICAL METHODS FOR NO
J\
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 Federal Reference Method, the continuous chemiluminescence method.
The method is specific for NO but may easily be modified for measurement of
N02 by first quantitatively reducing the N02 to NO. The regulatory
specifications relating to the Federal Reference Method (FRM) are pre-
scribed in Title 40 of the Code of Federal Regulations, Part 50, Appendix
F.
4.2.1 The Federal Reference Method for NO.,: Gas-Phase Chemi luminescence
———• • — £
Atmospheric concentrations are measure4 indirectly in the FRM by first
4-3
-------
reducing the N02 quantitatively to NO, then reacting the resultant NO with
0, and measuring the light intensity from the reaction.
0
The use of the gas-phase chemiluminescent reaction of NO and 03 for
2
quantitative measurement of NO was reported initially by Fontijn et a!.,
3
and some improvements were described by Stedman et al. The sample air
stream is mixed with air containing a high 03 concentration (approximately
1 percent). The reaction of NO and 03 forms excited N02 molecules, the
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. The reaction chamber
is held at reduced pressures to decrease the collisional deactivation, and
the emitted radiation is measured with a photomultiplier tube and asso-
ciated electronics. To reduce interferences of the chemi luminescent
reactions of ozone with other species, optical filters can be employed.
Typical commercial chemi luminescence instruments can detect concentrations
as low as 9.5 yg/m (0.005 ppm).
Since the detection of N02 by the FRM 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 concen-
trations.
Catalytic reduction of N02 to NO is commonly employed in chemi lu-
minescence NO-NOX instruments. These instruments measure NO alone by
passing the sample directly to the detector. The total concentration of NO
and N02 (N0x) is measured by drawing the sample through a catalytic re-
duction unit prior to entering the detector. N0£ concentrations are
obtained by subtraction.
4-4
-------
Winer et al. studied the reactions of various nitrogen compounds over
carbon and molybdenum converters. It was found that not only NCL but PAN
and a wide variety of organic nitrogen compounds were reduced to NO
quantitatively; nitroethane and nitric acid were partially reduced. Joshi
o
and Bufalini 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 by FeSO. converters, however
this technique has not been thoroughly evaluated. There is also evidence
that converters operating at high temperatures may oxidize amnonia (NH3) to
NO. This can be of importance in measuring N02 exposures in animal
studies, where elevated levels of NH3 may be present as a result of
biologic processes.
While care must be exercised in the use of chemiluminescence instru-
ments because of potential interferences, in most ambient situations NO
plus NOp are present in much higher concentrations than interfering species.
Results of the USEPA's collaborative quality assurance testing of the
Q
method showed that, for 1-hour instrumental averaging times for N0«
concentrations ranging from 50 to 300 yg/m (0.027 to 0.16 ppm), the
method has an average negative bias of 5 percent with a standard deviation
of about 14 percent for equivalent samples measured by different laboratories,
The method is satisfactory for averaging times of 1 hour or more.
4.2.2 Other Analytical Methods for N00
1 ~ _.-.-.- !____ _.. ~£
4.2.2.1 Griess-Saltzman Method--
This chemical method for collection and analysis of N02 was originally
4-5
-------
proposed by Ilosvay. Many variations of this method exist.
The principle of the reaction is thought to be the formation of
nitrous acid by the reaction of N02 with water. This in turn is reacted
with an aromatic amine to form a diazonium salt. In a further step,
addition of an organic coupling agent forms a deeply-colored azo dye. The
amount of N02 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 is one of the most widely used. This
method has been designated as a Tentative Method by the Intersociety
12
Committee on Methods for Ambient Air Sampling and Analysis, and was
adopted as a standard method by the American Society for Testing and
13
Materials. It has been shown that many different reagent formulations
are possible so long as they all contain a diazotizer, a coupler, a buffer,
14
and a surfactant.
If an extended sampling time is required, the azo dye may suffer
bleaching by S02. Saltzman recommended addition of acetone to prevent
this. In addition, if the sample is collected in an evacuated bottle or
syringe, a long waiting period may cause some NO to be oxidized to NOp.
Since the conversion of N02 to azo dye is not quantitative, a factor
is introduced to represent the conversion efficiency under a given set of
experimental conditions. This is often termed the "stoichiometric factor."
If the experimental conditions are the same as Saltzman's original formu-
lation or his modified version, the stoichiometric factor has been
shown to be 0.72.11'15'17 Scaringelli et al.18 obtained a value .of 0.764.
When fritted bubblers are employed, the method has been reported
o
to have a usable range of 10 to 9,400 yg/m (0.005 to 5.0 ppm). A
4-6
-------
precision of 1 percent of the mean concentration is obtainable.12
19
The Saltzman procedure has recently been evaluated by EPA. The
results show that static calibration (with colored nitrite solutions) is
not uniformly reliable, due to variable collection efficiency of the
absorption system. Dynamic calibration procedures by means of a reliable
N02 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 is a negative
20
interferent in the method. Two specific variants of the method are
currently in widespread use for ambient air monitoring. Although both are
continuous colorimetric techniques suitable for averaging times of 1 hour
or more, they differ in the use of two distinct absorbing solutions, in
which azo dyes are formed. The first 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. The second, sometimes known
as the instrumental colorimetric Griess-Saltzman method, uses a modi-
fication of the originally proposed reagent for manual analysis and
contains 0.5 percent sulfanilic acid, 5.0 percent acetic acid, and 0.005
percent NEDA. Both variants are useful in the range of ambient
concentrations from 19 to 9,400 yg/m (0.01 to 5.0 ppm). Results of the
USEPA's quality assurance testing indicate a maximum negative bias of 15
percent with a 12 percent standard deviation among different laboratories
21
testing equivalent samples.
4-7
-------
4.2.2.2 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 epi-
demiological studies.
22
The method was developed by Jacobs and Hochheiser to avoid the
bleaching of the azo dye by S0« 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 S02 is oxidized with
hydrogen peroxide. The nitrite in solution is not affected. The solution
may then be stored up to 48 hours before analysis. To quantitate the
nitrite in solution, the solution is first acidified with phosphoric acid.
An azotizer 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,
yt OA
was employed by the National Air Sampling Network (NASN) ' and was
adopted as the Federal Reference Method in 1971.
?6
The National Academy of Sciences document on nitrogen oxides 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-container material, incoming pollutant
concentration, and contaminants present in the sample. Sampling efficienciesi
in the work reviewed, ranged from 15 to 78 percent when 0.1N NaOH alone was
4-8
-------
used as an absorbant. In addition to the varying efficiency with which NCL
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
23 24 27-29
the presence of hydrogen donors. ' ' A composite of 11 sites sampled
23
in the NASN network gave an average stoicismetric factor of 62 +_ 7 percent.
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 yg/m3 (0.01 to 0.4 ppm) N02.6 Katz6
reported relative standard deviations of 14.4 and 21.5 percent at N02
o
concentrations of 140 and 200 yg/m (0.07 and 0.11 ppm), respectively.
Because the sampling efficiency and stoichiometric factor are signi-
ficantly affected by the details of the method employed and constituents of
the sample other than N02, 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.
4.2.2.3 Triethanolamine Method—
30
The method described by Levaggi et al. 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 of 95 to 99
12 30
percent have been reported. * The USEPA has recently evaluated the
31
method under somewhat different conditions. For those conditions, the
results indicate the collection efficiency to be constant, at approximately
80 percent, over the range of 20 to 700 yg/m (0.01 to 0.37 ppm) if glass
frits are used. If restricted orifices, which are less fragile and cheaper
4-9
-------
than glass frits, are used, the collection efficiency falls to about 50
percent. For this reason, the USEPA did not subject the method to quality
assurance testing. No interference is expected from SOg, 0^, or NO at
ambient levels and the sample solutions are stable for 3 weeks after
sampling. The accuracy is considered to be comparable to that of the
Gri ess-Sal tzman method6 with bias errors less than 2 percent at a
stoichiometric factor of 0.764.18 This method is presently considered to
be a 24-hour method.
4.2.2.4 Sodium-Arsenite Method—
The use of an alkaline solution of sodium arsenite (NaAsO) to
27 32
absorb N02 was described by Christie et al. and Merryman et al.
Christie et al. reported a collection efficiency of 95 percent using an
orifice bubbler. The USEPA recently has evaluated the sodium-arsenite
33
procedure and has designated it an equivalent method as of December 14,
1977. The method is presently considered to be a 24-hour method. The
results showed that the procedure has a constant collection efficiency for
N0« of 82 percent over the recommended useful concentration range, 20 to
750 yg/m3 (0.01 to 0.4 ppm). Results of the USEPA's collaborative quality
assurance testing of the method indicate a negative bias of 3 percent with
o
an interlaboratory standard deviation of 11 ug/m independent of concentra-
tion.21
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, NO in the air sample can produce a positive interference
by increasing the N02 response in the sample by 5 to 15 percent of the N02
4-10
-------
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 6 weeks. Recently, the USEPA also has conducted an evaluation
of potential NO and CXL interferences. Results show that, in the range
50 to 310 yg/m3 (0.04 to 0.25 ppm) NO and 360,000 to 900,000 yg/m3 (200 to
500 ppm) C02, the average effect of these interferents is to increase the
3 3
indicated N02 response by only 10 yg/m over the range 50 to 250 yg/m N02
(0.03 to 0.13 ppm).
4.2.2.5 TGS-ANSA Method—
A 24-hour manual method for the detection and analysis of NOp in
ambient air, the TGS-ANSA method was first reported by Mulik et al.35 It
has been designated an equivalent method to the FRM as of December 14,
1977. Ambient air is bubbled, via a restricted orifice, through a solution
containing triethanolamine, o-methoxyphenol, and sodium metabisulfite. The
N02 gas in the ambient sample is converted to nitrite ion (NOI) 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
30
provide a basic collecting medium. The addition of o-methoxyphenol
raises the collection efficiency to 93 percent when using a restricted
29
orifice. 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 NOp is constant at concentrations
between 20 and 700 yg/m (0.01 and 0.37 ppm), which is the range of the
4-11
-------
method with 50 ml of absorbing reagent and a sampling rate of 200 cm /min
for 24 hours. No interferences were reported at an NOp^ concentration of
100 yg/m3 (0.05 ppm) for the following pollutants at the levels shown in
parentheses: ammonia (205 yg/m3 or 0.29 ppm); CO (154,000 yg/m3 or 134
•3 O
ppm); formaldehyde (750 yg/m or 0.61 ppm); NO (734 yg/m or 0.59 ppm);
phenol (150 yg/m3 or 0.04 ppm); 03 (400 yg/m3 or 0.2 ppm); and S02 (439
yg/m or 0.15 ppm). The absorbing reagent is stable for 3 weeks before
sampling and the collected samples are stable for 3 weeks after sampl-
35,36
ing.
37
Results of USEPA's collaborative quality assurance testing indicate
o
a lower detectable limit < 15 yg/m (0.008 ppm), an average bias of 9.5
3 3
yg/m (0.005 ppm) over the range of 50-300 yg/m (0.03 to 0.16 ppm), and an
Inter!aboratory standard deviation of 8.8 yg/m (0.005 ppm).
4.2.2.6 Other Methods—
In addition to the standard wet chemical methods for NOp measurement,
many other techniques have been explored. Molecular correlation spectro-
metry compares a molecular absorption band of a sample or plume with the
38
corresponding absorption band of NOp stored in the spectrometer. Spectro-
meters processing the second derivative of sample transmissivity with
39
respect to wavelength have been employed to measure NOp as well as NO.
Infrared lasers and infrared spectrometry have been applied by Hanst,
Hinkley and Kelley,41 and Kreuzer and Pate!.42'
4.2.3 Analytical Methods for NO
Numerous methods, other than the chemiluminescence procedure (discussed
in Section 4.2.1), can be used for direct measurement of NO; however, none
are widely used presently for air quality monitoring. These methods include:
4-12
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ferrous sulfate (FeSO,) absorption and spectrophotometric measurement of
the resulting colored complex ion, and ultraviolet and infrared
spectroscopy. The spectroscopic techniques 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.
4.2.4 Sampling for NO
/\
Sampling technique is a particularly important consideration for the
measurement of NO and NO,,. Nitric oxide and N02 in the atmosphere during
the day are involved in very rapid reactions which keep 0« in a photostationary
state. The rate of photolysis of N0« (forming NO and 0 and thus 03) is
nearly equal to the reaction of the NO and 03 to form N02. When a sample
is drawn into a dark sampling line, photolysis ceases while NO continues to
react with Og to form N02. 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.46
In general, due to the reactive properties of NO , only glass or
A
Teflon materials should be used in sampling trains.
If NO and NO^ 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 and granules
impregnated with triethanolamine. ' The triethanolamine is reported to
be the best absorbent, with only 2 to 4 percent of the incoming N02 converted
4-13
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to NO.
When NO is to be measured by a method specific to ML, either with or
without removal of NOp from the sample, it is necessary to oxidize NO to
NOg in the gas phase. The most frequently used oxidizer is chromic oxide
on a fire brick granule support. ' 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 S02.
Considerations relating to the reduction of ML to NO have been
discussed in Section 4.2.1.
4.2.5 Calibration of NO and N00 Monitoring Instruments
~ J c_
Calibration of monitoring instruments or methods may be accomplished
either by measuring a gas of known concentration or by comparing measure-
ments of a stable source with measurements of the same source made by a
primary reference method.
Standard gas sources are the principal means by which NO and NOp
measurement instruments are calibrated. The preparation of standard mix-
tures of NO in nitrogen was studied by the National Bureau of Standards.
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 of several hundred ppm is satisfactory with only 0 to 1
percent average change in concentrations over a 7-month period. Other
sources which have been employed include permeation of compressed NO through
membranes to produce dilute NO streams, electrolytic generation, catalytic
CO
reduction of a known concentration of N0p, or photolysis of known NOp
53
concentrations and rapid dilution.
4-14
-------
The permeation tube is the only direct source of dilute NC2 mixtures
in widespread use. ' It may be calibrated by weighing or by micro-
manometric measurements. The other common procedure used to calibrate an
N02 measurement instrument is gas-phase titration. Stable sources of known
concentrations of both NO and 03 are required. A dilute stream of NO is
measured by NO methods. Then 0, is added to the stream at a constant rate.
The decrease in NO by reaction with the added ozone is equal to the NOp
57
formed. Thus, a known N02 concentration is created. The USEPA recommends
the combined use of permeation tubes and gas-phase titration, using one
technique to check the other.
4.3 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 HNOg.
A microcoulometn'c method designed to measure nitric acid was developed
by Miller and Spicer.58'59 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,
4-15
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nitric acid concentrations are obtained by subtraction.
The sensitivity of this method at a signal-to-noise ratio of 2 to 1 is
approximately 2 ppb. No detectable interferences have been reported from
S02, N02, PAN, H2S04 and formaldehyde (CH20). It should, however, be
noted that Spicer, et al. report significant artifact nitrate formation
on nylon filters under conditions of very high N02 concentrations (56,400
yg/m ; 30 ppm) and high humidity. Although concentrations of this magnitude
would not be expected to occur in ambient situations, the possible implica-
tions of these reported interferences 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. report collection efficiencies for nitric
acid ranging from 93 to 100 percent. Interferences from N02 were reported
over a range of N02 concentrations up to 15,000 yg/m (8.0 ppm). The
3
equivalent of about 1 yg NOg-N/m of artifact gaseous nitrate corresponded
o
to 188 yg/m (0.1 ppm) N02 being passed through the filter at relative
humidities of 55 to 72 percent. Ozone did not enhance artifact formation
at a concentration of 980 yg/m (0.73 ppm) in the presence of 1,372 yg/m3
(0.73 ppm) N02. Interferences from PAN and n-propyl nitrate were cited as
negligible or very small. Nitrate formation from N02 increased with
increasing relative humidity.
62
Recently, Tuazon et al. 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
4-16
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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 auto-
matically by appropriate data processing.
4.4 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 concentrations is similar
for samples drawn from air, water, and soil.
4.4.1 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. 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 particulate
matter. The upper size limit of particulate matter collected depends on
the geometry of the sampler housing but is generally above about 30 ym. in
aerodynamic diameter, well above the respirable size range. The sampler
thus collects all of the respirable material and some fraction of the non-
respirable material suspended in ambient air. In typical nitrate moni-
toring, a portion of the HIVOL filter is subjected to aqueous extraction
and the water-soluble nitrate analyzed as described below in Section 4.4.2.
Recent reports point to serious difficulties associated with the
routine use of glass fiber filters. In a study of nitrate in auto exhaust,
4-17
-------
Pierson et al. 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
65
artifact formation from gaseous constituents. Spicer reported that glass
fiber filters completely removed gaseous nitric acid when in low concentra-
tion in gas streams, while Teflon and quartz filters showed no corresponding
effect. O'Brien et al. describe very unusual results of particle 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 conver-
sion of gaseous nitrate precursors on the filter masked the true nitrate
size distribution.
Okita et al. report that untreated glass fiber filters collect
nitric acid vapor with a highly variable collection efficiency (0-56
percent), suggesting erratic nitrate artifact formation in urban atmos-
pheres containing nitric acid.
In an intensive laboratory investigation of interferences in atmo-
spheric particulate nitrate sampling, Spicer, Schumacher and co-workers60'67
concluded that all five types of glass filters investigated exhibited
serious artifact formation due to collection of gaseous nitric acid and, to
some extent, N02 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. Inter-
ferences on quartz fiber filters varied with the filter type, with ADL
Microquartz showing the least effect at moderate N0« concentrations (592
4-18
-------
yg/m , 0.315 ppm). When a variety of quartz filter types were tested, the
greatest quantity of artifact nitrate was formed on the Gelman AE filter.
Artifact nitrate formed on this filter was calculated to be less than 2
o
yg/m (0.001 ppm) during a standard 24-hour H1VOL measurement. The estimate
was derived from drawing air samples of about 1 m3 containing 4,512 yg/m3
(2.4 ppm) N02 through the filters. The relative humidity was 30 +_ 10
percent.
fiR
Most recently, Spicer and Schumacher 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 4-1).
During the experiment, meteorological conditions 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 manufacurer's
-specifications. The ratio of nitrate collected on Glass 1 to that col-
lected 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.
These results point to the conclusion that most of the existing data
on urban ambient nitrate concentrations must be considered to be of doubt-
ful 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 artifact formation, is not routinely monitored.
It is, however, possible that data from certain background monitoring
sites may be validated where it can be shown that HN03 and N02 (also
4-19
-------
implicated in artifact nitrate formation) were both sufficiently low
during the monitoring period of interest.
4.4.2 Analysis of Nitrate from Airborne Parti cul ate 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
69
extracts of particulate matter and in solutions obtained through absor-
ption of nitrogen oxides contained in streams of air. '
The oldest procedures for analyzing nitrate used brucine
(C23H26N2°4^ " or Pnenoldisulfonic acl"d- " Newer procedures exten-
sively used to analyze nitrate in atmospheric particulate matter extracts
involve the nitration of xylenols [(CHOgCgHgOH] and separation of the
81 87
nitro-derivative by extraction or distillation. Recent comparison of
85
a 2,4-xylenol procedure with the automated copper-cadmium reduction and
88
diazotization method in samples collected near high density vehicular
traffic, demonstrated a negative interference in the former up to a factor
of 3.89
Nitration of chromotropic acid [C10H4(OH)2(S03H)2]90 and coumarin
91 92
(CgHg02) analogs • also have been reported. Small amounts of nitrate
can be assayed by the quenching of the fluorescence after nitration of
93
fluorescein (C20Hi2°5^ Nitrate analysis can also be accomplished through
reduction with Devarda alloy to ammonia (NH,)94'95 or reduction of nitrate
to nitrite by zinc,96 cadmium,97"99 or hydrazine (NH2NH2).100 Automation
instituted by the NASN improved the hydrazine reduction process by cur-
tailing the unwanted effects resulting from its sensitivity to motion.24
The addition of antimony sulfate [Sb2(S04)3] eliminates the chloride
4-20
-------
90
interferences found in most nitration methods. One brucine procedure
circumvents the effect of chlorides by adding an excess of sodium chloride
72
before nitration.
Nitrate analysis by ion-selective electrodes has been used but has
several disadvantages: potential drifts caused by agitation speed, necessity
of frequent re-standardization, interferences 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.
In atmospheric analysis, the electrode procedure has no advantage over
104
direct UV determination of either nitrite formed in an alkaline absorbent
or nitrate obtained after oxidation and absorption of nitrogen oxides in
alkaline permanganate. ' Microscopic techniques also allow analysis of
individual nitrate particles.
Small et al. report an application of ion exchange chromatography
to the measurement of a wide variety of cations and anions including the
nitrate and nitrite ion. The novel feature of the method is the use of a
second ion exchange "stripper" column (after a conventional 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
108
simple and sensitive conductometric technique. Mulik et al. 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, respectively. Since carbonic acid has
4-21
-------
low conductivity, the nitrate ion alone is effectively measured in a
conductivity detector. Under the experimental conditions, sensitivity
of 0.1 yg/mfe was reported. The related standard deviation was 1 percent
(95 percent confidence level) for ten replicate injections at the 5 yg/m£
level. At this concentration level, no interferences were found from
fluoride, chloride, nitrite, sulfite, sulfate, silicate, or carbonate.
Positive interferences were found for bromide and phosphate but the authors
suggest techniques for eliminating these.
In other recent work, Glover and Hoffsommer and Ross et al.
report a technique 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 cali-
bration 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 cali-
bration with added nitrotoluene. The lower detection limits reported by
12
Ross et al. are in the range of 10 g nitrobenzene in a 1 yfc 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, respectively. 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 4.4.3 and 4.4.4).
4-22
-------
4.4.3 Nitrate in Water
Current methodology for determination of nitrate in water is summarized
in Table 4-2. 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 techniques have been
used to preserve them during storage, including refrigeration, freezing,
and addition of sulfuric acid and of mercuric chloride. Simple refrigera-
tion is adequate for periods up to a day; freezing is effective for longer
preservation. Mercuric chloride is effective, especially when coupled
with refrigeration or freezing, but the mercuric ion slowly degrades columns
112 113
used in various reduction methods (Table 4-2) and also is toxic. '
The strong absorption of the nitrate ion in the range 210-220 nm
allows direct spectrophotometric measurement. * * 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 spectro-
photometric method is three times more sensitive than the brucine method.
Nitrate ion selective electrodes have also been used for measurement
of nitrate in water. ' The method, however, is not currently in
widespread use.
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 hydrogen in an aromatic compound by
the N02 moiety, and (2) reduction of nitrate to nitrite.
Nitration and oxidation reactions generally require a strong acid
4-23
-------
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
72
can be eliminated from the brucine method, experience has shown that
results obtained using this method are difficult to reproduce. Interferences
119
from nitrite and chlorine can be eliminated in the chromotropic acid method.
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 (NOI) ion (Section 4.2.1).
Although nitrate is readily reduced by a variety of agents including
hydrazine, metallic zinc or cadmium, difficulties with quantitative re-
covery have been reported.88j98'100'113'120"122 Techniques presently
recommended to avoid these difficulties have been documented by the
American Public Health Association. Columns using copperized cadmium '
120 123
or amalgamated cadmium granules or copperized cadmium wire give
stoichiometric or near stoichiometric reductions. These methods are widely
113
used and are regarded as accurate, sensitive and acceptable procedures. '
' Nitrate can be reduced quantitatively to ammonia by Devarda's
alloy and subsequently analyzed by titration or colorimetrically.
4.4.4 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,
4-24
-------
denitrification and flushing of nitrate. Biocides have been used to
prevent microbial activity but they are often ineffective.125 Cold storage126
and rapid air or oven drying have also been used. Most extraction methods
employ a salt solution such as CaS04, K2S04 or KC1.125 Methods of removing
turbidity include flocculation with aluminum hydroxide 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
125
content. Ultraviolet methods used in analysis of atmospheric nitrate
samples require similar flocculation techniques to remove turbidity, color
and other interferences.
Analytical methods are summarized in Table 4-3.
4.4.5 Nitrate in Plant and Animal Tissue
Methods analogous to those described above have been applied to measure-
ment of nitrate in plant and animal tissue. Nitrate ion concentrations
have been.measured in tobacco extracts using a spectrophotometric pro-
127 128
cedure. Wegner has described a procedure for determining both nitrate
129
and nitrite in biological fluids. Fudge and Truman described the analysis
of nitrate and nitrite in meat products. Methods of analysis for plant
tissue have been recently described by Carlson and Keeney.
4.5 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 atmos-
pheric 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,
4-25
-------
food and water.
4.5.1 Nltrosanrines in Air
Because of the low nitrosamine concentrations in air, sample con-
centration methods are necessary. One suitable concentration procedure is
the adsorption of nitrosamines on a solid substance. Bretschneider and
Matz report using chemically pure active carbon. Another effective
132
technique is the use of chemically bonded stationary phases. In this
method, nitrosamines are collected by passing air through a cartridge
packed with a solid sorbent. 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 Jl/min. Results showed that they maintained effi-
ciencies 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 ' 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 concentration, 2,2,4 trimethylpentate
was added as a keeper. It is important in using either solid sorbents or
liquid KOH traps, that the procedure be carefully checked to ensure that
the measurement is free of artifacts.
135
Fine, et al. have developed a specific method for detecting N-
nitroso compounds based on catalytic cleavage of the N-NO bond and the
subsequent infrared detection of chemiluminescence. The technique,
4-26
-------
called thermal energy analysis (TEA), is coupled with gas chromatography
and, sometimes, with high-pressure liquid chromatography.136 The technique
is highly sensitive (detection limit of about 1 ng/mfc) and specific for
heat-labile nitrosyl group. The TEA detector operates by splitting the
m'trosyl radical off N-nitroso compounds coming from a chromatographic
column. 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 formation has not
137
been reported to be a significant problem in the method.
4.5.2 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
138
compounds in water have been reported. Fine et al. reported two concen-
tration 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
1 ^8
been used by Fine and co-workers to measure part per trillion concentra-
tions 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 polarography139 and colorimetry, but neither method has the
4-27
-------
sensitivity required for environmental samples. Furthermore, the colori-
metric method has exacting experimental conditions and cannot be used for
complicated mixtures.
4.5.3 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 nitrosamines. 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 spectrometry (GC-MS) is presently the most acceptable
procedure for the measurement of nitrosamines in food. Wassermann and
142
Eisenbrand have published surveys of analytical techniques 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
143
been used.
4-28
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4.6 REFERENCES FOR CHAPTER 4
1. U.S. Environmental Protection Agency. Tentative method for con-
tinuous measurement of nitrogen dioxide (chemiluminescent).
Fed. Reg. 38: 15177-15178.
2. Fontijn, A., A. J. Sabadell, and R. J. Ronco. Homogeneous chemil-
uminescent measurement of nitric oxide with ozone. Implications
for continuous selective monitoring of gaseous air pollutants.
Anal. Chem. 42; 575-579, 1970.
3. Stedman, D. H., E. E. Daby, F. Stuhl, and H. Niki. Analysis of
ozone and nitric oxide by a chemiluminescent method in laboratory
and atmospheric studies of photochemical smog. J. Air Pollution
Control Assoc. 22; 260-263, 1972.
4. Clough, P. N., and B. A. Thrush. Mechanism of chemiluminescent
reaction between nitric oxide and ozone. Trans. Faraday Soc.
63: 915, 1967.
5. Stevens, R. K., and J. A. Hodgeson. Applications of chemiluminescent
reactions to the measurement of air pollutants. Anal. Chem. 45:
443A-449A, 1973.
6. Katz, M. Nitrogen compounds and oxidants. In: Air Pollution,
Vol. III. A. C. Stern (ed.), Academic Press, Inc., New York, 1976.
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nitrogen-containing compounds. Environ. Sci. Technol. 8; 1118-
1121, 1974.
8. Joshi, S. B., and J. J. Bufalini. Halocarbon interferences in
chemi luminescent measurements of NO . Environ. Sci. Technol.
12: 597-599, 1976. x
9. Constant, P. C., Jr., M. C. Sharp and G. W. Scheil. Collaborative
test of the continuous chemiluminescent method for measurement
of nitrogen dioxide in ambient air. EPA-650/4-74-046, U.S.
Environmental Protection Agency, Research Triangle Park, North
Carolina, 1974.
10. Treadwell, F. P. and W. T. Hall. Analytical chemistry. In_:
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11. Saltzman, B. E. Colorimetric microdetermination of nitrogen
dioxide in the atmosphere. Anal. Chem. 26_: 1949-1955, 1954.
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12. Intersociety Committee for Ambient Air Sampling and Analysis.
Tentative method of analysis for nitrogen dioxide content of the
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Public Health~A~ssociation, 2nd ed. Washington, D.C., 1977.
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Sampling and Analysis of Atmospheres. Standard method of test
for nitrogen dioxide content of the atmosphere (Griess-Saltzman
reaction) ASTM Designation: D1607-69. In: 1974 Annual Book of
ASTM Standards, Part 26. Gaseous fuels; Coal and Coke; Atmospheric
Analyses. American Society for Testing and Materials, Philadelphia,
Pennsylvania, 1974. pp. 317-322.
14. Kothny, E. L., and P. K. Mueller. Sub-minute continuous nitrogen
dioxide analysis. In: Proceedings of First International Clean
Air Congress, Part I. London, Leagrave Press Ltd. 1966. pp.
182-184.
15. Saltzman, B. E. Modified nitrogen dioxide reagent for recording
air analyzers. Anal. Chem. 32_: 135-136, 1960.
16. Saltzman, B. E., and A. F. Wartburg, Jr. Precision flow dilution
system for standard low concentrations of nitrogen dioxide. Anal.
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17. Shaw, 0. T. The measurement of nitrogen dioxide in the air.
Atmos. Environ. !_: 81-85, 1967.
18. Scaringelli, F. P., E. Rosenberg, and K. A. Rehme. Comparison
of premeation devices and nitrite ion as standards of colorimetrie
determination of nitrogen dioxide. Environ. Sci. Techno!. 4_:
924-929, 1970.
19. Evaluation of a continuous colorimetric method for measurement of
nitrogen dioxide in ambient air. EPA-650/4-75-022. U.S. Environmental
Protection Agency, Research Triangle Park, North Carolina, 1975.
20. Baumgardner, R. E., T. A. Clark, and R. K. Stevens. Comparison of
instrumental methods to measure nitrogen dioxide. Envir. Sci.
Techno!. 9_: 67-69, 1975.
21. Constant, P. C., Jr., M. C. Sharp and G. W. Scheil. Collaborative
testing of methods for measurements of N0? in ambient air. Vol.
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Triangle Park, North Carolina, 1975.
22. Jacobs, M. B., and S. Hochheiser. Continuous sampling and ultra-
mi crodetermi nati on of nitrogen dioxide in air. Anal. Chem. 30:
426-428, 1958.
23. Morgan, G. B., C. Golden, and E. C. Tabor. New and improved
procedures for gas sampling and analysis in The National Air Sampl-
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24. Morgan, G. B., E. C. Tabor, C. Golden, and H. Clements. Auto-
mated laboratory procedures for the analysis of air pollutants.
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4-40
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Table 4-1. COMPARISON OF NITRATE COLLECTED ON VARIOUS FILTER1" TYPES60'68
—
Date
Oct. 15
Oct. 18
Oct. 19
Oct. 20
Oct. 21
Oct. 22
Oct. 25
Filter
Quartz
Quartz
Glass
Quartz
Glass
Quartz
Glass
Quartz
Glass
Quartz
Glass
Quartz
Glass
Quartz
NO"
3
yg/m
1
2
1
2
1
2
1
2
1
2
1
2
2
2
1.
1.
14.
0.
17.
1.
28.
2.
18.
0.
11.
0.
38.
0.
6
6
4
39
0
2
7
3
8
82
2
49
4
78
Date
Oct. 26'
Oct. 27
Oct. 28
Oct. 29
Nov. 1
Nov. 2
Nov. 3
Filter
Quartz
Quartz
N03>
yg/m3
1
2
Glass 2
Quartz 2
Glass
Quartz
Quartz
Quartz
Quartz
Quartz
Glass
Quartz
Quartz
Quartz
1
2
1
2
2
2
2
2
1
2
1.
2.
3.
0.
9.
1.
1.
2.
1.
1.
9.
1.
0.
1.
3
1
9
52
1
9
8
9
7
7
1
6
68
1
Date Filter
Nov. 4 Glass 2
Quartz 2
Nov. 5 Glass 2
Quartz 2
Nov. 9 Glass 2
Quartz 2
Nov. 10 Quartz 1
Quartz 2
Nov. 11 Quartz 2
Quartz 2
Nov. 12 Glass 2
Quartz 2
Nov. 15 Glass 2
Quartz 2
NO",
yg/m3
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
t 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 - Pall flex QAST.
4-41
-------
Table 4-2. ANALYTICAL METHODS FOR NITRATE IN WATER
Method
Range Interferences
(mg/1 nitrate-nitrogen)
Reference
1. UV absorbance
2. Ion selective
electrode
0.1 - 10
0.2 - 1400
Nitration and Oxidation Reactions
3. Phenoldisulfonic
acid
4. Brucine 0.1 - 2.0
5. Chromotropic 0.1 - 5.0
6. Automated 0.05 - 4.0
fluorimetric
with substituted
benzophenone
7. Szechrome 0.05 - 1.0
Reduction Methods
8. Zinc 0.02 - 1.0
9. Amalgamated
cadmium
10. Copperized
cadrni urn
11. Hydrazine-
copper
12. Devarda's alloy
<0.01 - 1.0
<0.01 - 1.0
<0.01 - 1.0
2 - >200
Organic Matter
Chloride,
ionic strength
Chloride
Many, but all
readily removed
Organic color,
chloride, sulfi.de,
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
A.P.M.A., 1976
A.P.M.A., 1976
119
119
A.P.H.A., 1976
119
A.P.M.A., 1976
119
A.P.M.A., 1976
Afghan and
Ryan,
119
Szekely, 1975
146
O'Brien and
Fiore, 1962
121
A.P.H.A., 1976
119
Technicon, 1973
88
E.P.A.,
A.P.M.A., 1976
Strickland and
Parsons, 1972
Kemphake, 1976
144
A.P.H.A., 1976
119
4-42
-------
Table 4-3 METHODS FOR DETERMINATION OF NITRATE IN SOILS
Method
1. Ion electrode
2. Phenoldisulfonic
acid
3. Brucine
4. Reduction to NO"
by Cd Griess- *
Ilosvay method.
Range, mg/V
2 - 1400
0.1 - 2
0.1 - 2
0.02 - 0.1
5. Reduction to NH3 by 1 - 1000
Devarda alloy, Steam
distillation of NH3
6. UV absorbance
Interferences
Chloride, bromide,
nitrite, iodide,
sulfide, ionic
strength.
Chloride, organic
matter, nitrite
None
Labile amide,
phosphate, nitrite
References
Carlson and
Keeney, 1971
130
125
Bremner, 1965
Bremner, 1965125'147
APHA, 1976119
Bremner, 1965125'147
APHA, 1976119
Bremner, 1965
125
Cawse, 1967
105
CO
«*
Range on soil basis varies widely depending on soil: solution ratio of extractant.
-------
CHAPTER 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 parti-
cipate in atmospheric chemical pathways leading to effects on human health
and welfare. Particular emphasis in this Chapter is placed on emissions of NO
A
for two reasons: (1) N02 is a pollutant of major concern for human health
(Chapter 13) and (2) atmospheric transformation products of NO such as nitric
A
acid (HN03) and particulate nitrates are of concern both for their effects on
human health and their role in the acidification of precipitation (Chapter 9).
Agricultural usage of nitrogenous compounds is discussed because of recent
concern about possible perturbations of the stratospheric ozone layer by
nitrous oxide ^0), which is produced in part from fertilizer not utilized by
plants (Chapter 9). Sources of N-nitroso compounds and their possible pre-
cursors are reviewed in order to evaluate potential exposure and accompanying
health effects (Chapter 7). Sources of ammonia are discussed because some
researchers have suggested that NH_ is converted to NO in the atmosphere.
O A
5.2 ANTHROPOGENIC EMISSIONS OF N0x
Global estimates of natural emissions of nitrogenous compounds including
N0x will be discussed in detail in Chapter 8. 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.
J\
In highly industralized or populous localities, anthropogenic emissions of
NO and/or NOp assume primary importance. Mobile combustion and fossil-fuel
power generators are the two largest source categories. In addition, industrial
5-1
-------
processes and agricultural operations produce minor quantities. Although
certain industrial processes, such as nitric acid plants, and certain agri-
cultural activities, such as the application of fertilizer or the operation
of animal feedlots, may result in localized emissions of other nitrogenous
compounds, only NO and NCL are, in general, considered to be the primary
pollutants; the other nitrogen oxides are mainly products of atmospheric
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
A
though the compound being emitted were N02. This method of presentation serves
the purpose of allowing ready comparison of different sources. Because of
the interconvertibility of NO and N02 in photochemical smog reactions,
such an approach is realistic and avoids the difficulty in interpretation
associated with different ratios of N0/N02 being emitted by different
sources.
5.2.1 Global Sources of NO
~~ ~~ ^
Table 5-1 presents historical estimates of the man-made global
production of NO^1'2 These estimates are based on 1966 fuel consumption
figures and emissiort factors available in 1965.4 From these data,
o
Robinson and Robbins estimated global NO emissions from combustion
rt
processes to be 44.4 x 10° metric tons per year (expressed as NOJ. These
authors also estimated that natural emissions of NO from terrestrial
^
and aquatic sources exceed those from anthropogenic sources by a factor of
7 to 1. An earlier estimate by Robinson and Robbins1 had natural emissions
exceeding anthropogenic emissions by 15 to 1. The downward revision of
their ratio was based on a 55 percent lower estimate of the amount of N00
5-2
-------
emitted by natural sources.
A different estimate was provided by Soderlund and Svensson, who
concluded that NO emissions from natural versus anthropogenic sources
A ~
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
A
emissions (Chapter 9). In particular, estimates of different authors on
the magnitude of NO emissions from soils vary greatly. Definitive experi-
A
ments have yet to be performed.
5.2.2 Sources of NO in the United States
Table 5-2 and Figure 5-1 provide historical data on estimated emissions
of NO in the United States for the years 1940 through 1970. A significant
A
upward trend in the two major source categories, transportation and stationary
fuel combustion, is discernible over this 30-year period. Total NO
/\
emissions increased almost 3-fold. 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 NOX 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 exceed-
5-3
-------
ing 1,000,000, accounted for more than half (53 percent) of the NO
y\
emissions. The population in these same SMSA's was only 38.5 percent of
the total U.S. population in 1970.6
A clear picture of the nationwide distribution of NO emissions can
rt
be obtained from the U.S. maps reproduced in Figures 5-4 through 5-6.
Figure 5-4 shows total NO emissions by U.S. counties as compiled in the
A
National Emissions Data System (NEDS) file of February 1978.7 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 considered. Areas of relatively high
emission densities are still evident throughout the eastern states and the
midwest and on the west coast. The percent contribution of major point
sources to total NO emissions is plotted by U.S. county in Figure 5-6.
/\
Comparison of this figure and Figure 5-4 reveals that, in general, major
point sources make a significant contribution to total NO emissions in
/\
those areas where NO emissions are high. (In this discussion, a major
A
point source is defined as one for which the yearly NO emissions exceed
/\
100 tons.)
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
A
in Sacramento, California. In San Francisco, California, they are esti-
o
mated to contribute about 56 percent, while in northwestern Indiana the
9
estimate is 8 percent. Motor vehicle emissions in Los Angeles County,
5-4
-------
California, increased 6-fold from 1940 to 1970, compared to a 3-fold
national increase.
While not of major national importance, NO emissions from aircraft
A
11 12
are believed to be a major source around airports. High-altitude emissions
could become a major source in the stratosphere.
National trends also do not portray seasonal variations. For example,
emissions of NO from electric generating plants have been reported to
J\
vary up to 60 percent seasonally; this appears to be due to fluctuations
in heating and cooling loads.
While industrial process losses (NO emissions from noncombustion
/\.
industrial sources) are minor on a national level, these emissions can be
important near individual sources. Manufacturing of nitric acid, explosives
and fertilizers, and petroleum refining are the principal activities in
these source categories.
It is important to note 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 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,
sources and meteorological parameters exhibit both seasonal and diurnal
variability, which can greatly affect the impact of particular sources on
5-5
-------
ambient pollution levels.
5.3 EMISSIONS OF AMMONIA
On a global basis, abiotic emissions of ammonia (NH3) represent only
a small fraction of the total emissions of NH3. f * Soderlund and
Svensson calculated that anthropogenic emissions (from coal combustion)
accounted for between 4 x 10 to 12 x 10 metric tons per year. A global
loss of 7 x 10 metric tons NH--N per year from inefficiencies in handling
and applying ammonia-based fertilizers was reported by the Council for
Agricultural Science and Technology (CAST). A recent report indicated
that the United States accounts for about 25 percent of the global use of
ammonia-based fertilizer. Another source has reported estimated NH-,
emissions for the United States at a much lower level, as shown in Table
5-4. Discrepancies in these estimates by various authors preclude any
firm judgements at this time as to NH~ emissions resulting from fertilizer
usage.
In addition to volatilization of NH3 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.16 As urea is rapidly hydrolyzed into NH~ and C00,
»3 £
atmospheric contributions of NH, from feedlot-generated urine of an
estimated cattle population of 132 million in the United States could
amount to 2 x 10 to 4 x 106 metric tons NH3-N per year. This amount is
between one-fourth and one-half of the rate of anthropogenic emissions of
nitrogenous compounds (excluding NgO) to the atmosphere in the United
States.13
5-6
-------
5.4 AGRICULTURAL USAGE IN NITROGENOUS COMPOUNDS
Nitrogenous material applied as fertilizer participates in the
nitrogen cycle via a variety of pathways (Chapter 8). Emissions of
ammonia from agricultural sources have been discussed above in Section
5.3. Excess fertilizer may be of concern also: (a) by contributing an
anthropogenically produced burden to stratospheric concentrations of N20
with consequent potential for attenuation of the ozone layer and (b) by
contributing, through run-off from agricultural lands, to both nitrate
pollution of drinking water and to changes in natural aquatic ecosystems.
The data presented in Figure 5-7 and Table 5-5 are intended to place usage
of nitrogenous materials applied as fertilizer in the U.S. in historical
perspective. Examination of Table 5-5 reveals that the total nitrogen
applied as fertilizer has increased more than a factor of 5 from 1955 to
1976. Applications of anhydrous ammonia have increased more than 14-fold
and applications of nitrogen solutions have increased more than fifty
times in the same period.
5.5 SOURCES OF N-NITROSO COMPOUNDS AND POSSIBLE PRECURSORS
N-nitroso compounds may be emitted to the atmosphere during their
production or use, and have been postulated to occur by atmospheric
formation or volatilization from water or soil. Additional routes
of human exposure to N-nitroso compounds may include drinking water, foods
and tobacco products.
5.5.1 Anthropogenic Sources of N-Nitroso Compounds
Possible direct anthropogenic sources of N-nitroso compounds include
Industrial processes in which these compounds are intermediate or final
products, reactants or additives; or in which they may occur incidentally as
impurities. While over 20 N-nitroso compounds are listed as products in
5-7
-------
recent commercial directories,17" 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
20
regulatory actions have apparently discouraged their general use.
The two N-nitroso compounds produced in greatest quantity, diphenyl-
nitrosamine and dinitrosopentamethylenetetramine, are used in the rubber
21
industry as a vulcanizing retarder and a blowing agent, respectively.
22
Neither has been found carcinogenic in laboratory tests on male rats.
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 contain N-nitroso concentrations rarely
23-27
exceeding 1.0 ppm. Release of small quantities of N-nitroso compounds
may occur in the processing of such products. Emissions occurring as a
result of certain combustion processes have also been suspected. Analysis
for emissions of nitrosamines (usually only N-nitrosodimethylamine) has
been carried out as part of research programs involving automobiles,
diesel engines, emission control systems, and fuels and fuel additives.
Other tests by five different groups using different techniques all pro-
29 ?8
duced negative results, although Fine, et-al. reported the presence of
several unidentified N-nitroso compounds in the exhaust of a truck diesel
engine and an automobile internal 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
5-8
-------
weights, may reach the atmosphere through volatilization from soil and
water. These compounds may be present in soil or water as deposits or
effluents from industrial or agricultural sources, or may be formed de_
novo from appropriate precursors in water or soil. Nitrosamines have
been found in several commercial herbicides which, upon application,
could be volatilized from surface water or soil. Volatilization may
also occur from N-nitroso compounds formed in situ. Formation of N-nitroso
compounds in soil and water samples has been demonstrated under laboratory
conditions.31"35 Most of these experiments involve pesticides 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 resist-
ivity.^*3^ A study, however, reported no detection of nitrosamines in
emissions from a power plant using such amine additives.
In general, preliminary considerations of the atmospheric mechanisms
suggested that ambient concentrations 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. Sources leading to ambient concentrations of the
nitrogen compounds have been discussed above in Section 5.2. With regard
5-9
-------
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. 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 poultry
manure, air sampled over cattle feedlots, and exhaust from rendering of
29 38 39
animal matter. ' * Volatility and water-solubility of various amines
results in extensive dispersal of these compounds in the atmosphere, water
and soil. Results of investigations of ambient concentrations of N-
nitroso compounds in the vicinity of suspected sources are discussed in
Section 7.3.
5.5.4 N-Nitrosamines in Food, Water and Tobacco Products
A variety of raw and processed foods have been tested for N-nitroso
compounds. A review of earlier qualitative studies was published by
41 42
Sebranek and Cassens. Scan!on has summarized a number of the studies
reported since 1970. These recent studies concentrate on processed meats
and fish, in which nitrosamines, 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). 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 diethylnitrosamine (DEN) and 50 to 60 ppb nitrosopiperidine
(NPi).44'51"56 Raw and processed fish products have shown 1 to 26 ppb DMN
44 45 57
and 1 to 6 ppb NPY, ' ' with some fish meal samples containing as much
5-10
-------
CO
as 450 ppb DMN. Cheese samples were found to contain up to 4 ppb DMN,
1.5 ppb DEN and 1.0 ppb NPY.44'45 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.43
Contamination of drinking water with N-nitroso coumpounds may occur
through water-borne emissions from the industrial sources discussed in
Section 5.4.1 or by nitrosation of precursors found in natural bodies of
water or water supply and treatment systems. N-nitroso coumounds have
been found in industrial wastewater, and in samples taken from water near
industrial facilities. Nitrosation in lake water samples has been domon-
33
strated in the laboratory. Analyses of drinking water have either
failed to detect N-nitroso compounds or have shown concentrations in the
t
0.1 ppb range.62*63
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 ni-
trosodiethylamine (<5). N'-nitrosonornicotine found in a variety of
chewing tobacco products indicates that such unsmoked products may also
27
be sources of exposure to N-nitroso compounds.
5-11
-------
5.6 REFERENCES FOR CHAPTER 5
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fate of gaseous atmospheric pollutants. In: Air Pollution
Control, Part II, W. Strauss, ed. Wiley-Interscience, New York,
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2. Robinson, E. and R. C. Robbins. Gaseous atmospheric pollution
from urban and natural sources. In: The Changing Global Environment.
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3. U. S. Statistical Abstract, 1967.
4. Mayer, M. A compilation of air pollution emission factors. U.S.
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5. Soderlund, R. and B. H. Svensson. The global nitrogen cycle. Jjn:
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6. U.S. Bureau of the Census. City and County Data Book, 1972. U.S.
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7. Data extracted from the National Emissions Data System (NEDS),
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8. California Board of Air Sanitation. The Oxides of Nitrogen
in Air Pollution. California Department of Public Health, 1966.
9. Ozolins, G. and G. Rehmann. Air pollution emission inventory of
northwest Indiana. A preliminary survey. U.S. Dept. of Health,
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5-12
-------
14. Council for Agricultural Science and Technology. CAST Report No.
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>
21. Magee, P. N. Possibilities of hazard from nitrosamines in in-
dustry. Ann. Occup. Hyg. 15: 19-22, 1972.
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cinogenic properties of certain rubber additives. Eur. J. Cancer
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Ceh. Isolation and denitrification of a hepatotoxic factor in
herring meal produced from sodium nitrite preserved herring.
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5-13
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33. Ayanaba, A. and M. Alexander. Transformation of methyl amines and
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5-14
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Estimation of steam-volatile N-nitrosamines in foods at the 1
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51. Fazio, T., R. H. White, and J. W. Howard. Analysis of nitrite-
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Assoc. Off. Anal. Chem. 54_: 1157, 1972.
52. Sen, N. P. The evidence for the presence of dimethylnitrosamines
in meat products. Food Cosmet. Toxicol. 10: 219, 1972.
53. Wasserman, A. E., W. Fiddler, E. C. Doerr, S. F. Osman, and
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Toxicol. 10: 681, 1972.
5-15
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54. Panalaks, T., J. R. lyengar, and N. P. Sen. Nitrate, nitrite
and dimethylnitrosamine in cured meat products. J. Assoc. Off.
Anal. Chem. 56_: 621, 1973.
55. Sen, N. P., W. F. Miles, B. Donaldson, T. Panalaks, and J. R.
lyengar. Formation of nitrosamines in a meat curing mixture.
Nature 245: 104, 1973.
56. Panalaks, T., J. R. lyengar, B. A. Donaldson, W. F. Miles, and
N. P. Sen. Further survey of cured meat products for volatile N-
nitrosamines. J. Assoc. Off. Anal. Chem. 57_: 806, 1974.
57. Fazio, T., J. N. Damico, J. W. Howard, R. H. White, and J. 0. Watts,
Gas chromatographic determination and mass spectrometrie confir-
mation of N-nitrosodimethylamine in smoke-processed marine fish,
J. Agric. Food Chem. 19: 250, 1971.
58. Sen, N. P., L. A. Schwinghamer, B. A. Donaldson, and W. F. Miles.
N-nitrosodimethylamine in fish meal. 0. Agric. Food Chem. 20:
1280, 1972. ~~~
59. Reconnaissance of Environmental Levels of Nitrosamines in the
Central United States. EPA-330/1-77-001. National Enforcement
Investigations Center, U.S. Environmental Protection Agency,
Denver, Colorado, January 1977.
60. Reconnaissance of Environmental Levels of Nitrosamines in the
Southeastern United States. EPA-330/1-77-009. National Enforce-
ment Investigations Center, U.S. Environmental Protection Agency,
Denver, Colorado, August 1977.
61. Scientific and Technical Assessment Report on Nitrosamines. EPA-
600/6-77-001. U.S. Environmental Protection Agency, Office of
Research and Development, June 1977.
62. Fine, D. H., D. P. Rounbehler, N. M. Belcher, and S. S. Epstein. N-
Nitroso compounds in air and water. Paper presented at the Fourth
Meeting of the Int'l. Agency for Research on Cancer, Tallinn,
Estonia, USSR, October 1-2, 1975.
63. Fine, D. H., D. P. Rounbehler, N. M. Belcher, and S. S. Epstein. N-
Nitroso compounds in the environment. Paper presented at Int'l.
Conf. on Environmental Sensing and Assessment, Las Vegas, Nevada,
September 22-26, 1975.
64. Hoffman, D., 6. Rathkamp, and Y. Y. Lin. Chemical studies on
tobacco smoke. XXVI. On the isolation and identification of
volatile and non-volatile N-nitrosamines and hydrazines in cig-
arette smoke. IARC Scientific Publications No. 9, Lyon, France,
1975.
5-16
-------
65. Nationwide Air Pollutant Emission Trends, 1940-1970. AP-115,
U.S. Environmental Protection Agency, Research Triangle Park, North
Carolina, January 1973.
66. National Air Quality and Emissions Trends Report. EPA 450/1-77-022.
U.S. Environmental Protection Agency, Office of Air Quality Plan-
ning and Standards, Research Triangle Park, North Carolina,
December 1977.
67. Hargett, N. L. Fertilizer Summary Data. National Fertilizer
Development Center, Tennessee Valley Authority, Muscle Shoals,
Alabama, 1976.
68. National Research Council. Air Quality and Stationary Source
Emission Control. A report by the Commission on Natural Resources,
National Academy of Sciences for the Committee on Public Works,
U.S. Senate, 94th Congress, 1st Session, Committee Serial No.
94-4, Washington, D.C., 1975.
5-17
-------
Table 5-1. ESTIMATED ANNUAL GLOBAL EMISSIONS OF
NITROGEN DIOXIDE (Anthropogenic).2
(10 metric tons per year, expressed as ML)
Source Emissions Emissions as N % Total
Total combustion and refining 48.0 14.6 100
Coal combustion 24.4 7.4 51
Petroleum refining 0.6 0.2 1
Gasoline combustion 6.8 2.1 14
Other oil combustion 12.8 3.9 27
Natural gas combustion 1.9 0.5 4
Other combustion 1.5 0.5 3
5-18
-------
Table 5-2 HISTORIC NATIONWIDE NO
EMISSION ESTIMATES 1940-1970
(10 metric tons per year, expressed as N02)65
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.
5-19
-------
ro
o
Table 5-3. RECENT NATIONWIDE NOX EMISSION ESTIMATES 1970-197666
(10 metric tons/yr, expressed as NO,,)
Source Category
TRANSPORTATION
Highway vehicles
Nonhighway vehicles
STATIONARY FUEL COMBUSTION
Electric utilities
Industrial
Residential, commercial
and institutional
INDUSTRIAL PROCESSES
Chemicals
Petroleum refining
Metals
Mineral products
Oil and gas production
and marketing
Industrial organic
solvent use
Other processes
SOLID WASTE DISPOSAL
MISCELLANEOUS
Forest wildfires and
managed burning
Agricultural burning
Coal refuse burning
Structural fires
Miscellaneous organic
solvent use
Totals
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
0.3
0.2
0.1
0
0.1
0
0
20.4
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
0.3
0.3
0.2
0
0.1
0
0
21.3
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
0.2
0.2
0.1
0
0.1
0
0
22.2
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
0.2
0.2
0.1
0
0.1
0
0
22.9
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
0.2
0.2
0.1
0
0.1
0
0
22.6
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
0.2
0.2
0.1
0
0.1
0
0
22.2
1976
10.1
7.8
2.3
11.8
6.6
4.5
0.7
0.7
0.3
0.3
0
0.1
0
0
0
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.
-------
Table 5-4. ESTIMATED AMMONIA EMISSION FROM FERTILIZER APPLICATION
AND INDUSTRIAL CHEMICAL PRODUCTION IN U. S. (1975)15
Source of Emission
Ammonia Production
Direct application of
anhydrous ammonia
Ammonium nitrate
Petroleum refineries
Sodium carbonate
(Solvay process)
Di ammonium phosphate
Amnioniator-granulators
Urea
Miscellaneous emission from
fertilizer production
Beehive coke ovens
Total
Ammonia
tons/yr
19,000
168,000
59,000
32,000
14,000
10,000
10,000
4,000
2,000
1,000
319,000
Emission Rate
tons N/yr
15,600
138,400
48,600
26,400
11,500
8,200
8,200
3,300
1,600
800
262,600
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.
5-21
-------
ro
ro
Table 5-5. NITROGENOUS COMPOUNDS APPLIED AS FERTILIZER IN THE U. S. 1955-1976
(usage 1n 10 tons of material3)
67
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
1.75
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
a Numbers are rounded to three decimal places
-------
o
•r—
J-
PO
oo
25.
0)
e 20.
c
o
•r—
£ 15.
j=^
c
° 10.
5.
All other sources
(Industrial, Solid Waste)
tationary Fuel Combustion
Transportation Sources
1950
1960
1970
Figure 5-1. Historic NO Emissions By Source Groups^
A
^Values shown for each year are cumulative over source groups.
-------
25
01
I
ro
O)
E 20
o
.7 15-
^
10
I 10-|
10
CO
5 5.
X
o
All Other Sources
(Industrial, Solid Haste)
Stationary Fuel Combustion
Transportation Sources
« ~l 1 1 1 1 1—
1970 1971 1972 1973 1974 1975 1976
Figure 5-2. Recent NO Emissions By Source Groups66
A
Values shown for each year are cumulative over source groups,
-------
Medium-Sized
Urban AQCR's
24%
Emissions
AQCR Urbanization3 (10 tons/yr)
Large Urban 11.71
Medium-sized Urban 5.30
Small Urban 2.36
Rural 2.88
Total 22.25
a Urbanization is based on largest SMSA population
in an AQCR:
Large Urban=SMSA population 1,000,000
Medium-sized Urban=SMSA population 250,000-1,000,000
Small Urban= SMSA population 50,000-250,000
Rural= AQCR containing no SMSA
b Miscellaneous sources accounting for 160,000 tons/yr
are not included.
Figure 5-3. Distribution of 1972 Nationwide NO Emissions
By Degree of Urbanization 68
5-25
-------
TONS / YEflR
< 3.000
3.000 - 10.000
10.000 - 30.000
30.000 - 100.000
> 100.000
Figure 5-4. Total NOY Emissions by U. S. County'
-------
TONS/SO MI
Figure 5-5. Total NO Emission Density by U. S. County'
-------
, n
rv>
00
PERCENT
Figure 5-6. Percent N0x Emissions Contributed by Major Point Sources, by county.
(over 100 T/yr)7
-------
TONS
Anhydrous
Ammonia
Nitrogen
Solutions
Ammonium
Nitrate.
1955
I960
1965
1970
1975
FIGURE 5-7 TRENDS IN U.S. USAGE OF NITROGENOUS
MATERIAL APPLIED AS FERTILIZER6'
(Usage is in million tons of applied material)
5-29
-------
CHAPTER 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 transformations 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 transformation 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 transformation
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 NOp levels and precursors is cited.
Finally, chemical reactions occurring in plumes are discussed. The
formation of nitrites and nitrates is surveyed in Section 6.2. The
transport and removal of nitrogeneous species are discussed in Section
6.3. Section 6.4 is devoted to the chemistry of nitrosamine formation.
6-1
-------
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 photochemical smog. To understand the chemistry of the oxides of
nitrogen in the lower atmosphere, it is necessary to consider the in-
teractions that take place between the oxides of nitrogen and organic
constituents. Several reviews of atmospheric chemistry are available,
4-8 9
as are detailed discussions of reaction mechanisms and rate constants.
In this section the chemistry of the oxides of nitrogen in the lower
atmosphere is briefly reviewed. The above-cited references should be
consulted for more detail.
Most of the chemistry that occurs in a sunlight-irradiated urban
atmosphere involves the interaction of a variety of unstable, excited
molecules and molecular fragments that have only a transitory existence.
These species include: the unexcited and first excited electronic states
of the oxygen atom, triplet-P oxygen atoms [0(''P)]> and singlet-D oxygen
atoms [0( D)]; ozone (03); symmetrical nitrogen trioxide (N03); dinitrogen
pentoxide (N205); hydroxyl radicals (HO); alkylperoxyl radicals (R02);
acylperoxyl radicals RC(0)02; and other less important species. In the
formulas, R represents a methyl (CH3), ethyl (CpH.,), or another, more
complex hydrocarbon radical. The paths by which these intermediates are
formed and destroyed are important keys in explaining the chemical changes
that occur in the polluted atmosphere.
6-2
-------
6.1.1. Reactions Involving Oxides of Nitrogen
The major portion of the total oxides of nitrogen emitted by com-
bustion sources is nitric oxide (NO). The rate at which NO is converted to
nitrogen dioxide (N02) 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 concentration. Reaction 6-1 can be important in
generating a small level of nitrogen dioxide (up to 25 percent of total
NO ) during the initial state of dilution with air when the concentration
A
of NO is still quite high. Reaction 6-1 is much too slow, however, to
account for any significant fraction of the nitric oxide to nitrogen
dioxide conversion observed in the atmosphere for typical ambient levels
of nitric oxide.
Since sunlight triggers the phenomenon of photochemical smog for-
mation, it is important to recognize those constituents that will absorb
light energy. In some cases, these constituents decompose or become
activated for reaction. A dominant sunlight absorber in the urban at-
mosphere is the brown gas, nitrogen dioxide. Light absorption at wave-
lengths < 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
6-3
-------
frequently with oxygen molecules. 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 mole-
cule that absorbs the excess vibrational energy released, thereby
stabilizing the ozone produced. For most concentration conditions
common in polluted atmospheres, the very reactive ozone molecules re-
generate 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, symmetrical 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)
Dinitrogen pentoxide may redissociate to form symmetrical nitrogen
trioxide and nitrogen dioxide or possibly react with water to form
nitric acid (HON02):
N2°5 "" N03 + N02 (6'7)
or
N205 + H20 -> 2HON02 (6-8)
The following reactions may take place between oxygen atoms and N02
and NO:
6-4
-------
NO, + Q(3P) + NO + Op (6-9)
or - ^
NOp + 0(3P) + M -> N0? + M (6-10)
or * d
NO + 0(3P) + M -»• N02 + M (6-11)
Also, NO and NOg may react to regenerate N02:
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:
HONO + HONO -»• NO + N02 + H20 (6-14)
The unexcited and first excited electronic state of the oxygen atom are
produced by ozone photolysis in sunlight:
03 + sunlight
290-350 nm
450-700 nm
0(!D) or 0(3P) (6-15a)
»• 02 + 0(3P) (6-15b)
The singlet-D oxygen [Of^)] atom is much more reactive than the ground
state triplet-P oxygen [0(3P)] atom. For example, it reacts efficiently dur-
ing collision with a water molecule to form an important transient
species in the atmosphere, the hydroxyl radical:
0(JD) + H20 + 2HO <6-16)
Ibis radical is also formed through the photodecomposition of nitrous acid
(HONO):
HONO + sunlight (290-400 nm) •*• HO + NO (6-17)
6-5
-------
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 -> MONO + M (6-19)
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 NOp observed in the ambient atmosphere. 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 in-
creases. Thus, the hydroxyl radicals produced'by reactions 6-16 and 6-17
can react with a hydrocarbon:
OH + HC -»• R- + H20 (6-20)
where HC represents a hydrocarbon molecule (paraffin, olefin, aromatic
or any compound having C-H bonds). 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 peroxy radical R02':
R- + 02 % R02- (6-21)
6-6
-------
Typically, the next reaction in the series converts NO to NCL and produces
an oxyl radical, RO-:
R(y + 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 (HOp) can react with a second NO to form
N02 to complete the cycle:
H02- + NO -> OH- + N02 (6-24)
Although this description is very simplified, these series of reactions
contain the essential features of NO to NO^ 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. 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 concentrations sufficient to explain the
observed induction time for smog chemistry, but the concentrations ne-
cessary to initiate smog chemistry in the atmosphere are below the limits
ffleasured by most modern instruments.
Another possible source of radicals in the atmosphere is the photo-
lysis of aldehydes:
RCHO + hv -> tilQ + R- (6-25)
6-7
-------
Aldehydes are emitted from many sources, including automobiles. They are
also formed in smog.
During the course of the overall smog formation process, the free
radical pool is maintained by several sources, but the dominant one appears
to be photolysis of the aldehydes formed from the initial hydrocarbons.
Since the formation of free radicals is a cyclic process, any additional
source radicals will add to the pool and increase the cycle rate. Con-
versely, any reaction that removes one of free radicals will slow the cycle
rate. For example, a primary radical sink and a primary sink for oxides of
nitrogen is reaction 6-18 to form nitric acid.
The hydrocarbon classes important in the chemistry of the polluted
troposphere are alkanes, olefins, and aromatics. In addition, the
oxygenated hydrocarbons, such as aldehydes, ketones, esters, ethers, and
alcohol are also important. A great variety of chemical reactions take
place among these organic species and the free radicals cited above. The
reactions of typical hydrocarbon species are now discussed briefly.
Throughout the discussion references to more extensive coverages are given.
The most important atmospheric reaction involving alkanes is with the
OH radical. For n-butane, for example, the reaction is
CH3CH2CH2CH3 + OH- ->• CH3CH2CH2CH2- + H20 (6-26a)
and
-»• CH3CH2C"HCH3 + H20 (6-26b)
The alkyl radicals will rapidly add 02 to form the corresponding per-
oxyalkyl radicals, e.g.
CH3CH2CH2CH2- + 02 + M -* CH3CH2CH2CH202- + M (6-27)
(subsequently the third body M will not be indicated).
6-8
-------
A reaction of substantially lesser importance is with oxygen atoms,
* °2
CH3CH2CH2CH3 + 0(3P) -> OH- + CH^CH^H^ (6-28a)
and
°2 ?°"
-*• OH- + CH3CH2CHCH3 (6-28b)
o
The importance of both the OH and 0( P) reactions with alkanes is the
generation of the peroxyalkyl radical R02', which plays a substantial role
in the conversion of NO to NO,,. Rate constants for alkane reactions are
q
summarized by Hampson and Garvin.
The atmospheric chemical reactions involving olefins have been widely
studied. ' The most important reactions in which olefins participate
are with OH radicals, ozone, and atomic oxygen, in that order. The re-
action of OH with an olefin, such as propylene, may proceed by addition of
OH to the double bond or by abstraction of a H-atom from the olefin. For
propylene, for example, the reaction paths with OH are
CH3CH = CH2 + OH- •*• CH3£HCH2OH (6-29a)
OH
-»• CH3CHCH2- (6-29b)
H- CH££H = CH2 + H20 (6-29c)
In each case the free radical product will quickly react with 02 to produce
a peroxyalkyl radical that is capable of converting NO to N02.
Ozone-olefin reactions are an important source of free radicals and
stable products in air pollution chemistry. The initial attack of 03 on an
olefin produces an unstable intermediate, which may decompose by several
pathways.10'11 For propylene, for example, the initial step in the reaction
with 03 is believed to be:
6-9
-------
CH3CH = CH2
A
A CH,CH-CH
0 0
•00
CH3CH-CH2
Subsequent composition of the products leads to a variety of free radicals
12 13
and stable products. * 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:
CH3CH = CH2 + 0(3P) •»• CH3CH2- + HtO (6-31a)
or
•*• CH3fr) + CH3« (6-31b)
or
-»• CH3CH2CHO (6-31c)
The mechanism of photooxidation of aromatic species in the atmosphere
is perhaps the area of greatest uncertainty in atmospheric hydrocarbon
chemistry. The principal reaction of aromatics is with the hydroxyl
radical. » For aromatic-OH reactions, the initial step can be either
addition to or abstraction from the aromatic ring.103 The free radical
addition products may then react, most likely, with either 02 or N02,
leading to the creosols 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
6-10
-------
pollutants and are direct precursors of free radicals in the atmosphere.
Consequently, aldehyde chemistry represents an important subject area in
atmospheric chemistry. Although aldehydes are the main oxygenated hydro-
carbons generally considered with respect to their role in atmospheric
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 olefins, and radical decomposition products.
In addition, aromatic aldehydes can be formed as an ultimate consequence of
the reaction of OH with aromatics, e.g. benzaldehyde. The aldehydic hydro-
gen-carbon bond in aldehydes is relatively weak (CH bond strength is 86
kcal/mol ). Consequently, this hydrogen atom will be susceptible under
3 1
atmospheric conditions to attack by radical species, such as 0( P), 0( D),
OH, and HOp. 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 -> H20 + 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, respectively.
The photodissociation of aldehydes is an important radical generation
nechanism in the formation of photochemical air pollution. The reactions
that are most significant can be generalized in terms of a radical and a
Wlecular route:
6-11
-------
RCHO + hv -> R + HtO (6-33a)
and
-> RH + CO (6-33b)
(Reaction 6-33a was previously given as reaction 6-25.)
The radical route is the more important one from the point of view of
atmospheric chemistry. Considerable attention has been given to formal-
dehyde 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)
In order to compare the rates of photolysis with the depletion of forma-
ldehyde by OH reaction, one can calculate a photolysis rate of approxi-
mately 13 percent per hour for a solar zenith angle of 20° using the value
of the photodissociation rate given by Horowitz and Calvert.
The interaction with NO and N0« of the organic free radicals produced
by hydrocarbon oxidation represents an extremely important aspect of the
chemistry of the oxides of nitrogen in the polluted atmosphere. The ra-
dicals can be classed according to:
R-
RO-
ROO-
alkyl
alkoxyl
peroxyal kyl
0
it
RC»
0
M
RCO-
0
it
RCOO.
acyl
acylate
peroxyacyl
In air it can be assumed that combination with 02 is the sole fate of alky!
(R*) and acyl (RCOO radicals and that the reaction is essentially in-
stantaneous. Consequently, in reactions with alkyl or acyl radicals as
6-12
-------
products, these products are often written as the corresponding peroxy
radicals. Also, acylate radicals will decompose rapidly to give an alky!
radical and C02. Therefore, only alkoxyl, peroxyalkyl, and peroxyacyl
radicals need to be considered explicitly in terms of NO chemistry. Table
^
6-1 shows the various reaction combinations that are important between
these radicals and NO and N02-
The reactions of OH with N02 and NO are reasonably well understood and
have been previously listed as reactions 6-18 and 6-19. Rate constants for
Q
these two reactions are available.
The rate constant for the reaction of H07 and NO has recently been
determined by direct means and is substantially larger than previously
1Q
calculated indirectly. The FKL-NO reaction, as noted earlier, is a key
reaction in the atmospheric conversion of NO to NO,,.
The reaction of H02 and N02 has the following two possible mech-
anisms:
H02 + N02 + H02N02 (6-35a)
and
H02 + N02 -»• MONO + 02 (6-35b)
In addition, the peroxynitric acid formed in reaction 6-35a thermally
21
decomposes as follows:
i
H02N02 -»• H02 + N02 ' (6-36)
At the present time it appears that, at the temperatures prevalent in
summer smog episodes (>20°C), peroxynitric acid does not represent an
appreciable sink for N02 because of the rapid thermal decomposition
reaction 6-36. At lower temperatures H02N02 will achieve higher con-
6-13
-------
centrations and its importance as a sink for NCL increases.
The reactions of RO, R02 and RC03 with NO and N02 represent key
reactions in the conversion 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 (6-38a)
or
+ RCHO + HONO (6-38b)
The reaction of alkylperoxyl radicals with NO is generally assumed to
proceed by the oxidation of NO to NOp 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 atmosphere (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 photooxidation will add to NO to form an excited complex that
22
can be stabilized to produce an alkyl nitrate:
R02- + NO -»• RON02 (6-39)
The peroxyalkyl-N02 reaction proceeds principally by
R02- + N02 •»• R02N02 (6-40)
The peroxynitrate may thermally decompose according to
R02N02 -*• R02- + N02 (6-41)
6-14
-------
Measured rate constants for the R02-N02 reaction and the FK^NCL decomposition
are not currently available.
Peroxyacyl nitrates have long been recognized as important components
i 27
of photochemical air pollution. Peroxyacetyl nitrate (PAN) exists in
equilibrium with the peroxyacyl radical and N02:
0 0
CH3COO- + N02 j CH3COON02 (f>-W)
There exists a competition between NO and N02 for the peroxyacyl radical
through:
0 0
CH3COO- + NO -»• CH3CO- + N02 (6-43)
The acetyl radical will rapidly decompose as follows:
CH3CO- -> CH3- + C02 (6-44)
followed by:
CH3- + 02 -*• CH302- (6-21)
CH302- + NO -> CH30- + N02 (6-22)
CH30- + 02 -> HCHO + H02' (6-23)
H02- + NO •* OH- + N02 (6-24)
Thus, PAN chemistry is intimately interwoven in the NO to N02 conversion
process. Rate constants for reactions 6-42 and 6-43 have recently been
of- OC
.reported by two groups of investigators. '
> The chemistry of the oxides of nitrogen in a hydrocarbon-containing
atmosphere can be summarized as follows: The major observed phenomenon in
6-15
-------
the system is conversion of NO to N0« 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 03. N02 serves as both an initiator
and terminator of the chain reactions that result in conversion of NO to
N02 and buildup of 03. Termination of the chain reactions leads to nitric
acid and organic nitrates. The nature of the system can be explained by
considering its behavior as a function of the initial concentrations of NO
f\
and hydrocarbon in the irradiation of a static system, as well as the ratio
of two reactants, i.e, the [HC]/[NOJ ratio.
A
At low [HC]/[NO ] ratios, usually ratios of less than 1/1, the rate at
A
which NO is converted to N02 is influenced by the availability of organic
compounds. Therefore, the effects of reducing organic compounds are to
slow the conversion of NO to NOg, thereby lowering the NOp/NO ratio. When
this occurs, a larger proportion of the NO that is converted to NOp 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 signi-
ficant amounts of N02 are created, photodissociation of NOp will be diminished
and less ozone will accumulate on that day. At moderately high £HC]/[NO ]
^
ratios (usually greater than 5/1), 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 N02 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
A
additional organic precursors. At very high [HC]/[NO ] ratios (greater than
/\
20/1), ozone cannot accumulate because either the ozone is consumed by
6-16
-------
reaction with hydrocarbons or radical-radical termination reactions occur
which reduce oxygen atom and, hence, ultimate ozone concentration. Of
course, this discussion is applicable for a definite distribution of
hydrocarbons. If the hydrocarbon distribution is altered, say to all
aromatic, the concentration of ozone may build up even at high HC/NO
A
ratios since the ozone once produced would not be destroyed by further
reactions with the hydrocarbons.
Identification of the nitrogen-containing products in atmospheric
28 30
reactions has been under investigation for a number of years. 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
«
NOp with free radicals produce, in addition to nitrous, nitric, and
peroxynitric acids, a variety of organic nitrogen-containing 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 formation and decomposition of peroxynitrates,
WLNCL, is unknown, .and rate constants for the key reactions in the series,
ROg + NO, are yet to be determined.
S-1^ Laboratory Evidence of the NOp-to-Precursor Relationship
In the previous section, the nature of chemical reactions involving
oxides of nitrogen and hydrocarbons in the atmosphere was discussed. These
reactions have traditionally been studied experimentally in laboratory
vessels called smog chambers. These chambers characteristically employ
radiation sources that closely approximate the UV portion of the solar
spectrum as observed at the earth's surface and clean, chemically inert
interior surfaces. It is believed that the chemical processes that take
6-17
-------
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
injection 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 under-
standing of atmospheric chemical mechanisms.
Considerable effort has been devoted to the development of chemical
reaction mechanisms that are capable of describing the processes observed
23 31
in smog chambers. ' Smog chambers have been used extensively to deter-
mine how concentrations of NOX and other photochemical products respond to
changes in the initial composition of nitrogen oxides and organics. A
27
previous Criteria Document discusses smog chamber evidence concerning the
relationship between ozone/oxidant and the photochemical precursors. This
section focuses on how N02 concentrations respond to changes in the input
levels of organics and nitrogen oxides.
Several researchers have used smog chambers to investigate the depen-
dence of nitrogen dioxide concentrations on the levels of precursor inputs:
o The University of North Carolina (UNC) study using an 11,000 cubic-
o
foot (311 m ) outdoor Teflon chamber, a simulated urban hydrocarbon
op
mix, and twelve-hour irradiations
o The Bureau of Mines study, using a 100 cubic-foot (2.8 m3) aluminum-
glass chamber, auto-exhaust hydrocarbons, and six-hour irradiations33'
6-18
-------
o The General Motors study, using a 300 cubic-foot (8.5 m3) stainless
steel-glass chamber, a simulated Los Angeles hydrocarbon mix, and six-
hour irradiations
o The Health, Education and Welfare (HEW) study using a 335 cubic-foot
o
(9.5 m ) chamber, auto-exhaust hydrocarbons, and up to ten-hour
oe
irradiation time and
0 The HEW study using a 335 cubic-foot (9.5 m ) chamber, toluene and m-
xylene, and 6-hour irradiations.
38 39
Trijonis * has recently reviewed the results of these studies, as
sumnarized in Table 6-2. As indicated in Table 6-2, the various chamber
studies basically agree concerning the dependence of maximal N02 and
average N02 on NO input. With other factors held constant, maximal N02
and average N0~ tend to be proportional to initial NO . The minor devia-
£ X
tions away from proportionality that sometimes occur tend to be in the
direction of a slightly less than proportional relationship, i.e. a 50%
reduction in NO input sometimes produces slightly less than a 50% re-
X
duction in N02.
There is less agreement among the chamber studies concerning the
dependence of N02 on initial hydrocarbon concentrations. With respect to
maximal NO,., the Bureau of Mines study indicates essentially no dependence
on hydrocarbons. However, two other studies suggest that hydrocarbon
reductions decrease maximal N02 concentrations. The UNO results indicate
that 50% hydrocarbon control tends to decrease maximal N02 by about 10% to
202. The General Motors studies imply that 50% hydrocarbon control reduces
maximal N02 by about 25%.
With respect to average N02, the Bureau of Mines study indicates that
6-19
-------
hydrocarbon reductions would tend to increase NOg dosage. This result is
40
consistent with the theoretical argument of Stephens, who hypothesized
that hydrocarbon reduction would increase average NOp because these re-
ductions would delay and suppress the chemical reactions that consume N0?
after it reaches a peak. However, the General Motors chamber study and the
two HEW studies indicate that hydrocarbons produce no consistent effect on
average N02 concentrations. Furthermore, in direct contradiction to
Stephens' hypothesis, the UNC experiments imply that a 50% reduction in
hydrocarbons produces about a 20% decrease in average N02> There is some
question about the UNC conclusion, however, because the UNC chamber runs
were of a 10-hour duration and the N02 levels at the end of the experiments
were greater when hydrocarbons were reduced. The extra N02 remaining after
the 10-hour period could cause an increase in 24-hour average N02, even
though average N02 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 N02 concentrations (a change of + 10 percent) but would yield
moderate decreases in maximal N02 (a reduction of about 10 to 20 percent).
It should be noted that these conclusions are meant to apply to one basic
type of ambient situation - the situation of well-mixed urban air.
Some additional support for these conclusions was provided recently by
studies of actual ambient data on NOX and hydrocarbon levels from a number
of cities in the U. S. Using empirical modelling and historical trend
38 39
analysis, Trijonis ' concluded that the ambient data were generally
consistent with the consensus of chamber results. The exact form of the
6-20
-------
NOp/precursor relationship, however, was found to vary somewhat from one
location to another, presumably depending on local hydrocarbon/NO ratios,
J\
on the details of the hydrocarbon mix, and on specific meteorological
conditions.
6.1.3 NO Chemistry in Plumes
' TA ""
The atmospheric chemistry involving oxides of nitrogen in plumes from
major fuel burning installations is essentially that described earlier.
However, the relatively high concentratins of NO and N02 in such plumes com-
pared with those in the ambient urban atmosphere leads to certain chemical
phenomena particularly characteristic of plumes. For example, ambient
ozone is quickly scavenged in the plume by the large quantities of NO
through reaction 6-4. Because the rate of the N0-03 reaction is fast
relative to that of dilution of the plume, the rate of conversion of NO to
NOg is controlled by the rate at which ambient 03 is entrained into the plume
by turbulent mixing. There is some nitric acid produced in power plant
plumes during the daylight hours through the oxidation of nitric oxide
{reaction 6-1) and the subsequent photodissociation of N02 (reaction 6-2),
then followed by the combination of N02 with N03 and H20 (reactions 6-10
and 6-8). The generation of nitrous acid is also probable since the stack
gases will contain NO, N02, and H20 (reaction 6-13). Since nitrous acid
will photodissociate to give hydroxyl radicals (reaction 6-17), more
nitric acid can be produced by reaction 6-18. Thus, although the free
radical concentration is expected to be low in power plant plumes, some
N0xwill be converted to nitric acid. In addition, after sufficiently long
travel times during which ambient hydrocarbons have been mixed with the
plume constituents, the usual free radical reactions described earlier
occur, possibly leading to 03 production.
6-21
-------
There are several studies in which measurements have been made of the
concentrations of pollutants in power plant plumes.43' 5' The most
difficult current problem is predicting the rate at which NO is converted to
N02 in such a plume since the 'rate of conversion is controlled by the rate
of mixing of the plume.
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 were identified:
MONO nitrous acid
HON02 nitric acid
H02N02 peroxynitric acid
RONO alkyl nitrite
RON02 alkyl nitrate
0
RCOON02 peroxyacylnitrate (PAN)
R02N02 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 concentration 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 HONO, MONO,,, H00N09,
L. «_ £
6-22
-------
RONO, RON02, RC(0)OON02 and R02N02 for smog chamber experiment EC-237
carried out at the Statewide Air Pollution Research Center of the Univer-
sity of California, Riverside, using the chemical mechanism of Falls and
Q
Seinfeld. 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, N02 Og, PAN, and hydrocarbons, agreed well.
The concentrations of HONO, H02N02, and RONO are predicted to be small
relative to those of NO and N02. Each of these species has decomposition
reactions,
HONO + hv -> OH- + NO (6-17)
H02N02 -»• H02- + N02 (6-36)
RONO + hv f RO- + NO (6-45)
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,
HOpN02 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 destruc-
tion route for HONO is reaction 6-14. Depending on the relative impor-
tance of reactions 6-19, 6-13, and 6-14, HONO may reach substantial con-
centrations under nighttime conditions. A lower limit on the nighttime
concentration of HONO can be estimated from the equilibrium HONO concen-
tration based on reactions 6-13 and 6-14.
6-23
-------
[MONO] =
k13[NO][NO ][H20]
1/2
14 <6-46)
At [NO] = [N02] = 0.1 ppm, [H£0] = 2.4 x 104 ppm (50 percent relative
humidity), the equilibrium MONO concentration calculated from equation 6-46
is 1.9 x 10~ ppm, using the values k,o and k^ reported by Chan et al.
Like MONO, H02N02 and RONO, PAN undergoes both formation and decom-
position steps (reactions 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 N02> 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 H02N02 and PAN. It was presumed in the mechanism on which the
results of Table 6-3 are based that R02N02 thermally decomposes at a rate
between those for H02N02 and PAN. Assessment of the importance of R02N02
as a sink for NOX 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 alky!
nitrates apparently do not undergo appreciable decomposition reactions.
Thus, these two species potentially serve as important atmospheric sinks
for N02. Both nitric acid and alky! 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
6-24
-------
particles or homogeneously nucleate to form particles.
Figure 6-1 depicts the potential paths by which particulate nitrate
species may be formed from NO and NCL. 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 experi-
ment have been given in Table 6-3. Comparisons of the individual rates of
reactions 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 NFL, a ubiquitous
atmospheric constituent with both natural and anthropogenic sources, to
produce ammonium nitrate, NH,N03 (path 2), which at standard temperature
and pressure, exists as a solid. Alternatively, the nitric acid vapor may
be absorbed directly into a particle (path 3), although thermodynamic and
kinetic considerations favor reaction with NHL to form NH-NOo as the path
of conversion of gaseous nitric acid to nitrate in particulate form.
Path 4 involves the direct absorption of NO and N02 into an atmospheric
particle, a route that is likely for certain aqueous particles, particularly
52
when accompanied by the absorption of ammonia (path 5). Path 6 depicts
the formation of organic nitrates through reactions 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 deepicted by
path 6.
There have been a number of measurements of nitric acid and parti-
culate nitrate concentrations in ambient air, and several of these are
simmarized in Chapter 7. Many of the measurements have identified the
particulate nitrate as NH4N03, suggesting that the aerosol may consist of
6-25
-------
solid NH4N03 or NH^ and N03 in solution in approximate stoichiometric
balance. It is difficult 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 reaction is
probably rapid and, in fact, can be presumed to be in equilibrium with the
dissociation of solid ammonium nitrate.
NH3(g) + HON02(g) * NH4N03(s) (6-47)
Second, the rate of absorption of NO and N02 into existing particles
depends on the composition and size of each particle and cannot generally
be predicted a priori. In either case it is apparent that the presence of
NH3 is required, either to form NH,N03 or to neutralize the acidity of a
liquid droplet in which NO and NOp dissolve.
The current state of understanding of atmospheric nitrate formation
can be summarized 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 6-47 is established.
In competition with the nitric acid/ammonium nitrate path is the path
consisting of direct absorption of NO and ML into aqueous droplets. The
relative rates of these two paths cannot be determined in general.
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
6-26
-------
and N02 may also be absorbed into existing particles. The mixture of
gases and particles is transported downwind of the source region, accom-
panied by continuous conversion of more of the NO gases to particulate
/\
nitrates. Also occurring simultaneously is surface absorption of NO and
NOg 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 nitro-
genous 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 complexes in order to obtain material balances on gaseous and
52 53
particulate pollutants. ' A goal of these studies is to determine the
relative roles of transport, removal and conversion of gaseous to par-
ticulate pollutants on the overall pollutant material balance downwind of a
major urban source. On the basis of the previous discussion 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 inter-
relations. 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 distributions of the
particles. However, at this time, the understanding necessary to
6-27
-------
formulate and apply such a model does not exist. 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 par-
ticulate 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
54
model of this type has been developed by Peterson and Seinfeld and
applied to the prediction of airborne concentrations of gaseous and
particulate pollutants in the case in which gases are converted to
54
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 estimates 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.
In this section the general nature of the transport and removal of
nitrogeneous species is briefly discussed.
6-28
-------
6.3.1 Transport and Diffusion
Some atmospheric processes play an important role in the dispersion
of air pollutants on large spatial scales, and others are important on
small spatial scales. The interactions among these processes, and their
overlapping influences on eventual pollutant distributions, are very
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 diurnally and seasonally. They also vary spatially if nonuniform
terrain or inhomogeneous heating is present. Aside from the dominant
atmospheric motions, divergence in the synoptic and mesocale horizontal
wind regimes leads to vertical air motions. Vertical currents, which
give rise to the phenomenon known as Ekman pumping, are also generated
by viscous forces in the boundary layer and can be particularly large in
regions of complex terrain. Although the vertical velocities generated
6-29
-------
by these processes have a magnitude of only 1 to 10 centimeters per
second, they can have significant effects on the net transport of air
pollutants. Accurate estimates of the vertical components of the wind
vectors on this scale are extremely difficult to obtain. While vertical
diffusion is over-whelmingly dominant, lateral (or horizontal) diffusion
is also marginally important in pollutant transport over large dis-
tances.
6.3.2 Removal Processes
The following two processes must be considered in assessing the
removal of nitrogeneous species from the atmosphere:
o dry deposition
o wet deposition (rainout and washout)
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 concentration c. (micrograms per cubic meter) is removed
across a horizontal surface of unit area at an elevation zs is often
expressed at c-v- where v- is the so-called "deposition velocity," which
depends on the value of zg.
Vegetation has been shown capable of removing significant amounts
of N02 and NO from the atmosphere. Tingey showed that alfalfa and
12
oats absorbed N02 from the air in excess of 100 x 10 moles per square
3
meter per second when exposed to an atmosphere containing 460 yg/m
N02 (or 1 x 10 moles per cubic meter). More recent work by Rogers et
al. , using a continuous reactor technique, indicated that the N02
uptake in both corn (Zea mays 1.) and soybean (Glycine max. L.) could be
6-30
-------
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 NCL concentrations and leaf surface area, but
55
directly dependent upon inverse total diffusion resistance. Tingey
extrapolated his data to estimate the removal of N0? from the Salt Lake
Valley in Utah. On an annual basis, removal of N02 from the valley with
an ambient N02 concentration of 9.6 yg/m (0.005 ppm) which is about 3-4
times greater than background N02 levels, would total about 3 x 10 kg
NtL. This may be compared with an estimated total global anthropogenic
9 57
annual N02 emissions of 53 x 10 kg.
ro
Hill 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 N02 was absorbed at a velocity of 2 cm/sec when present in
o
the air of the chamber at a concentration of 96 yg/m (0.05 ppm). Using
ambient N02 concentrations found in those areas of Southern California
from August to October of 1968, and assuming a continuous alfalfa cover,
2
Hill estimated that N02 could be removed at a rate of 0.1 gram/m /day.
Nitrogen oxides (especially N20) have long been known to be pro-
duced by biological action in soils. Recently, however, Abeles et
al.59 found that soils could absorb N02 from the atmosphere as well.
They found that when air containing N02 was passed over soil in a test
chamber, the concentration of N02 in the air was reduced from an initial
value of 190 x 103 yg/m3 (100 ppm) to 5.7 x 103 yg/m3 (3.0 ppm) over a
24-hour period. When soil was autoclaved, the total N02 present over the
same time period was reduced from 186 x 103 yg/m3 (97 ppm) to only 25 x
103 yg/m3 (13 ppm). This result would point to a biological sink for
6-31
-------
NOp in soils. Ghiorse and Alexander , 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, autoclaved or
y-irradiated. The authors point out that autoclaving may drastically
alter the physical and chemical properties of soil and thus introduce
artifacts in such studies. They conclude that the role of microorgan-
isms in the fate of NOp 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 NO^. Mortland has noted that transition metal ions in
the soil promote NO absorption. If the soil is saturated with alkaline
cp
earth cations though, absorption of NO is halted. Sundareson et al.
found that alkaline-earth zeolites readily absorb NO and release it as
NO and HNO^ when heated. To date, the role of organic matter in the
absorption of nitrogen oxides by soil is unknown.
6.3.2.2 Dry Deposition of Particles—
The deposition of particles can occur through sedimentation,
Brownian diffusion, or impaction. Impaction occurs when, because of its
inertia, a particle is unable to follow the streamlines of air around an
obstacle and is intercepted by the object. The removal of particles
through impaction on an object can be defined in terms of a pseudo-
deposition velocity, v . The loss of particles per unit surface area of
the object per unit time can then be expressed as:
LD = -vgN, (6-48)
6-32
-------
where N is the number density of particles in the size range corresponding
to the deposition velocity, v .
y
The transfer of aerosol particles from the turbulent atmosphere to an
underlying boundary depends upon the flow near the surface, as well as upon
the nature of the surface itself. Particles are transferred through a
turbulent boundary layer, the transport properties of which depend on the
eddy motion of the turbulence. Near the surface, the particles move
through a laminar sublayer, where the thermal motion of the particles
becomes important.
Particle removal from the atmosphere by deposition strongly depends on
the properties of the surface on which material deposits, the surface
roughness, and the wind speed. For the purposes of an order-of-magnitude
63
estimate of deposition rates, one can use the results of Chamberlain to
estimate v .
6.3.2.3 Wet Deposition-
Precipitation can remove gases and particles by two methods, rainout
and washout. Rainout involves the various processes taking place within a
cloud that lead to the formation of raindrops. Washout refers to the
removal of aerosols below the cloud by falling raindrops.
Rainout and washout, together with dry deposition, are the major sinks
for atmospheric nitrogen-containing species. The efficiency of rainout and
washout as removal mechanisms depends on three factors:
o The quantity of clouds
o The efficiency of the capture mechanism of gases and
particles by clouds and raindrops
o The frequency of rains
.Particles are removed by rainout through their serving as condensation
6-33
-------
nuclei for cloud formation. The extent of absorption of gases by cloud
droplets depends on the chemical compositions of both the gases and the
droplets. Whereas the removal of SOp by cloud droplets has received con-
siderable attention, the processes taking place during the absorption of NO
and NCL by water droplets have not yet been thoroughly studied. In a study
51
of aerosol nitrate formation routes, Orel and Seinfeld elucidated many of
the chemical processes that occur when NO and N0« are absorbed in water
droplets. The most important factor in the overall efficiency of rainout
in removing oxides of nitrogen from the atmosphere is the frequency of
rains. Because of the difficulty in describing the detailed processes
occurring in rainout, it is generally assumed that removal of pollutants by
rainout can be described adequately by a characteristic mean residence
time, and that the amount of pollutant removed by rainout at any one place
is proportional to the ambient concentration of that pollutant.
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 generally much lower than those near the ground where washout occurs.
Thus, rainout and washout can be of similar importance. The uptake of NO
/\
by rain depends on physical parameters such as rainfall intensities and
raindrop size distributions, and on chemical characteristic^, such as 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
6-34
-------
drop controls the quantity absorbed. The study of Dana et al. suggests
that under typical atmospheric conditions washout is often mass-transfer-
11mlted.
6.4 MECHANISMS OF ATMOSPHERIC NITROSAMINE FORMATION
This section is limited to a discussion of specific reactions possibly
leading to the formation of nitrosamines and related compounds in the
atmosphere.
Three mechanisms will be discussed in this section:
o Non-photochemical reactions of gaseous amines with oxides of
nitrogen and nitrous acid
o Photochemical reactions of amines with oxides of nitrogen in
the gas phase
o Heterogeneous nitrosamine formation processes in atmospheric
aerosols
The first two processes have been the object of recent experimental studies,
including simulation 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 discussed 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 Matz65' reported the fast formation of diethyl-
nitrosamine (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. Dimethylnitrosamine was formed in
6-35
-------
the same way from dimethylanrinfe 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 , who achieved in a few minutes a 90 percent conversion
to diethylnitrosami ne at 25°C. They proposed the following rate equation:
-d(N02)/dt = k (dimethylamine) (N02)2 (6-49)
8 2 -2 -1
with a rate constant k.g = 6.5 x 10 1 Mol s . Initial reactant con-
-6 -5 -1
centrations ranged from 4 x 10 to 6 x 10 Mol. 1 . 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 (6-50)
Neurath and co-workers ' 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 (6-51)
N203 + 2 R2NH H- 2 R2NNO + HgO (6-52)
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 and diethylamine
with NO in the presence of 10 percent oxygen were also followed by directly
6-36
-------
measuring the (decreasing) amine concentration. No reaction was observed
between diethylamine and NO in nitrogen.
Dushumin and Sopach also report a rapid reaction between dimethylamine,
N«0. (in equilibrium with NCL) 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 [(CH3)2NN02L it
is suspected that photochemical reactions took place as well, as is dis-
cussed 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 nitro-
71 72
samines were obtained by Hanst et al., Grosjean et al., and Pitts et
al.73 in experiments involving dark reactions of ppm levels of alkylamines
and nitrogen oxides in humid air.
Hanst, Spence and Miller,71 using long path infrared spectroscopy,
followed the reaction of 1 ppm dimethylamine with 0.5 ppm HONO (in equi-
librium with 2 ppm NO, 2 ppm N02 and 13,000 ppm water vapor) in air in
a 9 m x 0.3 m diameter cylindrical glass cell. Dimethylnitrosamine was
formed in yields of 10 to 30 percent, and the rate of amine disappearance
Wis ^ percent min .
72 73
Grosjean et al. and Pitts et al. also report .low yields of ni-
trosamine in the dark reaction of ^.5 ppm amine with 0.8 ppm NO and 0.16
ppm N02 in air at 30 percent relative humidity in 50 m Teflon chambers.
Hitrosamine yields were 2.8 percent from diethylamine and ^1 percent from
dimethylamine. The tertiary amine triethylamine also yielded diethylni-
Irosamine (0.8 percent yield), while trimethylamine yielded traces of
6-37
-------
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. , Hanst et
al. estimated an amine disappearance rate of 0.8 ppm min . This would
constitute an upper limit for nitrosamine formation since (a) the nitro-
samine 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 reaction, and (c) nitrous acid formation may be controlled by
heterogeneous rather than homogeneous processes.
With respect to the latter, Cox and Derwent reported decomposition
of 150 ppm MONO 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 reinvestigated the kinetics of formation and decomposition
of nitrous acid:
NO + N02 -f H20 ->. 2 MONO (6-53)
2 HONO -»• NO + N02 + HgO (6-54)
They found the reactions to be heterogeneous under all surface conditions
tested. They also estimated upper limits for the homogeneous rate constants;
kj < 4.4 x io'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.74 Thus,
homogeneous (gas phase) formation of nitrous acid seems too slow to account
6-38
-------
for HONO formation in the studies of Hanst at al. and Grosjean and
72 73
Pitts ' , and heterogeneous formation (being itself very slow) may
account for the low nitrosamine yields reported by these authors. Pitts et
73
al. 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.77'?8
Finally, it should be noted that the accepted mechanism for the
liquid phase nitrosation of secondary amines involves N^Oo according
to the reactions:
2 HONO j N203 + H20 (6-55)
N203 + R2NH + R2NNO + HONO (6-56)
p
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 heterogeneous processes. The mechanisms
of Gehlert and Rolle and Neurath et al. for the gas phase reaction also
involve N203 (or NO and N02). Furthermore, Hanst et al. 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 not conducive
to the formation of nitrous acid) was comparable to that measured in the
amine-HONO-NO -water mixture in air (1 percent min and 4 percent min" ,
X
respectively). Thus, the conflicting evidence currently available does not
permit firm conclusions regarding the rates, yields and mechanisms of
nitrosamine formation from amines and oxides of nitrogen in the dark.
6-39
-------
6.4.2 Photochemical Reactions of Amines
79 T\
In the smog chamber experiments described in the previous section, *°
amine-NO -air mixtures were also exposed to sunlight for ^ 2 hours. Diethyl-
A
and triethylamine reacted rapidly to form ozone, peroxyacetylnitrate (PAN) and
acetaldehyde 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 including diethylnitramine [(CpHgLNNOp] and
several ethyl substituted amides. These products and the corresponding yields
are listed in Table 6-4.
Irradiation of dime thy! amine and trimethyl amine under the same conditions
yielded ozone, formaldehyde, dimethylnitramine [(CH3)2NN02] and several methyl
7"?
substituted amides in the gas phase as well as aerosol products. Reaction
products of dimethylamine that have also been identified by other investigators
include formaldehyde ', dimethylnitramine ', and the amine nitrate
aerosol.67'70
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 nitrosamine65'66*71 and diethylnitrosamine.65*66
In contrast, the concentration of diethylnitrosamine formed in the dark from
the tertiary amine, triethylamine, increased upon irradiation for «v 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 *73 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)2N£HCH3 (6-57)
6-40
-------
followed by the well-known sequence ft + 02 -»• R62, R6? + NO •> N0? + RO".4
The alkoxy radical R6 then decomposes to give two of the major products,
acetaldehyde and diethylacetamide:
6
(C2H5)2 NCHCH3->- CH3CHO + (C2H5)2ft (6-58)
-> (C2H5)2NCHO + £H3 (6-59)
Further reactions of acetaldehyde lead to PAN, another major product.
The diethyl ami no radical, (C2H5)2N, reacts with NO and N02 to form
diethylnitrosamine and diethylnitramine, respectively:
(C2H5)2N + NO •*• (C2H5)2NNO (6-60)
(C2H5)2N + N02 H- (C2H5)2NN02 (6-61)
It is assumed, by analogy with the simplest dialkylamino radical, NH2, that
reaction of (C2H5)2N with oxygen is very slow (this has received confir-
mation very recently in the case of NH283).
A recent study by Calvert et al.84 of the photolysis of dimethyl-
nitrosamine has shown that the dimethylamine radical, (CH3)2N, can react
with NO almost 10 times faster than with 02 and with N02 approximately 107
times faster than with 02. Nitrous acid and CH3N=CH2 were 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
6-41
-------
yield indicates that the di ethyl ami ne radical is also produced by other
reactions, including OH abstraction on the N-H bond:
(C2H5)2NH + OH + (C2H5)2N + H20 (6-62)
Rate constants for the OH-amine reaction have been measured recently '86
and are consistent with both N-H and C-H abstraction. Alkylamines react
quite rapidly with OH, with atmospheric half-lives of 2-3 hours at typical
pC
OH concentrations in the lower troposphere.
The efficient formation and accumulation of nitramines (reaction 6-61)
72 73
is due to their stability in sunlight. * In contrast, nitrosamines
photodecompose readily:
hv
R2NNO •+ R2N + NO (6-63)
and their concentration in sunlight is dictated by the competing reactions
6-60 and 6-63. Results shown in Figure 6-3 for triethylamine indicate that
photochemical formation (reaction 6-60) may prevail upon photodecomposition
during daytime under certain conditions, in contradiction with the
generally accepted idea that any nitrosamine present at night in the
71 87
atmosphere should be rapidly destroyed after sunrise. 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
oo
Heterogeneous formation in acid aerosols has been suggested as a
possible 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,
6-42
-------
nitrous acid, or other species, could theoretically lead to the formation
of nitrosamines. The acid media would favor nitrosamine formation and
wuld prevent rapid photodecomposition during daylight hours since the
absorption of nitrosamines is greatly attenuated in acid solutions.89
This hypothetical mechanism, which is intuitively plausible, warrants
several comments. First, basic species, such as ammonia, which are present
in ambient air at higher concentrations than amines, may compete effectively
for absorption in acidic aerosol droplets. Second, nitrosamines photolyze
89 90
readily in aqueous solutions * 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 necessarily
required, since several studies have shown that nitrosation proceeds quite
91
effectively at neutral and/or alkaline pH by free radical processes or
92 93
due to catalysis by carbonyl compounds or metal ions. * Finally,
irrespective of the aerosol acidity, reactions of nitrosamine with oxi-
dizing species in aqueous aerosol droplets may lead to the formation of,
for example, ni trami nes.
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.
Nighttime production of nitrosamines: Conflicting results are pre-
sented in the literature concerning nitrosamine formation rates and yields
from secondary and tertiary amines. Several investigators report low
6-43
-------
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.
71-73
Nitrosamines have been shown to form from secondary and tertiary
amines72'73 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
94
phase.
If one accepts the low yields of Hanst et al .71 and Grosjean, Pitts et
al. ' nighttime concentrations of nitrosamines in typical urban atmos-
pheric conditions should be quite low. However, .caution should be exer-
cised 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 photodecomposi-
tion. However, photochemical formation of diethyl nitrosamine from the
tertiary amine, triethylamine, has been shown to prevail over photodecom-
position 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 in-
dustrial environments where, for example, 50-500 ppb of amine might be
6-44
-------
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.
95 96 97 98
Dimethylnitramine ' and acetamide ' are carcinogenic, while
99
dimethyl formamide has been identified in urban air and has been shown to
undergo nitrosation. ' Another amide, N.N-dirnethyl-acetamide, has
102
been identified in diesel crankcase emissions.
6-45
-------
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M
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tertiary amines. J. Amer. Chem. Soc. 89: 1197, 1967.
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temperature range 299-426°K. J. Chem/Phys. 66-. 1578, 1977.
86. Atkinson, R., R. A. Perry and J. N. Pitts, Jr. Rate constants of
for the reactions of the OH radical with (CH~)?NH, (CH^)2N and
C«HCNH9 over the temperature range 298-426°K: J. Chem? Phys. 68_:
1850, 1978.
87. Scientific and Technical Assessment Report on Nitrosamines. EPA-
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89. Chow, Y. L., M. P. Lau, R. A. Perry, and J. N. S. Tarn. Photo-
chemistry of nitroso compounds in solution. XX. Photoreduction,
photoelimination and photoaddition of nitrosamines. Can. J. Chem.,
50: 1044, 1972.
6-52
-------
90. Polo, J., and Y. L. Chow. Efficient degradation of nitrosamines
by photolysis. Int. Agency for Research on Cancer (IARC) Scientific
Publication No. 14: 473. Lyon, France, 1976.
91. Challis, B. C., and S. A. Kyrtopoulos. Rapid formation of car-
cinogenic N-nitrosamines in aqueous alkaline solutions. Brit. J.
Cancer 35: 693, 1977.
92. Keefer, L. K., and P. P. Roller. N-nitrosation by nitrite ion in
neutral and basic medium. Science 181: 1245, 1973.
93. Keefer, L. K. Promotion of N-nitrosation reaction by metal complexes.
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No. 14_: 513. Lyon, France, 1976.
94. Wartheson, J. J., R. A. Scanlan, D. P. Bills, and L. M. Libbey.
Formation of heterocyclic nitrosamines from reaction of nitrite
and selected primary diamines and ami no acids. J. Agric. Food
Chem. 23: 898, 1975.
95. Goodall, C. M., and T. H. Kennedy. Carcinogenicity of dimethyl-
nitramine in NZR rats and NZO mice. Cancer Lett. 1: 295, 1976.
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chemical constitution and carcinogenic effects of the nitrosamines.
Naturwissenchaften 48_: 134, 1961.
97. Jackson, B., and F. I. Dessau. Liver tumors in rats fed acetamide.
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98. Weisburger, J. H., R. S. Yamamoto, R. M. Glass, and H. H. Frankel.
Prevention by arginine glutamate of the carcinogenicity of
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99. Pellizzari, E. D. The Measurement of Carcinogenic Vapors in
Ambient Atmospheres. EPA-600/7-77-055. U. S. Environmental
Protection Agency, Research Triangle Park, North Carolina, June
1977.
100. Walker, P., J. Gordon, L. Thomas, and R. Oulette. Environmental
Assessment of Atmospheric Nitrosamines. Rep. No. MTR-7512, The
Mitre Corp., McLean, Virginia, February 1976.
101. Lijinsky, W., L. Keefer, E. Conrad, and R. van de Bogart. Nitro-
sation of tertiary amines and some biologic implications. J. Natl.
Cancer Inst. 4£: 1239, 1972.
102. Diesel Crankcase Emissions Characterization. Southwest Research
Institute, San Antonio, Texas, September 1977. National Technical
Information Service Report No. PB-275 950, 1977.
103. Kenley, R. A., J. E. Davenport, D. G. Hendry. Hydroxyl radical reactions
in the gas phase. Products and pathways for the reaction of OH with
toluene. J. Phys. Chem. 82: 1095, 1978.
6-53
-------
Table 6-1. REACTIONS OF ALKOXYL, ALKYLPEROXYL AND ACYLPEROXYL RADICALS WITH
NO AND NOo
i
tn
Free Radical
OH
H02
RO
R02
RC03
NO
Reaction Reference
OH + NO -> HONO Hampson and
Garvin, 19789
H0? + NO -> N09 + OH Howard and
10
Evenson, 1977iy
RO + NO •»• RONO Batt et al.23
(RONO + hv -»• RO + NO)
R02 + NO + N02 + RO
H. RON02
RC03 + NO •*• N02 + RC02 Cox and Roffey25
Hendry and
Kenley26
N02
Reaction
OH + NO, •*• HON09
H02 + N02 •*- HONO + 02
•*• H02N02 2
(H09NO,-^ H00 + N00)
C. c. £. £.
RO + N02 -»• RON02
-»• RCHO + HONO
2 2 22
(R02N02 -»• R02 + N02)
RC03 + N02 -»• RC03N02
(RC03N02 -»• RC03 + N02
Reference
Tsang et al . ,
197718
on
Howard, 1977^u
Graham et al. ,
197721
Wiebe et al.24
Cox and Roffey'
Hendry and
Kenley26
25
-------
Table 6-2. SUMMARY OF CONCLUSIONS FROM SMOG CHAMBER EXPERIMENTS
en
en
CHAMBER STUDY
University of North
32
Carolina
MAXIMAL N02
Dependence Dependence
on NO on HC
A
Proportional 50% HC reduc-
or slightly tion reduces
less than maximal N02
proportional by 10% to 20%
AVERAGE
Dependence
on NO
A
Proportional
or slightly
less than
proportional
N02
Dependence
on HC
Uncertain, 50% HC
reduction may de-
crease average
N02 by 20% or may
increase average
N00
•5-5 -54,
Bureau of Mines ' Proportional No effect
General Motors
35
HEW, Auto Exhaust
HEW, Toluene37
36
Slightly less
than propor-
tional
50% HC reduc-
tion reduces
maximal NO,
by 25% *
Proportional
Proportional
to slightly
less than
proportional
Proportional
Proportional
50% HC reduction
increases average
N02 by 10% to 30%
No effect
No consistent
effect
No effect
-------
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 SEINFELD8
HONO
HON02
H02N02
RONO
RON02
0
RCOON02
R02N02
60 min.
0.0061
0.067
0.00083
0.0030
0.0041
0.025
0.034
Concentration, ppm
180 min.
0.00040
0.22
0.0019
0.00054
0.0070
0.089
0.075
300 min.
0.00036
0.29
0.0025
0.000080
0.0072
0.13
0.098
Conditions of the experiment: T = 303°K, kg = 0.3 min"1, [N02]Q = 0.106,
[NO]Q = 0.377, [H20] = 2.4 x 104, [CO] = 0.96, [Aldehydes]Q = 0.0012,
[Alkanes]Q = 1.488, [Non-ethylene 01efins]Q = 0.15, [C2H4]Q = 0.875,
[Aromaticsl = 0.177, [HONOl (assumed) =0.1 (All concentrations in
A 1
ppm). Dilution rate = 2.93 x 10 min .
6-56
-------
6-4. MAXIMUM CONCENTRATIONS AND VIELDS OF THE PRODUCTS OF DIETHYVAMINE
AND TRIETHYLAMINE72'73
tn
Product
GAS PHASE
Ozone
Acetaldehyde
PAN
GAS PHASE (by GC-MS)
Dark
Di ethyl nitrosamine (c)
SunVight
Di ethyl nitrosamine (c)
Di ethyl nitramine
Diethylformamide
Diethylacetamide
Ethyl acetamide
Unidentified, MW=87 (d)
Di acetamide
Formula
°3
CH3CHO
CH3CO-OON02
(C2H5)2NNO
(C2H5)2NNO
(C2H5)2NN02
(C2H5)2NCHO
(C2H5)2NCOCH3
C2H5NHCOCH3
(CH3CO)2NH
From (C2Hg)2NH
Maximum Molar
Concentration Conversion
3 Yield,
yg/m ppb % (a)
290
300 30 (b)
41 4 (b)
59 14 2.8
-(destroyed)
780 162 32
29 7.0 1.4
3.6 0.8 0.2
42 12 2.4
-
- -
From (C2H5)3N
Maximum
Concentration
yg/m"3 ppb
260
700
"72
17 4.1
38 9.1
177 37
178 43
15 3.2
48 13
41 12
trace
Molar
Conversion
Yield,
% (a)
47 (b)
5 (b)
0.8
1.8
7.4
8.6
0.6
2.6
2.4
(continued)
-------
Table 6-4. (continued)
From (C2Hg)2
NH
From (C2H5)2N
Maximum
Concentration
Product
Formula
yg/m
-3
ppb
Molar
Conversion
Yield,
« (a)
yg/ni
Maximum
Concentration
-3
ppb
Molar
Conversion
Yield,
% (a)
I
tn
00
AEROSOL PHASE (e)
Sunlight
'•'scat (rnax^rnum value)
4 x KT'V1
46 xlO'
TSP
Acetamide
Di ethyl hydroxyl ami ne
Nitrates
CH3CONH2
(C2H5)2NOH
N03-
60
3
-
42
370
0.2 8.7
7.6
158
0.7
0.4
(a) Initial amine concentrations = 0.5 ppm (calculated from amount injected).
(b) Taking into account the number of ethyl groups in DEA and TEA.
(c) Not corrected for artifact formation (maximum ^ 10% of the observed concentration).
(d) Assuming same mass spectrometer response as diethylacetamide.
(e) Based on volumes sampled: 27.9 m3 (DEA) and 30.8 m3 (TEA).
-------
NOX(NO + N02)
6
Figure 6-1. Paths of Nitrate Formation in the Atmosphere51
6-59
-------
o
•9
>J
to
V
f
106
1 week —
10S
1 day —
104
Iw
1 hr.
103
102
IU
1 win, —
10
j
-
Domain of Interest
to Regional
Air Quality Studies-^
•
-
Planetary
Waves
{Extra-
— — —-J Trooical
1 Cyclones,
*C clonic Anti"
F^»^r»**^ r^«-. _»• ^^ tyc I onss /
\ r ~~ ~~ iX3,VC» *^
'->"•.'' '{Hum'-i
"•"•-',_ '- '- • t -,^ -.„.,. rn . . J ..
• » " 1 ^"^ X-
•Cumulonimous-con-r |. * x- x^
fvection (Land- Sea* i '; %,_".-] ^-^ -^
m
0 0
Atnosoheric
Turbulence
. \
"" """""JBresies and
'tain-Valley
Cumulus '
Convec-
tion j ^
\ ^-S
-------
©FROM (C2H5)2NH
O FROM(C2H5)3N
LJ
z:
CO tO
0 F
filled circles) and
from triethylamine (open circles).
-------
CHAPTER 7
OBSERVED ATMOSPHERIC CONCENTRATIONS OF NOY AND OTHER NITROGENOUS COMPOUNDS
/\
7.1 ATMOSPHERIC CONCENTRATIONS OF NOY
/\
In this section, selected examples of ambient concentrations of NO
/\
are presented in order to place possible human exposure in nationwide
perspective. NOp is given particular emphasis since it is the oxide of
nitrogen of most concern to human health. The data presented are not
intended to be a compendium of ambient monitoring activities. They have
been summarized to give a representative picture of N02 concentrations in
the United States.
7.1.1 Background Concentrations of NO
Data on background concentrations of nitrogen oxides are extremely
limited. Robinson and Robbins 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 N02 concen-
trations for land areas between 65°N and 65°S are 3.8 yg/m3 (0.002 ppm) and
7.5 yg/rn3 (0.004 ppm), respectively. The measurements cited for North
Carolina and Pike's Peak indicate that the background concentrations, in
remote areas of the United States, of NO and N02 combined can range from
0.001 to 0.005 ppm.1
More recent measurements using modern methods have yielded results
pointing to lower values. Noxon2 reports lower tropospheric N02 concen-
trations at a remote site in Colorado mountains of up to 0.20 yg/m
{0.0001 ppm) measured by ground-based absorption spectroscopy. In a more
7-1
-------
3
extensive study, Noxon reports detailed background measurements at the
Colorado site and at a number of other widely dispersed locations using
o
methodology with a sensitivity of 0.03 yg/m (0.015 ppb) at sea level. The
author concludes that in the truly unpolluted troposphere the column
1 /I O
abundance of N02 is less than 5 x 10 molecules/cm . Assuming an effec-
4 5
tive length for the N02 column of about 2 km, * this implies a ground
level N02 background concentration of less than 0.3 yg/m (0.15 ppb). If
the length of the column is 0.5 km, background N02 concentrations of
0.94 yg/m (0.5 ppb) would be implied. In addition, Noxon reports that the
ground level N02 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 Ritter et al. using chemiluminescence
analyzers at a site in Michigan showed NO concentrations in presumably
A
clean air coming from Canada to be in the range of 0.56 to 0.94 yg/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 7-1, taken directly from Ritter et al., summarizes
background NO measurements.
A
7.1.2 Ambient Concentrations of NO
^^^~^™"^^^^~ ' " A
7.1.2.1 Monitoring for NO
A
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 concentrations and relative amounts of
nitrogen oxides are the sources encountered along the trajectory and a
variety of meteorological variables. Atmospheric reactions, such as those
7-2
-------
that oxidize NO to NC^, are functions of the concentrations of pollutants
emitted to the atmosphere, temperature, sunlight, and time. Other meteoro-
logical 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 product of atmospheric reactions. Given the
complex nature of the processes which give rise to potential human expo-
sures, the most reliable and practical means of estimating these exposures
is by monitoring atmospheric concentrations.
Air monitoring data relevant to assessing ambient levels of NO or
A
NO -derived pollutants are collected to meet a variety of specific objec-
A
tives including:
o Determination of current air quality and in trend analysis
o Determination of the state of attainment of National Ambient
Air Quality Standards
o Preparation of environmental impact statements
o Development of effective control strategies and in evaluation
of their effectiveness
o Development and validation of mathematical models which relate
the strength of sources to predicted concentrations for a variety
of meteorological and topographic conditions
o Research, such as studies of the effects of ambient air pol-
lution on human health and welfare.
The ambient air quality data reported in this chapter relate mainly to the
first objective cited.
In general, each specific objective requires special consideration as
7-3
-------
to site location, frequency and techniques of sampling, and the total
amount of data collected. For example, several years of N02 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 very
detailed measurements of various pollutant concentrations, and emissions,
and meteorological parameters might suffice for the validation of mathe-
matical air quality models.
Once a station's location is chosed, additional practical considera-
tions arise relating to the actual placement of probes for sampling ambient
air. Building surfaces and other obstacles may possibly scavenge N02
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
the atmospheric chemical reactions, such as the conversion of NO emissions
to N02* which are characteristic of the polluted atmosphere. For this
reason, and also to avoid sampling air dominated by any one source, probes
must be located at least a minimum distance from primary sources.
Siting considerations have been reviewed recently and EPA has pro-
posed quidelines for air quality surveillance and data reporting which
p
include the considerations discussed briefly in this section. Refer
to these documents for a more complete discussion of the subject.
7.1.2.2 Sources of Data--
The emphasis in monitoring NO has been primarily on NOp, since it is
7-4
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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 received
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 insturmental
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, albiet only in 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 bases (minute-by-
nrinute data are also available) as obtained with chemiluminescence monitors
as 25 Regional Air Monitoring Sites (RAMS). These data are archived in a
special RAPS data base maintianed at EPA's Research Triangle Park Environ-
mental Research Center.
7.1.3 Historical Measurements of NO Concentration
' • -I - 1 -------- m--,.-...-m-_ £
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 avialable in this country. Some caution is necessary in
7-5
-------
using these data since collection and reporting procedures have not been
subject to detailed checks for data quality and since more than one ana-
lytical technique may have been used over the years at a given site. It
should be noted, however, that the data base presented does not include
data taken by the Jacobs-Hochheiser method since this method has been
withdrawn by EPA (Chapter 4). The data collected provide a useful
historical perspective on trends of NO concentrations. Table 7-2 presents
A
12 years of measurements of NO at CAMP stations for the time period 1962-
1973. The annual average NO concentrations are plotted in Figure 7-1.
Trends in concentrations are generally upward for all sites monitored.
When the annual means are grouped by 5-year periods, 1962-1966 and 1967-
1971 (Table 7-3), both the second highest value and the annual means
averaged over all CAMP cities show an increase of about 15 percent. Similar,
though more geographically variable results obtain for N02 concentrations
at most CAMP sites (Table 7-4, 7-5; Figure 7-2). St. Louis data show a
marked decrease, however, in both annual average concentrations and average
of second highest value between the two 5-year periods (Table 7-5). Upward
trends in annual average M^ concentrations are observed in 3 of the 5 CAMP
cities over the 9-year period, 1963 to 1971. Figure 7-3 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 is about 20 percent, but individual area results vary
widely.
7.1.4 Recent Trends in N0g Concentrations
Examination of data on trends in N02 concentrations in recent years
presents a variable picture at selected sites across the nation (Figures 7-
7-6
-------
4 through 7-8). 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 parameters, the only
data presented are those from the same site over the years plotted. Down-
ward trends are observed at Camden, New Jersey, for all statistics pre-
sented (Figure 7-4). A downward trend since 1971 is discernible at a site
in downtown Los Angeles (Figure 7-5) but in Azusa, California, an up-ward
trend is indicated (Figure 7-6). Nitrogen dioxide air quality seems to be
improving as of 1975 in'Newark, New Jersey (Figure 7-7). No clear-cut
trend is discernible in Portland, Oregon (Figure 7-8). Figure 7-9 shows
trends in a 4-year running average of annual averages 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 has increased over the same period. Changes in
N02 concentrations spanning the years 1969 to 1974, for the sites described
above as well as several other sites, are summarized in Table 7-6.
7.1.5 Seasonal Variations in NO,, Concentrations
In this section, a few examples of seasonal variations in N02 concen-
trations 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
x x
emissions of hydrocarbons, and area-specific meteorological conditions
throughout the year.
The data presented are, for the most part, averaged over several years
7-7
-------
of monitoring, a procedure which may be expected to yield representative
patterns for the regions reported. Examination of Figures 7-10 and 7-11
reveals that Chicago, Illinois, experiences a marked peak in N02 concentra-
tions during the summer months while concentrations in both Denver,
Colorado, and Lennox, California, peak in the winter. In contrast to the
Lennox pattern, other sites in California (Los Angeles, Azusa, and Pomona)
do not exhibit a marked seasonal!"ty.
7.1.6 Recently Observed Atmospheric Concentrations of NO,,
In this section, some representative examples of observed concen-
trations of N02 in recent years have been selected for presentation. In
summary, the data cited illustrate the following points:
o Annual average concentrations of NC^, are not a reliable index
of short-term (3-hr or less) human exposure.
o Although a distinct and fairly recurrent diurnal pattern is
discernible in some areas of the country, in many areas peak
diurnal values may occur almost any time of the day.
o 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.
Examination of Tables 7-7 and 7-8 for 1975 reveals that exposures to
NOp concentrations of 1,000 yg/m (0.53 ppm) or greater for 1-hr duration
were experienced in Los Angeles, California. Peak 1-hr exposures
3
equalling or exceeding 750 yg/m (0.4 ppm) were reported also at other sites
sites in California, and in Ashland, Kentucky; Joliet, Illinois; and
Cincinnati, Ohio. Additional sites reporting at least one peak hour NOp
concentration equalling or exceeding 500 yg/m (0.27 ppm) included Denver,
7-8
-------
Colorado; Phoenix, Arizona; St. Louis, Missouri; and New York City, New
fork, as well as several more California sites. Other sites, distributed
nationwide, reported maxima close to this value. Finally, it may be seen
that repeated N02 hourly concentrations in excess of 250 yg/m3 (0.13 ppm)
Here quite common nationwide in 1975.
Examination of Table 7-9 for 1976 shows that peak
3
equalling or exceeding 750 yg/m (0.4 ppm) were experienced in Anaheim,
California, and Port Huron, Michigan. A total of 28 of the 38 sites listed
in Table 7-9 reported concentrations equalling or exceeding 470 yg/m
(0.25 ppm). Table 7-10 presents data for 24-hr average N02 concentra-
tions at various sites. It is important to note that only data from
ronitoring stations meeting EPA National Air Data Branch (NADB) sampling
*
criteria were chosen for listing in this section. The number of stations
reeting these criteria varies from year to year, so that many of the areas
* 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 per-
cent of the total number of possible observations for the
applicable year.
2) For noncontiguous observations with sampling intervals of 24 hours or
greater:
a) Data representing quarterly periods must reflect a minimum of five
observations for the applicable quarter. Should there be no
measurements in 1 of the 3 months of the quarter, each remaining
month must have no less than 2 observations reported for the
applicable period.
b) Data representing annual periods must reflect four quarters of
observation that have satisfied the quarterly criteria.
7-9
-------
reported in Table 7-9 for 1976 are not identical with those listed in
Tables 7-7 and 7-8 for 1975. The data for the wide range of areas repre-
sented in these four tables do show, however, that peak N02 concentrations
of possible concern for human health occurred in the nation in recent
years.
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 7-7, taken from SAROAD, show the ratios
of the maximum hourly N02 concentrations to the annual mean. These ratios
range 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 N02 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
7-12 shows the distribution of maximum-to-mean N02 ratios averaged over
q
the years 1972, 1973, and 1974 for 120 urban sites. Over 70 percent of
the sites have maximum-to-mean ratios in the range of 5 to 8; about 8 per-
cent of the sites have ratios exceeding 10. Figure 7-13 shows long-term
trends in the maximum-to-mean NO,, ratios for groups of sites in New Jersey
and in the Los Angeles basin. (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. It may
be concluded that the annual mean is not a good indicator of the highest
short-term exposure level in the geographic areas considered.
7-10
-------
Table 7-8 shows the frequency distribution of 1-hr NCL measurements
at various sites in 1975. It may be seen here that there was great
variability across the nation for all the percentile values presented.
Also, it is obvious that the median value is not always indicative of the
potential for short-term exposure. For instance, Los Angeles, Riverside,
and San Diego, California, had high median values of 94 (0.05 ppm),
113(0.06 ppm), and 113 yg/m (0.06 ppm) respectively. St. Louis, Missouri,
on the other hand, had the moderate median value of 75 yg/m3 (0.040 ppm),
but exceeded more than half the California sites reported for the one-per-
cent! le level. It may also be seen from this table that some small cities
may experience peak concentrations of NO^ even higher than those observed
In center-city locations in major metropolitan areas. Ashland, Kentucky,
reported a maximum of 895 yg/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 7-9, in that Port Huron, Michigan,
reported a peak value of 832 yg/m (0.44 ppm), which is exceeded in the
listing only by Anaheim, California.
Two major factors that affect NO,, concentrations, mobile source
emissions and photochemical 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
a rapid increase in N02 in the morning as the result of NO emissions and
photochemical conversion to NO^. This is followed by a decrease of NO,,
in the midmorning hours due to advection and increasing vertical disper-
sion and also loss of N02 in various atmospheric transformation reactions.
Peaks in the NO concentration are often observed corresponding to
7-11
-------
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 NCL, concentration data from the month of
the highest observed 1-hr N02 concentration -in three cities are presented
in Figure 7-14. The monthly average 1-hour measurements were computed
separately for each hour of the day. This gives the composite diurnal
pattern as shown in Figure 7-14 for the month containing that year's high-
est 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 NCL 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 approximately 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-hour N02 concentration in 1975 are
plotted (Figure" 7-15). 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 7-16, 1-hr average N0« concentration data are plotted
versus time for periods of 3 days during which high N02 levels were
7-12
-------
observed. The Los Angeles data showed a diurnal profile typical for the
area on the afternoon of January 15, during which the NO,, concentration
climbed steadily after a small morning peak. This situation was probably
the result of low wind speeds and a strong elevated inversion restricting
both advection and dilution. The data for Ashland, Kentucky, show the same
basic diurnal trend seen in Los Angeles on the first two days and much
lower levels on the third day. The data from McLean, Virginia, at much
lower overall concentration values, had quite a different pattern. The
major increase in NO,, concentration did not take place until 5:00 or
6:00 p.m.
Figure 7-17 shows the N0_ and NO concentration profiles obtained from
a center-city station in St. Louis, Missouri, and the N0? concentration
12
from a rural site, 45 km north of the center-city location. The center-
city site showed a rapid buildup of NO during the morning with a slower
rise in the N02 concentration. The rural site, at this time, reported N02
concentrations at or near the instrumental limits of detection. During the
morning and early afternoon, the winds experienced at both sites were
light and from the northwest. Between 1:00 and 2:00 p.m. the wind direction
at the center-city site shifted and began coming from the south and south-
east over the next several hours. A similar change occurred between 5:00
and 6:00 p.m. at the rural site. After the shift in direction, the wind
speed increased somewhat at the rural site, and more gradually increased
in the downtown area. Since other monitoring sites in and around
St. Louis did not show a consistent, concomitant variation of N02 concen-
trations, the most likely explanation for the data presented is dispersion
or plume impaction from a variety of industrial sources, located roughly
7-13
-------
to the south of the sites reported herein.
The above discussion indicates that short-term excursions of N0? con-
centrations 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 7-17 are considerably
lower than those associated with the morning peaks shown in Figures 7-15
and 7-16. To further illustrate this phenomenon, the monthly maximum con-
centrations observed at each hour of the day are listed for selected
individual months from six geographically-dispersed urban locations in
Table 7-11.11
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 N0? 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 exposures 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, NCL
concentrations exceeded the monthly mean.
To summarize, the above data indicate that very high N0« concentra-
tions, 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
7-14
-------
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 7-18.
This figure presents data from RAPS on NO, NO,,, 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 7-18 shows a significant and constant N02 concen-
tration, presumably carried over from the previous day. During these hours,
the 0- concentration is quite low, near the instrumental detection limits.
0
Nitric oxide concentrations are high, most probably the result of contin-
uous emissions during the night and early morning hours. There is no dis-
cernible N02 formation. After sunrise, the N02 concentration increased
sharply as a result of photochemical reactions. Photochemical generation
of N00 is followed by a concomitant rapid increase in 0_ concentrations,
c j
which depresses the NO concentrations until the later afternoon hours
when decreasing radiant energy and increasing 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. The "ozone
^scavenging" mechanism would seem to be identical to that observed in plumes
ifrom power plants (Section 6,1.3). Significant quantities of NO are
oxidized leading to high nighttime N02 concentrations. It may be postulated
7-15
-------
that this mechanism is operative also in other localities exhibiting ele-
vated N02 levels after photochemical activity, including NCL photodissocia-
tion, decreases in the evening. Rapid reaction of NO and 03 leading to
increased NCL concentrations has also been observed across a high-traffic-
14
volume freeway in Los Angeles.
Although the data presented in Figure 7-18 were carefully chosen as
an unusually good example of ozone scavenging, Table 7-12 shows that ele-
vated N0? 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 7-12 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 7-12 are also an indication of the possible importance of local
sources and small-scale meteorological and topographical features in
determining ambient pollutant concentrations.
7.2 ATMOSPHERIC CONCENTRATIONS OF NITRATES
Although extensive monitoring has been carried out for nitrates
suspended in ambient air, recent reports (Section 4.4.1) 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. 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
7-16
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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 yg/m in the fine
particle fraction (<2.4y) of a sample collected by a dichotomous sampler
using Teflon filters. jl 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 yg/m3 in the fine fraction with a
3
mean of 0.28 yg/m . Concentrations from the coarse fraction (particles
with aerodynamic diameter between 2.4 y and 16 y) range from 0.06 to 0.83
3 3
yg/m with a mean of 0.22 yg/m . Measurements at a number of sites near
freeways in Los Angeles gave fine fraction nitrate concentrations up to 2.0
3 3
yg/m and similar readings up to 2.1 yg/m at nearby background sites.
19
Nitrate did not increase significantly in the roadway. Other data from
California obtained using quartz filters are summarized in Table 4-1 and in
on
Spicer et al.
Few measurements of ambient nitric acid vapor concentrations have been
carried out. Sampling from aircraft in non-urban areas at altitudes ranging
21
from 0.2 to 8 km was conducted by Huebert and Lazrus during August and
September of 1977i Those areas not influenced by urban plumes evidenced
concentrations ranging from 0.05 to 0.75 yg/m (0.02 to 0.3 ppb), with most
values below 0.4 yg/m (0.15 ppb).
Miller and Spicer, using a modified microcoulometric method, report up
to 25 yg/m3 (10 ppb) HN03 in Los Angeles, California. In a more extensive
report, Spicer23 cites measurements in St. Louis, Missouri, for 26 days
during July and August 1973, yielding maximum 23-hr average HN03
7-17
-------
3 3
concentrations of 30 yg/m (12 ppb) and a 1-hr maximum of 200 yg/m (80 ppb).
In West Corvina, California, 29 sampling days during August and September
1973, gave 23-hr average values up to 65 yg/m (26 ppb) and a 1-hr maximum
O ?A
of 78 yg/nr (31 ppb). Hanst et al., in failing to detect HN03 in Pasadena,
California, set an upper limit of 25 yg/m (10 ppb) on its concentration in
oc o
this area. Recently, Tuazon et al. report observing up to 15 yg/m
(6 ppb) in Riverside, California, during approximately one day of monitor-
ing in October 1976.
The data available are not sufficient to place human exposure to
suspended nitrates or nitric acid vapor in nationwide perspective. Further-
more, 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.
7.3 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.
Fine26*27 first reported dimethylnitrosamine (DMN) in ambient air in
1975. Levels ranged up to 0.95 yg/m in Baltimore, Maryland, and up to
0.051 yg/m3 in Belle, West Virginia. Later, Fine28 reported concentrations
. ~ «
up to 151 yg/m near the same site in Baltimore and, independently,
?Q 3
Pellizzari reported values up to 32 yg/m from the same area using
nn O
a different analytical method. Fine reported a level of 0.8 yg/m for a
7-18
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3-minute sample taken in New York City, New York. Fine26'27 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) showed little indication of N-nitroso
compounds in the vicinity of suspected sources at 32 locations in Kansas,
Missouri, Illinois, Indiana, Iowa, and Nebraska when contamination problems
were resolved. No evidence was found by NEIC to substantiate secondary
production in the vicinity of amine sources. In other monitoring by NEIC31
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 yg/m DMN) in the atmosphere.
32
Fine reports monitoring for atmospheric DKN at several sites in New York,
Jtew 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.
7-19
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7.4 REFERENCES FOR CHAPTER 7
1. Robinson, E.,andR. C. Robbins. Emissions, concentrations, and fate
of gaseous atmospheric pollutants. In: Air Pollution Control,
Part II. W. Strauss, ed. Wiley-Interscience, New York, 1972.
pp. 1-93.
2. Noxon, J. F. Nitrogen dioxide in the stratosphere and the troposphere
measured by ground-based absorption spectroscopy. Science 189:
54?-549, 1975.
3. Noxon, J. F. Tropospheric N02. J. Geophys. Res. 83: 3051-3057, 1978.
4. Chameides, W. L. Tropospheric odd nitrogen and the atmospheric water
vapor cycle. J. Geophys. Res. 80: 4989, 1975.
5. Crutzen, P. J., I. S. A, Isaksen, and J. R. McAfee. The impact of the
chlorocarbon industry on the ozone layer. J. Geophys. Res. 83: 345,
1978.
6. Ritter, R. A., D. H. Stedman, and T. J. Kelly. Ground level measure-
ments of NO, N0? and 0- in rural air. In: Proceedings, ACS Symposium
on Atmospheric nitrogen Compounds, Anaheim, Ca., March 1978.
7. Ludwig, F. L., and E.Shelar. Site Selection for the Monitoring of
Photochemical Air Pollutants. EPA-450/3-78-013. U.S. Environmental
Protection Agency, Research Triangle Park, N.C., 1978.
8. Federal Register. 40 CFR Parts 51, 52, 53, 58, 60. August 7, 1978.
9. Trijonis, J. Empirical Relationships Between Atmospheric Nitrogen
Dioxide and Its Precursors. EPA-600/3-78-018. Environmental Sciences
Research Laboratory, Office of Research and Development, U.S.
Environmental Protection Agency, Research Triangle Park, N.C.,
February 1978.
10. Air Quality Data - 1975 Annual Statistics including summaries with
reference to standards. EPA-450/2-77-002. U.S. Environmental
Protection Agency, 1977.
11. SAROAD, 1975. Data reported were abstracted from the 1975 SAROAD raw
data file maintained at the National Air Data Branch of the U.S.
Environmental Protection Agency, Durham, N.C.
12. RAPS, 1976. Data reported are abstracted from the 1976 data file for
the Regional Air Pollution Study program maintained at the
Environmental Research Center, U.S. Environmental Protection Agency,
Research Triangle Park, N.C.
7-20
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13. Possible mechanisms operating are due to David Iverach and John Trijonis
Their addresses are: David Iverach, Guest Worker, Technology Develop-
ment Section, AMTB, U.S.E.P.A., Research Triangle Park, N.C. 27711;
and John Trijonis, Technology Service Corporation, 2G11 Mil sin're Blvd.,
Santa Monica, Ca. 90403.
14. Fankhauser, R. K. Nitric Oxide, Nitrogen Dioxide, Ozone Interrelation-
ships Across the Freeway. In: The Los Angeles Catalyst Study Symposium.
EPA-600/4-77-034. U.S. Environmental Protection Agency, Research
Triangle Park, N.C., June 1977.
15. Harker, A. B., L. W. Richards, and W. E. Clark. The effect of atmos-
pheric S09 photochemistry upon observed nitrate concentrations in
aerosols. Atm. Env. Ij.: 87-91, 1977.
16. Stevens, Robert K., T. G. Dzubay, G. Russwurm, and D. Rickel. Sampling
and analysis of atmospheric sulfates and related species. Atm. Env.12:
55-63, 1978.
17. Dzubay, Thomas G., and R. K. Stevens. Ambient air analysis with dicho-
tomous sampler and X-ray flouresence spectrometer. Environmental
Science and Technology 9. (7): 663-668, 1975.
18. Stevens, Robert K., T. G. Dzubay, D. T. Mage, R. Burton, G. Russwurm,
and E. Tew. Comparison of nitrates and sulfates collected by Hi-vol
and dichotomous samplers. Presented to American Chemical Society,
Division of Environmental Chemistry, Miami, Fl., September 1978.
19. Dzubay, T. G., R. K. Stevens, and L. W. Richards. Composition of
aerosols over Los Angeles freeways. Accepted for publication in
Atm. Env.
20. Spicer, C. W., P. M. Schumacher, J. A. Kouyoumjian, and D. W. Joseph.
Sampling and Analytical Methodology for Atmospheric Particulate
Nitrates. EPA-600/2-78-067. Environmental Sciences Research
Laboratory, U.S. Environmental Protection Agency, Research Triangle
Park, N.C., April 1978.
21. Huebert, B. J., and A. L. Lazrus. Global tropospheric measurements
of nitric acid vapor and parti culate matter. Geophys. Res. Lett. 5_:
557-589, 1978.
22. Miller, D. F., and C. W. Spicer. A continuous analyzer for detecting
nitric acid. Presented at Air Pollution Control Association 67th
Annual Meeting, Denver, Co., June 9-13, 1974.
23. Spicer, C. W. The fact of nitrogen oxides in the atmosphere. I_n_:
Advances in Environmental Science and Technology, Vol. 7.
0. N. Pitts, Jr. and R. L. Metcalf, eds. John Wiley and Sons,
New York, 1977.
7-21
-------
24. Hanst, P. L., E. W. Wilson, R. K. Patterson, B. W. Gay, Jr.,
L. W. Chaney, and C. S. Burton. A Spectroscopic Study of California
Smog. EPA-650/4-75-006. U.S. Environmental Protection Agency,
Research Triangle Park, N.C., 1975.
25. Tuazon, E. C., R. A. Graham, A. M. Winer, R. R. Easton, J. N. Pitts, Jr.,
and P. L. Hanst. A kilometer pathlength Fourier-transform infrared
system for the study of trace pollutants in ambient and synthetic
atmospheres. Atm. Env. 12: 867-875, 1978.
26. Fine, D. H., D. P. Rounbehler, N. M. Belcher, and S. S. Epstein.
N-nitroso compounds in the environment. Paper presented at Int'l.
Conf. on Environmental Sensing and Assessment, Las Vegas, Nv.,
September 22-26, 1975.
27. Fine, D. H., D. P. Rounbehler, N. M. Belcher, and S. S. Epstein.
N-nitroso compounds in air and water. Paper presented at the Fourth
Meeting of the Int'l. Agency for Research on Cancer, Tallinn,
Estonia, USSR, October 1-2, 1975.
28. Walker, P., J. Gordon, L. Thomas, and R. Ouelette. Environmental
Assessment of Atmospheric Nitrosamines. Report under EPA Contract
No. 68-02-1495, Strategies and Air Standards Division. U.S. Environ-
mental Protection Agency, February 1976.
29. Pellizzari, E. D. The Measurement of Carcinogenic Vapors in Ambient
Atmospheres. EPA-600/7-77-055. Environmental Sciences Research
Laboratory, U.S. Environmental Protection Agency, Research Triangle
Park, N.C., June 1977.
30. Reconnaissance of Environmental Levels of Nitrosamines in the Central
United States. EPA-330/1-77-001. National Enforcement Investigations
Center, Office of Enforcement, U.S. Environmental Protection Agency,
Denver, Co., August 1977.
31. Reconnaissance of Environmental Levels of Nitrosamines in the South-
eastern United States. EPA-330/1-77-009. National Enforcement
Investigations Center, Office of Enforcement, U.S. Environmental
Protection Agency, Denver, Co., August 1977.
32. Fine, D. H. Final Report of Monitoring for N-nitroso Compounds in
the States of West Virgina, New York, New Jersey, and Massachusetts.
EPA Contract No. 68-02-2363, U.S. Environmental Protection Agency,
Research Triangle Park, N.C., November 1976.
33. Junge, C. E. Recent investigations in air chemistry. Tellus 8:
127-139, 1956.
34. Lodge, J. P., Jr., and J. B. Pate. Atmospheric gases and particulates
in Panama. Sciences 153: 3734, 408-410, 1966.
7-22
-------
35. 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 (30): 7057-7064, 1973.
36. Moore, H. E. Isotopic,measurement of atmospheric nitrogen compounds.
Tell us 26: 169-174, 1974.
37. Drummond, J. W. Atmospheric Measurements of Nitric Oxide Using a
Chemiluminescent Detector. Ph.D. thesis, University of Wyoming, 1976.
38. Cox, R. A. Some measurements of ground level NO, N02 and 0~ concen-
trations at an unpolluted maritime site. Tellus 29_: 356-36Z, 1977.
39. Galbally, I. E. In: Air Pollution Measurement Techniques, Special
Environmental Report No. 10, World Meteorological Organization No. 460,
WMO, Geneva, 1977. pp. 179.
40. National Aerometric Data Bank, U.S. Environmental Protection Agency,
1975.
41. The National Air Monitoring Program: Air Quality and Emissions Trends -
Annual Report. Volume 1, Chapter 4. EPA-450/1-73-001. U.S. Environ-
mental Protection Agency, Washington, D.C., 1973. pp. 26-28.
42. Trijonis, J. C., et al. The Relationship of Ambient ML to Hydro-
carbon and NO Emissions. Draft report from Technology Service
Corporation t6 EPA under Contract No. 68-02-2299. U.S. Environmental
Protection Agency, Office of Research and Development, Research
Triangle Park, N.C.
43. National Air Quality and Emissions Trends Report, 1975. EPA-450/1-76-
002. Office of Air Quality Planning and Standards, U.S. Environmental
Protection Agency, Research Triangle Park, N.C., November 1976.
44. SAROAD, 1976. Data reported were abstracted from the 1976 SAROAD raw
data file maintained at the National Air Data Branch of the U.S.
Environmental Protection Agency, Durham, N.C.
7-23
-------
.E
a.
c/>
tu
C3
ec
<
z
•at
200
100
0
100
50
0
100
50
0
100
50
0
100
50
0
1 ' I I I I
J2 - a - o - o - d -
LJv-
°—
CHICAGO CAMP
I I I
I I I- I I
I I I I I I I i
DENVER CAMP
O O -
PHILADELPHIA CAMP
I I I I I
I I I I
ST. LOUIS CAMP
I I I I
•62 '63 '64 '65 '66 '67 '68 '69 '70 '71
YEAR
Figure 7-1. 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). *Note change in
ordinate scale for these data.41
7-24
-------
1
CO
ac
<
_J
<
200
100
0
100
50
0
100
50
0
100
50
0
100
50
0
o _
CINCINNATI CAMP
_Q n_
DENVER CAMP
I I I
i 1 LJuJ
I I !
q
I I \ \
o o 0
n n a
ST. LOUIS CAMP
I I I I I I I I I I I
'62 '63 '64 '65 '66 '67 '68 '69 '70 '71
YEAR
Figure 7-2.
Trend lines for nitrogen dioxide annual averages
in five CAMP cities. D, Data satisfying NADB
minimum sampling criteria; O , invalid average
(based on incomplete data). *Note change in
ordinate scale for these data.41
7-25
-------
ro
cr>
AVERAGE NO, CONCENTRATION CHANGE (11 STATIONS): +20%
Figure 7-3. Trends in N02 air quality, Los Angeles Basin, 1965-1974
42
-------
Annual statistics
Three-year moving averages
From less than 75% of
possible observations
Maximum one-hour
observation
99th percent! le
90th percent!le
0 Arithmetic mean
74 75
Figure 7-4.
Annual air quality statistics and three-year moving
averages ^at Carnden, New Jersey. (Data adapted from
Trijonis, augmented with data from SAROAD.)
7-27
-------
S-i
10
o
o-
in
Annual statistics
Three-year moving averages
0>
O
o
C\T
O
CD-
O
o-
O
I/)
I 8-
2 w
Maximum
^one-hour
observation
X
o
5 i
c u
o^
•r- in
o
O'
99th
percent! 1e
^
CD-
CO
CD,
CD-
CM
CD
o-
90th
percentile
Arithmetic
mean
63
64 65
66
67 68
69 70
Year
71 72
73
74
•75
Figure 7-5.
Annual air quality statistics and three-year moving averages 9
at downtown Los Angeles, California. (Data adapted from Trijonis,
augmented with data from SAROAD.)
7-28
-------
o.
§
o .
o
o
en
c o
i- O
1C
i/I
c
o
o o
o o
0)
•o
•r-
X
OJ
en
•P C
^- CsJ
y.
CJ
o
Annual statistics
Three-year moving averages
Missing data
Maximum
one-hour
observation
99th
percentile
,90th
percentile
Ari thmeti c
mean
, ^ , 1 1 1 r
63 64 65 66 67 68 69 70
Year
71 72 73 74
75
Figure 7-6.
Annual air quality statistics and three-year moving averages
at Azusa, California. (Data adapted from Trijonis,y
augmented with data from SAROAD.)
7-29
-------
o
o
CD
O
VO
O
O'
LO
o
o
O>
c
o
4J
(O
C
0>
o
c
o
So
g»
c
-------
Annual statistics
Three-year moving
averages
Maximum one-hour
observation
99th Percentile
90th Percentile
Mean
74 75
Year
Figure 7-8. Annual air quality statistics and three-year moving
averages at Portland, Oregon. (Data adapted from
Trijonis, augmented with data from SAROAD.)
7-31
-------
™
340
320
300
280
260
5 240
CJ
JB
O
(J
«N
2 220
200
180
HIGHEST AVERAGE
BASIN WIDE
MEAN (5 SITES)
LOWEST AVERAGE
I
I
1970 1971
1972
YEAR
1973 1974 1975
Figure 7-9. Annual average of daily maximum 1-hour N0?
(4-yean^running mean) in the Los Angeles
Basin.
7-32
-------
_ Mill Illll I I 1 ill til 111 I I ll
10 —
I I I I I I I I I I I I I I I I I I I I 1 I
HOUSTON/MAE 1975-1976
II II ( I I ! I I I i I I I I I I I I I I I 1 I I I I I I I I I I I I I I I I I M I 1 I I I 1 I i I I
> I I I I I I I I i
1 Z 3 «4 5 C 78 9 10 11
MONTH
I I I I I ! I I I 1 I I I M I I M I I I I I I I I I I I ! I n I I I I I I I I I 1 I I I I I I I _
is
s
NQ2
DENVER 1967-1973
1lil|llll]llll|l Illjl II Mill I III! I jll! Ill III II III |l I II
1 2 3 1 5 6 7 8 9 10 II 12
KWTH
m 1x1' | i 1111111111111111 j i i 1111111 i 11 i 11111111111111111U. _
CHICAGO 1969-1973
11 111 »^
Figure 7-10.
1 2 3 H S 6 7 8 9 10 11 12
KWTH
Seasonal N02 concentration patterns of three U.S.
urban sites (monthly averages of daily maximum
1-hr concentrations). Adapted from Trijonis.9
7-33
-------
00
8
I: o _
o •—
L( 11 n 11111111HIII1111 n 11111111 M i i 111111111 III IJ
AZUSA
1 2 3
III III IIIII11 III.U. —
LOS ANGELES
5 G 7 8 9 10 11 12
WWTH
g 3 it 5 6 7 B 9 10 11 12
1111 ] 11 n 11111 j 11111 iTriji n 11111111111111111111111111
J 2 3 M 5 G 7 6 9 10 11 12
K3NTH
mil n nl i nil i tn I ii.ii In i ill ntli ii iliiit Inn In n _
— §
LENNOX
TTTmnnnni'H Mill III 1II JIIM|TTTTyTVTT|MTI |T1TT
56 7 8 9 10 11 12
1 2 3 M
tQ.'TII
Figure 7-11. Seasonal N0? concentration patterns of four U.S. urban sites (monthly
averages of daily maximum 1-hr concentrations). Adapted from Trijonis.y
-------
30%-
c
o
to
**-
o
cn
-------
UJ
SO
•-I
01—
CM 6
5-
1
64
i
65
i
66
i
67
I
68
YEAR
I
69
i
70
i
71
72
i
73
i
74
IS
so
CVJ
8 -
7 -
6 -
5 -
V
6*4
65
66
67
— I —
63
69
70 7*
1 72 7*
3 74
Figure 7-13.
Trends
groups
growth
in
YEAR
the maximum mean
N0? ratio
of sites: (a) average of five
for two
high
locations within the Los Angeles Basin
(Anaheim, La Habra, Azusa, Pomona, San Berna-
dino); (b) average of two New Jersey sites g
(Bayonne and Newark). Adapted from Trijonis.
7-36
-------
&
»*«.
3.
Q-
G_
Xs*
LU
C_>
z:
o
o
UJ
Q
I—I
X
o
o
o;
0.16 .
(300.8)
0.14
(253.2)
0.12
(225.6)
O.LO .
(188.0)
0.08
(150.4)
0.06
(112.8)
0.04
(75.2)
0.02
(37.6)
12
(NOON)
TIME OF DAY
Figure 7-14. Average diurnal pattern for the month during which the highest 1-hour N02 concentrations
were reported: (•) Los Angeles, California, January 1975; (o) Denver, Colorado, Aprif 1975; (x)
Chicago, Illinois, June 1975.H
-------
0.50
(940)
CO
00
01
3.
CL
Q.
as
UJ
o
o
UJ
o
*— I
X
o
.
UJ
CO
o
a:
0.40
(752)
0.30
(564) t
0.20
(376)
0.10
(188) +
24
12
(NOON)
15
18
21
24
TIME OF DAY
Figure 7-15. One-hr average concentration profiles on day of peak N09 concentration for three U.S. cities'
(•) Los Angeles , California January 17, 1975; (o) Denver, Colorado, April 5, 1975; (x) Chicago, ITTinofs,
Oune 21. 1975.Ai
-------
I
CO
CO
3.
a.
a.
2*
o
UJ
o
o
CJ
X
o
i—i
o
UJ
CD
O
a:
0.50
(940)
0.40
(7152)
0.30
(564)
0.20
(376)
0.10
(188)4:
J!
n
MIDNIGHT
NOON
MIDNIGHT
NOON
MIDNIGHT
NOON
MIDNIGHT
TIME OF DAY
Figure 7-16. One-hour N0? concentrations' during three days of high pollution in three U.S. cities:
(t) Ashland, Kentucky, November 19-20, 1975; (o) Los Angeles, California, January 15-17, 1975;
(x) McLean, Virginia, August 27-29, 1975.n
-------
*>
3L-
QL.
o.
c5
LU
O
X
o
O
r.-:
0.10
(188.0)-
0.08
(150.4)
O.C6
(112.8)
0.04
(75.2)
0.02
(37.6)
15
18
21
(NOON)
TIME OF DAY
Figure 7-17. Nitric oxide and nitrogen dioxide concentrations at an urban and a rural site 1n
St. Louis, Missouri, on January 27-28, 1976: (t) N02 at RAMS Station 5 (center city); (o)JO?
at RAMS Station 22 (45 km north of center city); (xj NO at RAMS Station 5 (center city).1<: c
-------
Q.
Q_
•z.
o
o
z
o
o
0.20 -
0.10 -
o
o.
Ozone scavenging
•> formation <
of NO
No Photochemical
format1on->}< formation
Afternoon NO
Nighttime NO
Carryover
18
20
Sunrise
TIME OF DAY (CENTRAL STANDARD TIME)
Figure 7-18 Pollutant concentrations in Central City St. Louis,
October 1, 1976, average of RAMS sites 101, 102, 106,
and 107. Illustration of photochemical and ozone
scavenging formation of NO. '
-------
Table 7-1. BACKGROUND NO MEASUREMENTS'
A
Author
Junge
Lodge et al.
Breeding et al.35
Moore36
.37
Drummond
Cox38
Gal bally39
Ritter et al.6
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
7-42
-------
Table 7-2. YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITRIC OXIDE AT CAMP STATIONS,
MEASURED BY THE CONTINUOUS SALTZMAN COLORIMETRIC METHOD4Q
•vj
co
Concentration, pg/ni
Year
1962
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
Denver
Mean
—
—
—
—
—
37
(30)
49
(39)
49
(39)
49
(31)
49
(39)
62
(SO)
- 62
(SO)
74
(60)
74
(60)
J (ppb), 25°
C
Washington
Mas
—
—
—
—
—
652
(522)
627
(502)
590
(472)
738
1590)
677
(542)
750
(600)
677
(542)
788
(630)
652
(522)
Mean
37
(30)
49
(39)
49
(39)
37
(30)
49
(39)
62
(50)
49
(39)
49
(39)
62
(SO)
49
(39)
86
(69)
123
(98)
Max
7K8
(630)
1,060
(8-18)
1,070
(8S6)
751
(600)
1.240
(1,000)
1,340
(1,112)
837
(670)
959
(767)
1,430
(1.144)
775
(620)
825
(6<>0)
640
(512)
Chicago
Mean
123
(9«)
123
(98)
123
(9H)
123
(98)
123
(98)
98
(78)
86
(77)
135
(108)
172
(137)
135
(108)
160
(128)
221
(177)
Max
739
(704)
615
(492)
1,105
(884)
750
(600)
775
(620)
763
(610)
739
(591)
1,920
(l,S3h)
2,240
(1.792)
824
(659)
787
<630)
775
(620)
St. Louis
Mean
—
_
—
49
(39)
37
(30)
37
(30)
44
(39)
37
(30)
37
(30)
62
(50)
62
(50)
62
(50)
74
(60)
Cincinnati
Max
—
_
—
923
(738)
443
(354)
688
(550)
343
(314)
492
(394)
873
(698)
689
(551)
615
(492)
7M
(571)
750
(600)
Mean
37
(30)
37
(JO)
49
(39)
37
(30)
49
(39)
37
(30)
74
(60)
49
(39)
49
(39)
62
(50)
49
(39)
49
(39)
Max
702
(562)
615
(492)
787
(630)
750
(600)
1,230
(984)
1,685
(1,348)
1,242
(994)
861
(689)
960
(768)
750
(600)
76,1
(610)
689
(551)
Philadelphia
Mean
25
(20)
62
(50)
62
(50)
62
(50)
74
(M))
74
(60)
62
(50)
49
(39)
74
(60)
49
(39)
62
(50)
—
—
Max
431
(345)
1,845
(1,476)
1,400
(1,120)
1 ,083.
(866)
2.290
(1.832)
1,820
(1,456)
1,735
(1,388)
1 ,083
(806)
1,072
(1,338)
935
(748)
800
(640)
—
—
-------
Table 7-3. FIVE-YR AVERAGES OF NITRIC OXIDE CONCENTRATIONS AT CAMP STATIONS,
MEASURED BY CONTINUOUS SALTZMAN COLORIMETRIC METHOD41
CAMP average
Average concentration,
3 (ppb), 25° C
Average of annual 2nd highest value,
Mg/mJ (ppb). 25° C
Station
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
1962-1966
122
43
44
55
39
.6
.8
.9
.2
.8
(98.1)
(35.0)
(35.9)
(44.2)
(31.8)
1967-1971
125.4
53.6
54.4
65.4
47.6
(100.3)
(42.9)
(43.52)
(52.3)
(38.1)
Change. %
+ 2
+ 22
+ 21
+ 18
+ 19
1962-1966
731
782
633
1,331
541
(584.8)
(625.6)
(506.4)
(1.064.8)
(287.8)
1967-1971
969
1,067
620
1,395
578
(775.2)
(853.6)
(496.0)
(1,116.0)
(462.4)
Change,
-------
Table 7-4. YEARLY AVERAGE AND MAXIMUM CONCENTRATIONS OF NITROGEN DIOXIDE AT CAMP STATIONS,
MEASURED BY THE CONTINUOUS SALTZMAN COLORIMETRIC METHOD40
^J
-------
Table 7-3. FIVE-YR AVERAGES OF NITROGEN DIOXIDE CONCENTRATIONS AT CAMP STATIONS,
MEASURED BY THE CONTINUOUS SALTZMAN COLORIMETRIC METHOD41
Average concentration,
jig/m' (ppb). 25° C
Average of annual 2nd highest
value. Mg/mJ (ppb), 25° C
Station
Chicago
Cincinnati
Denver
Philadelphia
St. Louis
CAMH average
!%2-!%b
Bb.l (45.8)
62.0 (33.0)
bb.O (JS.l)
b7.7 (3b.O)
58.5 (31.1)
t>8.l Ub.2)
1467-1471
101,2 (53. 8)
bO.U (31. 4)
67.9 (3b.t)
77.6 (41.3)
54.2 (28.8)
72.2 (38.4)
Change. %
+ 18
- 3
+ 3
+ 15
- 7
+ 6
14h2-l4(>6
444 (230.2)
341 (208.0)
448 (264.9)
361 (192.0)
320 (170.2)
403 (214.4)
1407-1471
444 (2(>5.4)
3b7 (195.2)
493 (2b2.2)
414 (220.2)
267 (142.0)
408 (217.0)
Change, %
+ 12
- 6
- 1
+ 15
-16
+ 1
4*
cn
-------
Table 7-6 . FIVE-YEAR CHANGES IN AMBIENT N02 CONCENTRATIONS"
STATIONS
LOS ANGELES BASIN SITES
Orange County: Anaheim
(rapid growth) La Habra
Average for Orange County
Los Angeles County: Azusa
(slow growth) Lennox
Los Angeles
L.A. (Westwood)
L.A. (Reseda)
Average for Los Angeles County
OTHER CALIFORNIA SITES
Oakland
Pittsburg
Redwood City
Salinas
San Rafael
Santa Cruz
Stockton
Average for Other California Sites
NEW JERSEY SITES
Bayonne
Camden
Newark
Average for New Jersey Sites
OTHER SITES
Chicago, IL
Portland, OR
NET PERCENTAGE CHANGE
TRATIONS
Annual
Mean
+ 9%
+99%
+54%
+17%
- 7%
- 5%
+ 8%
- 4%
+ 3%
- 7%
- 8%
-24%
- 1%
+ 5%
+15%
- 3%
- 3%
-27%
- 9%
+ 2%
-14%
+32%
-.7%
FROM 1969 TO
90th
Percent! le
+ 5%
+60%
+33%
+ 7%
-11%
- 2%
+11%
-10%
- 1%
- 9%
- 4%
-25%
- 1%
.0%
-24%
-44%
-15%
-18%
- 7%
0%
- 8%
+51%
+44%
IN N02 CONCEN-
1974
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'
7-47
-------
Table 7-7. RATIO OF MAXIMUM OBSERVED HOURLY NITROGEN DIOXIDE
CONCENTRATIONS TO ANNUAL MEANS DURING 1975 FOR SELECTED LOCATIONS10
State
California
.pa
00
Colorado
Georgia
Illinois
Kentucky
yg/m
Maximum hourly concentration * yearly arithmetic mean
Location
Anaheim
Azusa
Costa Mesa
Los Angeles
a
Lynwood
San Bernadlno
Napa
San Francisco
Barstow
Fontana
Chula Vista
Visalia
Denver3
Atlanta
Chicago3
East St. Louis
Paducah
Louisville
Ashland
Method A1
940/101= 9.3
696/112= 6.2
658/58 =11.3
1053/126= 8.4
1128/129= 8.7
602/97 =6.2
470/76 =6.2
188/49 = 3.8
432/62 = 7.0
432/39 =11.1
714/66 =10.8
895/85 =10.5
(Continued)
Method Bc
489/78 =6.3
451/64 =7.1
226/48 =4.7
555/96 = 5.8
489/76 = 6.4
395/104= 3.8
395/109= 3.6
244/41 =6.0
293/65 =4.5
348/84 = 4.1
-------
Tablet r-y C'COntrtt»U<(M*.>
I
£>
vo
yg/m
Maximum hourly concentration * yearly arithmetic mean
State
Maine
Maryland
Michigan
Oregon
Texas
Location
Bangor
Essex
Grand Rapids
Detroit
Portland
Dallas
Method Ab Method Bc
270/49 =5.5
282/53 =5.3
279/67 = 4.2
338/58 =5.8
207/50 =4.1
432/32 =13.5
a) More than one station reporting.
b) Method A: Instrumental Colorimetric-Lyshkow (MOD) method, a variation of
the continuous Greiss-Saltzman Method.
c) Method B: Instrumental Chemiluminescence Method.
-------
Table 7-8. FREQUENCY DISTRIBUTION OF 1975 HOURLY N02
CONCENTRATIONS AT VARIOUS SITES IN U.S. URBAN AREAS10
Concentrations (yg/m )
equalled or exceeded by
stated percent of
observations
Location
Arizona
Phoenix3
California
Los Angeles
Redlands?
RedlandsDa
Riverside?
Riverside^
San Diego?
San Diego
Colorado
Denver?
Denver
Illinois
JolietD
Kentucky.
Ashland3
Michigan.
Detroit0
Missouri
St. Louis3
New Jersey
Newark^
Newark
1%
271
526
282
226
301
395
226
395
282
265
220
297
150
338
273
226
5% 10%
188 152
301 226
169 132
150 132
226 188
282 226
150 113
282 226
188 150
177 149
137 115
209 173
113 94
244 207
169 150
169 132
50%
69
94
56
56
94
113
38
113
94
90
55
68
56
75
81
75
Maximum
observed
concentration
(yg/m3)
660
1053
545
357
564
658
508
865
432
483
857
895
338
658
494
376
(Continued)
7-50
-------
Table 7-8 (Continued)
Location
Concentrations (yg/m )
equalled or exceeded by
stated percent of
observations
1% 5% 10% 50%
Maximum
observed
concentration
(yg/m3)
New York .
New York City1
Ohio
Cincinnati.
Cincinnati
Pennsylvania .
Philadelphia0
Bethlehem0
Texas .
Dallas0
226 169 132 56
301 207 169 75
282 150 103 47
301 226 207 113
432 282 222 79
132 94 75 19
526
865
395
451
669
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.
7-51
-------
Table 7-9. FREQUENCY DISTRIBUTIOM.OF 1976 HOURLY NITROGEN DIOXIDE CONCENTRATIONS
AT VARIOUS U.S. SITES*4
Location
Arizona
Phoenix
Tucson
California
Anaheim
Chi no
..g
I
ro Costa Mesa
El Cajon
Fontana
Fremont
La Habra
SAROAD Site ID
030600002G01
030860002G01
050230001101
051300001101
051740001101
055300004F01
052680001101
052780001101
053620001101
Method
Instrumental
Cheml luminescence
Instrumental
Cheml luminescence
Grless-Saltzman
(Lyshkow)
Instrumental
Cheml luminescence
Grless-Saltzman
(Lyshkow)
Instrumental
Chemllumlnescence
Instrumental
Cheml 1 uml nes cence
*
Grless-Saltzman
(Lyshkow)
it
Grless-Saltzman
(Lyshkow)
Concentrations (ug/m )
equalled or exceeded by
stated percent of observations
IX 10X SOX
226
132
395
414
301
320
244
301
320
150
94
188
132
132
188
132
150
169
56
56
94
19
19
94
56
56
75
Maximum 2nd Maximum
observed observed
concentration concentration
(ug/m3) (wg/m3)
451
451
865
602
639
545
564
526
526
432
357
752
583
639
489
508
526
508
Yearly
arithmetic
mean
-------
Table 7-9 (continued).
in
CO
Location SAROAD Site ID
California
Sunnyvale 058080001101
Temple City1" 058220001F01
Upland 058440004F01
Colorado
Denver 060580002F01
District of Columbia
Washington 090020003A05
Geprgl a
Atlanta 110200001A05
Method Concentration (ug/m )
equalled or exceeded by
stated percent of obser-
vations
1% 10X
Grless-Saltzman 338 150
(Lyshkow)
Instrumental
Chemllumlnescence 357 226
Instrumental
Chemllumlnescence 282 169
Instrumental
Chemllumlnescence 280 150
Instrumental
Chem1lun1nescence 169 113
Instrumental
50%
75
113
94
90
66
Maximum
observed
concentration
(ug/m3)
564
696
526
457
338
O44
2nd Maximum Yearly
observed arithmetic
concentration mean
(ng/m3) (ug/m3)
526 83
470 128
526 98
442 97
329 70
91fi fi7
Chemllumlnescence 160
(continued)
-------
Table 7-9 (continued).
Location
California
Oakland
Oceans 1de
Redlands
Riverside1"
•vj
*» Riverside*
San Diego
San Diego
San Jose
San Jose
SAROAD Site ID
055300004F01
055320003101
056200001101
056400003F01
056400003F01
056800006101
056800004101
056980004A05
056980004101
Method
Instrumental
Chemllumlnescence
Instrumental
Cheml 1 uml nes cence
Instrumental
Chemllumlnescence
Instrumental
Cheml 1 uml nes cence
Instrumental
Chemllumlnescence
Instrumental
Cheml 1 uml nescence
Instrumental
Chemllumlnescence
Instrumental
Chemllumlnescence
Gr1ess-Sal tzman
(Lyshkow)
Concentrations (pg/m )
equalled or exceeded by
stated percent of obser-
vations
1%
301
263
169
282
338
244
357
301
320
10%
150
113
75
150
207
113
188
169
169
50%
56
38
38
75
94
56
94
66
75
Maximum 2nd
observed Maximum
concentration observed
3 concentration
545
620
470
470
564
451
585
479
526
489
620
451
470
526
451
564
461
507
Yearly
arithmetic
mean
(ug/m3)
77
57
47
92
113
63
105
86
86
(continued)
-------
Tabla 7-0 (continued).
en
Location
Illinois
Chicago
Chicago
Springfield
Kentucky
Ashland
Michigan
Port Huron
Saglnaw
Southfield
SAROAD Site ID Method
141122002P10 Instrumental
Chemllumlnescence
141122002A05 Instrumental
Chem1lum1nescence
147280003F01 Instrumental
Chemi 1 uminescence
180080008F01 Grless-Saltzman*
(Lyshkow)
234340003F01 GMess-Saltzraan*
(Lyshkow)
234760002F01 GHess-Saltzman*
(Lyshkow)
if
234880002F01 Grless-Saltzman
(Lyshkow)
Concentrations (ug/m3) Maximum 2nd
equalled or exceeded by observed Maximum
stated percent of obser- concentration observed
vatlons ., concentration
1*
273
263
90
209
222
291
363
(pg/mJ) , , 3,
10% 50X (W/m '
179 113 461 442
169 94 461 442
55 19 519 293
113 55 572 464
121 65 832 815
154 76 643 622
181 83 645 585
Yearly
arithmetic
mean
(,9/m3)
116
108
25
63
73
86
100
(continued)
-------
Table 7-9 (continued).
i
en
Location SAROAD Site ID
Method
Concentrations
(ug/m3)
equalled or exceeded by
Missouri
Kansas City 171800001H01
New Jersey
Newark 313480002A05
New York
Buffalo 330660007F01
Ohio
Cincinnati 361220019A05
Pennsylvania
Philadelphia 397140023H01
Utah
Salt Lake City 460920001F01
Salt Lake City 460920001A05
Coulometrlc
Instrumental
Cheml luminescence
*
Griess-Saltzman
(Lyshkow)
Instrumental
Cheml luminescence
*
Griess-Saltzman
(Lyshkow)
Instrumental
Cheml luminescence
Instrumental
Cheml 1 um1 nes cence
stated percent
vatlons
1% 10%
150 80
226 122
361 81
147 94
188 113
244 132
226 132
of obser-
50X
20
75
36
56
75
75
75
Maximum
observed
concentration
•>
(ug/nf)
500
338
645
677
451
470
470
2nd Maximum
observed
concentration
•>
(yq/m3)
480
320
645
508
451
451
432
Yearly
arithmetic
mean
•»
(yg/mj)
36
80
46
60
74
80
75
*Data obtained using dynamic calibration procedures
tData not satisfying NADB minimum sampling criteria
-------
I
en
Table 7-10. FREQUENCY DISTRIBUTION OF 1976 24-HR AVERAGE N09
CONCENTRATIONS AT VARIOUS SITES IN U.S. URBAN *
AREAS (ALL DATA OBTAINED BY SODIUM ARSENITE METHOD).
44
Location
Alabama
Birmingham
Alaska
Fairbanks
Arizona
Tucson
Arkansas
Little Rock
California
Fresno
Long Beach
San Bernadino
Colorado
Denver
Site Code
010380003P01
020160001P01
030860001 F01
041440003F01
052800002F01
0541 00001 F01
056680001 F01
060580001 P01
1st Max
(ug/m3)
127
110
127
105
147
339
156
163
2nd Max
(yg/m3)
117
103
96
100
133
285
154
140
Concentrations
or Exceeded by
of Observations
10%
107
85
69
65
118
215
124
102
(yg/m ) Equalled
Stated Percent
50%
66
59
45
32
49
101
78
46
Annual
Arithmetic
Mean o
(yg/nT)
69
59
47
37
58
119
85
55
(continued)
-------
Table 7-10(continued).
I
cn
CD
Location
Connecticut
Bridgeport
Greenwich
Florida
Jacksonville
Orlando
Georgia
Atl anta
Macon
Site Code
070060123F01
070330008F01
101960033H01
101960002P01
101960032H01
103280004F01
110200038G02
110200001P01
110200039G01
110200041G01
113440008F01
Concentrations (yg/m ) Equalled Annual
1st Max 2nd Max or Exceeded by Stated Percent Arithmetic
-, o of Observations Mean ->
(yq/rn ) (yq/rn ) 10% 50% (yg/rn )
143
101
138
100
93
91
133
123
120
100
109
139
80
91
89
81
76
81
95
115
92
85
123
54
90
79
67
50
72
94
92
83
71
66
33
55
59
50
32
48
56
64
45
36
70
36
59
58
53
32
52
61
59
51
40
Idaho
Boise City
Illinois
Chicago
Peon'a
130220007F01 96 - 83
141220002P01 172 140
141220001P01 117 113
146080001P01 94 72
66
130
99
68
47
91
70
52
50
91
73
51
fcontinued)
-------
Table 7-10(continued).
•vj
I
en
ID
Location
Indiana
Indianapolis
Iowa
Bellevue
Kentucky
Ashland
Paducah
Louisiana
Baton Rouge
Maine
Bangor
Maryl and
Baltimore
Silver Spring
Site Code
152040025H01
1 5204001 5H01
280180002F01
180080003F01
180080008F01
183180020F01
190280002F01
200100001F01
210120018F01
210120007H01
211480005G01
Concentrations (pg/m ) Equalled Annual
1st Max 2nd Max or Exceeded by Stated Percent Arithmetic
o o of Observations Mean ->
(yq/rn ) (pq/ni ) 10% 50% (pq/nr)
308
128
126
94
93
90
102
126
137
90
98
132
122
97
93
89
82
88
103
134
88
82
86
89
87
79
76
71
75
80
95
80
66
50
53
41
46
43
40
48
50
60
57
38
56
54
46
48
47
44
51
51
63
57
39
(continued)
-------
Table 7-10(continued).
^>!
O
Location
Michigan
Detroit
Minnesota
St. Paul
Missouri
Kansas City
St. Louis
Nebraska
Lincoln
New Hampshire
Nashua
North Carolina
Belmont
Charlotte
Wins ton-Sal em
Site Code
231180001P01
231180018F01
231180016F01
243300031P01
171800012P01
26428007 2P01
264280001 P01
281560004601
300480005F01
340300001G02
340700004G01
344460003G01
Concentrations (yg/m ) Equalled Annual
1st Max 2nd Max or Exceeded by Stated Percent Arithmetic
o ., of Observations Mean ^
(yq/rn ) (yg/nT) 10% 50% (yq/ni )
138
123
99
91
147
136
111
112
151
107
97
114
122
115
88
83
147
127
105
91
116
103
80
76
91
105
67
71
69
109
94
70
76
96
73
70
62
62
45
52
49
71
64
45
46
67
50
50
66
68
48
54
50
73
59
46
54
73
51
51
(continued)
-------
Table 7-10(continued).
Location
Ohio
Akron
Camp be 1 1
Cincinnati
Cleveland
Moraine
Toledo
Oklahoma
Tulsa
Oregon
Portland
South Carolina
Mount Pleasant
Spartanburg
Tennessee
Chattanooga
Eastridge
Knoxville
Nashville
Site Code
360060006H01
360060004H01
360960001101
361220018H01
361220019P01
361300033H01
361300012H01
364550001G01
366600007H01
373000112F01
381460001P01
421700001F01
422040001 F01
440380025G01
440900001G01
441740005G01
442540002G01
1st Max
(yg/m3)
96
100
128
158
121
193
189
126
117
193
102
118
121
94
124
119
145
2nd Max
(ug/m3)
91
91
125
139
98
181
175
91
115
157
98
74
90
92
95
114
115
Concentrations
or Exceeded by
of Observations
10%
70
82
92
106
89
127
127
84
80
119
90
37
74
74
64
101
97
(ug/m ) Equalled
Stated Percent
50%
45
48
60
61
61
83
87
52
53
68
53
16
38
48
46
70
64
Annual
Arithmetic
Mean ^
(wi/nr)
46
53
63
70
62
88
87
53
56
74
57
20
42
51
47
70
69
(continued)
-------
Table 7-10(continued).
^J
ro
Location
Texas
Austin
Dallas
Fort Worth
Houston
Utah
Salt Lake City
Washington
Seattle
Wisconsin
Milwaukee
Site Code
450220004F01
450220012F01
451310023H01
451310002F01
451310002H01
451880021H02
451880022H02
452560009H01
460920001P01
491840001P01
51 2200045 F01
Concentrations (ug/m ) Equalled Annual
1st Max 2nd Max or Exceeded by Stated Percent Arithmetic
^ ^ of Observations Mean ^
(yg/mj) (uq/mj) 10% 50% (uq/nT)
117
93
91
97
108
153
138
162
364
119
148
71
79
88
96
105
143
124
137
182
114
115
47
58
77
83
80
102
95
127
120
91
88
27
20
50
52
57
74
63
56
57
66
62
30
24
51
52
57
71
61
64
70
65
60
-------
Table 7-11. DISTRIBUTION BY TIME OF DAY OF ONE-HOUR MAXIMUM NOp
CONCENTRATIONS3 FOR ONE MONTH IN 1975 FOR SELECTED URBAN SITES U
Newark
New Jersey
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 pm
1 pm
2 pm
3 pm
4 pm
5 pm
6 pin
7 pm
8 pm
9 pm
10 pm
11 pm
Monthly
average
of all
hours
July
160
160
160
160
140
140
160
180
200
210
230
200
200
180
200
200
200
230
200
160
180
230
350
330
96
Los Angeles
California
September
320
280
240
210
240
240
260
430
850
1100
660
260
240
230
190
170
170
230
240
260
260
280
300
300
T30
(ug/m3)
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
"SB-
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
"IT
Chicago
Illinois
September
180
160
160
150
150
160
220
260
210
220
240
300
340
260
260
260
250
230
210
210
200
200
180
200
no
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
~5T
aData presented to two significant figures only.
bNo data available.
7-63
-------
Table 7-12. MEAN AND TOP FIVE NITROGEN DIOXIDE CONCENTRATIONS BEPORTED FROM 18
INDIVIDUAL RAMS STATIONS IN ST. LOUIS DURING 1976."
Site Number Date of Measurement Time of Measurement
101
(Center-city)
104
inc
1\J-J
107
Nov. 21
Nov. 21
Nov. 21
Nov. 21
Nov. 21
May 3
Oct. 3
May 3
Oct. 3
Oct. 4
Oct. 3
Oct. 3
Oct. 3
Oct. 3
Oct. 3
Oct. 3
Oct. 4
Aug. 27
Oct. 4
10 p.m.
9 p.m.
8 p.m.
7 p.m.
11 p.m.
7 a.m.
6 p.m.
8 a.m.
5 p.m.
6 p.m.
7 p.m.
10 p.m.
8 p.m.
9 p.m.
6 p.m.
7 p.m.
7 p.m.
9 a.m.
8 a.m.
Concentration
pg/m ppm
481
454
443
434
411
293
291
287
284
284
350
337
334
332
358
353
271
266
263
0.2556
0.2415
0.2358
0.2310
0.2187
0.1559
0.1549
0.1526
0.1512
0.1509
0.1864
0.1795
0.1776
0.1768
0.1907
0.1880
0.1441
0.1413
0. 1400
Arithmetic Mean Distance from
«""3 •» 5£,101
53 0.0282 0
48 0.0253 <4
~
44 0.0235 <»
~
57 0.0305 <4
(continued)
-------
Table 7-12 (continued).
•vj
tn
Site number
103
109
114
115
116
Date of Measurement
Sept. 3
Sept. 1
July 28
Sept. 1
Oct. 4
May 2
Oct. 3
Oct. 3
Oct. 3
Apr. 9
Oct. 4
Oct. 4
Oct. 4
Oct. 3
Oct. 4
Dec. 6
Oct. 4
Hay 12
Sept. 24
July 8
Hay
Hay
Oct. 4
Oct. 3
Oct. 3
Time of Measurement Concentration
ug/m ppm
7 a.m.
8 a.m.
11 a.m.
9 a.m.
8 a.m.
8 a.m.
6 p.m.
7 p.m.
8 p.m.
12 a.m.
8 a.m.
12 a.m.
3 a.m.
9 p.m.
9 a.m.
10 a.m.
8 a.m.
10 a.m.
9 a.m.
11 p.m.
11 p.m.
10 p.m.
7 p.m.
8 p.m.
7 p.m.
636
566
321
312
291
289
216
197
186
173
305
281
276
275
273
286
170
152
145
128
457
326
228
206
206
0.3383
0.3010
0.1707
0.1659
0.1548
0.1537
0.1147
0.1049
0.0991
0.0922
0.1624
0.1495
0.1466
0.1462
0.1452
U.I 520
0.0903
0.0809
O.C771
0.0682
0.2430
0.1734
0.1214
0.1098
0.1094
Arithmetic Mean Distance from
«">3 - SItt J01
33 0.0174 *20
26 0.0138 <20
32 0.0172 s20
22 0.0116 <20
23 0.0120 s20
(continued)
-------
Table 7-12 (continued).
Site number
--J
en
Date of Measurement
Time of Measurement
Concentration
Arithmetic Mean Distance from
ug/m ppm
102
106
110
111
112
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Feb.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Oct.
Aug.
Oct.
Oct.
3
4
4
3
3
3
3
3
3
3
24
3
3
3
3
3
3
3
3
3
3
3
25
3
3
7 p.m.
8 a.m.
9 a.m.
6 p.m.
8 p.m.
10 p.m.
9 p.m.
11 p.m.
7 p.m.
8 p.m.
7 a.m.
7 p.m.
6 p.m.
10 p.m.
11 p.m.
8 p.m.
7 p.m.
9 p.m.
6 p.m.
10 p.m.
11 p.m.
10 p.m.
8 a.m.
7 p.m.
9 p.m.
374
365
363
354
331
460
446
442
408
405
405
263
257
201
200
419
406
399
387
368
318
317
315
308
308
0.1990
0.1940
0.1929
0.1882
0.1762
0.2449
0.2375
0.2352
0.2169
0.2156
0.2155
0.1398
0.1366
0.1069
0.1067
0.2230
0.2161
0.2121
0.2060
0.1956
0.1689
0.1686
0.1677
0.1637
0.1636
(km)
62 0.0329
-------
Table 7-12 (continued).
-vj
CT>
Site number
117
118
119
120
Date of Measurement
May 21
May 21
May 21
May 21
May 21
Sept. 19
Sept. 17
Nov. 8
Nov. 8
Nov. 8
Feb. 3
Feb. 3
Feb. 3
Feb. 3
Feb. 3
Oct. 13
Sept. 5
Oct. 13
Oct. 13
Aug. 25
Time of Measurement
2 a.m.
6 a.m.
4 a.m.
3 a.m.
5 a.m.
8 a.m.
10 a.m.
9 p.m.
8 p.m.
7 p.m.
11 p.m.
10 p.m.
8 p.m.
9 p.m.
7 p.m.
6 p.m.
7 a.m.
8 a.m.
7 p.m.
8 a.m.
676
566
544
461
360
149
136
134
132
127
360
343
336
336
316
360
269
253
248
236
Concentration Arithmetic Mean Distance from
ug/m3 pom yg/m3 ppm S1(km)01
0.3594 21 0.0110 s20
0.3008
0.2891
0.2450
0.1914
0.0791 21 0.0111 <20
0.0722
0.0715
0.0705
0.0677
0.1917 35 0.0184 <20
0.1825
0.1787
0.1786
0.1681
0.1916 37 0.0198 <20
0.1430
0.1372
0.1322
0.1254
-------
8. NATURAL ECOSYSTEMS, VEGETATION AND MICROORGANISMS
8.1 EFFECTS OF NITROGEN COMPOUNDS ON NATURAL ECOSYSTEMS
It is difficult to assess the complex cause and effect relationships
of any pollutant; even when they are studied using only a single organism.
When attempting to assess such relationships within populations, communi-
ties and ecosystems, the problems become even greater. Additional
complications in determing the effects of a single pollutant on natural
communities are created by the presence of multiple contaminants that may
promote synergistic or antagonistic effects. Evaluating the contribution
of functioning natural ecosystems to human welfare is a very complex task
and involves weighing both economic and human social values. As life
support systems, their values should not be quantified in economic terms.
Ecosystems are integrated communities of organisms functioning together
as a unit within which there occurs an exchange of energy, materials and
1~3
information with each other and with their environment. After centuries
of stable annual climatic and geochemical conditions, ecosystems become
1-4
self-perpetuating, or climax units.
Climatic, physicochemical, or biologic changes, regardless of their
source or nature, will affect the nature of the ecosystem. Some ecosystems
are durable and relatively stable when subjected to a given environmental
change; others become unstable given the same change.
Woodwell5 has decribed the possible effects of pollutants on ecosystems
as falling into two categories; short-term and long-term effects. In
most terrestrial ecosystems, Woodwell pointed out that short-term effects
are dominated by the consequences of differential species sensitivity to
8- 1
-------
environmental change. The long-term effects are established by those same
consequences plus effects on reproductive capacity and genetic effects.
The disturbance or destruction of a climax community or ecosystem
results in its being returned to an earlier and successionally simpler
stage. ' Existing studies indicate that changes occurring within
ecosystems, in response to pollution or other disturbances, follow definite
patterns that are similar even in different ecosystems. It is, therefore,
possible to predict broadly the basic biotic responses to the disturbance
of an ecosystem. These responses to disturbances are: (1) an alteration
in reproductive capacity; (2) modifications in the genetic constitution of
the population; (3) reduction in standing crop; (4) inhibition of rate of
photosynthesis; (5) selective destruction of individual species; (6)
perturbations in biological food chains; (7) setbacks in the successional
sequence; and (8) modifications in the rates of cycling of plant nutrients.
Diversity and structure are most changed by pollution as a result of
the elimination of sensitive species of flora and fauna, and the selective
removal of the larger overstory plants in favor of plants of small stature.^'
The result is a shift from the complex forest community toward the less
complex hardy shrub and herb communities. The opening of the forest canopy
changes the environmental stresses on the forest floor, causing differential
survival and, consequently, changed gene frequencies in subcanopy species.
Associated with the reduction in diversity and structure is a shortening
of food chains, a reduction in the total nutrient inventory, and a return
to a simpler successional stage. ' In addition, the pollutants act as
predisposing agents, and an increase in the activity of insect pests and
certain diseases occurs.6'10 At the ecosystem level there are no thresholds;
21
only effects.
3- 2
-------
Mature ecosystems, because of their greater diversity, are less
susceptible to the disruption of their normal structure end function by any
type of perturbation. For example, a forest ecosystem in which the
communities are composed of many species would show less immediate damage
by stress than successional stages having only a few species. Even greater
damage would be anticipated in an agroecosystem, which may be considered
the simplest of successional stages, since often only a single producer
species is present.
Terrestrial, marine, and freshwater ecosystems are functionally important
to the integrity of the biosphere. They are important: (1) in the production
of food; (2) the maintenance of forests; (3) as global support systems for
the regeneration of essential nutrients and atmospheric components; (4) for
their aesthetic value in maintaining natural vegetative communities; and
(5) in the assimilation or destruction of many pollutants from the air,
water, and soil.
Of the many functions occurring within ecosystems, the flow of energy
and nutrients are among the most important. Energy flows through an ecosystem
1-4
in only one direction while nutrients are recirculated.
Nitrogen 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
1 4
molecular nitrogen composes 78 percent. ' 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 biologically available
8- 3
-------
compounds. These transformations of nitrogen are regulated almost entirely
by terrestrial and aquatic microorganisms through a complicated series of
reactions that are collectively termed the "nitrogen cycle." These
transformations are more accurately discribed as a "nitrogen web" because
the image of a simple loop of compounds through which nitrogen successively
passes bears little resemblance to reality.
cr-
The nitrogen cycle^en 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 is illustrated in Figure 8-1 and
discussed below in order that the modifications caused by man's activities
may be better understood. Figure 8-2 indicates the quantitative flows of
major nitrogen forms among the atmospheric terrestrial, and aquatic phases
of the global nitrogen cycle. Although the biospheric nitrogen cycle is
driven primarily by biological transformations, the atmospheric reactions
in the cycle (shown in Figure 8-1) are chemical and photochemical.
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 particulate forms of
organic nitrogen; and sorption (e.g., of ammonium ion by clays). Under-
standing of the biospheric nitrogen cycle and of the factors that control
the cycle depends primarily on an understanding of biological principles,
especially those of microbial ecology.
The diagrams of the nitrogen cycle in Figures 8-1 and 8-2 appear to be
highly dissimilar and complex, however, the biological transformations
shown in these diagrams involve only six major processes (Figure 8-3).
8- 4
-------
03
I
0>
/ //I 2T~t)
'- ' UPTAKE I '
— ORGAMC-N fc- NM* •= V NOj
DEMT«'F1L;AT!ON
"O; ^5E£°A&t
FIGURE 2ri" Schematic representation of the nitrogen cycle, emphasizing human activities that affect fluxes of nitrogen.
-------
00
Figure A. As the reactions of nitrogen are ex-
amined in detail they are tound to constitute a
complex web of processes, some of them
strongly influenced by human activities. These
are summarized in this Figure, which gives vari-
ous pool sizes and reaction possibilities. Figures
given tor pool sizes within the compartments are
in Tg of N. Transfer rates in Tg nitrogen per year
are given in the following table with identifying
letters for the reactions corresponding with those
shown in the figure. The discrepancy between
figures given here and those of other scientists
does not represent any real controversy but
rather is an expression ol our uncertainties with
regard to many pool sizes and transfer rates.
a
b
c
d
e
f
g
h
i
i
k
1
m
n
0
P
q
r
s
t
u
V
w
Reaction
N ixation, land
N ixation, ocean
N ixation, atmospheric
N ixation. industrial
N ixation, combustion
Weathering processes
Runoff, organic
Runoff, inorganic
Assimilation, land
Assimilation, sea
Mineralization, land
Mineralization, sea
Demtrification, land
Denitrification. sea
NH^ fallout, rainout
and washout, land
NHj fallout, rainout
and washout, sea
N from fossil fuel
(largely NHj)
NHj volatilization.
plants and animals
NHj volatilization, soil
NO, fallout, rainoul.
and washout, land
NO, fallout, rainout
and washout, sea
To organic pool, land
To organic pool, tea
Process rate
inTg N
per year
9.9
3.0
7.4
4.0
1.8
4.4
2.2
1.3
1.8
1.4
1.9
1.4
1.2
4.0
6.5
1.4
3.5
5.3
2.2
2.5
8.8
1.9 •
1.4 «
> W
x 10'
y 10'
» 10'
• 10'
• 10'
v 103
V 103
* 101
• 10J
> 10'
x 10'
x 10'
x 10'
, 10'
- 10'
• 10'
10'
10'
////////X7///////////X/// SEDIMENTS I//}////// //////////////
/ORGANIC / INORGANIC
,7 9 - 10' \ 19- 10'
-------
(3) (4) (4)
Organic N ^ NH3 ^ NO2~ v
(1) i (I) /, (1,5)
N03'
FIGURE^.3 Simplified biological nitrogen cycle, showing major
molecular transformations. Numbers in parentheses correspond to
numbered processes discussed in text: (1) assimilation; (2) hetero-
trophic conversion; (3) ammonification; (4) nitrification; (5) denitri-
t'ication; (6) nitrogen fixation.
8-4c
-------
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 NHL and collectively for NH +
o 4
plus NH3, when there is no need or intention to distinguish between these
forms. Ammonium (ion) is used specifically to indicate the cationic form
NH4+.).
2. Heterotrophic conversion of organic nitrogen from one organism (food or
prey) to another organism (consumer or predator); Nitrogen is bound in
plant or animal protein until the organisms die or as in the case of
animals certain products are excreted).
3. Ammom'fication, 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 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 ammonia 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. the bacterial reduction of nitrate to nitrous oxide
(N20) and molecular nitrogen (N£) under anaerobic conditions; (Nitrates
(N03~) are converted into nitrites (N02~), to nitrous oxide (a gas) (N20)
and finally into nitrogen gas (N2) which goes off into the atmosphere. in
8-5
-------
the soil, nitrites rarely accumulate under acidic conditions but are
decomposed spontaneously to nitric oxide (NO), and under alkaline condi-
14 15
tions they are biologically converted to N^O and N^. ' 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.
6. Biological Nitrogen Fixation is the transformation of atmospheric
nitrogen gas into ammonia, nitrates and other nitrogen-containing com-
pounds. 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 ammonifi-
cation in soils; autolysis of cells and excretion of ammonia by zooplankton
and fish are important processes in aquatic systems. Ammom'fication is
important in renewing the limited supply of inorganic nitrogen for further
assimilation and growth by plants. Nitrification is mediated primarily by
aerobic bacteria that obtain their energy by oxidizing ammonia to nitrite
and nitrate. Nitrification converts ammonia, which is volatile but readily
absorbable, into nitrate, a nonvolatile but easily leached form.
8-6
-------
On an ecosystem scale, denitrification is considered a nitrogen sink
since the products (N~ and N,,0) 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.
Nitrogen fixation is important as a source of available nitrogen for
plant growth in both natural and managed agricultural ecosystems. On a
global scale and over millions of years, nitrogen fixation balances the
losses by denitrification; on time scales of decades to thousands of years
the two processes may be out of phase without significantly affecting the
nitrogen content of the global atmosphere.
Nitrogen fixation is only an indirect source of nitrate in the biospher
but this process is important in global nitrogen balances, and in the
current controversy over the depletion of stratospheric ozone by N 0. (See
Chapter 9-1).
Numerous texts, monographs, and papers review the nitrogen cycle 13,16-23
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 understanding of the accumulation of nitrate and its transformations
in the biosphere. Because the literature dealing with nitrate and the
i
nitrogen cycle is so extensive, no attempt has been made to provide exhaust*
documentation here.
8.1.1 Effects of Nitrates
Ecological effects of nitrate can be beneficial or detrimental.
Nitrogen is an essential nutrient for biotic productivity, and in managed
agricultural ecosystems nitrogen fertilizer enhances crop yields. However
8-7
-------
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 9) and some nitrates and related compounds are to^ic to plants,
animals and microorganisms.
In most nonagricultural terrestrial ecosystems, the major processes
that provide nitrogen for plant growth are mineralization of soil organic
nitrogen and biological fixation of atmospheric nitrogen. When fluxes of
nitrogen enter such systems as a result of human activities, the added
inputs in many cases represent a significant fraction of total nitrogen
inputs. On the basis of such mass-balance considerations, it seems likely
that such fluxes are important nutrient sources that could support
increased biotic productivity.
Except in ecosystems that receive fertilizer or nitrogenous wastes,
the most important anthropogenic inputs (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, calculated total nitrogen inputs from precipi-
tation and from gaseous deposition over the Florida peninsula exceed by a
factor of two the amount of nitrogen applied as fertilizer to the
12
agricultural land area within the region.
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
8-8
-------
nitrogen inputs to most ecosystems; this is especially true for terrestrial
systems, where the major influxes are from atmospheric deposition. Second,
far less is known of the responses of nonagricultural plant communities to
increased supplies of fixed nitrogen than is known for cultivated crops.
It is possible, however, to estimate the approximate magnitude of anthropogenic
nitrogen fluxes to ecosystems, using the limited amount of monitoring data
available or mass-balance calculations (see Appendix A of the National
1 ?
Academy of Sciences: Nitrates; an Environmental Assessment). 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 approached.
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 environmental processes of transport and
transformation (illustrated in Figure 8-4).
frl.l.l Aquatic Ecosystems Nitrogen and Eutrophi cation—The overenrichment
of surface waters, usually lakes, with nutrients is termed eutrophication.
This process results in an array of water quality changes that are generally
regarded as undesirable. Phosphorus and nitrogen are the most important
nutrients that stimulate 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 limiting nutrient, and nitrogen inputs may control eutrophication.
8- 9
-------
PANs, NO~
Aerosols
AIR
oo
I
vr>
Q)
LAND
Runoff
NO:
WATER
Denitrification
Food
Production
NH;
1
NO.,
1
Waste
Disposal
NO:
Nitrification
Uptake by
Vegetation
NO:
Accumulation
in Soil and
Groundwater
Increased
UV
Vegetation,
Litter Buffering
Climate
Modification
J
Toxicity
NH
NO:
Increasing
N : P
Imbalance
t
FIGURE 8-rl 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 (Cx3) on the arrows representing the appropriate pathways.
-------
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. Hhe role of nitrogen in cultural eutrophication
therefore appears to be important, although it is complex and poorly
quantified relative to the role of phosphorus.
rcuK-Ai'v?
The sources of anthropogenic nitrogen^surface waters include sewage,
industrial wastes, animal manures, surface runoff and sub-surf ace transport
of nutrients from urban and agricultural lands, and atmospheric fluxes. It
12
has been estimated that more than 90 percent of the nitrogen entering
surface waters comes from nonpoint sources, and that more than 80 percent
of that portion is' from agricultural lands (including livestock feedlots).
Because nitrogen forms in aquatic systems are readily interconvertible, all
nitrogen inputs, rather than nitrate per se, must be considered.
The average atmospheric input of 10 to 20 kg N/ha-yr that is typical
for most of the United States is also a sufficient nutrient loading to
support a moderate increase in biotic productivity in some lakes,
especially shallow, oligotrophic lakes that may be nitrogen-limited.
Atmospheric nitrogen fluxes may contribute to slight eutrophication in such
cases; however, it is unlikely that these inputs alone would induce serious
water quality problems:
-'3- Eutrophication of Lakes. Cultural or man-induced eutrophication has been
-i '
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
8'10
-------
lifetime. However, addition of excessive amounts of nutrients from sewage
effluents, agricultural runoff, urban runoff and other anthropogenic
sources can greatly modify the characteristics of a lake in a matter of a
few years; the literature is replete with examples of this phenomenon.
The over-enrichment or eutrophication of surface waters, usually
lakes, with nutrients results in an array of water quality changes that are
generally considered undesirable. These changes most commonly include the
proliferation or "blooms" of algae and aquatic macrophytes, the depletion
of dissolved oxygen in bottom water, a decrease in water clarity, the loss
of cold water fisheries, shortened food chains, and takeover by rough fish.
Table 8-1 summarizes changes in common trophic state indicators that occur
when lakes become eutrophic, and Table 8-2 lists some common water use
problems that may result from eutrophication.
Eutrophication is usually considered undesirable. This somewhat
narrow viewpoint, however, ignores the fact that nutrient-rich waters are
more productive not only of algae, but also of fish. Lakes are not now a
significant source of protein in the United States, but lake fish may be an
important food resource in a food-hungry world. Many sports fishermen
prefer moderately eutrophic lakes, unless they are seeking coldwater fish,
which cannot survive in such lakes because of oxygen depletion in the cold
bottom waters. A conflict thus exists between the desires of some fisher-
men and the preferences of swimmers and other recreational users of lakes,
who generally favor the clearest and most oligotrophic situation. On the
other hand, continued nutrient enrichment eventually is undesirable to
sport fishermen also, since game fish disappear, rough fish predomonate,
and excessive aquatic weed growths may hinder or prevent boating in highly
eutrophic lakes.
8-11
-------
TABLE 8-1. COMMON TROPHIC STATE INDICATORS
AND THEIR RESPONSES TO EUTROPHICATION
Physical Indicators
Transparency (D)
(Secchl 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: After Reference 24.
8-12
-------
TABLE 8-2. 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
swin, 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: Ref. 24
8-13
-------
Jbme functions of some oligotrophic lakes, where nitrogen may be the
A^
limiting nutrient, the input from runoff or atmosphere fluxes may be
essential to maintaining biological productivity. The point at which the
effects on productivity of nitrate input to 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
rt»ese
in most lakes, thts two nutrients are most important in stimulating eutro-
phication.25 Oligotrophic lakes (low in nutrients) are commonly thought to
?fi ?7
be phosphorus-limited, ' because of the relative paucity of phosphorus
in the biosphere compared 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
frequently the limiting nutrient, most often because domestic sewage, the
tf b
chief nutrient source for many eutrophic lakes, is imjpalanced with respect
to nitrogen and phosphorus. The total N/P ratio (by weight) in sewage is
about 3:1 to 4:1, largely because of the widespread use of phosphate detergents.
By comparison, the annual N/P ratio of healthy plants is about 7:1 to 8:1
(by weight).
28
Miller et al. conducted algal nutrient bioassays on waters from 49
lakes throughout the United States and found that phosphorus limited growth
in 35 lakes; nitrogen was limiting in eight lakes; and some other nutrient
was limiting in six. The incidence of phosphorus limitation was lower
among lakes that were more productive. The same relationship has been
12
noted in National Eutrophication Survey data on Florida lakes.
8-14
-------
g.U.3 Eutrophlcation In Coastal Waters. Studies of estuarine waters at
several locations along the east coast of the United States have indicated
that low concentrations of dissolved nitrogen limit primary production.2
Additions of nitrate to such estuarine systems stimulate primary
production and can produce changes in the dominant species of plants,
leading to cultural eutrophication and ultimately to deterioration of
water quality. However, the significance of nitrogen as a limiting
nutrient varies in different estuaries and even on a spatial and temporal
basis within a single estuarine system (e.g., Thayer,30 Estabrook,33
OO O A
Goldman ). Furthermore, not all estuaries are nitrogen-limited; Myers
n
found that phosphate was the primary limiting fcutrient in near-shore
waters of the Gulf of Mexico near Appalachicola, Florida. The high
degree of heterogeneity in the role of nitrogen as a control of produc-
tivity 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 sediment and water in saline waters
is one possibility. It has also been suggested that denitrification 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 considerable detail.35'38 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
8-15
-------
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 contributes to eutrophication problems.
OQ
Sawyer was the first to determine critical nutrient levels associ-
ated with water quality degradation in lakes. He concluded from a study of
17 lakes in southeastern Wisconsin that lakes with spring maximum concentra-
tions of more than 300 ug/1 of inorganic nitrogen and more than 10 to 15
ug/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 base
from which they were developed.
25
Vollenweider, 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 8-5 presents
25
Vollenweiger's loading graph for nitrogen. Vollenweider presented a
semi theoretical masspalance 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 guide-
lines (e.g.,Dillon and Rigler ). 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.
8-16
-------
10.0
10 20 50
MEAN DEPTH, m
SOURCE: VoHgnwoidOf 11068).
l-'IGURj; «-.£ Areal loading rates for nitrogen plotted against mean depth of lakes.
100
8-16a
-------
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. ' Although blue-green algae are cosmopolitan, they are seldom
the dominant phylum in oligotrophic lakes, and nitrogen-fixing species
(e.g., Anabaena spp., Apham'zomenon 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-gree algae requires an adequate
supply of phosphorus, and dissolved phosphorus is usually growth-
43
limiting in oligotrophic waters. For example, Vanderhoef et al.
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 Apham'zomenon increased with
rft
dec!inige-combined nitrogen concentrations and showed increased efficiency
of fixation as inorganic nitrogen levels decreased. The standing crop
of this species decreased with decreasing phosphate concentrations.
Finally, diatoms predominated in the northern reaches of the bay (40 km
from the Fox River, the major tributary and source of nutrients for the
bay).
8-17
-------
The importance of nitrogen fixation in the nitrogen budgets of
lakes is controversial. Most reports indicate relatively low contribu-
tions (<15 percent) in lakes where fixation occurs at all, but a few
cases where fixation supplies up to 50 percent of the annual nitrogen
input have been reported. Even in the typical case where fixation makes
only a small contribution to the total loading, however, the process is
still significant in maintaining nuisance blue-green algal blooms in
lake surface waters.
Denitrification occurs in the anoxic hypolimnia of stratified
eutrophic lakes, and can represent a significant term in lacustrine
12
nitrogen balances (see NRC, Nitrates ). Denitrification also occurs in
the anoxic sediments of lakes. The source of nitrate for sediment
s~* t
denitrification may be upward see page of roundwater, downward diffusion
of nitrate from the lake water column, or nitrification in the oxygenated
surface layer of sediment. Sediment denitrification can occur in oligo-
trophic lakes, since their sediments are also anoxic. However, Chen et
al. reported much higher rates in sediments from a hard water eutrophic
lake than in those from a soft water oligotrophic lake.
ftlLq-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, Wisconsin12 represents one of the few cases where
nitrogen loading rates have been broken down according to form. Table
8-3 indicates that 47 percent of the total nitrogen loading to Lake
Wingra was in the form of nitrate.
3-18
-------
Table 8-3. NITRATE-N LOADINGS TO LAKE WINGRA
Kilograms Percent Total
Source N03~-N/yr N as N03"-N
Precipitation on
lake surface 440 40
Dry fallout 480 22
Spring flow 4,140 96
Urban runoff 600 13
Average —
SOURCE: 47.
8-19
TOTAL 5,660 47
-------
Inorganic nitrogen forms in lake water are so readily interconverti-
ble 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
12
variations occur. Rainfall in industrialized and urbanized regions
45
has exhibited increasing nitrate levels over the past several decades.
Urban runoff and sewage effluents vary widely in their nitrogen composi-
ton, making generalizations tenuous. Kluesener and Lee summarized
average nitrogen component concentrations from several urban runoff
studies. The grand means of the data they collected are: NH--N, 0.44
i,fisr _ |.T,rr 1'Tt*1
mg/(G; N03 -N, 0.51 mg/A; organic nitrogen, 2.0 mg/t.
In summary, the specific contribution of nitrate to eutrophication
is uncertain, because of a relative lack of data on nitrate inputs per
se_, and because of the ease of interconversion of nitrogen forms.
Nitrogen inputs from human activities can promote increased biological
productivity in aquatic systems, but the role of nitrogen in eutrophica-
tion is understood much less quantitatively than the role of phosphorus.
The effects that nitrogen inputs may have on productivity, phytoplankton
succession, and other processes of aquatic ecosystems are certain to be
influenced by other variables, such as light and temperature; but few
quantitative statements about the relationships among these factors can
be supported with present knowledge.
8-20
-------
8.\-i,f> Terrestrial Ecosystems-Nitrates
Input of nitrate and other nitrogen forms from the atmosphere is an
integral component of the terrestrial nitrogen cycle. Higher plants and
microorganisms can assimilate the inorganic forms rapidly. The flux 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; but total nitrogen fluxes,
including organic nitrogen, in bulk precipitation (rainfall plus dry
fallout) can be significant, especially in unfertilized natural systems.
In absolute terms, atmospheric inputs of nitrate can range from
48
less than 0.1 kg N/ha-yr in the Northwest (e.g., Fredericksen ) to 4.9
kg N/ha-yr in the eastern United States. ' Inorganic nitrogen
(ammonia-N plus nitrate-N) loadings in wet precipitation ranged from
51
less than 0.5 kg/ha-yr to more than 3.5 kg/ha-yr in Junge's 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 inputs of nitrogen from the atmosphere commonly range
12
from about 10 to 20 kg N/ha-yr for most of the United States.
In comparison, rates of annual uptake by plants that range from 11
12
to 125 kg N/ha-yr in selected ecosystems from several bioclimatic zones.
Since the lowest fluxes are generally associated with desert areas,
where rates of uptake by plants are low, and the highest fluxes usually
occur in moist areas characterized by high plant uptake, the inputs of
8-21
-------
ammonia and nitrate from rainfall to terrestrial ecosystems are equivalent
to about 1 to 10 percent of annual plant uptake. The typical fluxes 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
suggest that plant growth in terrestrial ecosystems depends to a signifi-
cant extent on atmospheric loadings, it is not yet possible to estimate
the importance of these inputs compared to biological nitrogen fixation
and mineralization of soil nitrogen. In nutrient-impoverished ecosystems,
such as badly eroded abandoned croplands or soils subjected to prolonged
leaching by acid precipitation, nitrogen inputs from atmospheric fluxes
are certainly important to biological productivity. Such sites, however,
are relatively limited in extent. In largely unperturbed forests,
recycled nitrogen form 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 anthropogenic inputs could play a
significant ecological role in a relatively large portion of the forested
areas near industrialized regions.
8-22
-------
8.1.2 Effects of Nitrogen Oxides
8.1.2.1 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
community under stress is the elimination of the more sensitive popula-
tions and an increasing abundance of species that tolerate or are favored
by the stress. The response of plant populations or species to an
u
environmental perturbation will depend upon life cycles of the plants,
•\
microhabitats in which they are growing, and their genetic constitution
(genotype). Abundant evidence exists to show that new species become
prominent in plant communities undergoing structural changes that reduce
environmental or biological variability. ' Furthermore, the
specific pollutant to which a community is exposed for prolonged periods
of time will govern the capacity of the community to recover. In turn,
an alteration in the community-composition, size of the community, or
its rate of energy fixation will influence the animal populations in the
vicinity and microorganisms in the underlying soil. These changes, in
their turn, will modify the behavioral patterns or alter competition
among the prevalent organisms.
Investigations of the influence of nitrogen oxides on economically
important plant species have revealed differences in susceptibility of
dissimilar plant species, the effect of plant age on the toxicity, and
the difficulties in predicting synergistic effects when a plant popula-
tion is exposed to more than one pollutant. MtiMOUgTi .attention has been
focused on agriculturally-important species? little information is
8-23
-------
available on the effect of nitrogen oxides on plants in natural communi-
ties. Evidence for visible damage to plant communities is not common.
Visible damage may represent only a fraction of the actual harm done to
terrestrial communities. The vigor and survival rate of plants have been
affected deleteriously by air pollution.62 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
frequently 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.62
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.
A number of studies have been conducted on the effect of air pollutants
on ecosystems and plant communities. It is the general conclusion
8-24
-------
of these investigations that further research on the influence of nitrogen
oxides on plant communities is required. The available information
clearly is too small to warrant meaningful generalizations at this time;
however, there is information detailing the effects on individual plant
species. These effects are discussed in Section 8.2.
8.1.2.2 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 labora-
tory tests on animals maintained under careful conditions, to populations
in the field. The intereaction of the various stresses in nature and
c
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., 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.
Beyond this limited amount of knowledge, the literature concerning
the effects of nitrogen oxides on natural animal populations or communi-
ties is extremely sparse. No conclusions can be drawn about whether
8-25
-------
ambient levels of nitrogen oxides in the atmosphere have an effect on
the composition or functioning of animal communities or populations
8.1.2.3 Effects of Nitrogen Oxides on Microbial Processes in Nature—
Microorganisms are essential for the functioning of key process in
terrestrial, marine, and freshwater communities. They are the chief
agents for regenerating the limited supply of carbon dioxide (C02) in
the atmosphere through decomposition of 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 solely by these microscopic
organisms, which also maintain soil structure and form the humus important
to abundant plant growth. In addition, many of the pathogens that are
constantly discharged into soils and waterways are elimianted 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 potential 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
f\
found in the atmosphere.
8-26
-------
Therefore, the knowledge concerning the potential impact of nitrogen
oxides on microbial processes in soils and waters is sparse. AlthofZrh
ambient concentrations probably do not significantly affect biologic
processes in natural ecosystems, it is not possible to support this view
with experimental data.
8.1.3 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 dependent on the extent to which man
can manipulate the ecosystem for his own purpose. This single-purpose
point of view makes it difficult to explain the many benefits of a
natural ecosystem to man's welfare in terms of the conventional cost-
benefit analysis. Natural forests are among the most efficient in the
fixation of solar energy. Most agriculture, by comparison, is inefficient
in total energy fixed; however, in transforming solar energy into food
for man it may be highly efficient, so agriculture is emphasized.
Many functions of natural ecosystems and their benefits to man are
unknown to the decisionmakers. Gosselink, Odum, and Pope have, however,
placed a value on a tidal marsh by assigning monetary values to the
multiple contributions to man's welfare such as fish nurseries, food
suppliers, and waste-treatment functions of the marsh. They estimate
the total social values to range from $50,000 to $80,000 per acre.
68
Westman also evaluated the benefits of natural ecosystems by
estimating the monetary costs associated with the loss of the free
services (absorption of air pollution, production of oxygen regulation
of global climate and radiation balance, and soil binding) provided by
8-27
-------
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 quali-
ties such as clean air and water, untamed wildlife, and wilderness, once
regarded as priceless, are an attempt to rationalize the activities of
68
civilization. When estimating the monetary cost in currency of the
values lost through the damaging of ecosystems, the assumption is usually
made that the decisionmakers will choose the alternative which is most
socially beneficial as indicated by costs compared to benefits. As
68
Westman points out, the assumption "that decisions that maximize
benefit cost ratios simultaneously optimize social equity and utility"
are based on certain inherent corollaries. These are:
"(1) The human species has the exclusive right to use and manipulate
nature for its own purposes. (2) Monetary units are socially
acceptable as means to equate the value of natural resources destroyed
and those developed. (3) The value of services lost during the
interval before the replacement or substitution of the usurped
resource has occurred is included in the cost of the damaged resource.
(4) The amount of compensation in monetary units accurately reflects
the full value of the loss to each loser in the transaction. (5)
The value of the item to future generations has been judged and
included in an accurate way in the total value. (6) The benefits
of development accrue to the same sectors of society, and in the
same proportions, as the sectors on whom the costs are levied, or
acceptable compensation has been transferred. Each of theseggssump-
tions, and others not listed, can and have been challenged."
8-28
-------
In the case of (4) above, for example, the losses incurred when the
development of natural ecosystems are involved, include species other
than man. These losses are seldom, if ever, compensated. The public at
large also is usually not consulted to determine whether the dollar
compensation is adequate and acceptable. Frequently, there is no direct
compensation. Corollary (5) can never be fulfilled because it is impossible
to determine accurately the value to future generations.
It should be remembered that ecosystems are life support systems
and therefore their value cannot be measured in dollars and cents.
SUMMARY
Human impacts on the nitrogen cycle begin either with a source of
input of fixed nitrogen into the environment or with a major perturbation
of the nitrogen cycle. The net result is a change in either the sizes
of or the transfer rates to or from one or more pools of fixed nitrogen
in the environment. The pollution problems most pertinent to this
report ensue when an excessive amount of nitrate or an associated nitrogen
compound accumulates in one or more compartments of the environment.
Examples include potentially toxic amounts of nitrate in drinking water,
food, or forage; excessive nutrient enrichment of lakes, rivers, or
coastal waters; nitric acid in precipitation; or increased nitrous oxide
content of the atmosphere.
Human activities have unquestionably increased the amounts of
nitrates and related compounds in some compartments of the eivnronment.
The effects of such increased concentrations of nitrogen compounds may
be beneficial or adverse, or both. Effects of both kinds may occur
8-29
-------
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. In addition, the inhibition of a particular function of an
ecosystem may have a deleterious effect on the total community. At the
are.
present time there fe insufficient data to determine &BS, the impact of
nitrogen oxides as well as other nitrogen compounds on terrestrial plant,
animal or microbial plant communities. The effects of nitrates on eutrophication
in fresh and marine coastal waters have been much better quantified.
8.2 EFFECTS OF NITROGEN OXIDES ON VEGETATION
Of the variety of oxides of nitrogen (NO ) occurring in ambient air
/%.
(Chapter 7), only nitric oxide (NO) and nitrogen dioxide (NOp) are considered
to be important phytotoxins.
The various nitrogen oxides by themselves are usually considered to
have only minor effects as the doses required to produce injury are typically
larger than those which would occur in the ambient air. However, nitrogen
4
oxides, particularly NOp, when experimentally administered with other
pollutants such as S02, may produce injury at much lower doses than have
been suggested in some earlier studies. This finding suggests that in
certain instances N0y in conjunction with other substances in the ambient
air can behave synergistically. N02 and S02 together do not always cause
injury below the injury threshold of each individual gas.
8-30
-------
The pH of the precipitation for several regions of the world, including
the eastern United States, is becoming more acidic with time (Chapter 9.).
Nitrogen oxides contribute significantly to the increased acidity of
precipitation. The effects of acidic precipitation on ecosystems is
discussed in Chapter 9.
8.2.1 Factors Affecting Sensitivity of Vegetation to Oxides of Nitrogen
Plants vary in their sensitivity to nitrogen oxides. There is a range
of variability, based on genetic factors, for plant tolerance of NO . This
range is narrow enough that one species of plant can consistently be shown
to be more sensitive to NO than another, if both are grown and exposed
/\
under specified conditions. This principle also extends to cultivars
within a species. However, the variance can be great enough that, given
different sets of environmental parameters or other variables, the relative
sensitivity to NO of species, or cultivars within species, can change.
Therefore, relative sensitivity charts, such as the one presented in Table
S~£
8^, seem to present some conflicting results, possibly due to changes in
sensitivity of certain plants under different environmental settings.
A given plant, as well as its individual leaves, will vary in
sensitivity with time. Sensitivity to N02 varies with the age of the leaf
91 92 93
on a given plant. In Ixora, mustard and m'cotiana glutinosa the
older leaves are more sensitive. In other species such as chickweed,
dandelion (Taraxocum officinale) and pigweed (Aneranthus retroflexus) the
92
middle aged leaves are more sensitive. Middle aged and older leaves
92
respond similarily in sunflower. In citrus, necrosis was most severe on
91
the youngest leaves.
8-31
-------
TABLE 8~4. KELAT1VS SENSITIVITY OP SEVERAL fLANT SPECIES TO NITHO«EN DtOXtoe"•>fa-"°-lmz•
Plant Type
Coniferous
Field Crop
» firass
Fruit Trees
Susceptible
Intennediate
Larix decidua Mill. (European larch)
Larix Teptolepsis Gord. (Japanese larch)
Avert a sativa L. (Oats)
Clfntland 64
329-RO
Pendek
Bromus Inermis, L_. (Bromegrass)
Sac Smooth
Hordeum distichon I. (Barley)
HecTicago sativa, i. (Alfalfa)
Nicotiana' glutinosa (Tobacco)
Sjcorzpnera_ iLLs^anTca (Viper's grass)
Tri foil urn pratense L. (Red clover)
J. incarnatum (Spring)
Triticum vulgare, Vill. (Wheat)
Wells
Vicja sativa L. (Spring vetch)
Mai us sp. (Wild apple)
Mai us sylvestris Mill. (Apple)
Pyrus cominunis j.. (Wild Pear)
Abies alba Mill. (White fir)
Shies ba_1samca Hill. (Balsam)
Ml.?§ b?J]l°JpPls 5J^- * Succ.(Nikko fir)
Abies pectinata (Coiunon sTlver fir)
Chaniaocyparis Tav;soniana (Layson's
cypress"]
Picea alba (White Spruce)
F4£?5 ilLa_uJL3 (Moench) Voss (Hhite spruce)
PTcen purujens cv. s]auca, Regel
TColorado~b"lue spruce)
Gossypium hirsutum, L. (Cotton)
'Rex
Acala4-42
Paymaster
Glycij[ie_ max, mcrr. (Soybean)
Scott
Bonsei
Kanrich
llordoum vulgare, L. (Barley)
Nicotiana tacacum, L. (Tobacco)
Whfte Gold
Bel-B
Beltsville W3
Beltsville C
§£ca_\e_ cereaje. L. (Rye)
TJliiJjL1™ sativum Lam (Wheat)
Triticum aestiy'um L. (Wheat)
Zea mays JL. (Sweet corn)
Golden Cross
Citrus sp. (Orange, grapefruit, tangelo)
Citrus sinensis Osbeck (Navel orange)
Tolerant
Pinus montarta mughus (Knee pine or dwarf
mountain pine)
fiQiLS nigra Arnold (Austrian pine)
Taxus baccata L. (English yew)
Dactylis glonierata, J.. (Orchard grass)
Potomac
^!c.°Ji?n.a -ts^iCLSl' L- (Tobacco)
"Beltsvi'lle" B~
W3
Burley 21
L?A £DIiyA> k- (Annual blwgrass)
Poa pratensis L. (Kentucky bluegrass)
Pioneer
Golden Cross
Sorghum, sp. (Sorghum)
Martin
Zea mays L. (Sweet corn)
Pioneer
Hosta plantaqiriea (Lam,) Archers (Plantain)
-------
TABLE 8-4 . (Continued)
Plant Type
Susceptible
Intermediate
Tolerant
Garden Crops
oo
All 1 urn porrum L (Leek)
Apium graveoTens L. (Celery)
Irasslca sp. (Mustard)
Brassica oTeracea L. (Broccoli)
Brasslca TTeracea Fotrytls. L. (Broccoli)
var. CaTabrese
Capsicum frutesceans L. (Bell Pepper)
Cal chill 505
Daucus carota L (Carrot)
LactucaTativa, L. (Lettuce)
Ruby
Early Prize Head
Iceberg
Grand Rapids
Great Lakes
Romalne
Burpee Bibb
Black Seeded Simpson
Butter King
Big Boston
Butter Crunch
Petrosellnum hortense Nym. (Parsley)
Phaseolus vulgaris. L. (Bean)
TTnto
Pi sum satlvum L_. (Pea)
Raphanus satlvus L. (Radish)
Cherry leTTe
Rheum rhapontlcum L. (Rhubarb)
Splnacea oleracca U. (Spinach)
Bloons dale Long Standing
SI nap Is alba (White mustard)
Apium grayeolens L (Celery)
Rapaceum
Brasslca aryensls, Rabenh. (Mustard)
CTcbrluin endlvla, L. (Endive)
"Tiuffee
Cucumls satlvus, L^. (Cucumber)
Heinz Pickling
Black Diamond
London
CucurbJta, S£. (Squash)
Early White Bush
Golden Summer Crookneck
FraqaHa chlloensls (Strawberry)
CfiTToe
Fragarla chlloensls var. grandlflora
T/Plne strawberry)
Fuchsia sp. (Fuchsia)
LycopersTcum esculentum, Mill (Tomato)
Roma
A
B
C
D
Pearson Improved
Phascoins lunatus, J.. (Lima Bean)
Henderson
BF
Thaxter
Phaseolus vulgaris cv. humlUs Alef. L.
(Bush beanj~
Solanuni tuberosum L. (Potato)
SlrinacTa olerace?, L_. (Spinach)
Noble"
Early Hybrid #7
American
A1 1 1 u_m cejm L. (Onion)
Asparagus ofTlcl nails L (Asparagus)
Beta vulgaris, L. (Beet)
Perfected Detrol t
Brass^lca oleracea cv. gongylodes (Kohlrabi)
Brass ica caulorapa Pasq. (Kohlrabi)
B~ras"sTca' oleraceaa'cephala (Kale)
Brasslca aTiraca ^cv. capita ta_ i.- (^M te
cabbage f
Brasslca oleracea var. capltata rubra ( Red
cabbagd)
Cucumls satlvus. L. (Cucumber)
Long Marketeer
Daucus carota L. (Carrot)
-------
TABLE H-4 . (Continued)
Plant Type
Ornamental Shrubs
and Flowers
CO
i
oo
Trees & Shrubs
Weeds
Susceptible
Antirrhinum niajus L. (Snapdragon)
Bejonia_ sp. {Tuberous begonia)
5.?32!lli £§?.' Put*. (Begonia)
Thousand Wonders White
IK.cta bj l_^s_ Wind.
IE- "(Chrysanthemum)
Oregon~~~
!!§•''^l^iy?- annuus_ t.. (Sunflower)
Hjbisojs sp7~(Hibiscus)
liJ'litLCUs rqsa-sinensis L. (Chinese
hibiscus)
Lathy rus_ odoratus L_. (Sv/eet pea)
Lupjnus S£. Augustrifolius (Lupin)
Nerium oleander JL. (Oleander)
Pyracantha coccinea Ro
-------
Primary leaves of bean (Phaseolus vulgorus L.) were most sensitive to
N02 when apparent photosynthesis and dark respiration were at their highest
94
rate. Since these varied with leaf age so did sensitivity to N02-
Plants vary in their sensitivity to NO^ according to the time of day
as
with dark hours being more frequently reported 1» the most sensitive time
but this variability is not consistent between species. For example, sugar
beets (Beta vulgaris L.). alfalfa (Medicago sativa L.). are most sensitive
to N02 at night. Rye (Secale cereale) is most sensitive between noon and 2
p.m.79
97
Moist soil, may promotet sensitivity to nitrogen oxides. The protective
aspect afforded by drought may be due to mechanisms other than just stomatal
98
closure. Recent work by Mohanty and Boyer calls attention to the wide
range of effects of physiological drought on plant metabolism, especially
photosynthesis. Plants probably present a different array of chemical
receptors during drought conditions.
One would anticipate that dissolving N02 in the water surrounding a
plant cell could provide precursors for normal nitrate metobolism: nitrate
99
—> nitrite —> ammonia —> amino acids-^protein. Fallen was able to
grow sunflower for three weeks with only NOp as a nitrogen source. In
1974, Zeeuaart demonstrated that N02 exposure increases the activity of
y
nitrate reductose. The enzyme concreting nitrate to nitrite. In further
work on pea grown with only NH3 as an N source, Zeevaart was able to
show that NO* provided as a gas showed up in leaves as nitrate, nitrite,
ammo acid and protein. This further demonstrated the potential beneficial
effects of NQ-2 and the potential for uptake to be dependent on the status
8-32
-------
of N- .Metabolism in a given plant. Rogers102 was unable to demonstrate
differences in uptake of N02 in corn (Zea mays L.) or soybean (Glycine
maxmur.) that were grown in varying levels of soil nitrogen. However
96
Zahn has suggested that a lack of available soil nitrogen may reduce leaf
injury caused by N02. This is supported in work on tobacco (Nicotiona
glutinosa) byfroiano and Leone.103
102
The findings of Roger suggest that N02 uptake in corn (Zea mays L.)
and soybean (Glycine max merr.) is directly related to diffusion resistance
over the range 0 to 1090 ug/m3 (0.58 ppm). Similar results were obtained
on the primary leaves of beans (Phaseolus vulgaris).94'104 Uptake of N0?
was poorly correlated with such processes as apparent photosynthesis and
dark respiration, but was highly correlated with transpiration, which is a
measurement of diffusion resistance. Leaf boundary layers and cell wall
hydration, environmental factors that are involved with the regulation of
stomatal opening, have an important influence on N0x uptake. The ease with
which the experimenter can manipulate these regulating factors may have led
to results inconsistent with what occurs in nature. Plant tolerance of NO
is probably related to two general mechanisms: (1) regulation of the
excessive entry of NO into the plant, inadvertently by the experimenter or
/s
by the plant's own mechanisms, and (2) regulation or detoxification of the
pollutant after it has entered the plant. Acutal NO uptake data may be
helpful in understanding mechanisms of tolerance and relative sensitivity
of plants.
8.2.2 Mechanisms of Action
When plants are exposed to high levels of N02, the injured leaf often
first exhibits a waxy or water-soaked appearance prior to necrosis. This
8-33
-------
suggests that cell membranes are probably disrupted beyond repair.
Felmeister and his colleagues have discussed the ability of N02 to
attack lipid monolayers, especially those monolayers containing unsaturated
lipids. Such lipids have been proposed to be components of biological
membranes. The work of Estefan suggests that the products of N02 action
on lipid monolayers include both transient and stable free radicals.
Because of the high concentrations used in these esperiments, it is not
clear whether a similar response would occur in nature.
Nitrites and nitrates in plants are normally reduced to ammonia (NH~).
The energy to reduce nitrates and nitrites comes from reduced nicotinamide
adenine dinucleoTide (NADIH). It has been demonstrated that the rate of
carbon dioxide (C02) fixation is reduced by either N02 or nitrite. Part of
the energy for C02 fixation comes from reduced nicotinamide-adenine
dinucleotide phosphate (NADPH), which is produced during the photolysis
step of photosynthesis. Potential exists for competition for this reducing
power between the CCL fixation process and the reduction of nitrate and
nitrite. The result could be that less C02 is fixed.
88
Hill and Bennett have hypothesized an alternative reductive source
involving reduced ferredoxin possibly in the chloroplast. This reduction
could also lead to less reduced NADPH and, in turn, less CCL fixation.
Whichever pathway is involved, the reduction in C02 fixation is not
permanent. Fixation rates recover 1 hour after NO is removed and 4 hours
after N02 is removed.88 The diminished rate of C02 fixation due to nitrite
exposure returns to normal when the nitrite becomes reduced.
108
Kandler and Ullrich demonstrated a reduced amount of carotene and
chlorophyll in leaves following an acute N02 exposure. Some species of
8-34
-------
lichens exposed to 3,760 ug/m3 (2.0 ppm) N02 for 6 hours had reduced
chlorophyll content.109 A dose of 7,520 ug/m3 (4.0 ppm) N02 for 6 hours
was even more effective in reducing chlorophyll content in lichens.
Measurements had been made 12 hours after the exposure. In contrast,
Taylor and Eaton found an increase in chlorophyll content following
chronic exposures to N02. Similarly, Horsman and Will burn87 found that 188
3
to 1,880 ug/m (0.1 to 1.0 ppm) N02 applied to pea seedlings increased the
chlorophyll content 5 to 10 percent. They also noted the defer green color
and downward curling of the leaves observed by Taylor and Eaton.110 In
addition to NOX having the potential to alter pigments,it has been shown
that thylakoids in the chloroplasts of broad bean (Phaseolus sp) swell in
response to N02> Structural changes can be expected to result from a
disruption of the chemical components of the grana.
Several iji vitro studies employing very high levels of NOX implicate
other possible biochemical processes. A 1.0 M nitrous acid solution slowly
inactivated p-amylase extracted from barley, according the Weil! and
112
Caldwell. These authors suggest that sulfhydryl groups in the enzyme
may have been oxidized. Bacillus subtil!is cramylase also was demonstrated
to be affected by nitrous acid in the experiments of Di Carlo and
113
Redfern. These authors proposed that nitrate attacks the essential
ami no groups of this enzyme. Nitrous acid also may reduce infectivity of
some viruses by causing oxidative deamination of amino groups on their
nucleic acids. A 1.0 M nitrite solution also was shown to inactivate
115
horseradish peroxidase from Amoracia rusticana.
11C 0
Matsushima found that exposure to 75,200 ug/m (40 ppm) N02 for 16
hours stimulated amino acid synthesis, as indicated by C labelling.
8-35
-------
Amino acid synthesis was stimulated at the expense of organic acid
synthesis, which increased very little.
On a more general cytological level, Berge suggested that NOp may
cause plasmolysis of exposed cells, implying damage to the membrane. He
also noted a decline in starch grains.
In summary, a variety of response to NO have been noted. Effects may
s\
relate directly to pH changes, as pointed out by Maclean. Certainly,
cell membranes are disrupted. Photosynthesis is affected either by
competition for reductive power, interference in chlorophyll metabolism, or
by structural cnnges occurring in the chloroplast. Apparently enzymes and
certain nucleic acids also are subject to interference by NO in jjn vitro
/\ ~ ^^^~^^^^~
systems at very high doses.
8.2.3 Visual Symptoms
No one visual symptom or set of symptoms reliably indicate that
exposure of vegetation to NOp occurs. The diagnosis of injury resulting
from N0? exposure is often very difficult. The injury pattern will vary
with the species, cultivar, age of leaf, season of the year, and pollutant
dose. The general symptoms of chlorosis (yellowing of leaves) produced by
chronic exposures, and bifacinjajnecrotic lesions caused by acute exposures,
also are characteristic, of exposure to other pollutants, such as SO,,.
Even the distinction between acute and chronic exposure is confounded when
the lower leaves of some plants become chlorotic while their upper leaves
develop necrotic lesions. The following descriptions represent some of the
symptoms that have been reported in association with N02 exposures.
Occurrence of these symptoms does not necessarily indicate exposure to N02,
nor does thepbsence of such symptoms rule out such exposure.
8-36
-------
8.2.3.1 Broad-leaved (Dicotyledonous) Plants
8-2.3.1.1 Acute necrotic leaf injury. In some deciduous trees, necrotic
lesions originate as small spots scattered over the leaf. These spots may
persist, or expand and fuse to form larger necrotic areas. The larger
necrotic areas may rupture, forming holes in the leaf. In clover, the
necrosis begins at the leaf margin and progresses inward. The initial
symptoms develop on the same day as the exposure. In some citrus varieties
and a few ornamentals, marginal necrosis and intercostal necrosis develop
within 1 hour after exposure to N02. The tissue first collapses on the
upper leaf surface, but later the lesion becomes bifacial.118 In some
species, the marginal necrosis progresses inward with continuation of
exposure, resulting in bands of necrotic tissue between green major veins
or, in very severe cases, green only along the midrib. In pear, the spots
which develop are black-brown in color; on maple and oak leaves they are
light red-brown, and on apple leaves they are dark red-brown. Gray-green
spots precede the formation of necrotic lesions in many other plants.119
97
Benedict and Breen also noted a general waxy appearance on the leaves of
several weed species. The necrotic lesions are the result of cell collapse
and death. The colorations are probably the result of pigment loss coupled
with phenolic formation, phenolic oxidation, or both.
8.2.3.1.2 Chrbnic chlorotic leaf injury. Chlorosis, the yellowing of the
leaf, may occur over the entire leaf surface or may be concentrated in
spots. As with necrotic lesions, the yellow-green chlorotic spots may.be
randomly distributed over the leaf or they may be concentrated on the leaf
margins or tips. This chlorotic syndrome has the same appearnace as leaf
senescence. Chlorosis is most common on the older, lower leaves and often
8-37
-------
results in early leaf abscission. Leaves in the intermediate age group may
119
possess both acute and chronic symptoms.
8.2.3.2 Narrow-leaved (Monocotyledonous) Plants
8.2.3.2 Acute Necrotic Leaf Injury—Leaves of corn and cereal grains
develop tip necrosis which may extend back along the leaf margins. The
position of the lesion varies somewhat with leaf age. In young leaves,
lesions form just below the tip; in older leaves the lesions may concen-
trate more at the base of the lamina (leaf), von Haut and Stratmann
state that cells that have just completed the expansion phase of growth are
the most sensitive. In many narrow-leaved plants, the growth of the lamina
proceeds from the base, producing a gradient of cell age with the oldest
cells concentrated at the leaf tip. Necrotic lesions also may occur
between the veins, giving the leaf a stripped appearance. These lesions
begin soon after exposure, when cells in the affected area turn a
brownish-green color. In cereals, this area turns gray-white in color 1
day after exposure. This bleaching continues to spread for several days.
119
One week following exposure, a thin red-brown border may develop. In
barley and rye, the awns of the inflorescence also are very sensitive and
may bleach and become necrotic, initially at the tips and then progressing
79
toward the base.
8.2.3.2.2 Chronic chlorotic leaf injury—Chiorotic spots or general chlorosis
may be initiated at or near the leaf tip and progress downward, either
along the margins or between the veins, following the same pattern as the
necrotic lesions developing upon acute exposure. In older leaves, necrotic
lesions often occur. This is often mainfested as a distinct band of chlorotic
119
tissue between the upper necrotic area and the lower green tissue.
8-38
-------
8.2.3.3 Coniferous Plants
8.2.3.3.1 Acute necrotic leaf injury—Conifer needles, which grow from
their bases as do the leaves of many monocotyledonous flowering plants
(monocots), have injury patterns similar to those of monocots. The initial
injury site in younger needles is usually at or near the tip and, in older
needles, in a band some distance from the tip or at the base. The injured
area appears to first lose its gloss and turn gray-green in color. This
initial stage sometimes is restricted to that portion of the needle
receiving the most direct sunlight. Upon continued exposure to sunlight, a
brownish color will develop in a few hours, with the final red-brown color
appearing within 7 to 14 days, depending on the intensity of the sunlight.
Needles on the same tree may show different degrees of discoloration: those
in the direct sunlight becoming red-brown much sooner than those in the
shade. In later stages, the lesions may bleach and some may turn pale
red-brown in color. In pines and firs, there is distinct boundary between
the affected and unaffected tissue. This boundary zone can appear as a
dark, red-brown ring following exposure to NO . Needle retention time
s\
varies greatly among species. Some pines may retain their needles for more
than a year after the red-brown lesion forms, while larches may keep their
needles for several months; spruces drop their needles immediately after
119
the lesion is fully developed.
8.2.3.3.2 Chronic chlorotic leaf injury—Chlorosis usually develops first
at the tips of needles or on the leaf surface receiving the greater exposure
of sunlight. This yellow-green color gradually spreads over the entire
8-39
-------
needle. In the final stages, the leaf tips may bleach further and become
11Q
necrotic.
8.2.4 Dose Response
The term dose is defined as a certain concentration of a particular
pollutant administered over some stated time period. Acute doses are
defined as a relatively high concentration (well above ambient levels) of
the pollutant over a relatively short time (several hours or less).
Chronic doses are defined as relatively low concentrations (near ambient
levels) administered over a long time period (several days or longer).
120
Thomas observed that leaves of plants growing near nitric acid
factories had brown and black spots, often near the leaf margins. This was
an early indication that oxides of nitrogen might be phytotoxic. In a
study of Los Angeles smog components, however, it was noted that a mixture
•7S*»9l+? 121
containing ft.4 ppmjNO did not injure the vegetation tested. Several
4. . 122-124 noted that chronic levels of NO did not seem to
other researchers x
injure vegetation in their tests. Subsequent research seemed to support
this belief Korth et al ^ found that beans (Phaseolus vulgaris), tobacco
(Nicotiana tabacum). and petunia (Petunia multiflora) were not injured by
o 1 yc
1,800 ug/m (1.0 ppm) N02 for 2 hours. However, Thompson extended the
N0» exposure period, for several concentrations of NCK, to 35 days and
found that the two highest levels caused chlorosis and defolieation of
navel oranges (Citrus sinensis). Concentrations tested were 113; 226; 470;
3 127
940; and 1,880 ug/m (0.06, 0.23, 0.25, 0.5, and 1.0 ppm). Spierings
noted that tomatoes exposed to between 752 and 940 ug/m (0.4 and 0.5 ppm)
N02 for 45 days became etiolated and their yield of fruit was decreased by
22 percent. Taylor et al. reported leaf drop and reduced fruit yield in
8-40
-------
navel oranges exposed to 470 ug/m3 (0.25 ppm) N0£ for 8 months. However,
Taylor and his colleagues concluded that exposure to 1,880 ug/m3 (1.0 ppm)
N02, for 1 day, could induce damage in sensitive plants. The same paper
cited work by Stratmann, who found taht the growth of bush beans (Phaseolus
vulgaris) was slowed by exposure to 1,880 ug/m3 (1.0 ppm) N0 for 14 days.
Stratmann suggested t a likely threshold dose for injury would be 752
|jg/m (0.4 ppm) N02 over prolonged time periods.
Pinto bean (Phaseolus vulgaris). endive (Cicorium endivia). and cotton
(Gossypium hirsutum) exhibited slight leaf spotting after a 48-hour
3
exposure to 1,880 ug/m (1.0 ppm) NOg. ° Exposure of these same plants to
6,580 ug/m (3.5 ppm) N02 for 21 hours produced mild necrotic spots on
cotton and bean while endive became completely necrotic. No injury was
seen in these plants after exposure to lower doses of NO,,. A summary of
* ?-S.
the results of several chronic exposures is presented in Table
129
Using more acute doses, Heck and co-workers conducted a series of
experiments in which field and vegetable crops were exposed to various
concentrations of N02- In one experiment, 10 field and vegetable species
o
were exposed to 15,040; 30,080, or 60,160 ug/m (8,0, 16, or 32 ppm) N02
3
for 1 hour. At the 60,160 ug/m (32 ppm) level of N02 exposure, tobacco
(Nicotiana tobacum), bromegrass (Bromus ineamis), soybean (Glycine max.),
orchard grass (Dactylis glomerata), cotton (Gossypium sp.), beet (Beta
vulgaris). Swiss chard (Beta chilensis), and wheat (Triticum sp.) all
evidenced injury. However, injuries observed were not all of the same
severity. Bromegrass and tomato (Lycopersicumpsculentum) were the only
species to show injury at 15,040 ug/m (8.0 ppm). The same dose
combinations were presented in another experiment involving 22 different
crops. One important conclusion drawn from these experiments was
8-41
-------
TABLE R-5. EFFECTS OF CHRONIC HITPalGF.H DIOXIDE EXPOSURES ON SF.Vt.RAL CROP SPECIES
00
tu
* " ' — . . .- — _ ... . _.
Species
Cjchorlum endlva
rendTve)
C1tras_ sjjiensls
friaver orange)
Gossyplum hlrsutum
1 cotton)
LycopjRrslcum esculentuin
ftoiitatoT
Phaseolus vulqarls
(pinto bean)
EollRtanA.Cpncentratjion
ug/m ppm Exposure Time
1,880
1,880
940
470
1,880
280
490
750
V.880
560
1.0
1.0
0.5
0.25
1.0
0.15
0.26
0.4
1.0
0.3
2 days
35 days
34 days
8 mo.
2 days
10 to 22 days
10 to 22 days
45 days
2 days
10 to 19 days
Symptom
Slight leaf spotting
chlorosis and leaf abscission
chlorosis and loaf abscission
leaf abscission and yield
reduction
Slight leaf spotting
dry weight and leaf area
decrease etiolation, 225!
yield reduction
Slight leaf spotting
dry weight loss, chlor-
Referaices
Heck, 1964128
Thompson et al., 1970126
Ibid 7q
Taylor et al., 1975
1 7R
Heck, 1964
Taylor and Eaton, 1966
Sp1er1ngs, 1971127
ipn
Heck, 1964
110
110
(bush bean)
1,880
1.0
14 days
ophyll Increase
Growth depression
Taylor et al., 1975'
-------
that the extent of injury was greatest when N0£ levels were high, even
for short time periods. For example, cotton exposed to 30,080 ug/m3
(16 ppm) N02 for 1 hour (dose = 16) had an injury rate of 27 percent for
the three most sensitive leaves. When cotton was exposed to 16,920
yg/m (9.0 ppm) N02 for 2 hours (dose = 18) the comparable injury rate
was 2 percent. Thus, dose is not always a good predictor of injury.
118
Maclean et al. exposed 14 ornamental and 6 citrus species to NO
in the concentration range of 18,800 to 470,000 ug/m3 (10 to 250 ppm)
for 0.2 to 8 hours. Necrosis occurred in the citrus species when the
leaves were exposed to 376,000 ug/m3 (200 ppm) for 4 to 8 hours or
470,000 ug/m (250 ppm) for 1 hour. Non-specific marginal and intercostal
necrosis developed within 1 hour after exposure. Young citrus leaves
wilted and abscised at some lower doses.
oq
Taylor and Cardiff exposed several field crops to N02 in sunlight
chambers. They found that several crops exposed to 18,880 ug/m3 (10
ppm) N02 for 90 minutes suffered little or no injury, while exposure to
3
28,200 ug/m (15 ppm) for 90 minutes increased the extent of injury by
90 percent in tomato. They concluded that the threshold of injury for
>2
several field crops would be 18,800 to 28,200 ug/m3 (10 to 15 ppm) NO,
for 90 minutes.
The 1971 Air Quality Criteria for Nitrogen Oxides130 contained
information relating exposure dose to plant sensitivity. That information
is still useful for exposures to N02 within the range of concentrations
presented. Some of the data reported include much lower concentrations
S~S
over longer durations. This information is included in Tables S^ and
8-42
-------
CO
I
4=>
PO
0)
Table 8-ff. PROJECTED N02 EXPOSURES FOR 5 PERCENT INJURY LEVELS
ON SELECTED VEGETATION134
Concentrations Producing Injury
Time (hr)
0.5
1.0
2.0
4.0
8.0
ppm
6-10
4-8
3-7
2-6
2-5
Sensitive3
ug/m
11,280-18,800
7,520-15,040
5,640-13,160
3,760-11,280
3,760-9,400
Low
ppm
9-17
7-14
6-12
5-10
4-9
sensitive3
vi g/m
16,920-31,960
1,316-26,320
11,180-22,560
9,400-18,800
7,520-16,920
Resistant3
ppm
>. 16
>. 13
>. 11
21 9
>_ 8
vg/m3
>. 30,080
£ 24,440
>_ 20,680
>. 16,920
>. 15,040
a Plant type
-------
Two dose-response graphs have been constructed. Maclean separates
types of symptomology related to dose of N02 (Figure JST). These curves
are useful starting points in looking at acute and chronic exposures.
79
Taylor and co-workers have plotted N00 concentration versus the time
s-%2 r
required to produce injury (Figure a^fc). Qhe studies used in Figures 9-1
and 9-2 are also included individually in this report.! The curve generated
79 / &"*l\
by Taylor et al. (^Figure £5*) is very similar to the one presented by
Maclean.131
8.2.5 Effects of Mixtures
Mixtures of dissimilar pollutants often occur in nature. A combination
likely to occur includes N02 with ozone (0~) and/or sulfur dioxide (S02).
78 79
Heggestad et al. and Taylor et al. have reviewed information on these
types of pollutant combinations. The assumption that NO in normal ambient
J\
concentrations is important only on the basis of its participation in the
photochemical oxidant complex has been tested during the past few years by
exposing plants to combinations of pollutants, including NOX- The results
of these studies are described below.
In considering the impact of ambient air pollution on vegetation, N02
80
and S02 have bean evaluated for their combined effects. Taylor found
that 3,760 ug/m3 (2.0 ppm) N02 for 4 hours would not injure Bel W3 tobacco.
Also, 1,834 ug/m3 (0.7 ppm) S02 for 4 hours had no effect. However, 188
pg/m3 (0.1 ppm) N02 in combination with 262 ug/m3 (0.1 ppm) S02, for 4
hours, produced moderate leaf injury. The effect was greater than additive.
Tingey et al.81 found that neither 3,760 ug/m3 (2.0 ppm) N0£ nor 1,310
ug/m3 (0.5 ppm) S02 caused injury; however, a mixture of 282 ug/m (0.15
ppm) NO, an 262 ug/m3 (0.1 ppm) S02, administered for 4 hours, caused some
8-43
-------
OOI
IOOO
OL
a.
10
cc
§ 1.0
o
u
0.1
0.1
01
DAYS
I.O
10
100
Death
Threshold for
Foliar Lesions
IOOO
K>0
IO
I.O
E
^.
C?
z
t>
£
ID 10 100 IOOO
DURATION OF EXPOSURE (HOURS)
IOJOOO
Figure 8-7. Threshold curves for the death of
plants, foliar lesions, and metabolic or growth
effects as related to the nitrogen dioxide con-
centration and the duration of exposure.
8-43a
-------
lOOOr
• G
IOO
• 6
• •F »D
K>
(C
V)
o
0.
X
IU
IJO
•E
•E
j _ t
I.O IO IOO
NOt, ppm
7
Figure 8-6. Summary of effects of N02 on
vegetation. The points describe a dosage
79
line above which injury was detected.
Individual points were taken from the
123
following references: (A) Middleton et al.,
QA QR
(B) Hill et al., (C) Czech and Nothdurft,
(D) H. Strattman (in Taylor et al. 9),
(E) Heck,128(F) Taylor and Eaton,110
i ?fi
(G) Thompson et al., and
(H) Matsushima.116
8-43b
-------
leaf injury to pinto bean (Phaseolus vulgaris), radish (Raphanus sp.),
soybean (Gycine max. ), tomato (Lycopericum esculentum sp.), oat (Avena
82
sativa). and tobacco (Nicotiana tobacum). Fugiwara found greater-than-
additive effects when green peas (Pi sum sativum) were exposed to 188
3
(0.1 ppm) N02 in combinations with 262 pgAi (0.1 ppm) SO^. When 376
o
N02 and 524 ug/m SO^ (0.2 ppm of each gas) was employed, the effect was
only additive. If S02 exposure was followed by an N0? exposure, the effect
83
was sometimes greater- than additive but the reverse sequence did not show
this effect. Desert species have not exhibited greater-than-injury effect
after exposure to various combinations of N0? and $0,^84
85
Bennett et al. studied the effects of N02-S02 mixtures on radish
(Raphanus sativus L ), Swiss chard (Beta chilensis) oats (Avena sativa),
and sweet peas (Pi sum sativa). When applied together in equal concentra-
tions, N02 and SO,, were more phytotoxic than when applied separately over
the dose range of 0.125 to 1.0 ppm for 1 or 3 hours. Radish (Raphanus
sativus L. ) was the most sensitive of the group, but only the higher doses
within range produced visible injury symptoms.
Alfalfa exhibited a synergistic response in the form of a greater
inhibition of apparent photosynthesis (CO, uptake) when S09 and NO, were
applied Ljor 2 hrs at 25 pphm each. Even a mixture of 15 pphm each for 2
hours caused a decrease in apparent photosynthesis 7 percent greater than
the total of the two gases applied independently. At higher concentrations
ftfi
(50 pphm) there was no synergistic effect.
87
Horsman and Wellman looked at the effect of N02~S02 mixtures on
several enzyme systems in peas (Pi sum sativum). Peroxidase activity was
enhanced somewhat by S02 alone, but not by N02, However, 188 ug/m (0.1
8-44
-------
ppm) N02 plus 525 ug/m (0.2 ppm) S02 for 6 days increased the activity by
3
24 percent. A 100 percent increase was obtained when 118 (jg/m (0.1 ppm)
3
N02 plus 5,240 ug/m (2.0 ppm) SO,, was used for 6 days. The effect was
much greater-than-additive. The increase in peroxidase activity was assumed
to be a rather typical stress response by the plant. Some enhancement of
3
the inhibitory effect of SOp was obtained when 188 ug/m (0.1 ppm) NOp was
3
given in conjunction with 5,240 ug/m (2.0 ppm) S0? in a 6-day exposure
period.
8.2.5.2 Nitrogen Dioxide With Other Pollutants—Nitrogen dioxide and
nitric oxide often occur together in the ambient atmosphere. Hill and
OQ
Bennett exposed alfalfa (Medicago sativa L.) and oats (Avena sativa) to
o 3
1,128 ug/m NO,, and 1,080 m g/m NO (0.6 ppm of each gas) separately and
to a combination of both at the same concentration. The combination of
gases produced an additive effect. Carbon dioxide uptake was reduced more
rapidly by NO, and recovery of C02 uptake was more rapid following NO
89
exposure than after exposure to N02- Taylor and Cardiff achieved similar
results after exposing pinto bean (Phaseolus vulgaris L.) and tomato
(Lycopersicum esculentum) to NO.
Combinations of 03 and N02 were less injurious to pepper (Capsicum
frutesceans L.) and tomato (Lycopersicum esculentum) than similar cofi-
83
•centrations of either gas alone.
Reinert and Gray90 obtained somewhat different results using different
pollutant combinations. Using radish (Raphanus sativus L.), pepper (Capsicum
protescerus L.), and tomato (Lycopersicum esculentum), they found that N02,
S0?, or 03 were less injurious when used individually than they were in
combinations of N02+S03, N02+S02, or S02+03- The dose in each experiment
8-45
-------
involved equal concentrations of gases, ranging from 0.1 to 0.6 ppm for
either 3 or 6 hours.
Ttusff*
It is clear from tWf limited data that low levels of N02 (those doses
generally considered below the injury threshold) may participate with other
common air pollutants to induce vegetation injury. Much more work needs to
be done to verify this phenomenon under field conditions in which plants
are exposed to pollutants. If the results can be verified in field
o
studies, it would appear that levels of N02 between 188 mg/m (0.1 ppm) to
470 mg/m (0.25 ppm) are of concern in producing direct effects on
vegetation when in combination with certain other pollutants.
8.2.6 Summary and Conclusions
Sensitivity of plants to nitrogen oxides varies with species, time of
day, stage of maturity, type of injury assayed, and soil moisture.
When exposures to NO* alone in controlled studies are considered, the
ambient concentrations producing measurable injury are above those normally
occurring in this country (Chapter 7). Tomato plants exposed continuously
to 750 to 940 mg/m (0.4-0.5 ppm) for 45 days became etiolated and suffered
decreased yield of 22 percent. Leaf drop and reduced yield occurred in
naval oranges exposed to 470 ug/m (0.25 ppm) continuously for 8 months.
Pinto beans, endive and cotton exhibited slight leaf spotting after 48
o
hours of exposure to 1,880 ug/m (1.0 ppm). Growth depression in bush bean
o
was observed with a 14 day exposure to 1,880 ug/m (1.0 ppm). Other reports
cited no injury in beans, tobacco, or petunia with a 2-hour exposure of the
same concentration.
8-46
-------
Nitrogen dioxide concentrations ranging from 188 to 1,880 pg/rn3 (0.1
to 1.0 ppm) increased chlorophyll content in pea seedlings form 5 to 10
percent. Some species of lichens, a plant sometimes used as an indicator
•3
of presence of toxic gases, exposed to 3,960 ug/m (2.0 ppm) for 6 hours
showed a reduction in chlorophyll content. The significance of these
observations is, however, not clear at present.
In contrast to the studies cited above on the effects of N02 alone, a
number of controlled greenhouse studies on mixtures of N0? with sulfur
dioxide (SOp) show effects greater, in some cases much greater than those
effects caused by the individual pollutants alone. Concentrations at which
observable injury occur are well within the ranges occurring in some areas
of this country. Neither 3,960 ug/m (2.0 ppm) N02 nor 1,300 ug/m (0.7
ppm) SOp alone caused injury in Bel W3 Tobacco. However, a combination of
'
3 > 3
190 |jg/m (0.1 ppm) NCL and SB ug/m (0.1 ppm) S02 for 48 hours caused
moderate leaf injury. Pinto bean, radish, soybean, tomato, oat, and tobacco
exhibited some leaf injury after a 4-hour exposure to 280 ug/m (0.15 ppm)
3
N02 in combination with 260 ug/m (0.1 ppm) SO,,. Separate exposures to
3,960 ug/m3 (2.0 ppm) N02 and 1,300 pg/m (pm) S02 caused no injury.
Similar results were observed in green peas and Swiss chard. Few field
studies have been conducted.
In one report, combinations of ozone and N02 were less injurious to
pepper and tomato than similar concentrations of either gas alone. Another
report cites some increased injury from combinations of NO^SO^j+O^ and
S0?+03 in radish, pepper, and tomato compared to exposure to the individual
pollutants. Doses ranged from 0.1 ppm to 0.6 ppm for 3 to 6 hours for each
pollutant.
8-47
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1971.
8-56
-------
128. Heck, W. W. Plant injury induced by photochemical reaction products
of propylene-nitrogen dioxide mixtures. J. Air Pollut. Control Assoc.
14:255-261. 1964.
129. Heck, W. W., and D. T. Tingey. Cited in Mudd, J. B. and T. T.
Kozowski. Responses of Plants to Air Pollution. Academic Press, Inc.
New York. 1975.
130. U.S. Environmental Protection Agency. Air Quality Criteria for
Nitrogen Oxides. No. AP-84. U.S. Govt. Printing Office. Washington,
D.C. 1971.
131. Maclean, D. C. Stickstoffoxide als phytotoxische luftverunreinigungen.
Staub Reinhalt. Luft. 35(5):205-210. 1975.
132. Diagnosing Vegetation Injury Caused by Air Pollution. N. L. Lacasse
and M. Treshow. eds. U.S. Environmental Protection Agency, U.S.
Government Printing Office. Washington, D.C. 1976.
133. Taylor. 0. C. and D. C. Maclean. Nitrogen oxides and the peroxyacyl
nitrates. _In: Recognition of air pollution injury to vegetation: A
pictorial atlas. J. S. Jacobson and A. C. Hill, eds. Air Pollution
Control Association. Pittsburgh, Pennsylvania. 1970. p E1-E14.
134. Heck, W. W., 0. C. Taylor, and D. T. Tingey. Responses of plants to
acute doses of nitrogen dioxide. Bioscience. 21:21-24. 1971.
8-57
-------
CHAPTER 9
GLOBAL EFFECTS
Traditionally the effects of man's activities are thought of as being
local, regional or nationwide. There are, however, specific activities of
man which influence the environment on an international and even a global
scale. The contributions to the perturbation of the stratospheric ozone
layer and the increasing acidity of precipitation through the increased
production of nitrogen oxides are two examples.
9.1 PERTURBATIONS OF THE STRATOSPHERIC OZONE LAYER
Since the beginning of this decade it has become 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
1 2
nitrogen (NO and NOO from high-flying aircraft. ' It had been proposed
by Crutzen that NO (NO + N0?) could catalyze the destruction of ozone and
s\ £
control its stratospheric abundance by the set of photochemical reactions
induced by solar radiation:
03 + hv ^ 0 + 02 (9-1)
(wavelengths shorter than 1140 nm)
0 + N02 •» NO + 02 (9-2)
NO + 0 -> N0 + 0 (9-3)
20- -> 3 02 net
9-1
-------
The main source of NO in the stratosphere is probably the oxidation
A
245
of nitrous oxide (N20) via the reactions: ' '
03 + hv -> O^D) + 02 (9-4)
(wavelengths shorter than 310 nm)
0(1D) + N20 -» 2 NO (9-5)
Because of its relatively low solubility and low reactivity in water,
nitrous oxide is not removed in clouds and through precipitation in the
troposphere. In contrast, direct transport of NO and N02 into the strato-
sphere from the earth's surface is strongly prohibited by wet removal of
NOp and especially its oxidation product HNO,, which is formed by the
reaction:
OH + N02 (+M) -» HN03 (+M) (9-6)
The hydroxyl radical (OH) is primarily formed by the attack of 0( D)
on water vapor, following reaction 9-4, above:
0(1D) + H20 -> 2 OH (9-7)
This radical, and therefore, also ozone, play an extremely important
role in the photochemistry of the atmosphere. In the troposphere (0 to 10
km in middle and high latitudes, or 0 to 18 km in the tropics) it attacks a
host of gases, which otherwise would be inert, such as CO, H2, hydrocarbons
and chlorinated hydrocarbons. This ensures that only a small portion (vLO
percent 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 otherwise larger destruction.
Nitrous oxide, however, is nearly inert to attack by all known tropospheric
gases, including OH.
9-2
-------
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 NO
/\
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 photochemical 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 02 •» RO + 03. The radical R can here stand for
such radicals as CH^CO and H. In the non-urban troposphere, ozone production
may, however, still take place in the oxidation of hydrocarbons emitted
from 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 distinct possibility of worldwide ozone
increases, especially in the Northern Hemisphere's troposphere.
9-3
-------
It should be added that the origin of tropospheric ozone is not well
known. Traditional thinking in the meteorological community explained the
o
presence of ozone in the troposphere by its formation in the stratosphere
via the reaction
02 + hv -> 2 0 X < 240 nm (9-13)
0 + 02 + M -> 03 + M (x2) (9-14)
3 Op -»• 2 03 net
and its downward transport into the troposphere in the vicinity of frontal
Q
zones or tropopause breaks. The tropospheric ozone production taking place
near urban centers was thought to be only of minor global importance.
However, it seems now that ozone production can also take place in the
"clean" troposphere as long as NO volume mixing ratios are not too small
J\
(>10 ), because of the fast rate of reaction 9-8.
In the lower stratosphere (V10 to 24 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)
H0 + 0 -» OH + 2 0 (9-16)
2 0- -*• 3 02 net
by deferring it into the sequence
OH + 03 -» H02 + 02 (9-15)
H02 + NO -> OH + N02 (9-8)
N0£ + hv -> NO + 0 (9-9)
0 + 02 + M -> 03 + M (9-10)
no net chemical effect net
9-4
-------
Additions of NO to the lower stratosphere, therefore, tend to increase
local ozone concentrations 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, 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 photochemical action of NO , we
/\
notice also a decrease in altitude of the center of gravity of stratospheric
ozone by transfer of mass from above 24 km to below 24 km. As NO is
/\
produced by the oxidation of N20 via reactions 9-4 and 9-5, the same conclusions
are valid regarding the possible effects of a future rise in the atmospheric
content of nitrous oxide. Such an increase may be caused by man's intervention
in the nitrogen cycle through an increasing use of nitrogen fertilizer and
other agricultural activities.
It should be noted that the present stratospheric content of
chlorine is not well known. From the known tropospheric abundances of
CH^Cl, CFC13, CF2C12 and CH3CC13, which are believed to be the main sources
of stratospheric chlorine, the maximum stratospheric total chlorine volume
-9
mixing ratio can be estimated at 2 ppbv (2 x 10 ). Observations of Cl and
11 12
CIO in the stratosphere by Anderson and co-workers ' have, however,
shown substantial variability and on one occasion volume mixing ratios of
-9
CIO alone of about 7 x 10 near 20 km. In the stratosphere the active
forms of chlorine, Cl and CIO, are formed from the stable organic forms by
photolysis and reaction with the OH radical:
9-5
-------
CFC13 + hv -» CF2C12 + Cl -»• .... 3(C1 or CIO) (9-17)
CF2C12 + hv -*• CF2C1 + Cl -»• 2(C1 or CIO) (9-18)
CH3C1 + OH -> l(d or CIO) (9-19)
CH3CC13 + OH -> 3(C1 or CIO) (9-20)
As in the case of NO and N02, Cl and CIO attack ozone, but in an even
more efficient catalytic cycle:
03 + Hv -»• 0 + 02 (9-21)
0 + CIO -» Cl + 02 (9-22)
Cl + 03 -> CIO + 02 (9-23)
2 03 -» 3 02 net
Other important stratospheric chlorine compounds are HC1, C10N02, and
possibly C10H, which are formed from the reactions
Cl + CH4 -> HC1 + CH3 (9-24)
Cl + H02 -» HC1 + 02 (9-25)
CIO + H02 -» C10H + 02 (9-26)
CIO + N02 + M -* C1N03 + M (9-27)
making the conflict between at least one of Anderson's observations of CIO
and known sources of stratospheric chlorine even more serious (there is a
lot of HC1 expected near 20 km).
NO additions to the stratosphere will lessen the effect of Cl and CIO
on ozone by binding more of these compounds in HC1 or C10NO?, which do
not react with ozone, through the reaction sequences
NO + CIO -» Cl + N02 (9-28)
Cl + CH4 -»• HC1 + CH3 (9-29)
CIO + N02 + M •» C1N03 + M (9-30)
9-6
-------
Therefore, if there is much active chlorine present in the stratosphere,
NOX additions may moderate the powerful Cl and CIO catalytic action on
ozone and actually lead to ozone increases.
Two points should be made in this context:
(a) The high CIO volume mixing ratio mentioned above may not be
correct. More and independent observations of stratospheric CIO are needed.
(b) If the use of fluorocarbons -11 and -12 (CFClj and CF2C12) outside
the U.S. continues, very high background values of Cl and CIO in the stratosphere
may develop. NO additions to this background may lead to total ozone
/\
increases. They cannot, however, neutralize the damaging effects of the Cl
and CIO catalysts themselves (for further details see the different reports
prepared by the National Academy of Sciences and NASA14).
Among the most important kinetic factors determining the sensitivity
of stratospheric ozone concentration to NO additions are the rate co-
y\
-1C -i /•
efficients for the reactions: '
H02 + 03 ^ OH + 2 02 (9-16)
H02 + NO -> OH + N02 (9-8)
OH + H02 -» H20 + 02 (9-31)
For instance, quite different total ozone changes due to changes in
N20 concentrations were calculated, only making two different choices of
the rate coefficient for reaction 9-31 (K31 = 2.1 x 10 cm3 mol"1 s"1
against 5.1 x 10 cm mol s ) as given in Table 9-1. The computa-
tional results were obtained with a one-dimensional, detailed photochemical-
diffusive model of the stratosphere, which simulates the average vertical
distributions of stratospheric constituents, thereby smoothing out the
global horizontal variations. There is an expectation that such simplified
9-7
-------
models can describe the more important features of average conditions in
the atmosphere and give an idea about the possible changes in atmospheric
composition that may result fron anthropogenic activities. Atmospheric
observations are used to validate such models. Unfortunately, several rate
constants of important reactions and atmospheric transport parameters are
not sufficiently well known. Although superficially good agreement is
often obtained between observations and theoretical calculations, this is
not sufficient for a validation of the models because of a limited sensitivity
to choice of rate constants and because of atmospheric variability.
Previous theoretical predictions of total ozone reductions, using the
then-recommended rate constants, yielded the following approximate relationship
between total ozone changes (6V3) and atmospheric nitrous oxide volume
mixing ratio (6uN?0) increase:
6V3 = ^ 6|jN20
V3 5 pN20
A doubling in the atmospheric abundance of N«0 was, therefore, expected
to yield a 20 percent decrease in total ozone. We notice from the results
presented in Table 9-1 the likelihood of a much smaller dependence of the
total ozone column on changes in the atmospheric abundance of nitrous
oxide. This is due to the increase in ozone concentrations caused by the
increased NO concentrations below 24 km, which was not previously calculated.
^\
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 atmosphere. An effective
lowering of the "center of gravity" of the ozone layer, which would be the
9-8
-------
Table 9-1. CALCULATED CHANGES IN TOTAL STRATOSPHERIC OZONE DUE TO HYPOTHETICAL
CHANGES IN THE GLOBAL TROPOSPHERIC BACKGROUND MOLE FRACTIONS OF NO
The rate constants used for reaction 9-8 (H02 + NO -> OH + N02) and
reaction 9-16 (H09 + 0, -> OH + 2 0,) were kft = 3 x 10"11 exp (-390/T)
-i3 "\ -1 -2
and k,g = 2 x 10 exp (-1250/T) cm mol s . These choices of rate
coefficients for reactions 9-8 and 9-16 seem to agree most closely with
the laboratory rate constants recently determined by Howard and co-workers.
Extracted from Crutzen and Howard.
Mole fraction of NpO in atmosphere (assumed) and calculated total
ozone changes in stratosphere (in percent)
K31
(cm3 mol I s"1) 3'30 x 10~7 (current) 4-95 x 10"7 <50% UP) 6-60 x 10'7 (doubling)
2.1 x 10"11 - +0.9 - 0.1
5.1 x 10"11 - - 2.3 - 5.1
-------
result of NO additions to the stratosphere, may have significant climatic
/\
18
implications, as it may cause a warming of the lower stratosphere and the
earth's surface by the increased absorption of ultraviolet solar radiation
and enhanced trapping of thermal 9.6 pm radiation emitted from the warm
surface of the earth.
The significance of nitrous oxide is also not restricted to its impor-
tance as a source of stratospheric NO via reactions 9-4 and 9-5. Because
y\
of its absorption bands at about 7.8 urn and 17.0 urn, nitrous oxide likewise
contributes significantly to the atmospheric "greenhouse" effect by trapping
outgoing terrestrial radiation. It has, therefore, been estimated that a
doubling of the atmospheric N,,0 content could cause an increase in surface
19
temperatures by as much as 0.7°K.
The results presented in Table 9-1 do not take into consideration the
already discussed photochemical processes in the troposphere, where anthro-
pogenic activities leading to ozone increases may not be totally ignored
from the point of view of total ozone changes, as the troposphere contains
roughly 10 percent of the total atmospheric ozone burden. In addition, we
repeat that the role of ozone in producing the OH radical by reaction 9-7
is of crucial importance for the chemical composition of the atmosphere.
Therefore, the effect of NO additions to tropospheric ozone concentrations
/\
is not only of importance to the air quality in urban areas, but also to
the overall chemical composition of the atmosphere.
Several recent studies have been designed to estimate the possible
extent of future nitrous oxide build-up due to increased utilization of
17 ?f)~?fi
nitrogen fertilizer. ' Three important but poorly understood factors
determining the release of nitrous oxide from the soil and water to the
9-10
-------
atmosphere are the following: (1) the release of NpO in the denitrification
process. This microbiological process, which is currently considered to be
the main source of atmospheric N20, takes place in anaerobic micro-environments,
and involves the reduction of nitrate to nitrous oxide and molecular nitrogen.
It is this process which presumably balances nitrogen fixation, i.e., the
conversion of N2 to fixed nitrogen. A growing amount of observational
evidence is now accumulating, which indicates that the yield of NJ) versus
?~1 28
N« in agricultural and aquatic environments is less than 20 percent. '
It remains, however, important to gather 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, leaching of nitrate in groundwater, volatilization of ammonia and
its transport and conversions 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.,22 McElroy et al.,24 and Crutzen and Ehhalt;23 (3) the role of the
oceans in the worldwide N20 budget. While initial studies indicated the
pq
oceans to be a large source of N20, recent investigations point toward a
much smaller role for the world's oceans in the global N20 budget.
The scientific problems connected with possible future increases in
atmospheric N20 concentrations are being investigated by several research
groups and the issue has been reviewed by an ad hoc committee of the National
Academy of Sciences in a recently published report.31 The issue is further
9-11
-------
complicated by the fact that the nitrogen cycle is coupled to other cycles,
32
such as those of carbon and phosphorus. It is, therefore, fair to say
that many years of active research are needed to assess reliably this
potentially important global environmental issue.
9.2 ACIDIC PRECIPITATION
Substances in the atmosphere are transferred to terrestrial and aquatic
ecosystems via wet deposition (precipitation as rain or snow) or dry deposition
(impaction of aerosols and absorption of gases). Precipitation is the
main process through which water is cycled from the atmosphere to the
ground. Precipitation begins as water vapor. Cooling of the water vapor
results in condensation and the formation of droplets. When present in the
atmosphere, parti cul ate matter smaller than 10 urn may act as nuclei on
which the water vapor condenses. If temperatures are cold enough, ice
34
crystals may form instead. The large surface area of raindrops and
snowflakes as well as certain physical properties of water make precipi-
tation an excellent carrier and scavenger of other atmospheric constituents
such as gases (e.g., COp, S02), aerosols (e.g., (NH^pSO^), large particles
(e.g., CaCO-, silicates) and organic matter (e.g., pollen, microorganisms).
The chemical composition of precipitation resulting from these scavenging
processes will vary from region to region and from storm to storm depending
on the composition of the atmosphere at the time precipitation occurs.
The acidity of precipitation falling on widespread areas of the world
has been increasing during the past two decades.
9.2.1 Formation and Composition
Rainwater from unpolluted atmospheres has a pH ranging from 5.5 to
6.O.3 Since the mi d- 1950' s, the rainfall and snow over northern Europe has
9-12
-------
been continuously sampled and analyzed. These analyses have revealed a
steady decline in the pH of precipitation from a range of 6.0 to 5.5 in
1956 to one of 4.5 to 4.0 in 1966.35
The hydrogen ion concentration of a solution determines its acidity.
The pH of precipitation from unpolluted atmospheres is determined by the
presence of carbonic acid, a weak acid naturally formed by the combination
of C02 and water in the atmosphere. Increasing amounts of strong inorganic
acids, primarily nitric (HN03) and sulfuric (h^SO^) acids have appeared in
the precipitation falling over wide areas surrounding the industrialized
OC_ OQ
regions of the world during the past two decades.
The occurrence of highly acidic rainfall over large areas of the
eastern United States and northern Europe has received much attention in
39-42
recent years. Studies to date have demonstrated trends toward decreasing
pH of rainfall in the northeastern United States and expansion of the area
receiving acidic rains (Figure 9.1). Acidic rain is defined here as having
a pH less than 5.6, the minimum pH expected from atmospheric carbon dioxide.
Currently the average annual pH of precipitation in the northeastern United
States is between 4.0 and 4.2, and average pH values around 4.5 have been
reported as far south as northern Florida. The pH of rainfall throughout
southern Scandinavia is less than 4.5, and the hydrogen ion content of
precipitation in some parts of Scandinavia has increased 200-fold (a change
37 42 44
of 2.3 pH units) in the past two decades. ''^'^
While it is clear from recent studies that acidic rainfall is a man-
made problem with potentially serious ecological impacts over widespread
geographic areas, several aspects of the problem remain controversial
because existing data are ambiguous or inadequate. Important unresolved
9-13
-------
Figure 9-1. Average pH of annual precipitation in the eastern United States. In (A) and (B), pH values are computed from cation/anion balances;
in (C), the values represent actual measurements of pH of precipitation. [(A) and (C) from Ref. 42; (B) from Ref. 45.j
9-14
-------
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 cause(s) of the widespread acidification of rain in
the eastern United States over the past 20 years; (4) the relative extent
to which the acidity of rainfall in a region depends on local emissions of
sulfur and nitrogen oxides versus emissions transported from distant sources;
and (5) 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.
The following sections discuss evidence related to these five issues,
and in particular assess the contributions of NO emissions and the resulting
nitric acid to the problem.
9.2.1.1 Temporal and Spatial Trends in Rainfall Acidity
9.2.1.1.1 Long-Term Trends. The isopleth maps of rainfall pH presented in
Figure 9-1 show that the acidity of rainfall over the eastern United States
has increased during the past 20 years, but the rate of change at a given
location is difficult to quantify, largely because historical data on the
pH of rainfall are extremely rare. Even where fairly long-term records are
available (e.g., measurements have been made since 1964 at Hubbard Brook,
New Hampshire), values are scattered over a wide range. Likens et al.
reported that the mean annual pH of rainfall at Hubbard Brook varied from
4.03 to 4.21 over the period 1964 to 1973, with no statistically signif-
icant trend. When concentrations were multiplied by the amount of precip-
itation to give areal deposition rates (equivalents of H /ha-yr), a trend
of increasing H+ deposition (a 36 percent increase over the decade) was
9-15
-------
noted [Figure 9-2 (A)]. Increases in the annual amount or frequency of
precipitation will increase the rate of deposition in the same way that
increases in acidic emissions will; and as Figure 9-2 (B) shows, the annual
amount of rainfall at Hubbard Brook increased significantly over the decade.
However, deposition rates for cations other than H at the same site were
not related to the annual amount of precipitation [Figure 9.2 (C)]; thus,
the increase in H deposition over time cannot be explained solely by
increases in annual rainfall.
40
Cogbill reviewed the temporal trends and the geographic distribution
of rainfall acidity in the northeastern United States, and summarized the
sparse information on rainfall pH available prior to the 1960s. He found
that the acidity of rainfall at nine stations near the periphery of the
central isopleth in 1955-1956 (see Figure 9-1) showed an average increase
of 12 ug H /I by 1965-1966. More recent data for two of the stations near
the northern limit of the acidic region showed an apparent stabilization in
rainfall pH after the initial decrease in the 1960s. At Caribou, Maine,
the pH values for 1955-1956, 1965-1966, and 1972-1973 were 4.94, 4.63, and
4.76, respectively, and at Sault Ste. Marie, Michigan, the pH values for
the same years were 5.76, 4.76, and 4.69, respectively. Other reviews of
available data suggest that the average pH is decreasing in the most affected
areas, from about 4.4 in the 1950s to 4.0 to 4.1 in the 1970s,42'47 but
quantitative inferences should be made cautiously.
9.2.1.1.2 Seasonal Variations. The pH of individual rain events may be as
low as 2.2 to 3.0. Seasonal variations in pH measured at several sites in
New York during 1970-1971 (Likens ) were erratic and site-specific, but pH
values tended to be lower in summer than in winter. Horbeck et al. also
9-16
-------
120
110
100
90
2
3 on
|
1 70
60
I I I I I I I I j I I
1964 '65 '66 '67 '68 '69 70 71 72 73 74 75
YEAR
2
u
ui
-------
reported that precipitation was most acidic at nine stations in the northeastern
United States during the growing season (May to September) and least acid
during winter (December to February). At Hubbard Brook, New Hampshire, the
mean H content of precipitation was 46 ug/1 (pH = 4.34) in winter, and 102
ug/1 (pH = 3.99) in summer. The seasonal trends in pH were mirrored by
seasonal trends in sulfate content of precipitation, and the trends in both
components could be explained by the lower efficiency of snow (compared to
rain) in scavenging substances from the atmosphere. No significant seasonal
trends were noted in pH of bulk precipitation rainfall at Gainesville,
49
Florida, during 1976-1977 (Hendry ), but wet-only precipitation showed a
trend of highest pH in fall and winter months and lowest pH in spring
months (see Figure 9-3).
9.2.1.1.3 Geographic Extent of Acidic Rain. The isopleth maps in Figure
9-1 indicate that the area affected by acidic rainfall has grown signifi-
cantly over the past 20 years, and that it now covers nearly all of the
United States east of the Mississippi River. However, this apparent trend
must be accepted with caution for two reasons: (1) the pH values in the
1955-1956 and 1965-1966 maps are computed rather than measured values, and
(2) the number of sampling stations is too small for accurate placement of
the isopleths in all of the maps. In the absence of measured pH values, it
is possible to calculate the pH of a rain sample by taking the difference
between the sums of the anions and cations (expressed in equivalents/1)
measured in chemical analysis of the rain. This method is based on the
fact that the total positive and negative charges must balance in any
sample, and on the assumption that the chemical analyses account for all
major ions except H+. Cogbill and Likens39 stated that pH can be computed
9-18
-------
i
2
K
4.80
4.60
4.40
4.20
0.40
0.30
0.20
0.10
M
I I I I I I I I I I I I
A S 0 N
1978
M A
-1977-
MONTH
Figure 9-3. 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.***
9-19
-------
by this method to within 0.1 units of the measured pH, but this may over-
estimate the accuracy of data from most routine monitoring programs.
The second reason for caution about the rate of expansion of the area
receiving acidic rainfall is the small number of data points used to draw
isopleths. The pH 5.00 isopleth was drawn through the border between North
and South Carolina in the first two maps in Figure 9-1, but in Likens1
map for the early 1970s the pH 5.00 line was moved to central Florida.
This change was based on recent acquisition of data for two Florida cities,
Tallahassee and Gainesville, in a region where pH measurements had not
previously been made, and it does not necessarily imply a rapid expansion
of the acidic rainfall area.
Data from the San Francisco Bay area indicate that precipitation has
become more acidic in that region since 1957-1958. The pH has decreased
from 5.9 in 1952-1958 to 4.0 in 1974. Another article, using data from the
California Air Resources Board (CARB) states that acidic precipitation has
been reported from such widespread areas as Pasadena, Palo Alto, Davis and
Lake Tahoe. Due to the geological composition of the soil, the areas most
likely to be affected by acidic precipitation are the national forests,
state parks and preserves, Bureau of Land Management forested areas, many
national parks and private forest holdings concentrated in the southern
California mountains, the western slope of the Sierra Nevada and the Coast
Range. All of the areas have acidic soils and are being adversely affected
by photochemical oxidant air pollutants.
There are also some tentative and unpublished reports of the increasing
acidity of pH in Colorado.
9-20
-------
9.2.1.1.4 Contributions of Nitric Acid to Total Acidity. The relative
importance of sulfuric and nitric acid contributions to rainfall acidity
has changed with time. Following the reasoning of Granat,50 Likens et al.46
found that the contribution of sulfate declined from 83 to 66 percent
of the total acidity between 1964 and 1974 at Hubbard Brook, and the con-
tribution 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
+• AQ
between H input and sulfate input (Figure 9-4). Hendry found that
sulfate contributed 69 percent, nitrate 22 percent, and chloride 6 percent
of the free acidity in rainfall at Gainesville, Florida, during 1976. On
53 54
the other hand, Gorham ' reported that hydrochloric acid was the domi-
nant acid in urban precipitation in Great Britain. Coal used in Great
Britain is high in chloride, but low in sulfur.
Available data for eastern North America indicate a roughly three-fold
increase in nitrate in rainfall since 1955, whereas sulfate in rain has
47
roughly doubled in this period. According to Nisbet, 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 calculated
that the fraction of H deposition attributable to nitric acid rose from 19
percent in 1955-1956 to 24 percent in 1972-1973 (Table 9-2). He also
projected trends in acid deposition from 1970 to 1980 for a number of
scenarios assuming continued control of S02 emissions, but no controls on
projected NO emissions. Even if S02 emissions were held constant by
source controls on new power plants, a small increase in acidity would be
likely because of increases in NO emissions.
x\
9-21
-------
VD
I
r\>
r>o
u
8
GC
120
110
100
90
70
10
O O
20
30
40
NITRATE INPUT, mill«qui«l«nti/itiS'
120
100
BO
40
20
O
O
I
I
I
I
I
60 0 20 40 60 80 100 120
SULFATE INPUT, milli«quiv.ltnti/m2-yr
Figure 9-4. Hydrogen ion deposition in precipitation plotted against (A) nitrate deposition and (B) sulfate deposition. Data from Hubbard Brook,
New Hampshire, 1964 1973.46
-------
TABLE 9-2. DEPOSITION OF SULFURIC AND NITRIC ACIDS IN
PRECIPITATION IN EASTERN NORTH AMERICA
Total deposition of
acid (as H )
Estimated deposition
as sulfuric acid
(percent of total)
Estimated deposition
1955-56
4.0
3.2 (80)b
0.76 (19)b
1972-73
10.8
7.9 (73)b
2.60 (24)b
Percent
change 1956-73
+170
+150
+240
as nitric acid
(percent of total)
Total deposition 16.4 31.8 +94
of sulfates
Sulfuric acid as % 19.7 24.8 +27
of sulfates
Deposition rates are expressed as multiples of the chemical equivalent
weight, so that ra|,es for different chemical species can be compared
directly. 1 ton H is equivalent to 49 tons sulfuric acid or to 63
tons nitric acid.
A small but increasing fraction of the acid in precipitation is attribut-
able to hydrochloric acid.
SOURCE: Modified from Ref. 47.
9-23
-------
42
Likens has pointed out that although sulfuric acid has been by far
the dominant acid in precipitation at the Hubbard Brook Experimental Forest
in New Hampshire for the past decade; the increased deposition of hydrogen
ion has been due chiefly to an increase in the amount of nitric acid in the
precipitation (rain and snow) falling there. The components and their
contribution to acidity in precipitation are listed in Tables 9-3 and 9-4.
Nearly all of the nitrate in rainfall is formed in the atmosphere from
NOX, and little is derived from wind erosion of nitrate salts in soils.
Similarly, nearly all of the sulfate in rainfall is formed in the atmos-
phere from S02. The reactions that produce nitrate and sulfate from NO
and S02 are well known and result in the production of equivalent amounts
of hydrogen ion, regardless of the reaction mechanism:
OH + N02 »HN03, or
N205 + H20 »*2HN03, and
S02 + 1/2 02 »*S03 + H20 »*H2S04.
Thus, all atmospherically derived nitrate and sulfate contribute to the
acidification of rainfall, 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 neutrali-
zation occurs, the free acidity of rainfall will be reduced. Reuss
noted, however, that even ammonia in rain can contribute to the acidifi-
cation of soil, since ammonia that enters the soil may be nitrified, resulting
in the formation of nitric acid.
9-24
-------
TABLE 9-3. SULFURIC AND NITRIC ACIDS ARE MAJOR
SOURCES OF ACIDITY IN PRECIPITATION
Substance
Concen-
tration in
precipitation
(mg per
liter)
Contri-
bution to
free acidity3
(microequiv-
alents per liter)
Contri-
bution to .
total acidity
(microequiv-
alents per liter)
H2C03
NH4
Al, dissolved
Fe, dissolved
Mn, dissolved
Total organic acids
HN03
H2S04
TOTAL
0.62C
0.92
0.05d
0.04d
0.0005d
0.34
4.40
5.10
0
0
0
0
0
2.4
39
57
98
20
51
5
2
0.1
4.7
39
57
179
*At pH 4.01.
cln a titration to pH 9.0.
.Equilibrium concentration.
Average value for several dates.
Note: Data from a sample of rain collected at Ithaca, N.Y., on Oct 23, 1975.
9-25
-------
TABLE 9-4. HYDROCHLORIC, SULFURIC, AND NITRIC ACIDS ARE
STRONGEST OF SEVERAL POTENTIALLY IMPORTANT PROTON
DONORS IN RAIN AND SNOW
Acid Relative strength (pKa)
a.
HCl —3
H2S04 -3
Ref. 42.
HN03
1.9
HS04 2.0
Fe(H20)6+3 2.2 to ~3
FH 3.2
Organic acids 3 to 7
A1(H20)6+3 4.9
H2C03 6.3
HS03 72
HN4+ 9.3
HC03" 10.3
9-26
-------
9.2.1.1.5 Causes of the Acid Rainfall Problem. Several lines of evidence
suggest that the widespread acidification of rain began no earlier than
1950-1955, but although this shift has been linked to changes in the amounts
of S09 and NO emissions, the precise causes are still unclear. Likens and
£. X
Bormann suggested that acidification was partially a consequence of the
decrease in emissions of alkaline fly ash from coal-burning power plants,
coupled with increasing emissions of S09 and NO (from power plants, smelters,
tL. x\
42
and industrial processes), and Likens noted that the trend toward higher
smokestacks to disperse pollutants may be responsible in part for the
widening geographic extent of the acid deposition problem.
39
Cogbill and Likens associated acidic rainfall in New York with high
altitude air masses transported into the region from the Midwest, implying
that the SO,, and NO that cause acidic rain may be transported distances of
£- *\
300 to 1500 km. Gatz criticized the procedure used by Cogbill and Likens
to track air masses, and recommended that trajectories of lower altitude
air masses be used to trace the source of acids in rainfall. He suggested
that the major source of rainfall acidity in the Northeast is the Ohio
Valley region of Ohio, Pennsylvania, West Virginia, plus Maryland, an area
of large S02 emissions (Figure 9-5). The high-altitude trajectories used
by Cogbill and Likens showed little variation in pH of rainfall borne in by
air masses from different directions, even though the sources of SO,, are
concentrated to the south and southwest of the rainfall collection area at
Ithaca, New York.
Evidence from northern Europe also supports the idea that acidic rain-
fall is a large-scale regional problem involving long distances between
emission sources and deposition of acidic rain. The acidic rains that have
9-27
-------
Figure 9-5. Trajectory map indicating source strengths for SC^ emis-
ions affecting the eastern United States.5*" Emission rates of SO2
are shown by shading of the map. 500 mbar trajectory corridors
from Cogbill and Likens™ are superimposed on the map to indicate
directions of movement of air masses at ca. 5500 m altitude for
several days preceding specific rain events at Ithaca, New York, the
numbers between the lines are mean pH values for rain events assoc-
iated with each trajectory corridor.
9-28
-------
received intensive study in southern Scandinavia have been shown to result
primarily from emissions of sulfur and nitrogen oxides in Great Britain and
the industrial regions of continental Western Europe (e.g., Holland, Belgium,
37
West Germany).
47
Nisbet compared estimated total S02 emissions with total deposition
of sulfate in precipitation in eastern North America for the years 1955-1956,
1965-1966, and 1972-1973. Only 30 to 38 percent of the emitted sulfur
could be accounted for by rainfall deposition. The fate of the remainder
is uncertain; presumably some was deposited as dry fallout within the
region studied, and the rest was transported eastward over the Atlantic
Ocean. A similar calculation is not available for the fraction of NO -N
/\
deposited as nitrate in rainfall.
In summary, the causes of widespread acidification of rainfall in the
eastern United States are still controversial. The principal agents of
acidity, sulfuric and nitric acids, are derived primarily from combustion
of fossil fuels and consequent emissions of S09 and NO . The atmospheric
£- r\.
reactions involved in transforming these gases into acids are reasonably
well understood on a qualitative basis, but rates of transformation, atmos-
pheric residence times for the acids, and the scale of transport prior to
deposition are not known with precision. The lack of more definite quanti-
tative estimates of linkages among sources, transport processes and depo-
sition patterns hinders the development of appropriate control measures.
While the intensity and geographic extent of the problem have increased
over the past few decades, recent trends and the exact geographic extent of
the problem still are not well known. Nitric acid accounts for only about
one-fourth of the acidity of rainfall in the eastern United States, but its
9-29
-------
proportional contribution has been increasing as controls on stationary
emissions of sulfur dioxide have taken effect.
9.2.2 Effects on Freshwater Ecosystems
The increasing acidity of rain and snow is threatening the freshwater
ecosystems in eastern North America and in northern Europe that lie in and
are adjacent to the regions where acidic precipitation occurs. The lakes
in these areas are extremely vulnerable to additions of acidic precipitation
because the geological composition of their watersheds is highly resistant
to chemical weathering. Lakes of this type are usually soft water lakes
with a low buffering capacity. The pH of lake water reflects both the
acidity of precipitation and the ability of the lake and the watershed
CQ
surrounding it to neutralize acid contributions. The potential of such
effects occurring can be placed into some perspective by examining patterns
of the buffer capacity of soils and waters in the United States. Figure
9-6 shows the distribution of hardness in surface waters of the United
States, and Figure 9-7 shows the distribution of calcium which can be taken
as an approximate index of cation exchange capacity in soils of the United
States. Hardness is closely correlated with alkalinity, and hence with
buffer capacity, and cation exchange capacity is related to the buffer
capacity of soil. The figures show that the regions in which rainfall
acidity is highest include large areas with soft water (hence low buffer
capacity) and low ion exchange capacity in the soil.
During the past 30 to 40 years the pH of many soft-water lakes has
decreased from a pH 6 to a pH below 5 due to changes in the chemistry of
the lakes. Measurements of the pH of a large number of lakes in the Adirondack
Mountains of New York State illustrate the changes that have taken place.
9-30
-------
u.
HARDNESS AS CaCOj
IN PARTS PER MILLION
[ | Under 60
Yflflh 60-120
120 180
180-240
Over 240
Figure 9-6. Hardness of surface waters in the United States.60
-------
r-'~9~\
I
a
' I
SYMBOL AND PERCENTAGE OF TOTAL SAMPLES
18 21
CALCIUM IN PERCENT
Figure 9-7. Calcium content of surface soils in the United States.61
-------
Of 320 lakes measured in the 1930s, most lakes were in a pH range of 6.0 to
59
7.5. Data from 216 lakes measured in June, 1975, indicated that a large
group of lakes with a pH below 5.0, another group with a pH range of 6.0 to
CLQ
7.5, and a few lakes with a range in pH from 5.5 to 6.0. The long-term
deposition of acidic precipitation and runoff from the watershed have
caused the decrease in pH.
9.2.2.1 Effects at the Ecosystem Level—The effects of acid precipitation
on aquatic ecosystems have been dramatic and well documented. The susceptibility
of lakes to acidification is greater in base-poor areas (for example, for
lakes with adjacent podzol soils, or formed on hard crystalline rock) and
cc /• o
for lakes with low watershed: surface area ratio. '
Observed effects include: depauperate phytoplankton communities of
low productivity; similarly impacted macrophyte .communities, declining fish
populations, and, particularly in extremely poorly buffered lakes, community
changes that further reduce the availability of nutrients because of decreased
remineralization of detritus. Gorham and Gordon reported that levels
of dissolved heavy metals were elevated in waters receiving acidified
precipitation, but they could not determine the relative contributions to
this effect of leaching due to rainfall acidity and of fallout of metallic
contaminants from a nearby smelter complex. If acidity does in fact lead
to higher levels of potentially toxic cations, the secondary biological
effects of such changes in the pH of rainfall could be. substantially multiplied.
Likens reviewed the effects of acid precipitation on lakes and
concluded that widespread loss of biological and potential economic produc-
tivity has occurred in several regions. In Norway, populations of fish,
9-33
-------
especially trout and salmon, have been decimated south of 63° latitude N.
Although such losses were initially noted 50 years ago, they have increased
sharply during the past 15 years, a period that coincides with increases in
fossil fuel combustion. Similar changes have been observed in Sweden.
About 10,000 lakes have been acidified to a pH value less than 6.0, and
5000 below pH 5.0. Declines in fish populations have been correlated with
the acidity of the lakes (Figure 9-8). A recent survey of the Adirondack
Mountains of New York has revealed that 50 percent of the lakes above 600 m
elevation have pH values below 5.0, and that 90 percent of those lakes are
devoid of fish; a similar survey in the 1929 to 1937 period showed that
only 4 percent of the same lakes had a pH <5 or were devoid of fish.42
A number of studies have delineated the effects of pH on aquatic
vertebrates. Table 9-4 summarizes some general patterns of pH effects on
fish. Of note are the differences in effects according to species and
stages of life history in a given species. Clearly, a significant pH
change can cause substantial and rapid changes in the composition of an
aquatic community. The mechanism(s) of pH effects on fish are incompletely
understood but interference with the metabolism of calcium, sodium, and
31
other elements has been strongly implicated.
Analysis of samples of invertebrate organisms collected from 84 lakes
in Sweden indicated that acidification caused the limitation of many species
and led to a simplification of zooplankton communities. In 47 lakes of a
region of Ontario, Canada, the distribution and association of crustacean
zooplankton were also shown to be strongly related to pH and to the number
of fish species present in the lakes. For invertebrates in general a
number of pH patterns are apparent, and organisms can be grouped according
to such responses as the width of their tolerance limits, or sensitivity at
9-34
-------
100
80 -
.
O
I-
6 0
pH OF LAKE WATER
Figure 9-8. Status of fish populations in Norwegian lakes in relation
to pH of water.42
9-35
-------
TABLE 9-5. SUMMARY OF EFFECTS OF pH CHANGES ON FISH
pH Effects
3.0 - 3.5 Toxic to most fish; some plants and invertebrates
survive.
3.5 - 4.0 Lethal to salmonids. Roach, tench, perch, pike survive
4.0 - 4.5 Harmful to salmonids, tench, bream, roach, goldfish,
common carp; resistance increases with age. Pike can
breed, but perch, bream and roach cannot
4.5 - 5.0 Harmful to sal mom" d eggs and fry; harmful to common
carp; tolerable lower limit for most fish.
5.0 - 6.0 Not harmful unless >20 ppm COp, or high concentrations
of iron hydroxides present
6.0 - 6.5 Not harmful unless >100 ppm C02
6.5 - 9.0 Harmless to most fish
9.0 - 9.5 Harmful to salmonids, perch if persistent
9.5 - 10.0 Slowly lethal to salmonids
10.0 - 10.5 Roach, salmonids survive short periods, but lethal
if prolonged
10.5 - 11.0 Lethal to salmonids; lethal to carp, tench, goldfish,
pike if prolonged
11.0 - 11.5 Lethal to all fish
SOURCE: Ref. 72.
9-36
-------
different stages of their life cycles. With some exceptions, pH values
below 5.0 pose a serious threat to aquatic invertebrates. Because inverte-
brates are important components of aquatic food webs, and because the
observed pH in areas affected by acidic precipitation is often below 5.0
(Figure 9-1), potentially serious effects on aquatic ecosystems seem likely
and could be much more widespread than is currently appreciated.^8
Limited data are available on the effects of pH on algae. Giddings
and Galloway reviewed work by Moss ' and Sorokin71, and concluded that
lowered pH of lakes would favor species normally excluded by lack of free
C02- They state that below pH 4.5, growth of most species would be reduced;
the result would be erratic blooms by the few tolerant species remaining.
Interference with nutrient recycling is another major consequence of
changes in microdecomposers brought about by acidification of lakes.
Organic debris and fungus mats accumulating in lake bottoms, as observed in
Swedish lakes, both tend to seal off the mineral sediments from interactions
with the overlying water and hold organically bound nutrients which would
have become mineralized and available if normal decomposition had occurred.
These changes may affect the invertebrate populations which feed on detritus
which has first been "conditioned" by microorganisms.
Little information is available on reclamation of acidified lake
ecosystems, but addition of lime has produced beneficial effects in some
lakes. Much of the experimentation with liming has been done in Scandinavia.
73
Wright reviewed an early attempt in which addition of chalk to Swedish
lakes increased pH and led to increased phytoplankton growth and improved
fish survival. Addition of CaCO, and Ca(OH)2 to two acidic lakes in Sudbury,
9-37
-------
Ontario increased pH, decreased heavy metal concentrations, and caused a
temporary decline in chlorophyll (Michalski and Adamski, cited in Wright ).
73
Reviews of liming experiments in Norway, cited by Wright concluded that
this practice would be feasible only for small ponds and streams.
9.2.2.2 Summary--Many changes, most of which involve decreases in biological
activity and important changes in nutrient cycling result from the acidifi-
cation of freshwater ecosystems. Increased accumulations of organic matter
result from decreased decomposer activity. Phytoplankton and zooplankton,
bottom fauna and several other groups of invertebrates decrease in numbers
of species when the pH drops below 6, thus affecting the variety of food
available for fish and other animals that depend on aquatic ecosystems.
Fish populations are seriously affected by pH's less than 5.5. The
elimination of fish is often a result of chronic reproductive failure in
acidic conditions and damage done to the newly hatched larvae and other
sensitive stages. Fishery yields do not indicate such an insidious process
until extinction is imminent. There is strong evidence that the main cause
of extensive losses of salmonid fish stocks as well as other populations of
economic importance in Scandanavia, the northeastern part of the United
States and parts of southwestern Canada is the increased acidity of precipi-
tation.
9.2.3 Effects on Forest Ecosystems
Forest ecosystems are complex organizations composed of many different
biological elements which respond each in its own way to environmental
changes. The effects of acidic precipitation on forest ecosystems are
being discussed separately from fresh water ecosystems, though in reality
they are interdependent with a continuing interchange of energy and matter.
9-38
-------
The effects of acidic precipitation on entire terrestrial communities
or ecosystems are unknown. Several investigators have suggested that
acidic precipitation is the major cause of observed declines in forest
growth. ' Quantitative relationships have not been established, however,
and must await additional research. The effects of acidic precipitation on
forest growth are difficult to separate from the many other factors that
may also limit growth. For example, the period of decline in forest
growth observed by Whittaker et al. in an area affected by acidic rain
also corresponded to a severe drought in the northeastern United States.
Studies are needed to determine whether a trend toward slower forest
growth will continue in years when rainfall is more abundant. The
geographic pattern of rainfall pH exhibits a series of gradients across
the eastern United States. The existence of these gradients should
permit comparative long-term studies of forest growth.
Another major uncertainty in estimating effects of acidic rain on
forest productivity is the capacity of forest soils to buffer against
leaching by hydrogen ions. Where the evidence is strongest for a direct
effect of acidic precipitation on forest growth (e.g., Sweden), the soils
are already highly leached, and the buffer capacity has been reduced.
For much of the eastern United States, however, the soils still retain
the major portion of their natural buffering capacity. This may explain
why effects are not yet apparent in this region. Many questions remain
unanswered on this subject, including the rate of forest soil degradation,
the ultimate consequences of this degradation to forest productivity,
and the time frame in which those consequences will occur under the
present rates of hydrogen ion leaching.
9-39
-------
Increasing acid inputs may cause decreases in the fertility of
forest soils. Laboratory investigations by Overrein have demonstrated
that leaching of potassium, magnesium and calcium, all important plant
nutrients, is accelerated by increased acidity of rain. Field studies
in Sweden correlate decreases in soil pH with increased additions of
78
acid. On the other hand, 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 likely to be short-lived as depletion of nutrient cations
35
through accelerated leaching should eventually retard growth.
79
Norton has reviewed the potential effects of acidic rain on soils
(Table 9-3). Most of the available information is from northern latitudes;
much less is known about soils of temperate regions, where the largest
increases in rainfall acidity are presently occurring. The types of
effects that have been observed are destabilization and solution of clay
minerals, loss of cation exchange capacity, increased rates of mineral
losses and, consequently, increased rates of podzolization. Overrein
has provided perhaps the most extensive studies of effects of acidic
precipitation on soils. Both accelerated leaching of calcium and loss
of the capacity of the soil to buffer pH have been observed in lysimeter
studies.
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,
especially those containing carbonates, and least in soils derived from
80
hard crystalline rocks such as granites and quartzites. Soil buffering
9-40
-------
TABLE 9-6. POTENTIAL EFFECTS OF ACID PRECIPITATION ON SOILS
Effect
Comment
Increased mobility of
most elements
Increased loss of
existing clay minerals
A change in cation
exchange capacity
A general propor-
tionate increase in
the removal of all
cations from the soil
An increased flux
nutrients through the
ecosystem below the
root zone
Mobility changes are essentially
in the order: monovalent,
divalent, trivalent cations.
Under certain circumstances may
be compensated for by production
of clay minerals which do not
have essential (stoichiometric)
alkalies or alkali earths.
Depending on conditions, this
may be an increase or a decrease.
In initially impoverished or
unbuffered soil, the removal
may be significant on a time
scale of 10 to 100 years.
SOURCE: Re. 79.
9-41
-------
capacity varies widely in different regions of the country (Figures 9-6
and 9-7). Unfortunately, many of the areas now receiving the most
acidic precipitation also are those with relatively low natural buffering
capacities.
The effects of acidic precipitation on soils are potentially long-lasting.
81
Oden has estimated that rainfall at pH 4.0 would be the cation equivalent
+2
of 30 kg Ca /ha, which represents a considerable potential loss of cations
82
essential for plant growth. McFee et al. calculated that 1000 cm of
rainfall at pH 4.0 could reduce the base saturation of the upper 6 cm of a
midwestern U.S. forest soil by 15 percent and lower the pH of the Al 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 counter-
acting forces could reduce the final effect of acidic precipitation, including
the release of new cations to exchange sites by weathering and through
nutrient recycling by vegetation.
Reuss makes an excellent case for placing the incoming H in the
perspective of the H+ produced within the soil from carbonic acid forma-
tion, sulfur oxidation, and nitrification.
Should pH changes occur in agricultural soils, the effects could
probably be offset by extensive liming of the soil in regions where that is
practical.
Lowered soil pH also influences the availability and toxicity of
metals to plants. In general, potentially toxic metals become more available
as pH decreases. Comprehensive reviews have been published on this subject. '
As mentioned previously, the loss of nutrients from the soil through
leaching by acidic rain could have major impacts on plant growth unless
9-42
-------
corrected by applications of fertilizer. Direct effects upon higher plants
are summarized in Table 9-4. They include necrosis, loss and/or reduction
85 fifi 87
in leaf area, accelerated loss of elements from foliage, ' and erosion
88
of cuticular surfaces. Experimental studies in which plants have been
subjected to experimental rain have generally used dilute sulfuric rather
than dilute nitric acid solutions.
Plants such as mosses and lichens are particularly sensitive to changes
in precipitation chemistry because many of their nutrient requirements are
obtained directly through precipitation. These plant forms are typically
absent from regions with high chronic air pollution and acidic precipitation.
on CO
Gorham and Giddings and Galloway have written reviews concerning this
problem.
Information on the effects of acidic precipitation on plant-symbiont
or host-parasite relationships is sparse. The most complete study is that
87
of Shriner who found that rainfall at pH 3.2 inhibited root nodulation by
Rhizobium on common beans and soybeans. A number of plant parasites were
influenced positively or negatively by acidic precipitation, depending upon
the status of infection, the condition of the plant and the timing of the
precipitation events. The vigor of the host plant appears to be the key to
the response of the plant to a pathogen. The potential for serious additive
or synergistic effects of acidic precipitation and pathogens on host plants
is great.
Little is known about the effects of acidic precipitation on soil
microorganisms. Alteration of the soil chemistry would be expected to
cause changes in the soil microorganismal populations. Increased soil
acidity generally favors fungal populations rather than bacterial populations.
Such selective effects can alter rates of decomposition and remineralization
9-43
-------
TABLE 9-7. POTENTIAL EFFECTS OF ACIDIC PRECIPITATION ON VEGETATION
Effect Reference
Direct Effects
88
Damage to protective surface QQ
structures such as cuticle
Interference with guard cell
function (potential disruption
of gaseous exchange processes)
Poisoning of plant cells
after diffusion through
stomata or cuticle
Disturbance of normal
metabolism without
tissue necrosis
88
Alteration of leaf- and gg
root-exudation processes
Interference with reproduc-
tive processes
Synergistic interaction
with other environmental
stress factors
Indirect Effects
Accelerated leaching of 85,86,87
substances from foliar organs
Increased susceptibility to
drought or other stress factors
88
Alteration of symbiotic
associations
88
Alteration of host-parasite
interactions
SOURCE: Ref: 91
9-44
-------
of elements essential for plant growth. Nitrification, a process carried
qp
on by bacteria, is inhibited by highly acidic soils.
9.3 SUMMARY
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
possible 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, and the extent to which synergisms may occur between acidic
precipitation and other forms of environmental stress is unknown. The
long-term effects of acidification on aquatic ecosystems have been better
documented. These effects are widespread, regionally and globally, and can
include decimation of fish populations. Little is known about the recovery
of ecosystems from such effects, but liming of soils and lakes has been
successful in a limited number of cases.
9-45
-------
9.4 REFERENCES FOR CHAPTER 9
1. Johnston, H. S. Reduction of stratospheric ozone by nitrogen oxide
catalysts from SST exhaust. Science. 173:517-522, 1971.
2. Crutzen, P. J. Ozone production rates in an oxygen-hydrogen-nitrogen
oxide atmosphere. J. Geophys. Res. 76:7311-7328, 1971.
3. Crutzen, P. J. The influence of nitrogen oxides on the atmospheric
ozone content. Quart. J. Roy. Met. Soc. 96:320-325, 1970.
4. Nicolet, M., and E. Vergison. L'oxide azoteux deus la stratosphere.
Aeronimica Acta. 90:1-16, 1971.
5. McElroy, M. B., and J. C. McConnell. Nitrous oxide: A natural
source of stratospheric NO. J. Atmos. Sci. 28:1095-1098, 1971.
6. Biermann, H. W., C. Zetzch, and F. Stuhl. Rate constant for the
reaction of OH with N90 at 298k. Ber. Bunsengess. Phys. Chem.
80:909-911, 1976. £
7. Fishman, J., and P. J. Crutzen. The origin of ozone in the tropo-
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CHAPTER 10
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. This causes consumer disappointment and economic losses,
both to the product manufacturer, and to the nation at large. The most in-
jurious nitrogen oxide is nitrogen dioxide (N02-)- 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 pollu-
tant 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.
10.1 EFFECTS OF NITROGEN OXIDES ON TEXTILES
The types of damage to textiles attributed to NOX action include:
o Fading of dyes on cellulose acetate (also known as acetate and
cellulose acetate rayon), cotton, viscose rayon, and nylon.
o Color changes on permanent press garments containing polyesters.
o Yellowing of white fabrics.
10-1
-------
10.1.1 Fading of Dyes by NOX
10.1.1.1 Fading of Dyes on Cellulose Acetate--
The NO fading of acetate, dyed blue, or in shades in which blue is
A
2
a component, results in pronounced reddening. Rowe and Chamberlain demon-
strated 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 nitro-
A
sation and oxidation by NO . The fading of Disperse Blue 3 as a result of
A
NO action is caused by the formation of a nitrosamine at the vulnerable
A
alkylamine site(s), or the production of a phenolic group (-OH) at the amine
3
site(s), through oxidation. Both of these reaction products have a red
color, which is seen when certain fabric-dye combinations are exposed to NOp.
4
Salvin et al. found that cellulose acetate is an excellent absorber
of N02« Absorption characteristics of fibers also are believed to play an
important role in dye-fading mechanisms. Polyester and polyacrylic fibers
have low N02 absorption rates while nylon, cotton, viscose rayon and wool
have intermediate rates. While cellulose acetate and cellulose triacetate
have high N02 absorption rates, the N02 is released upon heating. Nylon and
and wool, materials which contain reactive amino groups, hold the N02 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 suscep-
tible to NO action. These dyes include Disperse Blue 7, Disperse Blue 3,
10-2
-------
Disperse Red 11 and Disperse Red 55. The fading of these dyes is recog-
nized and noted in shade books published by dye suppliers. Asquith and
Campbell have noted that fading also occurs with certain yellow dyes of
the diphenylamine class.
Dye fading associated with NCL exposure of cellulose acetate and
in L
cellulosics is summarized Table 10-1. Testing methods predictive of dye
fading have been summarized in the literature. Selected anthraquinone-b
and blue dyes exhibit high resistance to fading by NO ,10"12
f\
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 N02 concentrations of 380 yg/m3 (0.2 ppm).9 (See Table 10-1)
Also, the additional acid introduced by S02» frequently present in signi-
ficant concentrations in ambient air, appears to accelerate the fading by
N02 even though S02> by itself, produces no change.
10.1.1.2 Fading of Dyes on Cotton and Viscose Rayon (Cellulosics)—
Although the effects of NO on dyed acetate are well documented, the
A
effects on dyes used for the cellulosic fibers have received much less atten-
tion. Anomalous cases of fading were reported by McLendon and Richardson
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 10-1.
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. ' Urban and rural
sites were chosen in areas of high and low atmospheric contaminant concentra-
tions: Phoenix, Arizona (low), Sarasota, Florida (low), Los Angeles,
10-3
-------
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
10-2). The fabric samples were exposed to ambient air for 30 and 120 days
in covered cabinets which excluded the action of light. Fading was demon-
strated on a range of fabrics, including cotton and rayon, for which the
cause could be NO , 0^ or SOg, The dyes applicable to cellulosics which
exhibited appreciable color change represented four major classes: direct,
vat, sulfur and fiber-reactive dyes.
Table 10-3 presents typical atmospheric pollutant concentrations in
Los Angeles, Chicago and the rural exposure sites. Chicago's high SOg
concentration was principally due to burning of coal; ozone concentrations
were low. The concentrations of NO are high in both Los Angeles and
A
Chicago, and are of similar magnitude. These differences in pollutant
concentrations correlate with the fact that the Disperse Blue 3, which
characteristically reacts to NO , showed pronounced reddening changes
A
in both Los Angeles and Chicago while being almost unchanged (in the Inter-
national Grey Scale ratings) in the rural exposure areas of Phoenix and
Sarasota (Table 10-2). 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 designed to produce changes similar to
those shown on service exposure, the AATCC N0x 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, oxides of nitrogen are generated by the addition of phosphoric
10-4
-------
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 ex-
posures in Los Angeles and Chicago showed similar changes upon laboratory
exposure under the high humidity conditions of the German Fastness Commission
test procedure.
The effect of NO on fiber reactive dyes has been reported by Imperial
A
Chemical Industries in its shade card of Procion Dyes. The vulnerability
18
of certain reactive dyes on cotton to NO also has been reported by Hertig
A
in his critical study of the International Standards Organization test pro-
cedure for fastness to NO . This method employs high humidity conditions.
rt
The effects of air pollutants were examined by the U.S. Environmental
19
Protection Agency (USEPA) in laboratory trials, using the same dye-fabric
combinations employed in the AATCC15 study (Table 10-2). The dye-fabric
combinations were exposed to air to which diluted auto exhaust and S02
were added over a 54-hour period. Neither the auto exhaust nor S02 produced
significant fadi.ng. However, irradiation of the auto exhaust, which
contains both hydrocarbons and oxides of nitrogen, gave products which
caused significant fading. The addition of S02 at a concentration of
3
2,520 yg/m (1.0 ppm) produced additional fading. The synergistic effect
of S02 is suggested as being responsible for the observed results.
Beloin20 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 10-2. The exposures were carried out in
10-5
-------
eleven nationwide urban and rural sites for consecutive three-month periods
over a period of two years.
The exposure sites are listed in Table 10-4. 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 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 dif-
21
ferent dyes tested totalled over $30 million dollars. Of the 67 dye-fabric
combinations, 25 were cellulosics.
The sites were monitored for 03, N02 and S02. The gas fading control
(Disperse Blue 3 on cellulose acetate) showed high correlation with NO con-
centration. Fadings on the 0^ test 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 per-
cent 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 S02, 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.
22
Beloin also conducted laboratory studies designed to determine the
effects of the individual air pollutants on dyed fabrics. Exposure was made
10-6
-------
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 10-5) used in the trials. Reactive dyes and one type
of vat dye were used. The p'ollutants were S02, NO, N02, and 0-. Two con-
centration levels were used for nitrogen dioxide: 940 and 94 yg/m3 (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 concentra-
tion of 940 yg/m (0.5 ppm), caused severe changes on 8 of the 9 samples.
Significant fading also occurred at high humidity with an ML concentration
3 22
of 94 yg/m (0.05 ppm). 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
23
tests with added contaminants using Xenon arc irradiation. The objective was
to establish a relationship between light-fastness tests made in natural day-
light in Florida and Xenon arc exposure in the laboratory Weatherometer. The
3 3
contaminants included separate additions of 940 ug/m (0.5 ppm) N02> 294 yg/m
(0.15 ppm) 03 and 786 yg/m (0.3 ppm) S02. In one trial, all three contami-
nants were added to the exposure cycle under Xenon arc irradiation. Of the
29 dyed fabric combinations exposed, 14 were cellulosic (cotton or rayon).
The addition of N02 alone caused increased fading compared to the control in
over half of dyed cellulosic fabrics examined.
Upham and co-workers 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 (134 and 1340 yg/m3), 03 (98 and 980 yg/m3),
and N02 (94 and 940 yg/m3) under Xenon arc irradiation, at various humidities.
10-7
-------
The effect of NOp was pronounced, especially on a vat-dyed drapery fabric.
o
The most noticeable color changes were at 940 yg/m (0.5 ppm) and 90 percent
relative humidity.
20
In summary, the investigations by Beloin both in the field study
22
and the chamber study show that, at concentrations of N0« present in
urban atmospheres, representative dyes for cotton and rayon will suffer
serious fading. WL resistant dyes are available; however, limitations
of brightness of shade and difficulty of application introduce production
problems and the need for greater quality control resulting, generally,
in increased costs. The AATCC work confirms the vulnerability to NOp
of several dyes widely used on cellulosic fibers, especially certain blue
dyes.
10.1.1.3 Fading of Dyes on Nylon—
The fading of dyed nylon in polluted atmospheres has been noted in
1C
exposure trials carried out by the AATCC and by the U.S. Environmental
20
Protection Agency. 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 N02» which demonstrated the vulnerability
of the disperse dyes used on acetate, showed little change when the same
dyes were used on nylon (Table 10-6). The problem of fading on nylon be-
came of considerable interest as nylon found use in carpets. The quantity 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
10-8
-------
dyes. ' In contrast, the same dyes on polyester showed no changes
(Table 10-6). The fading of disperse blue dyes on nylon carpets was
shown to be due to 03 in the presence of high humidity.25 Acid dyes,
which are more resistant to 03, were substituted as a remedial measure.
However, the remedy presented additional problems. The vulnerability of
acid dyes on nylon to N02 was the basis of a bulletin issued by Imperial
2fi
Chemical Industries on a range of acid dyes marketed as Nylomines. The
fading effect of N02» derived from combustion gases, was determined 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 manufacturers point out the importance of dye selection
in carpets and in home furnishings which are likely to be exposed for long
pen'ods in air contaminated with NCu from gas burner fumes.
Acid dyes on nylon were included in the range of dyes exposed to
visible light radiation and N02 by Hemphill in the AATCC study.23 Under
o
high humidity conditions and at an N02 concentration of 940 vg/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 N02-free air (Table
10-6).
10.1.1.4 Fading of Dyes on Polyester-
Polyester dyed with disperse dyes did not show NOg-induced fading
changes in AATCC field exposures in urban atmospheres of Chicago and Los
Angeles (Table 10-6). The same fabrics in various urban sites also
showed no changes; high or low humidity had no effect. However, a large
number of complaints regarding fading of permanent press garments (65
10-9
-------
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
27
press fabrics by Salvin indicated that fading did not take place on dye
contained within the polyester fiber matrix. Fading was found to take
place on the surface of the fiber as a result of dye migration from the
fiber subsurface to the modified urea-formaldehyde resin used on the blend
to stabilize the cotton. When exposed to NO^ or 0~, the components of the
resin finish absorb the contaminants and fading occurs. The measures which
can be used to eliminate the problem are (a) selection of dyes with lower
rate of migration, (b) substitution of the magnesium chloride catalyst with
zinc nitrate and, (c) reduction in quantity of non-ionic surfactant which
acts as an acceptor for the dye and an absorber for either N0« or 03.
28
Urbanik 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 N02 or 03. The fading attributed to N02 was noted in these 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.
10.1.1.5 Economic Costs of NO -induced Dye Fading—
A
29
Barrett and Waddell , in a 1973 status report to the U.S. Environmental
Protection Agency, reported that annual economic costs of NO -induced dye
A
fading in textiles amounted to $122.1 million. These estimates were based
on figures reported by Salvin.
10-10
-------
The economic costs to the nation as a result of Og damage to tex-
tiles is approximately 70 percent of the costs attributed to NO damage.
A
These costs of N0x and 03 action are tabulated in Table 10-7.
The basis for the estimates included not only the reduced wear life
of textiles of moderate fastness to NO but also the costs of research
/\
and quality control. The major share of the cost is the extra expense
involved in using dyes of higher NO resistance and in the use of inhi-
J\
bitors. Additional costs also are incurred in dye application and in
increased labor expenditures.
The factors relating to higher costs in the textile indudstry as a
result of NO action are discussed in Chapter 8, The Effects of Nitrogen
^ —^—»-^—™^"^»«^—•—^^^^^^—•^^»—^^•^•i—^j*»^»*».
Oxides on Materials, in the National Academy of Sciences report on nitrogen
oxides.30
10.1.2 Yellowing of White Fabrics by N00
""""^ ~ " ------ £
The survey of the effects of air pollutants on textiles reported a
number of instances in which white fabrics yellowed. This discoloration
occurred in areas protected from light. Causes of yellowing were not es-
tablished, except for the observation that contact with ambient air currents
seemed to be a causative factor.
Using 18 fabric samples which were the subjects of manufacturers' com-
plaints, Salvin investigated the effects of specific air pollutants or
combinations and the effects of humidity and temperature. The products
tested included polyurethane segmented fiber, rubberized cotton, optically-
brightened acetate, nylon, nylon treated with permanent antistatics, and
resin-treated cotton containing softeners (Table 10-8).
10-11
-------
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 Og, S02, or hydrogen sul-
fide (H2S).
The standard AATCC test procedure (conducted in low humidity) for
effects of N0~ 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
A
showed change on cellulose acetate fabrics, high humidity test procedures
demonstrated yellowing in nylon.
Although fibers without additives do not show yellowing following
exposure to N02, the polyurethane-segmented fibers (e.g., Lycra and
Spandex) are exceptions. These fibers contain urethane groups which react
directly with N02 to form yellow-colored nitroso compounds. Yellowing of
Spandex and Lycra fibers occurred in the standard AATCC test for N02
31
fading. 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
•50
where rubber is present.
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.
10-12
-------
Optical bn'ghteners, 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.
33
The AATCC 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 N0«. The yellowing was especially noted on those softeners of a cationic
nature. Softeners have been synthesized which are resistant to yellowing
34
by oxides of nitrogen.
The unexpected yellowing of nylon treated with an antistatic agent
31
has been reported. 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.
10.1.3 Degradation of Textile Fibers by NO
/\
Cotton and nylon are the two fibers whose strength is reduced by the
hydrolytic action of acid aerosols. This problem assumes economic impor-
tance 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 strength are costly and create safety hazards.
A chamber study of the combined action of N02 and light on cotton did
35
demonstrate that NO- contributed to strength loss . Cotton yarns were ex-
posed to sunlight. In one cabinet, air was filtered through carbon to
10-13
-------
remove oxides of nitrogen. The second cabinet contained fibers exposed to
sunlight and air containing monitored levels of 03 and N02- Exposure was
carried out for a total of 72 days. Since the test area (Berkeley, California)
was low in S02, 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 gave increased deterio-
A
ration over sunlight alone. The contributions of 0, and other oxidants was
not determined.
It is not possible to isolate the effects of nitrogen oxides from
that of sulfur oxides in field studies which have shown strength loss in
35-38
cotton. The effect of NOg on fiber degradation of cotton requires
further investigation.
on
Inconclusive results were shown by Zeronian et al. in a study of
the effect of N0«, 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 yg/m (0.2 ppm) NO^ 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 conditions but without N02. Modacrylic
(Dynel), acrylic (Orion), and polyester showed only slight differences in
degradation in exposures with and without NOg. These materials are considered
resistant to the action of acids. The results for nylon were not conclusive,
although significantly greater degradation (loss of tensile strength, in-
creased viscosity) at 48°C occurred in the present of NOp, under irradiation.
10-14
-------
Further experimentation would be suggested to test NCL effects in the absence
of irradiation and under higher humidity conditions.
10.2 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 im-
portance.
40
A 1977 survey predicts a market for these materials in 1982 of
1.78 billion pounds. Under the generic term of plastics are included
polyethylene, propylene, polystyrene, poly vinyl chloride, polyacrylonitrile
and polyamides.
Ageing is the term used to denote deterioration of chemical and
physical properties which can occur upon weathering. This degradation has
been blamed on the known effects of sunlight. The comparative resistance
to sunlight can be shown upon exposure in the laboratory to carbon or
Xenon arc irradiation. The effects of air pollutants, such as N02, has
been approached in laboratory trials. The substitution of plastics for
metals, particularly in automobiles, where long periods of outside exposure
are involved, brings this problem into focus.
The polymers which represent the structures in plastics, as well as
textiles, were subjected by Jellinek at al.41 to the action of S02, N02, and
ozone obtained by action of UV radiation on the oxygen-containing mixture.
These combinations of S02, N02, and ozone represent the components of smog.
The polymers include polyethylene, polypropylene, polystyrene, polyvinyl-
chloride, polyacrylonitrile, butyl rubber and nylon. All polymers suffered
deterioration in strength. The deterioration was considerable over longer
time periods. The elastomer, butyl rubber, was more susceptible to S02 and
10-15
-------
N02 than other polymers. However, the effect of 03 on the rubber was more
pronounced than that of the S02 or the N02.
Jellinek42 examined the reaction of linear polymers, including nylon
and polypropylene, to N02 at concentrations of 1,880 to 9,400 ug/m (1.0 to
5.0 ppm). Nylon 66 suffered chain scission. (Chain scission results in
polymers having lower molecular weights and lower strength.) Polypropylene
tended to crosslink. Chain scission of polymers caused by small concen-
trations of S02 and N02 took place in the presence of air and UV radiation.
The action of ML and 03 on polyurethane also was investigated by
Jellinek. The tensile strength of linear polyurethane was reduced by
N00 alone and also by N00 plus 0,. Chain scission resulting in lower
L. C •J
molecular weights and formation of nitro- and nitroso-groups along the
polymer backbone occurred upon exposure to NOp.
10.3 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 pro-
tective oxide layer, exposing new surfaces to electrolytic corrosion.
10-16
-------
An analysis of the contributing effects of air pollutants was offered
in the examination of the contributions of NCL to corrosion in the review
44
by the National Research Council.
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 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.
10.3.1 Pitting Corrosion
Pits or pitting corrosion is generally associated with the presence
of the chloride ion which may be related to the formation of the strong,
highly-ionized, hydrochloric acid. Nitrates also may be strong pit-formers.
Since solutions containing ferric chloride and cupric chloride or nitrate
are aggressive because of the presence of the acid anion and the
reducibility of the cation, oxygen is not necessary. In both crevice and
pitting corrosion, the rate at which metal dissolves, when in contact
with the solution, is accelerated by the presence of the chloride ion.
10.3.2 Stress Corrosion
Stress corrosion requires the presence of corrosive media and a
mechanical force. The corrosive media initiate the stress riser from which
10-17
-------
the crack propagates. The applied stress cracks any protective scale
that separates the corrodent from the substrate. The application of
stress initiates corrosion.
10.3.3. Selective Leaching
Material failure caused by selective leading of a component of an
alloy is represented by dezincification; loss of zinc is a well-established
form of corrosion common to brasses. The materials engineer must apply an
understanding of the various corrosion processes that occur in order to
remedy the problem and minimize the economic losses.
10.3.4 Correlation of Corrosion Rate with Pollution
The general approach taken by investigators to the effects of air pol-
lutants 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
45
corrosion due to air pollutants. Waddell in his estimates of the economic
damages of air pollution includes a section on costs of metal corrosion. Using
29
data supplied by the Rustoleum Corporation, Waddell and Barrett estimated
costs at $7.5 billion in 1958.
Material damage due to air pollutants emphasizes SCL as the major
46 47 47
causative agent in the corrosion of metals. * Fink and co-workers
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 electrolyte for galvanic
corrosion, becomes important. The potential of nitrates in upsetting the
10-18
-------
homogeneity of the protective oxide film becomes a factor.
48
Haynie et al. investigated the separate or combined effects of S02,
N02 and 03 under controlled conditions of pollutant, humidity and tempera-
ture. 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
49
conclusion was reported by Yocum and Grappore in a review of the effect
of air pollutants emanating from power plants.
The premature failure of nickel brass springs in telephone equip-
ment primarily in the Los Angeles area has been investigated by Hermance
and co-workers. 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.
51 52
Previous laboratory studies by Hermance and McKinney and Hermance
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 cracking at the nitrate concentra-
2
tn'on levels found in Los Angeles. Up to about 15 yg/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.
A field study was made of the incidence of breakage as related to
10-19
-------
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 hygroscopic than the chloride and sulfate salts. As such,
they may lower the threshold humidity requirements for the formation
of an aqueous medium, which can serve as the electrolyte or solvent
for wet corrosion.
Hermance also reported on the failure of other telephone equip-
ment, 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 cap of the contacts.
The heavy nitrate deposits were greater than 15.5 wg/cm2. Stress cor-
rosion occurred in the absence of anodic electrical current.
The function of N02 in changing the defect structure of many oxides,
thereby increasing or decreasing the rate of oxidation of metals and alloys,
CO
was suggested by Lazareva et al. in the study of the oxidation of tung-
sten alloys.
A field study of the effect of air pollutants on electrical contact
materials was carried out by Chiaranzelli and Joba,54 in which the forma-
tion of corrosion films in various areas of pollution was correlated with
the concentration of pollutants present. Nitrogen dioxide, SO^, H^S and
dust were monitored. This study did not isolate the specific contribution
10-20
-------
of N02 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
50
al. did show that nitrates were a contributory factor, although no re-
lation to the concentration of N02 in the air was established.
Gerhard and Haynie examined the cases of catastrophic failure of
metals in which structures failed unexpectedly, leading to loss of life
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 re-
lationship 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. Nitro-
gen dioxide was not considered a factor.
A review of the voluminous literature on corrosion has produced no
further references to investigations of NOp action, in the absence of SO^.
The above studies are summarized in Table 10-9.
10-21
-------
10.4 REFERENCES FOR CHAPTER 10
1. Upham, J. B., and V. S. Salvin. Effects of air pollutants on textile
fibers and dyes. Ecological Res. Series. EPA-650/3-74-008. U. S.
Environmental Protection Agency, Washington, D. C. 1975.
2. Rowe, F. M., and K. J. Chanjberlain. The fading of dyeings on cellulose
acetate rayon. J. Soc. Dyers Colour. 52: 268-278, 1937.
3. Couper, M. Fading of a dye on cellulose acetate by light and gas fumes:
1,4 bis methyl ami no-anthraqui none. Textile Res. J. 21: 720-725, 1951.
4. Salvin, V. S., W. D. Paist, and W. J. Myles. Advances in theoretical and
practical studies of gas fading. Amer. Dyestuff Reporter 41: 297-302,
1952. ~~
5. 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.
6. Seibert, C. A. Atmospheric (gas) fading of colored cellulose acetate.
Amer. Dyestuff Reporter 29_: 366-374, 1940.
7. American Association of Textile Chemists and Colorists. AATCC Technical
Manual. Volume 48. Research Triangle Park, North Caroline. 1972, 370 pp.
8. Salvin, V. S. Color fastness to atmospheric contaminants. Textile
Chem. and Color. £{7): 164-166, 1974.
9. Hemphill, J. Color fastness to light and atmospheric contaminants.
Textile Chem. and Color. 8_(4): 60-62, 1976.
10. Salvin, V. S., and R. A. Walker. Relation of dye structure to properties
of disperse dyes. Amer. Dyestuff Reporter 48: 35-43, 1959.
11. Straley and Dickey. Eastman Kodak. U. S. Pat. 2,641,602. June 9, 1953.
12. Seymour, 6. W., and V. S. Salvin. Celanese Corporation. Process of react-
ing a nitro hydroxy anthraquinone with a primary amine and a product
thereof. U. S. Pat. 2,480,269. August 30, 1949.
13. McLendon, V., and F. Richardson. Oxides of nitrogen as a factor in color
changes of used and laundered cotton articles. Amer. Dyestuff Reporter
54(9): 15-21, 1965.
14. Schmitt, C. H. A. Light fastness of dyestuffs on textiles. Amer. Dye-
stuff Reporter 49_: 974-980, 1960.
15. Salvin, V. S. Relation of atmospheric contaminants and ozone to light
fastness. Amer. Dyestuff Reporter 53: 33-41, 1964.
10-22
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16. Salvin, V. S. Testing atmospheric fading of dyed cotton and rayon.
Amer. Dyestuff Reporter 5: 8-29, 1969.
17. Rabe, P., and R. Dietrich. A comparison of methods for testing the fast-
ness to gas fading of dyes on acetate. Amer. Dyestuff Reporter 45: 737-
740, 1956.
18. Hertig, J. Priifung der Stickoxidechtheit-Erfahrungen und Vorschlaqe.
TextiIveredlung 3; 180-190,' 1968.
19. Ajax, R. W., C. J. Conlee, and J. B. Upham. The effects of air pollution
on the fading of dyed fabrics. J. Air Pollut. Control Assoc. 17: 220-
224, 1967. —
20. Beloin, N. J. A field study - fading of dyed fabrics by air pollution.
Textile Chem. and Color. 4_: 43-48, 1972.
21. U. S. Tariff Commission. U. S. production of dyes and synthetic chemicals.
Washington, D. C., 1967.
22. Beloin, N. J. A chamber study - fading of dyed fabrics exposed to air
pollutants. Textile Chem. and Color. 5; 29-33, 1973.
23. Hemphill, J. E., J. E. Norton, 0. S. Ofjord, and R. W. Stone. Color fast-
ness to light and atmospheric contaminants. Textile Chem. and Color. 8:
25-27, 1976.
24. Upham, J. B., F. H. Haynie, and J. W. Spence. Fading of selected drapery
fabrics by air pollution. J. Air Pollut. Control Assoc. 26_(8): 790,
25. Salvin, V. S. Color fastness to atmospheric contaminants - ozone. Tex-
tile Chem. and Color. £: 41-45, 1974.
26- Imperial Chemical Industries. ICI bulletin D1322. Synthetic fiber
4yeing - nylomine dyes - effect of burnt gas fumes.
27. Salvin, V. S. The effect of dry heat on disperse dyes. Amer. Dyestuff
Reporter 55_: 490-510, 1966.
28' Urbanik, A. Reduction in blooming of disperse dyes on durable press
fabrics. Textile Chem. and Color. 6: 78-80, 1974.
29. Barrett, L. B., and T. E. Waddell. Cost of air pollution damage. A stat-
tus report. NTIS Publication No. PB-220-040. U. S. Environmental Protec-
tion Agency, AP-85. February, 1973.
30. National Academy of Sciences. Effects of N02 on Materials. In: Nitrogen
Oxides. Chapter 6. National Research Council, Subcommittee on Nitrogen
Oxides, Washington, D. C. 1976.
31. 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, 1974. pp. 40-51.
10-23
-------
32. Burr, F. K., and T. E. Lannefeld. Yellowing of white fabrics by gas
fume fading. Asian Textile J. 2.:27, 1974.
33 American Association of Textile Chemists and Colorists. Cationic
softeners - Their secondary effects on textile fabrics. Intersectional
contest paper. Philadelphia. Amer. Dyes tuff Reporter 46.: 41, 1957.
34. Dexter Chemical Company. Dextrol softeners resistant to oxides of
nitrogen. Technical bulletin.
35 Morris, M. A. Effect of weathering on cotton fabrics. California
Agricultural Experiment Station Bulletin 823, Davis, Calforma, 1966.
29 pp.
36. Brysson, R. J., F. B. Trask, 0. B. Upham and S. G. Booras. The effects
of air pollution on exposed cotton fabrics. J. Air Pollut. Control
Assoc. 17: 294-298, 1967.
37 Travnicek, Z. Effects of air pollution on textiles, especially syn-
thetic fibers. International Clean Air Congress Proceedings, London,
1966. pp. 224-226.
38. Brysson, R. J., B. J. Trask and A. S. Cooper, Jr. The durability of
cotton textiles - The effects of exposure in contaminated atmospheres.
Amer. Dyestuff Reporter 57: 14-20, 1968.
39. Zeronian, S. H., K. W. Alger and S. T. Omaye. Reaction of fabrics made
from synthetic fibers to air contaminated with nitrogen oxide, ozone, or
sulfur dioxide. Proceedings of the Second International Clean Air Congress,
Washington, D. C., December, 1970. Academic Press, Inc., New York, 1971.
pp. 468-476.
40. Chemical and Engineering News. November 7, 1977.
41. Jellinek, H. H. G., F. Flajeman and F. J. Kryman. Reaction of S02 and
N02with polymers. J. App. Poly, Sci. 13(1): 107-116,1969.
42. Jellinek, H. H. G. Chain scission of polymers by small concentrations
(1-5 ppm) of sulfur dioxide and nitrogen dioxide, respectively, in
the presence of air and near UV radiation. J. Air Pollut. Control
Assoc. 20: 672-674, 1970.
43. Jellinek, H. H. G. Degradation of polymers at low temperatures by N02,
00, and near-ultraviolet light radiation. Cold Regions Res. Eng. Lab.,
HSnover, New Hampshire. USN TIS AD 782950/OGA, 1974. 31 pp.
44. National Academy of Sciences. Nitrogen oxides. National Research Coun-
cil, Committee on Medical and Biological Effects of Environmental Pol-
lutants, Subcommittee on Nitrogen oxides. Washington, D. C. 1976.
45. Waddell, T. E. Economic damage of air pollution. NTIS Publication No. PB
235 761 PGF, 1974.
10-24
-------
46. Gillette, D. G. S09 and material damage. J. Air Pollut. Control Assoc.
25.: 1238, 1975. i
47. Fink, F. W., F. H. Buttner, and W. K. Boyd. Economic costs of corrosion.
NTIS Publication No. PB 198 453, EPA Publication No. APTD 0654. February,
1971. 160 p.
48. Haynie, F. H., J. W. Spence, and J. B. Upham. Effect of gaseous pollu-
tants on materials - a chamber study. NTIS Publication No. PB 251-580 7
ga. EPA-600/3-76-015. February, 1976. 98 pp.
49. Yocum, J. E., and N. Grappore. Effects of power plant emissions on
materials. NTIS Publication PB 257-537 7 ga. July, 1976. 92D. EPRI EC
139. EPRI RB 575.
50. 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. Tech. 5.: 781-789, 1971.
51. Hermance, H. W. Combatting the effects of smog on wire-sprung relays.
Bell Lab. Rec. 48-52, 1966.
52. McKinney, N. and H. W. Hermance. Stress corrosion cracking rates of a
nickel-brass alloy under applied potential. In: Stress Corrosion Testing,
ASTM STP 425, Amer. Soc. Testing Mat., Philadelphia, Pennsylvania. 1967.
p. 274-291.
53. Lazareva, I. Y., D. A. Prokoshkin, E. V. Vasileva, and S. A. Skotnikov.
Reactional diffusion during oxidation of tungsten alloys in an atmosphere
with a high concentration of NO,. Protective Coating Metals 5; 57-60,
1973. *•
54. Chiaranzelli, R. V., and E. L. Joba. Effect of air pollution on electri-
cal contact materials. J. Air Pollut. Control Assoc. 16: 123, 1966.
55. Gerhard, J., and F. H. Haynie. Air pollution effects and catastrophic
failure of metals. NTIS Publication No. PB 238-290. November, 1974.
56. Romans, H. B. Stress Corrosion Test. Environments and Test Periods
Report of ASTM Task Group B. January, 1965. p. 58.
57. Salvin, V. S., and R. A. Walker. Service fading of disperse dyes by
chemical agents other than oxides of nitrogen. Textile Res. J. 25:
571-585, 1955.
10-25
-------
Table 10-1. FADING OF DYES ON CELLULOSE ACETATE AND CELLULOSICS
(COTTON AND RAYON) BY NITROGEN DIOXIDE
o
no
Concentration
of Pollutant
Dyed Fiber
Acetate
Acetate
Acetate
Acetate
Cotton-Rayon
Acetate-
Cotton, Rayon
Exposure
Gas heated
rooms
Chamber
Pittsburgh-
Urban,
Ames -Rural
Chamber
Clothes dryer
Los Angeles8
Chicago3
Pollutant
N09
£
N02
N0,-0,
c O
NO,
C
NO,
c
NO,
*0,
4-
S02
I^Urt
°3
* SO,
yg/m3
3,760
3,760
N/A
3,760
1,128-
3,760
489
+ 312
+ 131
414
+ 10
+ 655
ppm
2.0
2.0
2.0
0.6-
2.0
0.26
+0.21
+0.05
0.22
+0.005
+0.25
Time
N/A
16 hr
6 mo
16 hr
1 hr
cycle
30 to
120
days
Effect
Fading
Fading
Fading
Fading
Fading
Fading
Reference
Rowe and 2
Chamberlain, 1937
Selbert, 19406
Salvln and c7
Walker, 1955
Salvln, A
et al., 19524
McLendon and .~
Richardson, 19651J
Salvln, 196415
(continued)
-------
Table 10-1 (continued)
o
r>o
Concentration
of Pollutant
Dyed Fiber
Cotton-Rayon
Cotton-Rayon
Range of
Fibers
Range of
Fibers
Range of
Fibers
Acetate-
Cotton, Rayon
Acetate-
Cotton, Rayon
Exposure
Chamber
Chamber
Field-Urban,
Rural
Chamber
Chamber
Chamber
Survey
Pollutant
S02-N02
S02-N02
and Og
S02-N02*03
N02
N02+Xenon
arc radiation
N02
N0?,
S02, H£S
yg/m
ppm
3,760 2.0
94 to
940
940
94 to
940
N/A
N/A
0.05 to
0.5
0.5
0.05 to
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, 196916
Ajax et al., 196719
Beloin, 197220
Beloin, 197322
Hemphill ,,.,
et al., 1976"
Upham p*
et al., 197r
Upham and •>
Salvin, 19751
Concentrations also shown in Table 10-3
-------
Table 10-2.
COLOR CHANGES ON DYED FABRIC—EXPOSED WITHOUT
SUNLIGHT IN POLLUTION AND RURAL AREAS15
International Grey Scale; 5 = no change;
Y = yellow; W = weaker; G = greener; R =
redder; and B = bluer
Code Index No.
ACETATE
Disperse Red 35
Disperse Blue 27
Oxides of nitrogen
fading control
Disperse Blue 3
Ozone control —grey
dyed with:
Disperse Blue 27
Disperse Red 35
Disperse Yellow 37
POLYESTER
Disperse Yellow 37
Disperse Blue 27
Disperse Red 60
WOOL
Acid Black 26A
Acid Red 89
Acid Violet 1
Acid Blue 92
Acid Red 18
COTTON
Direct Dyes
Direct Red 1
Congo Red B
Direct Red 10
Direct Blue 76
Direct Blue 71
Direct Blue 86
if •
Vats
Vat Yellow 2
Vat Blue 29
Vat Blue 6
Vat Red 10
Phoenix
4.5Y
3.0W
3.5
3.0
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
Los Angeles
4.0Y
2.0W
1.5R
1.5
5.0
4.0
5.0
4.5
3.5
4.0
4.0
4.0
1.5
2.5
3.5
2 grey
2.5R
1G
4.0
3G
3.5R
4.5
Chicago
4.5Y
2.5W
2. OR
3.5
4.0
3.5
w • w
4.0
3.5
3.5
3.0
2.5
fc- • *j
3.5
1.5
2.5
3B
1R
2R
1G
3G
2.5G
3.0
3.5
Sarasota
4.5Y
2.0W
3.5
v • »/
2.5
4 0
• • v
4 5
*T» J
4.5
4 5
~ • w
2 5Y
£• • */ 1
4 0
~ • w
4 0
*t« V
4.5
3 0
*/ * V
2Y
4.0
4.0
3R
2. 56
5.0
1.5G
4R
5.0
(continued)
10-28
-------
Table 10-2 (continued)
International Grey Scale; 5 = no change.
Y = yellow; W = weaker; G = greener; R =
redder; and B = bluer
Code Index No.
Fiber React ives
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
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
C 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
3.0R
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
36
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.
10-29
-------
Table 10-3. TYPICAL CONCENTRATIONS9 OF ATMOSPHERIC
CONTAMINANTS IN EXPOSURE AREAS15
Oxides of Nitrogen
Sulfur Dioxide
Carbon Monoxide
Ozone
Aldehydes
Rural
(Phoenix - Sarasota)
(ppm) (yg/m )
0.01
0.03 90
—
0.06-0.11 120 - 220
—
Los
(ppm)
0.26
0.05
23.00
0.21
0.'3
Angeles
(yg/m3)
140
26,000
410
Chicago
(ppm) (yg/m3)
0.22
0.25
16.00
0.005
—
700
18,000
10
Concentrations shown are average concentrations measured over a two-month period,
relative humidity data not available.
10-30
-------
Table 10-4. EXPOSURE SITES'
20
City
Washington, DC
Poolesville, MD
Tacoma, VIA
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*
Units
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.
10-31
-------
CO
ro
Table 10-5. AVERAGE FADING OF 20 DYE-FABRIC COMBINATIONS8 AFTER 12 WEEKS EXPOSURE
TO NITROGEN DIOXIDE23
Hunter Color Units5
90 ug/m3 NO,,
Material
Cotton
Rayon
Wool
Cotton
Acrylic
Cotton
Nylon
Wool
Acrylic
Cotton
Wool
Cotton
Cellulose Acetate
Nylon
Dye
Direct
Direct
Acid
Reactive
Basic
Azo1cc
Add
Add
Basic
Sulfur
Add
Direct
Disperse
Disperse
Color Index No.
Red 1
Red 1
Red 151
Red 2
Red 14
Red
Orange 45
Yellow 65
Yellow 11
Green 2
Violet 1
Blue 86
Blue 3
Blue 3
Low Temp.
Avg.,
12.78°C
7.2
3.4
T
T
T
T
5.6
T
T
T
T
5.9
29.0
5.5
High Temp.
Avg. .
32.22°C
8.0
T
T
T
T
T
17.0
T
T
3.3
T
9.5
42.3
14.7
Low
Humidity
Avg. •
(SOX RH)
7.4
T
T
T
T
T
10.1
T
T
T
T
9.4
37.7
5.9
High
Humidity
Avg.
(90% RH)
7.8
T
T
T
T
T
9.5
T
T
T
T
6.0
33.6
14.2
Low Temp.
Avg. ,
12.78°C
18.0
13.4
T
10.4
T
T
21.5
T
T
6.5
T
14.1
86.9
39.6
940 uq/m3 N0n
High Temp.
Avg.,
32.22°C
20.4
16.3
T
6.9
T
T
27.9
T
T
6.6
T
17.2
75.6
45.5
Low
Humidity
Avg.
(50% RH)
16.1
12.6
T
9.7
T
T
24.3
T
T
6.1
T
14.2
88.0
34.0
High
Humidity
Avg.
(90% RH)
22.3
17.0
T
7.6
T
T
25.1
T
T
7.1
4.1
17.1
74.4
51.1
(continued)
-------
Table 10-5. (continued)
CO
CO
90 ug/m3 NO,
Material
Cellulose Acetate
Polyester
Cotton
Cotton
Cotton
Acetate
Dye
Disperse
Disperse
Reactive
Reactive
Vat
d
Color Index No.
Blue 27
Blue 27
Blue 1
Blue 2
Blue 14
AATCC Ozone Ribbon
Low Temp.
Avg.,
12.78°C
6.4
T
3.9
6.4
6.3
T
High Temp.
Avg.,
32.22°C
4.9
T
13.6
10.6
6.7
T
Low
Humidity
Avg.
(SOX RH)
3.8
T
9.6
8.2
3.3
T
High
Humidity
Avg.
(90X RH)
7.5
T
7.9
8.9
9.7
T
Low Temp.
Avg. ,
12.78°C
20.5
T
31.8
30.5
34.3
5.7
940 uq/m3 NO,,
High Temp.
Avg.,
32.22°C
26.8
T
41.7
41.6
30.4
11.7
Low
Humidity
Avg.
(50% RH)
17.0
T
35.4
33.8
23.4
5.7
High
Humidity
Avg.
(90% RH)
29.6
T
38.1
38.4
41.3
11.7
Each average, e.g. the low temperature average, was calculated by averaging the color change
of.duplicate samples from both the low temperature-low humidity and low temperature-high
humidity exposure periods.
T=trace (less than 3 units of fading). The higher the number, the greater the fading.
Hunter Color Units approximate the NBS color scale.
Coupling Component 2, Azoic D1azo Component 32.
dC.I. Disperse Blue 27, C.I. Disperse Red 35, C.I. Disperse Yellow 37.
-------
Table 10-6. EFFECT OF NITROGEN DIOXIDE ON FADING OF
DYES ON NYLON AND POLYESTER
o
CO
Concentration
of Pollutant
Dyed Fibers
Nylon
Polyester
Nylon
Polyester
Nylon
Polyester
Nylon
Nylon
Polyester
Permanent Press
Polyester
Textured
Double Knit
Exposure
Chicago
Los Angeles
Chicago
Los Angeles
Urban Sites
Urban Sites
Chamber
High Humidity
Chamber
High Humidity
Chamber
High Humidity
Chamber
High Humidity
Xenon Arc
Chamber
Chamber
Pollutant
NO,
£.
NO,
£
N02
N02
NO,
c
NO,
£
NO,
c.
NO,
L
NO,
£
NO,
£
yg/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 mo
3 to 24 mo
12 wk
12 wk
48 hr
30 to 120 hr
16 hr
16 hr
Effect
Fading
Unchanged
Fading
Unchanged
Fading
Unchanged
Fading
Reference
Salvin, 196415
Ibid
Beloin, 197220
Ibid
Beloin, 197322
Ibid
Imperial
Chemical ,7
Industries
More fading Hemphill, 197623
than without
N02
Fading
Fading
Salvin, 196627
00
Urbanik, 1974"
-------
Table 10-7. ESTIMATED COSTS OF DYE FADING IN TEXTILES29
Pollutant
M0x
°3
Effect
Fading on acetate and triacetate
Fading on viscose rayon
Fading on cotton
Yellowing of white acetate-nylon-Spandex
Subtotal
Fading on acetate and triacetate
Fading on nylon carpets
Fading on permanent-press garments
Subtotal
Total
$ million
73
22
22
6
122
25
42
17
84
206
*A11 costs rounded to nearest million, therefore some totals do not agree.
10-35
-------
Table 10-8. YELLOWING OF WHITES BY NITROGEN DIOXIDE
o
I
CO
Concentration
of Pollutant
Fiber
Survey
Rubberized
Cotton
Rubberized
Cotton
Spandex
Acetate
Optical
brightener
Nylon
Optical
brightener
Nylon
Anti-stat
finish
Cotton
Cationic
softener
Exposure
Service
Complaints
Chamber
Chamber
Chamber
Chamber
Chamber
High Humidity
Chamber
High Humidity
Chamber
Pollutant
N/A
NO,
c.
NO,
c
NO,
£
NO,
b
NO,
c.
NO,
c.
NO,
£
yg/m3
564
376
ppm
0.3
0.2
Time
N/A
16 hr
Effect
Yellowing
Yellowing
Reference
Upham and
Salvin, 1975
Burr and
i
i
•V)
Lannefeld, 1974"
376
376
376
376
376
376
0.2
0.2
0.2
0.2
0.2
0.2
16 hr
8 hr
8 hr
16 hr
16 hr
16 hr
Yellowing of
anti-oxidant
Action on
fiber
Yellowing
Yellowing
Yellowing
Yellowing
Salvin, 1974
Ibid
Ibid
Ibid
Ibid
Ibid
31
-------
Table 10-9. CORROSION OF METALS BY NITROGEN DIOXIDE
o
CO
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
N02-S02-H2S
N02-S02-03
Effect
Strength
Loss
Strength
Loss
Corrosion
Change oxide
surface
Corrosion
film
Failure
Economic Costs of Corrosion
Reference
National Research
Council, 1975 w
Hermance et al., 197150
McKinney and g2
Hermance, 1967
Hermance, 1966
Lazareva, 1973 53
Chiaranzein and
Ooba, 196#4
Gerhard and Haynie, 197455
Fink et al., 197147
-------
CHAPTER 11
EFFECTS OF NITROGEN OXIDES ON VISIBILITY
Air pollution degrades the appearance of distant objects and re-
duces the range at which they, can be distinguished from the background.
These effects are manifested not only in visible smoke plumes, but also
in large-scale, hazy air masses. In regions of good visibility, such
as the southwestern United States, haze and smoke plumes can result
in the deterioration and loss of scenic vistas. In other areas, re-
duced visual range due to haze and plumes may impede air and surface
traffic. It has long been known that N02 is responsible for a signi-
ficant portion of the brownish coloration often observed in polluted
2
air. In addition, recent work indicates that particulate nitrates
may contribute to the reduction of visual range. '
11.1 NITROGEN OXIDES AND LIGHT SCATTERING AND ABSORPTION
Deterioration in visibility is due to the absorption and scattering
c
of light by gaseous molecules and suspended solid or liquid particles.
Absorbed light is transformed 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 ab-
sorption and scattering coefficients, b. and b . These coefficients
a S
specify the rate at which a beam of light is attenuated in passing
through the atmosphere:
and
dla/l = -badx,
dls/l = -b$dx,
11-1
-------
where I is the intensity of the beam, and dl and dl are the changes
a s
in I due to absorption and scattering over the incremental distance
dx. The sum of the absorption and scattering coefficients is the
total extinction coefficient, b = b + b.
a s
The absorption and scattering coefficients of parti cul ate 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 parti cul ate matter can be distinguished as follows
(the subscripts g and p denote the respective contributions from gases
and parti cul ates):
= b + b + b +b
ag ap sg sp
In polluted atmospheres, the term b3/1 is dominated, at visible wave-
ay
lengths, by the contribution from NCL, 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. In some locations,
nitrate compounds may constitute a significant fraction of the material
in the particle size range that is optically important.
11.2 EFFECT OF NITROGEN DIOXIDE ON COLOR
Under typical ambient conditions, light scattering dominates
total extinction, i.e., reduction of visual range. The most significant
optical effect of NOp involves discoloration. The absorption coefficient
for NOp can be used to calculate the visual impact of ML in the atmos-
phere.
11-2
-------
11.2.1 Nitrogen Dioxide and Plumes
Nitrogen dioxide in the plume from a combustion source, for example,
acts as a blue-minus filter for transmitted light. It tends to im-
part 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., similar
effects would be produced by a 1 kilometer-wide plume containing 0.1
o
ppm (190 yg/m ) of N02 or a 0.1 kilometer-wide plume containing 1.0 ppm
(1,900 yg/m3) of NOg.
Figure 11-1 shows the calculated transmittance of particle-
free N02 plumes for several values of the concentration-distance pro-
duct. As little as 0.1 ppm-km NOp is sufficient to produce a color
shift which is distinguishable in carefully-controlled, color-matching
o
tests. . Under more usual viewing conditions, a pale color would be
produced in a white target at a concentration-distance product of 0.5
2
ppm-km.
Plume coloration due to N02 is modified by particulate matter,
g
which may include a substantial nitrate fraction. The effect of
particles in the plume is strongly dependent on the viewing angle.
Small particles scatter the shorter wavelengths of sunlight preferentially
so that their filtering effect on transmitted light is similar to that
of N02.10 For an observer with the sun at his back, particle-scattering
can thus intensify the apparent brown coloration of the plume. When the
sun is in front of the observer, however, light scattered toward him
by the plume tends to wash out the brownish light transmitted from
beyond. Under these conditions, particle scattering diminishes the
plume coloration.
11-3
-------
11.2.2 Nitrogen Dioxide and Haze
A common feature of pollutant haze is its disagreeable brown color.
The discoloration of the horizon sky due to N02 absorption is determined
by the relative concentrations of N02 and light-scattering particles. In
a uniform atmosphere, the effect of N02 is described by the following
relationship:
"horizon/Wizen"1^ ' 0) ' H^y = (1 + V"5'"'
where Bnorjzon and Bhorizon^N02-' = °^ are the bri9ntness of tne horizon
sky, with and without NCL.
The ratio b.,Q /b is more easily related to experience when ex-
pressed in terms of concentration, [N02], and visual range, VR. Samuels
12
et al. compared human observations with instrumental measurements
and found indications that VR and b are related by the formula,
VR = (3 - l)/bs. Since, in addition, bNQ is proportional to [N02], it
follows that the ratio bNQ /bs is proportional to the product [N02] VR.
Figure 11-2 shows, for several values of this product, the cal-
culated alteration in horizon brightness produced by N02-
The interpretation of Figure 11-2 is similar to that of Figure
11-1. Concentration-visual range products of 0.3 ppm-km and 2 ppm-km
of N02 correspond to color shifts which should be, respectively, de-
tectable in color-matching tests and noticeable under ordinary viewing
conditions. At a visual range of 100 kilometers, typical of the rural
southwestern United States, 0.02 ppm (40 pg/m ) N02 would suffice to
color the horizon noticeably. At a visual range of 10 kilometers,
2
typical of urban haze, 0.2 ppm (400 yg/m ) N02 would be required to
produce the same effect.
11-4
-------
Independently of absorption by N02, wavelength-dependent scattering by
small particles can also produce a noticeable brown coloration in polluted
13
air masses. Unlike the coloration due to absorption, which is independent
of sun angle, the brown coloration contributed by scattering is most
intense when observed in the hemisphere opposite the sun as discussed in
Section 11.2.1.
11.3 EFFECT OF PARTICULATE NITRATES ON VISUAL RANGE
The visual range in a uniform atmosphere is inversely proportional to
the extinction coefficient. For a "standard" observer, the Koschmeider
formula expressing this relationship is:
VR = 3.9/b
where b is the extinction coefficient.
For example, in a pure atmosphere containing no aerosols and no light
absorbing gases, the extinction coefficient from Rayleigh light scattering
by air molecules is b ^ 0.15 x 10 m; this corresponds to a visual
range of 260 kilometers.
A definitive assessment of the contribution made by nitrate aerosols
to total extinction (and therefore to degradation of visual range) 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 , it would be
expected, on theoretical grounds, that they would be efficient scatterers
of light. As shown in Figure 11-3, light scattering per unit mass of
aerosol exhibits a pronounced resonance at a particle size of 0.5 microns,
near the wavelength of visible light.
11-5
-------
Theoretical calculations based on the Mie theory of light scattering
from aerosols indicate that particles found in the 0.1 to 1 micron size
range (such as in secondary aerosols) should exhibit extinction coeffi-
cients per unit mass on the order of 0.06 - 0.03, where the units are
(10 mrVfyg/m3).3'15'16 Similar calculations indicate that particles
occurring in the coarse size range above 2 microns, such as dust or sea
17 18
spray, » should exhibit much lower extinction coefficients per unit
mass, on the order of 0.006 - 0.003 where the units are (104m)~1/(yg/m3).3'15'16
These results are confirmed by empirical studies, 3»4>19»20»21 which
typically find extinction coefficients per unit mass of sulfates (a
prevalent secondary aerosol) to be 0.04 to 0.10 (104m)"1/(yg/m3). For
the remainder of TSP (mostly coarse particles), the extinction coef-
ficient per unit mass is 0.004 to 0.01 (lO^mJ'Vfyg/m3).
With the following assumptions, one could conclude that nitrates
account for 3 to 10 percent of total extinction in the Southwest and 2
to 8 percent of total extinction in urban haze:
(1) Scattering coefficient for nitrates is in the range of 0.004 to
0.08, where the units are (104m)~1/(pg/m3).
q
(2) nitrate concentrations are taken to be typically 0.25 to 0.5 yg/m
in the southwestern United States, where visibility is approximately
100 kilometers.
q
(3) nitrate concentrations are taken to be typically 2 to 4 yg/m in
urban haze, with 10 kilometer visibility (see Chapter 7).
Although the assumed scattering efficiency is relatively high for nitrates,
the nitrate contributions to total extinction are low because the assumed
atmospheric concentrations are very low compared to concentrations of other
atmospheric aerosols.
11-6
-------
11.4 REFERENCES FOR CHAPTER 11
1. Husar, R. B., N. V. Gillani, J. D. Husar, and D. E. Patterson. A
study of long range transport from visibility observations, tra-
jectory analysis, and air pollution monitoring data. Paper pre-
sented at the Seventh Annual Technical Meeting on Air Pollution
Modeling and its Applications.
2. Hodkinson, J. R. Calculations of colour and visibility in urban
atmospheres polluted by gaseous NO,. Intern. J. of Air and Water
Pollut. 10_: 137, 1966. i
3. White, W. H. and P. T. Roberts. On the nature and origins of
visibility-reducing aerosols in the Los Angeles Air Basin. Atmos.
Environ. 11: 803, 1977.
4. Trijonis, J. and K. Yuan. Visibility in the Southwest—an explor-
ation of the historical data base. EPA-600/3-78-039. U.S. Envir-
onmental Protection Agency, 1978.
5. Middleton, W. E. K. Vision Through The Atmosphere. University of
Toronto Press, Toronto, Canada, 1952.
6. U.S. Department of Health, Education and Welfare. Air Quality
Criteria for Participate Matter. NAPCA Publ. No. AP-49, Public
Health Service, Environmental Health Service, National Air Pollution
Control Administration, Washington, D.C., January 1969.
7. Nixon, J. K. Absorption coefficient of nitrogen dioxide in the
visible spectrum. J. Chem. Phys. 8_: 157, 1940.
8. MacAdam, D. L. Visual sensitivities to color differences in day-
light. J. Opt. Soc. Amer. 32; 247, 1942.
9. Williams, M. D. and R. Cudney. Predictions and measurements of
power plant plume visibility reductions and terrain interactions.
In: Proceedings of the Third Symposium on Atmospheric Turbulence,
Diffusion, and Air Quality. American Meteorological Society,
1976.
10. Ahlquist, M. C. and R. J. Charlson. Measurement of the wavelength
dependence of atmospheric extinction due to scatter. Atmos.
Environ. 3k 551, 1969.
11. Robinson, E. Effect on the physical properties of the atmosphere.
In: Air Pollution, A. C. Stern, (ed.). Academic Press, Inc.,
New York, 1968.
11-7
-------
12. Samuels, J. J., S. Twiss, and E. W. Wong. Visibility, light
scattering and mass concentration of particulate matter. A report
of the California Tri-City Aerosol Sampling Project, California Air
Resources Board, 1973.
13. Husar, R. B. and W. H. White. On the color of the Los Angeles
smog. Atmos. Environ. 19_: 199-204, 1976.
14. Lee, R. E. and R. K. Pattbrson. Size determination of atmospheric
phosphate, nitrate, chloride, and ammonium particulate in several
urban areas. Atmos. Environ. 3; 249, 1969.
15. Latimer, D. A., et al. The Development of Mathematical Models for
the Prediction of Anthropogenic Visibility Impairment. Draft Final
Report, Contract No. 68-01-3947. U.S. Environmental Protection
Agency, 1978.
16. Ursenbach, W. 0., et al. Visibility models for the arid and
semi arid western United States. Paper presented at the Seventy-
First Annual Meeting of the Air Pollution Control Association,
1978.
17. Whitby, K. T. and 6. M. Sverdrup. California aerosols: their
physical and chemical characteristics. To Be Published in ACHEX
Hutchinson Memorial Volume. Particle Technology Laboratory Pub.
No. 347. University of Minnesota, 1978.
18. Bradway, R. M. and R. A. Record. National Assessment of the Urban
Particulate Problem, Volume II Particulate Characterization. EPA-
450/3-76-025. U.S. Environmental Protection Agency, 1976.
19. Trijonis, J. and K. Yuan. Visibility in the Northeast: long-term
visibility trends and visibility/pollutant relationships. EPA-
600/3-78-075. U.S. Environmental Protection Agency, 1978.
20. Cass, G. R. The Relationship between Sulfate Air Quality and
Visibility in Los Angeles. Caltech Environmental Quality Lab-
oratory Memorandum No. 18, California Institute of Technology,
Pasadena, California, 1976.
21. Waggoner, A. P., A. J. Vanderpol, R. J. Charlson, S. Larsen, L.
Granat, and C. Tragardh. Sulfate-light scattering ratio as an
index of the role of sulphur in tropospheric optics. Nature 261:
5556, 1976.
11-8
-------
Ul
z
«c
0
WAVELENGTH, A
Figure 11-1. Transmittance exp(-bNn x) of NCL plumes for selected values
MU2 c o
of the concentration - distance product.
11-9
-------
o
II
CM
O
O
M
•r—
J_
O
JZ
CO
c
o
Nl
•r—
S-
o
JC
CQ
WAVELENGTH, A
Figure 11-2. Relative horizon brightness b /(b + bMn ) for selected
S S HUp
values of the concentration - visual range product,
O
assuming b = 3/(visual range).
11-10
-------
V)
to
•4->
•r~
C
Z3 *-*
J_ E
*£*
.03 .05 .07 O.I 0.2 0.3 0.5 0.7 1.0 2.0 3.0 5.0 7.0 10.0
Figure 11-3.
Particle Diameter (microns)
Normalized light scattering by aerosols as a function of particle
diameter. Computed for unit density spherical particles of
refractive Index 1.5.3
-------
CHAPTER 12
STUDIES OF THE EFFECTS OF NITROGEN COMPOUNDS ON ANIMALS
12.1 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, the National Academy of
Sciences monograph, the North Atlantic Treaty Organization document3 and
the U.S. EPA document concerning short-term effects of N02.208 A World
4
Health Organization monograph has been recently published as have two
excellent interpretive reviews by Coffin and Stokinqer5 and by Morrow.6
The reader is referred to these publications for a general background on
the toxicity of the oxides of nitrogen (NO ).
^\
Host of the data presented in this chapter relate to nitrogen dioxide
(N02) because it appears to be the most toxic oxide of nitrogen and most
widely distributed in a manner affecting human health. The data presented
are confined to animal studies as they relate to human health. Table 12-1
presents a summary of effects of N0~ on animals at a wide range of concen-
trations.
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 concentrations below 9,400 ug/m (5.0 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 tabular form only.
12-1
-------
12.2 NITROGEN DIOXIDE
12.2.1 Respiratory Tract Transport and Absorption
Nitrogen dioxide is soluble and is approximately 50 percent 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. Ichioka constructed a glass tube and
filter paper model of the trachea and found only negligible uptake of N02
in the moistened filter papers lining his model. An estimate of the total
N02 removed from the stream can not be calculated from his results.
Yokoyama8 used isolated upper airways of the dog and rabbit to measure N02
removal, which amounted to 42.1 percent of the incoming N02 concentration.
Q
Dahlman and Sjoholm measured the concentration of N02 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. Consider-
able variation occurred between animals, but about 50 percent of the
incoming N02 was removed on a single passage through the nasopharyngeal
cavity.
Goldstein et al.10 exposed monkeys for 9 minutes to 560 to 1,710 pg/m
(0.3 to 0.91 ppm) N02 plus 13N02. During auiet respiration,
50 to 60 percent of the inspired pollutant was retained by the animal;
radioactivity was distributed throughout the lungs. Once absorbed, N02 or
chemical intermediates derived from N02 remained within the lung for pro-
longed periods following exposure. 13N-radioactivity was detectable in
extrapulmonary sites as well. The authors postulated the reaction of N02
with water in the nasopharynx and lungs to form nitric and nitrous acids
which then react with pulmonary and extrapulmonary tissues.
12-2
-------
Observed effects at much higher concentrations of N02 include
cessation of cilia beating and detection of nitrates and nitrites in urine
of animals exposed to N02.
12.2.2 Mortality
In a survey of the acute toxicity of N02 to mice, rats, guinea pigs,
rabbits, and dogs, Hine et al. found that concentrations below 94,000
pg/m3 (50 ppra) rarely produced mortality from exposures up to 8 hours. The
effects varied from species to species. Dogs and rabbits appear to be
relatively resistant to acute toxicity. Factors associated with increased
aortality at high concentrations of N02 include cold stress and adrenal-
ectomy.
Strain and sex differences in the susceptibility of mice to N02 alone
and in combination with other air pollutants have been reported. Emik et
al.13 noted that males of the C57BL/6 strain of mice, exposed to ambient
air in California, died sooner than either C57BL/6 females, or males and fe-
nales 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
3
exposed to clean or polluted air. Concentrations of about 40 ug/m (0.02
ppio) N02 were observed during the study. In an investigation of the sus-
ceptibility of inbred mouse strains to ozone, Goldstein et al. observed
no differences in the susceptibility of males or females to either ozone or
N02.
Dietary supplementation of Vitamin E (45 to 100 mg d,l-a-tocopherol)
has been shown to protect against mortality and increase mean survival of
animals exposed, for long periods of time, to high concentrations of N02
(37,600 to 62,000 ug/m3; 20 to 33 ppm)/5'16 The effects of dietary com-
ponents are discussed more fully in Section 12.2.3.2.1.
12-3
-------
12.2.3 Pulmonary Effects
12.2.3.1 Host Defense Mechanisms—In the past, environmental toxicologists
have been concerned with measurement and description of effects of single
17 18-20 21
toxic agents such as S02, N02, and °3. Considerable information
has been accumulated indicating a pathophysiological interrelationship
between exposure to atmospheric pollutants and enhanced respiratory suscep-
tibility 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 exposure studies have been undertaken using
several models.
Normally, the lungs are protected from viral and bacterial infection
by the combined activities of the mucociliary, phagocytic (alveolar macro-
phage), and immune systems. The mucociliary system, which extends from the
nares to the terminal bronchioles, removes 50 to 90 percent of deposited
?35 236
articles within hours after they enter the lung. ' It is important to
emphasize that the discontinuous nature of the mucous blanket precludes
237
complete cleansing of microbes and particles from the bronchial tree.
Surviving microbes and residual particles are phagocytized, killed, and/or
removed by nacrophages that are attracted to the foreign bodies by chemo-
tactic factors. Microorganisms, upon entrance to the lung, also stimulate
the formation of various humoral defense mechanisms. Interference, by N02,
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.
12.2.3.1.1 Interaction with infectious agents. The effect of N02 on the
susceptibility to airborne infection has been studied extensively and
12-4
-------
reviewed by Ehrlich, ° Coffin et al.20 and Gardner and Graham24 using the
infectivity model. The infectivity model system has been employed success-
fully with hamsters,22 mice,17"21 and squirrel monkeys.23 Animals are
randomly selected for exposure to either a test substance in air (in this
case NOg) or filtered air. After exposure, control and exposed animals are
placed in another chamber and exposed for a brief period (approximately 15
linutes) to aerosols of a specific infectious agent, such as Streptoccoccus
pyogenes (S. pyogenes), Klebsiella pneumom'ae (K._ pneumoniae), Diploccoccus
pneumom'ae (DL. pneumom'ae), influenza A2/Taiwan virus, or A/PR/8 virus.
The animals are then returned to clean air for a 15-day holding period and
the mortality rates in the Nt^-exposed and control groups are compared.
Theaortality of the control group is usually 15 to 20 percent. Death is
due to pneumonia and its consequences. The investigators tested the
relationships of concentration and time to susceptibility to respiratory
infection and to subsequent mortality in infections with £. pyogenes. They
3
varied the concentrations of N02 from 1 to 14 ppm (1,880 to 26,320 ug/m )
and the duration of exposure from 0.5 to 7 hours so that the product of
concentration and time equalled a value of 7. Exposure to high concen-
trations 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 N02. This indicated that susceptibility to infection was influ-
26 209 210
enced lore by concentration of NO2 than by duration of exposure. ' *
As depicted in Figure 12-1, Gardner et al., using the same model,
examined the effect of varying durations of continuous exposure on the
•ortality of mice exposed to .6 constant concentrations of N02
12-5
-------
3 3
[940 yg/m to 52,670 yg/m (0.5 to 28 ppm)]. A linear dose-response
(p < 0.05) indicated that mortality increases with time at a
given concentration of N0«. Mortality also increased with increasing
concentration of N0«. When C x T was held constant, the relationship
between concentration and time produced significantly different mortality
responses. At a constant C x T of approximately 28 (ppm x hour), an
18-hour exposure at 2,800 ug/m (1.5 ppm) N02 increased mortality by 25
percent whereas a 2-hour exposure at 27,300 ug/ra (14.5 ppm) N02 enhanced
Mortality by 65 percent. These studies confirmed the previous conclusion
that concentration is more important than time in determining the degree of
injury induced by N02 in this model.
27
Gardner et al. also compared the effect-of continuous versus inter-
mittent exposure to N02 followed by bacterial challenge with S. pyogenes
(Figures 12-2, 12-3). Mice were exposed either continuously or intermitt-
ently (7 hours/day, 7 days/week) to 2,800 ug/m or 6,600 ug/m (1.5 or 3.5
ppm) N0«. Figure 12-2 illustrates the results of continuous and inter-
m'ttent exposure to 6,600 ug/ra (3.5 ppm) N02 for periods up to 15
days. There was a significant increase in mortality for each of the exper-
imental groups with increasing duration. 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 or intermittent exposure
of mice to 2,800 ug/m (1.5 ppm) N02 increased mortality. During the first
week of exposure, the mortality was significantly higher in mice exposed
continuously to N02 than those exposed intermittently. By the 14th day
of exposure, the difference between intermittent and continuous exposure
became indistinguishable (Figure 12-3).
12-6
-------
IN3
—I
I
Q 3
H JS
J O
2 u
tj I
P« 0
O O
X 2
CO
M
Pi
90
80
70
60
50
40
30
20
10
0
-10
I III I III
Mill II III III
3.5 ppm —
28 ppm
5 ppm
0.5 ppm
I III I I I I I I I I I I II I I I I I I
15 253035 1
minutes—
2357 14 24 48 96 7 1416 30 2 3 6 912
I— I I
"9 days,' ^M months H
TIME (Io910 scale)
Figure 12-1. Regression lines of percent mortality of mice versus length of continuous
exposure to various N02 concentrations prior to challenge with streptococci
-------
ro
i
CO
m
po
o
m
80
70
60
50
40
30
20
10
0
I H H H II M II II II II II II II II ||
O CONTINUOUS
D INTERMITTENT
0-
a
ha
o
2%%%%5%^^ N0 EXPOSURI
^^^^^^^^kiii^2^^2Z^
K A ^INTERMITTENT NC*f EXPOSUN
1 1 1 1
07 31 55 ™ 103 127 151 175 199 223 247 271 295 319 343
TIME, hours
Figure 12-2. Percent mortality of mice versus the length of either continuous or
intermittent exposure to 6,600 ug/m3 (3.5 ppm) NO., prior to challenge
with streptococci 26.209,210
-------
ro
i
8
40
30
20
10
U 0
§
O* CONTINUOUS
O
a
]
0*
D
0*
0*
D INTERMITTENT
* CONTINUOUS AND INTERMITTENT
TREATMENT MEANS ARE
SIGNIFICANTLY DIFFERENT AT
p < 0.05
ENTEPMITTENT NOJ EXPOSURE^
JgL
0 7 79 151 319
TIME, hours
Figure 12-3. Percent mortality of mice versus length of either continuous or
intermittent exposure to 2,800 pg/m (1.5 ppm) N0_ prior to
challenge with streptococci26'209'210
487
-------
When mice were exposed continuously or intermittently (6 or 18 hours
per day) to 940 ug/ra (0.5 ppra) N0« for up to 12 months, neither exposure
regimen affected murine resistance to K. pneumom'ae infection during the
first month.28 After 6 months, however, mice exposed intermittently to N02
showed decreased resistance to the infectious agent. Those exposed con-
tinuously exhibited increased mortality after 90 days. Therefore, while it
is not possible to directly compare the results of studies using S. pyogenes
to those using J(. pneumom'ae, the data suggest that as exposure to NCL is de-
creased, a longer exposure is necessary for the intermittent exposure regimen
to produce the level of effect equivalent to continuous exposure.
Mice, hamsters, and monkeys have been exposed to N02 for 2 hours
followed by a challenge of K. pneumom'ae. Nitrogen dioxide enhanced the
23
mortality due to the pathogen in all species tested. Differing sensi-
tivities among species were found for both NO? and the pathogen tested.
In squirrel monkeys which were tested with a small sample size, 94,050
ug/m (50 ppm) N02 was required to produce a significant increase in mor-
tality due to NO-. The hamster model, which exhibited enhanced mortality
due to N02 at > 65,830 ug/ra (35 ppm), had intermediate sensitivity. The
mouse model was sensitive to N02 exposure as evidenced by the enhanced
mortality following exposure to 6,580 ug/m (3.5 ppm) N0~ for 2 hours. No
effect on mortality, however, was observed in mice exposed to 4,700 yg/m3 (2.5
28
ppm). However, when S^ pyooenes was the infectious agent, a 3-hour exposure
to 3,760 yg/m (2.0 ppm) N02 caused an increase (p<0.05) in mortality.29
18
The persistence of the N02 effect was investigated by Purvis et al.
who exposed mice for 2 hours to N02 before or after an aerosol challenge
with K. pneumoniae. At 9,400, 18,800, 28,200 and 47,000 ug/m3 (5, 10, 15,
12-10
-------
or 25 ppm) NOg there was a significant enhancement of mortality in mice
challenged with bacteria 1 and 6 hours after the N02 exposure. When bac-
terial challenge was delayed for 27 hours, there was an effect only in the
group exposed to 28,700 ug/m (15 ppra). Exposure to 4,700 ug/m3 (2.5 ppm)
caused no effect at any of the bacterial challenge times tested. Exposure
of 47,000 ug/m (25 ppm) N02 for 2 hours with subsequent K. pneumoniae
challenge 6 and 14 days later did not affect mortality. When the experi-
mental regimen was reversed and mice were exposed for 2 hours to 47,000
ug/B (25 ppm) NO,,, mortality was significantly increased 1, 6, 27,
48 and 72 hours after bacterial challenoe. Dose response studies in which mice
were challenged 1 hour after a 2 hour N02 exposure showed that 6,580 ug/m
(3.5 ppm) had a significant effect; exposure concentrations of 2,820 and
4,700 ug/m (1.5 and 2.5 ppm) did not.
Environmental stress has been shown to enhance the toxic effect of
NO*. Mice placed on continuously moving exercise wheels during exposure to
1,880 ug/ra (1.0 ppm), 3,760 ug/m (2.0 ppm), or 5,600 ug/m (3.0 ppm) N02
for 3 hours showed enhanced mortality (p < 0.05) using the infectivity
nodel. The presence of other environmental factors, ozone (0,) or
tobacco smoke, also augments the deleterious effect of N02 on host resis-
tance to experimental infection (see Section 12.3).
Squirrel monkeys, exposed continuously to N02 levels of 18,800 ug/m
and 9,400 ug/m (10 ppm and 5.0 ppm) in air for 1 and 2 months, respec-
tively, showed increased susceptibility to a challenge with K. pneumoniae
23
and influenza A/PR/8 virus and reduced lung clearance of viable bacteria.
All animals exposed to 19,000 ug/ra3 (10 ppm) died within 2 to 3 days of
infection with the influenza virus. At 9,400 ug/m3 (5.0 ppm), one of three
12-11
-------
monkeys died. Susceptibility to viral infection also was enhanced when the
NO* exposure occurred 24 hours after infectious challenge. Exposure to
94,000 ug/m (50 ppm) NO- for 2 hours was not fatal, whereas the same
exposure followed by challenge with K. pneumom'ae was fatal to three out of
32
three monkeys. After challenge with K. pneumom'ae, two of seven monkeys
exposed to 9,400 ug/m (5.0 ppm) for 2 months died and the rest had bac-
teria in the lungs on autopsy. After an exposure to 19,000 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) N02 followed by challenge with A/PR/8 influenza virus demonstrate
33
significant pulmonary pathological responses. Motoraiya reported a
greater incidence of adenomatous proliferation of bronchial epithelial
cells following both exposures. Viral exposures or N02 alone caused less
severe alterations. Continuous NO- exposure for an additional 3 months did
not enhance further the effect of N02 or the subsequent virus challenge.
34
Ito challenged mice with influenza A/PR/8 virus after continuous
exposure to 940 to 1,880 ug/m (0.5 to 1.0 ppm) N02 for 39 days and to
18,800 ug/w (10 ppm) N02 for 2 hours daily for 1, 3, and 5 days. Acute
and intermittent exposure to 18,800 .ug/m (10 ppm) N02 increased the
susceptibility of mice to influenza virus as demonstrated by increased
33
mortality. Motomiya also observed increased proliferation of the bron-
chial and bronchiolar epithelium with advanced interstitial pneumonia
3
following continuous exposure for 3 and 6 months to 560 to 940 ug/m (0.3
to 0.5 ppm) N02.
12-12
-------
The enhancement in mortality following exposure to N02 and a patho-
genic organism could be due to several factors. One could be a decreased
ability of the lung to kill bacteria. Studies by Goldstein et al.35'36
illustrated this concept in a series of experiments which show decreased
bactericidal activity following exposure to various pollutants. In the
first experiments, mice breathed aerosols of Staphylococcus aureus (S.
aureus) labelled with radioactive phosphorus (32P) and were then exposed to
35
N02 for 4 hours. Physical removal of the bacteria was not affected by
N02 concentrations of 3,570 and 7,140 ug/m3 (1.9 and 3.8 ppm). Concen-
trations of 13,200, 17,200, and 27,800 ug/m3 (7.0, 9.2, and 14.8 ppm) N02
lowered bactericidal activity by 7, 14, and 50 percent, respectively, when
compared to controls (p < 0.05). In another experiment, mice breathed N02
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/m3 (2.3 and 6.6 ppm) N02
decreased pulmonary bactericidal activity by 6 and 35 percent, respectively,
compared to control values (p < 0.05). Exposure to 1,880 ug/m3 (1.0 ppm)
N02 had no effect. Goldstein et al. hypothesized that the decreased bacter-
icidal 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 12.2.3.1.3.
12.2.3.1.2 Mucoci1iary transport. -Mucociliary transport is the principal
mechanism for removal of inspired and aspirated particles from the tracheo-
3
bronchial tree. Concentrations of N02 greater than 9,400 ug/m (5.0 ppm)
38
decrease rates of ciliary beating, as measured ir\ vitro, and i_n vivo
12-13
-------
measurements of raucociliary transport. The effect of lower concentra-
tions of N02 on mucociliary function is unknown.
Schiff^ exposed hamster trachea! ring cultures to 3,760 ug/m (2.0
ppm) N02 for 1.5 hours/day, 5 days/week, for 1, 2, and 3 weeks. Tracheal
cultures infected with the virus immediately after the initiation of the
N02 exposure were not different from control infected cultures. However,
when the explants were infected after 1 or 2 weeks of NO* exposure, there
was decreased ciliary activity and morphological changes compared to con-
trols held in filtered air. After 14 days exposure to N02 there was a
decrease in ciliary activity and morphological changes in non-infected
cultures. 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.
12.2.3.1.3 Alveolar macrophage. Exposures of animals to N02 concen-
trations ranging from 13,160 to 112,800 ug/m (7.0 to 60 ppm) causes a
variety of structural and physiological abnormalities in alveolar macro-
phages. Alveolar macrophages (AM) isolated from animals exposed to high
41
concentrations of N02 show diminished phagocytic activity, appearance of
A O
intracellular deuse bodies, increased congregation of AM on epithelial
cells,43 enhanced wheat germ lipase-induced binding of autologous and
heterologous red blood cells to AM, increased j_n vitro penetration of AM
by virus, reduced iji vitro production of interferon, and increased
48 49
mitochondria! and decreased cytoplasmic NAD+/NADH ratios. * Increased
proportion of polymorphonuclear leukocytes was observed in lung lavages of
41
animals exposed to high levels of N02.
12-14
-------
40
Aranyi et al. used scanning electron microscopy (SEM) to study the
effect of exposure to N02 on the anatomic integrity of mouse alveolar
lacrophages which were lavaged from the lung. No changes in the AM surface
wre observed after continuous exposure of mice for 4, 12, and 24 weeks to
940ug/ra3 (0.5 ppm) or 1,880 ug/m3 (1.0 ppm) N02 with 3-hour peaks at 1,880
pg/B (1.0 ppm) for 5 days/week. Macrophages from mice continuously
3 3
exposed to 3,760 ug/m (2.0 ppm) or 940 ug/m (0.5 ppm) N02, with 1-hour
peaks of 3,760 ug/m (2.0 ppm) N02 for 5 days/week, showed distinctive
•orpnological 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 indicative of cell death were observed also at the same
NO. concentrations after continuous exposure for 28 or 33 weeks. These
observations appear to correlate well with a reduction in iji vitro phago-
cytic activity and increased susceptibility to infection.
47
Acton and Myrvik administered an intratracheal injection of parain-
fluenza-3 virus to rabbits prior to 3-hour exposures to 9,400, 28,200,
3
47,000, or 94,000 ug/m (5.0, 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
bad increased resistance (75 percent) to pox virus. However, there was
partial loss of resistance 48 hours following exposures to 28,200 ug/m (15
ppn) N02. No decrease in resistance was observed with 9,400 ug/m (5.0
ppn) N02. Phagocytic capabilities were adversely affected in macrophages
from animals exposed to 28,200 to 94,000 ug/m3 (15 to 50 ppm) N02. At a
concentration of 94,000 pg/m3 (50 ppm), N02 stimulated oxygen uptake and
hexose monophosphate shunt activity in the AM.
12-15
-------
Nitrogen dioxide induced alteration of receptor sites of the alveolar
2T2
nacrophages have been studied by Goldstein et al. It was found that
in vitro exposure of rat alveolar macrophages to 4,512 ug/ra (2.4 ppm) N00
~ ~ — ~"~— ^™*
-------
formate to C02 by approximately 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 N02 alone did not inhibit its
activity.
12.2.3.1.4 Immune system. The effects of exposures of animals to N02 on a
few parameters of the immune response have been investigated by a small
number of workers. It should be emphasized that local responses
within the lung are critical in regard to antimicrobial defense and that
these responses are, for the most part, unstudied. Ehrlich et al.
exposed male SPF Swiss albino mice continuously to 3,760 ug/m (2.0 ppm) or
940 ug/ra (0.5 ppm) N02 with daily 1-hour peaks of 3,760 \iq/m (2.0 ppm)
for 5 days/week for 3 months. After exposure, all mice were vaccinated
with influenza bJ Taiwan/1/64. A four-fold lower mean serum neutralizing
antibody titer occurred with N02 exposure (p < 0.05) than with controls.
Control mice breathing filtered air also showed a depressed serum neutral-
izing antibody titer 2 weeks after vaccination (p < 0.05). However, there
were no differences 4 to 8 weeks after vaccination between controls and
treated. The hemagglutination inhibition titer was not affected. Non-
vaccinated mice exposed to either N02 regimen had decreased serum IgA and
increased serum IgG, (p < 0.05). Mice breathing 940 ug/m (0.5 ppm) N02
with peaks of 3,760 ug/m (2.0 ppm) also had increases in IgM and IgG2
(p < 0.05). A different picture was seen after the mice received the virus.
Serum IgA increased only (p < 0.05) when mice were held in filtered air,
vaccinated and exposed to 940 or 3,760 ug/m (0.5 or 2.0 ppm) N02. Immuno-
globulin M (IgM) concentrations were elevated in all N02-exposed groups. A
significant increase (p < 0.05) took place in only the following groups:
12-17
-------
(a) continuous exposure to 940 or 3,760 ug/ra3 (0.5 or 2.0 ppra), (b) contin-
uous exposure to 940 or 3,760 ug/m3 (0.5 or 2.0 ppm) or to 3,760 ug/m3 (2.0
ppra), pre- vaccination and clean air afterwards, and (c) 3 months filtered
air and 3,760 ug/ra (2.0 ppm) N02 post- vaccination. Similar results were
observed for IgG2 and IgG, determinations.
The immune system of monkeys exposed to N02 was studied in an addi-
tional series of experiments. Renters et al. injected mouse-adapted
influenza A/PR/8/34 intratracheally 24 hours prior to continuous exposure
to 9,400 ug/m (5.0 ppm) N0«. Hemaggluti nation inhibition titers to influ-
enza titers were not changed. Initially serum neutralization titers were
depressed by NO-. By 133 days the effect had disappeared. The amnestic
response was not affected.
53
Renters et al. described the effects of continuous exposures of
1,880 ug/m (1.0 ppm) N0~ for 493 days on monkeys challenged five times via
intratracheal injection to live monkey-adapted influenza virus A/PR/8/34
during NO- exposure. Again, hemaggluti nation inhibition titers were not
significantly affected by N02 exposures. However, the mean serum neutral-
izing antibody titers were significantly higher in animals exposed to N02
for 93 days. Twenty-one days post- vaccination, animal titers were increased
2-fold over controls. Forty-one days post-challenge, N02-treated animals
exhibited an 11-fold enhancement. Even after 266 days of N02 exposure,
titers were higher when compared to controls. Again, the authors hypoth-
esized that N02 enhanced the ability of the monkey-adapted virus to become
established and multiply.
Antweiler et al.54 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/ffi3 (5.3 ppm) N0>
12-18
-------
On the basis of experiments in which the continuous exposure of guinea
3
pigs to 1,880 ug/m (1.0 ppm) NCL for 6 months resulted in an increased
incidence of infection, particularly within the lung, Kosmider and colleagues
postulated an adverse effect of N0« on immune function. These investi-
gators also claimed that NO* causes decreases in complement concentrations
when measured by a hemolysis assay; reductions in all immunoglobulin
fractions, when tested by immunoelectrophoresis and mortality, was increased
3
in mice exposed to 1,880 ug/m (1.0 ppm) of N02 when infected intranasally
with 0. pneumom'ae. Because of the importance of these observations, they
require confirmation.
Balchum et al. exposed guinea pigs to 9,400 ug/m (5.0 ppm) N02 for
4 hours/day, 5 days/week and to 9,400 ug/m3 (5.0 ppm) N02 or to 28,200
M9/m3 (15 ppm) N02 for 7-1/2 hours/day, 5 days/week. There was a notice-
able increase in the titer of serum antibodies against lung tissue in all
3 3
guinea pigs exposed to 9,400 ug/m (5.0 ppm) or 28,200 ug/m (15 ppm) N02
as early as 160 hours after N02 inhalation. The antibody titers increased
with the intensity and duration of exposure to N02.
12.2.3.2 Lung biochemistry—
12.2.3.2.1 Introduction. Nitrogen dioxide-related studies of lung biochemistry
have been directed to either an investigation of the mechanism of toxic
action of N02 or to the detection of indicators of early damage by N02
exposure. Two theories of action of N02 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 N02 inhalation. The second theory is that N02
oxidizes low molecular weight reducing substances and proteins. This
oxidation results in a metabolic dysfunction which evidences itself as the
12-19
-------
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 N02 intoxication have
been proposed. The effects of NO* exposure on lung biochemistry will be
discussed in this context.
12.2.3.2.2 Lipid and diet effects. The dietary background of animals
affects their response to all types of toxicants. For the most part, diet
effects concerning N02 have been neglected and are unreported in the liter-
ature. 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 N02 exposure. Roehm et al. studied
the jn vitro oxidation of unsaturated fatty acids by 0^ and N02. A common
mechanism of action was suggested for these two oxidizing air pollutants.
Both NO- and 0~ initiated the oxidation of unsaturated fatty acids through
free radicals. Typically, an induction period was noted with either anhy-
drous thin films or aqueous emulsions of linolenic acid exposed to 2,800
ug/m (1.5 ppm) N02. The addition of free radical scavenging agents such
as vitamin E, butylated hydroxytoluene (BHT), or butylated hydroxyanisol
(BHA) delayed the onset of oxidation iji vitro. The rate of oxidation of
linolenic acid in thin films was proportional to concentrations of N02
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 conver-
sion to polar nitrogen-containing compounds and to peroxides. A proposed
mechanism of formation of these products is as follows:
12-20
-------
00.
C=C + NO, -»• -C-C-NO, ->* -C -C-NO,
^ i i Z i i Z
00* OOH
-C -C-NO- + RH •» -C -C-NO + R.
R* + 02 -»• ROO* + ROOM
Products produced from the oxidation of unsaturated fatty acids by N02 are
nitrohydroperoxides and fatty acid hydroperoxides. Phenolic antioxidants
prevent the autoxidation of unsaturated fatty acids by N0« 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 t i i <-
ROO- + AOH * ROOH + AO'
where AOH represents a phenolic antioxidant.
Rats evidenced increased mortality ' and decreased content of un-
16 62
saturated fatty acids in lung lavage fluid ' when exposed to N02
concentrations ranging from 18,800 to 62,000 vg/m (10 to 33 ppm).
The severity of these effects was reduced for those animals whose diets
which were not Vitamin E depleted.
Arner and Rhoades63 exposed rats to 5,450 ug/m3 (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
12-21
-------
in lung wet weight was the same as the increase in lung water content. The
lipid content of the lung was depressed by 8.7 percent, and both of these
effects were found to be statistically significant (p < 0.05). An analysis
of the lungs showed that a decrease occurred in the total saturated fatty
acid content. Unfortunately, values for unsaturated fatty acids of biolog-
ical importance such as the essential fatty acid arachidonic acid were
not reported. The surface tension of extracts of the lung increased,
and the author suggests that the increased surface tension corresponded to
a decrease in the lunq surfactant concentration.
64 3 3
Trzeciak et al. exposed guinea pigs to 940 ug/m (0.5 ppm), 94 pg/m
(0.05 ppm), or these same N02 concentrations plus an equal amount of ammonia,
for 8 hours per 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 phosphatidic acid. Increases were noted in the
lysophosphatidyl ethanolamine content, while the phosphatidyl choline (lecithin)
content remained constant or was slightly depressed. Such changes could be
indicative of change in cell type or cell function.
Lecithin synthesis appeared to be depressed in the lungs of rabbits
3 65
exposed to 1,880 yg/m (1.0 ppm) N02 for 2 weeks. The most marked effect
was observed after 1 week of exposure and appeared to decline in effect
after the second week of exposure.
Csallany exposed mice continuously for 1.5 years to 750 to 940 pg/m
(0.4 to 0.5 ppm) or 1,790 to 1,880 ug/ra3 (0.95 to 1.0 ppm) N02 and fed the
animals a basal diet which was either deficient or supplemented with vitamin
12-22
-------
E at 30 or 300 mg/kg of diet. The author indicated that N02 reduced the
growth rate in all four diet groups, but the vitamin E-supplemented 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 vitamin E in the diet. Ayaz and Csallany, in another
study, exposed female weanling mice to 940 or 1,880 ug/m (0.5 or 1.0 ppm)
NO- continuously for 17 months. Animals were divided into three groups
receiving the basal diet with either a normal supplement of vitamin E (30
ng/kg) or 300 mg/kg and a third group supplemented with the synthetic
antioxidant N.N'-diphenylphenylenediamine (DPPD) at 30 mg/kg. After 17
•onths of exposure, the presence of lipofuscin pigment in the liver, lungs,
spleen, heart, brain, kidney, and uterus was determined. While no effect
could be ascribed to N02 exposure, vitamin E supplementation decreased the
concentration of lipofuscin 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) NOg,
5 hours/once a week for 4 weeks caused lung damage as compared to NO^-
91 T
exposed, non-vitamin A deficient hamsters.
12.2.3.2.3 Sulfhydryl compounds and pyridine nucleotides. Oxidation of
sulfhydryl compounds and pyridine nucleotides in the lung is well-established
68
for 0, exposures, but little evidence has been reported for NOg .
In experiments involving exposure of mice to very high (>143,000
|ig/in3; 76 ppm) concentrations of N02, several investigators reported that a
wide variety of sulfur-containing compounds reduced the toxicity of N02.
For example when mice were first exposed to benzenethiol (14 ppm). for 24 to
12-23
-------
72 hours prior to N02 exposure only 1/20 died whereas 10/20 of the N02-
exposed mice not pretreated with benzenethiol died. Inferences drawn from
the protective effect of these compounds suggest that sulfhydryl compounds
within the lung were being oxidized to disulfides. Included among the
compounds observed to exert a protective effect are (1) hydrogen sulfide
(H-S), (2) benzenethiol, (3) d,a-napthylurea, (4) phenylthiourea, and (5) a*
number of thyroid-blocking agents.
73 3
Ospital et al. reported that exposure to 9,400 ug/m (5.0 ppm) N02
for 8 hours altered the glucose metabolism of slices made from the lungs of
exposed rats. Glucose utilization and lactate production were increased by
28- and 43 percent, respectively, while pyruvate production rose by 6
percent. Exposure of rats to 9,400 ug/m (5.0 ppm) N02 for 1, 2, and 4
days produced similar alterations, but individual values were not reported.
Neither increased hexose monophosphate shunt nor citric acid (Krebs) cycle
activity could account for the increased glucose utilization. The authors
concluded that N02 exposure increased the activity of the glycolytic path-
way and suggested that this increase may be related to an increased bio-
synthesis due to injury.
12.2.3.2.4 Effects on lung amino acids, proteins, and enzymes. High
concentrations of N02 produce lung edema with concomitant infiltration of
serum protein and enzymes. Alterations in the cell types of the lung also
occur (see Section 12.2.3.3). Thus, some reports of changes in lung enzymes
and proteins may reflect either edema or altered cell populations rather
than direct effects of N02 on lung enzymes.
Sherwin et al.74 exposed guinea pigs to 3,760 ug/m3 (2.0 ppm) N02 for
3 weeks. They examined lung sections histochemically for lactic acid
dehydrogenase (LDH). LDH is primarily an indicator of Type II pneumocytes
12-24
-------
rather than Type I. The number of Type II pneumocytes per alveolus was
deterained. 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 pneunocytes per alveolus
Mas found in the lower lobes. Exposure to N02 increased the LDH content of
the lung by increasing the number of Type II cells per alveolus (p < 0.05)
over a 3-week exposure period. The authors then contended that the increase
in lung LDH content was due to the replacement of Type I pneumocytes by
Type II pneumocytes as suggested from morphological studies (see Section
12.2.3.3).
Several other biochemical indicators of lung damage have been studied.
Sherwin et al. exposed guinea pigs to 750 ug/m (0.4 ppm) NCL for 4
hours/day for 7 days and found an increase in acid phosphatase activity (p
78
<0.05). An increased aldolase activity was reported by Kosmider et al.
in the blood, liver, and brain of NOp-exposed guinea pips, but was statistically
significant only in liver samples. Values for the lung and exposure levels
wre not reported.
The effect of NO. on the important enzyme benzpyrene hydroxylase was
79
studied by Palmer et al. Since lung cancer in man is predominantly of
bronchial rather than parenchyroal 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 (5.0, 20, or 50 ppm) N02 for
I hours. No effect was observed on the benzpyrene hydroxylase activities
inN02 exposure, but 03 exposure of 1,400 to 19,600 ug/m (0.75 to 10 ppm)
•arkedly decreased benzpyrene hydroxylase activity in a dose-related manner.
lw et al. studied the effect of N02 on the benzpyrene hydroxylase,
•icrosomal 0-methyl transferase, catechol 0-methyl transferase, and the
12-25
-------
supernatant catechol 0-methyl transferase activity of the lung. While
benzpyrene hydroxylase activity of the lung could be induced by treatment
with the carcinogen, 3-methylcholanthrene, exposure to 75,200 or 132,000
ug/ra (40 or 70 ppm) N02 for 2 hours had no effect. Thus, the studies of
Palmer et al. and Law et al. are in agreement that N02 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 meta-
bolize the important catecholamine hormones. This metabolism does not
appear to be affected by N02 treatment.
82 83
Donovan et al. and Menzel et al. exposed guinea pigs continuously
to 940 ug/m (0.5 ppm) N02 for 4 months. After an initial exposure of 7
days, serum LDH, total creatine phosphokinase (CPK), glutamic-oxalacetic
transaminase (SGOT), and glutamic-pyruvic transaminase (SGPT) were ele-
vated. Lung 6SH peroxidase and acid phosphatase were not affected. In con-
81
trast to the findings of Chow et al., lunp 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 statis-
tically significant (p < 0.05) while the elevations in LDH, SGOT, 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.
86
Bils reported a thickening of the collagen fibrils in squirrel monkeys
exposed to 5,640 ug/m (3.0 ppm) NO* for 4 hours/day for 4 days. Kosmider
et al. reported that the urinary hydroxyproline and acid mucopolysac-
2
charide content of guinea pigs exposed to 1,880 ug/m (1.0 ppm) N0« for 6
months was increased (p < 0.05). Presumably these increases represented
88
degradation of collagen. Hacker et al. measured the incorporation of
12-26
-------
C-proline into soluble and insoluble collagen fractions in the lungs of
rats exposed to 9,400 ug/m (5.0 ppm) N02 for 12 hours. Incorporation of
14
C-proline into insoluble collagen was 58 percent greater in the N0«-
exposed animals than in air-exposed control groups, supporting the bio-
chemical evidence for greater collagen turnover in NOg-exposed animals.
Enzymes observed to have increased activity following exposure to high
concentrations of NOg included aldolase (in vitro) * and serum antiprotease (in
vivo). Plasma lysozyme activity was reported to be unaffected (in vivo).81
12.2.3.2.5 Poteotial defense mechanisms. Menzel61'89 proposed that
antioxidants might protect the lung from damage by N0« by inhibiting lipid
peroxidation. Data related to this hypothesis have been reported.15'16'62'66'67
90
Chow and Tapper proposed an enzymatic mechanism for the protection of the
lung against lipid peroxidation damage by ozone. They proposed the following
scheme:
p-oxidation
t
ROH v , GSH y * NADP t / Glucose-6-P04
GSH Reductase JIG-6-P Dehydrogenase
RH +* ROOH /* GSSG /x NADPH <* * 6-Phosphogluconate
where R- is an aliphatic organic radical
Chow et al.81 exposed rats to 1,880, 4,330, or 11,560 ug/m3 (1.0, 2.3, or
6.2 ppm) N02 continuously for 4 days to determine the effect on the glu-
tathione peroxidase system. They determined the activity of GSH reductase,
glucose-6-phosphate dehydrogenase, and GSH peroxidase in the soluble fraction
12-27
-------
of exposed rat lungs. Linear regression analysis of the correlation
between the NO- concentration and enzymatic activity was found to have a
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 peroxldase activity and the NO- exposure concen-
tration.
82 83
Donovan et al. and Menzel et al. exposed guinea pigs continuously
to 940 ug/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) GSM
peroxldase levels were determined. Short-term exposure to NO- depressed
RBC GSH peroxldase but did not affect lung levels. Long-term exposure, on
the other hand, affected neither lung nor RBC GSH peroxldase. These
studies confirm the results In rats and Indicate a distinct difference In
the effect of N02 and 03 on the lung.
Since protection against NO- occurs with vitamin E, lipid peroxidatlon
most likely occurs, but the GSH peroxldase defense system does not appear
to be Induced. Chow et al.81 concluded: "Since exposure of rats to N02
has insignificant effect on lung GSH peroxldase activity, but had signifi-
cantly 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." Dietary vitamin E remains the only proven natural
defense mechanism against NO-.
12-28
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12.2.3.3 Morphology Studies—Nitrogen dioxide produced morphological
alterations starting in the terminal airways and adjacent alveoli. A
comprehensive summary review has been prepared by Coffin and Stokinger.5
The events leading to emphysema from N02 exposure of the rat have been
described by Freeman and co-workers.68'98~107'214»215 The earliest alter-
ations resuiting from exposures to concentrations above 22,600 yg/m3 (12 ppm)
were seen within 24 hours of continuous exposure. These alterations included
increased macrophage aggregation, desquamation of the Type I pneumocytes and
ciliated bronchiolar cells, and accumulation of fibrin in the small airways.
The cuboidal Type II pneumocytes slowly differentiate into the squamous Type I
cells as replacements and alter the appearance of the parenchyma into a "gland-
like" tissue in the region of the ducts. Incorporation of H-thymidine 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-
102
exposure levels by 6 days, despite persistent exposure. This pattern of in-
corporation of H-thymidine, indicative of cell replication, was documented at
3,760 ug/m3 (Z.O^pm) N02 as well as at 32,000 M9/m3 (17 ppm).103 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 noncili-
232
ated (Clara) cells and the exfoliation of ciliated cells. Later, aberra-
tions in ciliogenesis occur and cilia often appear within vacuoles surrounded
by cytoplasm.
Age is a factor in determining the response of the lungs to NO*.
Newborn rats up to the age of about 3 weeks are relatively resistant to
high subacute concentrations (about 28,000 ug/m3; 15 ppm) compared to more mature
233
animals. On the contrary, old rats about 2 years of age or more have a
12-29
-------
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.
108
Buell reported the isolation of swollen, damaged, insoluble collagen
fibers from the lungs of rabbits exposed to 470 ug/m3 (0.25 ppm) for 4
hours/day, 5 days/week for 24 to 36 days. Modifications of collagenous
tissue are evident early and late and may be reflected in the increased
excretion of collagen degradation products in the urine.
While hyperplasia of the terminal bronchiolar and alveolar epithelium
is reversible on discontinuation of exposure to 28,200 ug/m3 (15 ppm), the
interstitial structural alterations of alveoli are not.234 Bronchiolar
epithelial alterations are observed during lifetime exposure to 3,760 ug/m3
93 96
(2.0 ppm). ' Similar changes in rats without enlargement of lungs have
been seen after a lifetime exposure to 1,500 ug/m (0.8 ppra) N02.96
Embryonic and adult hamster tracheal cells were exposed as cultures to
3
1,880 ug/or (1.0 ppm) N02 for 6 hours. Cells so treated lost their
ability to grow and form colonies. Hamster lung fibroblasts (V-79), when
3
exposed to 216 yg/m (0.12 ppm) NO,, for periods up to 6 hours, also failed
to divide and form colonies.
109
Blair et al. studied the temporal alterations of lung morphology in
nice exposed to 940 ug/m (0.5 ppm) N02 for 6, 18, and 24 hours per day,
microscopically. Exposed mice were found to have expanded alveoli after 3
to 12 months of exposure. However, interstitial pneumonia may have con-
fused the interpretation. Continuous exposures of mice to 940 to 1,500
3
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,
12-30
-------
edema In alveolar epithelial cells, loss of cilia, and an influx of
.onocytes.110'111
113
Furiosi et al. investigated the.influence of a 14-month continuous
exposure to 3,800 ug/m3 (2.0 ppm) N02 and 330 ug/m3 (0.1 ppm) NaCl (0.1 to
10.3 u), alone and in combination, on monkeys (Macaca speciosa). Rats were
exposed simultaneously but received approximately 1,880 ug/m (1.0 ppm) NCL
due to differences in the exposure cages. The NaCl exposure alone caused
no effects. In monkeys, the N0~ exposure resulted in hypertrophy of the
bronchiolar epithelium, particularly in the area of the respiratory bron-
chiole which is confluent with the alveolar duct. Morphological changes
were observed also in the more proximal bronchiolar epithelium. When NaCl
was combined with NO*, there appeared to be no.influence by the NaCl.
Neither were alveolar epithelial changes noted. In rats, the results were
99
similar to an earlier study with equivocal findings, in which rats were
exposed to about 1,500 ug/m (0.8 ppm) N02 for over 2 years. In the latter
QQ
study, it was reported that animals exposed continuously up to 33 months
exhibited an essentially normal gross and microscopic appearance with
suggestive evidence of changes in the terminal bronchioles.
114 232
Recovery from exposure to N02 has been reported. ' In mice sacri-
ficed after exposure to 1,900 to 2.800 ug/m3 (1.0 to 1.5 ppm) N02 for 30
days, the morphological changes were found to be similar to those described
above.114 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.
Bils36 observed connective tissue changes in squirrel monkeys that
respired 5,640 ug/m3 (3.0 ppm) N02 for 4 hours/day for 4 days with inter-
12-31
-------
ro
CO
ro
2'
I ""I 'I I
- EXPOSURE
I I ' ' I
CHEMICAL REACTION
SUSCEPTIBIUTYTO
MICROORGANISMS
—.- CELL DEATH (max. at 24 hr.l
| -— BIOCHEMICAL INDICATORS
OF INJURY (max. at 18 br.) '~
REPLACEMENT OF DEAD
AND INJURED CELLS'
AND BIOCHEMICAL'
INDICATORS OF REPAIR
(max. at 48 hr.) '
I I . .1
(log scale) 4
10 24 (48
14
I
houn
days
30
I
2 3
months
Figure 12-4. Temporal sequence of injury and repair hypothesized
from short-term single exposures of less then 8 hours.
12
-------
(S3
CO
OJ
II I '
CHEMICAL' REACTION
CELL DEATH
PULMONARY
FUNCTION
'CHANGES
BIOCHEMICAL
INDICATOR '
OF DEATH
ANDi"
INJURY
REPLACEMENT OF DEAD
AND INJURED CELLS
AND BIOCHEMICAL'
'INDICATORS OF REPAIR
• INCREASE
SUSCEPTIBILITY TO
MICROORGANISMS
LEVATED
. CELL*
TURNOVER
INCIDENCE
OF EMPHYSEMA
-LIKE PATHOLOGY
YPOTHETICA
TOLERANCE
10
24 48
14
hour*
day*
4' 6 12 | (log scale)
months
Figure 12-5. Temporal sequence of injury and repair hypothesized
from continuous exposure to NO^ as observed in experimental
animals.
-------
ro
CO
4 24 48 7 14 30 60 (log scale)
hour* day*
TIME AFTER BEGINNING EXPOSURE
Figure 12-6. Proportionality between effect (cell death) and
concentration of NC^ during a constant exposure period.
The maximum in cell death is reached ~ 18 hours after
exposure and the extent is proportional to the dose
(concentration x time).
-------
littent 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 suggest that fenestrations are related to the
pores of Kohn. Since the frequency of such pores differs among species,
attenuation of alveolar septae and distent ion of their pores may be recog-
nized* 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
•ay be largely irreversible once the pores are enlarged. Thus, the mechan-
ists resulting in their appearance, although fe'nestration may not be promi-
nent in all species, may be a hallmark of pathogenesis.
TT2
Port et al. investigated the effects of NO^ on several species
and normal controls using light and scanning electron microscopy.
Exposure to 188 ug/m (0.1 ppm) was continuous for 6 months. Upon this
o
regimen were superimposed daily 2-hour peaks of 1,880 yg/m (1.0 ppm)
IL. Although bronchioles and alveolar ducts were not found to be remark-
ftle, occasional foci of distended alveoli were seen under the pleura.
Urge 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 N02 in some species and not in others.
12.2.3.4 Pulmonary Function—Exposures of animals to 9,400 ug/m (5.0 ppm)
»2 or lower have been reported to have produced a variety of effects on
|rtU»nary function. Elevated respiratory rates throughout the life-span of
3
rats were observed after the animals were exposed to 1,500 ug/m (0.8 ppm)
91 99
K>2 for periods up to 2.75 years. '
12-35
-------
Rats exposed to 5,400 ug/m (2.9 ppm) NOg 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. Freeman
et al., however, observed that resistance to airflow and dynamic compli-
ance were not affected when rats were exposed, for 2 years, to 3,800 ug/m
(2.0 ppn) NOg. Tachypnea (rapid breathing) was observed.
Rats and cats exhibited a tendency toward increased respiratory rates
and decreased arterialized Og partial pressure when exposed to 940 to 3,800
o 24
UO/B (0.5 to 2.0 ppn) NOg. Oxygen uptake in the blood was impaired and
125
persisted several hours after exposure was terminated.
Murphy et al. exposed guinea pigs to various concentrations of N02
between 5.2 and 13 ppm (9,776 and 24,440 ug/m3). At 5.2 ppra (9,776 ug/ra3),
there were no significant increases in respiratory rate until after 3 hours
of exposure. When guinea pigs exposed to this concentration for 4 hours
were returned to clean air, there was recovery within approximately 1 hour.
At higher concentrations, respiratory rates increased earlier. Tidal
volume also decreased during the 4-hour exposure to 5.2 ppm (9,776 ug/m ).
The net effect was to maintain minute ventilation at a nearly constant
level. No significant alterations in respiratory function in rabbits were
observed when animals were exposed to 9,400 ug/m (5.0 ppm) NOg for 6
hours/day over a period of 18 months.
23
: Henry et al. exposed male squirrel monkeys continuously to 18,800
and 9,400 ug/m (10 and 5.0 ppm) NOg for 1 and 2 months, respectively.
Elevation in minute respiratory volume due to increased tidal volume and
respiratory rate was apparent by 2 weeks and persisted throughout exposure
to 18,800 ug/m (10 ppm) NOg. At the end of the exposure period, monkeys
12-36
-------
were challenged with K. pneumonlae: 3 days later there was a marked reduc-
tion in minute volume. Only minor changes in minute respiratory volumes
were noted in monkeys exposed to 9,400 ug/m3 (5.0 ppm) N02 for 2 months.
The tidal volumes displayed a gradual reduction during the 2 months, while
it the same time respiratory rates increased. After challenge with bac-
teria, minute volumes decreased and remained depressed.
Fenters et al. found that monkeys exposed to 1,880 ug/m3 (1.0 ppm)
NOg 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 N02
134
exposure have been examined. Monkeys continuously exposed to 9,400 and
18,800 ug/ra (5.0 and 10 ppra) N02 for 90 days were stressed at a temper-
ature of 31°C versus 24°C for controls. At the higher concentration, N02
{•paired the distribution of ventilation of the lungs, increased respira-
tory rates, and decreased tidal volumes. The addition of heat stress did
not further impair distribution of ventilation but it did decrease dynamic
conpliance of the lungs whereas N02 alone did not. No synergistic effect
was seen at N02 concentrations of 9,400 ug/m (5.0 ppm) with heat.
Freeman and Juhos exposed pregnant monkeys to N02 continuously and
raised their offspring in similar environments. Adult and juvenile monkeys
were exposed to 3,800 and 16,900 ug/m (2.0 and 9.0 ppm) N02 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.
12.2.3.5 Studies of Hyperplasia—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,,.
12-37
-------
138
The studies by Ide and Otsu revealed evidence of some tumor produc-
tion in mice exposed to 9,400 to 18,800 ng/ra (5.0 to 10 ppm) N02 after
receiving injections of 0.25 mg 4-nitroquinoline-l-oxide (a lung-tumor-
specific carcinogen). No tumors were observed in mice exposed to N02
alone. These data indicated that N02 had no synergistic or inhibitory
properties with a known carcinogen but these data are of questionable value
for predicting potential interactions with the broader classes of carcino-
gens.
139
Loosli et al. exposed specific pathogen-free mice to synthetic smog
23 to 24 hours/day for 8 to 12 months. The smog was composed of 1,500
ug/m3 (0.8 ppm) N02, 5,750 \ig/a? (5.0 ppm) CO, 760 yg/m3 (0.38 ppm) Oj, and
5,700 pg/n (2.2 ppm) SOg. The lungs of mice exposed for 20 days revealed
thickened bronchial membrane due to cell proliferation. By 60 days the
membranes were markedly thickened and appeared to have villas-like hyper-
plastic folds, whereas evidence of hyperplasia in control animals was
absent. When mice were removed from smog exposure after 4 months, the
hyperplasia regressed.
Rejthar and Rejthar exposed rats to 9,400 vg/m (5.0 ppm) N02 con-
tinuously 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 found in adjacent alveoli.
By 7 weeks, hyperplasia was apparent in all bronchioles, thus narrowing the
12-38
-------
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 inter-
cellular spaces. A return to a single layer of epithelium without cilia
was observed after 11 weeks. Seven weeks after exposure to N02, the lungs
appeared to be in a state of repair moving towards reversal of the lesions.
141 ^
Nakajima et al. A exposed mice to 940 to 1,500 ug/nr (0.5 to 0.8 ppm)
N02 for 30 days. Examination revealed hyperplasia from the terminal bron-
chiole to the alveolus. Mice exposed to the same concentrations of N02
with CO (58,000 ug/m3; 50 ppm) for 30 days revealed the same hyperplastic
foci in the terminal bronchioles. At exposure concentrations up to 115,000
3
pg/n (100 ppm) for 30 days, CO by itself failed to induce hyperplasia in
•ice.
142
Stupfel et al. 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 different concentrations of NO (0.2 and 23
• . ^\
ppaO, C02 (0.07 and 0.37 percent), along with aldehydes (0.1 and 2.0 ppm).
There were no effects observed at 0.2 ppm NO while at 23 ppm NO more
^* ^\
spontaneous tumors, cutaneous abscesses, and bilateral renal sclerosis were
observed.
12.2.3.6 Teratogenesis and Mutagenesis—There is little or no evidence in
the literature demonstrating that exposure to N02 is teratogenic or muta-
* m A A
genie in animals. Shalamberidze et al. exposed rats to 2,360 ug/m (1.3
ppo) 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.
12-39
-------
There was a statistically significant decrease in litter size and neonate
weight (p < 0.001). In utero death due to N02 exposure resulted in smaller
litter sizes, but no direct teratogenic effects were observed in the off-
spring. In fact, after several weeks, N02-exposed litters approached
weights similar to controls.,
144
Gooch et al. exposed C3H male mice to 190, 1,880, 9,400, and 18,800
3
ug/m (0.1, 1.0, 5.0, and 10 ppra) 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 N02 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.
12.2.3.7 Edemaqenesis and Tolerance—Sherwin and Carlson reported an
increase of protein in the lavage fluid from lung of guinea pigs exposed
continuously to 750 ug/ra (0.4 ppm) N02 for 1 week (p < 0.001). Proteins
were identified and measured by disc electrophoresis. No remarkable
differences were noted in the composition of the filtered proteins obtained
3 3
by pulmonary lavage. Mice injected with H-rabbit albumin accumulated H
in their lungs following exposure to 7,500 to 13,000 ug/m (4.0 to 7.0 ppm)
146
N02. 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) N02 for 5 days/week for 3
147
weeks. Greater retention of horseradish peroxidase occurred after 7
weeks of exposure.
The development of tolerance to lethal concentrations of N02 has been
correlated with lethal edema production. Wagner et al. examined the
question of tolerance along with several other characteristics. They found
12-40
-------
that tolerance could be evoked by prior exposure to low or high concen-
trations of NO*, in young and old animals. Mice were made tolerant to an
3 3
LC50 dose of 113,000 \ig/m (60 ppra) by prior exposure to 9,400 ug/m (5.0
ppro) NO* for 7 weeks. Tolerance disappeared after 3 months following
removal from the NO* exposure. Rats also were made tolerant.
12.2.4. Extrapulmonary Effects
12.2.4.1 Nitrogen dioxide-induced Changes in Hematology and Blood
Chemistry—Exposure of experimental animals and humans to NOg alone or in
combination with other pollutants produces an array of hematological pertur-
bations of questionable biological significance (see Chapter 13 for human
studies).
Shalaraberidze exposed rats continuously to 100 vg/m (0.05 ppm) NO*
for 90 days with no change in blood hemoglobin or erythrocyte levels.
A 7-day exposure to 940 pg/m (0.5 ppm) NO* resulted in a depression
in GSH peroxidase levels of RBC in guinea pigs (p < 0.001) which was not
82 83
observed after exposure for 4 months. '
78
Kosmider et al. exposed guinea pigs for 8 hours/day for 120 days to
940 ug/m3 (0.5 ppm) NO* with 1,000 ng/m3 (0.39 ppm) SO* or 940 ug/m3 (0.5
3 3
ppm) NO* with 1,000 ug/m (0.39 ppm) SO* and 70 ug/m (0.1 ppm) ammonia.
Animals exposed to NO* and SO*, with and without ammonia, displayed an
increase in white blood cells (WBC) and a decrease in RBC and hemoglobin.
Following exposure, a differential count of white cells revealed a decrease
in neutrophils and eosinophils and an increase in lymphocytes.
Mersch et al.149 exposed guinea pigs to 680 ug/m3 (0.36 ppm) N02 con-
tinuously for 1 week. Following exposure, RBC D-2,3-diphosphoglycerate was
significantly increased (p < 0.05), a measure which could reflect tissue
deoxygenation.
12-41
-------
Studies reported by Nakajima and Kusumoto showed that addition of
58,000 ug/m3 (50 ppm) CO to 940 to 1,500 pg/m3 (0.5 to 0.8 ppm) N02 did not
change the carboxy hemoglobin 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 ppra) N02 for 5 days and found that methemoglobin levels were not
affected.151
3
Metina exposed rabbits to 2,400 to 5,700 pg/m (1.3 to 3.0 ppm) HQ
o
and/or 5,240 ug/m (2.0 ppra) S02 2 hours/day for 15 and 17 weeks. Exposure
to N02 alone produced a significant rise in leukocytes followed by a decrease
in their phagocytic activity. Exposure to NO^ alone reduced the number of
RBC, while a mixture of NO^ and S02 or S02 alone had no effect.
53
Renters et al. showed that exposing male squirrel monkeys to 1,880
ug/m (l.O ppm) N02 continuously for 493 days had no significant effect on
hematocrit, hemoglobin, total protein, globulins, chloride, sodium, calcium
potassium, glucose, blood urea, nitrogen, glutamic-pyruvic transaminase,
lactate dehydrogenase , and lactate dehydrogenase isoenzymes. Challenge
with influenza A/PR/8/34 increased leukocytes in N02-exposed animals above
levels in similarly challenged controls.
Coate et al. exposed monkeys to 9,400 and 18,800 ug/m (5.0 and 10
ppm) NO - for 90 days with no direct effect on hemato logical parameters.
Monkeys and rats were exposed to 330 pg/m (0.14 ppm) Nad and 3,800 ug/m'*
(2.0 ppm) N02 for 14 months. Exposure to N02 with or without NaCl
produced polycyt hernia with reduced mean corpuscular volume and approximately
normal mean corpuscular hemoglobin concentration. In monkeys and rats
exposed to N02 with and without NaCl, the ratio of neutrophils to lympho-
cytes was greater.
12-42
-------
Block et al. conducted several hematological studies on dogs exposed
16 hours/day, 7 days/week, for 4 years to 940 ug/m3 (0.76 ppm) NO, 1,880
ug/m3 (1.0 ppm) N02> or 1,840 yg/m3 (1.5 ppm) NO plus 2,450 yq/m3 (1.3 ppm)
NO,. No changes in hematocrit, viscosity, carboxyheraoglobin, or metherao-
globin were found.
12.2.4.2 Central Nervous System and Behavioral Effects—Information
regarding the effects of N02 on the central nervous system or on animal
behavior is limited to a few studies, most of which have uncertain rela-
tionships to humans.
Tusl et al. exposed rats to 9,400 ug/m (5.0 ppra) N0« for 8 weeks.
The influence of N0« on swimming of rats was measured. By the 5th and 6th
weeks of exposure, swimming performance had decreased 25 percent. Rats
exposed to 1,880 ug/m (1.0 ppm) maintained a constant performance with a
slight tendency of performance to deteriorate.
Jakimcuk and Celikanov reported that rats exposed to 600 \ig/m
(0.32 ppm) NO- for 3 months developed a delay in their conditioned reflexes
to sound and light. Shalamberidze exposed rats to 100 ug/m (0.05 ppm)
N02 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. There was a decrease in brain
malate dehydrogenase, alanine aminotransferase, sorbitol dehydrogenase,
lactate dehydrogenase, adenosine triphosphatase, and 5'-nucleotidase.
There were increases in 1,6-diphosphofructose aldolase, isocitrate dehy-
drogenase, a-hydroxybutyrate dehydrogenase, phosphocreatine kinase, and
cholinesterase.
12.2.4.3 Biochemical Markers of Organ Effects—A major goal has been the
detection of early enzymatic markers of N00 effects. Studies of enzyme
«.
levels in different animal species indicate that the earliest enzymatic
12-43
-------
changes of nitrogen dioxide effects occur in guinea pigs. Several such marker
enzymes have been determined in blood. Release of lysozyme into the blood from
81*83
pulmonary damage was cited above. The CPK isoenzyme patterns seen in
NOg-exposed guinea pigs are difficult to differentiate from CPK patterns
82
caused by myocardial damage and are not particularly useful. Plasma
cholinesterase (CHE) was significantly (p < 0.001) elevated after a 7-day
exposure to N02 but fell on long-term exposure (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. * Increased CHE is seen with cardiac surgery but values are
159
depressed consistently with myocardial infarction. Aside from meta-
static 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
82
pig studies are related to N02"induced hepatic damage. The persistent
alteration in CHE, albeit lower activity, after 4- months exposure to 940
|jg/m (0.5 ppra) NO*, suggests an hepatic lesion.
Another study indicating hepatic damage revealed decreased plasma
levels of albumin, seromucoid, alanine and aspartate transaminases when
guinea pigs were exposed to 2,000 MS/m (1.05 ppm) N02 for 8 hours/day for
82 160
180 days. In agreement with Donovan et al., Drozdz et al. reported
decreased plasma cholinesterase levels. This group also found increased
serum levels of or,-and Bg-immunoglobins. Electron micrographs of the liver
suggested intracellular edema. Kosmider reported decreased serum
cholesterol, total lipids, and beta and gamma lipoproteins in guinea pigs
exposed to 1,000 pg/m3 N0x (mainly N02), 8 hours/day for 120 days. At the
12-44
-------
same time, there was an Increase in serum alpha (a) lipoproteins. Blood
serum sodium and magnesium were reduced while liver and brain were depleted
of magnesium and zinc as well. Cell permeabilities were changed and Ions
displaced. Edema of the liver mitochondria occurred. At the same time,
there was an increased secretion in the urine of nitrite, nitrate, and
coproporphyrin. There was a significant rise in respiratory rate with
little or no excitement or aggressiveness. Kosmider also exposed these
animals to the same schedule of NO and added ammonia. Nitrogen oxides
A
reacted with ammonia (1,000 ug/m ; 1.4 ppm) reducing the lipid and elec-
trolyte disturbances seen with NOX exposure alone. Blood serum lipids,
lipoproteins, and cholesterol were not significantly altered from those of
control guinea pigs breathing filtered clean air. There was a decrease in
the urinary excretion of nitrites, nitrates, and coproporphyrin from N0y-
ammonia treated animals. Blood serum sodium and potassium were lowered
while magnesium and calcium were higher than controls. No effect on serum
calcium levels was seen with NOX alone. Liver mitochondria contracted, in
contrast to the edematous state seen in NO -exposed groups. Earlier,
^\
74
Kosmider et al. 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 (1.0 ppm) N02 for 6 months.
An Interesting observation of proteinuria in the guinea pig was reported
by Sherwin and Layfield, who found consistently higher levels of urinary
protein (p < 0.01) in animals breathing 940 ug/m (0.5 ppm) NOg contin-
uously for 7 to 14 days. Proteinuria was detected in another group of
3
animals exposed for 4 hours per day to 750 ug/m (0.4 ppm) NO- (p < 0.05).
Disc electrophoresis of the urinary proteins demonstrated the presence of
12-45
-------
albumin, and alpha, beta, and gamma globulins. The presence of high molec-
ular weight proteins in urine is characteristic of the nephrotic syndrome.
Histopathological studies of the kidney were negative.
12.2.4.4 Effects of NO,, on Body Weights—Dogs, rabbits, guinea pigs, rats,
hamsters, and mice have been exposed to 100 to 47,000 \ig/nr N02 (0.05 to 25
ppm) without reported body weight loss.133'141'148 Oda et al.,165 however,
observed reduced body weights of rats exposed to ambient air containing 135
ug/m (0.07 ppm) NO? in over a 100-day period.
12.3 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 atmos-
pheric 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.
Hysell et al. studied the toxicological effects on animals of auto-
motive emissions, with or without a catalytic converter and with or without
irradiation. Female lactating rats and their 2-week-old offspring were ex-
posed for 7 days. Infant mortality was increased following exposure to
3
auto emissions containing 9,400 ug/m (5.0 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. Following exposure to raw
exhaust with no catalyst there was an increase in hemolysis-resistant RBC
due to high ambient CO. There was no effect on blood eosinophils in rats
exposed to converted exhaust. Animals developed extensive pulmonary
12-46
-------
changes when exposed to irradiated, unconverted auto exhaust. Hamsters
developed purulent bronchitis, bronchiolitis, and bronchopneumonia when
exposed to such exhaust. There was an initial increase in the number of
alveolar macrophages at the level of the terminal bronchioles, a prolifer-
ation of respiratory epithelium in the ducts, and a thickening of the
alveolar septae. Extramedullary hematopoiesis in rat livers resulted from
high CO concentrations, and occasional degenerative changes in renal and
hepatic tissue were seen in these animals.
Lee et al. 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 ug/m (4.6 and 5.2 ppm) for the irradiated and
non-irradiated samples, respectively. For exhausts with catalytic conver-
sion, N02 concentrations were 5,640 and 3,380 |jg/m (3.0 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 hemato-
crit 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 trans-
ami nase (SGOT) was not affected by any exposure regimen. Reduction of
effects in converted exhaust-exposed groups was attributed to the decreased
CO levels in *he chamber.
12-47
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Stupfel et al.,142 in two separate experiments, exposed specific
pathogen-free rats to auto exhaust fumes 6-8 hours/day, 5 days/week, for
periods of 2.5 months to 2 years. The exhaust gas contained either 0.2 or
3
23 ppra NO , 0.07 or 0.37 percent C02, 58 mg/m (50 ppm) CO and 0.1 or 2.0
^\ *•
ppm aldehydes. With low concentrations of NOX, no biological effects were
observed. When NO was increased to 23 ppm, there was a reduction in body
^\
weight, an increase in spontaneous tumors, and emphysema. There was no
effect on the heart rate or on the QRS wave of the EKG. Sound avoidance
reflexes were decreased.
Cooper et al. exposed rats 24 hours/day for 38 to 88 days to auto-
mobile exhaust with and without catalytic converters. During three exper-
iments, N02 levels were 0.3, 0.4, and 5.1 ppm (564, 752, and 9,588 ug/m3);
nitric oxide (NO) levels were 7.1, 10.8, and 8.3 ppra (8,733; 13,284; and
10,209 |jg/m ); 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.
ysc
Murphy 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, subsequent studies were performed with
irradiated exhaust maintained at equilibrium values or at cyclic values.
For the equilibrium group, the following pollutant concentrations were
measured: 2.42 ppm formaldehyde, 0.2 ppm acrolein, 0.8 ppm oxidant, 2.66
ppm (5,000 ug/m3) N02> and 300 ppm carbon monoxide (CO). For the "cyclic"
12-48
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exposure, concentrations varied: 1.3 to 1.9 ppm formaldehyde, 0.06 to 0.1
ppm acrolein, 0.56 to 0.95 oxidant, 0.79 to 2.17 ppm (1,485 to 4,079 ug/m3)
N02i 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 depressed,
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,
168 169
and 61 months of exposure. * The animals were then allowed to recover
for 2 years and examined again. Vaughan et al. reported no alter-
ations in CO diffusing capacity, dynamic compliance, or total expiratory
169
resistance to air flow after 18 months of exposure. By 36 months, there
were no significant changes indicated by analysis of variance; however, a
significant number of animals exposed to high N0« and low NO had an abnorm-
ally (p < 0.005) low CO diffusing capacity. More changes were observed
169
after 61 months of exposure. 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 NCL 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 NOp and low NO had a lower mean carbon monoxide diffusing
12-49
-------
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 N02-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.170 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
N02 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.
Orthoefer et al., utilizing the same beagles exposed for 68 months,
evaluated biochemical alterations 2.5 to 3 years after the animals had re-
covered. In groups exposed to irradiated auto exhaust with and without SO
^
and high NQ2 with low NO, there was a rise in lung prolyl hydroxylase (p <
0.05). There was a high correlation between lung weights and hydroxy-
proline content 1n animals exposed to NO . No effects were observed in the
rt
hydroxyproline/total ninhydrin reactive material, nor did histological and
morphological examinations reveal significant differences in collagen
content of exposed tissues. There was no difference in the collagen/
protein ratios between tissues. Beagle lung morphology was evaluated by
237
Hyde et al. Air spaces in the proximal acinar regions were enlarged
with and without increases in the number and size of interalveolar pores.
i
Hyperplasia of the nonciliated bronchiolar cells was evident. Proximal
enlargement of air spaces was severe in dogs exposed to oxides of nitrogen,
12-50
-------
sulfur or oxides of sulfur, and photochemically reacted auto exhaust.
Hyperplasia of nonciHated bronchiolar cells was more severe in animals
exposed to raw exhaust alone or with oxides of sulfur. Occasional obser-
vance of foci of ciliary loss with and without squamous metaplasia was seen
in the trachea and bronchi.
172
Coffin and Blommer investigated the effects of a 4-hour exposure to
irradiated auto exhaust containing varying concentrations of N02, NO, CO,
and oxidant on mice which were also challenged with S. pyoqenes. Those
3 3
mixtures containing greater than 752 ug/m (0.4 ppm) N02 and 25 |jg/m (0.02
ppm) NO in the presence of 115 ug/ra (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 combin-
ations were also tested. Concentrations between 376 and 1,500 \ig/m (0.2
o
and 0.8 ppm) N02, 0.15 and 0.48 ppm oxidant, and 29 and 115 mg/m (25 and
100 ppm) CO were found to increase mortality in the infactivity model.
Using the infectivity model in which the mortality of pollutant-
29
exposed mice challenged with S. pyogenes is measured, Ehrlich et al.
investigated the effects of combinations of 0_ and N0~. 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
was a mixture of 0.05 ppm 03 and 2.0 ppm (3,760 ug/m ) N02. This effect
was additive. This concentration of 03 alone caused no significant change;
3
2.0 ppra (3,760 ug/m ) N02, however, resulted in a significant enhancement
of mortality. Multiple 3-hour daily exposures also were tested. With the
mixture of 0.05 ppm 0- and 2.0 ppm (3,760 ug/m ) N02, excess mortalities
were evident after five daily exposures. At 0.1 ppm 03 plus 1.5 ppm (2,800
ug/m3) N02, there was a significant effect when the mice were examined
12-51
-------
after 20 daily exposures, but not after 10. In the latter case, the author
attributed the effect to the presence of 03; in the former case, the author
suggested a synergistic relationship. When mice were exposed to a combin-
3 3
ation of 6,580 ug/m (3.5 ppm) N02 and 100 ug/m (0.5 ppm) 03 for 3 hours,
followed 1 hour later by challenge with S. pyogenes t 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 N02 concentration was reduced to 3,760 ug/m^
(2.0 ppm) and the initial 0- concentration maintained, no distinguishable
effect on bacterial clearance was observed.
Goldstein et al. found that mixtures of NO,, and 03 would decrease
bactericidal activity of the lungs. Mice received S. aureus aerosols
before a 4-hour N02 exposure. A reduction (p < 0.01) in bactericidal
activity of 36.9 and 111 percent was seen after exposure to 7,520
(4.0 ppra) N02 plus 700 ug/m (0.36 ppm) 03, and after 12,860 ug/m3 (6.84
ppm) N02 plus 760 ug/ra (0.39 ppm) 03 respectively. Lower gas concen-
trations had no effect. The protocol was then changed so that mice were
exposed to pollutants for 17 hours before S. aureus challenge. Bacter-
icidal activity was generally more impaired at higher gas concentrations.
The lowest gas concentrations to cause a significant effect (p < 0.05) was
4,320 ug/m (2.3 ppm) N02 plus 390 ug/m (0.2 ppm) 03 which decreased
bactericidal activity 13 percent. However, decreases in pulmonary bac-
terial deposition were observed at these concentrations. 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.
12-52
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Furiosl et al.113 exposed monkeys and rats to aerosols containing
330 yg/m3 (0.14 ppm) NaCl and 3,760 yg/m (2.0 ppm) N02 continuously
for 14 months in order to delineate the effect of participate aerosols on
o
N02 toxicity. Of the total NaCl aerosolized, only 5 ug/ra (< 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 N02 with and
without NaCl developed polycythemia with reductions in mean corpuscular
volumes although mean corpuscular hemoglobin concentration was normal.
Kosmider et al.75 exposed guinea pigs 8 hours/day for 6 months to
1,880 ug/m3 (1.0 ppm) oxides of nitrogen (N02 + N204) or 1,880 ug/m3 (1.0
ppm) oxides of nitrogen (N02 + N204) 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 also was
A
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 also was observed. Hemorrhage
and emphysematous-like conditions were noted in the lungs of NO -exposed
^k
animals. Emik et al. reported that alkaline phosphatase activity
decreased in the lungs of rats exposed 2.5 years to ambient air containing
approximately 0.019 ppm (36 pg/m ) N02, 0.011 ppm NO, 03, PAN, etc.
12-53
-------
129
Antweiler and Brockhaus exposed female guinea pigs 6 days/week for
6 months to 10,000 ug/m3 S0£ (3.8 ppm), 10,000 ug/m3 (5.3 ppm) N02> OP a
combination of the two pollutants. 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.
143
Shalamberidze et al. reported on the effects of low concentrations
of S0« and N02 on the estrous cycle and reproductive functions of rats.
Female albino rats were exposed 12 hours/day for 3 months to one of the
following: (1) 2,360 ug/m3 (1.3 ppm) N02; (2) 5,000 ug/m3 S02 (1.9 ppm);
(3) 160 ug/m3 S02 (0.06 ppm); (4) 130 ug/ra3 (0.07 ppm) N02; (5) 2,500 ug/m3
S02 (0.95 ppm) and 1,130 ug/m (0.6 ppm) N02< Low concentrations of SCL
and N02 did not affect the rat's estrous cycle, or induce morphological
changes in reproductive organs. Exposure to high concentrations did not
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, there was a depletion of
glandular epithelium in the uterus, a depletion of thyroid connective
tissue between follicles with a mild cellular degeneration of the adrenals,
ovaries, and uterus. There was also a decrease in the number of ovarian
primordial follicles. Long-term exposure had no effect on the rats' ability
to conceive, although there was a significant reduction in litter size and
average weight of progeny (p < 0.001).
Oda et al. ' exposed female mice and male rats and rabbits for 1
3 3
hour to 13,040 pg/m (10/6 ppm) NO containing 1,500 ug/m (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.
12-54
-------
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 ^n vitro with sodium dithionate.
12.4 NITRIC OXIDE
The toxicological assessment of nitric oxide (NO) exposure data is not
extensive and most of it has been done in recent years.
217 3
Azouley et al. exposed rats continuously for 6 weeks to 2,460 ug/m
(2.0 ppra) NO. Following exposure, no significant differences were seen in
blood oxygen saturation, pH, or oxygen combining capacity, 2,3-diphospho-
glycerate, ATP, glucose, lactate, hemoglobin concentration, hematocrit, and
red blood cell count. Methemoglobin was not detected. No striking histo-
logical 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 emphysematory-like changes with increased incidence
until 6 weeks of exposure.
Arnold et al. exposed various tissues from male rats in vitro to
250 ul NO gas for 15 seconds. Guanylate cyclase (GC) activity in various
tissues 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, trachea!
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
12-55
-------
activity decreased with a half-life of 3 to 4 hours at 4°C. When tissue
was re-exposed, the GC activity was reactivated. Sodium nitrite increased
GC activity as well. Nitric oxide increased cyclic GMP (cGMP) but had no
effect on cyclic AMP (cAMP).
Minced rat lungs were exposed to 98 percent cigarette smoke for 30
seconds or 417 pi NO for 10 seconds. Similar increases in cGMP levels (2-3
fold) were observed for cigarette-exposed tissue as well as for NO-exposed
tissue. Combination of NO with 98 percent cigarette smoke had no accumu-
lative effect on cGMP levels. No effects on tissue cAMP levels were
218
observed following exposure to cigarette smoke.
Kosmider and Chorazy reported that following the exposure of guinea
3
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.
12.5 NITRIC ACID AND NITRATES
178
Gray et al. conducted some of the earliest experiments investi-
gating inhalation toxicity for rats, guinea pigs, and mice exposed to N09
generated from nitric acid (HNCL). No measurement of vapor particle size was
made. Results were expressed as evidence of N0« toxicity, whereas the
experimental method could not adequately distinguish the difference between
NOg and HN03 effects. Concentrations of 17,000 and 26,000 ug/m3 (9.0 and
14 ppm) N0« administered 4 hours/day, 5 days/weak for 6 weeks produced lung
pathology. When exposure concentration was reduced to 9,400 ug/m3 (5.0
ppm), no lesions were observed.
179
Gardiner and Schanker investigated the effects of nitric acid-
induced lung damage on the absorption of drugs from the lungs. Rats v/ere
12-56
-------
given an intratracheal Injection of I 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. There was no difference in wet or dry weight of the exposed lungs.
Treatment with nitric acid enhanced the pulmonary absorption rates (20
percent) of jraminohippuric acid, procaineamide ethobromide, procaineamide,
and mannitol.
Sackner et a!.180 exposed dogs for 7.5 minutes to aerosol, with
particles less than 1 urn in diameter, containing 740 and 4,000 yg/m (0.1 and
1.0 percent) of sodium nitrate in order to observe potential effects on cardio-
pulmonary function. Sodium nitrate at either concentration had no effect
on functional residual capacity, static lung compliance, or total respir-
atory resistance.
1ST.
Charles and Menzel incubated 100 mM ammonium nitrate with guinea
pig lung fragments for 30 minutes and measured the release of histamine.
Ammonium nitrate released 58.1 percent of the total histamine.
12.6 N-NITROSO COMPOUNDS
Reviews of the acute toxicity, carcinogenicity, mutagenicity, and de-
182 183 191
tection of nitrosamines have appeared recently. ' ' These compounds
and nitrosamides are highly toxic and potent carcinogens. N-Nitrosamines
require metabolic activation to their mutagenic and carcinogenic active
intermediates and are most toxic to the liver and kidneys. Nitrosamides,
12-57
-------
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
diraethylnitrosamine in air has been reviewed in the Scientific and
Technical Assessment Report on Nitrosamines. Henschler and Ross
investigated the possible formation of nitrosamines from tissue amines
exposed to N02- Mice were exposed intermittently to 75,200 ug/m (40 ppm)
N02 for 38 hours every tenth day for periods up to 1.5 years. No lung
tumors were found in exposed animals. In fact, when compared to controls,
there was^a slight inhibition of the formation of lung adenomas and spon-
taneous skin fibro-adenomas. The formation of nitrosamines by reaction of
amines with nitrogen oxides has been observed in the laboratory but has not
226 227
been observed to occur in the atmosphere. ' Nitrosamines would not be
expected to accumulate to any great extent in ambient air because they are
228 229 185
readily decomposed by sunlight. ' Kaut 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 in
vivo, whereas they were found in 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
3
to 41,000 ug/m being the LD50 for dimethylnitrosamine to the rat. Diethyl-
nitrosamine, another compound detected in the air, is much less toxic with
3 186
an LD50 of 216,000 ug/m . Inhalation toxicity has not been reported.
Industrial use of nitrosamines as solvents suggest that they are rapidly
absorbed and exert their toxic action equally well on inhalation and
12-58
-------
ingestion. These compounds were acutely toxic to every animal species
187 188
tested and were also poisonous to humans. '
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 dominanat feature of the kidney
189
damage. Dimethylnitrosamine produces venous occlusions in the liver.
Ultrastructural changes in the liver after diethyl- and dimethylnitrosamine
include separations of the fibrillar and granular components of the hepa-
tocyte and the formation of electron dense plaques at the periphery of the
190
nucleolus. Lysosomal alterations occur within 35 minutes of exposure to
190
dimethylnitrosamine and reached a maximum at 12 hours.
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
199
and kidneys. N-Nitrosoheptamethyleneimine produced squamous neoplasia
192
of the lung in rats, histologically similar to human lung cancer.
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
193
have been shown to be mutagenic in microbial systems.
N-Nitroso compounds are also teratogens. The nitrosamide, N-nitroso-
194
ethyl urea, given to rats on the 12th day of gestation or N-nitrosomethyl-
12-59
-------
195
urea given on the 13th or 14th, 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 osteo-
196
sarcomas or chondrosarcomas of the lower vertebrae in rats.
In several instances, a single exposure to neonatal animals has induced
197 198
tumors as the animals reached adulthood. ' Single-exposure induction
199
of tumors can also occur in adult rats that are pregnant or recovering
from a partial hepatectomy.
N-Nitroso compounds can induce cancers transplacentally. Brain and
201 202
spinal cord tumors and renal tumors were found in progeny of pregnant
rats treated with N-nitrosoethylurea. Diethylnitrosamine has transpla-
203
centally induced tracheal papillomas in rats.
Small amounts of carcinogenic nitrosamines have been detected in some
204 205
samples of urban air and in the food supply.
N-Nitroso compounds could present a hazard, not only because people
are exposed to these compounds but also because they can be produced rn
vivo, at least in experimental animals. Nitrosation reactions are cata-
lyzed by acid and hence should occur preferentially in the stomach. Their
reactions have been induced in animals by feeding nitrite with amines or
907 230 231
amides. ' Also, under these situations acute toxic effects have
been observed and N-nitroso compounds have been detected by chemical analy-
sis.206
12-60
-------
12.7 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
(NOp). A summary of the biological effects observed from N02 exposure is
presented in Table 12-1. These effects are dependent upon both the concentration
and the duration of exposure.
The response of the lung to NOp follows a temporal sequence which helps
to clarify the potential hazards of such environmental exposure. In Figures
12-4 and 12-5, this sequence of events is summarized with approximate time
scales for single short-term exposure and continuous long-term exposures.
Because strictly comparable exposures and experimental designs for the various
species are neither available nor possible (exemplified by the
large differences in longevity between rodents and primates), the time scale is
approximate and arbitrary.
Short-Term Exposure
Figure 12-4 represents a hypothetical response to a single short-term expo-
sure of less than 8 hours. The chemical reactions leading to the toxic response
are essentially instantaneous when compared to the subsequent response of the
animal. Inhaled N02 is taken up rapidly and distributed throughout the lung as
shown by radiotracer studies. A large fraction of NOp is retained in the lung,
probably representing the fraction that has reacted chemically with the pulmonary
tissue. The rates of reaction of N02 with water vapor at ambient, and then
intrapulmonary, temperatures and concentrations are considerable. The chemical
species reaching the pulmonary surface to produce the observed lesion is most
likely NOp, but nitrous acid (HNOp), nitric acid (HNOg), and, perhaps, NO may
bfe formed in the liquids overlying the epithelium. Both acids may be neutralized
12-61
-------
in the liquid layer at rapid rates.
In vitro experiments in which N02 was reacted with tissue constituents,
such as unsaturated fatty acids, small molecular weight reducing substances,
and proteins, revealed that N02 oxidizes these substances within seconds to
minutes. These experiments indicate that inhaled NO^ reaching cells of the
lung would react rapidly and would fail to attain a measurable concentration
within the blood. However, some nitrate formed as a consequence has been
detected in blood and urine at levels unlikely to induce the biological responses
observed. The predominant response is direct injury of the tissue in the lung.
Effects on organs distant to the lung are likely to result from products formed
in the lung and circulated to other parts of the body. Direct proof of this
hypothesis has not been found.
Cellular injury and death following initial exposure of the lung occurs
during a period of less than 24 hours. The magnitude and site of injury depend,
in part, upon the concentration of NCL inhaled, so that the absolute degree of
response, as depicted schematically in Figure 12-4, will depend on both the
rate and magnitude of respiration and concentration. The moderate solubility
of NCL in water also accounts for significant doses to alveoli, even at low
inhaled concentrations, because NCU is not completely removed by passage through
the upper airways. At ambient and near-ambient concentrations (concentrations
usually found in urban environments), the region of the terminal and respiratory
bronchioles and adjacent alveoli is most affected. In rodents, the respiratory
bronchiole is much shorter than in man. Higher concentrations (above 9,400 pg/m3;
5.0 ppm) may affect segments of the upper airways as well and penetrate deeper into
the alveoli. Protein and nucleic acid synthesis are stimulated in surviving stem
cells, and a wave of mitosis reaches its maximum at about 48 hours during or after
exposure. The Type I pneumocytes are more sensitive than the Type II cells and
12-62
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may be sloughed off, leaving debris within the affected alveoli. Ciliated cells
are similarly sensitive and are replaced by differentiating Clara cells. In
time, mucous-secreting cells appear more peripherally.
Biochemical indicators of injury to the lung can be detected by a wide
variety of means. Changes in cell permeability have been reported at concen-
trations as low as 752 pg/m (0.4 ppm) N0?, when sensitive parameters such as
those of plasma proteins or radiolabeled albumin within the airways have been
measured. Pulmonary macrophages themselves also are damaged in turn by inhaled
N02» as noted by alterations in their respiration and intracellular ratio of
MAD/NADH. Similar effects can be observed on direct exposure of pulmonary macro-
phages to N02 in vitro. Often the biochemical parameters of injury return to
normal or near normal values within a week or two after cessation of exposure.
Pulmonary defenses against exogenous elements also are affected by short-
term exposures. The infectivity model has proven to be a particularly sensitive
indicator of pulmonary injury. When mice are exposed to N0? by varying both
concentrations and periods of exposure, mortality from infectious agents is
influenced more in proportion to the concentration of NO,, than to the duration
of the exposure (see Figure 12-1). Such effects are consistent with the hypo-
thetical temporal sequence of injury, suggesting that pulmonary damage occurs
rapidly on exposure but that its effects may be observed later, depending on the
extent of damage and the system used to measure the damage. The infectivity
model tends to incorporate many of the defense mechanisms of the lung and to
reflect the overall damage. The results of infectivity experiments are measured
in terms of mortality in excess of that observed in infected controls not exposed
to N02 (approximately 20% mortality in air-exposed mice). Thus, short-term,
high-level effects from exposure to greater than 13,160 ug/m3 (7.0 ppm) for approxi-
mately 14 hours are underestimated. Lew concentrations, such as 1,880 yg/m (1.0
12-63
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ppm) N0?, may result in only a small excess mortality on a single exposure of
o
3 hours which can be repaired by £4 to 36 hours. High concentrations (47,000 yg/m ;
25 ppm) may initiate other mechanisms such as edema, which may complicate inter-
pretation of the excess mortality observed.
LopSzI^JJH Exposure
The sequence of events on continuous exposure is similar to that seen with
short-term exposure (Figure 12-5). During the first 14 days of exposure, cell
death and replacement of pulmonary cells are the dominant features. The wave of
mitosis reaches its maximum at about 48 hours from the onset of exoosure. The extent
of cell death and, consequently, all of the other indicators of N0~ exposure so far
examined are dose dependent. The rate of chemical reaction is very rapid compared
to other observable responses of the lung to NOp. Biochemical and physiological
or functional indicators of damage change rapidly with injury and repair and
reach a relatively steady state after about a week or two. Some enzymes indicative
of cellular injury, such as LDH, CPK, SGOT, and cholinesterase, could be found in
2
elevated amounts in the serum of animals exposed to 940 pg/m (0.5 ppm) N0? during
the injurious phase (greater than 7 days). The enzyme lysozyme is associated with
the aggregation of pulmonary macrophages and its elevation in the lung, and release
into serum may be indicative of damage to pulmonary tissue. Susceptibility to
infection, as measured by the infectivity model, rises almost linearly during this
period. Excess mortality may be very little at concentrations in the range of
940 to 2,820 pg/m (0.5 to 1.5 ppm) NO,,. Because of the small differences in
mortality, experimental designs that would assure adequate sample size in exposed
and control groups of animals are difficult.
The temporal sequence of morphological alterations is difficult to interpret
because of the slow gradation of response once the initial phase of replacement
of susceptible cells has passed. The development of an emphysema-like disease
12-64
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in the experimental animal requires considerable time, as indicated by the studies
on rats. The development of obstruction to airflow and distension and destruction
of alveolar tissue in experimental animals required considerable time, approxi-
mately proportional to that for man in the development of emphysema. The process
is complex, but the role of continuous N02 exposure on the dynamics of the cell
populations and the structural alterations of the lung is clear. Increased
thickness and attenuation of the interstitial alveolar tissue, loss of cilia
and their cells, narrowing of the small airways, alterations in the morphology
of Clara cells, transformation of Type II to Type I cells, the appearance of
altered collagen within the interstitium, and aggregation of macrophages are
apparent in rats exposed continuously to 3,760 yg/m3 (2.0 ppm) N02 or greater.
The development of bulbous-like air spaces, expanded lung, and chest deformity
3
resembling emphysema in the rat occurs after lifetime exposure to 28,200 yg/m
(15 ppm) N02.
Changes in the fatty acid composition of lung membranes have been noted
when careful dietary control has been imposed to allow the measurement of small
changes. These and the reduction of mortality from continuous exposure to high
concentrations of N02 by supplementation with vitamin E and other free radical
scavengers support the hypothesis that membrane damage by the chemical oxidation
of unsaturated fatty acids is a major mechanism of toxicity by N02. It is
understood that the changes in both enzyme and lipid content may reflect alter-
ations in the types of cells found in the lung at a particular time as well as
serve as a measure for the mechanism of toxicity.
The question of tolerance or resistance and recovery on continuous exposure
remains unresolved. In Figure 12-5, the dashed line indicates replacement of
dead and injured cells resulting from N02 exposure and represents the hypothesis
that tolerance may develop during long-term exposure. Tolerant cells, as compared
12-65
-------
to naive cells, may be more resistant to N0? because they are younger or because
of the induction of protective mechanisms. The elevated levels of the lung
enzymes glutathione peroxidase, glutathione reductase, and glucose-6-phosphate
dehydrogenase in the rat may represent the induction of such a protective
mechanism or, more likely, may reflect the state of proliferation of specific
lung cells with the organ. Enzyme induction does not appear to occur in the
o
guinea pig when it is exposed to 940 jjg/m (0.5 ppm) for 4 months. When
cultured lung cells are coated with a very thin layer of nutrients (less than
0.1 mm), direct exposure to NCL is highly toxic. This supports the idea that
all cells are relatively sensitive to NCL.
2
When rats are exposed continuously to 3,760 pg/m (2.0 ppm) N02 for long periods
and then exposed to an abrupt increase in concentration, a second wave of mitosis
follows, suggesting that continuous exposure may stimulate cell turnover
above the normal rate. This hypothesis is represented by the elevated level of
cell death indicated in Figure 12-5. Adaptation to NOp, when viewed in this
context, is a questionable concept and must be resolved by further experimentation.
Unfortunately, interpretation of the "adaptive" mechanisms is difficult, and the
extent to which they are protective to the host is not known. While it is
possible that these mechanisms could conceivably ameliorate a toxic response,
the ultimate development of an emphysema-like condition occurs in their presence.
No evidence has been found for an enhanced rate of tumor formation or
malignant metaplasia. Because N02 stimulates a rapid turnover of cells, a
transient hyperplasia of Type II pneumocytes and nonciliated bronchiolar cells
may be seen. Such hyperplasia represents part of the natural repair mechanism.
o
Intermittent exposures of mice to 2,820 pg/m (1.5 ppm) N02 eventually
become equivalent to continuous exposure when the infectivity model is used.
A total of 319 h°urs of exposure (13.3 days) is required before a 7 hour/day
12-66
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exposure becomes equivalent to continuous exposure.. The time period for
equivalence between intermittent and continuous exposures will be shortened
relative to the concentration of NCL. The intervening 17 hours between each 7
hour exposure to 2,820 \ig/m (1.5 ppm) N0? are inadequate for complete recovery.
Excess mortality upon challenge with bacterial pathogens could be observed after
o
7 days of continuous exposure to 2,820 yg/m (1.5 ppm), however, or even to
3
940 pg/m (0.5 ppm).
Considerable differences occur in the response to N0? when animal species
and infectious agents other than mice and S^. pyogenes are used. Resistance to
J(. pneumoniae is less affected by NO^ exposure than resistance to S. pyogenes.
Squirrel monkeys were the least sensitive animals tested using this end point,
and hamsters demonstrated intermediate sensitivity when compared to mice. The
extension of such data to man is difficult because analogous human data are not
available. The infectivity model may be viewed as a general indicator of
sensitivity, even though both 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.
In terms of the probable temporal sequence of events, NO^ affects almost
all cell types of the lung. The cell populations most susceptible to death and
followed by replacement will vary with the animal species, the concentration,
and the duration of exposure. Because the rate of chemical reaction of WL with
cell constituents is almost instantaneous compared to the biological expression
of injury, it may be expected that the concentration of N02 during exposure has
a greater effect on an end point than does the duration. Such factors complicate
the interpretation and correlation of physiological, morphological, and bio-
chemical parameters. Biochemical parameters generally are more sensitive than
12-67
-------
physiological or morphological ones, because injured or dying cells release
their cellular contents which may be detectable by representative enzymes in
the blood of the affected animal. Dead cells recruit phagocytic cells to the
lung where they also may release digestive or phagocytic enzymes during the
removal of previously affected cells.
The suppression or elevation of activity of a circulating enzyme following
long-term exposure to NO- may represent some effect of N0? or its reaction
products on organs other than the lung. Again, direct correlates with specific
human disease are lacking, but the data represent a measurable biological effect
of NOp. Some experimental results reported here of effects of N0? on hepatic,
renal, and central nervous tissue need to be confirmed. Their relevance to
possible underlying pathologic processes also needs clarification.
Physiological parameters, such as smooth muscle reflex changes in pulmonary
function upon acute exposure, may not be altered until considerable tissue is
injured. Historically, small animals have been unsuitable for sensitive physio-
logical measurements because of technical difficulties. Morphological alterations
are not seen until cells are severely injured or killed, and often not until
replacement of such cells has been initiated. Histopathologic changes have
been demonstrated unequivocally, however, at 3,760 yg/m (2.0 ppm) or more NO
i
Because the infectivity model is a combination of many of these effects, the
noxious influences of N02 are observed at the same or lower levels than those
found either with biochemical indices or at levels where physiological and
morphological effects have been observed. The major characteristic of the
infectivity model is that a progressive increase in susceptibility occurs at
a time in the exposure of animals to NO^ when morphologic changes have become
stable and are approaching anatomic rather than pathologic alterations.
12-68
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Additive toxicity, by other air pollutants to NCL, is most likely. Air
pollutants such as ozone, sulfuric acid, and sulfur dioxide are likely to injure
many of the same cells within the lungs, but no evidence for potentiation has
been found. Tobacco smoking a.nd occupational exposure may add very significantly
to the toxicity of ambient N0?, but presently insufficient data are available
for detailed evaluation. Interactions with other pollutants are likely to present
an increased or altered response. For example, since N0? causes pulmonary damage
similar to ozone, it can be hypothesized that sequential exposure to NCk and
hLSCL could be additive, as lias been observed with ozone using the infectivity
model.
In summary, then, the lowest dose at which either biochemical changes or
reduction in resistance to infectivity can be detected in experimental animals
is 940 iig/m (0.5 ppm) NOp for 4 hours or more. The time needed for recovery from
a single short exposure to NCL will depend on the concentration and duration of
exposure. The duration is probably greater than 17 hours, as this recovery period
was insufficient to prevent an eventual reduction in bacterial resistance of
mice. The temporal sequence of NCL toxicity in man is unknown but is likely to
be similar to that found in animals, because cells must be renewed. The issue
of true adaptation is not resolved. The influence of diet and of vitamin E on
toxicity suggests that effects observed in animals may be observed in man. Such
effects may be exacerbated during dietary deficiencies and may also be obscured
by complex diets.
Toxicity p_f Other Oxjd e_s £f Nitrogen
Nitric oxide (NO) is less toxic than N02 but may have important biochemical
effects related to the cyclic nucleotide concentration of cells. Nitric oxide
stimulates quanyl cyclase and increases the level of intracellular cyclic GMP, but not
cyclic AMP. Cyclic GMP acts on a number of intracellular receptors of considerable
12-69
-------
physiological importance, particularly those involved in exocytosis. Increased
cyclic GMP may cause a destabilization of the cell membrane. The biological
significance of these effects is obscure, especially since NO,, is an inevitable
contaminant in all NO exposures. The toxicity of NO is poorly understood and
should be studied further and reviewed periodically, because trace amounts of
NO-hemoglobin appear to exist in man and animals.
Other potential areas of toxicity involve the formation of nitroso
compounds, because nitrosamines and nitrosamides are known carcinogens. Gas
phase reactions forming nitrosamines have been reported, and inhaled, injected,
or ingested nitrosamines produced tumors in exposed animals. No direct evidence
that nitrosamines or nitrosamides are formed in ambient air from nitrogen oxides
is available; nor has it been demonstrated that they are found jn vivo from the
inhalation of nitrogen oxides. Similarly, the role of inhaled nitrates found
in atmospheric particles is unknown and should be studied. Continued surveillance
of these important areas is needed.
12-70
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in the rat by dimethylnitrosamine (N-nitrosodimethylamine). Acta
Union Int. Contra Cancrum 15: 187-190, 1959.
198. Oruckrey, H., R. Preussmann, G. Blum, S. Ivankovic, and J. Afkham.
Erseugung van Karzionmen der Speiserohre durch unsymmetrische Nitrosamin.
Naturwissenschaften 50: 100-101, 1963.
199. Druckrey, H., R. Preussmann, S. Ivankovic, 0. Schmahl, J. Afkham, G.
Blum, H. 0. Mennel, M. Mailer, P. Petropoulos, and H. Schneider.
Organotropic carcinogenic effects of 65 different N-Nitroso compounds
in BO rats. 2. Krebsforsch. 69: 103-201, 1967.
200. Craddock, V. M. Liver carcinomas induced in rats by single administration
of dimethylnitrosamine after partial hepatectomy. J. Natl. Cancer
Inst. 47: 899-907, 1971.
201. Ivankovic, S., and H. Druckrey. Trasplazentare Erzeugung maligner
Tumoren des Dervensysterns. I. Althylnitroso-harnstoff an BD IX-Ratten.
A. Krebforsch. 71: 320-260, 1968.
202. Wrba, H., K. Pielsticker, and U. Mohr. Die displazentarcarcinogene
Workun von Diathyl-nitrosamin bei Ratten. Naturwissenschaften 54: 47,
1967.
203. Mohr, U., J. Althoff, and A. Anthaler. Diaplacental effect of the
carcinogen diethylnitrosamine in the Syrian golden hamster. Cancer
Res. 26: 2349-2352, 1966.
204. Fine, D. H., D. P. Rounbehler, N. M. Belcher, and S. S. Epstein.
N-Nitroso compounds: Detection in ambient air. Science 192: 1328-1330,
1976.
205. Crosby, N. T., and R. Sawyer. N-Nitrosamines: A review of chemical
and biological properties and their estimation in foodstuffs. Adv.
Food Res. 22: 1-71, 1976.
206. Mirvish, S. S. Formation of N-nitroso compounds: chemistry, kinetics
and in vivo occurrence. Toxicol. Appl. Pharm. 31: 325-351, 1975.
12-86
-------
207. Rounbehler, D. P., R. Ross, D. H. Fine, Z. M. Igbal, and S. S. Epstein.
Quantisation of diraethylnitrosamine in the whole mouse after biosynthesis
in vivo from trace levels of precursors. Science 197: 917-918, 1977.
208. U.S. Environmental Protection Agency. Health Effects of Short-Term
Exposures to Nitrogen Dioxide (Air Quality Criteria). Final Draft,
May 1978.
209. Gardner, 0. E., D. L. Coffin, M. A. Pinigin, and G. I. Sidorenko.
Role of time as a factor in the toxicity of chemical compounds in
intermittent and continuous exposures. Part I. Effects of continuous
exposure. J. Toxicol. Environ. Health 3: 811-820, 1977.
210. Coffin, D. L., D. E. Gardner, G. I. Sidorenko, and M. A. Pinigin.
Role of time as a factor in the toxicity of chemical compounds in
intermittent and continuous exposures. Part II. Effects of intermittent
exposure. J. Toxicol. Environ. Health 3: 821-828, 1977.
211. Schiff, L. J. Effect of nitrogen dioxide on influenza virus infection
in hamster trachea organ culture. Proc. Soc. Exp. Biol. Med. 156:
546-549, 1977.
212. Goldstein, B. 0., S. J. Hamburger, G. W. Falk, and M. A. Amaruso.
Effect of ozone and nitrogen dioxide on the agglutination of rat
alveolar macrophages by Concanavalin A. Life Sciences 21: 1637-1644,
1977. ~~
213. Kim, J. C. S. Virus activation by Vitamin A and N02 gas exposures in
hamsters. Environ. Health Perspectives 19: 317-3207 1977.
'o
214. Cabral-Anderson, L. J., M. J. Evans, and G. Freeman. Effects of NO,
on the lungs of rats. I. Morphology. Exp. Mol. Pathol. 27: 353-3^5,
1977. ~~
215. Evans, M. J., L. J. Cabral-Anderson, and G. Freeman. Effects of N02
on the lungs of aging rats. II. Cell proliferation. Exp. Mol.
Pathol. 27: 366-376, 1977.
216. Samuel son, G. S., R. E. Rasmussen, B. K. Nair, and T. T. Crocker.
Novel culture and exposure system for measurement of effects of airborne
pollutants on mammalian cells. Environ. Sci. Technol. 12(4): 426-430,
1978.
217. Azoulay, E., P. Soler, M. C. Blayo, and F. Basset. Nitric oxide
effects on lung structure and blood oxygen affinity in rats. Bull.
Europ. Physiopath. Resp. 13: 629-644, 1977.
218. Arnold, . P., R. Aldred, and F. Murad. Cigarette smoke activates
guanylate cyclase and increases guanosine 3', S'-uronophosphate
in tissues. Science 198: 934-936, 1977.
12-87
-------
219. Blank, M. L., W. Dalbey, P. Nettesheim, J. Price, 0. Creasia, and F.
Snyder. Sequential changes in phospholipid composition and synthesis
in lungs exposed to nitrogen dioxide. Am. Rev. Resp. Die. 117:
273-280, 1978.
220. Viosin, C., C. Aerts, E. Jakubczak, J. L. Houdret, and A. B. Tonne].
Effects du bioxyde d'azote sur les macrophages alveolaires en survie
en phase gazeuse. Bull. Europ. Physiopath. Resp. 13: 137-144, 1977.
221. Viosin, C., C. Aerts, J. L. Houdret, A. B. Tonnel and Ph. Ramon.
Action du bioxyde d'azote sur les macrophages alveolaires en survie
"in vitro" en phase gazeuse. Lille Med. 21(2): 126-130, 1976.
222. Langloss, J. M., E. A. Hoover, and D. E. Kahn. Diffuse alveolar
damage in cats induced by nitrogen dioxide or feline calicivirus.
Amer. J. Pathol. 89(3): 637-644, 1977.
223. Hackett, N. A. Cell renewal of Chinese hamster lung and trachea
following NO, exposure. Abstract. Annual Meeting Supplement, Am. Rev.
Resp. Dis. 117(4): 25, 1978.
224. Campbell, K. I. Effect of Nitrogen dioxide on swimming endurance in
rats. Clin. Toxicol. 9(6): 937-942, 1976.
225. Crapo, J. D., K. Sjostrom, and R. T. Drew. Tolerance and cross-
tolerance using NO, and 0,. I. Toxicology and biochemistry. J.
Appl. Physiol. 441(3): 364-369, 1978.
226. Gehlert, P. and W. Rolle. Formation of diethylnitrosamine with
nitrogen dioxide in the gas phase. Experentia 33: 579-581, 1977.
227. Challis, B. C. Rapid formation of carcinogenic N-nitrosamines in
aqueous alkaline solutions. Brit. J. Cancer 35: 693-696, 1977.
228. Chow, Y. L. Nitrosamine photochemistry: reactions of ammonium
radicals. Accounts of Chem. Res. 6: 354-360, 1973.
229. Polo, J. and Y. L. Chow. Efficient degradation of nitrosamines by
photolysis. In: Environmental N-Nitrosocompounds, Analysis and
Formation. P. Bogovski, L. Griarte, and W. Davis, eds. IARC
Publication No. 14, Lyon, 1976. p. 473-476.
230. Mirvish, S. S. Kinetics of N-nitrosatron reactions in relation to
tumorigenesis experiments with nitrite plus amines or ureas. In:
N-Nitroso Compounds: Analysis and Formation. P. Bogovski, P.
Preussman, E. A. Walker, and W. Davis, ed. IARC Publication No. 3,
Lyon, 1972, pp. 104-108.
231. Mirvish, S. S. N-Nitroso compounds: Their chemical and HI vitro
formation and possible importance as environmental carcinogens. J.
Toxicol. Environ. Health 2: 1267-1277, 1977.
232. Evans, M. J., L. J. Cabral-Anderson, and G. Freeman. Role of the
Clara cell in renewal of the bronchiolar epithelium. Lab. Invest.
38(6): 648-655, 1978.
-------
233. Lunan, K. D., P. Short, D. Negi, and R. J. Stephens. Glucose-6-
phosphate dehydrogenase response of postnatal lungs to NO,, and 0,.
In: Pulmonary Macrophage and Epithelial Cells, ERDA Symposium Series
43, CONF-760927, 2977. pp. 236-247.
234. Freeman, G., S. C. Crane, and N. J. Furiosi. Healing in rat lung
after subacute exposure to nitrogen dioxide. Amer. Rev. Resp. Dis.
100: 662-676, 1969.
235. Cooper, G. P., J. P. Lewkowski, I. Hastings, and M. Malanchuk.
Catalytically and noncatalytically treated automobile exhaust.
Biological effects in rats. J. Toxicol. Environ. Health. 3:
923-934, 1977.
236. Murphy, S. D. A review of effects on animals of exposure to auto
exhaust and some of its components. J. Air Pollut. Control Assoc.
14: 303-308, 1964.
237. Hyde, D., J. Orthoefer, D. Dungworth, W. Tyler, R. Carter, and H. Lum.
Morphometric and morphologic evaluation of pulmonary lesions in beagle
dogs chronically exposed to high ambient levels of air pollutants.
Lab. Invest. 38: 455-469, 1978.
12-89
-------
TABLE 12-1. SUMMARY OF OBSERVED EFFECTS ON ANIMALS OF EXPOSURE
TO N02 CONCENTRATIONS BELOW 30 PPM
RESPIRATORY TRACT TRANSPORT AND ABSORPTION
EFFECTS ON RESISTANCE TO RESPIRATORY INFECTIONS
i
•J3
o
MUCOCILIARY TRANSPORT
ALVEOLAR MACROPHAGE
N02 evenly distributed in lungs and absorbed into blood of monkeys
exposed to 560 to 1,710 ug/m (0.3 to 0.9 ppm)
In mice increased mortality from bacterial pneumonia after
single 2 hr exposure to 3760 ug/m (2.0 ppm) and respira-
tory challenge with S. pyogenes. Challenge with K.
pneumoniae after 3 months of continuous exposure or 6
months of intermittent (6 or 18 hr/day) exposure to
940 ug/m also produced increased mortalities. In squirrel
monkeys increased mortality after 1 mo exposure to,
19000 ug/ra (10 ppm) or 2 mo exposure to 9400 ug/m
(5.0 ppm) followed by respiratory challenge with k.
pneumoniae or influenza virus.
Mice showed high incidence of adenomatous proliferation of
peripheral and bronchial epithelial cells after continuous
exposure to 560 to 940 ug/m (0.3 to 0.5 ppm) over 3 to
6 mo which was exacerbated by influenza virus challenge.
Lowes bactericidal activity in mice exposed to 13,200
pg/m (7.0 ppm) for 4 hr followed by S_. aureus challenge;
at 27,800 [ig/m (14.9 ppm), bactericidal activity was 50%
lower but unchanged at 7,140 ug/m (3.8 ppm).
After female rats were exposed to 11,280 ug/m
for 6 wk, TPTT and FET increase was observed.
within 1 wk.
(6.0 ppm) for 6 days/wk,
Impairment reversed
After 21 wk exposure to 940 or 3,760 ug/m (0.5 or 2.0 ppm), mice showed
distinct morphological alterations. Rabbits exposed to 19,000 (jg/m
(10 ppm) for 3 hr exhibited 5QX inhibition of phagocytic activity.
After exposure to 43,300 pg/ra (23 ppm), the NAD /NADH ratio was
decreased but ascorbate reversed it. Rabbits also had increased
resistance to pox virus after exposure to 9,400jpg/m (5.0 ppm).
Guinea pigs exposed continuously to 18,800 ug/m (10 ppm) for 7 wk
evidenced 63% increase in epithelial cells.
(continued)
-------
TABLE 12-1 (CONTINUED).
IMMUNOLOGICAL EFFECTS
EFFECTS ON LUNG BIOCHEMISTRY
IN3
VO
EFFECTS ON LUNG MORPHOLOGY
pg/m v^.u ppm; snowea aecrease in serum igA and increase
IgM.-IgGj and IgG- Imnunoglobullns. Guinea pigs exposed
pg/m (5.0 ppm) evidenced Increased lung tissue and serum
Exposure to 1,880 pg/m (1.0 ppm) for 6 mo followed by a
Monkeys challenged flwe times with Influenza virus during continuous
exposure to 1880 pg/m (1.0 ppm) for 493 days had Increased serum
neutralizing antibody tlters which persisted for approximately 21 days
aftej? the challenge. Mice exposed continuously for 3 mo to either 3760
pg/m3 (2.0 ppm) or to 940 vg/m3 (0.5 ppm) with dally 1-hr peaks of 3760
vg/m (2.0 ppm) showed decrease In serum IgA and Increase 1n serum
" " " " for 160 hr to 9,400
serum antibodies.
.... „ challenge with
0. pneumonlae demonstrated: (a) decreased Immunity, (b) decreased
Femolytlc activity of complement and, (c) Increased mortality.
Rats exposed to 1,880 to 47,000 gg/m3 (1.0 to 25 ppm) showed increased
GSH reductase and G6P dehydrogenase activities, an increase in total
lung lipid, and a decrease in lung tissue fatty acids. Vitamin E re-
duced N02 effects on lung fatty acids,
Growth of mice was retarded after continuous exposure to 940 or 1,880
(0.5 or 1.0 ppm) for 1 yr. Vitamin E improved growth. Certain enzyme
levels increased after exposure to 11,000 to 53,000 yg/m (6.0 to 28
ppm) for varying time periods. Also, guinea pigs showed increased en-
zyme,levels and lung protein content after exposure to 740 to 3,760
ug/m (0.4 to 2.0 ppm).
Rabbits exposed continuously to 1,880 pg/m (1.0 ppm) for 1 wk evidenced
decreased lecithin synthesis. Hamsters exposed continuously to 56,400
pg/rn (30 ppm) for 2 days showed increased lung proteolytic activity.
Rats exposed to 3,760 to 32,000 ug/m (2.0 to 17 ppm) for varying periods
demonstrated: (a) cilia loss, (b) decreased length and weight of neo-
nates, (c) delayed lung development, (d) connective tissue damage,
(e) emphysema-like conditions, (f) increased cell division.
Monkeys exposed to 5,640 gg/m (3.0 ppm), 4 hr/day for 4 days,
had thickening of alveolar walls and basal lamina. Mice exposed con-
tinuously to 940 pg/m (0.5 ppm) evidenced damage to tracheal mucosa and
cilia. Longer exposures resulted 1n bronchial hyperplasla, alveolar
edema, and fibrosis. Rabbits and dogs exposed to 47,000 pg/m'5 (25 ppm)
had emphysema and increased mortality.
(continued)
-------
TABLE 12-1 (CONTINUED).
EFFECTS ON PULMONARY FUNCTION
POTENTIAL HYPERPLASIA, MUTAGENESIS, AND TERATOGENESI5
ID
ro
TOLERANCE TO NO,
PRODUCTION OF LUNG EDEMA
Rats exposed continuously to as low as 1,500 uP/m (0.8 ppm) for ?.75
yrs showed Increased respiratory rates. Higher N02 levels and'longer
exposure times resulted in increased tidal volume, decreased fung com-
pliance, ahd increased incidence of emphysema.
Cats exposed continuously to as low as 940 ug/m (0.5 ppm) had impaired
Op uptake in blood. Higher concentrations and longer exposure times
resulted in increased R and a decrease in static lung compliance.
oW
Squirrel monkeys exposed to 18,800 vjg/m (10 ppm) showed increased
minute volume after 1 mo. There was no effect at 940 ug/m (5.0 ppm).
Exposure of pregnant monkeys to 16,900 ug/m (9.0 ppm) had no effect
on functional residual capacity of mother and offspring.
Mice, when exposed to 940 to 1500 ug/m (0.5 to 0.8 ppm) NO- plus
50 ppm CO, for 1 mo, evidenced hyperplasia in terminal brocrnoles.
Each pollutant alone had no effect. Auto exhaust containing 0.2 ppm
NO had no biological effects on rats; however, at 23 ppm there was
anxincreased number of spontaneous tumors but none in lungs.
Pregnant rats exposed to 18,800 ug/m (10 ppm) continuously through
pregnancy and up to 3 mo after delivery had decreased litter size and
increased mortality of neonates. .No teratogenic effects were noted. Mice
exposed to this level for 6 hr showed no mutagenic effects.
Rats exposed to 9,400 ug/m3 (5.0 ppm),for 13 mo had no mortality upon
subsequent challenge with 47,000 ug/m (25 ppm) for 6 wk. Controls
had 67% mortality. Mice, exposed continuously to 47,000 iig/m" (25 ppm)
for 7 wk showed a tolerance to 132,000 ug/m (70 ppm) for 5 hr. The
tolerance disappeared in 3 mo.
Mice exposed to 940 to 13,000 ug/m3 (0.5 to 7.0 ppm) showed indications
of edema. Guinea pigs exposed to 750 ug/m (0.4 ppm) for 1 wk evidenced
increased serum proteins in lavage fluid.
(continued)
-------
TABLE 12-1 (CONTINUED).
CHANGES IN HEMATOLOGY
Guinea pigs, exposed to 940 |ig/m (0.5 ppm) had decreased R|C GSH
peroxidase; increased D-2, 3-d^phosphoglycerate at 690 yg/m (0.36 ppm).
Exposure of mice to 1,500 iig/m (0.8 ppm) for 5 days had no effect on
methemoglobin.
Rabbits exposed to as low as 2,400 pg/m (1.3 ppm) showed an increase in
leukocytes followed by decreased phagocytic activity. Decrease in RBC was
also noted. At 45,100 yg/m (24 ppm), blood contained increased nitrate
and nitrite.
ro
i
10
CO
CENTRAL NERVOUS SYSTEM EFFECTS
MARKERS OF ORGAN DAMAGE
EFFECTS ON BODY WEIGHT
Monkeys exposed to 9,400 yg/m (5.0 ppm) for 90 days showed no changes
in hematological parameters. Polycythemia was observed in monkeys ex-
posed to 3,800 iic]/m (2.0 ppm) for 14 mo.
Dogs exposed to 48,900 yg/m (26 ppm) for 6.5 mo evidenced decreased
hematocrit and hemoglobin; UBC increased but returned to normal following
cessation of N0£ exposure.
Mice exposed to 14,000 yg/m (7.7 ppm) for 6 hr had decreased voluntary
running activity. Rats exposed to 100 iig/m (0.05 ppm) for 3 mo evi-
denced no effects but 600 yg/m (0.32 ppm) showed decreased conditional
reflexes. Guinea pigs exposed to 1,000 yg/m (0.53 ppm) for 8 hr/day,
for 180 days, had many enzyme levels increased.
Exposure of guinea plqs to 940 uq/i" (0.5 ppm) for varying periods showed
Increased SROT, SGPT, and Ivsozyme. Cholinesterase activity was depressed upon
long exposure. Albumin and globulins v/ere found 1n urine. At l,800jiq/m (1.0
ppm)", exposure for 6 mo inhibited protein synthesis. At 47,000 yg/nr
(25 ppm) for 2 hr, rats had increased plasma corticosterone levels. Hamsters
exposed to 56,400 iig/m (30 ppm) continuously for 30 days evidenced increased
serum antiprotease levels.
Rats showed decreased body weight after exposure to concentrations, as low
as 5,000 yg/m (2.7 ppm) for 8 wk. Monkeys exposed to 18,800 yg/m (10
ppm continuously for 90 days had decreased body weight when exposure VBS com-
bined with heat stress.
-------
TABLE 12-2. RESPIRATORY TRACT TRANSPORT AND ABSORPTION
ro
i
vo
N02
concentration n..-,4-^«
Species
Dog, and
rabbit
Rabbit
Monkey
3
|jg/m
Not
Reported
188,000
560-
1,710
ppm (min)
Not Not
Reported Reported
100 < 45
0.3 to 9
0.9
Effect
Removal of 42.1% by isolated upper
airways. Concentration and flow rates
not given.
Absorption of approximately 50% N02 in
the nasopharyngeal cavity
Concurrent exposure to N02 demon-
strated that N0? was evenly distri-
Reference
Yokoyama, 19688
Dahlhamn and
Sjoholm, 19639
Goldstein et al. ,
197710
into the blood.
-------
TABLE 12-3. MORTALITY FROM N02 EXPOSURE FOR 1 TO 8 HOURS
en
N02
concentration
Species
Mouse
Rat
Guinea pig
Rabbit
Dog
ug/ra
141,000
173,000
94,000
to
141,000
141,000
141,000
141,000
141,000
ppm
75
92
50
to
75
75
75
75
75
Duration
(hr)
1 to 8
< 8
4 or 8
1 to 8
1 to 8
1 to 8
1 to 8
Effect
Estimated LT50* 2.3 hr
Genetic effects on mortality of inbred
mouse strains. LT50 for CF1, 3.33 hr;
C57BL/6, 6.53 hr
Increased mortality with cold stress,
adrenal ectomy, and exercise.
No increase with heat or prior N02
Estimated LT50 3.7 hr
Estimated LT50 4.0 hr
Estimated LT50 2.7 hr
Estimated LT50 >8 hr
Reference
Nine et al, 197012
Goldstein et al. ,
197314
Mine et al., 197012
Ibid
Ibid
Ibid
Ibid
*LT50=Time at which 50% of the animals would die during continuous exposure to the indicated
concentration.
-------
TABLE 12-4. INTERACTION WITH INFECTIOUS AGENTS
concentration
Species
ppm Exposure Infective agent
Effect
Reference
Mouse SPF
female Swiss
albino,
strain CD-I
940 to 0.5 to
52,670 28.0
2,800 1.5 18 hr
27,800 14.8 2 hr
ro
vo
en
S. pyogenes
S. pyogenes
S. pyogenes
2,800 1.5 continuous S. pyogenes
or inter-
mittent
7 hr/day,
7 days/wk
6,600 3.5 continuous S. pyogenes
or inter-
mittent
7 hr/day,
7 days/wk,
15 days
Increased mortality with in-
creased time and concentra-
tion.
Gardner et al.,
in press
C X T*=28. Increased mortality by
25% (p < 0.05).
C X T=28 Increased mortality by 65%,
(p < 0.05). Short-term exposure to
high concentration produced greater
effect than exposure to lower con-
centrations for longer periods.
After 1 wk, mortality with
continuous exposure greater
(p < 0.05) than that for
intermittent. After 2 wk,
no significant difference
between continuous and in-
termittent exposure
Increased mortality with increased
duration of exposure. No signifi-
cant difference between continuous
and intermittent exposure. With
data adjusted for total difference
in C X T, mortality essentially
the same.
(continued)
-------
TABLE 12-4 (continued).
10
concentration
Species
Mouse, female
Swiss albino
Mouse
Hamster
Squirrel
monkey
Mouse
Mouse
ug/m
940
940
6,580
65,830
94,050
3,760
1,880
3,760
5,600
ppm Exposure
0.5 Intermit-
6-18 hr/day,
6 mo
0.5 continuous
90 days
3.5 2 hr
35 2 hr
50 2 hr
2.0 3 hr
1 3 hr
2 3 hr
3 3 hr
Infective agent
K. pneumoniae
K. pneumoniae
challenge after
exposure
S. pyogenes
S. pyogenes
S. pyogenes
S. pyogenes
Effect Reference
Increased mortality (p<0.05) Ehrlich and
after 6 mo intermittent H 1Qco28
exposure or after 90 days con- "enry» 13O°
tinuous exposure.
Most sensitive Ehrlich, 196622
Intermediate sensitivity
Least sensitive
NOp toxic to all species and
increased mortality. Each
species had resistance to NO,,
and bacteria.
Increased mortality (p<0.05) Ehrlich et al.,
Exercise on continuously Gardner and ?.
moving wheels during ex- Graham, 1976
posure increased toxicity
to 2 and 3 ppm N02 as
evidenced by increased
mortality.
(continued)
-------
TABLE 12-4 (continued)
vo
oo
N02
concentration
Species
Squi rrel
monkey
Squirrel
monkey
Mouse
ug/m
19,000
9,400
94,000
94,000
9,400
19,000
560
to
940
ppm Exposure
10 continuous
1 mo
5.0 continuous
2 mo
50 2 hr
50 2 hr
5.0 2 mo
10 1 mo
0.3 continous
to 3 mo
0.5
Continued
3 mo. more
Infective agent
K. pneumoniae
and A/PR/-8 virus
K. pneumoniae
and A/PR/-8 virus
None
K. pneumoniae
K. pneumoniae
K. pneumoniae
A/PR-8 virus
Effect Reference
Death within 2-3 days after Henry et al. ,
infection. Increased suscep- 1970^
tibility to infection.
Decreased Tung clearance of
viable bacteria.
One-third died after infection. Henry- et al.,
1970Z<3
Henry, et al. ,
32
Mortality 3/3 1969
Mortality 2/7. Bacteria present
in lung of survivors upon autopsy.
Mortality 25%. Bacteria present
in lungs of survivors at autopsy.
High incidence of adenomatous Motomiya, et
proliferation of peripheral , 1973^^
and bronchial epithelial cells. "'
N0« alone & virus alone caused
less severe alterations.
No enhancement of effect of N02 &
virus.
(continued)
-------
TABLE 12-4 (continued)
ro
i
-------
TABLE 12-4 (continued)
N02
concentration
Species
Mouse
ug/m
3,570
PPiu
1.9
Exposure
4 hr
Infective agent
Infected with
Effect
Physical removal at ar
Reference
w ex- Goldstein et
Mouse
Hamster
Trachea
Ring cultures
7,140 3.8 4 hr
13,200 7.0 4 hr
17,200 9.2 4 hr
27,800 14.8 4 hr
1,880 1 17 hr
4,280 2.3 17 hr
12,400 6.6 17 hr
3,760 2.0
1.5 hr/day
5 days/wk
1,2,3 weeks
S. aureus prior
to NO exposure
Infected with
S. aureus prior
to NOp exposure
NO,
one group
infected with
A/PR/8/34 (HON1)
after NO
posure concentration un-
changed.
Bactericidal activity un-
changed.
7% lower bactericidal activity
(p<0.05).
14% lower bactericidal activity
(p<0.05)
al., 197335
50% lower bactericidal activity
(p<0.05)
S. aureus after No significant effect.
Goldstein et al.,
6% decrease in bactericidal
activity.
35% decrease in bactericidal
activity (p<0.05).
3 to 4 wk following NO,,
significant decrease in
ciliary activity (25 and
63%). Minimal damage
to epithelium.
1973
35
Schiff, 1977
211
-------
TABLE 12-5. MUCOCILIARY TRANSPORT
Species
Rat, female
Guinea pig
trachea
ciliated
cells
N02
concentration
o
ug/m ppm Exposure
11,280 6 7 days/wk,
6 wk
71,500 38 6 min
Effect
Increase in TPFF and FET: decrease in muco-
ciliary velocity, p<0.02. Functional
impairment reversed within 1 wk.
In Vitro: 90% reduction in ciliary beat.
Reference
Giordano and~7
Morrow, 19724
Kita and Omichi
197438
ro
O
-------
TABLE 12-6. ALVEOLAR MACROPHAGES
o
PO
N02
concentration
Species
Mouse
Rats
ug/m
940
or
1,800
940
or
3,760
18,800
47,000
ppm
0.5
1.0
1.0
0.5
or
2.0
10
25
Exposure
continuous 940
ug/nT 4, 12, 24 wk
with 3 hr oeaks at
1,800 ug/m3, 5
days/wk
continuous 3,760
ug/m 4, 12, 24
wk with 1 hr
peaks at 3,760
Mg/m , 5 days/wk
24 hr
24 hr
Effect Reference
AM* surface unchanged. Aranyi et al. ,
197640
Distinct morphological alterations after Ibid
21 wk total exposure.
Loss of surface processes, appearance of
fenestrae, bleb formation, denuded surface
areas, and complete deterioration of
cells were noted.
Phagocytic activity was unchanged. «atz anc' Laskin,
42
Depressed phagocytosis was seen 1975
Guinea pig
on 3rd day of culture. Macrophages
apparently recovered by 7th day
of culture.
18,800 10
7 wk
continuous
63% increase in epithelial cells
positive for macrophage congregation.
Presence of 7 or more AM on a single 1968
epithelial eel 1-2.5 times more frequent.
8% more instances of macrophage congrega-
tion relative to control.
Sherwin et al.
43
(continued)
-------
TABLE 12-6 (continued)
N02
concentration
Species
Guinea pig
Rabbit
Rabbit
ug/ra
188
1,880
3,760
and
9,400
13,200
47,000
ppm Exposure
0.1 30 min
1.0
2.0
and
5.0
7 24 hr
25 3 hr
Effect
Decreased bactericidal activity,
reduction in ATP content, and changes
in morphology were noted. Cyto-
plasma projections were seen at
at 0.1, 1.0. and 2.0 ppm. At 2
ppm nucleus was hard to identify.
Increased rosette formation in AM
treated with wheat germ lipase.
No development of resistance with
Reference
Voisin et al. ,
1977220,221
Hadley et al. ,
197744
Valand et al. ,
O
co
Rabbit
Rabbit
47,000 25
3 hr
9,400
28,200
47,000
94,000
5.0
15
25
50
3 hr exposure
after infection
N02 exposure immediately after in-
infection with parainfluenza-3
virus or up to 24 hr before viral
inoculation. Increased lung ab-
sorption of virus, and no effect
on viral potency were noted.
Viral uptake not affected when in-
fected with para-influenza-3 virus
after N02 exposure.
No inhibition of viral RNA synthesis
Twice as many virus attached and
penetrated exposed AM.
Normal AM had increased resistance
(75%) to pox virus.
1970
45
Williams et al.,
197246
Actop7and Myrvik,
1972^'
Partial loss of resistance, decreased
phagocytic capabilities, infection with
para-influenza-3 virus, AM challenged
with rabbit pox virus. Reduction in
resistance, stimulation of Op uptake plus
hexose-monophospate shunt activity.
-------
TABLE 12-6 (continued)
Species
Rabbit
Rabbit
concent!
ug/m
19,000
15,000
to
112,800
0
43,300
Cation
ppm
10
8
to
60
0
23
Exposure
3 hr
2 hr
1 hr
1 hr
Effect Reference
50% inhibition of phagocytic activity Gardner et a!.,
Increased proportion of polymorpho- 1969
nuclear leukocytes in lavage fluid
persisted for more than 72 hr.
Increased mitochondria!, and Mintz, 197248
Rabbit 43,300 + 23 + 1 hr
2.5 2.5
mmole iranole
ascorbate ascorbate
Rat alveolar 4,512 2.4 1 hr
macrophages
Rat alveolar
macrophages
Rat alveolar
macrophages
22,748 12.1 2 hr
6,768
3.6
1 hr
decreased cytoplasmic NAD /NADH
were observed.
Addition of ascorbate abolished
mitochondrial NAD /NADH changes.
In Vitro: 64 percent increase in
agglutination by concanavalin A,
completely inhibited by ormethyl-
mannose
48
Mintz, 1972
Goldstein et al.,
1977212
In Vitro: 40 percent increase in agglu-
tination of concanavalin A to macrophages.
Completely inhibited by ormethylmannose
n Vitro: Incubation of macrophages with -
H-concanavalin A revealed no significant
alterations in binding. At this concen-
tration, agglutination was enhanced 47%.
*AM = Alveolar macrophage
-------
TABLE 12-7 IMMUNOLOGICAL EFFECTS
Pollutant concentration
Species Pollutant ug/m
pprn
Exposure
Effects
Reference
o
01
House,
male, SPF
Swiss albino,
CD strain
NO.
Monkey N02
3,760
or
940 with
dally 1 hr
3,760
Monkey hX>2 9,400
1,880
Guinea pig N02 10,000
Guinea pig N02 9,400
Guinea pig NO. 9,400
or
28,200
2 or 0.5
with
daily 1 hr
2.0
5.0
1.0
5.3
5.0
5.0
or
15
24 hr/day, 5 days/wk
3 mo followed by
vaccination with
influenza
A2/Taiwan/l/64
virus
Intratracheal
injection of mouse
adapted influenza
A/PR/8/34 virus
24 hr prior to NO,
exposure for 133 nays
Continuous 493 days;
challenge 5 times
with monkey adapted
influenza A/PR/8/34
virus
33 days, continuous
4 hr/day, 5 days/wk
7.5 hr/day, 5 days/wk
4-fold decrease in serum neutraliz- Ehrlich et
al., 1975
50
ing antibody.
Hemagglutination inhibition titers
unchanged before virus challenge.
Decreased serum IgA.
Increased serum IgG,, IgM, and IgG~
(p < 0.05).
Serum IgA unchanged IgM increased
(p < 0.05) after virus.
Hemagglutination inhibition titers Fenters et
or amnestic response unchanged.
Initial depression in serum neu-
tralization titers with return to
normal by 133 days.
al., 1971
51
1973
,53
Hemagglutination inhibition titers Fenters et al.,
unchanged.
Increased mean serum neutralizing
antibody titers 93 days exposure.
Titers increased 7-fold 21 days post
virus.
Titers Increase 11-fold 41 days post
virus.
No effect on antibody production.
Increased lung tissue serum anti-
bodies in all groups after 160
hr N02.
Antweiller
197554
Balchum et
al., 196555
(continued)
-------
TABLE 12-7 (continued)
Pollutant concentration
Species Pollutant
ppm Exposure
Effects
Reference
Guinea pig N02 1,880
1.0 6 mo followed by
intranasal
challenge with
D. pneumoniae
Increased respiratory infection
Decreased hemolytic activity of
complement.
Decrease all iimtunoelectrophoretic
fractions.
Increased mortality following D.
pneumoniae
Kosmider et
al.,197356
Guinea pig
ro
i
N02
°3
so2
37,600,
75,200, or
131,700
1,960,
9,810, or
19,600
52,400
157,200
471,000 or
864,600
20,
40, or
70
1.0,
5.0, or
10
20,
60.
180, or
330
Gas 30 min, then
aerosol of egg
albumin or bovine
serum albumin for
45 min, repeated
5-7 times on
different days
Anaphylactic attacks in 50% ex-
posed animals by 5th aerosol
administration. No effect at
low levels. Hemagglutination tests
unchanged. Less antigen needed
in active cutaneous anaphylaxis
test at high levels (p<0.05).
Animals died of systemic anaphylaxis
following 5th and 6th albumin exposure
Less antigen needed in active cutaneous
anaphylaxis test at high S02 (p<0.05).
Matsumura,
1970a57
(continued)
-------
TABLE 12-7 (continued)
ro
C3
Species Pollutant
Guinea pig 0,
j
NO,
e.
SO,
£.
Guinea pig 0,
o
NO.
£.
so2
Pollutant
M9/«3
9,800 or
3,900
150,000 or
75,200
c
1.0 x 10°
2,900
3,900,
5,900, or
6,900
56,400,
75,200.
84,600, or
94,000
1,170,000
i ccn nnn
concentration
ppm
5.0 or
2.0
80 or
40
400
1.5,
2.0,
3.0, or
3.5
30.0,
40.0,
45.0, or
50.0
450.0,
**>_ c.f\f\ n f\»>
Exposure
Sensitized to egg
and bovine serum
albumin by intra-
peritoneal injection;
3 days later exposure
for 30 rain to pollu-
tants then antigen
30 min later
Exposure 30 win
then nebulized
acetylcholine
Effects Reference
Mortality Matsumura,
75% Ig70b58
35% ly/UD
37%
20%
3% (not significant)
Mortality increased at 0,>2 ppm Matsumura et al
197259
U 1 f.
Mortality increased at N02 >50 ppm.
No adverse effects.
1,820,000 700.0
-------
TABLE 12-8.
EFFECTS OF N02 ON LUNG BIOCHEMISTRY
N0_
concentration
Species
Rat
Rat
Rat
ug/m
1,880
4,330
11,560
5,600
5,400
ppm
1.0
2.3
6.2
2.9
2.9
Exposure
4 days
continuous
Continuous
20 days
24 hr/day,
5 days/wk,
9 mo
Effect
GSH reductase (EC 1.6.4.2) and glucose-6-
phosphate dehydrogenase (EC 1.1.1.49)
increased at 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.
Decrease in linoleic and linolenic acid
of lavage fluid.
Increase in lung weight (12.7%) and de-
crease 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.
Reference
Chow et al. ,
1Q-7y|81
J.3/4
Menzel et al . ,
197216
Arner and
Rhoades, 197363
ro
i
_^
o
00
Rat 75,200 40 5 hr Increased incorporation of C-palmitic
acid in lung lecithin. Accumulation of
disaturated lecithin by 6 hr post-NO?
with maximum accumulation by 48 hr
Rat 18,800 10.0 Continuous Decrease in unsaturated fatty acids in
4 wk lavage and lung tissue.
Vitamin E as (d,l-a-tocopheryl acetate
100 mg/kg diet) reduced N0_ effect.
Rat 37,600 20 8 hr/day x 2 High level of dietary antioxidants pre-
and and 8 hr/day x 1 vented acute mortality and weight loss of
47,000 25 survivors.
Blank. el al.
^15
Menzel et al.,
197216
Ibid
(continued)
-------
TABLE 12-8 (continued)
ro
o
10
NO
concentration
Species
Rat
House
Guinea
pig
ng/n.3
75,200
132,000
940
or
1,880
940
or
1,880
9,400
11,000
15,000
28,000
or
53,000
740
ppm
40
70
0.5
or
1.0
0.5
or
1.0
5
6
8
15
or
28
0.4
Exposure
2 hr
continuous
1 yr, 5 mo
continuous
1.5 yr
14-72 hr
4 hr/day x
30 days
continuous
14 days
7 days
4 hr/day,
7 days
Effect
Benzo(a)pyrene hydroxylase (EC 1.14.12.3),
phenol-0-methyl transf erase (EC 2.1.1.25)
and catechol-0-methyl transfcrase (EC 2.1.1
not affected.
No increase in lipofuscin or glutathione
peroxidase.
Vitamin E (30 or 300 mg/kg) prevented
Upofuscin accumulation (EC 1.11.1.9).
Growth reduced;
Vitamin E (30 or 300 mg/kg diet) improved
growth.
Increase in lung protein (14-58 hr) by
radio-label.
Increase in GSH reductase (EC 1.6.4.2) and
gl ucose-6-phosphate dehydrogenase
(EC 1.1.1.49) activities.
Increase in lung protein.
Increase in GSH levels, GSH reductase,
gl ucose-6-phosphate dehydrogenase, and GSH
peroxidase.
Increase in acid phosphatase (EC 3.1.3.2).
Reference
Law et al. ,
.el'"8"
Ayaz and Csallany,
197767
Csallany, 197566
Ibid
Ibid
Ibid
Ibid
Sherwin et al. 1974
76
(continued)
-------
TABLE 12-8 (continued)
ro
NO.
concentration
Species ug/m3 ppm
Guinea 740 0.4
pig
Guinea 940 0.5
pig
Guinea 940 0.5
Pig
Guinea 3,760 2.0
Pig
Hamster 56,400 30
Exposure
continuous
1 wk
8 hr/day.
7 days
continuous
8 hr/day,
4 mo
continuous
1-3 wk
continuous
to 30 days
Effect
Increase in lung protein content, most
likely due to plasma leakage (See edema
section 4.2.3.6)
some may result from cell death.
Increase in serum LDH, CPK, SCOT, SGT and
cholinesterase, lung and plasma lysozyne.
Decrease in RBC GSH peroxidase.
Lung GSH peroxidase unchanged.
Decrease in plasma cholinesterase and
RBC or lung GSH peroxidase unchanged.
Increase in lung acid phosphatase, and
plasma and lung lysozyme.
Increase in number of lactic acid
dehydrogenase (EC 1.1.2.3) positive cells
with time of exposure.
Suggests Type 1 (LDH negative) cells
decrease as Type II (LDH positive) cells
increase.
Increase in lung proteolytic activity and
in serum antiproterase at 2 days.
Declined to normal values at 50 days.
Reference
Sherwin and
145
1973
Donovan et
Menzel, et
no
1977. 83
Donovan et
1 fi~jrO£
Carlson
al. ,
al..
al.,
1976
Menzel et al. ,
O3
197783
Sherwin et
74
1972
Kleinerman
Rynbrandt,
al.,
and
197684
(continued)
-------
TABLE 12-8 (continued)
ro
i
Species
Hamster
concentration
ug/m ppm
56,400 30
Exposure
continuous
to 50 days
Effect
Increase in lung proteolytic activity
Reference
Rynbrandt and
Klpinprman 19;
,,85
Hamster 18,800 10
(Vitamin A
deficient)
Rabbit
1,880 1.0
9,400 5
to to
94,000 50
5 hr
once a week
4 wk
continuous,
2 wk
3 hr
Not active at physiological pH of 7.2
Attributed to cathepsins, A, B,, B., C, 0,
and E.
lipid droplets in alveolar walls.
Alveolar necrosis and thickening of
epithelial basement membrane and
calcium deposits on inner and outer
surfaces. Presence of virus particles
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.
Decrease in lecithin synthesis after 1 wk;
Less marked depression after 2 wk.
Benzo(a)pyrene hydroxylase (EC 1.14.12.3)
activity or tracheal mucosa not affected.
0. decreased activity.
Kim, 1977"
Seto et al., 1975
Palmer et al.,
197279
65
-------
TABLE 12-9. EFFECT OF N02 ON LUNG MORPHOLOGY
ro
i
concentration
Species
Rat
Rat
Rat
Rat
Rat
Rat
Rat
M9/«3
3,760
32,000
18,800
28,200
28,200 to
32,000
28.200
28,200 to
32.000
ppm
2.0
17
10
15
15 to
17
15
15 to
17
Exposure
continuous,
43 days
continuous,
43 days
continuous,
90 days
continuous,
75 days
continuous,
lifetime
48 hr
48 hr
Effect
No changes in terminal bronchi.
Cilia lost and altered by 72 hr.
Greater cilia loss and focal hyperplasia
by 7 days.
Regeneration of cilia by 14 days.
Substantial recovery by 21 days.
Earlier and greater injury of same type
and sequence as at lower level with loss
of Type I cells.
Decrease in length and weight of neonates
exposed, delivered and reared in N0?.
Delayed lung development in progeny exposed
in utero and raised in N0~.
75 days required to make Dp deficit.
Bronchial epithelium hypertrophic and meta-
plastic.
Increased mucus.
Connective tissue damage.
Fibrosis at junction of respiratory bronchiole
and alveoli.
Emphysema.
Increased cell division, especially Type II
cells.
Alveolar macrophage division seen with DNA
synthesis.
Reference
Stephens et al. ,
1972105
Ibid
Freeman et al . ,
1974117
Sherwin et al . ,
1973118
Freeman et al . ,
1972106
Stephens et al. ,
1971107
Freeman et a! . ,
196896
Evans et al. ,
197468
Evans et al . ,
1973100
(continued)
-------
TABLE 12-9 (continued)
NO.
concentration
Species
Guinea pig
Rabbit
Dog
Dog
Cat
ug/m
18,800
470
18,800 to
47,000
69,000
19,100 to
21,500
ppm
10
0.25
10 to
25
37.2
10.2 to
11.4
Exposure
continuous,
6 wk
4 hr/day,
5 days/wk
24 or 36 days
4 hr
12 mo
Effect
Type II cell hypertrophy, 1 to 6 wk exposure
with increased lamellar bodies within Type II
cells.
Isolated swollen collagen fibers.
Emphysema and death.
Interstitial edema.
Some alveolar desqtiamation.
Intraluminal mucus.
Increase in goblet cells.
Reference
Yuen and Sherwin,
1971122
Buell, 1970108
Riddick et al. ,
196892
Guidotti and
Liebow, 1977116
Kleinerman et al . ,
1976115
Cat
co
150,000
80
3 hr
Thickening of epithelium. ,
Fly ash (9,950 to 10,200 \ig/m ) had no effect.
12 and 24 hr post-N02, 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 based lamina in lungs 12 and 24 hr post-NOg.
Serous and serofibrinous edema, neutrophilic
emigration and extravasation of erythrocytes
evident through 24-hr post-NO- tissues. Peri-
bronchiolar congestion and edema. 50% proximal
alveolar spaces filled with serous edema fluid.
Increased number of AM and hyperplasia of type
II pneumocytes.
Langloss et al.,
1977222
-------
Table 12-9 (continued)
I
-t»
concentration
Species
Mouse
Mouse
Mouse
Mouse
Guinea pig
Guinea pig
ug/m3
940
940
1,030 to
3,000
1,880 to
2,820
188 +
daily 2 hr
spike of
1,880
3,760
3,760
ppm
0.5
0.5
0.55 to
1.6
1.0 to
1.5
0.1 +
daily
spike
of 1.0
2.0
2.0
Exposure
12 mo,
continuous
6, 18, or
24 hr/day, up
to 12 mo
5 wk.
continuous
1 mo,
continuous
6 mo.
conintuous
continuous.
3 wk
continuous,
3 wk
Effect
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:
Fibrosis
At 12 mo:
Bronchial hyperplasia
Alveolar damage.
Damaged cilia, increase in mucus secretion
by nonciliated cells.
Same morphology as others.
Recovery for 1 to 3 mo showed lymphocyte
inf ilitration up to 3 mo.
Emphysematous alterations.
Increased number of LDH positive cells/
alveolus (presumably Type II cells)
Type II cell hypertrophy.
Reference
Hattori, 1973119
Hattori and
Takemura, 1974
Blair et al. ,
1969109
191
Miyoshi, 1973"1
Chen et al. ,
1972114
i J / f.
Port et al.,
1977112
Sherwin et al . ,
197274
Sherwin et al . ,
1973118
-------
Table 12-9 (continued)
ro
i
concentrati on
Species
Rat
Rat
Rat
Rat
Rat
Rats
House
ug/m3
32,000
32,000
28,000 to
32,000
28,000
* 28,000
28,000 to
31,960
940
ppm
17
17
14 to
17
15
15
15 to
17
0.5
Exposure
conti inious ,
1 day
continuous,
90 days
24 hr
continuous
1,4,10,16 and
20 wk
subacute
12 and 24 hr.
30 to 45 days,
continuous
Effect
Cell division seen at 24 hr, peak at 2 days,
decreased to preexposure by 6 days.
At 3,760 ug/m cell devision of Type II cells
peripheral to terminal brochiolar-alveolar
junction seen.
Collage damage.
Large fibers and thickened basement membrane.
Division of Clara cells replaced damaged
ciliated cells.
Hyperplasia of terminal bronchiolar
and alveolar epithelium reversible
on discontinuation of exposure;
alterations of interstitial structural
features of alveoli are not.
Newborn rats up to age 3 wk relatively
persistent to exposure compared to
mature rats
Loss of cytoplasmi c projections
of nonciliated (Clara) cells and
exfoliation of ciliated cells
Damage to tracheal mucosa and cilia.
Reference
Evans et al. ,
1972103
Stephens et al. ,
1971107
Evans et al. ,
1976104
Freeman et al. ,
1978233
711
Lunan et al. J
Evans.et al. ,
1978233
Hattori et al . ,
1Q7,1W
Nakajina et al.,
1969111
-------
TABLE 12-9 (continued)
N02
concentration
Species
Monkey
Monkey
Monkey
Monkey
pg/m3
470
1,130
1,510
2,820
1,880
3,800
9,400
and
18,800
ppm
0.25
0.60
0.75
1.5
1.0
2.0
5.0
and
10
Exposure
4 hr/day,
4 days
continuous,
493 days
14 mo
continuous,
90 days
Effect
Thickening of alveolar wall and basal lamina.
Instertitial collagen.
Virus-challenged animals had slight emphysema,
thickened bronchial and bronchi alar epithelium.
Hypertrophic bronchiolar ephithelium, particu-
larly in the area of respiratory bronchiole.
Nad aerosol had no added effect.
Infiltration of macrophages , lymphocytes, and
occasionally polymorphonuclear leukocytes.
Hyperplasia of bronchiolar epithelium and Type
II cells.
Reference
Bils, 19768G
Renters, 197353
Furiosi et al . ,
1973113
Busey et al. ,
1974123
Hamsters
Hamster
trachea
cells
28,200
1,880
15
24 hr
1.0
6 hr
H-thymidine (TdR) 24 hr post-N02, 1 and 24
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% AH labelled. No change in
AM population.
Iji Vitro: Cells lost ability to form
macroscopic colonies
Hackett, 1978
223
Samufilson et al. .
1978216
225
0.12
up to
6 hr
Lung cells (V-79) failed to divide and
form micro-colonies.
-------
TABLE 12-10. PULMONARY FUNCTIONS
ro
i
Pollutant
concentration
Species Pollutant \ig/n
Rat N02 1,500
Rat NO. 28,200
Rat NO, 5,400
tm
Rat N02 3,800
Rat, cat NO, 940 to
* 3,800
Hamster N02 38,400
ppm Exposure
0.8 Continuous,
2.75 yr
15 Continuous,
lifetisio
2.9 24 hr/day.
5 days/wk
9 mo
2.9 2 yr
0.5 to Continuous
20
20.4 20 to 22
hr/day ,
7 days/wk
12 to 14 mo
Effect
Increased respiratory rates.
Increased tidal volumes 50 to 350%.
Minor increased resistance and de-
creased compliance 15 to 20 wk.
Increased emphysema.
Decreased (13% p < 0.05) lung com-
pliance and lung volume.
Resistance or dynamic compliance
unchanged.
Tachypnea.
Increased respiratory rates
Decreased arterial oxygen pressure.
Impaired 0_ uptake in blood.
Increased total pulmonary resistance
during passive ventilation and maximal
airflow with concurrent decreased flow
values.
Reference
Freeman et al. ,
QQ
1966^
Haydon et al. ,
195691
Freeman et al. ,
,07,106
1972
Arner and Rhoades,
197363
Freeman et al . ,
iqfift96
J..7OO
Zorn, 1975124
Kleinerman, 1977
Return to normal within 3 mo.
Static lung compliance unchanged.
Decreased surface area.
(continued)
-------
TABLE 12-10 (continued)
00
Pollutant
concentration
Species
Hamster
Cat
Guinea pig,
female
Guinea pig
Pollutant
NO,
N02
fly ash
elutriated
dust of fly
ash
NO,
so;
"°2 * SO,
NO,
M9/™
56,400 to
65,800
19,200 to
21,400
10,000 to
10,200
2,100 to
1,600
10,000
10,000
10,000 +
10,000
9,400
ppm
30 to
35
10.2 to
11.4
5.3
3.8
5.3 +
3.8
5.0
Exposure
7 to 10 days,
followed by
papain
Continuous,
12 mo
6 days/wk,
6 mo
7.5 hr/day,
5 days/wk,
5.5 mo
Effect
N02 + papain increased lung volumes.
N0» + papain increased pulmonary
resistance (p < 0.05).
Pulmonary resistance unchanged by papain.
Increased total airway resistance and
upstream resistance.
Decrease in static lung compliance.
Internal surface area unchanged.
No effect due to fly ash.
Respiratory frequency, flow rate, or
minute volume unchanged in all regimens.
No increase in total resistance to airflow.
Reference
Niewoehner and
Kleinerman, 1973128
Kleinerman et al. ,
1976115
Ibid
Antweiler and
Brockhause, 1976
Balchum et al . ,
196555
Guinea pig
NO
9,800
5.0
4 hr
Increased respiratory rate.
Decreased tidal volume.
Return to normal levels in clean air.
Murpbyn
"U
et al . ,
(continued)
-------
TABLE 12-10 (continued)
PO
i
Species Pollutant
Rabbit N02
Rabbit, male N02
and female
albino
Rabbit N02
Squirrel N02
monkey, male
Pollutant
concentration
ug/m3 ppm Exposure Effect
56 goo 30 15 rain Redistribution of lung perfusion resulting
' in reduced storage activity in peripheral
zones of lung.
15,000 to 8 to 24 hr/day, Increased nonelastic resistance and
22*600 12 12 wk functional residual capacity.
' Static lung compliance unchanged.
9^00 5.0 6 hr/day Respiratory function unchanged.
94,000 50 2 hr Respiratory rate increased 2-fold.
Decreased tidal volumes.
Reference
von Nieding et al
1973131
Davidson et al. ,
1967132
Wagner et al . ,
19G5133
Henry et al. ,
196932
and female
Squirrel N02
monkey, male
and female
Squirrel N02
monkey, male
and female
Squirrel N02
monkey, male
and female
Squirrel N02
monkey, male
and female
94,000
94,000
65,800
18,800
28,200
50
50
35
10
15
Respiratory rates high for 72 hr, return
to normal by 7 days.
2 hr, immediate Tidal and minute volume decreased by 4 hr.
challenge with Mortality: 2/3 within 5 to 72 hr.
K. pneumonias Increased respiratory rate.
2 hr, challenge Tidal volume decreased.
with K. pneu- Respiratory rate increased.
monlae after Death within 72 hr.
24 hr
Ibid
2 hr, K. pneu-
monlae chal-
2 hr, K. pneu-
mon1ac~chal-
lenge
(continued)
No mortality.
Less drastic effects on respiratory
function.
Decreased tidal volume, increased respira-
tory rate 2 to 4 hr post exposure.
No enhancement by K. pneumoniae.
Ibid
Ibid
-------
TABLE 12-11. STUDIES OF POTENTIAL HYPERPLASIA, MUTAGENESIS, TERATOGENESIS
Pollutant
concentration
Species
Mouse
Mouse
Mice, male &
female, SPF
CD-I
_^ Mouse, C3H
ro male
1
ro
o Mouse, female
strain ddo
Pollutant
N02
N02
Synthetic
N02
CO
°3
so2
NO,
N02
CO
ug/m
18,800
9,400 to
18,800
Smog
1,500
5,750
760
5,700
190, 1,880
9,400, 18,800
940 to
1,500
57,500
PPm
10
5.0 to
10
0.3
5.0
0.38
2.2
0.1,
1.0,
5.0,
10
0.5 to
0.8
50
Exposure
2 hr/day,
5 day/wk
50 wk
2 hr/day
5 day/wk
50 wk
23 to 24
8 to 12 mo
6 hr
continuous,
30 days
Effects
Mice given 4-nitroquinol ine-1-oxide (carcinogenic agent)
+ N02 decreased incidence of lung tumors.
Mice given 4-nitroquinoline-l-oxide and NO-; no effect
on tumor production.
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 .
2 wk post-exposure no increase in chroniatid or chromo-
some-type alterations in leukocytes or primary spenna-
tocytes.
No mutagenic effects noted.
Increased hyperplasia terminal bronchioles to alveolus.
No difference from N0? alone.
CO (100 ppm) alone for 30 days failed to induce hyper-
plasia.
Reference
Otsu and Ide ,
1975137
Ide and Otsu
1973
Loosl i et al . ,
1972139
Gooch et al
,,,-,144
1977
Nakajima et al.
141
1972 L
(continued)
-------
TABLE 12-11 (continued)
Species
Rat
ro
ro
Rat
Rat, prior
to breeding
Pollutant
concentration
Pollutant
NO-
9,400
NO,
NO-
18,800
2,360
5.0
10
1.26
Exposure
Effects
continuous for
periods up to
11 wk
continuous from
pregnancy up to
3 mo after de-
livery
12 hr/day
3 mo
Appearance of hyperplastic foci in the shape of 2 to 4
layer pyramids by 3 wk.
Decreased ciliated cells.
Extensive hyperplasia (3 to 4 layers of epithelium),
cuboidal metaplasia in adjacent alveoli by 5 wk.
Hyperplasia in all bronchioles, decreased bronchiolar
lumina.
Polymorphous epithelium extensive.
Bronchiolar epithelium contained only 2 layers.
Appearance of 1 layered epithelium as well.
Increased number of ciliated cells.
By 11 wk return to 1 layer epithelium.
Lungs at indefinite state of repair from week 7 on.
Decreased litter size and increased mortality of neo-
nates up to 15 days post delivery.
No teratogenic effects noted.
No effect on fertility.
Decrease in litter size and neonatal weight.
No teratogenic effects.
Reference
Rejthar and
Rejthar, 1974
140
Freeman et al.,
1974117
Shalamberidze
and
Tsereteli, 19711
Rats, SPF
Auto Exhaust
CO
NO.
C0? (0.07 and
0.37%)
Aldehydes
58,000
50
(0.2
and
23)
(0.1
and
2.0)
6 hr/day, Auto exhaust had no biological effects when NO was
5 days/wk, 0.2 ppm. x
2 mo to Exposure to NO (23 ppm) increased number of
2 yr spontaneous tumors, cutaneous abscesses, and bilateral
renal sclerosis.
No tumors or abscesses in lungs.
Stupfel et al.,
1973142
-------
TABLE 12-12.
TOLERANCE TO N02 EXPOSURES
ro
i
ro
ro
Species
Mouse
Rat
Concentration
pg/m ppm Duration
9,400 5.0 continuous
7 wk
47,000 25 continuous
7 wk
9,400 5.0 13 mo
47,000 25 6 hr/day
2 days
Effects
Challenge with IC50 (113 pg/m3 for 5 hr)
caused 28% less mortality than naive mice
Challenge with 132 pg/m x 5 hr gave no
mortality but 29% in naive mice. Tolerance
disappeared in 3 mo.
Zero percent mortality to 47 pg/m for 6
wk compared to 67% in controls.
Increased tolerance to 75 ppm N0«.
Increased G6PO, catalase, 41% increase
cytochrome oxidase. No effect on
superoxide dismutase.
Reference
Wagner et,,..
al., 19651"
Ibid
Ibid
Crapo et al. ,
9?^
1978"*
-------
ro
ro
CO
TABLE 12-13. PRODUCTION OF LUNG EDEMA BY N0?
Pollutant
concentration
Species ug/m ppm Duration
Mouse 940 0.5 5 days/wk for
3 or 6 wk
Mouse 7,500 to 4 to continuous
13,000 7 14 days
flamster 56,400 30 continuous
up to 30 days
Guinea pig 750 0.4 1 wk
Effect
Horseradish peroxidase used as a marker for
proteins showed greater sequestering in exposed
mice at 3 wk than 6 wk.
Suggests edema.
H rabbit albumin infiltration indicates lung
edema .
Lung wet weight elevated at 1 and 30 days.
Increased proteins in lung lavage fluid of
exposed animals detected by disc gel
electrophoresis.
Reference
Sherwin et al. ,
1977147
Sherwin and
Richters, 1971146
Kleinerman and
Rynbrandt, 197684
Sherwin and
Carlson, 1973145
-------
TABLE 12-14. NITROGEN DIOXIDE-INDUCED CHANGES IN HEMATOLOGY
ro
Species Pollutant
Rat N02
Guinea pig NO-
Guinea pig N02
so2
N02
so2
NH3
Guinea pig N02
Mouse NO-
CO
House, male NO-
Rabhit NO,
C
Pollutant
concentration
3
ug/m ppm
100
940
940 +
1.000
or
940 +
1,000 +
70
680
940 to
1,500 +
58,000
1,500
2,400 to
5,200
0.05
0.5
0.5 +
0.39
or
0.5 +
0.39 +
0.1
0.36
0.5 to
0.8 +
50
0.8
1.3 to
3.n
Exposure
90 days
7 days
8 hr/day
120 days
7 days
1 to 1.5 mo
5 days
2 hr/day
15 f. 17 wk
Effects
No effect on blood hemoglobin or
erythrocytes.
Decrease in RBC GSH peroxidase (p < 0.001).
Same effects in both exposures.
Increased WBC, decreased RBC, decreased
neutrophils and eosinophils, increased
lymphocytes.
Increased red blood cell 0-2,3-diphospho-
glycerate.
Addition of CO and N02 failed to affect
carboxyhenionlobin.
Mo effect on methenoglobin.
Increased leukocytes followed by decreased
pliagocyf.ic activity.
Reference
;Shalamberidze,
1969148
Donovan et al . ,
1976R2
Menzel et al . ,
197783
Kosmider et al . ,
197578
Mersch et al . ,
19731"9
Nakajima and
Kusumoto, 1970lf'°
Nakajima. and
Kusumoto 1968151
Mitina, I96?1"2
Decreased RBC.
(continued)
-------
TABLE 12-14 (continued).
Pollutant
concentration
ro
i
ro
en
Species
Rabbit
Rabbit
Rabbit
Monkey
Monkey
Monkey and
Rat
Pollutant
S0?
e.
N02
so2
NO,
2
NO,
£.
NO,
C.
NO 2
Nad
uq/m
5,000
2,400 +
5,000
45,100
1,880
9,400 +
18,800
3,800 +
330
ppm
1.9
1.3 +
1.9
24
1.0
5.0 +
10
2.0 +
0.1
Exposure
2 hr/day
15 wk
2 hr/day
15 wk
4 hr
493 days
followed by
influenza
A/PR/8/34
vi rus
90 days
14 mo
Effects
Decreased phagocytic activity leukocyte.
No effect on RBC.
No effect on RBC.
Increased nitrite & nitrate in blood.
Thought to react with hemoblobin producing
methemoglobin.
No effect on hematocrit or hemoglobin.
Following viral challenge increased leuko-
cyte count.
No effect on hematological parameters.
With or without Nad produced polycythemia
in rats & monkeys with reduced mean corpus-
/•iilav wnlnma 4- nnv"tnal rni-niie rn 1 A r" homnnlnhin
Reference
Mitina, 1962152
Ibid
Svorcova and
Kaut, 197111
Renters et al. ,
107-3^3
iJ/O
Coate and Badger
1974134
Furiosi et al . ,
^y^113
Dog
NO,
48,900
26
191 days
Neutrophi I/lymphocyte ratio tendency to shift
upwards.
Increased WBC disappeared following cessa-
tion of NO-.
Decreased Rematocrit, hemoglobin, increased
mean corpuscular volume, increased mean
corpuscular hemoglobin.
Lewis et al.,
1973136
(continued)
-------
TABLE 12-14 (continued).
Pollutant
concentration
Species
Dog
Dog
Pollutant pg/rn
NO-
NO
N02
NO
NO,
73,000 to
310,000
940 or
1,880 or
1,840 -t-
2,450
ppm
39 to
164
O.R or
1.0 or
1.5 +
1.3
Exposure
5 to 60 min
16 hr/day
7 days/wk
4 wk
Effects
No effect on hematocrit or platelet counts.
No effects on hematocrit carboxyhemoglobin
or methemoglobin
Reference
Carson et al. ,
1962153
Block et al.,
1973154
ro
i
ro
-------
TABLE 12-15. CENTRAL NERVOUS SYSTEM AND BEHAVIORAL EFFECTS
Pollutant
concentration
Species Pollutant
Rat, male NO
SPF x
Rat N02
Rat N02
Rat N02
Rat N02
Rat N02
Mouse, male NO.
Guinea pig N02
uq/m3
not reported
9,400
1,880
600
100
75,200
37,600
15,040
14,000
1,000
ppm
0.2 and
23
5.0
1.0
0.32
0.05
40
20
8
7.7
0.53
Exposure
6 hr/day,
5 days/wk,
2.5 mo to
2 yr
8 wk
8 wk
3 mo
3 mo
5 hr
1 day
19 days
6 hr
8 hr/day,
180 days
Effect
Decreased sound avoidance reflexes,
learning rate lowered.
Rate performance decreased 25% by 5th and
6th wk of exposure
More or less constant performance with
only slight tendency to deterioration.
Decreased conditioned reflexes.
No effect on CNS.
20% decrease swimming endurance
10% decrease swimming endurance
No effect swimming endurance
Decreased voluntary running activity.
Return to normal within 24 hr post
exposure.
Increased mal ate, sorbitol, lactate
dehydrogenase.
Reference
14?
Stupfel, 19731
Tusl et al.,
1973155
Jakimcuk and
Celikanov, 1958156
Shalamberidze,
1969148
Campb.il
1976ZZ4
Murphy et al . ,
1964130
Drozdz et al . ,
1975157
Decreased ATPase and 5-nucleotidase.
Increased 1,6-diphosphofructose aldolase.
Increased isocitrate, alpha-hydroxybutyrate
dehydrogenase. Increased phosphocreatine
kinase and cholinesterase.
-------
TABLE 12-1S. BIOCHEMICAL MARKERS OF ORGAN EFFECTS
ro
i
«*
ro
oo
N02
concentration
Species pg/m
Guinea pig 940
Guinea pig 940
Guinea pig 940
Guinea pig 1,000
Guinea pig 1,880
Guinea pig 2,000
Guinea pig 2,000
ppm
0.5
0.5
0.5
(NO :
mainly N0_)
1.0
1.1
1.1
Exposure
7 days
4 mo
continuous,
14 days
8 hr/day,
180 days
6 mo
8 hr/day ,
180 days
8 hr/day,
180 days
Effects
Serum lactic dehydrogenase, total creatinine phosphokinase,
SCOT & SGPT elevated cholinesterase and lysozyme elevated.
Lysozyme elevated; cholinesterase depressed.
Albumin and globulins found in urine.
Nitrates and nitrites excreted in urine.
Serum cholesterol slightly elevated; total lipids depressed.
Urinary Mg increased while liver & brain Mg decreased.
Hepatic edema reported.
Protein synthesis inhibited.
Body weight, total serum proteins, and imniunoglobulins
decreased.
Plasma changes observed were:
Decreased: albumin, seromucoid, cholinesterase,
alanin and aspartate transminases.
Increased: Alpha- and beta^ innunoglobulins.
Hepatic changes similar to plasma.
Reference
Donovan et al . ,
197682
Menzel et al . ,
197783
Ibid82'83
Sherwin and .,,
Layfield, 197410
Kosmider, 197S161
Kosmider et al . ,
197375
Drodz et al. .
1976160
Iki.4
(continued)
-------
TABLE 12-16. (continued)
Species
Rat
Rat
Hamster
N02
concentration
yg/m ppm Exposure
11,660 6.2 continuous,
4 days
47,000 to 25 to 2 hr
179,000 95
56,400 30 continuous,
30 days
Effects
No effect on serum lysozyme.
Plasma corticosterone increased proportional to^NOp
concentration from 47 to 179 mg/m , at 85 mg/m x ,
5 hr/day levels returned to normal 19 days; at 56 mg/m
x 5 hr/day levels returned to normal in 5 days.
Serum antiprotease levels increased
Reference
Chow et al . ,
197481
Tusl et al. ,
1975162
Kleiner-man and
Rynbrandt, 197fi8/1
Rynbrandt and
Kleinerman, 19778!
ro
vo
-------
TABLE 12-17. EXTRAPULMONARY EFFECTS OF N02: BODY WEIGHT
NO-
concentration
Species
Rat
Rat
Rat
Rat
Rat
Monkey
,
7* Monkey
co
o
Mouse
Dog, rabbit,
guinea pig.
rat, hamster,
mouse
uq/m
135
5,000
18,800
24,000
100
18,800
42,000
1,300 to
1,500
1,900 to
47,000
ppm
0.072
2.7
10
12.5
0.05
10
22.5
0.7 to
0.8
1.0 to
25
Exposure
continuous ,
100 days
8 wk
from birth
213 days
90 days
continuous,
90 days
continuous.
1 yr
30 da_ys
18 mo
Effects
Ambient air exposure (6.3 ppm CO, 0.206 pom NO, 0.047
SO,,, 0.0048 mg/m acid mist and 0.88 mg/m dust) de-
creased body weight.
Decreased body weight.
Decreased body weight & length of pups.
Decreased body weight.
No effect.
In combination with heat stress decreased body weight.
Auto exhaust (including 0.92 ppm NO) caused lower body
weight and anorexia.
No effect.
No effect.
Reference
Oda et al. ,
1973165
Kaut et al.,
1966164
Freeman et al
1974117
Freeman and
Haydon, 196494
Shalamberidze,
1969148
Coate and Badger,
1974134
Stupfel et al..
1973142
Natcajima et al. ,
Wagner et al . ,
171
1965IJJ
-------
TABLE 12-18 NITRIC OXIDE
ro
l
Species
Mice, female
Rat, male
Rabbit, male
Mouse tissue
Guinea pig
Guinea pig
Rat lung
tissue
Pollutant
concentration
Pollutant ug/m3 ppm Exposure Effects
NO 13,040 + 10.6 + 1 hr Mice and rats showed increased nitrosyl hemo-
NO 1,500 0.8 globin {NOHb); dose related to concentration
2 of NO.
By 20 minutes equilibrated, 0.13% total hemo-
globin. NOHb half-life 10 minutes.
No NOHb produced in rabbits exposed to NO
until sodium dithionate added to blood.
NO 14,800 12 5 hr Edema and dilation of vessels in submucosal
tissue of trachea.
Congested alveoli.
24 hr later proliferation of trachea!
mucosal epithelium.
Anomalies in CNS, heart and cell
metabolism.
NO 19,700 to 16 to 4 hr No significant alteration in
94,000 50 respiratory rate or tidal volume
NO 1,000 0.8 8 hr/day, Decreased blood sodium, magnesium,
120 days and chloride in blood calcium
Decrease brain and liver Zn, Mg.
Increased excretion Mg.
NO 417 pi 30 sec In Vitro: Similar increases in tissue
and/or cGMP levels seen for cigarette smoke
Cigarette and No. Combination had no
Smoke accumulative effect on cGMP.
Reference
Oda ft,al.,
1975I/J
Oda 5748!.,
1975174
Udai,at al. ,
1973177
Murphy et al. ,
1964130
Kosmider and ,7,
Chorazy, 19751/b
Arnold et al. ,
1977218
-------
TABLE 12-18. Continued
Pollutant
concentration
Species
Rat
Pollutant
ug/m
ppm
Exposure
Effects
Reference
NO
2,460
Rat tissue
NO
250 ul
ro
co
ro
2-° 6 wk Cellular infiltration of alveolar-
walls and areas of intra-alveolar
edema observed. After 3 wk exposure,
emphysema-1 ike changes observed.
Methemoglobin undetected. No differ-
ences in blood oxygen saturation, pH,
oxygen combining capacity, ATP, 2,
3-diphosphoglycerate, glucose, lactate,
hemoglobin concentration, heraatocrit,
or RBC count.
10 sec In Vitro: Increased guanylate cyclase
(GC), dependent upon concentration of NO.
Increased GC 19- to 33-fold in
supernatant of liver, lung, tracheal
smooth muscle, heart, kidney, cerebral
cortex and cerebellum.
Increased GC 5-to 14-fold in super-
natant of skeletal muscle, spleen,
intestinal muscle, adrenal, and
epididymal fat pads.
Half-life 3 to 4 hr at 4° C.
Sodium nitrite increased GC as well.
Nitric oxide increased cGMP, no
effect on cAMP.
Azoulay
et al., 1977
217
Arnold.et al.
197717b
-------
TABLE 12-19. NITRIC ACID AND NITRATES
CO
to
Species Pollutant
Rat, mouse, HN03
guinea pig
Rat HN03
Dog sodium
nitrate
Guinea pig ammonium
nitrate
Pollutant
concentration
2,313 to ,
3,598 ug/nT
(9 to 14 ppm)
1%
0.1 to 1.07,
0.74 to 3
410 pg/m
100 nH
Exposure
4 hr/day,
5 days/wk
intratracheal
injection
7.5 min
30 min
Effects
Increased lung pathology.
24 hr post-injection increased inflammation
of bronchioles; epithelium lost normal scal-
loped appearence.
Increased cytoplasm in epithelium.
Inflamed alveolar septae.
No difference in lung wet and dry weight.
HNO, enhanced pulmonary absorption rates of
p-aminohippuric acid, procaineamide ethobromide,
procaineamide and mannitol.
No effect on pulmonary function.
Accounted for the release of 58% of the
total histamine release.
Ammonium sulfate released.
Reference
Gray et al. ,
1952178
Gardiner and
Schanker, 1976179
Sackner et al . ,
.......180
1976
Charles and
Menzel,1975181
— ••
-------
CHAPTER 13
EFFECTS ON HUMANS OF EXPOSURES TO OXIDES OF NITROGEN
The effects of exposure of humans to nitrogen dioxide (N02) have
been the subject of three literature reviews since 1971. Each was
concerned with the effects of short-term exposures.
The Committee on Toxicity of the National Academy of Sciences-
National Research Council issued guides to short-term exposures of the
public to oxides of nitrogen (NO ) in April 1971. A review of the then
A
current literature showed: (1) that the individuals most susceptible to
NOp action are those predisposed by age, heredity, and preexisting
respiratory disease; (2) that many of these individuals will respond
most sensitively at concentrations to which healthy individuals would be
unresponsive; and (3) that the effects of N02 are, within limits, rever-
sible 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 ack-
nowledged that too much critical information was missing to permit
highly conclusive recommendations about short-term exposure to NO^, but
did conclude that the exposure limit for the general public for 10
minutes, 30 minutes, or 60 minutes should be established at 1,880 ug/m3
(1.0 ppm).
A more complete review was published by the National Academy of
p
Science in 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.
13-1
-------
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" should include, in addition
to the morphological and other changes produced by high N02 concentra-
tions, increased airway resistance, increased sensitivity to bronchocon-
3
strictors, and enhanced susceptibility to respiratory infections. This
group selected 940 yg/m (0.5 ppm) as their estimate of the lowest
concentration of N02 at which adverse health effects due to short-term
exposure might be expected to occur.
The following discussions appraise most of the studies included in
these previous reviews plus additional, more recent, pertinent publications,
13.1 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 expected
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 con-
trolled exposure studies over several months limits the extent to which
human studies have been useful in determining the effects of repeated,
short-term exposures 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.
13-2
-------
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 obtained from animal
studies. Prudence requires, however, that exposure times be limited to
those causing initial response's. When effects are detected, additional
studies are undertaken to collect evidence of the lowest concentration
at which effects can be measured in both healthy and selected, sensitive
volunteers.
13.1.1 Studies of Sensory Effects
13.1.1.1 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 biochemical transmission of the
stimulation.
Changes in the intensity of light to which an individual is exposed
initiate such a biochemically 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 impairment. 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 N02 than is any
other physiologic system tested.
Shalamberidze reported that impairment of dark adaptation occurred
at N02 concentrations as low as 140 yg/m3 (0.07 ppm) (Table 13-1). The
tests, as reported by the investigator, demonstrated changes in ocular
sensitivity to light by determining reflex changes in the functional
13-3
-------
state of the cerebral cortex. This study, however, gave results that
conflicted with those reported by Bondareva (Table 13-1). This latter
investigator determined normal dark-adaptation curves for five volunteers
and then exposed them to concentrations of N0~ varying from 150 to 500
yg/m (0.08 to 0.26 ppm) to determine alterations that might be related
to the changed atmosphere. While her results indicated that exposure
q
to concentrations of 300 yg/m (0.16 ppm) had no effect on dark adaptation,
time for adaptation increased significantly as a result of exposure to
o o
500 yg/m (0.26 ppm). Repeated daily exposures to 500 yg/m (0.26 ppm) N0?
over a period of 3 months, however, induced an apparent physiological
adjustment that largely reversed the initial increase in the time for
2
adaptation. It has been suggested that, since Bondareva did not indicate
whether NCL 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 occurs ordinarily upon 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 aware-
ness of potentially hazardous situations arising from increasing levels
of the pollutant.
Studies of odor perception show that sensitive individuals can
detect the characteristic pungent odor of N02 at a concentration of 200
-------
atmosphere. Other studies have indicated that, by increasing relative
humidity in the exposure atmosphere, odor perception is improved and
respiratory irritation also is increased.
Henschler et al.6 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 immediately. The odor of N02 was perceived by
three of nine volunteers when the concentration was 230 ug/m (0.12
o
ppm), by 8 of 13 subjects when the concentration was 410 yg/m (0.22
ppm), and by all of eight subjects when the concentration of N02 in the
exposure chamber was 790 yg/m3 (0.42 ppm). The duration of exposure
over which odor could be perceived varied considerably among subjects
and was unrelated to the concentration of N02. At concentrations of up
to 20,000 yg/m3 (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 capability returned within 1 to 1.5
minutes after subjects left the exposure chamber. Some subjects
exposed to N02 concentrations as low as 230 yg/m (0.12 ppm) reported a
metallic taste, dryness, and constriction in the upper respiratory
tract. Such symptoms lessened and eventually disappeared with repeated
exposures. When N0« was added gradually to the exposure chamber over a
i-1
period of approximately 1 hour, exposed subjects did not perceive the
odor even when it reached a level of 51,000 yg/m (27 ppm). When sub-
«j
jects were exposed to an atmosphere containing 2,260 yg/m N02 (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 correspondingly sharp increase in irritation of the mucous
membranes of the respiratory tract. It is possible that the increased
13-5
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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.
Additional odor perception studies were conducted by Feldman, who
2
reported that 200 yg/m (0.11 ppm) was the lowest concentration at which
the odor of N02 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 NOp. The sensory effects involved are the impairment of
dark adaptation and the perception of odor. Effects were reported at
levels as low as 140 to 200 yg/m3 (0.08 to 0.1 ppm) and occurred almost
immediately upon exposure.
13.1.1.2 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 13-2. 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 con-
centrations causing impairment of dark adaptation, odor perception, and
changes in the amplitude of alpha rhythms in the brain.
Shalamberidze exposed 15 healthy subjects for periods of 5 or 25
minutes to various combinations of N02 and sulfur dioxide (SOg). 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 found the minimum levels for
impairment of dark adaptation for single pollutants to be 600 yg/m3
13-6
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(0.23 ppm) for S02 and 140 yg/m3 (0.07 ppm) for N02> The thresholds for
alteration of odor perception for subjects exposed to a single gas were
230 yg/m3 (0.12 ppm) for N02 and 1,600 yg/m3 (0,61 ppm) for S02. In
these studies, combinations of the gases produced an impairment of dark
adaptation or odor perception whenever the fractional threshold concen-
trations for the separate gases totaled one or more. The lowest N02
concentration causing impairment of dark adaptation was approximately 60
percent lower than the minimum concentration needed for odor perception.
For S02, dark-adaptation impairment occurred at a concentration about 38
percent below that at which the odor was detected.
Q
Kornienko determined odor-perception capabilities in a group of
subjects exposed to individual gases or combinations of NOp, SCL,
sulfuric acid aerosol, and ammonia. He reported also that the odor of
any gas mixture was perceived whenever the sum of the fractional thres-
hold concentrations of the component gases totaled one or more. Kornienko
also investigated 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.
13.1.2 Pulmonary Function
13.1.2.1 Controlled Studies of the Effect of Nitrogen Dioxide on Pulmonary
Function in Healthy Subjects—•
q
Nakamura determined the effect of exposure to combinations of N0?
and sodium chloride aerosol (mean diameter 0.95 ym) on airway resistance
(Rail) measured by an interruption technique (Table 13-3). Two groups of
aw
13-7
-------
seven and eight healthy subjects, 18 to 27 years old, were exposed for 5
minutes to 1,400 yg/m sodium chloride aerosol alone. After resting for 10
to 15 minutes, subjects were exposed for 5 minutes to 5,600 or 11,300 yg/m3
(3.0 or 6.0 ppm) NO,,. Nitrogen dioxide concentrations were measured by the
Saltzman method. After resting again for 10 or 15 minutes, they were
exposed for 5 minutes to a mixture of the same concentration of sodium
chloride and N09. Each group showed increased R after exposure to the NO
£ ciw 2
alone, but the sodium chloride aerosol alone exerted no effect on airway
resistance. Nitrogen dioxide alone at concentrations of 5,600 and 11,300
yg/m (3.0 and 6.0 ppm) caused increases in Raw of 19 and 24 percent,
respectively. When the-sodium chloride aerosol (mean diameter 0.95 ym) was
added to the exposure atmospheres, the increases in Raw were approximately
40 percent, about twice that produced by the gas alone. A sodium chloride
aerosol comprised of smaller particles (mean diameter 0.22 ym) at 1,400
3
yg/m , in combination with the same concentrations of N02, produced no
increase in R over that caused by the gas alone.
uW
Schlipkbter and Brockhaus determined, in three subjects, the
effects of exposure to N02, carbon monoxide (CO), and S02 on pulmonary
deposition of inhaled dusts. A suspension of homogenized soot (particle
sizes 0.07 to 1.0 ym) was combined with either 9,OOOMg/m (4.8 ppm)
N02, 55,000 yg/m3 (50 ppm) CO, or 13,000 yg/m3 (5.0 ppm) S02 and admin-
istered to experimental subjects by inhalation. The individual pollutant
concentrations were the maximum acceptable concentrations in the Federal
Republic of Germany. Pulmonary retention was determined 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
13-8
-------
percent of the dust was retained. Retention increased to approximately 76
percent when the dust was administered in an atmosphere containing 9,000
yg/m (4.8 ppm) NCL. Greater proportions of dust particles in the range of
0.3 to 0.8 um were retained than were other size particles. This study is
significant in that it demonstrates a potential additive or synergistic
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 particulates. If the particulates
include toxic materials, the additional impact on health could be signi-
ficant.
11 12
von Nieding and his co-workers ' have conducted a number of studies
of the effects of N0? on pulmonary function in healthy and bronchitic sub-
jects. 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 American investigators have used constant-volume body
13
plethysmographs and measure R during panting.
uW
Investigators in this country also measure arterial partial pressure
of oxygen (Pa02) 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 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 resistance or
changes in PaC2.
13-9
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von Nieding et al. reported, at the Second International Clean Air
Congress, the results of exposures of 13 healthy subjects to NO,, levels of
940 to 9,400 yg/m (0.5 to 5.0 ppm) for 15 minutes (Table 13-3). Concen-
trations were measured by the coulometric "Picos" analyzer and checked
intermittently by the colorimetric Saltzman method. Pulmonary measure-
ments showed that these healthy subjects were affected only by the high-
est exposure concentration (9,400 yg/m ; 5.0 ppm). At this level, a
significant decrease in arterialized oxygen partial pressure was induced,
but the end expiratory oxygen partial pressure remained unchanged. A reduced
oxygen pressure in arterial blood would suggest a reduction in the trans-
fer 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 increased difference between the alveolar and arterialized oxygen
partial pressures (AaDTL) was accompanied by a significant increase in
systolic pressure in the pulmonary artery.
von Nieding et al. also exposed 11 healthy subjects, aged 24 to
38 years, to 9,400 ug/m (5.0 ppm) N02 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 AaD00.
aw 2
The effect of N02 at a concentration of 9,400 yg/m3 (5.0 ppm) was not
increased by the addition of ozone (O) to the experimental atmosphere
13-10
-------
o o
at a concentration of 200 yg/m (0.1 ppm) or by adding 13,000 yg/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 measure-
ments 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.
Yokoyama14 measured airway resistance in volunteers exposed to
various concentrations of N02 for periods of 10 to 120 minutes. He
o
measured increases in airway resistance at 13,200 yg/m (7.0 ppm) and
higher. He also recorded wide variations in individual sensitivity.
Some volunteers tolerated concentrations as high as 30,000 vg/m (16
ppm) with no increase in airway resistance. Because atropine effecti-
vely blocked the bronchoconstrictive effect of S02 but not of N02, this
investigator suggested that the mechanism for the increase in airway
resistance was unrelated to vagal stimulation.
Folinsbee et al.15 concluded from studies of three groups of five
healthy males, ranging in age from 19 to 29 years, that no significant
alterations in the measurements of pulmonary, cardiovascular, or metabolic
factors were produced by 2-hour exposures to 1,150 yg/m (0.61 ppm) N02
monitored by a continuous chemiluminescence technique (Table 13-3.
Pulmonary measurements included: ventilatory volume (V£); tidal volume
(VT); 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 (C02) percentages in inspired and expired air, cardiac output, blood
13-11
-------
pressure, heart rate, steady state diffusion capacity of the lungs for
carbon monoxide (DL^) and closing volume, with slow vital capacity (VC).
Hackney found no significant changes in pulmonary function in 16
healthy individuals exposed for 2 hours to 1,800 yg/m (1.0 ppm) NOp.
Nitrogen dioxide was monitored by a continuous chemi luminescence analyzer
and checked by the Saltzman method. Pulmonary functions measured included
FVC, FEV, peak and maximum expiratory flow, closing volume (CV), R , and
dW
others.
Beil and (Jlmer exposed healthy volunteers (groups of 8 or 16) for
2 hours to 1,800, 4,700, 9,400, and 14,000 yg/m3 (1.0, 2.5, 5.0, and 7.5
ppm) N02. Nitrogen dioxide concentrations were monitored by the contin-
uous chemi luminscence method. An additional group was exposed for 2
hours to clean air. Following exposure to N02 at concentrations of
o
4,700 yg/m (2.25 ppm) or above, these investigators measured significant
increases in Raw compared to the controls, but no decrease in Pa02 or
increase in PaC02. Airway resistance was not increased at a concen-
•3
tration of 1,800 yg/m (1.0 ppm). Nitrogen dioxide concentrations of
o
9,400 or 14,000 ug/nr (5.0 or 7.5 ppm) did not produce significantly
greater increases than did 4,700 yg/m3 (2.5 ppm). In these healthy
subjects, increased sensitivity to a bronchoconstrictor (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 yg/m3 (7.5
ppm) NOg but not after exposure to 4,700 or 9,400 yg/m (2.5 or 5.0
ppm). When the duration of exposure was increased from 2 to 14 hours,
9,400 yg/m (5.0 ppm) N0« caused an initial increase in Ra during the
£ oW
13-12
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first 30 minutes. Airway resistance tended to return toward normal during
the second hour. This was followed by even larger increases in Rgw
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 ini-
clW
tiation of exposure (10 hours after exposure was terminated) had returned to
pre-exposure levels. Exposure of healthy subjects for 14 hours to 9,400
yg/m3 (5.0 ppm) increased sensitivity to acetylcholine; the effects of
longer exposures to lower concentrations were not tested.
18
von Nieding and co-workers observed significant decrease in the
lung's diffusion capacity for CO (DLCQ) in 16 healthy subjects resulted from
a 15-minute inhalation of 9,400 yg/m3 (5.0 ppm) N02 (Table 13-3). Abe1
found that concentrations of 7,500 to 9,400 yg/m3 (4.0 to 5.0 ppm) for 10
minutes produced increases in both expiratory and inspiratory flow res-
istance 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 subjects exposed to NO* concentrations ranging from 1,300
2
to 3,800 yg/m (0.7 to 2.0 ppm) for 10 minutes, were reported by Suzuki
20
and Ishikawa (Table 13-3). 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
13-13
-------
levels were reported by the authors to have varied during the studies,
results are difficult to interpret. It is unlikely that concentrations
of N02 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.
When von Nieding and co-workers1 exposed 11 healthy subjects to a
o O
combination of N02 at 100 yg/m (0.05 ppm), 03 at 50 yg/m (0.025 ppm),
S02 at 300 yg/m"3 (0.11 ppm) for 2 hours, no effect on Raw or AaD02 was
reported (Table 13-3). Exposure to this combination of pollutants did,
however, produce what was interpreted by the investigators as dose-dependent
increases over controls (not exposed to the pollutants) in the sensitivity
of the bronchial tree to administered acetylcholine as measured by in-
creases in Raw. Constriction of the bronchi is a physiological alteration
similar to that experienced by many individuals as asthma attacks. The
suggestion provided by this study is that exposure to air pollutants may
increase susceptibility in some individuals to asthma attacks.
21 23
Hackney et al. exposed four healthy male volunteers to 0.,
O
(1,000 yg/m ; 0.5 ppm) and subsequently to mixtures of 03 and ML (560
3 ?
yg/m ; 0.3 ppm) or 03> N02 and CO (45,900 yg/m ; 30 ppm) (Table 13-
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, Raw and others) were measured when test subjects were exposed to 0
13-14
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alone. These 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 irritants, was exposed under a
similar protocol with an exposure time of 2 hours and to 500 yg/m (0.25
ppm) Og. Again, little or no change in pulmonary function was found with Og
exposure alone, or with addition of N02 (560 yg/m3; 0.3 ppm) or of N02 plus
CO (45,900 yg/m3; 30 ppm).
In summary, studies on the effects of N02 on pulmonary functions in
healthy volunteers (Table 13-3) indicate that exposure of 2 hours or less to
concentrations of 3,000 to 9,400 yg/m3 (1.6 to 5.0 ppm) can induce increases
in Raw> Other changes in pulmonary function have been reported at higher
concentrations. Exposure of a low-level mixture of N02, 0-, and S02 was
reported to increase sensitivity to a bronchoconstrictor.
13.1.2.2 The Effects of Nitrogen Dioxide Exposure on Pulmonary Function
in Sensitive Subjects—
18
von Nieding et al. exposed 14 patients with chronic bronchitis to N02
at a concentration of 9,400 ug/m3 (5.0 ppm) for 15 minutes (Table 13-4).
Alveolar partial pressures of oxygen measured before, during, and after
inhalation of N02 were not altered significantly (p > 0.05). The earlobe
arterialized blood partial pressure of 02, however, decreased from an
average of 102 x 102 to 95 x 102 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 in earlobe
arterialized blood from an average of 34 x 102 to 43 x 102 pascals (25.5 to
32.3 torr). When exposure was continued for an additional 60 minutes,
further significant disturbances of respiratory gas exchange were not
observed.
13-15
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Significant elevations in Rflw (p < 0.1) were seen in 15 patients
with chronic bronchitis after exposure to N0? concentrations of 3,000 to
3,800 yg/m3 (1.6 to 2.0 ppm) for 15 minutes24 (Table 13-4). This increase
became more pronounced at concentrations above 3,800 yg/m (2.0 ppm),
and disappeared completely below concentrations of 2,800 yg/m (1.5 ppm).
von Nieding et al. also reported on studies of pulmonary function
in 88 patients with chronic bronchitis, who were exposed for 15 minutes
•3
to N02 concentrations ranging from 940 to 9,400 yg/m (0.5 to 5.0 ppm).
o
Inhalation of 2,800 yg/m (1.5 ppm) N02 or lower concentrations had no
significant effect on the parameters measured. Between 3,000 and 9,400
yg/m (1.6 to 5.0 ppm) a significant increase in R was produced, and
uW
at levels of 7,500 to 9,400 yg/m3 (4.0 to 5.0 ppm) patients also showed
a significant decrease in Pa02 and an increase in AaDO,,.
Kerr et al.25 studied the effects of 2 hours of exposure to N02 at
a concentration of 940 yg/m (0.5 ppm) on healthy and sensitive sub-
jects. A 15-minute program of light to medium exercise on a bicycle
ergometer was included in the exposure protocol. One of 10 healthy
subjects and one of seven chronic bronchi tics reported a slight nasal
discharge associated with the exposure to NO,,. Seven of 13 asthmatics
reported some evidence of slight discomfort with exercise. No significant
changes were found in any of the pulmonary function parameters measured
by spirometry, plethysmography, or esophageal balloon techniques.
?fi
Orehek et al. studied the effects of low levels of N02 exposure
on the bronchial sensitivity of asthmatic patients to carbachol, a
bronchoconstricting agent. In this study the carbachol was used to in-
duce a response in asthmatics similar to the response occurring when
they are exposed to particular natural agents to which they are sensitive.
Nitrogen dioxide concentrations were monitored by the Saltzman method.
13-16
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For 20 asthmatics, dose-response curves were developed for changes in
specific airway resistance (SRaw) as a result of the subjects inhaling
carbachol after a 1-hour exposure to clean air, and after a 1-hour
exposure to 190 yg/m3 N02 (0.1 ppm). Following the initial N02 exposure,
marked increases in SR,,, were observed in only 3 of 20 test subjects;
uW
however, these three observations, together with smaller increases in 10
other subjects identified after carbachol treatment, gave a small but
statistically significant increase in SRaw for the 13. The N02 exposure
also increased the effect of the bronchoconstrictor in the 13 of 20
subjects. The mean dose of carbachol producing a two-fold increase in
SR in the 13 sensitive subjects was decreased from 0.66 mg to 0.36 mg
wW
as a result of N02 exposure. Seven of the asthmatic subjects showed
neither an increase in Raw in response to the exposure to N02, nor an
enhanced effect of carbachol.
The statistical significance of the data was affected greatly by
the small sample size. For example, the mean dose of carbachol produc-
ing a 100 percent increase in Rflw was 0.36 mg for 7 non-responders and
0.66 mg for 13 responders. However, the difference is not statistically
significant. On the other hand, the mean doses of carbachol producing a
100 percent increase in R.1( for 13 responders, before and after the N09
uW £
exposure, were 0.66 mg and 0.36 mg, respectively. In this instance, the
same difference in means was statistically significant. Similarly, a 15
percent difference in mean R for 13 responders, before and after NO,
uW £
exposure, was significant statistically, but a 20 percent difference in
the initial mean between responders and non-responders was not significant.
The results of this study are of interest because it is one of very
few reports available concerning a supposedly highly sensitive group ~
13-17
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asthmatics. The study suggests that measurable responses can be produced
in some asthmatics by very low concentrations of N02. It is believed,
however, that the results of this study do not provide conclusive evidence
of significant adverse responses attributable to NCL exposure. The
system used in the study was an extremely sensitive one, i.e., 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 pronounced measurable variations as a
result of exposure to NCL alone. However, the mean of measurements of
Rai. in 13 responders to the carbachol treatment was significantly higher
dW
after the NCL exposure than it had been prior to exposure. The criticism
of this reported change was that the comparisons of Rai, were made in sub-
nW
jects selected not at the time of N02 exposure, but after the fact, follow-
ing the carbachol exposure. There was no report of the initiation of an
asthma attack, or even wheezing, or lack of such symptoms in any subjects,
as a result of the combined insults of carbachol and N02> The study
does have health implications, however, since it suggests that those
asthmatics whose illness results from vagal stimulation could be pre-
disposed to more severe attacks as a result of breathing NCL. The study
discussed here suggested that, in an experimental situation, the effects
of a potent vagal stimulus may be increased by the inhalation of low
levels of NCL. In this respect it seems to be at odds with the report
of Yokoyama discussed earlier, who found that atropine blocked the
bronchoconstrictor effect of SCL but not NCL and for this reason con-
cluded that NCL did not act by stimulating the vagus nerve. This study
reports what may be a useful method for determining the possible effects
of exposure to low concentrations of N02 on asthmatics, but the data
13-18
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included with this first published report of the method do not provide
reliable evidence of such effect. It remains to be determined which
concentrations of NCL may produce significant adverse effects under
ambient exposure conditions.
A suggestion that measurably greater impact of exposure to N02
occurs in highly susceptible individuals is obtained from the studies of
?7
Barter and Campbell. These investigators studied a group of 34 sub-
jects with mild bronchitis and showed that decreases in FEV, n, over a
J. • U
period of 5 years, were related to the subjects' degree of reactivity to
the bronchoconstrictor, methacholine. Even minimal cigarette smoking, a
28
source of significant concentrations of nitrogen oxides, 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 methacholine
was slight. It is not certain that the effective material in the
cigarette smoke causing the impairments in ventilatory function was N02,
although this seems to be a good possibility. It also is not known how
these study results relate to ambient N02 exposures of individuals who
are highly reactive to methacholine.
Studies of the effects of exposure to N02 on pulmonary function in
susceptible groups of the population have been presented in Table 13-4.
These studies show that, in persons with chronic bronchitis, concen-
2
trations of 9,400 yg/m (5.0 ppm) produced decreases in Pa02 and increases
in AaD02; exposures to concentrations of N02 above 2,800 yg/m (1.5
ppm), for periods considerably less than 1 hour, produced significant
Increases in R,,, (p < 0.1). Thus, results from bronchi tic individuals
aW
and healthy individuals differed very little. Exposures to 190 yg/m
13-19
-------
(0.1 ppm) N0? for 1 hour were reported to have increased mean R in 13 of
20 asthmatics and increased the sensitivity to a bronchoconstrictor in these
same individuals. However, in another study, no measurements of pulmonary
function were altered in 13 asthmatics as a result of 2 hours of exposure to
940 yg/m3 (0.5 ppm) N02.
An exposure sufficient to produce increased Raw in healthy individuals,
or in those with some symptoms of chronic respiratory illness, may indeed
produce much greater and more severe responses in highly susceptible segments
of the population. Studies to date are inadequate for determining the
effects in the more susceptible groups.
on
Thomas et al. showed no effect of exposure to N02 at concentrations of
«j
940 to 6,580 yg/m (0.5 to 3.5 ppm) on histamine concentrations in sputum or
on total sputum weight, in five healthy subjects, or four patients reported
to have chronic respiratory disease.
13.2 COMMUNITY EXPOSURE STUDIES
Epidemiological studies of the effects of air pollution are complicated
because there is a complex variety of pollutants constantly present in
ambient atmospheres. Thus, the most that can be obtained from such studies
is an association of effects with the ambient concentrations of a mixture of
pollutants. The association must remain consistent throughout a variety of
conditions for acceptable causality to be attached to such observations.
Epidemiological studies on air pollution effects also ha^e been hampered by
the difficulty in defining actual exposures of study populations. Very few
community studies of the effects of N02 exposure have been undertaken.
Furthermore, those conducted prior to 1973 are of questionable validity due
to a number of analytical and instrumental difficulties inherent in the
13-20
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techniques for measuring atmospheric concentrations of NCL. For this reason,
the contribution of community studies to knowledge concerning the effects of
exposure to N02 is limited.
13.2.1 Effects of NQ^ on Pulmonary Function
30 32
Shy et al. observed slightly lower ventilatory function, adjusted
for age, sex, and height, in 306 school children, ages seven and eight,
living in an industrial area of high NOg concentration in Chattanooga,
Tennessee (Table 13-5). Determinations of 0.75-second forced expiratory
volume (FEV75) were made weekly during 2 months of the school year. Measure-
ments on children living in areas of relatively high NOp concentrations were
compared with similar measurements on children living in areas having
intermediate or low concentrations of NOp. Tests on children living in
areas having intermediate and low N02 concentrations gave comparable results
which, when taken together, were lower than the values obtained from
children exposed in the high concentration area. Test results, however,
were not consistent during the 2 months of testing. Consequently, the
association of impaired lung function with higher N0? concentration is not
strongly supported. Estimated annual means of daily NOp concentrations at
three monitoring stations in the high concentration area were 150, 150, and
o
280 yg/m (0.08, 0.08, and 0.15 ppm). Nitrogen dioxide was measured by the
Saltzman method. On the basis of the relationships between annual mean and
maximum hourly concentrations discussed in Chapter 7, the highest short-term
exposure levels are estimated to have been at least 1,400 yg/m (0.75 ppm)
and may have been as high as 2,800 yg/m3 (1.5 ppm). The validity of results
of this study has been questioned because direct measurements of N0? could
not be used, and because significant concentrations of sulfate and nitrate
13-21
-------
participate seemed likely to have been present in the study area. Parti-
culate matter may have been a contributing cause of any observed adverse
effects.33
34
Hasselblad reported, in'a U.S.E.P.A. publication, the results of
additional study during the 1971-72 school year in the same areas of
Chattanooga. Air quality had improved in the interval since the Shy et al.
studies in 1968. The additional study was undertaken to investigate whether
the more intense exposures to air pollutants during early life might have
produced effects in children that persisted for a number of years. FEVn ,c
u. /o
measurements were obtained from 4,704 children (6 to 13 years old) in the
winter, and again in the spring. Air monitoring included measurements of
total suspended particulates (TSP). Strips of the TSP filters were used to
determine both water-soluble sulfates and nitrates. Measurements using the
Saltzman method indicated that the concentration of NOg in the area desig-
nated by Shy and co-workers as being an area of high NOg concentration had
decreased by more than 50 percent between 1969 and 1972.
Analyses showed that population in the high, intermediate, and low
pollution areas did not differ with regard to parental smoking habits,
educational level of parents, or length of residence; therefore, those
factors were not considered in the analyses of pulmonary function test data.
No statistically significant impairments of pulmonary function were asso-
ciated with the designated high pollution area, suggesting that the effects
of earlier, higher concentrations of pollution were reversible, and that
recovery was essentially complete after 3 years. The study did show a less
than statistically significant lower FEVQ>75 in the higher N02 area during
the winter; however the aerometric data did not show a corresponding increase
13-22
-------
in either N02 or suspended nitrates. It is possible that previous exposures
to high concentrations of pollutants may have increased sensitivity to cold
air, but if this occurred, the effect had almost disappeared after 3 years.
Another possibility is that the earlier study30"32 incorrectly gave evidence
of reduced pulmonary function in the high pollution area.
Speizer and Ferris administered pulmonary function tests to 128
traffic policemen in urban Boston and to 140 patrol officers in nearby
suburban areas (Table 13-5). Mean 24-hour NCL concentrations determined
from 1-hour sampling data, measured by the Saltzman technique, were 100
- *3
yg/m (0.055 ppm) in the downtown urban area, and 75 yg/m (0.04 ppm) in the
suburban area. Sulfur dioxide levels averaged 92 yg/m (0.035 ppm) in the
i
city and 36 yg/m (0.014 ppm) in the suburban area. No differences in
pulmonary function were observed.
•JC
Cohen et al. found no difference in the results of several venti-
latory 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 13-5). The average N02 concentration in
o
the Los Angeles basin was 96 yg/m (0.05 ppm). The ninetieth percentile of
the daily averages in this area, i.e., the level exceeded only 10 percent of
o
the time, was 188 yg/m (0.1 ppm). In San Diego, the average and ninetieth
percentile were, respectively, 43 and 113 yg/m (0.02 and 0.06 ppm).
37
Linn et al. 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
13-23
-------
pollution, but information regarding N02 was provided as well. Most results
of FEV, single breath N? tests, and interviews showed no differences between
cities. Los Angeles women did report nonpersistent cough and phlegm more
often than did San Francisco women, and smokers in both cities showed
greater changes in pulmonary function than did nonsmokers. Median hourly
oxidant values (primarily O.J were 0.07 and 0.02 ppm in Los Angeles and San
Francisco, respectively. Ninetieth percentile oxidant values were 0.15 and
q
0.03 ppm. The median hourly NCU concentrations were 130 and 65 yg/m (0.07
and 0.035 ppm), respectively, for Los Angeles and San Francisco. The 90th
2
percentile hourly N02 concentrations were 250 and 110 yg/m (0.13 and 0.06
ppm) for Los Angeles and San Francisco, respectively.
Measurements of pulmonary function in Japanese employees exposed to
38
diesel exhausts in railroad tunnels were reported by Mogi et al. and by
Yamazaki et al. 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 NOp concentrations,
measured by the Saltzman method, ranged from 300 to 1,130 yg/m3 (0.16 to
0.60 ppm). Highest measured N0? concentrations ranged from 340 to 3,000
yg/m (0.18 to 1.60 ppm). Test results [VC, FEVj 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 NO
concentrations in their work areas. There also were some questions about
the adequacy of the statistical analyses of the data collected on this
study, particularly concerning weight and height adjustments.
13-24
-------
The relationships of ambient temperature and air pollutants (NCL.
NO, 03, hydrocarbons, S02, and particulate matter) to weekly variations
in pulmonary function in 20 school children, 11 years of age, were
40 41
studied in Tokyo by Kagawa and Toyama and Kagawa et al. Of all the
factors, temperature was most closely correlated (p < 0.05) with vari-
ations in specific airway conductance, and with maximum expiratory flow
rate (\L, ) at 25 and 50 percent of FVC. In children believed by the
max
investigators to be sensitive to air pollution, a significant negative
correlation was observed between exposure to 0^ and specific airway
conductance; other negative correlations were found between NO/> (as measured
by the Saltzman technique), NO, SO,,, and particulate matter, with Vmav at 25
L. IIIQA
percent or 50 percent FVC. At high outdoor temperatures N02, SO^, and
particulate matter were significantly correlated (negatively) with both
*
V at 25 percent or 50 percent FVC, and specific airway conductance
•
(p < 0.05). In one particularly sensitive subject, Vm^ at 50 percent FVC
iMuX
-5
decreased sharply at any N02 concentration above 75 yg/m (0.04 ppm). In
the ambient situation, however, the effect was not associated with N02
alone, but with the combinations of air pollutants, including $02,
particulate matter, and 0,. During the period of high outdoor temperatures,
correlations between, lung function and N02 concentrations were calculated
using the pollutant level in the ambient air at the specific time of testing
(1:00 p.m.). These hourly N02 values ranged from 40 to 360 yg/m (0.02 to
0.19 ppm).
The effects of community exposures to ambient levels of N0? on
pulmonary function have been summarized in Table 13-5. These studies
gave no indication that the mean concentrations of N0« or of N0?
13-25
-------
in combination with other pollutants had a significant effect on lung
function in the exposed populations. One study did show some associations
•
between Vm,M or specific airway conductance and concentrations of N00
max
-------
exposure neighborhood. The incidence of acute respiratory illness,
averaged over all family members, was found to be 18.8 percent higher
than the average incidence in the intermediate- and low-N02 areas.
In this study, NCL concentrations were determined by the Jacobs-
Hochheiser method. This method has since been shown to be unreliable
44
due to a variable collection efficiency at different NC^ concentrations.
Population exposures were re-evaluated using data, obtained by the
Saltzman method, from an 11-station monitoring network operated by the
•
U.S. Public Health Service and the U.S. Army in Chattanooga from
September 1967 through November 1968. The re-evaluation provided the
pertinent data, which have been included in Table 13-6, and indicate that
the largest differences in pollutant exposures were in the concentra-
tions of NCL and suspended nitrates. It is possible that the mixture of
these pollutants in this area, associated with a prolific point source,
may have been quite different from that found in urban areas where they
are produced primarily by mobile sources. It is probable also that
atmospheric sulfuric acid and nitric acid aerosols were present in
addition to the measured pollutants. Such pollutant combinations may
or may not have been responsible for the increased illness rates ob-
served in the communities exposed to high concentrations of NCL. It is
extremely difficult to identify one individual pollutant, at any con-
centration of exposure, as the sole cause of the effects.
46
In a retrospective study in the same area, Pearlman et al. deter-
mined the frequency of lower respiratory disease among first- and second-
grade school children and among children born between 1966 and 1968
(Table 13-6). Responses from subjects' families were validated by
13-27
-------
physician and hospital records. Bronchitis rates per 100 children were
highest in the area of maximum N02 concentration. For children who had
lived in the same neighborhood for 3 or more years, the bronchitis rates
in the area of high N02 concentration were significantly greater (32.2
per 100) than those for children living for comparable periods in the
low concentration area (23.2 per 100). Rates in the intermediate area
(31.2 per 100) were nearly as high as those determined from the children
in an area of high NOp concentration. Bronchitis rates in children who
had lived in the area for less than 2 years, however, did not follow the
exposure gradient. Bronchitis rates for children born between 1966 and
1968, grouped by length of residence, showed a tendency for the highest
rates to occur in the areas of high or intermediate N02 concentrations,
but results were inconsistent.
Giguz studied illness rates and other factors in 16- to 19-year-
old vocational trainees in the Soviet Union (Table 13-6). One-hundred-
forty individuals training in fertilizer or chemical manufacturing
plants were compared with 85 individuals of the same age, but who were
not exposed to the pollutants found in the manufacturing plants. Ex-
posure concentrations of N02 and ammonia, the gases expected by the
investigators to occur in highest concentrations in this situation, did
not exceed the maximum permissible concentrations (average daily mean; for
O AQ
N02, 100 yg/m or 0.53 ppm in 1964) in the U.S.S.R. 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. Studies indicated that, during the second year
of training, exposed individuals had an increased incidence of acute
13-28
-------
respiratory disease and increased serum levels of beta-lipoproteins,
cholesterol, and albumin. This report lacks important information
related to the sampling frequencies and methods. The results do suggest,
however, an association between increases in respiratory illness and
exposure to nitrogen oxides at concentrations that frequently occur in
ambient situations in the United States.
49
Petr and Schmidt studied acute respiratory illness among 7- to
12-year-old Czechoslovakian children living near a large chemical com-
plex. They found a disease incidence twice that occurring 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 the relative con-
centrations of N02 and S02. These investigators determined that measure-
ments affected by exposure to higher N02 concentrations were: (1) the
lymphocytogram (ratio of lymphocytes with narrow cytoplasm to lympho-
cytes with broad cytoplasm), (2) an index of proliferation of monocytes
(ratio of promonocytes to polymorphic monocytes), and (3) an index of
monocytic differentiation (ratio of monocytes to polymorphic monocytes).
Children from the area having the lower concentrations of NO had much
A
lower lymphocytogram values and higher indices of proliferation and
differentiation of monocytes. Parameters for children from the town
with higher concentrations of NO and lower concentrations of sulfur
A
oxides deviated most from those for the children of the low-pollution
area. The clinical significance of these differences is not known. The
results of the study are difficult to interpret also because data on
13-29
-------
concentrations of NO and N02 individually were not presented, nor were
measurements of other pollutants such as acid aerosols, particulate
nitrates, sulfates, or total suspended particulate matter. It is prob-
able that, in the environs of a large chemical complex, a variety of
pollutants was present. Any of these pollutants, individually or in
combination with N02, may have contributed to the observed alteration of
health indicators.
13.2.2.2 Effects Associated With Indoor Exposures--
Tobacco smoke is a major source of nitrogen oxides, and may include
28
significant concentrations of N02. Norman and Keith demonstrated that the
•3 C O
concentration of NO may vary between 492 x 10 and 1.23 x 10 yg/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 con-
tained higher concentrations than did the fourth puff. Often N02 could not
be measured in the cigarette smoke but, in other instances, concentrations
as high as 47,000 yg/m (25 ppm) were found. In confined spaces such as
meeting rooms, concentrations of N02 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, parti-
cularly cigarette smoking. It has not been possible, however, to incri-
minate conclusively any single factor in cigarette smoke as the one primarily
responsible for the effects observed. Other major pollutants in cigarette
smoke include CO and tars. Each of these materials, in experimental
situations, causes a fairly unique type of effects. Consequently, even
though no specific adverse effects can be attributed conclusively
only to the N02 in cigarette smoke, the increases in some adverse
13-30
-------
health parameters point strongly in this direction. The specific parameters
possibly related to the NOp in cigarette smoke include the incidence of
acute respiratory illnesses or prevalence of chronic respiratory disease.
Combustion of natural or manufactured gas within confined spaces
also leads to increases in N02 concentrations. Although some CO may
also be produced by gas-burning appliances, the relative efficiencies of
the combustion process cause larger quantities of NCu to be produced
when CO production is lowest. The inclusion in this document of studies
related to the adverse health effects associated with the use of gas
stoves is not an indictment of gas-burning appliances. Effects, if they
occur, are the result of pollutant production, and exposure to these
toxic materials. Measurements of pollutant concentrations may well be
the sum of that produced by the gas stove plus that from other sources
such as smoking in the home. Social characteristics, as well as the
size and type of housing, will dictate the intensity of exposure for
those people living in homes with the pollution produced by the gas
appliances or from 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. If the social custom is to heat as
little of the home as possible, most or all of the family may spend
considerable time in or near the kitchen, especially while meals are
being prepared and the room is warm.
The U.S. Environmental Protection Agency compared the incidence of
acute respiratory illness among women using gas cook stoves with the
Incidence among women using electric cook stoves45 (Table 13-6). The
high temperature of a gas flame oxidizes atmospheric nitrogen and, in
this study, resulted in peak concentrations of N02 as high as 940 yg/m3
13-31
-------
(0.5 ppm) for durations of 1/2 to 1 hour each time the gas stove was used
for the preparation of a meal. Electric stoves, which operate at lower
temperatures, do not form NC^. The results of the study indicated that
women using gas stoves did not show evidence of increased respiratory
disease. This suggests that possible intermittent exposure of these
o
women to NCL concentrations potentially as high as 940 ug/m (0.5 ppm)
did not impair respiratory defense mechanisms.
Mitchell et al.50 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, pulmonary
function tests (FEVQ 75 and FVC) were conducted on a 42 percent sample
of the participants representative of both sexes and both types of
households. No differences in illness rates or in the results of pul-
monary 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. Continuous
chenriluminescence 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
q
1,880 yg/m (1.0 ppm). The location of the peak concentrations within
t.he home was not reported, but probably was within a few feet of the
stove. On the basis of the range of mean M^ concentrations reported,
it can be determined that peak N02 concentrations in most homes with gas
stoves must have ranged between 75 and 1,650 yg/m (0.04 and 0.88 ppm).
q
The average peak value would have been approximately 750 ug/m (0.4
ppm). In homes with electric stoves, the mean NOg concentration was
lower than the mean of 53 outdoor determinations.
13-32
-------
51 52
Lutz et al. ' confirmed the earlier results obtained by Mitchell and
co-workers in an indoor epidemiology study involving over 400 families using
both gas and electric stoves. Nitrogen dioxide and NO concentrations were
monitored over periods of 24 hours using a sodium arsenite procedure and
continuous chemiluminescence.
A study of 2,554 children in England and Scotland living in homes in
which gas was used for cooking reported that the children had significantly
higher incidences of respiratory illness than did 3,204 children from homes
in which electric stoves were used. In this study, the analysis of data
collected took account of age, of individuals' social class, latitude of
residence, population density, family size, crowd-ing in the home, outdoor
level of smoke and S02 and the type of fuel used for heating the home.
Smoking habits of parents were not ascertained. The investigators, however,
believed that the statistical bias attributed to smoking was reduced by the
known relationships between smoking and social class. The prevalence of
bronchitis in homes using gas stoves was 5.7 and 4.7 percent for boys and
girls, respectively. The prevalence in homes with electric stoves was 3.1
and 2.0 percent for boys and girls, respectively. Smaller but still
statistically significant (p < 0.05) excesses in "day or night cough," and
"colds going to chest" were found for both boys and girls living in homes
with gas stoves. Girls in these homes also had a significantly higher
prevalence rate for "morning cough" and for "wheeze." The investigators
concluded that elevated levels of NO might have caused the increased
A
respiratory illness.
These same investigators subsequently measured N02 concentrations
at 1.2 meters (4 feet) above floor level and 0.6 and 2.2 meters (2 and 7.5
feet) from either gas or electric stoves. The mean N02 concentrations
13-33
-------
over a 96 hour test period, during which the stoves were in use from
o
8.5 to 10 hours, were 136 yg/m (0.072 ppm) when gas was burned and
q
18 yg/m (0.01 ppm) when electricity was used.
Wade et al.55 reported that, over a 2-week period, the average
concentration of NO,, in kitchens with gas stoves exceeded 94 yg/m3 (0.05
ppm) and that in different parts of the house, the concentrations fluct-
uated with use of the stoves. Nitrogen dioxide was monitored by a
chemiluminescence method. Average levels of 280 yg/m (0.15 ppm) N0?
for 2 hours were measured in the kitchen. Other studies discussed above
of N02 concentrations in homes during the preparation of meals have
demonstrated that gas stoves produce N02 concentrations usually within
the range of 470 to 940 yg/m3 (0.25 to 0.5 ppm) in the immediate vicinity
of the stove.45'50 The highest level recorded was 1,880 yg/m3 (1.0
ppm). The high concentrations were reduced within 2 hours after the
stove was turned off.
Information developed by studies of the effects of exposure to NO
on the incidence of acute respiratory illness has been summarized in
Table 13-6. These studies provide evidence of increased occurrences of
acute illness in areas in which ambient concentrations of N0? are high.
The data suggest that peak hourly concentrations in the range of 470
2
to 1,880 yg/m (0.25 to 1.0 ppm) may be associated with the occurrence
of a greater number of respiratory illnesses.
There are major problems inherent in efforts to interpret the
information contained in Table 13-6. One is the lack of data, in some
instances, pertaining to hourly levels of N02. The second problem is
the inability to attribute illness to exposure to the N02 occurring in
the atmosphere, to one of the other air pollutants present concurrently,
13-34
-------
or to combinations of the various pollutants. A third problem is the
inability to equate indoor NO,, concentrations with exposure. It has
been possible to estimate, through mathematical modeling, the maximum
hourly peak values that might be associated with specific annual mean
values or cooking with a gas stove. Such estimates must be viewed with
caution since their validity cannot be determined except in a statis-
tical sense. Data obtained from animal studies cited earlier in this
document indicate that intermittent peak exposures to NOp for shorter
periods probably are more significant in the development of increased
susceptibility to respiratory infections than are concentrations averaged
over longer periods of time. Thus, the estimated peak exposures in
ambient or indoor situations might be very significant. In the studies
summarized in Table 13-6, however, while the concentrations of some
other pollutants have sometimes been given (e.g. S02 or total suspended
particulate matter), in most instances, concentrations of materials such
as suspended sulfates or suspended nitrates were not monitored and
concentrations of the potentially toxic acids (nitrous or nitric and
sulfurous or sulfuric acids) that represent the intermediate products of
transformation also were not determined. These other pollutants also
could have contributed to any adverse human health effects observed.
13.2.3 Effects of NO,, Pollution on Prevalence of Chronic Respiratory
Disease—
A study of chronic bronchitis among 400 women identified by the
investigators as housewives (30- to 39-years-old) living in six local-
ities in Japan was reported by the Central Council for Control of
Environmental Pollution (Table 13-7). This study, conducted during the
winter of 1970-71, found the prevalence rate of chronic bronchitis to
13-35
-------
exceed 5 percent only in areas in which the annual NOp concentration was
70 ng/m3 (0.042 ppm) or above. Although population exposure in this
study was confounded by extremely high total suspended particulate
pollution, which ranged from 2 to 6 times the U.S. primary standard, the
Japanese set a 24-hour annual mean standard for N02 of 37.6 yg/m (0.02
ppm) on the basis of this study. It was the opinion of many air pollution
researchers that the high TSP levels precluded a determination that the
observed effects were due to N02 exposure.
The prevalence of chronic bronchitis among Japanese post office
employees in 1962 and in 1967 were reported by Fujita et al. 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 in-
creased, 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
believed that the increases were caused by increases in the atmospheric
concentrations of N02, NO, and S02. Annual mean particulate data measured
as coefficient of haze indicated that concentrations had decreased
during the study period but weight data were not provided in the report.
Cigarette smoking was not believed to have changed significantly among
study groups.
The aerometric data available for the study period are insufficient
to show meaningful association between the prevalence of chronic bron-
chitis and any single pollutant. Nitrogen dioxide was not monitored
13-36
-------
in 1962; however it was believed by the investigators that annual mean
N02 concentrations may have increased rather modestly in all three
environmental categories. Thus, N02 concentrations may have correlated more
closely with chronic bronchitis rates than did S02 or TSP. The estimated
annual mean concentration of N02 associated with the increased rates, based
3
on data obtained with automatic instruments in 1967, was about 36 yg/m
(0.019 ppm) and did not show a gradient from downtown to suburban areas.
Some atmospheric measurements suggested that annual mean SC^ concentrations
probably increased significantly in the downtown areas but remained
constant in the suburban areas. Annual mean S02 concentrations from 1962 to
o
1967 increased from 147 to 214 yg/m (0.056 to 0.082 ppm) in the downtown
o
area and remained unchanged at 54 yg/m (0.021 ppm) in the suburban areas.
CQ
Speizer and Ferris compared the prevalence of chronic respiratory
disease among 128 policemen who patrolled on foot in congested business and
shopping areas of central Boston with that of 140 suburban patrol car
officers. The exposure of each group to N02 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 increases in the prevalence of chronic respiratory
disease, while not statistically significant were found among nonsmokers and
smokers but not among ex-smokers. Estimates of annual mean pollution
levels, based on approximately 1,000 hourly samples, were, for the urban
area, 103 yg/m (0.055 ppm) N0« together with SO, concentrations of 90
Cf C.
o
yg/m (0.05 ppm); the N02 concentrations for the suburban area averaged 75
3 "\
yg/m (0.04 ppm) and S02 concentrations averaged 26 yg/m (0.01 ppm).
13-37
-------
Chapman et al. determined the prevalence of chronic bronchitis in
3,500 parents of high school children living in three study areas of
Chattanooga (Table 13-7). Higher N02 concentrations had been present in
this area from 1966 to 1969 than were present in 1970, at the time of the
study. Concentration data for neither period were related to the pre-
valence of chronic respiratory illness found in the three study popu-
lations.
36
Cohen et al. (Table 13-7) also found no differences in the pre-
valence of chronic respiratory 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 N02 between 90 and 100
3 3
yg/m (0.05 ppm) plus oxidant levels of about 90 yg/m (0.045 ppm); the
San Diego group was exposed to N02 concentrations of approximately 40 to
g
45 yg/m (0.02 ppm) and concentrations of oxidants of approximately 76
ug/m3 (0.038 ppm).
37
Linn et al. also found no increase in chronic respiratory
disease in Los Angeles women exposed to a median hourly NOp concentration
of 130 yg/m3 (0.07 ppm) with a 90th percentile value of 250 yg/m3 (0.13
ppm), over that occurring in San Francisco women where the median hourly
NO concentration of N02 was 65 yg/m3 (0.035 ppm) and the 90th percen-
tile was 110 yg/m3 (0.06 ppm). Median hourly oxidant values in the two
areas were respectively 0.07 and 0.02 ppm. These investigators con-
cluded that cigarette smoking was much more significant than was Los
Angeles air pollution in the development of chronic respiratory illness.
Studies concerned with the effects of exposure to N02 pollution on
the prevalence of chronic respiratory disease are summarized in Table
13-7. These studies failed to establish an association between disease
13-38
-------
prevalence in populations and the concentrations of NO^ to which these
populations were exposed.
Chronic respiratory disease is a condition that develops over many
years. If, in fact, air pollution is a contributing factor, the disease may
develop as a result of long-term exposure to the annual mean, to 24-hour
concentration, or to the daily peak level to which individuals are exposed
routinely and repeatedly. This is a topic,.however, which cannot be decided
on the basis of presently available epidemiological data.
13.2.4 Extrapulmonary Effects Of Exposure To NO
J\
Nitrogen oxides, as well as other components of polluted air, have
been reported to be correlates of daily mortality, heart disease, and lung
cancer. Lebowitz studied variations in daily mortality in relation to
daily air pollution and weather variables in New York City, New York;
Philadelphia, Pennsylvania; and St. Louis, Missouri, from 1962 to 1965
(Table 13-8). An association between air pollution, weather variables, and
daily mortality was found in each of the cities. In New York City, multiple
regression analysis revealed a significant but negative influence of daily
nitrogen oxide concentration on mortality in winter. Particulate matter
(measured as coefficient of haze), low temperature, and wind speed were also
significant determinants of daily mortality. Nitrogen oxide concentrations
were not statistically associated with mortality in summer. In Los Angeles,
California, winter mortality of persons 45 to 64 years old, 65 years and
older, and all ages combined was significantly and positively related to
daily nitrogen oxide concentrations during the period of 1962 to 1969.
Sulfur dioxide, temperature, and wind speed also were significant determinants
of daily winter mortality variations. In summer, nitrogen oxides were not a
13-39
-------
significant variable whereas S02, CO, relative humidity, and wind speed were
statistical determinants of daily mortality. These results failed to
provide convincing evidence of a relation between N02 and daily mortality.
Findings in New York City were opposite to those in Los Angeles and the
associations were not consistent for all seasons.
/~O
Mickey et al. compared air pollution measurements made at the
National Air Sampling Network 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 NO,,, S02, 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
S02 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. It is
believed that the quality of both the monitoring data, and the mortality
data, and the fact that exposures of individuals dying of these specific
diseases could not be evaluated is such that the findings do not allow
conclusions regarding risk of death or disease due to pollutant exposure.
Nevertheless, the consistency of the findings precludes complete dis-
missal of the conclusions of the investigators.
/TO
Sprey correlated geographical differences in death rates from
hypertensive and arteriosclerotic heart disease and lung cancer with
annual N02 concentrations in each of 42 metropolitan areas. He found
13-40
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significant linear relationships for 1962. Higher death rates, when
compared with areas having the lowest concentrations of NCL, were found
even in areas in which the NCL concentrations were below the primary
national ambient air quality standard. Adjustments for area differences
in family income and education, population density, temperature, and
sulfate and nitrate concentrations, did not affect the basic geographical
association between NCL and death rates. This investigator also found a
similar linear relationship between lung cancer deaths among males and
females over 65 years of age and NCL concentrations. This relationship
was maintained even after adjustments were made for area differences in
SC^. sulfates, nitrates, climate, socio-economic factors, and population
density. The significance of these results has been questioned by some
investigators because individual exposures were not assessed, because
the monitoring was limited to 26 observations during the period of 1959
to 1961, and because NCL. measurements utilized the Jacobs Hochheiser
analytical method, which has now been discredited.
The interactions of atmospheric NO pathways with those of photo-
A
chemical oxidants, discussed elsewhere in this document and also in the
Air Quality Criteria for Ozone and Other Photochemical Oxidants,64 may
lead to increases in the incidence of skin cancer in certain population
groups. Epidemiological studies have demonstrated that solar UV
65
radiation is carcinogenic. Outdoor workers, such as farmers or fisher-
men, 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 N0« may lead to a decrease in the strato-
spheric concentration of 03 and a resultant increase in the amount
of UV radiation penetrating to the earth's surface.
13-41
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13.3 ACCIDENTAL AND OCCUPATIONAL EXPOSURES
o
Acute exposure to high concentrations (> 47,000 yg/m ; 25 ppm) of NOp
produces an almost immediate reaction consisting usually of cough, dyspnea,
and a tightness of the chest and respiratory tract caused by acute bron-
chitis 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 apparently
fully recover. Such a biphasic reaction to exposure to N02 was described by
Milne who also determined, from a literature review, that it represented a
rather typical response.
There are a number of occupational situations in which workers are
intermittently or continuously exposed to high concentrations of N02 or
other oxides of nitrogen.
There have been a few cases of unusually high levels of exposure for
short periods of time which confirm the potential hazard associated with
short-term exposure to N02< Lowry and Schuman reported the development of
illness of four farmers who entered freshly-filled silos in which high
concentrations of N02 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
13-42
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scattered in both lungs. Two of the patients died while the other two
improved dramatically after receiving high doses of steroids. Concen-
trations of N02 were estimated to be in the range of 380,000 to 7,500,000
yg/m3 (200 to 4,000 ppm). Grayson reported on two other cases of N02
o
poisoning from silage gas estimated at 560,000 to 940,000 yg/m (300 to
500 ppm) N02. Indications from this study are that exposure to concen-
trations in this range is likely to result in fatal pulmonary edema or
asphyxia. The study further indicates that concentrations in the range of
280,000 to 380,000 yg/m3 (150 to 200 ppm) are likely to produce bron-
chiolitis; exposure to 94,000 to 190,000 yg/m3 (50 to 100 ppm) are
associated with reversible bronchiolitis, and exposure to concentrations
in the range of 47,000 to 140,000 yg/m (25 to 75 ppm) are associated with
bronchitis or bronchial pneumonia with complete recovery probable.
Gregory et al. 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 concentrations 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 conditions,
several factors, including various atmospheric pollutants, may have
contributed to the immediate deaths. The conditions at the time of the
fire, however, and the symptoms in many of the individuals who subseq-
uently died, were most consistent with symptoms expected as a result of
inhalation of very high N02 concentrations. In spite of the significant
number of deaths within 30 days of the fire, the survival rate over the
next 30 years for exposed clinic employees, firemen, policemen, and rescue
13-43
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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.
13.4 EFFECTS OF NO-DERIVED COMPOUNDS
X
Many compounds may be derived from the 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 in-
clude nitric acid, nitrates, nitrites, and nitrosamines.
13.4.1 Nitrates. Nitrites and Nitric Acid
Nitrate poisoning occurs when a sufficient quantity of nitrate ions
is reduced by intestinal bacteria to nitrites, which, in turn, oxidize the
iron in hemoglobin from the ferrous to the ferric state. The resultting
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. However, Goldsmith et al. 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
13-44
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reducing methemoglobin to hemoglobin is deficient in infants, and (4)
because intake of water per kilogram body weight is higher in the infant
72
than in adults. 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
7 O ™T A
United States and in England has been estimated to average about
400,000 to 500,000 ug. Because concentrations in water, in cured meats,
and in vegetables vary greatly, as do the quantities of these materials
consumed by individuals, the ingestion estimates must be applied with
caution. However, since the worst case situation would probably find less
3 75
than 40 yg/m nitrate in ambient air, an adult engaged in heavy
exercise, who might inhale 20 m of air per day could be expected to
inhale no more than 5,600 yg 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 stand-
point in that they are the final stage in the atmospheric oxidation of
NOX, a process that includes the formation of various nitrogenous acids.
The discussions of measurement techniques (Section 4.4.1) 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 including nitric acid. The
13-45
-------
following discussion of the effects of atmospheric nitrates, then, relate
to the experience of populations exposed to atmospheric conditions from
which the indicated nitrate levels were obtained from collections of
particulate matter on glass filters.
Data from unpublished reports of French et al., as included in
the Environmental Health Criteria document on nitrate, issued by the World
Health Organization (WHO), indicated that in six of seven study com-
munities in the New York City-Newark metropolitan area, when minimum
temperature exceeded 50°F., increases in asthma attacks were correlated to
a significant degree with increases in concentrations of atmospheric
nitrates. Pooled data from all seven communities indicated that when
minimum temperatures exceed 50°F, 40 percent more asthma attacks could be
3
expected when 24 hour mean nitrate levels were 8 yg/m or higher than when
the nitrate levels were 2 yg/m or lower. Concentrations of N02, measured
by the chemilumescence method, were not associated with asthma attacks.
An earlier study in three of the seven communities failed to show as
strong a relationship between asthma attacks and suspended nitrate levels.
In this study suspended sulfate levels appeared to have greater influence
on the occurrence of asthma attacks; however, the suspended nitrate
levels during this earlier study were, on the basis of median, 90th per-
centile and maximum hourly values, lower than they were during the second
study.
Additional unpublished data of French et al. reported in the WHO
document showed evidence that the asthma attack rate in a study
population, in the southeastern United States, was related to combined
concentrations of suspended nitrates and suspended sulfates. The com-
bination correlated more closely than did the concentrations of either
13-46
-------
pollutant alone.
In both of these studies, the concentration of nitrates were deter-
mined as the water soluble nitrates extracted from a strip of the
fiberglass filter from a h,igh volume particulate sampler. Thus, all of the
problems associated with determination of total suspended particulates,
plus those related to possible increase or decrease of nitrate on the
filter, are concerned with the accuracy of the quantitive data collected
in these studies; qualitatively, it is considered that the associations
probably are valid. An additional potential problem with these studies is
autocorrelation that might have affected the statistical analyses. This
same question must be addressed in all time series analyses in which data
for a given day may have been affected by events on preceeding days. No
adequate means for handling such data with complete satisfaction are
available. Nevertheless, the consistency of the association of asthma
attacks with suspended nitrate measurements warrants consideration of the
issue.
78
Utell et al. studied the effects of a nitrate aerosol on pulmonary
function and on the sensitivity of test subjects to the bronchocon-
stricting 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
oW
carbachol. Subjects were exposed for 16 minutes in a double-blind manner
to either sodium nitrate (NaNOj) or sodium chloride (aerodynamic diameters
0.49 ym, ag = 1.7, and 0.46 urn, ag = 1.7, respectively) at a concentration
3
of 7,000 ug/m . Following exposure, subjects inhaled a predetermined
quantity of carbachol sufficient to increase R 20 to 30 percent.
13-47
-------
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), Raw, FEV, FEV1 Q, 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 NaN03 at concentrations approx-
imately 100 times the total nitrate in ambient exposures, does not effect
pulmonary function. These investigators did point out that their study
results might have been quite different had they (1) used an "acidic"
nitrate in their exposure atmosphere rather than the neutral NaNO^,
(2) had the exposure time been extended beyond the 16 minutes, or (3) had the
study included symptomatic asthmatics.
It is possible that nitrates suspended in the atmosphere may contri-
bute indirectly to human health problems by their participation in chemical
reactions that result in a decrease in the concentration of stratospheric
ozone. A lower concentration of stratospheric 0, (Chapter 9), could in-
crease the amount of ultraviolet radiation that would reach the earth's
surface. This could produce significant increases in the incidence
of skin cancer particularly in individuals with little pigment in their
skin.79'80 A study by the Climatic Impact Committee of the National
01
Research Council concluded that a 1 percent decrease in stratospheric
ozone would likely cause an increase in the incidence of skin cancer
of about 2 percent. However, a decrease in 03 of 10 percent would
13-48
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likely cause an increase in cancer incidence greater than 20 percent and
possibly as much as 30 percent. The Council for Agricultural Science and
oo
Technology estimated that if the stratospheric concentration of NO were
A
to double, the stratospheric concentrations of 03 would be reduced by
about 20 percent. Thus, while insufficient data are available to permit
quantitative estimates of relationships among emissions of NO, N09, NO ,
£ A
and concentrations of nitrate in the lower atmosphere and in the stratosphere,
the role of NO and NO -derived compounds such as nitrates for increasing
X A
this particular health hazard cannot be discounted.
Peroxyacetyl nitrate (PAN) is a strong eye irritant at a concen-
o
tration of 4,945 yg/m (1.0 ppm). The effects of this compound are
discussed at length in Air Quality Criteria for Ozone and Other Photo-
64
chemical Oxidants.
"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 for exposed
individuals depends upon the concentration of the acid plus its products
of reaction and the duration of exposure. The clinical picture sometimes
is biphasic and similar to that shown by individuals exposed to high
83
concentrations of N0«. In other instances, the picture is quite
different and may reflect the toxicity of reaction products, particularly
R4
those produced by the reaction of nitric acid and some metals. Extended
exposure to lower concentrations of nitric acid vapors have been postu-
lated as the probable cause of chronic bronchitis or a chemical pneu-
85
monitis. Neither these effects nor the concentrations that might
13-49
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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.
13.4.2 Nitrosamines
A few epidemiological studies have attempted to link environmental
nitrates, nitrites, and nitroso compounds with human cancer. The Inter-
national 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
fifi
and in nearby areas where the tumor rates are lower. Fifteen of 29
samples of cider contained 1 to 10 yg/kg of dimethylnitrosamine and two
samples also contained diethylnitrosamine (1 yg/kg). Benzo(a)pyrene also
occurred in some samples. Correlations between dietary intake of N-nitroso
oc
compounds and esophageal cancer were not established.
A similar study was conducted in the Anyang region of China, where 20
percent of deaths from all causes reportedly result from esophageal
87
cancer. Twenty-three percent of the food samples from the areas with
the highest cancer rates were reported to contain dimethyl-, diethyl-, and
methyl benzyl-nitrosamine. Confirmation of this analysis by gas chroma-
tography and mass spectroscopy, 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
13-50
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of similar tumors, suggesting an environmental etiology for the disease.
88 89
Zaldivar and Wetterstand and Armijo and Coulson 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 in vivo nitrosation of secondary amines, contained in
the diet, to form carcinogenic nitrosamines, which can induce stomach
cancer. The suggested causal relationship remains highly speculative.
90
Hill et al. 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 pro-
91
vided. Gelperin et al. 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 consumption of salt-
op
preserved foods. Reference is made to Chapter 7 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 evidence that atmospheric nitrates contribute signi-
ficantly to the in vivo formation of nitrosamines or that inhaled
nitrosamines represent significant health hazards.
Nitrosation of amines in the stomach has been demonstrated to occur
13-51
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in humans,9 in rodents, and in dogs. Preformed nitrosamines have
Q/" QT QO QQ
been found in tobacco ' and in tobacco smoke. '
13.4.3 Other Compounds
Recent studies by Pitts et al. have demonstrated that, in sun-
light, very low concentrations of diethylamine and triethyl amines behaved
like hydrocarbons and reacted with NO, N02 or nitrous acid to form 03,
PAN, acetaldehyde plus diethylnitramine and several amides including
acetamide. In addition to nitrosamines, diethylnitramine ' and
acetanride ' have been shown to be carcinogenic in test animals.
However, the significance of these materials as human carcinogens
is unknown.
13.5 SUMMARY OF EFFECTS ON HUMANS
Controlled exposure studies have indicated that sensory responses
in humans may be elicited or altered by exposure to NOp concentrations
2
of approximately 200 yg/m (0.11 ppm). When the exposure atmosphere
contained 0^. S02, or ammonia in addition to N02, the effects on sensory
receptors were reported to be additive.
No increases in respiratory flow resistance were produced in healthly
individuals by short term exposures to N02 in concentrations of 2,800
ug/m3 (1.5 ppm) or less. Increased airway resistance was produced by
short exposure in the range of 3,800 yg/m (2.0 ppm) and several additional
alterations in pulmonary functions were produced by a 2-hour exposure to
to 9,400 yg/m (5.0 ppm) NO,,. In one study, exposure for 2 hours to 100
yg/m3 (0.05 ppm) N02, combined with 50 yg/m3 (0.025 ppm) 03, and 300
«j
yg/m (0.11 ppm) S02 resulted in an increased sensitivity to a broncho-
constricting agent (acetylcholine), which may or may not be indicative
of health impairment.
13-52
-------
•J
Exposure to N02 at concentrations above 2,800 yg/m (1.5 ppm) for
15 minutes to 2 hours produced significant increases in Rail in subjects
aW
with chronic bronchitis. No effects on pulmonary function even in
chronic bronchi tics were observed at N02 concentrations of 2,800 yg/m
(1.5 ppm) or less. There is little information on effects of N02
exposure on asthmatics. One study indicated that exposure to 190 yg/m
(0.11 ppm) for 1 hour may increase the sensitivity of asthmatics to
bronchoconstricting agents. This study also suggested that the exposure
increased airway resistance in 13 of 20 asthmatics studied; however,
another investigation found no increase in airway resistance in 13
o
asthmatics exposed to 940 yg/m (0.5 ppm) for 2 hours.
Community exposure studies during which pulmonary function or the
incidence of acute respiratory disease were measured suggest that some
impairments in health may be associated with ambient situations in which
the daily mean N02 concentrations on 10 percent of the days exceed 940
•3
yg/m (0.50 ppm). The data available, however, are insufficient to
permit a confident determination of the relative effects of exposure to
long-term mean concentrations of pollutants and of repeated exposure to
short-term peak concentrations. Available data also relate to health
status in ambient situations that include, in addition to the N02>
significant concentrations of S02, particulate sulfates and nitrates,
and such intermediate products as may be part of the atmospheric trans-
forming processes. Studies of children suggest that gas stoves produc-
ing recurrent concentrations of N02 in the home ranging from 470 to 940
yg/m (0.25 to 0.50 ppm) may cause increases in respiratory symptoms and
13-53
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illness. Studies of chronic respiratory disease have failed to associate
prevalence of such disease with the ambient concentrations of NOp to
which the study populations were exposed.
There is some evidence that atmospheric nitrates may act as res-
3
piratory irritants when 24-hour average concentrations exceed 8 yg/m ;
however, it is unlikely that atmospheric nitrates contribute to acute
nitrate poisoning resulting from the formation of methemoglobin.
There is no evidence that nitrate in the atmosphere contributes to
the in vivo formation of nitrosamines, or that inhaled nitrosamines
represent significant health hazards.
13-54
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13.6 REFERENCES FOR CHAPTER 13
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Public to Air Pollutants I. Guide for Oxides of Nitrogen. Pre-
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2. Committee on Medical and Biological Effects of Environmental
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3. Environmental Health Criteria 4, Oxides of Nitrogen. World Health
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7. Feldman, Y. G. The combined action on a human body of a mixture
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u., o. n. nurvaui, u. r. ocu i , emu u. u. LICICI
I ppm NO,, on cardiopulmonary function in young
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22. Hackney, J. D., W. S. Linn, J. G. Mohler, E. E. Pedersen, P.
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24. von Nieding, G., and H. Krekeler. Pharmakologische Beeinflussung
der akuten N02-Wirkung auf die Lungenfunktion von Gesunden und
Kranken mit eTner chronischen Bronchitis. Intern. Arch. Arbeitsmed.
29: 55-63, 1971.
25. Kerr, H. D., T. J. Kulle, M. L. Mcllhany, and P. Swidersky. Effects
of nitrogen dioxide on pulmonary function in human subjects. An
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92 Sato, R., T. Fukuyama, T. Suzuki, J. Takayanagi, T. Murakami, N.
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94* Sander, J., F. Schweinsberg, and J. P. Menz. Untersuchgenen liber
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13-63
-------
Table 13-1 EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON SENSORY
RECEPTORS IN CONTROLLED HUMAN STUDIES
CO
N02
concentrations
3
ug/m
790
410
230
230
200
0
to
ppm
0.420
0.220
0.120
0.120
0.110
0
to
No. of
subjects
8
(males)
13
(males)
9
(males)
14
(males)
28
6
Time until
effect
Immediate
Immediate
Immediate
Immediate
Immediate
54 minutes
Effects
Perception of odor
of N02
Perception of odor
of N02
Perception of odor
of N02
Perception of odor
of N02
No perception of odor
of N02
No perception of odor
of N00 when concentration
No. of
subjects
responding
8/8
8/13
3/9
most
26/28
0/6
Reference
Henschler fi
et al. , 1960
Ibid
Ibid
Shalamberidze,
1967^
Feldman, 19747
Henschler ,.
et al., 1960b
51,000 27
2,260 1.2
was raised slowlv from
0 to 51,000 yg/nr
Immediate Perception improved when
relative humidity was
increased from 55% to 78%
6/6
Ibid
(continued)
-------
Table 13-1 (continued)
co
i
cn
N02
concentrations
3
yg/m
140
150
to
500
No. of
ppm subjects
0.07 4
0.08 5
to
0.26
Time until
effect
5 and 25
minutes
Initial
Repeated
over 3
months
Effects
Impairment of dark
adaption
Increased time for
dark adaption above
500 yg/mj (0.26
ppm)
Initial effect reversed
No. of
subjects
responding
4/4
Not
Reported
Reference
Shalamberidze,
Bondereva,
1963*
-------
Table 13-2.
EFFECTS OF EXPOSURE TO COMBINATIONS OF POLLUTANTS
ON SENSORY RECEPTORS IN CONTROLLED HUMAN STUDIES
Pollutant
Subjects
Exposure
Effects
Reference
Various combi-
nations of N09
and SO,, '
15 healthy
subjects
5 or 25 min;
oral or nasal
inhalation
CO
I
01
en
The lowest effective concentration
for dark^adaptation was: N0?,
140 yg/mf (0.07 ppm) and S0~,
600 yg/m (0.23 ppm). When in-
haled together, the gases acted
additively. Dark adaptation was
impaired when the sum of the frac-
tional threshold concentrations
for the separate gases equaled
1.0 or more.
Lowest effective concentration
for odor^perception was: N0«,
230 yg/rr (0.12 ppm) and SOf,
1,600 ug/rrr (0.61 ppm). When
inhaled together these gases
additively. Odor was perceived
when the sum of the fractional
threshold concentrations equaled
1.0 or more.
Shalamberidze,
1967^
(continued)
-------
Table 13-2 (continued).
Pollutant
Subjects
Exposure
Effects
Reference
Various Mix-
tures of NO
S02, H2SO.
aerosol arid
NH.,
x>
Not reported Not reported
Lowest effective concentrations
for odor perception of a combina-
tion of gases were reported to
be: NO , 20 ug/rrT (0.01 ppm);
S02, 170 yg/m (0.06 ppm);
H9SO. aerosol, 110 yg/m, (0.03
ppm), and NH3, 300 yg/nf (0.43
ppm). When inhaled together
the odor was perceived when-
ever the fractional threshold
totaled 1.0 or more.
KornienkOj
1972b
CO
cr>
Mixture of NO
SO,, NH-, and
3
x»
Not reported
Threshold for changes in the am-
plitude of alpha rhythms occurred
when the sum of the fractional
concentrations of the individual
gases equaled 1.0 or more.
Ibid
-------
Table 13-3. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY
FUNCTION IN CONTROLLED STUDIES OF HEALTHY HUMANS
co
i
(Ti
CO
Concentration ?°:,°f.
yg/m3
13,200
5,600
or
11,300
9,400
1,150
1,880
uea i ui.y
ppm Pollutant subjects
7.0 N02 Several
3.0 N02 8
or
6.0 N02 7
5.0 N02 11
0.62 N02 15
1.0 N02 8
Exposure
time
10-120
min.
5 min
5 min
2 hr.
2 hr
2 hr
Effects
Increased R * in some sub-
jects. Others tolerated
30,000 yg/m (16 ppm) with
no increase in R .
uW
Increase in R * compared to
to pre-exposure values (en-
hanced by NaCl aerosol)
Increase in R * and a de-
crease in AaD52** with inter-
mittent light exercise. No
enhancement of the effect when
200 yg/m (Q.I ppm) 0-, and
13,000 yg/rtT (5.0 ppm) S02
were combined with N02 but re-
covery time apparently
extended.
No significant change in
cardiovascular, metabolic,
or pulmonary functions after
15, 30, or 60 min of
exercise.
No increase in R *
Reference
Yokoyama,
1972™
Nakamura,
1964y
von Nieding ,9
et al., 1977"
Folinsbee- et.
al. 197815
Beil and .,
Ulmer, 19761'
(continued)
-------
Table 13-3 (continued)
CO
I
VO
Concentration
ug/nr
ppm Pollutant
4,700 2.5
14,100 7.5
9,400 5.0
No. of
healthy
subjects
Exposure
time
Effects
NO,
NO,
NO,
8
16
Not
Reference
2 hr Increased R with no Beil and
further impairment at Ulmer, 1976
higher concentrations. 111
No change in arterial P02
pressure or PCO,/** pressure.
2 hr Increased sensitivity to a Ibid
bronchoconstrictor (acetyl-
choline) at this concen-
tration but not at lower
concentration.
14 hr Increase in R during first Ibid
30 min that w$!§f reduced
through second hour followed
by greater increases measured
at 6, 8, and 14 hr. Also in-
creased susceptibility to a
bronchoconstrictor (acetyl-
choline).
17
1,880 1.0
9,400 5.0
N02
N02
16
16
2 hr
15 min
No significant changes in
pulmonary function.
Significant decrease in
ni * *
ULCO
Hackney, 19761'
von Nieding,1fi
et al., 1973itt
(continued)
-------
CO
I
Table 13-3 (continued)
Concentration ^°;,?f
3
yg/m
7,500
to
9,400
1,300
to
3,800
1 1 ea i uiy
ppm Pollutant subjects
4.0 N02 5
to (males)
5.0
0.7 N00 10
to Z
2.0
Exposure
time Effects Reference
19
10 min 40% decrease in lung compli- Abe, 1967
ance 30 min after exposure
and increase in expiratory
and inspiratory flow resis-
tance that reached maximum
30 min after exposure.
10 min Increased inspiratory and Suzuki and 20
expiratory flow resistance Ishikawa, 1965
of approximately 50% and
10% of control values
measured 10 min after
exposure.
9,400
5.0
NO,
13
15 min
Significant decrease in
PaOpiiibut end expiratory
P02 unchanged with signi-
ficant increase in systolic
pressure in the pulmonary
artery.
von Nieding ,,
et a!., 197011
100
combined
with
50
and
300
0.05
0.025
0.11
N02
0-5
3
so2
11 2 hr No effect on R * or AaDOp**; von Nieding
exposed subjects showed in- et a].,
creased sensitivity of bronch- 1977
ial tree to a bronchoconstrictor
(acetylcholine) over controls
not exposed to pollutants.
(continued)
-------
Table 13-3 (continued)
GO
I
Concentration
yg/m3
1,000
1,000
combined
with
560
or
1,000
combined
with
560
and
45,000
ppm
0.50
0.50
0.29
0.50
0.29
30.0
No. of
healthy Exposure
Pollutant subjects time Effects
03 4 4 hr
°3
o
N02
°3
3
NO,
CO
With each group minimal alter-
ations in pulmonary function
caused by 0^ exposure.
Effects were not increased by
addition of ML or N02 and CO
to test atmospneres.
Reference
Hackly—
1975" ZJ
(continued)
-------
Table 13-3 (continued)
CO
I
-•si
ro
Concentration
yg/m3
500
or
500
combined
with
560
or
500
combined
with
560
and
45,900
ppm
0.25
0.25
0.29
0.25
0.29
30.0
No. of
healthy Exposure
Pollutant subjects time Effects Reference
0, 7 2 hr
j
0.
3
N09
°3
j
NO,
CO
Little or no change in pul- Hackney—
monary function found with 1975
0^ alone. Addition of NO,,
of of N02 and CO did not
noticeably increase the ef-
fect. Seven subjects in-
cluded some believed to be
unusually reactive to
respiratory irritants.
AaDO,
DLco'
Pa00
PCO,
airway resistance
difference between alveolar and arterial blood partial pressure of oxygen
diffusion capacity of the lung for carbon monoxide
arterial partial pressure of oxygen
partial pressure of oxygen
partial pressure of carbon dioxide
-------
Table 13-4. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON PULMONARY
FUNCTION IN CONTROLLED STUDIES OF SENSITIVE HUMANS
CO
I
CO
N02
concentration
o
yg/m
9,400
3,000
to
3,800
7,500
to
9,400
3,000
to
9,400
940
to
2,800
ppm
5.0
1.6
to
2.0
4.0
to
5.0
1.6
to
5.0
0.5
to
1.5
No. of Exposure
subjects time
14 with 15 min
chronic
bronchitis
15 with 15 min
chronic
bronchitis
88 chronic 15 min
bronchitis
patients
studied
15 min
15 min
Effects
No change in mean PaOp*, during
or after exposure compared with
pre-exposure values, but Pa02*
significantly.
Continued exposure for 60 minutes
produced no enhancement of effect.
Increase in R~w*** more pronounced
at higher exposure concentrations.
(0.05 < p < 0.1)
No significant change at exposure
concentrations below 2,800 yg/m
(1.5 ppm).
Significant decrease in PaOp and
increase in AaD00**.
L.
Significant increase in &aw***-
No significant effect.
Reference
von Nieding
et al., 1973
von Nieding
et al., 1971
von Nieding
et al., 1970
Ibid
Ibid
1ft
1O
24
(continued)
-------
Table 13-4 (continued).
OJ
concentration M^ nf c»nne.
yg/m3
940
190
I«U. *J 1 l_ApUJ
ppm subjects time
0.5 10 healthy 2 hrs
7 chronic
bronchi tics
13 asthmatics
0.1 20 asthmatics 1 hr
ure
Effects
One healthy and one bronchi tic subject
reported slight nasal discharge. Seven
asthmatics reported slight discomfort,
but showed no changes in pulmonary
function.
Significant increase in SR \\. Ef-
fect of bronchoconstriction enhanced
after exposure in 13 of 20 subjects.
Neither effect observed in 7 of 20
subjects.
Reference
Kerr, et al.25
Orehek, 197626
PA09
** £-
: alveolar partial pressure of
oxygen
AaD0:
***
Raw
SR
aw
difference between alveolar and arterial blood partial pressure of oxygen
airway resistance
arterial partial pressure of oxygen
specific airway resistance
-------
Table 13-5. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON
PULMONARY FUNCTION IN COMMUNITY STUDIES
-j
in
N02 exposure
concentrations
Measure
Annual mean 24-hr
concentrations in
high exposure area
90th percenti le
in high exposure
area
Estimated 1-hr
maximum :
high ex-
posure area
Estimated 1-hr
maximum :
low ex-
posure area
yg/m
150
to
280
280
to
940
1400
to
2800
750
to
1500
ppm
0.08
to
•0.15
0.15
to
0.50
0.75
to
1.50
0.40
to
0.80
Study
population
In the high
exposure area
306 school
children
ages seven
and eight
were tested;
in the inter-
mediate level
area, 264
school child-
dren; and in
the low ex-
posure area,
225 school
children of
the same age
group
Effect Reference
FEVQ 75* for children in areas Shy et al.,
of n1gn concentration were sig- 1970
nificantly lower than for other
areas (p < 0.05).
Differences were of borderline
significance since they were not
consistent. Significant concen-
trations of atmospheric sulfate
and nitrate parti culates probably
were also present but they were
not measured.
(continued)
-------
Table 13-5 (continued)
Measure
Los Angeles:
Median hourly
N02
90tn percen-
tile N02
Median hourly
0
9o£h percen-
tile Ov
X
San Francisco:
Median hourly
N02
90tn percen-
tile N02
Median hourly
0
90£h percen-
tile Ox
N02 exposure
concentrations
3
ug/m ppm
130 0.07
250 0.13
0.07
0.15
65 0.35
110 0.06
0.02
0.03
Study
population Effect Reference
37
205 office No differences in most tests. Linn, et al.
workers in Smokers in both cities showed
Los Angeles greater changes in pulmonary
function than non-smokers.
439 office (See Above)
workers in
San Francisco
(continued)
-------
Table 13-5 (continued)
CO
N0« exposure
concentrations
Measure
Mean "annual "b 24-
hr concentrations
high ex-
posure area
low ex-
posure area
1-hr mean
high ex-
posure area
low ex-
posure area
yg/m
103 +
92 S00
L.
75 +
36 SO,
c
260
to
560
110
to
170
ppm
0.055 +
0.035
SO,
L.
0.04 +
0.014
S09
2
0.14
to
0.30
0.06
to
0.09
Study
population Effect Reference
Pulmonary No difference in various pul- Speizer and
function nonary function tests. Ferr^§'58
tests admin- 1973 '
istered to
128 traffic Burgess et al.,
policemen in 1973
urban Boston
and to 140
patrol offi-
cers in near-
by suburban
areas
(continued)
-------
Table 13-5 (continued)
OJ
00
NOp exposure
concentrations
Measure yg/m ppm
High exposure
groups:
Annual mean 96 0.051
24-hr concen-
trations
Study
population
Nonsmokers
Los Angeles
(adult)
Effect Reference
No differences in several Cohenfiet al.,
ventilatory measurements in- 1972
eluding spirometry and flow
volume curves
90th percent!le 188
Estimated 1-hr
maximum
Low exposure
group:
480
to
960
0.01
0.26
to
0.51
Annual mean
24-hr concen-
trations
90th percentile
Estimated 1-hr
maximum
43
113
205
to
430
0.01
0.06
0.12
to
0.23
Nonsmokers
San Diego
(adult)
(continued)
-------
Table 13-5 (continued)
CO
I
10
Measure
N02 exposure
concentrations
3~~
yg/m ppm
Study
population
Effect
1-hr
concentration
at time of
testing
(1:00 p.m.)
40
to
360
0.02 20 school
to children
0.19 11 years of
age
During warmer part of the year
(April -October) N02> S02 and
TSP" significantly correlated
with V ** at 25% and 50%
FVC***m§fid with specific air-
way conductance. Significant
correlation between each of
four pollutants (N0~, NO, SO,
and TSP and V ** at 25% c
and 50% FVC***. Temperature
was the factor most clearly
correlated with weekly
variations in specific air-
way conductance with V **
at 25% and 50% FVC***. a5ne
sensitive subject had sharp
decrease in V ** at 75
pg/m3 (0.04
above.
N0 and
Reference
Kagawa and
Toyaraa
W
Kagawa et al . ,
1976^
a
b
*
FEV
0.75
max
***
FVC
'TSP
Estimated at 5 to 10 times annual mean 24-hour averages
Mean "annual" concentrations derived from 1-hour measurements using Saltzman technique
Forced expiratory volume, 0.75 seconds
Maximum expiratory flow rate
Forced vital capacity
Total suspended particulates
-------
Table 13-6 EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON THE INCIDENCE
OF ACUTE RESPIRATORY DISEASE IN COMMUNITY STUDIES
Pollutant
concentrati on
00
I
00
o
Pollutant
High Exposure
NCL
£
so2
ss
SN
TSP
Intermediate
N02
S09
c.
SS
SN
yg/m ppm
150 0.08
to to-
282 0.15
<26 <0.01
13.2
to
3.8
7.2
to
3.8
96
to
63
113 0.06
<26 <0.01
9.8
2.6
OLUuy
population
871 familes
comprising
4043 indivi-
duals
Families with
children born
1966-1968
School chil-
dren born
1966-1968
(See Above)
Effects
Respiratory illness rate
Grade 2 children: 22.1/100
Siblings: 18.8/100
Mothers: 14.2/100
Fathers: 12.1/100
Bronchitis rate: 32.2/100 for
children 3 yr or more in area
Bronchitis rate compared on
length of residence basis shows
highest rates in high exposure
areas
Respiratory illness rate
Grade 2 children: 18.0/100
Siblings: 15.6/100
Mothers: 11.8/100
Fathers: 8.8/100
Bronchitis rate 31.2/100 for
children 3 yr or more in area
Reference
Shy at al . ,
1970^
01
Shy, 1970Ji
Shy et al . ,
*/ j y
-1973^
Hauser and Shy,
1972^
/IC
USEPA, 1976 b
Pearlman et
al., 197rD
(See Above)
(continued)
-------
Table 13-6 (continued)
GO
CO
Pollutant
TSP
1 nw Fvnnciiv*£
so2
ss
SN
TSP
Pollutant
concentration
yg/m ppm
62
56 0.03
<26 <0.01
10.1
1.6
62
St d
population Effects
Bronchitis rate compared on length
of residence basis shows higher
rates than in low exposure areas
(See Above) Respiratory illness rate
Grade 2 children 20.1/100
Siblings: 17.0/100
Mothers: 12.3/100
Fathers: 9.6/100
Bronchitis rate 23.2/100 for
children 3 yr or more in area
Reference
(See Above)
NO,
940 0.5
1/2-1 hr
peak
Housewives
cooking with
gas stoves,
compared to
those cooking
with electric
stoves
No increased respiratory illness USEPA, 197645
NO, 470
* to
940
0.25
to
0.50
2554 children
from homes
using gas to
cook compared
to 1304 chil-
dren from
homes using
electricity
Bronchitis, day or night cough,
morning cough, cold going to
chest, wheeze, and asthma in-
creased in children from homes
using gas
Melia.et al. ,
J.977
Wade^et al . ,
1975DD
USEPA, 197645
(continued)
-------
Table 13-6 (continued)
Pollutant
Pollutant
concentration
yg/m ppm
Study
population Effects
Reference
NO,
<100 <0.053
24-hr mean
oo
00
PO
140 vocational
trainees, 16
to 19 years
old, in fer-
tilizer or
chemical manu-
facturing.
Exposure: 3
hr/day, 150
days during
1st yr; 6 hr/
day, 200 days
during 2nd yr
Controls: 85
trainees of
similar age in
nonexposed
occupations
During year 2 of training, in-
creased incidence of acute respira-
tory disease and increased serum
levels of B-lipoproteins, choles-
terol , and albumin
Giguz, 1968
47
N09
c.
so2
HoSO,
2 4
580
to
1200
225
400
0.31
to
0.64
0.12
Nonemployees
living with-
in 1 km of a
chemical
plant
Similar sub-
jects who lived
more than 3 km
from the plant
44% more visits to health clinic
for respiratory, visual, nervous
system, and skin disorders than
population more than 3 km from
the plant
Polyak, 196842
Pollutants: SS, suspended sulfates; SN, suspended nitrates; TSP total suspended particulates
-------
Table 13-7.
EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON THE PREVALENCE
OF CHRONIC RESPIRATORY DISEASE IN COMMUNITY STUDIES
Pollutant
NO *
L
SO *
f.
N00
2
Pollutant
concentration
yg/m3 ppm
Annual Mean
103 0.055
92 0.035
75 0.04
Study
population
128 urban
(Boston)
traffic
policemen
and 140 sub-
urban patrol
car officers
Effects Reference
Reported prevalence (%) of 100 sub- Speizer and
jects for chronic respiratory dis- Ferris, 1973 j:q
ease associated with exposure to Burgess, 1973
higher levels of air pollution was
as follows:
light heavy
nonsmokers smokers smokers ex-smokers
(urban officers)
17 50 60 28
(suburban officers)
15 43 55 31
CO
I
CO
CO
N02 Mean
High exposure group
6/70 to 12/70
92 0.05
12/67 to 11/68
15-282 0.08-0.15
Intermediate exposure group
6/70 to 12/70
71 0.04
12/67 to 11/68
117 0.06
Low exposure group
6/70 to 12/70
58 0.03
12/67 to 11/68
117 0.06
Test popula-
tions con-
sisted of
parents of
high school
students in
the high,
intermediate
and low ex-
posure cate-
gories.
High:
650 parents
Intermediate:
755 parents
Low:
234 parents
Prior exposure to higher levels of
NOp was not associated with in-
creased prevalence of chronic res-
piratory disease. Prevalence (%)
of chronic bronchitis adjusted for
smoking, sex, race, and age:
early disease: advanced disease:
30 11
Chapman et al.
197350
33
25
20
13
(continued)
-------
Table 13-7 (continued)
CO
I
CO
Pollutant
N02
°3
N02
°3
N02
°3
N02
°3
Pollutant
concentration
yg/m ppm
Annual Mean,
1963 to 1967
96 0.05
92 0.046
Annual Mean,
1963 to 1967
42 0.023
76 0.038
Median Hourly:L.A.
130 0.07
Median Hourly :L. A.
137 0.07
Median HourlyrS.F.
65 0.035
Median Hourly :S.F.
39 0.02
_ .
population
136 nonsmokers
living in Los
Angeles Basin
207 nonsmokers
living in
San Diego
205 office
workers in
Los Angeles
439 office
workers in
San Francisco
Effects Reference
No difference in prevalence of Cohegget a!.,
chronic respiratory disease 1972
between the two groups.
No difference in chronic respiratory Linnet a!.,
disease between the two groups; 1976
cigarette smoking was much more
significant.
-------
Table 13-7 (continued)
oo
en
Pollutant
concentration
Pollutant yg/m ppm
N02
TSP
so2
N02
so2
so2
Annual Mean
70 0.042
111-498
29-143 0.01-0.05
Annual Mean
36
Annual Mean
54-147
Annual Mean
54-214
(1966)
0.019
(1962)
0.021-0.056
(1966)
0.021-0.082
Study
population
Housewives in
six Japanese
communities
7,800 Post
Office
employees
in Japan
Effects
Prevalence rate for chronic
bronchitis exceeded 5%. Results
confounded by the high TSP con-
centrations
Increases in chronic bronchitis
prevalence rates in 1967 following
a period of increasing air pollution
correlated more closely with N09
than S02 - TSP levels fell. L
Reference
Central Counci
for Control of
Environmental
Pollution 1977
Fujita et al. ,
196937
1
56
* These are averages of 2 sampling days per season of the year for 1 year at each of 16 work
stations. The values, however, differ little from^nnual pollutant concentrations in Boston
and nearby suburbs reported by Speizer and Ferris.'
-------
Table 13-8. EFFECTS OF EXPOSURE TO NITROGEN DIOXIDE ON EXTRAPULMONARY PARAMETERS
Pollutant
Study Population
Effects
Reference
TSP
so2
or
Deaths in New York,
Philadelphia and
St. Louis 1962-1965
No consistent evidence of a relation-
ship between nitrogen oxide concen-
tration and mortality.
Lebowitz, 1971
61
NO,
so£
Suspended
Sulfate
TSP
oo
01
NO,
Deaths from cancer,
cardiovascular
disease and res-
piratory disease
in 38 SMSAs.
N0« and S02 concentration positively
associated with geographical differences
in mortality rates for various cancers,
and for arteriosclerotic heart disease.
However, the quality of the air monitor-
ing and the nature of geographical studies
limit the inferences that can be drawn
regarding risk of disease.
Mickey et al.
62
Deaths from heart
disease and lung
cancer.
Higher death rates found even in areas
in which the annual mean.,N02 concen-
trations were < 100 yg/m (6.05 ppm).
Lung cancer rates in the over 65 group
correlated with N0? concentration.
Data are of questionable validity since
aerometric measurements were limited to
26 per year and Jacobs-Hochheiser
technique was used for N02 measurement.
Sprey
63
------- |