&EPA
United States
Environmental Protection
Agency
Environmental Criteria and
Assessment Office
Research Triangle Park NC 27711
EPA-600/8-82-029a
December 1982
Research and Development
FINAL
Air Quality Criteria for
Particulate Matter and
Sulfur Oxides
Volume I
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EPA-600/8-82-029a
December 1982
Air Quality Criteria
for Participate Matter
and Sulfur Oxides
Volume I
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Research and Development
Environmental Criteria and Assessment Office
Research Triangle Park, NC 27711
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NOTICE
Mention of trade names or commercial products does not
consititute endorsement or recommendation for use.
ii
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PREFACE
This, document is Volume I of a three-volucne revision of Air Quality
Criteria for Particulate Matter and Air Quality Criteria for Sulfur Oxides
first published in 1969 and 1970, respectively. By law, air quality criteria
documents are the basis of the National Ambient Air Quality Standards (NAAQS).
The Air Quality Criteria document of which this volume is a part has been
prepared in response to specific requirements of Section 108 of the Clean Air
Act, as amended in 1977. The Clean Air Act requires that the Administrator of
the Environmental Protection Agency periodically review, and as appropriate,
update and reissue criteria for NAAQS.
As the legally prescribed basis for deciding on national air quality
standards, this •-document, Air Quality Criteria for Parti cul ate Matter and
Sulfur Oxides, delineates health and welfare effects associated with exposure
to particulate matter and sulfur oxides and concentrations of those pollutants
which cause such'effects. The major health and welfare effects of particulate
matter and sulfur oxides are discussed, in Chapters 8 through 14 in Volume III
of the document. To assist the reader in putting the effects into perspective
with the real-world environment, Chapters 2 through 7 in Volume II of the
document have .been prepared and discuss: physical and chemical properties of
particulate matter and sulfur oxides; air monitoring and analytical measure-
ment methods; sources and emissions; transport, transformation and fate; and
observed ambient concentrations of the pollutants. Also, Chapter 7 in Volume
II introduces the reader to the contemporary problem of acidic deposition and
potential contributions of sulfur oxides to acidic deposition processes and
effects.
This volume, Volume I, introduces the criteria document, explains the
rationale behind combining the criteria for particulate matter and sulfur
oxides, and briefly summarizes the content of the entire air quality document.
However, for a fuller understanding of the health and welfare effects of par-
ticulate matter and sulfur oxides, the materials in Volumes II and III of this
document should be consulted.
The Agency is pleased to acknowledge the efforts of all persons and
groups who have contributed to the preparation of this document. In the last
analysis, however, the Environmental Protection Agency accepts full respon-
sibility for its content.
m
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ABSTRACT
The document evaluates and assesses scientific information on the health and
welfare effects associated with exposure to various concentrations of sulfur
oxides and particulate matter in ambient air. Although the literature through
1980-81 has been reviewed thoroughly for information relevant to air quality
criteria, the document is not intended as a complete and detailed review of
all literature pertaining to sulfur oxides and particulate matter. , An attempt
has been made to identify the major discrepancies in our current knowledge and
understanding of the effects of these pollutants. -~\
Although this document is principally concerned with the health and
welfare effects of sulfur oxides and particulate matter, other scientific data
are presented and evaluated in order to provide a better understanding of
these pollutants in the environment. To this end, the document includes
chapters that discuss the chemistry and physics of the pollutants; analytical
techniques; sources; and types of emissions; environmental concentrations and
exposure levels; atmospheric chemistry and dispersion modeling; acidic deposi-
tion; effects on vegetation; effects on visibility, -climate, and materials;
and the respiratory, physiological, toxicological, clinical, and epidemiologi-
cal aspects of human exposure. •
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CONTENTS
PREFACE...-.-. ill
ABSTRACT. iv
FIGURES xvii
TABLES xxx
ABBREVIATIONS AND SYMBOLS xxxvi
AUTHORS, CONTRIBUTORS AND REVIEWERS xlv
CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE Ixiii
1. EXECUTIVE SUMMARY 1-1
1.1 INTRODUCTION 1-1
1.1.1 Legal Requirements.... ' 1-1
1.1.2 Organization of the Document 1-2
1.2 PHYSICAL AND CHEMICAL PROPERTIES OF SULFUR OXIDES AND
•PARTICULATE MATTER 1-4
1.3 TECHNIQUES FOR COLLECTION AND ANALYSIS OF PARTICULATE
MATTER AND SULFUR OXIDES 1-7
1.3.1 Summary of Sulfur Dioxide Measurement Techniques 1-9
1.3.2 Summary of Measurement Techniques for Particulate
Matter. 1-11
1.4 SOURCES AND EMISSIONS OF PARTICULATE MATTER AND SULFUR
OXIDES 1-15
1.5 CONCENTRATIONS AND EXPOSURE 1-18
1.6 ATMOSPHERIC TRANSPORT, TRANSFORMATION, AND DEPOSITION 1-22
1. 7 ACIDIC DEPOSITION 1-24
1.8 EFFECTS ON VEGETATION 1-32
1.9 EFFECTS ON VISIBILITY AND CLIMATE 1-37
1.10 EFFECTS' ON MATERIALS. 1-45
1.11 RESPIRATORY TRACT DEPOSITION AND FATE OF SULFUR OXIDES AND
PARTICULATE MATTER 1-52
1.12 TOXICOLOGICAL STUDIES , 1-57
1.13 CONTROLLED EXPOSURE STUDIES. .' 1-70
1.14 EPIDEMIOLOGICAL STUDIES ON HEALTH EFFECTS OF PARTICULATE
MATTER AND SULFUR OXIDES 1-82
1.14.1 Methodological Considerations 1-82"
1.14.2 Air Quality Measurements 1-87
1.14.3 Acute Particulate Matter/Sulfur Oxide Exposure
Effects. 1-90
1.14.4 Chronic Exposure Effects 1-97
1.14.5 Implications of Epidemiglogical Findings for
Criteria Development Purposes... 1-103
1.15 REFERENCES • 1-106
ADDENDUM: Discussion of Newly Available Information A-l
GLOSSARY G-l
2. PHYSICS AND CHEMISTRY OF SULFUR OXIDES AND PARTICULATE MATTER 2-1
2.1 INTRODUCTION. 2-1
2.2 ATMOSPHERIC DOMAIN AND PROCESSES. 2-3
2.3 PHYSICS AND CHEMISTRY OF SULFUR OXIDES. 2-8
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CONTENTS (continued)
2.3.1 Physical Properties of Sulfur Oxides.in the Gas :
Phase 2-8
2.3.2 Solution Physical Properties 2-8
2.3.2.1 Sulfur Dioxide 2-8
2.3.2.2 Sulfur Trioxide and Sulfuri-e Acid... 2-12
2.3.3 Gas-Phase Chemical Reactions of Sulfur Dioxide 2-12
2.3.3.1 Elementary Reactions 2-14
2.3.3.2 Tropospheric Chemistry of Sulfur Dioxide
Oxidation 2-15
2.3.4 Solution-Phase Chemical Reactions 2-22
2.3.4.1 S(IV)-02 - H20 System 2-23
2.3.4.2 S(IV) - Catalyst - 02 - H2Q System 2-27
2.3.4.3 S(IV) - Carbon Black - 02 - H20..' 2-35
2.3.4.4 S(IV) - Dissolved Oxidants - H20 2-35
2.3.4.5 The Influence of Ammonia 2-37
2.3.5 Surface Chemical Reactions 2-38
2.3.6 Estimates of S02 Oxidation 2-40
2.4 PHYSICS AND CHEMISTRY OF PARTICULATE MATTER 2-41
2.4.1 Definitions 2-42
2.4.2 Physical Properties of Gases and Particles 2-45
2.4.2.1 Physical Properties of Gases. ;,..., 2-45
2.4.2.2 Physical Properties of Particles ;.... 2-46
2.4.3 Dynamics of Single Particles., .. 2-60
2.4.4 Formation and Growth of Particles ........ 2-62
2.4.4.1 Growth Dynamics 2-65
2.4.4.2 Sulfuric Acid - Water Growth Dynamics 2-67
2.4.4.3 Dynamics of Growth by Chemical Reaction 2-67
2.4.4.4 Dynamics of Desorption .: 2-68
2.4.5 Characterization of Atmospheric Aerosol 2-69
2.4.5.1 Distribution ', 2-69
2.4.5.2 Composition of Particles 2-75
2.4.6 . Particle-Size Spectra Evolution ' 2-80
2.4.6.1 General Dynamics Equation (GDE) '2-80
2.4.6.2 Application of the GDE 2-81
2.5 REFERENCES , 2-86
3. TECHNIQUES FOR THE COLLECTION AND ANALYSIS OF SULFUR OXIDES,
PARTICULATE MATTER, AND ACIDIC PRECIPITATION. 3-1
3.1 INTRODUCTION 3-1
3.2 MEASUREMENT TECHNIQUES FOR SULFUR DIOXIDE 3-2
3.2.1 Introduction. 3-2
3.2.2 Manual Methods I 3-2
3.2.2.1 Sample Collection 3-2
3.2.2.2 Calibration '. 3-3
3.2.2.3 Measurement Methods. . ........ 3-4
3.2.3 Automated Methods 3-12
3.2.3.1 Sample Collection...... 3-12
3.2.3.2 Calibration 3-12
3.2.3.3 Measurement Methods 3-13
3.2.3.4 EPA Designated Equivalent Methods 3-17
3.2.4 Summary 3-21
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CONTENTS (continued)
3.3 PARTICULATE MATTER 3-24
3.3,1 Introduction ' 3-24
3.3.2 Gravimetric PM Mass Measurements "..... 3-30
3.3.2.1 Filtration Samplers 3-32
3.3.2.2 Impactor Samplers 3-49
3.3.2.3 Dustfall Sampling...... . 3-54
3,3.3 Nongravimetric Mass Measurements. 3-54
3.3.3.1 Filtration and Impaction Samplers 3-54
3.3.3.2 In Situ Analyzers . 3-60
3.3,4 Particle Composition .-. 3-62
., 3.3.4.1 Analysis of Sulfates *. 3-63
3.3.4.2 Ammonium and Gaseous Ammonia Determination... 3-70
3.3.4.3 Analysis of Nitrates 3-71
3.3.4.4 Analysis of Trace Elements 3-75
3.3.4.5 Analysis of Organic Compounds 3-79
, 3.3.4.6 Analysis of Total Carbon and Elemental
Carbon • .....'..,... 3-80
3.3.5 Particle Morphology Measurements 3-81
3.3.6 Intercomparison of Particulate Matter Measurements 3-81
3.3.7= Summary :..,.. 3-83
3.4 MEASUREMENT TECHNIQUES FOR ACIDIC DEPOSITION 3-85
3.4.1, Introduction 3-85
3.4.2 U.S. Precipitation Studies 3-86.
3.4.3 Analytical Techniques 3-89
3.4.3.1 Introduction ".....• 3-89
3.4.3.2 Analysis of Acidic Deposition Samples 3-89
3.4.4 Inter!aboratory Comparisons 3-93
3. 5 REFERENCES 3-96
APPENDIX 3-A 3-120
4. SOURCES AND EMISSIONS 4-1
4.1 INTRODUCTION ' 4-1
4.2 DATA SOURCES AND ACCURACY 4-2
4.3 NATURAL SOURCES AND EMISSIONS 4-3
4.3.1 Terrestrial Dust 4-4
4.3.2 Sea Spray 4-7
4.3.3 Biogenic Emanations 4-7
4.3.4 Volcanic Emissions. 4-9
4.3.5 Wildfires 4-10
4.4 MANMADE SOURCES AND EMISSIONS 4-11
4.4.1 Historical Emission Trends 4-11
4.4.2 Stationary Point Source Emissions 4-13
4.4.2.1 Fuel Combustion..., 4-24
4.4.2.2 Industrial Processes 4-27
4.4.3 Industrial Process Fugitive Particulate Emissions 4-30
4.4.4 Nonindustrial Fugitive Particulate Emissions 4-33
4.4.5 Transportation Source Emissions 4-35
4. 5 SUMMARY 4-36
4. 6 REFERENCES 4-38
vn
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CONTENTS (continued)
5. ENVIRONMENTAL CONCENTRATIONS AND EXPOSURE 5-1
5.1 INTRODUCTION 5-1
5.2 AMBIENT MEASUREMENTS OF SULFUR DIOXIDE 5-2
5.2.1 Monitoring Factors 5-4
5.2.2 Sulfur Dioxide Concentrations 5-5
5.2.3 Sulfur Dioxide Concentration by Site and Region 5-7
5.2.3.1 Analyses by Various Site Classifications..... 5-7
5.2.3.2 Regional Comparisons .• 5-7
5.2.4 Peak Localized Sulfur Dioxide Concentrations 5-12
5.2.4.1 1978 Highest Annual Average Concentrations... 5-12
5.2.4.2 1978 Highest Daily Average Concentrations...:. 5-12
5.2.4.3 Highest 1-Hour Sulfur Dioxide Concentra-
tions-1978 National Aerometric Data Bank
(NADB) Data. 5-12
5.2.5 Temporal Patterns in Sulfur Dioxide Concentrations..1. 5-13
5.2.-5.1 Diurnal Patterns 5-13
5.2.5.2 Seasonal Patterns • .'.. 5-16
5.2.5.3 Yearly Trends 5-16
5.3 AMBIENT MEASUREMENTS OF SUSPENDED PARTICULATE MASS 5-22
5.3.1 Monitoring Factors -..;.. 5-23
5.3.1.1 Sampling Frequency •'.'... 5-23
5.3.1.2 Monitor Location .;. 5-27
5.3.2 Ambient Air TSP Values 5-27
5.3.3 TSP Concentrations by Site and Region. 5-30
5.3.3.1 TSP by Site Classifications 5-31
5.3.3.2 Intracity Comparisons. 5-31
5.3.3.3 Regional Differences in Background
Concentrations— .• — .. *.. 5-33
5.3.3.4 Peak TSP Concentrations 5-33
5.3.4 Temporal Patterns in TSP Concentrations 5-35
5.3.4.1 Diurnal Patterns „ 5-35
5.3.4.2 Weekly Patterns 5-35
5.3.4.3 Seasonal Patterns 5-37
5.3.4.4 Yearly Trends 5-37
5.4 SIZE OF ATMOSPHERIC PARTICLES 5-46
5..4.1 Introduction 5-46
5.'4.2 Size Distribution of Particle Mass . 5-47
5.5 FINE PARTICLES IN AIR 5-57
5.5.1 Sulfates 5-58
5.5.1.1 Spatial and Temporal Variations 5-58
5.5.1.2 Urban Variations 5-64
5.5.2 Nitrates 5-73
5.5.3 Carbon and Organics. 5-77
5.5.3.1 Physical Properties of Particulate Organics.. 5-78
5.5.3.2 Carbon and Total Organic Mass 5-79
5.5.3.3 Chemical Composition of Particulate Organic
Matter 5-85
5.5.4 Metallic Components of Fine Particles 5-87
5.5.4.1 Lead 5-92
5.5.4.2 Vanadium, Nickel, and Other Metals.. 5-92
5.5.5 Acidity of Atmospheric Aerosols 5-96
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CONTENTS (continued)
5.6 COARSE PARTICLES IN AIR 5-99
5.6.1 Introduction 5-99
5.6.2 Elemental Analysis of Coarse Particles 5-100
5.6.3 Evidence from Microscopical Evaluation of Coarse
Particles. 5-103
5.6.4 Fugitive Dust 5-106
5.6.5 Summary 5-109
5.7 SOURCE-APPORTIONMENT OR SOURCE-RECEPTOR MODELS 5-109
5.8 FACTORS INFLUENCING EXPOSURE 5-115
5.8.1 Introduction .... 5-115
5.8.2 Indoor Concentrations of Sulfur Dioxide ,.... 5-117
5.8.3 Particle Exposures Indoors..... 5-118
5.8.3.1 Introduction 5-118
5.8.3.2 Coarse-Particle Concentrations Indoors 5-122
5.8.3.3 Fine Particles Indoors 5-127
5.8.4 Monitoring and Estimation of Personal Exposures 5-131
5.9 SUMMARY OF ENVIRONMENTAL CONCENTRATIONS AND EXPOSURE 5-136
5.10 REFERENCES. 5-139
6. ATMOSPHERIC TRANSPORT, TRANSFORMATION, AND DEPOSITION. 6-1
6.1 INTRODUCTION 6-1
6.2 CHEMICAL TRANSFORMATION PROCESSES 6-1
6.2.1 Chemical Transformation of Sulfur Dioxide and
Particulate Matter. , 6-3
6.2.2 Field Measurements on the Rate of Sulfur Dioxide
Oxidation f /. 6-3
6.3 PHYSICAL REMOVAL PROCESSES 6-6
6.3.1 Dry Deposition 6-7
6.3.1.1 Sulfur Dioxide Dry Deposition 6-8
6.3,1.2 Particle Dry Deposition. 6-10
6.3.2 Precipitation Scavenging 6-17
6.3.2.1 Sulfur Dioxide Wet Removal 6-19
6.3.2.2 Particle Wet Removal 6^20
6.4 TRANSPORT AND DIFFUSION ,. 6-23
6.4.1 The Planetary Boundary Layer 6-23
6.4.2 Horizontal Transport and Pollutant Residence Times 6-27
6.5 AIR QUALITY SIMULATION MODELING 6-30
6.5.1 Gaussian Plume Modeling Techniques 6-31
6.5.2 Long-Range Air Pollution Modeling , 6-32
6.5.3 Model Evaluation and Data Bases 6-36
6.5.4 Atmospheric Budgets 6-37
6.6 SUMMARY -. 6-38
6.7 REFERENCES 6-39
7. ACIDIC DEPOSITION 7-1
7.1 INTRODUCTION 7-1
7.1.1 Overview of the Problem 7-1
7.1.2 Ecosystem Dynamics 7-6
ix
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CONTENTS (continued)
Page
7,2 CAUSES OF ACIDIC PRECIPITATION . 7*13
7.2.1 Emissions of Sulfur and Nitrogen Oxides... .;«'.... 7-13
7.2.2 Transport of Nitrogen and Sulfur Oxides............... 7*14
7.2.3 Formation 7-21
7.2.3.1 Composition and pH of Precipitation...... 7-22
7.2.3.2 Geographic Extent of Acidic Precipitation..., 7-29
7.2.4 Acidic Deposition ...... 7-34
7.3 EFFECTS OF ACIDIC DEPOSITION :.. 7-36
7.3.1 Aquatic Ecosystems 7-36
7.3.1.1 Acidification of Lakes and Streams...'........ 7-38
7.3.1.2 Effects on Decomposition 7-46
7.3.1.3 Effect on Primary Producers and Primary
Productivity 7-49
7.3.1.4 Effects on Invertebrates 7-55
7.3.1.5 Effects on Fish........ , 7-59
7.3.1.6 Effects on Vertebrates other than Fish.. 7-65
7.3.2 Terrestrial Ecosystems ....................;..... 7-66
7.3.2.1 Effects on Soils V....-.• 7-70
7.3.2.2 Effects on vegetation 7-79
7.3.2.3 Effects on Human Health. 7-90
7.3.2.4 Effects of Acidic Precipitation on Materials. 7-92
7.4 ASSESSMENT OF SENSITIVE AREAS 7-94
7.4.1 Aquatic Ecosystems. 7-94
7.4.2 Terrestrial Ecosystems 7-97
7.5 SUMMARY 7J99
7.6 REFERENCES 7-105
8. EFFECTS ON VEGETATION 8-1
8.1 GENERAL- INTRODUCTION AND APPROACH...,..; 8-1
8.2 REACTION OF PLANTS TO SULFUR DIOXIDE EXPOSURES 8-2
8.2.1 Introduction 8,-2
8.2.2 Wet and Dry Deposition of Sulfur Compounds on
Leaf Surfaces 8-3
8.2.3 Routes and Methods of Entry Into the Plant.. ...... 8*3
8.2.4 Cellular and Biochemical Changes 8-5
8,2.5 Beneficial "Fertilizer" Effects : 8-7
8.2.6 Acute Foliar Injury 8-10
8.2.7 Chronic Foliar Injury ...» , 8-10
8.2.8 Foliar Versus Whole Plant Responses. 8-11
8.2.9 Classification of Plant Sensitivity to Sulfur Dioxide. 8-13
8.3 EXPOSURE-RESPONSE RELATIONSHIPS - SULFUR DIOXIDE 8-13
8.4 EFFECTS OF MIXTURES OF SULFUR DIOXIDE AND"OTHER POLLUTANTS... 8-28
8.4.1 Sulfur Dioxide and Ozone 8-28
8.4.2 Sulfur Dioxide and Nitrogen Dioxide "., 8-30
8.4.3 Sulfur Dioxide and Hydrogen Fluoride 8-31
8.4.4 Sulfur Dioxide, Nitrogen Dioxide and Ozone............ 8-31
8.4.5 Summary 1 8-31
8.5 EFFECTS OF NON-POLLUTANT ENVIRONMENTAL FACTORS ON SULFUR
DIOXIDE PLANT EFFECTS. 8-32
8.5.1 Temperature ..*... .' 8-32
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CONTENTS (continued)
Page
8.5.2 Relative Humidity 8-32
8.5.3 Light 8-33
8.5.4 Edaphic Factors 8-33
8.5.5 Sulfur Dioxide and" Biotic Plant Pathogen Interactions. 8-34
8.6 PLANT EXPOSURE TO PARTICULATE MATTER. 8-34
8.6.1 Deposition Rates. 8-34
8.6.2 Routes and Methods of Entry Into Plants 8-35
8.6.2.1 Direct Entry Through Foliage 8-35
8.6.2.2 Indirect Entry Through Roots 8-36
8.7 REACTION OF PLANTS TO PARTICLE EXPOSURE 8-36
8.7.1 Symptomatology of Particle-Induced Injury... 8-36
8.7.2 Classification of Plant Sensitivity—Particles 8-41
8.8 EXPOSURE-RESPONSE RELATIONSHIPS—PARTICLES 8-41
8.9 INTERACTIVE EFFECTS ON PLANTS WITH THE ENVIRONMENT—
PARTICULATE MATTER. 8-42
8.10 EFFECTS OF,SULFUR DIOXIDE AND PARTICULATE MATTER ON NATURAL
ECOSYSTEMS f 8-43
8.10.1 Sulfur Dioxide in Terrestrial Ecosystems. 8-43
8.10.2 Ecosystem Response to Sulfur Dioxide 8-46
8.10.3 Response of Natural Ecosystems to Particulate Matter.. 8-54
8.11 SUMMARY 8-56
8.12 REFERENCES 8-60
APPENDIX 8-A , 8-78
9. EFFECTS ON VISIBILITY AND CLIMATE 9-1
9.1 INTRODUCTION. 9-1
9.2 FUNDAMENTALS OF ATMOSPHERIC VISIBILITY 9-2
9.2.1 Physics of Light Extinction. . 9-11
9.2.2 Measurement Methods " 9-14
9.2.2.1 Human Observer (Total Extinction); 9-16
9.2.2.2 Photography (Total Extinction) 9-16
9.2.2.3 Telephotometry (Total Extinction) 9-17'
9.2.2.4 Long-path Extinction (Total Extinction) 9-17
9.2.2.5 Nephelometer .(Scattering) '. 9-18
9.2.2.6 Light Absorption Coefficient 9-18
9.2.3 Role of Particulate Matter in Visibility Impairment.. 9-19
9.2.3.1 Rayleigh Scattering 9-19
9.2.3.2 Nitrogen Dioxide Absorption 9-20
9.2.3.3 Particle Scattering....... 9-20
9.2.3.4 Particle Absorption « 9-30
9,2.4 Chemical Composition of Atmospheric Particles 9-31
9.2.4.1 Role of Water invisibility Impairment 9-34
9.2.4.2 Light Extinction Budgets 9-38
9.2.5 Considerations in Establishing a Quantitative
Relationship Between Fine-Particle Mass Concentration
and Visual Range.... 9-40
9. 3 VISIBILITY AND PERCEPTION 9-43
9.4 HISTORICAL PATTERNS OF VISIBILITY 9-49
9.4.1 Natural Versus Manmade Causes 9-63
XI
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CONTENTS (continued)
Page
9.5 THE EVALUATION OF IMPAIRED VISIBILITY 9-66
9.5.1 Social Awareness and Aesthetic Considerations 9-67
9.5.2 Economic Considerations... 9-68
9.5.3 Transportation Operations 9-71
9.6 SOLAR RADIATION 9-75
9.6.1 Spectral and Directional Quality of Solar Radiation^. 9-86
9.6.2 Total Solar Radiation:- Local to Regional Scale 9-92
9.6.3 Radiative Climate: Global Scale :... 9-94
9.7 CLOUDINESS AND PRECIPITATION 9-95
9.8 SUMMARY 9-97
9.9 REFERENCES 9-100
10. EFFECTS ON MATERIALS :.... 10-1
10.1 INTRODUCTION 10-1
10.2 SULFUR OXIDES 10-4
10.2.1 Corrosion of Exposed Metals 10-4
10.2.1.1 Physical and Chemical Considerations . 10-4
10.2.1.2 Effects of Sulfur Oxide Concentrations
on the Corrosion of Exposed Metals 10-12
10.2.2 Protective Coatings 10-23
10.2.2.1 Zinc-Coated Materials 10-23
10.2.2.2 Paint Technology and Mechanisms of Damage... 10-28
10.2,3 Fabrics 10-32
10.2.4 Building Materials 10-34
10.2.4.1 Stone 10-34
10.2.4.2 Cement and Concrete 10-35
10.2.5 Electrical Equipment and Components 10-37
10.2.6 Paper 10-37
10.2.7 Leather 10-37
10.2.8 Elastomers and Plastics 10-38
10.2.9 Works of Art. '...' 10-38
10,2.10 Review of Damage Functions Relating Sulfur Dioxide
to Material Damage " 10-39
10.3 PARTICULATE MATTER 10-41
10.3.1 Corrosion and Erosion 10-41
10.3.2 Soiling and Discoloration.... 10-42
10.3.2.1 Building Materials 10-43
10.3.2.2 Fabrics 10-45
10.3.2.3 Household and Industrial Paints 10-45
10.4 SUMMARY, PHYSICAL EFFECTS OF SULFUR OXIDES AND PARTICULATE
MATTER ON MATERIALS. 10-47
10.5 ECONOMIC ESTIMATES 10-49
10.5.1 Introduction. 10-49
10.5.2 Economic Loss Associated with Materials Damage and
Soi 11 ng. 10-50
10.5.2.1 Metal Corrosion and Other Damage to
Materials Associated with Sulfur Oxides . 10-50
10.5.2.2 Soiling of Paint and Other Materials.
Associated with Particulate Matter 10-54
10.5.2.3 Combined Studies 10-64
XI 1
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CONTENTS (continued)
10.5.3 Estimating Benefits from Air Quality Improvement,
1970-1978 10-70
10.5.4 Summary of Economic Damage of Particulate Matter/
Sulfur Oxides to Materials 10-73
10.6 SUMMARY AND CONCLUSIONS, EFFECTS ON MATERIALS 10-74
10. 7 REFERENCES ." 10-75
11. RESPIRATORY TRACT DEPOSITION AND FATE OF INHALED AEROSOLS AND
SULFUR DIOXIDE 11-1
11.1 INTRODUCTION 11-1
11.1.1 General Considerations 11-1
11.1.2 Aerosol and Sulfur Dioxide Characteristics 11-2
11.1.3 The Respi ratory Tract 11-4
11.1.4 Respiration and Other Factors 11-7
11.1.5 Mechanisms of Particle Deposition 11-12
11. 2 DEPOSITION IN MAN AND EXPERIMENTAL ANIMALS 11-16
11.2.1 Insoluble and Hydrophobic Solid Particles 11-16
11.2.1.1 Total Deposition 11-16
11.2.1.2 Extrathoracic Deposition 11-20
11.2.1.3 Tracheobronchial Deposition. 11-23
11.2.1.4 Pulmonary Deposition 11-27
• 11.2.1.5 Deposition in Experimental Animals 11-29
11.2.2 Soluble, Deliquescent, and Hygroscopic Particles 11-32
11.2.3 Surface-Coated Particles 11-33
11.2.4 Gas Deposition 11-33
11.2.5 Aerosol-Gas Mixtures 11-37
11.3 TRANSFORMATIONS AND CLEARANCE FROM THE RESPIRATORY TRACT.... 11-38
11.3.1 Deposited Particulate Material 11-39
11.3.2 Absorbed Sulfur Dioxide 11-47
11.3.3 Particles and Sulfur Dioxide Mixtures 11-48
11.4 AIR SAMPLING FOR HEALTH ASSESSMENT 11-48
11. 5 , 11-54
11.6 REFERENCES 11-57.
12. TOXICOLOGICAL STUDIES 12-1
12.1 INTRODUCTION 12-1
12.2 EFFECTS OF SULFUR DIOXIDE 12-2
12.2.1 Biochemistry of Sulfur Dioxide 12-2
12.2.1.1 Chemical Reactions of Bisulfite with
Biological Molecules. . 12-3
12.2.1.2 Metabolism of Sulfur Dioxide 12-5
-12.2.1.3 Activation and Inhibition of Enzymes by
. • Bisulfite.. ' 12-6
12.-2.2 Mortality 12-7
12.2.3 Morphological Alterations 12-8
12.2.4 Alterations in Pulmonary Function 12-13
12.2.5 Effects on Host Defenses 12-19
12.3 EFFECTS OF PARTICULATE MATTER 12-22
xm
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CONTENTS (continued)
12.3,1 Mortality; .. 12-24
12.3.2 Morphological Alterations 12-24
12.3.3 Alterations in Pulmonary Function ,. 12-28
12.3.3.1 Acute Exposure Effects 12-28
12.3.3.2 Chronic Exposure Effects 12-39
12.3.4 Alteration in Host Defenses ; ..... 12-41
12.3.4.1 Mucoeiliary Clearance, 12-41
12.3.4.2 Alveolar Macrophages 12-46
12.3.4.3 Interaction with Infectious Agents 12-51
12.3.4.4 Immune Suppression 12-53
12.4 INTERACTION OF SULFUR DIOXIDE AND OTHER POLLUTANTS. ..... 12-54
12.4.1 Sulfur Dioxide and Particulate Hatter 12-54
12.4.1.1 Acute Exposure Effects 12-54
12.4.1.2 Chronic Exposure Effects ; .'... 12-56
12.4.2 Interaction with Ozone :..... 12-63
12.5 CARCINOGENESIS AND MUTAGENESIS OF SULFUR COMPOUNDS AND
ATMOSPHERIC. PARTICLES 12-66
12.5.1 Airborne Particulate Matter 12-68
12.5.1.1 Jjn vitro Mutagenesis Assays of Particulate
Matter 12-68
12.5.1.2 Tumorigenes is of Particulate Extracts... 12-70
12.5.2 Potential Mutagenic Effects of Bisulfite and Sulfur
Dioxide 12-72
12.5.3 Tumorigenesis in Animals Exposed to Sulfur Dioxide
or Sulfur Dioxide and Benzo(a)pyrene 12-74
12.5.4 Effects of Trace Metals Found in Atmospheric
Particles , 12-75
12.6 CONCLUSIONS. 12-75
12.6.1 Sulfur Dioxide 12-75
12.6.2 Particulate Matter 12-78
12.6.3 Combinations of Gases and Particles 12-81
12.7 REFERENCES 12-83
APPENDIX 12-A: U.S. EPA Analysis of the Laskin et al.
and Peacock and Spence Data (Memo from V. Hasselblad
to L.D. Grant) 12-102
13. CONTROLLED HUMAN STUDIES 13-1
13.1 INTRODUCTION 13-1
13.2 SULFUR DIOXIDE .... 13-2
13.2.1 Subjective Reports 13.2
13.2.2 Sensory Effects. 13-3
13.2.2.1 Odor Perception Threshold 13-3
13.2.2.2 Sensitivity of the Dark-Adapted Eye 13-5
13.2.2.3 Interruption of Alpha Rhythm 13-6
13.2.3 Respiratory and Related Effects 13-6
13.2.3.1 Respiratory Function... 13-6
13.2.3.2 Water Solubility , 13-12
xiv
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CONTENTS (continued)
13.2.3.3 Nasal Versus Oral Exposure 13-12
13.2.3.4 Subject Activity Level 13-13
13.2.3.5 Temporal Parameters 13-15
13.2.3.6 Mucoci 1 iary Transport 13-17
13.2.3.7 Health 'Status ; 13-19
13. 3 PARTICULATE MATTER.: 13-23
13.3.1 Sulfuric Acid and Sulfates 13-23
13.3.1.1 Sensory Effects 13-23
13.3.1.2 Respiratory and Related Effects 13-24
13.3.2 Insoluble and Other Non-sulfur Aerosols 13-31
13.4 PARTICULATE MATTER AND SULFUR DIOXIDE 13-36
13.5 SULFUR DIOXIDE, OZONE, AND NITROGEN DIOXIDE 13-39
13.6 SUMMARY AND CONCLUSIONS 13-46
13.6.1 Sulfur Dioxide Effects 13-47
13.6.2 Sulfuric Acid and Sul fate Effects 13-52
13.6.3 Effects of Other Particulate Matter Species 13-53
13.7 REFERENCES 13-55
APPENDIX 13A 13-62
14. EPIDEMIOLOGICAL STUDIES ON THE EFFECTS OF PARTICULATE MATTER AND
SULFUR OXIDES ON HUMAN HEALTH 14-1
14.1 INTRODUCTION 14-1
14.1.1 Methodological Considerations 14-2
14.1.2 Guidelines for Assessment of Epidemiological Studies. 14-5
14.2 AIR QUALITY MEASUREMENTS 14-7
. 14.2.1 Sulfur Oxides Measurements.: 14-7
14.2.2 Particulate Matter Measurements 14-8
14.3 ACUTE PARTICULATE MATTER/SULFUR OXIDE EXPOSURE EFFECTS 14-11
14.3.1 Mortal ity : 14-11
14.3.1.1 Acute Episode Studies 14-11
14.3.1.2 Mortality Associated with Non-episodic
Variations in Pollution 14-15
14.3.1.3 Morbidity 14-26
14.4 CHRONIC PM/S02 EXPOSURE EFFECTS 14-35
14.4.1 Mortal ity 14-35
14.4.2 Morbidity 14-44
14.4.2.1 Respiratory Effects in Adults 14-44
14.4.2.2 Respiratory Effects in Children 14-46
14. 5 SUMMARY AND CONCLUSIONS ~. 14-49
14.5.1 Health Effects Associated with Acute Exposures to
Particulate Matter and Sulfur Oxides- 14-50
14.5.2 Health Effects Associated with Chronic Exposures to
.Particulate Matter and Sulfur Oxides 14-53
14. 6 REFERENCES. .-• 14-56
APPENDIX 14-A: Annotated Comments on Community Health Epidemio-
logical Studies Not Discussed in Detail in Main Text of
Chapter 14 14-73
xv
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CONTENTS (continued)
APPENDIX 14-B: Occupational Health Studies on Particulate Matter
and Sulfur Oxides
APPENDIX 14-C: Summary of Examples of Sources and Magnitudes of
Measurement Errors Associated with Aerometric Measurements
of PM and SOg Used in British and American Epidemiologica]
Studies
APPENQIX 14-D: EPA Reanalysis of Martin and Bradley (1960) Data
on Mortal ity Ouri ng 1958-59 London Wi ntef
APPENDIX 14-E: Summary of Unpublished Dawson and Brown (1981) Re-
analysis of Martin and Bradley (1960) Data
APPENDIX 14-F: Summary of Unpublished Roth et al. (1981) Year-
by-Year Analysis of London Mortality Data for Winters of
1958-59 to 1971-72 ............. f.....
APPENDIX 14-G: Summary of Mazumdar et al. Year-by-Year Analysis
of London Mortality Data for Winters of 1958-59 to 1971-72...
14-102
14-107
14-116
14-126
14-135
14-138
xvi
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CONTENTS (continued)
FIGURES
Figure Page
1-la Idealized size distribution for particles found in typical
urban aerosols (mainly from anthropogenic sources) under
varying weather conditions 1-5
1-lb Idealized size distribution for atmospheric particles from
anthropogenic sources. 1-5
1-lc Idealized size distribution for atmospheric particles from
natural sources in a marine setting 1-6
1-ld Idealized size distribution for atmospheric, particles from
natural sources in a continental setting 1-6
1-2 Idealized representation of typical fine- and coarse-particle
mass and chemical composition distribution in an urban aerosol... 1-8
1-3 Characterization of 1974-76 national SO, status is shown by
second highest 24-hr average concentration 1-19
1-4 One example of rapid increase in ambient S0? concentra-
tion from near zero to 1.30 ppm (3410 jjg/m37 during
a period of approximately two hours 1-20
1-5 Seasonal variations in urban, suburban, and rural areas for
four size ranges of particles. The data were obtained from
a relatively small number of monitoring sites 1-21
1-6 Complex processes affecting transport and transformation of
airborne particulate matter and sulfur oxides 1-23
1-7 Average pH isopleths as determined from laboratory analyses of
precipitation samples, weighted by the reported quantity
of precipitation 1-26
1-8 Idealized conceptual framework illustrating the "law of
tolerance," which postulates a limited range of various
environmental factors within which species can.survive 1-28
1-9 Conceptual model of the factors involved in air pollution's
effects on vegetation 1-34
1-10 Median yearly visual range (miles) and isopleths for suburban/
nonurban areas, 1974-1976 * 1-38
1-11 Inverse proportionality between visual range (V) and the
scattering coefficient (OSD) as measured at the point of
observation v. 1-40
1-12 Simultaneous in situ monitoring of cr and fine-particle
mass concentration in St. Louis in April 1973 showed a high
correlation coefficient of 0.96, indicating that cr depends .
primarily on the fine-particle concentration.......?............. 1-41
1-13 The spatial distribution of 5ryear average extinction coeffi-
cients shows the subtantial increases of third-quarter extinc-
tion coefficients in the Carolines, Ohio River Valley, and
Tennessee-Kentucky area 1-42
xvn
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CONTENTS (continued)
Figure Page
1-14 Season'al turbidity patterns for 1961-1966 and 1972-1975 are
shown for selected regions in the Eastern United States ......... 1-44
1-15 Steel corrosion behavior as a function of average SO, con-
centration at 65% rel ati ve humidity ...................... . ...... 1-48
1-16 Steel corrosion behavior as a function of average relative
humidity at three average concentration levels of sulfur
dioxide ...... . ...... . . ....................................... ... 1-49
1-17 Isopleths of annual mean relative humidity in the
United States ...................................... . _____ . ____ ... 1-50
1-18 Features of the respiratory tract of man used in the descrip-
tion of inhaled particles and gases .................. ... . ...... 1-53
1-19 Division of the thoracic fraction of deposited particles into
pulmonary and tracheobronchial fractions. .... ...... . ------ . ...... 1-56
1-20 These data show hypothetical dose-response curves derived from
regressing mortality on smoke in London, England during winters
1958/59 to 1971/72 ..... . ..... . .............. . .................. 1-95
1-21 History and clinical evidence of respiratory disease (percent)
in 5-year-olds, by pollution in areas of residence .............. 1-101
1-22 Penetration of aerosol through the inlet of the British Smoke
Shade Sampler and through the complete system ........... .... ..... ''1-104
2-1 The global sulfur cycle, showing the major reservoirs, pathways,
and forms of occurrence of sul fur ................... : . . ......... 2-4
2-2 Interrelations of pathways, processes, and properties of
sulfur oxides and parti cul ate matter and effects. ........... ..... 2-7
2-3 The distribution of species for the S02 • H20-HS03-S03" system
as a function of pH. Also, the ratio of the concentrations of
SOZr Q\ to the total quantity dissolved in water is shown. ..... ... 2-11
2-4 Schematic of the polluted atmospheric photooxidation cycle ....... 2-18
2-5 The theoretical rate of reaction (percent per hour) of various
free-radical species with S02 is shown for a simulated sunlight-
irradiated (.solar zenith angle of 40°) polluted atmosphere ....... 2-20
2-6 Percentage conversion at midday of sulfur dioxide to sulfate
by HO and by HO, H02, and CH302 radicals as a function of °N
latitude in summer and winter ......................... ........... 2-21
+ + 2_
2-7 Solubility diagram for the H -NH«-SQ4 -H20 system at
equi 1 ibrium (30°C) .............. . ................................ 2-49
+ + 2.
2-8 Growth of H -NH4-S04 particles as a function of RH ........ . ..... 2-50
2-9 Condensational growth and evaporation of (NH4)2S04 particles as
a function of relative humidity at 25°C ..................... . ---- 2-52
2-10 The -equilibrium size of sulfuric acid solution droplets as a
function of relative humidity. . ...... ... ---- •. ................. ... 2-54
2-11 NHg and HN03 partial pressures as a function of droplet" s nitrate
-) and sulfate (Ccg2~) concentrations at 85 percent relative
humidity, 25°C ...................... . ....................... . ---- 2-58
xvm
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CONTENTS (continued)
2-12 Frequency plots of number, surface, and volume distributions for
1969 Pasadena smog aerosol . 2-71
2-13a Idealized size distribution for particles found in typical urban
aerosols (mainly from anthropogenic sources) under varying
weather conditions 2-73
2-13b Idealized size distribution for atmospheric particles from
anthropogeni c sources • 2-73
2-13c Idealized size distribution for atmospheric particles from
natural sources in a marine setting 2-74
2~13d Idealized size distribution for atmospheric particles from
natural sources i n a conti nental setti ng 2-74
2-14 Idealized representation of typical fine- and coarse-particle
mass and chemical composition distribution in an urban aerosol... 2-76
3-1 Respiratory deposition models used as patterns for sampler
cutpoints 3-25
3-2 Plots illustrating the relationship of particle number,
surface area, and volume distribution as a function of
particle size 3-27
3-3 , Typical ambient mass distribution data for particles
up to 200 |jm 3-28
3-4 Sampling effectiveness of a Hi-Vol sampler as a function of
windspeed ,.: 3-31
3-5 Sampling effectiveness of the dichotomous sampler inlet as a
function of wi ndspeed 3-33
3-6 Sampling effectiveness of the Wedding IP inlet 3-34
3-7 Sampling effectiveness of UM-LBL IP inlet 3-35
3-8 Effect of sampler flowrate on the performance of a Hi-Vol for
30 urn particles at a windspeed of 8 km/hr 3-38
3-9 Separator efficiency and wall losses of the dichotomous
sampler at 25 pm 3-41
3-10 Sampling .effectiveness for the 3.5 |jm cutpoint CHESS
cycl one sarapler 3-43
3-11 ^ Fraction of methylene blue particles deposited in a cyclone .
sampler as a function of the aerodynamic particle diameter ,. 3-45
3-12 Sampling effectiveness for the size-selective inlet Hi-Vol
sampler 3-46
3-13 Effect of windspeed upon cutpoint size of the size-selective
inlet. 3-47
3-14 Effect of sampler flowrate on the sampling effectiveness of
the size-selective inlet Hi-Vol for a particle size of
15.2 pin and windspeed of 2 km/hr 3-48
3-15 An example of mass size distribution obtained using a cascade
impactor. 3-50
3-1.6 Fractional particle collection of the CHAMP fractionator inlet
at a sampler flowrate of 1133 liters/min under static windspeed
conditions 3-52
3-17 Efficiency of the single impaction stage of the CHAMP Hi-Vol
sampl er 3-53
3-18 Sampling effectiveness of the inlet alone and through the
entire flow system of the British Smoke Shade sampler 3-56
3-19 Response of a Piezoelectric Microbalance to relative humidity
for vari ous parti cl e types : ' 3-60
xix
-------
CONTENTS (continued)
Figure Page
3-20 Light scattering and absorption expressed per unit volume of
aerosol 3-61
5-1 Distribution of annual mean sulfur dioxide concentrations across
an urban complex, as a function of various spatial scales 5-3
5-2 Histogram delineating annual average sulfur dioxide concentrations
for valid continuous -sampling sites in the United States in 1978. 5-6
5-3 Characterization of 1974-76 national S02 status is shown by
second highest 24-hour average concentration. 5-10
5-4 Composite diurnal pattern of hourly sulfur dioxide concentrations
are shown for Watertown, MA, for December 1978 5-14
5-5 Monthly means of hourly sulfur dioxide concentrations are shown
for St. Louis (city site 26-4280-007, "Broadway & Hurck") for
February 1977 and 1978 ,. ,5-15
5-6 Monthly means of hourly sulfur dioxide concentrations are
shown for Steubenville, Ohio (NOVAA site 36-6420-012) for
June 1976 and July 1977 5-17
5-7 Seasonal variations in sulfur dioxide levels are shown for
Steubenville, St. Louis, and Watertown 5-18
5-8 Annual average sulfur dioxide concentrations are shown for 32
urban NASN stations / 5-19
5-9 Nationwide trends in annual average sulfur dioxide concentrations
from 1972 to 1977 are shown for 1233 sampling sites 5-20
5-10 Distribution shows the number of TSP observations'per-valid site
in 1978; total of 2882 sites 5-24
5-11 The 95 percent confidence intervals about an annual mean TSP
concentration of 75 ug/m3 is shown for various sampling
frequencies 5-26
5-12 Distribution of mean and 90th percentile TSP concentrations is
shown for valid 1978 sites 5-28
5-13 Histogram of number of sites against concentration shows that
over one-third of the sites had annual mean concentrations
between 40 and 60 ug/m3 in 1978. ... 5-29
5-14 Histogram of mean TSP levels by neighborhood shows lowest levels
in residential areas, higher levels in commercial areas, and
highest levels in industrial areas 5-32
5-15 Average estimated contributions to nonurban levels in the East,
Midwest, and West are most variable for transported secondary
and continental sources 5-34
5-16 Severity of TSP peak exposures is shown on the basis of the
90th percentile concentration. Four AQCR's did not report 5-36
5-17 Seasonal variations in urban, suburban, and rural areas
for four size ranges of particles 5-38
5-18 Monthly mean TSP concentrations are shown for the Northern Ohio
Valley Air Monitoring Headquarters, Steubenville, Ohio. No
el ear seasonal pattern i s apparent ; 5-39
5-19 Annual geometric mean TSP trends are shown for selected NASN
sites 1 < 5-40
5-20 (Top) Nationwide trends in annual mean total suspended
particulate concentrations from 1972 to 1977 are shown for
2707 sampling sites. (Bottom) Conventions for box plots 5-42
5-21 Regional trends of annual mean total suspended particulate
concentrations, 1972-1977, Eastern states.. 5-44
xx
-------
CONTENTS (continued)
Figure •• • Page
5-22 Regional trends of annual mean total suspended particulate
concentrations, 1972-1977, Western states 5-45
5-23 Linear-log plot of the volume distributions for the four
background distributions 5-49
5-24 Linear-log plot of the volume distributions for two urban
aerosols and a typical distribution measured in the Labadie
coal-fired power plant plume near St. Louis, Size distri-
' butions measured above a few hundred meters above the
ground generally have a rather small coarse particle mode 5-50
5-25 Incursion of aged smog from Los Angeles at the Goldstone
tracking station in the Mojave Desert in California 5-51
5-26 Sudden growth of the coarse particle mode due to local dustv
sources measured at the Hunter-Liggett Military Reservation
in California. This shows the independence of the
accumulation and coarse particle mode ,.-, 5-52
5-27 Inhalable particle network sites established as of
March 19, 1980 5-54
5-28 Contour maps of sulfate concentrations for 1974 are shown for:
(a) annual average; (b) winter average; (c) summer average 5-59
5-29 Intensive Sulfate Study area in eastern Canada shows the
geometric mean of the concentration of soluble particulate
sulfate during the study period. Units are micrograms of
sulfate per cubic meter 5-61
5-30 Map of SURE region shows locations of ground measurement
stati ons 5-62
5-31 Cumulative plots show the frequency of sulfate concentrations
in the SURE region on the basis of the 1974-75 historical data... 5-63
5-32 Maps show the spatial distribution of number of days per month
that the sulfate concentration equaled or exceeded 10 ug/m3 5-65
5-33 1977 seasonal patterns of S02 emissions and 24-hr average S02
and S04 ambient levels in the New York area are normalized to
the annual average val ues 5-66
5-34 Monthly variation in monthly mean of 24-hour average sulfate
concentration at downtown Los Angeles is compared with monthly
mean 1973 Los Angeles County power plant S02 emissions 5-67
5-35 Map shows annual mean 24-hr average sulfate levels in micrograms
per cubic meter in the New York area, based on 1972 data from
Lynn et al. (1975). Squares are locations of three CHAMP site
stations. The fourth station is at the tip of Long Island
about 160 km from Manhattan 5-70
5-36 Distribution of annual average sulfate concentration in
micrograms per cubic meter in the greater Los Angeles area
based on 1972-1974 data 1 5-71
5-37 Map shows U.S. mean annual ambient nitrate levels in micrograms
per cubic meter , 5-74
5-38 Mean nitrate concentrations in micrograms per cubic meter at
nonurban sites in the U.S. based on valid annual average from
1971 through 1974. , 5-75
xxi
-------
CONTENTS (continued)
Figure Page
5-39 Calculated distribution'of aerosol constituents for two aerosol
samples taken in the Los Angeles Basin, .-v...." 5-82
5-40 Benzo(a)pyrene seasonality and trends (1966-75) in the
50th and 90th percentiles for 34 NASN urban sites.... 5-84
5-41 Seasonal patterns and trends in quarterly average urban lead
concentrations 5-94
5-42 Regional trends in the 90th percentile of the annual averages
for vanadi urn ".... 5-95
5-43 Seasonal variation in quarterly averages for nickel and
vanadium at urban sites in the northeast 5-97
5-44 Elemental compositions of some coarse particle components... 5-102
5-45 Diurnal variation of particle concentrations and Plymouth
Avenue traffic volume at Falls River, Mass., during March
through June 1979 (weekdays only), shows contribution from
reentrained particles 5-108
5-46 Types of receptor source apportionment models 5-110
5-47 Source contributions at RAPS sites for July-August 1976 estimated
by chemical element balance ...- 5-112
5-48 Monthly averages of size fractionated Denver aerosol mass and
composition for January and May, 1979 5-113
5-49 Aerosol source in downtown Portland, annual stratified
arithmetic average. Does not include the 17%, on,the average,
of material collected with the standard Hi-Vol sampler which
was not collected and characterized with the ERT-TSP sampler..... 5-114
5-50 Retention of Au198 labeled FegOs particles from human lungs,
comparison of 9 non-smoking subjects with three smoker
subjects 5-116
5-51 Annual sulfur dioxide concentrations averaged across each
community's indoor and outdoor network (May 1977-April 1978) 5-119
5-52 Monthly mean SQ2 concentrations averaged across Watertown's
indoor and outdoor network (November 1976-April 1978) 5-120.
5-53 Monthly mean SQ^ concentrations averaged across Steubenville's
indoor and outdoor network (November 1976-April 1978) 5-121
5-54 Annual respirable particulate concentrations averaged across
each community's indoor and outdoor network (May 1977-
April 1978) 5-130
5-55 An example of personal exposure to respirable particles 5-132
5-56 Normalized distribution of personal (12-hour) exposure samples
(pm/m3) for non-smoke exposed and smoke exposed samples 5-134
5-57 Daily mean indoor/outdoor and personal concentrations (jjg/m3)
of respirable particles. Daily means averaged over 24 homes
and outdoor locations and up to 46 personal samples. Samples
collected during May and June 1979 5-135
6-1 Pathway processes of airborne pollutants 6-2
6-2 Predicted deposition velocities at 1 m for M*=30 cm s and
-3
particle densities of 1,4, and 11.5 g cm 6-16
6-3 Basic factors influencing precipitation scavenging 6-18
6-4 Relationship between rain scavenging rates and particle
size. . 6-24
6-5 Percentages of aerosol particles of various sizes removed by
precipitation scavenging 6-25
xxi i
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CONTENTS (continued)
Figure Page
6-6 Estimated residence times for select pollutant species and
their associated horizontal transport .scale 6-29
6-7 Trajectory modeling approaches are shown... 6-34
7-1 Schematic representation of the nitrogen cycle, emphasizes human
activities that affect fluxes of nitrogen ....; " 7-10
7-2 Law of tolerance 7-12
7-3 Historical patterns of fossil fuel consumption in the
United States 7-15
7-4 Forms of coal usage in the United States. 7-16
7-5a Trends in emissions of sulfur dioxide 7-17
7~5b Trends in emissions of nitrogen oxides 7-17
7-6 Characterization of U.S. SO emissions density by state 7-18
7-7 Characterization of U.S. NO emissions density by state 7-19
7-8 Trends in mean annual concentrations of sulfate, ammonium,
and nitrate in precipitation 7-24
7-9 Comparison of weighted mean monthly concentrations of sulfate in
incident precipitation collected in Walker Branch Watershed,
Tennessee (WBW) and four MAP3S precipitation chemistry monitoring
stations in New York, Pennsylvania, and Virginia 7-27
7-10 Seasonal variations in pH (A) and ammonium and nitrate
concentrations (B) in wet-only precipitation at Gainesville,
Florida... 7-28
7-11 Seasonal variations of precipitation pH in the New York
Metropol itan Area 7-31
7-12 History of acidic precipitation at various sites in and
adjacent to State of New York 7-32
7-13 pH of rain samples as measured in the laboratory and used in
combination with the reported amount of precipitation..... 7-35
7-14 Annual mass transfer rates of sulfate expressed as a percentage
of the estimated total annual flux of the element to the forest
floor beneath a representative chestnut oak stand 7-37
7-15 Schematic representation of the hydrogen ion cycle. 7-39
7-16 pH and calcium concentrations in lakes in northern and northwestern
Norway sampled as part of the regional survey of 1975, in lakes in
northwestern Norway sampled in 1977 (o) and in lakes in southernmost
and southeastern Norway sampled in 1974 (o) 7-43
7-17 The pH value and sulfur loads in lake waters with extremely
sensitive surroundings (curve 1) and with slightly less
sensitive surroundings (curve 2)...., 7-44
7-18 Total dissolved Al as a function of pH level in lakes in
acidified areas in Europe and North America.. 7-45
7-19 pH levels in Little Moose Lake, Adirondack region of New York
State, at a depth of 3 meters and at the lake outlet ,:... 7-47
7-20 Numbers of phytoplankton species in 60 lakes having different
pH values on the Swedish West Coast, August 1976 are compared 7-51
7-21 Percentage distribution of phytoplankton species and their
biomasses. September 1972, West Coast of Sweden 7-52
7-22 The number of species of crustacean zooplankton observed in
57 lakes during a synoptic survey of lakes in southern Norway.... 7-56
7-23 Frequency distribution of pH and fish population status in .
Adirondack Mountain lakes greater than 610 meters elevation 7-60
xx i i 1
-------
CONTENTS (continued)
Figure Page
7-24 Frequency distribution of pH and fish population status in 40
Adirondack lakes greater than 610 meters elevation, surveyed
during the period 1929-1937 and again in 1975 7-61
7-25 Norwegian salmon fishery statistics for 68 unacidified and 7
acidified rivers 7-62
7-26 Showing the exchangeable ions of a soil with pH 7; the soil
solution composition, and the replacement of Na by H from
acid rain 7-71
7-27 Regions in North America with lakes that are sensitive to acidi-
fication by acid precipitation by virtue of their underlying
bedrock characteristics 7-96
7-28 Soils of the eastern United States sensitive to acid rainfall
are mapped 7-100
8-1 Map of the United States indicating major areas-of sulfur-
deficient soils 8-8
8-2 Conceptual model of the factors involved in air pollution
effects (dose-response) on vegetation 8-16
8-3 The sulfur cycle 8-45
9-1 Map shows median yearly visual range (miles) and isopleths for
suburban/nonurban areas, 1974-76 9-3
9-2 Median summer visual range (miles) and isopleths for suburban/
nonurban areas, 1974-76 9-3
9-3 (A) A schematic representation of atmospheric extinction,
illustrates (i) transmitted, (ii) scattered, and (iii) absorbed
light. (B) A schematic representation of daytime visibility
illustrates: (i) light from target reaching observer,
(ii) light from target scattered out of observer's line of
sight, (iii) air light from intervening atmosphere, and
(iv) air light constituting horizon sky 9-4
9-4 The apparent contrast between object and horizon sky decreases
with increasing distance from the target. This is true for
both bright and dark objects 9-5
9-5 Mean contrast threshold of the human eye for 50% detection
probability as a function of target angular diameter and adaption
brightness (candles/m ) for targets brighter than their background.
Daytime adaptation brightness is usually in the range 100 to
10,000 candles/m2 9-8
9-6 Inverse proportionality between visual range and the scattering
coefficient, a , as measured at the point of observation 9-10
9-7 Extinction efficiency factor (Qex+.) of a single spherical
particle as a function of diameter for a non-absorbing par-
ticle of refractive index (1.5-O.Oi) and wavelength 0.55 urn 9-12
9-8 Extinction efficiency factor (Qext) of a single spherical
particle as a function of diameter for an absorbing particle
of refractive index (2.0, -1.0) and wavelength 0.55 urn 9-12
xxiv
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CONTENTS (continued)
9-9 For a light-scattering and absorbing particle, the scattering
per volume concentration has a strong peak at particle
diameter of 0.5 urn (m = 1.5-0.05i; wavelength = 0.55 pm).
However, the absorption per aerosol volume is only weakly
dependent on particle size. Thus the light extinction by
particles with diameter less than 0.1 pm is primarily due to
absorption. Scattering for such particles is very low. A
black plume of soot from an oil burner is a practical
example. , ., 9-22
9-10 (A) Calculated scattering coefficient per unit mass
concentration at a wavelength of 0.55 pm for absorbing and
nonabsorbing materials is shown as a function of diameter for
single-sized particles 9-23
9-11 For a typical aerosol volume (mass) distribution, the calculated
light-scattering coefficient is contributed almost entirely by
the size range 0.1-1.0 (jm. The total a and total aerosol
volume concentration are proportional to the area under the
respective curves 9-24
9-12 Scattering-to-volume concentration ratios are given for various
size distributions. The ratio values for accumulation (fine)
and coarse modes are shown by dashed lines corresponding to
average empirical size distributions reported by Whitby and
Sverdrup (1980) , ;....... 9-26
9-13 Simultaneous in situ monitoring of a and fine-particle mass
sp
concentration in St. Louis in April 1973 showed a high correla-
t4ion coefficient of 0.96, indicating that a depends primarily
on the fine-particle concentration P 9-28
9-14 Aerosol mass distributions, normalized by the total mass, for
New York aerosol at different levels of light-scattering
coefficient show that at high background visibility, the fine-
particle mass mode is small compared with the coarse-particle
mode. At the low visibility level, C, 60 percent of the mass
i s due to f i ne parti cl es , 9-29
9-15 Humidograms for a number of sites show the increase in o
which can be expected at elevated humidities for specific sites
or aerosol types (marine, Point Reyes, CA; sulfate, Tyson, MO)
and the range observed for a variety of urban and rural sites
(composite) 9-35
9-16 Relative size growth as a function of relative humidity for an
ammonium sulfate particle at 25°C 9-37
9-17 Fine mass concentration (determined from equilibrated filter)
corresponding to 4.8 km visual range, as a function of K and y,
where K equals the Koschmieder constant (-log E), and y equals
0 +0 /fine mass concentration 9-44
9-18 Visual range as a function of fine mass concentration (deter-
mined from equilibrated filter) and y, assuming K = 3.9 9-45
9-19 Hi-storical trends in hours of reduced visibility at Phoenix
and Tucson are compared with trends in SOX emissions from
Arizona copper smelters 9-50
xxv
-------
CONTENTS (continued)
Figure Page
9-20 Seasonally adjusted changes in sulfate during the copper strike
are compared with the geographical distribution of smelter SO
emissions 9-51
9-21 Seasonally adjusted percent changes in visibility during the
copper strike are compared with the geographical distribution of
smelter SO emissions 9-52
9-22 The locations of sampling sites and smelters and the mean surface
wind vectors at each sampling site from August 1979 through
September 1980. 9-55
9-23 Particle light extinction (cr + cr ) budget for the low visibil-
sp ap
ity southern California incursion (June 30) and a clear day
(July 10) 9-56
9-24 Compared here are summer trends of U.S. coal consumption
and Eastern United States extinction coefficient. 9-58
9-25 In the 1950's, the seasonal coal consumption peaked in the winter
primarily because of increased residential and railroad use. By
1974, the seasonal pattern of coal usage was determined by the
winter and summer peak of utility coal usage. The shift away
from a winter peak toward a summer peak in coal consumption is
consistent with a shift in extinction coefficient from a winter
peak to a summer peak in Dayton, OH, for 1948-52 9~58
9-26 In 1974, the United States winter coal consumption was well
below, while the summer consumption was above, the 1943 peak.
Since 1960 the average growth rate of summer consumption was 5.8
percent per year, while the winter consumption increased at only
2.8 percent per year 9-59
9-27 Trends in the light extinction coefficient (°~ext) in the Eastern
United States are shown by region and by quarters; 1 (winter), 2
(spring), 3 (summer), 4 (fall) 9-60
9-28 The spatial distribution of 5-year average extinction coeffi-
cients shows the substantial increases of third-quarter extinc-
tion coefficients in the Carolines, Ohio River Valley, and
Tennessee-Kentucky area 9-62
9-29 Average annual number of days with occurrence of dense fog.
Coastal and mountainous regions are most susceptible to fog 9-65
9-30 Annual percent frequency of occurrence of wind-blown dust
when prevailing visibility was 7 miles or less, 1940-70.
Dust is a visibility problem in the Southern Great Plains
and Western desert regions 9-65
9-31 Percent of daily midday measurements (1971-75) in which
visibilities were three miles or less in the absence of fog,
precipitation, or blowing material 9-76
9-32 Percent of daily midday measurements (1976-80) in which visibi-
lities were three miles or less in the absence of fog,
precipitation, or blowing material 9-77
9-33 Solar radiation intensity spectrum at sea level in cloudless
sky peaks in the visible window, 0.4-0.7 urn wavelength range,
shows that in clean remote locations, direct solar radiation
contributes 90 percent and the skylight 10 percent of the
incident radiation on a horizontal surface 9-85
xxvi
-------
CONTENTS (continued)
Figure ' ^ Page
9-34 Extinction of direct solar radiation by aerosols is depicted 9-87
9-35 On a cloudless but hazy day in Texas, the direct solar radiation
intensity was measured to be half that on a clear day, but most
of the lost direct radiation has reappeared as skylight 9-88
9-36 To interpret these 1961-66 monthly average turbidity data in
terms of aerosol effects on-transmission of direct sunlight, use
—R
the expression I/I = 10 , where B is turbidity and I/I is the
fraction transmitted 9-90
9-37 Seasonal turbidity patterns for 1961-66 and 1972-75 are shown for
selected regions in the Eastern United States 9-91
9-38 Analysis of the hours of solar radiation since the ,1950's shows
a decrease of summer solar radiation over the Eastern United
States. There may be several causes for this trend, including
an increase of cloudiness; some of the change may also be due
to haze 9-93
9-39 Numbers of smoke/haze days are plotted per 5 years at Chicago,
with values plotted at end of 5-year period 9-96
10-1 Relationship among emissions, air quality, damages and
benefits, and policy decisions.... 10-2
10-2 Steel corrosion behavior is shown as a function of average
relative humidity at three average concentration levels of
sulfur dioxide 10-6
10-3 Steel corrosion behavior is shown as a function of average
sulfur dioxide concentration and average relative humidity 10-7
10-4 Empirical relationship between average relative humidity and
fraction of time relative humidity exceeded 90 percent (time
of wetness) is shown for data from St. Louis International
Ai rport. 10-9
10-5 Relationship between corrosion of mild steel and corresponding
mean S02 concentration is shown for seven Chicago sites. (Corro-
sion is expressed as weight loss of panel). ,,-.... 10-17
10-6 Adsorption of sulfur dioxide on polished metal surfaces is
shown at 90 percent RH 10-22
10-7 Relationship between retained breaking strength of cotton fabrics
and corresponding mean sulfation rate measured at selected sites
in St. Louis area 10-33
10-8 Dust deposit patterns with corresponding coverage (% surface
covered) are shown 10-44
10-9 Representation of soiling of acrylic emulsion house paint
,as a function of exposure time -and particle concentrations 10-48
10-10 Increases in particulate matter concentrations are plotted
against reductions in outdoor cleaning task benefits (1978
dollars). The range of benefits increases progressively as
pollution is reduced 10-63
10-11 Improvement in U.S. annual average S02 levels from 32 yg/m3
in 1970 to 18 ug/m3 in 1978 has resulted in approximately $0.4
billion in estimated economic benefit for 1978 10-72
xxv n
-------
CONTENTS (continued)
Figure Page
11-1 Features of the respiratory tract of man used in the description
of inhaled particles and gases with insert showing parts of a
silicon rubber cast of. a human being showing some separated
bronchioles to 3 mm diameter, some bronchioles from 3 mm
diameter to terminal bronchioles, and some separated respiratory
acinus bundles -. 11-5
11-2 Representation of five major mechanisms of deposition of inhaled
airborne particles in the respiratory tract 11-13
11-3 Deposition of monodisperse aerosols in the total respiratory
tract for nasal breathing in humans as a function of aerody-
namic diameter, except below 0.5 urn, where deposition is plotted
vs. physical diameter '. 11-18
11-4 Deposition of monodisperse aerosols in the total respiratory
tract for mouth breathing as a function of aerodynamic diameter,
except below 0.5 urn, where deposition is plotted vs. physical
diameter. 11-19
11-5 Deposition of monodisperse aerosols in extrathoracic region for
nasal breathing as a function of D2Q, where Q is the average
inspiratory flowrate in liters/min 11-21
11-6 Deposition of monodisperse aerosols in extrathoracic region for
mouth breathing in humans as a function of D2Q, where Q is the
average inspiratory flowrate in liters/min 11-22
11-7 Deposition of monodisperse aerosols in the tracheobronchial
region for mouth breathfng in humans in percent of the aerosols
entering the trachea as a function of aerodynamic diameter,
except below 0.5 pm, where deposition is plotted vs. physical
diameter as cited by different investigators 11-24
11-8 Total and regional depositions of mono-disperse aerosols with
mouth breathing as a function of the aerodynamic diameter for
three individual subjects as cited by Stahlhofen et al. (1980)... 11-26
11-9 Deposition of monodisperse aerosols in the pulmonary region for
mouth breathing in humans as a function of aerodynamic diameter,
except below 0.5 urn, where deposition is plotted vs. physical
diameter , 11-28
11-10 Deposition of inhaled polydisperse aerosols of lanthanum oxide
(radio-labeled with 140La) in beagle dogs exposed in a nose-
only exposure apparatus showing the deposition fraction of
(A) total dog, (B) tracheobronchial region, (C) pulmonary
alveolar region, and (D) extrathoracic region 11-30
11-11 Deposition of inhaled monodisperse aerosols of fused .alumino-
silicate spheres in small rodents showing the deposition in the
extrathoractc (ET) region, the tracheobronchial (TB) region,
the pulmonary (P) region, and in the total respiratory tract 11-31
11-12 Single exponential model, fit by weighted least-squares, of the
buildup (based on text equation 7) and retention (based on text
equation 9) of zinc in rat lungs 11-45
11-13 Comparison of sampler acceptance of BMRC and ACGIH conventions
with the band for the experimental pulmonary deposition data of
Figure 11-9 11-51
xxvi n
-------
CONTENTS (continued)
11-14 Division of the thoracic fraction of deposited particles into
pulmonary and tracheobronchial fractions for two sampling con-
ventions (ACGIH and BMRC) as a function of aerodynamic diameter,
except below 0.5 urn, where physical diameter is used (Interna-
tional Standards Organization, 1981). Also shown are bands for
experimental pulmonary deposition data from Figure 11-9 and for
tracheobronchial (TB) deposition as a percent of particles
entering the month, 11-53
14-1 Martin and Bradley (1960) data as summarized by Ware et al.
(1981) showing average deviations of daily mortality from 15-day
moving average by concentration of smoke (BS) and $02 (London,
November 1, 1958 to January 1, 1959) 14-17
14-2 Linear and quadratic dose-response curves plotted on the
scattergram of mortality and smoke for London winters 1958-59
to 1971-72 14-22
14-3 Hypothetical dose-response curves derived from regressing
mortality on smoke in London, England, during winters 1958-59
to 1971-72 14-23
14-4 History and clinical evidence of respiratory disease- (percent) in
5-year-olds, by pollution in area of residence.. 14-48
XXIX
-------
CONTENTS (continued)
TABLES
Table ... , ,. page
1-1 National estimates of particulate and sulfur oxide emissions 1-17
1-2 Selected physical damage functions related to S02 exposure 1-46
1-3 Effects of acute exposures to sulfur oxide on pulmonary
function *,.. 1-58
1-4 Relative irritant potency of sulfate species in guinea pigs
exposed for one hour. 1-61
, 1-5 Responses to acute sulfuric acid exposure 1-62
1-6 Responses to chronic sulfuric acid exposure 1-63
1-7 Responses to various particulate matter mixtures 1-65
1-8 Responses to acute exposure combinations of S02 and some types
of particulate matter 1-67
1-9 Responses to acute exposure combinations of sulfuric acid and
ozone , 1-68
1-10 Pathological responses following chronic exposure to S02 alone
and in combination with particulate matter 1-69
1-11 Summary of studies on respiratory effects of S02 1-73
1-12 Excess deaths and pollutant concentrations during severe air
pollution episodes in London (1948-62) 1-91
1-13 Summary of quantitative conclusions from epidemiolog.ical studies
relating health effects to acute exposure to ambient air
levels of S02 and PM 1-94
1-14 Summary of quantitative conclusions from epidemiological studies
relating health effects of chronic exposure to ambient air
PM and S02 1-100
1-15 Comparison of measured components of TSP in U.S. cities (1960-
1965) and maximum 1-hour values in London (1955-1963) 1-102
2-1 Estimates of environmental sulfur annual fluxes (tg/year) 2-5'
2-2 Characteristic times and lengths for observation of effects 2-6
2-3 Dilute sulfur dioxide-water system 2-10
2-4 Relative strengths of acids in water solution (25°C) 2-13
2-5 Rate constants for hydroxy 1, peroxy, and methoxy 2-15
2-6 Investigations of S02 - 02 aqueous systems 2-24
2-7 Values of k and k, for reaction type 1 2-26
2-8 Values of 1C for reaction types 2... 2-27
2-9 Investigations of S02 - manganese - 02 aqueous system 2-29
2-10 Rate expression for the manganese-catalyzed oxidation 2-30
2-11 Investigations of S02 - iron - 02 aqueous system 2-31
2-12 Rate expression for the iron-catalyzed oxidation 2-32
2-13 Investigations of S02 - copper - 02 aqueous systems 2-34
2-14 Estimates of S02 oxidation rates in well-mixed troposphere 2-40
2~15 Estimate of global tropospheric particulate matter production
rates. 2-43
2-16 Particle shapes and source types. 2-46
2-17 Deliquescence and efflorescence points of salt particles........ 2-51
2-18 Sulfuric acid solution values (25°C) 2-55,
2-19 Conditions for the single-particle regime 2-60
2~20 Mass transport parameters for air 2-63
2-21 Dependence of particle behavior on air temperature, pressure,
and viscosity. 2-64
xxx
-------
CONTENTS (continued)
Table ^ Page
2-22 Classification of major chemical species associated with
atmospheric particles.» 2-77
2~23 Application of GDE to describe particle size evolution. 2-82
3-1 Temperature effect on collected S02-TCM samples (EPA reference
method) 3-6
3-2 Performance specifications for EPA equivalent methods for S02
(continuous analyzers)., 3-18
3-3 List of EPA designated equi'valent methods for S02 (continuous
analyzers). 3-19
3-4 Interferent test concentrations (parts per million) used in the
testing of EPA equivalent methods for S02 3-20
3-5 Comparison of EPA designated equivalent methods for S02
(continuous analyzers) 3-22
3-6 Recommended physical/chemical parameters for analysis 3-90
3-7 Results of WMO intercomparisons on synthetic precipitation
samp! es , ..... . • 3-94
3-8 Coefficients of variation of WMO intercomparisons on :
synthetic precipitation samples 3-95
4-1 Two EPA estimates of 1977 emissions of particulate matter
and sulfur oxides (106 metric tons per year).. 4-2
4-2 Summary of natural source particulate and sulfur emissions...... 4-5
4-3 Aerosol enrichment factors relative to A"K 4-6
4-4 Summary of estimated annual manmade emissions (1978) 4-11
.4-5 (a) National estimates of particulate emissions (106 metric
tons per year) 4-13
(b) National estimates of SO emissions (106 metric tons per
year) 4-13
4-6 1978 estimates of particulate and sulfur oxide emissions
from stati onary poi nt sources 4-14
4-7 State-by-State listing of total particulate and sulfur oxide
emissions from stationary point sources (1977), population,
and density factors 4-16
4-8 Examples of uncontrolled particulate emission characteristics'... 4-20
4-9 Size-specific particulate emissions from coal-fired boilers 4-23
4-10 Trace element air emissions vs. solid waste: percent from
conventional stationary fuel combustion sources, and total
(metric tons per year). 4-25
4-11 Uncontrolled industrial process fugitive particulate emissions... 4-31
4~12 Estimated annual particulate emissions from nonindustrial
fugitive sources '... 4-34
4-13 Estimated particle size distributions for several
nonindustrial fugitive source categories in California's
south coast air basin. 4-34
5-1 Crosstabulation of annual mean S02 concentration by method
(bubbler or continuous) for population-oriented and for
source-oriented center-city sites 5-8
xxxi
-------
. CONTENTS (continued)
Table Page
5-2 Continuous S02 monitor results by region, |jg/m3 5-9
5-3 Eleven S02 monitoring sites with the highest annual mean
concentrations in 1978 (valid continuous sites only) 5-11
5-4 Comparison of frequency distribution of S02 concentration (ppm)
during 1962-67 and during 1977 . 5-21
5-5 Range of annual geometric mean concentrations in areas with
high TSP concentrations in 1977 5-33
5-6 Regional summaries of TSP values from valid monitors 5-43
5-7 Fine and coarse aerosol concentrations from some urban
measurements compared to clean areas 5-53
5-8 Fine fraction and coarse fraction dichotomous sampling by
Environmental Science Research Lab, US EPA in four locations 5-55
5-9 Recent dichotomous sampler and TSP data from selected sites--
arithmetic averages 5-56
5-10 Some characteristics of pollution in the New York and
Los Angeles areas .... 5-69
5-11 Primary ranking of variables for correlating airborne S0|
in two cities based on a stepwise linear regression of
15 variables from CHAMP and related monitoring stations 5-72
5-12 Typical values of aerosol concentration for different
geographic areas (annual averages) 5-81
5-13 Annual averages of organic fractions in TSP, New York City,
dispersion normalized : 5-83
5-14 Composition of the organic fraction of airborne PM
collected in Detroit 5-85
5-15 Comparison of urban and nonurban annual average concentrations
for selected metals, 1970-74 (|jg/ni3) 5-88
5-16 Ratios of urban (U) to suburban (S) concentrations in air,
Cleveland, Ohio, area 5-89
5-17 Correlations of chemical content with particle size 5-90
5-18 Particulate analyses from'selected urban locations 5-91
5-19 Trends in reported urban metal concentrations and their possible
causes 5-93
5-20 Coarse particle silicon, aluminum, calcium, and iron 5-101
5-21 Relative amounts of fine, coarse, and super coarse particles at
selected sites 5-104
5-22 Fourteen-city study - microscopical identification of coarse
particles collected in urban atmospheres 5-105
5-23 Summary of indoor/outdoor (I/O) PM monitoring studies by
method 5-123
5-24 Measurements in principal room of study 5-128
5-25 Measurements in various closed rooms 5-128
5-26 Respirable particulate concentrations outdoors and indoors by
amount of smoking .- 5-129
6-1 Field measurements on the rates of S02 oxidation in plumes 6-4
6-2 Average dry deposition velocity of S02 by surface type 6-9
6-3 Laboratory measurements of deposition velocities of particles.... 6-11
6-4 Field measurements of deposition velocities of particles 6-13
xxxn
-------
CONTENTS (continued)
Tab!e Page
6-5 Predicted particle deposition velocities 6-17
6-6 Field measurements of scavenging coefficients of particles 6-21
6-7 Summary of select long range transport air pollution models 6-35
7-1 Composition of ecosystems , 7-8
7-2 Mean pH values in the New York metropolitan area ............. 7-30
7-3 Storm type classification 7-30
7-4 Chemical composition (Mean ± standard deviation) of acid lakes
(pH <5) acidic precipitation (pH <4.5), and of soft-water
lakes in areas not subject to highly acidic precipitation
(pH>4.8) 7-41
7-5 pH levels identified in field surveys as critical to
long-term survival of fish populations 7-63
7-6 Changes in aquatic biota likely to occur with increasing
acidity 7-67
7-7 Summary of effects on aquatic organisms associated with a
range in pH 7-68
7-8 Potential effects of acid precipitation on soils...... 7-72
7-9 ' Types of direct, visible injury reported in response to
simulated acidic wet deposition 7-81
7-10 Thresholds for visible injury and growth effects associated with
experimental studies of wet deposition of acidic substances. 7-84
7-11 Lead and copper concentration and pH of water from pipes
carrying outflow from Hinckley Basin and Hanns and Steele
Creek Basin, near Amsterdam, New York 7-91
7-12 Composition of rain and hoarfrost at Headingley, Leeds 7-93
7-13 The sensitivity to acid precipitation based, on: buffering
capacity against pH-change, retention of H , and adverse
•effects on soi 1 s 7-98
8-1 Relationship of biochemical response to visual symptoms of
plant injury. .- 8-6
8-2 Sensitivity groupings of vegetation based on visible injury
at different S02 exposures. 8-14
8-3 Effects of exposure to S02 on plants under field
conditions -... 8-20
8-4 The degree of injury of eastern white pine observed at various
distances from the Sudbury smelters for 1953-63 : ., 8r22
8-5 Ambient exposures to sulfur dioxide that caused injury
to vegetation. 8-23
8-6 Summary of the effects resulting from the exposure of
seedling tree species in the laboratory .( 8-26
8-7 Plants sensitive to heavy metals, arsenic, and boron as
accumulated in soils and typical symptoms expressed 8-39
9-1 Particle light scattering coefficient per unit fine-mass
concentration 9-27
9-2 Median percent frequency of occurrence of selected RH classes
for 54 stations in the contiguous U.S 9-42
xxxi
-------
CONTENTS (continued)
Table Page
9-3 Correlation/regression analysis between airport extinction
and copper smelter SO emissions 9-53
9-4 Seasonal average percent of time when midday visibility was
3 miles (4.8 km) or less at U.S. airports from 1951 to 1980 9-74
9-5 Percent of visibility measurements at 3 miles (4.8 km) or less
at 26 U.S. airports during the summer quarter :... 9-78
9-6 Some solar radiation measurements in the Los Angeles area 9-92
10-1 Some empirical expressions for corrosion of exposed ferroalloys. 10-20
10-2 Critical humidities for various metals 10-21
10-3 Experimental regression coefficients with estimated standard
deviations for small zinc and galvanized steel specimens
obtained from six exposure sites 10-25
10-4 Corrosion rates of zinc on galvanized steel products exposed to
various environments prior to 1954 10-26
10-5 Paint erosion rates and t-test probability data 10-31
10-6 Mechanisms contributing to stone decay. Principal atmospheric
factors participating these mechanisms are denoted by solid
circles: secondary factors are indicated by solid triangles 10-36
10-7 Selected physical damage functions related to S02 exposure 10-40
10-8 Results of regression for soiling of building materials as a
function of TSP exposure 1Q-46
10-9 Summation of annual extra losses due to corrosion damage by air
pollution to external metal structures for 1970 10-52
10-10 Selected characteristics of households in four air po-llution
zones 10-56
10-11 27 cleaning and maintenance operations separated by sensitivity
to air particulate levels in four pollution zones.... 10-57
10-12 Annual welfare gain from achieving primary and secondary
standards for TSP concentration 10-62
10-13 Economic loss, materials damage attributed, to .ambient exposure
to SOV and PM, estimated by Salmon, 1970 (in bill ions of 1970
dollars) | 10-65
10-14 Estimates of materials damage attributed to SO and PM in 1970
(in millions of 1970 dollars) 10-66
12-1 Lethal effects of S02 12-9
12-2 Effects of S02 on 1 ung morphol ogy 12-10
12-3 Effects of S02 on pulmonary function 12-20
12-4 Effects of S02 on host defenses. 12-23
12-5 Effects of H2S04 aerosols on lung morphology 12-26
12-6 Respiratory response of guinea pigs exposed for 1 hour to
particles in the Amdur et al. studies 12-29
12-7 Effects of acute exposure to sulfate aerosols on pulmonary
function 12-40
12-8 Effects of chronic exposure to H2S04 aerosols on
pulmonary function 12-42
12-9 Effects of H2S04 on mucociliary clearance 12-45
12-10 Effects of metals and other particles on host defense mechanisms 12-47
xxxiv
-------
CONTENTS (continued)
Table Page
12-11 Effects of acute exposure to ,SQ2 in combination with certain
particles 12-57
12-12 Pollutant concentrations for chronic exposure of dogs 12-60
12-13 Effects of chronic exposure to SO and some PM 12-64
12-14 Effects of interaction of SO and 03 12-67
12-15 Potential mutagenic effects 8f S02/bisulfite 12-73
13-1 Sensory effects of S02 13-4
13-2 Respiratory effects of S02 13-7
13-3 Pulmonary effects of sulfuric acid 13-25
13-4 Pulmonary effects of aerosols 13-33
13-5 Pulmonary effects of combined exposures to S02 and other gaseous
air pollutants , 13-40
14-1 Excess deaths and pollutant concentrations during severe air
pollution episodes in London (1948 to 1962). 14-12
14-2 Summary of results, selected patients, 1964-65 and 1967-68 14-29
14-3 Average deviation of respiratory and cardiac morbidity from 15-
day moving average, by smoke level (BS)(London, 1958-60) 14-31
14-4 Average deviation of respiratory and cardiac morbidity from 15-
day moving average, by S02 level (London, 1958-60) 14-31
14-5 Summary of key results regarding mortality-air pollution relation-
ships in U.S. cities based on Lave and Seskin Model analyses for
1960, 1969, and 1974 data. 14-39
14-6 Summary of Lave and Seskin (1977) analysis of residuals from
regression analysis for 1960 and 1969 U.S. SMSA data 14-42
14-7 Summary of quantitative conclusions from epidemiological studies
relating health effects to acute exposure to ambient air levels
of S02 and PM 14-52
14-8 Summary of quantitative conclusions from epidemiological studies
relating health effects to chronic exposure to ambient air
levels of S02 and PM : 14-54
14-9 Comparison or measured components of TSP in U.S. cities (196Q-
, 1965) and maximum 1-hour values in London (1955-1963) — 14-55
XXXV
-------
ABBREVIATIONS AND SYMBOLS
o
A
A-aDQ2
ACGIH
ACHEX
ACM
AEC
AISI
Al
AM
AQCD
AQCR
AQSM
ASTH
ATP
BaP
BHRC
BPH
BS
C
Ca2+
CA
CAA
CBM
CAMP
Angstrom
Alveolar-arterial 'difference in partial pressure of oxygen
American Conference of Governmental Industrial Hygienists
Aerosol Characterization Experiment
Atmospheric Corrosion Monitor
Atomic Energy Commission
American Iron and Steel Institute
Alumi num
Alveolar macrophage
Air Quality Criteria Document
Air Quality Control Region
Air Quality Simulation Model
American Society for Testing and Materials
Adenosine triphosphate
Benzo[a]pyrene
British Medical Research Council
Breaths per minute
British Smokeshade
Carbon
Calcium ion
Clean air '
Clean Air Act
Chiorobenzilidene malonitrile
Continuous Air Monitoring Program
xxx vi
-------
CAPITA
CC/TLC%
CH302
CH3SH
CHAMP
CHESS
Cl
CMD
CMC
CoH
co2
COPD
COS
cs2
CV
cv
Dae
Dar
DMDS
DMS
D.S.I.R.
EAA
EAC
Center for Air Pollution Impact and Trend Analysis
Closing volume
Methyl peroxy radical
Methyl mercaptan'
Community Health Air Monitoring Program
Community Health Environmental Surveillance Program
Chloride ion
Count mean diameter
Condensation nuclei counter
Coefficient of haze
Carbon dioxide
Chronic obstructive pulmonary disease
Carbonyl sulfide
Carbon disulfide
Coefficient of variation; standard deviation divided
by the mean
Cultivar
Aerodynamic equivalent diameter
Aerodynamic resistance diameter
Project area diameter
Delta nitrogen
Dimethyl disulfide
Dimethyl sulfide
Department of Scientific and Industrial Research
Electrical aerosol analyzer
Effective area coverage
xxxv11
-------
EDTA Ethylenediaminetetraacetic acid....
EPA Environmental Protection Agency
EPRI Electric Power Research Institute
ESCA Electron spectroscopy for chemical analysis
ET Extrathoraci c
Fe Iron
FegO. Magnetite
FeOOH Ferric oxyhydroxide
FeSO, Ferrous sulfate
FEF Forced expiratory flow
FEV, Q Forced expiratory volume in 1 second
FGO Flue gas desulfurization
FMC Fine mass concentration
FPD Flame-photometric detector
FRC Functional residual capacity
FVC Forced expiratory volume/forced vital capacity
GC Gas chromatography
GRALE Gamma-ray analysis of light elements
H Hydronium ion; hydrogen ion
Hb Hemoglobin
HpCQ, Carbonic acid
HpO, Hydrogen peroxide
HpSOn Sulfurous acid
HgSO, Sulfuric acid
HCOg Bicarbonate ion
hi-vol High-volume
xxxviil
-------
HN03 Nitric acid
HO Hydroxyl radical
HO, Peroxy radical
HPLC High-pressure liquid chromatography
Bisulfite ion
ICRP International Commission on Radiological Protection,
Task Group on Lung Dynamics
IFR Instrument Flight Rules
IP Inhalable particle
IR Investigative report
ISP Interstate Surveillance Program
Kg Kilogram
K Potassium ion
KPH Potassium acid phthalate
LC Lethal concentration
LDH Lactate dehydrogenase
LEB Light extinction budget
M Meter
MAP3S Multi-state Atmospheric Power Production Pollution Study
MEF Maximum expiratory flow (pulmonary measurement)
MEFj-nVC Maximum expiratory flow measured when half the vital
capacity tias been expelled
MEFR Maximum expiratory flowrate
mg Milligram
ug Microgram
2
rag/m" Milligrams per cubic meter
•q
Mg/m Micrograms per cubic meter
xxx ix
-------
mm
Mm
MM
MMAD
MMAO
ar
MHFR
MRI
MTB
MVD
Mg2*
MnCl£
NAAQS
Na+
NaCl
NAD/NAOP
NADB
NAMS
NAPCA
NASN
NBS
NEDS
NH*
NH3
NH4N03
MilH meter
Micrometer
Million metric
Mass median aerodynamic diameter
Mass median aerodynamic resistance diameter
Mass median diameter
Maximal mid-expiratory flowrate. Also known as
Midwest Research Institute
Methyl thymol blue
Mean volume diameter
Magnesium ion
Manganese chloride
National Ambient Air Quality Standard
Sodium ion
Sodium chloride
Pyrimidine nucleotides
National Aerometric Data Bank
National Air Monitoring Station
National Air Pollution Control Association
National Air Surveillance Network
National Bureau of Standards
National Emissions Data System •
Ammonium ion
Ammonia
Ammonium nitrate
Ammonium sulfate.
xl
-------
NIOSH
N02
HO'
NPK
NRC/NAS
°3
OBAQI
ODS
OECD
OH
P
PaC02
Pa02
PAH
Pb02
PEFR
PFT
pHa
PM
PMT
POM
ppb
ppm
PVC
Raw
Ammonium bisulfate
National Institute for Occupational Safety and Health
Nitrogen dioxide
Nitrate ion
Nitrogen, phosphorus, potassium
National Research Council/National Academy of Sciences
Ozone
Observer-based air quality index
Octadecylsilyl
Organization for Economic Cooperation and Development
Hydroxyl radical
Pulmonary
Partial pressure of carbon dioxide in the arterial blood
Partial pressure of oxygen in the arterial blood
Polycyclic aromatic hydrocarbons
Lead dioxide
Peak expiratory flowrate
Pulmonary function test
Arterial pH
Particulate matter
Photomultiplier tube
Polycyclic organic matter
Parts per billion
Parts per million
Polyvinyl chloride
Airway resistance (pulmonary measurement)
xli
-------
Rt
R'APS
RH
RHC
Rl
RMS
RSD
RSSO~
RUDS
RV
S
SAROAD
SEM
SES
SGaw
Si02
SLAMS
SMSA
SO,
SO,
S0x
SPM
SRaw
SRM
SSI
Total respiratory flow resistance (pulmonary measurement)
Regional Air Pollution Study
Relative humidity
Reactive hydrocarbons
Pulmonary flow resistance
Root mean square
Recommended site distances
Plasma S-sulfonate
Reflection unit dirt shade
Residual volume (pulmonary measurement)
Sulfur
Storage and Retrieval of Aerometric Data
Scanning electron microscopy
Socioeconomic status
Specific airway conductance
Silicon dioxide
State and Local Air Monitoring Stations
Standard metropolitan statistical area
Sulfur dioxide
Sulfur trioxide ion
Sulfite ion
Sulfate ion
Sulfur oxides
Suspended particulate matter :
Specific airway resistance
Standard reference material
Size selective inlet
xlii
-------
SURE
TB
TB,2
TCM
TGV
TiO£
TLC
TLV
TMR
TMTR
TSP
"t" test
TV
UNAMAP
u. v.
o
V
max 50% and
75%, etc.
VC
Ve or Ve
VFR
VISTTA
WHO
WMO
Sulfate Regional Experiment
Tracheobronchial
Bronchial mucociliary clearance half-time
Tetrachloromercurate
Thoracic gas volume
Titanium dioxide
Total lung capacity
Threshold limit value
Total mortality rates
Tracheal mucus transport rate
Total suspended particulate matter
Student's statistical test
Tidal volume (pulmonary measurement)
User's Network for Applied Modeling of Air Pollution
Ultraviolet
Flowrate during forced expiration (pulmonary measurement)
Maximum flowrate calculated at 50 and 75% of expired vital
capacity from a partial flow volume curve begun from approxi-
mately 60% of inspired vital capacity
Vital capacity (pulmonary measurement)
Minute ventilation or minute volume (pulmonary measurement)
Visual Flight Rules
Visibility Impairment Due to Sulfur Transport and Transformation
in the Atmosphere
World Health Organization
World Meteorological Organization
xl i i i
-------
WTA Willingness to accept compensation
WTP Willingness to pay
ZAPS Zonal air pollution system
xl i v
-------
AUTHORS, CONTRIBUTORS AND REVIEWERS
The following people served on "the EPA task force responsible for the
preparation of this document. Within categories of principal author,
contributors and reviewers, names are in alphabetical 'order.
Chapter1. Executive Summary
Authors and Contributors
Mr. Robert D. Bauman, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Mr. Michael A. Berry, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Ronald L. Bradow, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Ms. F. Vandiver P. Bradow, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Robert M. Bruce, Environmental Criteria and Assessment Office,-
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. J. Michael Davis, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Kenneth L. Demerjian, Environmental Sciences Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Jack L. Durham, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Mr. Thomas G. Ellestad, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Dr. J. H. B. Garner, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
xlv
-------
Dr. Judith A. Graham, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Lester D. Grant, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Steven M. Horvath, Institute of Environmental Stress, University of
California, Santa Barbara, California 93106.
Mr. James Kawecki, Center for Health and Environmental Studies, Biospherics
Incorporated, Rockville, Maryland 20852.
Dr. Si Duk Lee, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Daniel B. Menzel, Department of Pharmacology and Medicine, Duke University,
Durham, North Carolina 27710.
Dr. Frederick J. Miller, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. Charles E. Rodes, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711,
Dr. David E. Weil, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Chapter 2. Physical and Chemical Properties
of Sulfur Oxides and Parti cut ate Matter
Principal Author
Dr. Jack L. Durham, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Contributors
Dr. Kenneth L. Demerjian, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
xlvi
-------
Dr. Harold M. Barnes, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. William E. Wilson, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Reviewers
Dr. A. Paul Altshuller, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Bruce Appel, Air and Industrial Hygiene Labs, California Department of
Health Services, Berkeley, California .94704.
Dr. James Brock, University of Texas, Austin, Texas 78712,
Dr. Warren Galke, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. -Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Walter John, Air and Industrial Hygiene Labs, California Department of
Health Services, San Francisco, California.
Dr. Dale Lungren, University of Florida, Gainesville, Florida 32611.
Dr. Robin Martin, Aerospace Corporation, Los Angeles, California.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office,. Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
•*'''«. • ' > '
Dr. David Natusch, Department of Chemistry, Colorado State University, Fort.
Collins, Colorado 80523.
Dr. Leonard Newman, Brookhaven National Labs, Upton, New York. 11973.
Dr. David Pui, Mechanical Engineering Department, University of Minnesota,
Minneapolis, Minnesota 55455.
Mr. Robert Shaw, Environmental Sciences Research Laboratory, Office of
Research and Development,.U.S. .Environmental protection Agency, Research
Triangle Park, .North Carolina 27711.
Dr. Roger Tanner, Brookhaven National Labs, Upton, New York 11973.
Dr. James Wedding, Colorado State University, Fort Collins, Colorado 80523.
Dr. Kenneth Whitby, Mechanical Engineering Department, University of
Minnesota, Minneapolis, Minnesota 55455.
xlvii
-------
Chapter 3. Techniques for the Collection and
Analysis of Sulfur Oxides,Particulate Matter,
and Acidic Precipitation.
Principal Authors
Mr. Larry J. Purdue, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina. 27711.
Mr. Kenneth A. Rehme, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. Charles E. Rodes, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
V. Ross Highsmith, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Contributors
Mr. Thomas Hart!age, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. James Kawecki, Center for Health and Environmental Studies, Biospherics
Incorporated, Rockville, Maryland 20852.
Dr. William McClenny, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Reviewers
Dr. Bruce Appel, Air and Industrial Hygiene Labs, California Department of
Health Services, Berkeley, California 94704.
Dr. James Brock, University of Texas, Austin, Texas 78712.
Dr. Robert J. Charlson, Department of Atmospheric Chemistry, University of
Washington, Seattle, Washington 98195.
Dr. Douglas Dockery, Harvard School of Public Health, Boston, Massachusetts
02115.
Dr. Warren A. Galke, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
xlviii
-------
Dr. Thomas R. Mauser, Environmental Monitoring Systems Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. John Holmes, California Air Resources Board, Sacramento, California 95819.
Dr. Walter John, Air and Industrial Hygiene Labs, California Department of
Health Services, San Francisco, California.
Dr. Daris Levaggi, Bay Area Air Quality Management District, San Francisco,
California.
Dr. Dale Lungren, Environmental Engineering Department, University of Florida,
Gainesville, Florida 32611.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. David Natusch, Department of Chemistry, Colorado State University, Fort
Collins, Colorado 80523.
Dr. Leonard Newman, Brookhaven National Labs, Upton, New York 11973.
Dr. David Pui, Mechanical Engineering Department, University of Minnesota,
Minneapolis, Minnesota 55455.
Ms. Laura.Scoville, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agencyt Research
Triangle Park, North Carolina 27711.
Mr. Robert Shaw, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. Robert Stevens, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Roger Tanner, Brookhaven National Labs, Upton, New York 11973.
Dr. James Wedding, Engineering Research Center, Colorado State University,
Fort Collins, Colorado 80523.
Chapter 4. Sources and Emissions
Principal Authors
Dr. James N. Braddock, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina .27711.
xlix
-------
Mr. Jeff Mel ing, Radian Corporation, Austin, Texas.
Dr. John W. Winchester, Department of Oceanography, Florida State University,
Tallahassee, Florida .32306.
Contributors
Dr. Lester D. Grant, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. Elmer Robinson, Chemical Engineering Department, Washington State University,
Pullman, Washington 99164.
Reviewers
Dr. August T. Rossano, Civil Engineering Department, University of Washington,
Seattle, Washington 98195.
Chapter 5. Environmental Concentrations
and Exposure
Principal Authors
Dr. Ronald L. Bradow, Environmental Sciences Research Laboratory, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Dr. John D. Spengler, Environmental Health, Harvard School of Public
Health, Boston, Massachusetts 02115.
Contributor
Dr. John S. Evans, Environmental Health, Harvard School of Public
Health, Boston, Massachusetts 02115.
Mr. Douglas B. Fennel!, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Reviewers
Dr. Robert Braman, Department of Chemistry, University of South Florida, Tampa,
Florida 33620.
Dr. Cliff I. Davidson, Department of Civil Engineering, Carnegie-Mellon
University, Pittsburgh, Pennsylvania 15213.
Dr. Douglas Dockery, Harvard School of Public Health, Boston, Massachusetts
02115.
1
-------
Dr. John Holmes, Research Division, California Air Resources Board,
Sacramento, California 95812.
Dr. Paul Lioy, Institute of Environmental Medicine, New York University
Medical Center, New York, New York 10016.
Dr. James P. Lodge, Boulder, Colorado 80303.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Kenneth E. Noll, Department of Environmental Engineering, Illinois
Institute of Technology, Chicago, Illinois 60616.
Dr. August T. Rossano, Civil Engineering Department, University of
Washington, Seattle, Washington 98195.
Chapter 6. Atmospheric Transport, Transformation
and Deposition
Principal Author
Dr. Kenneth L. Demerjian, Environmental Sciences Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Reviewers
Dr. 'A. Paul Altshuller, Environmental Sciences Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Frank Binkowski, Environmental Sciences Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Jeremy Hale, Battelle Pacific Northwest Research Laboratory, Richland,
Washington 99352.
Dr. Rudolf Husar, Department of Mechanical Engineering, Washington
University, St. Louis, Missouri 63130.
Dr. Paul Lioy, Institute of Environmental Medicine, New York University
Medical Center, New York, New York 10016.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr; Jarvis L. Moyers, Department of Chemistry, University of Arizona,
Tucson, Arizona 85721.
11
-------
Dr. Kenneth E. Noll, Department of Environmental Engineering, Illinois
Institute of Technology, Chicago, Illinois 60616.
Dr. August T. Rossano, Civil Engineering Department, University of
Washington, Seattle, Washington ,98195.
Dr. Jack Shreffler, Environmental Sciences Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. Warren H. White, CAPITA, St. Louis, Missouri 63130.
Chapter 7. Acidic Deposition
Principal Authors
Dr. Joan Baker, School of Forestry and Environmental Studies, Duke University,
Durham, North Carolina 27706.
Dr. J..H. B. Garner, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Contributors
Mr. Angelo P. Capparella, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Dr. J. Michael Davis, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711.
Reviewers
Dr. Martin Alexander, Department of Agronomy, Cornell University, Ithaca,
New York 14853.
Dr. David S. Anthony, Department of Botany, University of Florida,
Gainesville, Florida 32611.
Dr. Carl W. Chen, Tetratech, Inc., Lafayette, California 94549.
Dr. Charles Cogbill, Private Consultant, Denver, Colorado 80220.
Dr. Ellis B. Cowling, School of Forest Resources, North Carolina State
University, Raleigh, North Carolina 27650.
Dr. Lance S. Evans, Department of Biology, Manhattan College, Bronx, New
York 10471.
lil
-------
Mr. Patrick J. Festa, Bureau of Fisheries, New York State Department of
Environmental Conservation, Albany, New York 12233.
Dr. Robert A. Goldstein, Environmental Assessment Department, Electric Power
Research Institute, Palo Alto, California 94303.
Or. Bertil Hagerhall, Ministry of Agriculture, Stockholm, Sweden.
Dr. George R. Hendrey, Department of Energy and Environment, Brookhaven
National Laboratory, Upton, New York 11973.
Dr. Patricia M. Irving, Argonne National Laboratories, Argonne, Illinois
60439.
Dr. Jay S. Jacobson, Boyce Thompson Institute at Cornell University,
Ithaca, New York 14853.
Dr. Rick Linthurst, Botany Department, North Carolina State University,
Raleigh, North Carolina 27650, •
Dr. Samuel N. Linzon, Air Resources Branch, Ontario Ministry of the
Environment, Toronto, Canada.
Dr. William W. McFee, Natural Resources and Environmental Sciences,
Purdue University, West Lafayette, Indiana 47907.
Dr. Charles Powers, Environmental Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Corvallis,
Oregon 97330.
Dr. Carl L. Schofield, Department of Natural Resources,-Cornell University,
Ithaca, New York 14853.
Dr. David Shriner, Oak Ridge National Laboratory, Oak Ridge, Tennessee
37830.
Dr. David Weber, Office of Research and Development, U.S. Environmental
Protection Agency, Washington, D.C. 20460.
Chapter 8. Effects on Vegetation
Principal Authors
Dr. Lance W. Kress, Radiological and Environmental Research Division, Argonne
National Laboratory, Argonne, Illinois 60439.
Dr. Samuel B. McLaughlin, Oak Ridge Union Carbide, Oak Ridge, Tennessee
37830.
Dr. John M. Skelly, Department of Plant Pathology and Physiology, Virginia
Polytechnic Institute & State University, Blacksburg, Virginia 24061.
1111
-------
Contributors
Mr. Michael A. Berry, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection .Agency, Research
Triangle Park, North Carolina 27711. -
Mr. Angelo P. Capparella, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Dr. 0. H. B. Garner, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Lester D. Grant, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Sagar V. Krupa, Department of Plant Pathology, University of Minnesota,
St. Paul, Minnesota 55108.
Dr. George E. Taylor, Oak Ridge National Laboratory, Oak Ridge, Tennessee
37830.
Reviewers
Dr. Donald Davis, Pennsylvania State University, State College,
Pennsylvania 16801.-
Dr. Lance S. Evans, Department of Biology, Manhattan College, New York,
New York 10471.
Dr. Walter Heck, Science and Education Administration, U.S. Department of
Agriculture, Botany Department, North Carolina State University, Raleigh,
North Carolina 27650.
Dr. Allen Heagle, Science and Education Administration, U.S. Department of
Agriculture, Department of Plant Pathology, North Carolina State
University, Raleigh, North Carolina 27650.
Dr. Howard E. Heggestad, Science and Education Administration, U.S. Department
of Agriculture, Beltsville, Maryland 20705.
Dr. Herbert C. Jones, Air Resources Program, Tennessee Valley Authority,
Muscle Shoals, Alabama 35660.
Dr. Allan H. Legge, Environmental Science Center, University of Calgary,
Alberta, Canada.
Dr. Samuel N. Linzon, Air Resources Branch, Ontario Ministry of the Environ-
ment, Toronto, Canada.
Dr. Delbert C. McCune, Boyce Thompson Institute at Cornell University, Ithaca,
New York 14853.
liv
-------
Dr. David Shriner, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830.
Dr. Raymond Wilhour, Environmental Research Laboratory, Office of Research and
Development, U.S. Environmental Protection Agency, Corvallis, Oregon 97330.
Chapter 9. Effects 'on Visibility and Climate
Principal Authors
Mr. Thomas G. Ellestad, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Mr. James Kawecki, Center for Health and Environmental Studies, Biospherics,
Incorporated, Rockville, Maryland 20852.
Contributors
Ms. F. Vandiver P. Bradow, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Dr. Rudolf Husar, Department of Mechanical Engineering, Washington University,
St. Louis, Missouri 63130.
Dr. David Patterson, CAPITA, Washington University, St. Louis, Missouri 63130.
Dr. Charles Sternheim, University of Maryland, College Park, Maryland 20742.
Dr. Warren H. White, CAPITA, Washington University, St. Louis, Missouri 63130.
Reviewers
Dr. Janja Husar, Washington University, St. Louis, Missouri 63130.
Dr. James P.. Lodge, Boulder, Colorado 80303.
Chapter 10. Effects on Materials
Principal Author
Ms/ F. Vandiver P. Bradow, Environmental Criteria and Assessment Office,
Office of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Contributors
Mr. Michael A. Berry, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Iv
-------
Dr. John A. Jaksch, Rogers, Golden & Halpern, Reston, Virginia 22091.
Mr, James Kawecki, Center for Health and Environmental Studies, Biospherics,
Incorporated, Rockville,. Maryland 20852.
Dr. David Maase, Center for Health and Environmental Studies, Biospherics,
Incorporated, Rockville, Maryland 20852.
Dr. Victor S. Salvin, University of North Carolina, Greensboro, North Carolina
27408.
Reviewers
Dr. Ronald L. Bradow, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Donald J. Gillette, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Mr.- Fred Haynie, Environmental Sciences Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Dr. James P. Lodge, Boulder, Colorado 80303.
Mr. Thomas B. McMullen, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection .Agency, Research
Triangle Park, North Carolina 27711.
Mr. John W. Spence, Regional Support Services, Office of Research and Develop-
ment, U.S. Environmental Protection Agency, Research Triangle Park, North
Carolina 27711.
Mr. James B. Upham, Environmental Sciences Research Laboratory, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Phillippus Willems, Biospherics, Incorporated, Rockville, Maryland 20852.
Mr. John Yocom, TRC Environmental Consultants, Wethersfield, Connecticut
06109.
Chapter 11. Respiratory Deposition and
Biological Fate of InhaledAerosols and SOp
Principal Authors
Mr. Frederick J. Miller, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Ivi ' '
-------
Dr. Otto G. Raabe, Department qf Civil Engineering, University of California,
Davis, California 95616;
Contributors
Ms. Margaret Grady, Northrop Services, Inc., Research Triangle Park, North
Carolina 27709.
Dr. Amit Patra, Northrop Services, Inc., Research Triangle Park, North Caro-
lina 27709.
Dr. David E. Weil, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Reviewers
Dr. Douglas Craig, Toxicology Division, Litton Bionetics, Rockville,
Maryland 20850.
Dr. Richard Cuddihy, Lovelace Biomedical and Environmental Research Institute,
.Albuquerque, New Mexico 87115.
Dr. Warren Johnson, SRI International, Menlo Park, California 94025.
Dr. George Kanapilly, Lovelace Biomedical and Environmental Research Institute,
Albuquerque, New Mexico 87115.
Dr. Myron Mehlman, Toxicology Division, Mobil Oil Corporation, Princeton,
New' Jersey 08540.
Dr. Paul Morrow, University of Rochester Medical Center, Rochester, New York
14642.
Dr. Mohammad Mustafa, School of Public Health, University of California, Los
Angeles, California 90024.
Dr. Robert Phalen, Department of Community and Environmental Medicine,
University of California, Irvine, California 92717.
Dr. David L. Swift, School of Hygiene and Public Health, The Johns Hopkins
University, Baltimore, Maryland 21205.
Dr. Walter Tyler, Department of Anatomy, California Primate Research Center,
University of California, Davis, California 95616.
Dr. Ron Wolff, Lovelace Biomedical and Environmental Research Institute,
Albuquerque, New Mexico 87115.
Dr. C. P. Yu, Department of Engineering Science, State University of New York
at Buffalo, Buffalo, New York 14214.
Ivii
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Chapter 12. Toxicological Studies
.Principal Authors
Dr. Judith A. Graham, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Dr. Daniel B. Henzel, Department of Pharmacology and Medicine, Duke
University, Durham, North Carolina 27710.
Ms, Elaine Smolko, Department of Pharmacology and Medicine, Duke University,
Durham, North Carolina 27710.
Contributors
Mr. Steven Silbaugh, Duke University, Durham, North Carolina 27710.
Dr. Vic Hasselblad, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Dr. Andrew Stead, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Dr. David E. Weil, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park,,North Carolina 27711.
Dr. M. Jean Wiester, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Reviewers
Dr. Douglas K. Craig, Toxicology Division, Litton Bionetics, Rockville,
Maryland 20850.
Dr. T. Timothy Crocker, College of Medicine, University of California, Irvine,
California 92717.
Dr. Richard Ehrlich, IIT Research Institute, Chicago, Illinois 60616.
Dr. Jack Hack'ney, Rancho Los Amigos Hospital, Downey, California 90242.
Dr. F. Gordon Hueter, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Dr. Myron Mehlman, Toxicology Division, Mobil Oil Corporation, Princeton,
New Jersey ' 08540.
Iviii
-------
Dr. Paul Morrow, University of Rochester Medical Center, Rochester, New
York 14642. ,
Dr. Mohammed Mustafa, School of Public Health, University of California, Los
Angeles, California 90024.
Dr. Joseph Santodonato, Life and Material Science Division, Syracuse Research
Corporation, Syracuse, New York 13210.
Dr. Robert Shapiro, Department of Chemistry, New York University, New York,
New York 10003.
Dr. Walter Tyler, Department of Anatomy, California Primate Research Center,
University of California at Davis, Davis, California 95616.
Dr. Ron Wolff, Lovelace Biomedical and Environmental Research Institute,
Albuquerque, New York 87115.
Chapter 13. Controlled Human Studies
Principal Author
Dr. Steven M. "Horvath, Institute of Environmental Stress, University of
California, Santa Barbara, California 93106.
Contributors
Dr. Robert M. Bruce, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. J. Michael Davis, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Lester D. Grant, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. David J. McKee, Environmental Criteria and Assessment Office, Office of
Research and Development, Research Triangle Park, North Carolina 27711.
Reviewers
_ =
Dr. Homer Boushey, Cardiovascular Research Institute, University of
California, San Francisco, California 94143.
Dr. Phillip Bromberg, Department of Medicine, University of North Carolina,
Chapel Hill, North Carolina 27514.
Dr. Anthony Colucci, Colucci and Associates, Morgan Hill, California 95037.
lix
-------
Dr. Douglas K. Craig, Toxicology Division, Litton Bionetics, Rockville,
Maryland 20850,
Dr. Richard Cuddihy, Lovelace Biomedical and Environmental Research Institute,
Albuquerque, New Mexico 87115,
Dr. Richard Ehrlich, IIT Research institute, Chicago, Illinois 60616.
Dr. Robert Frank, Environmental Health, University of Washington, Seattle,
Washington 98195,
Dr. Jack Hackney, Rancho Los Amigos Hospital, Downey, California 90242.
Dr. Milan Hazucha, Center for Environmental Health, University of North
Carolina, Chapel Hill, North Carolina 27514.
Dr. Thomas J. Kulle, School of Medicine, University of Maryland, Baltimore,
Maryland 21201.
Dr. Myron Mehlman, Toxicology Division, Mobil Oil Corporation, Princeton,
New Jersey 08540.
Dr. Donald Proctor, The Johns Hopkins School of Hygiene, Baltimore, Maryland
" 21205.
Dr. David L. Swift, The Johns Hopkins University, Baltimore, Maryland 21205.
Chapter 14. Epidemiology Studies on the Effects
of Sulfur Oxidesand Particulate Matter on Human
Health
Principal Author
Dr. Lester D. Grant, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Contributors
Dr. Benjamin G. Ferris, Harvard School of Public Health, Boston, Massachusetts
02115.
Dr. Warren A. Galke, Environmental Criteria and Assessment Office, Office of
Research and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina 27711.
Dr. Victor Hasselblad, Health Effects Research Laboratory, Office of Research
and Development, U.S. Environmental Protection Agency, Research Triangle
Park, North Carolina 27711.
Ix
-------
Dr. Dennis J. Kotchmar, Environmental Criteria and Assessment Office, Office
of Research and Development, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
Dr. Michael D. Lebowitz, Arizona Health Sciences Center, Tucson, Arizona
85724.
Dr. Frank Speizer, Harvard School of Public Health, Boston, Massachusetts
02115.
Dr. James H. Ware, Harvard School of Public Health, Boston, Massachusetts 02115.
Reviewers
Dr. Karim Ahmed, Natural Resources Counsel, New York, New York 10017.
Dr. Albert Bennett, St. Georges Hospital, London, England.
Dr. Steven D. Colome, Harvard School of Public Health, Boston, Massachusetts
02115.
Dr. Anthony Colucci, Colucci and Associates, Morgan Hill, California 95037.
Dr. Inga Goldstein, Division of Epidemiology, Columbia University, New York,
New York 10032.
Dr. Douglas I. Hammer, Private Consultant, Raleigh, North Carojina 27607.
Dr. Ian T. Higgins, School of Public Health, University of Michigan, Ann
Arbor, Michigan 48109.
Dr. Lawrence Hinkle, Cornell University Medical School, New York, New York
10021.
Dr. Emanuel Landau, Environmental Health Hazards Project, Chevy Chase,
Maryland 20015.
Dr. Gory J. Love, Institute for Environmental Studies, University of North
Carolina, Chapel Hill, North Carolina 27514.
Dr. Thaddeus J. Murawski, New York Department of Health, Albany, New
York 12337.
Dr. Herbert Schimmgl, Neurology Department, Albert Einstein Medical
College, Pleasantville, New York 10570,
Dr. Carl M. Shy, Institute for Environmental Studies, University of
North Carolina, Chapel Hill, North Carolina 27514.
Dr. Larry Thibodeau, Harvard School of Public Health, Boston, Massachusetts
02115.
Ixi
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Technical Assistance
Editing Reference Verification
Andrea Dykstra Lucie Chu Chen
William Epple Deborah Doerr
Patricia Hodgson Mildred Farrington
Susan McKee - Douglas Fennel!
Helen Qscanyan John Ferrell
Matthew Schudel Kathryn Flynn
Alan Senzel Bettie Haley
Scott Smith Frances Lederer
Joyce Lindsay
Elizabeth Smith
Carolyn Stevens
Patricia Tierney
Graphics Word Processing
Jim Faunce Penny Andrews
Wayne Fulford Susan Bass
Jennie Fuller Del a Bates
Allen Hoyt • Catherine Boykin
Charles Keadle Bobbi Creech
Charles Rodriguez Peggy Creighton
Terry Smith Wanda Currin
Ruth Takemoto Jacki Epperson
Cecil Winstead Anita Flintall
Gloria Gallant
, Pam Jones
Evelynne Rash
Jo Reynolds
Sarah Stumley
Aimee Tattersall
Constance Van Oosten
Proofreading Data Sourcesand Verification
Diane Chappell Neil Frank
Lisa Friedkin Bill Hunt
Peggy Lacewell Charles Masser
Sharon McCoy Tom Pace
Holly Singer Jake Somers
Donna Wicker
Ixii
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CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE
The substance of this document was independently peer-reviewed in public
session by the Subcommittee on Health Effects of Particulate Matter and Sulfur
Oxides and the Subcommittee on Welfare Effects of Particulate Matter and
Sulfur Oxides, Clean Air Scientific Advisory Committee, Environmental
Protection Agency Science Advisory Board.
Chairman, Clean Air Scientific Advisory Committee:
Dr. Sheldon K. Friedlander, Vice Chairman of Chemical Engineering, Department
of Chemical, Nuclear, and Thermal Engineering, School of Engineering and
Applied Science, University of California at Los Angeles, Los Angeles,
California 90024
Acting Director, Science Advisory Board:
Dr. Terry F. Yosie, Science Advisory Board, United States Environmental
Protection Agency, Washington, D.C. 20460
SUBCOMMITTEE ON HEALTH EFFECTS OF PARTICULATE MATTER AND SULFUR OXIDES
Chai rman
Dr. Vaun Newill, Associate Medical Director, Exxon Corp., 1251 Avenue of
the Americas, New York, New York 10020
Members
Dr. Mary Amdur, Department of Nutrition and Food Science, Massachusetts
Institute of Technology, Cambridge, Massachusetts 02139.
Dr. Judy A. Bean, College of Medicine, Department of. Preventive
Medicine and Environmental Health, University of Iowa, Iowa
City, Iowa 52242.
Consultants
Dr. Edward Crandall, Division of Pulmonary Disease, Department
of Medicine, University of California at Los Angeles,
Los Angeles, California 90024.
Dr. Bernard Goldstein, Rutgers University Medical School, Department of
Environmental and Community Medicine, Piscataway, New Jersey 08854
Dr. Herschel Griffin, San Diego State University, School of
Public Health, San Diego, California 92192.
Dr, Timothy Larson, Department of Civil Engineering, Mail Stop
FC-05, University of Washington, Seattle, Washington 98195.
Dr. Morton Lippmann, Institute of Environmental Medicine, New
York University, New York, New York 10016.
Dr. Roger 0. McClellan, Director of Inhalation Toxicology
Research Institute, Lovelace Foundation, P.O. Box 5890,
Albuquerque, New Mexico 87115
Ixiii
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SUBCOMMITTEE ON WELFARE EFFECTS OF PARTICIPATE MATTER AND SULFUR OXIDES
Chairman
Dr. Sheldon Friedlander, School of Engineering and.Applied Science, University
of California at Los Angeles, Los Angeles, California 90024
Members
Mr. Harry Hovey, New York Department of Environmental Conservation, 50 Wolf
Road, Albany, New York 12233.
Mr. Donald Pack, 1826 Opalocka Drive, McLean, Virginia 22101
Consultants
Dr. Robert Dorfman, Department of Economics, Harvard University, 325 Littauer,
Cambridge, Massachusetts 02138
Dr. Ronald Hall, Section on Ecology and Systematics, Langmuir Laboratory,
Cornell University, Ithaca, New York 14850
Dr. Andrew McFarland, Department of Civil Engineering, Texas A & M University
College Station, Texas 77843
Dr. Peter McMurry, Department of Mechanical Engineering,
University of Minnesota, 111 Church Street S.E., Minneapolis,
Minnesota 55455
Dr. Michael Treshow, Department of Biology, University of Utah,
Salt Lake City, Utah 84112.
Ixiv
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1. EXECUTIVE SUMMARY
1.1 INTRODUCTION
1.1.1 Legal Requirements
The purpose of this document is to present air quality criteria for participate matter
and sulfur oxides in accordance with Section 108(a)(2) of the Clean Air Act, 42 U.S.C.
§7408(a)(2), which specifies that:
"Air quality criteria for an air pollutant shall accurately reflect the latest
scientific knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the presence of such
pollutant in the ambient air, in varying quantities. The criteria for an air pol-
lutant, to the extent practicable, shall include information on—
(A) those variable factors (including atmospheric conditions) which of them-
selves or in combination with other factors may alter the effects on public
health or welfare of such air pollutant;
(B) the types of air pollutants which, when present in the atmosphere, may
interact with such pollutant to produce an adverse effect on public health or
welfare."
National ambient air quality standards are based on such criteria [Clean Air Act Section
109(b), 42 U.S.C. §7409(b)]. Both the criteria and standards are to be reviewed and, as
appropriate, revised at five-year intervals beginning not later than December 31, 1980
[Section 109 (d)(l), 42 U.S.C. §7409(d)(l)].
This document constitutes a revision of separate criteria documents previously issued for
participate matter and sulfur oxides (National Air Pollution Control Administration, 1969 and
1970, respectively). A combined document has been prepared for various reasons: (1) Signi-
ficant amounts of gaseous sulfur dioxide are transformed into particulate sulfate by chemical
processes in the atmosphere; (2) It is difficult to separate the relative contributions of
sulfur oxides and particulate matter to the mortality and morbidity effects observed in epi-
demiological studies; (3) Combining the criteria review of the two pollutants, as was done by
the World Health Organization, was recommended by the U.S. Environmental Protection Agency's
advisory committee on matters related to air quality criteria documents, the Clean Air Scien-
tific Advisory Committee of EPA's Science Advisory Board. .
This document describes what is known or anticipated with regard to both the health and
welfare .effects of particulate matter (PM) and sulfur oxides (SO ). For purposes of this doc-
X
ument, PM is considered to consist of any airborne solid particles and low vapor pressure
liquid droplets with an effective diameter smaller than a few hundred micrometers. Important
classes of particle sizes within this broad range are identified in subsequent sections of
this summary (see Section 1.2, for example). Of the sulfur oxides, only sulfur dioxide (S02)
occurs at significant concentrations in the atmosphere and is discussed here. Other related
sulfur compounds, notably sulfates and sulfuric acid, are covered in the discussion of PM.
With regard to health effects, the document is intended to evaluate the' nature and signi-
1-1
-------
ficartce of all identifiable effects of PM and SO . Under Section 109(b) of the Clean Air Act,
the Administrator of EPA is to consider such information in this document in judging which ef-
fects are to be considered adverse and to set national primary ambient air quality standards
which, based on the 'criteria and allowing an adequate margin of safety, are requisite to pro-
tect the public health. This requires-careful assessment of the relationship between levels
of exposure to PM and SO , via all routes and average'd oVer appropriate time periods, and bio-
logical responses to those exposures. Temporal and spatial distributions of PM and SO are
/\
considered, as well as such complicating factors as breathing patterns, individual activity
levels, special populations of sensitive persons, interactions with other pollutants, and the
complex and diverse chemical composition of PM.
The welfare effects to be identified in the criteria document include effects on vegeta-
tion, crops, soils, water, animals, manmade materials, weather, visibility, and climate, as
well as damage to and deterioration of property, hazards to transportation, and effects on
economic values, personal comfort, and well-being [Clean Air Act Section 302(h), 42 U.S.C.
§7602(h)]. Under Section 109(b) of the Clean Air Act, the Administrator must consider such
information in this document to set national secondary ambient air quality standards that are
based on the criteria and are requisite to protect the public welfare from any known or antici-
pated adverse effects associated with the presence of such pollutants.
1.1.2 Organization of the Document
This document is being issued in three volumes. The first volume (Volume I) includes
Chapter 1 of the document, which contains the general introduction and the executive summary
and conclusions for the entire document*; an addendum to the document (discussing certain new-
ly available information on health effects of S02) is also included in Volume I, following
Chapter 1. Volume II contains Chapters 2 through 7 of the document. Chapters 2 through 5
provide background information on: physical and chemical properties of PM and SO ; methods
for the collection and measurement of such air pollutants; their sources and emissions; and
their ambient air concentrations, along with factors affecting exposure of the general popu-
lation to these pollutants. Chapter 6 evaluates information on atmospheric transport, trans-
formation, and fate of PM and SO , followed by an overview discussion in Chapter 7 of poten-
* /C
tial involvement of PM and SO in acidic deposition processes and effects. Volume III contains
A
Chapters 8 through 14 of the document. Chapter 8 evaluates PM and SO effects on vegetation,
; s\
whereas Chapters 9 and 10, respectively, describe effects on visibility and damage to materials
attributable to either PM or SO . Chapters 11 through 14 evaluate information concerning the
/\
health effects of PM and SO . More specifically, Chapter 11 discusses respiratory tract depo-
A.
'sition of SO,, sulfur-related particulate matter (especially sulfates), and other types of PM,
as well as factors affecting their deposition and biological fate. Chapters 12 and 13 discuss
information derived respectively from experimental toxicological studies of animals and from
controlled human cli-nical studies. Chapter 14 discusses epidemiological studies.
*Note that the second digits of the numerical headings throughout this chapter (Chapter 1)
correspond to respective later chapters in the document (e.g., Section 1.2 refers to Chapter
2, Section 1.3 to Chapter 3, etc.)-
1-2
-------
The extensive literature on PM and SO is critically reviewed and evaluated in this docu-
)\ *
ment with emphasis on valid studies relevant to the assessment of human health and welfare
effects. Air quality information and measurement techniques are discussed in early chapters
of the document only to the extent that such information pertains to and helps elucidate the
health and welfare effects of PM and SO discussed in later chapters. As indicated by the
discussion of air quality information, airborne particles of a wide variety of sizes, shapes,
and chemical composition are found in the ambient air of the United States in quantities and
combinations that vary with time and geographic location. Analysis of the effects of airborne
particles is further complicated by comp'lex transformations of various parti'culate species or
their precursor substances during atmospheric transport from sources of emissions that may be
hundreds or thousands of kilometers away from humans, other organisms, or materials ultimately
exposed to the pollutants. Sulfur dioxide, capable of causing notable health and welfare
effects as a gaseous air pollutant, is also the main precursor emitted from manmade sources
contributing to the secondary formation of sulfuric acid and sulfate salts. The latter
products are in turn major constituents of the PM present as urban aerosols to which large
segments of the U.S. population are exposed. Sulfur dioxide and sulfur-related PM species and
their associated health and welfare effects are accordingly discussed in considerable detail
in the present document. Other individual particulate species of concern, however, are not
discussed in as much detail here. Instead, the reader is referred to other EPA air quality
criteria or health assessment documents where the effects of such substances are thoroughly
reviewed, e.g., Air Quality Criteria for Lead (U. S. Environmental Protection Agency, 1977)
anc' Air Quality Criteria for Oxides of Nitrogen (U. S. Environmental Protection Agency, 1982).
In evaluating available information on the health effects of PM and SO in humans, the
s\
main focus is on the inhalation-.of these substances as the most direct and important route of
exposure, although it is recognized that some species of PM may cause biological effects via
other routes of exposure, such as ingestion or contact with skin. Important issues considered
in the document include: (1) patterns of inhalation, deposition, and biological fate of SOg,
sulfur-related PM, and other particulate substances, -as a function of their physical and
chemical properties; (2) mechanisms of action by which such substances may exert biological
effects of potential concern; (3) qualitative characterization of such biological effects; (4)
quantitative characterization of dose-response or exposure-effect relationships; and (5)
identification of populations at special risk from the effects of PM and SO .
A
In the evaluation of welfare effects of PM and SO , consideration is accorded to the
)\
direct, acute effects of such substances on visibility, manmade materials, and plant and
animal species. Also assessed are the more indirect, long-term effects that might be
reasonably anticipated to occur as a consequence of repeated or continuous chronic exposures
1-3
-------
to low levels of such pollutants. The interactions of PM and SO with other factors, such as
* /\
meteorological variables, and the subsequent deposition of PM and SO on and movement through
/\
aquatic and terrestrial ecosystems are also addressed.
1.2 PHYSICAL AND CHEMICAL PROPERTIES OF SULFUR OXIDES AND PARTICULATE MATTER
Of the four known gas-phase sulfur oxides (sulfur monoxide, sulfur dioxide, sulfur tri-
oxide, and disulfur monoxide), only sulfur dioxide occurs at significant concentrations in
the atmosphere. A colorless gas with pungent" odor, SOj, is emitted from combustion of sulfur-
containing fossil fuels, such as coal and oil, as well as from many other sources,
Sulfur dioxide is removed from the atmosphere by gaseous, aqueous, and surface oxidation
to form acidic sulfates. Also important are physical removal pathways for S0~,
-------
Figure 1-1. Idealized size distributions for atmospheric particles under various conditions.
tn
•a
m
S1
o
K
10s
10"
10"'
1 I
1 1
TTT
1 1
SERIOUS "SMOG"
EPISODE ^
/ V
PARTICLE DIAMETER (D),;
105
4
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3 102
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3 1!)1
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__ COMBUSTION / ' / / /
— x^ * / /
/"*
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= //^x-
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~i ii iinil I ii mill 1 1 11 mil
10"3 10"2 10"^ 10
1 1 nini| i iiiiinj IIIIH
FOREST FIRE ~
/'"N _z
1 / » =
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/ 2 ^- ^FRACTURING
/ /FLYASH\ Z
j/y~\ -=
/ / 4 E
1 X ^r *^ **** — <*
/ / —
f =
f —
___
™
—
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—
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*~=
—
-=
I __.cn A R*?P • k.
™™r| ^^BMM. ^,Urt*«OC ^^^-
i iniiiii i 11 mill 1 1 nun
0 101 102 1C
Figure 1-1a. Idealized size distribution for particles found in
typical urban aerosols (mainly from anthropogenic sources)
under varying weather conditions. Note bimodal distribu-
tion under usual conditions and shift in distribution (in-
creasing fine-mode particles, decreasing coarse-mode par-
ticles) under stagnation (1) and serious "smog" conditions
(2), respectively.
Source: Adapted from Slinn (1976).
10 • iu" io-
PARTICLE DIAMETER (D),jum
Figure 1-1b. Idealized size distribution for atmospheric par-
ticles from anthropogenic sources, showing fine particle con-
tributions from "clean" high-temperature combustion and
coarse particle contributions from "dirty" fly ash sources,
forest fires, and crushing and grinding operations. Note
change in distribution near sources (1) and at increasing
distances (2,3,4) from sources.
Source: Adapted from Slinn (1976).
-------
Rgure 1-1. (Continued)
10s
10"
10
102
< 10'
UJ
s
| 10°
UJ
o
oc 10
10'
10"'
,-2
10"
=i 11 mill 11 mill 11
i i
— c
111 linn 111 linn i ui =
IlllliJ I ! 11 111!j
HURRICANE
2
•#'«A\ \\
/.•/SPRAY • \ \
iK\ \ \\
-FINE-) COARSE-
111 mill 11 mini 11 in
10
,-3
10"'
10
,-1
10U
10'
102
CO
J
uj
5
_i
O
O
oc
10
103
102
10
10
,-1
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10"J
El Illllij I
= d
10"
I llllllll I Illllllj I llllllll 1 1 ll^
/•N4 ~
DUST STORM
iTYPICAL CONTINENTAL
: (WITHIN MIXED LAYER)
MOUNTAIN
ELEVATIONS
(ABOVE MIXED LAYER)
-FINE—I — COARSE i
ill i 11 mill 111 mill i iiiniil i
10
,-3
10'2 10'1
10U
101 102 103
PARTICLE DIAMETER (
PARTICLE DIAMETER (
Figure 1-1c. Idealized size distribution for atmospheric par-
ticles from natural sources in a marine setting. Note, in com-
parison to typical background levels over open ocean, in-
creasing levels of coarse-mode particles ranging from those
found in sea spray (1,2) to the extreme cases of storms (3)
and hurricanes (4).
Source: Adapted from Slinn (1976).
Figure 1-ld. Idealized size distribution for atmospheric par-
ticles from natural sources in a continental setting. Note, in
comparison to usual background profiles over typical con-
tinental and high-elevation mountain areas, increasing con-
tributions of coarse-mode particles from wind-blown dusts
(1,2,3), ranging to the extreme case of a dust storm (4).
Source: Adapted from Slinn (1976).
-------
sulfate mass occurs in the accumulation mode. Accumulation-mode particles normally do not
grow -into the coarse mode. Coarse particles include re-entrained surface dust, salt spray,
and particles formed by mechanical processes such as grinding.
Primary particles are directly discharged from manmade or natural sources. Secondary
particles form by chemical and physical .reactions in the atmosphere, and most of the reactants
involved are emitted to the air as gaseous pollutants'.
In the atmosphere, particle growth and chemical transformation occur through gas-particle
and particle-particle interactions. Gas-particle interactions include condensation of low
vapor pressure molecules, such as sulfuric acid (H^SO.) and organic compounds; such condensa-
tion occurs principally on fine particles. The only particle-particle interaction important
in atmospheric processes is coagulation among fine particles.
As shown in Figure 1-2, major components of fine atmospheric particles include sulfates,
carbonaceous material, ammonium, lead, and nitrate. Coarse particles consist mainly of oxides
of silicon, aluminum, calcium, and iron, as well as calcium carbonate, sea salt, and material
such as tire particles and vegetation-related particles (e.g., pollen, spores). Note that the
distributions of fine and coarse particles overlap and that some chemical species found pre-
dominantly in one mode may also be found in the other mode.
The carbonaceous component of fine particles contains both elemental carbon (graphite and
soot) and nonvolatile organic carbon (hydrocarbons emitted in combustion exhaust and secondary
organics formed by photochemistry). In many urban and nonurban areas, these species may be
the most abundant fine particles after sulfates. Secondary organic particles form by oxida-
tion of primary organics by a cycle that also involves ozone and nitrogen oxides. Atmospheric
reactions of nitrogen oxides yield nitric acid vapor (HNO~) that may accumulate as nitrate
particles in the fine and coarse modes. Details of the chemical pathways for forming nitrate
particles and secondary organics are not well established, and the validity of historical
nitrate data is questionable. ,
Most atmospheric sulfates and nitrates are water-'soluble and have a tendency to absorb
moisture. Hygroscopic growth of sulfate-containing particles has a profound effect on their
size, reactivity, and other physical properties which in turn influence their biological and
physical effects.
1.3 TECHNIQUES FOR COLLECTION AND ANALYSIS OF PARTICULATE MATTER AND SULFUR OXIDES
Various instruments are used to measure levels of particulate matter and sulfur oxides.
The instruments used in laboratory studies of the effects of PM and SO may differ greatly
from those used to monitor ambient air levels. Differences in exposure characterization
obtained from these various methods may have important implications for the derivation of
quantitative dose-response relationships from different types of studies. Ambient air
monitoring methods are most important for epidemiological studies on the health effects of PM
and SO and for assessing compliance with related NAAQS; such monitoring methods are, there-
)\
fore, considered in detail in Chapter 3.
1-7
-------
cc
Ul
Ul
en
tn
CD
TTT
I I I I I I
FINE
COARSE
SULFATES, ORGANICS,
AMMONIUM, NITRATES,
CARBON, LEAD, AND
SOME TRACE CONSTITUENTS
I I ll
/ CRUSTAL MATERIAL \
(SILICON COMPOUNDS, \
IRON, ALUMINUM), SEA
SALT, PLANT PARTICLES
I I I I M
\
0.1
1.0
PARTICLE DIAMETER,jum
10.0
Figure 1-2. Idealized representation of typical fine- and coarse-particle mass and chemical
composition distribution in an urban aerosol. Although some overlap exists, note substan-
tial differences in chemical composition of fine versus coarse modes. Chemical species of
each mode are listed in approximate order of relative mass contribution. Note that the or-
dinate is linear and not logarithmic.
1-8
-------
1.3.1 Summary of Sulfur Dioxide Measurement Techniques
Methods for the measurement of S02 can be classified as: (1) manual methods, which
involve collection of the sample over a specified time period and subsequent analysis by
a variety of analytical techniques, or (2) automated methods, in which sample collection and
analysis are performed continuously and automatically.
In the commonly used manual methods, the techniques for the analysis of the collected
sample are based on colorimetric, titrimetric, turbidimetric, gravimetric, x-ray fluorescent,
chemiluminescent, and ion exchange chromatographic measurement principles.
The most widely used manual method for the determination of atmospheric S0? is the
pararosaniline method developed by West and Gaeke. An improved version of this colori-
metric method, adopted as the EPA reference method in 1971, is capable of measuring ambient
SO, concentrations as low as 25 (jg/rn (0.01 ppm) with sampling times ranging from 30 minutes
to 24 hours. The method has acceptable specificity for SO™, if properly implemented to mini-
mize interference by nitrogen dioxide or metal oxides; but samples collected in tetrachloro-
mercurate (I!) are subject to a temperature-dependent decay which can result in an under-
estimation of the ambient SOp concentration. Temperature control during sample collection,
shipment, and storage effectively minimizes this decay problem. A recent variation of the
pararosaniline method uses a buffered formaldehyde solution for sample collection and is
reported to be less susceptible to the temperature-dependent decay problem. Some American
epidemiological studies employed the West-Gaeke method for measurement of SO- concentrations
to assess possible health effects of SO,.
.A titrimetric method based on collection of SOp in dilute hydrogen peroxide, followed by
titration of the resultant HpSQ« with standard alkali, is the standard method used extensively
in Great Britain. Although simple to perform, the method requires long sampling times (24
hours) and is subject to interference from, atmospheric acids and bases. Additional sources of
error include evaporation of reagent during sampling, titration errors, and alkaline con-
tamination of glassware. The hydrogen peroxide method was also adopted as a standard method
by the Organization for Economic Cooperation and Development (OECD) and was employed to pro-
vide aerometric S0? estimates reported in many British and European epidemiological studies.
Methods that employ alkali-impregnated filter papers for the collection of SOp and subse-
quent analysis as sulfite or sulfate have also been developed. Most of these methods involve
an extraction step prior to analysis, although nondispersive x-ray fluorescence has been used
for«the direct measurement of S0? collected on sodium carbonate-impregnated membrane filters.
These methods, however, have not yet found wide-spread use in the. United States for routine
ambient air monitoring purposes or in generating SQp aerometric data used in epidemiological
studies of the health effects of SOp.
1-9
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Two of the most sensitive methods now available for measurement of SCL use principles
base'd on chemiluminescence and ion exchange chromatography. In the chemiluminescence method,
SOp is absorbed in a tetrachloromercurate solution and subsequently oxidized with potassium
permanganate. The oxidation of the absorbed SOp is accompanied by a chemiluminescence that is
detected by a photomultiplier tube. One method uses ion exchange chromatography to determine
ambient levels of SO- which have been absorbed into dilute hydrogen peroxide and oxidized to
sulfate. Another ion chromatographic approach using a buffered formaldehyde absorbing reagent
has also been reported. These methods, however, have not yet been widely employed for routine
monitoring or other field uses.
Sulfation methods, based on reaction of airborne sulfur compounds with lead dioxide
paste to form lead sulfate, have commonly been used to estimate ambient SO^ concentrations
over extended time periods. However, the accuracy of sulfation methods is subject to many
physical and chemical variables and other interferences (such as wind speed, temperature, and
humidity). Moreover, the method is not specific for SO,, since it is affected by other sulfur
2
compounds (such as sulfates) as well. Thus, although sulfation rate (mg S03/100 cm /day) is
commonly converted to a rough estimate of S02 concentration (in ppm) by multiplying the sulfa-
tion rate by the factor 0.03, this cannot be accepted as an accurate measure of atmospheric
SO, concentrations. This fact is important in view of the past widespread use of lead dioxide
gauges in the United Kingdom as the basis for aerometric S0? data reported in some pre-1960s
British epidemiological studies. Also, sulfation-rate methods were used in some American
epidemiological studies, as noted in Section 1.14.
Automated methods for measurement of ambient levels of sulfur dioxide have gained wide-
spread use in the air-monitoring community. Certain of the earliest continuous S0y analyzers
« ' <-
were based on conductivity and coulometry. These first generation analyzers were subject to
interference by a wide variety of substances present in typical ambient atmospheres. However,
.more recent commercially available analyzers using these measurement principles exhibit
improved specificity for S02 through the incorporation of sophisticated chemical and physical
scrubbers. Early continuous colorimetric analyzers using West-Gaeke type reagents and having
good sensitivity and acceptable specificity for S02 were fraught with various mechanical
problems, required frequent calibration, and thus never gained widespread acceptance.
Continuous sulfur dioxide analyzers using the techniques of flame photometric detection
(FPD), fluorescence, and second-derivative spectrometry have been developed over the past 10
years and are commercially available from a number of air monitoring instrumentation companies.
Flame photometric detection of ambient SO, is based on measurement of the band emission of
* &
excited S, molecules formed from sulfur species in a hydrogen-rich flame. The FPD analyzers
exhibit- high sensitivity and fast response, but must be used with selective scrubbers or
coupled with gas chromatographs when high specificity is required.
1-10
-------
Fluorescence analyzers are based on detection of .the characteristic fluorescence of the
SCL molecule when it is irradiated by UV light. These analyzers have acceptable sensitivity
and response times, are insensitive to sample flowrate, and require no support gases. They
are subject to interference by water vapor (due to quenching effects) and certain aromatic
hydrocarbons, and therefore must incorporate ways to minimize these species or their effects.
Second-derivative spectrometry is a highly specific technique for measurement of S02 in
the air, and continuous analyzers based on this principle are commercially available. The
analyzers are insensitive to sample flowrate and require no support gases, but relatively high
sample flowrates are required to achieve reasonable response times. Excessive electronic
noise and -inherent lack of precision can be problems with these analyzers.
Continuous analyzers based on many of the above measurement principles (conductivity,
coulometry, flame photometry, fluorescence, and second-derivative spectrometry) have been
designated by EPA as equivalent methods for the measurement of SO, in the atmosphere. Testing
of these analyzers by the manufacturers prior to designation has demonstrated adequate per-
formance for use when an EPA reference or equivalent method is desired or required. Testing
of these methods by EPA has verified their performance and has also demonstrated excellent
comparability among these designated methods under typical monitoring conditions.
1.3.2 Summary of Measurement Techniques for Particulate Matter
Sampling particulate matter suspended in ambient air presents a complex task because of
the spectrum of particle sizes and shapes. Separating.particles by aerodynamic size provides
a simplification by disregarding variations in particle shape and relying on particle settling
velocity. Note that the aerodynamic diameter of a particle is not a direct measurement of its
size but is the equivalent diameter of a spherical particle of specific gravity which would
settle at the same rate as the. particle in question. Samplers can be designed to collect
particles within sharply defined ranges of aerodynamic diameters or to simulate the deposi-
tion pattern of particles in the human respiratory system, which exhibits a more gradual
transition from acceptance to exclusion of particles. High-volume (hi-vol) samplers with
selective inlets, dichotomous samplers, cascade impactors, and cyclone samplers are the most
common devices with specifically designed collection characteristics. Carefully collected
size distributions of ambient particle mass have shown that most particle samplers under-.
estimate the concentration of particles in the air because of sensitivity to external factors
such as wind speed or because of internal particle losses.
Mass concentrations can be estimated using methods that measure an integral property
of particles such as optical reflectance. Empirical relationships between mass concen--
trations and the integral measurement have been developed and can be used to predict mass
concentration. However, without a valid physical model relating to the measurements, plus
empirical data to demonstrate the model, these techniques have a limited ability to estimate
mass concentrations. These conditions are poorly met in the case of reflectance or trans-
mission tape samplers, fairly well met in the integrating nephelometer, and very well met in
the case of beta-ray attenuation analysis.
1-11
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Sampling accuracy can be estimated through key sampling components, such as flowrate and
inlet sampling effectiveness. These component measurements provide a means of intercomparing
methods, even though a reference measurement technique is not available. Recent interest in
larger particle sampler cutpoints (e.g., 15 |jm) have resulted in wind tunnel test procedures
that determine sampling effectiveness of particle samplers under controlled conditions.
Such measurements have added significantly to the ability to estimate particle sampling
accuracy.
The hi-vol sampler collects particles on a glass-fiber filter by drawing air through the
filter at a flowrate of approximately 1.5 m /min, thus sampling a higher volume of air per
unit of time than the above sampling methods for PM. The hi-vol sampler is widely used in the
United States to measure what is known as "total suspended particulate matter" (TSP). Recent
evaluations show that the hi-vol sampler has cutpoints of =25 urn at a wind speed of 24 kph and
45 |jm at 2 kph. Although the sampling effectiveness is wind-speed sensitive, wind speed is
estimated to produce no more than a 10-percent day-to-day variability for the same ambient
concentration for typical conditions. The hi-vol is one of the most reproducible particle
samplers currently in use, with a typical coefficient of variation of 3 to 5 percent. A
significant problem associated with the glass-fiber filter used on the hi-vol is the formation
of artifact mass caused by the presence of acid gases in the air (artifactual formation of
3
sulfates from SO, being one example). These artifacts can add 6 to 7 |J9/m "to a 24-hour
sample. The hi-vol sampler has been extensively used in the United States for routine
monitoring purposes and has provided estimates of total suspended particulate (TSP) mass used
in many American epidemiological studies of the health effects of PM.
The dichotomous sampler was designed to collect the fine and coarse ambient particle
®
fractions, typically providing a separation at 2.5 pm. This sampler uses Teflon filters to
minimize artifact mass formation and is available in versions for manual or automatic field
operation. The earlier inlets used with this sampler were very wind-speed dependent, but
newer versions are much improved. Because of low sampling flowrate, the dichotomous sampler
collects submilligram quantities of particles and requires microbalance analyses, but is
capable of reproducibill ties of ±10 percent or better. The method, however, has only
recently begun to be evaluated for possible routine field use and has not yet been extensively
employed for generating size-selective data on PM mass in relation to health effects evaluated
in epideroiological studies.
Cyclone samplers with cutpoints in the vicinity of 2 (jm have been used for years to
separate the fine particle fraction. A version is also available for personal dosimeter
sampling." Cyclone samplers can be designed to cover a range of sampling flowrates and are
available in a variety of physical sizes. Applications of cyclone samplers are found in 10-
and 15-pm cutpoint inlets for the dichotomous sampler. Cyclone sampling systems could be
expected to have coefficients of variations similar to that of the dichotomous sampler and
have also found only limited use until recently in epidemiological studies of PM health
effects.
1-12
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The Size .Selective Inlet (SSI) hi-vol collects samples containing particles less than 15
urn for comparison with TSP. Except for the inlet, this sampler is identical to the TSP
hi-vol. It is expected to have the same basic characteristics and is presently being evaluated
for possible routine monitoring use in the field.
Cascade impactors have been used extensively to obtain mass distribution by particle
size. Because care must be exercised to prevent errors, such as those caused by particle
bounce between stages, these samplers are normally not operated as routine monitors. A study
by Miller and DeKoning (1974) comparing cascade impactors with hi-vol samplers showed
inconsistencies in the mass median diameter and total mass collections of the impactors.
Samplers that derive mass concentrations by analytical techniques other than direct
weight have been used extensively. One of the earliest was the British smokeshade (BS)
sampler, which measures the reflectance of particles collected on a filter and uses empirical
relationships to predict mass concentration. These relationships have been shown by Bailey and
Clayton (1980) to be more sensitive to carbon concentrations than mass, and hence are very
difficult to interpret as either total or size-selective PM mass present in the atmosphere.
More specifically, the BS method and its standard variations typically collect PM with an =4.5
urn DCQ cutpoint under field conditions (McFarlajid et al., 1982). thus, regardless of whether
larger particles are present in the atmosphere, the BS method collects predominantly small
particles. The BS method neither directly measures mass nor determines chemical, composition
of collected PM. Rather, it measures light absorption of particles as indicated by
reflectance from a stain formed by the particles collected on filter paper, which is somewhat
inefficient for collecting very fine particles. The reflectance of light from the stain
depends both on the density of the stain, or amount of PM collected, and the optical proper-
ties of the collected PM. Smoke particles composed of elemental carbon found in incomplete
fossil-fuel combustion products typically make the greatest contribution to darkness of the
stain, especially in urban areas. Thus, the amount of elemental carbon, but not organic
carbon, present in the stain tends to be most highly correlated with BS reflectance readings.
Other nonblack, noncarbon particles also have optical properties such that they can affect the
reflectance readings, although their contribution to optical absorption is usually negligible.
Since the relative proportions of atmospheric carbon and noncarbon PM can vary greatly
from site to site or from one time to another at the same site, the same absolute BS reflect-
ance reading can be associated with markedly different amounts (or mass) of collected parti-
cles or, in unusual circumstances, even with markedly different amounts of carbon. Site-
specific calibrations of reflectance readings against actual mass measurements obtained by
collocated gravimetric monitoring devices are therefore necessary to obtain estimates of
atmospheric concentrations of particulate matter based on the BS method. A single calibration
curve relating mass or atmospheric concentration (in |jg/m ) of particulate matter to BS re-
flectance readings obtained at a given site may serve as a basis for crude estimates of the
levels of PM (mainly small particles) at that site over time, so long as the chemical composi-
1-13
-------
tlon and relative proportions of elemental carbon and noncarbon PM do not change substantially.
However, the actual mass or smoke concentrations present at a particular site may differ
markedly from the values calculated from a given reflectance reading on either of the two most
widely used standard curves (the British and OECD standard smoke curves). Thus, great care
o
must be taken in interpreting the meaning of any BS value reported in. terms of fjg/m ,
especially as employed in many of the British and European epidemiologies! studies discussed
in Chapter 14.
The AISI light transmittance method is similar in approach to the BS technique and has
been employed for routine monitoring in some American cities. The instrument collects parti-
cles with a DJ-Q cutpoint of =5.0 |jm aerodynamic diameter and uses an air intake similar to
that of the BS method. Particulate matter collects on a filter-paper tape that is
periodically advanced to allow accumulation of another stain. Opacity of the stain is deter-
mined by transmittance of light through the deposited material and the tape, with results
expressed in terms of optical density or coefficient of haze (CoH) units per 1000 linear feet
of air sampled (rather than mass units). Readings in CoH units are somewhat more responsive
to noncarbon particles than are BS measurements; but, again, the AISI method does not directly
measure mass or determine chemical composition of the PM collected. Any attempt to relate
CoHs to pg/m would require site-specific calibration of CoH readings against mass measure-
ments determined by a collocated gravimetric device, but the accuracy of such mass estimates
could still be subject to question. This type of calibration, however, has only been
attempted for New York City and has only very limited possible applicability for certain New
York City aerometr'ic data reported in some epidemiological studies.
Regan et al. (1979) showed that this sampler correlates favorably with gravimetric
measurements limited to the smaller particle sizes. Waggoner and Weiss (1980) and Groblicki
et al. (1980) also reported good correlation between the integrating nephelometer and gravi-
metric fine particle mass. The Electrical Aerosol Analyzer (EAA), however, was shown to have
difficulties in reliably predicting gravimetric mass measurements (Mulholland et al., 1980).
These latter methods, unlike the AISI method, have not been used in gathering PM data used in
epidemiological studies; but the nephelometer. has yielded information useful in quantifying
the effects of fine-mode PM on visibility (see Section 1.9).
Since the hi-vol method collects particles considerably larger than those collected by
the BS or AISI methods, intercomparisons or conversions of PM measurements by the BS or AISI
methods to equivalent TSP units, or vice versa, are severely limited. For example, as shown
by several studies, no consistent relationship exists between BS and TSP measurements taken at
various sites or even at the same site during various seasons. One exception appears to be
the relationship between BS and TSP observed during severe London air pollution episodes when
low wind-speed conditions resulted in settling out of larger coarse-mode particles. Since
fine-mode particles consequently predominated, TSP and BS levels (in excess of about 500
o
) tended to converge, as would be expected if only fine-mode particles were present.
1-14
-------
Optical particle morphology techniques are very useful for identifying the character and
sources of collected particles; Bradway et al. (1976),' 'however, noted that these techniques
are dependent on the skill of the microscopist and stressed the need for careful quality
assurance procedures. In general, such methods have not found wide-spread use beyond highly
specialized research applications.
An extensive list of analytical techniques is available to determine chemical properties
of particles collected on a suitable substrate. Many of the analytical techniques, such as
those for elemental sulfur, have been demonstrated (Camp et al., 1978) to be more precise than
the analyses for gravimetric mass concentration. Methods are available to provide reliable
analyses for sulfates, nitrates, organic fractions, and elemental composition (e.g., sulfur,
lead, silicon). Not all analyses can be performed on al,l particle samples because of factors
such as incompatible substrates and inadequate sample size. Misinterpretation of analytical
results can occur when samples have not been appropriately segregated by particle size and
when artifact mass is formed on the substrate rather than collected in particulate form.
Positive artifacts are particularly likely in sulfate and nitrate determinations, and negative
nitrate artifacts also occur.
Sampling technology is available to meet specific requirements such as providing sharp
cutpoints, outpoints that match particle deposition models, separate collection of fine and
coarse particles, automated sample collection capability, collection of at least milligram
quantities of particles, minimal interaction of the substrate with the collected particles,
ability to produce particle size distribution data, low purchase cost, and simple operating
procedures. Not all of these sampling requirements may be needed for a measurement study.
Currently, there is no single sampler which meets all requirements, but samplers are available
to meet most typical requirements if the overall accuracy and reproducibility of the method
are consistent with the objectives of a study.
1.4 SOURCES AND EMISSIONS OF PARTICULATE MATTER AND SULFUR OXIDES
Both natural and manmade sources emit particulate matter and sulfur oxides into the
atmosphere. Natural particulate emissions include dust, sea spray, volcanic emissions, bio-
genie emanations (e.g., from plants), and emissions from wildfires. Manmade emissions ori-
ginate from stationary point sources, fugitive sources (such as roadway and industrial dust),
and transportation sources (vehicle exhausts). See Section 1.2 for information regarding
physical (e.g., size) and chemical properties of PM emitted from these different sources.
Reliable estimates for natural emissions of PM and SO specific to the United States are
not available. Proportional interpolations from global estimates indicate that in the United
States natural sources may emit 84 million metric tons of particles yearly ; estimates of
biogenic sulfur emissions in the United States suggest a total in the range of 0.2 to 0.5
million metric tons annually. Additional contributions from coastal and oceanic sources may
also be significant. In contrast, manmade sources are estimated to emit 125 million to 385
1-15
-------
minion metric tons of PM and 27 million metric tons of SO (mostly S09) per year in the
X £.
United States. However, these numbers should be considered no more than rough estimates
because of the assumptions and crude approximations inherent in most emissions calculations.
The proximity of emissions to humans often is more important than relative intensity.
For example, emissions from combustion of home-heating fuels and transportation sources are
minor on a national level. However, because they are emitted in densely populated areas and
close to ground level, the possibility of effects on human health and welfare is thereby
greatly increased. On the other hand, dust from unpaved roads appears to be significant, but
usually occurs in rural areas, and tends to settle out quickly, lessening any possible con-
sequences. Conversely, although some natural source emissions can be fairly intense (volcanic
ash or sulfur from marshlands, for example), in general their effects are lessened because
they tend to be distributed fairly broadly nationwide. Consequently, simple comparisons of
total national tonnages of manmade versus natural emissions will seldom reflect the impact
that localized manmade sources can have on an area's air quality. For such reasons, certa'in
manmade sources, particularly stationary point sources, have been given special attention in
this document. Historical trends in anthropogenic emissions of PM (excluding fugitive
emissions) and SO are shown in Table 1-1.
X
Most manmade sulfur oxide emissions come from stationary point sources, and more than 90
percent of these discharges are in the form of SO-. The balance consists of sulfates. Most
natural sulfur is emitted as reduced sulfur compounds, some portion of which probably become
oxidized in the atmosphere to S0? and sulfates.
Characteristics of particle emissions vary with the source and a host of other factors.
Primary particles from natural sources tend to be coarse. About 50 percent are larger than 10
urn. Particles from nonindustrial fugitive sources, such as unpaved roads and wind-eroded
farmland, are significant on a mass basis, constituting an estimated 110 to 370 million metric
tons a year. However, only about 20 percent of this particulate matter is less than 1 |jm in
size. On the other hand, most particles emitted by stationary and transportation sources are
less than 2.5 urn in .diameter. In addition, the variety of different toxic elements found in
fine material from stationary point sources tends to exceed that typically found in emissions
from manmade or natural fugitive sources.
Fugitive dust emissions exceed those from stationary point sources in most Air Quality
Control Regions having high TSP loadings. However, the impact of this pollution on populated
areas may be lessened because: (1) a major portion of these emissions consists of large
particles that settle out in a short distance, and (2) most sources, such as unpaved roads,
exist in rural areas and their emissions spread over areas with Tow population densities.
1-16
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TABLE 1-1. NATIONAL ESTIMATES OF PARTICIPATE AND SULFUR OXIDE EMISSIONS
(a). PARTICULATE EMISSIONS3
(10 metric tons per year)
SOURCE CATEGORY
Stationary fuel
combustion
Industrial processes
Solid waste disposal
Transportation
Miscellaneous
TOTAL
1940
8.7
9.9
0.5
0.5
5.2
24.8
1950
8.1
12.6
0.7
1.1
3.7
26.2
1960
6.7
14.1
0.9
0.6
3.3
25.6
1970
7.2
12.8
1.1
I.I
1.0
23.2
1975
5.1
7.4
0.5
1.0
0.6
14.6
1978
3.8
6.2
0.5
1.3
0.7
12.5
(b). SULFUR OXIDE EMISSIONS
(10 metric tons per year)
SOURCE CATEGORY
1940
1950
1960
1970
1975
1978
Stationary fuel
combustion
Industrial processes
Solid waste disposal
Transportation
Mi seellaneous
TOTAL
15.1
19.5
16.6
22.0
15.7
22.7
21.4
29.8
20.9
26.2
22.1
3.4
0.0
0.6
0.4
4.1
0.1
0.8
0.4
4.8
0.0
0.5
0.4
6.2
0.1
0.7
0.1
4.5
0.0
0.8
0.0
4.1
0.0
0.8
0.0
27.0
Table does not include industrial-process fugitive particulate emissions, and non-
industrial fugitive emissions from paved and unpaved roads, wind erosion, construc-
tion activities, agricultural tilling, and mining activities.
Table includes forest fires, agricultural burning, coal-refuse burning, and
structural fires.
Source: U.S. Environmental Protection Agency (1978, 1980)
1-17
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1.5 CONCENTRATIONS AND EXPOSURE
Sulfur oxide concentrations in the air have been markedly reduced during the past 15
years by restrictions on sulfur content in fuels, control devices on stationary and other
major sources, and tall stacks that disperse power plant exhausts. Currently, only I percent
of the SO, monitoring sites show annual levels above 80 jjg/m (0.03 ppm), as compared with 16
percent of the monitoring stations that reported annual means above this level in 1970.
Despite this change, some areas still report high short-term SO,, concentrations (see areas
3
indicated in Figure 1-3). Hourly values of 4000 to 6000 pg/m (1.5 to 2.3 ppm) are common
3
near large smelters. Maximum hourly values above 1000 pg/m (0.4 ppm) exist in about 100
locations in the United States. Near isolated point sources, such peaks may be reached very
rapidly and be of only short duration (see, for example, Figure 1-4).
Following a downward trend between 1970 and 1974, TSP concentrations have not changed
significantly in recent years. Dusty, arid parts of the country still have somewhat elevated
TSP values, as do industrialized cities in the East and Far West. Ninetieth percentile values
(values exceeded 10 percent of the time) of 24-hr TSP >85 pg/m are reported in every part of
the United States except Alaska. Annual mean TSP values generally range from 55 pg/m in New
•j
England to 100 pg/m in the arid Southwest.
As discussed in Section 1.2, particulate matter is generally distributed in fine- and
coarse-mode size ranges of differing chemical- compositions. A comparison of dichotomous
sampler data (fine and coarse) and hi-vol particle measurements (TSP) for selected urban,
suburban, and rural sites is shown in Figure 1-5. The figure suggests a seasonal pattern of
high summer and low winter concentrations that is most evident for fine particles. Fine
particles typically contribute about one-third of TSP mass in urban areas. The sulfate ion
usually accounts for about 40 percent of the fine-mode mass; sulfate compounds collectively
account for the Majority of the fine-mode mass. Large areas of the United States experience
a
10 |jg/m or greater sulfate levels for one or two periods of a month or more every year.
These areas are so large that no background levels of fine particles can now be measured east
of the Mississippi River. Southern California experiences high levels of sulfates and
nitrates, particularly during photochemical smog incidents. Extremely high levels (>100
3
pg/m ) of organic aerosols also occur in this area, particularly during afternoon periods of
intensive ozone formation. These organic aerosols consist largely of dicarboxylic acids and
other polyfunctional compounds. Concentrations of toxic organic particulate matter and trace
metals are highest in cities. Levels of some fine-particle components have decreased because
of control measures, such as reduction of lead in gasoline.
Coarse particles tend to settle close to sources. In most cases, these particles account
for two-thirds of the TSP mass. During the summer, in dry regions such as Phoenix, Oklahoma
City, El Paso, and Denver, they may contribute even higher proportions. The primary cause of
high TSP appears to be local dust; but, in industrialized cities, evidence exists for signifi-
cant contributions of soot, fly ash, and industrial fugitive emissions.
1-18
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r
M
10
Figure 1-3. Characterization of 1974-76 national SO2 status is shown by second highest 24-hr,
average concentration. Asterisks denote counties for which this level exceeded 365 /ug/m3.
(The current 24-hr, primary standard is 365 ptg/m3, which is not to be exceeded more than once
per year. Alaska and Hawaii reported no such exceedences.)
Source: Monitoring and Reports Branch, Monitoring and Data Analysis Division, Office of
Air Quality Planning and Standards, U.S. Environmental Protection Agency.
-------
E
&
z
o
ts
UJ
o
2
O
o
CM
O
W
150
1.40
1.30
1.20
1.10
1.00
.90
.80
.70
.60
.50
.40
.30
.20
.10
o
i I I i I I I i I I I I I I I I I I I i I I
— —
_^ ' _«_
__^ 130ppm^J"33ppm JACKSON CO., ALABAMA
II SOURCE-ORIENTED SITE
~
1 —
__ • •
—
1 1
I 1
__ —
1 1
_ . _
-
I 1
— II
I 1
1 1
««. - . "lr;;1™
I
1
_ _
1
1
IV
1 \
! I I i i I I/ I V 1 1 1 I 1 1 i 1 I I I 1 1
12; 24 6. 8 10 12, 2 8 10 12 2 4 6. 8 10 12 2 4 6 8 10 12
NOON' PM. MID" NOON P.M. MID A.M, NOON
NIGHT NIGHT
JULY 29, 1979 JULY 30, 1979 JULY 31, 1979
Figure 1-4. One example of rapid increase in ambient sulfur dioxide concentration from near zero to
1.30 ppm (3410 pg/m } during a period of approximately two hours.
Source: U.S. Environmental Protection Agency (1981).
1-20
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TSP (HI-VOL)
"• 4 URBAN
SUBURBAN
RURAL
. _. DURBAN
"" SUBURBAN
RURAL
JAN FEB MAR APR MAY JUN JUL AUG SEPT OCT NOV DEC
MONTH
Figure 1-5. Seasonal variations in urban, suburban, and rural areas for four
size ranges of particles. The data were obtained from a relatively small num-
ber of monitoring sites.
Source: After Trijonis et al. (1980).
1-21
-------
Coarse particles are composed mainly of silica, calcium carbonate, clay minerals, and
soot. Chemical constituents in the coarse fraction include silicon, aluminum, potassium,
calcium, and iron, together with other alkaline-earth and transition elements. Organic
materials are also found in coarse particles, including plant spores, pollens, and diverse
biogenic detritus. Much of this coarse material is road dust suspended by traffic action.
Street levels of resuspended dust can be very high. Traffic on unpaved roads generates huge
amounts of dust that deposits on vegetation and can be resuspended by wind action. Rain and
snow can reduce these emissions, but as one study suggests, salting of roads when precipita-
tion occurs under freezing conditions may be a major source of winter TSP. Industrial fugi-
tive emissions, particularly from unpaved access roads, construction activity, rock crushing,
and cement manufacturing, can be a major category of coarse particles.
A number of calculational methods, generally categorized as source-apportionment or
source-receptor models, are being used to trace particle levels to their sources. The results
from chemical element balance calculations or factor analysis are available for several
cities. Apportionments for these cities are presented in Chapter 5 as examples of results to
be expected by future applications of these methods.
Ambient air monitors measure pollutant concentrations at fixed locations. Most indi-
viduals in our highly mobile society move through a variety of exposure levels that can be
higher or lower than might be deduced solely from the values reported by a community's ambient
air monitors. Most people spend a majority of their time indoors, where lower respiratory
rates are associated with lower activity levels. Indoor levels of SOp, which are almost
entirely attributable to penetration from outdoors, can range from 10 to 90^percent of outdoor
levels, depending on such factors as the tightness of house construction and the absorptive
properties of walls, floors, and furniture. Presence or absence of air conditioning, rates of
air exchange, and activities that resuspend dust influence indoor particulate matter levels.
In addition, outdoor fine particles penetrate into buildings. Peak indoor TSP levels corre-
late to some degree with outdoor values, with a time lag that depends on a building's air-
exchange rate. Because stationary ambient-air pollution monitors provide general statistics
on composite population exposures, it would be extremely difficult (if not impossible) to pre-
dict an individual's actual exposure to SO and PM on the basis of community air-monitoring
data alone.
1.6 ATMOSPHERIC TRANSPORT, TRANSFORMATION, AND DEPOSITION
The concentration of a pollutant at some fixed time and place beyond its source depends
on; (1) the rate of emission and configuration of the source, (2) the chemical and physical
reactions that transform one pollutant species to another, (3) the transport and diffusion
(dilution) of the pollutant as a result of various meteorological variables, and (4) the re-
moval of the pollutant through interaction with various surfaces on land and water (dry
deposition) and interaction with rain drops or cloud particles (wet deposition). Figure 1-6
schematically illustrates some of these processes.
1-22
-------
FREETROPOSPHERIC
EXCHANGE
VERTICAL
DIFFUSION
AEROSOL
CONDENSATION
COAGULATION
CHEMICAL REACTIONS
ABSORPTION IN
CLOUD ELEMENTS
SEDIMENTATION
AS AEROSOL
DRY DEPOSITION ON »///,'>,', //////// '/'////
THE GROUND //////A///'/////////-'
«£7.H5» ANTHROPOGENIC
SOURCES
SOURCES
ABSORPTION IN
PRECIPITATION
WASHOUT IN PRECIPITATION
Figure 1-6. Complex processes affecting transport and transformation of
airborne paniculate matter and sulfur oxides.
Source: Adapted from Drake and Barrager (1979).
1-23
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Processes governing transport and diffusion, chemical transformation, and wet and dry
removal of S0« and particulate matter are extremely complex and not completely understood.
The oxidation rate of SCL observed in urban and rural atmospheres is only partially accounted
for by gas-phase reactions. Liquid-phase catalytic reactions involving manganese, iron, and
carbon may contribute to observed rates, but further research is required to determine the
rates and detailed mechanisms of these processes under typical atmospheric conditions.
Dry deposition of SCL is fair.ly well understood as a result of extensive measurements
over various surfaces. The study ,of particle deposition has focused on modeling physical
aspects of the process, namely, aerodynamics. Few measurements for -particles with composi-
tions typical of those in polluted atmospheres exist to support these modeling efforts.
Coarse particles are removed from the atmosphere much more rapidly than fine particles, for
the residence time of fine particles in the atmosphere is apparently on the order of 1 week
and their transport distance may exceed 500 km.
Understanding of wet-removal processes for S0? has progressed considerably in recent
years, particularly in the area of solution-phase chemistry of rain drops. Removal of gases
as well as particles depends mainly on the physical character of precipitation events, which
in many instances may be the determining factor in how accurately wet-removal rates can be
predicted.
Characterization of the dynamics of the planetary boundary layer is essential to an
adequate understanding of pollutant transport and diffusion over all spatial, scales. Though
considerable advances have been made in this area, the ability to predict mean transport and
diffusion over long distances is less than adequate, partly because of sparse spatial and
temporal measurements of upper-air wind activity.
The long-range transport of the fine-particle/SOp complex results in the superposition
and chemical interaction of emissions from many different types of sources. Present long-
range air pollutant transport models are characterized by simple terms representing chemical
transformation and wet and dry removal, and by varying degrees of sophistication in their
treatment of transport and diffusion. None of the models adequately treats the dynamics of
the planetary boundary layer. Although always limited by the adequacy of their underlying
/ •
data bases, with further research and development long-range transport models should be able
to address issues associated with the movement of pollutants over long distances.
1.7 ACIDIC DEPOSITION .
The occurrence of acidic deposition, especially in the form of acidic precipitation (rain
and snow), has become a matter of environmental concern. Acidic precipitation in various
regions of the United States and elsewhere in the world has been associated with acidification
of ponds, lakes, and streams, with a resultant disappearance of aquatic animal and plant life.
Acidic precipitation is also believed to have the potential for leaching elements from sensi-
tive soils and causing direct and indirect injury to forests and vegetation. It is also
believed to play a role in damaging stone monuments and buildings and in corroding metals and
deteriorating paint.
1-24
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Chapter 7 of this document emphasizes the, effects of the wet deposition of sulfur and
nitrogen compounds on aquatic and terrestrial ecosystems. Dry deposition also plays an
important role, but contributions by this process have not been well quantified. Because
sulfur oxides and nitrogen oxides are closely linked in the formation of acidic precipitation,
the present discussion is not limited to sulfur oxides. A critical assessment of the various
causes as well as effects of acidic deposition will be presented in a future EPA document.
Acidic precipitation has been conventionally defined.as precipitation with a pH less than
5.6, because precipitation formed in a geochemically clean environment would have a pH of
approximately 5.6 due to the combining of carbon dioxide with water in the air to form
carbonic acid. As shown in Figure 1-7, the acidity of precipitation in the Eastern United
States currently averages frpm pH 3.9 to 5.0; and even in regions of the.United States with
average pH levels above 5.0, precipitation episodes with pH levels as low as 3.0 have been
reported. Measurements have been weighted according to rainfall amounts in the calculation of
the average values shown in Figure 1-7.
The pH level can vary during a precipitation event, from event to event, from season to
season, and from geographical area to geographical area. Other substances in the atmosphere
besides oxides of sulfur and nitrogen can also cause a shift in the pH of precipitation by
making it more acidic or more basic. For example, dust and debris swept up from the ground by
winds may become components of precipitation and affect its pH. In the West and Midwest, soil
particles tend to be basic, but in the Eastern United States they tend to be acidic. Further-
more, in coastal areas sea spray strongly influences precipitation chemistry by contributing
calcium, potassium, chlorine, and sulfates. In the final analysis, the pH of precipitation
reflects the contributions of all of these components.
It is not known when precipitation in the United States began to become markedly acidic.
Some scientists argue that it began with the burning of large amounts of coal in the indus-
trial revolution, and others estimate that it began in the United States with the introduction
in the 1950s of tall stacks on power plants. Still other scientists disagree completely and
argue that rain has always been acidic. No definitive answer to the question exists at the
present time. Because the pH of rain has not been monitored without interruption over
extended periods of time, there are insufficient data, to characterize with confidence long-
term temporal trends in the pH of precipitation in the United States.
Though wet deposition is,usually emphasized, it is not the only process by which acids or
acidifying substances are added to bodies of water or to the land. Dry deposition also
occurs. Dry-deposition processes include gravitational settling of particles, impaction of
aerosols, and absorption of gases by soil or water or by objects at the earth's surface. Dew,
fog, and frost are also involved in deposition processes but do not strictly fall into the
category of wet or dry deposition. Dry deposition of particulate matter is not as well under-
stood as wet deposition; however, it is known that both deposition processes contribute to
1-25
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B'° V 6.5 6,0
ro
01
5,0
ProdycHMi PoUutlon 8lody (HAPSS)
A ElteMePoMrtUMantilMIIUitXEPRn
Figure 1-7, Average pH isopleths as determined from laboratory analyses of
precipitation samples, weighted by the reported quantity of precipitation.
Source: Wisniewski and Keitz (1981).
-------
the gradual accumulation of acidic or acidifying substances in the environment. Therefore,
the reported effects of acidic deposition should not be attributed to wet deposition alone.
The most notable changes associated with acidic deposition are those observed in lakes
and streams in New York's Adirondack Mountains, in Maine, in northern Florida, in the
Precambrian Shield areas of Canada, in Scotland, and in the Scandinavian countries. In these
regions, the decrease in the pH of freshwater bodies has been associated with changes in
aquatic animal and plant populations. The chemistry of freshwaters is determined primarily by
the geological structure (soil system and bedrock) of the lake or stream catchment basin, by
the ground cover and by land use. In coastal regions marine salts also may be important in
determining the chemical composition of freshwater streams, rivers, and lakes. The capability
of a lake and its drainage basin to neutralize incoming acidic substances, however, is deter-
mined largely by the composition of the bedrock. Acidification of surface waters results when
the sources of hydrogen ion exceed the ability of an ecosystem to neutralize the hydrogen ion.
In general, the soils and crust of the earth are composed principally of basic materials with
large capacities to buffer acids. However, areas where bedrock.is particularly resistant to
weathering and where soils are thin and poorly developed have much less neutralizing ability.
This inability to neutralize hydrogen ions does not usually arise from a Timited soil or
mineral buffering capacity. Instead, low cation exchange capacity and slow mineral dissolu-
tion rates in relation to the relatively short retention time of water within the soil system
may result in incomplete neutralization of soil waters and acidification of surface waters.
The capacity of organisms to withstand injury from weather extremes, pesticides, acidic
deposition, or polluted air follows the ecological principle of limiting factors: For each
physical factor in the environment there exists for each organism a minimum and a maximum
limit beyond which no members of a particular species can survive. Either-, too much or too
little of a factor such as heat, light, water, or minerals can jeopardize the survival of an
individual and, in extreme cases, a species. The range of tolerance (see Figure 1-8) may be
broad for one factor and narrow for' another. The tolerance limit for each species is deter-
mined by its genetic makeup and therefore varies from species to species. The range of toler-
ance also varies depending on the age, stage of growth, and/or growth form of an organism.
Limiting factors are, therefore, those components of an ecosystem which, when scarce or over-
abundant, limit the growth, reproduction, or distribution of an organism.
The stability of natural ecosystems under stress from marked environmental changes or
perturbations depends upon the ability of the constituent organisms to adapt and to continue
reproduction of their species. The most sensitive species decline or die out first. However,
the capacity of an ecosystem to maintain internal stability is determined by the ability of
all constituent organisms to adjust and survive. Thus, other species may be subsequently
affected due to the loss of the most susceptible species.
1-27
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ZONE OF
INTOLERANCE
LOWER LIMITS
OFtOUBANCE
ZONE OF
PHYSIOLOGICAL
STRESS
TOLERANCE RANGE
RANGE OF OPTIMUM
UPPER LIMITS
Of TOLERANCE
ZONE OF
PHYSIOLOGICAL
STRESS
• ZONE OF
INTOLERANCE
ORGANISMS
INFREQUENT
ORGANISMS
ABSENT
ORGANISMS
INFREQUENT
GREATEST
ABUNDANCE
ORGANISMS
ABSENT
LOW-*-
-GRADIENT-
Figure 1-8. Idealized conceptual framework illustrating the "law of tolerance," which
postulates a limited range of various environmental factors within which species can
survive.
Source: Adapted from Smith (1980).
1-28
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Continued or severe disturbance of an ecosystem 'can overcome its resistance or prevent
its recovery, with the result that it is replaced by a new system. In the Adirondack
Mountains of New York State, in eastern Canada, and in parts of Scandinavia the original aqua-
tic ecosystems have been and are continuing to be replaced by ecosystems different from the
original because of acidification of the aquatic habitat. Forest ecosystems, however, appear
thus far to have been resistant to changes due to perturbation or stress from acidifying sub-
stances.
The disappearance of fish populations from freshwater lakes and streams is usually one of
the most readily observable signs of lake acidification. The death of fish in acidified
waters has been attributed to the modification of a number of physiological processes. The
sensitivity of fish to low pH levels has also been shown to depend on aqueous calcium levels.
The reproductive failure of fish has been cited as the primary factor leading to the gradual
extinction of fish populations. Long-term gradual increases in acidity, particularly below pH
5, interfere with reproduction and spawning, producing a decrease in population density and a
shift in size and age characteristics of the population toward larger and older fish. Such
effects often are not recognizable until the population is close to extinction, particularly
in the case of late-maturing species with long lives. Even relatively small increases (as low
as 5 percent) in mortality of fish eggs and fry can decrease reproduction and bring about
extinction.
Acidic pollutants deposited during the winter accumulate in the snowpack and ice, and may
be released in a relatively short time during the melting of the snowpack and ice cover in the
spring. The resulting sudden short-term changes in water chemistry may have a significant
impact on aquatic biota, especially if they occur during spawning or during early stages of
development or other points in the life cycle when the organisms are particularly vulnerable.
In some acidified lakes, concentrations of aluminum may be equally and perhaps more
important than pH levels as a factor causing a decline in fish populations. At low pH levels
certain aluminum compounds in the water may' be mobilized, thereby upsetting the osmoregulatory
function of the blood in fish. Aluminum toxicity to aquatic organisms other than fish has not
been assessed.
When evaluating the potentia-1 effects of acidification on fish or other biotic popula-
S.
tions, it is very important to keep in mind the highly diversified nature of aquatic systems
spatially, seasonally, and year-to-year. As a result of this diversity, it is necessary to
evaluate each system independently in assessing the reaction of a population to acidification.
Survival of a fish population may depend more on the availability of refuge areas from acid
conditions during spring melt than on mean annual pH, calcium, or inorganic aluminum levels.
Other organisms ranging from bacteria to waterfowl may also be affected by lake and
stream acidification. Organisms at all levels in the food web appear to be vulnerable.
Reductions in the number and diversity of species may occur, biomass (total mass of living
organisms in a given volume of water) may be altered, and processes such as primary production
and decomposition may be impaired.
1-29
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Significant changes that have occurred in aquatic ecosystems with increasing acidity,
particularly as the pH drops below 5.5, include the following:
1. Fish populations are reduced or eliminated.
2. Bacterial decomposition is reduced, and fungi may become dominant in aquatic
communities that feed on organic debris. Consequently, such matter accumulates
rapidly, tying up nutrients and limiting nutrient mineralization and cycling.
3. Species diversity and total numbers of species of aquatic plants and animals are
reduced. Acid-tolerant species predominate".
4. Phytoplankton productivity may be reduced because of changes in nutrient cycling and
nutrient limitations.
5. Biomass and total productivity of benthic macroscopic plants and algae may increase,
in part because of increased lake transparency.
6. The number and biomass of herbivorous invertebrates decline. Tolerant invertebrate
species, such as air-breathing insects, may become abundant primarily because of
reduced fish predation.
7. Changes in community structure occur at all levels in the food web.
An indirect effect of acidification potentially of concern to human health is the possi-
ble contamination of edible fish and of water supplies. Studies in Canada and Sweden reveal
high concentrations of mercury in fish from acidified regions. Potentially toxic levels of
lead have been found in plumbing systems with acidified water, and persons drinking the water
could be affected by the lead. However, no cases have yet been documented of human health
effects being directly linked to the impact of acidic precipitation on water supplies or
edible aquatic organisms.
Soils may become gradually acidified from an influx of hydrogen ions. Leaching of the
mobilizable forms of mineral nutrients may occur. The rate of leaching is-determined by the
buffering capacity of the soil and the amount and composition of precipitation. Anion mobil-
ity is also an important factor in the leaching of soil nutrients, for cations cannot leach
without the, associated anions also leaching. The capacity of soils to adsorb and retain
anions increases when hydrated oxides of iron and of aluminum are present.
Sulfur and nitrogen are essential for optimal plant growth. Plants usually obtain sul-
fur in the form of sulfate from organic matter during microbial decomposition. Wet and dry
deposition of atmospheric sulfur is also a major source. In soils where sulfur and nitrogen
are limiting nutrients, such deposition may increase growth in some plant species. The amount
of sulfur entering the soil system* from the atmosphere depends on proximity to industrial
areas, sea coast, and marshlands. The prevailing winds and the amount of precipitation in a
given region are also important. Near fossil-fuel power plants and industrial installations
the amount of sulfur in precipitation may be as much as 168 kilograms per hectare (150 pounds
per acre) or more.
At present there are no documented observations or measurements of changes either in
natural terrestrial ecosystems or in agricultural productivity directly attributable to acidic
precipitation under ambient conditions. Information regarding effects on vegetation comes
1-30
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from controlled research studies, which mainly use some form of simulated acidic rain such as
+ 2-
dilute sulfuric acid. These simulated rains have deposited hydrogen (H ), sulfate (SO* ),
and nitrate (NO., ) ions on vegetation and caused necrotic lesions in a wide variety of plant
species under greenhouse and laboratory conditions. Such results must be interpreted with
caution, however, because the growth and morphology of leaves under such conditions are not
necessarily typical of field conditions. Studies of the effects of simulated acidic precipi-
tation on field crops have reported beneficial, detrimental, or no effects on yield, depending
on the particular species as well as the portion of the plant that is of economic value (e.g.,
root, leaf, fruit).
Damage to monuments and buildings made of stone, corrosion of metals, and deterioration
of paint may be caused by acidic precipitation, but the effects resulting from dry or wet
deposition of sulfur compounds cannot be clearly distinguished. Also, deposition of sulfur
compounds on stone surfaces may cause damage indirectly by providing a medium for microbial
growth that can result in deterioration.
Several aspects of the phenomenon of acidic precipitation remain subject to debate
because of ambiguous or inadequate data. Important unresolved issues include:
(1) the rate at which rainfall is becoming more acidic and/or the rate at which the
phenomenon is becoming geographically more widespread;
(2) the relative extent to which the acidity of rainfall in a region depends on local
emissions of nitrogen and sulfur oxides versus emissions transported from distant
sources;
(3) the relative importance of changes in total mass-emission rates compared to changes
in the nature of the emission patterns (e.g., ground-level versus tall-stack emis-
sions) in contributing to the regional acidification of precipitation;
(4) the relative contribution of wet and dry deposition to the acidification of lakes
and streams;
(5) the geographic distribution of natural sources of SO , nitrogen oxides (NO ), and
ammonia, and the significance of their seasonal as well as annual contributions;
(6) the existence and significance of anthropogenic, non-combustion sources of SO , NO ,
and hydrogen chloride,(HC1);
(7) the dry deposition rates- for SO,, NO , sulfate, nitrate, and HC1 over various ter-
rains and at different seasons of the year;
(8) the existence and reliability of long-term pH measurements of lakes and headwater
streams;
(9) the acceptability of current models for predicting long-range SO and NO transport
and of models for predicting the acid-tolerance of lakes;
(10) the feasibility and costs of 'using liming or other corrective procedures to prevent
or reverse damage from acidification;
1-31
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(11) the differential effects of sulfate, nitrate, and hydrogen ion deposition on eco-
system dynamics in both aquatic and terrestrial ecosystems;
(12) the effectiveness of fertilization resulting from sulfate and nitrate deposition on
soils;
(13) the ultimate effects of acidic deposition on agricultural crops, forests, and other
native plants; and
(14) the effects of acidic deposition on soil microbial processes and nutrient cycling.
A comprehensive critical assessment of scientific evidence bear-ing on these and other
issues will be presented in a future EPA document on the causes and effects of acidic
deposition.
1.8 EFFECTS ON VEGETATION
Plants may be exposed to sulfur dioxide and particulate s-ulfate through dry and wet
deposition. Of the two, sulfur dioxide is potentially more injurious to vegetation, partic-
ularly when it is in combination with other airborne pollutants. The effects of S0? through
external exposure of vegetation or through contact with the soil substrate are much more
difficult to assess than the effects associated with the entry of S02 into the plant.
To cause injury, sulfur dioxide must enter a plant through leaf openings, or stomata.
After entering plant cells through the stomata, sulfur dioxide is converted to sulfite and
bisulfite, which may then be oxidized to sulfate. Sulfate is about 30 times less toxic than
sulfite and bisulfite. Absorption rates and plant resistance to sulfur have been shown to
vary with different species exposed to S0?. For example, sulfur dioxide has been shown to
induce stomatal closure in some plants and to induce stomatal,, opening in others. In some
instances, tolerance to SO, may depend less on the amount of pollutant absorbed than on the
ability of the plant to move S0? out of the leaf and into other plant tissues. As long as the
absorption rate of S0« in plants does not exceed the rate of conversion to sulfate, the only
effects of exposure may be changes in opening or closing of stomata, or subtle changes in the
biochemical or physiological systems. Such effects may abate if SO, concentrations are
reduced. Pollutant uptake by plants may be influenced by such dynamic physical factors as
light, leaf surface moisture, relative humidity, and soil moisture. Such factors influence
internal physiological conditions in plants as well as stomatal opening and closing and,
therefore, play a major role in determining the sensitivity of the plant species or cultivars.
Symptoms of S02~induced injury in higher plants may be quite variable, since response is
governed by pollutant dose (concentration multiplied by duration of exposure), conditions of
exposure (e.g., day Vs. night, peak vs. long-term), physiological status of the plant, matura-
tions! stage of plant growth, environmental influences on the pollutant/plant interaction, and
environmental influences on the metabolic status of the plant itself. Although the product of
time and concentration may remain constant, the effect of exposure may vary for a given dose.
The relationship between exposure and injury is generally more influenced by changes in con-
centration than by changes in duration of exposure.
1-32
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Possible plant responses to SO- and related sulfur compounds include: (1) increased
growth and yield due to fertilization effects; (2) no detectable response; (3) injury mani-
fested as -growth and yield reductions without visible symptoms on the foliage or with very
mild foliar symptoms that would be difficult to attribute to air pollution without comparing
control plants grown under pollution-free conditions; (4) injury exhibited as chronic or acute
symptoms on foliage with or without associated reduction in growth and yield; and (5) death of
plants or plant communities.
Under certain conditions, atmospheric S0« can have beneficial effects on agronomic
vegetation. The amount of sulfur accumulated from the atmosphere by leaf tissues is
influenced by the amount of sulfur in soil relative to the sulfur requirement of the plant.
After exposure to low doses of S0?, plants grown in sulfur-deficient soils have exhibited
increased productivity.
As the concentration of S0~ increases, plants may develop more predictable and more
obvious visible symptoms. Foliar symptoms progress from chlorosis, or other types of pigmen-
tation changes, to the development of necrotic areas, the extent of which increases with
exposure. Studies of the effects of SQp on growth and yield have demonstrated a reduction in
the dry weight of foliage, shoots, roots, and seeds, as well as a reduction in the number of
seeds. At still higher doses there are further reductions in growth -and yield. Extensive
mortality has been noted in forests continuously exposed to S0? for many years. The presence
of acute or chronic foliar injury does not necessarily indicate that growth or yield is
affected, nor does foliar injury always portend subsequent growth or yield effects. However,
plant productivity and visible damage to foliage are the best available indicators of plant
response to S0?.
A number of species of plants, particularly lichens, are sensitive to low concentrations
of SOp, and some may be used as bioindicators of such pollution. Even sensitive species may
be asymptomatic, however, depending on the environmental conditions before, during, and after
exposure to SO,. Because of the absence of empirical data quantifying losses in growth or
yield in relation to S0? exposure, sensitive species are generally identified on the basis of
visible symptoms.
Dose-response studies aid in quantifying plant response to air pollutants. Useful gener-
alizations on the relationship between parameters of plant response and measurable indices of
dose may be developed. "Response" may be considered to be a measurable change in parameters
such as gas-exchange rates, photosynthetic rates, biochemical pathways, physiological func-
tions, degree of visible leaf injury, and subsequent effects on growth and yield. In
interpreting dose-response studies, it is important to realize that the ultimate effect of
a given exposure dose may be influenced significantly by environmental factors that control
the rate of pollutant flux into plant leaves and by plant factors that determine the metabolic
fate of the pollutant within leaf tissues (see Figure 1-9).
1-33
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NUMBER OF,
EXPOSURES"
POLLUTANT
CONCENTRATION
DOSE-*-
DURATION OF
"EACH EXPOSURE
CLIMATIC FACTORS
EDAPHIC FACTORS
BIOTIC FACTORS
PLANT RECEPTOR
MECHANISM OF ACTION
GENETIC MAKEUP
STAGE OF PLANT
DEVELOPMENT
EFFECTS
ACUTE
CHRONIC
SUBTLE
Figure 1-9. Conceptual model of the factors involved in air pollution's effects on vegetation.
Source: Heck and Brandt (1977).
1-34
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Concentrations of SOp from point sources may fluctuate widely within short periods.
Laboratory experiments have demonstrated that short-term exposures at high concentrations of
SO, are relatively more toxic than longer-term exposures with the same total dose. In studies
of the effects on kidney beans of short-term (3-hr) SO, exposures, increasing the peak-to-mean
ratio of SOp concentrations from 1.0 to 2.0 did not alter the degree of depression in photo-
synthetic activity; however, increasing the peak-to-mean ratio to 6,0 tripled the depression
in post-fumigation photosynthetic activity, although the total dose delivered remained
approximately the same (i.e., in the 1.0 to 2.0 ppm-hr range).
Another important aspect of exposure dose is the frequency and duration of periods of low
SO, stress. Such periods may be critical to the recovery of plant 'systems following exposure
to elevated levels of SQp. Thus, experimental studies using continuous exposure systems
probably overestimate the toxicity of the delivered dose in many cases. Recovery would be
more likely to occur under field conditions, where fluctuating meteorological conditions
strongly influence exposure patterns.
Plant growth and development represent an integration of cellular and biochemical
processes. The response of a given species or variety of plants to a specific air pollutant
cannot be precisely predicted on the basis of the known response of related plants to the same
pollutant; neither can the response of a plant be predicted on the basis of its response to
similar doses of other pollutants. Each plant species is different genetically, and therefore
its genetic susceptibility and the influence of the environment at the time of exposure must
be considered for each plant and each pollutant. Because of the variation in response shown
by different plant species and different cultivars of the same species, making generalizations
is difficult. For example, studies (Dreisinger and McGovern, 1970) of S0? effects on vege-
tation in non-arid regions (where environmental conditions such as high temperature, high
humidity, and abundant sunlight enhance plants' responsiveness to SOp) indicate that many
species of sensitive and intermediately responsive vegetation would likely, from time to time,
show visible injury when exposed to peak (5-min), 1-hour, and 3-hour SQp concentrations as low
as 2.6-5.2, 0.13-5.2, and 0.78-2.1 mg/m3 (1-2, 0.5-2, and 0.3-0.8 ppm) respectively. In
contrast, other studies (Hill et al., 1974) indicate that some species of vegetation in .arid
regions would probably not show visible signs of injury even at SOp concentrations as high as
28.82 mg/m3 (11 ppm) for 2 hours.
In general, studies discussed in Chapter 8 indicate that regardless of the conditions of
exposure, for a given plant species or variety there is a critical SOp concentration and
.duration of exposure above which plant injury will occur. Such injury results from exceeding
the plant's capability to transform toxic SOp and sulfite into much less toxic sulfate and
ultimately to transfer or break down the sulfate.
At present, data concerning the interactions of S0? with other pollutants indicate that,
on a regional scale, SQp occurs at least intermittently at concentrations high enough to pro-
duce significant interactions with other pollutants, principally ozone. A major weakness in
the understanding of pollutant interactions, however, is the lack of in-depth analysis of
existing regional air-quality data sets for the three principal pollutants (SOp, ozone, and
1-35
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nitrogen dioxide). Analysis of these data should show how frequently and at what concentra-
tions the pollutants occur together both spatially and temporally within regions of major
concern. The relative impact on plants of the simultaneous versus sequential exposure to
these pollutants is also not well documented and is crucial in evaluating the likelihood and
extent of potential pollutant interactive effects under field conditions.
A few studies have reported that combinations of particulate matter and SO,, or particu-
late matter and other pollutants, may increase foliar uptake of SO,, increase foliar injury of
vegetation by heavy metals, and/or reduce growth and yield. Because of the complex nature of
particulate pollutants, conventional methods for assessing pollutant injury to vegetation,
such as dose-response relationships, are poorly developed. Studies have generally reported
responses relative to a given source and the physical size or chemical composition of the
particles. For the most part, studies have not focused on effects associated with specific
ambient concentrations. Coarse particles, such as dust, directly deposited on leaf surfaces
can reduce gas exchange, increase leaf surface temperature, reduce photosynthesis, and lead to
chlorosis, reduced growth, and leaf necrosis. Heavy metals deposited either on leaf surfaces
or on the soil and subsequently taken up by a plant can accumulate and reach toxic concentra-
tions within the tissues of the plant.
Natural ecosystems are integral to the maintenance of the biosphere, and disturbances of
these ecosystems may have long-range effects that are difficult to predict. In the United
States anthropogenic contributions to atmospheric sulfur exceed natural sources; most of these
emissions are deposited (by wet and dry deposition) on terrestrial and aquatic ecosystems.
The subsequent fate and distribution of sulfur in these systems is not well understood. The
wet deposition of sulfur compounds is discussed in Chapter 7.
Natural ecosystems do not respond to environmental perturbations in the same manner as do
a few isolated individuals or crop monocultures. The responses observed in ecosystems under
ambient conditions are a complex function of many variables, which cannot conclusively be
attributed to any particular substance such as sulfur dioxide or particulate matter alone.
Data relating responses of ecosystems to specific doses of SO^ and other pollutants are diffi-
cult to obtain and interpret because of the generally longer periods of time over which these
responses occur and "because of the many biotic and abiotic factors that modify them.
Vegetation within terrestrial ecosystems is sensitive to SO, toxicity, as evidenced by
changes in physiology, growth, development, survival, reproductive potential, and community
composition. Indirect effects may result from the modification of the habitat through change
in the decomposition of litter and the cycling of nutrients or through altered structure of
the community. At the community level chronic exposure to SCL, particularly in combination
with other pollutants such as ozone may cause shifts in community composition as evidenced by
elimination of individuals or populations sensitive to the pollutant. Differential effects on
individual species within a community can occur through direct effects on sensitive species
and through alteration of the relative competitive potential of species within the plant
1-36
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community. In one study'of a forest chronically exposed to gaseous sulfur emissions, changes
were observed in the mineral nutrient balance and in the biological relationships among the
various components of the ecosystem. However, a reduction in gaseous sulfur emissions
occurred during the study, and it appeared that the changes resulting from the ecological per-
turbations were reversible.
Particulate emissions have their greatest impact on terrestrial ecosystems near large
sources of emission. Particulate matter in itself constitutes a problem only in those few
areas where rates of deposition are very high. However, ecological.modification may occur if
the particles contain toxic elements, even though deposition rates are moderate. Solubility
of particle constituents is a critical factor determining the impact of particulate matter
deposited on terrestrial ecosystems since water-insoluble elements are not mobile within
ecosystems. Most of the material deposited by wet and dry deposition on foliar surfaces in
vegetated areas is transferred to the soil where accumulation in the litter layer occurs.
Such accumulation may affect recycling of the nutrients in litter.
1.9 EFFECTS ON VISIBILITY AND CLIMATE
"Atmospheric visibility" is a term often used by airport weather observers to connote
visual range, which refers to the farthest distance at which a large, black object can be seen
against the horizon sky in the daytime. In the everyday -sense, visibility relates to
atmospheric clarity and the perceived characteristics of viewed surroundings, including the
contrast and the color of objects and sky. Pollution affects visibility in two primary ways:
(1) as coherent plumes or haze layers visible because of their contrast with background; and
(2) as widespread, relatively homogeneous haze that reduces contrast of viewed targets and
reduces visual range. The kind and degree of effects are determined largely by the distribu-
tion and characteristics of atmospheric particulate matter, which scatters and absorbs light.
The currently available methods for monitoring visibility measure different aspects of
visibility impairment. Generally, contrast-type measurements (such as photography, telephoto-
metry, and human eye observations) relate well to the perception of visual air quality, while
extinction or scattering measurements (such as transmissometry and nephelometry) relate to the
cause of visibility degradation. Each of these measurement methods can be used to approximate
visual range. No single method is yet widely accepted for measuring light absorption.
Visibility in the United States, as indicated by airport observations, is depicted in
Figure 1-10. Some uncertainty arises from the use of airport data to characterize regional
visibility because of differences in target quality and observers between sites and at the
same site. Despite these limitations, the data should be at least indicative of regional
trends. The best visibility occurs in the mountainous Southwest where annual median visi-
bility exceeds 110 km (70 miles). East of the Mississippi and south of the Great Lakes,
annual median visibilities are less than 24 km (15 miles) and are significantly lower in
summer, particularly during sporadic episodes of regional haze. To some extent, these
regional differences reflect naturally occurring meteorological patterns, such as the higher
humidity of the Southeast versus the Southwest.
1-37
-------
25
M
00
oo
P: BASED ON PHOTOGRAPHIC
PHOTOMETRY DATA
N: BASED ON NEPHELOMETRY DATA
*: BASED ON UNCERTAIN EXTRAPOLATION
OF VISIBILITY FREQUENCY DISTRIBUTION
15
Figure 1-10. Median yearly visual range (miles) and isopleths for suburban/nonurban areas,
1974-1976. (1 mile =1.6 km)
Source: Trijonis and Shapland (1979).
-------
Visual range is inversely related to total extinction and can be estimated, if extinction
is known, by the Koschmieder relationship (see Figure 1-11). Total extinction is the sum of
scattering and absorption by particles and by gases. Because extinction is dependent on wave-
length and sun angle, particle-derived haze may appear blue, white, gray, or brown under
varying conditions. On a regional scale, visibility reduction is generally dominated by light
scattering by fine particles, particularly those in the 0.1 to 2 urn size range. In urban
areas, absorption of light by fine carbonaceous particles (and, to a lesser extent, N02) can
become important.
Extinction due to scattering is closely proportional to the fine-particle mass concentra-
tion (Figure 1-12), with typical extinction/fine mass concentration ratios (for <70-percent
2
relative humidity) of about 3 m /g. Measurements suggest that extinction due to fine-particle
scattering will increase by a factor of two to three as relative humidity (RH) is increased
from 50 to 90 percent. This increase is due to absorption of atmospheric water vapor by
aerosol constituents such as sulfates. Despite the well-established functional relationship
between visual range and fine-particle mass concentration, the choice of fixed coefficients
for the relationship is complicated by the spatial and temporal variation of RH, particle
composition, and observer contrast thresholds.
The major constituents of fine particles from natural and anthropogenic sources contri-
bute in varying degrees to the impairment of visibility. Theoretical and empirical findings
suggest that two .constituents, sulfates and elemental carbon, generally tend to be most signi-
ficant. Sulfate, with associated ammonium and water, often dominates the fine-particle mass
and hence impairment of visibility. In urban areas, elemental carbon can be a major
visibility-reducing species. In both cases, significant variations can occur at different
times and sites. Other species, such as nitrates and organics, may also be important, but
understanding of their roles is hindered by lack of reliable data.
Studies of trends in airport visibility in the Eastern United States indicate that, while
wintertime visibilities improved in some northeastern locations, visibility in the East
declined overall (Figure 1-13). Summer, often the season of best visibility in the early
1950s, is currently the season of worst visibility. From 1948 to 1974, summertime haze
(extinction) increased by more than 100 percent in the Central Eastern States, by 50 to 70
percent in the Midwest and the Eastern Sunbelt States, and by 10 to 20 percent in the
New England area. Although the results of airport surveys'should be viewed with caution, the
results are consistent from site to site. Similarities exist in the long-term record of the
spatial and seasonal trends in airport visibility, sulfate concentrations, and point-source
emissions of SO . These similarities suggest, but do not prove, that historical visibility
J\
trends in the East were caused, at least in part, by regional sulfur oxides emissions and
resultant sulfate aerosol concentrations.
Reductions in visibility can adversely affect transportation safety, property values, and
aesthetics. When visibility (visual, range) drops below 4.8 km (3 miles), Federal Aviation
1-39
-------
O.i0
0,40
0.30
*
f
°-20
z
LU
5
.
Ul
8 0,10
a
z
LU
0.05
0.03
IT
I I I I I I
I
I
10 20 SO
VISUAL RANGE, km
100
Figure 1-11. Inverse proportionality between visual range (V)
and the scattering coefficient (osp) as measured at the point
of observation. The straight line is derived from the Kosch-
mieder formula for visual range, assuming V = 3.9/asp and
nonabsorbing media (0ext = °spJ- The correlation coefficient
for V and osp is —0.89.
Source: Horvath and Noll (1969).
1-40
-------
59
tu H
60
40
z 5
iu a. 20
,- 0.2
& 0.1
4/17
4/18
4/19
4/20
4/21
4/22
TIME, days
Figure 1-12. Simultaneous in situ monitoring of osp and
fine-particle mass concentration in St. Louis in April 1973
showed a high correlation coefficient of 0.96, indicating
that osp depends primarily on the fine-particle
concentration.
Source: Macias and Husar (1976).
1-41
-------
1S48-S2
196064
1970-74
EXTINCTION
COEFFICIENT, km
VISIBILITY, miles
(km)
-1
>0.36
<6.B
«11)
0.3-0,36
6.6-8
(11-13)
0.24-0.30
8-10
(13-16)
0.18-0.24
10-13.3
(16-21)
<0,18
>13.3
Figure 1-13. The spatial distribution of 5-year average extinction
coefficients shows the substantial increases of third-quarter ex-
tinction coefficients in the Carolinas, Ohio River Valley, and
Tennessee-Kentucky area. In the summers of 1948-1952, a 1000-
km size multistate region around Atlanta, GA, had visibility greater
thaq 24 km (15 miles); visibility had declined to less than 13 km
(8. miles) by the 1970s. The spatial trend of wmter (first quarter)
visibility shows improvements in the Northeast megalopolis region
and some worsening in the Sunbelt region. Both spring and fall
quarters exhibit moderate but detectable increases over the entire
Eastern United States.
Source: Husar et al. (1979).
1-42
-------
Administration regulations restrict flight in controlled air spaces to those aircraft equipped
with instrument flight rules (IFR) instrumentation. ^ Under these conditions, most small air-
craft would be grounded. In addition, for some airports operating under IFR conditions during
periods of peak tra'ffic, delays in arrivals and departures might occur. Airport visibility
data from the National Weather Service indicate that during the summer months about half of
all visibilities less than 4.8 km (3 miles) at noontime occur in the absence of fog, precipi-
tation, or blowing material. Preliminary studies of the economic value of visibility, con-
ducted in both urban and nonurban settings, show that the public is concerned and willing to
pay for improved visual air quality. These studies are still too limited, however, to permit
any large-scale quantitative evaluation.
The relatively long residence time and, light-attenuating properties of fine particles may
lead to slow and subtle changes in the nature of the atmosphere and, possibly, in climate.
Three possible effects have been recognized, each of which may have far-reaching and inter-
related consequences. First, the amount of solar energy reaching ground level may be reduced,
some being backscattered to space and some being diverted to increased atmospheric heating.
Thus, less energy will be available at ground level for photosynthesis and commercial exploi-
tation of solar energy. Second, reductions in solar radiation may lead to alterations in
local or regional temperatures, which may lead to changes in atmospheric stability, agricul-
tural production, energy usage, and sea level. Third, increased cloud formation may alter
precipitation patterns, which may lead to changes in agricultural production. The complex
radiative interactions between atmosphere and earth have obscured the influence of fine
particles on temperature balance and precipitation patterns. The role of fine particles in
reducing grqund level solar radiation is better understood.
If there are no clouds between the observer and the sun, the intensity of direct solar
radiation for a given solar elevation depends on the variable amount of dust, haze, and water
vapor in the atmosphere. The extinction produced by these constituents is called "atmospheric
turbidity." Data from a 29-station turbidity network showed that there are strong spatial and
temporal variations of turbidity across the United States. The mean annual net loss of ground
level solar radiation due to particles for 1961-1966 was estimated at 2.6 percent for the
Southwestern United States and 4 percent for the Midwestern states, based on reasonable
assumptions for the amount backscattered to space or lost to heat-absorbing particles.
Turbidities in the Eastern United States in the summer imply net losses to haVe been about 6
percent. More recent reports from the network (1972-1975) imply net .losses of about 10
percent for average summer conditions in the East. Long-term trends in atmospheric turbidity
in the Eastern United States are qualitatively consistent with those for airport visibility
(Figure 1-14).
1-43
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TURBIDITY TREND
1961-66 » —«
1872-75
0 t.l.l.l.l.t.l-l.'»l-' '•' II.1.1.1.1.I.I.1.1.1.1.1.1 ii.l.l.l.l
1. 1. 1, 1.1.
J F M A M
J J A S O N O
MdNTH
Figure 1-14. Seasonal turbidity patterns for 1961—1966 and 1972—1975 are
shown for selected regions in the Eastern United States.
Source: Flowers et al. (196i), and WMO (1974 through 1977).
1-44
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1.10 EFFECTS ON MATERIALS
Physical damage to materials by sulfur oxides and particulate matter has been investi-
gated in field and laboratory studies. Various approaches have been used to estimate economic
damage. Economic determinations have directly related ambient pollutant levels to economic
damage estimates, or they have estimated economic damage on the basis of physical damage func-
tions. The latter method, called here the physical damage function approach, has been the
method of choice in the past. Other studies, especially in the last decade, have employed the
first approach. Both approaches share a common element: an estimation of willingness to pay to
reduce the damage.
Approaches employing physical damage functions have been most widely used and, therefore,
have received the most extensive treatment. The damage function is a mathematical expression
linking exposure to damage, expressed in terms appropriate to the interaction of the pollutant
and material. For example, corrosion of metal would be expressed in units of thickness lost,
and deterioration of paint in units of reflectance or thickness lost. A major problem in
establishing reliable damage functions for a given pollutant involves separating influences of
the pollutant from those of meteorological parameters (e.g., temperature, relative humidity,
sunlight, windspeed, wind direction) and other air pollutants. For the corrosion of metals,
the duration of surface wetness is the most important variable.
Economic valuations may require determinations of a critical damage level. This level
represents the point at which the service life or utility of the material ends or is severely
impaired. When this point is reached, replacement or repair costs are incurred. For example,
if a typical coat of paint is 60 (jm thick, the critical damage level at which repainting is
necessary might be about 10 |jm. Monetary value is determined through economic damage func-
tions, which may be developed from physical damage functions. This approach includes exposure,
replacement cost, protection cost, and other data, but it cannot account for damage to
irreplaceable items, such as works of art, where the only measurable cost is that of preserva-
tion. However, only a few of the functions developed to date are relatively reliable in
determining damage, and none has been generally accepted for estimating costs. •
The best documented and most significant damages from sulfur oxides and particulate
matter involve accelerated corrosion of metal, erosion and soiling of paint, and soiling of
buildings and other structures. Erosion of stone and other building materials due to sulfur
oxides is also well established, but the importance of sulfur oxides relative to other
pollutants is not clear. Although evidence of damage to fibers (e.g., cotton and nylon),
paper, leather, and electrical components has been reported, reliable damage functions have
not been developed for these materials.
Table 1-2 displays damage functions developed for effects of SOp on zinc, steel, and
house paint. These equations and the data from which they are derived imply that temperature
and particulate matter are relatively unimportant factors in metal corrosion and that the most
important factor is surface wetness. Corrosion will not take place when the metal surface is
1-45
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TABLE 1-2. SELECTED PHYSICAL FUNCTIONS RELATED TO S02 EXPOSURE
Material
Reference
Exposure-Response relationships
Zinc
Haym'e and Upham, 1970 Y = 0.001028 (RH - 48.8) S02
0.92
Galvanized steel Haynie et al., 1976 corr = (0.0187 SO, + e 4L85 " 23»240/RT)t 0.91
c. W
Galvanized steel Haynie, 1980
corr = 2.32 t+ 0.0134v°'781SO,t,
w /, w
Oil-base house paint Spence et al., 1975 Y = 14.3 + 0.0151 S02 + 0.388 RH
Enameling steel
Weathering steel
Haynie and Upham, 1974 corr = 325 & e^'00275 S02 '
Haynie et al. , 1976 corr = [5.64 ^ * e(55'44 ' 31,150/KT)]
Not provided
by author.
0.61
Not provided
by authors.
0.91
corr = depth of corrosion or erosion, (Jin
Y = corrosion/erosion rate, |jm/yr "
S02 = |jg/m3 S02
R = gas constant (1.9872 cal/gm mol K)
RH = percent annual average relative humidity
f = fractional time of panel wetness
= time of wetness in years
= wind velocity in m/s
= geometric mean temperature of panels when wet, K
= time exposure, years
w
v
T
t
Note: 1 ppm S09 = 2620 ng/m .
-------
dry. This dominant factor is usually approximated by a "time-of-wetness" term, that is, the
amount of time the relative humidity (RH) exceeds some critical level (60 to 80 percent RH),
which varies for different metals. There are, of course, several sources of moisture (e.g.,
rain, snow, fog, condensation), but RH is the usual proxy for moisture from all sources.
Corrosion initiated by surface wetness is accelerated by SCL. An increase in either the con-
centration of SOp or the relative humidity is accompanied by an increase in the rate of cor-
rosion. The relative importance of the two factors in accelerating corrosion is shown in
Figures 1-15 and 1-16, based on analyses of 'field data. As shown in Figure 1-16, a 100-
percent increase in the average concentration of sulfur dioxide has about the same effect as a
10-percent increase in relative humidity above a critical humidity level. In some areas of
the country (see Figure 1-17) the humidity is usually at or above the critical level of 60 to
80 percent RH; in other areas, the critical level is rarely reached.
The impact of relative humidity must be taken into account in estimating nationwide
damage to metals from SOp. Average annual RH can vary 10 percent even within one region of
the country; for instance, included in the data base for Figures 1-15 and 1-16 are average
RH's of 29 and 39 percent for Las Vegas and Phoenix, respectively. The range in RH for 57
sites covering 34 States and the District of Columbia was 29 to 76 percent. Average S09 con-
3 '
centrations measured at these sites ranged from 9 to 374 ug/m (0.003 to 0.14 ppm) during the
same period. This wide variation is useful in regression analysis .for developing damage func-
tions, but it greatly complicates estimation of aggregate damage. Relative humidity and SOp
concentrations vary spatially and seasonally. Their respective spatial and temporal varia-
tions, however, are not the same across the country. In some areas, the highest SOp concen-
trations coincide with periods of highest relative humidity; in other areas, the reverse is
true.
Even if there were a means to predict with perfect precision the amount of corrosion in-
curred by a metal surface due to a specified level of S0?, it would still be difficult to
arrive at an acceptable aggregate damage estimate. One would have to know the total thickness
of the metal layer in-question, the critical thickness below which repair or replacement is
necessary, and the total area of surface exposed. This information has not been compiled;
instead, various surrogates have been used, typically annual production data modified by some
service-life .factor. These surrogates do not account for such influences as indoor versus
outdoor use, use of protective coatings, or subjective judgments as to the point at which the
object in use should or could be repaired or replaced. The latter judgment is influenced both
by willingness to pay and ability to pay, and is tied to the economic status of the user or
owner. Because of these complex factors, recent attempts to relate atmospheric pollutant
levels to economic damage have focused on the development of direct relationships between pol-
lutant concentrations and economic benefit or loss of utility.
1-47
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100
150
200
250
SO2 CONCENTRATION, jig/m3
Figure 1-15. Steel corrosion behavior as a function of average SO2
concentration at 65% relative humidity.
Source: Adapted from Haynie and Upham (1974).
1-48
-------
100
90
80
70
E
w- 60
»-
1 50
O
1 40
cc
o
g
10
I
_L
fill
_L
10 20 30 40 50 60 70 80 90 100
AVERAGE RELATIVE HUMIDITY, %
Figure 1-16. Steel corrosion behavior as a function of average
relative humidity at three average concentration levels of sul-
fur dioxide.
Source: Haynie and Upham {1974}.
1-49
-------
Figure 1-17. Isopleths of annual mean relative humidity in the United States,
Source: U.S. Environmental Protection Agency (1979).
1-50
-------
Estimates of nationwide erosion of paint and building materials are limited by the same
kinds of factors limiting estimates of metal corrosion. Factors such as humidity, nature and
extent of exposure, and critical damage points are quantifiable for the nation as a whole only
with a great deal of uncertainty. Costs assigned to repair or replacement are often neces-
sarily arbitrary. Furthermore, damage functions for paint and building materials' are not as
well documented as are those for metals.
The least reliable of the damage functions are those for soiling from PM. Regression
analyses show that the relationship between soiling .(loss of reflectance) of building
materials, including paint, and TSP exposure is tenuous. (See Chapter 3 for information on the
lack of a consistent general relationship between reflectance and TSP). Furthermore, reflec-
tance is not the only property of PM important to soiling; also important is particle size,
for the deposition velocity of particles depends on their size. Characteristics such as
stickiness, oiliness, and tarriness, which would increase adherence of deposited particles to
a surface, should also be considered. There is at present no single technique that combines
all relevant measurements of reflectance, adherence, and particle size.
The limitations of these and other physical-damage functions hinder accurate estimates of
total material damage and soiling. Coupled with these limitations is the lack of material-
exposure estimates. These problems currently preclude complete and accurate estimates of the
costs of damage based on a physical-damage function approach. Nevertheless, the best estimate
of economic loss in 1970 due to 50,,-related materials damage is $900 million (1978 dollars).
Reduction in S0? levels from 1970 to 1978 are estimated to have resulted in an annual benefit
of up to $400 million (1978 dollars) in reduced materials damage. Because of the above-cited
difficulties, most soiling-cost estimates developed since 1970 have departed from the physical
damage function approach to examine cost and frequency of household cleaning and maintenance
tasks. The evidence to date indicates that though cleaning and maintenance expenditures are
not a function of TSP levels, the monetary value of increased cleanliness resulting from TSP
reduction can be calculated, based on an estimated economic loss of $2000 million (1978
dollars) in 1970 due to exterior household soiling. "Reductions in TSP levels from 1970 to
1978 are judged to have resulted in annual benefits of $200 to $700 million from less soiling.
The above estimates for SO, and TSP reductions are quite rough, but they can serve to
represent the direction and magnitude of changes in benefits associated with improved air
quality. ' Other estimates of costs for materials damage and soiling have related ambient pol-
lutant concentrations directly to economic benefit or loss of utility. The value of such
approaches is currently limited by their inability to distinguish the different types of
effects of a pollutant, the relative roles of different pollutants, and the influence of
socioeconomic variables. Though they show promise for future application, it is not clear at
present that these approaches are adequate for decisionmaking guidance.
1-51
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1.11 RESPIRATORY TRACT DEPOSITION AND FATE OF SULFUR OXIDES AND PARTICIPATE .MATTER
Information on the deposition and fate of sulfur oxides and particulate matter in various
regions of animal and human respiratory systems aids in understanding the findings from animal
toxicological, human clinical, and epidemiclogical studies discussed in subsequent chapters of
this document. In both animal laboratory and human clinical studies, exposure levels can
usually be measured near the point of inhalation. Moreover, animal studies can often deter-
mine the relationship between exposure level and the amount actually reaching the target
organ. The monitoring instruments used in- these studies, however, vary considerably from
those used for ambient air sampling. The resulting differences in exposure characterizations
have important implications for quantifying the dose-response relationships that may be
derived from the various types of studies described in the health-effects chapters (12, 13,
14) of this document.
The respiratory tract (Figure 1-18) includes the passages of the nose, mouth, nasal phar-
ynx, oral pharynx, epiglottis, larynx, trachea, bronchi, bronchioles, and small ducts and
alveoli of the pulmonary acini. With respect to respiratory tract deposition and clearance of
inhaled aerosols, three regions can be considered: (1) extrathoracic (ET), the airways ex-
tending from the nares down to the epiglottis and larynx at the entrance to the trachea (the
mouth is included in this region during mouth breathing); (2) tracheobronchial (TB), the
primary conducting airways of the lung from the trachea to the terminal bronchioles (i.e.,
that portion of the lung respiratory tract having a ciliated epithelium); and (3) pulmonary
(P), the parenchyma! airspaces of the lung, including the respiratory bronchioles, alveolar
ducts, alveolar sacs, atria, and alveoli (i.e., the gas-exchange region). The extrathoracic
region, as defined above, corresponds exactly to the definition of the nasopharynx used by the
International Commission on Radiological Protection Task Group on Lung Dynamics (Morrow et
al., 1966).
The nose is a complex structure of cartilage and muscle supported by bone and lined with
mucosa. The vestibule of the nares is unciliated but contains a low-resistance filter con-
sisting of small hair.s. The nasal volume is separated into two cavities by a 2- to 7-mm thick
septum. The inner fossae and turbinates are ciliated, with mucus flow in the direction of the
pharynx. The turbinates are shelf-like projections of bone covered by ciliated mucous mem-
branes with a high surface-to-volume ratio that facilitates humidification of the incoming air.
The larynx consists of two pairs of mucosal folds that narrow the airway.
The trachea, an elastic tube supported by 16 to 20 cartilaginous rings that circle about
three-fourths of its circumference, is the first and largest of a series of branching airway
ducts. The left and right lungs are entered by the two major bronchi thai; branch off of the
trachea (Figure 1-18). The left lung consists of two clearly separated lobes, the upper and
lower lobes; the right lung consists of three lobes, the upper, middle, and lower lobes. The
conductive airways in each lobe of the lung consist of up to 18 to 20 dichotomous branches
from the bronchi to the terminal, bronchioles.
1-52
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LEFT WALL OF NASAL CAVITY
AND TURBINATES
ORAL CAVITY
RIGHT MAIN BRONCHUS
UPPER LOBE BRONCHUS
MEDIAL LOBE
BRONCHUS
I
LOWER LOB!
BRONCHUS
LUNG PARENCHYMA
AND ALVEOLI
UPPER LOBE BRONCHUS
LOWER LOBE BRONCHUS
Figure 1-18. Features of the respiratory tract of man used in the description of the deposition of
inhaled particles and gases with insert showing parts of a silicon rubber cast of a human lung show-
ing some separated bronchioles to 3 mm diameter, some bronchioles from 3 mm diameter to term-
inal bronchioles, and some separated respiratory acinus bundles.
Source; Adapted from Hatch and Gross (1964) and Raabe (1979).
1-53
-------
The pulmonary gas-exchange region of the lung begins with the partially alveolated respi-
ratory bronchioles. Pulmonary branching proceeds through a few levels of respiratory bronchi-
oles to completely alveolated ducts and alveolar sacs. Alveoli are thin-wallefd polyhedral air
pouches that cluster about the acini through connections with respiratory bronchioles,
alveolar ducts, or,alveolar sacs. Oxygen uptake and carbon dioxide excretion occur via cells
located in the alveoli.
Because sulfur dioxide is highly soluble in water, it is readily absorbed upon contact
with the moist surfaces of the nose and upper respiratory .passages. Removal of- $0« by the
upper airways during inhalation determines how much SC^ penetrates to the tracheobronchial and
pulmonary regions of the lung. Sulfur dioxide is almost completely removed (95 to 99 percent)
by nasal absorption under resting conditions in both man and laboratory animals. However,
animal studies indicate that SCL removal from the respiratory tract is significantly lower
during oral breathing than during nasal breathing. Since increasing activity levels and
respiratory workloads generally lead to a shift from nasal to oronasal breathing, SO^ penetra-
tion to the lower respiratory tract increases accordingly. In addition, some persons tend to
breathe orally or oronasally even at rest, thereby increasing their exposure. Furthermore,
fine particles in the inhaled air may increase the penetration of sulfur compounds into the
lower respiratory tract.
The majority of studies concerning the deposition of S09 in animals and people have been
•5 t
done at concentrations greater than 2.62 mg/m (1 ppm). The 95 to 99 percent removal of S02
by the upper respiratory tract noted above has not been confirmed at levels ordinarily found
•a
in ambient air (generally less than 0.1 mg/m [0.038 ppm]). It is anticipated, however, that
similar deposition patterns would be observed at these lower concentrations of SO,.
Once inhaled, SQ2 is absorbed quickly into the secretions lining the respiratory
passages. Host is transferred rapidly into the systemic circulation from all regions of the
respiratory tract. However, of the total S02 inhaled, less than 15 percent is likely to be
exhaled immediately, with only small amounts (about 3 percent) to be exhaled later.
The deposition of inhaled particles in the respiratory tract is complex. Deposition in
different regions of the respiratory tract depends upon breathing patterns and upon the
physical properties of the inhaled particles. Particles .inhaled through the nose are
deposited in patterns markedly different from particles inhaled through the mouth. During
nasal breathing, most particles greater than 4 urn i.n aerodynamic diameter* are deposited in
the respiratory tract. With oral breathing, on the other hand, nearly complete deposition is
observed only for particles greater than 10 urn. In both modes of breathing, larger particles
*Aerodynamic diameter is, defined as the diameter of a unit density sphere having the same
settling speed under gravity as tha particle in question, whatever its shape and density.
Unless stated otherwise in this chapter, all particle sizes are given as aerodynamic
diameters.
1-54
-------
are deposited mainly in the upper airways above the trachea. However, 20 to 30 percent of
particles between 5 and 10 (j"1 inhaled during oral breathing are deposited farther down the
respiratory tract in the trachea and bronchial airways. At levels of light physical activity,
only about 10 percent of particles as large as 15 urn are thought to be deposited in the
tracheobronchial region.
The deeper penetration of particles into the respiratory tract when a person breathes
through the mouth is reflected in the deposition data of Figure 1-19. Generally, between 10
and 20 percent (see lighter shaded area of figure) of inhaled particles less than about 1 |jm
are deposited in the pulmonary region. About 20-percent pulmonary deposition is typical for
particles 1 to 4 urn when inhaled through the nose; when particles are inhaled through the
mouth, substantially greater (20 to 70 percent) pulmonary deposition results, especially for
particles around 3-. 5 urn. For nasal breathing, the peak of the pulmonary deposition curve
shifts downward from 3.5 to 2.5 pm. Depending upon breathing frequency and the volume of air
inhaled or exhaled during a breathing cycle (tidal volume), pulmonary deposition of 5-|jm
particles can vary from as little as 5 percent to as much as 50 percent during oral breathing.
However, only about 5 to 13 percent of particles as large as 8 to 9 urn are deposited in the
pulmonary region.
Studies of the regional deposition of particles less than 3 pm have been conducted using
dogs, rats, and hamsters. In these animals the relative distribution of the particles along
the respiratory tract during nasal breathing follows a regional deposition pattern that is
similar to that, found in humans during nasal breathing. Hence, it is possible, with appro-
priate corrections, to extrapolate from these animals to humans for particles, in this size
range.
Children are usually considered to be more susceptible than adults to the effects of
environmental pollutants, but deposition data for children are not currently available, nor
are they likely to be obtained soon because of ethical and other constraints on using children
as experimental subjects. The few data that are available on other populations, such as
persons with asthma or chronic bronchitis, indicate that tracheobronchial deposition appears
to increase while pulmonary deposition decreases in most abnormal respiratory conditions.
By taking into account the biological effects of the particles and the population at
risk, air-sampling procedures can be formulated to focus on the region or regions of the
respiratory tract pertinent to accurate health assessment. The particle-collection charac-
teristics of certain standard samplers intended to reflect selective deposition patterns in
different regions of the respiratory tract are depicted in Figure 1-19.
Particles deposited in different regions of the respiratory tract are cleared by
different pathways and at different rates. Particles deposited in the anterior regions of the
nasal passages are cleared forward by nose-blowing and sneezing. Beyond the middle turbinate
1-55
-------
11
ACGIH CONV.
— — BMRCCONV.
_„._ PULMONARY VIA
NOSE
PULMONARY VIA
MOUTH
TRACHEOBRONCHIAL
VIA MOUTH
PULMONARY FRACTION
TRACHEO-
BRONCHIAL
FRACTION
0.1 0.2 03 04 0.5
PHYSICAL DIAMETER, Mm—*-•*
1JD 2 3457
- AERODYNAMIC DIAMETER, pm
20 30 40 50
Figure 1-19. Division of the thoracic fraction of deposited particles into pulmonary
and tracheobronchial fractions for two sampling conventions (ACGIH and BMRC) as
a function.of aerodynamic diameter, except below 0.5^m, where physical diameter is
used (International Standards Organization, 1981). Also shown are bands for ex-
perimental pulmonary deposition data from Figure 11-9 and for tracheobronchial (TB)
deposition as a percent of particles entering the mouth. The band for TB deposition
was derived using the overall regression line of Chan and Lippmann (1980) for ex-
trathoracic deposition with oral breathing and their equation for TB deposition,
which was evaluated at bronchial deposition size values one standard deviation
from the mean, given an average inspiratory flow rate of 30 liters per minute. The TB
band is shown up to about the largest particle size used by Chan and Lippmann
(1980).
Source: ACGIH (Threshold Limits Committee, 1968); BMRC (Orenstein, 1960);
Pulmonary via nose (Lippmann, 1977); Pulmonary via mouth (see Figure 11-9);
Tracheobronchial via mouth (Chan and Lippmann, 1980).
1-56
-------
region of the nose, clearance to the pharyngeal regions occurs by mucociliary action, after
which the particles are generally swallowed. Likewise, most clearance of material deposited
in the oral cavity is by swallowing. All of these processes are relatively rapid and remove
most of the deposited material from the respiratory tract within minutes to hours.
Insoluble particles deposited in the tracheobronchial region are cleared upward in the
respiratory tract by mucociliary action and are then swallowed. This clearance is usually
complete within one or two days after deposition. In contrast, particles deposited in the
pulmonary region may be retained for several hundred days before th'ey are cleared to the con-
ducting airways or to the pulmonary lymphatic system.
As particles are cleared by mechanical processes from all regions of the respiratory
tract, chemical dissolution may remove soluble compounds, which can then be absorbed directly
into the systemic circulation. Since dissolution and absorption of substances from particles
deposited in the respiratory tract compete with mechanical clearance processes, the amount
absorbed depends upon the rate of dissolution as compared to the rate of mechanical clearance.
The proportion of deposited material that is absorbed into the body varies markedly for
different regions of the respiratory tract because of the large variations in clearance rates.
1.12 TOXICOLOGICAL STUDIES
Toxicological studies of the metabolism and effects of sulfur oxides and various forms of
particulate matter in experimental animal subjects are discussed in Chapter 12, Although in-
haled sulfur compounds are rapidly absorbed into the systemic circulation, their main effect
is observed in the respiratory tract. Prior to or during inhalation, SO, may react with water
to form sulfurous acid (H?SO~) or be oxidized to form sulfur trioxide (SO.,). The latter
reacts rapidly with water to form sulfuric acid (HLSO.), 4/hich subsequently forms ammonium
sulfate in the presence of ammonia. Sulfurous acid readily dissociates to sulfite and
bisulfite ions, which are In rapid chemical equilibrium. Bisulfite ions react with biological
molecules by sulfonation, by auto-oxidation, and by addition to cytosine. Most of the inhaled
SO, is presumed to be detoxified in the liver and other organs by the sulfite-oxidase pathway,
which forms sulfate that can then be excreted in the-urine.
The metabolism of toxic substances that may be inhaled with atmospheric particles is
specific to the individual compounds. A discussion of the metabolism of all potentially
inhalable compounds in urban air is beyond the scope of this document. Detailed studies on
the deposition and clearance in laboratory animals of coal combustion products, automobile
exhausts, and silicates have been reported elsewhere in the scientific literature.
A number of studies have been conducted o'n the effects of exposing various species of
laboratory animals to different concentrations of S0?. Some of these studies examined the
effects of short-term S0? exposures on pulmonary function in animals (see Table 1-3). From
these investigations it appears that constriction of the bronchial air passages (broncho-
constriction) is the most likely effect of 1-hour exposure to SO,; but at levels below 2.62
3 ^
mg/m (1 ppm) such effects are not consistently observed.
1-57
-------
TABLE 1-3.- EFFECTS OF ACUTE EXPOSURES TO SULFUR DIOXIDE ON PULMONARY FUNCTION
Source
table
Concentration
Duration
Species
Results
Reference
en
oo
12-3 0.42 or 0.84 mg/m3
(0.16 or 0.32 ppiu)
12-3 :0.52, 1.04, 2.1 «g/i»a
(6.2, 0.4, 0.8 ppra)
12-3 2.62, 5.24, 13.1,
26.2 mg/m3
(1, 2, 5, 10 ppi)
32-3 0, 44.5, 83.8, 162,
233, 322, 519, 781 mg/m3
(0, 17, 32, 62, 89, 123
198, 298 ppm)
1 hr
Guinea pig
1 hr Guinea pig
1 hr Dog
10 min Mouse
Increase in airway.resistance.
No significant increase
in airway resistance.
Increased bronchial reactivity
to aerosols of acetylcholine,
a potent bronchoconstrictive
agent.
Respiratory rate decreased
proportionally to the log of
the concentration. Time,for
maximum response was inversely
related to the log of the
concentration; recovery complete
within 30 min following all
exposures.
Aradur and Underhill,
1970; Amdur et al.,
1978a
Amdur et al., 1978c
Islam et al,, 1972
Alarie et al., 1973d
-------
It has been hypothesized that S02 induces bronchoconstriction by stimulating bronchial
epithelial receptors that initiate reflexive contraction of smooth muscles in the bronchial
air passages. This reflex is pharmacologically mediated by portions of the autonomic nervous
system, particularly the vagus nerve, and apparently involves the release of acetylcholine or
histamine. Sulfur dioxide is thought to produce bronchoconstriction in humans also through
the same autonomic reflex arc (see Section 1.13).
Since similar, if not identical, bronchoconstrictive effects are produced by histamine
aerosols and SQy, there is some plausibility in the view that histamine may also be involved
in the bronchoconstriction initiated by SQy. Other similarities tend to support this hypothe-
sis. For example, the effects of SQy and of histamine aerosols are both seen over broad
ranges of concentrations. To wit, as much as a 200-fold difference in dose has been reported
for histamine-induced bronchoconstriction. In addition, as in the case of S02, histamine sen-
sitivity may decrease with age, depending upon the species. Further studies are needed to
substantiate this hypothesis about the role of histamine and to determine if the variation in
response to $02 represents sensitive populations.
Another alteration in breathing caused by S02 'is a transient decrease in respiratory
rate. This effect may involve a chemoreceptor in the nasal passages (similar to the one
thought to be responsible for bronchoconstriction). It also may involve the release of
acetylcholine and is thought to be mediated by the trigeminal nerve. The decrease in
respiratory rate induced by SOy requires a higher concentration than the bronchoconstrictive
effect (see Table 1-3) and differs in other respects, among which are a concentration-
independent transience and a concentration-dependent period of desensitization.
The primary host-defense mechanism of the respiratory tract is the clearance of foreign
objects from the lung, whether by mechanical means (mucociliary transport) or biological means
(phagocytosis or immunological processes). The effects of SO, on these mechanisms are
3
variable and species-dependent. For example, rats exposed to S02 at 0.26 mg/m (0.1 ppm), 7
hours/day, 5 days/week for either 2 or 3 weeks exhibited accelerated clearance of radioisotope-
labeled particles 10 days and 23 days after SO, exposure terminated. In the same study,
3
2.6-mg/m (1-ppm) S02 exposures also accelerated clearance of particles 10 days later but
depressed clearance rates 25 days later. In other studies, mucus flow in the trachea of dogs
decreased following intermittent exposure for 1 year to S09 at a concentration of 2.62 mg/m
3
(1 ppm), whereas a single 30-minute exposure of 65 mg/m (25 ppm) did not affect clearance in
donkeys. Also, from limited work with infectivity models, it appears that susceptibility to
bacterial infection is not affected by high concentrations/of S02 (}3 mg/m [5 ppm] for up to
3 months). Antiviral defenses were impaired by S09 in-mice, but only at exposures to a mini-
, o ' ^ 3
mum of 18.3'to 26.2. mg/m (7 to 10 ppm) for 7 days. Chronic exposure to S02 (5.2 mg/m [2 ppm]
for 192 days), however, can cause alterations of the pulmonary and systemic immune systems.
In summary, acute exposure to S02can alter some aspects of host defenses, but concentrations
1-59
-------
in excess of those currently found in the ambient air appear to be required. Unfortunately,
few studies have examined effects of chronic exposures at lower concentrations.
In regard to possible respiratory tract pathology, no remarkable alterations in lung
o
morphology have been observed following chronic exposure to SO, in monkeys (0.36 to 13.4 mg/m
3
[0.14 to 5.1 ppm] for 540 days) or dogs (13.4 mg/m [5.1 ppm] for 620 days). However, only
conventional light microscopy was used, a method far less sensitive than scanning- or trans-
mission-electron microscopy for observing alterations in surface membranes and cilia. Shorter
o
exposures to much higher concentrations (26 to 1050 mg/m [10 to 400 ppm]) generally did cause
morphological changes in mice, rats, and pigs.
The issue of whether SO, is a mutagen in humans is currently unresolved. Although
mutagenesis in response to S0? has been demonstrated in two microorganisms _in vitro at acidic
pH levels, no evidence supports its occurrence in at least two higher systems, viz. Drosophi1 a
and mouse oocytes.
With regard to the tumorigenic properties of BOy, in vivo investigations of its potential
oncogenicity are quite rare. Tumorigenesis has been examined in mice and rats after exposure
to SO, or to a combination of SO, and benzo(a)pyrene, respectively. In one study, mice were
exposed to S02 intermittently over an entire lifetime. Increased incidence of primary lung
carcinoma was reported for females, but not for males. Because an adequate statistical
analysis was not presented in the report of the study, a subsequent statistical analysis was
performed, revealing that the increase in primary lung carcinoma was significant (p = 0.011)
in SOg-exposed females but not males. However, the exact duration of exposure and concen-
tration cannot be determined accurately from the published .report.
q
The effects of lifetime simultaneous exposure to SO, (10.5 mg/m [4 ppm]) and benzo(a)-
3
pyrene (10 mg/m ) were studied in rats. The biological significance of this study is
difficult to interpret, particularly since statistical analyses were not given. However,
subsequent statistical analysis of the data reported for a combined exposure revealed that the
increased incidence of lung tumors was statistically significant (p = 0.005), whereas the
effects of exposure to S0? and to benzo(a)pyrene alone were not significant.
Numerous animal studies have investigated mortality induced by sulfur dioxide. However,
2
SO, causes increased mortality only at high concentrations (>131 mg/m [50 ppm]) that are not
relevant to ambient air exposure levels.
Characterizing exposures to particles in the atmosphere may be even more difficult than
characterizing exposures to SO,. This difficulty is due, in large part, to the fact that the
toxicity of particulate matter depends greatly upon its chemical composition. In general,
urban air is quite heterogeneous in composition and may vary widely from one community to the
next, or even within a single community. It may contain both inert and chemically toxic
constituents, with the potential impact of the latter being complicated by such considerations
as dissolution, solubility, and biological availability. Although adequate physical and
1-60
-------
chemical information can be obtained from studies with laboratory animals exposed to
homogeneous aerosols, the above-mentioned types of data are not available for the
heterogeneous mixture of particles found in the environment. Therefore, the comparisons that
can be made between toxicological studies of animals exposed to well-defined, laboratory-
produced aerosols and epidemiological studies of people exposed to environmental aerosols are
extremely limited.
Sulfur compounds that have been used in particulate form in inhalation studies include:
sulfuric acid, ammonium sulfate and bisulfate, and sulfate salts of zinc, iron, copper,
manganese, and other metals. Alterations of pulmonary function, particularly increases in
pulmonary flow resistance, provide a measure of response to acute exposure to aerosols of
particulate sulfur compounds. Reports of the irritant potency of various sulfate species are
variable, perhaps due to differences in animal species and strains and to different particle
sizes, pH, composition, and solubility. Generally, however, sulfuric acid appears to be more
irritating than any of the sulfate salts, as reflected in Table 1-4, which ranks various sul-
fate species in terms of their irritant potency (measured as increased airway resistance),
based on short-term (1-hour) exposures. As Table 1-5 indicates, for short-term exposures the
lowest concentration of sulfuric acid found to increase airway resistance was 100 |jg/m . This
finding was obtained with guinea pigs, which appear to be more sensitive than other laboratory
animal species to aerosols of sulfuric acid.
TABLE 1-4. RELATIVE IRRITANT POTENCY OF SULFATE SPECIES IN
GUINEA PIGS EXPOSED FOR ONE HOUR3
Sulfuric acid 100
Zinc ammonium sulfate 33
Ferric sulfate 26
Zinc sulfate 19
Ammonium sulfate 10
Ammonium bisulfate 3
Cupric sulfate 2
Ferrous sulfate 0.7
Sodium sulfate (at 0.1 jjm) 0.7
Manganous sulfate . -0.9
Data are for.0.3-pm mass median diameter particles. Increases in airway
resistance were related to sulfuric acid (0.41 percent increase in resistance
per pg of sulfate as sulfuric acid), which was assigned a value of 100.
Source: Amdur et al. (1978a).
The irritant potency of sulfuric acid aerosol depends in part on particle size. As
reflected to some extent by the findings reported in Table 1-6, sulfuric acid particles
approximately 2 urn or smaller (mass median diameter) generally have more effect on respiratory
function. The irritant potency of sulfuric acid may also be affected by its partial neutra-
lization by ammonia present in the breath or in the air of exposure chambers. The resulting
1-61
-------
TABLE 1-5. RESPONSES TO ACUTE SULFURIC ACID EXPOSURE
Source
table Concentration Duration Species
Results
Reference
12-6 100 |jg/m3
12-9 500 pg/m3
1 hr
1 hr
Guinea pig Pulmonary resistance increased
47%; pulmonary compliance
decreased 27%.
Dog Slight increases in trachea!
mucoci-liary transport veloc-
ities immediately and 1 day
after exposure. One wk later
clearance was significantly
decreased.
Amdur, 1977;
Amdur et al., 1978b
Wolff et al., -1979
12-6 510 ug/m3
12-6 1000 pg/m3
12-9 1000 pg/tn3
12-9 1400 |jg/m3
1 hr
1 hr
12-9 190-1400 pg/m3 1 hr
1 hr
1 hr
Guinea pig Pulmonary resistance increased
60%; pulmonary compliance
decreased 33%.
Guinea pig Pulmonary resistance increased
78%; pulmonary compliance
decreased 40%.
Donkey Bronchial mucociliary
clearance was slowed.
Dog Depression in"trachea!
mucociliary transport
rate persisted at 1 wk
after exposure.
Donkey No effect on trachea!
transport.
Amdur et al., 1978b
Amdur et al., 1978b
Schlesinger et al., 1978
Wolff et al., 1979
Schlesinger et a!., 1978
-------
TABLE 1-6. RESPONSES TO CHRONIC SULFURIC ACID EXPOSURE
Source Concentration
table and particle size*
Duration
Species
Results
Reference
12-9
cr>
OJ
12-5
12-8
12-5
12-8
100 (jg/m3
(0.3-0.6 MHI)
80
(0.84 Mm)
100 M9/m3
(2.78 Mm)
380
(1.15 pm);
480 M9/m3
(0.54 Mm)
1 hr/day,
5 day/wk,
6 mo
Donkey
52 wk
cont.
78 wk
cont.
Guinea pig
Monkey
Within the first few weeks
all four animals developed
erratic bronchial mucociliary
clearance rates, either slower
than or faster than those
before exposure; animals not
exposed to H2S04 before this
study had slowed clearance during
the second 3 mo of exposure
and for 3-4 mo after the end of
of the exposure.
Schlesinger et a!., 1978
No significant blood
effect; no lung alter-
ations; no effect on
pulmonary function.
No significant blood
effect; 380 pg/m3 increased
respiratory rate; 480Mg/m3
had no effect on respiratory
rate but altered distribution
of ventilation early in
exposure period but not
later.
Alarie et al., 1973a,
1975
Alarie et al., 1973a
12-13 900
(2.78 Mm)
52 wk
cont.
Guinea pig No significant effects on
hematology, pulmonary
function, or morphology.
Alarie et al., 1975
*A11 particle sizes in mass median diameter (geometric median size of a distribution of particles, based on weight).
-------
ammonium sulfate and ammonium bisulfate lessen the effects of sulfuric acid, but the extent to
which they have affected the results of available animal studies cannot be quantified.
As summarized in Tables 1-5, 1-6, and 1-7, chronic exposure effects of sulfuric acid and
sulfate salts are less certain than acute exposure effects. Exposure to sulfuric acid at a
concentration of 380 ug/m for 78 weeks was reported to produce small increases in respiration
rate in monkeys, but measurable respiration-rate changes did not occur at a concentration of
3 •
480 ug/m . Duration of exposure, concentration, particle size, and chemical composition all
appear to be important in determining changes in pulmonary function.
Exposure to, sulfuric acid mist causes an alteration in mucociliary. clearance of viable as
well as nonviable bacterial particles from the lung. The effects are variable. For example,
trachea! mucociliary transport in dogs increased after exposure to sulfuric acid aerosol at
o
500 ug/m for 1 hour but decreased in rats and hamsters after 1- to 3-hour exposures to 1000
3 3
ug/m . Prolonged daily 1-hour exposures of donkeys to 100 ug/m of 0.5-um sulfuric acid
aerosols caused a persistent slowing of mucociliary transport.
Resistance to bacterial infection is not affected by exposure to sulfuric acid mist.
However, various metal sulfates adversely affect this defense mechanism. The potency of these
metal sulfates, based on a 3-hour exposure causing an increased susceptibility to bacterial
infection, may be ranked as: cadmium sulfite > cupric sulfate > zinc sulfate > aluminum sul-
3
fate > zinc ammonium sulfate. At concentrations greater than 2.5 mg/m , sulfuric acid and the
following sulfates were ineffective in this bacterial infection paradigm: ammonium sulfate,
ammonium bisulfate, sodium sulfate, ferric sulfate, and ferric ammonium sulfate. It should be
noted, however, that various nonsulfate metallic aerosols, especially compounds containing
nickel or cadmium, have substantial inhibitory effects on host-defense mechanisms in general.
Changes in pulmonary morphology due to particulate matter have been studied mostly after
chronic exposure to sulfuric acid. Morphological changes were evident in the lungs of monkeys
3
after a long-term (78-week) exposure to relatively high levels of sulfuric acid (>2.43 mg/m ).
The major findings included thickening of the bronchial wall and bronchiolar epithelium, which
may contribute to changes in lung function. In other studies, involving chronic exposure of
guinea pigs (for 1 year) and dogs (for about 2 years) to sulfuric acid, neither morphological
3
nor physiological changes were noted at concentrations of less than 1 mg/m .
The lethal effects of sulfate aerosols depend in part on an animal's age. For example,
3 3
18 mg/m sulfuric acid was lethal to 1- to 2-month-old guinea pigs, as opposed to 50 mg/m for
18-month-old animals. Particle size is also important: for guinea pigs the LC™* was 30
3 3
mg/m with particles of 0.8-um diameter, as opposed to 109 mg/m with particles of 0.4-um
diameter. Bronchial spasm appeared to be the major cause of death.
Suspended particles not related to sulfur oxides are also of concern. However, because
of the wide variety of such substances, it is difficult to summarize pertinent toxicological
results. Information on the inhalational toxicology of several individual substances found in
*LCe« refers to the lethal concentration of a substance for 50 percent of tested subjects.
1-64
-------
TABLE 1-7. RESPONSES TO VARIOUS WWTICULATI MATTER MIXTURES
Source
table
12-6
12-6
12-6
12-6
12-10
12-13
12-13
Concentration Duration
100 ug/«3 1 hr
open hearth dust
500 ug/ra3 1 hr
(NH4)2SO«
750 ug/m3 1 hr
Na3V04
1000 M9/ns 1 hr
FeS04
1000 ug/n* 1 hr
HnCl2
75-1940 ug/m3 2 hr
Cd as CdCl2
100-670 ug/m3
Ni as N1C12
500-5000 ug/«3
Hn as Mn304
» 1500 ug/m3 3 hr/day
carbon; 5 day/wk,
H2S04 + 20 wk
1500 ug/»3
carbon
1100 M9/«* 3 hr
H2S04i. or
1500 yg/B3
carbon, or
combination
Species Results
guinea pig Pulmonary resistance Increased
9%; no change in pulmonary
compliance.'
Guinea pig Pulmonary resistance increased
231; pulmonary compliance
decreased 27%.
Guinea pig Pulmonary resistance Increased 7%.
Guinea pig Pulmonary resistance increased 2X.
Guinea pig Pulmonary resistance increased 4X.
House Increased mortality from sub-
sequent standard airborne
streptococcal infection at:
100 ug/m3 for CdCl2. 500 ug/n4
for NiClz, and 1550 pg/m3 for
a 4*
House Immune system altered. Morphologi-
cal changes observed; more severe
with exposure to carbon alone.
Hamster No change in ciliary beat
frequency after carbon
exposure; frequency
depressed after H2S04
exposure. Combination
produced similar effects,
but recovery occurred by
48 hr postexposure. Up to
48 hr after exposure, B2SO«
+ carbon resulted in more
tissue destruction than either
pollutant alone.
Reference
Amdur and Underbill,
1968, 1970
Amdur et al., 1978a
Amdur and Underbill,
1968
Amdur and Underbill,
1968
Amdur and Underbill,
1968
Gardner et al., 1977t>
Adkins et al., 1979,
1980
Fenters et al., 1979
Schiff et al., 1979
-------
ambient air participate matter is .summarized in Table 1-7. Relevant information
can also be derived from noninhalational toxicological studies. For example, numerous trace
metals have been found as components of airborne particulate matter. In addition to being
generally toxic, certain compounds of some of these metals, including arsenic, beryllium,
cobalt, and nickel, have been identified as carcinogenic under specific, nonrespiratory
laboratory-exposure conditions.
Silicon is ubiquitous in the earth's crust and in airborne coarse-mode particles.
Silicon dioxide (SiOg), which is responsible for the disease silicosis, is found in three
crystalline forms, which occur in the following general order of toxicity: tridymite >
cristobalite > quartz. These uncombined forms of SiO, are generally called "free silica."
Silicon dioxide is also found combined with cations in silicates. There have been few animal
toxicological studies of silicates. Several hypotheses on the etiology of silicosis have
been developed, but none has been proven. Although many animal toxicological studies of SiCL
exist, comparisons are difficult because of differences in the species and strains of animals
used, the occurrence of accidental infections, and the variations in size and crystalline form
of the SiO,, particles. Silicosis similar to that observed in man has been produced in animals
exposed to high concentrations of quartz and other Si02 dusts via intratracheal instillation
(30-50 mg) or chronic inhalation. Chronic (2.5-year) exposures of dogs to aerosols of diato-
maceous earth containing 61-percent cristobalite produced fibrotic nodules in hilar lymph
nodes, but not in the lungs.
It is difficult to assess with accuracy the toxicity of complex sulfur-containing aero-
sols in urban atmospheres based simply upon their sulfuric "acid or. sulfate content. The
chemical composition of aerosol sulfate compounds, particularly the metal or cation component,
is important in determining their relative toxicity. Since atmospheric aerosols may contain
varying proportions of sulfuric acid and ammonium or metal sulfates, it is not possible to
extrapolate from animal toxicological data obtained with single compounds to ambient environ-
mental conditions.
Liquid or solid particles, which may act as carriers for SO,,, seem to enhance the toxic
effects of the gas in some cases. Table 1-8 shows examples where the aerosols contain
solutions of salts such as sodium chloride (NaCl), manganese chloride (MnC^), or ferrous
sulfate (FeS04). Although the evidence is not clear, synergistic as well as additive toxic
effects have been observed by some investigators using sulfuric acid and ozone (see Table
1-9). In addition, conversion of SC^ to fUSO. may increase the toxic potency of SOg. On the
other hand, it may be seen from Table 1-10 that the addition of fly ash to mixtures of SO^ and
H^SO* had no significant effect.
1-66
-------
TABLE 1-8.
RESPONSES TO ACUTE EXPOSURE COMBINATIONS OF S0£ AND SOME TYPES OF PARTICULATE MATTER
Source
table Concentration Duration Species
Results
References
12-11 2.62 ug/m3 1 hr
(1.0 ppm) S02
+
1 mg/m3 NaCl
aerosol (<40% RH
and >80% RH)
12-11 2.62 jjg/m3 1 hr
(1.0 ppm) S02
+
Aerosols of
various salts
12-11 5.24 Mg/m3 1 hr
(2.0 ppm) S02
+
4, 10 mg/m3
NaCl aerosol
Guinea pig No increase in pulmonary flow
resistance at low RH; at high
RH, potentiation was marked
and evident during both early
and late parts of exposure.
McJilton et al., 1973
Guinea pig Presence of soluble salts
increased pulmonary flow
resistance about threefold.
The potentiation was evident
early in the exposure.
Guinea pig S02 alone produced an
increase of 20% in pulmonary
flow resistance; with 10 mg/rn3
NaCl the increase was 55% and
the potentiation occurred later
in exposure; with 4 mg/m3
potentiation was reduced.
Amdur and Underhill, 1968
Amdur, 1961
-------
TABLE 1-9. RESPONSES TO ACUTE EXPOSURE COMBINATIONS OF SULFURIC ACID AMD OZONE
Source
table
12-14
Concentration
880 ug/m3
H2S04
Duration
3 hr 03
2 hr H2S04
Species
Hamster
Results
H2S04 depressed ciliary beat
frequency; by 72 hr after
Reference
Grose et al . ,
1980
1
an
CO
0.1 ppm
12-14 900 pg/m3
H2S04
+
0.1 ppm 03
12-14 1000 pg/m3
H2S04
+
0.4-0.5 ppm 03
3 hr 03
2 hr H2S04
3 days
cont.
Mouse
Rat
exposure, recovery had
occurred. Og exposure had no
effect. Sequential exposure
to Os then H2S04 decreased
ci1iary beat frequency
significantly but to a lesser
extent than that caused by
H2S04 alone.
Significant increase in
mortality in response to
airborne infections only
when 03 was given
immediately before exposure
to HgS04j in which case the
effect was additive.
Synergistic effects.
Glycoprotein synthesis was
stimulated in trachea! ring
explants; lung DNA, RNA and
protein content increased.
Gardner et al., 1977a
Last and Cross, 1978
-------
"TABLE 1-10.
i
en
to
PATHOLOGICAL RESPONSES FOLLOWING CHRONIC EXPOSURE TO SO,
IN COMBINATION WITH PARTICULATE MATTER i
ALONE MO
Source
table
12-2
12-2
12-13
12-13
Concentration
26.2 mg/ra3
(10 ppn) S02
0.37, 1.68,
3.35 ng/m3
(0.14, 0.64,
1.28 ppm) S02
0.29, 2.62,
13.1 Bg/M3
(0.11, 1.0,
5.0 ppnt) S02
560 ug/ra3
fly ash
2.62 mg/a3
(1.0 ppin) S02
Duration
72 hr
cont.
78 wk
cont.
78 wk
cont.
18 mo
Species
Mouse
Cynomolgus
monkey
Cynomolgus
monkey
Cynomolgus
monkey
Results Reference
Pathological changes in the Giddens and Fairchild,
nasal nucosa appeared after 1972
24-hr exposure and increased
in severity after 72-hr exposure.
Mice free of upper respiratory
pathogens were significantly
less affected than the control
animals. Morphological altera-
tions were qualitatively iden-
tical in both groups.
No remarkable morphological Alarie et al., 1972,
changes in the lung. 1973c
No effects on morphology. Alarie et al., 1973b
No significant effects on Alarie et al., 1975
heaatology or pulmonary
1000 ug/n3
H2S04 (MMD=0.5 ua)
500 |jg/a3
fly ash (KMD=5 us)
function during exposure. At
end of exposure to S02 +
H2S04 lungs had morphological
alterations in the bronchial
nucosa. Exposure to S02 +
H2S04 + fly ash produced similar
alterations; thus fly ash did
not enhance effect. Exposure
to H2S04 + fly ash produced
only slight alterations.
12-13
12-13
0.29, 2.62,
13.1 mg/iii3
(0.11, 1.0,
5.0 ppn) S02
560 ug/"s
fly ash
13.4 mg/ffl3
(5.1 ppn) S02
900 ug/«a
H2S04
52 wk
Guinea pig No effects on morphology.
21 hr/day
620 days
Dog
After 225 days, dogs receiving
H2S04 had a lower diffusing
capacity for CO than those
that did not receive H2S04.
No morphological changes
after 620 days. H2S04 de-
creased net lung volume and
total weight.
Alarie et al., 1973b
Lewis et al., 1969,
1973
-------
1.13. CONTROLLED HUMAN EXPOSURE STUDIES , ,
Chapter 13 discusses clinical studies of the effects of sulfur dioxide and particulate
matter on humans. Such studies provide a necessary bridge between epidemiological and animal
toxicological data for characterizing health effects induced by air pollution. Unlike com-
munity epidemioTogical studies that investigate health responses of large population groups
under highly variable ambient exposure conditions, controlled human .exposure (clinical)
studies typically evaluate much smaller numbers of subjects but under much better defined and
carefully controlled exposure conditions. In the latter type of studies, exposures to either
single pollutants or combinations of pollutants are usually carried out in environmentally
controlled chambers in which relative humidity, temperature, and pollutant concentrations are
designed to approximate representative ambient air exposure conditions, especially those
thought to be associated with the induction of acute effects.
Generally inherent in the design of controlled human exposure studies carried out in the
United States are limitations on the range or types of pollutant exposures and types of sub-
jects studied so as to assure (as approved by human rights and medical ethics committees) that
the experimental exposures to the pollutants being tested per se will not lead to serious
morbidity, irreversible illness, or death. Consequently, the types of pulmonary responses
assessed in controlled exposure studies are typiqally "transient", and "reversible." However,
depending upon the population at risk, the method of exposure, and the level of subject
activity, the so-called mild and reversible health effects measured in controlled human
exposure studies may be indicators of other, more serious, associated health effects likely to
occur if more prolonged or repeated ambient exposures to the same concentrations of pollutants
were encountered by study subjects; or the observed effects per se may be sufficient to inter-
fere with normal work or social activities of certain individuals under some ambient circum-
stances. For example, relatively small increases in airway resistance of no particular health
concern for healthy, nonsensitive adults may be of medical importance for asthmatic individ-
uals or "other sensitive groups with already compromised pulmonary functions, especially when
accompanied by symptoms associated with or indicative of the onset of more severe breathing
difficulties *for them under ambient conditions.
In general, the population groups at special risk to air pollution include the young, the
elderly, and individuals predisposed by some particular disease, such as asthma, bronchitis,
cystic fibrosis, emphysema, and cardiovascular disease. In the normal population, there are
also nondiseased but hypersensitive individuals. Such nondiseased "hyperreactors" have been
found among at least three of the distinct population groups (normal, chronic bronchitic, and
asthmatic) that have been evaluated under controlled exposure conditions in. regard to their
responses to S0? and particulate matter (Lawther, 1955; Frank et a!., 1964; Nadel et al.,
1965; Burton et al., 1969; Lawther et al., 1975; Jaeger et al., 1979; Sheppard et al.., 1980,
1981; Stacy et al., 1981).
1-70
-------
In evaluating responses of the above population groups, various investigators have as-
sessed the effects of varying the activity levels of the subjects, the mode of exposure (e.g.,
nasal, oral, oronasal, or open chamber), and the duration of exposure. One purpose of in-
creasing the activity level during exposure is to simulate outdoor exposures during daily
activities by increasing minute ventilation (Ve), i.e., the volume of air expired in one
minute. A large majority of normal subjects at rest breathe almost exclusively through the
nose with a Ve of approximately 5 to 10 liters. However, some healthy individuals may have
abnormally obstructed nasal passages or, for other reasons, regularly breathe oronasally even
at rest (Niinimaa, 1980, 1981; D'Alfonso, 1980) Also, certain population groups at risk (such
as those with asthma) include some individuals who tend to breathe orally even at rest. At
some level of increased ventilation, individuals who normally breathe through the nose at rest
also shift over to oronasal breathing. In regard to ventilation levels at which that shift
has been observed to occur, Niinimaa et al. (1980, 1981) reported a switch from nasal to
oronasal breathing at a minute volume of 35.3 ± 10.8 (mean ± S. D.) liters, and after the
switch to oronasal breathing by persistent nasal breathers (at rest), the nasal portion of Ve
decreased to 56 percent of total Ve. In addition to the studies recently published by
Niinimaa et al. (1980, 1981), D'Alfonso (1980) has also observed the shift to oronasal
breathing in response to increasing ventilation rate and found that subjects who are nasal
breathers at rest move to oronasal breathing at a mean Ve of 30 liters per minute. At maximum
exercise levels (Ve = 90 liters/minute), subjects breathe, at most, 40% of the total minute
volume through the nose.
The results of such studies are extremely important in aiding our understanding of re-
sults reviewed here as being derived from controlled human exposure studies of PM and S02-
Sulfur dioxide, for example, is very soluble in water and, when inhaled nasally, is readily
(95 to 99 percent) absorbed on the moist surfaces of the nose and upper respiratory passages
(Frank et al.., 1973). This may protect individuals breathing nasally at rest from even
relatively high levels of SOp exposure. At some level of ventilation, however, breathing
shifts from nasal to oronasal, thereby increasing the dose of S02 .reaching the tracheo-
bronchial region of the lung and probably leading to enhanced SO^ effects at ambient exposure
levels below those affecting the same individuals while breathing nasally at rest or at lower
activity levels. Forced 'oral breathing yields less nasopharyngeal absorption than either
nasal, or oronasal breathing and would be expected to yield a more intense exposure-effect
relationship than observed with either nasal or oronasal breathing. The significance of these
exposure variables can be discerned clearly when examining the results of available controlled
human exposure studies summarized below, especially in regard to S02 effects.
Sulfur dioxide has been found to affect a variety of physiological functions. These in-
clude sensory processes, subjective perceptions of irritative or painful SO effects, and more
1-71
-------
objectively measured changes in respiratory function parameters. Although the reliability of
subjective reports of perceived effects of SOp has been questioned by some, certain statements
can be made with confidence concerning SC^ effects on sensory processes. For example, exposure
to 5 ppm of SOg results uniformly in the detection of the odor of the gas,, while odor de-
tection below that level varies considerably. Other changes (e.g., alterations in electro-
encephalogram alpha rhythms or in the response of the dark adapted eye to. light) have been
reported to occur at St^-exposure levels as low as 0.20 to 0.23 ppm. The health significance
of such "sensory effects" is unclear at this time, but they would appear to be of relatively
little concern unless any .resulting discomfort or other outcome would markedly alter normal
activities of affected subjects.
Of much more concern are cardiovascular or respiratory effects found to be associated
with exposure to S0?. For healthy subjects at rest, in general, such effects have not been
^ o
consistently observed except at exposure levels above 5 ppm (13.1 mg/m ). These include, for
example, observations by Frank et al. (1962) of marked increases in pulmonary flow resistance
o
(mean = 39%) at 5 ppm (13.1 mg/m ) and consistent observations by numerous other investigators
listed in Table 1-11 of increased airway resistance or other bronchoconstrictive effects with
' o
exposures of healthy adult subjects to SO, levels of 5 ppm (13.1 mg/m ) or higher. Only Amdur
et al. (1953) have reported observations of significant cardiorespiratory effects in healthy
adults at rest following SO, exposures below 5 ppm (13.1 mg/m ), including exposures as low as
3
1 ppm (2.6 mg/m ). Other investigators (e.g., Lawther, 1955; Frank et al., 1962) have not
observed similar results in attempting to replicate the findings of Amdur et al. (1953) at
q
levels below 5 ppm-(13.1 mg/m ). Numerous accounts could be offered for this apparent dis-
crepancy in reported exposure-effect relationships for bronchoconstriction effects in healthy
adults at rest, but no clear resolution of the issue is currently available. Nevertheless,
q
available evidences points to 5.0 ppm (13.1 mg/m ) as being the most probable lowest observed
effect level for induction of bronchoconstrictive effects in healthy adults exposed to SO?
while at rest.
Probably of more crucial importance are the findings of several investigators suggesting
potentiation of SO, airway effects in normal subjects as the result of increased oral inhala-
tion of SO,, due either to forced mouth breathing or increased exercise levels or both. As in-
• ' 3
dicated in Table 1-11, for example, deep breathing of S02 at 1 ppm (2.6 mg/m ) increased spe-
cific airway resistance (SR ) significantly in comparison t& breathing air alone (Lawther et
QW •
al., 1975). Also, Melville (1970) reported greater decreases in specific airway conductance
o
(SG_.,) with oral breathing than with nasal breathing at 2.5 ppm (6.6 mg/m ) SO,; and Snell and
OiW ' fm
Luchsinger (1969) found significant decreases in maximum expiratory flow (MEFgQv) at 1 ppm
(2.6 mg/m ) S02 with oral breathing at rest but not at 0.5 ppm (1.3 mg/m ) S02- Similarly,
Jaeger et al. (1979) observed no pulmonary effects in resting normal subjects with forced oral
•3 " * '
breathing at 0.5 ppm (1.3 mg/m ) SQ~. These studies suggest possible bronchoconstriction
3
effects in healthy adults with oral breathing of 1.0 to 2.5 ppm (2.6 to 6.8 mg/m ) SOg,
1-72
-------
TABLE 1-11. SUMMARY OF STUDIES ON RESPIRATORY EFFECTS OF SO,
I
-«J
CO
Oral (0) or
Concentration Duration of Number of nasal (N) Rest (R) or h
SO- (ppra) exposure (orfns) subjects exposure exercise (E)* . Effects
HEALTHY ADULT SUBJECTS AT REST
10,15,25,50 60 1 -
9-60 5 10 Hask
5, 10 10 18 0, N
20 10 60
1-80 10-60 8-12 Hask. chaeber
N
1-45 10 46 Mask
1-8 10 14 Hask
.
R
R
R
R
R
R
Hucoclllary activity decreased
at higher cone. (>15 ppn SO.)
Airway resistance Increased
No changes In pulse rate.
resp. rate or tidal vol.
(5, 10 ppm). Bronchospasn
In two subjects at 10 pp«
Bronchoconstrlctlon
above 5 ppm
Decreased peak flow.
decreased expiratory
capacity at 2 1.6 ppn
Pulse and respiratory rates
Increased; tidal volume
Reference
Cralley, 1942
Nakanura. 1964
Lawther, 1955
Sin and Pattle, 1957
Tonono, 1961
Andur et al.,
1953
1(1-2), 5(4-7), 10 - 30
13(10-16)
1(1-2), 5(4-6),
15(14-17)
4-6
4-5
"•Mouthpiece
30
10
10
11
12 0* R
70 R
5 0« R
rate decreased at 21.0 pp*
Pulmonary flow resistance
for groups increased 39X-.
at 5 ppm and 72% at 13 ppn.
At 1 ppm, one subject had 7X
increase In flow resistance,
another a 23% decrease
Increases .In Rl (pulmonary
flow resistance) at £5 pp» SO.
Airway conductance decreased
39%. Blocked by atroplne
Increased respiratory and
Insplratory resistance
Frank et al., 1962
Frank etal., 1964
Nadel et al., 1965
Abe, 1967
-------
TABLE 1-11. (continued)
Oral (0) or
Concentration Duration of Number of nasal (N) Rest (R) or
SO, (ppa) exposure («1ns) subjects exposure exercise (E) Effects
IS, 28 10 8
1.0, 5.0 2*4 hr/d 15
and 25.0
5 270 hr 16 controls
16 exposed
5 120 9
O.N R
Charter (N) R
Charter (N) R
0 R
5-30 10 10 CO, stimulus (0)* R
1 60/08 13/12 ^Charter N/0 R
3 OS 17
0* R
Pulmnary flow resistance
Increased less with N
breathing
Significant decreases In
expiratory flow and FEV. « .
at' 25 ppn. Decreased nasal
MUCUS f Iworate at £ 5 pp«.
Responses greater after 4 hr
than after 2 hr
50% decrease In nasal MUCUS
f lowrate but number of colds
sivilar In both groups
No effect on MUCUS transport
For group as whole (12 sub*
jects) snail but significant
(14X) Increase in SR follow-
ing 25 DB by air aloRl and 26X
increase' after 25 DB SO- at 1 ppa;
but no changes detected after
nornal quiet breathing of 1-3 ppn
soz
Reference
Speizer and Frank,
19GG
Anders tn et al., 1974
Andersen et al., 1977
Wolff etal.. 19751
Uwther, 1975
2.5. 5.0. 10.0 10
0.5. 1.0, 5.0 15
1.1-3.6 30
0.50 • 1BO
Mouthpiece
OB • deep breaths
15
9
S
10
40 Chamber (0)
Nose clips
«, N
0* R
0. N* R
Greater percentage decrease In
In SG,W with 0 breathing at
all concentrations
Decreases 1n MEFcnv «C *or
group were sig, at I and S
for H lot sig. different frea
0 breathing
Deep breathing produced no
effects
No pulnonary effects seen
Nelwllle, 1970
Snell and Luchslnger,
1969
Burton et §1., 1969
Jaeger et al., 1979
-------
TABLE 1-11. (continued)
Concentration Duration of Number of
SO, (ppa) exposure (nlns) subjects
EXERCISING
5.0
5.0
5.0
5.0
3.0
1.0
0.5
0.75
0.75
i
01 0.50
0.40
0.40
0.37
0.37
RESPIRATORY
HEALTHY ADULTS
120
120
120
3
3
3
3
120
120
120
120
120
120
120
DISEASE SUBJECTS
0.3, 1.0 and 95 - 120
3,0
7.7
0.3-4
hr
6 d
6-7 d
10
11
10
10
8+9
10+8
5
4
15 controls
16 exposed
24
9
11
8
4-12
J
12 (normal)
7 (COPD)
32 normals
27 subjects
w/obstrutive
Oral (0) or
nasal (N)
exposure
0
Chamber
Chamber (0)
0
0
0
0
Chamber
Chanber
Chamber
Chanber
Chanber
Chamber
Chamber
Chamber
Chanber (N)
Chamber (N)
Rest (R) or
exercise (E)
E
E
E
R
R •*• E
«* E
R
E
E
E
E
E
E
E
R
R
R
Effects
Increased tracheobronchlal
clearance
Insignificant changes in
v .airway resistance and
arterial P0g
HHFR decreased 8.5%; Increased
tracheobronchlal clearance
Light exercise potentiates
effect of SO.. MEF.pv
decreased at 3 ppm ina above
Decrease in HMFR. FVC. FEV.0
(-8-10X) and 201 in HEFRj^
.Significantly elevated Raw
and trend toward decreased
FEF50 and FEV/FVC after SO.
exposure during heavy exercise
No pulmonary effects seen
with 0.50 ppm SO. + 0.5 pp»
No pulmonary effects
No pulmonary effects seen
with 0.4 ppm S02 alone
No pulmonary effects
No pulmonary effects
No difference In response
between groups. Slight
decrease in pulmonary
compliance but of question-
able significance
No significant changes in
airway resistance or other
effects in health subjects
Reference
Wolff et al., 1975b
von Neiding et al., 1979
Kewhouse et al., 1978
Krelsmn et al., 1976
Bates and Hazucha, 1973
Stacy et al., 1981
Linn et al., 1980
Horvath and Folinsbee, 1977;
Bedi et al. , 1979
Bedl et al., 1981
iates and Hazucha, 1973;
Hazucha and Bates, 197S
Bell et al., 1977.
Weir and Broraberg, 1972
Reichel. 1972
or patients
-------
TABLE 1-11. (continued)
i
•NJ
en
Concentration
S02 (pp«)
Glint/Ion of
exposure (ilns)
Nuaber of
subjects
Oral (0) or
nasal (N) Rest (R) or
exposure exercise <£)
Effects
Reference
ASTHMATIC SUBJECTS
I. 3, 5
1.0
0.1, 0.25, 0.5
10
5
10
7 normals
7 atopies
7 asthmatics
£ asthmatics
7 asthaatics
0» R
0* E
SB Increased significantly
at all cone for asthnatics;
only at 5 ppro for normals and
atoplc subjects. Some asth-
natics exhibited narked
dyspnea requiring bronchodlla-
tion therapy.
SR significantly increased
in the asthmatic group at
Sheppard et al. , I960
Sheppard et al., 1981
0.50
0.5
0.25, 0.5
0.30
180 40 Chamber (0)
(asthmatics) Nose clips
10 5 asthaatics
SO
120
24 asthoatlcs
19
(astlwatlcs)
0«
Charter
Chandler
0.5 and 0.25 ppii SO, and at
0.1 ppm in the two host re-
sponsive subjects. At 0.5 pp«
three asthnatics developed
wheezing and shortness of
breath.
MHFR significantly decreased
2.7i; recovery within 30 min.
Specific airway resistance
(SR ) increases were ob-
served over exercise base-
line rates for 80% of the
subjects.
No statistically significant
changes in forced vital
capacity (FVC) or specific
airway resistance (SR )
aw
No pulmonary effects seen
with 0.3 ppm S0? and 0.5
ppm N0_ exposure compared
to exercise basline
Jaeger et al., 1979
Linn tt al., 1982
Linn et al., 1982
Linn et al., 1980
1.0 ppa s 2620 pg/m3
5.0 ppa s 13,100 Mg/«3
10 ppn s 26,200 M9/B3
50 pp« s 131,000 pg/>3
afl.l pp« S02 S 262 pg/«a
0.5 ppa S02 s 1310 jig/a3
Significant increase or decreases noted here refer to "statistically significant* effects, independent of whether the
observed effects are "•edically significant" or not..
Chronic obstructed pulaonary disease.
•Mouthpiece 08 = deep breaths
-------
raising the possibility of such effects being seen at similar concentrations in healthy adults
exercising at sufficient workloads to induce .a shift to oronasal breathing.
Examining the effects of~ exercise, Kreisman et a.1. (-1976) found that light exercise
potentiated the effect of SO,, with ^^AQ% being significantly decreased with exercise during
oral exposure of normal subjects to 3 ppm (7.9 mg/m.) SO, or above. Another study, by Bates
and Hazucha (1973), reported a 20 percent (but not statistically significant) decrease in MEFR
o
with 0.75 ppm (2.0 mg/m ) exposure of exercising adults in an open chamber; «md Stacy et al.
(1981) reported slight but statistically significant SR increases in healthy adults exposed
•3 clW
to 0.75 ppm (2.0 mg/m ) SO, while exercising in a controlled exposure chamber. These effects
were the only significant ones found among numerous pulmonary function test results even under
rather extreme exercise conditions employed in the Stacy et al. (1981) study. These results
(Bates and Hazucha, 1973; Stacy et al . 1981) therefore provide only very weak evidence for
3
effects in exercising healthy adults at SO, levels <1.0 ppm (2.6 mg/m ). In other studies, no
pulmonary effects were observed with chamber exposures of exercising healthy adults at SO,
3 •
exposure levels of 0.50, 0.40, or 0.37 ppm (1.31, 1.05, or 0.97 mg/m ) (Horvath and Folinsbee,
1977; Bedi et al., 1979; Bates and Hazucha, 1973; Hazucha and Bates, 1975; Bell et al., 1977;
Linn et al., 1980; Bedi et al., 1981). The weight- of available evidence, therefore, appears
to indicate that induction of pulmonary mechanical function effects may occur with exposure to
2
concentrations of 1 to 3 ppm (2.6 to 7.9 mg/m ) SO, or higher in exercising healthy adults but
3
not at S0.50 ppm (1.31 mg/m ) S02 even with exercise or forced oral breathing.
In attempting to define populations at special risk for SO, effects, Weir and Bromberg
(1972) and Reichel (1972) exposed patients with obstructive pulmonary disease to SO, levels
3
across the range of 0.3 to 4.0 ppm (0.8 to 10.5 mg/m ) and observed no statistically signifi-
cant increase in airway resistance or other pulmonary function effects. The exposures were
carried out while the subjects were at rest in a controlled exposure chamber, but no assess-
ment was conducted regarding possible enhanced effects of increased oral inhalation due to
exercise or forced mouth breathing. Thus, although no evidence was obtained for increased
susceptibility of these patients at rest, possibly enhanced vulnerability to SO, effects of
such subjects at elevated activity levels cannot be ruled out based on the reported results.
A clearer picture of probable enhanced susceptibility or special risk for SO^-pulmonary
function effects appears to be emerging now in regard to asthmatic subjects. For example,
Jaeger et.al. (1979) reported observing small, statistically significant (mean = 2.7%) de-
creases in MMFR levels (which recovered in 30 minutes) following forced oral exposure (by use
of nose clips) to 0.5 ppm (1.3 mg/m ) S02 of 40 asthmatic subjects at rest in a controlled
exposure chamber. Two subjects experienced delayed effects requiring medication that may have
been due to the SO, exposures. (Other uncontrolled factors, however, cannot be ruled out as
possibly having caused the delayed symptoms.) While the small pulmonary function decrements
observed by Jaeger et al. (1979) may be physiologically insignificant per se, they are
1-77
-------
suggestive of possible SCL effects occurring in asthmatic individuals at SO- levels below
those affecting nonsensitive healthy adults.
Consistent with this possibility, Sheppard et al. (1980) observed statistically signifi-
cant SR.,,, increases in subjects with clinically defined mild asthma exposed to 1, 3, or 5 ppm
ctW «j
(2,6, 7.7 or 13.1 mg/m ) SO, via mouthpieces while at rest; however, significant SR in-
creases in normal and atopic subjects occurred only at 5 ppm (13.1 mg/m ). In further
studies, Sheppard et al. (1981) observed statistically significant increases in SR with oral
n 9W
exposure of asthmatic subjects to 0.25 and 0.5 ppm (0.7 and 1.3 mg/m ) S02 via forced mouth
breathing while exercising at a moderately elevated level (Ve = 30 liters). The two most
responsive subjects of six tested experienced increased SR with oral exposure to levels as
o Q.W
low as 0.10 ppm (260 mg/m ) SO-. At 0.5 ppm three of the subjects experienced wheezing and
shortness of breath, and at 1.0 ppm all six subjects experienced such symptoms. Sheppard" et
al. (1980) also employed pharmacologic tests, which indicated that the very rapid-onset
bronchoconstriction effects seen in the asthmatic subjects are under parasympathetic neural
control, as was earlier demonstrated (Nadel et al., 1965) to be the case for normal subjects
experiencing bronchoconstriction in response to exposure to SO- at a higher level (i.e., 5
ppm) while at rest.
The Sheppard et al. (1980, 1981) results appear to demonstrate that some asthmatic sub-
jects may be approximately an order of magnitude more sensitive to SO^ exposure than normal,
nonsensitive healthy adults. That is, whereas nonsensitive healthy adults display increased
bronchoconstriction at 5 to 10 ppm while at rest and at levels possibly as low as 1 ppm with
oral or oronasal breathing, persons with clinically defined mild asthma appear to be sensitive
(as a group) down to 0.25 ppm S0? and the most sensitive (as individuals) down to 0.1 ppm
under moderate exercise (Ve = 30 liters/minute) conditions. Most importantly, with brief
10-minute exposures to SO- concentrations encountered in U.S. cities (0.1 to 0.5 ppm), Sheppard
et al, (1981) demonstrated that moderate exercise increased the bronchoconstriction produced
by S02 in subjects with mild asthma. These results were qualitatively confirmed by Linn et
al. (1982) using techniques similar to those employed by Sheppard et al. (1981). In a pilot
study by Linn et al. (1982), five asthmatic subjects were exposed, via mouthpiece, to 0.5 ppm
S0« for a period of 10 minutes while exercising (at a rate equivalent to ~400 kg-m/ min), and 4
of the 5 showed increased SR in response to the S09 exposure. Similar results using oronasal
, clW £*
0.5 ppm SO- exposure via a face mask have been recently described (see Addendum following
Chapter 1 in this volume). However, caution should be employed in regard to any attempted
extrapolation of these observed quantitative exposure-effect relationships to what might be
expected under ambient conditions. Additional research results from studies using open chamber
oronasal breathing conditions more analogous to those encountered in daily activities have
also recently been described by Linn et al. (1982). In this large-scale* chamber study employ-
ing 24 asthmatic subjects, no statistically significant pulmonary function decrements were
found with 0.5 ppm S0« exposures for 1 hour under intermittent exercising conditions. These
1-78
-------
negative results are in contrast to the findings of Sheppard et al, (1981) and Linn et al.
(1982) obtained with 0.5 ppm SO, exposure via mouthpiece while exercising. These differences
may be due to the delivery of a higher proportion of inhaled SO, to the tracheobronchial and
lung regions with mouthpiece exposure or to individual variations in bronchial reactivity to
S02 among subjects used in the different studies.
The health significance of pulmonary function changes and associated symptomatic effects
demonstrated to occur in response to SO, by the above human exposure studies is an important
issue for present air quality criteria development purposes. In contrast to the sensory
effects of SO- earlier described as probably being of little health significance, much more
concern is generally accorded to the potential health effects of pulmonary function changes
(such as increased bronchoconstriction) and associated symptomatic effects (such as coughing,
wheezing, and dyspnea or shortness of breath) observed with human exposures to SO,, especially
in sensitive population groups such as those having asthma. Temporary, small decrements in
pulmonary airway functions observed in some of the above studies for nonsensitive healthy
adults at SO- concentrations of greater than 1 to 5 ppm are generally of less concern in terms
of their implications regarding the potential health impact of ambient air. SO, exposures than
are the pulmonary function and symptomatic effects observed in mildly asthmatic persons at
similar (1 to 5 ppm) or lower (<1 ppm) concentrations of SO-. Probably of most concern are
marked increases (>10 percent) in airway resistance and symptomatic effects (wheezing,
dyspnea) observed by Sheppard et al. (1981) in a group of mildly asthmatic subjects with oral
3
exposure via mouthpiece to 0.5 ppm (1.3 mg/m ) SO- during exercise, although the level of SO,
exposure at which such effects might occur under ambient conditions cannote be precisely
stated at this time. A recent article (Fischl et al., 1981) and accompanying editorial
(Franklin, 1981) in the medical literature discuss the inclusion of indices of airway
obstruction and symptoms such as wheezing and dyspnea among factors to be considered in
attempting to predict the need for hospitalization of asthma patients following initial
emergency room treatment (e.g., bronchodilator therapy, etc.) for asthma attacks.
Particulate matter, especially hygroscopic salts, has been shown to be potentially
important in enhancing the. pulmonary function effects of SO- exposure. Airway resistance in-
creased more after combined exposure to SO, and sodium chloride in several studies, although
others have failed to demonstrate the same effect. This difference in response to the
SO--NaCl aerosol mixtures may be due principally to the relative humidity at the time of the
exposure. McJilton et al. (1973) have demonstrated that changes in pulmonary mechanical
function were seen in guinea pigs only when the SQp-NaCl mixture was administered at high
relative humidity (RH >80%). The effect is ascribed to absorption of the highly soluble S02
into the droplet before inhalation, whereas at RH <40% the aerosol was a crystal. Significant
reduction in MEFcnwwr was observed for the group mean after .oral exposure to a combination of
saline aerosol and 5 ppm (13.3 mg/m ) SO,; however, no effects were observed at S0£ levels of
0.5 and 1.0 ppm (1.3 and 2.6 mg/m3) (Snell and Luchsinger, 1969). The validity of this study
1-79
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has been questioned because of the lack of an air sham control group and also based on the
methodology used to measure MEFrAvr- More recently, studies have been reported showing
pulmonary function changes in extrinsic asthmatic subjects both at rest (Koenig et a!., 1980)
3 3
and during exercise (Koenig et al., 1981) with exposure to 2.62 mg/m (1 ppm) SO- and 1 mg/m
NaCl. Statistically significant decreases in certain measures of maximum expiratory flow
(V maxcfw and V 7g«) were observed both at rest and during exercise for asthmatic subjects
but not for all normal subjects. Although NaCl alone produced no such effects, the lack of a
group exposed to SO- alone and the difference in the number of subjects used with NaCl alone
or in combination with SO- make interpretation difficult.
In contrast to the apparent enhancement of S02-induced pulmonary airway effects by com-
bined exposure with certain particulate matter aerosols, there is less evidence that syner-
gistic interactions between S0? and other gaseous pollutants, such as ozone or nitrogen
dioxide, produce greater- than-additive effects on pwlmonary mechanical functions. None of the
controlled human exposure studies reviewed in Chapter 13 convincingly demonstrated such
synergistic effects.
Evidence from controlled human exposure studies regarding SO- effects on respiratory
defense mechanisms, such as mucus clearance processes, is highly limited at present. For
healthy adults exposed to S0? while at rest, nasal mucus flowrate appeared to decrease
markedly (by 50 percent) at 5.0 ppm SOy (Andersen et al., 1977), but tracheobronchial
mucociliary clearance appeared to be unaffected by SO, exposure at the same level while at
rest (Wolff et al., 1975a). These observed differences may be due to the much greater dose of
S09 delivered to nasal passages than to tracheobronchial regions by nasal breathing at rest.
3
Oral exposure of healthy adults to 5.0 ppm (13.1 mg/m ) SOg during exercise (which notably
increases tracheobronchial deposition of S02), however, was observed to- increase tracheo-
bronchial clearance rates in two studies (Wolff et al,, 1975b; Newhouse et al., 1978). No
studies, to date, have investigated whether or not repeated exposures to 5.0 ppm SD? would
continue to induce increased nasal or tracheobronchial clearance or, possibly, cause eventual
slowing of mucus clearance. (Note that one early study by Cralley [1942] reported decreased
mucociliary activity in a healthy adult exposed to high [>15 ppm] SOp concentrations while at
rest.) Nor have any controlled exposure studies investigated the effects of SO- exposure on
mucus clearance activities in asthmatic or other potentially sensitive human population
groups, such as individuals with chronic obstructive pulmonary diseases. Thus, while SOg
effects on nasal and tracheobronchial mucus clearance processes cannot be said to have been
demonstrated to occur, in sensitive population groups at exposure levels below those affecting
healthy adults, such a possibility cannot be ruled out at this time.
In addition to S02 being absorbed by hygroscopic particles, whereby its effects may be
potentiated, sulfur dioxide is also transformed during transport into sulfur trioxide which in
turn in combination with moisture forms sulfuric acid. The latter may exist as a sulfuric
acid droplet or can be converted to sul fates in the presence of ammonia, which is found in the
ambient air and in expired human breath.
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Sulfurie acid and other sulfates have been found to affect both sensory and respiratory
function in study subjects. The odor threshold for sulfuric acid has been estimated to be at
3 *i
0.75 mg/m based on one study and at 3.0 mg/m based on another.
2
Respiratory effects from exposure to sulfuric acid mist (0.35 to 0.5 mg/m ) have been
reported to include increased respiratory rate and decreased maximal inspiratory and ex-
piratory flowrates and tidal volume (Amdur et al., 1952). However, several other studies of
pulmonary function in nonsensitive healthy, adult subjects (Newhouse et al., 1978; Sackner
et al., 1978; Kleinman et al., 1978; Avol et al., 1979; Leikauf et al., 1981; Kerr et al.,
1981; Horvath et al.5 1981) indicated that pulmonary mechanical function was little affected
q
when subjects were exposed at 0.1 to 1.0 mg/m sulfuric acid for 10 to 120 minutes, although
in one study (Utell et al., 1981) the bronchoconstrictive action of carbachol was potentiated
by the sulfuric acid and sulfate aerosol, more or less in relation to their acidity.
In regard to mucociliary clearance effects, tracheobronchial clearance was significantly
o o
increased at 100 ug/m HUSCh, was not significantly altered at 300 ug/m , but was signifi-
cantly decreased at 1000 ug/m (Leikauf eta!., 1981). Although transiently depressed
q
following a single 60-minute exposure, the decreased'clearance rates seen at 1000 ug/m raise
the possibility of more persistent or chronic depression of tracheobronchial clearance after
repeated exposures to the same concentrations of sulfuric acid. The possible occurrence of
such an effect in humans would be consistent with observations of persistently slowed
clearance for several months following repeated exposures of donkeys to comparable FUSQ.
concentrations (Schlesinger et al., 1978, 1979).
In studies with asthmatic subjects, no changes in airway function have been demonstrated
O
after exposure to sulfuric acid and sulfate salts at concentrations less than 1000 ug/m .
•a
However, at concentrations higher than 1000 ug/m , reductions in specific airway conductance
(SG ) and forced expiratory volume (FEV-, g) have been observed after sulfuric acid and
ammonium bisulfate exposures, as reported by Utell et al. (1981). No studies, on the other
hand, have as yet evaluated the effects of sulfuric acid or other sulfate salt aerosols on
nasal or trancheobronchial mucus clearance functions.
Water-soluble sulfates have been the most frequent ingredients of experimental aerosol
exposure atmospheres because ambient sulfate levels were earlier reported as likely being
epidemiologically associated with morbidity. However, in addition to sulfuric acid and sul-
fates, other nonsulfur particulate matter species exist in the ambient air. These include
polycyclic organic matter (POM), lead, arsenic, selenium, ammonium salts, and carbon as dust.
Although controlled human exposure to some of these inherently toxic compounds is forbidden
for obvious reasons, several investigators have conducted clinical studies using carbon and
other inert particles.
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The relatively sparse results involving insoluble and other nonsulfur aerosols under con-
trolled human exposure conditions preclude drawing conclusions regarding quantitative exposure-
effect or dose-response relationships fo.r the particulate chemical species studied. This is
due to the fact that extremely high 'aerosol concentrations were typically employed in such
studies. Nor can any clear conclusions be drawn, based on the available controlled human
exposure data, in regard to size ranges of insoluble and other nonsulfur aerosols that may be
associated with the induction of significant respiratory system effects at, concentrations
commonly found in the ambient air (although most of the controlled exposure studies generally
appear to have employed either fine particles of <2.5 pm diameter or inhalable particles of
<10-15 urn diameter). However, the effects in polydispersed aerosol studies cannot be ascribed
to fine particles alone. Only studies by McDermott (1962), Anderson et al. (1979), and Toyoma
and Nakamura (1964) have explicitly studied the effects of larger particles but at highly
elevated levels of insoluble particulate matter not usually associated with ambient conditions.
1.14. EPIDEMIOLOGICAL STUDIES ON HEALTH EFFECTS OF PARTICULATE MATTER AND SULFUR OXIDES
Chapter 14 evaluates epidemiological literature concerning health effects associated with
ambient air exposures to particulate matter and sulfur oxides. The main focus of the chapter
is on; (1) qualitative characterization of human health effects associated with exposure to
airborne SO,, related particulate sulfur compounds, arid other PM; (2) quantitative delineation
of exposure-effect and exposure-response relationships for induction of such effects; and (3)
identification of population groups at special risk for experiencing the effects at ambient
exposure levels. The epidemiological data discussed both complement and extend information
presented as part of analyses in other health-related chapters (11, 12, and 13) of the
document. Epidemiological studies offer several advantages beyond those of animal toxicology
or controlled human exposure studies. Health effects of both short- and long-term pollutant
exposures (including complex mixtures of pollutants) can be studied and sensitive members of
populations at special risk for particular effects at ambient air concentrations identified.
Also, epidemiological evaluations allow for investigation of both acute and chronic disease
effects and associated human mortality. Epidemiological studies, then, together with
controlled animal and human exposure studies, can contribute to a more complete understanding
of the health effects of PM and SO , especially in helping to delineate human health effects
}\ "
occurring under ambient exposure conditions. Despite these advantages, however, important
limitations exist regarding the conduct, analysis, interpretation, and use of available
epideraiological studies on the health impact of PM and SOp. Such limitations, summarized
next, are discussed in more detail in Section 14.1.1 of Chapter 14 and must be taken into
account in any evaluation of epidemiological studies on PM and SO .
X
!• 14.1 Hethodologi cal Consi derations
Epidemiological studies employed to generate information for human risk assessment pur-
poses typically focus on the following: (1) defining exposure conditions; (2) identifying
1-82
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health effects; (3) relating exposures to effects; and (4) estimating overall risk of par-
ticular health effects occurring among specific population groups under ambient exposure
conditions.
One important limitation of most epidemiological studies reviewed in Chapter 14 is less-
than-optimum characterization of community air quality parameters used to estimate exposures
of population groups to atmospheric concentrations of PM and SO,,. Such characterization of
air quality generally involved relatively crude estimates of levels of pollutants present,
often allowing for only limited qualitative statements to be made regarding exposure condi-
tions (e.g., whether a given site or time period had higher or lower atmospheric levels of PM
or SOy than some other site or time period). Only rarely were measurement methods used that
provided reasonably precise determinations of ambient air concentrations of pollutants, which
were sufficient to permit quantification of approximate PM or SCL levels associated with
observed health effects; Even when reasonable quantification of community air quality para-
meters was achieved, however, the use of such data in estimating actual population exposures
was typically further constrained by factors such as siting of air sampling devices in
relation to study populations, frequency and duration of sampling periods, activity patterns
of study population members, and contributions of indoor air pollution to overall exposures of
study groups. These limitations arise in part from the fact that most presently-avail able
epidemiological studies utilized air monitoring data from sampling networks originally esta-
blished for purposes other than health-related research and, therefore, not optimally designed
to provide aerometric data of the type or quality needed for precise epidemiological
assessment of health effects related to PM and S0?. Therefore, the aerometric data reported
should be, viewed as yielding, at best, only approximate estimates of actual study population
exposures.
Inadequate characterization of health effects associated with PM and SO,, exposure condi-
tions represents another major problem with many of the epidemiological studies evaluated.
Various health endpoint measurements (mortality, morbidity, and indirect, measures of
morbidity) were employed in such studies and each has advantages and disadvantages. Some
involved direct observations of signs and symptoms of disease states or objective indicators
thought to be associated with the occurrence of illnesses, e.g., patient visits to hospitals
or clinics or absenteeism from school or work. Direct quantification of health effects also
Included measurement of biochemical or physiological changes in study populations, as in
recording of pulmonary function changes by spirometric methods. Indirect measures or indices
of health effects were also used, e;g., by gathering information on frequency and duration of
respiratory illnesses by telephone interviews, written questionnaires, or self-reported en-
tries in diaries. The validity of such indirect measurements of health effects, however, is
highly dependent on the ability and motivation of respondents to recal.l and report accurately
past or present health-related events; this can be influenced by numerous extraneous factors
such as age, cultural and educational background, instructions from experimenters, sequencing
1-83
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of questions, and interviewer variability or bias. Confidence in results obtained by either
direct or indirect measurement methods is enhanced if potentially interfering or biasing
factors are appropriately controlled for and if results are validated against corroborating
evidence, but very> few of the available epidemiological studies on PM and S02 effects
adequately addressed such methodological issues.
Adequately relating observed health effects to specific parameters of ambient exposure
conditions is another objective not often .achieved by the epidemiological studies reviewed,
such that few allow for confident qualitative or quantitative characterization of PM or S02
exposure-health effect relationships. For example, competing risks such as cigarette smoking
and occupational exposures may contribute to observed health effects results and must usually
be taken into account in order for confidence to be placed in reported air pollution-health
effects relationships; however, many studies on PM or S0? effects did not adequately control
for such factors. Similarly, possible effects of other covarying or confounding factors
(e.g., socioeconomic status, race, and meteorological parameters) were not always adequately
evaluated. Also, further complicating evaluation of the epidemiological data is the fact that
exposure parameters are not subject to experimenter control; thus, ambient levels of a given
pollutant often varied widely over the course of most studies, making it extremely.difficult
to determine whether mean concentrations, peak concentrations, rapid fluctuations in levels,
or other air quality factors were most important as determinants of reported health effects.
Significant covariation between concentrations of PM, SOo, and other pollutants also often
made it difficult to distinguish among their relative contributions to observed health
effects.
Estimation of overall risk by means of epidemiological studies requires still further
steps beyond delineation of exposure-effect relationships that define exposure conditions
(levels, durations, etc.) associated with induction of specific health effects. That is, risk
estimation also requires: (1) identification of particular population groups likely to mani-
fest health effects under exposure conditions of concern; and (2) ideally, determination of
numbers or percentages of such individuals (responders) likely to be affected at various
exposure' or dose levels. Delineation of the former, i.e., identification of population groups
at special risk at comparatively low exposure levels of SO, and PM, has only started to be
accomplished via presently available epidemiological studies. Also, epidemiological
delineation of quantitative dose-response (or, more correctly, exposure-response) relation-
ships, defining percentages of population groups likely to manifest a given health effect at
various levels or durations of exposure to PM and SO,, is largely lacking at this time.
Another limitation of the .epidemiological information concerns its usefulness in
demonstrating cause-effect relationships versus merely establishing associations (which may be
non-causal in nature) between PM or SO, and various health effects. Interpretation of epide-
miological data as an aid in inferring causal relationships has been addressed by previous
expert committees or deliberative bodies faced with evaluation of controversial biomedical
1-84
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issues (U.S. Surgeon General's Advisory Committee on Smoking and Health, 1964; U.S. Senate
Committee on Public Works, Subcommittee on Air and Water Pollution, 1968). Among criteria
selected by each group were: (1) the strength of the association; (2) the consistency of the
association, as evidenced by its repeated observation by different persons, in different
places, circumstances, and time; (3) the specificity of the association; (4) the temporal
relationship of the association; (5) the coherence of the association in being consistent with
other known facts; (6) the existence of a biological gradient, or dose-reponse curve, as
revealed by the association; and (7) the biological plausibility of the association. In dis-
cussing such criteria, Hill (1965) further noted that strong support for likely causality
suggested by an association may be derived from experimental evidence, where manipulation of
the presumed causative agent (its presence or absence, variability in intensity, etc.) also
affects the frequency or intensity of the associated effects. Importantly, Hill (1965) and
the above committees emphasized, regardless of the specific set of criteria selected by each,
that no one criterion was definitive by itself nor was it necessary that all be fulfilled in
order to support a determination of causality. Also, Hill and the committes noted that
statistical methods cannot establish proof of a causal relationship in an association nor does
lack of "statistical significance" of an association necessarily negate the possibility of a
causal relationship. That is, as stated by the U.S. Surgeon General's Advisory Committee on
Smoking and Health (1964): "The causal significance of an association is a matter of judgment
which goes beyond any statement of statistical probability." All of the above points are
important to consider in arriving at conclusions regarding the meaning and implications of the
epidemiological data evaluated in the present document.
Taking into account the above methodological limitations, the following set of guidelines
are stated in Chapter 14 and were used to judge the relative scientific quality of epidemio-
logical studies and their findings reviewed there:
1. Was the quality of the aerometric data sufficient to allow for meaningful character-
ization of geographic or temporal differences in study population pollutant ex-
posures in the range(s) of pollutant concentrations evaluated?
2. Were the study populations well-defined and adequately selected so as to allow for
meaningful comparisons between study groups or meaningful temporal analyses of
health effects results?
3. Were the health endpoint measurements meaningful and reliable, including clear defi-
nition of -diagnostic criteria and consistency in obtaining dependent variable
measurements?
4. Were the statistical analyses appropriate and properly performed and interpreted,
including accurate data handling and transfer during analyses?
5. Were potentially confounding or covarying factors adequately controlled or taken
into account in the study design and statistical analyses?
6. Are the reported findings internally consistent, biologically plausible, and coher-
ent in terms of consistency with other known facts?
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Few, if any, of the epidemiological studies reviewed dealt with all of the above points
in a.completely ideal fashion; nevertheless, these guidelines provided benchmarks for judging
the relative quality of various studies and for selecting the best for detailed discussion in
Chapter 14.
Detailed critical analysis of all epidemiological studies on health effects of PM and SOp
represents an undertaking beyond the scope of the present document. Of most importance for
present purposes are those studies which provide useful quantitative information on exposure-
effect or dose-response relationships for health effects associated with ambient air levels of
PM and SOg likely to be encountered in the United States during the next 5 years. Accordingly,
the following criteria were employed in selecting studies for detailed discussion in the text
of Chapter 14:
1. Concentrations of both PM and S02 were reported, allowing for potential evaluation
of their separate or combined effects.
2. Study results provided information on quantitative relationships between health
effects and ambient air PM and S02 levels of current concern (i.e., generally < 1000
ug/m3).
3. Important methodological considerations were adequately addressed, especially (a) in
controlling for likely potentially confounding factors and (b) in carrying out data
collection, analysis, and interpretation so as to minimize errors or potential
biases which could be reasonably expected to affect the results.
4. The study results have been reported in the open literature or are in press, typi-
cally after having undergone peer review.
In addition, some studies not meeting all of the above criteria are briefly discussed in
Chapter 14 as appropriate to help elucidate particular points concerning the health effects of
PM and/or SO-. Other studies found to be of very limited usefulness for present criteria
development purposes are noted in Appendix 14A of Chapter 14, along with annotated comments on
methodological or other factors tjiat limit their usefulness for present purposes.
The extensive epidemiological literature on the effects of occupational exposures to PM
and SO- presently is not reviewed in Chapter 14 for several reasons:
1. Such literature generally deals with effects of exposures to S02 or PM chemical spe-
cies at levels many times higher than those encountered in the ambient air by the
general population.
2. Populations exposed occupationally mainly include healthy adults, self-selected to
some extent in terms of being better able to tolerate exposures to S02 or PM
substances than more susceptible workers seeking alternative employment or other
groups often at special risk among the general public (e.g., the old, the
chronically ill, young children, and asthmatic individuals).
3. Extrapolation of observed occupational exposure-health effects relationships (or
lack thereof) to the general public could, therefore, be potentially misleading in
demonstrating health effects among healthy workers at higher exposure levels than
would affect susceptible special risk groups in the general population.
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The occupational literature does, however, demonstrate links between acute high level or
chronic lower level exposures to SO, or many different PM chemical species and a variety of
health effects, including: pulmonary function changes, respiratory tract diseases, morpholog-
ical damage to the respiratory system, and respiratory tract cancers. The reader, is referred
to National Institute of Occupational Safety and Health (NIOSH) criteria documents and other
assessments listed in Appendix 14B of Chapter 14 for information on.health effects associated
with occupational airborne exposures to SO,-and various PM species.
1.14.2 Air QualityMeasurements
Of key importance for evaluation of epidemiological studies reviewed in Chapter 14 is a
clear understanding of physical and chemical properties of PM and S0? indexed by measurement
methods (and associated limitations) used to collect aerometric data employed in those
studies. The most crucial points discussed in Chapters 3 and 14 on the subject are summarized
here.
Three main measurement methods or variations were used to generate SO, data cited in the
epidemiological studies reviewed: (1) sulfation rate; (2) hydrogen peroxide; and (3) the
West-Gaeke (pararosaniline) methods. As noted earlier (Section 1.3), sulfation rate (lead
dioxide) methods are not SOg-specific, and atmospheric concentrations of SO, or other sulfur
compounds cannot be accurately extrapolated from the results. However, lead dioxide gauges,
widely used in Britain prior to 1960, provided aerometric data reported in some British epide-
miological studies, and sulfation rate methods were also used in some American studies. Use
of a better method, the hydrogen peroxide method, was expanded in Britain during the 1950s,
usually in tandem with apparatus for PM (smoke) monitoring, and the method was adopted in the
early 1960s as the standard S02 method for the United Kingdom National Survey of Air Pollution
and, as an QECD-recommended method, elsewhere in Europe. The method can yield reasonably
3
accurate estimates of atmospheric S0~ levels expressed in jjg/m.; but results can be affected
by factors such as temperature, atmospheric ammonia, and titration errors. Unfortunately,
little quality assurance information exists on sources and magnitudes of errors encountered in
the use of the method to obtain SO, data reported in specific British or European epidemio-
logical studies, making it difficult to assess the accuracy or precision of reported SOp
values. The West-Gaeke (pararosaniline) method was more widely used in the United States' and
is specific for SO, if properly implemented to minimize interference by nitrogen or metal
oxides; but results can also be affected by factors such as temperature and mishandling of
reagents. -Again, unfortunately, only very limited quality assurance information (see Appendix
14B of Chapter 14) has been reported for some American SO, measurements by the West-Gaeke
method but is otherwise generally lacking by which to evaluate the quality of SOg data
reported in most published American epidemiological studies.
Measurement approaches for suspended sulfates and sulfuric acid, used mainly in the
United States,, include turbidimetric and methylthymol blue methods, which usually involve
collection of samples on sulfate-free glass fiber filters by high-volume PM samplers. How-
ever, as discussed in Section 1.3, such methods usually do not differentiate between sulfates
1-87
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and sulfuric acid, and secondary formation of such products from S0~ in air drawn through the
filter can affect estimation of atmospheric sulfate levels. Essentially none of the available
epidemiological studies using sulfate aerometric data derived from these measurement methods
adequately controlled for such artifact formation; and few other studies have employed more
recently developed better sulfate measurement methods.
To be of maximum value, epidemiological studies on PM effects must utilize aerometric
methods that provide meaningful data regarding not only the mass but also the size and
chemical composition of particles present. In actual practice, most epidemiological studies
on PM effects relied on air quality data from air monitoring instruments of questionable
sampling accuracy and not specifically designed for health-related research. The resulting
data thus typically provided only limited information regarding mass, size, or chemical pro-
perties of the PH sampled.
Three measurement approaches were mainly used to obtain PM data cited in .the epidemio-
logical studies reviewed: (1) the British Smokeshade (BS) light reflectance method or vari-
ations used in Britain and Europe; (2) the American Society for Testing and Materials (ASTM)
filter-soiling light transmittance method or AISI variation used in the United States; and (3)
the high-volume sampling method widely employed in the United States. As noted in Section
1.3, the BS method in routine use typically employed standard monitoring equipment with a DJ-Q
cutpbint of ~4.5 pm. Also, as noted earlier, the BS method neither directly measures the
mass nor determines chemical composition of collected particles. Rather, reflectance of light
from the stain is measured and depends both on density of the stain and optical properties of
the collected materials, of which smoke particles composed of elemental carbon typically make
the greatest contribution. Because highly variable proportions of carbon and non-carbon PM
exist from site to site or from time to time at the same site, the same BS reflectance can be
associated with different concentrations of particles. Site-specific calibrations of reflect-
ance readings against gravimetric mass measurements are therefore necessary to obtain approxi-
mate estimates of airborne PH concentrations by the BS method. Unfortunately, such site-
specific calibration of BS reflectance readings against gravimetric mass measurements was
carried out only once in London during the 1950s. Later, in the early 1960s, additional
calibrations were carried out, e.g., some site-specific BS mass calibration curves were deter-
mined for urban areas in Britain and Europe for British National Survey and OECD work, respec-
tively. Such curves were interrelated or normalized to. define two "standard" curves: (1) a
British standard smoke curve defining relationships between PH mass and BS reflectance read-
ings for London's atmosphere in 1963, which was used to yield BS concentration estimates (in
3
|jg/m ) reported in many published British epidemiological studies; and (2) an OECD interna-
tional standard smoke curve, against which smoke reflectance measurements made elsewhere in
2
Europe were compared to yield smoke concentration estimates (in pg/m ) reported in European
studies on PM effects. Of crucial importance in assessing such studies is the fact that the
actual PM mass or smoke concentration .at a particular site may differ markedly (e.g., by
1-88
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3
factors of two or more) from the corresponding mass or concentration (in pg/m ) associated
*
with a.given reflectance reading on either of the two standard curves ; therefore, great care
must be applied in interpreting what any reported BS value in ug/m means at all. Further
complicating interpretation of smoke data used in most epidemiological studies is the lack of
specific quality assurance information for cited aerometric measurements.
The ASTM or AISI light transmittance method is similar in approach to the BS method,
having a D™ cutpoint of ~5 pm and accumulating PM as a stain on filter paper. Thus, coef-
ficient of haze (CoH) readings (like BS readings) roughly index the soiling capacity of PM in
the air, are most strongly affected by fine-mode elemental carbon particles, and do not
directly measure mass or chemical composition of PM. Attempts to relate CoHs to pg/m also
require site-specific calibration of CoH readings against side-by-side gravimetric mass
measurements, but the accuracy of such mass estimates is questionable and clearly only
applicable for the particular location(s) where carried out for a limited time period.
The high volume (hi-vol) sampler method, used in the United States to measure TSP,
directly measures the mass of the PM collected by gravimetric means. The D,-,, cutpoint for the
sampler is typically around 25 to 50 pm, and collection of larger particles tends to drop off
rapidly above such cutpoints. Thus, the hi-vol sampler, as typically employed, collects both
fine- and coarse-mode particles that may include windblown crustal material of natural origin
(especially in dry,rural areas). Only rarely have cyclone samplers or other variations of the
hi-vol sampler with smaller size cutpoints been used in epidemiological studies to limit
collected particles to an inhalable range, but even then the cutpoints achieved were not sharp
or independent of w}
comparisons of amounts of PM present at a given time versus another time at the same site and
generally do not permit meaningful comparisons between PM levels at different geographic areas
having airborne PM of different chemical composition (especially in terms of relative porpor-
tions of elemental carbon).
1-89
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Holland et a!,, 1979). One exception was during severe London air pollution episodes, when
low wind speeds resulted^in settling out of large coarse-mode particles and smaller particles
3
increased to levels (>500 ug/m ) such th'at BS and TSP nfeasWemefits tended to converge (as ex-
pected when fine-mode and small coarse-mode particles predominate in the PM sampled).
Taking into account the foregoing information, aerometric data cited in published epi-
demiological studies must be viewed only as very approximate estimates'of atmospheric levels
of SO-, particulate sulfur compounds, or other PM associated with reported health effects.
Further, to the extent that (1) the cited aerometric data are derived from use of techniques
with limited specificity for the substance(s) purportedly measured or (2) the relative con-
tributions of PM or SOo to observed health effects cannot be distinguished from each other or
from the effects of other covarying pollutants, then the aerometric data and associated health
effects reported might be more appropriately viewed as relatively nonspecific indicators of
the effects of air pollutant mixtures containing PM and SO .
f\
1-14.3 Acute Exposure Effects
Detailed study of human health effects due to severe air pollution episodes spans a
period of less than 50 years. The first reliable account of such episodes describes a 1930
incident in the Meuse Valley of Belgium. Dense fog covered the valley from December 1 to 5,
with low winds and large amounts of PM present. About 6,000 residents became ill and 60
deaths associated with the fog occurred on December 4-5. The people who died were only
briefly sick and the onset of acute illnesses abated rapidly when the fog dispersed. The
death rate was 10.5 times normal. During a later event, when Donora, Pennsylvania, was
blanketed by a dense fog in October 1948, 43 percent of the population of ~10,000 people was
adversely affected. Twenty persons, mostly adults with preexisting cardiopulmonary diseases,
died during or shortly after the fog due to cardiorespiratory causes. In a followup study,
increased mortality rates and morbidity effects (e.g., heart disease and chronic bronchitis)
were found among residents who reported acute illness during the 1948 episode in comparison to
those reporting no acute illness. The Meuse Valley and Donora incidents demonstrated that
severe air pollution can cause death and serious morbidity effects in human populations and
raised the possibility of PM and S02 being among the causative agents.
As shown in Table 1-12, a series of episodes was also documented in London between 1948
and 1962. Excess mortality during those episodes occurred mainly among the elderly and
chronically ill adults during periods of marked air pollution for several days. Various
factors might help to explain the excess mortality, including possible influences not only of
increased air pollution but also of high humidity (fog) and low temperatures. Regardless of
the relative contributions of such factors, a clear consensus exists that increases in mor-
tality were associated with air pollution episodes when 24-hr concentrations of both SO, and
•5 £-
BS exceeded 1000 ug/m in London; but the effects of specific pollutants acting alone or in
combination cannot be clearly distinguished.
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TABLE 1-12. EXCESS DEATHS AND POLLUTANT CONCENTRATIONS DURING SEVERE
AIR POLLUTION EPISODES IN LONDON (1948-62)
Date
Nov. 1948
Dec. 1952
Jan. 1956
Dec. 1957
Jan. 1959
Dec. 1962
Duration,
days
6
4
4
4
6
5
Deviation from
X of total
excess deaths*
750
4000
1000
750
250
700
Maximum 24-hr pollutant
concentration, |jg/md
Smoke
(BS)
2780
4460**
2830
2417
1723
3144
S02
(H202 titration)
2150
3830
1430
3335
1850
3834
*Note that the numbers of excess deaths listed represent 15 to 350 percent
increases in normal London baseline death rates during the years listed.
**Note that peak and 24-hr BS levels were likely much higher than 4460
due to rapid saturation of filter paper by collected PM.
Source: Holland et al. 1979.
Acute episodes of high air pollution also occurred in the United States since the 1948
Donora episode, but no single event reached the magnitude of the London episodes. Some pub-
lished studies (Greenburg et al., 1962, 1967; Glasser et al., 1967) suggested that increases
in mortality may have occurred during certain New York City episodes in the 1950s and 1960s,
3
when PM levels exceeded 5.0 to 8.0 CoHs and S02 exceeded 1000 |jg/m , as measured at a single
monitoring station in central Manhattan. Independent evaluation of the same New York City
data led to one published report (McCarroll and Bradley, 1966) confirming apparent associa-
tions between increased mortality and acute episodes of high PM and SOg. However, later
reexamination of the New York data and the published analyses by the Greenburg group and by
McCarroll and Bradley (1966) led Cassell et al. (1968) to question the validity of the earlier
published conclusions, especially in view of difficulties in separating air pollution episode
effects on mortality from effects of competing factors such as temperature and humidity ex-
tremes and epidemic illnesses, which appeared to exert much larger effects on death rates than
the air pollution episodes. Still further doubts about the reported associations between New
York City air pollution episodes and mortality are raised by inconsistencies in the data, such
as no evident mortality increases being associated with some days of PM and/or SO, elevations
as high or higher than those on other days reported to be associated with excess mortality.
Thus, the results of the New York City episode studies do not provide much evidence for an
association between increased mortality and episodic elevations of PM and SO,.
When a marked increase in air pollution is associated with a sudden rise in the death
rate or illness rate that lasts for a few days and when both return to normal shortly there-
after (as documented in some of the above studies), a causal relationship is strongly sug-
gested. But sudden changes in weather, which may have caused the air pollution incidents,
1-91
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must also be considered as a possible cause of the death rate increase. However, the
consistency of associations between SCL and PM elevations in London and increases in mortality
make it very unlikely'that weather changes alone provide an adequate explanation for all such
observations. This view is further reinforced by: (1) some episodes not being accompanied by
sharp falls in temperature; and (2) other weather changes of similar magnitude to those during
the pollution episodes not being associated with dramatic mortality increases in the absence
of increased levels of SO,, PM, or other pollutants. In summary, the London episode studies
provide clear evidence for substantial increases in excess mortality when the general popula-
tion was exposed over several successive days to air pollution containing SO, concentrations
3 3
S1000 ug/m in the presence of PM levels over 1000 pg/m (BS). Certain New York studies also
tentatively suggest that small increases in excess mortality may have resulted from simul-
o
taneous elevations of SO, at 1000 jig/m and PM at greater than 5.0-8.0 CoHs, but this is
much less clearly established.
Comparison of the New York City episode data and those for the Meuse Valley, Donora, and
London episodes reveals further important observations. Perhaps most striking are the much
lower estimates of excess mortality reported for the New York episodes (at most 4 to 20 per-
cent) compared to the 15 to 350 percent increases in death rate during the London episodes and
even larger mortality rate increases in Oonora and the Meuse Valley. Numerous factors might
be cited to explain the striking differences, including likely variations in the specific
chemical composition of the pollutant mixes present in the different areas and the much
greater peak levels of pollutants (including PM and/or S02) that were probably present during
the non-New York episodes. Also of probable considerable significance are two other features
typifying the episodes in the Meuse Valley, Donora, and London: (1) the presence of extremely
dense fog together with accumulating air pollutants, possibly providing the basis for trans-
formation of pollutants to potentially more toxic forms (e.g., formation of sulfuric acid
aerosol or absorption of PM into water droplet particles) resulting in more deposition of
toxic substances in tracheobronchial regions of the respiratory tract and possible effects on
mucociliarly clearance processes (see Chapters 11 and 13); and (2) the generally much more
prolonged, continuous exposures of the non-New York populations to marked elevations of the
pollutants. Examination of published New York City episode reports reveals that during such
episodes the contributing temperature inversion conditions typically intensified during
evening hours, thus accumulating air pollutants overnight. However, the inversions dissipated
during morning hours, thereby resulting in much higher peaks in PM and SO, in the mornings
than in the afternoons (when PM and S02 levels fell back to near-normal levels). This is in
contrast to the continuously high pollutant and fog levels that apparently persisted for
several (4 or more) successive days during the Meuse Valley, Donora, and London episodes, with
largest increases in mortality tending to occur on later days of each episode. Thus, although
24-hr concentrations of PM and SO, SIOOO pg/m can be stated as levels at which mortality has
notably increased, great care must be exercised in generalizing from these observations in
attempting to predict likely effects associated with comparable concentrations at other times
and locations. In particular, the prolonged or continuous nature of the high pollutant ex-
1-92
-------
posures and other interacting factors, e.g., high humidity levels, must be taken into account
as additional important determinants of mortality increases observed so far during major air
pollution episodes. Moreover, marked increases in mortality should not be expected to occur
regularly as a function of short-term peak excursions of 24-hr PM or SO, levels barely
3 '
exceeding- 1000 ug/m • Consistent with this statement are numerous examples in the epidemio-
logical literature where no detectable increases in mortality were found to occur on scattered
days when PM and/or SOy levels reached comparably high (felOOO ug/m ) 24-hr levels as on other
days (or sets of successive days) when mortality was more clearly increased.
Even more difficult to establish are to what extent smaller but significant increases in
mortality and morbidity are associated with nonepisodie 24-hr average exposures to SO, and/or
3
PM levels below 1000 (jg/m . Concisely summarized in Table 1-13 are findings from several key
studies reviewed in Chapter 14 which appear to demonstrate with a reasonably high degree of
certainty mortality and morbidity effects associated with acute (24-hr) exposures to these
pollutants. The first two studies cited, by Martin and Bradley (1960) and Martin (1964), deal
with a relatively small body of data from London in the late 1950s. No clear "threshold"
levels were revealed by their analyses regarding SOp or BS levels at which significantly
increased mortality began to occur. However, based on their findings and a reanalysis of the
Martin and Bradley data by Ware et al. (1981), mortality in the elderly and chronically ill
was clearly elevated in association with exposure to ambient air containing simultaneous S09
3
and BS levels above 1000 ug/m ; and some indications exist from these analyses that slight
increases in mortality may have been associated with nonepisodic BS and PM levels in the range
of 500 to 1000 ug/m (with greatest certainty demonstrated for levels in excess of 750 ug/m ).
Much less certainty is attached to suggestions of mortality increases at lower levels possibly
based on the Ware et al. (1981) or other reanalyses (Appendices 14D and 14E, Chapter 14) of
the Martin and Bradley data, especially in view of wide 95 percent confidence intervals
demonstrated by the reanalyses to be associated with estimation of dose-response relationships
between mortality and BS or S0~ using the Martin and Bradley (1960) data. Analyses by
Mazumdar et al. (1981) for 1958-59 to 1971-72 (Figure 1-20) are generally consistent with the
above findings but seem to suggest that the 1958-59 London winter may represent a worst-case
situation in comparison to most later winters. Still, the Mazumdar et al. (1981) and certain
other analyses (Appendix 14E, Chapter 14) of 1958-59 to 1971-72 London winter mortality data
are strongly indicative of small, but significant, increases in mortality occurring at BS
levels below 500 ug/m and, possibly, as low as 150 to 200 ug/m .
Only very limited data exist by which to attempt to delineate any specific physical and
chemical properties of PM associated with the observed increases in mortality. Taking into
consideration information noted earlier (Section 1.14.2), marked increases in fine-mode and
small coarse-mode particles to levels above 500-1000 ug/m appear, based on the reported BS
aerometric measurements, to be most clearly associated with increased mortality, although
1-93
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TABLE 1-13. SUMMARY Of THJANTITATIVE CONCLUSIONS FROM EPIDEHIOLOGICAL STUDIES RELATING HEALTH
EFFECTS TO ACUTE EXPOSURE TO AMBIENT AIR LEVELS OF S0g AND PH
Type of study
Effects observed
24-hr average pollutant level (ug/m )
BS SO,
Reference
Mortality
i
ID
Morbidity
Clear increases in daily total
mortality or excess aortality above
a 15-day moving average among the
elderly and persons with preexisting
respiratory or cardiac disease during
the London winter of 1958-59.
Analogous increases in daily
mortality in London during
1958-59 to 1971-72 winters.
>1000
>1000 Martin and Bradley
(1960); Martin (1964)
Mazuiidar et al. (1981)
Sone indications of likely increases
in daily total mortality during the
1958-59 London winter, with greatest
certainty (95X confidence) of increases
occurring at BS and SO, levels above
750 ug/ss £
Analogous indications of increased
mortality during 1958-59 to 1971-72
London winters, again with greatest
certainty at BS and S02 levels above
750 ug/nr but indications of small
increases at BS levels <500 (if/m3 and
possibly as low as 150-200 ug/ra3.
500-1000
500-1000 Martin and Bradley (1960)
Mazumdar et al. (1981)
Worsening of health status among
a group of chronic bronchitis
patients in London during
winters from 1955 to 1960.
>250-500* >500-600 Lawther (1958); Lawther
et al. (1970)
No detectable effects in most
bronchitics; but positive
associations between worsening
of health status among a
selected group of highly
sensitive chronic bronchitis
patients and London BS and S0?
levels during 1967-68 winter.
<250*
<500
Lawther et al.
(1970)
*Mote that the 250-500 ug/m3 BS levels stated here may represent somewhat higher PH concentrations than those actually
associated with the observed effects reported by Lawther et al. (1970). This is because their estimates of PM mass
(in ug/ra3 BS) were based on the D.S.I.R. calibration curve found by Waller (1964) to approximate closely a site-specific
calibration curve developed by Waller in central London in 1956, but yielding somewhat higher mass estimates than another
site-specific calibration developed by Waller a short distance away in 1963. However, the precise relationship between
estimated BS mass value based on the D.S.I.R. curve versus the 1963 Waller curve cannot be clearly determined due to
several factors, including the non-linearity of the two curves and their convergence at low BS reflectance levels.
-------
60
1 =0
I
O
i*
111
o
z
111
o
GC
Ul
a.
40 —
30
20
10
/ QUADRATIC MODEL
500
1000 1500
SMOKE (fjg/m3)
2000
2600
Figure 1-20. Hypothetical dose-response curves derived from regressing
mortality on smoke in London, England during winters 1958/59 to 1971/72,
Results obtained with linear (—) and quadratic (- -) models are depicted for
comparison.
Source; Mazumdar et al. (1981).
1-95
-------
contributions from larger coarse-mode particles cannot be completely ruled out. Nor is it
possible to state with certainty which PM chemical species were associated with the increases
in mdrtaTity. It is known that large amounts of pollutants (e.g., elemental carbon, tarry
organic matter, etc.) from incomplete combustion of coal were present in the air, and mor-
tality levels appeared to decrease as PM concentrations declined over the years? but no single
component or combinations of particu.late pollutants can clearly be'.implicated/ Neither can
the relative contributions of SO- or PM be clearly separated based on these study results, nor
can possible interactive effects with increases in humidity (fog) be completely ruled out.
Teiperature change, however, does not appear to be a key determinant in explaining mortality
effects demonstrated by the above analyses to be associated with atmospheric.elevations of PM
or SQ2.
Analysis of the Lawther morbidity studies listed in Table 1-13 suggests that acute ex-
posure to elevated 24-hr PM levels in the range of 250-500 ng/m (BS) in association with
24-hr SOo levels of 500-600 ug/m were most clearly associated with exacerbation of respi*
ratory disease symptoms among large (>1000) populations of chronically ill London bronchitis
patients. Most such patients were apparently not affected at lower BS or SO- levels. How-
ever, a smaller population (~80) of selected, highly sensitive London bronchitis patients
appeared to be affected at somewhat lower BS and S02 levels, but specific exposure-effect
levels cannot be determined on the basis of the reported data. Again, little can be said,
however, in terms of specifying physical or chemical properties of PM associated with the
observed effects beyond the comments noted above in relation to Martin's mortality studies.
Other studies, besides those of Lawther, tend to suggest that the elderly, people with
chronic cardiorespiratory diseases, and children may constitute populations at risk for mani-
festing morbidity effects in response to acute exposure to elevated atmospheric levels of SO*
and PM. Qualitatively, increases in the occurrence of cardiac and upper respiratory tract
disease symptoms, including exacerbation of preexisting chronic bronchitis (but not asthma
attacks), appear to be among the morbidity effects most clearly associated with exposures to
the ambient levels of PM and S0« evaluated in those studies and are most clearly seen at
markedly elevated levels of the two pollutants. For example, increased applications by adults
aged 45-79 for admissions to London hospitals for cardiac and respiratory morbidity most
clearly occurred^ based on the Martin (1964) study, when 24-hr BS and SO, levels approached or
3
exceeded 900-1000 |jg/m ; but Martin's data also suggest that such effects may have occurred at
somewhat lower levels, i.e., down to 500 yg/m for both S02 and BS. Similarly, American
studies by Greenburg's group appear to most clearly suggest increased cardiac and upper
respiratory morbidity, especially among the elderly, during air pollution episodes in New York
City when extremely high levels of PM (5.0-8.0 CoHs) and S02 (>1000 pg/m ) were present. On
the other hand, much less clearly demonstrated were morbidity effects related to nonepisodic
elevations in New York City of air pollution containing PM and S02- The findings of
McCarroll's group (especially as reported by Lebowitz et al., 1972), for example, suggest at
1-96
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most an increase in upper respiratory tract symptoms (e.g., coughs and colds) in certain
"sensitive" children at lower nonepisodic levels of PM or S0? in New York City. Insufficient
epidemiological information from such studies exists, however, by which to determine specific
quantitative acute exposure levels at which such "sensitive" children may have been affected.
1.14.4 Chronic ExposureEffects
Numerous studies have been performed to compare general or cause-specific mortality in
areas of lowest-to-highest pollution concentrations. However, virtually all of these studies
(1) used aerometric data of questionable accuracy or representativeness of study population
exposures, and (2) did not adequately account for the potential effects on-mortality rates of
such confounding factors as cigarette smoking, occupation, social status, or mobility differ-
ences between areas (see Appendix 14A, Chapter 14). These methodological problems preclude
accurate characterization of any quantitative relationships between mortality and air pollu-
tion parameters. Therefore, essentially no epidemiological studies are presently well-
accepted as providing valid quantitative data relating respiratory disease or other types of
mortality to chronic (annual average) exposures to PM or SO . On the other hand, the findings
f\
of certain published studies of chronic air pollution effects on mortality appeared to warrant
consideration in regard to their potential for establishing qualitative links between morta-
lity and chronic exposures to "-PM or SO . Two types of general approaches were employed in
such studies: (1) aggregation, of mortality and other information, e.g. smoking or socio-
t*
economic status data, in relation to specific individuals within the study population(s); and
(2) aggregation of analogous data for entire populations across large geographic areas, e.g.
cities, counties, or standard metropolitan statistical areas.
Among the best known examples of the first approach are the Winkelstein et al. (1967),
Winkelstein and Kantbr (1967), and Winkelstein and Gay (1971) studies of total and cause-
specific mortality in Buffalo sand Erie County, New York, during 1959 to 1961. A network of 21
sampling stations provided data on TSP (hi-vol sampler) and oxides of sulfur (non-specific
sulfation methods) for the period July 1961 to June 1963; and these aerometric data were used
to categorize geographic areas>as "low" to "high" air pollution areas. Chronic respiratory
disease mortality for white males 50 to 69 years old was reported to be about three times
higher in the high-pollution areas than in the low-pollution areas, across all economic groups
(Winkelstein et al., 1967). ffdditional positive associations in relation to TSP concentrations
were reported for both stomach cancer (Winkelstein and Kantor, 1967) and deaths from cirrhosis
of the liver (Winkelstin and Gay, 1971). However, numerous criticisms can be noted which
raise serious doubts regarding the validity of the reported findings, including the following
methodological problems: (1) the use of 1961-1963 TSP and SO measurement data as a basis for
retrospectively classifying geographic areas according to presumed past air pollution gradients
against which to compare mortality among the elderly during 1959 to 1961; (2) inadequate
controls for possible age differences between study groups that may have covaried with the air
pollution gradient used; (3) lack of information on lifetime (including occupational) exposures
1-97
-------
to PM or SOp; (4) failure to correct for smoking habits; and (5) the implausibility of some of
the reported findings, e.g., air pollution increasing mortality due to liver cirrhosis.
Later, Winkelstein (1972) attempted to correct for some of these problems by looking at smok-
ing patterns among populations living in the same study areas included in the earlier studies,
but the 1972 analyses do not adequately counter major concerns about the earlier studies. For
example, the reported 1972 follow-up investigation found no significant differences in smoking
patterns among the different study areas for females, but this finding does not adequately
control for possible smoking effects in different specific population cohorts evaluated in the
earlier studies. These studies, therefore, are of questionable validity in regard to pro-
viding credible qualitative evidence for links between PM air pollution and mortality.
The second type of approach listed as being used for evaluation of chronic air pollution
effects on mortality is typified by the work of Lave and associates. Lave and Seskin (1970)
carried out regression analyses on relationships between PM air pollution (indexed by deposit
gauges and BS measurements) in Britain and bronchitis mortality data, taking into account the
effects of socioeconomic status (SES). They reported positive associations between such
mortality and PM pollution. However, the Lave and Seskin (1970) study has been extensively
criticized in detail by others who noted difficulties in justifying inclusion of SES and air
pollution levels in the analyses as if they were completely independent variables and failure
to make direct allowance for smoking habits in the analyses. Still more basic difficulties
with the analyses derive from: (1) use of qualitative BS aerometric data expressed in terms
o
of mass concentration estimates (in [jg/m ) not appropriately obtained by means of site-
specific calibrations of reflectance readings against local gravimetric mass data; and (2)
ambiguities regarding locations of sampling devices in relation to study population resi-
dences, which raise serious questions regarding the representativeness of the aerometric data
used in estimating population PM exposures.
In three later publications (Lave and Seskin, 1972, 1977; Chappie and Lave, 1981), the
results of further extension of their cross-sectional analysis approach (Lave and Seskin,
1970) to standard metropolitan statistical areas (SMSAs) in the United States were reported.
Significant positive associations between mortality and certain air pollution variables (e.g.,
TSP and sulfate levels) were reported for 1960, 1969, and/or 1974 U.S. data, suggesting that
air pollution variables made a significant contribution to explaining differences in mortality
rates among the SMSAs. However, based on their analyses, it was not possible to quantify the
individual contributions of each air pollutant and other variables to the observed mortality
rates. Many criticisms similar to those indicated above for the earlier Lave and Seskin
(1970) publication apply here. Of crucial importance are basic difficulties associated with
all of their analyses in terms of: (1) use of aerometric data without regard to quality
assurance considerations, including use of sulfate measurements known to be of questionable
accuracy due to artifact formation during air sampling (see Sections 1.3 and 1.14.2); (2)
questions regarding the representativeness of the air pollution data used in the analyses
as estimates of actual exposures of individuals included in their study populations;
1-98
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and (3) overgeneralization of findings in extrapolating results obtained for limited air
pollutant levels or selected localities across much broader ranges of pollutants and geo-
graphic areas despite indications to the contrary. Clearly, then, no useful information on
quantitative relationships between specific concentrations of PM or SO and mortality can be
3\
derived from these published analyses. Similarly, only very limited qualitative conclusions
can be stated regarding PM or SO air pollution-mortality relationships, based on the results
A,
of these and other analogous "macroepidemiological" studies, as discussed in Chapter 14.
In regard to morbidity effects associated with chronic exposure to PM and S0?, the best
pertinent epidemiological health studies are summarized in Table 1-14. The studies by Ferris
et al. (1973, 1976) suggest that lung function decrements may occur in adults at TSP levels in
3
excess of 180 ug/m in the presence of relatively low estimated SO, levels, whereas no effects
3
were observed by the same investigators at TSP levels below 130 ug/m . Other studies (Lunn
et al., 1967) listed in Table 1-14 suggest that significant respiratory effects occur in
children in association with long-term (annual average) PM levels in the approximate range of
3 3
230-301 pg/m (BS) in association with $02 levels of 181-275 pg/m , although no clearly dis-
tinct thresholds are evident (see Figure 1-21). A later 3-year followup study (Lunn et al.,
1970) of cohorts of children from the same study population (in Sheffield, England), however,
failed to find demonstrable respiratory effects attributable to air pollution following marked
decreases in PM and S02 levels. This suggests possible recovery from earlier-detected
respiratory disease symptoms and associated decrements in pulmonary function as a result of
decreased exposure to PM or SQ2-
No particular PM chemical species can clearly be implicated as causal agents associated
with the effects observed in the studies listed in Table 1-14. Nor can potential contri-
butions of relatively large inhalable coarse-mode particles be ruled out on the basis of these
study results. It should be remembered that various occupational studies listed in Appendix
14B of Chapter 14 at least qualitatively suggest that such sized particles of many different
types of chemical composition can be associated with significant pulmonary decrements,
respiratory tract pathology, and morphological damage—at least at relatively high exposure
levels.
Only very limited information has (summarized in Table 1-15) been published (Commins and
Waller, 1967) on the chemical composition of particulate matter present in London air during
the period of some of the above epidemiological studies of associations between mortality or
morbidity effects and elevations in PM levels. Such data may provide important clues as to
possible causative agents involved in the etiology of health effects observed in London during
the 1950s and early 1960s. For the sake of comparison, information on measured chemical
components of TSP matter in U.S. cities during the early 1960s is also provided in Table 1-15.
It must be noted, however, that likely substantial differences in specific components of the
PM present in London air of the 1950s and 1960s versus the chemical composition of PM
currently present in urban aerosols over American cities argue for much caution in
1-99
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TABLE 1-14. SUMMARY OF QUANTITATIVE CONCLUSIONS FROM EPIDEMIOLOGICAL STUDIES
RELATING HEALTH EFFECTS TO CHRONIC EXPOSURE TO AMBIENT AIR PM AND S02
o
o
Type of study
Effects observed
Annual average pollutant levels (ug/m )
participate matter
BS TSP S02
Reference
Cross-sectional
(4 areas)
Longitudinal
and cross-
sectional
Longitudinal
and cross-
sectional
Likely increased frequency
of lower respiratory symp-
toms and decreased lung
function in children in
Sheffield, England
Apparent improvement in
lung function of adults
in association with decreased
PM pollution in Berlin, NH
Apparent lack of effects
and symptoms, and no apparent
decrease in lung function in
adults in Berlin, NH
230-301* - 181-275 Lunn et al.
(1967)
180 ** Ferris et al.
(1973, 1976)
80-131 ** Ferris et al.
(1973, 1976)
*Note that BS levels stated here in (jg/m3 must be viewed as only crude estimates of the approximate PM (BS) mass levels
associated with the observed health effects, given ambiguities regarding the use or non-use of site-specific calibrations
in Sheffield to derive the reported BS levels in |jg/m3.
**Note that sulfation rate methods indicated low atmospheric sulfur levels in Berlin, NH during the time of these studies.
Crude estimation of S02 levels from that data suggest that SOp levels were generally <25-50 ug/m3 and did not likely
contribute to observed health effects.
-------
iOi-
50
40
lu
t-
<
u
z
30
20
CHIST COLDS
PERSISTENT COUGH
J_
100
200
BS {pgfm3}
300
Figure 1-21, History and clinical evidence of respira-
tory disease (percent) in 5-year-olds, by pollution in
area of residence. BS (pg/m-*) levels indicated above
must be taken as only very crude approximations of
actual PM mass present due to ambiguities regarding
use of site-specific calibrations in deriving the mass
estimates.
Source: Lunn et al. (1967);
1-101
-------
TABLE 1-15, COMPARISON OF MEASURED COMPONENTS OF TSP IN U.S. CITIES (1960-1965)
AND 1-HOUR VALUES IN LONDON (1955-1963).
UNITED STATES0
LONDON
b •-•
Pollutant
Concentration ug/m
Number of Arith. Maximum
stations average 24-hour
Maximum
1-hour
Suspended Particles 291
Fractions:
Benzene-soluble organics 218
Chloride (water soluble)
Nitrates 96
Sul fates 96
Sulfuric acid
Ammonium ,_ 56
Antimony 35
Arsenic 133
Beryllium 100
Bismuth __ _ 35
Cadmium 35
Calcium
Chromium 103
Cobalt 35
Copper,. 103
Iron____, , ' 104
Lead 104
Manganese 103
Molybdenum 35
Nickel 103
Tin '_ ,_ 85"
Titanium 104
Vanadium 99
Zinc 99
Gross beta radioactivity 323
105
6.8
2.6
10.6
1.3
0.001
0.02
<0.0005
<0.0005'
0.002
0.015
<0.0005
0.09
1.58
0.79
.0.10
<0.005
0.034
0.02
0.04
0.050
0.67
1254 (TSP)
39.7
101.2
75.5
0.160
0.010
0.064
0.420
0.330
0.060
10.00
22.00
8.60
9.98
0.78
0.460
0.50
1.10
2.200
58.00
9700 (Smoke)
410
5
666
680
i
32
2
<1
2
25
22
'5
<1
1
2
1
2
24
(0.8 pCi/m3) (12.4 pCi/ra4)
3U.S. Department of Health, Education, Welfare (1970)
"Obtained from one London site.
Commins and Waller (1967)
1-102
-------
extrapolating results of London epidemiclogical studies for present criteria development
purposes.
1.14.5 ImplicationsOf Epidemiological Findings For Criteria Development Purposes
Several epidemiologies! investigations of health effects associated with exposures to PM
and SO, in London during the 1950s and 1960s (summarized in Table 1-13) appear to provide a
reliable basis by which to estimate quantitatively ambient air levels of PM a>id S02 at which
acute exposure effects are likely to be seen, under some circumstances, among certain human
population groups at special risk. More specifically, the elderly and those with preexisting
cardiorespiratory disease conditions appear to be at greatest risk for acute PM and S02 expo-
sure effects, based on the London mortality and morbidity studies summarized in Table 1-13.
As noted above, however, great care must be exercised in extrapolating from the observed
exposure-effect relationships indicated in Table 1-13 to what might be expected to occur at
other times or geographic locations. That is, acute exposure effects of the type listed in
the table may not occur at the indicated pollutant levels under different meteorological
conditions or with varying atmospheric aerosols that differ substantially in particle size and
chemical composition from those present in London during .the 1950s and 1960s. High humidity
levels (fog conditions) occurring jointly with prolonged simultaneous elevations of PM and
SOg, for example, may be required before the most marked mortality effects listed in Table
1-13 would occur.
In relation to aerosol composition, as noted earlier, it is not possible to delineate
precisely specific particle sizes or chemical species that may have been crucial in inducing
the observed health effects noted in Table 1-13. Only reasonable possibilities can be deduced
from the available epidemiologies! data and other types of information presented elsewhere in
the present document. For example, concerning the size of particles likely associated with
observed health effects, both mortality and morbidity effects increased in relation to ele-
vations in PM concentrations as indexed by BS measurements. Recently, McFarland et al. (1982)
demonstrated that the BS sampling apparatus, as typically employed in the field, was capable
of collecting particles up to about 7-9 urn MMAD, with 50 percent efficiency for ~ 4.5 pro-sized
particles, under low (2 km/hr) wind-speed conditions (see Figure 1-22). Variations in exact
configurations of BS sampler apparatus inlet tubing in the field and other conditions (e.g.,
different wind speeds) present at the time of actual BS sampling in London during the 1950s
and 1960s, however, likely resulted in some deviations (both higher and lower) in collection
efficiencies for various size particles in comparison to those depicted in Figure 1-22.
Nevertheless, it appears that, in general, particles less than 7-9 urn were sampled by the BS
apparatus, with greatest efficiency for those below 4-5 \im MMAD.
In light of the above, the mortality and morbidity effects found by studies summarized
in Table 1-13 to be associated with increases in BS levels might be most reasonably and
directly attributed to fine- and small coarse-mode particles of <7-9 pm MMAD. This would be
consistent with the potential for respiratory effects occurring as the result of significant
1-103
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100
80
60
Ul
z
ff.
40
20
1 I
I I
INLET ONLY
O 2 km/hr-
& 8 km/hr.
COMPLETE SYSTEM
O 2 km/hr
I
I I I I I
J_
2 4 6 8 10 20 30 40
AERODYNAMIC PARTICLE DIAMETER, /urn
Figure 1-22. Penetration of aerosol through the infet of the British
Smoke Shade Sampler and through the complete system,
Source: McFarland et al. (1982).
proportions of fine- and coarse-mode particles (<10~15 pm MMAD) being deposited in thoracic
(i.e., tracheobronchial and pulmonary) regions of the respiratory tract with mouth breathing,
as demonstrated by deposition studies summarized in Figure 1-19. It is unfortunate, however,
that more precise estimates of concentrations of particles in the thoracic particle (TP) range
(i.e., <10-15 urn MMAD) present in London air during the periods studied by the epidemiological
investigations listed in Table 1-13 do not exist, as would have been measured better by
presently available modified hi-vol sampling devices with relatively sharp 10- or 15-|jm
cutpoints (see Section 1.3 and Chapter 3). As it is, no simple, precise, or invariable
relationship(s) can be stated between atmospheric TP concentrations and PM levels indexed by
BS measurements demonstrated by epidemiological studies listed in Table 1-13 to be associated
with mortality and morbidity effects in London of the 1950s and 1960s. Nor can there now be
stated any precise, consistent relationships between such TP levels and fine-particle (<2.5
urn) mass or TSP (<25-50 urn) mass, as measured by presently available dichotomous or hi-vol
samplers of types alluded to in Section 1.3 or Chapter 3. However, based on present know-
ledge, it would appear that the following relationships are, in general, probably correct:
fine-particle mass < reported London BS values expressed in ug/m3 < TP mass (as defined by
particles < 10 - 15 pm MMAD) < TSP mass. Further, based on recently reported observations by
Pace et al. (1981), comparing seasonal variations in concentrations of fine-mode (<2.5 |jm)
particle, inhalable (<15 urn) particle, and TSP (<25-50 urn) particle mass in several Eastern
and Midwestern U.S. cities, it appears that TP mass may generally constitute roughly 40 to 60
percent of TSP mass currently found in atmospheric aerosols over many U.S. cities.
1-104
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In regard to chronic PM and SO, exposure-effect relationships indicated by studies
summarized in Table 1-14, it should be noted that the Lunn et al. (1967) study demonstrates
that increased risk for respiratory symptoms and pulmonary function decrements among young
school age children are associated with long-term chronic exposures to the PM and SO, levels
listed in the table. However, no clear threshold levels can clearly be discerned based on the
Lunn et al. (1967) study results, such that some small but undefined degree of risk might
exist at or below the lowest pollutant levels depicted for the "control" study population in
Figure 1-21. On, the other hand, the possibility of any increased risk existing at such
exposure levels can neither be scientifically confirmed nor denied in the absence of
additional data. The lack of any detectable similar effects being found 3 years later (in a
followup study by the same investigators) among other children of the same age or cohorts of
the same children studied earlier tends to suggest, -however, that such risks are likely
nonexistent or minimal at annual average PM or SO, levels lower than those listed in Table
1-14. The same comments presented above regarding possible relationships between BS values
listed in Table 1-13 and TP mass levels possibly associated with listed health effects also
apply here for Table 1-14.
In regard to the other chronic exposure studies (by Ferris et al.) listed in Table 1-14,
it should be noted that the results reported are for relatively small study cohorts investi-
gated for brief intervals of time over the course of several years. Also, the improvements in
lung functions (as measured by spirometric methods) in study subjects from one time point to
another (coincident with decreases in TSP levels during the same time periods as indicated by
limited air monitoring data) represent only a rather modest basis upon which to attempt to
estimate ambient air PM levels at which health effects are likely to occur in the general
population.
1-105
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Newly Available Information on Health Effects Associated with
Exposure to Sulfur Dioxide as Evaluated by Controlled Human Exposure Studies:
An Addendum to the EPA Criteria Document Entitled
Air Quality Criteria for Partial late Matter and Sulfur Oxides (December, 1982)
A-l
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The EPA document entitled "Air Quality Criteria for Particulate Matter
and Sulfur Oxides" (to which this addendum is appended) was substantively
completed in December, 1981, and made available for use in decision making
regarding possible revision by EPA of National Ambient Air Quality Standards
(NAAQS) for particulate matter (PM) and sulfur dioxide (S02). Since the 1981
completion of the Criteria Document and during its editorial preparation for
publication in its present form (December, 1982), several scientific articles,
newly published or accepted for publication in peer-reviewed journals, have
become available and appear to provide important information pertinent to
development of criteria for primary (health-related) NAAQS for SQ2. This
addendum to the Criteria Document summarizes and evaluates the newly available
studies and attempts to place their findings in perspective in relation to the
results of certain other key studies and conclusions discussed in Chapter 13
of the Criteria Document. This includes discussion of data and conclusions
bearing on such important issues as:
(1) S02 exposure levels associated with the induction of pulmonary
mechanical function effects (e.g., bronchoconstriction) in sensitive
individuals under increased activity conditions;
(2) Mechanisms of action by which such pulmonary function effects may be
mediated in sensitive individuals;
(3) Possible enhancement in sensitive individuals of SO^-induced pul-
monary function effects by combined SCL-PM aerosol exposures.
In relation to the first issue, various studies discussed in Chapter 13
of the Criteria Document indicate that the level of physical activity of human
subjects (both nonsensitive and sensitive individuals) is an important deter-
minant of SO/, exposure concentrations at which measurable changes in pulmonary
function and symptomatic effects are manifested. This is mainly due to the
fact that most human subjects, while at rest, breathe nasally (i.e., through
the nose), where more than 90 percent of inhaled S0« is normally absorbed by
the nasal mucosa and does not penetrate deeper into tracheobronchial regions
of the respiratory tract. In contrast, with increased levels of physical
activity or exercise, human subjects eventually reach a point where they shift
over to oronasal breathing, during which time up to 40-50 percent of the
inhaled air enters .via the mouth and allows for substantial amounts of S02 to
bypass nasal defense mechanisms and reach tracheobronchial regions of the
respiratory tract (Niinimaa et al., 1981). The exercise level at which such
A-2
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a shift to oronasal breathing .occurs varies vtidejy fo,p different subjects, the
mean minute volume (V ) at which such a shift occurs being 35.3 ± 10.8 1/min.
Such ventilation rates are equivalent to those experienced while engaged in
moderately strenuous day-to-day physical activities, e.g. walking at a fast
pace for some individuals or jogging for others, climbing a flight ffr two of
stairs, or lifting and carrying relatively lightweight packages or other
materials.
As discussed in Chapter 13 of the Criteria Document, various published
studies indicate that most nonsensitive, healthy adult subjects do not exper-
ience pulmonary function changes or symptomatic effects (e.g. dyspnea, chest
pains, etc.) at SO, levels below 5 ppm. However, with increased delivery of
SO- to tracheobronchial regions of the respiratory tract, due either to forced
oral breathing via a mouthpiece or increased oronasal breathing under light to
heavy exercise conditions, nonsensitive adult subjects have been reported to
experience pulmonary mechanical function changes..at SO^ exposure levels of 3
ppm or, in some cases, at levels as low as 0.75 ppm under heavy exercise
conditions without a mouthpiece. In other studies (Sheppard et al.,1981b)
certain sensitive population group subjects, i.e. individuals with clinically
defined mild asthma, were shown to be about an order of magnitude more sensi-
tive than the nonsensitive individuals. That is, statistically significant
increases in airway resistance (SR_.,) indicative of bronehoconstriction and
3w
associated symptomatic effects were reported to occur in such subjects (as a
group) at 0.5 ppm SO, under conditions of light exercise (Vjv 30 £/min) and
forced oral breathing via a mouthpiece; and in some of the most sensitive
individuals, SR increases were reported at S00 levels as low as 0.1 ppm.
3W £,
Qualitatively similar results were independently obtained in a pilot-study by
other investigators (Linn et a!., 1982a) with forced oral breathing of 0.5 ppm
S02 by mild asthmatics under light exercise conditions (at V *» 27 I/min).
The possibility was raised, then, that bronehoconstriction might be
experienced by mild asthmatic subjects in response to ambient air S02 ex-
posures at levels below 1.0 ppm. However, direct extrapolation of specific
dose-effect levels established in these controlled human exposure experiments
to ambient situations was not possible due to the use of an artifical airway
(mouthpiece) in these studies whereby the efficient SO, removal processes in
the nasal passages are bypassed. Moreover, airflow characteristics of the
oral airway show very marked differences between breathing through a mouthpiece
A-3
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and breathing through the spontaneous positioned mouth (Cole et a!., 1982),
lending support to the suggestion that SO^ removal in the oral cavity during
mouthpiece breathing is less efficient than that which occurs for unencumbered
oronasal breathing. Thus, additional research would be necessary, using
non-mouthpiece SCL exposure methods more closely approximating natural oro-
nasal breathing, before dose-effect relationships established by controlled
human exposure experiments could be extrapolated to ambient conditions.
In an initial study evaluating the effects of non-mouthpiece exposure to
SOg on exercising asthmatic subjects, Linn et al. (1982a) exposed 24 adult
mild asthmatic subjects (11 females and 13 males ranging in age from 21 to 27
years) to 0, 0.25, and 0.5 ppm SCL while engaged in unencumbered breathing
during exercise in an open chamber. The SO, exposures, conducted in a
control!ed-exposure chamber at 23°C and R.H. = 90% or higher, lasted one hour
during which 10-min. periods of exercise (mean V = 27 £/min) were alternated
with 10-min. rest periods. No statistically significant increases in SR or
associated symptoms were found in the mild asthmatic subjects with the open
chamber exposures, either to 0.25 or 0.5 ppm SOp under the light exercise
conditions employed by Linn et al. (1982a). However, given a mean V of 27
Jd/min,, it is highly probable that the exercise conditions used were not
sufficiently high to assure a shift to oronasal breathing by the study
subjects and most of them probably breathed predominately nasally during SCL
exposure while exercising. This study, then, left unresolved the issue of
whether or not significant bronchoconstriction or symptomatic effects could be
induced by SCL in mild asthmatic subjects under unencumbered oronasal
breathing conditions simulating ambient circumstances.
In another study providing important evidence bearing on this issue,
Kirkpatrick et al. (1982) compared pulmonary function and symptomatic effects
obtained with SCL exposure of exercising mild asthmatic subjects via: (a)
oral breathing; (b) oronasal breathing; or (c) nasal breathing. More
specifically, Kirkpatrick et al. (1982) studied six non-smoking young adult
subjects (4 men, 2 women), with medical histories suggestive of asthmatic
disease but neither receiving medication nor recently exhibiting respiratory
disease symptoms. These individuals exercised on a bicycle ergometer for 5
rain, at 550 kpm/min which resulted in minute ventilation rates that averaged
41-44 A/min ± 5.0-6.9 S.D. during different exposure conditions that included
A-4
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exposure to:, (a) humidified air via mouthpiece; (b) humidified air plus 0.5
ppm SOp via mouthpiece with nasal airways obstructed (oral breathing); (c)
humidified air plus 0.5 ppm SOp via a facemask (oronasal breathing); and (d)
humidified air plus 0.5 ppm SO, via facemask but with mouth occluded (nasal
breathing). Dose-response curves were additionally defined for two subjects
exposed to 0, 0.25, 0.50 and 1.0 ppm S02 or to 0, 0.50, 1.0 and 2.0 ppm SOp
via mouthpiece (orally) and facemask (oronasally). Both v"t and SRaw were
measured before and after exercise for all six subjects; and the four highest
consecutive baseline SR values for each subject were compared with their
four highest consecutive post-exposure SR values for each exposure condition,
cfW
using unpaired t-tests. In addition, further statistical evaluations of the
group response under the different exposure conditions were made by analyses
of variance (ANOVA's). The increase in SRaw resulting from breathing S02
orally was significantly (P < 0.01) greater than the increase observed after
breathing humidified air orally. SRai, was also significantly greater when
aw
breathing SOp either by the oronasal or nasal routes. An independent analysis
of variance confirmed that SO, inhalation by these asthmatic subjects produced
bronchoconstriction regardless of the mode of entry into the lungs (personal
communication from Horvath, 1982). For the group, although the increase in
SR_. was greater when subjects breathed SO, through a mouthpiece (oral) than
aw c.
when they breathed SOp from a facemask (oronasal), the difference did not
achieve statistical significance at P < 0.05. Specific symptomatic responses
(e.g. eye, nose and throat irritation or shortness of breath and cough), were
variously reported to occur for some subjects under each of the different SOp
exposure modes. The exposure of two subjects to several concentrations of SOp
demonstrated clear dose-response relationships; that is, increases in SOp
exposure levels resulted in increasingly larger SR,.( values with either oral
aLW
or oronasal breathing for each subject. However, only one subject had a
greater increase in SR to oral inhalation of SOp at 0.5 and 1.0 ppm SOp than
with oronasal exposure, whereas there were no differences seen between oral or
oronasal exposures for the other subject even up to 2 ppm SOp.
The results obtained by Kirkpatrick et al. (1982) using mouthpiece ex-
posure to 0.5 ppm SOp are in agreement with those previously described by
Sheppard et al. (1981b) and Linn et al. (1982a), in their pilot study, using
the same exposure mode. When the results of these studies on asthmatic subjects
A-5
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are compared with results from studies of nonsensitive, healthy adults it
appears that, with oral or oronasal breathing under moderate exercise .con-
ditions, asthmatic subjects are approximately an order of magnitude more
sensitive to SOy exposure than nonsensitive, healthy adults. The results of
the Kirkpatrick et al. (1982) and other studies of asthmatic subjects also
demonstrate that specific exposure-effect relationships for S0--induced in-
creases in bronchoconstriction are influenced by the level of exercise. For
example, holding exercise levels constant at a moderately high level and using
exposure to 0.5 ppm S09 via a face mask and/or mouthpiece, Kirkpatrick et al.
^ .j
(1982) demonstrated that the intensity of SO^-induced bronchoconstriction
effects in asthmatics varied as a function of mode of exposure in the fol-
lowing order: oral > oronasal > nasal. However, the observation by Kirk-
patrick et al. (1982) of significant increases in SR with facemask (oro-
<*w
nasal) exposure to 0.5 ppm SOy differs from the results obtained by Linn et
al., (1982a) in their study in which they exposed mild" asthmatics to 0.5 ppm
S0£ during exercise (V = 27 £/min) in an open chamber. This contrast in
results is most likely due to the difference in exercise levels employed in
the two studies, the exercise levels used in the Kirkpatrick et al. (1982)
study resulting in ventilation rates (mean Vg ~ 40-44 £/min) sufficiently high
to ensure orbnasal breathing with facemask exposure' whereas the exercise
levels in the;Linn et al. (1982a) study were probably nbt sufficient to induce
oronasal breathing during their open chamber exposure of exercising subjects.
This suggests that significant increases in bronchoconstriction could be
induced in asthmatic subjects with exposure to SO, levels below 1.0 ppm, if
sufficiently high exercise levels were used to ensure a shift to oronasal
breathing and, thereby, delivery of a greater proportion of inhaled SO, to
tracheobronchial regions of the respiratory tract.
In an effort to assess this possibility, Linn et al. (1982b) effectively
doubled (relative to their earlier study reported by Linn et al., 1982a) the
SO, dose rate (concentration times ventilation) by exposing 23 young adult
asthmatic subjects (21 to 27 years old) in an open chamber to 0.75 ppm SOg
during moderately heavy exercise (V = 40 £/min) for 10 min., once with un-
encumbered breathing and once under forced oral breathing conditions using
nosedips and mouthpiece. Similar exposures to clean air alone, under iden-
tical temperature (23°C) and R.H. (90%) conditions, served as the control
exposure condition. During clean-air exposures, SR... and symptoms increased
A-6
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significantly but with no meaningful differences seen between mouthpiece and
unencumbered breathing. Exposures to 0.75 ppm S02 under these conditions
produced significantly greater increases in SR than clean-air exposures,
clW
regardless of the breathing mode (the SR increases, however, being signif-
clW
icantly greater with mouthpiece exposure than with unencumbered breathing).
Symptom score changes and post-exposure forced expiratory function changes
were qualitatively similar (i.e., little or no difference between unencumbered
and mouthpiece, breathing of clean air, increased symptom scores and a large
decrement in expiratory function measures with unencumbered breathing of S02,
and a large decrement in expiratory function measures with mouthpiece breath-
ing of SCL) to ASR under SCL exposure conditions, but the excess responses
seen with mouthpiece breathing did not attain statistical significance. These
results of Linn et al. (1982b), like those of Kirkpatrick et al. (1982),
demonstrated that mouthpiece breathing can compromise upper-respiratory de-
fenses against SQ~ to the extent that respiratory function decrements are
greater than or equal to those seen with oronasal breathing via chamber and
facemask, respectively. In addition, the results of each study strongly
reinforce each other and jointly demonstrate that SQ?-induced bronchocon-
striction effects are possible at S02 levels below 1.0 ppm under exposure
conditions which closely approximate the ambient situation during exercise.
The mechanisms by which bronchoconstriction is induced by SCL appear to
include a neurally-mediated reflex, based on previous work by Nadel et al.
(1965) and Sheppard et al. (1980). It has been hypothesized that release of
chemical substances, eg. histamine, by degranulation of airway mast cells may
also be indirectly involved in the mediation of the bronchoconstriction
response. Sheppard et al. (1981 a) evaluated this possibility by means of
pharmacologic studies of the effects of disodium cromoglycate (cromolyn) on
SOp-induced bronchoconstriction. Disodium cromoglycate is known to inhibit
the release of mediators from airway mast cells. In their study, Sheppard,
Nadel and Boushey (1981a) evaluated SR responses of six exercising asth-
matics (who had marked bronchial hyperreactivity to inhaled histamine aerosol)
to oral inhalation of 0.5 ppm (3 subjects) and 1.0 ppm (3 subjects) SO,,. Each
subject was studied on three occasions, once breathing SO^-free air, once
breathing S02 with cromoglycate treatment, and a third test breathing SO*
after a lactose placebo. Data were obtained before and after 10 minutes of
exercise at a level inducing a minute ventilation of approximately 37-38
A-7
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liters. In the cromolyn study, subjects inhaled 40 mg of cromolyn 20 minutes
before the exercise and SO? exposure began. The effects of cromolyn alone were
not determined. Statistical analyses were made by t-tests. Exercise alone
did not increase SR . However, SO, inhalation resulted in increases of SR
CtW £. 3W
similar to the bronchoconstriction effects reported in the previous study by
Sheppard et al (1980). Prior treatment with cromolyn significantly (P <
0.025) decreased S0~-induced bronchoconstriction. This response was observed
in all six subjects, although the dose utilized did not completely block
bronchoconstriction in 2 of the 3 subjects breathing 1.0 ppm SO-. No sub-
jective symptomatic responses were reported. The results obtained support the
view that SO- activates parasympathetic pathways indirectly by causing de-
granylation of mast cells and the consequent release of some chemical mediator
such as histamine.
In another study, Koenig et al. (1982a) first exposed atopic adolescent
subjects (having no clinical diagnosis of asthma) to either filtered air, 1
2
mg/m NaCl droplet aerosol, 1 ppm SOp, or 1 ppm S02 + NaCl aerosol for 30
minutes while at rest. No changes in pulmonary functions were observed as a
consequence of exposures while at rest. (This is in contrast to observations
made on extrinsic asthmatics exposed for 30 or 60 minutes while at rest in an
earlier study by Koenig et al, 1980). Approximately 5-7 minutes later, the
subjects in the present study walked on a treadmill at a level of exercise
sufficient to increase their minute ventilation 5-6 times greater than their
resting ventilation (absolute ventilatory volumes not reported). The subjects
did not experience exercise-induced bronchospasm (EIB) following either of the
sham exposures (i.e. air, NaCl droplet aerosol); however, in the presence of
SO, (1 ppm) exercise-induced bronchospasm was observed in these atopic adoles-
cents. The magnitude of the exercise-induced bronchospasm for SOy alone or
SO, and NaCl droplet aerosol were the same. That is, oral inhalation of SO,
or S0? + NaCl aerosol each produced essentially similar alterations in pul-
monary functions: FEV, ~ decreased by 24% (P < 0.05; paired t-Test); V ,.g~
an(^ ^max 75% were recluced by 29 and 34% respectively (P < 0.05; paired t-Test).
While RT (total airway resistance) increased significantly following the S02 +
NaCl exposure, this measure of pulmonary function was not significantly al-
tered following S02 exposure. No statistically significant pulmonary alter-
ations were noted when these subjects exercised while breathing filtered air
or NaCl aerosol alone. Koenig et al. (1982b) have also reported on the effects
A-8
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of SOp exposure of adolescents with no. evidence of pulmonary disease. No
significant changes in pulmonary functions were observed following exposure to
S02 (1.0 ppm) or NaCl aerosol droplet alone while at rest. Only minor (but
statistically significant) reductions in FEV-, 0, (P <0.025; 3% decrease) were
seen after exposure at rest to SCk (1.0 ppm) + NaCl aerosol droplet. Table 1
summarizes the xJata obtained by Koenig et al. (1981, 1982a, 1982b) on the
three groups of adolescents they have studied. The data suggest that the
degree of sensitivity to SO- depends on the relative magnitude of preexisting
general hypersensitivity in the airways of human adolescents.
TABLE A-l. AVERAGE CHANGE (%) IN PULMONARY FUNCTION VALUES IN THREE GROUPS
OF ADOLESCENT SUBJECTS AFTER EXPOSURE TO S09 (1 ppm) PLUS NaCl DROPLET AEROSOL
(1 mg/ms) DURING MODERATE EXERCISE C2-5 min. POST EXERCISE)
Pulmonary
functional
value
RT (3 Hz)
Vmax 50
Vmax 75
FEV1.0
FRC
Extrinsic
asthmati cs
+67*
-44*
-50*
-23*
+7.0
Atopies
with EIB
+41*
-29*
-44*
-18*
+0.3
Normal s
+3.0
-8.0*
-7.0
-6.0*
+.10
* Statistically different from baseline.
Sources: Koenig, et al. (1981, 1982a, 1982b)
Previous work by Koenig et al. (1980, 1981) demonstrated that extrinsic
adolescent asthmatics, unlike all normals, were sensitive to 1 ppm SO, in the
3 •
presence of 1 mg/m NaCl droplet aerosol under conditions of either rest or
exercise via a mouthpiece. Although NaCl alone produced no such effects
(decrease in V cnw + V 75%). ^e lack of an "SO^ alone" group made
interpretation difficult.
A-9
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The most recent study by Koenig et al. (1982a) described above on atopic
non-asthmatic adolescents demonstrates that oral inhalation (mouthpiece) of
either SO^ or SOy + Nad aerosol produced essentially similar alterations in
pulmonary function parameters (FEV1 Q Vmax 5Q^ and 75^ Rj) and affects both
large and small airways. With these less sensitive adolescents, no changes in
pulmonary functions were observed after exposure at rest, in contrast to
observations (Koenig et al, 1980) made on extrinsic asthmatics at rest and
exposed for 30-60 minutes to 1.0 ppm SOp plus Img/m NaCl. The responses in
atopic non-asthmatics were less in magnitude than those in a group of previ-
ously studied adolescent extrinsic asthmatics.
The studies by Koenig et al. (1980, 1981, 1982a,b) collectively demon-
strate, in terms of pulmonary function parameters, that the sensitivity of
adolescents to SOp-induced bronchoconstriction decreases in the following
order: extrinsic asthmatics > atopies > normals.
In summary, early studies indicated that some individuals in the presumed
normal population were substantially more sensitive (i.e., hyperreacters)
under controlled exposure conditions in regard to their responses (significant
bronchospasm) to 1 ppm SOy- These subjects were often noted to have histories
of childhood asthma or of wheezing with viral upper respiratory infections.
Despite these observations, systematic study of .the effect of sulfur dioxide
on clinically defined asthmatics was not initiated until 1980, when Sheppard
et al. at the University of San Francisco and Koenig et al. at the University
of Washington both reported that, in groups of asthmatic subjects, significant
bronchoconstriction occurred on inhalation of 1.0 ppm sulfur dioxide. In some
subjects the physiologic responses were accompanied by wheezing and shortness
of breath. Subsequent studies by both of these research groups, using the
same exposure mode (mouthpiece breathing), demonstrated that extrinsic asth-
matics are more sensitive to 1 ppm SOp, under exercising conditions (V ~ 30
£/min) insufficient to induce bronchospasm. The Sheppard et al., (1980,
1981b) results and other studies (Kirkpatrick et al., 1982; Linn et al.,
1982a, b) demonstrate that some asthmatic subjects are an order of magnitude
more sensitive to SOp than nonsensitive, healthy adults. That is, whereas
nonsensitive healthy adults display increased bronchoconstriction at 5 to 10
ppm while at rest and at levels possibly as low as 1 ppm with oral or oronasal
breathing, clinically defined asthmatics appear to be more sensitive, as a
group, down to 0.25 ppm SOp and the most sensitive (as individuals) down to
A-10
-------
0.1 ppm under light to moderate exercise (V *> 30 £/min.) conditions. This
potentiation of the effect of. sulfur dioxide is attributed to both the greater
dose (concentration times volume) and the rise in inspiratory flow that ulti-
mately results in the penetration of more sulfur dioxide to the tracheobron-
chial region of the respiratory tract. Increased sensitivity to S02, less
marked than in asthmatics, has also been observed among individuals without
any signs of asthma (Koenig et a!., 1982a; Stacy et a!., 1981; Sheppard et
al., 1980), These findings, that people with asthma and atopic disorders are
more sensitive to sulfur dioxide and this sensitivity is further potentiated
by mild exercise, are consistent with the theory that bronchial hyper-re-
activity is associated with an increase in parasympathetically mediated reflex
responses in the airways (Boushey et al. 1980).
In order to circumvent the criticism associated with direct extrapolation
of the effects of SOp to the ambient situation in studies involving forced
mouth (mouthpiece) breathing, additional experiments* have been conducted by
Nadel's group (Kirkpatrick et al., 1982) at the University of San Francisco
and by Hackney's group (Linn et al., 1982a, 1982b) at the University of South-
ern California using different exposure modes. Both sets of studies demon-
strate that, mouthpiece breathing can compromise upper-respiratory defenses
against SOp' to the extent that respiratory decrements are greater than or
equal to oronasal breathing via chamber and facemasjc, respectively. In ad-
dition, these results strongly reinforce each other with respect to the im-
portance of exposure mode and exercise in inducing* bronchoconstriction and
jointly demonstrate that SO^-induced bronchoconstriction effects and assoc-
iated symptoms are possible under exposure conditions that closely approximate
the ambient situation during exercise.
The health significance of the pulmonary function changes and symptomatic
effects reported in the above studies is/jf importance in regard to decision-
making related to the setting of standards for S02. Clear and indisputable
resolution of what constitutes adverse health effects from among the effetts
demonstrated by these studies is probably not possible at this time. However,
some important considerations can be stated which may assist in making reason-
able and appropriate interpretations as to what the present results may imply
regarding the potential or likely impact of S02 exposures on sensitive members
of the general population under ambient conditions.
A-11
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First, we should note that little controversy exists regarding the seri-
ousness of full-fledged asthma attacks. That is, in the most extreme case,
status asthmaticus, which occurs in as many as 10% of adults hospitalized for
asthma (Senior and Lefrak, 1980), clearly represents a life-threatening med-
ical condition. In less extreme cases of asthma attacks, also typified by
airway constriction and various symptoms such as wheezing and dyspnea (but of
lesser degree than is seen in cases of status asthmaticus) the day-to-day
activities of affected individuals are often markedly disrupted or curtailed
until medication is administered to relieve the symptoms and to ease their
breathing.
In relation to the effects observed in the controlled human exposure
studies discussed here, it .should be emphasized that such studies are de-
signed, in accord with currently accepted medical and research ethics, to
avoid precipitating very serious asthmatic attacks or irreversible effects in
exposed subjects. The question arises, then as to what the responses observed
in the above studies may imply as far as being indications of potentially more
serious effects among members of the general population exposed to SO, in
ambient settings.
As stated in the Criteria Document, the temporary small changes in pul-
monary function observed with S0« exposures of healthy ("normal") adults to
SI. 0 ppm SO, are of much less concern than the functional changes and symptoms
observed in asthmatics in the present studies at SO, exposure levels below 1.0
ppm. Probably of most concern are the statistically significant increases in
airway resistance and symptomatic effects (wheezing, dyspnea, etc.) observed:
2
(1) with oral exposure to 0.5 ppm (1.3 mg/m ) SO- during exercise (Sheppard et
al. 1981b); (2) with oronasal exposure via facemask to the same SO, level
during exercise (Kirkpatrick et al,, 1982); or (3) with oronasal exposures to
0.75 ppm S02 during exercise in an open chamber most closely simulating likely
ambient exposure conditions (Linn et al., 1982b). Such combined airway func-
tional changes (bronchoconstriction) and symptomatic effects (wheezing, dysp-
nea, etc.) are likely to occur at 0.5-0.75 ppm SO,, in the ambient air and are
of concern in view of reports of indices of airway obstruction and presenting
symptoms such as wheezing and dyspnea being among factors considered by phy-
sicians in determining the need for hospitalization of asthma patients fol-
lowing initial emergency room treatment (e.g., bronchodialator therapy) for
asthmatic attacks.
A-12
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The numbers of individuals in the general population potentially affected
by SOy in terms of increased susceptibility to induction of airway constric-
tion and for symptoms indicative of asthmatic attacks are difficult to esti-
mate with precision, based on currently available data. However, individuals
with non-asthmatic atopic disorders (e.g., hay fever, other allergies) make up
13.25% of the U.S. population in comparison to asthmatics (NIAID, 1979) that
'are estiipated to comprise 4.5% (higher estimates have been made by Dodge and
Burrows, 1980). Also, the undetected presence of asymptomatic atopic indi-
viduals in ..studies of presumed "normal" subjects may account for the recurrent
finding of subjects "hyperreactive" to SO* who generally make up 10-20% of
study groups evaluated in controlled human exposure studies of "normal" adults.
A-13
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REFERENCES FOR ADDENDUM
1. Boushey, H.A., Holtsman, M. J., Sheller, J. R., Nadel, J. A.: State
of the art. Bronchial hyperractivity. Am. Rev. Respir. Dis. ]^[:389, 1980.
2. Cole, P., R. Forsyth and J. S. J. Haight. Respiratory Resistance
of the Oral Airway. Am. Rev. Respir. Dis. 125: 363-365 (1982)
3. Dodge, R. R., and B. Burrows. The prevalence and incidence of asthma and
asthma-like symptoms in a general population sample. Am. Rev. Respir.
Dis. 122:567-575, 1980.
4. Kirkpatrick, M. B., D. Sheppard, J. A. Nadel, and H. A. Boushey.
Effect of the oronasal breathing route on sulfur dioxide-induced
brochoconstriction in exercising asthmatic subjects. Am. Rev.
Respir. Dis. 125: 627-631 (1982)
5. Koenig, J. Q., W. E. Pierson, and R. Frank. Acute effects of inhaled S02
plus NaCl droplet aerosol on pulmonary function in asthmatic adolescents.
Environ. Res. 22:145-153, 1980.
6. Koenig, J. Q., W. E. Pierson, M. Horike, and R. Frank. Effects of SO,
plus NaCl aerosol combined with moderate exercise on pulmonary function
in asthmatic adolescents. Environ. Res. 25:340-348, 1981.
7. Koenig, J. Q., W. E. Pierson, M. Horike, and R. Frank. Bronchoconstrictor
responses to sulfur dioxide or sulfur dioxide plus sodium chloride drop-
lets in allergic, nonasthmatic adolescents. J. Allergy Clin. Immunol.
69:339, 7982(a).
8. Koenig, J. Q., W. E. Pierson, M. Horike, and R. Frank. Effects of
inhaled SO, alone and SOp + NaCl droplet aerosol on pulmonary
function in healthy adolescents exposed during rest and exercise.
Arch. Environ. Health 37: 5-9, 1982(b).
9. Linn, W. S., R. M. Bailey, D. A. Medway, T. G. Venet, L. E. Wigttman
and J. D. Hackney. Respiratory Responses of Young Adult Asthmatics to
Sulfur Dioxide Exposure under Simulated Ambient Conditions. Environ.
Res. (In press, 1982a)
10. Linn, W. S., D. A. Shamoo, C. E. Spier, L. M. Valencia, U. T. Anzar,
T. G. Venet and J. D. Hackney. Respiratory Effects of 0.75 ppm Sulfur
Dioxide in Exercising Asthmatics: Influence of Upper-Respiratory Defenses.
Environ. Res. (In press, 1982b) \
11. Nadel, J., H. Salem, B. Tamplin, and Y. Tokiwa. Mechanism of
bronchoconstriction during inhalation of sulfur dioxide. J. Appl.
Physio!. 20:164-167, 1965.
12. NIAID Asthma and other allergic diseases. U.S. Department of
Health, Education, and Welfare. NIH Publication 79-387, Washington,
D.C., 1979.
A-14
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13. Niinimaa, V., P. Cole, S. Mintz and R. J. Shephard. Gronasal distribution
of respiratory flow. Resp. Physio! 43; 69-75, 1981.
14. Senior, R.M., and S. S. Lefrak. Status Asthmaticus. In: Pulmonary
Diseases and Disorders. A.P. Fishman, ed. McGraw-Hill, New York.
pp. 593-599, 1980.
15. Sheppard, D., J. A. Nadel, and H. A. Boushey. Inhibition of sulfur
dioxide-induced bronchoconstriction by disodium cromoglycate in
asthmatic subjects. Am. Rev. Respir. Dis. 124: 257-259, 1981a.
16. Sheppard, D., A. Saisho, J. A. Nadel, and H. A. Boushey. Exercise increases
sulfur dioxide-induced bronchoconstriction in asthmatic subjects. Am.
Rev. Respir. Dis. 123:486-491, 1981b.
17, Sheppard, D., W. S. Wong, C. F. Uehara, J. A. Nadel, and H. A. Boushey.
Lower threshold and greater bronchomotor responsiveness of asthmatic
subjects to sulfur dioxide. Am Rev. Respir. Dis. ^22:873-878, 1980.
18. Stacy, R. W., D. E. House, M. Friedman, M. Hazucha, J. Green, L. Raggio,
and L. J. Roger. Effects of 0.75 ppm sulfur dioxide on pulmonary function
parameters of normal human subjects. Arch. Environ. Health, 36:172-178,
1981.
A-15
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GLOSSARY
Abiotic: Pertaining to the nonliving components of the environment, usually
refers to a physical or chemical feature of the environment or ecosystem.
Absorption: Penetration of a substance into the bulk of a solid or liquid
(cf. adsorption).
Accumulation mode: Particles formed principally by coagulation or growth
through vapor condensation of short-lived particles in nuclei mode (see
Aitken nuclei).
Acidic deposition: See Deposition.
Acidity: The quantity of hydrogen ions in solution; having a pH less than 7
(see pH).
Acute toxic effects: Effects of, relating to, or caused by a poison or toxin
and having a sudden onset, sharp rise, and short course.
Adsorption: Solid, liquid, or gas molecules, atoms, or ions retained on the
surface of a solid or liquid, as opposed to absorption, the penetration
of a substance into the bulk of the solid or liquid.
Aerodynamic diameter: The diameter of a unit density sphere having the same
settling speed (under gravity) as the particle in question of whatever
shape and density.
Aerometry: Relating to measurement of the properties or contaminants of air.
Aerosol: A suspension of liquid or solid particles in a gas.
Aitken nuclei: Those particles and ions measured by means of an instrument in
which water vapor is made to condense on particles by supersaturating the
vapor; the term "condensation nuclei" is often used synonymously.
Atmospheric aerosols: A suspension in the atmosphere of microscopic particles
of a liquid or a solid.
AISI light transmittance method: Technique for measuring ambient particulate
matter by collecting the particles on a filter paper tape to determine
the opacity of the stain expressed in terms of optical density or CoH
units per 1000 feet of air sampled.
AISI tape sampler: See AISI light transmittance method.
Alkalinity: The quantity of hydroxide ions in solution; having a pH greater
than 7 (see pH).
Anion: A negatively charged ion.
Anthropogenic emissions: Emissions resulting from the impact of human activ-
ities on the natural world.
G-l
-------
Artifact: 1. A structure in a fixed cell or tissue formed by manipulation or
by the reagent. 2. An erroneous estimate of the atmospheric 'concentra-
tion of a gaseous or parti cul ate species due to chemical or physical
modification during sampling, storage, or analysis. 3. A structure or
substance not normally present, but produced by somer external agency or
action. -ft .
Atmospheric aerosols: A suspension in the atmosphere of microscopic particles
of a liquid or a solid.
• [>•
Atmospheric turbidity: Any condition of the atmosphere that reduces its
transparency to radiation, especially to visible radiation. Cloudy or
hazy appearance in an atmosphere caused by a suspension of colloidal
liquid droplets or fine solids.
1 • 6.
Benthic macroscopic plants: Flora and fauna large enough: to be observed by
the naked eye occurring on the bottom underlying a body of water.
Beta attenuation analysis: A method of estimating mass concentrations of
particles by using the differential attenuation of electrons.
Biogenic: Produced by actions of living organisms. , <•:.
Bioindicator: Any species of plant or animal that is particularly sensitive
to a specific pollutant.
Biomass: The total amount of living organic matter in a 'given ecosystem,
usually expressed as dry weight per unit area. ;
Biosphere: The portion of the earth in which living systems are encountered,
including the lower part of the atmosphere, the hydrosphere, and the
lithosphere to a depth of about 2 kilometers.
Biota: Pertaining to the living systems of the environment, animals, plants,
and microorganisms.
Blue sky scattering: See Rayleigh scattering. -;
British Smokeshade (BS) sampler: Device used to measure the reflectance of '
particles collected on a filter and to predict mass concentrations.
Bronchoconstriction: Constriction relative to or associated with the bronchi
or their ramifications in the lungs.
Bronchospasra: Temporary narrowing of the bronchi due to violent, involuntary
contraction of the smooth muscle of the bronchi.
Carbachol (C6H15 CIN^Oa): The choline ester, carbamycholine chloride, used
principally as a miotic (pupil constrictor) in the local treatment of
glaucoma and as a bronchoconstrictor.
Carcinogenesis: The production of cancer.
G-2
-------
Cardiorespiratory effects: Influence of a substance on the functioning of the
heart and lungs.
• "f- ' ...
Cascade impactors: A device for sampling an aerosol that consists of sets of
jets of progressively smaller size and collection plates designed so that
each plate collects particles of one size range.
Catchment basin: The geological structure of a lake or stream.
Cation: A positively charged ion.
Chemoreceptor: Any isensory organ that responds to chemical stimuli.
Chemiluminescence: Emission of light as a result of a chemical reaction
without an apparent change in temperature. Used in determining concen-
tration of some pollutant gases.
Chlorosis: A disease condition of green plants seen as yellowing of green
parts of the plant.
Chronic toxic effects: Characterized by a slow progressive course of toxicity
of indefinite duration.
Ciliary beat frequency: Rate of pulsation of the minute vibratile, hairlike
processes attached to the cells lining some airways.
Cloud: A free aerodisperse system of any type having a definite form and
without regard to particle size.
Coarse particles: Airborne particles larger than 2 to 3 micrometers (MW) in
diameter, ,
Coefficient of haze (CoH): Measurement of the optical density of a sample of
suspended particulates collected by the AISI light transmittance methods.
Cohort: A group of individuals or vital statistics about them having a statis-
tical factor in common in a demographic study (as year of birth).
C°H: See Coefficient of haze.
Colorimetry method: Chemical analysis in which the amount of a chemical
substance present is found by measuring the light absorption due to its
intrinsic color or the color of another substance into which it can be
completely converted. Used in determining presence of atmospheric S02-
Condensation nuclei: See Aitken nuclei.
Condensed organic vapors: See Polycyclic organic matter.
Coulometry: A chemical technique for measuring average current strength.
G-3
-------
Critical damage point; The point at which the service life or utility of the
material ends or is severely impaired.
Crop monoculture: The agricultural practice of growing a single crop species.
Opposite of a natural ecosystem in which a wide variety of flora and
fauna interact.
Cultivar: A cultivated variety or species of crop plants. Abbreviated cv.
Also known as cultigen. ;,
r
Cyclone samplers: A centrifugal device for separating particles from an
aerosol.
Deposition: ?.
£
Acidic—Removal of acidic pollutants from the atmosphere by dry and wet
deposition. ^
Dry—Removal of pollutants from the atmosphere through interactions with
various surfaces of plants, land, and water.
Respiratory tract—Removal of inhaled particles by the respiratory tract
which depends on breathing patterns, airway geometry, and the
physical and chemical properties of the inhaled particles.
Wet—Removal of pollutants from the atmosphere by precipitation.
Dicarboxylic acids: Compounds with two carboxyl groups.
Dichotomous sampler: A device used to collect separately fine and coarse
particles from an aerosol.
Dust: Dispersion aerosols with solid particles formed by comminution or
disintegration, without regard to particle size.
Ecosystem: A functional unit of the environment that includes all organisms
and physical features within a given area. Derived from ecological
system.
Aquatic—An ecosystem functioning in a marine environment.
Terrestrial—An ecosystem functioning on the land surface of the earth.
Edaphic factors: Factor of or relating to the soil.
Electrical Aerosol Analyzer (EAA): A device for measuring the size distribu-
tion of particles of 0.01 to about 1.0 urn diameter. The particles pick
up electric charges according to their size and are then analyzed by
electrostatic precipitation and an electrometer.
Electroencephalogram alpha-rhythms: Alpha waves graphically depicted on an
electroencephalogram.
G-4
-------
Epithelium: A primary animal tissue, distinguished by closely packed cells
with little intercellular substance; covers free surfaces and lines body
cavities and ducts, such as in the respiratory tract.
Expiratory flowrate: See Pulmonary measurements.
Fine particles; Airborne particles smaller than 2 to 3 micrometers in diameter.
Flame photometric detection: A process by which a spray of metallic salts in
solution is vaporized in a very hot flame and subjected to quantitative
analysis by measuring the intensities of the spectrum lengths of the
metals present.
Fluorescence analysis: A method of chemical analysis in which a sample,
exposed to radiation of one wavelength, absorbs this radiation and reemits
radiation of the same or longer wavelength in about 10 9 second. The
intensity of reemitted radiation is almost directly proportional to the
concentration of the fluorescing material. Also known as fluorometry.
Fogs: Suspension of liquid droplets formed by condensation of vapor or atomi-
zation; the concentration of particles is sufficiently high to obscure
visibility.
Foliar uptake: Uptake through the leaves of plants.
Fugitive emissions: Air pollutants arising from human activities, such as
roadway and industrial dust, that do not emanate from a particular point,
such as an exhaust pipe or stack, and are not readily amenable to control.
Fumes: Condensation aerosols containing liquid or solid particles formed by
condensation of vapors produced by chemical action of gases or sublima-
tion.
FVC: The volume of air that can be forcibly expelled from the lungs after the
deepest inspiration.
Glycoprotein synthesis: The creation of a class of conjugated proteins con-
taining both carbohydrate and protein units.
Gravimetric mass method: Measurement technique in which the amount of the
constituents is determined by weighing.
Gravimetry: Measurement of a weight or density.
Haze: An aerosol that impedes vision and may consist of a combination of
water droplets, pollutants, and dust.
Hematology: The science of the blood; its nature, functions, and diseases.
High volume (hi-vol) sampler: A high flow-rate device used to collect par-
ticles from the atmosphere.
G-5
-------
Hilar lymph nodes: Nodes located in that part of a gland or of certain organs,
especially the lung, where the blood vessels, nerves, or ducts leave and
enter.
Hydrogen peroxide method: A titrimetric method for providing aeromatric SOg
estimates. &.
• ' - f
Hydroxyl radical: Chemical prefix indicative of the [OHJigroup.
Hygroscopic growth: Growth induced by moisture. g
IFR (Instrument Flight Rules) instrumentation: System put into effect by
Federal Aviation Administration which restricts flight in controlled air
spaces when visibility falls below 4.8 kilometers, causing the grounding
of most small aircraft. .<••..
Integrating nephelometer: See Nephelometry.
Intratracheal instillation: Process of placing material within or through the
trachea, >
Ion exchange chromatography: A chromatographic procedure in which the station-
ary phase consists of ion-exchange resins which may be acidic or basic.
Irritant potency: The relative strength of an agent that produces irritation.
Isopleth: 1. A line of equal or constant value of a given quantity with
respect to either space or time. Also known as an isogram; 2. A line
drawn through points on a graph at which a given quantity has the same
numerical value as a function of the two coordinate ^variables.
Koschmieder relationship: The inverse proportionality between visual range
and total extinction. !t
LC5o: Concentration of a substance lethal to 50 percent of tested species.
Leach: 1. The dissolving, by a liquid solvent, of soluble material from its
mixture with an insoluble solid; 2. The separation or dissolving out of
soluble constituents from a rock or ore body by percolation of water; 3.
Dissolving soluble minerals or metals out of the ore, as by the use of
percolative solutions, such as cyamide or chlorine solutions, acids, or
water. Also known as lixiviation.
Linear model: A model where all the interrelationships among the quantities
involved are expressed by linear equations which may be algebraic, dif-
ferential, or integral.
Mm: Micrometer.
Mechanical clearance: See Mucociliary action.
6-6
-------
MEFR: See Pulmonary measurement.
Megalopolis: 1. A very large city; 2. A thickly populated region centering
on a metropolis.
Methyl thymol blue method: Technique for measuring suspended sulfates and
sulfuric acid involving a collection of samples on sulfate-free glass
fiber filters by high-volume particulate matter samplers.
Middle turbinate region: Area encompassed by the concha nasalis media ossea.
Minute volume (Ve): 1 See Pulmonary measurements.
df '
Mist: Suspension of, liquid droplets formed by condensation of vapor or
atomization; the droplet diameters exceed 10 urn and in general the concen-
tration of particles is not high enough to obscure visibility.
MMFR: See Pulmonary measurements.
Morbidity: 1. The quantity or state of being diseased; 2. The ratio of the
number of sick individuals to the total population of a community.
Morphology: Structure and form of an organism at any stage of its life history.
Mortality rate: For,a given period of time, the ratio of the number of deaths
occurring per 1000 population. Also known as death rate.,
Mucociliary action: iCiliary action of the mucous membranes lining the airway
that aids in cleansing and removing irritants and aids in moving particles
to the pharyngeal regions.
Mutagenesis: An abrupt change in the genotype of an organism, not resulting
from recombinations; genetic material may undergo qualitative or quanti-
tative alteration, or rearrangement.
Nasopharyngeal absorption: The taking up of fluids, gases, or particles by
and within the nasopharynx. :
Necrotic lesions: A,cell or group of cells undergoing necrosis (i.e., dying
as a result of injury, disease, or other pathologic state).
Nephelometry: 1. The study of aerosols using the techniques of light scat-
tering. 2. Measurement of light scattering coefficient by certain
optical instruments.
Oncogenesis: Process of tumor formation.
Optical density: The degree of opacity of a translucent medium expressed by
log I_/I, where I is the intensity of the incident ray, and I is the
intensity of the transmitted ray, abbreviated OD.
G-7
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Optical particle morphology method: Techniques for identifying the character
and sources of collected particles. .«;
Oronasal breathing: Breathing through the nose and mouth.
Osmoregulation: A physiological regulatory mechanism for the maintenance of
an optimal and constant level of osmotic activity of the fluid in and
around the cells. ;
Oxidation (various types): A chemical reaction in which ascompound or radical
loses electrons 1/m that is, in which the positive valence is increased.
Pararosaniline method: Manual method for determining the concentration of
atmospheric S02. a
Bi1
Particle: Any object, solid or liquid, having definite physical boundaries in
all directions; in air pollution, practical interest concentrates on
particles less than 1 mm in diameter. f
Particulate matter (PM): Matter in the form of small airborne liquid or solid
particles. t
Pathogen: A disease-producing agent; usually refers to living organisms.
Personnel dosimeter sampling: Determination of the degree of exposure on
individuals, using survey meters, and determination of the dose received
by means of dosimeters.
pH: A measure of the effective acidity or alkalinity of a solution. It is
expressed as the negative logarithm of the hydrogen-ion_eoncentration.
Pure water has a hydrogen ion concentration equal to 10 moles per liter
at standard conditions (25°C). The negative logarithm of this quantity
is 7. Thus, pure water has a pH value of 7 (neutral). The pH scale is
usually considered as extending for 0 to 14. A pH less than 7 denotes
acidity; more than 7, alkalinity.
Phagocytosis: A mechanism by which macrophages engulf and carry away particles.
Pharyngeal regions: The chamber at the oral end of the vertebrate alimentary
canal, leading to the esophagus.
Photochemistry: The study of the effects of light on chemical reactions.
Physical damage functions: The mathematical expression linking exposure to
damage, expressed in terms appropriate to the interaction of the
pollutant and material.
Planetary boundary layer: First layer of the atmosphere extending hundreds of
meters from the earth's surface to the geostrophic wind level, including,
therefore, the surface boundary layer and the Ekman layer; above this
layer lies the free atmosphere.
G-8
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Polycyclic organic matter: Compounds including both polycyclic aromatic
hydrocarbons (homocyclics) and heterocyclic analogs, having low vapor
pressure and usually condensed on the surface of fine particles in the
atmosphere. Abbreviated POM.
Potentiation: The combined, action of two drugs, greater than the sum of the
effects of each used alone.
Primary particles (or primary aerosols): Dispersion aerosols formed from
particles that are emitted directly into the air that do not change form
in the atmosphere.
, $
Pulmonary Measurements: Measurements of the volume of air moved during a
normal or forced;inspiration or expiration, which is a reflection of
pulmonary compliance. Atmospheric pollutants can seriously impair the
volumes of air/gas exchanged during the ventilatory function. Specific
lung volume measurements include:
Tidal volume (TV)—The volume of air moved during normal inspiration.
Functional residual capacity (FRC)—The amount of air left in the lung at
the end of a normal expiration.
Expiratory reserve volume (ERV)—Air removed from the lung by forced
expiration.
Residual volume (RV)—Air that cannot be expelled from the lung.
Vital capacity—The sum of ERV, TV, and inspirational reserve volume
< (IRV).
Rales: An abnormal sound accompanying the normal sounds of respiration within
the air passages and heard on auscultation of the chest.
Rayleigh scattering: Scattering of electromagnetic radiation by bodies much
smaller than the wavelength of the radiation. For visible wavelengths,
the molecules constituting the atmosphere cause Rayleigh scattering.
Refractive index method: The ratio of the phase velocity of light in a vacuum
to that in a specified medium. Also known as refractive index; refracture
index.
RH (Relative Humidity): The dimensionless ratio of the actual vapor pressure
of water in the air to the saturation vapor pressure.
Secondary particles (or secondary aerosols): Dispersion aerosols that form in
the atmosphere as a result of chemical reactions, often involving gases.
Smaze: A combination of "smoke" and "haze".
Smog: A combination of "smoke" and "fog". Originally, this term referred to
episodes in Great Britain that were attributed to coal burning during
persistent foggy conditions. In the United States, "smog" has become
associated with urban aerosol formation during periods of high oxidant
concentrations.
G-9
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Smoke: Dispersion aerosol containing both liquid and solid particles formed
by condensation from supersaturated vapors.
Spectrometry, second-derivative: A technique for measuring ambient S02.
Spirometry: The measurement, by a form of gas meter (spirometer), of volumes
of air that can be moved in and out of the lungs.
Stomata: Plural of stoma. Any minute pore, orifice, or opening on a free
surface; specifically, one of the openings between epithelial cells of a
lymph space.
Sulfate: 1. A compound containing the [S0| ] group, as in sodium sulfate
(Na2S04); 2. A salt of sulfuric acid.
Sulfation methods: Tests used to estimate ambient SQ2 concentrations over
extended time periods.
Sulfur dioxide (S02): A toxic, irritating, colorless gas; soluble in water,
alcohol, and ether; boils at -1Q°C; used as a chemical intermediate in
paper pulping, a solvent, a disinfectant, and a preservative; emitted by
the combustion of sulfur-bearing fuels. Also known as sulfurous acid
anhydride.
Sulfur oxides: Oxides of sulfur, such as sulfur dioxide (S02) and sulfur
trioxide (SOS).
Synergism: The joint action of agents so that their combined effect is
greater than the algebraic sum of their individual effects.
Systemic: Pertaining to or affecting the body as a whole.
Telephotometry: Measurement of the apparent brightness of distant objects.
Thoracic: Of or pertaining to the chest.
Thorax: The chest.
Tidal volume (TV): See Pulmonary measurements,
Tracheobronchial region: The area encompassed by the trachea and bronchi,
Transmissometry: The technique of determining the extinction characteristics
of a medium by measuring the transmission of a light beam of known initial
intensity directed through that medium.
Troposphere: Free tropospheric exchange: The portion of the atmosphere from
the earth's surface to the tropopause; that is, the lowest 10 to 20
kilometers of the atmosphere.
Tumorigenesis: Formation of tumors.
G-10
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Turbidim'etry: A scattered-light procedure for the determination of the weight
concentration of particles in cloudy, dull, or muddy solutions; uses a
device that measures the loss in intensity of a light beam as it passes
through the solution.
Visual range: The maximum distance at which a large black object can be seen
against the horizon sky in daytime.
West-Gaeke method: See Pararosaniline method.
X-ray fluorescence: Emission by a substance of its characteristic X-ray line
spectrum upon exposure to X-rays. Also known as X-ray emission.
G-ll
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing)
1, REPORT NO,
EPA-600/8-82-Q29a
2.
3, RECIPIENT'S ACCESSION NO.
4. TITLE AND SUBTITLE
Air Quality Criteria for Participate Matter
and Sulfur Oxides. Volume I.
5, REPORT DATE
December 1982
6. PERFORMING ORGANIZATION CODE
7. AUTHOHIS)
See list of Authors, Contributors, and Reviewers
8. PERFORMING ORGANIZATION REPORT NO.
9, PERFORMING ORGANIZATION NAME AND ADDRESS
U.S. Environmental Protection Agency
• Environmental Criteria and Assessment Office
MD-52
Research Triangle Park, NG 27711
10. PROGRAM ELEMENT NO.
11. CONTRACT/GHANT NO.
12. SPONSORING AGENCY NAME AND ADDRESS
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
401 M Street, SW Washington, DC 20460
13. TYPE OF REPORT AND PERIOD COVERED
FINAL
14. SPONSORING AGENCY CODE
EPA/600/00
IB. SUPPLEMENTARY NOTES
10, ABSTRACT
The document evaluates and assesses scientific information on the health and welfare
effects associated with exposure to various concentrations of sulfur oxides and
particulate matter in ambient air. The literature through 1980-81 has been reviewed
thoroughly for information relevant to air quality criteria, although the document
is not intended as a complete and detailed review of all literature pertaining to
sulfur oxides and particulate matter. An attempt has been made to identify the major
discrepancies in our current knowledge and understanding of the effects of these
pollutants. :
Although this document is principally concerned with the health and welfare effects of
sulfur oxides and particulate matter, other scientific data are presented and evalu-
ated in order to provide a better understanding of these pollutants in the environment
To this end, the document includes chapters thatjdiscuss the chemistry and physics
of the pollutants; analytical techniques; sources; and types of emissions; environ-
mental concentrations and exposure levels; atmospheric chemistry and dispersion
modeling; acidic deposition; effects on vegetation; effects on visibility, climate,
and materials; and respiratory, physiological, toxicological, clinical, and
epidemiological aspects of human exposure.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Group
18. DISTRIBUTION STATEMENT
RELEASE UNLIMITED
19. SECURITY CLASS (ThisReport)
UNCLASSIFIED
21, NO. OF PAGES
208
2O. SECURITY CLASS (This page)
UNCLASSIFIED
22. PRICE
EPA Form 2220-1 (Rev. X-77) ' PREVIOUS EDITION is oosOLCTt
6U.S. QOVIRNMINT PWNTINQ OFFICf: J98Si-Si»6-ll6J 40635
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