United States Environmental Criteria and EPA-600/8-78-004 

Environmental Protection Assessment Office April 1978 

Agency Research Triangle Park, NC 27711 

Research and Development 

EPA Air Quality Criteria 

For Ozone and 

Other Photochemical 

Oxidants 
NOTICE 

This document is available through the Library Services Office, MD-35, U.S. 

Environmental Protection Agency, Research Triangle Park, N.C. 27711. It is also 

available from the Superintendent of Documents, U.S. Government Printing 

Office, Washington, D.C. 20402. Correspondence relating to the subject matter 

of the document should be directed to: 

Project Officer for Ozone - Photochemical Oxidants 

Environmental Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 27711 
EPA-600/8-78-004 

APRIL 1978 

AIR QUALITY CRITERIA 

FOR 

OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS 

U.S. .gcncy 

OFFICE OF RESEARCH AND UEVELOPMENT 

U.S. ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 
FOREWORD 

This document has been prepared pursuant to Section 108(c) of the Clean Air 

Act, as amended, which requires that the Administrator from time to time review 

and, as appropriate, modify and reissue criteria issued pursuant to Section 

108(a). Air quality criteria are required by Section 108(a)to reflect accuratelythe 

latest scientific information useful in indicating the kind and extent of all 

identifiable effects on public health and welfare that may be expected from the 

presence of a pollutant in the ambient air in varying quantities. 

The original criteria document for photochemical oxidants, AP-63, was issued 

in 1970. Since that time, new information has been developed, and this 

document represents the modification and reissuance of the air quality criteria 

for photochemical oxidants. 

The regulatory purpose of these criteria is to serve as the basis for national 

ambient air quality standards promulgated by the Administrator under Section 

109 of the Clean Air Act, as amended. Accordingly, as provided by Section 

109(d), the Administrator has reviewed the national ambient air quality 

standards for photochemical oxidants based on these revised criteria and is 

proposing appropriate action with respect to those standards concurrently with 

the issuance of this document. 

The Agency is pleased to acknowiedge the efforts and contributions of all 

persons and groups who have contributed to this document as participating 

authors or reviewers. In the last analysis, however, the Environmental 

Protection Agency is responsible for its content. 

DOUGLAS MtCOSTLE 

Administrator 

U.S. Environmental Protection Agency 
PREFACE 

This document consolidates and assesses current knowledge regarding the 

origin of ozone and other photochemical oxidants and discusses their effect on 

health, vegetation, certain ecosystems, and materials. 

Photochemical oxidants are products of atmospheric reactions involving 

hydrocarbons (HC), nitrogen oxides (NOx), oxygen, and sunlight. Oxid6nts consist 

mostly of ozone, nitrogen dioxide (NOz), and peroxyacetylnitrate (PAN), with 

smaller amounts of other peroxyacylnitrates, other oxy- and peroxy-compounds, 

formic and nitric acid, and formaldehyde. Usually referred to collectively as 

"oxidants," they originate mainly from human activities that produce HC and 

NOX emissions. 

This document summarizes current data on the effects of oxidant/ozone in the 

ambient air on man, vegetation, and ecosystems. The effects that have been 

observed will form the scientific basis for supporting the present National 

Ambient Air Quality Standard of 160 /ag/m3 (0.08 ppm) or a revised standard. 

Although nitrogen dioxide is considered one of the photochemical oxidants, 

oxides of nitrogen are-the subject of a separate report and are therefore 

discussed in this document only as they participate in the formation and 

reactions of other photochemical oxidants. Hydrocarbons and other organics are 

important air pollutants because they too are precursors of other compounds 

formed in the atmospheric photochemical system. In this document, toxic 

organics are considered only with respect to eye irritation. 

The studies and data cited constitute the best available basis for specific 

standards aimed at protecting human health and the environment from 

photochemical oxidants in ambient air. 
CONTRIBUTORS AND REVIEWERS 

The following individuals participated in the preparation of this document. 

Authors 

Dr. J. H. B. Garner 

Project Officer for Ozone and Other 

Photochemical Oxidants 

Environmental Criteria and Assessment Office 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Frank Black 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Robert Chapman 

Health Effects Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Kenneth L. Demerjian 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Basil Dimitriades 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Donald E. Gardner 

Health Effects Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Ms. Judith A. Graham 

Health Effects Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Fred H. Haynie 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. , 

Dr. Milan J. Hazucha 

Health Effects Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

iv 
Mr. John H. Margeson 

Environmental Monitoring and Support Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Frederick J. Miller 

Health Effects Research Laboratory 

U.S. Erlvironmental Protection Agency 

Research Triangle Park, N.C. 

Dr. Richard J. Paur 

Environmental Monitoring and Support Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Larry Purdue 

Environmental Monitoring and Support Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Robert K. Stevens 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Environmental Protection Agency Review Group 

Dr. J. H. B. Garner, Chairman 

Environmental Criteria and Assessment Office 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. John Clements 

Environmental Monitoring and Support Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Robert Fankhauser 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agencv 

Research Triangle Park, N.C. 

Mr. Thomas B. Feagans 

Strategies and Air Standards Division 

Office of Air Quality Planning and Standards 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Charles R. Hosler 

Environmental Sciences Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Mr. Michael H. Jones 

Strategies and Air Standards Division 

Office of Air Quality Planning and Standards 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. John H. Knelson 

Health Effects Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 
Mr. Ted Ripberger 

Industrial Environmental Research Laboratory 

U.S. Environmental Protection Agency 

Research Triangle Park, N.C. 

Dr. David Tingey 

Ecological Effects Division 

U.S. Environmental Protection Agency 

Corvallis, Ore. 

Dr. David Weber 

Ecological Effects Division 

U.S. Environmental Protection Agency 

Corvallis, Ore. 

Dr. Raymond Wilhour 

Ecological Effects Division 

U.S. Environmental Protection Agency 

Corvallis, Ore. 

Consultants 

Dr. Stephen M. Ayres 

Chairman, Department of Internal Medicine 

St. Louis University School of Medicine 

St. Louis, Mo. 

Dr. David V. Bates 

Dean, School of Med'+cine 

University of British Columbia 

Vancouver, B C., Canada 

Dr. T. Timothy Crocker 

Chairman, Department of Community and 

Environmental Medicine 

University of California College of Medicine 

Irvine, Calif. 

Dr. Richard Ehrlich 

Director, Life Sciences Division 

Illinois Institute of Technology Research Institute 

Chicago, III. 

Dr. Gustave Freeman 

Director, Department of Medical Sciences 

Life Sciences Division 

Stanford Research Institute 

Menlo Park, Calif. 

Dr. Bernard D. Goldstein 

Associate Professor, Department of Medicine 

and Department of Environmental Medicine 

New York University School of Medicine 

New York, N.Y. 

Dr. John R. Goldsmith 

Environmental Epidemiology Unit 

California State Department of Public Health 

Sacramento, Calif. 

vi 
Dr. Jack D. Hackney 

Chief, Environmental Health Laboratories 

Associate Professor of Medicine 

Rancho Los Amigos Hospital Campus 

of the University of Southern California 

Downey, Calif. 

Dr. Sagar V. Krupa 

Assistant Professor, Department of Plant Pathology 

University of Minnesota 

St. Paul, Minn. 

Dr. Daniel B. Menzel 

Associate Professor of Pharmacology and Medicine 

and Director, Laboratory of Environmental Pharmacology 

and Toxicology 

Duke University Medical Center 

Durham, N.C. 

Dr. Carl M. Shy 

Institute of Environmental Health 

University of North Carolina 

Chapel Hill, N.C. 

Dr. Boyd R. Strain 

Professor, Department of Botany 

Duke University 

Durham, N.C. 

Technical Assistance 

Environmental Protection Agency 

Research Triangle Park, N.C. 

Ms. F. Vandiver Duffield 

Mr. Douglas B. Fennell 

Mr. R. Wayne Fulford 

Mr. Allen Hoyt 

Ms. Evelynne R. Rash 

Ms. Beverly A. Tilton 

DOT Systems, Inc. 

Vienna, Va. 

Mr. Frank Broadwell 

Dr. John Preston 

Dr. Carolyn Pyrek 

Mr. Arthur Willey 

vii 

CONTENTS 

Page 

FIGURES........................................................ xiv 

TABLES......................................................... xviii 

ABBREVIATIONS AND SYMBOLS . . .. . .... . . .. .. . ... . . ... . ... . .. . . xxii 

ABSTRACT...................................................... xxix 

ASSOCIATION OF OZONE WITH OTHER CONSTITUENTS OR 

MANIFESTATIONS OF SMOG 

1. SUMMARY AND CONCLUSIONS . . . .. . . ... . ... . . ... ...... .. .... 1 

INTRODUCTION ............................................. 1 

NATURE AND ATMOSPHERIC CONCENTRATIONS OF PHOTOCHEMICAL OXIDANTS . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . .. .. 1 

SOURCES AND SINKS OF OXIDANTS . .... ...... . . . . . . .. . . ... . 1 

OXIDANT PRECURSORS ........ . .... . . . . . .. . . .. . . .. . . .. . .... 2 

RELATIONSHIPS BETWEEN AMBIENT OXIDANT AND PRECURSOR 

EMISSIONS ................................................. 3 

MEASUREMENT METHODS FOR OXIDANT AND OXIDANT PRECURSORS................................................... 3 

HEALTH EFFECTS OF OZONE AND OTHER PHOTO CHEMICAL 

OXIDANTS .................................................. 4 

Discussion of Threshold Concentrations . . . . . . . . . . . . . . . . . . . 4 

Human Studies .... . . ... . . .. . . ... ... . . .. . . .. . . ... ... . .... 4 

Animal Toxicology Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10. 

Ozone Versus Oxidant Health Effects . . ... . .. .. . . .. .. .. .. .. 11 

EFFECTS OF PHOTOCHEMICAL OXIDANTS ON VEGETATION AND 

CERTAIN MICROORGANISMS ................................ 11 

EFFECTS OF PHOTOCHEMICAL OXIDANTS ON ECOSYSTEMS .. 14 

EFFECTS OF PHOTOCHEMICAL OXIDANTS ON MATERIALS .... 16 

2. INTRODUCTION ............................................... 17 

3. NATURE AND ATMOSPHERIC CONCENTRATIONS OF PHOTOCHEMICAL OXIDANTS ........................................ 19 

NATURE OF OXIDANT .. . . .. . . .. . . ... . .. . ....... . . .. . . ...... . 19 

OXIDANT CONCENTRATIONS AND THEIR PATTERNS .......... 20 

Introduction ............................................. 20 

Oxidant Concentrations in Urban Atmospheres . . . .. .. .. .. .. 20 

Oxidant Concentrations in Rural Atmospheres ..... .. .. .... 21 

Patterns of Variation in Oxidant Concentrations .... .... .... 23 

ASSOCIATION OF OZONE WITH OTHER CONSTITUENTS OR 

MANIFESTATIONS OF SMOG ................................. 24 

SUMMARY .................................................. 27 

REFERENCES FOR CHAPTER 3 ............................... 27 

4. SOURCES AND SINKS OF OXIDANTS .......................... 29 

PHOTOCHEMICAL FORMATION OF OXIDANTS ... .. .. . . .. ..... 29 

, 

x 
Page 

Introduction ............................................. 29 

Atmospheric Reaction Mechanisms ... .... .... .... .... .... 30 

Effects of Meteorological Factors ......................... 35 

NATURAL SOURCES OF OXIDANTS .. .... .. .. .. . . .. .. . . .. .. . . 47 

Introduction ............................................. 47 

Stratospheric Ozone Intrusion ............................ 47 

Photochemistry of Natural Organics NO.................... 52 

SINKS OF OXIDANTS AND OF OXIDANT PRECURSORS ........ 55 

Introduction ............................................. 55 

Sinks for Oxidants and Oxidant Precursors . .. . ... . . . . . . .. . 56 

SUMMARY .................................................. 57 

REFERENCES FOR CHAPTER 4 .. . ... . . .. . . .. . . .. . ... . ... . . .. . 58 

5. OXIDANT PRECURSORS .. .... . . .. .. .. .... .. .. .. . . .... . . .. .. . . 65 

INTRODUCTION ............................................. 65 

AMBIENT LEVELS AND VARIATIONS OF OXIDANT/OZONE PRECURSORS .................................................. 65 

Organic Compounds in Urban Atmospheres .. . .. . . ... . ... . 65 

Organic Compounds in Rural and Remote Areas . . . . . . . . . . . 70 

Nitrogen Oxides ..... .... .... .... ................ .... .... 71 

SOURCES OF OXIDANT PRECURSORS ........................ 71 

Introduction ............................................. 71 

Summary of Organic Emissions Data . . . . . . . . . . .. . . . . . . . . . . 77 

Hydrocarbon Emissions From Natural Sources ............. 78 

Hydrocarbon Emissions From Anthropogenic Sources .. .. .. 81 

Emissions of Nitrogen Oxides ............................. 82 

REACTIVITY OF ORGANIC EMISSIONS .. .. .... .... .. .. .. . . .... 83 

SUMMARY .................................................. 88 

REFERENCES FOR CHAPTER 5 ............................... 89 

6. RELATIONSHIPS BETWEEN AMBIENT OXIDANTS AND PRECURSOR 

EMISSIONS .................................................. 93 

INTRODUCTION ............................................. 93 

MODELS BASED ON EMPIRICAL RELATIONSHIPS ... .. .. .. .... 94 

Rollback Model .. .. .. .. .. . . .. .. .. .... .... .. .. .. .. .... .. .. 94 

Modified Rollback: Observational Model .. . . .. . ..... .. . .... 95 

Statistical-Empirical Models .......... .... ............ .... 98 

MECHANISTIC MODELS OF Ox/HC/NOx RELATIONSHIPS ...... 101 

AIR QUALITY SIMULATION MODELS (AQSM) . ... . ... . . .. . .... 105 

SUMMARY.................................................. 111 

REFERENCES FOR CHAPTER 6 ............................... 113 

7. MEASUREMENT METHODS FOR OZONE, OXIDANTS, AND THEIR 

PRECURSORS ................................................ 116 

INTRODUCTION ............................................. 116 

SAMPLING FACTORS IN AMBIENT AIR MONITORING . . . . . . . . . . 116 

MEASUREMENT OF OZONE .. .. . . ... . .... ...... . . ... . .... .. . . 117 

Gas-Phase Chemiluminescence (EPA Reference Methods) .. 117 

Gas-Solid Chemiluminescence ............................ 118 

Ultraviolet Photometry . . . .... .. .... . . ... . .... ... . .... .... 118 

MEASUREMENT OF TOTAL OXIDANTS . .. . ... .... .... .. . . .... 119 

OZONE CALIBRATION PROCEDURES ......................... 120 

KI Calibration Procedures ............ ................ .... 120 

Recently Developed Calibration Procedures ................ 121 
Page 

RELATIONSHIPS BETWEEN AMBIENT OXIDANT AND OZONE 

DATA ....................................................... 122 

MEASUREMENT OF PEROXYACYLNITRATES .. . . .. . ... . ... .. .. 125 

MEASUREMENT OF HYDROCARBONS . .. . . ... . ... . .. .... . . .. . 126 

Measurement of Nonmethane Hydrocarbons . . . .. . . . . . . . . . . 126 

Measurement of Individual Hydrocarbons .. . . . . . ... .. . . .... 128 

Measurement of Reactive Hydrocarboris . . . . . . . . .. . . . . . . . . . 129 

Calibration .............................................. 129 

ME.4SUREMENT OF NITROGEN OXIDES ...................... 130 

Measurement of NO2 . .. . . . . . ... . . .. . . .. . . .. . . .... .. . .... 130 

Measurement of NO . .. .. . . . . .... ... . .. .. .. . . . ... . . .. .... 131 

SUMMARY .................................................. 131 

REFERENCES FOR CHAPTER 7 .. . .... ... . . .. . . .. . . ...... . .... 131 

8. TOXICOLOGICAL APPRAISAL OF PHOTOCHEMICAL OXIDANTS .. 136 

INTRODUCTION ............................................. 136 

EFFECTS OF OZONE ON EXPERIMENTAL ANIMALS . . .. . . . . . . . . 136 

Respiratory Tract Transport and Absorption . . . . . . . . . . . . . . . . 136 

Mortality ................................................ 138 

Pulmonary Effects .. .... . . . . . ... . ... . . .. . . .. . . ... ... . ... . 138 

Extrapulmonary Effects ....... ................. ........... 158 

Summary and Conclusions .. . .... .. . . . .. . . .. . . ... . .. . . ... 162 

EFFECTS OF PHOTOCHEMICAL OXIDANTS ON EXPERIMENTAL 

ANIMALS ................................................... 

165 

Experimental Data ....................................... 

165 

Summary ............................................... 

176 

EFFECTS OF PEROXYACETYLNITRATE ON EXPERIMENTAL 

ANIMALS ................................................... 

177 

Experimental Data ........... ............... . ............ 

177 

Summary ............................................... 

177 

REFERENCES FOR CHAPTER 8 ... .................... ........ 

177 

9. CLINICAL APPRAISAL OF THE EFFECTS OF OXIDANTS .......... 184 

OCCUPATIONAL AND ACCIDENTAL EXPOSURES TO OZONE ... 184 

CONTROLLED STUDIES OF HUMAN HEALTH EFFECTS ......... 186 

Hematology ............................................. 195 

Mutagenesis ............................................ 196 

Controlled Studies of Human Health Effects of Peroxyacetylnitrate .. 197 

SUMMARY .................................................. 197 

REFERENCES FOR CHAPTER 9 ... ................. ........... 197 

10. EPIDEMIOLOGIC APPRAISAL OF PHOTOCHEMICAL OXIDANTS . 200 

INTRODUCTION ........................................... 200 

EFFECTS OF SHORT-TERM PHOTOCHEMICAL OXIDANT EXPOSURES 200 

Daily Mortality in Relation to Variations in Oxidant Levels .. 200 

Hospital Admissions in Relation to Oxidant Levels .......... 206 

Aggravation of Existing Respiratory Diseases by Oxidant 

Pollution ................................................ 208 

Effects of Oxidant on the Promotion of Symptoms and Illness in 

Healthy Populations ...................................... 212 

Impairment of Performance Associated with Oxidant Pollution ... 221 

Eye Irritation in Relation to Variations in Oxidant Levels .... 230 

EFFECTS OF CHRONIC PHOTOCHEMICAL OXIDANT EXPOSURES .. 236 

Introduction .............................................. 236 

xi 
Page 

Mortality in Areas of High- and Low-Oxidant Pollution ...... 237 

General Morbidity in Areas of High and Low Oxidant Pollution 239 

Chronic Oxidant Exposure and Pulmonary Function ... .... . 244 

ATTITUDES OF LAYMEN AND PHYSICIANS TOWARD OXIDANT 

AIR POLLUTION ........ .... .... .... .... ........ .... ........ 246 

State of California General Health Survey . .. . . .. . . . ... ... . 246 

Survey of Los Angeles Physicians . . . . . . . . . . . . . . . . . . . . . . .. . 246 

Discussion of Attitudes of Respondents and PhysiciansToward 

Oxidant Air Pollution . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . 247 

SUMMARY OF EPIDEMIOLOGIC APPRAISAL OF PHOTOCHEMICAL 

OXIDANTS ................................................. 247 

Effects of Short-Term Photochemical Oxidant Exposures ... . 248 

Effects of Chronic Photochemical Oxidant Exposures ....... 249 

Attitudes of Laymen and Physicians Toward Oxidant Air 

Pollution ................................................ 250 

REFERENCES FOR CHAPTER 10 ............................. 250 

11. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON VEGETATION 

AND CERTAIN MICROORGANISMS ............... ........... . 253 

INTRODUCTION . . . . . . . . . . . . . . . . . .. . . . . . . .. . . . . . . . . . . . . . . . . . . 253 

VASCULAR PLANT RESPONSE TO PHOTOCHEMICAL OXIDANTS 253 

Physiological Processes .................................. 254 

Visible Symptoms . . . .. . . .. .. ..... . .. . .. .. . .. .. . . .. . . ... . 255 

Growth and Yield .. .. .. .. .. .. .... ... . .... .... .... . . .. .. .. 257 

Factors Affecting Plant Response . . . . . . . . . . . . . . . . . . . . . . .. . 270 

RESPONSES OF MOSSES, FERNS, AND MICROORGANISMS ... 280 

SUMMARY .................................................. 281 

REFERENCES FOR CHAPTER 11 .............................. 284 

12. ECOSYSTEMS ............................................... 294 

INTRODUCTION ............................................. 294 

GENERAL RESPONSES OF NATURAL AND AGROECOSYSTEMS 

TO STRESS BY OXIDANTS .. . . . .. .. . ... .. . ..... . . .. . . ... . ... . 297 

Agroecosystems ........................................ 297 

Natural Ecosystems ...................................... 297 

ORIGIN OF INJURIOUS CONCENTRATIONS OF OZONE AND 

OXIDANTS .................................................. 298 

Advection From Urban Centers to Remote Areas in Southern 

California ........................................... 298 

San Joaquin Valley and Adjacent Sierra Nevada Mountains . 301 

Seasonal and Daily Variations of Injurious Concentrations— 

Synoptic Weather Patterns Associated With Episodes 

of High Pollution ..................................... 301 

Annual Trends of Total Oxidant Concentrations at a San Bernardino 

Station and the Nearby City of San Bernardino ..... .. .. 304 

INVESTIGATING THE EFFECT OF OXIDANT STRESS ON ECOSYSTEMS 307 

Ecosystem Modeling ..................................... 307 

Modeling the Effects of Oxidant Stress on a Western Mixed 

Conifer Forest Ecosystem . ... . ... .... . ... ...... .. .. .. 308 

Effects on Primary Producers (Green Plants) . .. .. . . .. . . .. .. 308 

EFFECTS ON CONSUMER POPULATIONS ......... ........ .... 319 

Vertebrate Populations ................................... 319 

Plant Parasites and Symbionts ............................ 321 

Xii 
Page 

EFFECTS ON DECOMPOSERS ................................ 322 

SUMMARY .................................................. 324 

REFERENCES FOR CHAPTER 12 .. .. . . ... . ... . .... ... . .... ... . 326 

13. EFFECTS OF OZONE ON MATERIALS . .. . . .. . . .. . . .. . . .. . . .. .. 329 

INTRODUCTION ............................................. 329 

MECHANISMS OF OZONE ATTACK . .. .. .. .. .... .. .. . ... .. .... 329 

Effects on Elastomers .... .... .. .. .... .... ... . ... . .. .. .... 329 

Effects on Textiles .. . ....... . .... . . . . .... ... . . .. . ... . ... . 333 

Effects on Paints ........................................ 337 

Effects on Other Materials . . . ... . . ... ... . . .. . ... . . ....... 340 

SUMMARY .................................................. 340 

REFERENCES FOR CHAPTER 13 .. ................... ......... 340 

Xiii 
FIGURES 

Figure Page 

3-1. Trends in NO2 air quality and in HC and NOx emission, Los 

Angeles Basin, 1965-74 ............................... 25 

3-2. Pollutant trends in Los Angeles, annual and 3-year moving 

averages.............................................. 25 

3-3. Correlation between Bscat and maximal ozone concentration 26 

4-1 . Chemical changes occurring during photoirradiation of hydrocarbon-nitrogen oxide-air systems ...................... 30 

4-2. The major reaction paths for the degradation of trans-2-butene 

in an irradiated NOx-polluted atmosphere ............... 32 

4-3. Isopleths (m x 10 2 ) of inean summer morning mixing heights 38 

4-4. Isopleths (m x 10 2 ) of inean summer afternoon mixing heights 38 

4-5. Isopleths (m x sec -') of inean summer wind speed averaged 

through the afternoon mixing layer ..................... 39 

4-6. Isopleths (m x sec-') of inean summer wind speed averaged 

through the morning, mixing layer ...................... 39 

4-7. Isopleths of total number of forecast days of high meteorological potential for air pollution . . . . .. . . .. .. . . .... .. .. .. 40 

4-8 Monthly distribution of number of cases of 4 or more days of 

atmospheric stagnation, 1936-75 (September) ... .. .. .. .. 41 

4-9. Monthly distribution number of cases of 4 or more days of 

atmospheric stagnation, 1936-75 (August) . .. . . ... . . ... . 41 

4-10. Diurnal variations in actinic irradiance .................... 42 

4-11 . Long-term ozone variations at Quillayute .. .. .. : . .. . . . . . . . 50 

4-12. Monthly ozone variations at Mauna Loa, Hawaii .. .... .... . 51 

4-13. Average monthly ozone concentrations recorded at summit of 

Mount Whiteface .. . ... . . . . .. . . .. . . .. . . .... . . .. . . . . .. . 52 

4-14. Effect of NOx concentration increase on ozone formation at 

White River, Utah ..................................... 

55 

5-1 . Distribution of hydrocarbons in diesel exhaust gas ......... 67 

5-2. Distribution of hydrocarbons in jet-aircraft engine exhaust . 68 

5-3 Nonmethane hydrocarbon trends in Los Angeles, 1963-72 . 70 

5-4. Oxides of nitrogen trends in Los Angeles, 1963-72, 6- to 9-a.m. 

and maximum 1-hr concentrations . . . . . . . . . . . . . . . . . . . . . 77 

5-5. Correlation of observed and calculated Os reactivities ...... 87 

6-1 . Maximum daily 1-hr average oxidants as a function of 6- to 9- 

a.m. averages of nonmethane hydrocarbon ICAMP data from 

four U.S.cities ........................................ 96 

6-2. Upper limit oxidant values in the Los Angeles south coast air 

basin as a function of average 6- to 9-a.m. concentration 97 

6-3. Oxidant-hydrocarbon relationships from smog chamber and 

aerometric data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 

xiv 
Page 

6-4. Merz, Painter, and Ryason's relation of NOX and NMHC assumed 

as 50 percent of total HC and oxidant for downtown Los 

Angeles .............................................. 99 

6-5. California Air Resources Board aerometric-results, relation 

between 6- to 9-a.m. NOx, 6- to 9-a.m. HC, and maximum 

hourly oxidant concentrations in downtown Los Angeles . 99 

6-6. California Air Resources Board aerometric results, relation 

between 6- to 9-a.m. NOX, 6- to 9-a.m. HC, and maximum 

hourly oxidant concentration in Azusa .. .... .. .... . . .. .. 100 

6-7. California Air Resources Board aerometric results, relation 

between 6- to 9-a.m. NOX, 6- to 9-a.m. HC, and maximum 

hourly oxidant concentrations in San Bernardino .. .... .. 100 

6-8. California Air Resources Board aerometric results, relation 

between 6- to 9-a.m. NOx, 6- to 9-a.m. HC, and maximum 

hourly oxidant concentrations in Anaheim . .. .. .. .. . . .... 101 

6-9. Expected number of days per year exceeding 0.10 ppm versus 

NOx and reactive hydrocarbon emission levels for central 

LosAngeles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 

6-10. Oxidant/Os isopleths derived from combined use of smog 

chamber and photochemical and modeling techniques ... 103 

7-1. Diurnal ozone-oxidant averages from September 4 through 

September 30, 1971 .... .. .. .. .... ...... .. .. .. .... .. .. 123 

7-2. Ozone-oxidant ratios in Musashino, Japan ... .. .. .. .... ... 124 

7-3. Comparison of the KI, Mast, and chemiluminescence methods 

for measuring ozone in irradiated exhaust mixtures .. .. .. 124 

7-4. Relationship of total oxidant and ozone values greater than 10 

ppb, August through December 1973 . . . . . . . . . . . . . . . . . . . 125 

7-5. Comparative measurements of ambient oxidant/ozone by the 

potassium iodide (KI) chemiluminescence (Chem), and 

ultraviolet (UV) methods . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . 126 

9-'. Changes with time in dynamic lung function tests in nonsmokers during a 2-hour exposure to 0.75 ozone and during 

recovery .............................................. 189 

9-: 1 . Changes with time of minute ventilation, respiratory rate, and 

tidal volume in ozone-exposure (0.75 ppm) and subsequent 

recovery period in exercising nonsmokers . .. .. .. .. . . ... . 190 

9-3. Dose-response curves for Los Angeles and Montreal subjects 195 

10-1. Comparison of deaths of persons aged 65 years and over, and 

maximum daily temperature, Los Angeles County, July 1 to 

November 30, 1955 ... .... .. . ... .. .. . . .... .. . . ... . .... 202 

10-2. Comparison of nursing home deaths, maximum daily temperature, and smog-alert days in Los Angeles County, July 

through December 1955 . .. .. . . .. .. ...... .. .. . . .... .. .. 203 

10-3. Comparison of maximum concentrations of oxidant and carbon 

monoxide, maximum temperature, and daily death rate for 

cardiac and respiratory causes, Los Angeles County, 1956- 

58 ................................................... 204 

10-4. Monthly changes in symptom and complaint rates with daily 

maximum hourly oxidant content above and below 0.10 ppm 218 

10-5. Comparison of various symptom and complaint rates on days 

when oxidant concentrations were over 0.15 pphm and 

below0.10 ppm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219 

xv 
Page 

10-6. Relationship between oxidant concentration in the hour before 

an athletic event and percentage of the team failing to improve running time ... . . . .. .. . . .... .. .. .. .. . . .. .. .. . . .. 222 

10-7. Regression curves relating eye irritation scores and simultaneous oxidant concentrations from a number of stations 

in the Los Angeles area, 1954 . . . . . . . . . . . . . . . . . . . . . . . . . 231 

10-8. Variation of inean maximum eye irritation, as judged by a panel 

of scientists, with 'maximum oxidant concentrations, 

Pasadena, August-November 1955 . . .... .. . . .... .. .. ... 232 

10-9. Mean index of eye irritation versus oxidant concentration .. 234 

10-10. Monthly regression lines between oxidant levels and eye 

irritation .............................................. 235 

10-11. Combined weekly incidence rates of selected conditions 

(colds, hay fever, asthma, and other respiratory conditions) 

in persons of all ages, Los Angeles County and the remainder 

of California, August 7 to November 28, 1954 ... .... .... 240 

10-12. Weekly incidence rates of illness and injury for persons aged 

65 and over in Los Angeles County and the remainder of 

California, August 2 to November 28, 1954 ... .. .... .... 240 

10-13. Percentage of respondents in Los Angeles County and San 

Francisco Bay area attributing exacerbation of respiratory 

conditions to air pollution and other factors, 1956 ....... 242 

1 1-1. Sequence of ozone-induced responses . . . . . . . . . . . . . . . . . . . . 254 

1 1-2. Relation between ozone concentration, foliar injury, and a 

reduction in plant growth or yield . . . . . . . . . . . . . . . . . . . . . . 264 

1 1-3. Limiting values for foliar injury to trees and shrubs by ozone 265 

1 1-4. Limiting values for foliar injury to agricultural crops by ozone 266 

1 1-5. Ozone concentration versus duration of exposure required to 

produce a 5% response in three different plant susceptibility 

groupings ............................................ 267 

11-6. Dose-response relationships and limiting values for foliar 

injury to vegetation by peroxyacetylnitrate (PAN) . . . . . . . . . 269 

11-7. Conceptual model of factors involved in air pollution effects 

on vegetation ......................................... 271 

12-1. Law of tolerance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295 

12-2. Major topographic features of the Los Angeles Basin witn 

inland valleys and mountains . .... . . .. . . . . . . .. . . .. .. .. . 299 

12-3. Altitudinal sequence of ecosystems in the San Bernardino 

Mountains ............................................ 300 

12-4. Daytime changes in oxidant concentrations along a west-toeast transect in the southern coastal air basin, including the 

slopes of the San Bernardino Mountains ... . . .. .. . . .. .. . 301 

12-5. The relationship of time of occurrence of the daily peak oxidant 

concentration to temperature and vapor-pressure gradients 

in an elevational sequence ......... ........ ............ 302 

12-6. Monthly summation of'total oxidant concentration data at Rim 

Forest/Sky Forest, San Bernardino Mountains, California, 

June through September, 1968-75 . . . . . . . . . . . . . . . . . . . . . 305 

12-7. Number of hours of total oxidant, July through September, 

greater than or equal to 392 pg/m 3 (0.20 ppm) at the downtown San Bernardino County Air Pollution Control District 

Station, 1963-74, and Rim Forest/Sky Forest, 1968-74 .. 306 

xvi 
Page 

12-8. Hypothetical relationships of oxidant dose, natural ecosystems, 

agroecosystems and the relative values of their vegetation 

components along a transect of southern coastal air basin of 

California ............................................. 307 

12-9. Organism-level interactions in a mixed conifer forest ...... 309 

12-10. Tree-level interactions in a mixed-conifer forest ecosystem . 311 

12-11. Community-level interactions in a mixed-conifer forest 

ecosystem ............................................ 313 

12-12. Stand-level interactions in a mixed-conifer forest ecosystem 315 

12-13. Community-succession interactions in a mixed-conifer forest 

ecosystem ............................................ 317 

12-14. Topographic projection, San Bernardino Mountains, with 

comparison of oxidant injury to black oaks at major study 

sites, August 31, 1974, with accumulated total oxidant dose 

for June-August measured at nearby monitoring stations 318 

12-15. Topographic projection, San Bernardino Mountains, showing 

how ponderosa pines and Jeffrey pines in major study sites 

are distributed in six injury classes according to seasonal 

dose of total oxidant .. . .. . . .. . . .. . . .. . . .. .. . . . . . . . . .. . . 318 

12-16. Annual growth of the terminal shoot and first-order branches 

in upper half of ponderosa pine saplings maintained in 

filtered or unfiltered (ambient) air greenhouses, or in outside 

ambient air (1968-73) . .. . . .. .. . .. . . . .. .. . . .. . . .. . . . . .. 320 

12-17. Relationship of degree of oxidant injury in ponderosa pines 

with bark beetle attack and number of trees killed bywestern 

pine beetle, mountain pine beetle or both species ........ 323 

13-1. Effect of annual average ozone concentration on added costs 

resulting from damage to materials and preventive measures .................................................. 340 

xvi i 
TABLES 

Table Page 

3-1. Summary of maximum oxidant concentrations in selected 

urban areas .......................................... 20 

3-2. Oxidant concentrations observed in selected urban areas of 

the United States, 1974-75 ............................ 21 

3-3. PAN and oxidant (OX) measurements (10 a.m. to 4 p.m.), Los 

Angeles, Calif., 1968 .................................. 21 

3-4. PAN and ozone measurements (10 a.m. to 4 p.m.), Hoboken, 

N .J., 1970 ............................................ 22 

3-5. PAN, oxidant, and ozone measurements (10 a.m. to 4 p.m.), St. 

Louis, Mo., 1973 ...................................... 22 

3-6. Concentrations of tropospheric ozone before 1962 ......... 22 

3-7. Summary of ozone data from 1973-1975 oxidant studies, 

Research Triangle Institute . . .. . . . ... . . .. . . . . .. .. . . .. .. 23 

4-1. Calculated rates of attack on irans-2-butene by various reactive 

species in simulated smog system at several irradiation 

times................................................. 31 

4-2. Compounds observed in photochemical smog . . .. . . .. .. . . . 35 

4-3. Compounds that may be formed in photochemical smog .... 35 

4-4. Secondary organic aerosols . . .. . . . . . . . . .. .. . . .. .. . . .. .. . . 36 

4-5. Relative importance of aliphatic and aromatic precursors ... 37 

4-6. Percentage difference between the Peterson and the Leighton 

values at the Earth's surface over selected wave-length 

intervals and solar zenith angles . .. .. ... . . . .. .. . . .. .. . . 42 

4-7. Calculated values of NO2 photodissociation rate constant at 

Earth's'surface and percentage increase of the rate constant 

from the surface to various heights . . . . . . .. .. . . . . .. . . . . . 43 

5-1. Hydrocarbons identified in ambient air .. .......... ........ 66 

5-2. Frequency distributions for 6- to 9-a.m. nonmethane hydrocarbon concentrations at CAMP sites, 1967-72 .......... 69 

5-3. Volatile plant products identified by Rasmussen .. ...... ... 70 

5-4. Frequency distribution data for 6- to 9-a.m. nitric oxide 

concentrations at CAMP sites, 1962-72 . .. .. . . .. .. . . .. . . 72 

5-5. Frequency distribution for 6- to 9-a.m. nitrogen dioxide concentrations at CAMP sites, 1962-72 .. . . . . .. .. . . .. . . . . . . 73 

5-6. Nitric oxide concentration in California by averaging time and 

frequency, 1963-67 ................................... 75 

5-7. Nitrogen dioxide concentration in California by averaging time 

and frequency, 1963-67 ............................... 76 

5-8. Estimates of total hydrocarbon emissions from manmade and 

naturalsources ....................................... 77 

5-9. Total yearly hydrocarbon emission rate for the continental 

United States, based on leaf biomass ................... 77 

xvui 
Page 

5-10. 1974 nationwide estimates of total hydrocarbon sources and 

emissions ............................................ 78 

5-11. Nationwide total hydrocarbon emission trends, 1970-75 ... 78 

5-12. Hydrocarbon emissions from mobile sources . . . . .. . . .. .. .. 78 

5-13. Organic emission inventory for the metropolitan Los Angeles 

air quality control region, 1972 . . . . . . . . . . . . . . . . . . . . . . . . . 79 

5-14. Reactive emission inventories for the metropolitan Los Angeles 

air quality control region . . . .. : . . . .. .. . . . . . . . . . . .. . . .. . . 80 

5-15. 1974 nationwide estimates of nitrogen oxide sources and 

, emissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 

5-16. • Comparison of reactivities of different types of organics .... 84 

5-17. Reactivity data .......................................... 84 

5-18. Summary of data from studies on reactivities (toluene equivalents) 

. and classification of organics .... ........ ...... ......... 85 

5-19. Classification of organics with respect to their oxidant-related 

reactivity in urban atmospheres .... ...... .. ...... .... .. 86 

6-1. Forms of air quality simulation models . .. . . . . . . .. . . .. . . . . . 107 

6-2. Currently available air quality simulation models for photochemical oxidant ...................................... 108 

6-3. Treatment of ineteorological variables in air quality simulation 

' models ............................................... 109 

6-4. Uncertainties in predicted ozone concentrations from all 

mechanisms and input uncertainties ...... .. ...... .... .. 111 

6-5. Prior validation studies of air quality simulation models .... 112 

7-1. Performance specifications for automated methods ........ 118 

7-2. List of designated reference methods . .. . . . . . . .. . . .. . . . . .. 119 

7-3. List of designated equivalent methods ...... .. .... ........ 119 

7-4. Percent difference from known concentrations of nonmethane 

hydrocarbons obtained by sixteen users ................. 127 

8-1. Pulmonary effects of ozone: Host defense mechanisms ..... 166 

8-2. Pulmonary effects of ozone: Biochemistry ......... .... .... 167 

8-3. Pulmonary effects of ozone: Morphology .... .. .... ...... .. 170 

8-4. Pulmonary effects of ozone: Pulmonary function . . . . . . .. . . . 171 

8-5. Pulmonary effects of ozone: Edema and tolerance .... .... . 172 

8-6. Extrapulmonary effects of ozone: Hematology and serum 

chemistry ............................................. 173 

8-7. Extrapulmonary effects of ozone: Central nervous system and 

behavior .............................................. 174 

8-8. Extrapulmonary effects of ozone: Morphology . . . . .. . . . . .. .. 174 

8-9. Extrapulmonary effects of ozone: Miscellaneous ... .... .... 174 

8-10. Atmospheric mean concentrations and their standard deviations 

administered from 8 a.m. to midnight each day .......... 175 

8-11. Effects of oxidants on animals ............... ........ .. ... 176 

9-1. Summary of available data on occupational exposure of 

humans to ozone .. . . .. . . . . .. . . . . .. . . . . . . . . . . . . .. . . . . . . 185 

9-2. Summary of data on human experimental exposure to ozone 

before 1970 .......................................... 187 

1 G-1. Average number of deaths per day resulting from cardiac and 

respiratory causes among residents of Los Angeles Cojunty 

aged 65 and over, as related to oxidant concentrations and 

maximum daily temperature, by month 1954-55 

......... 201 

xix 
Pa4e 

10-2. Comparison of respiratory and cardiac deaths during smog and 

smog-free periods occurring in Los Angeles County, AugustNovember .1954 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206 

10-3. Correlation of morning and early afternoon oxidant levels with 

oxygen consumption and airway resistance of 15 patients 

with chronic respiratory disease . .. . . . . . . . . .. . . . . . . . . . . . 211 

10-4. Relationship of average daily simple and adjusted percentage 

of student nurses report to photochemical oxidant levels 

for 868 days, November 1961 through May 1964 .... .. .. 213 

10-5. Sign-test data for testing the association of oxidant levels with 

accidents in Los Angeles, August through October, 1963 

and1965 ............................................. 224 

10-6. Number of subjects for whom correlation coefficients between 

environmental and respiratory function measurements are 

significant at p < 0.05, Japan, 1972 . . . . . . . . . . . . . . . . . . . . 227 

10-7. Correlation of eye irritation with simultaneous oxidant concentrations, in order of decreasing eye irritation score, for 

a number of stations in the Los Angeles area, 1954 ..... 231 

10-8. Correlation between eye irritation and simultaneous environmental measurements, as judged by a panel of scientists, 1954 232 

10-9. Effect of filter on sensory irritation and chemical measurements 233 

10-10. Pearson product moment correlation of coefficients between 

eye irritation and environmental factors in a nonfiltered 

room ................................................. 234 

10-11. Total lung cancer mortality in an American Legion study population, California, 1958-62 ............................. 237 

10-12. Lung cancer deaths and relative risks per 100,000 man-years 

in an American Legion study population, by extent of cigarette 

smoking and residence, California, 1958-62 ............. 2:58 

10-13. Total chronic respiratory disease mortality in an American 

Legion study population, California, 1958-62 ............ 239 

10-14. Selected respiratory conditions reported by general population 

sample, California, May 1956 .......................... 241 

10-15. Percent of survey response of general and working population 

bothered by -air pollution, by major geographic areas in 

California, May 1956 .................................. 246 

10-16. Air pollution effects reported in general population survey, by 

type of community and by major geographic areas in California, May 1956 ........................................ 247 

1 1-1. Effects of oxidants (ozone) in ambient air on growth, yield, and 

foliar injury in selected plants .......................... 258 

11-2. Effects of acute exposure on growth and yield of selected 

plants ................................................ 260 

1 1-3. Effects of ozone on selected understory species from 

an aspen community . ............ ..... ... .. ........... 261 

1 1-4. Effects of long-term, controlled ozone exposures on 

growth, yield, and foliar injury to selected plants ......... 262 

11-5. Concentration, time, and response equations for three susceptibility groups and for selected plants or plant types with 

respectto ozone ...................................... 268 

1 1-6. Ozone concentrations for short-term exposures that produce 

5 or 20 percent injury to vegetation grown under sensitive 

conditions ............................................ 269 

xx 
Page 

11-7. Estimates of economic losses to crops and vegetation in the 

United States attributable to oxidant air pollution ... .... . 270 

1 1-8. Response of plants to ozone, as conditioned by humidity during 

growth and exposure .................................. 

274 

11-9. Effects of soil moisture on response of selected plants to 

oxidant stress ......................................... 275 

11-10. Effects of various nutrients on response of selected plants to 

ozone (oxidant) stress . . . . . . ... . . . . . ... . . . . . . .. . . . . . . .. . 276 

11-1 1. Summary effects of sulfur dioxide and ozone mixtures on foliar 

injury ................................................ 277 

11-12. Foliar response of selected plants to sulfur dioxide and ozone 

mixtures .............................................. 279 

11-13. Growth response of selected plants to sulfur dioxide and ozone 

mixtures .............................................. 279 

12-1. Composition of ecosystems .......... .... ... ..... .... .... 294 

12-2. Descriptions of ineteorologic patterns for five classes of spring 

and summer days in southern California .... ........ .. .. 304 

12-3. Changes in oxidant injury scores and mortality rates of ponderosa and Jeffrey pines at 18 major study plots, 1973-74 .. 319 

12-4. Changes of timber volume and percentage of total Jeffrey 

pines at Barton Flats in the San Bernardino National Forest 319 

12-5. Tree species and size composition in a study area affected by 

oxidant air pollution .... . ........... .... .. ............. 321 

12-6. Injury thresholds for 2-hour exposures to ozone ... .. .. .... 322 

13-1. Formulation of highly ozone-sensitive natural rubber .. .... . 331 

13-2. Effect of ozone on natural rubber . .. . . .. . . .. . . .. . . . . . . .. . . 331 

13-3. Tire sidewall formulation ................... ........ ..... 332 

13-4. Effects of ozone on sidewall formulations containing various 

antiozonant concentrations .. ............ . ............. 332 

13-5. Cracking rates of white sidewall tire specimens ........... 332 

13-6. Paint erosion rate coefficients for the effects of ozone in 

laboratory-controlled environments ........ .. ... ... ..... 338 

13-7. Paint erosion rates at field exposure sites . . . . . .. .. . . . . .. . . 339 

XXi 
ABBREVIATIONS AND SYMBOLS 

n 

Aa Doz 

AChE 

AIChE 

AM 

APCD 

AQSM 

Ar 

A203 

ATPase 

Avg 

BAKI 

bd it 

'Be 

Br2 

Bscat 

oC 

14c 

CAMP 

CARB 

C1'C3 

C1'C4 

C2+ 

C2H2 

C4+ 

C4,5 

C4-C6 

C5-C10 

C6H5 

C6H5C002NO2 

CC 

Cdyn 

CH(CH3)CHQ 

CH2CHCH0 

CH2 CH2 

CH2C0 

CH2O 

CH3 

CH3CH0 

CH3C002NO2 

CH4 

Chem 

C1 2 

Angstrom 

Alveolar-arterial gradient 

Acetylcholinesterase 

American Institute of Chemical Engineers 

Alveolar macrophages 

Air pollution control district 

Air quality simulation model 

Argon 

Arsenous oxide 

Adenosine triphosphatase 

Average 

Potassium iodide solution acidified with boric acid 

Board foot 

Radioisotope of beryllium 

Bromine 

Extinction coefficient due to scatter by aerosols 

Degrees Celsius 

Radioisotope of carbon 

Community Air Monitoring Program 

California Air Resources Board 

Hydrocarbons containing one to three carbon atoms 

Hydrocarbons containing one to four carbon atoms 

Hydrocarbons containing more than two carbon 

atoms 

Acetylene 

Hydrocarbons containing more than four carbon 

atoms 

Hydrocarbons containing four or five carbon atoms 

Hydrocarbons containing four to six carbon atoms 

Hydrocarbons containing five to ten carbon atoms 

Benzyl 

Peroxybenzoylnitrate (PBzN) 

Closing capacity 

Dynamic compliance 

Propionaldehyde 

Acrolein 

Ethylene 

Ketene 

Formafdehyde; also HCHO and H2C0 

Methyl group 

Acetaldehyde 

Peroxyacetylnitrate (PAN) 

Methane 

Chemiluminescence 

Chlorine 

xxn 
cm Centimeter 

cm3 Cubic centimeter 

CNS Central nervous system 

CO Carbon monoxide 

COz Carbon dioxide 

Coh Coefficient of haze 

COMT Catechol-o-methyltransferase 

conc. Concentration 

COOH Carboxyl group 

COONOz Peroxynitrate group 

Cros Chromium trioxide (chromic anhydride, chromic acid) 

Cst Static lung compliance 

Cyt. P450 Cytochrome Paso 

2,4-D 2,4-Dichlorophenoxyacetic acid 

dbh Diameter breast height 

DEN Diethylnitrosamine 

DIFKIN Diffusion Kinetics Model 

DLco Cdrbon monoxide diffusing capacity of lung 

DNA Deoxyribonucleic acid 

DOLA Downtown Los Angeles 

DW Dry weight 

EA Environment Agency (Japan) 

EC Electron capture detection 

EH Humidity during exposure 

EKMA Empirical Kinetic Modeling Approach 

EPA U. S. Environmental Protection Agency 

ESR Electron spin resonance 

Et Ethyl 

F, First filial generation 

F2 Second filial generation 

°F Degrees Fahrenheit 

FEF 25-50% Mean expiratory flow during rniddle half of FVC 

FEF 25-75% Maximal midexpiratory flow rate 

FEF 50% Instantaneous expiratory flow at 50% of FVC 

FEFinax Peak expiratory flow 

Fe203 Ferric oxide 

FEV Forced expiratory volume 

FEVo.,e 0.75-second forced expiratory flow 

FEV,.o 1-second forced expiratory flow 

FEVs.o 3-second forced expiratory flow 

FID Flame ionization detection (or detector) 

FRC Functional residual capacity 

FS Fourier-transform spectroscopy; also FT 

FT Fourier-transform spectroscopy; also FS 

ft Foot 

ft2 Square foot 

ft-c Foot-candle 

FVC Forced vital capacity 

g Gram 

Gaw/Vtg Specific conductance 

GC Gas chromatography 

GDI Gas distribution index 

gf Emission growth factor 

GH Humidity during growth 

xxiii 
GLC Gas-liquid chromatography 

GM General Motors Corporation 

G-6-P Glucose-6-phosphate 

G-6-PD Glucose-6-phosphate dehydrogenase 

GPT Gas-phase titration 

GSC Gas-solid chromatography 

GSH Reduced glutathione 

GSSG Oxidized glutathione 

GSSRase Glutathione reductase 

H Hydroge n 

H+ Hydrogen ion 

3 H Tritium 

ha Hectare 

HC Hydrocarbons 

HCHO Formaldehyde; also CH2O and H2C0 

HCOOH Formic acid 

He Helium 

Hg Mercury 

HI Hemagglutination inhibition 

HMP Hexose monophosphate 

HNOz Nitrous acid; also HONO 

HNOs Nitric acid; also HONO2 

HO Hydroxyl group; also OH 

HOz Hydropheroxy radical 

HONO Nitrous acid 

HONOz Nitric acid 

H02N0 Pernitrous acid 

H02NO2 Pernitric acid; also HOONO2 

HOONOz Pernitric acid 

hr Hour 

hv Photon 

H2C0 Formaldehyde; also HCHO and CH2O 

Hz0 Water 

HzOz Hydrogen peroxide 

H2S Hydrogen sulfide 

H2SO4 Sulfuric acid 

I Intensity of sunlight 

1 2 lodi ne 

1 3 - Triiodide ion 

131, Radioisotope of iodine 

in. Inch 

IR Infrared 

JA Actinic irradiance 

k Rate constant; or, dissociation constant 

K Potassium 

K' Potassium ion 

KBr Potassium bromide 

kg Kilogram 

KH Horizontal eddy diffusivity coefficient 

KI Potassium iodide 

K, Photodissociation rate constant 

km Kilometer 

kPa Kilopascal 

kV Kilovolt 

xxiv 
Kv Vertical eddy diffusivity coefficient 

LA Los Angeles 

LARPP Los Angeles Reactive Pollutant Project 

Ib Pound 

LD50 Dose lethal to 50% of recipients 

LDH Lactic acid dehydrogenase 

LIRAQ Livermore Regional Air Quality (Model) 

I/min Liters per minute 

In Natural logarithm 

LT50 Time in whjch 50% of recipients of stated dose died 

Ix Lux 

M Third body (in a reaction) 

m Meter 

m Meta 

m2 Square meter 

m 3 Cubic meter 

MAO Monoamine oxidase 

max Maximum 

mb Millibar 

MBC Maximum breathing capacity 

MCP McKee, Childers, and Parr (test) 

Me Methyl 

MEFR Maximum expiratory flow rate 

mg Milligram 

mi Mile 

miz Square mile 

ml milliliter, 

min Minute 

min. Minimum 

mm Millimeter 

MMC Mean meridional circulation 

MMEF Mid-maximal expiratory flow rate 

mmol Millimole 

Mn02 Manganese dioxide 

mo Month 

mph Miles per hour 

MS Mass spectroscopy 

n Normal 

Nz N itrogen 

ON2 Single breath N2 alveolar plateau 

n/a Not applicable 

NAD Nicotinamide adenine dinucleotide 

NAAQS National Ambient Air Quality Standard 

NADB National Air Data Bank 

NADH Reduced nicotinamide adenine dinucleotide 

NADP + Nicotinamide adenine dinucleotide phosphate 

NADPH Reduced nicotinamide adenine dinucleotide 

phosphate 

NAS National Academy of Sciences 

NATO/CCMS North Atlantic Treaty Organization/Committee on 

Challenges of Modern Society 

NBKI Neutral buffered potassium iodide 

NBS National Bureau of Standards 

ND No data; or, not detectable 

xxv 
Ne Neon 

NEDS National Emissions Data System 

NHs Ammonia 

nm Nanometer 

NMHC Nonmethane hydrocarbons 

NO Nitric oxide 

NO2 J ~ trogen dioxide 

NOx Ritrogen oxides 

N20 Nitrous oxide 

N205 Nitrogen pentoxide 

NPSH Nonprotein sulfhydryls 

o Ortho 

0 Atomic oxygen 

02 Oxygen 

03 Ozone 

OAQPS Office of Air Quality Planning and Standards, EPA 

O.D. Orthostatic dysregulation 

O('D) or 0( 1 A) Excited atomic oxygen 

OH Hydroxyl group; also HO 

OH° Hydroxyl radical 

Os.Olefin Ozonides 

O(3 P) Ground-state atomic oxygen 

OX Photochemical oxidants 

P Probability (of observed results occurring by chance) 

p Para 

32P Radioisotope of phosphorus 

PAN Peroxyacetylnitrate 

Paoz Arterial oxygen tension 

PAQ Present air quality 

PBN Peroxybutyrylnitrate 

PBzN Peroxybenzoylnitrate 

6-PG 6-phosphogluconate 

6-P-GD 6-phosphogluconate dehydrogenase 

pH Measure of acidity (negative logarithm of hydrogen 

ion concentration) 

P,,,BN Peroxyisobutyrylnitrate 

PMN Polymorphonuclear leukocytes 

PNH Paroxysmal nocturnal hemoglobinuria 

Poz Oxygen tension 

PP Photoperiod 

ppb Parts per billion 

ppb C Parts per billion expressed as carbon 

pphm Parts per hundred million 

ppm Parts per million 

ppm C Parts per million expressed as carbon 

PPN Peroxypropionylnitrate 

ppt Parts per trillion 

psi Pounds per square inch 

PST Pacific standard time 

Pst TLC Maximal transpulmonary pressure 

r Correlation coefficient 

R Roentgen 

RAPS (St. Louis) Regional Air Pollution Study 

Raw Airway resistance 

xxvi 
RBC Red blood cells; erythrocytes 

RCHO Higher aldehydes 

RC(0)02 Peroxyacyl radical 

RC002 Organic peroxy compounds 

RC002H Organic peracids 

RC(0)02NO2 Peroxynitrates 

RDW Root dry weight 

RH Relative humidity 

RHC Reactive hydrocarbons 

RL Pulmonary resistance 

ROz Alkoperoxy radical 

RONO2 Organic nitrates 

ROzNOz Organic peroxynitrates 

ROOH Organic hydroperoxides 

rpm Revolutions per minute 

Rt Flow resistance 

RTI Research Triangle Institute 

RTP Research Triangle Park 

RV Residual volume 

S Sulfur 

-S- Sulfide linkage 

SAI Systems Applications, Inc. (Model) 

SBR Styrene-butadiene rubber 

S.D. Standard deviation 

sec Second 

SEM Scanning electron microscopy 

S.F. San Francisco 

SGaw Specific airway conductance 

SGPT Serum glutamic-pyruvic transaminase 

SH Sulfhydryl group 

SMSA Standard metropolitan statistical area 

SOz Sulfur dioxide 

SOs Sulfur trioxide 

SOx Sulfur oxides 

SOD Superoxide dismutase 

sp. or spp. Species 

SPM Suspended particulate matter 

90Sr Radioisotope of strontium 

SRI Stanford Research Institute 

SRM Standard reference material 

-SS- Disulfide linkage 

SSET Small-scale eddy transport 

STA Seasonal tropopause adjustment 

Std Desired air quality (standard) 

t Student"s statistic 

TDW Top dry weight 

TF Tropopause folding 

TGV Thoracic gas volume 

TLC Total lung capacity 

UKI Unbuffered potassium iodide 

UV Ultraviolet 

V25 Maximum expiratory flow rate at 25% of VC 

V50 Maximum expiratory flow rate at 50% of VC 

VC Vital capacity 

xxv i i 
VMT Vehicle miles traveled 

Voz Oxygen uptake 

Voz max Maximum oxygen uptake 

v/v Volume/volume 

W Watts 

wk Week 

wt Weight 

XO, X02 Compounds in which X represents hydrogen or an 

organic radical (R or RO) 

yr Year 

a Level of statistical significance set by investigator 

lug Microgram 

Ng/m3 Microgram per cubic meter 

Nm Micrometer 

/imol or /lmole Micromole 

> Greater than 

< Less than 

Approxi mately 

xxviu 
ABSTRACT 

This document is an evaluation and assessment of scientific information 

relative to determination of health and welfare effects associated with exposure 

to various concentrations of ozone and other photochemical oxidants in ambient 

air. The•document is not intended as a complete, detailed literature review. It 

does not cite every published article relating to oxidants in the environment and 

their effects. The literature through 1976-1977 has been reviewed thoroughly 

for infprmation relative to criteria. An attempt has been made to identify the 

major discrepancies in our current knowledge, again relative to criteria. 

Though the emphasis is on presentation of health and welfare effects data, 

other scientific data are presented and evaluated to provide a better 

understanding of the pollutants in the environment. To this end, separate 

chapters are included on the nature and atmospheric concentrations, of 

photochemical oxidants, their sources and removal processes, oxidant 

precursorS, the relationships between ambient oxidants and precursor 

emissions, and measurement methodsfor ozone, oxidants, and their precursors. 

Specific areas addressed within a general area of health or welfare effects are 

as follows: Toxicological, clinical, and epidemiologic appraisals, and effects on 

vegetation, ecosystems, and materials. 

xxix 

1. SUMMARY AND CONCLUSIONS 

INTRODUCTION 

This document consolidates and assesses 

current knowledge regarding the origin of ozone 

and other photochemical oxidant pollutants and 

their effects on health, vegetation, certain 

ecosystems, and materials. This chapter 

summarizes the information contained in this 

document and includes conclusions that are 

believed to provide a reasonable basis for 

evaluating the effects on health or welfare that are 

produced by, various concentrations of ozone and 

other photochemical oxidants. Although nitrogen 

dioxide is considered one of the photochemical 

oxidants, oxides of nitrogen are the subject of a 

separate report and are therefore discussed in this 

document only as they participate in the formation 

and reactions of other photochemical oxidants. 

Hydrocarbor s(HC) and other organics are 

important air oollutants almost entirely because 

they are precu -sors of other compounds formed in 

the atmosph -ric photochemical system, not 

because thPy produce any direct effects 

themselves. -,:)xic organics are considered only 

with respect to eye irritation. 

The studies and data cited constitute the best 

available bas , 3 for specific standards aimed at 

protecting hu nan health and the environment 

from photochemical oxidants in ambient air. 

NATURE AND ATMOSPHERIC CONCENTRATIONS OF PHOTOCHEMICAL OXIDANTS 

Photochemical oxidants are products of atmospheric reactions involving organic pollutants, 

nitrogen oxides (NOx), oxygen, and sunlight. They 

consist mostly of ozone, NO2, and peroxyacetylnitrate (PAN), with smaller amounts of other 

peroxyacylnitrates and other peroxy compounds, 

and they are formed along with other 

photochemical products such as aldehydes, 

nitrous acid, nitric acid, and formic acid. 

Photochemical oxidants originate mainly from 

volatile organic and NOx emissions produced by 

human activities. Photochemical oxidant 

formation is a complex function of emissions and 

meterological patterns. 

Peak concentrations of oxidant, expressed as 

ozone, are generally higher in urban and suburban 

areas than in rural areas, reaching levels i excess 

of 590 Ng/m3 (0.3 ppm). In rural areas, peak 

concentrations are lower but often exceed the 1-hr 

National Ambient Air Quality Standard of 160 

pg/m3 (0.08 ppm). However, dosages or average 

concentrations in rural areas are comparable to or 

even higher than those in urban areas. Because of 

pollutant transport, oxidant pollution is a regional 

rather than a local problem. 

SOURCES AND SINKS OF OXIDANTS 

AII of the evidence presently available shows 

that in and around urban centers that have severe 

oxidant/ozone pollution, photochemical oxidant 

formed from anthropogenic organics and NO, is 

the majorcontributor. SinceAir Quality Criteria for 

Photochemical Oxidants was issued in 1970, the 

mechanisms of atmospheric oxidant/ozone formation have been studied intensively and are now 

understood in greater detail. Most noteworthy are 

recent findings pertaining to the roles of hydroxyl 

(OH•) and hydroperoxy (HO•z) radicals. The reaction 

with OH• has been established to be a majorhydrocarbon-consuming process, and OH• and 

HO•2 have been identified as having major roles in 

the atmospheric oxidation of NO to NO2. Aldehydes 

and PAN have also been found to play important 

roles in the atmospheric reaction. For olefins and 

paraffins, at least, these reactions are now 

understood to the extent that the kinetics of 

photochemical hydrocarbon-NO, reaction 

systems, as observed in the laboratory, can be 

described with reasonable accuracy. Additional 

research is needed to explain the atmospheric 

reactions of aromatic hydrocarbons and to clarify 

further the differences between laboratory and 

ambient atmospheric chemical systems. 

The photochemical formation of oxidant/ozone 

is the result of two coupled processes: (1) a 

physical process involving dispersion and 

transport of precursors to oxidants (e.g., HC and 
NOx), and (2) the photochemical reaction process. 

Both processes are strongly influenced by 

meteorological factors such as dispersion, solar 

radiation, temperature, and humidity. Recent data 

on wind velocity and mixing height show that 

episodes of limited dispersion are most common in 

the Far West and in the Rocky Mountains region, 

least common over the Plains States, and of 

intermediate frequency east of'the Mississippi. 

New measurements of solar radiation indicate that 

the distribution of light intensity among respective 

wavelength intervals is different from that 

previously reported, which results in higher 

photodissociation constantsfor NOz in the ambient 

atmosphere. Recent field and laboratory studies 

suggest that at temperatures below approximately 

550 to 60°F, concentrations of photochemical 

ozone are unlikely to exceed the national 1-hr 

standard of 160 Ng/m 3 (0.08 ppm). 

For understanding the sources of photochemical 

oxidants or ozone (oxidant/ozone), perhaps the 

most important recent development is the 

identification of short- and intermediate-range and 

synoptic-scale transport of photochemical 

oxidant/ozone. Short-range (urban-scale) 

transport causes the highest ozone concentrations 

some distance downwind from the core area 

(region of highest emission) of an urban center. 

Intermediate-range (mesoscale) transport occurs 

as urban oxidant/ozone plumes extending as far 

as 100 miles or more downwind and is also 

involved in land-sea breeze circulation. Finally, 

synoptic-scale transport over several hundred 

miles, associated with high-pressure systems, has 

been found to occur extensively. These findings 

have significant implications with respect to the 

location of oxidant/ozone monitoring stations. 

Conditions during long-range transport are such 

that ozone production per unit of precursor is 

enhanced. Also, many organics previouslythought 

to be unreactive are now believed to have 

significant ozone-producing potential. 

In addition to photochemical reactions of 

anthropogenic emissions, potential sources of 

oxidant/ozone in the troposphere are the intrusion 

of stratospheric ozone and the photochemical 

reactions of natural organic and NOX emissions. 

Estimates of ground-level concentrations of ozone 

originating in the stratosphere are based on two 

types of evidence: (1) global circulation patterns, 

namely, patterns in air interchange between 

stratosphere and troposphere; and (2) data on 

variations of ozone concentrations in remote rural 

areas. Based on the evidence of stratospheretroposphere interchange, the annual average 

stratospheric contribution to ozone concentrations at ground level is estimated to be 43 to 

98 Ng/m3 (0.022 to 0.05 ppm). The highest 

concentrations, at or above 160 Ng/m 3 (0.08 ppm), 

from that source are expected to occur mainly 

during April and May. Analysis of ozone data for 

rural areas indicated that major intrusions of 

stratospheric ozone also occur during the spring 

months in rnid-latitudes. The highest 1-hr 

concentration of stratospheric ozone reaching 

ground level during the smog season (usually late 

summer or early fall) has been found to range from 

29 to 78 pg/m3 (0.015 to 0.040 ppm), depending 

on the investigator. More recent data obtained at 

Whiteface Mountain, New York, suggest a 

maximum 24-hr concentration of 72 Ng/m 3 (0.037 

ppm) stratospheric ozone in July. 

Certain organic emissions from vegetation 

(terpenes) play the dual role of oxidant/ozone 

precursor and scavenger. Despite the substantial 

rates at which they are emitted in forested areas, 

the ambient concentrations of such organics, 

because of their reactivity and the areal dispersion 

of their sources, seldom exceed a few parts per 

billion (ppb). At these concentrations, the direct 

potential of terpenes for photochemical ozone 

formation is estimated to be negligible. It is 

conceivable, however, that the products of 

atmospheric reactions involving large amounts of 

terpenes do have a significant impact on 

oxidant/ozone-related air quality. 

OXIDANT PRECURSORS 

Organic pollutants in urban atmospheres 

consist mainly of hydrocarbons from automobile 

exhaust and fuel evaporation, and of oxygenated 

hydrocarbons and halocarbons emitted mainly 

from manufacturing and from the use of organic 

chemicals. In urban atmospheres, total organic 

concentrations, reported usually as 6- to 9-a.m. 

averages of total nonmethane hydrocarbons 

(NMHC), are typically in the 1-ppm range and can 

be as high as 10 ppm or even higher, as in Los 

Angeles. In rural and remote atmospheres, the 

composition and concentration of organic pollutants are uncertain, largely because of deficiencies 

in the analytical methods available for determining 

the concentrations involved. Evidence suggests 

that NMHC levels are generally less than 0.1 ppm, 

a fraction of which consists of vegetation-related 

terpenes. 

Concentrations of NOX in urban atmospheres 

vary within a wide range, with highest values 
exceeding 1 ppm. Such concentrations appear to 

decrease rapidly as the air mass moves away from 

the city In rural and remote areas, ambient 

concentrations do not exceed a few ppb and are 

often below the 5 ppb detection limit of current 

commercial NOx analyzers. 

Hydrocarbons and NOX are emitted to the 

atmosphere from both natural and manmade 

sources, with natural sources probably contributing more on a global scale. Natural and 

anthropogenic sources are, however, generally 

segregated geographically, so that anthropogenic 

emissions are concentrated in the populated urban areas. Thus it is the latter that are most 

relevant to oxidant/ozone pollution problems 

downwind from populous areas. At present, 

mobile sources appear to account for the major 

part of the organic compounds emitted in most 

urban areas. The imposition of emission standards 

for mobile sources has reduced the reactive 

hydrocarbon component of emissions from 

gasoline-powered vehicles. 

RELATIONSHIPS BETWEEN AMBIENT 

OXIDANT AND PRECURSOR EMISSIONS 

Quantitative relationships between ambient 

oxidant/ozone and precursor emissions are 

needed for predicting the impact of these 

emissions on air quality. Such relationships 

represent, with varying degrees of complexity, the 

physical and chemical processes taking place in 

the atmosphere. 

Air quality simulation models (AQSM's), a 

number of which are available, represent an 

approach to relating precursor emissions to 

oxidant air quality. However, AQSM's require a 

great deal of computation and have not been 

adequately evaluated. 

In summary, satisfactory methods of relating the 

emission of precursors to oxidant concentrations 

in ambient air are not yet available. Forthis reason, 

the U.S. Environmental Protection Agency has 

been sustaining an intensive research effort to 

develop and validate satisfactory models that 

relate emissions to air quality. Based on results of 

this research and on model performance standards 

yet to be defined, the Agency will recommend 

specific models for use in formulating optimum 

ozone control strategies. 

MEASUREMENT METHODS FOR OXIDANT 

AND OXIDANT PRECURSORS 

The chemiluminescence method, based on the 

gas-phase reaction of ozone with ethylene, was 

adopted by EPA as the reference method and is 

now being used extensively. Several commercial 

instruments based on reference methods specified 

in EPA's Ambient Air Monitoring Reference and 

Equivalent Methods have been found to perform 

better than required by these EPA regulations. 

Techniques for continuous measurement, based 

on gas-solid chemiluminescence and ultraviolet 

(UV) photometry, have been developed and 

designated as equivalent methods. 

Extensive studies in recent years have shown 

that various traditional KI calibration procedures 

for oxidant or ozone analyzers are deficient, and 

that these methods suffer from lack of both 

precision and accuracy. 

Methods for measuring total oxidants are based 

on the oxidation of potassium iodide (KI) and the 

electrochemical or colorimetric detection of iodine 

(Iz). Nitrogen dioxide, however, causes a positive 

interference, and S02 causes a negative 

interference in these methods; these interferences 

are very difficult to correctfor. EPA intends to study 

and evaluate several new calibration procedures 

and to amend Appendix D of 40 CFR Part 50 to 

revise the 1 percent neutral buffered potassium 

iodide (NBKI) calibration procedure or to replace it 

with one or more of several alternatives under 

consideration. These alternatives are: (1) gasphase titration (GPT) with excess N0; (2) UV 

photometry; (3) GPT with excess 03; and (4) boric 

acid KI. 

Commercial instruments for monitoring total 

nonmethane hydrocarbon (NMHC) in ambient air 

have been tested extensively and found to be 

inaccurate at NMHC levels approaching the 0.24- 

ppm C air quality standard. At present, 

hydrocarbons in ambient air can be accurately 

measured only by sophisticated gas chromatography. Routine methods are under development. 

On December 1, 1976, EPA promulgated a new 

principle and calibration procedure for measuring 

NO2. The measurement principle is the gas-phase 

chemiluminescent reaction of Os and NO. Two 

calibration procedures are prescribed. One is a 

GPT procedure referenced to an NO-in-nitrogen 

standard. The other calibration procedure is 

referenced to an NO2 permeation device. Before 

the development of chemiluminescence analyses, 

most NO2 data were collected using methods 

based on variations of the Griess-Saltzman 

procedure. For all practical purposes, these 

methods have been replaced by the 

chemiluminescence method 

3 
HEALTH EFFECTS OF OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS 

In this section, the influence of exposure to 

ozone and other photochemical oxidants on 

physiology and health is assessed, beginning with 

a brief discussion of the concept of "threshold 

pollutant concentrations" and itsapplicationtothe 

protection of public health. Then, the strength of 

association between exposure to ozone and other 

oxidants and changes in several types of 

biomedical indicators is evaluated. 

For each type of indicator, the discussion 

addresses four ma in topics: (1) the degree to which 

changes in each type constitute impairments in 

public health; (2) the available scientific evidence 

relating ozone and other oxidant exposures to 

changes within each type; (3) the reliability of 

existing scientific evidence; and (4) where 

appropriate, the confidence with which findings 

may be attributed to ozone alone, as opposed to 

other substances or combinations of substances. 

Whenever possible, clinical (human experimental) and epidemiologic studies will be 

discussed together. However, because of the great 

uncertainty inherent in the quantitative 

extrapolation of results of animal studies to 

humans, human and ariimal studies wiil be 

discussed separately. 

Discussion of Threshold Concentrations 

The Clean Air Act directs that National Primary 

Ambient Air Quality Standards be such that their 

attainment and maintenance shall, in the 

judgment of the Administrator, and allowing an 

adequate margin of safety, be requisite to protect 

the public health. The confidence with which a 

margin of safety can be defined depends on the 

precision with which a threshold pollutant 

concentration, (the level above which exposure to 

ozone or other oxidants promotes impairment of 

health and below which it does not) can be 

determined. 

In practice, no single overall threshold 

concentration for ozone or other pollutants exists. 

Thresholds have been shown to vary widely with 

the population segment studied and the biologic 

indicators measured. Also, since the great majority 

of known dose-response relationships do not show 

sharp discontinuities, it is most unlikely that a 

discrete threshold pollutant concentration can be 

established even for a single population segment 

and a single biomedical indicator. 

Despite these limitations, the environmental 

decisionmaker may find it useful to incorporate the 

concept of threshold concentrations into the 

standard-setting process. For a given population 

segment, a threshold concentration may be 

operationally defined as occurring somewhere 

between a concentration at which no effect on 

health or 'function has been observed, and a 

concentration at which such an effect has been 

demonstrated. In protecting public health, the 

population segments of primary concern are the 

most susceptible groups, in whom exposure to 

ozone or other pollutants is most likely to promote 

impairment of health. Such groups may include 

those with underlying illness, the very old, the very 

young, and the pregnant. (It has not 5een 

determined whether such susceptible population 

segments differ from the most sensitive population 

segments, which comprise those individuals most 

likely to show measurable responses to very low 

pollution concentrations.) 

Ideally, the environmental decisionmaker would 

know the pollutant concentrations with which no 

adverse effects are associated in susceptible 

groups, as well as the concentrations with which 

such adverse effects are unambiguously 

associated. Unfortunately, knowledge in both of 

these areas remains sparse. Recent experimental 

studies of healthy people and animals have greatly 

advanced our knowledge of the health effects of 

ozone. However, threshold concentrations 

deducible from such studies may not apply to the 

potentially susceptible groups described above. 

The opportunity to study such groups experimentally is severely limited by practical and ethical 

constraints. The relatively few epidemiologic 

studies of these groups that are extant have 

yielded inconclusive results. 

Human Studies 

SHORT-TERM OXIDANT EXPOSURES 

Mechanical Function Of The Lung 

Assessment Of Health Effect. There is considerable room for honest disagreement on 

whether pollution-induced alterations in 

mechanical lung function constitute bona fide 

impairments of health in and of themselves. In the 

great majority of experimental studies in which 

oxidant exposures have produced changes in lung 

function in healthy subjects, function has returned 

to normal within a few hours. Thus there is no 

reason to suspect that in healthy individuals such 

changes promote any measurable increase in risk 

4 
of future illness. Nor does any available evidence 

suggest that in healthy individuals a small change 

in ventilatory function, unaccompanied by 

symptoms or impairment of oxygen uptake orwork 

capacity, would interfere with normal activity or 

task performance. 

However, three considerations suggest that 

oxidant-associated changes in lung function may 

signal impairment of public health. First, in persons with underlying respiratory illness such as 

asthma, chronic bronchitis, and emphysema, even 

small decrements in lung function often interfere 

with normal activity. Second, at experimental 

ozone concentrations as low as 0.30 ppm, 

decrements in lung function have usually been 

accompanied by physical discomfort, as 

manifested i n symptoms such as sore throat, chest 

pain, cough, and headache. At times this 

discomfort has been great enough to prevent the 

completion of experimental protocols, particularly 

when subjects have been exercising vigorously. It 

appears quite likely that the pulmonary irritant 

properties of ozone (and perhaps other oxidants) 

underlie both the discomfort and the decrements 

in function. Thus, at least when associated with 

ozone exposure, changes in lung function often 

represent a level of discomfort that, even among 

healthy people, may restrict normal activity or 

impair the performance of tasks. 

Summary Of Data. Human experimental studies 

have demonstrated that the subject's level of 

exercise during ozone exposure is directly related 

to the magnitude of change in lung function and 

the severity of symptoms at any given ozone 

concentration. During exercise, subjects increase 

their expiratory flow rates, and they tend to breathe 

through their mouths. These factors increase the 

total dose of ozone delivered to the lung and may 

increase the depth to which it is delivered in the 

respiratory tree. 

After 2 hr of resting exposure to 1470 Ng/m 3 

(0.75 ppm), healthy young adults showed small 

changes in lung function in a study by Bates et al. 

Folinsbee et al. observed changes in respiratory 

pattern (increased respiratory frequency and 

decreased tidal volume) and reductions of vital 

capacity in healthy young adults exercising 

subm4ximally after a similar resting exposure. 

Immediately after 2 hr of exposure to 1470pg/m 3 

(0.75 ppm) ozone, during which they performed 

intermittent light exercise, subjects showed quite 

pronounced changes in lung function in studies by 

Folinsbee et al. and Hazucha et al. In subjects 

exposed under the same conditions, Folinsbee et 

al. observed changes in respiratory pattern, though 

not in minute volume or oxygen uptake. 

In subjects exercising maximally after 2 hr of 

exposure to 1470 Ng/m 3 (0.75 ppm) ozone and 

intermittent light exercise, Folinsbee et al. 

observed decrements in maximum work load, tidal 

volume, heart rate, and oxygen uptake. 

Folinsbee et al. observed decreases in tidal 

volume and maximum expiratory flow rate at 50 

percent of vital capacity (V so ) in subjects exercising 

submaximally after 2 hr of exposure to 980 pg/m 3 

(0.5 ppm) ozone and intermittent light exercise. In 

subjects giving no history of cough, chest 

discomfort, or wheezing in response to allergy or 

air pollution exposure (unreactive subjects), few 

changes in lung function occurred after 4 hr of 

exposure to 980 /jg/m 3 (0.50 ppm) and 

intermittent light exercise (Hackney et al.). 

However, in subjectsgiving such a history(reactive 

subjects) and receiving an identical exposure, the 

same investigators observed decrements in 8 of 14 

measured parameters. Interestingly, in a second 

group of unreactive subjects, the same investigators observed substantial decrements in 

lung function after only 2 hr of exposure to 980 

μg/m3 (0.5 ppm) ozone and intermittent light 

exercise. 

Statistically significant changes in forced vital 

capacity, maximum mid-expiratory flow rate, and 

airway resistance in 22 young males after 2 hr of 

exposure to 0.4 ppm ozone and intermittent 

moderate exercise were observed by Knelson et al. 

After subjects had been exposed for 4 hr, changes 

in these parameters had increased, and several 

other flow parameters had also changed 

significantly in comparison with control values. 

In studies by Hazucha and Bates, Hazucha et al., 

and Folinsbee et al., subjects showed changes in 

lung function after 2 hr of exposure to 730,Ug/m 3 

(0.37 ppm) ozone and intermittent light exercise. 

Hackney et al. observed such changes in reactive 

subjects but not in unreactive subjects. In a 

separate study by Hackney and colleagues, four 

Canadians and four southern Californians were 

exposed in the Los Angeles area to 730 Ng/m 3 

(0.37 ppm) ozone for 2 hr. The Californians showed 

few changes in lung function, whereas the 

Canadians showed decrements in most 

parameters measured. (At least partly because of 

the small sample sizes, no observed changes were 

statistically significant.) In subjects exposed to 730 

pg/m 3 (0.37 ppm)ozone together with 1000%jg/m 3 

5 
(0.37 ppm) SOz, Hazucha and Bates observed an 

effect on lung function substantially larger than 

the sum of the separate effects of the individual 

pollutants. 

DeLucia and Adams observed changes in lung 

function and respiratory pattern in healthy 

subjects exercising steadily and fairly heavily over 

a 1-hr exposure to 590 Ng/m 3 (0.30 ppm) ozone. 

Two of six subjects experienced such discomfort as 

to prevent them from completing the experimental 

protocol. 

Hazucha observed small changes in lung 

function in three nonsmokers exposed for 2 hr to 

490 /1g/m 3 (0.25 ppm) ozone and intermittent light 

exercise. No lung function changes of note were 

seen by Hackney et al. even among reactive 

subjects who were similarly exposed. 

After 1 hr of exposure to 290 Ng/m 3 (0.15 ppm) 

ozone and steady, fairly heavy exercise, subjects 

observed by DeLucia and Adams showed changes 

in respiratory pattern. In two of six subjects, the 

same investigators noted inconsistent increases in 

residual volume. 

Small but statistically significant increases in 

airway resistance, as measured by plethysmography, were observed in two of four healthy 

subjects immediately after a 1-hr exposure to 200 

ug/m3 (0.1 ppm) ozone. The investigators 

(Goldsmith and Nadel) did not state whether the 

subjects exercised during exposure. 

Von Nieding and Wagner reported that subjects 

showed decrements in arterial oxygen pressure 

(Pa12) and airway resistance after 2 hr of exposure 

to 200 /.rg/m3 (0.10 ppm) ozone and intermittent 

light exercise. 

Kagawa and Toyama reported the results of 

Japanese epidemiologic studies relating lung 

function in Japanese elementary school children 

to daily air pollution level. In approximately 25 

percent of the children studied, lung function 

parameters were significantly correlated with the 

average ozone concentration in the 2 hr before 

testing. During these studies, the ozone 

concentration ranged between 20 and 590/jg/m 3 

(0.01 and 0.30 ppm). Correlations of lung function 

with ozone exposure were generally greater than 

with total oxidant exposure, and correlations of 

ozone exposure with parameters reflecting upper 

airway function were generally greater than with 

those reflecting Iowerairwayfunction.Thedesign 

of these studies precludes the inference of specific 

dose-response relationships. 

Refiability Of Evidence. Available evidence 

showing that 730,ug/m 3 (0.37 ppm) ozone has an 

effect on the lung function of lightly exercising 

subjects is convincing. Though it remains 

unreplicated, the study of DeLucia and Adams 

raises the distinct possibility that an ozone 

concentration of 590 pg/m 3 (0.30 ppm) exerts a 

temporary effect on the lung function of healthy 

subjects exercising fairly strenuously. The same 

investigators have raised the question as to 

whether ozone concentrations as low as 290 

/jg/m 3 (0.15 ppm) exert effects in a portion of 

healthy subjects exercising strenuously. 

The findings of Nadel and Goldsmith suggest 

that certain changes in lung function may be 

detectable in some healthy subjects who have 

been exposed to 200 Ng/m 3 (0.1 ppm) of ozone. For 

three reasons, however, these findings do not 

suggest any endangerment of public health. First, 

the subjects experienced no physical discomfort 

while exposed to 200 Ng/m 3 (0.1 ppm) ozone. 

Second, the observed changes in airway 

resistance were small. Third, thetwo subjects who 

showed significant increases in airway resistance 

after exposure to 200 /ig/m 3 (0.1 ppm) ozone 

shovyed smaller, nonsignificant increases in 

airway resistance after exposure to 780ug/m 3 (0.4 

ppm) ozone. 

The studies of Von Nieding and Wagner, though 

interesting, are unconfirmed. These investigators 

did not use standard techniques to measure airway resista nce; nor did they draw arterial blood for 

Pa o z measurements. Instead, they drew 

arterialized blood from the subjects' ear lobes. 

Thus, until confirmed with generally accepted 

methods, these studies must be interpreted with 

caution 

The studies of Kagawa andToyama, likethoseof 

DeLucia and Adams and of Hackney, suggest that 

even among healthy individuals there is a 

considerable range of sensitivity to ozone 

exposure. Whether the lung function of respiratory 

disease patients is more sensitive to such 

exposure than that of healthy persons has not been 

determined. However, as mentioned above, the 

clinical significance of changes in lung function is 

likely to be greater in respiratory disease patients 

than in healthy subjects. 

The experimental study of Canadians and 

Californians by Hackney et al. is consistent with 

the hypothesis that repeated oxidant exposures 

promote adaptation toward the maintena nce of full 

lung function. More study is required to confirm 

this hypothesis and to investigate whether 

6 
adaptation in lung function is of any long-term 

consequence to health. 

Attributability Of Effects To Ozone. Experimental 

studies have shown that ozone at concentrations 

observed in the ambient air can produce changes 

in mechanical lung function. The epidemiologic 

studies of Kagawa and Toyama, in which lung 

function was correlated more strongly with ozone 

exposure than with total oxidant exposure, are 

consistent with this finding. However, the degree 

to which epidemiologic observations may be 

attributed specifically to ozone remains in doubt, 

since Kagawa and Toyama were not able fully to 

separate the effects of ozone from the effects of 

other environmental factors. 

Finally, the work of Hazucha and Bates suggests 

that the effect on lung function of ozone at 730 

Ng/m3 (0.37 ppm) may be enhanced by an identical 

concentration of sulfur dioxide. Observation of this 

enhancement argues in favor of providing a margin 

of safety in a primary National Ambient Air Quality 

Standard for ozone. However, this observation 

does not support a quantitative recommendation 

for a safety margin, since it has not yet been 

determined whether such enhancement occurs at 

lower ozone concentrations or with substances 

other than sulfur dioxide. 

Impairment Of Physical Performance — 

Decrements in physical performance are 

deterrents to personal satisfaction. In this respect, 

such decrements constitute impairment of public 

health. The degree to which oxidant exposures 

may promote decrements in physical performance 

has not been determined. However, Wayne et al. 

assessed the association between hourly oxidant 

concentrations and the proportion of a high school 

cross-country team failing to improve running 

times between successive track meets in southern 

California. Over six cross-country seasons, the 

correlation of average oxidant concentration inthe 

hour before the race with the proportion of runners 

failing to improve times was 0.88. The 

corresponding correlation for both the first and 

second three-season periods was 0.945. A 

correlation this high denotes a very close 

numerical relationship between two variables. 

During the period studied, hourly oxidant 

concentrations ranged from approximately 60 to 

590 /ag/m3 (0.03 to 0.30 ppm). Inspection of the 

data of Wayne et al. reveals no obvious 

relationship between unimproved running time 

and oxidant concentrations below 200 to 290 

Ng/m 3 (0.10 to 0.15 ppm), in spite of the high 

overall correlations mentioned above. Also, since 

the authors did not consider ozone separatelyfrom 

other oxidants, the specific contribution of ozone to 

the observed results cannot be determined from 

this study. 

As far as can be ascertained, no replication of the 

study of Wayne et al. has appeared in the published 

literature. For three reasons, however, the data 

from this study are more trustworthy than most 

results of a single epidemiologic study. First, the 

correlations between hourly oxidant concentration 

and unimproved running time were unusually 

high. Second, as mentioned in Chapter 10 of this 

document, Herman, at the University of North 

Carolina, has analyzed the data of Wayne et al. as 

well as data from two additional seasons, and he 

has observed results similar to those of Wayne et 

al. Third, the results of Wayne et al. are 

qualitatively consistent with the results of the 

experimental lung function studies meritioned 

above, especiallythose of Folinsbee et al. In viewof 

these experimental studies, it would also appear 

plausible that ozone contributed significantly to 

the results of Wayne et al. 

Oxidant Effects In Asthmatics - In the United 

States, there are an estimated 6 to 8 million 

asthmatics, about 70 percent of whom are 

estimated to live in urban areas. Thus, the number 

of asthmatics who may be exposed to elevated 

oxidant concentrations is substantial. 

Available epidemiologic evidence on the 

relationship between oxidant exposure and 

exacerbation of asthma is very limited. In 1961, 

Schoettlin and Landau reported that the proportion 

of selected asthmatics in the Pasadena area 

having attacks was significantly greater (p <0.05) 

on days when the maximum hourly oxidant 

concentration exceeded 490 /jg/m 3 (0.25 ppm) 

than on days when the corresponding 

concentration was below this level. However, the 

proportion of asthmatics having attacks on days of 

maximum hourly oxidant concentration above 250 

Ng/m 3 (0.13 ppm) was not significantly different 

from the corresponding proportion when the 

maximum hourly concentration was below this 

level. The authors did not state the actual 

percentage of asthmatics having attacks on days in 

any exposure category, though they did state that 

asthma attacks tended to coincide with elevated 

oxidant levels in 8(6 percent) of 137 patients 

studied. 

Because it does not present asthma attack rates, 

the Schoettlin and Landau report gives no 

7 
indication whether increases in attack rates might 

have been expected at maximum hourly oxidant 

concentrations below 490 Ng/m 3 (0.25 ppm). Nor 

does it allow any judgments as to the extent to 

which increased attack rates might be attributable 

specifically to ozone. Despite the considerable 

attention it has received, this report should be 

considered the preliminary investigation its 

authors intended it to be. 

Respiratory Symptoms and Headache 

Assessment Of Health Effect. As mentioned 

above, increased rates of respiratory symptoms 

and headache constitute impairment of public 

health. Even when mild, such symptoms are 

annoying. Even when reversible, they may restrict 

normal activity or limit the performance of tasks. 

Summary Of Data. In nearly all experimental 

studies in which ozone exposures have been 

sufficient to produce changes in lung function, 

most subjects have reported respiratory 

symptoms. The most common symptoms have 

been throat tickle, substernal tightness, pain on 

deep inspiration, and cough. Wheezing, dyspnea, 

and headache have occurred less commonly. 

Symptom severity has increased with ozone 

concentration and exercise. In studies of heavy 

exercise, symptoms have occasionally been severe 

enough to prevent subjects from completing 

experimental protocols. 

In an epidemiologic study in southern California, 

Hammer et al. assessed the association between 

daily maximum hourly oxidant concentration and 

rates of chest discomfort, cough, and headache 

among student nurses. Rates of each of these 

symptoms, whether unadjusted or adjusted for 

fever, began to increase in the following oxidant 

concentration ranges: chest discomfort, 490 to 

570 Ng/m3 (0.25 to 0.29 ppm); cough, 590 to 760 

Ng/m 3 (0.30 to 0.39 ppm); and headache, 290 to 

370 /ag/m3 (0.15 to 0.19 ppm). Adjusted and 

unadjusted rates of headache, however, were not 

unequivocally elevated below maximum hourly 

oxidant concentrations of 590 to 760 Ng/m 3 (0.30 

to 0.39 ppm). 

Several Japanese investigators have assessed 

the association between daily pollutant 

concentrations and symptom rates among 

students. In one Japanese study, rates of sore 

throat, dyspnea, and headache were somewhat 

higher during the summer months on days when 

the oxidant concentration exceeded 200 /jg/m 3 

(0.10 ppm) than on days when it did not. Over a 1- 

year period, rates of respiratory symptoms and 

headache were higher on days when the oxidant 

concentration exceeded 290 Ng/m 3 (0.15 ppm) 

than on days when it was lower than 200Ng/m 3 

(0.10 ppm). Though there is reason to believe that 

the stated oxidant concentrations were daily 

maximum hourly averages, averaging times were 

not clearly presented in the report of this study. 

Reliability Of Evidence. Because of their close 

correlation with the results of experimental 

studies, the results of Hammer et al. appear to be 

quite reliable, even though unconfirmed in this 

country. Their reliability is enhanced by the large 

number of person-days of observation (about 

53,000) L.,,:ompassed by the study. Though ozone 

levels were not considered in the Hammer et al. 

study, it is reasonable to hypothesize, in view of 

experimental studies, that ozone contributed 

substantially to observed increases in rates of 

cough, chest discomfort, and headache. 

As nearly as can be determined from 

translations of original articles, the Japanese 

epidemiologic studies cited in this document were 

appropriately designed. However, it is very difficult 

to interpret their results. Also, at least at present, 

the applicability of these results to any oxidant 

pollution problem in the United States must be 

considered very limited. 

In data analyses, Japanese investigators (like 

many U.S. investigators) have not been able fully to 

separate the effects of individual pollutants. It is 

conceivable that combinations of pollutants 

unique to Japan were necessary to promote the 

increased symptom rates observed there. 

Averaging times for pollutant measurements were 

not clearly stated in the Japanese studies. 

Therefore, it is often impossible to draw specific 

inferences as to dose and response. In addition, the 

degree to which differences in Japanese and U.S. 

cultural responses to air pollution may 

differentially affect symptom perception in the two 

countries has not been determined 

A problem more fundamental than any of these 

specific reservations, however, is that Japanese 

and U.S. investigators asyet have great difficulty in 

exchanging specific scientific concepts. Until the 

quality of scientific communication between these 

groups of investigators increases, the ability to 

interpret the Japanese studies and to apply them to 

situations in the United States will remain severely 

limited. 

Oxidants And Eye Irritation - In that it is annoying 

and uncomfortable, the reversible eye irritation 

8 
produced by exposure to ambient photpchemical 

oxidants may legitimately be considered a 

marginal impairment of public health. However, 

whether such eye irritation is sufficient to impair 

performance or restrict normal activity has not 

been determined. Nor has any association 

between oxidant-mediated eye irritation and 

chronic eye disease been observed. 

In epidemiologic studies, no symptom has been 

more consistently linked to oxidant exposure than 

eye irritation. In most studies reported before the 

publication in 1970 of Air Quality Criteria for 

Photochemical Oxidants, rates of eye irritation 

were observed to increase fairly steadily when 

oxidant cnncentrations ranged from 200 to 880 

Ng/m3 ,6.10to0.45ppm . Hammeretal.foundthat 

rates of eye discomfort began to increase at 

oxidant concentrations of 290 to 370 Ng/m 3 tJ.15 

to 0.19 ppm). 

Evidence linking ambient photochemial oxidant 

exposures to eye irritation is convincing. However, 

the specific etiologic agent or agents remain 

unknown. Experimental studies have shown quite 

conclusively that ozone at ambient conce'ntrations 

is not an eye irritant. 

Oxidants and Mortality - Reviewof existing studies 

shows no consistent association between daily 

oxidant concentrations and daily mortality rates. 

As far as can be ascertained, no studies of oxidant 

exposures and mortality have been performed 

sincethe publication in 1970 of Air Quality Criteria 

for Photochemical Oxidants. 

Other Effects Of Short-Term Ozone And Oxidant 

Exposure 

Changes ln Erythrocytes. In an experimental 

study, Buckley et al. observed increased rates of 

erythrocyte lysis in H2O2 after a 23/a-hr exposure of 

healthy subjects to 980/ag/m 3 (0.5 ppm) ozone and 

intermittent light exercise. These investigators 

also noted changes in the' activity of several 

erythrocytic enzymes. Hackney et al. observed an 

increased in vitro lysis rate in erythrocytes of Canadians, but not in that of Californians following a 2- 

hr exposure of subjects to 730 /!g/m 3 (0.37 ppm) 

ozone and intermittent light exercise. 

Chromosomal Aberrations. Merz et al. repdrted 

chromosomal abnormalities in the lymphocytes of 

six subjects after they were exposed to 980 /jg/m 3 

(0.5 ppm) ozone for 6 or 10 hrs. However, a study by 

McKenzie et al. showed no increased rate of 

leukocyte chromosomal aberration in the 

lymphocytes of 30 subjects exposed for 4 hr to 780 

Ng/m 3 (0.4 ppm) ozone. In the few epidemiologic 

studies of oxidant exposure and chromosome 

morphology performed to date, factors other than 

differences in oxidant exposure have confounded 

observed results to the extent that no inferences 

can be drawn. 

Biochemical Parameters. Buckley et al. observed 

reduced glutathione reductase activity and 

increased vitamin E and lipid peroxidation in 

human serum following exposure of subjects to 

980 Ng/m3 (0.5 ppm) ozone and intermittent light 

exercise for 2 3/a hr. Following a 2-hr exposure to 

730Ng/m3 (0.37 ppm) ozone and intermittent light 

exercise, the Canadians and Californians studied 

by Hackney et al. showed increases in serum 

vitamin E levels; but only in the Canadians were 

these increases statistically significant. 

After subjects exercised steadily and vigorously 

throughout a 1-hr exposure to 590 ug/m3 (0.30 

ppm) ozone, DeLucia and Adams observed no 

changes in the fol;owing biochemical blood 

parameters' hemoglobin level, nonprotein 

sulfhydryl level, erythrocyte glucose-6-phosphate 

dehydrogenase activity, and glutathione reductase 

activity. 

Clinical Significance. The clinical significance of 

ozone-mediated changes observed in studies of 

blood is not yet known. As yet, an epidemiologic 

study of oxidant effects on anemic individuals has 

not been done. Whether or not oxidant exposures 

promote changes in leukocyte chromosome 

morphology, the significance of the changes 

themselves is unknown. Finally, changes in serum 

parameters of the magnitude observed in 

ezperimental ozone studies have not yet been 

linked to any clinical diseases. 

LONG-TERM OXIDANT EXPOSURES 

With the exception of the Hackney et al study of 

Californians and Canadians, no experimental 

studies of humans have as yet assessed the effects 

of long-term oxidant exposures. The few available 

epidemiologic studies of such exposures have 

yielded inconclusive results. Mahoney has observed an association between broad patterns of 

oxidant distribution and annual respiratory disease 

mortality in the Los Angeles area. However, no 

convincing association between lung cancer 

mortality and oxidant exposure has been shown. In 

some studies, a limited association between the 

frequency of chronic obstructive lung disease and 

oxidant exposure has been observed. In other 

studies, however, no such association has been 

9 
apparent. No relationship between long-term 

oxidant exposure and acute respiratory disease 

incidence or change in lung function has been 

observed, though neither of these areas has been 

extensively investigated. 

Most available epidemiologic studies of longterm oxidant exposure are difficult to interpret. As 

usually acknowledged by the authors themselves, 

factors other than pollution exposure may often 

have influenced the results observed. Some 

studies have proved difficult to evaluate because 

areas in which health variables were compared did 

not show clear-cut differences in pollution 

exposure. Thus human studies cannot yet provide 

the environmental decisionmaker with concrete 

information as to the effects of long-term oxidant 

exposures on public health. 

Animal Toxicology Studies 

ANIMAL INFECTIVITY EXPERIMENTS 

Increased susceptibility of animals to bacterial 

infection following ozone exposure at 196 Ng/m 3 

(0.1 ppm) is described by several investigators 

(Coffin et al., 1968; Ehrlich et al., 1976; Gardner et 

al , 1974; Coffin and Gardner, 1972; Miller et al., 

1978). Others (Goldstein et al., 1971a, 1971b; 

Goldstein and Hoeprich, 1972; Goldstein et al., 

1974), using bacterial infection, have developed 

indices of infection for measuring the effects of 

ozone on the lungs of rodents. The effective 

concentration of ozone at which susceptibility to 

infection is increased is lower when either other 

pollutants or stress is combined with ozone 

exposure. These findings have definite human 

health implications, although different exposure 

levels may be associated with such effects in 

humans. These reactions in mice represent effects 

on basic biological responses to infectious agents, 

and there is no reason to believe that the pollutantinduced alterations of basic defense mechanisms 

that occur in mice could not occur in humans who 

possess equivalent defense systems. The 

extrapolation of these data to man is not supported 

by direct epidemiologic evidencethat susceptibility 

to infection increases in persons exposed to ozone 

and other photochemical materials. However, the 

biochemical and cellular alterations described 

below for animals suggest that multiple epithelial 

and biochemical targets are perturbed by ozone 

exposure. Ozone-induced irritation of the major 

bronchi in man does occur at ozone concentrations 

approximating 490/ag/m 3 (0.25 ppm). Fortracheal 

ozone concentrations greater than 100 pg/m 3 

(0.05 ppm), it is predicted that a smaller inspired 

concentration would be required in man than in 

rabbits and guinea pigs to result in a given 

respiratory bronchiolar dose (Miller et al., 1977). A 

3-hr exposure to 490 /jg/m 3 ozone (0.25 ppm) has 

been shown to be sufficiently high to injure rabbit 

alveolar macrophages. Thus, depending on the 

extent of nasopharyngeal removal of ozone in man, 

a given level may be expected to produce similar 

effects in man and certain animals. 

MORPHOLOGICAL ABNORMALITIES OF ANIMAL 

RESPIRATORY SYSTEMS 

A range of morphologica{ effects is noted in 

association with experimental ozone exposures of 

392 to 1 960 ug/m 3 (0.2 to 1.0 ppm). These effects 

vary from the reversible replacement of Type 1 

with Type 2 alveolar cells (e.g., 392 /jg/m 3 or 0.2 

ppm ozone for 3 hr/day over 7 days) to emphysematous changes and terminal bronchiolar and 

alveolar damage (e.g., 784 /jg/m 3 , or 0.4 ppm, 

ozone for 6 hr/day, 5 day/wk, for 10 months; and 

1058 Ng/m3 , or 0.54 ppm ozone continuous for 3 

months). Occurrence of these effects after longterm exposure to lowconcentrations increasesthe 

expectation that repeated or chronic exposures 

may have the potential for inducing similar effects 

in humans. 

BIOCHEMICAL EFFECTS 

There is an impressive variety of biochemical 

alterations associated with ozone exposures over 

the range of 196 to 1 960 Ng/m 3 (0.1 to 1.0 ppm). 

Though effects caused by levels of 980 pg/m 3 (0.5 

ppm) and greater have definite toxic potential, the 

biological significance of those changes detected 

in exposures to 196 to 392 ijg/m3 (0.1 to 0.2 ppm) 

are more difficult to assess. These biochemical 

changes are significant, however, in 

demonstrating that there are ozone-induced 

effects at cellular sites and in organ systems 

distant from the lung. Biological reactions to ozone 

include an increase in the activity of enzymes that 

detoxify oxidizing chemical species. Increased 

enzymatic activity, as well as increased oxygen 

consumption, has been shown in some instances 

to be prevented, reversed, or diminished by 

increased vitamin E levels (vitamin E is an 

antioxidant). Thus increased enzymatic activity 

may represent a reaction to potential toxicity rather 

than being a toxic response itself. Nevertheless, 

such reactions represent the organism's response 

to ozone. Such perturbations in biological systems 

may pose a health risk to the population, 

particularly for susceptible individuals. 

`[~7 
GENETIC AND TERATOGENIC POTENTIAL 

A report by Zelac (1971) on chromosomal 

abnormalities in peripheral leukocytes of intact 

hamsters which were exposed to 392 Mg/m3 (0.2 

ppm) ozone for 5 hr was not confirmed by Gooch et 

al. (1976). Although confirmation of the results 

may suggest another category of ozone-induced 

effects, the preliminary evidence does not suggest 

that these effects occur at lower levels of exposure. 

IMPLICATIONS OF ANIMAL TOXICOLOGY DATA 

Note that the difference between concentrations 

of ozone that produce toxicological effects in 

animals (as well as symptomatic and lung function 

changes in humans) and ambient air levels of 

ozone is much smaller than for nearly any other 

atmospheric pollutant. There is an unusual 

clustering and convergence of various 

toxicological, experimental human, and 

epidemiologically observed human effects in 

association with ozone concentrations ranging 

from 392 to 1 176 μg/m3 (0.2 to 0.6 ppm). 

Chronic effects of long-term ozone exposure in 

man cannot be quantitatively related to specific 

ozone concentrations of short (hourly or daily) 

averaging times because of the long period of 

disease induction and the varied exposures of 

individuals during the period of induction. 

Epidemiologic studies may establish relationships 

between long-term ozone exposure and the risk of 

human chronic disease, but toxicological studies 

must be relied on in quantifying the ozone levels 

that may induce chronic effects. 

Ozone Versus Oxidant Health Effects 

Two characteristics of ozone and oxidant 

exposures should be cited with reference to public 

health: (1) ozone itself is a primary cause of most of 

the health effects reported in toxicological and 

experimental human studies, and the evidence for 

attributing many health effects to this substance 

alone is very compelling; and (2) the complex of 

atmospheric photochemical substances is known 

to produce health effects, some of which (eye 

irritation, for example) are not attributable to pure 

ozone but may be caused by other photochemical 

substances in combination with ozone. 

EFFECTS OF PHOTOCHEMICAL OXIDANTS 

ON VEGETATION AND CERTAIN MICROORGANISMS 

Since injury to vegetation by oxidants was first 

identified in 1944 in the Los Angeles Basin, our 

understanding of oxidant effects and of the 

widespread nature of their occurrence has 

increased substantially. The major phytotoxic 

components of the photochemical oxidant complex 

are ozone and peroxyacetylnitrate (PAN), although 

some data suggest that other phytotoxicants are 

also present. The peroxyacylnitrates are the most 

phytotoxic of the known photochemical oxidants; 

but because ozone is ubiquitous and associated 

with widespread injury to vegetation, it is the most 

important phytotoxic component of the 

photochernical oxidant complex. 

The effects of photochemical oxidants on 

vascular plants occur at Several levels, ranging 

from the subcellular to the organismic, depending 

on the concentration and duration of exposure to 

the pollutant and the interval between cessation of 

exposure and examination of the plant. 

The earliest effect is an increase in cell 

membrane permeability. Following that, cellular 

and biochemical changes take place that are 

ultimately expressed on the organismic level as 

visible foliar injury, increased leaf drop, reduced 

plant vigor, reduced plant growth, and death. Such 

biochemical modifications in an individual plant 

are manifested by changes in plant communities 

and, finally, in whole ecosystems. 

Leaf stomata are the principal sites through 

which ozone and PAN enter plants. Oxidants affect 

photosynthesis, respiration, transpiration, 

stomatal opening, and metabolic pool 

development, as well as biochemical pathways 

and enzyme systems. 

Visible injury is identifiable as pigmented, 

chlorotic, or necrotic foliar patterns. Metabolic 

cellular disturbances can occur without visible 

injury and may be reversible. However, mostofthe 

growth effects reported until recently were 

accompanied by visible injury. 

Classic ozone injury is demonstrated by the 

upper-surface leaf fleck of tobacco and the leaf 

stipple of grape. Many plants show an uppersurface response with no associated injury to the 

lower surface of leaves. However, in monocotyledonous plants such as grasses or cereals, 

and in some non-monocotyledonous plants, there 

is no division of inesophyll tissue, and bifacial 

necrotic spotting (flecking) is a common symptom 

of ozone injury. 

Coniferous trees exhibit different symptoms. 

Ozone is probably the cause of emergence tipburn 

in eastern white pine (white pine needle dieback) 

and of chlorotic decline, a needle injury of 

ponderosa pine 

a 
Classic PAN injury appears as a glaze followed 

by bronzing of the lower leaf surface of many 

plants. Complete collapse of ieaf tissue ca n occur if 

concentrations are sufficiently high. Early leaf 

senescence and abscission usually follow the 

chronic symptoms. Patterns of chronic injury are 

generally not characteristic and may be confused 

with symptoms caused by biotic diseases, insect 

infestation, nutritional disorders, or other 

environmental stresses. 

A great deal of research has been done to define 

more accurately the effects of oxidants on plant 

growth and yield. Studies comparing the growth of 

plants in field chambers provided with carbonfiltered or nonfiltered ambient air containing 

oxidants have reported upto 50-percentdecreases 

in yield of citrus (orange and lemon) exposed to 

oxidants; a 10- to 15-percent suppression in grape 

yield in the first year and a 50- to 60-percent 

reduction over the following 2 years; and a 5- to 

29-percent decrease in yield of cotton lint and seed 

in California. Losses of 50 percent in some 

sensitive potato, tobacco, and soybean cultivars 

have been reported in the eastern United States. It 

is apparent that oxidants in the ambient air reduce 

the yields of many sensitive plant cultivars. 

Experimental chambers with controlled 

environments have been used to study both shortterm and long-term effects of exposure to ozone 

(Tables 1 1-2, 1 1-4, Chapter 11). Radishes given 

one, two, or three acute exposures (785 Ng/m 3 , or 

0.40 ppm) of 1.5 hr each at 7, 14, and/or 21 days of 

age exhibited reductions in root growth. The 

reductions in root growth from the multiple ozone 

exposures were equal to the additsve effects of the 

single exposures. In other words, the temporal 

distribution was nota significantfactor. When soybean plants were exposed to 1468 /jg/m3 (0 75 

ppm) ozone for 1 hr, root growth was consistently 

reduced more than top growth. There were also 

reductions in nodule weight and number. The 

greater reduction of root growth compared to top 

growth is related to the tra nsport of photosynthate. 

Ozone also affects nitrogen fixation in clover, 

soybean, and pinto bean through reduction in 

nodule number, even though nodule size and 

efficiency of nitrogen fixation are not influenced. 

The effect of ozone on the number of nodules 

formed by legumes, if widespread, could have a 

major impact on plant communities and could 

affect fertilizer requirements. There are 

indications that the effect of ozone on nodulation 

may be related to the carbohydrate supply in the 

host plant. 

Experimental long-term exposures to ozone of a 

variety of crops, as well as of ornamentaf and 

native plants, have resulted in a reduction in 

growth and/or yield. Exposure of 14 species 

representative of the aspen pfant community to 

ambient air containing 98 to 1 37 /Ug/m 3 (0.05 to 

0.07 ppm) ozone and to ozone concentrations of 

290 and 588 Ng/m 3 (0.15 and 0.30 ppm) for 3 

hr/day, 5 days/week, 2nd to charcoal-filtered air 

throughout the growing season, resulted in foliar 

injury to all species at the highest pollutant 

concentration. The growth of two soybean 

cultivars (Hood and Dare) was inhibited by 

intermittent exposure to ozone at 196 μg/m 3 (0.10 

ppm) for 3 weeks. Both root and top growth were 

decreased. Similar results were noted with radish, 

except that a lower concentration of ozone (98 

Ng/m 3 , or 0.05 ppm) inhibited growth. In these 

studies, the reduced growth occurred even though 

there were few visible symptoms of plant injury. 

A 30-percent reduction in the yield of wheat 

occurred when wheat at anthesis was exposed to 

ozone at 392 ,ug/m 3 (0.2 ppm) for 4 hr/day for 7 

days. A significant reduction in the yield of tomato 

was noted when plants were experimentally 

treated with ozone at 686 Ng/m3 (0.35 ppm); fewer 

fruit set, and thus fewer fruit were harvested. 

Chronic exposures to ozone at 98 to 290 Ng/m 3 

(0.05 to 0.15 ppm) for 4 to 6 hr/day reduced yields 

in soybean and corn grown under field conditions. 

The threshold for measurable effects for ozone 

appears to be between 98 to 196 Ng/m 3 (0.05 to 

0.10 ppm) for sensitive plant cultivars. This is well 

within the range of ozone levels monitored in the 

eastern United States. Growth orflowering effects 

were reported for carnation, geranium, radish, and 

pinto bean grown in greenhouse chambers and 

exposed to ozone at 98 to 294 Ng/m 3 (0.05 to 0.15 

ppm) for 2 to 24 hr/day. 

The two most critical factors in determining 

plant response to air pollution are duration of 

exposure and concentration of pollutants. These 

two factors describe exposure dose. In determining 

the response of vegetation to oxidants, 

concentration is more important than time. 

The concept of limiting values was used by 

Jacobson to define a boundary between doses of a 

pollutant that are likely to injure vegetation 

measurably and those that are not. Foliar injury 

was used as the index of plant response. The 

ranges for limiting values for effects of ozone are: 

1. Trees and shrubs - 

400 to 1,000 /jg/m 3 (0.2 to 0.51 ppm) 

for 1 hr 

12 
200 to 500 /ig/m 3 (0.1 to 0.25 ppm) for 

2 hr 

120 to 340 pg/m 3 (0.06 to 0.17 ppm) 

for 4 hr 

2. Agricultural crops - 

400 to 800 pg/m3 (0.2 to 0.41 ppm) for 

0.5 hr 

196 to 500 Ng/m 3 (0.1 to 0.25 ppm) for 

1 hr 

75 to 180 pg/m3 (0.04 to 0.09 ppm) for 

4 hr 

Limiting values for PAN are: 

1000 Ng/m 3 (0.2 ppm) for 0.5 hr 

500 pg/m3 (0.1 ppm) for 1 hr 

175 Ng/m 3 (0.035 ppm) for 4 hr 

Doses of ozone or PAN greater than the upper 

limiting values are likely to cause foliar injury. 

The data points used to determine the limiting 

values listed above are not necessarily threshold 

values, but are based on available published 

research data. More than 200 studies were 

surveyed. Any limitations that were present in the 

experimental techniques used in the studies are 

therefore expressed in the data points. The number 

of studies used to derive the data points for ozone 

exposure of trees and shrubs (19) and for PAN is 

another limitation on the values given above. 

For agricultural crops, the inaccuracies in 

measurements make the interpretation of results 

of repeated long-duration exposures difficult. Thus 

limiting values for ozone concentrations below 

100 Ng/m3 (0.05 ppm) are not useful. 

An ozone concentration of 98 to 137 pg/m 3 

(0.05 to 0.07 ppm) for 4 to 6 hr/day for 15 to 133 

days can significantly inhibit plant growth and 

yield of certain species (Table 1 1-4, Chapter 1 1). 

Plant sensitivity to ozone and PAN is conditioned 

by many factors. Genetic diversity in sensitivity to 

ozone between species and between cultivars 

within a species is well documented. Variations in 

sensitivity to ozone within a natural species are 

well known for several pine species, including 

white, loblolly, and ponderosa. Plant sensitivity to 

oxidants can be changed by both climatic and 

edaphic factors. A change in environmental 

conditions can initiate a change in sensitivity at 

once, but it will be 3 to 5 days before the response 

of the plant is totally modified. Plants generally are 

more sensitive to ozone when grown under short 

photoperiods, medium light, medium temperature, 

high humidity, and high soil moisture. Injury from 

PAN may increase with an increase in light 

intensity. Conditions during exposure and growth 

affect the response of plants to oxidants in similar 

ways. In general, environmental conditions 

optimum for plant growth tend to increase the 

sensitivity to ozone. Factors that increase water 

stress at the time of exposure tend to make plants 

more tolerant to ozone. Soil moisture is probably 

the most important environmental factor that 

affects plant response to oxidants during the 

normal growing season. Physiologic age affects 

the response of the leaf to oxidants. Young leaf 

tissue is most sensitive to PAN, whereas newly 

expanding and maturing tissue is most sensitive to 

ozone. Light is required for plant tissue to respond 

to PAN; a similar light requirement is not needed 

for plants to respond to ozone. 

The majority of effects observed, such as 

suppression of root growth, mineral uptake, and 

nitrogen fixation, apparently result from a 

suppression of photosynthesis and modifications 

in photosynthate distribution. This suppression of 

metabolic reserves ultimately slows plant growth 

and renders the plant more sensitive to other 

stresses. Physiological changes can provide a 

sensitive means of.monitoring the health and vigor 

of the plant with or without visible injury. Ozone 

affects pollen germination in some species and 

may affect yield through incomplete pollination of 

flowers. Investigations with Arabidopsis thaliana 

showed no mutagenic effects from ozone over 

seven generations. 

Mixtures of ozone and S02 can cause effects 

below the levels caused by either gas alone; 

however, there is some disagreement concerning 

the interactions of ozone with other gases. Ratios 

of gas - mixtures, intermittent exposures, 

sequential exposures to pollutants, and predisposition by one pollutant to the effects of a 

second pollutant may be important factors in 

nature, but insufficient knowledge is available for 

elucidation of the effects. 

The response of plants to oxidants may be 

conditioned by the presence or absence of biotic 

pathogens. Depending on the plant and the 

pathogen, oxidants may cause more or less injury 

to a given species. Oxidant injury to ponderosa 

pine predisposes the trees to later invasion by bark 

beetles. Ozone and ozone/sulfur dioxide mixtures 

can decrease the population of some plantparasitic nematodes. Variable plant responses 

were noted when herbicides were used in the 

presence of high oxidant concentrations. 

Little research on the effects of oxidants on 

ferns, nonvascular green plants, and microorganisms has been reported. Lichens and mosses 

13 
are responsive to acid gases, but there is no 

definite evidence that they respond to oxidants 

Ferns may be especially sensitive, but their injury 

response is different from that of higher vascular 

plants. Growth and sporulation of fungi on 

surfaces are usually, but not always, affected. 

Ozone from 0.1 to several milligrams per liter of 

solution is required to ktll many microorganisms in 

liquid media. Most work with microorganisms has 

been done to study the effectiveness of ozone as a 

biocide in the storage of vegetation or in the 

treatment of water or sewage. 

EFFECTS OF PHOTOCHEMICAL OXIDANTS 

ON ECOSYSTEMS 

Plants, animals, and microorganisms usually do 

not live alone but exist as populations. Populations 

live together and interact as communities. 

Communities, because of the interactions of their 

populations and of the individuals that make them 

up, respond to pollutant stress differently from 

individuals. Man is an integral part of these 

communities, and as such, he is directly involved in 

the complex ecological interactions that occur 

within the communities and within the ecosystem 

of which the communities are a part. 

The stresses placed on the ecosystems and their 

communities can befar-reaching, inasmuch asthe 

changes that occur may be irreversible. For 

example, it has been suggested that the arid lands 

of India are the result of defoliation and elimination 

of vegetation, which in turn induced local climatic 

changes that were not conducive to the 

reestablishment of the original vegetation. 

An ecosystem (e.g., the planet earth, a forest, a 

pond, or a fallen log) is a major ecological unit 

made up of living (biotic) and physical (abiotic) 

components through which the cycling of energy 

and nutrients occurs. A structured relationship 

exists among the various components. The biotic 

units are linked together by functional 

interdependence, and the abiotic units constitute 

all of the physical factors and chemical substances 

that interact with the biotic units. The processes 

occurring within the F,otic and abiotic units and 

the interactions among them can be influenced by 

the environment. 

Ecosystems tend to change with time. 

Adaptation, adjustment, and evolution are 

constantly taking place as the biotic component, 

the populations, and the communities of living 

organisms interact with the abiotic component in 

the environment. Recognizable sequential 

changes occur. With time, populations and 

communities may replace one another This 

sequential change, termed succession, may 

culminate in climax communities. Climax 

communities are structurally complex, are moreor 

less stable, and are held in a steady state through 

the operation of a particular combination of biotic 

and abiotic factors The disturbance or destruction 

of a climax community or ecosystem results in its 

being returned to a simpler stage. Existing studies 

indicate that changes occurring within 

ecosystems, in response to pollution or other 

disturbances, follow definite patterns that are 

similar even in different ecosystems. It istherefore 

possible to predict broadly the basic biotic 

responses to the disturbance of an ecosystem. 

Diversity and structure are most changed by 

pollution as a result of the elimination of sensitive 

species of flora and fauna and of the selective 

removal of the larger overstory plants in favor of 

plants of small stature. The result is a shift from the 

complex forest community toward the less 

complex hardy shrub and herb communities. The 

opening of the forest canopy changes the 

environmental stresses on the forest floor, causing 

differential survival and, consequently, changed 

gene frequencies in subcanopy species. 

Associated with the reduction in diversity and 

structure is a shortening of food chains, a 

reduction in the total nutrient inventory, and a 

return to a simpler successional stage. 

It should be emphasized that ecosystems are 

usually being subjected to a number of stresses at 

the same time, not just a single perturbation such 

as oxidant pollution. 

The effects of oxidants on the mixed-conifer 

forest of the San Bernardino Mountains 

graphically demonstrate the changes that occur in 

natural ecosystems as discus3ed above. Since the 

early 1940's, the San Bernardino Forest has been 

undergoing stress from oxidants transported longrange from Los Angeles, 144 km (90 miles) away. 

Losses of ponderosa and Jeffrey pines, the 

overstory vegetation, have increased dramatically 

as pollutant levels have risen. Black oak has also 

suffered oxidant injury. The composition of both 

plant and animal populations has been altered by 

the death of the ponderosa and Jeffrey pines. 

The interaction of pollutant and inversion layers 

at the heated mountain slope results in thevertical 

venting of oxidants over the mountain crest by upslope flow, thus establishing an elevational 

gradient of oxidant concentrations. Oxidant 

concentrations ranging from 100 to 200 pg/m 3 

(0.05 to 0.10 ppm) at altitudes as high as 2432 m, 

14 
approximately 1033 m above the mountain crest, 

have been measured by aircraft. 

Total oxidant concentrations in the San 

Bernardino Mountains have been measured 

continuously from May through September since 

1968 at the Rim Forest-Sky Forest monitoring 

station. During each of the first 7 years of 

monitoring, between June and September, the 

total number of hours in which concentrations of 

ozone were 160 Ng/m3 (0.08 ppm) or more was 

never less than 1300. The number of hours in 

which the total oxidant concentration was 390 

Ng/m3 (0.20 ppm) or higher increased from fewer 

than 100 in 1969 to nearly 400 in 1974. It was not 

uncommon to observe momentary oxidant peaks 

as high as 1 180 /jg/m3 (0.60 ppm). The duration of 

oxidant concentrations exceeding 200 Ng/m 3 

(0.10 ppm) was 9, 13, 9, and 8 hr/day going from 

the lower- to the higher-altitude stations. 

The most recent data firmly indicate that oxidant 

concentrations in the San Bernardino Forest will 

either increase annually or oscillate around the 

mean of present high concentrations in the 

foreseeable future. 

The transport of the urban plume from the coast 

northeastward to the mountains can be readily 

demonstrated. Because of this transport, the 

permanent vegetation constituting natural 

ecosystems receives much greater chronic 

exposure, while the short-lived vegetation 

constituting the economically more valuable 

agroecosystem of the Los Angeles coastal plain 

can be subject to injurious doses, but in 

intermittent, short-term fumigations. Each 

situation has measurable economic and aesthetic 

consequences, but on different time scales. The 

single-species agricultural ecologic system (the 

agroecosystem) has little resilience to pollutant 

stress. Losses are sometimes immediate and 

occasionally catastrophic. The complex natural 

ecosystem is initially more resistant to pollutant 

stress, but the longer chronic exposures cause 

disruption of both structure and function in the 

system that may be irreversible. 

The oxidant injury to the mixed conifer stands of 

the San Bernardino Mountains that began in the 

early 1940's, as indicated above, is well advanced. 

A similar problem is developing in the forests of the 

southern Sierra Nevada Mountains. Both areas 

show direct as well as indirect effects on all 

subsystems of the forest ecosystem - producers, 

consumers, and decomposers 

In summary: 

1. Ozone injury has limited the growth and 

caused the death of ponderosa and Jeffrey 

pines. An estimated 1.3 million trees have 

been affected. Decrease in cone production 

has resulted in a decrease in reproduction. 

Black oak has also suffered injury from 

ozone. 

2. Reduction in fruits and seeds that make up 

the diet of most of the common small 

mammals has influenced the populations 

of these organisms. 

3. Essential Nrocesses, such as recycling of 

nutrients, may have been disrupted, 

causing a limitation in the growth of 

vegetation. 

4. Death of the predominant vegetation has 

caused an alteration in the species 

composition and a change in the wildlife 

habitat. 

The San Bernardino Mountain study illustrates 

the complex;ty of the problems caused by 

environmental pollution. The changes that have 

occurred in this mountain ecosystem as the result 

of oxidant transport have already influenced the 

importance and value of this natural resource to 

the residents of Southern California. 

The injury to the eastern white pine in the 

Appalachian Mountains caused by oxidant 

transport from the urban northeast has begun a 

similar sequential change that could degrade this 

important recreational area. Total oxidant peaks as 

high as 220 Ng/m3 (0.11 ppm) were recorded for 

July 1975. Concentrations exceeding 160 Ng/m 3 

(0.08 ppm) were measured in June 1976. These 

episodes resulted in significant increases in 

oxidant injury to three categories of eastern white 

pine in the Blue Ridge Mountains (the eastern 

range of the Appalachian Mountains). 

Ecosystems are usually evaluated by modern 

man solely on the basis of their economic value. 

This economic value in turn depends on the extent 

to which man can manipulate the ecosystem for 

his own purposes. This single-purpose point of 

view makes it difficult to explain the many benefits 

of a natural ecosystem to man's welfare in terms of 

the conventional cost-benefit analysis. Gosselink, 

Odum, and Pope have, however, placed a value on 

a tidal marsh by assigning monetary values to its 

multiple contributions to man's welfare such as 

fish nurseries, food suppliers, and wastetreatment functions of the marsh. They estimate 

15 
the total social value to range from $50,000 to 

$80,000 per acre. 

Westman also evaluated the beneflts of natural 

ecosystems by estimating the monetary costs 

associated with the loss of the free services 

(absorptlon of air pollutlon, regulation of global 

climate and radlation balance, and soil bioding) 

provided by the ecosystems. Westman estimated 

that the oxidant damage to the San Bernardino 

National Forest could result In a cost of $27 million 

per year (1973 dollars) just for removal of 

sediments resulting from eroslon, as long as the 

forest remained in the early stages of succession. 

Estimates of the cost in currency of the values of 

items and qualities such as clean air and water, 

untamed wildllfe, and wilderness, once regarded 

as priceless, are an attempt to rationalize the 

activlties of civillzatlon. When estimating the 

monetary cost In currency of the values lost 

through damage to ecosystems, the assumption is 

usually made that the declslonmakers will choose 

the alternative that Is most soclally beneficlal as 

indlcated by costs compared to beneflts. As 

Westman points out, the assumption that 

declslons maximlzing benefit/cost ratios 

simultaneously optimlze social equity and utility is 

based on certain inherent corollaries: 

(1) The human species has the exclusive right to use and 

manipulate nature for its own purposes (2) Monetary units 

are socially acceptable as means to equate the value of 

natural resources destroyed and those developed (3) The 

value of services lost during the interval before the 

replacement or substitution of the usurped resource has 

occurred is included in the cost of the damaged resource (4) 

The amount of compensation in monetary units accurately 

reflects the full value of the loss to each loser in the 

transaction. (5) The value of the item to future generations 

has been judged and included in an accurate way in the total 

value (6) The benefits of development accrue to the same 

sectors of society, and in the same proportions, as the 

sectors on whom the costs are levied, or acceptable 

compensation has been transferred Each of these 

assumptions, and others not listed, can and have been 

challenged 

In the case of (4) above, for example, the losses 

incurred when developing natural ecosystems are 

involved affect species other than man. These 

losses are seldom, if ever, compensated The 

publlc at large also is usually not consulted to 

determine whether the dollar compensatlon Is 

adequate and acceptable. Frequently, there is no 

dlrect compensation. Corollary (5) can never be 

fulfilled because it is imposslble to determine 

accurately the value to future generatlons. 

Evaluating the contribution of functloning 

natural ecosystems to human welfare is a very 

complex task and involves weighing both 

economlc and human social values. As life support 

systems, they should not be evaluated in economic 

terms. 

With the passage of time, man has destroyed 

many of the naturally occurring ecosystems of 

whlch he was a part and has replaced them with 

slmplifled ecosystems wholly dependent on hls 

care and protection and requiring a large input of 

energy. 

Man favors the simple unstable and synthetic 

ecosystems because when extensively managed, 

and subsidized by the use of fossil fuels, they are 

highly productive. An agricultural ecosystem 

(agroecosystem) is an example of such a simplified 

ecosystem. The effects of oxidants on 

agroecosystems have been under study for more 

than 20 years. The study of effects on naturai 

ecosystems Is much more recent. 

Plants grown in agroecosystems are largely 

annuals and can be replaced when they are 

susceptible to pollutant stress. Natural ecosystems 

remain in place year after year. Manmade 

pollutants are undoing relatlonships developed 

within these ecosystems over milllons of years. 

EFFECTS OF PHOTOCHEMICAL OXIDANTS 

ON MATERIALS 

Ozone is a major factor In the overall 

deterloratlon of several different types of organic 

materlals. In fact, certain speclfic organlc 

compounds are more sensitive to ozone attack 

than are humans or anlmals. The magnitude of 

damage is dlfficult to assess because ozone is one 

of many oxidlzing chemicals In the atmosphere 

that contributes to the weathering of materials. 

Nevertheless, researchers have shown that ozone 

accelerates the deterioration of several classes of 

materials, Including elastomers (rubber), textile 

dyes and flbers, and certain types of paints and 

coatings. 

Although many organlc materials have been 

shown to be susceptible to ozone attack, only 

certain palnts, elastomers, and dyes sustaln 

damage representing slgnificant economic loss. 

Even the measures to prevent ozone damage to 

elastomers and dyes constitute a major cost. 

16 
2. INTRODUCTION 

Air quality criteria are expressions of the 

scientific knowledge of the relationships among 

various concentrations, averaged over an 

appropriate time period, of air pollutants in the 

atmosphere and their adverse effects on human 

health and the environment. Criteria are issued to 

assist in the formulation of decisions regarding the 

need for control of a pollutant and the development 

of air quality standards governing the pollutant. Air 

quality criteria are descriptive; that is, they 

describe the effects that have been observed when 

the ambient air concentration of a pollutant has 

reached or exceeded 'a specific figure for a 

specified period of time. 

Many factors must be considered when 

developing criteria. Consideration must be given to 

the chemical and physical characteristics of the 

polluta its, the techniques available for measuring 

these characteristics, and the exposure time, 

relativ; humidity, and other environmental 

conditi ms. Natural and anthropogenic emissions 

must t: considered and assessed. The number and 

distriL ition of sources and the extent to which the 

specif ; pollutant is emitted into the environment 

direct!- affect the levels to which the receptor is 

expos< d. In addition, the criteria must also include 

consid sration of the influence of all such variables 

on the effects of air pollution on human health, 

agriculture, vegetation, wildlife, visibility, and 

climate. Furthermore, the individual characteristics of the receptor must be taken into account. 

Air quality standards are prescriptive. They 

prescribe pollutant exposures or levels of effect 

that scientific judgment determines should not be 

exceeded in a specified geographic area, and they 

are used as one of several factors- in designing 

legally enforceable pollutant emission standards. 

This document focuses on photochemical 

oxidants and their precursors, HC and NOx, asthey 

are found in the ambient air. The nitrogen oxides 

are examined, but only for their oxidant-precursor 

role; a detailed examination of NO x as pollutants in 

their own right can be found in Air Quality Criteria 

for Nitrogen Oxides (U.S. Environmental 

Protection Agency, Publication No. AP-84, 

January 1971) andAirQualityCriteriaforNitrogen 

Oxides (Luxembourg: NATO/CCMS, Document N. 

15, June 1973). The discussion of HC in this 

document rests almost entirely on their role as 

precursors of other compounds formed in the 

atmospheric reaction system and not on the direct 

effects of HC themselves. Gas-phase HC and 

certain of their oxidation products that are 

associated with thn manifestations of photochemical air pollution are discussed. Toxic 

organics wili not be discussed here. Establishing 

health data for toxic organics is extremely complex 

and will be handled at a later date as more studies 

are completed. 

This publication reviews the sources of oxidants 

and of oxidant precursors and discusses the 

chemistry of the atmospheric oxidant formation 

process and the relationships between oxidants 

and their precursors. Air quality data, control 

techniques, and source and emission inventories 

are discussed briefly for orientation purposes only, 

inasmuch as these topics are discussed in detail in 

other documents. Measurement techniques and 

fate and transport of pollutants are discussed to 

the extent necessary to give a clear understanding 

of the health and welfare effects and of the bases 

for sound oxidant control strategies. 

The status of control technology for oxidants and 

their precursors has not been treated. For 

information on this subject, the reader is referred 

to Control Techniques for NOx and Hydrocarbons 

from Mobile Sources (U.S. Department of Health, 

Education, and Welfare, Publication No. AP-66, 

March 1977), and Control Techniques for 

Hydrocarbons and Organic Solvents (U.S. 

Department of Health, Education, and Welfare, 

Publication No. AP-68, March 1977). The subject 

of adequate margin of safety stipulated in Section 

108 of the Clean Air Act also has not been treated. 

Again, the reader is referred to documentation 

prepared by OAQPS. 

Methods and techniques for controlling the 

sources of photochemical oxidants as well as the 

17 
costs of applying these techniques are discussed in 

other documents. 

The scientific literature has been reviewed 

through 1976-77. This document is not intended 

as a complete, detailed literature review, and it 

does not cite every published article relating to 

oxidants in the environment and their effects. The 

iiterature has been reviewed thoroughly for 

information relative to criteria. Chapters 11 

(Effects of Photochemical Oxidants on Vegetation 

and Certain Microorganisms) and 12 (Ecosystems) 

in this document are based on the chapters by the 

same numbers and titles in the Nationai Academy 

of Sciences publication, Ozone and Other 

Photochemrcal Oxrdants (Washington, D.C., 

1977). An attempt has been made to identify the 

major deficiencies in our current knowledge 

relative to criteria. Between the issuance of the 

preprint volumes and the final publication of this 

document, a few minor changes were made to 

correct inadvertent omissions. 

18 
3. NATURE AND ATMOSPHERIC CONCENTRATIONS 

OF PHOTOCHEMICAL OXIDANTS 

NATURE OF OXIDANT 

Photochemical oxidants are chemical entities of 

concern because of their detrimental effects on 

biological systems and on certain materials. They 

are products formed in the atmosphere by 

sunlight-driven, chemical reactions that involve 

HC* and NOX. 

The term "photochemical oxidants" is used here 

to define those atmospheric pollutants that are 

photochemical reaction products and are capable 

of oxidizing neutral iodide ions. Extensive research 

has unequivocally identified several components 

of the photochemical oxidants mixture. Thus 

oxidants in ambient air are known to consist 

mainly of ozone, PAN, and nitrogen dioxide (NO2) 

and are suspected to include also (but in smaller 

amounts) other peroxyacyinitrates, hydrogen 

peroxide, alkyl hydroperoxides, nitric and nitrous 

acids, peracids, and ozonides. Collectively, they are 

measured by potassium iodide procedures and are 

referred to in this report as "oxidant." An 

important distinction to be made here is that the 

formation of NO2 in ambient air clearly precedes 

the formation of the other oxidants. For this 

reason, the relative levels of nitrogen dioxide and 

of the aggregate of the other oxfdants vary 

considerably during the day, with NOz being 

invariably the dominant oxidant earlier in the day. 

Because of this difference in the variation pattern 

and the differences in effects between NO2 and the 

aggregate of the other oxidants, the NO2 pollution 

problem has been treated independently of the 

other photochemical oxidant problem. Furthermore, because of its predominance among 

oxidants other than NOz, ozone has been singled 

out and treated as the sole representative of such 

oxidants and has been given most of the research 

attention. 

'The term ' hydrocarbon' is meant to include also all nonhydrocarbon organic 

compounds capable of participating in the atmospheric oxidant formation process 

Accordingly, the terms hydrocarbons" and ' organics' are often used 

interchangeably 

Photochemical air pollution is customarily 

defined in terms oF the concentrations of ozone and 

NOz only. This should not be interpreted to suggest 

that other photochemical pollutants are thought to 

be of less concern. Rather, it reflects (1) the fact 

that ozone and NO2 pollution problems are more 

easily quantified and hence are more amenable to 

research than problems associated with the other 

pollutants (e.g., eye irritation and visibility 

reduction), and (2) the assumption that abatement 

of the ozone and NO2 pollution problems will, in all 

probability, alleviate the other photochemical 

pollution problems. 

The ozone fou nd i n the lower levels of the earth's 

atmosphere has been traced to both natural and 

anthropogenic sources. One natural source of 

tropospheric ozone is the ozone abundantly 

present in the stratosphere, which can be 

transported into the biosphere. Ozone can also 

form naturally from eiectrical discharges in the 

atmosphere and from atmospheric photochemical 

reactions involving naturally emitted organic 

vapors and NOx. Obviously, the levels of ozone 

resulting from all such uncontrollable sources 

must be known if the anthropogenic sources and 

the effects of their control are to be assessed 

reliably. 

Ozone and other oxidants from anthropogenic 

sources are products of atmospheric photochemical reactions involving primary organic and 

inorganic pollutants and atmospheric oxygen. 

More specifically, the oxidant formation process Is 

inftfated by the photolysls of Ifght-absorbfng air 

contaminants such as NOz, aldehydes, and ozone, 

resulting in the formation of highly reactive 

radicals that react subsequently with organic 

pollutants. The net result of thfs photochemical 

activity is the accumulation of ozone, and other 

oxidants, to concentrations that depend on many 

factors, including local meteorologlcal conditions 

(sunlight intensity, air stagnation, temperature, 

etc.) as well as the concentrations, makeup, and 

variation patterns of the primary pollutants 

19 
present. Such dependence of oxidantformation on 

multiple factors makes this pollution problem 

immensely complex. 

those levels) of ozone and other oxidants and of 

some nonoxidant photochemical pollutants, the 

reader is referred to the literature. 26z' 

OXIDANT CONCENTRATIONS AND THEIR 

PATTERNS 

Introduction 

Although buildup of photochemical oxidants 

occurs in nearly every urban center in the United 

States, no pollutlon episodes involving a sudden 

and massive assault on human health have been 

attributed solely to photochemical oxidants. 

Accordingly, no case studies have been reported in 

which pollutants and their effects were comprehensively and systematically examined during 

an oxidant pollution episode. Photochemical 

oxldants are viewed as an air pollution problem 

mainly on the bases of (1) observations of humans, 

animals, plants, and materials In areas known to 

have hlgh oxidant levels, and (2) results from 

studies In which human subjects, animals, plants, 

and materials were exposed to smoggy 

atmospheres or to synthetic mixtures containing 

oxldant or ozone under controlled conditions. To 

present convincingly the case that photochemical 

oxidant alr pollution is a problem, it would be 

necessary and sufficient to present (1) data on the 

concentration and frequency of occurrence of 

photochemlcal oxidants, and (2) evidence 

regarding the adverse effects of oxidants. Data on 

the occurrence of oxldants are given In this 

chapter, but only in a brief summary form, since 

the occurrence of oxidant at problem levels is well 

established. Evidence on the effects of 

oxidant/ozone is presented and dlscussed in detail 

In subsequent chapters. For a more detailed 

discussion of amblent levefs (and variations in 

Oxidant Concentrations in Urban Atmospheres 

Concentrations of oxidant in ambient air were 

measured in 1974 at some 340 monitoring 

stations operated by state and local control 

agencies. Such data are gathered by EPA, stored in 

EPA's National Air Data Bank, analyzed for trends, 

and reported in summary form as EPA 

repo rts.28'29,30,31,32 

Table 3-1 shows the maximum hourly average 

as well as the number of day3 when the maximum 

hourly average oxidant concentration was equal to 

or exceeded 294, 196, and 98 Ng/m 3 (0.15, 0.10, 

and 0.05 ppm) for 12 monitoring sites in urban 

areas. Higher readings of 0.52 ppm in Philadelphia 

and 0.35 ppm in St. Louis were judged tc be 

spurious and were discarded. More recent data for 

16 urban areas are given in Table 3-2. 

In general, locations within the Los Angeles 

Basin urban area have the highest peak oxidant 

concentratlons (represented by the 99th percentile 

values) as well as the most frequent violations of 

the oxidant standard. High levelsare also observed 

in the northeast corridor between Washington, 

D.C., and Boston, Mass. In general, most cities for 

which extensive ozone data are available have 

been shown to exceed the national air quality 

standard for ozone of 160 Ng/m 3 (0.08 ppm). 

A number of these urban areas have 

experienced very high levels of oxidant, exceeding 

600 Ng/m3 (0.30 ppm). Los Angeles, for example, 

recorded maximum 1-hr values in excess of 1200 

Ng/m 3 (0.60 ppm). Denver, Philadelphla, Houston, 

and the area just east of New York - northeastern 

TABLE 3-1. SUMMARY OF MAXIMUM OXIDANT CONCENTRATIONS IN SELECTED URBAN AREAS 

Total 

days of 

valid 

Urban area Year data 

Number of days with at least 1 hourly 

average equalto or exceeding 

98 pg/m' 196 yg/m3 294 pg/m' 

(005 ppm) (0 10 ppm) (0 15 ppm) 

Maximum 

hourly 

average, 

PPm Ng/m' 

Los Angeles, Callf 1964-1967 730 540 354 220 058 1 137 

Pasadena, Callf 1964-1967 728 546 401 299 046 902 

San Dlego, Callf 1964-1967 623 440 130 35 038 745 

Sacramento, Callf 1964-1967 711 443 104 16 026 510 

Santa Barbara, Callf 1964-1967 723 510 76 11 025 490 

San Franclsco, Callf 1964-1967 647 185 29 6 022 431 

Phlladelphla, Pa 1964-1972 1783 723 186 39 033 647 

St Louls, Mo 1964-1972 2014 1042 152 27 022 431 

Clnclnnatl, Ohlo 1964-1972 1668 749 105 14 026 510 

Denver, Colo 1964-1972 1542 934 179 35 036 510 

Washington, D C 1964-1972 2157 1032 193 25 025 490 

Chlcago, III 1964-1972 2042 828 85 14 020 392 

oft 
TABLE 3-2. OXIDANT CONCENTRATIONS OBSERVED IN SELECTED URBAN AREAS 

OF THE UNITED STATES, 1974-75 

°ro of days 

Range of oxwdant 

Total No of sites 2nd max standard 

no of exceeding 1-hr violated 

vand oxidant values, atthe 

Urban area sitesa standard° Pg/m' (ppm) worst site 

New York, N Y- Northeastern N. J 8 8 259-510 (0 13-0 26) 197 

Los Angeles - Long Beach, Callf 3 33 255-784 (0 13-0 40) 38.6 

Chlcago, III - Northwestern Ind 6 6 1 63-427 (0 08-0.22) 80 

Phlladelphla, Pa. 10 10 216-625 (0.1 1-0 32) 382 

Detrolt, Mlch. 2 2 455-514 (0 23-0 26) 3 1 

Boston, Mass 7 7 186-376 (0.09-0 19) 82 

Washington, D C 8 8 363-451 (0 18-0 23) 274 

Cleveland, Ohlo 5 5 245-41 ,(0 12-0 21) 36 

Minneapolls - St Paul, Mlnn 2 1 141-206 (0 07-0.10) 42 

Houston - Galveston, Tex 4 4 304-588 (0 16-0 30) 235 

Baltlmore, Md 2 2 314-372 (0 16-0 19) 154 

Dallas - Fort Worth, Tex 2 2 274-323 (0 14-0 16) 148 

Mllwaukee - Raclne, Wfs 7 7 332-425 (0 17-0 22) 145 

Seattle - Tacoma, Wash 4 3 1 18-235 (0 06-0 12) 78 

Clnclnnatl, Ohlo - Northern Ky. 6 6 284-412 (0 14-0 21) 23 1 

Denver, Colo 6 6 212-349 (0.1 1-0 18) 275 

'Only sites having a minimum of 4000 observations were included in this summary 

'The oxidant standard is a 1-hr average of 160 pg/m', not to be exceeded more than once per year 

New Jersey have experienced levels in excess of 

600 Ng/m 3 (0.30 ppm). Hourly values exceeding 

400 Ng/m 3 (0.20 ppm) have occurred in most of the 

major urban areas. 

The data in Table 3-1 and some of those i n Table 

3-2 were obtained by the potassiuin iodide 

method, 26 and 'therefore they include both ozone 

and nonozone oxidant species. Data on ozone 

alone have been obtained only for the frtore recent 

years, after the chemiluminescence method for 

measurement of ozone was introduced. National 

summaries of such data are not available in a 

reported form, but detailed tabulations are 

ava i lab le.2a'29,30,31,32 

Nonozone oxidants are certain to exist in urban 

atmospheres, but in concentrations considerably 

lower than those of ozone. 7'

26' 2

' Measurements of 

such oxidants in ambient air are scant and consist 

mostly of PAN data. 21 '22 Some recent data on 

absolute concentrations of PAN and on ozone-toPAN or oxidant-to-PAN ratios both in urban and 

rural atmospheres are shown in Tables 3-3 

through 3-5. 21 The data currently available 

indicate, in general, that in urban atmospheres, 

PAN concentrations are considerably lower than 

those of oxidant or ozone, but nevertheless, they 

are not negligible. Hydrogen peroxide (H2O2) also 

has been reported to occur in smog chamber and 

ambient atmospheres at concentrations as high as 

0.18 ppm. 2 Peroxybenzoylnitrate (C6H5C002NO2) 

has been reported to occur in urban ambient air in 

the Netherlands, 23 but no evidence exists for its 

occurrence in U.S. urban ambient air. The 

significance of such PAN and other oxidant 

concentrations can only be assessed on the basis 

of their adverse effects on humans, vegetation, 

and materials. 

Oxidant Concentrations in Rural Atmospheres 

Ozone concentrations in rural atmospheres 

have been of interest because they were thought to 

be a measure of the composite contributions of 

TABLE 3-3. PAN AND OXIDANT (Ox) MEASUREMENTS (10 a.m. to 4 p.m.), LOS ANGELES, CALIF., 196821 ' a 

PAN Avg Range of Avg Range of 

No of conc , PAN conc , oxidant conc , oxidant conc , Ratio observed 

samples ppb ppb ppb ppb avg O./avg PAN 0,/PAN 

19 0-10 8.65 30-190 79.0 9.13 5 1-24 4 

59 10-20 130 44-220 97.0 758 3 3-18 3 

27 20-30 24.0 70-290 1440 604 2 8-13 0 

6 30-40 32.6 100-400 1680 523 3 0-9 7 

5 40-50 471 160-285 209.0 4.49 3.2-6.1 

2 > 50 65.5 243-410 3270 4.94 3 9-6.0 

' 1 96 pg/m' = 1 ppb as ozone, 5 pg/m3 = 1 ppb as PAN 

NE 
TABLE 3-4. PAN AND OZQNE MEASUREMENTS (10 a.m. to 4 p.m.), HOBOKEN, N,J., 1970 Z1 ' 8 

PAN Avg Range of Avg Range of 

No of conc , PAN conc , ozone cortc , ozone conc , Ratio observed 

samples ppb ppb ppb ppb avg Oa/avg PAN OziPAN 

14 0-2 15 15.0-1 12 0 420 280 5 6-77 5 

15 2-4 28 22.0-150 0 71.0 253 10 1-62 5 

4 4-6 47 100.0-135.0 113024 0 22 9-25 0 

8 6-8 71 97 0-219 0 1620 228 12 6-34 1 

2 8-10 99 214 0-278 0 2460 251 20 7-29 6 

' 1 96 /ig/m' = 1 ppb as ozone, 5 Ng/m' = 1 ppb as PAN 

TABLE 3-5. PAN, OXIDANT, AND OZONE MEASUREMENTS (10 a.m. to 4 p.m.), ST. LOUIS, MO.. 197321 '

1 

Range of Avg Ratio Range of Avg Ratio 

PAN Avg PAN oxidant oxidant avg ozone ozone avg 

No of conc, conc, conc, conc, 0./avg conc, conc, 03/avg 

samples ppb ppb ppb ppb PAN ppb ppb PAN 

3 0-2 1.7 46-100 80.6 475 10-40 286 163 

31 2-4 3.0 46-216 846 283 24-1 16 481 16.2 

60 4-6 50 30-250 673 134 10-140 502 100 

31 6-8 68 39-224 687 101 20-120 50.3 74 

14 8-10 93 40-180 846 81 10-96 502 54 

5 10-12 108 30-90 734 68 30-85 540 50 

10 > 12 186 52-100 856 46 32-80 59.5 32 

° 1 96 Ng/m' = 1 ppb as ozone, 5 pg/m' = 1 ppb as PAN 

natural sources to the ambient ozone problem. 

Recent studies, however, have established the 

occurrence of pollutant transport, thus refuting 

this early notion; and it is now widely accepted that 

rural areas are not necessarily unaffected by 

anthropogenic pollution. This conclusion has led 

air pollution specialists to use the term ""rural" to 

signify areas or atmospheres that are nonurban 

but are occasionally susceptible to anthropogenic 

pollutants, and the term ""remote" to signify areas 

or atmospheres so far removed from anthropogenic pollutant sources that their contamination by such pollutants is highly unlikely. 

Before 1962, ozone concentrations both'in rural 

and in remote areas appeared to be considerably 

below the NAAQS level of 160Ng/m 3 or 0.08 ppm 

(Table 3-6). 17 Comparable levels were observed 

also in rural North Carolina during 1964-67. 34 

Measurements in the last 5 to 6 years, however, 

showed that the ozone concentrations In several 

rural areas exceeded 160%rg/m 3 (0.08 ppm) with a 

frequency comparable to or even surpassing that 

observed in many urban areas. 

This fact is illustrated by the data in Table 3-7, 

which were obtained by recent multiyear fleld 

studies sponsored by EPA. 35 Similar data were also 

reported by New York State investigators. 6 Such 

increased ozone levels (i.e., >160Ng/m 3 , or>0.08 

ppm) in rural areas are almost certain to be caused 

largely by anthropogenic ozone and/or precursors 

generated locally or transported Into such areas 

from urban centers. 20,33,35,36,40,43 There Is evidence 

TABLE 3-6. CONCENTRATIONS OF TROPOSPHERIC OZONE BEFORE 1962 17 

03. ua/m' 

Observer Location, time, and remarks Altitude 

Cotz and Volz (1951) Arosa, Swltzerland, 1950-51, hlgh 

valley, dally maxlmum values 1860 m 19-90 50 

Regener (1957) Mt Caplllo and Albuquerque, 3100 m 18-85 45 

New Mexico, 1951-52 1600 m 3-120 36 

Regener (1957) O'Nell, Nebraska, 1953 12 5 m above ground 30-100 60 

Ehmert (1952) Welssenau, Bodensee, Germany, 1952 20 m 0-90 35 

above ground 0-70 30 

Telchert (1955) Llndenberg Obs., Germany, 1953-54 80 m 0-50 30 

above ground 0-50 27 

Kay(1953) Farnborough, England, 1952-53 0-12,000 m 26-50 38 

Brewer (1955) Tromso, Norway, 1954 0-10,000 m 60-70 65 

Rlce and Pales (1959) Mauna Loa Observatory, Hawall 3000 m 30-62 45 

Wexler et al. (1960) Llttle Amerlca Statlon, Antarctica 100 m 20-60 45 

' As interpreted from the pubhshed data The values sometimes represent absolute maxima, sometimes mean maxima 

22 
TABLE 3-7. SUMMARY OF OZONE DATA FROM 1973-76 OXIDANT 

STUDIES, RESEARCH TRIANGLE INSTITUTE 35 

% Hours 

Type of Average 0 3 No hours No 1-0 08 

Station Year station ppm yg/m' ?o 08 ppm hours ppm 

McHenry, Md. 1973 Rural 0.074 145 600 1662 37.0 

Kane, Pa. 1973 Rural 0.065 127 639 2131 300 

Coshocton, Ohio 1973 Rural 0056 110 357 1785 200 

Lewisburg, W Va 1973 Rural 0.0952 187 249 1663 15.0 

Wilmington, Ohio 1974 Rural 0.052 102 259 1751 149 

McConnelsville, Ohio 1974 Rural 0.057 112 262 2011 130 

Wooster, Ohio 1974 Rural 0.047 92 262 1878 140 

McHenry, Md. 1974 Rural 0.057 112 262 2011 130 

DuBois, Pa. 1974 Rural 0 056 110 341 1667 205 

Canton, Ohio 1974 Urban 0 035 69 148 1829 8.0 

Cincinnati, Ohio 1974 Urban 0.025 49 54 1548 3.5 

Cleveland, Ohio 1974 Urban 0.031 61 51 1652 30 

Columbus, Ohio 1974 Urban 0 033 65 113 1935 58 

Dayton, Ohio 1974 Urban 0 035 69 114 1576 7.2 

Pittsburgh, Pa 1974 Urban 0.028 55 106 1622 65 

Sradford, Pa 1975 Rural 0 040 78 100 2332 43 

Lewisburg, W Va. 1975 Rural 0.038 74 59 2386 25 

Creston, lowa 1975 Rural 0 035 69 17 2117 08 

Wolf Point, Mont 1975 Rural 0.028 55 0 2160 0.0 

DeRidder, La 1975 Rural 0.030 59 38 2994 1 3 

Pittsburgh, Pa 1975 Urban 0 030 59 227 2841 80 

Columbus, Ohio 1975 Urban 0.022 43 43 2885 1.5 

Poynette, Wis 1975 Rural 0.038 74 126 2663 4.7 

Cedar Rapids, lowa 1975 Urban 0 025 49 6 2781 0.2 

Des Moines, lowa 1975 Urban 0 036 70 124 2528 49 

Omaha, Neb. 1975 Urban 0 035 69 64 1787 36 

Nederland, Tex. 1975 Urban 0 027 53 138 2714 5.1 

Port O'Conner, Tex. 1975 Rural 0 027 53 99 2912 3.4 

Austin, Tex. 1975 Urban 0 025 49 19 2504 0.8 

Houston, Tex 1975 Urban 0.026 51 141 2104 6.7 

that some rural oxidant is anthropogenic in nature. 

This evidence is based on measurement of Freons 

or of acetylene, or on results of wind backtrajectory analysis, both of which are indications 

of the passage of the rural air over urban sources. 

20,33,36,40,43 Additional data on ozone concentrations in remote areas are presented in 

Chapter 4. 

Data on nonozone oxidants in rural or remote 

atmospheres are scarce. Recent data on PAN in the 

rural atmosphere at Wilmington, Ohio, showed 

levels considerably lower than those found in 

urban atmospheres, both absolutelyand relative to 

ozone concentrations. Earlier as well as recent 2 

measurements of PAN and oxidant/ozone showed 

that (1) the PAN concentrations are much lower 

than those of oxidant/ozone and (2) the PAN-tooxidant/ozone ratio varies with location, the rural 

areas showing lower values than the urban 

centers. 21 The maximum PAN concentration from 

1500 samples taken in August 1974 was 4.1 ppb, 

with the daily maximum rarely exceeding 3.0 

ppb, 21 even though the ozone concentration 

frequently exceeded 160 pg/m 3 (0.08 ppm). Such 

low rural PAN concentrations, expressed in 

absolute terms as well as in terms relative to 

ozone, can be explained in different ways. 

Accordingly, one explanation is that the chemical 

mechanism of oxidant formation is such that the 

lower reactant concentrations (of HC and NOX) and 

the prolonged irradiation conditions that 

characterize rural pollutant mixtures result in 

lower PAN yields and lower PAN-to-ozone product 

ratios. 21 Another explanation lies in the reverslble 

decomposltlon of PAN into NO2 and peroxyacyl 

radical; in rural areas where NO z is nearly absent, 

PAN decomposition is enhanced. 13 A third 

conceivable explanation is that the lower PAN-toozone ratios in rural atmospheres may reflect a 

greater proportion of stratospheric ozone relative 

to the photochemically produced ozone. The 

explanations based on the chemical mechanism 

are belleved to be the more plausible ones, at least 

for the Wilmington case. 21 The stratospheric ozone 

explanation may be a valid one in the cases in 

whlch PAN is undetectable. 

Patterns of Variation in Oxidant Concentrations 

Patterns of variation in oxidant or ozone 

concentrations are of interest for at least two 

23 
reasons. They provide a more detailed description 

of the oxidant problem, which in turn serves to 

guide the control effort better. Such patterns also 

help to explain the chemical and physical 

mechanisms by which emissions of precursors (or 

of ozone) disperse, react, and ultimately cause the 

observed oxidant problems. 

The most conspicuous variation patterns are the 

seasonal and diurnal ones. Such patterns result 

largely from (1) variations in emissions of oxidantforming pollutants, (2) variations in atmospheric 

transport and the dilution processes, and (3) 

variations in other atmospheric variables involved 

in the photochemical formation of oxidants. 

Detailed descriptions of the seasonal and diurnal 

patterns for oxidant/ozone concentrations and 

some explanatory discussions can be found in the 

literatu re.''9'

Zs 

Briefly, the striking characteristics of the seasonal and diurnal patterns are (1 ) the occurrence of 

higher oxidant concentrations in the summer 

months, and (2) the occurrence of a daily oxidant 

peak in the early afternoon hours. Of these, the 

seasonal pattern is consistent with and, in fact, 

supports the theory of photochemical formation of 

atmospheric oxidant in that the higher temperatures and sunlight intensities in the summer 

enhance the photochemical process. 19 

Unlike the seasonal patterns, the diurnal pattern 

can be explained in more than one way. Until 

recently, the only explanation accepted was based 

on the assumption that the daily oxidant peak at a 

particular location resulted from local emission 

sources or from those that had been transported to 

the site. The reactions normally occurred several 

hours before the oxidant peak. 19 

A more recent theory explains the oxidant peak 

as the net result of three simultaneouslyoccurring 

processes:s'25 (1 ) downward transport of 

oxidant/ozone from layers aloft; (2) destruction of 

oxidant/ozone on surfaces and in reaction with NO 

at ground level; and (3) photochemical in situ 

production of oxidant/ozone. Also, interpretation 

of reported evidence suggests that downward 

transport and destruction by reaction with NO, 

rather than photochemical formation, 6 ' 25 

determine the concentration of oxidant/ozone 

observed at ground level for the cores of some 

cities as well as remote areas. Whether the 

oxidant/ozone in the layers aloft originates from 

natural or anthropogenic sources is a question that 

some investigators consider unresolved; 5 ' s the 

bulk of the recent evidence on long-range pollutant 

transport, however, points to the anthropogenic 

origin. 2s' 3 ' 

ASSOCIATION OF OZONE WITH OTHER 

CONSTITUENTS OR MANIFESTATIONS OF 

SMOG 

The association of ambient levels of ozone and 

NO2 does not show well-defined patterns that 

would suggest a certain impact of ozone-related 

control on NO2. Trend analysis of Los Angelesdata 

shows the ambient NO2 concentration to increase 

and ozone to decrease during 1965-74 (see 

Figures 3-1 and 3-2). 42 These trends have been 

explained as reflecting the effects of the HC and 

NOX emission rate changes during that period. The 

effect of the ozone-related HC control alone on NO2 

cannot be delineated from the apparently 

overwhelming effect of the NOX emission change. 

A recent study by Trijonis of the ambient NO2- 

precursor relationships provided evidence that the 

hydrocarbon emissions factor had only a small 

codirectional effect on ambient NO2, whereas the 

NOx factor had a much stronger effect, equivalent 

to a 1:1 correspondence between NOX emission 

change and ambient NO2 concentration change. 41 

Laboratory (smog chamber) data also show (1) a 

nearly 1:1 correspondence between fractional 

changes in the NOX precursor factor and fractional 

changes in "daily" average or maximum 1-hr NOz, 

and (2) a small effect upon NO2 from change in 

HC. a.,s 

The association of ozone and PAN has been 

explored using the limited amount of ambient data 

available, and some explanations and 

interpretations have been given of the results. 

Earlier and recent measurements of PAN and 

oxidant/ozone showed (1) the PAN concentrations 

to be much smaller than those of oxidant/ozone, 

and (2) the PAN-to-oxidant/ozone ratio to vary 

with location, the rural areas showing lower 

values than the urban centers. 21 The lower PANto-oxidant/ozone ratios in rural areas can be 

explained mechanistically either as a result of 

enhanced PAN decomposition in NO2-free 

atmospheres or as a result of the relatively lower 

concentrations and prolonged irradiation 

conditions, as a result of pollutant transport, that 

characterize the reaction systems in rural 

atmospheres. Overall, the ambient data 

associations do not provide conclusive evidence on 

the impact of ozone-related control on PAN. The 

ev dence, however, from laboratory and 

theoretical studies is definitive and shows that for 

urban atmospheres, changes in HC and NOx 

24 
+42% 

~ 2% +25% 

~ 24 /° 

\ ' 17% 

f +15% +34% 

~ +7% • 

+3% 0% ( +50% 

, +17% .~ f 

.-•` ~ . 

-13% +68%'~ 

+7% +36% ' -4 

+6% `. a 

+89% 

BASINWIDE HC EMISSION CHANGE: 18% 

BASINWIDE NOXEMISSION CHANGE: +36% 

AVERAGE NO2 CONCENTRATION CHANGE (11 STATIONS): +20% 

Figure 3-1. Trends in NO2 air quality and in HC and NO. emission. Los Angeles Basin, 1965-74. 

18 __o\ 

~

r 16 0~_o ~ 

=p a 14 - \~ o 

Q X a O -O g O 12 \ 

\ O 

10 

0

~~ 

LL Z 30 

~ ~ c~E 25 9 ~0. Q w O L / \ 

20 'O % / ~O 

o' ~ 

O z 15 - ~0

.1 

y 30 

w z O Oa °m 25 - 

rnwv a 20 `~ /~— ` 20 a ~P--0\\ 

~ 7 b~ 

~ OO 15 10, ` O 

z> 

= 10 - 

1963 64 65 66 67 68 69 70 71 72 

YEAR 

• • ANNUALAVERAGE 

0— — — —0 THREE-YEAR MOVING AVERAGE 

Figure 3-2. Pollutant trends in Los Angeles, annual and 3- 

year moving averages. 42 

emissions should have greater impacts on ambient 

PAN than on ambient ozone. 8 

Ambient aldehydes, although nonoxidants, are 

also of interest here because they are constituents 

of the photochemical pollution complex and are 

known to have some physiological effects 

(Chapters 8 and 9). However, aldehydes are also 

directly discharged into the atmosphere as 

automotive emissions. 10 ' 39 Concentrations in 

urban atmospheres seem to rise quickly in the 

early morning hours, reach and maintain a broad 

plateau through most of the day, and then 

decrease in the afternoon. 7 This pattern probably 

reflects the dual origin (primary and secondary) of 

the ambient aldehydes as well as the factthat rapid 

photochemical formation of aldehydes, unlike 

oxidant/ozone, begins with the onset of 

irradiation. 19 Ambient data associations do not 

provide evidence on the impact of ozone-related 

control on aldehydes; laboratory data, however, do 

suggest a nearly 1:1 correspondence between 

fractional changes in HC and fractional changes in 

ambient (photochemical) aldehydes. 8 

The association of ambient oxidant/ozone with 

eye irritation has been explored extensively, but 

only in one location, the Los Angeles Basin. This 

association has been described in detail in the 

predecessor of this criteria document and need not 

25 
14 

12 

:

E 

0 

X 10 

m 

z w_ 

U 

~ 

w 6 

O 

U 

z 

0 

~ 4 

U 

Z ;7 

x 

w 

be elaborated here Briefly, amblent 

oxidant.lozone appears to correlate well with eye 

Irritation, a relationshlp whlch, however, is clearly 

not of cause-effect nature. Lack of causative 

relatlonship means that control of ozone is not 

expected to have a direct effect on eye irrltatlon. 

However, the hlgh degree of correlation between 

the ambient data, the laboratory evidence of good 

correlatlon between the photochemical process 

and eye irritation, 45 and, flnally, the fact that some 

eye irritants, (namely formaldehyde, acrolein, and 

PAN) are known to be products of atmospheric 

photo-oxidation of HC, when considered together 

all suggest that oxidant-related emission control 

will probably have a reducing effect on eye 

irritation for Los Angeles. Eye irritation has been 

observed also in other areas. A pollution episode, 

for example, In New York City during November 23- 

25, 1966, caused numerous eye irritation 

complaints from residents.' Oxidant/ozone 

measurements were not made during the episode, 

and therefore an assoclation could not be 

established. The problem could have been caused 

either by primary pollutants (afdehydes) mainly, or 

by both primary and secondary pollutants. In 

concluslon, based on present-day knowledge and 

understanding, the evidence and conclusions 

obtained for the Los Angeles area cannot be 

assumed to have unlversal validity. For such 

assumption to be supported (or refuted), additional 

evidence must be obtalned. 

The association of ambient ozone with visibility 

or visibillty- reducing aerosol is perhaps the most 

interesting of the associations discussed here. 

Publlc reaction to the vlsibility problem has been 

stronger than to the ozone problem, and there is a 

feeling among local air pollution control officials 

that the often upsetting ozone control programs 

will be more acceptable if they are shown to have a 

beneficial impact on the haze problem also. In spite 

of this strong interest in the ozone-haze 

association, relatively Ilttle evidence is currently 

available on this subject. The evidence available is 

mostly on the Los Angeles atmosphere. A 

considerable part was obtained in the course of 

conducting the California Air Characterization 

Study (ACHE7C)14 and has been summarized 

informatively In a recent National Academy of 

Sciences report. 42 The part of the evidence of most 

interest here is shown in Figure 3-3 in terms of 

diagrams indicating a good correlation for the Los 

Angeles Basin between vlslbility reduction and 

ambient ozone concentratlon. Somewhat similar, 

but weaker, evidence was reported by Husar et 

Bscat AT PEAK OZONE (BASED ON TWO HOUR 

AVERAGED DATA FROM LOS ANGELES AREA) 

(SUMMER 1973) (SUMMER 1972) 

o ROUBIDOUX (RIVERSIDE) • PASADENA 

e WEST COVINA • RIVERSIDE 

❑ POMONA • POMONA 

• DOMINGUEZ HILLS ♦ HARBOR FWY 

(TORRANCE) (DOWNTOWN LA) 

O BLIMP FLIGHT 

(9/6/73) 

1315-1500 PST 

BLIMP 

~ 

~~ — 0 0 0 

❑ 

n 

• 

• 

NO AEROSOL IN THE ATMOSPHERE 

01 0.2 0.3 0.4 0.5 06 

03, ppm (MAXIMUM) 

Figure 3-3. Correlation between B_, 

and maximal ozone concentration. 15 

a1. 15 and by Wolff et a1. 46 who showed that 

synoptic-scale areas with elevated ozone 

concentrations roughly corresponded in location 

and magnitude with areas of reduced visibility 

("haze blobs"). Such good correlations between 

ozone and haze are self-explanatory in the cases in 

which the haze-causing aerosols consist largely of 

photochemical reaction products. This clearly is 

the case with Los Angeles, as deduced from the 

findings that the optically active aerosol in the Los 

Angeles air consists primarily of photochemically 

generated sulfate with lesser amounts of nitrates 

and organics.

3'"' '2'°a 

The good ozone-haze correlation observed i n Los 

Angeles, the aerosol composition data, the good 

correlation between haze and ambient sulfates, 24 

and, finally, the experimental and theoretical 

evidence on the atmospheric photo-oxidation 

process18,3 all point to the conclusion that oxidantrelated control should also cause some reduction 

in haze in Los Angeles. This conclusion, with two 

26 
important qualifications, Is probably correct. The CalifornialnstituteofTechnology,Pasadena ,CA ,August 

qualiflcatlons are that (1) ozone-related control, 1976 

although beneficial, Is not necessarily the most 

4. City of Houston. Petition for Review and Revision of 

Ambient Air Quality Standard for Photochemical 

effective means for controlling haze, and (2) the Oxidants and Requirements for Control City of Houston 

Los Angeles evidence on the impact of ozone- Health Department, Houston, Tex., July 11, 1977 

related control on haze does not have universal 5 Coffey, P E, and W N Stasiuk Evidence of atmospheric 

validity. The second qualification is Supported by transport of ozone into urban areas. Environ. Sci 

the case of Denver, for example, where the haze Technol 9 59-62, 1975 

6. Coffey, P., W Stasiuk, and V Mohnen. Ozone in urban 

problem appears to be caused by primary and rural areas of New York State. /n International 

aerosolS. 38 '4 Such aerosols cannot possibly be Conference on Photochemical Oxidant Pollution and Its 

impacted by the ozone-related control except, of Control Proceedings Volume I. B Dimitriades, ed EPAcourse, when HC emission control measures 

600/3-77-001a, U.S. Environmental Protection Agency, 

happen to reduce vehiCDlar aerosol emiSSionS 

Research Triangle Park, N.C., January 1977 pp 89-96 

7 Committee on Challenges of Modern Society Air Quality 

(e.g., measures reducing autorllobile traffic). Criteria for Photochemical Oxidants and Related 

Houston also has been reported to show Hydrocarbons NATO/CCMS Publication No 29, North 

interpollutant relationships different from those Atlantic Treaty Organization, Brussels, Belgium, 

occurring in Los Angeles.4 February 1974 

8. Dimitriades, B On the function of hydrocarbon and 

SUMMARY nitrogen oxides in photochemical smog formation. Report 

of Investigation RI 7433, U S Department of the Interior. 

PhOtochemical oxldants are products of Bureau of Mines, Washington, D.0 , September 1970 

atmospheric reactions invOlving Organic 9 Dimitriades, B Photochemical Oxidants in the Ambient 

pollutants, NOX , oxygen, and sunlight. Theyconsist Air of the United States EPA- 600/3 -76 -017, U.S 

rTlostly of ozone, NO2, and PAN, with smaller Environmental Protection Agency, Research Triangle 

amounts of other peroxyacylnitrates and other 

Park, N C, February 1976 

10. Dimitriades,B,andT C Wesson Reactivities of exhaust 

peroxy -compounds, and are formed along with aldehydes J. Air Pollut. Control Assoc. 22 33 - 88, 1972. 

other photochemical products such as aldehydes , 11 Friedlander, S K Chemical element balances and 

gaseous and particulate nitrates, and sulfates. identification of air pollution sources Environ Sci. 

They originate mainly from volatile organic and Technol 7 235 -240, 1973. 

NOx e T1ISSIOr1S aSSOClated wlth hUman actlVltlBS. 

12. Gros~ ean, D, and S. K Friedlander Gas-particle 

distribution factors for organic and other pollutantsinthe 

Photochemlcal oxidant formation IS a complex Los Angeles atmosphere J Air Pollut Control Assoc 

function of emissionsand meteorological patterns. 25 1 038-1 044, 1975 

Peak concentrations of oxidant expressed as 13 Hendry, D G, and R A. Kenley Generation of peroxy 

ozone are generally higher within urban and radicals from peroxynitrates(R02NO 2 ) Decomposition of 

suburban areas, reaching levels in excess of 590 peroxyacyl nitrates J Am Chem Soc 99.3198 -3199, 

Ng/m 3 (0.3 ppm). In rural areas, peak con- 14 

1977 

Hidy, G M, B Appel, R J Charlson, W E Clark, S K 

centratlons are lower but often exceed the 1-hr Friedlander, R Giauque, S. Heisler, P K Mueller, R 

National Ambient Air Quality Standard of 160 Ragaini, L W Richards, T B Smith, A. Waggoner, J J 

,Ug/m 3 (0.08 ppm). Dosages or average conWesolowski, K T Whitby, and W White 

centrations, however, are comparable to or even 

Characterization of Aerosols in California (ACHEX) Final 

Report Volume I Summary California Air Resources 

higher than those in urban areas. Because of Board Contract No. 358, Rockwell International Science 

pollutant transport, the oxidant problem is viewed Center, Thousand Oaks, Calif , April 1975 

as having regional dimensions in the hundreds-of- 15 Husar, R B, D E Patterson, C C Paley,and N V Gillani. 

mileS range. Ozone in hazy air masses /n International Conference on 

Photochemical Oxidant Pollution and Its Control 

Proceedings Volume I B Dimitriades, ed EPA-600/3- 

REFERENCES FOR CHAPTER 3 77-001 a, U S Environmental Protection Agency, 

Research Triangle Park, N C, January 1977. pp 275- 

1 Becker, W. H., F J. Schilling, and M. P Verna. The effect 282 

on health of the 1966 eastern seaboard air pollution 16. Jeffries, H, D Fox, and R Kamens Outdoor Smog 

episode Arch Environ Health 16.414-419, 1968 Chamber Studies Effect of Hydrocarbon Reduction in 

2 Bufalini, J J, B W Gay, Jr., and K L Brubaker, Nitrogen Dioxide EPA-650/3-75-011, U S 

Hydrogen peroxide formation from formaldehyde Environmental Protection Agency, Research Triangle 

photooxidation and its presence in urban atmosphere Park, N C, June 1975 

Environ. Sci Technol 6816-821, 1972 17. Junge, C E Atmospheric Chemistry and Radioactivity 

3 Cass, G R The Relationship Between Sulfate Air Quality Academic Press, Inc , New York, 1963 

and Visibility at Los Angeles EQL Memorandum No 18, 18 Kocmond, W C, and J Y Yang Sulfur dioxide 

photooxidation rates and aerosol formation mechanisms 

27 
A smog chamber study EPA/600-3-76-090, U S. 34 

Environmental Protection Agency, Research Triangle 

Park, N C, August 1976 

19 Leighton,P A Photochemistry of Air Pollution, Academic 

Press, Inc , New York, 1961 

20 Lonneman, W A Ozone and hydrocarbon measurements 35 

in recent oxidant transport studies /n International 

Conference on Photochemical Oxidant Pollution and Its 

Control Proceedings Volume I B Dimitriades, ed EPA600/3-77-001a, U S Environmental Protection Agency, 

Research Triangle Park, N C, January 1977, pp 211- 

223 

21 Lonneman, W A, J J Bufalini, and R L Seila PAN and 

oxidant measurement in ambient atmosphere Environ 

Sci Technol 10 347-380, 1976 

22 Mayrsohn, H, and C Brooks The analysis of PAN by 

electron capture chromatography Presented at the 

Western Regional Meeting, American Chemical Society, 

November 18, 1965 

23 Meiter, G M, and H Nieboer Determination of 

peroxybenzoyl nitrate (PBzN) in ambient air /n Ozon und 

Begleitsubstanzen im photo-chemischen Smog VDI Ber 

(270) 55-56, 1977 

24 Miller, D F, and D W Joseph Smog-chamber studies on 

photochemical aerosol precursor relationships EPA600, 3-76-080, U S Environmental Protection Agency, 

Research Triangle Park, N C, July 1976 

25 Mohnen, V, and E Reiter International Conference on 

Oxrdants, 1976—Analysis of Evidence and Viewpoints 

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Research Triangle Park, N C, December 1977 

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No AP-63, U S Department of Health, Education, and 

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1970 

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and Air Quality Trends Report, 1972 EPA-450/1 -73- 

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29 Office of Air Quality and Planning Standards Monitoring 

and Air Quality Trends Report, 1973 EPA-450/1-74- 

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Research Triangle Park, N C, November 1976 

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Agency, Research Triangle Park, N C, August 1973 

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28 

36 

37 

38 

39 

40 

41 

42 

43 

44 

45 

46 

Ripperton, L A, and J J. B Worth Chemical and 

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Research Triangle Park„ N C, January 1977. pp 413- 

424 

Robinson, E, and R A Rasmussen Identification of 

natural and anthropogenic rural ozone for control 

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Pollutton Control Association, Pittsburgh, Pa., March 

1976 pp 3-13 

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February 1976 

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Emissions and Air Quality Trends in the South Coast Air 

Basin EQL Memorandum No. 16, California lnstitute of 

Technology, Pasadena, Calif , January 1976 

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Studies in Ohio-1974. EPA-600/3-78-007, U.S 

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the 68th Annual Meeting, Air Pollution Control 

Association, Boston, Mass , June 15-20, 1975 

WiIson, K W Survey of Eye-Irritation and Lachrymation 

in Relation to Air Pollution. Coordinating Research 

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Wolff, G T, P J Lioy, G D Wight, R F Meyers, and R. T 

Cederwall An investigation of long-range transport of 

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N C, January 1977 pp 307-317 
4. SOURCES AND SINKS OF OXIDANTS 

PHOTOCHEMICAL FORMATION OF OXIDANTS 

Introduction 

AII the evidence presently available indicates 

that in the urban centers and adjacent downwind 

areas where severe oxidant problems occur, the 

major cause by far is photochemical oxidant 

formation. In areas with less severe problems, and 

especially in remote areas, nonphotochemical 

sources (e.g., stratospheric ozone intrusion) may 

be significant and on occasions may be the 

dominant sources. 

When photochemical oxidants in air were 

identified as products of a photochemical process 

involving primary air pollutants, it became 

immediately apparent that the problem could not 

be abated by traditional methods of direct control. 

The chemistry of this process had to be clearly 

understood before rational abatement measures 

could be devised. Accordingly, in the ensuing 

years, numerous studies of the oxidant chemistry 

were conducted with the following specific 

objectives: 

1. To identify the precursors of photochemical 

oxidants (that is, those primary pollutants 

that participate as reactants in the oxidantforming process) for the purpose of 

directing the control effort to the right 

ta rgets. 

2. To determine the kinetics of the precursor 

reactions mainly for the purpose of 

deducing the impact of precursor control on 

oxidant formation. 

3. To determine the stoichiometry of the 

precursor reactions for the purpose of more 

fully assessing the pollution problems 

caused by such precursors. 

4. To elucidate in detail the oxidant-forming 

mechanism for the pLirpose of providing 

deterministic, as distinct from empirical, 

input to the oxidant abatement effort, and 

also for the purpose of relating oxidant 

formation to other manifestations of 

photochemical pollution. 

Several of these objectives have been achieved, 

at least to the degree of completion such that the 

information generated was sufficiently comprehensive and reliable to permit development of a 

crude but promising oxidant abatement strategy. 

These chemical studies clearly are relevant to the 

purposes of this document; however, they need not 

all be included in this review or expanded on in 

detail except where they pertain to applications 

directly related to the questions of oxidant control. 

To serve the purposes of this document better, 

the discussion of the chemistry pertaining to 

photochemical oxidants will be divided and 

presented in several sections. The following 

section on atmospheric reaction mechanisms 

includes a general discussion of the chemical 

processes and a review of recent atmospheric 

chemistry studies, focusing only on those findings 

that a re judged to have had the strongest impact on 

the understanding of the oxidant formation 

mechanism. It is intended and hoped that this 

introductory discussion and review will prepare 

the reader to understand better the subsequent 

sections dealing with the specific applications of 

the information used in formulating oxidant 

control strategies. In those sections, the reaction 

mechanisms and other pertinent aspects of the 

oxidant chemistry will be discussed critically and 

more comprehensively. For additional detailed 

discussions of the earlier studies of atmospheric 

chemistry, the reader is referred elsewhere. 54 '78 '92 ' 

93 

Finally, there is one important difference in 

emphasis between the following reaction 

mechanism section and the preceding chapters. In 

the preceding chapters, ozone and other oxidants 

were dealt with nearly always collectively, using 

the term "oxidant." In the discussions of reaction 

mechanisms, however, all mechanistic interpretations regarding oxidant, in actuality, pertain 

to ozone alone. Analogous mechanistic 

discussions addressed to other oxidants will not be 

included in this document mainly because the 

29 
emphasis is on ozone and because the mechanistic 

information available for other oxidants is 

considerably deficient. 

Atmospheric Reaction Mechanisms 

The pioneering work of Haagen-Smit in 1952 e4 

first demonstrated through laboratory experimentation that the photochemical oxidants 

present in an urban atmosphere may indeed be 

products "of atmospheric photochemical reactions 

involving organic (e.g., hydrocarbons) and 

inorganic (e.g., nitrogen oxides) pollutants. Since 

then, numerous studies of oxidant formation have 

been conducted," 5,7e,93 and a wealth of information 

is now available regarding the stoichiometry, 

kinetics, and mechanisms of these HC-NOX-airsunlight reactions. The following discussion 

summarizes the results of these studies and 

presents highlights of the chemical mechanism 

that is presently thought to explain best the 

phenomenon of photochemical oxidantformation. 

AII experimental reserach concerned with the 

mechanism of atmospheric oxidant formation was 

conducted in the laboratory using experimental 

conditions tFiat were,similar to but not nearly as 

cornplex as those prevailing in the ambient 

atmosphere. SLch simplifications of the natural 

system were necessary to facilitate research, but 

they also limited the validity of extrapolating 

research findings to ambient conditions. Thus 

most mechanistic evidence obtained to date 

pertains solely to the oxidant formation process 

occurring in laboratory systems. The mostthatcan 

be said at this time is that all of the reaction steps 

known to occur in the experimental reaction 

systems are almost certain to occur in the ambient 

atmosphere also, although perhaps with varying 

significance. The converse, however, may not 

necessarily be true; that is, unidentified reaction 

steps mayoccur in the ambient atmosphere but not 

in laboratory simulations. 

The overall chemical changes that are observed 

to occur when a mixture of HC and NOx pollutants 

is exposed to sunligF., under conditions similar to 

those in the atmosphere are illustrated in Figure 4- 

1. The curves of Figure 4-1 depict the overall 

photochemical process as consisting of two 

distinct reaction stages occurring consecutively. 

During the first stage, nitric oxide (NO) is converted 

into nitrogen dioxide (NOz)without anyappreciable 

buildup of ozone (03) or other non-NOz oxidants. 

The second stage starts when almost all of the HO 

has been converted into NO2 and is characterized 

\\\ 9R NTR 

\~ N OCFN 

\ o 

\ °+° 

\ E 

~~ . 

~ 

O ,O S O~ON~ 

F O QP ~ 

IRftAOIATION TINIE 

Figure 4-1. Chemical changes occurring during photoirradiationof hydro-carbon-nitrogen oxide-air systems 

by rapid accumulation of ozone and other oxidant 

and nonoxidant products. 

Several mechanisms explaining the observations depicted in Figure 4-1 have been 

postulated. Although these mechanisms differ 

substantially in chemical detail, they all explain 

ozone formation in the atmosphere to be the net 

result of the following main reactions: 

NOz UV=~NO + 0 (4-1) 

light 

0 + 02 M-0-03 + M (4-2) 

03 + NO ~ NOz + Oz (4-3) 

X02 + NO ~ NOz + XO (4-4) 

2N0 + 02 ~ 2NO2 (4-5) 

where M is the third body in a reaction, and X is 

hydrogen (H) or organic radical (R or RCO). Through 

this mechanistic procedure, the NO product from 

the photolysis of NO2 reacts rapidly with and 

consumes ozone to regenerate the photolyzed 

NOz. Therefore, unless other processes convert 

the NO into NOz, ozone is not allowed to 

accumulate to significant levels. However, other 

NO conversion processes do exist—mainly the 

reactions of NO with X02 and, to a much lesser 

degree, with molecular oxygen (02). The reaction 

with X02 occurs only when photochemically 

reactive organic compounds are present, in which 

case the reaction can be sufficiently rapid to cause 

atmospheric accumulation of ozone to significant 

levels. In the absence of reactive organics, the only 

NO conversion process parallel to the 03-NO 

reaction is the reaction of NO with Oz; this 

reaction, however, is relatively slow and does not 

cause significant ozone accumulation. 

In mathematical terms, the ozone buildup in the 

atmosphere obeys the equation2a 

[031 - [NOzI (4-6) 

[NO] 

30 
where I is light (sunlight) intensity, and k is a 

constant. This equation is derived by applying the 

steady state hypothesis to chemical reaction 

steps 4-1, 4-2, and 4-3. This equation illustrates 

the effect on ozone buildup of any process that 

converts NO into NO2 (e.g., the reaction of NO with 

X02); such effect istoward high [NO2] :[NO] ratios, 

and hence high levels of ozone buildup. Ambient 

measurements in downtown Detroit 132 in the 

summer of 1973 and from the Los Angeles 

Reactive Pollutant Project (LARPP) 18 have 

essentially verified the photostationary state 

equation in tie atmosphere within the stochastic 

limits of the turbulent atmosphere. 124 

Though the overall mechanistic scheme 

depicted by processes 4-1 through 4-5 was 

established long ago, the detailed reactions 

explaining the consumptlon of the organic and 

inorganic reactants and the formation of the X02 

radicals (e.g., reaction 4-4) have been relatively 

obscure. It is in this latter mechanistic area that 

some important developments havetaken place in 

the past 5 to 6 years. These new findings and their 

impact on current understanding are summarized 

here. The significance of these findings in the 

specific applications of reaction mechanisms in 

the development of mathematical models wlll be 

discussed in a subsequent section of this 

document. 

One important accompllshment [n recent years 

in the area of atmospheric reaction mechanisms is 

the development of computer techniques for 

simulating the atmospherlc smog-forming 

process. 19 ' 40 Such techniques have provlded a 

useful tool for selecting those reactions that play a 

key mechanistic role and for predlcting the 

existence of potentlally Important but as yet 

unidentified reaction products in the ambient 

atmosphere. 

The most important mechanlst[c find[ng, 

however, In recent years pertains to the Identities, 

sources, and roles of the radicals responsible for 

the oxidation of the organic and inorganic 

reactants. Unlike the early emphasis on atomic 

oxygen, O( 3 P), and ozone roles, the current 

thinking attributes to the hydroxyl radical (OH) 

most of the hydrocarbon- and aidehydeconsuming chemical activity. 5E,133 

Other radicals also, most notablyatoms and R02, 

can attack and consume the organ[c reactant 

signiflcantly, as illustrated bythe data inTable4-1. 

These data, derlved from a computer simulation of 

an irrad[ated trans-2-butene/NOx reaction system, represent calculated rates of attack of several 

TABLE 4-1. CALCULATED RATES OF ATTACK ON 

TRANS-2-BUTENE BY VARIOUS REACTIVE SPECIES IN 

SIMULATED SMOG SYSTEM AT SEVERAL 

IRRADIATION TIMES a 

Attack rate, ppb/min 

Species 2 min 30 min 60 min 

0 0 013 0 018 0.011 

03 0 026 016 016 

OH 1 72 055 0.27 

H02 0.16 0.15 009 

NO3 0.05 x 10-4 2 2 x 10-4 2.6 x 10- " 

02 (a'A) 2.9 x 10-6 2 1 x 10 -6 1.3 X 10 ~ 

'DatafromDemertianetal^Olnitialconditions [NO],0075ppm,[NOz1,0025ppm, 

[trans-2-butene], 0 10 ppm, [CO], 10 ppm, [CHzO], 0 10 ppm, [CH3CHO], 0 06 ppm, 

[CH<]. 1 5 ppm, relative humiuity, 50% 

reactive specles on butene, at several irradiation 

times. 

The radicals OH, H02, and X02 have also been 

identifled as having major roles in the oxidation of 

NO into NO2 (reaction 4-4). 93Sources of these 

[mportant radlcals are now believed to be the 

reactions: 

(Aldehydes, HONO, 03, others) 

h!'--,..OH, H02, R02, others (4-7) 

Ox[dat[on of NO Into NO2 occurs via a chain 

mechanism illustrated by the following sequence: 

OH + (hydrocarbons, aldehydes) 

H02, R02, others (4-8) 

H02 + NO — NO2 + OH (4-9) 

R02 + NO — RO (4-10) 

RO + 02 — H02 + aldehyde (4-1 1) 

Such chain processes are terminated when 

rad[cals react to form more stable products, for 

example. 

OH + NO2 — HONO2 (4-1 2) 

HOz + H02 (or R02) — H2O2 (or ROOH) (4-13) 

H02 + NO2 — HONO (or HOONO2?) (4-14) 

RC(0)02 ~ RC(0)02NO2 (i.e., PAN) (4-15) 

H02, R02 + surface —(H02, R02) surface (4-16) 

A more complete picture of the reactions 

accounting for the organic ox[dant degradat[on, 

oxidation of NO [nto NO2, and organ[c product 

formatlon [n the amb[ent atmosphere, is [Ilustrated 

in Figure 4-2 for the case in which the organic 

reactant Is an olefin. 40 Comparably complete 

mechanlstic information is now available for 

paraff[ns also, but not for aromatic hydrocarbons. 

In the inorganic part of the atmospheric reactlon 

mechan[sm, some steps recently have becomethe 

subjects of controversy because of the[r d[fferent 

roles In the ambient atmosphere and in the 

laboratory systems. Thus, the reactions 

a 
OE (' Ag ) 

CHs =CHCH(Oz H)CH E 

~ 

CH g CHOz+ 

~ O, 

CH E CH(O,)O, 

O ~ O 

I I 

OCH(CH 3 )O 

~ 

OOOCH(CH s )O 

O(' P) 

CH g CH(0)CHCH, 

O, H E /O 

CH s CH-CHCH s 

CH,CH=CHCH g 

03 

d°o 

CHe CH-CHCH$ 

~ CH,CH(U)CH(O,)C 

EHO*

] 

~ 

CH3 CH (U)O + 02 

O: 

NO 

CH3 COs + HOZ CH E CHO* + NO x 

CH, +OE 

CH 3 C0 + RH 1 °E ~01 

CH, O, 

CH 3 C061 NO 

NO 

~ CH 3 COE + NO, 

4 

NOE ~ AS BEFORE 

CH 3 0 + NOa 

~ O, CH3 COO Z NO2 =PAN CO, 

CH= O + HO, NO3 CH2 O* 

* ~ R 

NO CH, ONO= CO 

CH~ ONO* 

CHO + RH 

1 O, 

Fc—~+ HOD • These products undergc significant photodecomposition in sunlight 

Figure 4-2. The major reaction paths for the degradation of irans-2-butene in an irradiated NO,-polluted atmosphere. 

32 
CH y CH=CHCH i 

HQ/ `HO 

CH $ CH=CHCH a + H ' O CH j CHOHCHCH 3 

1 Oz ~ O 2 

CH S CH=CHCH,bA CH s CHOHCH(O = )CH3 

O1— O ~NO 

I I CH 3 CHOHCH(6)CH3 + NOz 

CH 3 CHCHCH1 

p= CH3 CH H + CH ~ CHO* 

O ~ O Oa 

I I ~ CH e CH(O= )OH 

CHs CHCH(6 = )CH 3 

i NO 

~ CH j CH(0)OH + N0 1 

O O ~ 

) ~ CH ; t HCOOH 

CH,CHCH(0)CH i + NO s ~ 

~ Oi 

CHg CH10 CHO + CH=O* 

CHaO' 

CH3 CH0* + tHO 

~ pa \*, 03 

CO + Hbs HCOb y 

NOi IVO 

HCOOz NOi HCbs + NO = 

HONO = + F01 H •-I F

O .1 

~ O = 

HO: 

t N0 

CH, O + NO X 

NO 

~ 02 NO . ~ CH3 0NOz 

CH~ O* + HO ~ CH a ONO* 

CH a CO + H z 0 -4 

HO 

1 AS BEFORE 

COa , CO 

PAN 

CH 2 O 

CH yONOy 

CH 3 0N0* 

Figure 4-2. (Continued). The major reaction paths for the degradation of irans-2-butene in an irradiated NOx polluted 

atmosphere. 

33 
NO + NO2 + H20 — HONO (4-17) 

N206 + H20 -- 2HNO3 (4-18) 

are known to occur both homogeneously (in the 

gas phase) and heterogeneously. Both reactions 

are thought to be of relatively little importance in 

the ambient atmosphere but are suspected to 

occur significantly on the reactor walls in 

laboratory systems. 17,71 Questions are thus raised 

about the applicability of the laboratory findings to 

the ambient atmosphere, which is an issue of 

crucial importance. 

Another noteworthy finding is that some 

nitrogenated products of the photochemical smog 

system, such as PAN and possibly peroxynitric acid 

(HOONO2) have a greater mechanistic role than 

thought earlier. Recent investigations of PAN 

chemistry 34,60,98 have revealed that PAN can 

thermally decompose to an acylperoxy radical and 

NO2. The rate of decomposition is extremely 

temperature dependent. Because of this temperature dependency, significant levels of PAN can 

build up early in the day when temperatures are 

relatively low. In the late afternoon when ambient 

temperatures are higher, the decomposition of 

PAN can proceed at a rapid rate, liberating NO2 

molecules that can lead to enhanced ozone 

production. 

The discovery that PAN can thermally 

decompose and enhance ozone formation 

suggests that there may be other peroxynitrates 

that can also affect the rate of smog formation. 

Recently, peroxynitric acid (HOONO2) was 

identified by Fourier-transform infrared spectroscopy (FS)79 ' 95 as an intermediate of 

photochemical smog systems. This species and the 

related peroxynitrates (ROONO2) could act as 

radical sinks and affect the rate of smog formation. 

The important H02 and R02free radicals, as well as 

NO2, could be temporarily stored as peroxynitrate 

and then released (through thermal decomposition 

of the peroxynitrate) at later stages in the reaction 

to enhance ozone production. However, recent 

experimental evidence33,so,12s indicates that the 

decomposition of HOONO2 proceeds so rapidly at 

room temperature that this species will not be a 

significant sink for H02 or NO2. Consequently, 

HOONO2 is not likely to be of significance in 

photochemical smog formation. 

This role of the peroxynitrate products raisesthe 

more general question regarding the role of 

atmospheric reaction products in the chemistry of 

polluted air masses irradiated for several days. 

Such multiday reaction of polVutant mixtures is 

now known to occur in the ambient atmosphere 

and specifically, within urban air masses subjected 

to long-range transport. 136 While the chemical 

mechanism of such aged systems cannot be 

different from that of fresh systems in terms of 

fundamental reaction steps involved, the relative 

rates of such steps may be sufficiently different 

that the relative roles of the organic and NOx 

reactants, as well as the relative reactivities of the 

various organics in producing oxidant/ozone, may 

be substantially different. Evidence attesting to 

such differences has recently been reported by 

researchers who did laboratory and computer 

simulation studies of fresh and aged HC-NOx 

reaction systems. Thus smog chamber studies 

have suggested that the oxidant-to-precursor 

dependencies in aged systems may be different in 

magnitude, and possibly in direction also, from the 

dependencies observed in fresh systems. 41 ' 71 

Current knowledge and understanding of the 

atmospheric chemistry of aged polluted air are 

considerably inferior to those pertaining to fresh 

atmospheres. 

The chemical transformation of S02 to particulate sulfates is of considerable interest, both in 

terms of understanding S02 removal mechanisms 

in the atmosphere as well as the potential health 

and welfare effects96 associated with particulate 

sulfates. Though it is beyond the scope of this 

document to provide a detailed review of the stateof-the-art of SOx chemistry, a short discussion 

regarding its interaction in the photochemical 

process seems warranted. 

In recent years, significant progress toward 

understanding the homogeneous S02 oxidation 

pathways in the atmosphere has been made. 16, 

119,122 One of the more important contributions has 

been the experimental gas kinetic rate constant 

determinations for the H02 and HO reactions with 

S02: 20,99 

H02 + S02 — HO + S03 

HO + S02 + M— HOS02 + M 

The quantification of these reaction rates in 

conjunction with theoretical estimates of the 

reaction rates for the organic radical analogies 

R02 and RO have explained major portions of the 

S02 transformation observed in both experimental 

smog chamber studies and field investigations. 

16,119,142 

In the presence of water vapor, S02 reacts 

rapidly to form H2SO4. The details of the reaction 

pathway for the HOS02 species is currently 

unknown, but evidence exists indicating that 

34 
H2SO4 is the resulting end product. In the 

atmosphere, H2SO4 may undergo complex interactions with aerosol particulate or react with 

gaseous ammonia to form a host of sulfate salts. 

Characterization of these condensable species via 

experimental and ambient observations will be a 

major area of continued research and will play a 

significant role in elucidating the mechanistic 

details of atmospheric SOx . 

Outside the reaction mechanism area, some 

significant developments have taken place in 

recent years in the area of reaction product 

identification. Table4-2 lists gaseous products and 

typical concentrations at which such products 

were found to occur in the ambient atmosphere. 

Table 4-3 lists gaseous products either observed in 

laboratory (smog chamber) systems or unreported 

yet but theoretically expected to exist in the 

ambient atmosphere. Particulate products also 

exist but are not easy to identify. Such products are 

certain to include nitrates and a variety of organic 

compounds. Tables 4-4 and 4-5 list some reaction 

products identified in ambient atmosphere 

aerosols. 93 The significance of these findings is 

that they provide a more complete description of 

the photochemical pollution problem and that they 

verify or further elucidatethe atmospheric reaction 

mecha nism. 

TABLE 4-2. COMPOUNDS OBSERVED 

IN PHOTOCHEMICAL SMOG 

Typical (or maximaQ 

concentration reported, 

Compound ppm 

Ozone, 03 01 (0 6) 

PAN, CH3C002NO2 0005(0.2) 

Hydrogen peroxlde, HzOz (0.18) 

Formaldehyde, CH2O 004 (0 16) 

Hlgher aldehydes, RCHO (0.36) 

Acrolein, CHzCHCHO (O 01 1) 

Fo rml c acld, H COO H (0 05) 

In conclusion, the information generated in the 

years since the issuance of the preceding criteria 

document provides a much more complete plcture 

of the atmospheric oxidant formation process. 

Nevertheless, it should be stressed that the 

present situation Is somewhat uncertain because 

most of the supporting evldence was obtained from 

laboratory atmospheres and is therefore mainly 

applicable to such an environment. The 

mechanism of the oxidant-forming process In the 

ambient atmosphere, containing a multitude of 

reacting pollutants, may Include reaction steps in 

addition to those presently recognized. Such 

TABLE 4-3. COMPOUNDS THAT MAY BE FORMED IN 

PHOTOCHEMICAL SMOG 

Compound Possible synthesis Reference 

Peroxybenzoylnitrate, 00002 + NO2 62 

C6H5C002NO2 

Nltrlc acld, HONO2 NOz + OH 55 

N205 + H20 91 

Organlc hydroperoxides, ROz + HOz 40 

ROOH 

Organlc peraclds, RCOOzH RC002 + HOz 40 

Organlc peroxynitrates, ROz + NO2 + Me 40 

RO2NO2 

Ozonldes, 03-olefin 03 + olefln + Ma 7 

Ketene, CH2C0 03 + olefln 88 

Nltrous acld, HONO OH + NO 8,32 

Pernitrlc acld, H0 2NO2 NOz + HOz + Ma 50,79,95 

Pernitrous acld, HOzNO NO + H02 + Ma 31 

Organlc nitrates, RONOZ RO + NO2 37 

R02 + NO 37 

'M represents any molecule that takes part in the three-body process 

additional reactlons, for example, known or 

suspected to occur in the ambient atmosphere, are 

those causing degradation of aromatic hydrocarbons and of numerous organics into gaseous 

and particulate products. To date, these 

degradations are largely unexplored Important 

reactions may also be occurring through energy 

transfer processes promoted by pollutants or other 

molecules capable of absorbing solar energy and of 

transferring such energy to nonabsorbing 

pollutants. Also, the nature and importance of 

heterogeneous reactlons occurring on the surface 

of ambient aerosol particles 49 and on the surface of 

laboratory chambers' have been explored but are 

not well understood. Further studies are needed to 

ascertain the appllcabillty of laboratory data to 

ambient atmospheres. 

Effects of Meteorological Factors 

INTRODUCTION 

The photochemical oxidant/ozone concentrations observed In the ambient air above 

urban and nonurban areas are the net resu It of two 

broadly deflned processes: First, a physical process 

involving dispersion and transport of the oxidantprecursor emisslons; and second, a chemical 

process involving reaction of the dispersed 

pollutants under the stimulus of sunlight. The 

potential effects of ineteorological factors on both 

these processes are obvlous. Thus the factors 

related to atmospherlc dllution and transport affect 

ambient levels of pollutant accumulation and the 

geographical relationship between source areas 

and corresponding oxidant problem areas. Solar 

radiation and ambient temperature are also 

important by virtue of their effects on the chemical 

35 
TABLE 4-4. SECONDARY ORGANIC AEROSOLS2 

Possible gas-phase hydrocarbon 

Compounds identified° orecursors 

Altphatic multl iunctlonal compounds 

1. X-(CH2)n-Y (n=3,4,5)• 1 Cycltc oleflns 

X y 

COOH CH2OH 

COOH COH (CH2) CH 

~ , 

COOH COOH CH 

COOHb CH2ON0 

or COH CH2ONO2 

COH CH2OH 

COH COH and/or dloleflns 

COOHb COONO 

or COH COONO2 >C=CH-(CH2)r,-CH=C< 

COH COONO 

COOH COONO2 

COOH CH2ONO2 

Others 2 Not known; posstbly from aromattc ring cleavage 

CH2OH-CH=C(COOH)-CHO 

CH2OH-CH2-CH=C(C0OH)-CHO 

CHO-CH-CH-CH(CH3)CHO 

CH2OH-CH=CH=CHb-C(CH3)CH0 

CsH803 Isomers 

Nttrocresols 

C6H602 Isomers° 

Aromattc monofunctlonal compounds 

3 C6H5-(CH2), - COOH (n = 0,1,2,3) 3 Alkenylbenzenes 

C6H5-(CH2)n-CH=CHR; also toluene for C6H5CO0H 

4 C6H5-CH2OH 4 Toluene, styrene, other monoalkylbenzenes? 

C6HsCH O 

Hydroxynttrobenzyl alcohol 

Terpene-dertved oxygenates. 

5 Ptnonlc acld 5 a-Ptnene 

Ptnlc acld 

Norpinonlc actd 

6 Isomers of pinonlc acld b 6 Other terpenes? 

C91-11402 Isomers 

C,oH1403 isomers 

C,oH1602 Isomers 

° Compounds identdied at West Covina, Calif , July 24, 1974 

°Isomers not resolved by mass spectrometry 

processes. Such meteorological influences 

obscure both the absolute and the relative effects 

of the emission-related factors to degrees thatvary 

with geographical location and season. Therefore, 

for proper assessment of emission-related factors, 

it is essential that meteorological factors and their 

effects on the oxidant problem be well understood. 

Such understanding often depends on meteoro4ogical details that are far beyond the scope of 

this discussion, but some general climatic factors 

may be discussed to illustrate their impact on air 

quality. 

ATMOSPHERIC MIXING 

The diurnal urban emission pattern for oxidantforming poflutants is falrly uniform from weekday 

to weekday. It is apparent, therefore, that 

variations in daily oxidant/ozone accumulation 

must be attributable largely to meteorological 

factors. Of these factors, atmospheric mixing has 

an extremely significant effect on oxidant 

formation. 

The rate and extent of atmospheric mixing and 

diffusion depends on stabllity, wind speed, and 

topography. Temperature inversions are relatively 

stable layers that inhiblt atmospheric diffusion. 

They are common at night in layers near the 

ground, but they may also occur at higher altitudes 

and at times other than at night. Also, several 

successive atmospheric layers with different 

degrees of stability are not unusual. The morning 

peak concentrations of oxidant/ozone precursors 

36 
TABLE 4-5. RELATIVE IMPORTANCE OF ALIPHATIC AND AROMATIC PRECURSORS a 

Gas-phase hydrocarbon 

precursors 

Secondary organic 

aerosols 

XACHzI- Y 

X Y n=3 

Concentration, ° Ng/m' 

n=4 

_ 

_ 

n=5 

COOH CH2OH 2 18 3.40 065 

COOH COH 1 39 259 082 

CH COOH COOH 1 35 0.78 015 

COOH CHzONO or 1 Ol 0.40 027 (CHz)^

CH COH CHzONOz 

COH CHzOH 031 0.40 013 

COH COH 0.30 024 — 

COOH COONO 014 024 — and/or or COH COONOz — — — 

COH COONO 1 01 0.14 — 

COOH COONOz — — — 

COOH CHzONOz 012 015 — 

>C=CH-(CHz)n-CH=C< Total 781 834 2.02 

COOH-CHrCOOH 0.15 — — 

COOH-(CHz)z-COOH 057 — — 

Total dlfunctlonal compounds 18.89 

CsHe-CH=CHR C6H5-(CH2)n-000H n=0.0.38 

n-1 0 41 

n-2 0 52 

n-3 0 03 

Total from aromatics. 1.34 

'Of aerosols in Pasadena, Calif, , Sept 22, 1972, sampling period, 7 30 a m,to 12 35 p m 

"The same response factor (that of adipic acid) was used for all difunctional compounds 

often result from emissibns from ground sources 

discharged into a stable atmosphere below an 

inversion layer. Typically, these low-level 

inversions begin to lift and provide a greater mixing 

height as the sun rises and heats the earth's 

surface. Thus mixing height (that is, the height 

above surface through which relatively vigorous 

vertical mixing occurs) varies during the day and 

with the season. Figure 4-3 65 shows average 

mixing heights in summer (usually the season of 

highest photochemical oxidant concentrations) 

that occur a few hours after sunrise. As surface 

heating continues, the low-level inversion is 

usually eliminated completely and, as depicted in 

Figure 4-4, 65 the mixing height increases to a 

maximum in the afternoon. Notice that these 

average afternoon mixing heights range from 600 

m(1970 ft) along the California coast to more than 

4000 m(13,000 ft) within the southern Rocky 

Mountain area. Over inland areas, the afternoon 

mixing heights are greatest in summer and least in 

winter (about half of the sLimmer values). However, seasonal variations in coastal regions are 

usually small. To a large extent, the height of the 

afternoon mixing layer has a significant impact on 

the day's accumulation of oxidant/ozone. 

The rate at which relatively unpolluted air moves 

into a region is related to wind speed. Wind speed 

and direction are highly variable in time and space 

(Figures 4-5 and 4-6). 65 The depicted wind speeds 

are averages of those speeds within the respective 

mixing layers. These averages tend to smooth out 

the greatervariations in space andtime thatwould 

occur if only surface winds had been considered. 

During summer mornings, the slowest average 

speeds are less than 2 m sec -1 and occur in the Far 

West. However, in the morning, average speeds of 

3 m sec -1 or less occur over most of California and 

Oregon as well as part of Nevada; in the East they 

occur over the Central Appalachians and 

Mississippi. On summer afternoons, the average 

wind speed pattern is similar to that in the 

morning, except that the average speeds in the 

afternoon tend to be 1 to 2 m sec 1 higher than in 

the morning. Thls diurnal variation is generally 

true for all seasons. 

Using daily values of morning and afternoon 

mixing height and wind speed, the occurrence of 

limited mixing episodes was determined for 62 

weather stations in the contiguous United 

States. 65 The most limiting conditionswere mixing 

heights of 500 m(1640 ft) or less, wind speeds of 2 

37 
16 

14 

12 

10 

.° 16 

Figure 4-4. Isopleths (m x 102 ) of inean summer afternoon mixing heights. 65 

38 
g---9 

Figure 4-5. Isopleths (m sec -

') of inean summer wind speed averaged through tfie afternoon mixing layer.65 

Figure 4-6. Isopleths (m sec -

') of inean summer wind speed'averaged through the morning mixing iayer.°° 

39 
DATA BASED ON FORECASTS ISSUED: 

1 AUGUST 1960 TO 3 APRIL 1970 FOR EASTERN PART OF THE UNITED STATES 

1 OCTOBER 1963 TO 3 APRIL 1970 FOR WESTERN PART OF THE UNITED STATES 

Figure 4-7. Isopleths of total number of forecast days of high meteorological potential for air pollution. 65 

m sec' or less, and no precipitation during at least 

5 consecutive days. Only six such epidoses 

occurred with a total of 39 episode-days at two 

stations (Medford, Oregon, and Lander, Wyoming) 

over a 5-year period. On the other hand, at least 

one episode of 2 days' duration, with mixing 

heights of 1000 m(3300 ft) or less and wind 

speeds of 6 m sec - ' or less, occurred at each of the 

62 stations. In general, limited mixing episodes are 

most common in the Far West and within the Rocky 

Mountain region, least common over the Plains 

States, and of intermediate frequency east of the 

Mississippi (Figure 4-7). 65 

Korshover 76compiled statistics on stagnation 

episodes occurring during the various months of 

the year east of the Mississippi. Such statistics are 

illustrated by graphs in Figures 4-8 and 4-9. 

Korshover's data, however, suffer from two 

limitations First, stagnation episodes were 

determined indirectly, using sea level pressure 

gradient data, rather than the more direct indices 

of mixing height and wind speed; second, the 

requisite pressure gradient data could be obtained 

only forthe relatively low and flat terrain east of the 

Rocky Mountains. A more detailed discussion of 

the Korshover statistics is included in the chapter 

dealing with the natural sources of oxidant/ozone. 

In conclusion, the atmospheric mixing 

parameters have a strong effect on both the 

accumulation of oxidant-precursor pollutants and 

the photochemical oxidant-forming process. The 

effect on the latter process, however, although 

certain to exist, has only recently been studied 

directly and comprehensively; 73,18changes in 

these mixing parameters cannot be simulated 

easily in smog chambers. Nevertheless, the 

information presented here is useful in that it 

suggests the areas and seasons in which 

atmospheric mixing conditions are relatively more 

conducive to oxidant formation and accumulation. 

SUNLIGHT 

The significance of sunlight is related to the 

intensity of sunlight and its spectral distribution, 

40 
50" 

45 

40° 

35 

30° 

25° 

105° 100° 95° 90° 85° 80° 75° 70° 65° 60 

2 1 

1 1 13 3 { 

2 1 

~ 3 

5 

s 4 

3 3 q5 8I 0 ~\ 

4 

i 

3 ] 

7 6 

3346 /11 2 

7 + 3 1 31~ / 

i 8 9 1 2 0 

1 I r 

4 ~ ~ n, 

\" i ' ~ /1 B 9 1 4 

3 10 a 

~ 2 ~ 

3 3 

12 2 

L r U` ~ ' 

\ ~ 

2 

1 1 10 9 

10 4 

3 3 6 ./ 2 

i .i•2 

2 ~ 

z t {rll 

, ^V`~✓1 

~ 

Figure 4-8. Monthly distribution of number of cases of 4 or 

more days of atmospheric stagnation, 1936-75 

(September). 76 

105° 100` 95° 90° 95° 80 75' 

ink 100' 95° 90` 85° 80` 75` 70° 65° 60° 

~- 

1 

1 z 

1 3 i i i { 

a 3 

5 S 6 I 6 4 

Z 

4 1 3 5 `/ 

A 

A 6 

~ 1 

17 ~b I 4/J 0 

~~''rr ~ 1 16 

3 S ] ' { / / ` 

I 2 1 2 1 3 ] R 

7 

3 ~ 9 8 6 

6 4 ] 

~ 

a loll ~ 

'Figure 4-9. Monthly distribution of number of cases of 4 or 

more days of atmospheric stagnation, 1936-75 (August).76 20` 

100° 95° 9 ° 85° 80° 75° 

50° 

45° 

40° 

35 ° 

30° 

25° 

45' 

40° 

35` 

30" 

45' 

40' 

35° 

30° 

25° 

20° 
z.5 

~ 

0 0 

r2.0 

N 

E U 

z 15 

O 

~ 

0 

x 

a 

0 1.0 

~ 

05 

both of which have direct effects on the specific 

chemical reaction steps that initiate and sustain 

oxidant formation. Steps of varying significance 

include the following (and possibly others also): 

NO2 + hv -- 0 + NO (4-19) 

HONO + hv -- OH + NO (4-20) 

H2C0 + hv — H + HCO (4-21) 

RCHO + hv -- CH3 + HCO (4-22) 

03 + hv -- 0 ('D) + 02 (4-23) 

H2O2 + hv -- 20H (4-24) 

HNO3 + hv — OH + NO2 (4-25) 

Whereas the effect of sunlight intensity is direct 

and amply demonstrated, 78 the effect of 

wavelength distribution on the overall oxidant 

formation process is a subtle one Experimental 

studies have shown the photolysis of aldehydes to 

be strongly dependent on radiation wavelength in 

the near-UV region. 28 Since aldehydes are major 

products in the atmospheric photo-oxidation of 

HC-NOx mlxtures, it Is inferred that the radiation 

wavelength should have an effect on the overall 

photo-oxidation process. This inference was 

directly verified, at least for the propylene/NO X a nd 

n-butane/NO x chemical systems, in recent smog 

chamber studies. 70 In the ambient atmosphere, 

some variation in the wavelength distribution of 

sunllght does occur as a result of variations in 

stratospheric ozone, ambient aerosol,t 31 and cloud 

cover. Obvlously, such variation should be 

recognlzed and properly considered in conducting 

and interpreting outdoor experimentation. Beyond 

this consequence, however, the wavelength 

distribution factor has no other practical 

significance. 

Sunlight intensity varies with season and 

geographical latltude, as shown in Figure 4-10.78 

The latltude effect is strong, but only during the 

winter months. During summer, throughout the 

contiguous United States, the maximum light 

intenslty Is fairly constant, and only the duration of 

the solar day varies to a sma{I degree with latitude. 

Some variations in Ilght intenslty also occur with 

longitude during the summer months, with the 

highest intensitles occurring in the western United 

States. 

Absolute levels of sunlight Intensities were 

calculated by Leighton nearly two decades ago. 78 

Since then, several investigators have recalculatedactinicfluxesandmeasured intensities 

by more direct methods. Thus recent 

measurements and recomputations by EPA 

investigators gave results somewhat different 

from those reported by Leighton. These differences 

VALUES OF SOLAR SPECTRUM SUMMER SOLSTICE 

ARE FOR THE 100 nINTERNAL 

CENTERED AT 3700 ,1. 

1 20 N. LAT 

II - 34 N. LAT 

N1 - 50 N. LAT. 

VVINTER SOLSTICE 

 I V- 20 N. LAT 

V - 35 N. LAT. 

VI - 50 N LAT 

Iv` ~~ 

/ \ 

/ _ \ 

/ / \ 

vi \\ \\ \\ 

~ 

! 

0 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 

a m P.m 

Figure 4-10. Diurnal variations in actinic irradiance. 78 

are summarized in Table 4-6. 100 The recomputed 

values are lower than Leighton's in the 295- to 

395-nm wavelength interval, slightly higher in the 

395- to 450-nm interval, and considerably higher 

in the 450- to 700-nm interval. The same EPA 

investigators expressed their recomputed light 

intensities also in terms of values for the NO2 

photodissociation constant, k t (min -1 ). 101 Resulting 

values are listed in Tab1e 4-7. These values are 

higher than the earlier values used in laboratory 

simulations of polluted atmospheres. Jackson et 

a1., 69 Zafonte, 747 and Harvey et a1. 56 measured k 1 

directly; their values also were higher than those 

based on Leighton's calcuiations or on data 

obtained by standard radiometric techniques. 

TABLE 4-6. PERCENTAGE DIFFERENCE BETWEEN THE 

PETERSON100 AND THE LEIGHTON VALUES AT THE 

EARTH'S SURFACE OVER SELECTED WAVELENGTH 

INTERVALS AND SOLAR ZENITH ANGLES 

Wavelength, Zenith angle (°) 

nm 0 20 40 60 

295-395 -6.1 -6 4 -5 5 -4 3 

395-450 +2.4 +21 +3.4 +5.9 

450-700 +18.8 +18.4 +17.0 +15.7 

42 
TABLE 4-7. CALCULATED VALUES OF NO2 PHOTODISSOCIATION RATE CONSTANTa AT THE EARTH'S 

SURFACE AND PERCENTAGE INCREASE OF THE RATE CONSTANT FROM THE SURFACE TO VARIOUS HEIGHTS 101 

Zenith angle (°) ` 

Height 0 70 20 30 40 50 60 70 78 86 

Surface 0.579 0 574 0.560 0 535 0 496 0 432 0 352 0 231 01140 025 

015km 60 6.1 6.4 69 77 89 111 143 167 80 

036 km 114 11 5 121 13.1 145 16.9 21 0 277 342 200 

0 64 km 16.6 169 177 191 21 2 244 304 407 52.6 350 

098 km 21.4 220 22.9 24.7 272 31 5 392 52.3 702 48.0 

1 84 km 29.9 303 31 6 340 377 434 53.7 732 1010 720 

2.91 km 364 37 1 35.8 41 7 462 537 666 91 3 132.0 1000 

r — 

aln umts of min' 

The light intensity factor has been studied in the 

laboratory both with respect to its effect on 

individual photolytic reaction steps and with 

respect to its effect on the overall process of 

oxldant formation. 94 AII of the early studies, 

however, employed constant light intensity 

conditions, in contrast to the diurnally varying 

intensity in the ambient atmosphere. Only within 

the last 3 years has the diurnal variation of light 

intensity been recognized and studied as a factor. 

Such studies have shown this factor to have a 

varying (with initial reactaiit concentration 

conditions), rather unpredictable, but somewhat 

significant effect.72 

TEMPERATURE AND RELATIVE HUMIDITY 

Effects of temperature and relative humidity on 

photochemical oxidant formation were suggested 

by early laboratory studies discussed in the 

predecessor of this criteria document. 92 Additional 

laboratory and field studies in more recent years 

verified a signiflcant, positive temperature 

effect1 0,73 Thus outdoor smog chamber studies of 

synthetic HC-NO X mixtures showed that in winter, 

with maximum daily temperatures at 50 ° to 60°F 

(10.00 to 15.6 0 C), oxidant yields were lower than 

those in the summer (800 to 90°F, or 26.7 0 to 

32.2°C) by 70 to 90 percent, depending on reactant 

composition.73 Also, an RTI analysls of field data 

showed (1) good correlation between daily 

maximum 1-hr oxidant levels and daily maximum 

temperature; and (2) no oxidant concentrations 

greater than 0.08 ppm on days when temperatures 

were below 62°F (16.70 C). The evidence' o '73 

suggests that below about 55 1 to 60°F (13 0 to 

16 0 C), photochemical oxidant concentrations are 

not likely to exceed the 0.08 ppm standard. Also, 

information on the temperature factor indicates 

that in the summer, temperature conditions are 

conducive to ambient oxidant formation throughout the United States as far north as Alaska. 

Unlike the temperature factor, the effect of 

relative humidity remains somewhat uncertain. 

Reveiws by Quon and Wadden 103 and byAltshuller 

and Bufalini 4 have pointed out inconsistencies In 

the available evldence. Model simulations of 

irradiated HC-NOX predict only a small humidity 

effect; 94 however, these predlctions have not been 

verified by consistent experimental evidence. 

TRANSPORT PHENOMENA 

Relative contrlbutions of natural and anthropogenic sources in a given region or area are a 

major question relevant to the ambient 

oxidant/ozone problem. This question has not 

been answered unequlvocally and quantitatively 

chiefly because anthropogenic pollutant transport 

makes it difflcult to assess the strength of the 

natural sources. The question has been answered 

qualitatively. The consensus is that oxidant/ozone 

and/or oxidant precursor transport does occur and 

contributes to oxidant/ozone buildup In areas far 

from the sources. The magnitude of this contribution and the magnitude of the contributions 

from the stratosphere and from other natural 

sources have been viewed as unresolved issues. 43 

Aside from its connection with the naturalversus-anthropogenlc-sources questlon, the 

phenomenon of oxldant transport Is important for 

another reason. The phenomena of urban 

oxidant/ozone plume formatlon and movement, 

rural oxidant/ozone occurrence (at problem 

levels), Sunday-weekday effect, and nighttime 

oxidant/ozone occurrence were previously either 

unnoticed or thought to be odd. They are now 

believed to be true manifestations of an extremely 

complex emission/pollutant disperslon process. 

Such complexities may be introduced by horizontal 

and/or vertical transport of oxidant/ozone and/or 

of precursor mlxtures for long distances wlthout 

excesslve dllutlon. 

43 
Consequences of pollutant transport are 

discussed here. Several studies concerned with 

oxidant transport have been conducted in the last 5 

years. Such studies have resulted in a wealth of 

information. This information and its implications 

are presented and discussed in the remainder of 

this section. 

The first item of interest is evidence on the 

occurrence and range of oxidant transport. It 

should be clarified that the term "oxidant 

transport" is commonly used to refer to transport 

of either oxidant/ozone or oxidant precursors. The 

distinction between oxidant/ozone and oxidant 

precursors should be kept in mind, as it is essential 

to the understanding of the nature, mechanisms, 

and imp ications of the oxidant pollution problem. 

Oxidant transport has been recognized to occur 

on three scales in terms of geographical distance 

or area subjected to the transport effects. These 

scales are. 

1. The urban-scale transport, as a result of 

which the peak oxidant concentrations 

deveiop in the suburbs some miles 

downwind from the city core area where 

the oxidant/ozone and their precursors 

orig i nated; 

2. The mesoscale transport that encompasses 

land- and sea-breeze circulation, and the 

formation of urban oxidant plumes that 

create oxidant problems asfaras 100 miles 

or more downwind from the source city; 

and 

3. The synoptic-scale transport, a much 

longer and broader range of transport 

associated with high pressure systems 

Urban-scale transport has been observed in Los 

Angeles, 134 New York, Houston, Phoenix, and 

several other urban centers. 3' 27 All of the evidence 

available points to the conclusion that conditions 

at the center of source-intensive areas are not the 

most conducive conditions for oxidant accumulation, mainly because of the strong scavenging 

effect of oxidant precursors, especially nitric oxide. 

At higher elevations or at horizontal distances 

downwind from the sources, whEre the precursor 

scavenging effect is less important, oxidant 

concentrations are, in general, greater, and their 

levels are determined primarily by the intensity of 

the photochemical activity and by ambient dilution. 

Measurements in severaV cities during days with 

various wind speeds showed the peak oxidant 

concentrations to occur at distances 8 to 136 km (5 

to 85 miles) downwind from the city center. 87 

During days of stagnation when the highest levels 

of oxidant/ozone occur, this peak-concentration 

distance was estimated by EPA to be between 15 

and 25 km (9 and 16 miles), 53 and more recently, to 

be 15 to 30 km (9 to 19 miles). 

This urban-scale transport of oxidant has two 

important implications. First, it suggests an 

obvious guideline to be used in siting stations for 

oxidant/ozone monitoring. The second implication, suggested by experimental data on the 

oxidant-to-precursor dependencies, 42 is that 

urban-scale transport may obscure the real impact 

of emission control on oxidant air quality. This 

latter implication may be clarified asfollows: small 

or even moderate decreases in emission rates for 

HC and NOX are expected to affect mainly the time 

at which the oxidant concentration will reach the 

day's peak levels; the effects on the peak level itself 

are of smaller magnitude. This time lag effect, in 

turn, translates into an increase in the distance 

from the source area where peak oxidant 

concentrations develop (i.e., the location of the 

peak concentration relative to the location of the 

core of the source area). Thus, for example, the 

actual effect of a modest HC emission reduction 

will be to shift the peak oxidant concentration 

farther downwind, rather than to effect a 

proportional reduction locally. Therefore, the 

impact of emission control will appear to be either 

beneficial or detrimental, depending on the 

location of the oxidant monitoring station. 

Evidence on occurrence of inesoscale and 

synoptic-scale transport has been obtained in 

numerous extensive and conclusive studies. These 

studies have been reported individually 10- 

12, 25,26, 28,30, 38, 39, 44,51,61,66,68, 85,86,115,116,129,130,136,138,139,- 

145 and collectively in reviews. 85,97,12o The evidence 

shows that many cities produce urban oxidant 

plumes that cause elevated oxidant concentrations 

in downwind areas as far as 300 km (190 miles) or 

more from the source CIty.12'25,61,74,128,136,143 

Transport associated with synoptic-scale high 

pressure systems, unlike such mesoscale 

transport, is not characterized by well defined 

urban oxidant plumes and can extend to distances 

several times greater than 300 km (190 miles). 

38,39,97,115,116,120,136,145 In either case, the significant 

implication is that urban emissions may be 

creating oxidant problems not only within and near 

their source areas, but also in other downwind 

urban areas, as well as oxidant problems in rural 

and even in remote areas. It should be stressed 

that the evidence on horizontal transport of 

oxidant/ozone suggests but does not prove that 

most of the oxidant observed in rural and remote 

44 
areas is transported from the cities. Also, 

horizontal transport of oxidant over long distances 

can only occur in air layers aloft; ozone at ground 

level is rapidly destroyed on surfaces and in 

reactions with NO and NC. 23•28,39,74,119,136 For 

oxidant/ozone to reach the surface, there must be 

vertical air movement, a movement that may also 

bring to the surface ozone from the stratosphere or 

from other natural sources. In general, because of 

the multiplicity of the sources that potentially 

contribute to surface oxidant/ozone buildup, the 

rural oxidant/ozone problem cannot automatically 

be attributed entirely to urban oxidant/ozone 

transport. The indications are that direct urban 

transport is a relatively important source of 

oxidants in many locales but not necessarily 

everywhere. 

Because of their elevated ambient oxidant/ozone levels, the State of California, the Gulf 

Coast and Texas, the upper Midwest, and the 

Northeast are the areas of the United States that 

have been studied most. The explanation for 

oxidant/ozone levels in California is relatively 

simple: Ozone levels in that area can be explained 

by local photochemistry and oxidant/ozone 

transport; nonanthropogenic explanations are not 

required. The most striking and clearly explained 

oxidant transport case reported for that area is the 

one involving overnight transport over water of Los 

Angeles air containing as much as 590 ,Ug/m 3 (0.3 

ppm) oxidant to San Diego. l2' 12° 

Unlike California, the situation in the Gulf 

Coast/ Texas area is considerably more complex 

and requires more careful examination. Early 

studies in Texas led investigators to conclude that 

widespread ozone concentrations were not of 

anthropogenic origin. The basis of that early 

conclusion was the observation that ozone was 

frequently high when there were onshore winds at 

coastal stations. 120 However, recent studies by 

Price 102 and by Decker et 81. 38 at the Research 

Triangle Institute (RTI) concluded that natural 

tropospheric ozone was not a factor in the high 

ozone events in Texas. The RTI study, in particular, 

invblved extensive aerial and ground measurements of ozone; HC, and NOx, and wind 

trajectory analysis. Results from that study 

showed the high ozone concentrations over the 

Gulf to be associated with recent passage of the air 

stream over land areas and often over sourceintensive areas. This finding, similar to that by Bell 

for the Los Angeles/San Diego case, 12 explains 

more rationally the observations made in the early 

studies of Texas and implies that the Texas ozone 

problem is at least partly of anthropogenic origin. 

The RTI study also indicated an association of high 

ozone concentration with the passage of high 

pressure systems, an association which had been 

recognized for years and which was more firmly 

established in the midwestern part of the United 

States. 

Transport of ozone for an unusually long distance was reported in an episode of widespread 

haze over southern Florida from May 21 to 27, 

1972. 123 The initial report concerned metropolitan 

Dade County and was supplemented by concurrent data obtained at the site of a proposed jetport 

65 km (41 miles) west of Miami. At this rural site, 

the ozone concentration equaled or exceeded 160 

Ng/m 3 (0.08 ppm) on 5 of those days, and the air 

quality standard was exceeded for 14 consecutive 

hr on both May 22 and 23. The analysis of the 

transporting trajectory that brought the haze and 

accompanying ozone was verified by the EPA 

Meteorological Laboratory. The source region 

appeared to be the industrial area among the 

states south of the Great Lakes, making a transport 

distance of over 1000 miles (1600 km), of which 

400 miles (640 km) were over the Gulf of Mexico. 

Both the haze and the ozone of its precursors may 

have been augmented along the route.46 

Most of the oxidant transport studies in the 

upper Midwest dealt with the role of high pressure 

meteorology in wide area oxidant problems. The 

connection between stagnating anticyclonic 

conditions and high oxidant concentrations over 

large areas was studied by several investigators 

and is now believed to be relatively well 

understood.3e,39,115,116,120,129,130,136,138,139,145 Thi$ 

belief is based on (1) data from direct monitoring 

with an aircraft of the ozone concentrations in the 

path of a moving high pressure system, and (2) 

presence of statistically supported correlation 

between high pressure systems and elevated 

ozone concentrations during days with such• 

conditions. This correlation has been verified by 

numerous studies. The reverse has not been 

established; that is, elevated ozone levels do not 

occur only during stagnating anticyclonic episodes. 

Within the moving and clockwise rotating 

anticyclone, the highest ozone concentrations are 

observed in the trailing or western portion of the 

cell where the air parcels have the longest 

residence time in the anticyclonic regime. RTI 

investigators made some detailed model 

calculations to show that air parcels initially in the 

northeast quadrant of the cell had a potential 

45 
residence time as long as 6 days, and that, air 

parcels on the western side of the circulation 

pattern had been in the cell the longest time. This 

latter conclusion is in general agreement with 

ozone measurements in source areas such as have 

been described by Westberg et a1. 138 Under 

conditions of the high intensity sunlight and 

stagnation or undiluted flow that typically prevail 

within the anticyclone, oxidant/ozoneformation is 

expected to be accelerated and depends on the 

emission density within the area covered by the 

high pressure system. This latter dependence 

seems to be manifested by the data obtained in the 

paths of high pressure systems moving from less to 

more densely populated areas. 38 

A significant percentage of the high oxidant/ozone episodes observed in the United 

States is associated with passage of high pressure 

systems. Statistics of high pressure episode 

occurrence have been obtained by Korshover 76 for 

the eastern part of the United States for all months 

of the year. The study could not be extended in the 

western United States because the extreme 

terrain irregularities result in unrepresented 

pressure distributions. Such statistics for the 

months'of August and September are shown by 

the plots in Figures 4-8 and 4-9. 

Oxidant transport in the Northeast received 

considerable attention because high oxidant/ozone concentrations have been measured 

almost routinely in rural and distant suburban 

areas for years. Careful analysis by Bell 

Laboratories and other investigators of aerometric 

data obtained in northern New Jersey, eastern 

New York, Connecticut, and Massachusetts 

provided strong evidence of extensive mesoscale 

transport, especially from the New York City/New 

Jersey area to the Northeast into Connecticut and 

Massachusetts. 12o,,a6 Such transport was characterized (1) by low oxidant/ozone levels within 

urban core areas because of scavenging by 

precursors, (2) by appearance of highest 

oxidant/ozone concentrations downwind from the 

main urban center ata distance equivalentto 1 to 2 

hr of midday wind travel, and (3) by shifting of peak 

oxidant/ozone concentrations with time and 

distance, refler:,og the regional movement of the 

main urban area plume along the wind trajectory. 

The results from Bell Laboratories seem to be in 

agreement with subsequent studies by other 

groups. Interestingly, the evidence descriptive of 

the Northeast situation suggests that weather 

patterns seem to play a minor role in establishing 

oxidant/ozone levels in that part of the United 

States. For example, oxidant/ozone concentrations seem to be less sensitive to the 

location or intensity of an anticyclonic system. 120 

This could be a result of the high population density 

in that area and the relative dominance of urban 

plumes over the nonanthropogenic background 

levels in the air mass. Finally, local circulations in 

the surface layers were found to play a dominant 

role in the coastal areas in the Northeast. 12o,,3s 

Such circulation systems, subjecting areas to nextday effects from their own emissions, were also 

observed in the Gulf Coast38 and MidwestS6 areas 

but were not as dominant. 

The evidence on transport has had another 

important impact on the understanding of the 

oxidant/ozone problem. It provided one plausible 

explanation to some phenomena previously 

thought to be paradoxical (e.g., the occurrence of 

elevated oxidant/ozone concentrations in rural 

areas and at night15 and the Sunday-weekday 

effect13,24,4s,ao,,s5 ) Thus downward intrusion, from 

layers aloft, of transported anthropogenic 

oxidant/ozone explains convincingly the occurrence of elevated oxidant/ozone concentrations in 

rural areas and during the night in the summer-fall 

months. The Sunday-weekday effect could also be 

explained in part as resulting from anthropogenic 

oxidant/ozone present in layers aloft. Although 

these explanations have not been supported by 

documentation in all cases, they at least have 

served to clarify these phenomena and to increase 

confidence in the current knowledge and 

understanding of photochemical processes. 

Identification and understanding of oxidant/ozone transport represents a significant 

advance in understanding photochemical pollution. However, it has also raised several 

questions that need to be addressed. For instance, 

the impact of pollutant transport on the oxidant 

concentration observed in a locality cannot be 

quantified at this time. 43 The difficulty here is not 

merely the absence of sufficient data (e.g., data on 

pollutant composition in transported, aged air 

masses), but also the absence of valid investigative 

methods. Clearly the need is for both laboratory 

and field sludies that would provide a better 

understanding of the quantitative aspects of the 

interaction of transported, aged pollutant mixtures 

with locally emitted fresh pollutants. More 

specifically, a method should be developed for 

estimating the proportion of local oxidant/ozone 

concentrations resulting from pollutant transport. 43 Evidence must also be obtained on the 

46 
photochemistry sources for which there is a 

relatively greater amount of information available. 

oxidant-to-precursor dependencies for transported oxidant/ozone. 43 

NATURAL SOURCES OF OXIDANTS 

Introduction 

The occurrence of ozone in remote areas and 

during the winter months constitutes strong 

evidence that natural sources of ozone must exist, 

providing an atmospheric bacrocground on which 

the anthropogenically generated ozone - is 

superimposed. Promulgation of the 160-Ng/m 3 

(0.08-ppm) National Ambient Air Quality Standard 

for ozone raised considerable interest in the 

quantity of emissions from natural sources 

because of the possibility that the natural sources 

alone could make it impossible to achieve the air 

quality standard. Additional interest was raised by 

the discovery that a widespread ozone problem 

existed in the rural areas, a problem that could 

conceivably have natural causes. The interest in 

these aspects of the question of natural sources is 

certainly justified, but it is also of a somewhat 

academic nature. More pragmatically, the 

question of the emission levels of natural sources 

needs to be answered to estimate more accurately 

the benefits to be derived from the reduction of 

anthropogenic emission. 

Early research on natural ozone ioentified a 

number of sources, of which stratospheric ozone 

intrusion, electric discharges, and photochemistry 

of natural emissions appeared to be the ones with 

the highest and most probable contributions. It 

should be noted that much of the evidence in those 

early studies was indirect, based on reasoning by 

elimination; that is, observed ozone was attributed 

to natural sources when explanations for 

anthropogenic origins were eliminated, either 

because they could not be made or because they 

were not acceptable to the researchers. 

Subsequent studies, however, did produce some 

direct evidence, mostly on the stratospheric source 

and to a smaller degree on the photochemistry of 

natural emissions. The case for a significant 

contribution to background ozone from natural 

electric discharges has not been made 

convincingly. Thunderstorms have been observed 

on occasion to cause elevated short-term 

concentrations of ozone, but it is not clear whether 

such ozone is electrically generated or reflects 

stratospheric intrusion brought about by the 

thunderstorm disturbance. 46 Therefore the 

discussion in the following sections will focus only 

on stratospheric ozone and natural emission 

Stratospheric Ozone Intrusion 

The magnitude of thL, tropospheric air quality 

problem caused by stratospheric ozone intrusion 

has long been an unresolved issue. 43 The specific 

questions at issue are whether such intrusions are 

sporadic, unpredictable incidents causing local, 

short-term ozone accumulations, or whether they 

are significantly extensive and predictable. Aside 

from the possibiiity that stratosphere-troposphere 

exchange contributes significantly to ground level 

ozone buildup, stratospheric ozone has also been 

proposed to have a reaction-trigger function that 

accelerates and enhances photochemical oxidant 

formation from HC-N0, precursors. 57 Evidence 

interpreted to show accumulation of stratospheric 

ozone within the troposphere varies widely in type 

and degree of directness. In most cases, the 

evidence reported is based on ozone measurements in remote areas, measurements that do 

not necessarily represent stratospheric effects 

alone. Recently, Reiter,"' Mohnen, 90 and Singh et 

a1. 126 independently reviewed and critically 

examined the information available on the 

stratospheric ozone issue and offered perhaps the 

most reliable and definitive assessments of the 

stratospheric ozone problem to date. Based chiefly 

on their reviews and on other available literature, 

the case regarding stratospheric ozone intrusion 

appears to be as follows. 

There are two types of evidence pertinent to the 

stratospheric ozone issue: (1) Evidence derived 

from analysis of global circulation patterns and, 

more specifically, from the quantification of the 

various known mechanisms or processes through 

which air is interchanged between the 

stratosphere and troposphere; and (2) evidence 

derived from analysis of data on tropospheric 

ozone concentration and concentration variation 

in remote areas. Estimates of stratospheric ozone 

concentrations at ground level may be drawn from 

both types of evidence, but with uncertainty. 

Estimates based on stratosphere-troposphere 

exchange data suffer mainly from uncertainties in 

the frequency and intensity of tropopause folding 

events and by the unquantified and hence 

inadequately considered ozone decay processes 

within the planetary boundary layer. Estimates 

based on tropospheric ozone measurements are 

also subject to uncertainty because of hidden 

influences from nonstratospheric ozone sources. 

47 
It is well established that air irlterchange 

between stratosphere and troposphere occurs via 

the following four mechanisms:"' (1) mean 

meridional circulation, (2) large-scale eddy 

transports (jet streams), (3) seasonal adjustment of 

tropopause level, and (4) mesoscale and smallscale eddy transport. Each of these mechanisms is 

characterized by short-term, seasonai, and longterm fluctuations, and their impact in terms of 

surface concentration of stratospheric ozone 

varies with geographical latitude. 

The mean meridional circulation (MMC) 

mechanism involves upward flux of tropospheric 

air mainly in the low latitudes and downward flux 

of stratospheric air in the middle latitudes. It varies 

somewhat in intensity from season to season, the 

most intensive period being in winter (DecemberFebruary). Reiter"' estimates the annual amount 

of stratospheric-MMC air mass transferred into 

the troposphere to be about 43 percent of the total 

mass of one stratospheric hemisphere, or about 

1.84 x 1020 g of air. Reiter further estimates that 

the upper limit of average ozone concentration 

shortly above the tropopause is 0.05 Ng/g. These 

estimates of mass exchange and the mean ozone 

concentration result in a calculated average ozone 

exchange of 9.22 x 10 13 g of ozone due to the MMC 

process. Furthermore, assuming that the MMC 

ozone flux exchange is concentrated over half the 

area of one hemisphere, Reiter calculates a yearly 

mean ozone flux of 0.23 x 10-' g/m2•sec. During 

the winter period, however, when the strongest 

cross-tropopause fluxes occur, this ozone flux 

could be 0.4 x 10-' g/m2 • sec. From this 

stratospheric mass flux (0.4 x 10 -' g/m2 • sec) and 

estimates of the mean tropospheric vertical 

velocity, Reiter calculated the mean background of 

stratospheric-MMC ozone in the springtime and in 

the midlatitudes to be 14.6Ng/m 3 (0.007 ppm). The 

yearly mean from Reiter's flux estimate would be 

about 8, Ng/m 3 (0.004 ppm). Junge, as cited in 

Reiter,"' using a somewhat higher flux value and 

a lower vertical velocity value, estimated such a 

mean background ozone concentration to be 35.6 

pg/m3 (0.017 ppm)."' 

Superimposed on the background concentration 

caused by the MMC process, there is an ozone 

increment of stratospheric origin caused by largescale eddy mixing occurring in the jet stream 

regions through a tropopause folding (TF) process. 

The intensity of this process relative to the MMC 

process is somewhat uncertain; however, its 

impact per unit of ozone mass transported on the 

lower troposphere is unquestionably stronger and 

48 

more localized. This is because relative to the MMC 

mechanism, stratospheric air during TF intrusion 

moves downward much faster and therefore is 

subject to much less tropospheric dispersion. 

Stratospheric ozone intrusions of the TF type occur 

mostly along the polar-front jet stream and yield, 

on the average, maximum stratospheric ozone 

accumulations at ground level in midlatitudes 

during March and April. 

Using the studies of Danielsen, Mohnen 90 has 

examined the intensity of the TF process, as has 

Reiter,"' using data from Mahlman. From case 

studies of TF events, Danielsen and Reiter 

estimated that the stratospheric air mass 

transported per TF event was 4 to 6 x 10" g. From 

the average number of TF events observed during 

1963-64, Reiter calculated the annual air mass 

transport to be equivalent to approximately 20 

percent of the air mass in the northern 

stratospheric hemisphere. In contrast, Danielsen's 

estimate was 90 percent. 

To estimate the impact of the TF-type 

stratosphere-troposphere interchange in terms of 

surface ozone concentration, it is necessary to 

know (a) the ozone concentration in the 

transported stratospheric air and (b) the 

(stratospheric) ozone decay process occurring 

within the troposphere. Indirect estimatesofthese 

have been made based on radioactive 90 Sr tracer 

methods and on isentropic trajectory analysis 

techniques. From measurements of the 90 Sr-toozone ratio within the lower stratosphere and from 

90Sr-related radioactivity data at ground level, 

Reiter re-estimated recently the 24-hr average 

surface concentration of stratospheric-TF ozone to 

be as high as 60 Ng/m 3 (0.033 ppm) in 1963 and 

120 ,ug/m3 (0.066 ppm) in 1964. 13 Reiter's 

estimate must be considered an upper limit, since 

it assumes that the 90 Sr-to-ozone ratio is 

conserved during transport from the lower 

stratosphere to ground level. From use of 

isentropic trajectory analysis techniques, it was 

deduced that exceptionally strong TF-type 

intrusions occur only occasionally, but can cause 

surface ozone concentrations of 160 pg/m 3 (0.08 

ppm) or higher. Such strong intrusions are 

expected to occur about once a year, usually in the 

southern and eastern United States. Reiter 

estimated the probability of such occurrence to be 

0.2 percent, measured in days of observations on 

an annual basis at a given location."' 

Direct evidence of the impact of stratospheric 

ozone on ground-level oxidant during TF events 

has been reported by Lamb." He tierformPd a 
detailed study of an incidentthat occurred in Santa 

Rosa, Calif., in which hourlyaveraged ground-level 

oxidant concentrations exceeded 160 Ng/m 3 (0.08 

ppm) for 5 consecutive hours just before dawn on 

November 19, 1972. The largest of the five hourly 

averaged concentrations was 450 pg/m 3 (0.25 

ppm). AII available evidence indicated that the 

ozone responsible for this episode originated in the 

stratosphere during a TF event off the south coast 

of Alaska 2 days earlier. Chatfield and Harrison 22 

found a positive correlation between increases in 

ozone concentration in the remote Olympic 

Mountains of Washington and the passage of low 

pressure systems originating in the same region 

that the TF event responsible for the Santa Rosa 

episode occurred. Attmannspacher and Hartmannsgruber9 have also reported ozone on an 

anomalous 1000-m (3300-ft) mountain peak in 

northern Germany attritiutable to stratospheric 

intrusion. On three different occasions during the 

winter of 1971, they observed fluctuations in 

ozone concentrations between 490 Ng/m3 (0.025 

ppm) and 980pg/m 3 (0.50 ppm) that lasted longer 

than 10 min. Each occurrence was during strong 

snow showers associated with passing cold fronts. 

(The Santa Rosa episode was initiated by a brief 

rain shower shcrtly after the passage of a cold 

front.) On three occasions, balloons were launched 

to measure ozon , concentrations aloft, and in all 

three cases, 3 strong, secondary ozone 

concentration m: ximum was observed just above 

the tropopause. 

Besides the NIMC and TF processes, stratosphere-tropospiiere interchange occurs also the 

seasonal tropop:iuse adjustment (STA) and the 

small-scale eddy transport (SSET) mechanisms. Of 

these, the STA mechanism has been estimated to 

cause a stratospheric air mass flux equivalent to 

10 percent of the entire stratospheric hemisphere, 

90'"' Such interchange occurs mainly in the same 

season and latitudes as the TF process. Therefore, 

its impact is included in the estimates madeforthe 

TF process. The SSET process is of much less 

importance and contributes to the tropospheric 

ozone problem only at the noise level. 90,111 

In conclusion, based on Reiter's estimates of 

stratosphere-troposphere interchange and on 90Sr 

data, the annual average total of stratospheric 

ozone accumulation expected at groundlevel 

amounts to 20 to 30 Ng/m 3 (0.01 to 0.015 ppm). 

84,113 If one considers the fact that some ozone can 

be destroyed during transport to ground level, the 

preferred mean ozone concentration calculated by 

Reiter would be closer to the lower limit of 20 

/.ig/m3 (0.08 ppm). Occasional excursions to about 

160 Ng/m 3 (0.080 ppm) can be expected, however. 

Danielsen's estimates of stratospheric ozone flux 

are a factor of two to three higher than Reiter's 

estimates and would lead to correspondingly 

higher yearly mean ozone concentrations. 

Danielsen estimates an ozone flux rate-of 8 x 1010 

molecules/cm2 • sec. Singh et a1. 127 suggests that 

this flux rate would be compatible with ground 

level ozone measurements at remote locations 

(yearly mean of 60 /ag/m 3 , or 0.030 ppm) if an 

ozone lifetime of about 4 months is assumed in the 

troposphere. The lifetime of ozone is unc ,rtain, 

and all estimates of ground level ozone 

determined from stratospheric ozone intrusions 

suffer from this uncertainty. Both of Reiter's and 

Danielsen's estimates apply to situations where 

stratospheric ozone is brought to ground level 

without the assistance of precipitation-driven 

downdrafts. The case studies cited above by 

Lamb" and Attmannspacher and Hartmannsgruber9 (and others) indicate that stratospheric 

ozone accompanying TF events can reach ground 

level in concentrationsexceeding 390/jg/m 3 (0.20 

ppm) when it is transported part of the way in 

downdrafts caused by precipitation. The frequency 

of this type of event is not yet known, butthe mean 

ozone contribution resulting from such events is 

expected to be minimal. 

Mohnen's estimate of the annual average 

stratospheric ozone at ground level is 40 to 70 

Ng/m3 (0.022 to 0.035 ppm). 90 Such background 

levels vary with season and latitude because the 

stratospheric ozone reservoir also varies with 

season and because the various stratospheretroposphere interchange mechanisms vary in 

intensity with season and latitude. Considering all 

these variables, there seems to be a consensus of 

opinion that at locations in the midlatitudes (e.g., 

the United States), the ground level ozone 

concentrations of stratospheric origin peak in 

winter and spring. 

The preceding paragraphs dealt mostly with the 

evidence and conclusions obtained from analysis 

of global circulation patterns. As stated earlier in 

this section, relevant evidence was obtained also 

from analysis of tropospheric ozone concentration 

data in remote areas. Such evidence, although 

seemingly more valid as being more direct, should 

be examined carefully, for it is often distorted or 

obscured by hidden interfering factors. Examples 

of such factors are destruction of ozone on 

surfaces or in reaction with HC and NO, and 

photochemical formation of ozone. 106 

49 
Mohnen 90 examined the evidence both on 

stratosphere-troposphere exchange and surface 

ozone concentration and concentration variation, 

but, unlike Reiter,"' he elected to base his 

conclusions on stratospheric ozone intrusion 

mainly on tropospheric ozone data. Utilizing the 

analytical method introduced by Junge 90 and data 

from monitoring stations in remote areas 

presumably free of local or regional anthropogenic 

emissions, Mohnen concluded that a range of 

annual mean concentrations equal to 40 to 70 

Ng/m3 (0.022 to 0.035 ppm) constitutes a 

representative tropospheric ozone level (of 

stratospheric origin) for 35 1 to 500 N latitudes. 

Mohnen also concluded that TF events may lead to 

ozone concentrations at ground level as high as 30 

Ng/m3 (0.15 ppm) and lasting from 2 or 3 hr up to 1 

to 3 days. 

Singh et a1. 126 examined aerometric data on 

ozone, HC, and NOx obtained at 10 stations 

selected to be as remote as possible and with air 

quality records of at least 2 years" duration. Seven 

of these stations were in the western continental 

United States, one in Hawaii, one on the summit of 

Whiteface Mountain in New York, and one on the 

Zugspitze in West Germany at a 3000-m (9800-ft) 

elevation. The ozone variation patterns observed at 

most of these stations are exemplified by the 

patterns observed at the Quillayute, Washington, 

and Mauna Loa, Hawaii, stations (Figures 4-1 1 and 

4-12). The striking features of these patterns are 

the maximum ozone concentrations observed in 

April and the 160-/jg/m 3 (0.08-ppm) or higher 

ozone concentrations of such maxima. 

Considering the low sunlight intensity and 

temperature conditions prevailing in April at 

Quillayute, it can be deduced that these high ozone 

concentrations must be primarily of natural, 

stratospheric origin. Such a deduction is further 

supported by the lack of the familiar diurnal ozone 

variation pattern that characterizes ozone 

formation from local photochemistry. Significantly, this stratospheric ozone declines as 

summer months approach, indicating that the 

effects of stratospheric intrusion are at a low ebb 

during the smog season. Singh eta1. 126 did observe 

elevated ozone concentrations during the summer 

months in some stations. Such maxima, however, 

were explained in terms of photochemical ozone, 

either locally produced or transported to the 

stations from upwind areas. 

0.120 

0.100 

0.080 

E 

a 

a 

Z 0.060 

0 

N 0 

0.040 

0.020 

STATION NO. 1 -- HIGHEST 1-hs MONTHLY 0 3 MAX 

(QUILLAYUTE) ••••••• MONTHLY AVERAGE OF DAILY 1-hr O, MAX 

— MONTHLY 0 3 AVERAGE OF ALL 1-hr 0 3 VALUES 

—.~ LOWEST 1-hr MONTHLY 0 3 MAX 

/ 

~ 

\ 

/~ 

,100,~ ~~~ i /;\•• ... ~ 

~ \.1••. 

. / •`./ • /• —. / 

/ •` • ~

.i' ..... 

,~ 

I 

DEC. APRIL AUG. DEC. APRIL 

(1973) (1974) (1975) 

MONTHS 

Figure 4-11. Long-term ozone variations at Quillayute. 126 

50 
0.120 

0.100 

0.080 

E 

a 

a 

W 0.060 Z 

O 

N 

O 

0.040 

0.020 

---' HIGHEST 1-hr MONTHLY 03 MAX ' 

STATION NO. 9 ....... MONTHLY AVERAGE OF DAILY 1-hr 03 MAX 

(MAUNA LOA, HAWA11) MONTHLY 03 AVERAGE OF ALL 1-hr 03 VALUES 

- LOWEST 1-hr MONTHLY 03 MAX - 

~ \ 

~ \ 

/ 

~ , , ` /'_ `, . .. 

•, 

~~ 

. • ~ ~ ~ 1 ,i•~• . 

/ ~~ ~ ' ~ ~~ ~ ~ ~• / 

% ~ ~ ' /•~•~• ~'~ - 

.`•`•/ ~• 

DEC. MAY OCT. MAR. AUG. JAN. 

(1973) (1976) 

Figure 4-12. Monthly ozone variations at Mauna Loa, Hawaii. 126 

Data collected by Singh et a1.126,'2' suggest 

yearly mean ozone levels of about 60Ng/m 3 (0.03 

ppm) between latitudes 18 0 N and 480 N. The 

springtime mean values are found to be about 80 

Ng/m 3 (0.04 ppm), and the fall mean is about 40 

/ag/m 3 (0.02 ppm). The yearly 1-hr maximum ozone 

concentrations also show large year-to-year 

variation. For example, at Mauna Loa (Figure 4- 

12), the 1-hr ozone maximum of 160 Ng/m 3 (0.08 

ppm) was exceeded on 1.6 percent of the days in 

1975 and on zero percent of the days in 1974. 

The Whiteface Mountain data were examined 

also by Coffey et a1. 28 along with data from other 

remote areas and from urban locations in New 

York State. The observations made by Coffey et 

a1. 28 from these data are: (1) Ozone concentrations 

at Whiteface Mountain often exceed the 160- 

/jg/m3 (0.08-ppm) IevPl; (2) a background ozone 

blanket covers the entire state; and (3) there is 

monthly variation of ozone with a strongly defined 

maximum in August (Figure 4-13). Presence of the 

ozone blanket suggests that the ozone source lies 

aloft and cannot be due to local photochemistry. 

However, occurrence of the peak concentrations in 

the summer (August), coupled with evidence on 

presence of manmade pollutants (halocarbons) 106 

can only be interpreted to mean thatthe Whiteface 

Mountain data did reflect anthropogenic influences, a conclusion pointed outalso by Reiter-" 1 

and by Singh et a1. 126 Thus transport, in paths aloft, 

of ozone and/or ozone precursors from upwind 

anthropogenic sources provides a more plausible 

explanation of the Whiteface Mountain data 

patterns, at least for 1973. 

More recently, Husain et a1. 67 obtained and 

analyzed ozone and 'Be data in Whiteface 

Mountain during the smog season. In their 

analysis, these investigators used data on'Be and 

air trajei;tory analysis to establish stratospheric 

origin, and NOx and aerosol concentrations and 03- 

7 13e correlation patterns to verify absence of 

photochemical ozone. Interpretation of results 

suggested an upper 24-hr concentration limitof 75 

Ng/m3 (0.037 ppm) stratospheric ozone at 

Whiteface Mountain during July 1975. 

Measurements of ozone on the Zugspitze, West 

Germany, were analyzed both by Reiter"' and by 

Singh et a1. 126 Reiter's frequency distribution 

analysis of data obtained during August 1973 to 

October 1975 indicates that (a) 0.2 percent of the 

hourly concentrations exceeded the 160-Ng/m 3 

(0.08-ppm) level, and (b) relatively high 

concentrations occurred during summer rather 

than spring. The latter indication again suggests 

an anthropogenic-influences explanation. However, in this case, such an explanation alone is not 

51 
0.070 

0.060 

0.050 

s 

a 

°' 0.040 

w 

z 

0 

p 0.030 

0.020 

0.010 

J F M A M J J A S O N D J F M A M 

I-- 1973 1974 -i 4 

Figure 4-13. Average monthly ozone concentrations recorded at summit of Mount Whiteface. 128 

convincing because the Zugspitze station, at the 

altitude of 3000 m(9800 ft), is above the planetary 

boundary layer where anthropogenic pollutant 

transport occurs. Reiter suggests that local 

circulation along the mountain slopes may be 

moving anthropogenicahy contaminated air from 

lower altitudes to the higher altitude of the station 

site. 

Finally, review of 1477 ozonesonde observations between December 1962 and December 

1965 showed that 2 percent of the ozone 

concentration values exceeded 150 pg/m 3 (0.075 

ppm). 12 However, of the 31 cases with such 

elevated concentrations, only three qualified as 

being unaffected by tropospheric source 

interferences. Thus only about 0.2 percent of the 

sampie exceeded the 150-,ug/m 3 (0.075-ppm) 

level. 

The tropospheric ozone data appear to agree 

with the theoretical deductions both on the 

intensity of the stratospheric ozone impact and on 

the seasonal variation of such impact. Both bases 

of evidence suffer from uncertainties, and 

additional research studies are needed for a fuller 

and more confident assessment of such impact. 

Specific research needs include: 

1. More definitive information on the 

frequency of occurrence and intensity of 

cyclogenetic events resulting in stratospheric ozone intrusion. 

2. More definitive information on the ozone 

decay (and formation, if any) attending the 

subsidence of stratospheric ozone within 

the lower troposphere, especially within 

the planetary boundary layer. 

3. Development of techniques for forecasting 

stratospheric ozone intrusions. 

4. Further analysis of tropospheric ozone 

measurements to de{ineate the stratospheric and anthropogenic contributions to 

such ozone. The need here incl udes also 

the measurement of trace contaminants 

characteristic of anthropogenic sources. 

The information and analysis presented in the 

preceding pages, although they do not answer all 

of the questions on the contribution of 

stratospheric ozone to ground level ozone 

concentrations, do provide important clarification. 

For example, it is now clear tliat violations of the 

oxidant/ozone NAAQS observed outside the smog 

season, particularly during the spring months, 

should not be attributed exclusively to 

anthropogenic causes. However, it is equally 

important that significant stratospheric ozo:le 

concentrations at ground level, though they may 

occur at any time, are less frequent during the 

summer months (that is, during the smog season). 

Within the summer months, such ozone is 

expected to occur at a background level somewhat 

lower than that of the annual average. Since the 

annual average ozone concentration has been 

estimated to be about 20 jjg/m 3 (0.01 ppm) by 

Reiter13 and about 60 /jg/m3 (0.03 ppm) by 

Mohnen90 and Singh et a1., 126 it follows that the 

summer average could be 14 to 40Ng/m 3 (0.007 to 

0.020 ppm) because of the spring-summer 

gradient. Data presented by Singh et a1. 126 indicate 

that the 1-hr ozone concentrations in any given 

season in a remote atmosphere are typically about 

twice the ozone mean values. Thus an hourly 

ozone concentration range of 30 to 80,ug/m 3 (0.15 

to 0.04 ppm) resulting from the stratospheric 

source alone can be expected in the summer 

season. The lower limit of 30 Ng/m 3 (0.015 ppm) 

would thus be suggested by Reiter's analysis,"' 

whereas Mohnen90 and Singh et a1.t 26 would 

support the upper limit of 80 /ag/m 3 (0.040 ppm). 

Photochemistry of Natural Organics/NOX 

As in the case of stratospheric ozone, the role 

and importance of naturally emitted orgarics and 

NOx in the formation of oxidant/ozone has Lpen an 

issue. 43 The issue was originally raised as -, result 

of early reports that the rates of organic emissions 

from vegetation are considerably higher, on a 

global basis, than thosefrom manmade sources.t 07 

52 
Although natural emissions and anthropogenic 

emissions are, for the most part, geographically 

segregated, it is nevertheless reasonable to 

suspect that the much more abundant natural 

organics, emitted either within an urban or 

nonurban area, or brought in through transport, 

could contribute to ambient oxidant/ozone 

concentrations to an important degree. These 

suspicions became considerably stronger as a 

result of two recent findings: (a) The occurrence of 

a pervasive rural oxidant/ozone problem, 18 and (b) 

the high reactivity of the terpenes. 48 ' 137 In either 

case, the finding could be interpreted to mean that 

natural organics may constitute a significant 

source of oxidant/ozone. As in the case of 

stratospheric ozone, the question regarding the 

role and importance of natural emissions as an 

oxidant/ozone source , needs to be answered. 

From a cursory examination of the current 

evidence, it becomes immediately apparent that 

certain questions regarding natural emissions 

have obvious answers or have been resolved by 

scientific evidence, whereas other questions 

appear unresolved. For example, it is certain that 

vegetation emits organic vapors and that some of 

these vapors (terpenes) play the dual role of ozone 

precursor and ozone scavenger. Questions that do 

not have obvious answers are: (1) What is the net 

effect on ozone concentrations of the atmospheric 

reactions of terpenes and of other natural 

organics? (2) What reactive organics, other than 

terpenes, are emitted by natural sources and at 

what rates? 

Evidence pertinent to these questions is 

available and is fairly complete and definitive in 

some respects, but it is incomplete and ambiguous 

in others. The main source of ambiguity is that 

most researchers are, in general, relatively 

unfamiliar with natural organic emissions. Thus, 

unless convincing documentation is provided, 

results and conclusions on chemical identity, 

ambient concentrations, and emission and sink 

processes of natural organics are viewed with 

considerable skepticism. In the remainder of this 

section, a brief review is given of the relevant 

evidence available, and an attempt is made to 

interpret such evidence so as to provide the best 

possible judgment regarding the importance of 

natural emissions as an oxidant/ozone source. 

The-e are two questions regarding the net 

impact of terpenes on ambient oxidant/ozone 

concentrations. First, what are the terpene 

concentrations actually observed in atmospheres 

with high oxidant/ozone levels? And second, what 

is the net effect of terpenes at such concentrations: 

Is it to produce or to destroy oxidant/ozone? The 

evidence available appears sufficiently complete 

and definitive 137 to resolve these questions. 

Most of the qualitative analysis on organic 

emissions from vegetation has been done by 

Rasmussen and his coworkers. Chromatographic 

analysis by Rasmussen and Holdren 108 of ambient 

organics collected at remote sites showed the 

presence of 10to 60 organic components in the C 5 - 

C,o range; individual component concentrations 

were usually below 2 Ng/m3 (0.001 ppm). 

Hydrocarbon concentrations in rural areas have 

also been reported formally by Whitby et a1. 14 ' and 

by Whitehead and Severs, 144 and ir,formally by 

others. 89'"' However, individual organicswere not 

identified in these studies. Because of this 

deficiency, and in view of the well documented 

occurrence of extensive urban pollutant transport, 

a natural origin for the organic compounds 

measured by these investigators cannot be 

supported. Nevertheless, their evidence leavesthe 

question somewhat open. Some better 

documentation on natural organic compounds in 

ambient air was obtained by Westberg and 

Holdren. 13' , ' ao Using a gas chromatograph linked 

to a mass spectrometer, these investigators 

identified in a forested area in Idaho, a-pinene, ,8- 

pinene, 0-carene, and limonene present at 

concentrations from a few ppt for limonene to 730 

ppt for /3-pinene. Westberg and Holdren also 

measured rates of emission of these terpenes from 

the forest and found such rates to be consistent 

with their measurements of the ambient 

concentrations. The most significant finding from 

this study, however, was that air samples taken 

outside the forest canopy showed no measurable 

terpenes, suggesting an extremely short life for 

those organic compounds. Measurements by 

Lonneman et a1. 82 ' 83 in a forested area near 

Durham, North Carolina, showed the presence of a 

a-pinene, /3-pinene, myrcene, and A-carene at 

concentrations from 0.3 ppb C(myrcene) to 90 ppb 

C (0-pinene)—roughly comparable to those 

reported by Westberg and Holdren. Other 

measurements in this same area showed the 

terpene concentrations to be at lower levels when 

the ambient ozone concentration was at higher 

levels. Finally, in addition to the monoterpenes 

already mentioned, isoprene was also found to be 

emitted by vegetation and to occur in ambient 

air.'oa 

In conclusion, there is sufficient evidence to 

show that monoterpenes do occur in the ambient 

53 
air but only within forested areas; in such areas, 

total terpene concentrations average 10 to 50 ppb 

C. 137 The evidence further shows that terpenes 

have extremely short lifetimes, such that, with the 

exception of isoprene, they are not transported 

downwind from their sources in appreciable 

quantities. Within urban areas, terpenes have not 

been detected. In their numerous efforts to search 

for and identify terpenes in urban atmospheres, 

EPA investigators only occasionally found 

isoprene, at ppb C concentrations. Thus the 

evidence does not support an important direct 

contribution of terpenes to urban oxidant/ozone 

concentrations; terpenes may contribute tc the 

urban problem indirectly, however, through 

terpene-induced oxidant formation in rural areas. 

This possibility will be examined next. 

Evidence of the potential of terpenes to form 

oxidant/ozone in rural areas has been observed 

both in laboratory and field studies. Smog chamber 

testing of terpene-NOx mixtures showed clearly 

that terpenes are potent oxidant precursors and, 

more important, that relative to the less reactive 

hydrocarbons, their oxidant-forming potential is at 

a maximum at low hydrocarbon-to-NOX ratios, 

typically at 2:1 to 2.5:1 molar concentrations. 4a,14o 

The latter finding is significant because it means 

that in rural atmospheres with hydrocarbon-toNOx ratios typically much higher than 2.5:1, the 

terpenes could be effective as oxidant producers 

only partially, if at all. In fact, in the absence of 

sufficient NOX, terpenes would act as ozone 

scavengers. 52 Under optimum hydrocarbon-toNOX ratio conditions, terpenes produced in smog 

chambers a maximum of 470pg/m 3 (0.24 ppm) of 

oxidant/ozone for 5 ppm C of reactant terpene. 

Assuming a proportionality dependence of oxidant 

on organic reactant, it follows that at their typical 

ambient concentrations of 10 to 50 ppb C in the 

rural air, terpenes can produce no morethan 2to4 

,ug/m 3 (0.001 to 0.002 ppm) of oxidant/ozone. 

137,140 

The potential of rural-atmosphere organic 

compounds to produce oxidant was also explored 

in studies in which rural air sampleswere captured 

in plastic bags, spiked with various amounts of 

NOX, and exposed to sunlight. Results by one 

investigator were interpreted to mean that in some 

rural areas, the ambient organic compounds have 

the potential to produce 40 to 1 20 /Ug/m 3 (0.02 to 

0.06 ppm) of oxidant/ozone. 105 A recent study in 

rural Wisconsin showed that irradiation of 

captured air samples spiked with NO did not 

produce significantly more oxidant/ozone than the 

54 

unspiked samples.z Finally, Singh et al. 1 26 analyzed 

ambient ozone monitoring data from a station at 

White River, Utah, and concluded that elevated 

levels of ozone in the summer occurred only when 

ambient NOX was present at concentrations 

sufficiently high to act as photochemical ozone 

precursors (Figure 4-14). This evidence is 

suggestive but far from being conclusive insofar as 

the role and importance of natural organic 

compounds are concerned. First, it is extremely 

difficult to establish with confidence that 

oxidant/ozone formation in the captured rural air 

samples results solely from natural organic 

compounds; the presence of anthropogenic 

pollutants and of experimental artifacts cannot be 

ruled out. 137 Also, relative to free ambient air, 

captured air samples probably yield higher 

oxidant/ozone concentrations. Singh et a1. 126 also 

agree that anthropogenic sources cannot be ruled 

out in explaining the elevated ozone concentrations observed in White River, Utah, in the 

summer (Figure 4-14). 126 Finally, substantial 

oxidant/ozone formation from natural organic 

compounds is not consistent with the laboratory 

evidence on terpenes, unless, of course, there are 

other yet unknown natural organic compounds 

with photochemical reactivities different from tha• 

of the terpenes. This latter possibility remains 

largely unexplored except for the case of inethane, 

which is somewhat uncertain. 

The modeling of the photochemical methane 

oxidation cycle in the lower troposphere has been a 

subject of considerable interest and controversy in 

recent years. 21,29,35,3s,a1 The importance of 

understanding the methane photo-oxidation cycle 

,is not only relevant in its potential role as a source 

for natural background ozone concentration, but 

also in elucidating the half-lives and budgets for 

chemical species present i n the atmosphere. M uch 

of the debate has centered on whether or not the 

methane photo-oxidation cycle in the unpolluted 

troposphere represents a net ozone production or 

destruction process. This in turn raflects on the 

classical concept of ozone intrusion from the 

stratosphere as being the dominant source of 

surface ozone in the unpolluted troposphere. 90 

Current models of the uncontaminated 

troposphere 2 ' 81 are sufficiently sensitive to 

uncertainties in initial and boundary conditions, 

rate constants, transport parameters, and 

heterogeneous removal rates that quantitative 

statements regarding net ozone production or 

destruction are still tenuous. In the final analysis, 

the importance of modeiing t.he clean troposphere 
1?0 — 

100 

_E 80 

~ 

X 

O 

Z 60 

d 

C. 

a 

w 

z 

O 

0 40 — 

20 

0 

NOV. 

(1974) 

--- HIGHEST 1-hr MONTHLY 0 3 MAX 

••••••••• IMONTHLY AVERAGE OF DAILY 1-hr 0 3 MAX 

MONTHLY 0 3 AVERAGE OF ALL 1-hr 0 3 VALUES 

LOWEST 1-hr MONTHLY 0 3 MAX 

—•• ~ MONTHLY AVERAGE OF ALL 1-hr NOx VALUES 

• ~ ~ ~ ~ / ~~ i~'~ 

~ ~ I 

\ ~ 

• r ``\ / '''''' ' • .. 

AVG.0 3 

 ` ~ 

- ' ~ ' •- 

\; AVG. NO 

V. 

x

s I 

~ ..~.../ o 

~• ` ~ 

.~ 

PROJECTED 0 3 

PROFILE WITHOUT 

NO ADDITION 

x 

/ 

• ~/''~~.. 

APR. SEPT. FEB. JU LY 

MONTHS (1976) 

Figure 4-14. Effect of NO, concentration increase on ozone formation at White River, Utah. 126 

resides in a clearer understanding of the physical 

and chemical processes in operation. This in turn 

will provide a better understanding of the effects of 

low-level anthropogenic contributions to rural 

oxidant/ozone contributions. 

One may conclude that natural organic 

emissions (at least terpenes) do not directly affect 

oxidant/ozone formation within urban areas. Their 

indirect effects, however, are not as well 

understood. Natural organic compounds do occur 

in rural atmospheres and could possibly contribute 

to the large-area oxidant/ozone concentrations 

associated with high pressure episodes. 

Furthermore, products from the atmospheric 

degradation of terpenes could also contribute to 

those concentrations. The evidence available, 

however, suggests that within rural areas where 

ambient HC-to-NOX ratios are high, terpenes act as 

scavengers rather than producers of ozone. 

Furthermore, terpenes decay too fast to survive 

transport into urbanized areas where the HC-toNOx ratios are more conducive to oxidant formation 

from terpenes. The limited evidence available 

suggests that chemical degradation products of 

terpenes are mainly particulates. Nevertheless, 

small amounts of gaseous products, including 

aldehydes, ketones, and organic acids are formed 

and could conceivably be transported into urban 

areas.48 Considering all the evidence, there is no 

convincing reason to believe that natural organic 

emissions have an important impact on the 

oxidant/ozone-related air quality. Such a view is 

supported by some. investigators90 but not by 

others. 29 

SINKS OF OXIDANTS AND OF OXIDANT 

PRECURSORS 

Introduction 

The preceding sections identified and described 

the various sources of ambient oxidant/ozone and 

discussed their absolute and relative contributions 

to surface accumulation of oxidant/ozone. Implicit 

in those discussions was the assumption that 

observed concentrations of oxidant/ozone do not 

reflect source emission levels alone; rather, they 

reflect the composite impact of the source and sink 

processes. Not all sink processes have the same 

significance and role. For example, removal of 

ambient NO2 in reactions forming PAN, nitrates, 

etc., is a sink process with entirely different 

significance than the removal of NO2 on surfaces. 

Sink processes relevant to oxidant/ozone are 

those that directly or indirectly lessen the impact of 

55 
the oxidant/ozone sources, thus reducing 

concentrations of ambient oxidant/ozone. 

Obviously, such sink processes include not only 

those for oxidant/ozone, but also those for 

oxidant/ozone precursors. For this reason, sink 

processes for hydrocarbons and NOx will be 

discussed here rather than in the subsequent 

chapter on oxidant precursors. 

Reviews of the various mechanisms by which 

pollutants are removed from ambient air have been 

made by Robinson and Robbins, 12 ' by Hidy, 63 and 

by Rasmussen et a1. 109 ' 10 The important 

mechanisms appear to be: (1) precipitation 

scavenging, including rainout (i.e., absorption in 

the cloud) and washout (i.e., capture by falling 

raindrops), (2) chemical reactions resulting in 

products that are not oxidants or that are rapidly 

removed from ambient air, (3) dry deposition (i.e., 

adsorption on aerosols and subsequent deposition 

on surfaces), and (4) adsorption on ground 

surfaces (soil, vegetation, etc.). Information on the 

occurrence of such processes for various 

pollutants exists, but it is mostly qualitative. For 

such information to be useful, it must be 

quantitative—that is, expressed in terms of data 

compatible with the available mathematical air 

quality simulation models. Such data, for example, 

are reaction rate constant and kinetic order values 

for the various chemical processes, and deposition 

rates for the various physical sink processes. 

Sinks for Oxidants and Oxidant Precursors 

Ozone is relatively insoluble in water. This, 

despite evidence that the oceans remove some 

ozone,' suggests that rainout and washout cannot 

be important sink processes for ozone. 

Reaction of ozone with NO and with HC is an 

important sink process accounting for the 

complete removal of ozone from the surface air 

layers in urban areas at night. On-surface 

adsorption/destruction, and some destruction 

from locally emitted NO and HC account for the 

nighttime absence of ozone from the rural 

atmospheres at ground level. Thus, under groundlevel conditions and at night, ozone appears to 

have a lifetime of only a few hours at most. 

In air layers aloft, relatively free of fresh 

precursor and surface influences, ozone has been 

observed to remain extremely stable, at least 

during the night. 39 During the day, ozone is 

photoiyzed rapidly by sunlight, but the resultant 

oxygen atoms react rapidly with molecular oxygen 

to regenerate the ozone. Thus sunlight has very 

little net effect on ambient ozone in the absence of 

other pollutants. In the presence of other 

pollutants at their global background levels, ozone 

participates in a photochemical destruction cycle 

resulting in an ozone haif-life estimated to be 7 to 8 

hr. 15 In the presence of other pollutants at or near 

urban concentrations, ozone is both produced and 

destroyed in such a way that the initial ozone loses 

its identity and significance. The ozone 

concentration that develops is the net result of the 

formation and destruction processes. The 

concentration and lifetime of such ozone depends 

on the composition and concentrations of the other 

reactants. From the evidence on long-range 

oxidant transport, it may be deduced that such 

transported ozone could have a lifetime of several 

days. 

Chemical sink processes for ozone are 

qualitatively we11 established. Quantitatively, the 

processes occurring at ground level have not been 

defined from direct, real-atmosphere data because 

of the difficulty in isolating the chemical process 

from the on-surface physical processes. 

Nevertheless, reasonably accurate quantification 

has been achieved since the main ozone 

destruction/reaction steps are well defined 

kinetically and are included in the mathematical 

models relating air quality to emissions. 

The dry deposition sink process for ozone is not 

well defined. Surfaces are known to act as ozone 

scavengers, but it is not certain that the 

composition and surface area of ambient aerosols 

are such that they cause substantial ozone 

destruction. The stability of ozone in polluted air 

layers aloft and in aerosol-containing smog 

chamber atmospheres suggests that removal of 

ambient ozone by aerosols cannot be an important 

sink process. 

Absorption and/or destruction of ozone on 

ground surfaces (soil, vegetation, water, etc.) 

constitute a major sink for this gas on a global 

basis. 109 Measurements of uptake rates of 

different pollutants by certain forms of vegetation 

(e.g., alfalfa) showed the ozone rate to be 

comparable to that for NO2 and somewhat lower 

than that for S02. 64 Recently, Garland and 

Penkett47 reported ozone deposition velocities of 

0.5 cro sec-' for grass, 1.6 cro sec -' for soil, and 0.4 

cro sec -' for sea water (compared to 2 8 cro sec-' 

and 0.2 to 0.7 cro sec -' for S02 for alfalfa and soils, 

respectively). These values are about three times 

lower than those reported by Hi11, 64 but they are 

claimed to be more representative of average field 

conditions. At any rate, even the low values of 

56 
Garland and Penkett indicate a substantial 

removal of ozone by ground surfaces. 

The evidence indicates that of the various 

possible sink processes for ozone, chemical 

destruction, chemical reaction, and on-surface 

destruction are probably the most important. The 

importance of the surface sinks, however, can be 

assessed only through use of models. One air 

quality •simulation model has been used to 

compute ozone concentrations in a moving 

polluted air parcel with and without the 

incorporation of surface losses. 75 Results showed 

that with representative surface loss rates for 

ozone and NOz included, the air parcei atthe end of 

an 8-hr trajectory was computed to have an 

average ozone concentration 25 percent lower 

than that with the surface losses excluded. 

Information on sink processes for oxidants other 

than ozone is limited to PAN and NO2. Judging 

from PAN solubility in water, rainout and washout 

are not expected to be significant sinks for PAN. 

The reaction of PAN with NO (0.16 ppm min-') is 

some two orders of magnitude slower than the 

reaction of ozone with NO; nevertheless, this sink 

process could be important in urban areas during 

evening hours when NO accumulates to high 

concentrations. PAN is not destroyed at a 

significant rate by sunlight photolysis (k = 5 x 10 -3 

hr')° but is subject to reversible thermal 

decomposition into NO2 59 (see also section on 

atmospheric reaction mechanisms). Because of 

this latter process, any removal process for NO2 

will also constitute an indirect sink for PAN. The 

low vapor pressure of PAN suggests that dry 

deposition could be an important sink for this 

oxidant; however, quantitative data are not 

available. In contrast, data for on-surface 

adsorption do exist and show PAN to be somewhat 

less adsorbable than ozone, with a deposition 

velocity of about 0.25 cro sec -' for grass and soil 

surfaces. 47 Such a value suggests that removal on 

surfaces is probabiy one of the major sinks for PAN 

in the lower troposphere. In air layers aloft, where 

the NO-reaction and surface sinks are ineffective, 

PAN can travel long distances. 

Nitric oxide and nitrogen dioxide can be removed 

to varying degrees by all four sink mechanisms. 

The primary sink for NO is the reaction with 

oxidizing radicals to produce NO2. Rainout and 

washout removal of NO are minimal because of its 

low solubility. Adsorption of NO by vegetation and 

by soil occurs very slowly, at deposition velocities 

around 0.1 cro sec-'.' os Noz is removed chiefly by 

oxidation into nitrates and peroxyacylnitrates and 

subsequent removal through precipitation, dry 

deposition, and surface adsorption. Removal of 

NOz on alfalfa surfaces was measured and found 

by Hi11 64 to occur with a deposition velocity of 2 cm 

sec '. The impact of surface sinks for NOz on 

ambient ozone and NO2 was computed by Killus 

and Jerskey. 75 

Information on sinks for HC is far more 

incomplete than for the other oxidant-related 

pollutants, probably because of the large variety of 

organic compounds (hydrocarbon and nonhydrocarbon) in ambient air. Hydrocarbons are, in 

general, insoluble in water and therefore cannot 

be removed significantly by precipitation. 

Chemical reactions converting the reactive HC to 

soluble and/or condensable products constitute 

the most important sink processes. Limited data 

reported by Hidy63 indicate that 1 to 10 percent (by 

weight) of reactive HC emissions are converted to 

removable aerosol. The remaining HC are 

eventually oxidized to CO2 and H2O, but with 

parallel formation of oxidant/ozone. Such a 

conversion does not, therefore, constitute a sink. 

Removal by soil apparently does occur, but data 

exist for a few hydrocarbons only (e.g., ethylene 

and acetylene). 109 The sink processes for 

unreactive hydrocarbons are the same, in general, 

as for the reactive ones, but they occur more 

slowly. 

SUMMARY 

Evidence shows that in and around urban 

centers with high oxidant/ozone concentrations, 

photochemicai oxidant and ozone are mainly 

formed from anthropogenic organic and NOX 

emissions. In the years since publication of the 

predecessor to this criteria document, the 

mechanisms of the atmospheric oxidant/ozone 

formation process have been studied intensively 

and are now better understood. Most noteworthy 

are recent findings pertaining to the roles of 

hydroxyl (OH•) and (HO•z). The reaction with OH 

has been established to be a major HC-consuming 

process, and OH and H02 have been identified as 

having major roles in the atmospheric oxidation of 

NO to NOz. Aldehydes and PAN were also found to 

play important roles in the atmospheric reaction. 

For olefins and paraffins, at least, these reactions 

are now understood to the extent that the kinetics 

of photochemical hydrocarbon-NO X reaction 

systems, as observed in the laboratory, can be 

described with reasonable accuracy. Additional 

research is needed to understand the atmospheric 

57 
reactions of aromatic hydrocarbons and to further 

clarify the differences between laboratory and 

ambient atmospheric chemical systems. 

The photochemical formation of oxidant/ozone 

is the result of two coupled processes: a physlcal 

process involving dlspersion and transport of the 

oxidant precursor emisslons (e.g., HC and NOx)and 

the photochemlcal reaction process. Both 

processes are strongly influenced by meteorological factors such as dispersion, solar 

radiation, temperature, and humidlty. Recently 

compiled statistics on wlnd velocity and mixing 

height showed that episodes of limlted disperslon 

are most common in the Far West and withln the 

Rocky Mountain reglon, least common over the 

Plains States, and of intermedlate frequency east 

of the Mississlppi. New measurements of solar 

radiation lead to results somewhat different from 

those reported earlier. Recent field and laboratory 

studles suggest that at terrlperatures below 

approximately 55 1 to 60°F (13 0 to 16 1 C), concentrations of photochemical ozone are unlikely to 

exceed the national 1-hr 160-Ng/m 3 (0.08-ppm) 

standard. 

Of all recent developments regarding the 

understanding of the sources of photochemical 

oxidant/ozone, perhaps the most Important ones 

were in the area of photochemical oxidant/ozone 

transport. Short-range (urban-scale) transport has 

been shown to occur and to cause the highest 

ozone concentrations some distance downwind 

from the core area (region of hlghest emisslon) of 

urban center lntermediate-range (mesoscale) 

transport has been identified in the form of urban 

oxidant/ozone plumes extending as far as 100 

mlles (160 km) or more downwlnd, and also 

Involved In land-sea-breeze circulation. Finally, 

synoptic-scale transport (over a range of several 

hundred miles) associated with high pressure 

systems has been found to occur extenslvely. 

These findings have significant Implicatlons with 

respect to the location of oxidant/ozone monitors. 

Conditlons under long-range transport are such 

that ozone production per unit of precursor is 

enhanced. Also, many organics previouslythought 

to be unreactive are now belleved to have 

slgnificant ozone-producing potential. 

In addition to the tropospherlc photochemistry of 

anthropogenic emissions, potential sources of 

tropospheric oxidant/ozone are the stratosphere 

and the photochemistry of natural organic and NO,, 

emissions. Estlmates of stratospheric ozone Intrusions at ground level are based on two types of 

evidence: (1 ) global circulation patterns, namely, 

58 

patterns In air Interchange between stratosphere 

and tropsphere, and (2) data on variations of ozone 

concentrations in remote rural areas. Based on the 

evidence of stratosphere-troposphere Interchange, the annual average stratospheric 

contribution to ozone concentrations at ground 

level is estlmated to be 0.022 to 0.05 ppm. The 

hlghest concentrations, at or above 0.08 ppm, from 

that source are expected to occur mostly during 

April and May. Occurrence of such major 

intruslons of stratospheric ozone concentration 

during the spring months in midlatitudes was 

indicated also by analysis of the ozone data for 

remote rural areas. The evidence suggests that the 

probable concentration of stratospheric ozone 

reaching ground level during the smog season 

(usually late summer or early fall) is about 60 

Ng/m3 (0.03 ppm). There are also more recentdata 

obtained at Whiteface Mountain, New York, 

suggesting a maximum 24-hr concentration of 72 

/Ig/m3 (0.037 ppm) stratospheric ozone in July. 

Certaln organic emisslons from vegetatlon 

(terpenes) were found to play the dual role of ozone 

precursor and destroyer. Despite the substantial 

rates at whlch they are emitted in forested areas, 

the ambient concentratlons of such organics, 

because of their reactivity and the areal dispersion 

of their sources, seldom exceed a few parts per 

billion. At these ambient concentrations, the direct 

potentlal of terpenes for photochemlcal ozone 

formatlon is estimated to be negliglble. It Is 

conceivable, however, that the products of 

atmospheric reactions involving large amounts of 

terpenes do have a significant impact on 

oxidant/ozone-related air quality. 

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Research Triangle Park, N.C., August 1976. 52. Grimsrud, E. P., H. H. Westberg, and R. A. Rasmussen. 

Decker, C E., J J. B. Worth, L. A. Ripperton, and W. D. Atmospheric reactivity of monoterpene hydrocarbons, 

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77-001 b, U.S. Environmental Protection Agency, Jr., L. W. Chaney, and C. S. Burton A spectroscopic 

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1154. National Meeting American Chemical Society. 

Dimitriades, B. Oxidant/Oa air quality benefits from American Chemical Society, Washington, D C., 1974. 

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key issues. J. Air Pollut. Control Assoc. 27:299-307, Control.Proceedings Volume I. B. Dimitriades, ed. EPA1977. 600/3-77-001 a, U.S. Environmental Protection 

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Pollution and Its Control. Proceedings Volume I. B. Publication No. 115-69, Pennsylvania State University, 

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Park, N.C., January 1977. pp. 109-118 59. Hendry, D. G, and R. A. Kenley Gas-phase free radical 

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Gay, B. W., Jr., and R. R. Arnts. The chemistry of 61 Hester, N. E., R. B. Evans, F. G Johnson, and E. L. 

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153. 

61. Killus, J. P., and T. N. Jerskey Surface sinks. /n: 

Continued Research in Mesoscale Air Pollution 

Simulation Modeling: Volume V-Refinements in 

Numerical Analysis, Transport, Chemistry, and 

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2216, Systems Applications, Inc., San Rafael, Calif., 

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62. Korshover, J. Climatology of stagnating anticyclones 

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63. Lamb, R. G. A case study of stratospheric ozone 

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78 Leighton, P. A. Photochemistry of Air Pollution. Academic Press, Inc., New York, 1961. 

79. Levine, S. Z., W M. Uselman, W. H. Chan, J. G. Calvert, 

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80. Levitt, S. B, and D. P. Chock. Weekday-weekend 

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81. Levy, H., 11. Photochemistry of the lower troposphere. 

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82. Lonneman, W. A. Ozone and hydrocarbon measurements in recent oxidant transport studies. /n 

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83. Lonneman, W. A., R. L. Seila, and S. A. Meeks. 

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measurements taken during the 1975 northeast oxidant 

transport study. /n: Proceedings of Symposium on 1975 

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017, U.S. Environmental Protection Agency, Research 

Triangle Park, N.C., February 1977. pp. 40-53. 

84. Ludwig, F. L., E. Reiter, E. Shelar, and W. B. Johnson. 

The Relation of Oxidant Levels to Precursor Emissions 

and Meteorological Features Vol. I Analysis and 

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September 1977. 

85. Lyons, W. A., and H. S. Cole. Photochemical oxidant 

transport: Mesoscale lake breeze and synoptic-scale 

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86. Marks, J. E., and J. L. Herman. Mesoscale transportation of ozone: An episode, August 18, 1974. /n. 

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87. Martinez, E. L., and E. L. Meyer, Jr. Urban-nonurban 

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Conference on: Ozone/Oxidants-Interactions with the 

61 

secondary pollution concentrations in the St. Louis 

urban plume. /n - International Conference on 

Photochemical Oxidant Pollution and Its Control. 

Proceedings. Volume I. B. Dimitriades, ed. EPA-600/3- 

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Research Triangle Park, N.C., January 1977. pp. 259- 

274. 

62. Heuss, J. M., and W. A. Glasson. Hydrocarbon reactivity 

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63. Hidy, G M. Removal processes of gaseous and 

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64. Hill, A. C. Vegetation. A sink for atmospheric pollutants. 

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65. Holzworth, G. C. Mixing Heights, Wind Speeds, and 

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66 Huffman, G. D., G. W. Haering, R. C. Bourke, P. P. Cook, 

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Conference on Photochemical Oxidant Pollution and Its 

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Agency, Research Triangle Park, N.C., January 1977. 

pp. 341-352. 

67 Husain, L., P. E. Coffey, R. E. Meyers, and R. T. 

Cederwall. Ozone transport from stratosphere to 

troposphere Geophys. Res. Lett. 4:363-365, 1977. 

68 Husar, R. B., D. E. Patterson, C. /n: International 

Conference on Photochemical Oxidant Pollution and Its 

Control. Proceedings. Volume 1. B. Dimitriades, ed. EPA600/3-77-OOta, U.S. Environmental Protection 

Agency, Research Triangle Park, N.C., January 1977. 

pp• 275-282. 

69. Jackson, J. 0., D. H. Stedman, R. G. Smith, J. H. Hecker, 

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Rev. Sci. Instrum. 46:376-378, 1975. 

70. Jaffe, R. J., F. C. Smith, Jr , and K. W. Last. Study of 

Factors Affecting Reactions in Environmental 

Chambers. Phase 111. EPA-650/3-74-004b, U.S. 

Environmental Protection Agency, Research Triangle 

Park, N.C., November 1974. 

71 Jeffries, H. E. Review and analysis. /n: International 

Conference on Oxidants, 1976-Analysis of Evidence 

and Viewpoints. Part 11. The Issue of Reactivity. EPA600/3-77-114, U.S. Environmental ProtectionAgency, 

Research Triangle Park, N.C., October 1977. pp 35-70 

72 Jeffries, H., D. Fox, and R. Kamens. Outdoor Smog 

Chamber Studies. Effect of Hydrocarbon Reduction on 

Nitrogen Dioxide. EPA-650/3-75-011, U.S. 

Environmental Protection Agency, Research Triangle 

Park, N.C., June 1975. 

73. Jeffries, H. E., R. M. Kamens, and C. E. Feigley. Outdoor 

Simulations of Air Pollution Control Strategies. 

Progress Report, 1975-1976. University of' North 

Carolina, School of Public Health, Chapel Hill, N.C., 

January 1977. 

74. Jerskey, T. N., T B. Smith, S. L. Marsh, and W. H. White. 

The effect of ozone layers aloft on surface 

concentrations. /n: International Conference on 
Total Environment. Air Pollution Control Association, 102 Price J. H A study of factors associated with high urban 

88 

89. 

90 

91.

92.

93.

94.

95.

96 

97.

98.

99 

100.

101.

Pittsburgh, Pa., 1976. pp. 221-133. ozone concentrations in Texas. /n Specialty Conference 

Mc,4fee, J. M, A. M. Winer, and J. N Pitts, Jr. Infrared on• Ozone/Oxidarrts—Interactions with the Total 

product analysis of ozone-olefin reactions by Fourier Environment. Air Pollution Control Association, 

interferometry. Presented at the Symposium on Pittsburgh, Pa., 1976. pp. 282-292. 

Chemical Kinetics Data for the Upper and Lower 103 Quon, J. E., and R A. Wadden. Oxidants in the Urban 

Atmosphere, Stanford Research Institute and National Atmosphere. IIEQ Publication No. 75-04, State of 

Bureau of Standards, Warrenton, Va., September 1 5- Illinois, Institute for Environmental Quality, Chicago, III., 

18, 1974. January 1975 

McKee, H. C Atmospheric Measurements at Seadock 104 Rasmussen, R. A. Isoprene: Identified as a forest-type 

Site Southwest Research Institute, Houston, Texas, emission to the atmosphere. Environ. Sci. Technol 

April 1974. 4:667-671, 1970 

Mohnen, V A. Review and analysis In - International 105. Rasmussen, R A Recent field studies. /n. Scientific 

Conference on Oxidants, 1976—Analysis of Evidence Seminar on Automotive Pollutants. EPA-600/9-75- 

and Viewpoints. Part III The Issue of Stratospheric 003, U.S. Environmental Protection Agency, Research 

Ozone and Intrusion. EPA-600/3-77-115, U.S Triangle Park, N.C., February 1975. Sect. 5, Subset J 

Environmental Protection Agency, Research Triangle 106. Rasmussen, R A. Surface ozone observations in rural 

Park, N C, December 1977 pp. 7-66. and remote areas. J Occup. Med. 18.346-350, 1976 

Morris, E. D, Jr., and H Niki Reaction of dinitrogen 107. Rasmussen, R A. What do the hydrocarbons from trees 

pentoxide with water J. Phys, Chem. 77.1929-1932, contribute to air pollution? J Air Pollut Control Assoc. 

1973. 22•537-543, 1972 

National Air Pollution Control Administration. Air 108. Rasmussen, R. A., and M. W. Holdren. Analysis of Cs to 

Quality Criteria for Photochemical Oxidants, NAPCA C,o hydrocarbons in rural atmospheres. Presented at 

Publication No AP-63, U.S Department of Health, the 65th Annual Meeting Air Pollution Control 

Education, and Welfare, Public Health Service, Associat'lon, June 18-22, 1972 

Washington, D C., March 1970. 109 Rasmussen, K. H., M. Taheri, and R. L. Kabel. Global 

National Research Council. Ozone and Other emissions and natural processesfor removal of gaseous 

Photochemical Oxidants National Academy of pollutants Water Air Soil Pollut 433-64, 1975. 

Sciences, Washington, D.C., 1977. 110. Rasmussen, K. H, M. Taheri, and R L. Kabel. Sources 

Niki, H., E. E. Daby, and B. Weinstock. Mechanisms of and Natural Removal Processes for Some Atmosphere 

smog reactions Adv. Chem Ser. 113:16-57, 1972. Pollutants EPA-650/4-74-032, U.S Environmental 

Niki, H., P D. Maker, C M. Savage, and L. P Protection Agency, Research Triangle Park, N C. 1974 

Breitenbach Fourier transform IR spectroscopic 111. Reiter, E. R/n. International Conference on Oxidants, 

observation of pernitric acid formed via HOO + NOz T 1976—Anatysis of Evidence and Viewpoints. Part III. 

HOONO2. Chem. Phys. Lett 45 564-566, 1977 The Issue of Stratospheric Ozone Intrusion. EPAOffice of Air Quality Planning and Standards Position 600/3-77-1 15, U.S. Environmental Protection Agency, 

Paper on Regulation of Atmospheric Sulfates. EPA- Research Triangle Park, N C., December 1977 

450/2-75-007, U.S Environmental Protection Agency, 112. Reiter, E. R. The role of stratospheric import on 

Research Triangle Park, N.0 , September 1975. tropospheric bzone concentrations. /n: International 

Conference on Photochemical Oxidant Pollution and Its 

Pack, D H. Review and analysis. /n International Control. Proceedings. Volume I. B. Dimitriades, ed. EPAConference on Oxidants-1976 Analysis of Evidence 600/3-77-001 a, U S. Environmental Protection 

and Viewpoints Part V. The Issue of OxidantTransport. Agency, Research Triangle Park, N C., January 1977. 

EPA-600/3-77-1 17, U S Environmental Protection pp 393-410 

Agency, Research Triangle Park, N.C., November 1977 113. Reiter, E. R The transport of radioactive debris and 

p• 9-20 ozone from the stratosphere to the ground. Arch 

Pate, C. T, R. Atkinson, and J. N Pitts, Jr Rate constants Meteorol. Geophys. Bioklimatol. Ser. A 26•323-340, 

for the gas phase reaction of peroxyacetyl nitrate with 1977. 

selected atmospheric constituents. J Environ Sci. 114 Renzetti, N A., and R. J Bryan. Atmospheric sampling 

Health Environ Sci Eng. A11(1) 19-31, 1976 for aldehydes and eye irritation in Los Angeles smog— 

Payne, W. A., L J. Stief, and D. D. Davis. A kineticsof the 1960. J Air Poilut. Control Assoc. 11 421-424, 1961. 

reaction of HOz with S02 and N0. J. Am. Chem. Soc. 115. Research Triangle Institute Investigation of Ozone and 

95.7614-7619,1973. Ozone Precursor Concentrations at Non-Urban 

Peterson, ; T Calculated Actinic Fluxes (290-700 nm) Locations in the Eastern United States. EPA-450/3-74- 

for Air Pollution Photoche,nistry Applications. EPA- 034, U.S. Environmental Protection Agency, Research 

600/4-76-025, U.S. Environmental Protection Agency, Triangle Park, N.C., May 1974. 

Research Triangle Park, N C., June 1976. 116 Research Triangle Institute. Investigation of Rural 

Peterson, J T., K L Demerjian, and K. L Schere Actinic Oxidant Levels as Related to Urban Hydrocarbon Control 

solar flux and photolytic rate constants in the Strategies. EPA-450/3-75-035, U.S Environmental 

troposphere /n• International Conference on Protection Agency, Research Triangle Park, N.C., March 

Photochemical Oxidant Pollution and Its Control. 1975 

Proceedings. Volume I. B Dimitriades, ed EPA-600/3- 117 Richardson, R. L, D. Johnson, and R. R. Wallis 

77-001a, U.S. Environmental Protection Agency, Background Concentrations of Hydrocarbons in the 

Research Triangle Park, N C, January 1977. pp. 763- Atmosphere of the Northwest Gulf of Mexico. Texas Air 

773. Control Board, Austin, Tex., September 20, 1973. 

62 
1 18. Ripperton, L. A., J. J. B. Worth, F. M. Vukovich, and C. E. 

Decker. Research Triangle Institute studies of high 

ozone concentration in nonurban areas. /n - 

International Conference on Photochemical Oxidant 

Pollution and Its Control. Proceedings. Volume I. B. 

Dimitriades, ed. EPA-600/3-77-001a, U.S 

Environmental Protection Agency, Research Triangle 

Park, N.0 , January 1977. 

119. Roberts, P. T., and S. K. Friedlander. Photochemical 

aerosol formation of S02, 1-heptene, and N0, in 

ambient air. Environ. Sci. Technol. 10.573-580, 1976. 

120 Robinson, E. Review and analysis. /n• International 

Conference on Oxidants-1976 Analysis of Evidence 

and Viewpoints. Part V. The Issue of Oxidant Transport. 

EPA-600/3-77-117, U.S. Environmental Protection 

Agency, Research Triangle Park, N.C., November 1977. 

pp 21-38 

121. Robinson, E., and Robbins, R C Sources, Abundance 

and Fate of Gaseous Atmospheric Pollutants. SRI 

Project PR-6755, Stanford Research Institute, Menlo 

Park, Calif , 1963. 

122 Sander, S. P., and J H. Seinfeld. Chemical kinetics of 

homogeneous atmospheric oxidation of sulfur dioxide. 

Environ. Sci Technol. 10 1114-1123, 1976. 

123. Schmitz, H. J., and D Cox. Local Air Pollution Episode 

from May 16 to May 27, 1972, Metropolitan Dade 

County Pollution Control, Miami, Fla., June 1972 

124. Seinfeld, J. H. Letter to the Editor. Environ. Sci Technol 

11•1218-1219, 1977. 

125 Simonaitis, R., and J Heicklen. The Temperature 

Dependence of the Reactions of H02 with NO and NO2. 

PSU-IRL-SCI-454, Pennsylvania State University, 

University Park, Pa , March 1977. 

126. Singh, H. B, F. L. Ludwig, and W B Johnson Ozone in 

Clean Remote Atmospheres Concentrations and 

Variabilities. SRI Project 5661, Stanford Research 

Institute, Menlo Park, Calif., June 1977. 

127. Singh, H. B, F L Ludwig, and W. B Johnson. 

Tropospheric ozone: Concentrations and variabilities in 

clean remote atmospheres. Atmos. Environ. 12.2185- 

2196, 1978. 

128. Siple, G. W., C. K. Fitzsimmons, K F. Zeller, and R. B. 

Evans Long range airborne measurements of ozone off 

the coast of the northeastern United States /n: 

International Conference on Photochemical Oxidant 

Pollution and Its Control Proceedings. Volume I. B. 

Dimitriades, ed. EPA-600/3-77-001 a, U S 

Environmental Protection Agency, Research Triangle 

Park, N.C., January 1977. pp 249-258 

129 Spicer, C W, J. L Gemma, D. W. Joseph, P R Sticksel, 

and G. F. Ward. The Transport of Oxidant Beyond Urban 

Areas. EPA-600/3-76-018a, U.S. Environmental 

Protection Agency, Research Triangle Park, N.C., 

February 1976 

130. Spicer, C. W., J. L. Gemma, and P. R. Sticksel. The 

Transport of Oxidant Beyond Urban Areas Data 

Analysis and Predictive Models for the Southern New 

England Study, 1975 EPA-600/3-77-041, U.S. 

Environmental Protection Agency, Research Triangle 

Park, N.C., May 1977. 

131. Stair, R The spectral radiant energy from the sun 

through varying degrees of smog at Los Angeles. /n 

Proceedings of the Third National Air Pollution 

Symposium. National Air Pollution Symposium, Los 

Angeles, Calif., 1955. pp 48-55. 

132 Stedman, D. H., and J. 0. Jackson. The photostationary 

state in photochemical smog. /n: Proceedings of the 

Symposium on Chemical Kinetics Data for the Upper 

and Lower Atmosphere. Int J. Chem. Kinet. Symp. 

(1)- 493-501, 1975. 

133 Stedman, D. H., F. D. Norvis, E E. Daley, H. Niki, and B. 

Weinstock The role of OH radicals in photochemical 

smog reactions. Paper presented at 160th National 

Meeting of American Chemical Society, Chicago, 

September 1970. 

134. Tiao, G. C, G. E. P. Boxand W J. Hamming Analysisof 

Los Angeles photochemical smog data: A statistical 

overview. J Air Pollut. Control Assoc. 25•260-268, 

1975. 

135. Tiao, G. C, M. S Phadke, and G. E. P Box. Some 

empirical models for the Los Angeles photochemical 

smog data Presented at 68th Annual Meeting, Air 

Pollution Control Association, Boston, Mass, June 15- 

20, 1975. 

136 Vukovich, F Review and analysis. /n. International 

Conference on Oxidants, 1976—Analysis of Evidence 

and Viewpoints. Part V. The Issue of OxidantTransport. 

EPA-600/3-77-117, U S. Environmental Protection 

Agency, Research Triangle Park, N C, November 1977. 

pp. 39-56 

137 Westberg, H Review and analysis /n: International 

Conference on Oxidants, 1976—Analysis of Evidence 

and Viewpoints. Part IV. The Issue of national Organic 

Emissions EPA-600/3-77-116, U.S. Environmental 

Protection Agency, Research Triangle Park, N.0 , 

October 1977. 

138 Westberg, H., K. J. Allwine, and D. Elias. Vertical ozone 

distribution above several urban and adjacent rural 

areas across the United States. /n: Specialty Conference 

on• Ozone/Oxidants—Interactions with the Total 

Environment Air Pollution Control Association, 

Pittsburgh, Pa., 1976. pp. 84-95. 

139 Westberg, H, K. J. Allwine, and E P,obinson The 

Transport of Oxidant Beyond Urban Areas. Light 

Hydrocarbon and Oxidant Data, New England Study 

1975 EPA-600/3-78-006, U.S Environmental 

Protection Agency, Research Triangle Park, N C., 

January 1978. 

140. Westberg, H, and M Holdren Quarterly Report U S. 

Environmental Protection Agency, Research Triangle 

Park, N C , 1976 

141, Whitby, R, L. Roland, V. Mohnen, and P. E Coffey. 

Measurement of background hydrocarbons in remote 

areas. Presented at the Symposium on the Non-Urban 

Tropospheric Composition American Geophysical 

Union and American Meteorological Society, 

Hollywood, Fla , November 10-12, 1976. 

142. White, W H, J. A. Anderson, W R Knuth, D. L. 

Blumenthal, J. C Hsiung, and R. B. Husar. Midwest 

Interstate Sulfur Transformation and Transport Project: 

Aerial Measurements of Urban and Power Plant 

Plumes, Summer 1974 EPA-600/3-76-110, U.S. 

Environmental Protection Agency, Research Triangle 

Park, N.0 , November 1976 

143 White, W. H, D. L. Blumenthal, J. A. Anderson, R. b. 

Husar, and W E. Wilson, Jr. Ozone formation in the St. 

Louis urban plume. /n - International Conference on 

Photochemical Oxidant Pollution and Its Control 

Proceedings Volume I. B. Dimitriades, ed. EPA-600/3- 

63 
77-001a, U.S. Environmental Protection Agency, 

Research Triangle Park, N.C., January 1977. pp 237- 

247. 

144. Whitehead, L. W, and R. Severs. Background 

hydrocarbon levels in east Texas. Presented at the 83rd 

Annual National Meeting, American Institute of 

Chemical Engineers, Houston, Texas, March 1977. 

Paper no. 21A. 

145. Wolff, G. T, P. J. Lioy, G. D. Wight, R E Meyers, and R. 

T. Cederwall. An investigation of long-range transportof 

ozone across the midwestern and northeastern U.S. /n: 

International Conference on Photochemical Oxidant 

Pollution and Its Control. Proceedings. Volume I B. 

Dimitriades, ed. EPA-600/3-77-001a, U.S 

Environmental Protection Agency, Research Triangle 

Park, N.C., January 1977 pp. 307-317 

146. Wo1ff, G. T., P. J Lioy, G. D. Wight, and R. E. Pasceri 

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64 
5. OXIDANT PRECURSORS 

INTRODUCTION 

As has been established, most of the oxidants 

found in urban atmospheres are secondary 

pollutants, and the primary pollutants that act as 

oxidant precursors are the hydrocarbons and the 

nitrogen oxides (i.e., nitric oxide and nitrogen 

dioxide, NO and NO2). Not all atmospheric 

hydrocarbons are significant oxidant producers. 

Methane is the most important exception. In 

addition, there are nonhydrocarbon organics (e.g., 

aldehydes) that are also capable of forming 

oxidants. However, the term "hydrocarbons," or, 

specifically, "nonmethane hydrocarbons," best 

describes the organic component of the oxidant 

precursor mixture in the atmosphere. 

Data on the nature, sources, concentration, and 

the concentration variation patterns for the 

oxidar t precursors are discussed in this chapter. 

Emphasis is placed on the organic precursors, as 

the NOx data are presented in detail in the 

litera ure. 22 The quantitative relationships 

betwEan oxidant and oxidant precursors are 

treatf i in a separate chapter. 

AMB9ENT LEVELS AND VARIATIONS OF OXIDAN''/OZONE PRECURSORS 

Orgar ic Compounds in Urban Atmospheres 

Information on the nature and relative amounts 

of the various organic compounds present in 

polluted atmospheres is needed to identify 

pollutants that have direct, adverse effects on 

human health and/or welfare. It is also needed to 

provide direct estimates, however rough they may 

be, of the levels of controllable and 

noncontrollable emissions. Data on the 

composition of polluted atmospheres are also 

necessary for characterizing in terms of their 

oxidant- producing potential the emissions 

discharged from various sources. A large part of 

the information needed can be obtained through 

analysis of the ambient air. The composition of 

emissions can also be determined from 

measurements at the sources. It is only from the 

combined use of such ambient air and source 

emission data that the impact of organic emissions 

on air quality can reliably and comprehensively be 

assessed. 

Most of the detailed stuL'es of organic 

compounds in the urban atmosphere were 

conducted during the 1960's. The results were 

summarized and discussed in the criteria 

document for hydrocarbons. 60 Those studies and 

other more recent ones identified a large number 

of hydrocarbons (Table 5-1) 4,62,78 and some 

aldehydes in the urban atmosphere.$ It is almost 

certain that such identification is far from 

complete because of the analytical problems 

created by the enormous complexity of the 

ambient organic mixtures and the trace 

concentrations of the various components. The 

composition of organics in urban atmospheres 

differs from city to city and reflects emission 

composition and the influences of chemical 

reaction. For example, industrial emissions and 

chemical reactions cause higher relative levels of 

paraffins and of other nonreactive organics in the 

ambient air. a5,5 ' Automobile emissions usually 

dominate the composition of organics in urban 

ambient atmospheres, especially during the peak 

traffic hours. 45 Some stationary emission sources, 

however, can be important also. More detailed but 

indirect information on the composition of 

organics likely to be present in urban ambient 

atmospheres has been provided by analysis of 

source emissions. Analyses of the exhaust and 

evaporative emissions from gasoline-fueled 

automobiles have identified some 200 

hydrocarbons 30 and several oxygenated 

hydrocarbons, 76 many of which could not be 

detected in the ambient air, although they were 

certain to be present. Data are also available in 

varying degrees of detail and specificity on the 

composition of organic emissions from dieselpowered automobiles (Figure 5-1 ), 39 from aircraft 

(Figure 5-2), 21 from natural gas lines, and from 

solvent evaporation. The presence of these latter 

organic emissions in the ambient air and, in fact, 

65 
their quantitative contrlbutions to the'ambient 

organic load have been explored by inves-, 

tigators 53 ' 79 with some definitive results. 

Contributions, for example, have been estimated 

by Mayrsohn and Crabtree in their source study 

(reconciling atmospherlc hydrocarbon data with 

known hydrocarbon sources and their emissions) 

of the Los Angeles atmosphere. 53 Mayrsohn's 

conclusions were that (1) automotive exhaust 

accounts for somewhat less than 50 percent of the 

nonmethane hydrocarbons; (2) gasoline and 

gasoline vapor together constitute the second 

largest source of atmospheric hydrocarbons, 

totaling 30 to 35 percent byweight; (3) commercial 

and geogenic natural gas makes up about 20 

percent of the total by welght; and (4) other 

emissions, such as those from solvent evaporation, diesel and alrcraft emisslons, and 

refrigerant and propellent usage are also present 

so that the percentage contrlbutions attributed to 

the preceding three sources should be regarded as 

upper iimits. 

Probably not all organics emitted by the various 

sources wlll be found intact in the ambient air. 

Many may be removed through sink processes 

(e.g., deposition on aerosol and ground surfaces 

and dissolution in water) before they can 

participate substantially in atmospheric reaction 

processes. Considering this latter uncertainty and 

the Ilmited compositional data available for most 

source emisslons (e.g., for the exhausts from 

gasoline- and diesel-powered automobiles and 

from aircraft), one can only assume that current 

knowledge of the composition of the organics in 

the urban atmosphere is incomplete and, 

therefore, that the search for and identification of 

unknown organic air pollutants should continue. 

TABLE 5-1. HYDROCARBONS IDENTIFIED lN AMBIENT AIR" ,sz,1e 

Carbon Carbon 

number Compound number Compound 

1 Methane 6 (cont.) 3-Methylpentane 

2,2-Dimethylbutane 

2,3-Dimethylbutane 

2 Ethane 

Ethylene cis-2-Hexane 

Acetylene trans-2-Hexane 

crs-3-Hexane 

trans-3-Hexane 

3 Propane 2-methyl-1-Pentene 

Propylene 4-methyl-1-Pentene 

Propadiene 4-methyl-2-Pentene 

Methylacetylene 

Benzene 

Cyclohexane 

4 Butane Methylcyclopentane 

isobutane 

1-Butene 

cis-2-Butene 7 2-Methylhexane 

trans-2-Sutene 3-Methylhexane 

Isobutene 2,3-Dimethylpentane 

1,3-Butadiene 2,4-Dimethylpentane 

Toluene 

5 Pentane 

Isopentane 8 2,2,4-Trimethylpentane 

1-Pentene o-Xylene 

cis-2-Pentene m-Xylene 

trans-2-Pentene p-Xylene 

2-methyl-1-Butene 

2-methyl-2-Butene 

3-methyl-1-Butene 9 m-Ethyltoluene 

2-methyl-1,3-Butadiene p-Ethyltoluene 

Cyclopentane 1,2,4-Trimethylbenzene 

Cyclopentene 1,3,5-Trimethylbenzene 

6 Hexane 10 sec-Butylbenzene 

2-M ethy lp e ntane 

66 
Z o 

O_E 

Q ~ 

f- r 

Z t 

W ~ 

U p 

Z ., 

Ow 

fU o 

w c J d 

O ° 

2 a 

32 

28 

24 

20 

16 

12 

8 

4 

0 

32 

28 

24 

20 

16 

12 

8 

4 

0 

2-CYCLE ENGINE 

AT IDLE 

2-CYCLE ENGINE 

FULL LOAD 

4-CYCLE ENGINE 

AT IDLE 

4-CYCLE ENGINE 

FULL LOAD 

4 8 12 16 20 24 1 4 8 12 16 20 24 

NUMBER OF CARBON ATOMS PER MOLECULE 

Figure 5-1. Distribution of hydrocarbons in diesel exhaust gas. 39 

Data on total levels of organic compounds in 

urban atmospheres are relatively abundant, but 

most of these data suffer from considerable 

measurement error (see Chapter 7). Some statistics on such data are shown for six urban centers 

in Table 5-2. 24 Total organic concentrations in 

ambient air are usually reported as totals of 

nonmethane hydrocarbons and as averages over 

the 6- to 9-a.m. period. Methane is excluded 

because it is nonreactive and chiefly of natural 

origin, and because its concentration usually 

overwhelms that of all other organics combined. 

The 6- to 9-a.m. period has been chosen and 

adopted in the early efforts by the Federal 

government to develop a model relating air quality 

to emissions (observational model). 22 The 

rationale behind that choice was that ambient 

concentrations during the early morning hours are 

a measure of the strength of the emissions only, as 

they are virtually unaffected bythechemical sinks. 

Speclfically, the 6- to 9-a.m. concentratlons refiect 

mainly the vehicuiar emissions, and such 

concentrations are relatively unaffected by 

changes in emissions from stationary sources. 

Some recent evidence suggests that a given 

amount of precursors, when injected into the 

reaction system, gradually, throughout the 

morning and afternoon, produce essentially the 

same ozone concentratlon as the same amount of 

precursors injected during the 6- to 9-a.m. 

period. 42 Such evldence was obtained from smog 

chamber studies and should be verifled 

The concentration levels listed in Tab(e 5-2 are 

typical of those in ordinary urban atmospheres, but 

they can be considerably higher. In Los Angeles, 

for example, total hydrocarbon concentrations 

have been as high as 30 ppm. This level is 

equivalent to a nonmethane hydrocarbon total of 

greater than 10 ppm. 16 In addition to the 

nonmethane organics upon which local 

contributions are superimposed methane also is 

present at a global background concentration of 

about 1.4 ppm.'o 

Seasonal and diurnal patterns of variation in 

nonmethane total organic levels have been 

discussed in the literature. 23' so Briefly, seasonal 

variations have not been well estabiished for lack 

of adequate data. In 14 of the 17 California cities 

for which adequate data exist, the highest 

hydrocarbon concentrations occurred in October 

or November. Such consistency is presumably a 

consequence of the generally similar meteorological conditions from year to year along the 

California coast. Cities elsewhere would be 

expected to show other patterns, depending on 

their particular meteorology. Diurnal patterns 

67 
observed in many cities show two distinct daily peak in the afternoon hours. Both peaks prepeaks, one during 6- to 9-a. m., and another broader sumably reflect the automobile traffic and local 

meteorological dispersion patterns. 

30 

F U E L-JP4 

20 

10 

0 1 4 8 12 16 19+ 

30 20 1 EXHAUST IDLE 

(TOTAL BY FID 686 ppm C) 

10 

0 ~ ■ . ■ . ■ ■ ■ ■ . ■ . . . . . . 

1 4 8 12 16 19+ 

Y 

C 

m 

V 

a', 30 

° APPROACH 

Z 20 (TOTAL BY FID <10 ppm C) 

O m 

m Q10 

U 

O 

m 0 

~ 1 4 8 12 16 19+ } 

_ 

30 

CRUISE 

(TOTAL BY FID < ppm C) 

20 

10 

0 1 4 8 12 16 19+ 

30 TA K E-OF F 

20 

(TOTAL BY FID <10 ppm C) 

10 

0 

1 4 8 12 16 19+ 

CARBON NUMBER 

Figure 5-2. Distribution of hydrocarbons in jet-aircraft engine exhaust (determined by gas 

chromatograph with flame ionization detector). 21 

68 
TABLE 5-2. FREQUENCY DISTRIBUTIONS FOR 6-TO 9-a.m. NONMETHANE HYDROCARBON CONCENTRATIONS 

AT CAMP SITES, 1967-72" 

(ppm C) 

Arithmetic Geometric 

Number Percentile' 

of Std Std 

Site Year samples Min 10 20 30 40 50 60 70 80 90 Max Mean dev. Mean dev 

Denver, Colo. 67° 29 0.0 0.0 0.3 0.4 0.6 0.9 1.1 1.8 2.3 2.7 5.2 1.3 1.2 0.74 3.69 

(060680002A10) 68° 161 0.0 0.2 0.4 0.6 0.8 1.0 1.1 14 1.7 2.7 5.3 1.2 1.0 0.87 • 3.62 

69° 219 0.0 0.0 0.1 0.3 0.5 0.7 0.8 1.0 1.3 1.7 4.9 0.8 0.8 0.50 3.26 

70° 231 0.0 0.0 0.2 0.3 0.5 0.6 0.8 1.0 1.1 1.6 5.9 0.8 0.7 0.52 2.96 

71 ° 178 0.0 0.3 0.6 0.7 0.9 1.1 1.3 15 1.8 2.4 5.7 1.3 0.9 0.99 2.29 

72 282 0.0 0.1 0.4 0.5 0.7 0.9 1.1 1.3 1.6 2.0 3.9 1.0 0.7 0.74 2.73 

Washington, D.C. 66° 250 0.0 0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 1.0 1.8 0.5 0.3 0.35 2.56 

(090020002A70) 68° 244 0.0 0.0 0.1 0.1 0.3 0.4 0.5 0.6 0.8 1.1 2.6 0.5 0.4 0.35 2.73 

69° 231 0.0 0.0 0.0 0.0 0.0 0.0 0.1 0.3 0.3 0.5 2.3 0.2 0.2 0.16 2.27 

70° 267 0.0 0.0 0.0 0.0 0.0 0.0 0.1 0.3 0.5 0.8 2.0 0.3 0.3 0.19 2.62 

71 279 0.0 0.0 0.0 0.0 0.1 0.1 0.2 0.3 0.5 0.8 3.3 0.3 0.3 0.20 2.64 

72° 187 0.0 0.0 0.0 0.0 0.1 0.1 0.3 0.5 0.6 1.1 2.6 0.4 0.4 0.25 2.82 

Chicago, III. 68° 146 0.0 0.1 0.2 0.4 0.6 0.8 1.0 1.1 1.4 1.8 2.8 0.8 0.6 0.64 2.58 

(141220002A10) 69 300 0.0 0.0 0.1 0.3 0.5 0.7 0.8 1.1 1.4 1.8 3.6 0.8 0.7 0.54 2.99 

70° 220 0.0 0.0 0.0 0.0 0.0 0.0 0.2 0.5 0.8 1.4 4.1 0.5 0.7 0.25 3.20 

71 ° 269 0.0 0.0 0.2 0.3 0.4 0.5 0.6 0.8 1.0 1.4 2.7 0.6 0.5 0.46 2.58 

Philadelphla, Pa. 66° 142 0.0 0.0 0.3 0.5 0.6 0.7 0.8 1.1 1.4 1.7 4.2 0.9 0.7 0.64 2.70 

(397140002A10) 67° 260 0.0 0.0 0.1 0.2 0.3 0.5 0.6 0.8 1.1 1.6 5.9 0.7 0.7 0.42 3.11 

68° 154 0.0 0.0 0.0 0.1 0.2 0.3 0.5 0.6 0.9 1.6 3.7 0.6 0.7 0.34 3.17 

69° 192 0.0 0.0 0.1 0.2 0.3 0.5 0.6 0.7 0.9 1-.3 3.7 0.6 0.5 0.42 2.74 

70° 264 0.0 0.0 0.1 0.2 0.3 0.4 0.6 0.7 1.0 1.3 2.3 0.5 0.4 0.37 2.90 

71 ° 234 0.0 0.0 0.0 0.1 0.2 0.2 0.4 0.4 0.6 0.9 3.0 0.4 0.4 0.27 2.74 

72° 59 0.0 0.0 0.0 0.1 0.3 0.4 0.4 0.6 0.7 1.1 2.4 0.5 0.4 0.31 3.02 

Cincinnati, Ohio 68° 109 0.0 0.0 0.0 0.1 0.2 0.3 0.4 0.6 0.8 1.4 3.4 0.5 0.6 0.31 3.18 

69° 188 0.0 0.0 0.0 0.2 0.2 0.4 0.4 0.5 0.7 1.1 3.1 0.5 0.5 0.32 2.79 

70° 99 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.1 0.4 2.3 0.1 0.3 0.23 2.22 

71 ° 104 0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.9 1.1 2.0 0.6 0.4 0.45 2.37 

72° 238 0.0 0.1 0.2 0.3 0.3 0.4 0.4 0.5 0.7 1.0 3.4 0.5 0.4 0.40 2.09 

St. Louls, Mo. 68° 198 0.0 0.0 0.0 0.2 0.4 0.6 0.8 0.9 1.1 1.6 4.4 0.7 0.7 0.44 3.25 

(264280002A10) 69 292 0.0 0.0 0.1 0.2 0.3 0.4 0.5 0.7 1.0 1.4 3.4 0.5 0.5 0.37 2.83 

70° 232 0.0 0.0 0.0 0.1 0.2 0.3 0.4 0.6 0.7 1.1 2.9 0.4 0.4 0.31 2.72 

71 314 0.0 0.0 0.0 0.0 0.0 0.1 0.2 0.3 0.4 0.7 2.5 0.2 0.3 0.19 2.54 

72° 235 0.0 0.0 0.0 0.0 0.1 0.2 0.2 0.3 0.4 0.7 1.8 0.3 0.2 0.21 2.42 

°Concentrations greater than or equal to specdied value in indicated percentage of samples 

"Yearly standard exceeded 

Since hydrocarbon emission controls went into 

effect in the 1960's, ambient air hydrocarbon 

concentrations have been observed to trend 

downward with time in some urban areas82but not 

in others. 80Figure 5-3 shows such a downward 

trend for the Los Angeles atmosphere. 40The trend 

is probably a real one, even though the 

nonmethane hydrocarbon data used to construct 

these trend plots were obtained indirectly (that is, 

they were computed from total hydrocarbon data 

and data on established relationships between 

total and nonmethane hydrocarbon for the Los 

Angeles atmosphere). Such data, as already 

stated, reflect control of automotive emissions 

only. In areas where substantial controls have 

been applied to stationary sources also, the impact 

of these latter controls on daily maximum or 6- to 

9-a.m. hydrocarbon concentrations will not be 

detectable; however, a detectable impact on the 

24-hr average hydrocarbon concentrations may be 

observed. In general, the analysis and interpretation of ambient air hydrocarbon data to 

assess the impact of emission controls should be 

done with great care to avoid biases and, hence, 

misleading results. Such biases can be introduced, 

for example, by ambient air measurement errors, 

by inappropriate definition of the ambient 

concentration, and by the disproportionate influence of a single emission source on measurements made at an improperly located 

measurement station. 

69 
z 

m V 

Cc E Q a V 

0Z O 

W Q 

z ~ 

QZ 

Lu 

w V 

Z C0.1 

0 

z 

MAX-HOUR AVERAGES - ALL DAYS OF YEAR 

MAX-HOUR AVERAGES - JULY, AUG., SEPT. 

o— 6-to-9-a rn. AVERAGES - JULY, AUG., SEPT. 

/ 

'00

.0~__~c~_ - 

~_ j ~ - o~. ~ .~ -o/ ~ 

~ 

1963 1964 1965 1966 1967 1968 1969 1970 1971 1972 

YEAR 

Figure 5-3. Nonmethane hydrocarbon trends in Los Angeles, 1963-1972. 82 

Organic Compounds in Rural and Remote Areas 

Occurrences of ambient organic compounds in 

rural and remote areas are of interest only to the 

extent that they constitute evidence on the role of 

natural organics in the ambient air oxidant 

problem. 28 Since such evidence has already been 

discussed (in the chapter on the natural sources of 

oxidant/ozone) and the conclusion was reached 

that the terpenes and methane have no important 

role, the information to be presented in this section 

will serve merely to provide additional detail and 

documentation for that previous discussion and 

conclusion. Specifically, more compiete and 

detailed evidence will be presented here on the 

occurrence of naturally emitted organics in rural 

and remote areas, but with the clear understanding that such evidence relates to occurrence 

alone and not to the impact of such organics on 

oxidant air quality. 

Besides the ubiqu+tous anthropogenic pollutants, rural atmospheres also should contain 

natural organics such as methane and organics 

emitted by vegetation. Several of these latter 

organics havP been identified either directly, 

through ambient air analysis, or indirectly, through 

analysis of the material emitted by vegetation 

samples processed in the laboratory. 6 e Organic 

compounds found by Rasmussen to be emitted by 

vegetation are listed in Table 5-3. 68 This list is by no 

means complete, since not all types of vegetation 

were examined. Studies reported in the Russian 

literature indicate that a considerable number of 

plant species release low molecular weight 

hydrocarbons and aidehydes and a wide variety of 

essential oil components. 41 

TABLE 5-3. VOLATILE PLANT PRODUCTS IDENTIFIED 

BY RASMUSSEN 6e 

Natural organic compounds 

a-Plnene Santene a-Ionone 

/3-Plnene Camphene (34onone 

Myrcene n-Heptane a-Irone 

D-Llmonene Isoprene 

Aside from the organics clearly associated with 

emissions from vegetation, measurements ,in 

remote areas have also shown the presence of 

ofganics that are commonly, but apparently not 

exclusively, associated with anthropogenic 

activities. For example, at Point Barrow, Alaska, 

Cavanagh et al. found benzerie, pentane, butane, 

ethane, ethylene, acetaldehyde, and acetone at 

sub-ppb levels (acetone at about 100 ppb) and 

attributed their origin to biological processes. 19 

70 
A few data on total organic concentrations in 

rural and remote atmospheres are available, but 

here again, as in the case of the urban 

atmospheres, most of the existing data are 

unreliable. One cause of unreliability is the 

relatively large error associated with the 

nieasurement of total non-methane organics. An 

additional problem, however, with the rural and 

remote atmospheric data arises from the lack of 

evidence on the composition of the organic 

pollutant mixture and, specifically, on the relative 

levels of vegetation-related and anthropogenic 

pollutants. This lack in compositional information 

has two consequences. First, it does not permit 

proper calibration of the ionization detector of the 

hydrocarbon analyzer, resulting in additional 

measurement error. Second, it attributes 

erroneously high concentration to the natural 

organics, since corrections for the anthropogenic 

components are not possible. Probably it is partly 

because of such errors that some of the reported 

values for total natural organic concentrations 

have been as high as 5 to 10 ppm C. 85 Extensive 

measurements in rural areas by EPA and other 

investigators using sampling and analysis 

procedures carefully designed to minimize such 

errors did not show the total of natural organics to 

be more than 0.1 ppm C. 69' 84 Whenever and 

wherever concentrations were higher, there was 

invariably evidence of anthropogenic contamination. 50' 72Finally, though it is probable that 

there are natural organic pollutants as yet 

unidentified, there are no strong indications that 

such unknowns could drastically change the 

current view regarding the role of natural organics 

in the oxidant/ozone problem. Such a role does not 

appear to be an important one, as was concluded 

also from the discussions in the preceding chapter 

dealing with the natural sources of ambient air 

oxidants. 

Nitrogen Oxides 

Information on the sources, concentrations, and 

variations in concentrations of nitrogen oxides has 

been reported elsewhere in detail. 2 '26 The 

information presented here is limited to data on 

ambient concentrations in urban and rural/remote 

atmospheres and is intended merely to 

complement the information on oxidant and 

oxidant pr.ecursor concentrations. 

Tables 5-4 and 5-5 include data on ambient NO 

and NO2 concentrations in seven urban centers 

outside California. 24 Data from selected California 

sites, where concentrations levels are generally 

higher, are shown in Tables 5-6 and 5-7. 2 Such 

data show a slight upward trend with time, as 

illustrated in Figure 5-4. 16 

Concentrations of NO and NO2 in rural and 

remote areas are extremely low, the average levels 

being at or below the limit of detectability for 

current monitoring instruments. Thus, early 

measurements of the NO2 background concentration showed levels generally below 5 

ppbaa,as More recent measurements of NO and 

NOz in rural areas in Ohio, Maryland, and 

Pennsylvania indicated NO and NO2 levels around 

5 ppb, with a few excursions to as high as 12 

ppb."'72Furthermore, it appears that the 

concentration of NOX in an urban air mass decays 

rapidly as the air mass moves away from the city. 

This is illustrated by ambient NOX data taken within 

and outside Dayton, Ohio. Such data showed the 

city core levels of NOX to range from 75 ppb to 450 

ppb, whereas the concentrations at a site 18 miles 

from the downtown area ranged only from 8 to 80 

ppb. » 

The extremely low levels of NO in the rural and 

remote areas or, alternativety, the lack of 

adequately sensitive analytical instruments, is a 

problem in that it limits the conclusiveness of the 

field studies on oxidant. Thus at present, it is not 

possible to establish reliably the levels of natural 

NOx and hence to estimate the relative 

contributions of the natural and manmade sources 

to rural NOX. This uncertainty, in view of the 

important role of the NO_ x factor in rural oxidant 

formation (see Chapter 4) makes it difficult to 

delineate completely and clearly the relative roles 

of anthropogenic hydrocarbon and NOx as 

precursors in the atmospheric oxidant/ozone 

formation process. 

SOURCES OF OXIDANT PRECURSORS 

Introduction 

Hydrocarbons and nitrogen oxides are emitted 

into the atmosphere from both natural and 

manmade sources, with the contribution of natural 

sources being the greater. However, the larger 

contribution by the natural sources does not 

significantly influence the oxidant problem, since 

the natural and anthropogenic emissions are 

geographically segregated, with the anthropogenic ones concentrated in the populated areas. 

Natural hydrocarbon emissions arise mostly from 

biological processes, trees, and localized sources 

such as seepage from natural gas and oil fields. Of 

the anthropogenic sources, combustion of fuels is 

71 
TABLE 5-4. FREaUENCY DISTRIBUTION DATA FOR 6-TO 9-a.m. NITRIC OXIDE CONCENTRATIONS AT CAMP SITES 

1962-72 24 

(ppm) 

Arithmetic Geometric 

Number Percentile' 

of Std Std 

S te Year samples Min. 10 20 30 40 50 60 70 80 90 Max Mean dev Mean dev 

San Francisco, 62° 112 0.00 0.00 0.00 0.01 0.01 0.02 0.02 0.03 0.04 0.06 0.13 0.02 0.02 0.02 2.51 

Calif. 63° 179 0.00 0.00 0.00 0.01 0.02 0.02 0.03 0.05 0.06 0.08 0.32 0.03 0.03 0.02 2.98 

(056860002A10) 64° 13 0.01 0.01 0.02 0.02 0.03 0.04 0.04 0.05 0.06 0.20 0.29 0.07 0.08 0.04 2.63 

Denver, Colo. 65b 223 0.00 0.01 0.02 0.03 0.03 0.04 0.05 0.06 0.08 0.11 0.31 0.05 0.04 0.04 2.14 

(060580002A10) 66 297 0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.08 0.11 0.15 0.30 0.06 0.06 0.05 2.61 

67° 191 0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.07 0.09 0.13 0.32 0.06 0.05 0.05 2.31 

68° 192 0 00 0.01 0.02 0.02 0.04 0.05 0.06 0.07 0.10 0.04 0.27 0.06 0.05 0.04 2.71 

69 285 0.00 0.01 0.02 0.03 0.04 0.05 0.07 0.0,9 0.12 0.16 0.45 0.07 0.07 0.05 2.76 

70° 252 0.00 0.02 0.03 0.04 0.06 0.07 0.09 0.11 0.13 0.16 0.42 0.08 0.06 0.06 2.52 

71 b 184 0.00 0.02 0.03 0.04 0.05 0.07 0.08 0.10 0.12 0.16 0.40 0.08 0.07 0.06 2.38 

72° 241 0.01 0.02 0.04 0.05 0.07 0.08 0.10 0.12 0.15 0.22 0.44 0.10 0.08 0.08 2.32 

Washington, D.C. 62 289 0.00 0.01 0.01 0.02 0.02 0.03 0.04 0.05 0.06 0.10 0.32 0.04 0.04 0.03 2.53 

(090020002A10) 63 279 0.00 0.00 0.01 0.02 0.02 0.04 0.05 0.06 0.08 0.13 0.40 0.06 0.06 0.04 2.82 

64 310 0.00 0.00 0.01 0.01 0.02 0.03 0.04 0.05 0.08 0.14 0.66 0.05 0.07 0.03 3.11 

65 274 0.00 0.00 0.01 0.02 0.02 0.03 0.04 0.06 0.08 0.12 0.38 0.05 0.06 0.03 2.83 

66 310 0.00 0.01 0.01 0.02 0.03 0.04 0.04 0.05 0.07 0.12 0.53 0.05 0.06 0.04 2.66 

67 304 0.00 0.01 0.02 0.03 0.04 005 0.06 008 0.10 0.16 074 0.07 0.08 0.05 2.74 

68' 270 0.00 0.01 0.02 0.03 0.03 004 0.05 0.06 0.08 0.13 0.49 0.06 0.06 0.04 2.56 

Washington, D.C. 69' 269 0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.07 0.08 0.14 0.62 0.07 0.08 0.05 2.73 

(090020003A10) 70 299 0.00 0.01 0.02 0.03 0.04 0.06 0.07 0.09 0.11 0.06 0.54 0.08 0.08 0.05 2.80 

71 308 0.00 0.01 0.02 0.03 0.04 0.04 0.05 0.07 0.09 0.13 0.54 0.06 0.06 0.04 2.52 

72° 219 0.00 0.00 0.02 0.03 0.04 0.06 0.08 0.11 0.13 0.15 0.41 0.08 0.08 0.05 3.10 

Chicago, III. 62 283 0.00 0.04 0.05 0.07 0.09 0.11 0.13 0.16 0.19 0.21 0.56 0.12 0.08 0.10 2.14 

(141220002A10) 63 315 0.00 0.04 0.06 0.08 0.09 0.11 0.12 0.13 0.16 0.20 0.38 0.11 006 0.10 1.99 

64 318 0.00 0.04 0.06 0.07 0.09 0.11 0.13 0.15 0.17 0.24 0.71 0.13 0.09 0.10 2.06 

65 317 0.00 0.04 0.06 0.08 0.10 0.12 0.13 0.15 0.17 0.21 0.430.12 0.07 0.11 1.98 

66 286 0.00 0.04 0.07 0.09 0.11 0.13 0.15 0.17 0.19 0.23 0.51 0.13 0.08 0.12 1.99 

67 311 0.00 0.03 0.05 0.07 0.08 0.10 0.12 0.13 0.15 0.18 0.43 0.10 0.06 0.09 2.16 

68 319 0.00 0.03 0.04 0.06 0.07 0.09 0.10 0.12 0.15 0.19 0.37 0.10 0.06 0.08 2.13 

69 318 0.01 0.04 0.06 0.09 0.10 0.13 0.15 0.18 0.21 0.26 1.02 0.15 0.11 0.12 2.03 

70 320 0.00 0.04 0.08 0.10 0.13 0.15 0.19 0.24 0.28 0.33 0.65 0.18 0.11 0.14 2.31 

71 ° 269 0.00 0.04 0.07 0.09 0.11 0.13 0.16 0.20 0.22 0.27 0.51 0.15 0.09 0.12 2.08 

72 321 0.01 0.04 0.07 0.10 0.13 0.15 0.18 0.21 0.24 0.29 053 0.16 0.09 0.13 2.10 

New Orleans, La. 62° 259 0.00 0.01 0.01 0.02 0.03 0.04 0.05 0.07 0.09 0.13 0.36 0.06 0.05 0.04 2.77 

(192020004A10) 63 325 0.00 0.00 0.00 0.01 0.01 0.01 0.02 0.02 0.03 0.04 0.24 0.02 0.12 0.02 2.45 

b1. Lows, Mo 64° 259 0.00 0.01 0.02 0.04 0.04 0.06 0.07 0.08 0.09 0.12 0.44 0.06 0.04 0.05 2.22 

(264280002A10) 65 333 0.00 0.00 0.01 0.01 0.02 0.03 0.04 0.05 0.06 008 0.19 0.04 0.03 0.03 2.70 

66 294 0.00 0.00 0.01 0.02 0.03 004 0.05 006 0.08 0.12 0.49 0.05 0.05 0.04 2.90 

67 326 0.00 0.01 0.01 0.02 0.03 0.04 0.05 0.07 0.08 0.11 0.26 0.05 0.04 0.04 2.68 

68° 256 0.00 0.01 0.01 0.02 0.03 0.04 0.05 0.06 0.08 0.11 0.28 0.05 0.04 0.04 2.80 

69 322 0.00 0.00 0.01 0.02 0.03 0.04 0.05 0.07 0.09 012 0.51 0.05 0.06 0.03 3.10 

70b 228 0.00 0.01 0.02 0.02 0.04 0.06 0.08 0.11 0.14 0.17 047 0.08 0.07 0.05 2.92 

71 311 0.000.01 0.02 0.03 0.05 0.16 0.08 0.10 0.12 0.15 0.36 0.07 0.06 0.06 2.47 

72° 234 0.00 0.01 0.02 0.03 0.05 0.07 0.10 0.12 0.14 0.19 0.40 0.09 0.07 0.06 2.48 

Cinclnnatl, Ohio 62 286 0.00 0.01 0.01 0.02 0.02 0.03 0.04 0.06 0.08 0.12 0.42 0.05 0.05 003 2.74 

(361220003A10) 63b 273 0.00 0.01 0.01 0.02 0.02 0.03 0.04 0.05 0.08 0.12 0.26 0.05 0.04 0.03 2.52 

64 334 0.00 0.01 0.01 0.01 0.02 0.03 0.04 0.05 0.09 0.13 0.45 0.05 0.07 0.03 2.90 

65 310 0.00 0.00 0.01 0.01 0.02 0.02 0.03 0.05 0.07 0.11 0.43 0.04 0.05 0.03 2.86 

66° 206 000 0.01 0.01 0.12 0.03 0.04 0.05 0.06 0.09 0.14 0.67 0.06 0.07 0.04 2.73 

67° 188 0.00 0.01 0.02 0.02 0.02 0.03 0.04 0.05 0.08 0.13 0.53 0.06 0.08 0.04 2.62 

68° 136 0.00 0.01 0.03 0.04 0.05 0.07 0.10 0.14 018 0.29 0.69 0.12 0.14 0.07 3.03 

69b 196 0.00 0.00 0.01 0.02 0.03 0.04 0.05 0.07 0.10 0.18 0.56 0.07 0.09 0.04 3.04 

70° 129 0.00 0.00 0.01 0.02 0.03 0.03 0.04 0.05 0.08 0.13 0.52 0.05 0.07 0.03 2.96 

71 ° 215 0.00 0.01 002 0.03 0.03 0.04 0.05 0.07 0.10 0.20 0.48 0.07 0.07 0.05 2.64 

72° 251 0.00 0.01 0.02 0.02 0.03 0.04 0.05 0.07 0.09 0.17 0.47 0.06 0.07 0.04 2.64 

IZ? 
TABLE 5-4 FREQUENCY DISTRIBUTION DATA FOR 6-TO 9-a.m. NITRIC OXIDE CONCENTRATIONS AT CAMP SITES, 

1962-72 26 (cont'd). 

(ppm) _ 

Site Year 

Number 

of 

samples 

Arithmetic 

Percentile' 

Std 

Min 10 20 30 40 50 60 70 80 90 Max Mean dev 

Geometric 

Std 

Mean dev 

Philadelphia, Pa. 62b 239 0.00 0.00 0.00 0.01 0.01 0.01 0.02 0.02 0.03 0.06 0.23 002 0.02 0.02 2.54 

63b 233 0.00 0.00 0.01 0.02 0.03 0.04 0.05 0.07 0.10 0.15 0.79 0.07 0.10 0.04 3.30 

64 302 0.00 0.01 0.02 0.03 0.03 0.04 006 0.07 0.10 0.14 0.42 0.06 0.06 0.05 2.61 

65 290 0.00 0.01 0.02 0.02 0.04 0.04 0.06 0.07 0.10 0.16 0.64 0.07 0.07 0.05 2.65 

66 336 0.00 0.01 0.02 0.03 0.04 0.05 0.06 0.08 0.10 016 0.79 0.07 0.08 0.05 2.50 

67 296 0.00 0.02 0.03 0.04 0.05 0.07 0.08 0.10 0.13 0.17 0.71 0.09 0.08 0.07 238 

68b 266 0.00 0.01 0.02 0.03 0.04 0.05 0.07 0.08 0.12 0.17 0.55 0.08 0.08 0.05 2.60 

69 276 0.00 0.01 0.12 0.03 0.04 0.05 0.06 007 0.09 0.12 0.38 0.06 0.05 0.05 2.48 

70 305 0.00 0.01 0.03 0.04 0.05 0.06 0.08 0.10 0.12 0.16 0.81 0.08 0.09 006 2.47 

71 278 0.00 0.01 0.02 0.02 0.03 0.04 0.05 007 0.09 0.13 0.42 0.06 0.06 0.04 2.78 

'Concentrations greater than or equal to specified value in indicated percentage of samples 

"1'early standard ezceeded 

TABLE 5-5. FREQUENCY DISTRIBI TION DATA FOR 6-TO 9-a.m. NITROGEN DIOXIDE CONCENTRATIONS 

AT CAMP SITES, 1962-72 20 

(ppm) 

Arithmetic Geometnc 

Number Percentile" 

of Std Std 

Site Year samples Min 10 20 30 40 50 60 70 80 90 Maz Mean dev Mean dev 

San Francisco, 62b 142 0.00 0.00 0.00 0.01 0.01 0.01 0.02 0.03 0.03 0.04 0.09 0.02 0.01 0.02 2.23 

Calif. 63b 155 0.00 0.01 0.02 0.02 0.03 0.03 0.04 0.04 0.04 0.06 0.19 0.03 002 0.03 1.80 

(056860002A10) 64° 10 0.0-7 0.01 0.02 0.03 0.04 0.04 0.04 0.04 0.05 0.05 0.06 0.04 0.01 0.04 1.54 

Denver, Colo. 65b 247 0.01 0.02 0.03 0.03 0.03 0.04 0.04 005 0.05 0.06 0.09 0.04 001 0.04 1 49 

(060580002A10) 66 324 0.00 0.02 0.03 0.03 0.03 0.04 0.04 0.04 0.05 0.05 0.10 0.04 0.01 0.04 1.47 

67b 180 0.00 0.02 0.02 0.03 0.03 004 0.04 0.04 0.05 0.06 0.09 0.04 0.01 0.04 1.57 

68b 226 0.00 0.02 0.02 0.03 0.03 0.04 0.04 005 0.05 0.06 0.11 0.04 0.01 0.04 1 64 

69 283 0.00 0.01 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.05 0.15 0.03 0.01 0.03 1.63 

70 282 0.00 0.02 0.02 0.03 0.03 0.04 0.04 005 0.05 0.07 0.13 0.04 0.02 0.04 1.76 

71 b 171 0.00 0.02 0.02 0.03 0.03 003 0.04 0.04 0.05 0.06 0.10 0.03 0.01 0.03 1.66 

72b 253 0.00 0.01 0.02 0.03 0.03 0.04 0.04 005 0.06 0.07 0.12 0.04 0.02 0.04 1.78 

Washington, D.C. 62 313 0.00 0.01 0.02 0.02 0.02 0.03 0.03 0.03 0.04 0.05 0.16 0.03 0.01 0.03 1.76 

(090020002A70) 63 312 0.00 0.01 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.06 0.13 0.03 0.02 0.03 1.75 

64 308 0.01 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.06 0.15 0.03 0.01 004 1.63 

65 336 0.00 0.02 0.02 003 0.03 0.03 0.03 0.04 0.05 0.05 0.18 0.03 0.01 0.03 1.55 

66 275 0.00 0.02 0.02 0.02 0.03 0.03 0.04 0.04 0.05 0.05 0.13 0.03 0.01 003 1.61 

67 305 0.00 0.02 0.02 0.03 0.03 0.04 0.04 0.05 0.05 0.06 0.14 0.04 0.02 0.04 1.65 

6R° 237 0.00 0.02 0.03 003 0.04 0.04 0.05 0.06 0.06 0.08 0.18 0.05 002 0.05 1 56 

Washington, D.C. 69b 254 0.00 0.02 0.02 0.03 0.03 0.04 0.04 0.04 0.05 0.06 0.11 0.04 0.01 0.04 1.56 

(090020003A10) 70 298 0.00 0.02 0.03 0.04 0.04 0.05 0.06 0.06 0.07 0.09 0.16 0.05 0.02 0.05 1.84 

71 318 0.01 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.04 0.05 0.11 003 0.01 0.04 1.50 

72b 214 0.00 0.00 0.02 003 0.03 0.04 0.04 0.05 006 0.09 0.40 0.05 0.06 0.04 2.55 

Chicago, III. 62 293 0.00 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.07 0.15 0.04 0.02 0.04 1 77 

(141220002A10) 63 318 0.00 0.02 0.03 0.03 003 0.03 0.04 0.04 0.05 0.06 0.11 0.04 0.01 0.04 1.49 

64 303 0.00 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.06 0.07 0.16 0.04 0.02 0.04 1.57 

65 330 0.01 0.02 0.03 0.03 0.03 0.04 0.04 0.04 0.05 0.06 0.11 0.04 0.01 0.04 1.43 

66 304 0.00 0.03 0.03 0.04 0.04 0.05 0.05 0.06 0.07 0.09 0.23 0.05 0.02 0.05 1.56 

67 290 0.00 0.02 0.03 0.03 0.04 0.04 0.05 0.05 0.06 0.07 0.17 0.04 0.02 0.04 1.62 

68 312 0.01 0.03 0.03 0.03 0.04 0.04 0.05 0.05 0.05 0.06 0.10 0.04 0.01 0.04 1.45 

69 330 0.00 0.03 0.03 0.03 0.04 0.04 0.05 0.05 0.06 0.07 0.17 0.04 0.02 0.05 1.51 

70 329 0.00 0.03 0.04 0.04 0.04 0.05 0.05 0.06 0.07 0.08 0.14 0.05 0.02 0.05 1.40 

71 285 0.02 0.03 0.03 0.04 0.04 0.04 0.05 0.06 0.07 0.08 0.39 0.06 0.05 0.05 1.67 

72 336 0.00 0.03 0.03 0.04 0.04 0.04 0.05 0.06 0.06 0.08 0.16 0.05 0.02 0.05 1.60 

New Orleans, La. 62 288 0.00 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.07 0.14 0.04 0.02 0.04 1.79 

(192020004A10) 63 289 0.00 0.00 0.01 0.01 0.01 0.01 0.02 0.02 0.02 0.03 0.05 0.01 0.00 0.02 1.86 

73 
TABLE 5-5. FREOUENCY DISTRIBUTION DATA FOR 6-TO 9-a.m. NITROGEN DIOXIDE CONCENTRATIONS 

AT CAMP SITES, 1962-72 24(cont'd). 

IPpml -- 

Site Year 

Number 

of 

samples 

Arnhmetic 

Percentile' 

Std 

Min 10 20 30 40 50 60 70 80 90 Max Mean dev 

Geometric 

Std 

Mean dev 

St. Louls, Mo. 64° 255 0.00 0.01 002 0.02 0.03 0.03 004 0.04 0.05 0.06 0.16 0.03 0.02 0.03 1.85 

(264280002A10) 65 348 0.00 0.01 0.01 0.01 0.02 0.02 0.02 0.02 0.03 0.04 0.08 0.02 0.01 0.02 1.80 

66 322 0.00 0.01 0.02 0.02 0.02 0.03 0.03 0.04 0.04 0.06 0.12 0.03 0.01 0.03 1.80 

67 352 0.00 0.01 0.01 0.01 0.02 0.02 0.02 0.03 0.03 0.03 0.06 0.02 0.01 0.02 1.83 

68 322 0.00 0.00 0.01 0.01 0.02 0.02 0.02 0.02 0.03 0.04 0.11 0.02 0.01 0.02 1.94 

69° 258 0.00 000 0.01 0.02 0.02 0.02 003 0.03 0.04 0.05 0.11 0.02 0.01 002 2.11 

70° 233 0.00 0.01 0.02 0.02 0.02 0.02 003 0.03 0.04 0.05 0.10 0.02 0.01 0.03 1.66 

71 309 0.00 0.02 0.02 0.02 0.02 0.03 003 0.04 005 0.06 0.11 0.03 0.01 0.03 1.61 

72° 231 0.01 0.02 002 0.03 0.03 0.04 0.05 006 0.07 0.08 0.16 0.04 002 004 1.66 

Cincinnatl, Ohlo 62 292 000 0.01 0.02 0.02 002 0.03 0.03 0.03 0.04 0.05 0.13 0.03 001 0.03 1.82 

(36122000A10) 63 304 • 0.00 0.01 0.02 0.02 0.02 0.03 0.03 0.03 0.04 0.05 0.13 0.03 0.01 0.03 1.71 

64 336 0.00 0.01 0.02 0.02 0.02 0.03 0.03 0.03 0.04 0.06 0.15 0.03 0.01 0.03 1.77 

65 313 0.01 002 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.11 0.03 0.01 0.03 1.45 

66° 238 0.00 002 0.02 0.02 0.03 0.03 0.04 0.04 0.05 0.06 0.10 0.03 0.01 0.03 1.69 

67° 223 0.00 0.01 0.02 0.02 0.02 0.03 003 0.03 0.03 0.04 0.09 0.02 0.01 0.03 1.52 

68 280 0.00 0.02 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.09 0.03 0.01 0.03 1.59 

69° 231 0.00 0.02 002 0.02 0.02 0.03 0.03 0.03 0.04 0.05 0.10 0.03 0.01 0.03 1.56 

70b 129 0.01 0.02 0.03 0.03 0.03 0.03 0.04 0.04 0.05 0.07 0.12 0.04 0.02 0.04 1.53 

71 ° 236 0.00 0.01 0.02 0.02 0.02 0.03 0.04 0.04 0.05 0.07 0.11 0.03 0.02 0.03 2.00 

72 b 227 000 0.02 0.03 0.03 0.04 0.04 0.04 0.05 0.05 0.06 0.13 0.04 0.01 0.04 1.64 

Phliadelphia, Pa 62° 211 0.00 0.00 0.01 0.01 0.02 0.02 0.02 0.03 0.03 0.04 0.10 0.02 0.01 0.02 1.56 

(397140002A10) 63 286 0.00 0.01 0.02 0.02 0.03 0.03 0.04 0.04 0.05 0.07 0.15 0.03 0.02 0.03 1.97 

64 281 0.00 0.02 0.02 0.03 0.03 0.03 0.04 0.04 0.05 0.07 0.20 0.04 0.02 0.04 1.72 

65 286 0.00 0.02 0 02 0.02 0.03 0.03 0.03 0.04 0.05 0.05 0.12 0.03 0.01 0.03 1.58 

66 340 0.00 0.02 0.02 0.02 0.03 0 03 0.04 0.04 0.05 0.06 0.11 0.03 0.01 0.03 1.66 

°Concentrations greater than or equal to specified value in indicated percentage of samples 

°Yearly standard exceeded 

by far the most important source of hydrocarbon 

and nitrogen oxide emissions. In addition, 

hydrocarbon and nonhydrocarbon organic 

emissions also arise from the use of such organics 

in the processing of raw materials. 

From a Qollution control standpoint, the 

distinction made between natural and manmade 

sources and the use that. is made of annual 

emission rate data are not entirely satisfactory. For 

example, anthropogenic emissions such as those 

from leaking fuel lines, home appliances, etc. 

cannot be subjected to systematic control because 

of their accidental nature. Thus from a control 

standpoint, such emissions may be considered to 

be natural. To generalize, classification of sources 

and emissions as controllable and uncontrollable 

may be more appropriate than the distinction now 

in use. Also, emission rate data reflecting annual 

or even daily averages are inadequate in that they 

mask seasonal and diurnal variations in emission 

rates. Considering that only the morning-to-noon 

emissions in the summer-to-fall season are of 

main photochemical consequence, it is evident 

that ignoring the seasonal and diurnal variations in 

emission rates does not permit equitable 

assessment of the various emission sources. 

The sections that follow deal with the main 

anthropogenic and natural emissions; emission 

rate data are presented in the form in which they 

are available-mostly as daily and yearly averages. 

74 
TABLE 5-6. NITRIC OXIDE CONCENTRATI014 e1N CALIFORNIA BY AVERAGING TIME AND FREnUENCY, 

1963-67z 

Ippml 

Place, site no , Maximum for year Percentile° 

averaging 

time 63 64 65 66 67 001 01 1 10 30 50 70 90 

Anaheim-176: 

1 hr 0.29 0.30 0.70 0.40 0.66 0.62 0.40 0.22 0.07 003 0.01 0.00 0.00 

8 hr 0.18 0.19 0.29 0.24 0.41 - 0.28 0.18 0.07 0.03 0.02 0.01 0.00 

1 day 0.11 0.09 0.17 0.15 0.18 - - 0.12 0.06 0.03 0.02 0.01 0.00 

1 mo 0.05 0.04 0.05 0.04 0.07 - - - 0.06 0.04 0.02 0.02 0.01 

1 yr 0.02 - - 0.02 0.04 - - - - - 0.02 - - 

Oakland-327: 

1 hr 0.93 0.93 0.66 0.68 0.91 0.92 0.70 0.41 0.15 005 0.02 0.01 0.00 

8 hr 0.57 0.60 0.34 0.34 0.52 - 0.55 0.32 0.14 0.05 0.03 0.01 0.00 

1 day 033 0.35 0.26 0.26 0.30 - - 0.26 0.13 0.06 0.03 0.02 0.01 

1 mo 0.02 0.14 0.11 0.13 0.11 - - - 0.11 0.07 0.04 0.02 0.02 

1 yr - 0.07 0.05 0.05 0.05 - - - - - 0.05 - - 

Riverside-126: 

1 hr - 1.10 0.57 0.43 0.52 0.74 0.47 0.29 0.11 0.04 0.02 0.01 0.00 

8 hr - 0.59 0.36 0.26 0.26 - 0.38 0.21 0.10 0.04 0.02 0.01 0.00 

1 day - 0.11 0.10 0.08 0.08 - - 0.18 0.09 005 0.03 0.01 0.00 

1 yr - - 0.04 0.04 0.04 - - - - - 0.04 - - 

Sacramento-276: 

1 hr 1.08 1.08 0.97 0.75 0.90 0.97 0.70 0.37 0.09 0.03 0.02 0.00 0.00 

8 hr 0.60 0.53 0.62 0.49 0.58 - 0.54 0.29 009 0.03 0.02 0.01 0.00 

1 day 0.35 0.26 0.28 0.23 0.33 - - 0.22 0.09 0.04 0.02 0.01 0.00 

1 mo 0.14 0.09 0.10 0.07 0.07 - - - 0.07 0.05 0.03 0.01 0.01 

1 yr 0.04 0.04 0.03 0.04 0.03 - - - - - 0.04 - - 

San Bernardino-151: 

1 hr 0.25 0.25 0.34 0.50 0.36 0.47 0.32 0.15 0.05 0.02 0.01 0.00 0.00 

8 hr 0.12 0.12 0.16 0.26 0.15 - 0.25 0.12 0.05 0.02 0.01 0.01 0.00 

1 day 0.06 0.06 0.10 0.20 0.11 - - 0.09 0.05 0.03 0.02 0.01 0.00 

1 mo 0.03 0.02 0.04 0.07 005 - - - -0.04 0.03 0.02 0.01 0.00 

1 yr 0.01 - - - 0.03 - - - - - 0.03 - - 

San Diego-101: 

1 hr 0.74 1.10 0.90 1.20 0.80 1.00 0.65 0.38 0.10 0.02 0.01 0.00 0.00 

8 hr 0.45 0.63 0.43 0.42 0.34 - 0.42 0.26 0.10 0.03 0.01 0.00 0.00 

1 day 0.24 0.21 0.23 0.26 0.22 - - 020 0.10 0.04 0.01 0.00 0.00 

1 mo 0.14 0.08 0.09 0.12 0.10 - - - 009 0.05 0.02 0.01 0.00 

1 yr 0.04 0.02 0.03 0.05 0.04 - - - - - 0.04 - - 

Stockton-252: 

1 hr 0.38 0.50 0.48 0.87 0.36 0.68 0.47 0.27 0.08 0.02 0.01 0.00 0.00 

8 hr 0.18 0.29 0.33 0.50 0.16 - 0.39 0.23 0.07 0.02 0.01 0.00 0.00 

1 day 0.14 0.15 0.23 0.26 0.09 - - 0.19 0.07 0.03 0.01 0.01 0.00 

1 mo 0.04 0.06 0.11 0.11 0.02 - - - 0.06 0.03 0.02 0.01 0.00 

1 yr - 0.03 0.03 0.03 0.01 - - - - - 0.03 - - 

'Determined by continuous Griess-Saltzman method 

'Concentrations greater than or equal to speciffed value in indicated percentage of samples 

75 
TABLE 5-7. NITROGEN DIOXIDE CONCENTRATIONa IN CALIFORNIA BY AVERAGING TIME AND FREQUENCY, 

1963-67 

(ppm) 

Place, site no, Maximum for year Percentile° 

averaging 

time 63 64 65 66 67 001 01 1 10 30 50 70 90 

Anaheim-176: 

1 hr 0.20 0.22 0.23 0.27 0.27 0.25 0.21 0.15 0.07 0.05 0.03 0.02 001 

8 hr 0.15 0.13 0.16 0.15 0.19 - 0.18 0.13 0.07 004 0.03 002 0.01 

1 day 0.11 0.11 0.13 0.12 0.13 - - 0.10 0.06 0.04 0.03 0.02 0.01 

1 mo 0.06 0.04 0.05 0.05 0.07 - - - 0.06 0.05 0.04 0.03 002 

1 yr 0.03 - - 0.04 0.04 - - - - - 0.04 - - 

Oakland-327• 

1 hr 0.28 0.41 0.23 0.29 0.33 0.33 0.23 0.14 0.07 0.04 0.03 0.02 0.01 

8 hr 0.19 0.25 0.15 0.18 023 - 0.20 0.13 0.06 0.04 0.03 0.02 0.01 

1 day 0.10 0.16 0.10 0.13 0.15 - - 0.10 0.06 004 0.03 0.02 0.02 

1 mo 0.05 0.05 0.06 0.05 0.06 - - - 0.05 0.04 0.03 0.03 0.02 

1 yr 0.03 003 0.03 0.03 0.04 - - - - - 0.03 - - 

Riverside-126 

1 hr 0.27 0.56 0.49 025 0.31 0.49 0.32 0.18 0.09 0.05 0.03 0.02 0.01 

8 hr 0.18 026 0.31 0.18 0.23 - 0.29 0.15 0.08 005 0.04 0.02 001 

1 day 0.14 0.19 0.25 0.13 017 - - 0.14 0.07 0.05 0.04 0.03 0.02 

1 mo 0.06 005 0.08 0.05 0.05 - - - 0.05 005 0.04 0.04 0.03 

1 yr - 0.04 0.05 0.04 0.04 - - - - - 0.04 - - 

Sacramento-276. 

1 hr 0.29 0.32 0.30 0.27 0.30 0.30 0.22 0.14 0.07 0.04 0.03 0.02 0.01 

8 hr 0.17 0.21 020 0.21 0.20 - 0.19 0.12 0.06 0.04 0.03 0.02 0.01 

1 day 0.13 013 0.13 0.15 0.13 - - 0.11 0.06 0.04 0.03 0.02 0.02 

1 mo 007 0.07 0.07 0.05 005 - - - 0.05 0.04 0.03 0.03 0.02 

1 yr 0.04 0.04 0.04 0.03 0.04 - - - - - 0.04 - - 

San Bernardlno-151. 

1 hr 0.14 0.06 0 1 1 0.25 0.22 0.23 0.19 0.13 0.07 004 002 0.01 0.00 

8 hr 0.12 0.03 007 0.14 0.17 - 0.16 0.12 0.06 0.04 002 0.01 0.00 

1 day 0.06 0.02 0.05 0.11 0.13 - - 0.10 0.06 0.04 003 0.01 000 

1 mo 0.03 - 0.03 0.06 0.07 - - - 0.05 0.04 0.03 0.01 000 

1 yr 0.01 - - 0.04 0.05 - - - - - 004 - - 

San Dlego-101: 

1 hr 0.33 0.35 0.52 0.40 0.34 0.35 0.22 0.12 0.06 0.03 0.01 0.00 0.00 

8 hr 018 015 0.22 0.19 017 - '0.18 0.11 0.06 0.03 0.02 0.01 0.00 

1 day 012 0.09 0.12 0.12 008 - - 0.09 0.05 0.03 0.02 0.01 0.00 

1 mo 006 0.06 0.04 0.06 0.03 - - - 0.04 0.03 0.02 0.01 0.01 

1 yr 0.03 0.02 0.02 0.03 0.02 - - - - - 0.02 - - 

Stockton-252 - 

1 hr 0.13 0.22 0.14 0.16 0.18 0.20 0.16 0.09 0.04 0.02 0.02 0.01 001 

8 hr 0.08 0.15 0.11 0.11 010 - 0.12 0.07 0.04 0.03 0.02 001 0.01 

1 day 0.06 0.08 008 0.07 0.06 - - 0.06 0.04 0.03 0.02 0.02 0.01 

1 mo 0.02 0.05 0.03 0.03 0.03 - - - 0.03 0.02 0.02 0.02 0.01 

1 yr - 0.03 0.02 0.02 0.02 - - - - - 0.02 - - 

"Determined by continuous Griess-Saltzman method 

'Concentration greater than or equal to specified value in indicated percentage of samples 

76 
50 

40 

30 

£ 

L 

a 

X 0 

Z 20 

10 

0 

1963 

~ \ 

~ / ~' \\ ~o~ 

/ — 

~~~/ \~~.~ ft.~ ~ 

~--~~ MAX-HOUR AVERAGES - ALL DAYS OF YEAR 

MAX-HOUR AVERAGES - JULY, AUG., SEPT. 

6-to-9-a.m. AVERAGES- JULY, AUG., SEPT. 

1964 1965 1966 1967 1968 1969 1970 1971 1972 

YEAR 

Figure 5-4. Oxides of nitrogen trends in Los -Angeles, 1963- 1972, 6-to-9-a.m. and maximum 1-hr average 

concentratio n s. ' 6 

Summary of Organic Emissions Data 

A summary of several estimates of the total 

hydrocarbon emissions from mobile, stationary, 

and natural sources within the United States is 

presented in Tables 5-8 and 5-9. 84 The differences 

between estimates are due primarilyto differences 

in calculation techniques, data sources, and 

underlying assumptions. Most investigators agree 

that emission estimates are improving as more is 

learned about sources and measurement 

techniques, and that the more recent estimates in 

Tables 5-8 and 5-9 are probably more reliable than 

earlier ones. 

TABLE 5-9. TOTAL YEARLY HYDROCARBON EMISSION 

RATE FOR THE CONTINENTAL UNITED STATES, BASED 

ON LEAF BIOMASS80 

Item Emissions, 10 6 tons/yr 

Summer (5 months) 52.4 

Vegetation emissions 482 

Leaf litter emissions 4.2 

Winter (7 months) 34.9 

Vegetatton emissions 34.9 

Leaf litter emissions —0 

Total yearly emissions from 

vegetation and leaf litter 87.3 

Total year emissions from 

anthropogenic sources 21.2 

Natural emissions as percent of total 

emissions from all sources 80% 

TABLE 5-8. ESTIMATES OF TOTAL HYDROCARBON 

EMISSIONS FROM MANMADE AND 

NATURAL SOURCES 

Estimate, 10' metric tons/yr 

1972 1912 MSA°8 197263 197283 197383 19748] 

Source type Rasmussen Research Corp. NEDS NADB NADB NADB 

Mobile ND ND 14.8 12.8 12:5 11.6 

Stationary ND 23.1 10.2 15.1 15.5 15.5 

Natural 2.3' ND ND ND ND ND 

°Emissions from tree fol,age only (see J Air Poll. Contr Assoc 22•537-543,1972) 

More detailed hydrocarbon emission inventories 

for the United States and hydrocarbon emission 

trends in 1970-75 are presented in Tables 5-10 

and 5-11. 83Information presented in Tables 5-10 

and 5-11 was taken from the EPA Data File of 

Nationwide Emissions 63,66 and has been validated 

recently. The data in Tables 5-10 and 5-11 should 

not be compared with previously published data on 

1970-75 emissions. 

77 
TABLE 5-10. 1974 NATIONWIDE ESTIMATES OF TOTAL 

HYDROCARBON SOURCES AND EMISSIONS 66 

Emissions, 10 6 metric tons/yr 

Source category 1974 1975 lorehnnarvl 

Transportation (lotal) (1 1 3) (10 6) 

Highway 9.8 91 

Non-highway 1.5 1 5 

Stationary fuel combustlon (total) (1.6) (1 3) 

Electric utilltles 0.1 0 1 

Other 1.5 1 2 

Industrial processes (total) (3.3) (3 2) 

Chemicals 1.6 1 5 

Petroleum reflning 0.8 08 

Metals 0.2 02 

Others 07 07 

Solld waste (total) (.9) ( 8) 

Miscellaneous (total) (12 7) (12 2) 

Forest wlldflres 0.5 05 

Forest-managed burning 0.2 02 

Agricultural burning 0.1 0.1 

Coal refuse burning 01 01 

Structural fires 0.0 <0 1 

Organlc solvents 8.1 7.5 

Oli and gas production and 

marketing 3.7 38 

Total 29.8 280 

TABLE 5-11. NATIONWIDE TOTAL 1fYDROCARBON 

EMISSION TRENDS, 1970-75" 

Year Emission, 10 6 metric tons/yr _ 

1970 30.7 

1971 30.2 

1972 30.9 

1973 30.8 

1974 298 

1975 28.0 

Table 5-12 presents a more detailed breakdown 

of hydrocarbon emissions from mobile sources 

than is given in either Table 5-10 or 5-11. Data for 

this table were obtained from the EPA Data File of 

Nationwide Emissions. 66 The table indicates the 

relatively large contribution that gasoline-fueled 

light vehicles make to total hydrocarbon emissions 

from mobile sources. Of course, it must be 

recognized that hydrocarbon emissions from lightduty, gasoline-fueled vehicles have been reduced 

since 1974, and the exhaust emission rate has 

decreasec; oy about 70 percent 6 5 Evaporative and 

crankcase emissions have remained essentially 

unchanged during this period. It is difficult to 

estimate national emission levels because of the 

uncertainties associated with vehicle populations, 

miles driven, and deterioration of emission control 

systems. But from the model developed by 

Heywood and Martin, a net decrease of about 28 

percent has been projected for aggregate 

hydrocarbon emissions from automobiles during 

the 1972-77 period. 38 Tables 5-13 and 5-14 give 

organic emission and reactive-organic emission 

inventories for the Los Angeles Air Quality Control 

Region. 81 

TABLE 5-12. HYDROCARBON EMISSIONS FROM 

MOBILE SOURCES 83 

Emissions, 

Source category 10s metric tons/yr % of total 

Land vehicles (total): 

Gasollne-fueled (total) (10.11) (89.23) 

Llght vehicles 8.41 74.23 

Heavy vehlcles 1.26 11.12 

Off-hlghway 0.44 3.88 

Dlesel-fueled (total) (0.46) (4.06) 

Heavy vehlcles 0.15 1.32 

Off-highway 0.13 1.15 

Rall 0.18 1 59 

Aircraft (total) (0 33) (2.91) 

Mllitary 0.22 1.94 

Clvil 0.04 0.35 

Commercial 0.07 0.62 

Vessels (total) (0.43) (3.79) 

Coal <0.01 <0.01 

Diesel 0.02 0.18 

Gasoline 0.41 3.61 

Total 11.33 - 

Hydrocarbon Emissions from Natural Sources 

The major natural sources that have been 

identified and for which quantitative estimates are 

available are the biologic decomposition of organic 

matter, seepage from natural gas and oil fields, and 

emission of volatile compounds from plants. 

However, there is information in the literature that 

indicates that there are many other natural 

sources of hydrocarbons and oxygenates that have 

not been considered heretofore. This section 

discusses the major natural sources for which 

quantitative estimates are available and indicates 

some of thP minor sources that have been 

identified. 

Methane is produced in the anaerobic bacterial 

decomposition of organic matter in swamps, lakes, 

marshes, paddy fields, etc. Koyama 46 has 

estimated the global production of inethane as 2.7 

x 10 14 g/year (300 million tons/year) on the basis 

of his measurements of inethane fermentation in 

various soils and lake sediments under controlled 

experimental conditions. Robinson and Robbins 74 

have estimated the production from swamps and 

humid tropical areas and added it to Koyama's 

figure to derive an estimate of inethane production 

of 14.5 x 1014 g/year (1.6 billion tons/year). Other 

sources of inethane are gas, oil, and coal fields. 5 

The seepage of natural gas from these areas has 

78 
been determined by Ehhalt, 33 through carbon-14 

measurements, to contribute as much as 25 

percent to the total atmospheric methane. The 

remaining 75 percent is of recent biogenic origin. 

Our understanding of the natural sources of 

methane is still highly limited. As a result, current 

estimates of global production remain speculative. 

Plants release a variety of volatile organic 

substances, including ethylene, isoprene, apinene, and a variety of other terpenes. 

Rasmussen 68 and Rasmussen and Went70 

measured and reported ambient concentrations of 

volatile plant organics (such as isoprene, a- and /3- 

pinene, limonene, and myrcene) in air at remote 

sites. From the average concentration of 10 ppb 

that they measured, a global production rate of 

volatile plant organics was estimated to be 438 

million tons/year. From the available estimates of 

methane and terpene emissions, it is estimated 

that worldwide natural hydrocarbon emissions are 

TABLE 5-13. ORGANIC EMISSION INVENTORY FOR THE METROPOLITAN LOS ANGELES 

AIR nUALITY CONTROL REGION, 1972 81 

Weight emissions Molar emiss_ions_ _ 

Average 

Tons/ Weight % 10 ' ton moles/ Mole % molecular 

Source category day of total day of total weight 

Stationary sources: Organic fuels and combustion 

Petroleum production and refining: 

Petroleum production 62 2.3 214 5.9 29 

Petroleum refining 50 1 9 54 1.5 93 

Gasollne marketing: 

Underground servlce statlon tanks 48 1.8 83 2.3 58 

Auto tank filling 104 4.0 141 3.9 74 

Fuel combustion 23 0.9 92 2.5 25 

Waste burning and fires 41 1.6 124 3.4 33 

Statlonary sources: Organic chemicals 

Surface coating• 

Heat treated 14 05 17 0.5 82 

Aly dried 129 50 148 4.1 87 

Dry cleaning: 

Petroleum-based solvent 16 0.6 13 0.4 126 

Synthetic solvent (PCE) 25 1 0 15 0.4 166 

Degreasing: 

TCE solvent 11 04 8 0.2 132 

1,1,1-T solvent 95 3.6 71 2.0 134 

Printing: 

Rotogravure 31 1 2 38 1.0 82 

Flexigraphic 15 06 26 0.7 57 

Industrial process sources. 

Rubber and plastic manufacturing 42 1 6 58 1.6 73 

Pharmaceutical manufacturing 16 06 21 0.6 75 

Mlscellaneous operations 83 3 2 104 2.9 80 

Mobile sources: 

Gasoline-powered vehicles: 

Llght duty vehicles. 

Exhaust emisslons 780 300 1130 31.2 69 

Evaporative emissions 481 185 529 146 91 

Heavy duty vehlcles: 

Exhaust emisslons 285 109 413 11.4 69 

Evaporative emissions 67 2 6 74 2.0 91 

Other ga,oline-powered equlpment: 

Exhaust emissions 110 4.2 159 4.4 69 

Evaporative emisslons 22 0.8 24 0.7 91 

Dlesel-powered motor vehlcles 12 05 13 04 89 

Aircraft: 

Jet 20 0.8 17 0.5 121 

Plston 22 0 9 39 1.1 56 

Total of weighted average 2604 100 3625 100 71.9 

79 
Moblle sources 

Gasollne-powered vehicles: 

Llght duty vehlcles: 

Exhaust emissions 

Evaporative emisslons 

Heavy duty vehlcles• 

Exhaust emisslons 

Evaporative emisslons 

Other gasoline-powered equipment. 

Exhaust emisslons 

Evaporative emisslons 

Dlesel-powered motor vehlcles 

Alrcraft 

780 30.0 562 562 562 32.1 33.9 34.2 

481 18.5 362 293 293 19.8 17.7 17.9 

285 10.9 205 205 205 11.7 12.3 12.5 

67 2.6 48 41 41 2.7 2.5 2.5 

110 4.2 79 79 79 4.5 4.8 4.8 

22 0.8 16 13 13 0.9 0.8 0.8 

12 0.5 8 9 9 0.5 0.5 0.5 

Jet 20 0.8 10 10 10 0.6 0.6 0.6 

Plston 22 0.9 18 20 20 1.0 1.2 1.2 

Total 2604 100 1749 1660 1641 100 100 100 

about 2 billion tons/year. However, there is 

evidence that many other volatile organics are 

emitted from natural sources into the atmosphere. 

These may be only trace amounts emitted on a 

local scale, but the total worldwide production can 

be very large. 

Annual hydrocarbon emissions from natural 

sources in the United States can be estimated from 

the preceding information. If the natural emission 

of inethane is uniform in all land areas, Robinson 

and Robbins'74 estimate of the worldwide emission 

of inethane (1.6 billion tons/year) can be used to 

calculate a U.S. emission of 100 million tons/year. 

The assumption that natural methane is emitted 

TABLE 5-14. REACTIVE EMISSION INVENTORIES FOR THE METROPOLITAN LOS ANGELES 

AIR OUALITY CONTROL REGIONa' 

Source category 

Total 

emissions 

Tons/ % of 

day total 

Reactive emissions 

Reactive tons/day' 

2-group° 5-group° 6-group° 2-group 

scheme scheme scheme scheme 

% of total 

5-group 

scheme 

6-group 

scheme 

Stationary sources. Organic fuels 

and combustion• 

Petroleum productlon and reflning: 

Petroleum productlon 62 2.3 24 28 18 1.4 1.7 1.1 

Petroleum reflning 50 1.9 33 27 27 1.9 1.6 1.6 

Gasoline marketing: 

Underground servlce 

statlon tanks 48 1.8 47 40 40 2.7 2.4 2.4 

Auto tank fllling 104 4.0 94 76 77 5.4 4.6 4.7 

Fuel combustlon 23 0.9 6 13 8 0.3 0.8 05 

Waste burning and flres 41 1.6 22 32 27 1.3 1.9 1.6 

Statlonary sources Organlc chemlcals: 

Surface coating: 

Heat treated 14 0.5 9 8 8 0.5 0.5 0.5 

Air drled 129 5.0 88 71 71 5.0 4.3 4.3 

Dry cleaning: 

Petroleum based solvent 16 0.6 9 6 6 0.5 0.4 0.4 

Synthetic solvent (PCE) 25 1.0 0 1 1 0.0 0.1 0.1 

Degreasing. ~ 

TCE solvent 11. 0.4 6 5 5 0.3 0.3 0.3 

1,1,1-T solvent 95 3.6 0 5 5 0.0 0.3 0.3 

Printing: 

Rotogravure 31 1.2 21 16 16 1.2 1.0 1.0 

Flexlgrapluc 15 0.6 15 14 14 0.8 0.8 08 

Industrlal process sources: 

Rubber and plastic manufacturing 42 1 6 33 39 39 1.9 2.3 2.4 

Pharmaceutical manufacturing 16 06 10 9 9 0.6 0.5 0.5 

Mlscellaneous operatlons 83 3.2 40 38 38 2.3 2.5 2.3 

'To convert to reactive ton moles per day, multiply by 0 0145 

° For reactivity definition, see reference 42 

80 
uniformly from all land areas is probably in error, 

since emission rates are higher in tropical than in 

nontropical areas. More realistically, assuming 

that the U.S. methane emission rate per unit of 

land area is half the world average, the U.S. natural 

methane emission would be 50 million tons/year. 

Similarly, if the estimate of Rasmussen and Went 70 

of worldwide terpene emission (438 million 

tons/year) is based on uniform distribution over 

the forested areas of the world, the U.S. emission 

would be 22 million tons/year. Emission of 

ethylene from plants in the United States has been 

estimated at 20,000 tons/year.' By combining 

these estimates, a natural hydrocarbon emission 

in the United States of about 72 million tons/year 

is obtained. 

Hydrocarbon Emissions from Anthropogenic 

Sources 

MOBILE SOURCES 

As indicated in Table 5-13, light-duty, gasolinefueled motor vehicles accou nt for a vast majority of 

the hydrocarbons emitted into the environment 

from mobile sources. There are three primary 

sources of hydrocarbon emissions from the motor 

vehicle: crankcase ventilation, gasoline 

evaporation, and combustion exhaust. Crankcase 

blowby emissi( ns were essentially eliminated by 

means of the positive crankcase ventilation system 

introduced in ' ~ 963; evaporative emissions were 

reduced by eaout 30 percent by means of 

adsorption-regoneration systems introduced in 

1971. 65 Exha st hydrocarbon emissions have 

been reduced ;by about 90 percent in new vehicles 

since 1968 wit) a variety of engine modifications, 

and most re cently with the application of 

oxidation -cataI,rst systems. Although the true 

reductions in emissions are somewhat less than 

these figures because of control device 

deterioration, it is reasonable, nevertheless, to 

believe that the current and the more advanced 

controls of the future will effect a further reduction 

in motor vehicle aggregate hydrocarbon emissions 

through the middle to late 1980's. 38 Vehicle 

population growth and miles traveled will become 

the controlling factors subsequent to that time. 

The patterns of hydrocarbon emissions from 

motor vehicles, as well as their mass, are 

dependent on a large number of factors. Driving 

patterns, emission - control system deterioration, 

ambient temperature, pressure, humidity, and the 

type of fuel used are all significant factors."'SB.a' 

The relative contributions of evaporative gasoline 

emissions and combustion exhaust in the 

aggregate are also important. Therefore, it is very 

difficult to speak in absolute terms about the 

relative abundances of hydrocarbon types in 

vehicle emissions. However, trends in emissions 

can be discussed with reasonable authority. 

Historically, combustion exhaust dominated the 

hydrocarbon emissions from automobiles, and its 

pattern was typical of atmospheric hydrocarbons 

from motor vehicle sources. The advances in 

emission controls, however, have changed this 

situation. The automobile manufacturers have 

been very successful in controlling exhaust 

hydrocarbons. Since the 1975 model year, 

evaporative hydrocarbons have constitU+ed the 

major fraction of the hydrocarbon aggregate from 

new automobiles. 65 It has been estimated that for a 

typical 1975 passenger car, evaporative gasoline 

accounts for about 60 percent of the total 

aggregate emissions, and combustion exhaust, 40 

percent.s 5 

The pattern of exhaust hydrocarbons has 

changed with the use of oxidation catalysts. Most 

catalytic control systems show greater activity for 

unsaturated hydrocarbons than saturated. They 

show very little activity for methane. 13''" Thus the 

relative abundance of paraffinic hydrocarbons in 

the exhaust has increased with recent generation 

automobiles. Typically, exhaust from a catalystequipped automobile would contain about 62 

percent paraffinic hydrocarbon, 17 percent 

aromatic hydrocarbon, 18 percent olefinic 

hydrocarbon, and 3 percent acetylenic 

hydrocarbon, as compared with 40, 24, 26 and 11 

percent, respectively, for noncatalytically equipped 

automobiles. The methane levels generally range 

from about 10 to 30 percent. Evaporative gasoline 

is also dominated by paraffinic hydrocarbons, with 

the Ca-Cs paraffins typically accounting for about 

70 percent of the total. 5s,as 

Thus, the trend in hydrocarbon emissions from 

passenger cars is toward an increased relative 

abundance of paraffinic hydrocarbons. 12 The 

oxidation-catalyst exhaust emission control device 

has generally resulted in an increased relative 

abundance of inethane and a decreased relative 

abundance of unsaturated hydrocarbons, 

particularly notable in the olefinic and acetylenic 

hydrocarbons. Evaporative gasoline has become a 

more significant fraction of the total aggregate of 

motor vehicle hydrocarbon emissions. 

Besides hydrocarbons, exhaust gdses contain 

oxygenated hydrocarbon compounds such as 

aidehydes, ketones, alcohols, ethers, esters, acids, 

and phenols. The total oxygenate concentration is 

81 
about 5 to 10 percent of the total hydrocarbon 

concentration. Aldehydes are generally believed to 

be the most important class of exhaust oxygenates. 

A reasonably complete quantitative analysis of 

exhaust aidehydes is possible with gaschromatographic techniques. Formaldehyde is by far 

the predominant aidehyde, constituting about 60 

to 70 percent of the total (on a volume basis); 

acetaldehyde is next, at about 10 percent; and propionaldehyde, acrolein, benzaldehyde, and the 

toluaidehydes are all found in appreciable 

amounts. As might be expected, the nature of the 

gasoline influences the aldehydes formed. 12,3a,sa, 

86,89 

There is little published information on 

noncarbonyl oxygenates such as ethers, alcohols, 

epoxides, and peroxides, but Seizinger and 

Dimitriades 75 ''s measured 10 aldehydes, 6 

ketones, and 16 noncarbonyl oxygenates in 

exhaust from 22 different simple fuels, each 

containing 1, 2, or 3 hydrocarbons. They developed 

formulas from their data that can be used to 

calculate the estimated concentrations of 

oxygenate in gasoline exhaust. 

The composition of organic emissions from the 

other mobile sources (diesels, aircraft, etc.) is not 

well defined. Diesel exhaust organics consist of a 

light fraction, in the C,-C arange, and a heavy 

fraction (C8-C22), with the relative amounts of the 

two fractions varying with engine load and speed 

(see Figure 5-1). 39 Several diesel exhaust organics 

have been identified in the course of researching 

diesel exhaust odor. 18 Such organics include 

indans, indenes, naphthalenes, and tetralins, as 

well as high molecular weight carbonyl and other 

oxygenated compounds. Exhaust organics from 

aircraft consist primarily of organics in the Ce-C22 

range (see Figure 5-2). 79 

There is little doubt that organic emissions from 

gasoline-powered mobile sources are oxidant 

producers almost in their totality. Emissions from 

diesels and aircraft will participate in gas-phase 

reactions only partly. A substantial part of such 

emissions is expected to condense on surfaces, 

thus contributing significantly, perhaps, to 

visibility reduct'ion. 

STATIONARY SOURCES 

A detailed description of the various stationary 

sources of organic emissions, including emission 

rate data, can be found in a recent National 

Academy of Sciences report. 61 Major constituents 

of the emissions associated with fuel combustion 

are organic acids, followed by hydrocarbons and 

aidehydes. 61 Such composition is entirely different 

from the combustion-related emissions from 

mobile sources in which hydrocarbons are the 

major constituent and organic acids are negligible. 

Industrial processes discharge a variety of organic 

compounds in the atmosphere, including Ca-Cs 

hydrocarbons from refineries and aromatic 

hydrocarbons and acid derivatives, aldehydes, 

alcohols, and phenols from chemical processing 

operations. Solvent evaporation from painting, 

coating, drycleaning, printing, etc., result in 

substantial levels of emissions consisting mainly 

of petroleum naphtha. Forestfires, structuralfires, 

and agricultural burning result in emissions that 

are difficult to characterize and nearly impossible 

to measure. Finaily, gasofine marketing 

operations, (i.e. storage, transportation, and 

service station handling of gasoiine) result in 

emissions consisting primarily of Ca-Cs 

hydrocarbons and secondarily of whole gasoline 

vapors. The relative importance of the stationary 

source emissions, in terms both of amounts and 

oxidant-producing potential, is illustrated by the 

Los Angeles data shown in Tables 5-13 and 5-14.a' 

Emissions of Nitrogen Oxides 

The distribution of nitrogen oxide (NOx) 

emissions by major source categories is indicated 

in Table 5-15. 63 Data shown in this table have been 

validated recently and are therefore more reliable 

than previously reported data on 1974 NO,, 

emissions. Fuel combustion is the major cause of 

technology-associated emissions. In 1974, 

combustion of coal, oil, natural gas, and motorvehicle fuel accounted for more than 22 of an 

estimated 23 million tons of manmade NOx in the 

United States. An estimated 9.6 million tons was 

emitted from transportation sources, 7.4 million 

tons of which was from motor vehicles. Industrial 

processes, solid waste disposal, and other 

miscellaneous sources accounted for about 1 

million tons of NOX. 

Relatively small quantities of NOx are emitted 

from noncombustion industrial processes, mainly 

the manufacturing and use of nitric acid. 52 Even 

though total quantities may be sma11, high 

concentrations of NOX can be emitted from some of 

these chemical processes. Electroplating, 

engraving, welding, metal cleaning, and explosive 

detonation also can be responsible for industriai 

NOX emissions, as can the maufacture and use of 

liquid-NO2-based rocket propellants. 

82 
TABLE 5-15. 1974 NATIONWIDE ESTIMATES OF 

NITROGEN OXIDE SOURCES AND EMISSIONS 63 

Source category Emission, 106 metric tons/yr 

Transportation (total) (9.6) 

Highway 7.4 

Nonhighway 2.2 

Stationary fuel combustion (total) (12.1) 

Electric utilities 6.3 

Other 5.8 

Industrial processes (total) (0.6) 

Chemicals 0.3 

Petroleum refining 0.3 

Other <0.1 

Solid waste (total) (0.2) 

Miscellaneous (0.2) 

Forest wildfires 0.1 

Forest-managed burning <0.1 

Agricultural burning <0.1 

Coal refuse burning 01 

Structural fires <0.1 

Total 22.7 

Natural sources of nitrogen oxide emissions 

include biological processes in soil, atmospheric 

oxidation of ammonia (NHs), and, possibly, 

photolysis of NO2. Estimates of NO ), emission rates 

from natural sources vary considerably among 

investigators. Robinson and Robbins 73 estirriated 

the annual NOX emissions from biological 

processes to be 770 million metric tons (as NO2), 

compared to 52 million metrictonsfrom manmade 

sources. Other investigators question the 

importance of the biological processes, and they 

offer the oxidation of NH3 resulting in 230 million 

tons of NOx per year, as the main source. 54 As in 

the case of the hydrocarbon emissions, the natural 

sources of NOx seem to dominate the anthropogenic ones. But again, as in the hydrocarbon 

case, this dominance has no significant relevance 

to the ambient oxidant probtem or even to the 

ambient NO2 problem, since the natural and 

anthropogenic emissions are, for the most part, 

segregated geographically, with the anthropogenic ones concentrated in the populated areas. 

REACTIVITY OF ORGANIC EMISSIONS 

From an air pollution standpoint, the 

photochemical reactivity of an organic pollutant 

denotes the intrinsic ability of the pollutant to 

participate in atmospheric chemical reactions that 

result in photochemical smog formation. The 

concept of hydrocarbon reactivity (the term 

"hydrocarbon" is meant here to encompass all 

organic substances) was developed when 

laboratory research showed that different organic 

substances, when exposed to atmospheric 

conditions, did not react similarly. Specifically, 

when traces of an individual organic and NO in air 

were irradiated with artificial sunlight, the 

resulting levels of smog, in terms of oxidant/ozone 

yield, eye irritation, plant damage, visibility 

reduction, etc., were found to vary widely with the 

chemical structure of the organic reactant. As a 

result of these studies, the concept of hydrocarbon 

reactivity has evolved to include several reactivity 

types, each type corresponding to a specific 

chemical-biological manifestation of photochemical smog.sThe reactivitytype of interest here 

is the one associated with the oxidant/ozone yield. 

The fact that organic substances differ greatly in 

reactivity is extremely significant in understanding 

the photochemical oxidant/ozone-forming 

process. Such reactivity data are presently 

available. The data and the methods used for 

obtaining them are discussed next. 

The procedure commonly used for reactivity 

measurements is to irradiate clean air mixed with 

the organic vapor, NO, and NO2 at prescribed 

concentrations in a smog chamber and to measure 

the formation of oxidant/ozone. Experimental 

conditions for such measurements are, to the 

extent feasible and practical, similar to the 

conditions typically present in polluted ambient 

atmospheres. Thus the reactant concentrations, 

the intensity and spectral characteristics of 

radiation, the temperature, and often the relative 

humidity are comparable to actual conditions in 

the real atmosphere during the summer. Because 

the concern traditionally has been for the oxidant 

problems observed in urban areas, nearly all of the 

reactivity data presently available were obtained 

under experimental conditions simulating urban 

atmospheres, and, more specifically, the Los 

Angeles atmosphere. Recent developments, 

however, led to recognition of two distinct 

atmospheric situations (to be referred to here as 

the urban, or no-transport, situation and the rural, 

or transport, situation) for which an organic may 

manifest different reactivitieS. 27 The terms 

"urban" or "no-transport" are used to designate 

the situation in which emissions react for a few 

hours and cause oxidant problems inthevicinityof 

their sources. Conversely, in the rural or transport 

situation, emissions undergo extensive transport 

and prolonged photochemical reaction and cause 

oxidant/ozone buildup in distant downwind areas, 

which may be rural or urban. Again, nearly all of 

the reactivity data currently available are 

applicable to the no-transport situation only; there 

83 
are very few measurements of reactivity under 

simulated transport conditions. 

The scientific evidence detailing the impact that 

the reactivity of the organic emissions has on air 

quality within the area of the sources and in the 

areas far downwind is examined in the following 

discussion. Scientific evidence pertinent to these 

questions does exist 25 and is presented next, first 

for the urban or no-transport situation, and then 

for the rural or transport case. 

Reactivity data obtained through 1965, all 

applicable to the urban situation, were compiled by 

Altshuller3 and presented in terms of a reactivity 

classification of hydrocarbons and aldehydes, as 

shown in Table 5-16. Since 1965, several reactivity studies have been reported, including 

detailed reactivity data on hydrocarbon and 

nonhydrocarbon organics. These studies and the 

types of reactivity data reported are tisted inTable 

5-17. 

TABLE 5-16. COMPARISON OF REACTIVITIES OF DIFFERENT TYPES OF ORGANICS 3 

Reactivity on 0 to 10 scale 

Peroxy- Eye 

Substances or Ozone or acyl- Formal- irnta- Plant Overall 

subclass oxidant nitrate dehyde Aerosol , ion damage .eactivity 

C,-C3 paraffins 0 0 0 0 0 0 0 

Acetylene 0 0 0 0 0 0 0 

Benzene 0 0 0 0 0 0 0 

C41 paraffinsa 0-4 0° 0° 0 0° 0 1 

Toluene (and other monoalkylbenzenes) 4 ND` 2 2 4 0-3 3 

Ethylene 6 0 6 1-2 5 +b 4 

1-alkenes° 6-10 4-6 7-10 4-8 4-8 6-8 7 

Dloleflns 6-8 0-2 8-10 10 10 0° 6 

Dlalkyl- and trialkyl-benzenes 6-10 5-10 2-4 +e 4-8 5-10 6 

Internally double-bonded olefins 5-10 8-10 4-6 6-10 4-8 10 8 

Allphatic aldehydes 5-10 +e +' ND` +e +" 

'Averaged over straight-chain and branched-chain paraffins 

'Very small yields or effects may occur after long irradiations 

`No experimental data available 

'Includes measurements on propylene through 1-hexene, 3-ethyl-l-butene and 2,4,4-trimethyl-1-1-pentene 

'Effea noted experimentally, but data insufficient to quannfy 

TABLE 5-17. REACTIVITY DATA 

Investigator Data reported 

Altshuller and Bufalinl 7 Reactivity data on hydrocarbons and aldehydes. 

Brunelle et aI 15 Reactivity data for solvent organlcs. 

Dimltrlades et a1. 31 Reactivity data for hydrocarbons and aldehydes. 

Dimltrlades et a{. 31 Rate of NOz formation and product yield reactivity data for hydrocarbons. 

Dlmltriades and Wesson 32 Rate of NOz formation and product yield reactivity data for aldehydes. 

(Bureau of Mines) 

Heuss, J. 36 Reactivity data on hydrocarbons. 

Heuss and Glasson37 Eye trritation, rate of NOz formation, and product yield reactivity data 

(General Motors) for hydrocarbons. 

Laity et a1. 47 Reactivity data for solvent organics. 

(Shell) 

Levy and Mlller4e Reactivity data for solvent organics. 

(Battelle) 

McReynolds et a1. 56 Reactivity data for hydrocarbon disappearance. 

Mlller et a1. 57 Aerosol activity data for hydrocarbons. 

Wllson and DoyleBe Reactivlty data for solvent organics. 

(Stanford Research Inst.) 

Yanaglhara et a1. 90 Reactivlty data for solvent organics. 

Of these studies, however, only a few included 

systematic testing of a variety of organic 

compounds. The data from these main studies, 

summarized in Table 5-18, were used by EPA to 

classify .organics into three reactivity classes, 

shown in Tables 5-18 and 5-19. The data in Table 

5-18 show that organics do differ widely in 

reactivity. 

84 
TABLE 5-18. SUMMARY OF DATA FROM STUDIES ON REACTIVITIES (TOLUENE EOUIVALENTS) AND 

CLASSIFICATION OF ORGANICS 

Organic Japan EA' BOM' GM' Battelle' Shell" Class 

Paraffinic hydrocarbons: 

Ct-C3 paraffins 0-0.1 0-0.2 I 

C.. paraffins -- 

Cycloparaffins 0.1-0.7 0.1 0.5-0.6(0.06)° 0.4-0.6 0.8-1.0 II 

Olefinic hydrocarbons 1.6-2.3 1.6-2.5 0.9-2.0 1.3-1.5 1.8-3.1 III 

Aromatic hydrocarbons: 

Benzene ~ 0 0 0.2 0 0.2 1 

Primary and secondary monoalkylbenzenes 0.9 0.8-1.0 0.6-1.0 0.9-1.0 1.0-1.2 III 

Tert-monoalkylbenzenes 0.4 0.6 0 5 II 

Dialkylbenzenes 1.4-2.0 1.4-1.5 0.9-1.3 1.0-1.2 1.3-1.7 III 

Tri-, tetraalkylbenzenes 1.7 1.5 1.5 3.2 III 

Styrene 0.7 I I I 

Me-styrene` 1.5 III 

Aldehydes: 

Allphatic aldehydes 1.5-2.0 III 

Benzaidehyde 0.1 I 

o-Tolualdehyde 0.4 II 

m,p-Tolualdehyde 0.2 II 

Ketones: 

Acetone 0 0 0.1 I 

Me-et-ketone ° 0.1 0.6 0.9 I 

n- Alkylketones 0.5-0.8 1.4 II 

Branched alkylketones 1.4 1.0-1 .8 1.3 III 

Cyclic ketones 0.35 0.2 0.5-0.6 II 

Unsaturated ketones 1.5-1 .7 III 

Alcohols: 

Methanol 0 I 

Ethanol 0 1.0 II 

Isopropanol 0.1 0.2 0.6 1 

Primary and secondary 0.7-1.0 III 

C,,s alcohols 

Tertiary alkyl alcohols 0.3 1 

Diacetone alcohol 1.4 III 

Ethers: 

Diethyl ether 2.5 III 

Tetrahydrofuran 1.9 1.4 111 

Ethyl cellosolves 1.9, 1.5 III 

Esters: 

Methyl acetate 0 

Primary, secondary alkyl 0.1 0.2 0.8-1.0 II 

C2+ acetates 

Tertiary alkyl acetates 0.5 II 

Phenyl acetate 0 I 

Methyl benzoate 0 I 

Amines: 

Ethyl amines 0.1-0.2 I 

N-Me-pyrrolidone 0.7 III 

N,N-dlmethyl-formamide 0.2 1 

N,N-dimethyl-acetamide 0.9 II 

N itroa Ika nes: 

2-Nitropropane 0.2 0.7 II 

Halocarbons: 

Perhalogenated hydocarbons 0.1 I 

Partlally halogenated paraffins I 

Partlally halogenated olefins 0.5 III 

Halogenated benzenes 0-0.2 I 

'Japan EA = Japan EnvironmentAgency, BOM = Bureau of Mines, U S Dept of Interior, GM = General Motors Corp, Battelle = Battelle Memorial Institute 

Laboratories-Columbus, Shell = Shell Oil Co 

°Values were obtained from two different GM studies in which test conditione were different. 

`Me = methyl, et = ethyl 

85 
TABLE 5-19. CLASSIFICATION OF ORGANICS WITH RESPECT TO THEIR OXIDANT-RELATED 

REACTIVITY IN URBAN ATMOSPHERES 

Class I Class II Class III 

(low reactivity) (moderate reactivity) (high reactivity) 

C,-C3 parafflns a Tert-monoalkyl benzenes Prlm., sec. monoalkyl benzenes 

Acetylenea Cycllc ketones Dlalkyl benzenes 

Benzene Tolualdehydes Styrene 

Benzaldehyde a Tert-alkyl acetates a N-Methyl pyrrolidone 

Acetone a 2-Nltropropane 8 Partlally halogenated 

Methanol Ca1 parafflns, cyclo- oleflns 

Isopropanol parafflnsa Allphatic olefins 

Tert-alkyl alcohols a Ethanol Tri-, tetra-alkyl 

Methyl acetate a Prlm , sec C z , alkyl benzene 

Methyl benzoate N, N-dlmethyl acetamlde a Methyl styrene 

Ethyl amines e n-alkyl C51-ketones a Branched alkyl ketones 

N, N-dlmethyl Unsaturated ketones 

formamlde a Allphatic aldehydes 

Perhalogenated Diacetone alcohol 

hydrocarbons Ethersa 

Partlally halogenated 2-Ethoxy-ethanol 

parafflns 

Mono, dlchlorobenzenes 

Methyl-ethyl-ketone 

'Currentiv classified as not photochemically reactive under Los Angeles County Rule 66 and similiar regulations 

For a practical application of these differing 

reactivities, it is necessary that the photochemical 

behavior of an organic pollutant mixture be 

consistent with the behavior of the individual 

components. This requirement was explored in 

smog chamber studies, and overall results, 

although not always conclusive, were positive. For 

example, for an ethane/butane/propylene/NO X 

mixture at the organic-to-NO X ratio of 10:1, 

removal of the extremely reactive propylene 

resulted in less smog, which is consistent with the 

individual component reactivities. At a ratio of 

20:1, however, removal of propylene had no 

effect. 9,44 Smog chamber data on solvent mixtures 

also showed that less smog was formed when less 

reactive solvents were substituted for more 

reactive ones. 29 For the more complex automotive 

exhaust mixtures, the values for the maxirlium 1- 

hr oxidant observed in the smog chamber did not 

correlate well with the reactivity values computed 

from exhaust composition and individual 

component reactivity data, as shown in Figure 5- 

5. 31 Such lack of correlation, however, was 

attributed primarily to misidentification of exhaust 

components and to the inappropriateness of the 

linear simulation method for calcu.lating mixture 

reactivities. 31 

Overall, the smog chamber data suggest that the 

relatively low organic-to-NOx ratios encountered 

in typical no-transport atmospheres will probably 

result in lower reactivity. In the real atmosphere, 

oxidant formation is expected to be different from 

that suggested by the chamber data because the 

main effect of a reduction in reactivity of the 

organic reactant is a delay in oxidant formation. 

This delay, in turn, means that the daily oxidant 

maximum will not be eliminated but, will rather be 

shifted some distance downwind. Thus the main 

result to be expected from reduced reactivity is a 

reduction in the peak oxidant concentration that 

results from the additional dispersion associated 

with the time delay. Of course, if the oxidant 

accumulation is delayed sufficiently, (i.e., until late 

afternoon), then such accumulation will not occur 

for lack of radiation. Note, however, that in this 

latter case, a greater part of the organic precursor 

will escape the photochemical process during the 

first solar day and will be transported downwind 

where, if sufficient NOX is also present, itwill react 

to form oxidant/ozone. This case is discussed 

further in a subsequent section of this chapter. 

The preceding discussion dealt with the urban or 

no-transport situation. Analogous evidence on 

reactivities of organics and on mixture behavior for 

the rural or transport situation is very scant; 

therefore, possible answers presented here will 

have to be surmised for the most part. 

Reactivities of organics under simulated 

transport conditions have not been measured 

systemically as they have in the case of notransport. Nevertheless, from the limited direct 

data available z9,3s and from current knowledge of 

the oxidant formation mechanism, it has been 

established that under transport conditions, the 

effective range of reactivities is more narrow than 

for the no-transport case. Therefore, and on this 

86 
W 0.3 

cc 

O 

2 

30.2 

~ 

X 

Q 

f 

00.1 

w 

H 

Q 

J 

~ 

U J 0 

Q 

U 

N 1.0 

H 

z 

W 

J 

Q 

~ 0.9 

~ 

c w 

w 

z 

ul 0.8 

} 

a 

O 

cc 

a 

: 0.7 

w 

J 

Q 

U 

N 

w 0.6 

z 

2 

LL 

O 

n 0.5 

Q 

w 

~ 

~ 

m 

} 0.4 

~ 

> 

~ L) 

LEAST-SQUARES CORRELATION LINE 

CORRELATION COEFFICIENT = 0.34 

0.1 0.2 0.3 0.4 0.5 0.6 0.7 

OBSERVED MAXIMUM 0 3 REACTIVITY, PROPYLENE EQUIVALENTS 

Figure 5-5. Correlation of observed and calculated maximum 03 reactivities. 31 

• • 

T• 

basis alone, the impact of emission substitution on 

air quality well downwind from the sources should 

be less than the impact within the source area. 

The evidence and reasoning discussed in the 

preceding paragraphs do not preclude the 

existence of organics that are so slightly reactive 

that they could be of almost no concern at all 

insofar as the oxidant problem is concerned. 

Evidence directly addressed to this possibility is 

neither adequate nor easy to obtain. One approach 

to identifying such organics has been offered by 

EPA recently29 and is based on the use of smog 

chambers. Briefly, the method entails smog 

chamber testing of organics under a variety of 

reactant concentrations (but within a realistic 

range), organic-to-NO X ratio, and prolonged 

irradiation conditions. Truly nonreactive organics 

are proposed to be defined as those that, when 

tested in an appropriate smog chamber do not yield 

more'than 160Ng/m 3 (0.08 ppm) ozone under any 

set of test conditions. An alternative method 

proposed by Chang and Weinstock 20 is based on 

the use of a photochemical model to predict the 

role and impact of less reactive organics in 

transport atmospheres. The two methods were 

critically examined by Calvert and Jeffries," and 

their relative merits and limitations were 

discussed. One problem with the chamber method 

87 
arises from the presence of chamber wall effects. 

Such effects create problems; first, because they 

cause reactivity manifestations that, when 

extremely unreactive organics are tested, are 

comparable to or even stronger than those caused 

by the test reactant mixture; and second, because 

they are not well understood. Thus, though chamber reactivities of the various organics are probably 

reliable in a relative sense, their absolute values 

are somewhat questionable. This latter weakness 

also affects the chamber-determined reactivity 

level that separates reactive organics from those of 

no concern insofar as the oxidant problem is 

concerned. 

The modeling method of Chang and Weinstock20 

also has weaknesses because of the questionable 

chemical mechanism and kinetic data used by the 

authors. Furthermore, because such models are 

derived theoretically, and because their validation 

is based mainly on comparison with smog chamber 

data, their predictions cannot be much more valid 

than those obtained by the smog chamber method. 

Finally, this modeling method has very Iimited 

utility, since photochemical models exist only for 

those very few organics for which the atmospheric 

photo-oxidation mechanism has been elucidated. 

The key problem here is to identify the boundary 

organic that separates the reactive organics from 

the nonreactive ones. Solving this probtem would 

probably require application of both the chamber 

method and modeling techniques. The chamber 

method would be used to determine the relative 

reactivities of organics, and photochemical 

modeling would be used to predict the absolute 

reactivity of the boundary organic. Because the 

chamber data suggest that propane may be a 

reasonable candidate for the boundary position, 29 

and because the mechanism of the atmospheric 

photo-oxidation of propane is relatively well 

established, it might be advisable to estimate the 

oxidant-forming potential of propane using the 

modeling method. 

As an alternative to smog chamber measurement, Pitts et a1.67 suggested thatthe rate constant 

for the reaction between the OH-radical and an 

organic be used as a measure of the reactivity of 

the organic. Such rate constants have been 

measured for over 100 hydrocarbon and nonhydrocarbon organics, and with exceptions, their 

relative values roughly parallel the relative 

reactivity values obtained by the smog chamber 

method. Relative to the smog chamber reactivities, 

these rate constant reactivities are superior in 

some respects but inferior in others. For example, 

they are more reliable measures of reactivity in the 

cases of extremely unreactive organics, and 

therefore they provide better bases for identifying 

such organics. On the other hand, this rate 

constant is not a direct measure of the organic's 

ability to produce oxidant/ozone; therefore, it has 

only limited validity." 

In summary, the use of the concept of reactivity 

is ~ generally accepted as sound `because organic 

emissions do differ widely in reactivity. Additional 

research should be done to provide more reliable 

bases for identifying those organic emissions that 

are of no concern insofar as the oxidant problem is 

concerned. 

SUMMARY 

Organic pollutants in urban atmospheres 

consist mainly of hydrocarbons emitted by 

automobiles and from fuel evaporation, and of 

oxygenated hydrocarbonsfrom manufacturing and 

the use of organic chemicals. In urban atmospheres, 

the ambient total organic concentrations, reported 

usually as 6- to 9-a.m. averages of total nonmethane hydrocarbons (NMHC), range typically 

around 1 ppm and can be as high as 10 ppm or even 

higher (e.g., in Los Angeles). In rural and remote 

atmospheres, the composition and concentrations 

of organic pollutants are considerably more 

uncertain, mainly because of deficiencies in the 

analytical methods available for the con- 

'centrations involved. Overall, the evidence 

suggests that natural NMHC levels are generally 

less than 0.1 ppm, a fraction of which consists of 

vegetation-related terpenes. 

Concentrations of NO,, in urban atmospheres 

vary within a wide range, with highest values 

exceeding 1 ppm. Such concentrations appear to 

decline rapidly as the urban air moves away from 

the city. In ruGal and remote areas, ambient 

concentrations do not exceed a few ppb and 

therefore are often belowthe 5-ppb detection limit 

of current commercial NO, analyzers. 

Hydrocarbons and NOx are emitted into the 

atmosphere from both natural and manmade 

sources, with the natural contribution being the 

greater. This greater contribution, however, does 

not inftuence oxidant/ozone formation, because 

the sources of natural and anthropogenic emissions are spatially segregated, with anthropogenic ones concentrated in the populated areas. At 

present, mobile sources account for a major part of 

the organic emissions in most urban centers. 

88 
Ongoing controls of mobile source emissions have 

reduced levels and changed the composition of 

emissions in favor of the paraffinic component. 

Organic emissions differwidely in reactivity(i.e., 

in their abilityto produce photochemical ozone and 

other oxidants). Thus some organics probably do 

not contribute to photochemical smog formation. 

More research is needed to provide reliable bases 

for identifying those organics that have no bearing 

on the axidant/ozone problem. 

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of Atmospheric Hydrocarbons State of California, Air 

Resources Board, Sacramento, Calif March 1975. 

54 McConnell, J. C, and M B. McElroy. Odd nitrogen in the 

atmosphere. J Atmos. Sci. 30:1465-1480, 1973. 

55 McEwen, D. J The analysis of gasoline vapors from 

automotive fuel tanks Paper presented at the 153rd 

National Meeting of the American Chemical Society, 

Miami Beach, Florida, April 1967 

56. McReynolds, L A., H. E. Alquist, and D B. Wimmer 

Hydrocarbon emisslons and reactivity as functlons of fuel 

and engine variables. SAE Trans. 74:902-91 1, 1966. 

57. Miller, D. F., A. Levy, and W. E. Wilson, Jr A Study of 

Motor Fuel Composition Effects on Aerosol Formation 

Part II. Aerosol Reactivity Study of Hydrocarbons. API 

Project EF-2, Battelle Memorial Institute Laboratories, 

Columbus, Ohio, February 21, 1972. 

58. Morris, W. E, and K. T. Dishart. Influence of vehicle 

emission control systems in the relationship between 

gasoline and vehicle exhaust hydrocarbon composition 

/n. Effect of Automotive Emission Requirements on 

Gasoline Characteristics. ASTM Special Technical Publ. 

90 
No 487, Amencan Society for Testing and Materials, 73. Robinson, E., and R. C Robbins. Gaseous nitrogen 

59. 

60 

61 

62.

63.

64.

65 

66 

67 

72 

Philadelphia, Pa , 1971. pp. 63-101. compound pollutants from urban and natural sources J. 

MSA Research Corp. Hydrocarbon Pollutant System Air Pollut Control Assoc. 20303-306, 1970. 

Study Volume I Publication No APTD-1499, U.S 74. Robinson, E, and R C Robbins. Sources, Abundarce, 

Environmental Protection Agency, Research Triangle and Fate of Gaseous Atmospheric Pollutants SRI Project 

Park, N.0 , 1972. PR-6755, Stanford Research Institute, Menlo Park, Calif , 

National Air Pollution Control Administration. Air Quality 1968. 

Criteria for Hydrocarbons. NAPCAPublication No AP-64, 75. Seizinger, D. E, and B. Dimitriades. Oxygenates in 

U S Department of Health, Education and Welfare, Automotive Exhausts. Effect of an Oxidation Catalyst 

Public Health Service, Washington, D.C., March 1970 Report of Investigations RI 7837. U.S. Department of the 

National Research Council Vapor-Phase Organic Interior, Bureau of Mines, Washington, D.C, 1973. 

Pollutants National Academy of Sciences, Washington, 76 Seizinger, D E, and B Dimitriades Oxygenates in 

D C, 1975 exhaust from simple hydrocarbon fuels J. Air Pollut. 

Neligan, R. E Hydrocarbons in the Los Angeles Control Assoc. 22.47-51, 1972. 

atmosphere A comparison between the hydrocarbons in 77 Spicer, C W, J L Gemma, D. W Joseph, P R. Sticksel, 

automobile exhaust and those found in the Los Angeles and G F Ward. The Transport of Oxidant Beyond Urban 

atmosphere Arch Environ. Health 5•581-591, 1962. Areas. EPA-600/3-76-018a, U S. Environmental ProOAQPS Data File of Nationwide Emissions U.S. tection Agency, Research Triangle Park, N.C., February 

Environmental Protection Agency, Office of Air Quality 1976 

Planning and Standards, Research Triangle Park, N C., 78 Stephens, E. R., and R F. Burleson. Distribution of light 

August 1976. (These reports are standard computer hydrocarbons in ambient air. Presented at 62nd Annual 

reports available from the National Air Data Branch, Meeting, Air Pollution Control Association, Nee^j York, 

Monitoring and Data Analysis Division, OAQPS ) June 22-26, 1969. 

Oberdofer, P E The determination of aldehydes in 79 Stephens, E R, E. F Darley, and F. R. Burleson Sources 

automobile exhaust gases SAE Tech. Pap No 670123, and reactivity of light hydrocarbons in ambient air Proc. 

Society of Automotive Engineers, Inc., New York, 1967 Div Refin Am Pet Inst 47•466-483, 1967 

Office of Air Quality Planning and Standards 80. Tannahill, G K The hydrocarbon/ozone relationship in 

Compilation of Air Pollutant Emission Factors. Part B. Texas /n: Specialty Conference On: Ozone/Oxidants— 

Third Edition AP-42, U S Environmental Protection Interactions with the Total Environment. Air Pollution 

Agency, Research Triangle Park, N C., February 1976 Control Association, Pittsburgh, Pa , 1976 pp. 26-37 

Office of Air QualityPlanning and Standards NationalAir 81 Trilonis, J. C, and K W Arledge Utility of Reactivity 

Quality and Emissions Trends Report, 1975 EPA-450/1- Criteria in Organic Emission Control Strategies. 

76-002, U S Environmental Protection Agency, Application to the Los Angeles Atmosphere EPA-600/3- 

Research Triangle Park, N C., November 1976 76-091, U S Environmental Protection Agency, 

Pitts, J N, Jr, , A M Winer, K R Darnall, A C. Lloyd, and Research Triangle Park, N C, August 1976 

G J Doyle Hydrocarbon reactivity and the role of 82. Trijonis, J, T Peng, G. McRae, and L Lees. Oxidant and 

hydrocarbons, oxides of nitrogen, and aged smog in the precursor trends in the metropolitan Los Angeles region. 

production of photochemical oxidants /n International /n International Conference on Photochemical Oxidant 

Conference on Photochemical Oxidant Pollution and Its Pollution and Its Control. Proceedings. Vol.11 B. Dimitriades, 

Control. Proceedings Vol II B Dimitriades, ed EPA- ed. EPA - 600 / 3-77-001 b, U.S. Environmental Protection 

600/3-77-001 b, U.S Environmental Protection Agency, Agency, Research Triangle Park, N. C., January, 1977. pp. 

Research Triangle Park, N.0 , January 1977 pp 687- 1077- 1093. 

704 83 Wade, D T. Factors influencing vehicle evaporative 

Rasmussen, R A Terpenes Their Analysis and Fate in emissions SAE Trans 76 (sect 2) 811-823, 1968 

the Atmosphere Ph.D Thesis, Washington University, 84 Westberg, H Review and analysis. /n. International 

St Louis, Mo , 1964 Conference on Oxidants, 1976—Analysis of Evidence 

Rasmussen, R A, R B Chatfield, M W Holdren, and E and Viewpoints Part IV The Issue of Natural Organic 

Robinson Technical Report on Hydrocarbon Levels in a Emissions EPA-600/3-77-116, U S Environmental 

Midwest Open-Forested Area Submitted to Coordination Protection Agency, Research Triangle Park, N.0 , October 

Research Council Washington State University, College 1977 

of Engineering, Pullman, Wash , October 1976 85 Whitehead, L W, and R Severs Background 

Rasmussen, R A., end F W Went. Volatile organic hydrocarbon levels in east Texas, Presented at the 83rd 

material of plant origin in the atmosphere Proc Natl Annual National Meeting, American Institute of 

Acad Sci. U S.A 53 215-220, 1965 Chemical Engineers, Houston, Texas, March 1977 Paper 

Research Triangle Institute. Investigation of High Ozone No 21A 

Concentration in the Vicinity of Garrett County, Maryland 86. Wigg, E. E, R J Campion, and W L Petersen. The effect 

and Preston County, West Virginia EPA-R4-73-019, U.S. of fuel hydrocarbon composition on exhausthydrocarbon 

Environmental Protection Agency, Research Triangle and oxygenate emissions SAE Tech Pap No 720251, 

Park, N C., January 1973 Society of Automotive Engineers, Automotive Engineers, 

Research Triangle Institute Investigation of Rural Inc., Warrendale, Pa , 1972 

Oxidant Levels as Related to Urban Hydrocarbon Control 87 Williams, M. E, J T. Whtte, L A Platte, and C J Domke 

Strategies EPA-450/3-75-036, U.S Environmental Automobile Exhaust Emission Surveillance—Analysis of 

Protection Agency, Research Triangle Park, N.0 , March the FY 72 Program EPA-460/2-74-001, U S. 

1975 

68 

69 

70 

71 

91 
Environmental Protection Agency, Ann Arbor, Mich , 

February 1974. 

88 Wilson, K. W, and G. J Doyle Investigation of 

Photochemical Reactivities of Organic Solvents APTD1232, U.S. Department of Health, Education and Welfare, 

Public Health Service, Cincinnati, Ohio, September 1970. 

89. Wodkowski, C S., and E E Weaver. The effects of engine 

parameters, fuel composition, and control devices on 

aldehyde exhaust emissions Presented at the Meeting of 

the West Coast Section, Air PolVution Control 

Association, San Francisco, Calif, October 1970. 

90. Yanagihara, S., I. Shimada, E. Shinoyama, F. Chisaka, 

K.Saito, and T.Ishii. Photochemical Reactivities of Organic 

Solvents. Environment Agency, Tokyo, Japan. Undated. 

[oYa 
6. RELATIONSHIPS BETWEEN AMBIENT OXIDANTS AND 

PRECURSOR EMISSIONS 

INTRODUCTION 

This chapter examines the functional relationships observed or theoretically derived 

between photochemical oxidants (OX), including 

ozone (03), and the two classes of oxidant 

precursors, hydrocarbons (HC) and nitrogen oxides 

(NOX). These 0,/HC/NOx relationships are 

extremely important in that they constitute the 

basis of the methods for predicting impacts of 

emissions on air quality. 

Since it is now well established that the impact 

of emissions is not confined solely and entirely 

within the emission source area, it is necessary to 

consider emission distributions and related 

processes that affect the requisite Ox/HC/NOx 

relationship. One concept used to clarify this 

geographic distinction of the emissions effects is 

the source-receptor relationship, that is, the 

spatial and temporal relationship between the area 

and time of emission discharge and the 

corresponding area and time of oxidant oc-- 

currence. Thus the requisite Ox/HC/NOx 

relationship(s) must be applicable to the sourcereceptor relationship encountered in the real 

atmosphere. 

Additional demands on the O,/HC/NOx 

relationships are posed by considerations of utility 

rather than validity. For example, it would be useful 

to have valid Ox/HC/NOx relationships for smallscale applications such as the prediction of 

localized impact from addition or deletion of an 

emission source within an urban area. 

AII of these requirements must be met by the 

O,/HC/NOx relationships if such relationships are 

to serve their purposes ideally. In reality, however, 

such ideal validity and utility are unattainable for 

various reasons. Two of the most important 

reasons are (1) it is extremely difficult to pinpoint 

the areas of the specific emission sources that are 

responsible for the oxidant problem observed in a 

given locality, and (2) the proposed Ox/HC/NOx 

relationships cannot be validated ideally or directly 

(i.e., by using real atmosphere data without 

substantial uncertainty). These reasons led to the 

adoption of the following two premises: first, 

perfectly accurate relationships will never be 

obtained; and second, the development of usable 

Ox/HC/NOx relationships will have to be pursued 

in the form of an iterative process in which 

judgment developed from and during the use of 

less accurate relationships is fed back into the 

development of improved ones. 

Consistent with these premises, relationships 

between oxidant/ozone-related air quality and 

emissions have been pursued following three 

distinct approaches that differ mainly in degree of 

empiricism. In order of decreasing empiricism, 

these approaches are as follows: 

1. Empirical Approach. This approach entails 

statistically or nonstatistically associating 

ambient oxidant-related air quality data 

either with ambient concentrations of 

precursors or with precursor emission 

rates. These associations are clearly not 

cause-effect in nature, and their intended 

use is not to predict absolute air quality; 

rather, it is to estimate changes in air 

quality resulting from changes in emission 

rates. 

2. Mechanistic Models of OX/HC/NOx. This 

approach entails deriving cause-effect 

relationships between oxidant and precursors through laboratory testing and 

chemical mechanistic simulations. As in 

the preceding case, this approach is 

intended to predict oniy changes in air 

quality resulting from changes in emission 

rates. 

3. Air Quality Simulation Model (AQSM) 

Approach. This approach entails deriving 

the requisite air quality-emission relationships through mathematical representation of the transport, dispersion, 

transformation, and deposition processes. 

93 
Its intended use is to predict absolute levels 

of air qualityfrom a given emission rate and 

meteorological data. 

The oxidant-emissions relationships or models 

developed to date through all these approaches are 

applicable only to the urban oxidant problem, and 

more specifically, to situations in which the 

geographical dimension of the source-receptor 

relationship is comparable to that of the urban 

area. Models relating local emissions and oxidant 

concentrations (caused by these emissions) in 

distant downwind areas are currently under 

development. 

Currently available models have received only 

limited testing; their vafidity, therefore, is only 

limited. Furthermore, assessments made of these 

models do not reflect a consensus of opinion. The 

problems in validating air quality models are 

considered to be prohibitive by some investigators, 

but not insurmountable by others. 14 

The following sections will cover the subject of 

the oxidant/ozone-emissions relationships by 

describing and discussing first the simpler 

empirical models and then the more sophisticated 

ones. Consistent with the previously stated 

premise that such models will never be perfect, the 

emphasis -in the following discussions will be 

placed on the relative merits and drawbacks of the 

various models rather than on their absolute 

validity and utility. For a more comprehensive 

coverage of models for predicting air quality, the 

reader is referred to a recent report bythe National 

Academy of Sciences. 3 a 

It should be noted that of the Ox /HC/NOx 

relationships currently derived and reported, some 

pertain to oxidant, as measured by the potassium 

iodide method (see Chapter 7), and some pertain to 

ozone. Relationships derived from the chemical 

mechanism of the atmospheric photochemical 

process pertain to ozone. 

MODELS BASED ON EMPIRICAL 

RELATIONSHIPS 

Rollback Model 

To relate precursor emission rates to oxidant or 

ozone air quality, it is necessary that two main 

processes be quantitated: (a) the combined process 

of dispersion and sink-removal of precursor 

emissions, and (b) the combined process of 

photochemical formation and sink-removal of 

oxidant/ozone. dne proposed method for 

quantitating the dispersion-removal process is by 

assuming a simple linear rollback model expressed 

by the following equation: 7 

c,=b+ke (6-1) 

where c, is the concentration of a pollutant at point 

i in the ambient air, b is the background concentration of the pollutant, e is the pollutant 

emission rate, and k is a constant dependent on 

meteorology, location of sources relative to point i, 

and on other factors (e.g., sinks) affecting the 

impact of the sources at point i. Equation (6-1), 

after processing and simplification,' yields 

equation (6-2): 

R _ (gf) (PAQ) - Std

x 100 

(gf) (PAQ) - b (6'2) 

where R is the percentage reduction needed to 

achieve the standard; PAQ and Std denote present 

and desired air quality (standard), respectively, in 

terms of pollutant concentration; and gf is the 

emission growth factor.' In the case of oxidant or 

ozone, the values for PAQ and Std are the second 

highest oxidant or ozone concentration observed in 

the base year and 160 pg/m 3 (0.08 ppm), 

respectively. By inserting those values and values 

for gf and b, calculation can be made of the percent 

reduction of oxidant/ozone needed to achieve the 

air quality standard of 160 ,ug/m 3 (0.08 ppm) of 

ozone. If ambient oxidant/ozone concentration is 

assumed to be proportional to the reactive organic 

emission rate, then the calculated oxidant/ozone 

control requirement equals numerically the control requirement for reactive organic emissions. 

Reactive organics are usually meant to include all 

hydrocarbons except methane; however, other 

reactivity definitions have been used in which 

other organics as well as methane were exempted 

as being nonreactive.so 

The preceding method for relating emissions to 

air quality is known as the simple or linear rollback 

model. It has several limitations, the main ones 

arising from the the assumptions used in the 

quantification of both the dispersion process and 

the photochemical process.' Thus the dispersionrelated equations (6-1) and (6-2) cannot be 

validated experimentally, since such validation 

would require that emission rates for each and 

every source be changed (reduced) identically, a 

requirement that obviously cannot be met in real 

situations. Also, the assumption of proportionality 

between oxidant and reactive organic emission 

rates is of questionable validity, as it is not 

supported by either smog chamber" or theoretical evidence. 37' 47 Finally, the method ignores 

the role of the NOX precursors, which have been 

94 
established as exerting an important role. Despite 

these and other limitations, the simple rollback 

method has received attention5s,5' mainly because 

of its computational simplicity and its relatively 

small demands for input information. In terms of 

accuracy and validity, this model is clearly the 

crudest of those currently available. 

Modified Rollback: Observational Model 

The main difference between simple and 

modified rollback models is in the quantification of 

the photochemical process. Thus, although in the 

simple rollback the percent control needed for HC 

emissions is taken to be equal to the percent 

control needed for oxidant/ozone, the modified 

rollback model utilizes an oxidant-to-precursor 

dependency derived from aerometric data. This 

latter derivation and resulting oxidant-tohydrocarbon dependency is often referred to as the 

observational model and is the quantitative basis 

of EPA's first proposed method, the Appendix-J 

method, for calculating oxidant-related control 

requirements. 59 The observational model has been 

described and discussed in detail elsewhere;'' 50 

therefore, only a brief description will be included 

here. 

The observational model is based on the 

assumption that early morning precursor 

concentrations are indicators of the oxidant levels 

that will occur later in the day. Consistent with this 

assumption, aerometric data taken in several 

urban centers were used to draw the upper limit 

curve shown in Figure 6-I. Specifically, this curve 

was constructed by plotting daily maximum 1-hr 

oxidant concentrations against 6- to 9-a.m. 

average nonmethane hydrocarbon (NMHC) 

concentrations. The curve was drawn through the 

uppermost points. Note that both the oxidant and 

NMHC data were taken at the same monitoring 

site—Continuous Air Monitoring Program (CAMP) 

site—invariably located in the downtown area of 

the respective urban center. Thus the upper limit 

curve is taken to depict the relationship between 

the hydrocarbon precursor and the oxidant formed 

within source-intensive areas under those 

meteorological conditions that are most conducive 

to oxidant formation (i.e., clear skies, high temperature, etc.). 

Accepting the upper limit curve as depicting the 

quantification of the photochemical process, 

control requirements for oxidant reduction can 

then be calculated using the rollback equation (6- 

2) as follows: From the curve in Figure 6-1, one can 

read off the NMHC value corresponding to PAQ 

(that is, to the second highest oxidant 

concentration observed in a location) as well as the 

NMHC corresponding to the standard (that is, to 

160 /jg/m 3 , or 0.08 ppm). This latter NMHC was 

determined to be 0.24 ppm C, and it is the air 

quality standard for hydrocarbon (to be used as a 

guide only and not as a true air quality standard). 58 

By using these NMHC values and assuming b= o 

(i.e., no background oxidant or NMHC), 58 the 

percentage control required for NMHC emissions 

was calculated as a function of oxidant 

concentration, and the resultant function was 

published by EPA in the form of the Appendix-J 

curve. 59 A somewhat different approach was used 

by Schuck and Papetti to construct an upper limit 

curve specific for Los Angeles. 60 By this latter 

approach, the NMHC values used were averages of 

data taken at several sites in the Los Angeles 

Basin; whereas, the oxidant values used were 

those for the highest oxidant concentration 

observed anywhere in the Basin. This Los Angeles 

curve is shown in Figure 6-2. 

This modified rollback, orAppendix-J, model has 

been critiqued extensively. 9,13,24 Briefly, the model 

has limitations and advantages related (1) to the 

rollback equation (6-2), (2) to the assumption of 

zero background oxidant or NMHC, and (3) to the 

upper limit curve. Limitations and justification of 

the rollback equation are discussed in the 

preceding section. The assumption that there is no 

background oxidant or NMHC is clearly incorrect, 

but it has been adopted in the interest of simplicity 

and because reliable data on the level of such 

background are lacking. The limitations and 

advantages of the upper limit curve are 

summarized as follows: 

1. The curve probably depicts the dependence 

of oxidant on the dispersion factor rather 

than the dependence on the hydrocarbon 

reactant factor. 13 

2. The curve depicts a purely empirical 

relation, not a cause-effect one, and it, 

therefore, cannot automatically be assumed to have predictive value; (it would 

have a more cause-effect nature if oxidant 

were measured within the same air mass in 

which the HC and NO X measurements were 

made). 

3. The curve disregards the N0, factor. 

4. Experimental error makes the low end of 

the curve (air quality standard for NMHC) 

highly uncertain. 

95 
5. Scarcity of data points makes the upper part 

of the curve highly uncertain. 

6. The curve is not necessarily valid in 

locations other than those from which it 

was derived. 

7. The curve disregards the oxidant transport 

phenomena. 

8. The curve has no statistical nature. 

Justification of the upper limit curve is mainly 

based on the following: 

1. The curve is derived from real atmospheric 

data, which is a more realistic alternative to 

laboratory smog chamber data, for 

example. 

2. The curve is in qualitative agreement with 

the smog chamber data, at least insofar as 

the oxidant-to-hydrocarbon dependence is 

concerned (Figure 6-3). 

3. The curvecan be improvedwith acquisition 

of additional data. 

0.30 

0.25 

0.20 

a 

a 

fN 

Z 0.15 

Q 

X 

O 

0.10 

0.05 

0 

0 

APPROXIMATE UPPER LIMIT 

OBSERVED OXIDANT 

/ • • 

• 

• 

• i • • 

• 

• • • • r • • • • • 

• • • • • • 

• • ~ ••~ • • 

•' i • •• • • • • • • 

: • ~ • • • • • ~•~ •~ •'•' • •t • • • • • 

•'• ~'~' • • .9 • •• • ~ • j • • • N • • 

0.5 1.0 1.5 2.0 2.5 

NONMETHANE HYDROCARBONS, ppm C 

Figure 6-1. Maximum daily 1-hr average oxidants as a function of 6-to-9-a.m average of 

nonmethane hydrocarbon (CAMP data from four U.S. cities).' 50 

96 
60 

Z 50 

O 

H 

Q ¢ 

Z E 40 

W j 

0 a Z a 

Oy 

~ Z 

Q 030 

Xy 

ON 

20 

~ Q 

~ 

~ 

~ 

Q 10 

~ 

0 . i 1 i 1 1 1 

0 1 2 3 

AVG. NONMETHANE HYDROCARBONS 

AT EIGHT STATIONS (1971), ppm C 

Figure 6-2. Upper limit oxidant values in the Los Angeles south coast air basin as a function of 

average 6-to-9-a.m. hydrocarbon concentrations. eo 

0.90 

0.80 

0.70 

O 

a 0.60 

H 

Z 

Q 

~ 0.50 

X 

O 

r 

.= 0.40 

f 

~ 

~ 

X 0.30 

Q 

~ 

0.20 

~ 

SMOG CHAMBER DATA HC/NOx = 12 

SMOG CHAMBER DATA NO x = 0.4 ppm 

AEROMETRIC DATA (UPPER LIMIT CU 

0.10 

SMOG CHAMBER DATA HC/NOx = 3.5 

0 r a ~ ~ 

0 1.0 2.0 3.0 4.0 5.0 

NONMETHANE HYDROCARBON, ppm C 

Figure 6-3. Oxidant-hydrocarbon relationships from smog chamber and aerometric data. 13 

97 
Overall, the Appendix-J method is judged to be 

no more valid than the simple rollback model 

because it is based on relatively few data taken 

from several cities. The method has more validity 

when it is derived from and used in one and the 

same locality, as, for example, in the case of the 

Schuck-Papetti curve for Los Angeles. This, 

however, requires an abundance of data, provided 

by multiyear rather than multistation measurements. Such data are currently available only 

for a very few cities.' Lack of adequate data, 

ambient measurement error, and influences 

associated with siting of the monitoring stations 

are probably the main reasons for the rather large 

differences observed among individual location 

upper limit curves. 61 

Statistica{-Empirical Models 

Statistical-empirical models are based on 

statistically defined associations among ambient 

air quality indices, meteorological parameters, and 

emissions rates. A considerable amount of work 

has been done in establishing such associations. 

However, much of that work was addressed to the 

air-quality-to-meteorology dependency and the 

development of_predictive models for short-term 

episode forecasting. Such models are not relevant 

to the subject of this document. Relevant models 

are those addressed to the air-quality-to-emission 

dependency—that is, models intended to predict 

long-term impact of emission controls on oxidant 

air quality and to calculate control requirements 

for oxidant reduction. The most notable of these 

models were recently reviewed by Myrabo et a1. 35 

The following discussion of such models is based 

partly on the Myrabo review. 

With one exception, the statistical-empirical 

models relating ambient oxidant to precursors 

neglect the spatial and temporal distribution of the 

precursor emissions. Accordingly, their utility is 

limited to relating changes in total levels of 

emissions within a region to changes in regionwide air quality. 

Merz et a1. 33 used regression analysis to relate 

daily 1-hr maximum oxidant to 6- to 9-a.m. 

concentrations of NOx and NMHC, with the latter 

taken to be 50 percent of total hydrocarbon. The 

data used were for downtown Los Angeles, and 

only for the months of August, September, and 

October. Results are shown in Figure 6-4. The 

diagrams of Figure 6-4 indicate that NO X control 

would have a slight but beneficial impact on 

oxidant air quality. 

Kinosian and Paskind 26 also used JulySeptember data from Los Angeles to relate, 

through regression analysis, daily maximum 1-hr 

oxidants to 6- to 9-a.m. NOX for constant NMHC. 

The NMHC data, again, were not obtained directly; 

they were computed from total hydrocarbon (HC) 

data using established HC-to-NMHC relationships. 

Results from four Los Angeles sites are shown in 

Figures 6-5 through 6-8. These results, unlike the 

Merz et al. mode1, 33 indicate that NOX control, 

unless drastic, is detrimental to oxidant air quality. 

Finally, Trijonis 55 used a stochastic model to 

relate emission rates in downtown Los Angeles 

(DOLA) to 7:30-9:30-a.m. ambient concentrations 

of hydrocarbon and NOx, which were then related 

to the oxidant concentrations observed in the 

sections of the Los Angeles Basin lying downwind 

from DOLA. Specifically, Trijonis used average 

values of oxidant concentrations measured at 

DOLA, Pasadena, and Burbank, weighted 

according to direction and speed of the morningto-noon wind. Trijonis expressed his results in 

terms of annual exceedance of the California 

oxidant standard (0.1 ppm as ozone) as a function 

of NOX and reactive hydrocarbon emission levels in 

DOLA(Figure 6-9). 55 These results again show NO x 

control to have a detrimental impact on oxidant air 

quality, at least for Los Angeles. 

AII three models discussed in the preceding 

paragraphs are not capable of treating spatial 

resolution of emissions. Thus, by those models, a 

region or urban center is treated as a single point 

source, a simplification that is obviously helpful, 

but that is also penalizing in that it makes it 

impossible to deal with questions of localized 

impact from addition or deletion of emission 

sources within the urban area. To lessen this fatter 

penalty, investigators from the University of 

California, San Diego, offered a statisticalempirical model with some spatial resolution 

incorporated. 5' 34 Specifically, their model related 

oxida nt a ir q ua I ity (expressed i n terms of nu mber of 

hourly violations of the Federal oxidant standard of 

0.08 ppm as ozone) to reactive hydrocarbon 

emission levels integrated over the prevailing 

windstream corridor leading to the oxidant 

monitoring station. Spatial resolution was 

achieved by defining the windstream corridor 

width to be approximately one-tenth of the 

maximum dimension of the urban area. Using data 

from 17 stations in San Diego and Los Angeles, the 

investigators generated a hydrocarbon-emissionto-air-quality relationship that they then proposed 

98 
1.0 

DATA BOUNDARIES 

E 

a 

a 

x 

z 10 

E 

~ ~ 

0 

E 

, 1 

1 

, 0.25 

~ 

0.20 

♦ 

♦ 

0.15 

MAX 1-hr OXIDANT 

(ppm) 

~ 

0.10 

~ 

01 4 0.05 10.08 

0.1 1.0 10 

6-to-9-a.m. NONMETHANE HYDROCARBONS, ppm C 

Figure 6-4. Merz, Painter, and Ryason's relation of NO. and NMHC assumed as 50 percent of 

total HC and oxidant for downtown Los Angeles. 33 

E 

L a 25 

a 

Z 

O 

Q 20 

a 

N 

z W 

U 

z 15 

O 

U 

Fz 

C,_ 10 

X 

O 

X 5 

Q 

~ 

N\ \ 713.6) 

613.0) 

512.4) 

~ 4(1.7) 

311.1) 

2(0.4) 

01 i i i i i i i _ i 

0 10 20 30 40 50 60 70 

6-to-9-a.m. OXIDES OF NITROGEN CONCENTRATION, pphm 

Figure 6-5. California Air Resources Board aerometric results, relation between 6-to-9-a.m. 

NO., 6-to-9-a.m. HC, and maximum hourly oxidant concentrations in downtown Los Angeles. 

(1ndividual curves show total and NMHC concentrations in ppm.) 26 

99 
35 

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512.3) 

1.5) 

3(0.8) 

35 

E 30 

t 

a 

a 

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Q 

¢ 

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¢ 

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Z 

W 

U 

~ 20 

U 

H 

z 

Q 

~ 15 

x 

O 

t 

Q 10 

2 

~ 7(2.6) 

^ 6(2.2) 

' `511.7) 

~ 

411.2) 

~ 

3(0.8) 

, 

2(0.3) 

for use for predictive purposes. The NOx factor, 

obviously, is ignored by this model. 

AII the statistical-empirical models described in 

the preceding paragraphs, and other similar 

ones, 2,38 are relatively simple in that they treat the 

conversion of emissions into ambient oxidant as 

one process. Thus distinct components of this 

process such as the vertical dispersion of 

emissions within a definable atmospheric layer 

(mixing layer), local (intracity) transport by wind, 

and chemical reactions are not delineated and 

treated separately. Because of this simplification, 

these models lose much of their validity when 

applied to areas with characteristics widely 

different from those of the area for which they 

were developed (for example, mixing heights, wind 

patterns, or photochemical conditions . To reduce 

this problem, Tiao et a1. 54developed a model that 

treats the dispersion, advection, and reaction 

processes separately, using separate terms in 

mass conservation equations for NO, NO2, and 

ozone. The coefficients of these terms were 

determined statistically by fitting the equations to 

the observations available. Because of its 

mechanistic detail, the Tiao et al. mode1 54is 

inherently more valid than the preceding models in 

treating diverse situations. However, because it 

does not include spatial resolution, this model, like 

the preceding ones, is not applicable in areas 

where a major fraction of the local oxidant is 

caused by extraneous sources. 

5 

0 

0 10 20 30 40 

6-to-9-a.m. OXIDES OF NITROGEN 

CONCENTRATION , pphm 

5 

0 

0 10 20 30 40 

6-to-9-a.m. OXIDES OF NITROGEN 

CONCENTRATION, pphm 

Figure 6-6 California Air Resources Board aerometric 

results, relation between 6-to-9-a.m. NO., 6-to-9-a.m. HC, 

and maxirnum hourly oxidant concentrations in Azusa. 

(Individual curves show total and NMHC concentrations in 

PPrn )26 

Figure 6-7. California Air Resources Board aerometric 

results, relation between 6-to-9-a.m. NO., 6-to-9-a.m. HC, 

and maximum hourly oxidant concentrations in San 

Bernardino. (Individual curves show total and NMHC 

concentration in ppm.) 26 

•• 
35 

E 

t 

a 30 

z 

0 

~ 

Q 25 

~ 

~ 

z 

W 

~ 

Z 20 0 

u 

~ 

z 

Q 

2 15 

X 

0 

t 

X 

a 10 

~ 

3(1.1) 

2(0.4) 

10 20 30 40 

6-to-9-a.m. OXIDES OF NITROGEN 

CONCENTRATION, pphm 

Figure 6-8. California Air Resources Board aerometric 

results, relation between 6-to-9-a.m. NO„ 6-to-9-a.m. HC, 

and maximum hourly oxidant concentrations in Anaheim. 

(Individual curves show total and NMHC concentrations in 

PPm.) 2e 

The statistical-empirical models have advantages arising from the fact that the models are 

constructed from real atmospheric data and are 

statistical in nature. Furthermore, such models are 

computationally simple and inexpensive, and 

unlike the rollback models, most of them consider 

both precursor factors, HC and NOx. 

Limitations of the statistical-empirical models 

arise mainly from the stochastic nature of such 

models. Because they are based on associative 

rather than cause-effect relationships, such 

models have limited predictive validity, especially 

when predictions call for extrapolating the model 

beyond the range of data from which it was 

derived. Furthermore, the models that relate 

oxidant to ambient concentrations rather than to 

the emissions of precursors are subject to the 

samevalidity limitation astheAppendix-J method, 

namely, that the model does not directly relate air 

quality to precursors. Instead, the direct relationship is between oxidant and the atmospheric 

dispersion factor. In general, the statisticalempirical models have less validity when they are 

derived from and are appiied to a variety of areas 

with significantly different meteorology and 

emission characteristics. 

In conclusion, when all the strengths and 

limitations of the statistical-empirical models are 

evaluated, such models are judged to be superior 

to the rollback models, especially when , they are 

designed for local use. 

MECHANISTIC MODELS OF OX/HC/NOx 

RELATIONSHIPS 

The development of reaction mechanisms 

describing the photo-oxidation processes of 

hydrocarbons and oxides of nitrogen has evolved 

extensively through the use of experimental data 

from smog chamber studies. 10 A basic 

understanding of the Ox/HC/NOX chemical 

relationship is a prerequisite to developing 

techniques for relating emission to ambient 

oxidant levels. It is important, therefore, that smog 

chamber studies be performed u nder conditions as 

similar as possible to those of real polluted 

atmospheres. Thus, considerations such as light 

intensity and its spectral distribution, temperature, 

humidity, and composition and concentration of 

reactants should be comparable to those in typical 

polluted atmospheres. The utility of one such smog 

chamber data set exhibiting many of the abovementioned attributes has been demonstrated via 

the development of a chemical kinetic model for 

predicting impacts of emission change on air 

quality and for calculating ozone-related control 

requirements.e This technique, given the acronym 

EKMA for Empirical Kinetic Modeling Approach, is 

one of several discussed by EPA in their report, 

Uses, Limitations and Technical Basis of Procedures for Quantifyin5 Relationships Between 

Photochemical Oxidants and Precursors. 39 Since 

application of the technique for air quality control 

is covered in detail in this work, only the scientific 

basis of the technique will be considered here. 

EKMA is based on the ozone-to-precursor 

relationship !03/1-!C/NOx) derived from a smog 

chamber study of automotive exhaust mixtures." 

The selection of this study over several other smog 

chamber data sets in existence 11 '40 was primarily 

based on the rather representative nature of the 

experimental conditions to that of urban polluted 

atmospheres. 10 Although the quality of the 

' 7(3.6) 

~ 6(3.0) 

512.4) 

411.7) 

om 
selected data set is considered high, deficiencies 

nevertheless still exist, as follows: 

l. The selected data are limited to those for 

hydrocarbon-to-NOX reactant ratios 

ranging from 1:1 to 1 2:1 , a range that does 

not extend to sufficiently high values. 

2. The ozone yield data are erroneously high 

for reactant concentrations close to zero, 

because at such low concentrations, the 

chamber background reactivity becomes 

important relative to the reactivity of the 

test mixture. 

-3. The selected data were obtained under 

fixed radiation intensity conditions in 

contrast to the diurnally varying sunlight 

intensity in the real atmosphere. 

Consideration of these and other minor 

deficiencies as well as practical constraints on the 

number of parameter variations that can be 

studied in smog chambers lead to the utilization of 

a photochemical kinetic mechanism to simulate 

and project the experimental data. The detailed 

photochemical mechanism was f irst f it to the smog 

chamber data on automotive exhaust mlxtures and 

then used to extrapolate ozone yields for varying 

initial hydrocarbon and NOx concentration and 

irradiation conditions. Resulting Os/HC/NOx 

relationships for conditions similar to those in the 

Los Angeles atmosphere during the smog season 

are depicted in Figure 6-10 in terms of a family of 

ozone isopleths. 

1200 

10 

50 

1000 100 

150 

800 

600 

400 

200 

0 

0 400 800 1200 1600 

L. A. COUNTY NO x EMISSIONS, tons/day 

Figure 6-9. Expected number of days per year exceeding 0.10 ppm versus NO, and reactive 

hydrocarbon emission levels for central Los Angeles. 55 

102 
E— H = 8.0 

NO 

x 

4.0 5.0 

0.6 

0.5 

0.4 

E 

a 

a 

X 0.3 

O 

Z 

0.2 

0.1 

0 

0 

OXIDANT/03, ppm 

0.08 0.20 0.30 0.40 0.50 0.55 0.60 0.65 

e 

1.0 2.0 3.0 

NMHC, ppm C 

Figure 6-10. Oxidant/03 isopleths derived from combined use of smog chamber and 

photochemical modeling techniques. 16 

The chemical kinetic modeling technique 16 used 

to derive the isopleths of Figure 6-10 is based on a 

75-reaction-step mechanism for a propylene and 

n-butane hydrocarbon mixture. The twocomponent hydrocarbon system is a surrogate for 

the automotive exhaust hydrocarbons, which in 

turn is a surrogate for atmospheric organic 

pollutant mixtures. Seventeen smog chamber 

experiments were modeled in which the 

agreement between observed and modelpredicted ozone yields was maximized by 

optimizing the butane-to-propylene ratio in the 

model. Chamber background reactivity was 

simulated in the model by assuming a source of 

propylene resulting from desorption from the 

chamber walls. After optimization, the model was 

extended to c©nsider conditions more realistic to 

urban polluted atmospheres. Major changes in the 

photochemical kinetic model included removal of 

the chamber background reactivity steps, 

consideration of diurnally varying photolytic 

reaction rate constants, simulations over 9-hr 

irradiation periods corresponding to the hours 

between 7 a.m, and 4 p.m., and consideration of 

dilution rate more appropriate to that of an urban 

atmosphere. 

With these adjustments, the model-generated 

isopleths shown in Figure 6-10 are taken to 

represent roughly the atmospheric situation in the 

Los Angeles Basin. The approximate nature of the 

representation arises since the isopleths, despite 

the model adjustment, reflect biases caused by the 

simplifications and possible perturbations 

inherent to the smog chamber experiment. Thus, 

for example, the absence of continuous fresh 

emission influx in the smog chamber simulation is 

one simplification that may have introduced a bias. 

The isopleths may also reflect biases introduced by 

unknown effects of the chamber walls, by use of 

unrealistic dilution and reactant mixing conditions 

in the smog chamber test, and possibly by other 

factors as well. 

In light of these uncertainties, the ozone 

isopleths derived from this model (Figure 6-10) are 

not assumed to have absolute validity and 

therefore should not be used to predict ambient 

ozone levels from given ambient 6- to 9-a.m. 

concentrations of NMHC and NOx or vice versa. 

Application of the isopleths is considered, in a 

relative sense, as illustrated in the foliowing 

example calculation for emission control 

requirements. The detailed reasoning behind this 

103 
calculation procedure and its advantages are given 

elsewhere." 

Control requirements for achievement of the 

ozone and NOz standards are calculated for a 

region from the second highest 1-hr 

oxidant/ozone concentration observed in the 

region's atmosphere, from the NMHC-to-NO x ratio 

during 6 to 9 a.m., and from the annual NOz mean 

concentration. For example, if the ozone 

concentration, the NMHC-to-NO x ratio, and the 

annual NO2 mean values are 0.4 ppm, 8.0 t 4.0, 

and 0.06 ppm, respectively, then the isopleth 

counterparts of the ambient NMHC and NOX 

concentrations causing the 0.4 ppm of ozone are, 

on the average, those defined by the point e; that is, 

the intercept of the 0.4 ppm ozone isopleth with the 

constant slope line ab corresponding to a NMHCto-NOx ratio equal to 8.0 (Figure 6-10). Next, the 

NO x reduction needed for achieving the national 

ambient air quality standard (NAAQS) for NO2 

(annual mean of 0.055 ppm) is calculated to be 10 

percent, assuming proportionality between 

ambient NOx reduction and ambient NO2 

reduction. Reducing NO X by 10 percent defines 

point 6. For achievement of the NAAQS for ozone, 

the NMHC must then be reduced along the line 6f 

to the point of being the intercept of line 6f with the 

0.08 ppm ozone isopleth. Such a NMHC reduction 

is calculated to be 81 percent. Similar calculations 

for the upper and lower limits of the NMHC-to-NO X 

ratio range give NMHC control requirements equal 

to 62 percent and 87 percent, the latter control 

being the one that will achieve the ozone standard 

regardless of NMHC-to-NO x ratio. 

Note that the EKMA is applicable only in those 

situations in which the source-receptor 

relationship is known and temporally consistent 

with that implied in the model. Thus since the 

model predictions are for 9-hr irradiation of 

emissions and the computed ozone peak appears 

usually after 5 to 6 hours of irradiation, the modelpredicted control requirements are only for 

emission sources lying within an upwind-distance 

equivalent to 5 to 6 hr (at the most, 9 hr) of wind 

transport. Situations in which a major fraction of 

the observed ozone appears to be caused by 

emissions from more distant upwind sources or 

from transported ozone aloft (anthropogenic or 

stratospheric in origin) cannot be appropriately 

treated by this model. 

The possibility of separating out the ozone 

contribution of the extraneous sources and of 

defining the local ozone component on which the 

isopleths are applicable has been explored, but 

without much success. At this time, the best 

judgment that can be made on this question is only 

qualitative. One of many conceivable scenarios 

describing the interaction between extraneous 

ozone and local ozone formation is as follows. 

Local emissions are discharged in the early 

morning into a relatively thin, stable layer (100 to 

200 m) of ozone-free air. As the day progresses, 

this inversion is eroded, and the reacting 

emissions disperse into the subsidence inversion 

layer that contains the extraneous ozone. By early 

afternoon, vertical mixing is complete, and 

pollutants (local and extraneous) are confined in a 

single layer under the subsidence inversion. For 

such a scenario, the extraneous ozone can be 

assumed to have undergone the following 

reduction processes: 

1. Dilution resulting from mixing with the 

ozone-free air in the radiation inversion 

layer. 

2. Destruction on surfaces. 

3. Destruction in reaction with precursors and 

other reaction mixture constituents. 

In contrast, this same extraneous ozone also 

enhances local oxidant formation processes. The 

quantification of the net impact of the extraneous 

ozone on ground-level ozone concentrations is 

beyond the capabilities of the EKMA approach and 

lies in the realm of the air quality simulation model. 

Nevertheless, there are some indications that the 

destructive processes outweigh those that 

enhance ozone formation. Thus, for example, 

Seinfeld performed modeling tests51 that showed 

that for an urban scenario similar to the one 

described here, extraneous ozone had a positive 

effect on ground-level ozone concentration, but 

that such an effect was less than additive. 

Therefore, subtracting the entire extraneous ozone 

concentration (measured upwind or aloft) from the 

maximum ozone concentration observed in an 

urban center may introduce substantial error in 

estimating the local ozone component for which 

the isopleth method is applicable. Conservative 

first-order approximation estimates can be made 

in areas subject to extraneous ozone by assuming 

negligible impact from the extraneous source. 

Further guidance regarding such calculations is 

provided elsewhere. 41 

From the preceding discussion, it is clear that the 

EKMA is not ideally applicable to situations in 

which the oxidant problem is largely of extraneous 

origin. The question that needs to be examined 

f[iL! 
next is whether, with the exception of these 

situations, the same set of isopleths can be used 

everywhere within the continental United States. 

Possible reasons for concern are that the 

meteorology- and emission-related factors that 

affect local ozone formation (and hence the ozoneto-precursor relationships) differ from location to 

location. Thus prevailing sunlight intensity, 

temperature, and dispersion conditions in Los 

Angeles are different from those in Chicago, for 

example. Likewise, the organic emission 

composition, organic-to-NOX ratio, and emission 

discharge patterns may be different for various 

urban areas. To explore the sensitivity of the EKMA 

to different urban areas with widely diverse 

conditions, the method was subjected to a 

sensitivity test," as follows. First, new sets of 

isopleths were generated by changing the model 

parameters related to light intensity, dilution rate, 

hydrocarbon composition (i.e., propytene-tobutane ratio), and emission discharge after 9 a.m. 

These new sets of isopleths were then used to 

compute emission control requirements for given 

ozone reduction strategies. Results showed that 

although the various sets of isopleths differed in 

isopleth shape and spacing, the control 

requirement estimates were nearly identical for all 

of them. Thus the same set of isopleths could be 

used in different locations without introducing a 

substantiai error in the calculation of control 

requirements. However, given that such error was 

substantial, it could be reduced by adjusting thq 

appropriate model parameters and generating a 

new set of isopleths that would more closely reflect 

the prevailing conditions in the region. 

Note that the sensitivity to parameter variations 

is that of the model and may not necessarily reflect 

responses of the real atmosphere. Therefore, this 

technique, like all others, must be verified as to its 

predictive accuracy. 

To complete the discussion on the modeling 

Os/HC/NOx relationships, it should be added that 

a model has been proposed by LosAngeles County 

investigators 12 that combines smog chamber and 

aerometric data. The method has been discussed 

in detail by Souten et a1., 52 who have pointed out 

several weaknesses in the approach. Because of 

these weaknesses, the model has not received 

much attention. 

In concluding this discussion on the mechanistic 

Os/HC/NOX models, it is stressed that such 

modeis, although clearly superior to the rollback 

and statistical models, are also acknowledged to 

have several imperfections, as discussed 

elsewhere."" ,16 Briefly, the specific model 

described here, (EKMA), has a conceptual 

limitation arising from the fact that the ambient 

atmosphere, with all its complexity, cannot be 

duplicated in the smog chamber. Furthermore, the 

model does not predict frequency of occurrence of 

ozone concentrations. The use of photochemical 

modeling techniques in deriving the EKMA 

03/HC/NOx relationships (Figure 6-10) has 

increased the utility of these relationships, but the 

photochemical model used also has its 

imperfections. The EKMA model is also limited in 

that it requires input information, some ofwhich is 

not available. Thus the required NMHC-to-NO X 

ratio data are not commonly available, mainly 

because measurement of ambient NMHC is not 

required by law. Finally, the model does not have 

the spatial andtemporal resolution neededtotreat 

distribution of ozone within an urban area. 

AII of these imperfections are real and of 

consequence, but certainly they do not altogether 

prohibit the use of this model. Viewing these 

imperfections in the context of the premise that a 

model shall be judged mainly in relation to other 

existing models, it would appear that the model 

described here is somewhat superior to the others 

presently ready for use. Thus many of the model's 

imperfections are also shared by the rollback and 

empirical-statistical models, whereas some of its 

strengths are not. For example, the strongest 

points of this model are the cause-effect nature of 

the model's ozone-to-precursor relationships, and 

the quantitative consideration of the NO x - 

precursor factor. The only models that have both 

these features are the air quality simulation 

models. Imperfections of the photochemical model 

used to supplement and adjust the smog chamber 

data are notcritical since the photochemical model 

is validated against laboratory data. Thus, future 

changes in - the chemical mechanism of the 

photochemical model can have only a small effect 

on the isopleths and an even smaller effect on 

control requirement estimates computed from the 

isopleths. 

AIR O.UALITY SIMULATION MODELS (AQSM) 

Air quality simulation models representthe most 

fundamental approach to relating primary 

pollutant emissions to secondary pollutant 

concentrations. This approach was first conceived 

and introduced by Friedlander and Seinfeld. 20 

Such models are based on a mathematical 

105 
description of the physical and chemical"processes 

involved in the atmospheric behavior of air 

pollutants. The basis of all AQSM's is the equation 

of conservation of mass, which with the help of 

certain simplifying assumptions is reduced to 

equation 6-3, commonly known as the atmospheric diffusion equation: 

ac, + u ac, + v ac, + w ac, 

at ax ay az 

= a K H ac ~ + a KH ac, 

ax ax ay ay 

+ a Kv ac, + R, (c,,...,cT) (6-3) 

az az 

where c, is the mean concentration of species i; 

x,y,z are the Cartesian coordinates; u,v,w are the 

mean velocity components; KH,Kv are the 

horizontal and vertical eddy diffusivities; R, is the 

rate of production (or negative of the rate of 

consumption); T is temperature; and t is time. 

The solution of the set of equations 6-3 yields the 

theoretical mean concentrations as a function of 

location and time. The solution of equation 6-3 

requires, as input information, initial and boundary 

concentrations of each of -the n species, the wind 

field, turbulent diffusivities, source emissions as a 

function of location and time (entering as boundary 

conditions), and a chemical reaction mechanism. 

AII air quality models are mathematical 

descriptions of the physical processes that are 

known to occur in the atmosphere. However, no 

model is a perfect descriptor; it is only as true a 

simulator of actual processes as the assumptions 

on which it is based are valid. Since models are 

known to be inaccurate, it is of interestto ascertain 

how inaccurate their predictions might be. 

Unfortunately, quantitative determination of the 

expected inaccuracy of a model is extremely 

difficult, if not impossible, to achieve. There are 

several reasons for this. 

First, meteorological processes are random in 

nature, whereas all of the current AQSM's are 

deterministic (as contrasted with stochastic). 

Outputs (and observations) are thus meaningfully 

expressed in terms of random variables. Predictive 

results of deterministic models are not 

commensurate with this requirement. Thus 

comparison of actual observations with model 

predictions is not entirely appropriate. The second 

and related reason for the difficulty of quantitative 

determination is that the atmosphere is highly 

variable in terms of all measures used by scientists 

to describe it. Spatial and temporal variations of 

virtually all parameters that serve as inputs to 

models are usually quite significant and, in fact, 

often rather large. Third, the data base one might 

use both for input to the model and for 

comparisons with predictions is virtually always 

sparse and sometimes inaccurate. Finally, it is not 

possible to derive a totally theoretically based 

estimate of expected errors associated with a 

particular formulation, because it is not possible to 

formulate a truly accurate representation of the 

natural system with which to compare. 

If equation 6-3 could be demonstrated to be an 

accurate representation of atmospheric processes, 

and if the necessary input information were known 

with sufficient accuracy, the AQSM would clearly 

be the preferred approach for relating primary 

emissions to secondary (e.g., oxidant) air quality. 

Commonly, however, there are inaccuracies 

associated with the use of equation 6-3. These 

inaccuracies can be categorized either as 

fundamental inaccuracies or input-related 

inaccuracies. The fundamental inaccuracies are 

those associated with the assumptions made in 

the derivation of equation 6-3. Such inaccuracies, 

for example, include those related to the 

assumptions made in modeling atmospheric 

turbulent flow. Input-related inaccuracies are 

those that result from uncertainties in the input 

information such as the source emissions, wind 

velocities, and the chemical reaction mechanism. 

A measure of the error resulting from all sources 

can be obtained through comparison of the 

concentrations predicted by the model with those 

measured. Ideally, such comparisons should be 

made (for a particular region) for a variety of 

meteorological and emission conditions. One 

discrepancy between predictions and data will 

arise because equation 6-3 predicts the mean 

concentrations, and ambient data reflect 

instantaneous conditions. Also, equation 6-3 must 

generally be solved numerically on a grid, so that 

the concentration, c,, implicitly involves some 

degree of spatial averaging; but the data usually 

consist of concentrations at a point. If a sufficient 

data base is available, extensive model evaluation 

over varying meteorological and emission 

conditions will provide insight into the accuracy of 

the model, thereby establishing the degree to 

which the model can be extrapolated to conditions 

beyond those in the domain of the evaluation. 

106 
Unfortunately, a data base that is truly suitable for 

model evaluation has only recently become 

available (see subsequent discussion), and thus 

conclusive model evaluation studies for AQSM for 

photochemical oxidant have yet to be carried out. 

The subject of this section is a brief review of the 

capabilities and limitations of AQSM for 

photochemical oxidant. More extensive 

discussions of AQSM's can be found in several 

recent reviews. 15' 3a ' 5

' AQSM's have the capability 

to predict oxidant (and other secondary pollutant) 

concentrations as a function of location and time 

over a region for any specified meteorological and 

emission conditions. Such prediction does require 

extensive data input requirements, such as a 

spatially and temporally resolved emission 

inventory and wind field, and a chemical reaction 

mechanism. The principal limitations associated 

with AQSM's result from the need for extensive 

input data and from inaccuracies in the input 

information. Because AQSM's have not yet been 

evaluated to the extent ultimately desired, it is 

difficult to provide precise indications of their 

ability to simulate oxidant formation accurately. 

An open issue is whether or not AQSM's 

presently exist that are sufficiently validated and 

appropriate for application in designing oxidant 

control strategies. 14 This section outlines the key 

aspects of this question. First, the basic types of 

AQSM's for photochemical oxidant are discussed, 

and several specific models that are available are 

summarized. Then follows a discussion of the 

general issue of the level of detail of treatments of 

chemistry and meteorology in AQSM's. Finally, an 

attempt is made to assess the level of accuracy of 

AQSM's for photochemical oxidant. Most of the 

analysis presented here is from a recent review by 

Seinfeld. 51 

A synopsis of the types of AQSM's is presented 

in Table 6-1, and several available AQSM's for 

photochemical oxidant are summarized inTable6- 

2. The AQSM's can be categorized according tothe 

level of detail of the treatment of both meteorological and chemical processes. From a meteorological point of view, the basicdistinction lies in 

the level of spatial resolution of the model. Socalled grid models are based on the solution of 

equation 6-3 on a three-dimensional grid representing the region of interest. An example of a 

model of this type is the SAI model summarized in 

Table 6-2. There is also a class of grid models 

wherein explicit computations of vertical transport 

are not carried out; the LIRAQ model exemplifies 

this type. So-called trajectory models represent the 

chemical and vertical transport processes taking 

place in an advecting air column. Table 6-3 

summarizes the meteorological treatments of each 

of the four AQSM's described in Table 6-2. 

TABLE 6-1. FORMS OF AIR QUALITY 

SIMULATION MODELS 

Form Distinguishing features 

Grid model Model is based on numerical solution of 

the coupled atmospheric diffusion 

equations in three spatial dimensions 

on a grid over the region of interest. 

Trajectory model Model is based on simulating chemistry 

and vertical transport in air column 

advecting with the local mean wind 

velocity 

Box model Model is based on simulating chemical 

processes in a well-mixed region in 

which no spatial inhomogeneities are 

assumed to exist and within which 

emissions are mixed instantaneously 

throughout the region 

With respect to chemistry, there are two types of 

chemical kinetic mechanisms employed in 

AQSM's: (1 ) lumped mechanisms, in which the 

various organic precursor species are grouped, 

based either on molecular structure or on 

reactivity, and (2) surrogate mechanisms, in which 

the organic species in a particular class, e.g., 

olefins, are represented by a single member of that 

class (e.g., propylene). The high degree of chemical 

detail in the surrogate mechanisms creates 

computational demands that prohibit detailed 

treatment of the dispersion processes. For this 

reason, surrogate mechanisms cannot be 

accommodated along with a detailed treatment of 

the transport process. Most AQSM's use lumped 

chemical mechanisms (SAI, LIRAQ, DIFKIN), 

whereas the Bell Laboratories model employs a 

surrogate mechanism. Which of these two 

approaches is more accurate depends on the 

relative errors that result from simplification of the 

chemical process versus the dispersion process. In 

his analysis of current AQSM's, Seinfeld 51 

suggested that the appropriate combination of 

organic and free radical species in the Bell 

Laboratories mechanism leads to a lumped 

mechanism essentially similar to the lumped 

mechanisms in the SAI and LIRAQ models. He 

notes that there is virtually no advantage gained as 

a result of the extensive chemical detail of the Bell 

model at the expense of a lack of treatment of 

transport and dispersion in that model. Thus, 

models that achieve a proper balance between 

107 
chemical and meteorological detail are the most 

appropriate for use in evaluating oxidant control 

strategies. 

Air quality simulation models represent the 

preferred approach for oxidant prediction if the 

necessary input information for exercise of the 

model is available and accurate. Because the 

necessary input information is not always 

available (and may be costly to generate), and 

because even when it is available it may not be of 

an accuracy that justifies use of the model, it has 

been necessary to utilize empirical and semiempirical methods for relating precursor 

emissions to oxidant concentrations. These 

methods have already been discussed earlier in 

this chapter. (Of course, there may be certain uses 

for which empirical or semi-empirical methods 

may be preferred over AQSM even if accurate 

input information for the AQSM were available. 

These uses would generally be those for which the 

cost of employing an AQSM might not bejustified.) 

Though conslderable time and money have been 

devoted to the development of AQSM's for photochemical oxidant, it has generally been stated that 

existing models do not possess sufficient accuracy 

to be judged reliable. Unfortunately (but for good 

reason), measures of the expected inaccuracies of 

model predictions are rarely available. As a 

consequence, the utility of AQSM has been 

debated on a subjective rather than an objective 

basis. The object of the remainder of this section is, 

where possible, to assess the major uncertainties 

in AQSM and estimate the level of accuracy of 

oxidant predictions. (Whether, given an estimated level of uncertainty in oxidant predictions for 

AQSM's, the AQSM is to be preferred over another 

method for evaluating oxidant control strategies 

given an estimated level of uncertainty in oxidant 

predictions for AQSM depends on the levels of 

uncertainty of the empirical and semi-empirical 

methods that are alternatives.) 

In deriving the atmospheric diffusion equation 6- 

3, the assumption of greatest concern is that of the 

turbuient mass flux [terms of theform u'c', where (' ) 

indicates the fluctuating component of velocity and 

concentration] being set equal to the product of a 

turbulent eddy diffusivity, K, and a concentration 

gradient. The problem is that K is not constant; 

rather it is a function of wind velocity, wind shear, 

the local vertical temperature gradient, and other 

variables. Thus K is a varlable in time and space 

and is a complex function of several other 

TABLE 6-2. CURRENTLY AVAILABLE AIR QUALITY SIMULATION MODELS FOR PHOTOCHEMICAL OXIDANT 52 

AQSM Description of AQSM 

SAI8,22,28,43,44,46,46,49,62 Thls three-dlmensional grld model Is based on numerlcal solutlon of the atmospherlc dlffuslon 

equatlon The three-dlmenslonal wlnd field Is derlved from ground-level measurements. 

Pollutants emltted from ground-level sources are Injected Into the bottom layer of grid cells; 

emisslons from stacks are dlstributed among the grld cells aloft. A 36-step klnetic mechanlsm 

dertved from the Hecht/Setnfeld/Dodge (1974) mechanlsmb,23 Is used. Numerlcal solutlon Is by 

the method of fractional steps wlth advectlon treated by the SHASTA algorlthm (Borls and Book, 

1973), 3 vertical diffusion and chemistry are by the Crank-Nicholson method 

LIRAQH' 31 Thls model predlcts the temporal variatlon of pollutant concentratlons In a two-dlmenslonal array 

of grld cells Each cell Is bounded on the bottom and top by the terraln and Inverslon base, 

respectively For computatlonal purposes, the pollutants a, e assumed to be well mlxed In each 

cell. An emplrlcal aVgorlthm is used to relate the cell-averaged concentratlon to the 

predlcted ground-level value. A two-dlmensional wlnd fleld Is used. Pollutantsemltted at ground 

level and aloft are Injected uniformly fnto the appropriate well-mlxed cell A 48-step chemlcal 

reactlon mechanlsm, slmllar In nature to the Hecht/Selnfeld/Dodge mechanlsm, Is used °23 

The governing equatlons are solved using a modffled verslon of Gear's method (Hfndmarsh, 

1974) 25 

DIFKINe,19,32 DIFKIN Is a trajectory model based on a moving column of alr In whlch vertical dlffuslon and 

chemlcal reactlons take place Pollutants are emltted Into the approprlate vertical cell. The 

column of afr follows a surface trajectory Interpolated from surface wlnd data A 12-step klnetic 

mechanlsm Is used. Governing equatlons are wrltten In the form of ordlnary dlfferentlal 

equatlons and solved using a Pade's approxtmatfon method. 

Bell Laboratory Thls model uses three well-mlxed cells In serles. Wlnd Is represented by volumetrlc alr flowfrom 

modele 21 cell to cell Emisslons are Instantaneously mlxed In cell A 143-step klnetic mechanlsm based 

on detalled chemistry of propylene, formaldehyde, acetaldehyde, and proplonaldehyde° Is used. 

(Interactlon between free radicals and aerosols Is Included.) Governing ordlnary dlfferentlal 

equatlons are solved by Gear's method (Edelson, 1976). 18 

'SAI = Systems Applications, Inc , mode., LIRAQ = Livermore regional air quality model, DIFKIN = diffusion kinetics model 

`rhe 36-step mechanism includes five reactions describing S0: oxidation 

`The 48-step LIRAQ mechanism does not include S0 2 oxidation 

°rhe 143-step mechanism includes 19 reactions describing S02 oxidation 

108 
variables. As a consequence, it is frequently quite 

difficult to estimate. 

Solution of equation 6-3 requires specification 

of a wind field, (u,v,w). As the wind velocity varies 

in space and time, its specification, whether based 

on the solution of the fluid dynamics equations or 

on the interpolation of a set of ineasurements, is 

very difficult, and as a consequence, it isfrequently 

one of the greatest sources of inaccuracy in model 

predictions. If one were to select two arbitrary 

locations separated by a mile or two and monitor 

the wind speed and direction on an hourly basisfor 

a day, the probability is considerable that one 

would find significantly different readings, both in 

TABLE 6-3. TREATMENT OF METEOROLOGICAL VARIABLES IN AIR QUALITY SIMULATION MODELS 

Model Advection Mixing depth Turbulent diffusion 

SAI a Model requires a three dimen- The mixing depth field is Vertical eddy diffusivlty coefflclents 

sional wind field. Hourly developed ustng areawide Kv have been dertved through 

averaged surface measurements Interpolatlon. Temperature use of a methodology developed 

are interpolated to a fine profiles from radlosondes by Lamb et a1. 2',28 In this 

mesh. The surface field and acoustic sounder procedure, which employs 

together with the lower bound- measurements are the basic flow flelds predlcted by 

ary conditlon, w=0, is used to Inputs used to determine the model of Deardorff, 6 particles 

derive the vertical velocities. the depth of the mlxed layer. are released from a point and 

The model employs upper level followed as they are transported 

wlnd measurements and objec- downwind. From the particle 

ttve analysts procedures to render trajectories, it is possible to 

the wlnd-fleld mass consistent. calculate the pollutant 

Theoretical wind-shear concentratlonfielddownwlndofthe 

relationships derived by Lamb 27 release polnt. Glven the 

using the predictions of a concentration and mean flowfields, 

planetary boundary layer model the diffuslvlty proflle is obtained 

developed by Deardorffs are through use of optlmal control 

employed. These relationshlps theory technlques. Horizontal 

are useful In instances when wlnd eddy dlffusivlty coefficient K„ 

measurements aloft are not specifled Is an input parameter. 

avallable. For situatlons in whlch 

wlnd measurements are avallable 

both at the surface and aloft, an 

objective technlque for preparing 

approprtate three-dlmensional 

wind inputs to the model has been 

developed by Reynolds. 42 

LIRAQa An approxlmate two-dimensional Mixing depths over the Spatlal and temporal varlations 

wind field ts constructed ustng region are inferred from of K„ calculated are based on 

a Gaussian weighting functlon sparse surface measure- simllarlty theory. Inputs are 

to Interpolate sparse, 3-hr ments o'f temperature, ele- root-mean-square disperslon, 

average wind measurements vated proflle data, topo- grtd cell size, energy 

to grld cells. An iterative graphy, and the temperature dlssipatlon rate, mixing depth, and 

varlatlonal procedure is used advection from prevalling reference helght wind velocities. 

to reftne the interpolated flows. These data are used Although LIRAQ Is a dimenslonal, 

values so as to render the to construct an interpolated vertically Integrated model, 

fleld mass consistent. A feature fleld The mixing depth Is an a value of Kv Is requlred to 

of the technlque Is that it allows Important Input parameter for establlsh boundary conditions for 

a parameterized treatment of the mass conslstent wlnd-fleld the vertical concentration profile. 

flow through the Inversion calculatlon Kv Is determined from a power-law 

base and around topographlc proflle for wlnd speed and the 

features assumptlon that the frlctlon 

velocity Is 0.1 x the horizontal 

veloclty at a helght of 1 m 

Bella A bulk wlnd flow along the The mixing depth Is averaged Dlffuslon In a cell Is Instantaneous. 

axis of the cells is assumed; no over each cell, and only three 

detalled vertical or horizontal spatlal values are required These 

resolutlon is employed In the data were determined from Ildar 

model. Wind speed variations measurements of vertical 

throughout the day are deftned aerosol extent In combtnatton 

from the medlans of seasonal wlth mixing height data obtalned 

observatlon These data are from other sources. 

smoothed to provide a conttnuous 

temporal wlnd variation. 

'8AI = Systems Applications, Inc , model, LIRAQ = Livermore regional air quahty model, Bell = Bell Laboratories model 

109 
magnitude and direction, between the locations. 

Thus an accurate model must allow for the 

possibility of a laterally varying wind field. In 

addition, variations of wind speed with height can 

often be substantial, so it is necessary that a model 

include wind shear. As noted, the problems 

associated with determining the spatially and 

temporally varying wind field for a particular time 

period in an area are substantial. Measurements of 

winds aloft are typically unavailable, and except for 

special circumstances, it is very difficult to predict 

wind speed and direction at elevations much 

removed from the surface, with only ground 

observations available. In addition, the density of 

ground-level wind stations is generally less than 

that required to interpolate a ground-level wind 

field with a resolution comparable to that of the 

AQSM. 

The chemical mechanism is that element of the 

AQSM that has undergone the most change over 

the period of time that models have been 

developed. This change has been the result of 

continuous investigation of the chemistry of 

photochemical smog and includes revised rate 

constants and new products for some of the 

individual reactions. Whereas the 'chemical 

mechanisms employed in various models differ 

(see Table 6-2), an increasing degree of uniformity 

in the treatment of the chemical processes is 

beginning to emerge as new chemical information 

is incorporated into the mechanisms in the 

AQSM's. The most direct evidence of the adequacy 

of a chemical mechanism isthat obtained through 

simulation of smog chamber data. 

In principle, every reaction appearing in a 

photochemical smog mechanism is subject to 

some degree of uncertainty, whether in the rate 

constant or the nature and quantity of the 

products. In validating a mechanism, the accepted 

procedure is to compare the results of smog 

chamber experiments, usually in the form of 

concentration-time profiles, with simulations of 

the same experiments using the proposed 

mechanism. A sufficient number of experimental 

unknowns exis: in all such mechanisms that a 

certain degree of adjustment of rate constants (and 

perhaps products) is possible. The inherentvalidity 

or accuracy of any mechanism should be judged on 

the basis of how realistic the parameter variations 

are. 

Uncertainties in the kinetic mechanism are 

related to inaccurately known rate constants or 

products for reactions in the mechanism. 

Uncertainties associated with comparison of the 

predictions of the mechanism to experimental 

smog chamber data arise, in addition, because the 

properties of the photochemical reactor, associated equipment, and experimental procedures 

are not completely known. The accuracy of any 

method based on smog chamber data for relating 

precursor emissions or concentrations to oxidant 

levels, (whether +t is based d'+rectly on ozone 

isopleths as a function of initial precursor 

concentrations or on a kinetic mechanism 

validated with smog chamber data) depends on the 

extent to which the influence of the smog chamber 

on the homogeneous kinetics is understood. Some 

of the specific chamber effects that must be 

considered are the spectral distribution and 

absolute intensity of the photolyzing lamps; the 

adsorption, desorption, and chemical reaction of 

species on the walls; the initial loading of impurity 

species in the chamber air or on the walls; and the 

effects of leakage, sampling, and possible 

temperature variations during the run. Of these 

effects, probably the most important are the effects 

of the photolyzing lamps and of species absorbed 

on the walls. Photolytic rates of absorbing species 

cannot be predicted with accuracy if the incident 

light intensity distribution is not known with 

accuracy. This information must be coupled with 

the absolute rate of photolysis of at least one 

species, such as NOz, in order to compute the 

appropriate photolytic rate constants. 

Characterization of the initial contaminant loading 

in the gas and on the walls is important in 

simulating the proper initial rates of conversion. 

In summary, the three classes of phenomena 

that often require treatment as parameters in 

kinetic mechanisms in simulating smog chamber 

data are: (1) unknown rate constants, (2) the 

photolytic properties of the reactor, and (3) wall 

absorption, desorption, and heterogeneous 

chemistry. Tuning the mechanism to account for 

unknown or uncertain chemical and physical 

effects is a legitimate procedure provided that the 

exact steps are spelled out in detail and lie within 

physically realistic bounds. Recent experimental 

elucidation of NOx/HOX chemistry (reactions of OH 

and H02 with NO and NOz) and PAN chemistry has 

significantly improved the accuracy of postulated 

mechanisms for photochemical air pollution. 

There still exist, however, important uncertainties 

in ROX/NOx chemistry (reactions of RO and R02 

with NO and NO2). Nevertheless, a properlytuned 

mechanism is capable of predicting the 

110 
concentration-time profiles of species such as NO, 

NOz, ozone, and hydrocarbons within 20 percent 

over a wide range of initial conditions. In theory, 

such a mechanism, minus the steps included to 

account exclusively for chamber effects, should be 

capable of predicting atmospheric concentrations 

with the same accuracy. 

Ozone prediction uncertainties due to 

uncertainties in the meteorological and emission 

inventory input data have been explored in a 

comprehensive sensitivity study by Liu et a1. 30 The 

uncertainties in predicted ozone concentrations 

from all mechanisms and input uncertaintieswere 

estimated by Seinfeld51 (Table 6-4). These estimates 

from the evaluation studies illustrate the magnitudes 

of the possible errors associated with the various 

components of an AQSM. The total error, of course, 

cannot be determined from such ciata alone. Seinfeld 

did estimate an overall uncertainty value of ± 50 percent. 

TABLE 6-4. UNCERTAINTIES IN PREDICTED OZONE 

CONCENTRATIONS FROM ALL MECHANISMS AND 

INPUT UNCERTAINTIES 

Uncertainty in predicted 

Source absolute ozone concentrations, % 

Chemlcal mechanlsm ±20 

Meteorology 

Wind speed and dlrectlon ±20 

Mixing depth ±25 

Llght Intenslty ±20 

Initlal and boundary condltlons ±50 

Emission Inventortes. 

NO. ±20 

Hydrocarbons ±30 

Evaluation studies using some of the current 

AQSM's are summarized in Table 6-5. As shown, 

the variety of regions and conditions for wrich the 

AQSM's have been evaluated is limited. In 

particular, there is a lack of evaluations under 

widely varying emission conditions. Most 

important, however, evaluation periods have been 

limited to 1 to 3 days, or 6 days atthe most. Overall, 

the past evaluations are inadequate in several 

respects. First, because of deficiencies in the data 

bases used, it is difficult to discern whether or not 

the disagreements between prediction and 

observations are the result of errors in the model, 

inaccuracies in input parameters, or deviations 

arising from comparison of point data and volumeaverage prediction. Second, the variety of 

conditions used in the verification tests was 

limited, as already mentioned. Third, and perhaps 

most important, the amount of verification in terms 

of number of test days is limited to the extentthat 

the resulting assessment of the model's accuracy 

is qualitative, at best; certainly, it'is not sufficient 

for statistically supported quantitative estimates. 

And finally, another problem in interpreting results 

from current verificatlon studies isthatoftuning of 

model parameters or inputs (adjustment of some 

influential parameters within their uncertainty 

limits to maximize agreement between predictions 

and observations). Such tuning varies in extent 

from study to study. However, even in the most 

serious studies, there are required data (e.g., initial 

and boundary concentrations aloft) that are simply 

not available and must be estimated; such input 

data are often adjusted to obtain the best fit. Thus 

the value of the model predictions is lessenedto an 

extent, depending on the amount of tuning 

performed and, more important, on the sensitivity 

of the model to the parameters tuned. 

A major verification study involving several of 

the current AQSM's is now close to completion 

a nd has been reported extensively.' 5 Known as the 

St. Louis Regional Air Pollution Study (RAPS), this 

study is a 5-year field program sponsored by EPA. 

The major objective is the development, evaluation, and verification of AQSM's. The magnitude of the study is such that the amount of data to 

be obtained will be adequate for a statistical 

assessment of AQSM performance. Thus some 50 

simulation days will be considered for statistical 

evaluation of each model. The statistical 

procedures to be used will be based on methods 

such as those reported by Brier, 4 Nappo, 36 and Liu 

et a1. 30 Following completion of this major effort, 

and based on AQSM performance standards to be 

defined, EPA will make judgments on the specific 

AQSM's to be recommended for use in the 

development of oxidant control strategies. 

SUMMARY 

Quantitative relationships between ambient 

oxidant/ozone and precursor emissions are 

needed for predicting the impact of emissions on 

air quality. Such reiationships represent, with 

varying degrees of complexity, the physical and 

chemical processes taking place in the atmosp here. 

The most fundamental approach to relating 

precursor emissions to oxidant air quality is that 

based on the equation of conservation of mass, 

which with the help of certain simplifying assumptions, is reduced to the atmospheric diffusion 

equation (equation 6-3). This approach, which 

uses AQSM's, requires knowledge of the wind 

IIIi 
field and boundary conditions of the region, the 

source emissions as a function of location and 

time, and a chemical reaction mechanism. The 

complexity of air quality simulation models 

(AQSM) is a source of both strength and weakness. 

The high degree of spatial and temporal detail 

makes the models suitable for a wide variety of 

applications, but at the expense of costly 

computations. No AQSM is a perfect description of 

the atmosphere; inaccuracies arise from 

assumptions needed to represent atmospheric 

turbulent processes in a manageable form and 

from uncertainties in the input information, such 

as chemical reaction rate constants. The largest 

sources of uncertainty in model predictions are 

caused by uncertainties in the initial and boundary 

conditions and in the chemical mechanism. 

Uncertainties are introduced also by errors in the 

wind, mixing height, and Ilght intensity, and in the 

HC and NOx emission inventory data. To date, 

verification of existing AQSM's has been 

inadequate in at least two respects. First, because 

of deficiencies in the data base used, it has been 

difficult to discern whether the disagreements 

between observations and model predictions are 

the result of errors in the model, inaccuracies in 

input parameters, or deviations arising from 

comparison of point data and volume-average 

prediction. Second, the amount of validation in 

terms of number of test days and the variety of 

conditions used in such validation have been 

limited to the extent that resulting assessments of 

model accuracy have been, at best, qualitative. 

Because AQSM's have not been developed to 

the point that their degree of accuracy is wellquantified, it has been necessary to employ 

empirical and semi-empirical methods for relating 

precursor emissions to oxidant air quality. Of the 

empirical methods for relating precursor 

emissions to oxidant air quality, linear rollback is 

the simplest; it is based on assumed 

proportionality between ambient oxidant/ozone 

concentration and the reactive organic emission 

rate. The method is of highly questionable validity 

and limited utility, since most information 

indicates that peak oxidant concentrations do not 

decrease linearly with reductions in hydrocarbon 

emissions. 

TABLE 6-5. PRIOR VALIDATION STUDIES OF AIR QUALITY SIMULATION MODELS 

Model Region Time periods Pollutants compared 

SAI e Portlons of south coast alr basln. 6 days In 1969 Valldation studles performed 

Both 50 x 50 ml and 80 x 100 ml 26 June 197441,45 wlth both the 15- and 31- step 

reglons. Denver, Colo (SAI, 1977) klnetic mechanlsms. In both versions, 

pollutants compared were NO, NO2, 

03, CO, reactive and unreactive 

hydrocarbons. 

LIRAQa San Franclsco Bay area. 26, 27 July 197331 Pollutants compared were NO, 

170 x 210 km reglon. A varlety 20 August 1973 31 NO2, 03, CO, reactive and unreactive 

of subreglons and grld slzes 26-28 September 1973 31 hydrocarbons. 

(1-5 km) were employed. 

DIFKIN e Trajectorles In south 6 days In 1969 Pollutants compared were N0, 

coast alr basln LARPP data 53 NO2, 03, CO, reactive and unreactive 

hydrocarbons 

Bell a Morrls, Essex, Hudson May-September 1972-1974. Cloud- 03, NO, NOz, S02 and computed 

countles, New Jersey less summer weekdays wlth 03 behavlor matches well the medlan 

(Comparlsons shown only for normal com-ective mlxing and of data. Computed concentratlon 

Hudson County). westerly wlnds Only days when levels of secondary specles agree 

the Integrated 0600-1300 hr solar qualltatively wlth levels measured In 

flux was greater than 200 New Jersey or elsewhere (acrolein, 

Langleys, average 0400-1300 hr acetaldehyde, formaldehyde, PAN, 

wlnd veloclty 6 7 ml/hr < v< H2O2, HNO2, HNO3) Levels of H02 

10 1 ml/hr, and 0400-1300 hr radlcals estlmated on the basis of 

wlnd dlrectlon was from 80 0 predlcted H2O2 levels. Levels of OH 

sector encompassing Essex County radicals estlmated on the basis of 

to the west-northwest 21 predlcted HNO3 levels 

°SAI = Systems Applications, Inc, LIRAQ = Livermore regional air quality, DIFKIN = diffusion kinetics, Bell = Bell Laboratories 

112 
The "Appendix-J method" is a modified version 

of linear rollback in which ambient oxidant/ozone 

is related to hydrocarbon precursors in the form of 

an upper limit curve derived from aerometric data 

from several cities on 6- to 9-a.m. NMHC and 

maximum oxidant concentration. The method is no 

more valid than linear rollback, except perhaps 

when used for one locality on the basis of data 

taken in that locality. Statistical methods that 

relate ambient oxidant/ozone to both HC and NOx 

precursors are superior to linear and modified 

rollback methods that are based only on 

hydrocarbon precursors. The methods, however, 

should be employed only for the locality from 

which the data on which they are based have 

come. 

An attempt to base the precursor/ozone 

relationship on chemical reality while avoiding the 

complex computational requirements ofAQSM led 

to the development by Dimitriades of peak oxidant 

isopleths as a function of initial hydrocarbon and 

NOX concentrations derived from smog chamber 

data. The advantage of the approach is that it is 

based on actual smog chamber data and also on 

the results of simulations with a chemical reaction 

mechanicm validated with smog chamber data. 

The limit jtions of the method arise from lack of 

spatial and temporal resolution and from the 

question• ble comparability of the atmosphere of a 

smog ch mber with the real atmosphere. 

In surimary, air quality simulation models 

represen the most fundamental approach to 

relating precursor emissions to oxidant air quality. 

Although AQSM's have now evolved to the point 

where ,hey can be employed with some 

confider ;e, they are still characterized by 

uncertainties that arise from our lack of ability to 

represent truly atmospheric processes. Based on 

extensive evaluation of several AQSM's with the 

St. Louis RAPS data, EPA will make judgments on 

speciflc AQSM's to be recommended. Because of 

their extensive computational requirements, even 

where fullyvalldated, theAQSM approach may not 

be suitable for all applications involving oxidant 

control planning. 

REFERENCES FOR CHAPTER 6 

Air Pollution Control Office Air Quality Criteria for 

Nitrogen Oxides APCO Publication No. AP-84, U S 

Environmental Protection Agency, Washington, D.0 

Bailey, B S Oxidant-HC-NO x relationships from 

aerometric data - L A. studies. /n: Scientific Seminar on 

Automotive Pollutants EPA-600/9-75-003, U S 

Environmental Protection Agency, Research Triangle 

Park, N C, February 1975 Sec 5, subsect C 

3 Boris, J. P., and D. L Book Flux corrected transport. I 

Shasta, a fluid transport algorithm that works. J. Comput 

Phys. 11:38-69, 1973. 

4. Brier, G W. Statistical Questions Relating to the 

Validation of Air Quality Simulation Models. EPA-650/4- 

75-010, U S. Environmental Protection Agency, 

Research Triangle Park, N C., March 1975. 

5. Caporaletti, J. M., L. N. Myrabo, P. Schleifer, A. Stanonik, 

and K R. Wilson. Statistical oxidant air quality prediction 

for land use and transportation planni ng. Atmos. Environ. 

11:449-458, 1977. 

6. Deardorff, J W A three-dimensional numerical 

investigation of the idealized planetary boundary layer. 

Geophys. Astrophys Fluid Dyn. 1 377-410, 1970. 

7. DeNevers, N, and J. R Morris Rollbac modeling Basic 

and modified. J. Air Pollut. Control Assoc 25.943-947, 

1975 

8 Dimitriades, B. An alternative to the Appendix-J method 

for calculating oxidant- and NOz-related control 

requirements. /n: International Conference on 

Photochemical Oxidant Pollution and Its Control 

Proceedings Vol. II. B. Dimitriades, ed. EPA-600/3-77- 

001 b, U.S. Environmental Protection Agency, Research 

Triangle Park, N.0 , January 1977 pp. 871-879 

9. Dimitriades, B Chemistry /n: Assessing TransportationRelated Air Quality Impacts. Special Report 167, National 

Academy of Sciences, Washington, D C., 1976. pp 8-20. 

10. Dimitriades, B. On the Function of Hydrocarbon and 

Nitrogen Oxides in Photochemical Smog Formation 

Report of Investigations RI 7433. U S Department of the 

Interior, Bureau of Mines, Washington, D C., September 

1970 

11 Dimitriades, B. Oxidant control strategies Part I. Urban 

control strategy derived from existing smog chamber 

data. Environ. Sci. Technol 11:80-88, 1977 

12. Dimitriades, B, chairman Smog Chamber Conference 

Proceedings U.S Environmental Protection Agency, 

Research Triangle Park, N C, April 1976 

13. Dimitriades, B The use of smog chamber data in 

formulating oxidant control strategies /n Report on UCARB Conference. Technical Bases for Control Strategies 

of Photochemical Oxidant. Current Status and Priorities 

in Research Univ of California Statewide Air Pollution 

Research Center Riverside, Calif , May 1976. 

14 Dimitriades, B. The use of smog chamber data in 

formulating oxidant control strategies /n. Report on UCARB Conference "Technical Bases for Control Strategies 

of Photochemical Oxidant Current Status and Priorities 

in Research." University of California, Statewide Air 

Pollution Research Center, Riverside, Calif , May 1976 

pp 76-95 

15 Dmerjian, K L Photochemical air quality simulation 

modeling. current status and future prospects /n. 

International Conference on Photochemical Oxidant 

Pollution and Its Control Proceedings Vol II B 

Dimitriades, ed EPA-600/3-77-001b, U S 

Environmental Protection Agency, Research Triangle 

Park, N C., January 1977 pp 777-794 

16 Dodge, M C. Combined use of modeling techniques and 

smog chamber data to derive ozone-precursor 

relationships /n: International Conference on 

Photochemical Oxidant Pollution and Its Control 

Proceedings. Vol II B Dimitriades, ed EPA-600i3-77- 

001b, U S Environmental Protection Agency, Research 

113 
Triangle Park, N.0 , January 1977 pp, 881-889 

17. Dodge, M. C Effect of Selected Parameters on Prediction 

of a Photochemical Model EPA-600/3-77-048, U S 

Environmental Protection Agency, Research Triangle 

Park, N.0 , June 1977. 

18 Edelson, D A simulation language and compiler to aid 

computer solution of chemical kinetic problems Comput 

Chem. 1:29-33, 1976 

19 Eschenroeder, A Q, and J R Martinez. Concepts and 

applications of photochemical smog models Adv Chem 

Ser.(113): 101-168, 1972. 

20 Friedlander, S K, and J H Seinfeld. A dynamic model of 

photochemical smog Environ. Sci. Technol 3 - 1175- 

1181, 1969 

21 Graedel, T E, L A Farrow, and T A Weber Y.inetic 

studies of the photochemistry of the urban troposphere. 

Atmos. Environ 10:1095-1116, 1976 

22. Hecht, T. A Urban Air Shed Photochemical Simulation 

Model Study Vol I Development and Evaluation 

Appendix B. Generalized Mechanism for Describing 

Atmospheric Photochemical Reactions EPA-R4-73- 

030c, U S Environmental Protection Agency, Research 

Triangle Park, N C, July 1973 

23 Hecht, T A, J H Seinfeld, and M. C Dodge Further 

development of generalized kinetic mechanism for 

photochemical smog Environ Sci Technol 8 327-339, 

1974 

24 Heuss, J M, G J Nebel, and J M Colucci National air 

quality standards for automotive pollutants - A critical 

review J Air Pollut Control Assoc. 21 535-544, 1971 

25 Hindmarsh, A C GEARB Solution of Ordinary 

Differential Equations Having Banded - Jacobian 

University ofCalifornia, Lawrence Livermore Laboratory, 

Livermore, Calif UCID-30059, Rev. 1, 1974 

26 Kinosian,J R.,andJ J Paskind Hydrocarbons, Oxides of 

Nitrogen, and Oxidant Trends in the South Coast Air 

Basin, 1963-1972 State of California, Air Resources 

Board, Sacramento, Calif , June 1973 

27. Lamb, R G Continued Research in Mesoscale Air 

Pollution Modeling Vol III Modeling of Microscale 

Phenomena EPA-600/4-76-016c, U S. Environmental 

Protection Agency, Research Triangle Park, N C, May 

1976 

28 Lamb, R G, W H Chen, and J H Seinfeld Numericoempirical analysis of atmospheric diffusion theories J 

Atmos Sci. 32 1784-1807, 1975 

29. Liu, M. K., and P. M Roth UrbanAir Shed Photochemical 

Simulation Model Study Vol. I Development and 

Evaluation. Appendix C Microscale Model of Local 

Vehicular Source Contributions to Measured Pollutant 

Concentrations EPA-R4-73-030d, U S Environmental 

Protection Agency, Research Triangle Park, N.0 , July 

1973. 

30 Liu, M K., D C Whitney, J H Seinfeld, and P M Roth 

Continued Research in Mesoscale Air Pollution 

Simulation Modeling Vol I Assessment of Prior Model 

Evaluation Studies and Analysis of Model Validity and 

Sensitivity. EPA-600/4-76-016a, U.S. Environmental 

Protection Agency, Research Triangle Park, N C, May 

1976. 

31. MacCracken, M C, and G D Sauter, eds Development 

of an Air Pollution Model for the San Francisco Bay Area 

Final Report to the National Science Foundation Vols. 1 

and 2. UCRL-51920, University of California, Lawrence 

Livermore Laboratory, Livermore, Calif , October 1975 

32 Martinez, J R User's Guide to Diffusion/Kinetics 

(DIFKIN) Code EPA-R4-73-012b, U S Environmental 

Protection Agency, Research Triangle Park, N C, October 

1972. 

33 Merz, P H, L J Painter, and P R Ryason Aerometric 

data analysis-time series analysis and forecast and an 

atmospheric smog diagram Atmos Environ 6 319-342, 

1972 

34. Myrabo, L N, P Schleifer, and K. R. Wilson Oxidant 

Prediction Model for Land Use and Transportation 

Planning. California Air Environment 4 3, 1974 

35 Myrabo, L N, K R Wilson, and J C Trijonis Survey of 

statistical models for oxidant air quality prediction. /n. 

Assessing Transportation-Related Air Quality Impacts 

Special Report 167, National Academy of Sciences, 

Washington, D.0 , 1976 pp 46-62 

36 Nappo, C J, Jr A method for evaluating the accuracy of 

air pollution prediction models Symposium on 

Atmospheric Diffusion and Air Pollution American 

Meteorological Society, Boston, Mass , 1974 pp 325- 

329 

37 National Academy of Sciences Air Quality and 

Automobile Emission Control A Report by the 

Coordinating Committee on Air Quality Studies Vol 3 

The Relationship of Emissions to Ambient Air Quality 

Studies prepared for the Committee on Public Works, 

U S Senate U.S Government Printing Office, 

Washington, D C., 1974. 

38. National Research Council Ozone and Other 

Photochemical Oxidants. National Academy of Sciences, 

Washington, D C , 1976. 

39 Office of Air Quality Planning and Standards Uses, 

Limitations and Technical Basis of Procedures for 

Quantifying Relationships Between Photochemical 

Oxidants and Precursors. EPA-450/2-77-021a, U S 

Environ'mental Protection Agency, Research Triangle 

Park, N C, November 1977 

40 Pitts, J N, Jr., A. M. Winer, K. R Darnall, G. J Doyle, and 

J M McAfee Chemical Consequences of Air Quality 

Standards and of Control Implementation Programs 

Roles of Hydrocarbons, Oxides of Nitrogen and Aged 

Smog in the Production of Photochemical Oxidant 

California Air Resources Board Contract No 4-214, 

University of California, Statewide Air Pollution Research 

Center, Riverside, Calif., May 1976 

41 Ranzieri, A., California Air Resources Board, 

Sacramento, Calif. Personal Communication to Prof J H 

Seinfeld, Calif Inst Technology, Pasadena, Calif , 1977 

42 Reynolds, S D, J Ames, T A Hecht, J P Meyer, D C. 

Whitney, and M A Yocke Continued Research in 

Mesoscale Air Pollution Simulation Modeling Vol II 

Refinements in the Treatment of Chemistry, 

Meteorology, and Numerical Integration Procedures. 

EPA-600/4-76-016b, U.S. Environmental Protection 

Agency, Research Triangle Park, N C, May 1976 

43. Reynolds, S D Urban Air Shed Photochemical 

Simulation Model Study Vol I Development and 

Evaluation. Appendix D. Numerical Integration of 

Continuity Equations. EPA-R4-73-030e, U S 

Environmental Protection Agency, Research Triangle 

Park, N C., July 1973 

114 
58. U,S. Environmental Protection Agency. National primary 

and secondary air quality standards Fed Regist 

36.•8186-8201, April 30, 1971 

59 U.S. Environmental Protection Agency. Requirementsfor 

preparation, adoption, and submittal of implementation 

plans Fed Regist. 36:15486-15506, August 14, 1971. 

60. U.S. Environmental Protection Agency. Technical 

Support Document for the Metropolitan Los Angeles 

Intrastate Air Quality Control Region Transportation 

Control Plan Final Promulgation Published in November 

12, 1973 Federal Register. U.S. Environmental 

Protection Agency, Region IX, San Francisco, Calif., 

October 30, 1973 

61. Walker, H M A"J" relationship for Texas. /n. 

International Conference on Photochemical Air Pollution 

and Its Control Proceedings Vol. I B Dimitriades, ed. 

EPA-600/3-77-001 b, U S. Environmental Protection 

Agency, Research Triangle Park, N.0 , January 1977. pp. 

851-869. 

62 Whitten, G. Z., and H. Hogo Mathematical Modeling of 

Simulated Photochemical Smog EPA-600/3-77-011, 

U.S. Environmental Protection Agency, Research 

Triangle Park, N C, January 1977. 

44 Reynolds, S D., M. K Liu,T A. Hecht, P. M Roth, andJ. H. 

Seinfeld. Urban Air Shed Photochemical Simulation 

Study Vol I Development and Evaluation. EPA-R4-73- 

030a, U S. Environmental Protection Agency, Research 

Triangle Park, N.C., July 1973. 

45 Reynolds, S D, M K. Liu,T A. Hecht, P M Roth, andJ. H 

Seinfeld Mathematical modeling of photochemical air 

poilution III Evaluation of the model. Atmos. Environ. 

8.563-596, 1974 

46. Reynofds, S. D, P. M Roth, and J H. Seinfeld. 

Mathematical mbdeling of photochemical air pollution. I. 

Formulation of the model Atmos. Environ. 7:1033-1061, 

1973 

47 Reynolds, S D, and J. H Seinfeld. Interim evaluation of 

strategies for meeting ambient air quality standard for 

photochemical oxidant Environ. Sci Technol 9:433- 

447, 1975. 

48. Roberts, P. J., M. K Liu, S D. Reynolds, and P. M Roth. 

Urban Air Shed Photochemical Simulation Model Study. 

Vol I Appendix A Contamrnant Emissions Model and 

Inventory for Los Angeles. EPA-R4-73-030b, U.S. 

Environmental Protection Agency, Research Triangle 

Park, N C., July 1973. 

49 Roth, P. M, P J. W. Roberts, M. K. Liu, S. D Reynolds, and 

J H. Seinfeld. Mathematical modeling of photochemical 

air pollution II. A model and inventory of pollutant 

emissions. Atmos. Environ. 8:97-130, 1974. 

50. Schuck, E. A., A. P Altshuller, D. S. Barth, and G. B 

Morgan. Relationship of hydrocarbons to oxidants in 

ambient atmospheres J. Air Pollut. Control Assoc. 

20:297-302, 1970 

51. Seinfeld, J. H. International Conference on Oxidants, 

1976—Analysis of Evidence and Viewpoints. Part VI. The 

Issue of Air Quality Simulation Model Utility. EPA600/3-77-118, U.S. Environmental Protection Agency, 

Research Triangle Park, N.C., November 1977. 

52. Souten, D. R., C. J. Hopper, and R. L Mueller A critical 

review of the Los Angeles County APCD method for 

simulating atmospheric oxidant based on smog chamber 

irradiation experiments. Presented at the 68th Annual 

Meeting, Air Pollution Control Association, Boston, 

Mass., June 15-20, 1975. 

53. Taylor, G. H., and A Q. Eschenroeder. Testsof the DIFKIN 

photochemical/diffusion model using Los Angeles 

reactive pollutant data /n: International Conference on 

Photochemical Oxidant Pollution and Its Control. 

Proceedings Vol. II. B Dimitriades, ed. EPA-600/3-77- 

001b, U.S Environmental Protection Agency, Research 

Triangle Park, N.0 , January 1977. pp. 817-825. 

54. Tiao, G. C., M. S Phadke, and G. E. P. Box Some empirical 

models for the Los Angeles photochemical smog data. 

Presented at the 68th Annual Meeting, Air Pollution 

Control Association, Boston, Mass., June 1975. 

55 Trijonis, J. C. Economic air pollution control model `,or Los 

Angeles County in 1975 General least cost air quality 

model Environ, Sci. Technol 8.811-826, 1974. 

56. U S. Environmental Protection Agency. Approval and 

promulgation of implementation plans Promulgation of 

Texas transportation control plan. Fed. Regist.38:30633- 

30650, November 6, 1973 

57. U S Environmental Protection Agency Approval and 

promulgation of implementation plans. Boston, Mass : 

Promulgation of transportation control plan. Fed. Regist. 

38:30960-30971, November 8, 1973 

115 
7. MEASUREMENT METHODS FOR OZONE, OXIDANTS, AND 

THEIR PRECURSORS 

INTRODUCTION 

Since the publication of the air quality criteria 

documents for photochemical oxidants, 60 hydrocarbons, s ' and nitrogen oxides,' there have been 

significant advances in the measurement of these 

pollutants in ambient air. The chemiluminescent 

reaction of Os with ethylene has been successfully 

exploited to produce instrumentation whose 

response is spectific for Os and is linear with 03 

concentrations over the range found in ambient 

air Advances in electronics technology have 

allowed development of photometers of adequate 

precision to measure Os by ultravioiet absorption 

photometry. Continuous analyzers based on the 

chemiluminescent reaction of NO with Os have 

been successfully developed for the measurement 

of NO, nitrogen dioxide (NO2), and oxides of 

nitrogen (NOx). Improved manual (integrated) 

methods for measuring NO2 have also been 

developed. Lesser advances have been reported in 

the measurement of ambient hydrocarbons and 

peroxyaclynitrates. 

The emphasis in this chapter will be placed 

primarily on methods for measuring Os, on the 03/ 

oxidant relationship, and on methods for 

measuring hydrocarbons and NO, NOz, and NOX. 

Continuous methods for measuring total oxidants 

based on the reaction of ambient air oxidants with 

potassium iodide (KI) will also be discussed briefly. 

A more detailed discussion of total oxidant 

methodology is given in the earlier criteria 

document.sa 

SAMPLING FACTORS IN AMBIENT AIR 

MONITORING 

In addition to analyttical principles and 

measurement procedures, sampling factors also 

have a crucial effect on the quality of ambient and 

experimental atmosphere measurements. In 

sampling the ambient atmosphere, it is extremely 

important that the sampling be performed in a 

manner that (1 ) is consistent with the specific 

purpose of the measurement, and (2) preserves the 

integrity of the pollutant mixture in the ambient air 

sample. These sampling factors and their 

significance in Os or oxidant-related air quality 

monitoring will be discussed here briefly. For more 

detailed discussions of this subject, the reader is 

referred to other EPA documents and to reports 

prepared for EPA by the National Academy of 

Sciences,62,63,67,72 

Air monitoring data relevanttotheambientO s or 

oxidant problem are collected for a diversity of 

specific purposes, including serving as an indicator 

of progress in attainment of the nationai ambient 

air quality standard for Os in the development of Os 

control strategies, in the development and validation of ozone-related air quality simulation 

models, in the investigation of causes of ozone 

problems, etc. Each of these specific purposes or 

needs requires special considerations in designing 

an air sampling strategy responsive to the 

respective need. For example, statistical 

considerations enter into the design of a monitoring network capable of detecting air quality 

changes over a given period of time. Other 

considerations arising from the chemical, physical, 

and meteorological aspects of the ambient ozone 

problem are explained briefly as follows. 

Ozone is a product of photochemical reactions 

that involve sunlight, hydrocarbon, and NOx reactants, which are heavily discharged into urban 

atmospheres by automobiles during the morning 

peak traffic hours. This photochemical process 

occurs at a rate such that the Os concentration 

reaches its daily peak level some time in midday at 

locations downwind from the source-intensive 

center-city area. Thus if peak Os concentrations 

are to be measured, monitoring stations should be 

located downwind from city centers at distances 

that have been determined by EPA to be 15 to 30 

km (9 to 19 miles), depending on the area's 

predominant wind patterns. s' Monitoring stations 

should also be located within the source-intensive 

116 
area for measurement of peak concentrations of 

oxidant precursors. Once a station is located, 

additional considerations arise because of the 

chemical reactivity and instability of the 03 

molecule. Ozone reacts extremely rapidly with NO 

and with some hydrocarbon compounds, including 

most of those emitted by vegetation. Also, 03 

decomposes readily on contact with the surface of 

many materials. Consideration of these effects led 

to the development of specific criteria for locating 

an 03 monitoring station. s2,s3,s7,7z Briefly, the inlet 

of the 03 analyzer's sampling probe should be 

positioned 3 to 15 m(10 to 49 ft) above ground, at 

least 4 m t13 ft from large trees, and 120 m(394 ft) 

from heavy automobile traffic. Sampling probes 

should be designed to minimize 03 destruction by 

surface reaction or by reaction with NO. 

Air monitoring data, as commonly obtained, 

have only limited validity as measures of absolute 

air quality. The reason is that at ground level, the 

ambient atmosphere is inhomogeneous as a result 

of a continuous influx of fresh emissions, 

incomplete mixing, and destruction of 03 by fresh 

and unreacted emissions. In view of such 

inhomogeneity, monitoring data from a fixed 

network provide measures of air quality at a 

discrete number of locations but may not detect 

possibly existing hot-spots. This problem can be 

alleviated by use of a greater density of monitoring 

stations or, perhaps at a lower cost, by use of an air 

quality model. Such models (Chapter 6) are 

capable of quantifying the emission dispersion and 

chemical reactions processes, and their outputs 

can provide data on the distribution of air qtlality 

concentrations between widely spaced ambient 

monitors. 

MEASUREMENT OF OZONE 

Gas-Phase Chemiluminescence (EPA Reference 

Methods) 

The U.S. Environmental Protection Agency 

promulgated National Ambient Air Quality 

Standards (NAAQS) for six pollutants on April 30, 

1971. 104 The standards are now codified at Title 

40, Code of the Federal Register (40 CFR), Part 50. 

At the same time, EPA published reference 

methods (presently described in the appendices to 

Part 50) to be used by EPA and by state and local 

agencies in measuring ambient concentrations of 

the six pollutants. Appendix D of 40 CFR Part 50 for 

the measurement of photochemical oxidants 

describes the measurement principle for an 

automated method (analyzer) based on the gasphase chemiluminescent reaction of 03 with 

ethylene.65 '99 Measurements made with analyzers 

based on this principle are therefore ozonespecific and differ from measurements made with 

analyzers designed to measure total oxidant. 

These analyzers are designed such that ambient 

air and ethylene are delivered simultaneously to a 

reaction cell where the 03 in the air reacts with the 

ethylene. The reaction produces a small fraction of 

an energetically excited species (thought to be an 

electronically excited formaldehyde molecule) that 

decays to the ground state with the emission of 

light. The intensity of' the emitted light 

(chemiluminescence), which is detected by a 

photomultiplier tube, is proportional to the 03 

concentration over the range of 4 to at least 5000 

/ug/m3 (0.002 to at least 2.5 ppm). The quantitative 

relationship between the intensity of the 

chemiluminescence and the 03 concentration 

must be established for each analyzer, using 

atmospheres containing known concentrations of 

03 • 

Analyzers utilizing the gas-phase chemiluminescence measurement principle have been 

evaluated under a variety of conditions. ' '

'b,22,9a 

These studies indicate that the performance of 

commercially available analyzers is generally 

satisfactory. However, the results of a 

collaborative test by McKee et al. indicated 

considerable variability and a negative bias of 16 to 

37 percent. 58 The reason for the variability is no 

doubt, in part, the variability in the 1 percent 

neutral buffered potassium iodide (NBKI) 

calibration procedure, which is discussed in detail 

in a subsequent section on 0 3 calibration 

procedures. The reported negative bias is in 

conflict with subsequent studies of the 1 percent 

NBKI procedure, which generally indicate that this 

procedure produces a positive bias of 5 to 30 

percent (see section on 03 calibration procedures). 

Under the provisions of the Ambient Air 

Monitoring Reference and Equivalent Methods 

Regulations 102 promuigated February 18, 1975 (40 

CFR Part 53), several commercial analyzers have 

been designated as reference methods for 

determining compliance with the NAAQS for 

photochemical oxidants. These analyzers have 

been subjected to the required testing and have 

met the EPA performance specifications for 

automated methods. These specifications are 

given in Table 7-1, and a list of the ozone analyzers 

(designated as of March 3, 1978) is given in Table 

117 
7-2. Information concerning the applications 

supporting the designation of these analyzers as 

reference or equivalent methods may be obtained 

by writing the Environmental Monitoring and Support Laboratory, U.S. Environmental Protection 

Agency, Research Triangle Park, North Carolina 

27711. 

TABLE 7-1. PERFORMANCE SPECIFICATIONS FOR 

AUTOMATED METHODS 

Performance parameter Ozone 

Range, ppm 0-0.5 

Noise, ppm 0 005 

Lower detectable limit, ppm 001 

Interference equivalent: 

Each interferant, ppm ±0.02 

Total interferant, ppm 006 

Zero drift, 12- and 24-hr, ppm ±0 02 

Span drift, 24-hr• 

20% of upper range limit, ppm ±20 0 

80% of upper range limit, ppm ±5 0 

Lag time, min 20 

Rise time, min 15 

Fall time, min 15 

Precision: 

20% of upper range limit, ppm 0.01 

80% of upper range limit, ppm 0.01 

A review of the performance data submitted in 

support of the designatlons listed in Table 7-2 

indicates that these analyzers exhibit performance 

better than that specified in Table 7-1. For the 

analyzers tested, the zero drift results (12- and 24- 

hr) were all lessthan 5 ppb and typically less than 3 

ppb. The span drift results (at 20 and 80 percent of 

the full-scale range of 0 to 0.5 ppm) were all less 

than 5 percent, and typically 2 to 3 percent. The 

precision results (at 20 and 80 percent of the fullscale range of 0 to 0.5 ppm) indicate a typical 

precision of 1 ppb. The response times (lag, rise, 

and fall) were all less than 2 min, and typically less 

than 1 min. The interference equivalent results 

(tests for carbon dioxide, hydrogen sulfide, and 

water vapor) were typically less than 1 ppb. 

However, under 40 CFR Part 53, the test procedure 

for water interference specifies that the test be 

conducted in the absence of 03. There have been a 

number of reports of a positive water interference 

of 3 to 12 percent under conditions of high 

humidity in the presence of 03,51,53,73 

Gas-Solid Chemiluminescence 

The measurement of 03 by a gas-solid chemiluminescence technique was first reported by 

Regener."'78 In Regener"s approach, air containing 

03 is passed across a surface of Rhodamine B and 

absorbed on slllca gel, resulting In the emisslon of 

light (chemiluminescence). The intensity of the 

erTiitted light is measured with a photomultiplier 

tube and is proportional to the concentration of 03 

in the air sample. The method is highly specific and 

extremely sensitive (lower detection limit less than 

0.001 ppm). Because the sensitivity of the 

chemiluminescence surface gradually decays with 

time, automated analyzers based on this 

measurement principle are designed to 

incorporate frequent internal calibration cycles. 

Prototype Regener 0 3 analyzers have been 

evaluated under fleld conditions and have given 

excellent performance. 6 

A commercial analyzer, based on a slight 

modification of the gas-solid chemiluminescence 

principle, has been designated as an equivalent 

method under the EPA40 CFR Part 50 regulations 

(Table 7-3). This analyzer, the Philips Model 

PW9771 03 Monitor, uses a detector disc 

containing Rhodamine B and an intermediate 

reagent, gallic acid. The 03 in the air sample reacts 

with the gallic acid to produce oxygen and a gallic 

acid derivative, which in turn reacts with the 

Rhodamine B to produce the chemiluminescence. 

Ultraviolet Photometry 

Older ozone monitors, based on the absorption 

of ultraviolet (UV) light, and their attendent 

problems are described in the earlier criteria 

document for photochemical oxidants. 60 Modern 

electronic techniques have permitted the 

successful development of an ambient 03 analyzer 

based on ultraviolet absorption. 12 This analyzer, 

the Dasibi Model 1003-AH Ozone Analyzer, has 

been designated as an equivalent method under 

the EPA 40 CFR Part 53 regulations (Table 7-3). 

The absorption of 254 nm ultraviolet light by 03 in 

an ambient air sample is measured, and a separate 

measurement is made on a similarairsamplefrom 

which the 03 has been removed by a manganese 

dioxide (Mn02) scrubber. These two 

measurements are processed electronically to 

produce a digital readout of the 03 concentration in 

the air sample. The 03 determination is based on 

the well established absorption coefficient of 03 for 

254 nm Ilght, 23,32,36,43,100 

Although not in wide use, this method is used 

extensively in California. Its main advantage is that 

it does not require the use of support gases such as 

ethylene (as is the case with the gas-phase 

chemiluminescence methods). In addition, the 03 

measurement can be referenced to the absorption 

118 
coefficient of 03 without reference to a dynamic 

calibration standard. In practice, however, 

analyzers may require dynamic calibration with 03 

standards because of problems associated with 

sample integrity. While potential interferences are 

few, there are some ambient pollutants, including 

sulfur dioxide and benzene, that absorb light at 254 

nm. Presumably, these potential interferants are 

unaffected by the Mn02 scrubber and therefore do 

not interfere with the ozone measurement. 

However, if the Mn02 scrubber eliminates or 

reduces such components, the analyzer gives 

erroneous readings. Field use of this analyzer is 

discussed by Zafonte et al.' oa 

MEASUREMENT OF TOTAL OXIDANTS 

The methods most frequently used in the past for 

measurement of ambient total oxidants were 

based on the oxidation of potassium iodide (KI) in 

solution and the electrochemical or colorimetric 

detection of the iodine(12) produced. The KI reagent 

produces 12 by reaction with 03, NO2, peroxyacylnitrates, chlorine (02), bromine (Br2), and peroxides. 4o,as,tol Reducing agents such as S02 are 

negative interferants because they react with the 1 2 

formed by the oxidizing species. Terms such as 

"corrected oxidant" or "adjusted oxidant" have 

often been used to indicate that the oxidant 

measurement has been corrected for 

interferences from NOx and/or S02. The corrected 

or adjusted measurement results are then taken to 

represent an oxidant mixturethat is predominantly 

03 with small amounts of other oxidizing compounds. 

TABLE 7-2. LIST OF DESIGNATED REFERENCE METHODS 

Designation Fed Register Notice 

number_ Identification and source Vol Page Date 

RFOA-1075-003 Meloy Model OA 325-2R Ozone Analyzer 40 54856 11 /26/75 

Meloy Laboratortes, Inc 

6715 Electrontc Drive 

Springfield, Virginia 22151 

RFOA-1075-004 Meloy Model OA 350-2R Ozone Analyzer 40 54856 11 /26/75 

Meloy Laboratortes, Inc 

6715 Electrontc Drtve 

Springfteld, Virginta 22151 

RFOA-1076-007 Bendtx Model 8002 Ozone Analyzer 41 5145 2/4/76 

The Bendix Corporation 

Post Office Drawer 831 

Lewisburg, West Virginta 24901 

RFOA-1076-014 MEC Model 1100-1 Ozone Meter 41 466747 10/22/76 

RFOA-1076-015 MEC Model 1100-2 Ozone Meter 30235 6/13/77 

RFOA-1076-016 MEC Model 1100-3 Ozone Meter 

Columbia Scientiftc Industrtes 

11950 Jollyville Road 

P 0 Box 9908 

Austin, Texas 78766 

RFOA-1176-017 Monitor Labs Model 8410E 41 53684 12/8/76 

Ozone Analyzer 

Monttor Labs, Inc 

4002 Sorrento Valley Blvd 

San Dtego, California, 92121 

RFOA-0577 Beckman Model 950A Ozone Analyzer 42 28571 6/3/77 

2500 Harbor Boulevard 

Fu llerto n, Ca lifornia 92634 

TABLE 7-3. LIST OF DESIGNATED EQUIVALENT METHODS 

Designation 

number Identification and source 

EQOA-0777-023 Phtltps PW9771 03 Analyzer,~ 

Phtltps Electronic Instruments, 

85 McKee Drtve 

Mahwah, New Jersey 07430 

EQOA-0577-019 Dastbt Model 1003-AH 

Analyzer 

Dasibt Environmental Corp 

616 E Colorado St 

Glenda le, Cat ifornta 91205 

Fed Reaister Notice 

Vol Page Date 

42 38931 8/1/77 

Inc 

42 28571 6/3/77 

119 
A variety of KI methods have been used for the 

continuous measurement of ambient total 

oxidants. Amperometric 85' 101 (often called coulometric) analyzers draw the air sample into a sensor 

cell where the oxidant reacts with the electrolyte 

(neutral buffered KI:KBr solution) to release 1 2 . The 

1 2is in turn reduced back to iodide, either 

electrolytically with a bias voltage across the cell, 

as used by mast, or galvanically, with different cell 

electrode materials according to Hersh and 

Deuringer. 37 Nitrogen dioxide is a positive 

interferant that causes a response equivalent to 3 

to 20 percent of that of Os, depending on a detector 

design, operating conditions, and other unknown 

factors. Sulfur dioxide results in a negative 

interference if 1 2is present in the electrolyte. When 

oxidant is present in excess, a given concentration 

of SOz reduces the oxidant response on a mole 

Os/mole SOz basis. 

Colorimetric analyzers utilize either a 10- or a 

20-percent neutral buffered Klao,so,,o, solution. 

Oxidants react with KI to produce I zand the triiodide ion (Ts ), which is formed in the presence of a 

large excess of iodide ion and is measured in a 

continuous colorimeter. Sulfur dioxide results in a 

negative response similar to the case for the 

amperometric analyzer. Nitrogen dioxide causes a 

positive response equivalent to 21 and 30 percent 

of that of 03 for the 10- and 20-percent KI 

analyzers, respectively. 

To eliminate errors resulting from S02 

interference with these KI methods, it is necessary 

either to measure SOz and adjust the total oxidant 

measurement appropriately, or to remove S02 by 

passing the air sample through a chromium 

trioxide (CrOs) scrubber. 40 In the first case, 

adjustments can be made only if the oxidant levels 

are in excess of the SOz levels. In the latter case, 

the Cr03 scrubber rriay cause new interferences by 

partially oxidizing the nitric oxide (NO) and 

hydrogen sulfide (H2S) possibly present in the 

sample to NO 2and S02, respectively, and by 

destroying part of the oxidant. Because of these 

potential problems, this method of correcting for 

SOz interference can be used reliably only in 

certain situations and only by skilled ana lysts. ss,95,, o, 

OZONE CALIBRATION PROCEDURES 

Calibration of 03 analyzers is complicated by the 

lack of Standard Reference Material (SRM) for Os 

analogous to those available from and certified by 

the National Bureau of Standards (NBS) for S02, 

NO, and carbon monoxide (CO). The instability of 

Oa prohibits the storage of Os standards for any 

practical length of time. Therefore, standard 

samples in air for calibration of Os analyzers must 

be generated and analyzed at the time and place of 

use. Typically, Os atmospheres are generated by 

means of an 03 generator that delivers a stable 

concentration of Os. These- atmospheres are 

assayed by some technique to determine their Os 

concentration and then are used to calibrate the 

analyzer. The Os assay procedure may be based on 

one of several different primary standards. 

KI Calibration Procedures 

Until recently, Os and total oxidant analyzers 

have been calibrated using Os atmospheres that 

have been assayed using various KI procedures. 

Such procedures, however, have been severely 

criticized lately for lack of accuracy and precision. 9ts,2a,,o, Some specifics of these procedures 

and associated criticisms are briefly reviewed 

here. 

The determination of the precise Os atmospheres by the KI procedures consists of bringing 

the air/Os mixture into contact with buffered or 

unbuffered KI solutions of various concentrations. 

In theory, absorption of one molecule of Os in any 

of these solutions should result in formation of one 

molecule of 12 as shown by the following equation: 

2H + +21 - + 03= I2+02+H20 

The 12 in the presence of a large excess of iodide ion 

forms the intensely colored triiodide ion (1 3). - The 

concentration of 1-3 is determined using a 

spectrophotometer calibrated with standard 

solutions of 12 /KI, standardized against a primary 

standard such as arsenous oxide (AszOs). The most 

commonly used procedures utilize a 1- or 2-percent 

NBKI solution, or a 2-percent unbuffered KI(UKI) 

solution. When EPA first promulgated the 

regulations (40 CFR Part 50) on April 30, 1971, 104 

the 1-percent NBKI procedure was considered to 

be the best available for calibration of inethods for 

measuring photochemical oxidants. This 

procedure is described in Appendix D of 40 CFR 

Part 50. 

Considerable evidence has accumulated to 

indicate that the use of NBKI calibration 

procedures can result in significant bias, 

variability, or both. These problems were 

documented in a joint EPA-NBS workshop held in 

August 1974. 19 Specific problem areas reported 

included purity of reagents, time for maximum 

color development, variability due to impinger type, 

120 
and a positive bias when compared to other ozone 

measurement methods such as UV photometry. 

An intercomparison of three KI procedures was 

carried out in California for the purpose of 

determining the relative (accuracy) responses and 

precisions of the three techniques. The three 

techniques were the 1-percent NBKI procedure (as 

used in the EPA reference method) the 2-percent 

NBKI procedure (as used by the California Air 

Resources Board), and the 2-percent UKI 

procedure (as used by the Los Angeles Air 

Pollution Control District). The absolute levels of 03 

were measured using UV photometry. The 

comparative results are fully described in a report 

by DeMore et a1. 24 and should be consulted for 

details. The major conclusions of the study are that 

the EPA (1-percent NBKI) and California Air 

Resources Board (2-percent NBKI) procedures give 

higher values by about 15 to 25 percent compared 

to the UV procedure. The Los Angeles County Air 

Pollution District procedure (2-percent UKI) gives 

values approximately 4 percent lower than the UV 

photometry measurements, but with considerable 

scatter in its values. Several other studies have 

indicated discrepancies and considerable 

variability between the various KI procedures and 

newly, developed procedures based on GPT and 

ultraviolet absorption (UV).9,15,99,41,91,53,73,79 AII of 

these and other studies have been reviewed 

recently'by Burton et al.' a 

Based on the results of the studies discussed or 

cited above, it can be concluded that the KI 

procedures for measuring 03, even when used in 

the laboratory by skilled operators, suffer from 

substantial systematic (accuracy-related) as well 

as random (precision-related) errors. The factors 

responsible for these errors, especiallythe random 

errors, are not well understood. They are probably 

related to differences in procedural detail among 

the various operators. When these KI procedures 

are used in the field by unskilled operators, such 

errors are certain to be considerably greater. The 

most important implication of these problems with 

the KI procedures is discussed later in the section 

on the relationships between ambient oxidant and 

ozone data. 

Recently Developed Calibration Procedures 

There ha& been a sustained effort to develop 

other techniques for measuring absolute concentrations of ozone in calibratipn atmospheres. 

These efforts have been successful, and it is all but 

certain that the KI calibration procedures will soon 

be replaced by one or more new techniques. 

0 n October 6, 1976, EPA published i n the Federr, 

alRegister 103a notice of its intent (1) to study and 

evaluate several alternative calibration procedures 

for reference methods for photochemical oxidants 

and (2) to amend Appendix D of 40 CFR Part 50 to 

revise the 1-percent NBKI calibration procedure or 

to replace it with one or more alternative 

procedures. Four alternative calibration 

procedures are currently under consideration: (1) 

GPT with excess NO, (2) UV photometry, (3) GPT 

with excess Os, and (4) boric acid KI (BAKI). A brief 

summary of each of these alternative proEedures 

follows. 

The Os calibration procedure utilizing GPT with 

excess NO is a relatively well developed procedure 

and very similar to that specified by EPA for 

calibration of NO2 reference method analyzers. 105 

The procedure is based on the reaction of Os with a 

known quantity of NO and uses available NO 

standards that can serve double duty in generating 

NO2 standards as well. However, an NO analyzer, 

which may not be readily available when 

calibrating Os analyzers, is required. In addition, 

the procedure is somewhat complex and requires 

accurate measurement of several gas flow rates. 

The UV photometry procedure is based on the 

absorption coefficient of Os at 254 nm, which has 

been well established by independent determinations. The procedure is quite easy to carry out, 

uses a physical measurement, and requires no 

other gases or critical flow measurements. 

However, the procedure as applied to the 

calibration of Os analyzers is relatively new and not 

in general use in the air monitoring community and 

has not been used extensively to measure Os in the 

sub-ppm range needed for ambient Os analyzer 

calibration. 

The procedure utilizing GPT with excess Os is 

similar to GPT with excess NO but has the 

advantage of not requiring an NO analyzer. If the 

residence time of the Os and NO reactants in the 

GPT reaction chamber is not carefully controiled, 

errors can resultfrom either incomplete reaction of 

NO or reaction of the resulting NO2 with residual 

Oa. For this reason, accurate use of the procedure 

is difficult, and further development may be 

required before it is recommended for use under 

field conditions. 

Boric acid KI is a modification of the NBKI 

calibration procedure. This procedure utilizes a 1- 

percent KI solution acidified with 0.1 molar boric 

121 
acid. Preliminary results indicate that this 

modification vastly improves both the variability 

and accuracy of the KI procedure. 27 

RELATIONSHIPS BETWEEN AMBIENT 

OXIDANT AND OZONE DATA 

The relationship, and more specifically the 

direction and magnitude of differences, if any, 

between chemiluminescence Os (chemilum-Oa) 

data and KI data taken in parallel from ambient 

atmospheres are of interest because they relate to 

the issue of the definition and justification of the 

numerical air quality standard for photochemical 

oxidants. 26 This issue arises from uncertainty 

regarding the specific species responsible for the 

health effects attributed to photochemical 

oxidants. The problem seems to be whether the 

epidemiological evidence or the ozone-specific 

toxicological evidence should be used as the main 

basis of the numerical air quality standard. Thus, 

for example, if the epidemiological evidence alone 

were selected as the main basis for the air 

standard, then the responsibility for the observed 

health effects would be placed on the entire 

photochemical pollution complex rather than on 

specific constituent(s), since epidemiological 

evidence is not pollutant specific. In that case, the 

smog constituent(s) measured and correlated with 

the epidemiological evidence (i.e., oxidants 

determined by KI) would be viewed as a surrogate 

species. This, in turn, introduces two , requirements. First, the numerical air quality 

standard must be defined either in terms of the 

same group of oxidants that was correlated with 

the epidemiological evidence (i.e., oxidants 

determined by the KI method) or in terms of an 

equivalent species (e.g., oxidants determined by 

the chemilum-O s method). An equivalent species 

is one present at concentrations equal to those 

determined by the KI method for measurement of 

oxidants. Second, the composition of the 

photochemical oxidants mixture, or at least the 

ratio of oxidants determined by the chemilum-Os 

method to oxidants determined by the KI method 

should be constant with location and time. 

In contrast to the preceding case, if toxicological 

evidence is used alone or in conjunction with 

epidemiological evidence to place the responsibility for the health effects on a specific 

species, Os for example, then the numerical air 

quality standard should be defined in terms of Os, 

and the correlation or lack of correlation between 

Os and other smog constituents could be disregarded as being irrelevant. 

The question of whether the air quality standard 

should be defined in terms of oxidant-bychemilum-03, oxidant-by-Kl, or any other 

measurable entity will not be examined here. The 

comparison, however, of oxidant data obtained by 

the KI method and by the chemilum-Os is relevant 

and will be discussed briefly. 

As discussed in the previous section on KI 

calibration procedures, the experiences from the 

laboratory application of KI procedures have 

demonstrated that such procedures, whether used 

in standardizing ozone mixtures or in measuring 

ambient oxidant, are substantially imprecise and 

inaccurate because of the effects from factors that 

are not completely understood. When the same 

standard Os mixtures are used to calibrate a KI 

method and the chemilum-O s method, then, 

obviously, any difference in ambient measurements obtained by the two methods reflects 

errors other than those related to calibration. Such 

errors include: (1) systematic errors related to the 

different response specificities of the two 

methods; (thus, for example, the KI method should 

give higher results because it responds to more 

oxidants than the chemilum-Os method), and 

perhaps more important, (2) disagreement 

between the two methods will reflect the 

unknown-origin random errors discussed in the 

preceding section. Because of the random nature 

of these latter errors, and because of their 

connection to the operator factor, the true 

difference in results between two methods cannot 

be determined from a single day"s side-by-side 

comparison of the two methods conducted by a 

single operator. Comparisons by a variety of 

operators using the same or equivalent calibration 

procedures over a span of many days are 

necessary if the comparison results are to be 

credible. 

Results from such multiday comparisons of KI 

procedures with other methods have been 

reported in an averaged form by several 

investigators. Such results have been reported in 

the predecessor to this criteria document 60 and 

more recently by Ballard et al.,' Stevens et al.,' oo 

Clark et a1., 18 and the California Air Resources 

Board. 16 These recent results show, in general, 

small differences between KI-oxidant data and 

ozone data. Although these differences are usually 

in the direction of higher oxidant than ozone, the 

122 
imprecision of the calibration and operation of the 

KI methods makes drawing conclusions from such 

studies difficult. Several studies are illustrated in 

Figures 7-1 to 7-5.64,69,89,91,100 

Results from side-by-side comparisons of the KI 

method and one 03-specific method have been 

reported also for individual days and will be briefly 

reviewed. Davis and Jensen 21 reported 

measurements in Florida in which a coulometric 

oxidant instrument (Mast) gave readings 

consistently lower than those of a chemiluminescence ozone detector by a factor of three. 

The coulometric instruments were operated using 

factory calibrations, while the chemiluminescence monitors were calibrated according 

to specified standards. The report contains nodata 

to demonstrate that the instrument would indicate 

similar ozone levels if both were sampling the 

same calibration atmosphere. Because of the 

imprecision of the calibration procedures, it is 

probable that a significant fraction of the 

discrepancy was caused by calibration. 

Furthermore, the differences betweert the two 

instrument readings were on the order of 20 to 30 

ppb. Since no measures were taken to remove or 

correct for interferences from reducing agents, at 

least part of the difference is probably due to 

interference in the Mast instrument from SOz. 

These uncertainties raise pertinent questions 

about the value of the Davis and Jensen21 report in 

estimating the equivalency of the ozone and 

oxidant methods. EPA measurements in St. Louis, 

Mo., showed consistently higher KI-oxidantvalues 

relative to chemilum-03 values. 1e Okita and 

Inugami69 reported their ozone measurements in 

Musashino, Japan, to be in excellent agreement 

with their KI-oxidant measurements (Figure 7-2). 

Carroll et al.," using smog chamber irradiated auto 

exhaust mixtures, conducted and compared 

parallel measurements of oxidant measured by KI 

and of ozone measured by chemiluminescence; 

their comparison showed the KI values to be higher 

by 0 to 10 percent (Figure 7-3). Finally, Seversand 

Neal64 '89 reported the results of their comparison of 

the KI-oxidant and chemilum-03 measurementsof 

the Houston atmosphere, which show the 

chemilum-03 values to be generally higher and, 

occasionally, to be considerably higher (Figures 7- 

4 and 7-5). 

Thus with the exceptlon of the Houston data 

obtained by Severs and his coworkers, 64 '69 the KIoxidant measurements appear, as a rule, to be 

either roughly equal to or somewhat higher than 

the chemilum-03 measurements, a differencethat 

is directionally consistent with the difference in 

response specificity between these methods. The 

significance of the Severs results, although 

difficult to assess, does not seem to be crucial. 

0.10 

E 

a a 

Z 0.08 

O 

~ 

Q 

~ 0.06 

Z 

W 

U Z 

O 

U 0.04 

0.02 

0 

I 

OZONE-CHEMILUM •—•— 

TOTAL OX-MAST • • • • • • 

TOTAL OX-TECHNICON 

~ 

~ 

4~ • ~ ~• • i • • Y• 

rr 

• ~ ~ ~ 

~ ~ ~• ~ 

•% . . * 

•e~ ► 

. ;` ~• 

.i ~ 

i . 

. . • 

ii.Y.•V.ii.s Y .... 

.~~ . ~. r~ • 

il..i.i•ryY•Mii• 

•.r~ 

• i • I • • 

•'. ~~ 

0 4:00 8:00 NOON 4:00 8:00 12:00 

j

f a.m. 0. 1 do p.m. 0. 1 

Figure 7-1. Diurnal ozone-oxidant averages from September 4 through September 30, 1971. 51 

123 
First, it is difficult to explain the "irrational" 

direction of the KI-oxidant-versus-chemilumozone disagreement reported by Severs. Second, 

there are several other studies that yielded rational 

results. Finally,there Is ample evidence attesting to 

the poor precision of the KI methods and, 

specifically, to the presence of a substantial 

operator error. In view of all these facts and 

indications, one would be inclined to conclude, 

presently at least, that the data analyzed by Severs 

reflect a strong operator error in the oxidant measurements. In a more recent study, Severs et a1. 90 

offer the explanation that the differences in results 

found in their method-comparison studies are 

largely the result of sampling turbulent 

atmospheres with instruments that use different 

sampling intervals. This explanation, however, is 

not consistent with the sustained method 

2.0 

AVERAGE 

INDIVIDUAL DAYS 

~ 

z 

Q 

0 

X 1.0 

O 

O 

0.5 

0.4i i 1 1 i i 

11:00 NOON 1:00 2:00 3:00 4:00 

~4_a.m. p,m. 0.

1 

LOCAL STANDARD TIME 

Figure 7-2. Ozone-oxidant ratios in Musashino, Japan. 69 

1.1 1.1 

j/ 1.0 

J ' 0.9 

0.8 

a 0.7 

a 

Y 0.6 

} 

m0.5 

w 

Z 

N 0.4 

O 

0.3 

0.2 

0.1 

•S 

1.0 

0.9 

E0.8 

O, 

a 0.7 

H 

Q 0.6 

~ 

m 0.5 

w 

~ 0.4 

N 

O0.3 

0.2 

0.1 

LEAST SQUARES- 

~ 

1 

•~.. 

~ 

LEASTSQUARES,,,,, ,/ • 

. 1 ~•! 

. / 

•/ 1 1 CORRESPONDENCE 

0 

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1•0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 

OLONE BY CHEMILUMINESCENCE, ppm OZONE BY CHEMiLUMINESCENCE, ppm 

Figure 7-3. Comparison of the KI, Mast, and chemiluminescence methods for measuring ozone in 

irradiated exhaust mixtures. 91 

124 
disagreement over a period of several hours, as 

shown in Figure 7-5. 64 The major and wellsupported conclusion from the discussion in this 

section on the data comparison of KI oxidant 

versus chemilum-03 is that definition of air quality 

and of air quality standards in terms of oxidant 

measured by the commonly used KI methods 

would create problems because of the inaccuracy 

and imprecision of such methods. These problems 

would be nearly eliminated, however, if the air 

quality and the air standard could be defined in 

terms of ozone. 

0 

N 

x 

.0 

a 

a 

Vl H 

z 

a 

0 

X 

0 

J 

Q 

~ 

O 

~ Z= a101+a111X 

 = 5.39+0.445X 

= 0.55 

X •Y) = 12.66 

3 

OZONE, ppb x 40 

Figure 7-4. Relationship of total oxidant and ozone values 

greater than 10 ppb, August through December 1973. 84 

MEASUREMENT OF PEROXYACYLNITRATES 

Peroxyacetylnitrate (PAN) is the principal 

member of a family of unstable, highly oxidized 

organic nitrogen compounds (peroxyacyl.iitrates) 

that are formed in polluted air by the 

photochemical action of sunlight on hydrocarbons 

and nitrogen oxides. PAN was first detected in the 

atmosphere and partially characterized with longpath infrared spectrometry. 87 's3 '95 This method, at 

one time, was the only means available for 

measuring PAN at concentrations approaching 

those found in polluted atmospheres. However, 

because of expense of the instrumentation 

required, the large volume of sample required, and 

a threshold of detectability of about 50 ppb, this 

method has serious limitations. 

Gas chromatography with electron-capture 

detection evolved as a method for measuring 

PAN2o,44,45,94 because electron-capture detectors 

are very sensitive to organic nitrates and much less 

sensitive to hydrocarbons and simple oxygenates 

that would befound in atmospheric samples. Since 

PAN is very unstable, and because its concentration in the air is in parts per billion, the 

operating variables of the gas chromatographic 

system must be carefully chosen. PAN can be 

measured in polluted atmospheres at 

concentrations less than 10 ppb with an electroncapture detector using very small, untreated 

samples. Ambient air samples can be analyzed by 

collecting samples in a gas-sampling syringe (100 

ml) and introducing this sample to the gassampling valve of the gas chromatograph. Samples 

must be analyzed at the time of collection because 

no reliable means of storing PAN-containing air 

samples is known at this time. The gas 

chromatographic system can be automated in such 

a way that samples can be taken directly from the 

ambient air and analyzed automatically on a cyclic, 

semi-continuous basis. 44 

Calibration standards for PAN cannot be 

purchased commercially; they must be 

synthesized. PAN can be synthesized at very low 

concentration levels by photolyzing known 

concentrations of ethyl nitrite vapor in an oxygencontaining atmosphere. 

Continuous methods for the measurement of 

PAN are under development. One such method 

utilizes the chemiluminescence produced from the 

gas-phase reaction of PAN with triethylamine 

vapor. 74 Application ofthis method could result in a 

technique for measuring atmospheric concentrations of PAN at concentrations as low as 1 

ppb. 

PAN generally occurs in ambient atmospheres at 

concentration levels much lower than those of 03. 

In addition, it is a highly reactive, unstable 

compound that must be treated with special 

precautions. For these reasons, PAN cannot be 

measured in a routine monitoring program. 

Considering the complicated methodology, the 

difficulty in obtaining standards, and the safety 

precautions required for handling PAN, only those 

laboratories with personnel experienced in this 

area should attemptto makethese measurements. 

Methods have been developed in which another 

member of the highly unstable PAN family, 

peroxybenzoyinitrate (PBzN), can be assayed by 

gas chromatography using either electroncapture2o,36,44,45,74,93,94,95 or flame-ionization 

detection (FID). 95 The latter method converts the 

125 
PBzN to the relatively more stable methybenzoate. 

The lower limit of sensitivity of this technique is 1 

ppb 5,20 ,38,44,45,74 ,94,95 With the exceptlon of one 

report from the Netherlands, 5,zo,3e,a4,4s,ssaa,sa the 

evidence indicates that PBzN does not occur in the 

ambient air in measurable concentrat I o n 

S.5, 20,38,44,45,74,94,95 

Gas chromatography with either electroncapture or FID appears presently to be the most 

viable method for the analyses of the PAN family. 

MEASUREMENT OF HYDROCARBONS 

The types of hydrocarbons covered in this 

discusslon are those gas-phase hydrocarbons that 

are likely to be found in urban atmospheres. 

Measurement methods for these hydrocarbons fal I 

into two classes. Those that measure nonmethane 

hydrocarbons (NMHC) and those that measure 

individual hydrocarbons. 

Measurement of Nonmethane Hydrocarbons 

In typical polluted air samples, the principal 

hydrocarbon component, methane(CH4), is usually 

more abundant than all other hydrocarbons 

combined. Methane, however, is inert in most 

photochemical reactions. Therefore, hydrocarbon 

measurements are usually corrected for CH 4 by a 

subtractive technique to better approximate the 

reactive component of the total hydrocarbon 

mixtures in the ambient air. Both CH 4 and total 

KI o--o 

Chem • • • • 

! UV 

~ 

i 

! 

i 

i 

h ~ • 

~• • • 

~ •t 

: M 

+ ~ G ~ . 

* • ~ 

• 

r • •: 

i 

: 

i• ~• ~ 

• 

!•~ 

•i 

8:00 11:00 2:00 5:00 8:00 11:00 

1-*— a.m. 10 1 .0 p.m. oi l 

TIME OF DAY 

Figure 7-5. Comparative measurer,G,... of ambient oxidant/ozone by the potassium iodide (KI), 

chemiluminescence (Chem), and ultraviolet (UV) methods. 60 

0.20 

0.15 

E 

a 

a 

w 

z 

O 

~ 

0.1 0 

0.0 5 

126 
hydrocarbons are measured by continuous 

monitoring analyzers that utilize the flameionization detector (FID) as the sensing element. 

Originally developed as a detector for gas 

chromatography, the FID was later adapted for 

total hydrocarbon analysis. 4In this technique, a 

sensitive electrometer detects the increase in ion 

intensity resulting from the introduction of air 

containing any hydrocarbon compounds into a 

hydrogen flame. 

The response of FID analyzers is reiated not only 

to the concentration of the hydrocarbon being 

measured, but also to the effective carbon number 

of the hydrocarbon compound. The effective 

carbon number varies depending on the number of 

carbon atoms in the molecule and on the type of 

compound (e.g., aliphatic, aromatic, olefinic, 

acetylenic, etc.). Thus, without knowing which 

hydrocarbon compound is being measured, the 

reading cannot be related to the actual 

concentration of the total hydrocarbons in the air 

sampled. 

For this reason, FID results are usually 

expressed in terms of the calibration gas used (for 

example, ppm C as CH4). Carbon atoms bound to 

oxygen, nitrogen, or halogens give reduced 

response or no response. 96 There is no response to 

nitrogen, carbon monoxide, carbon dioxide, or 

water vapor. An oxygen effect does occur, but it 

can be minimized by appropriate adjustment of 

operating condition. 

The response of the FID is rapid, and with careful 

optimization of operating parameters and proper 

calibration, it is sensitive to a fraction of a ppm C as 

CH4. A number of studies have been carried out on 

optimization of such operating variables as gas 

flow rates, detector temperature, and oxygen 

content of air, all of wh ich can affect F I D 

response." 28,31 

Early measurements of NMHC involved the use 

of a carbon column pretreated with CH 4

3,70,e2 This 

column was used to remove all other hydrocarbons 

from the ambient sample. A total hydrocarbon 

analyzer with a carbon column was operated either 

parallel or a..ernatively with a total hydrocarbon 

analyzer without a carbon column. Methane and 

total hydrocarbons were measured, and by 

difference, the NMHC value was computed. This 

method was subject to much variability because of 

the unpredictable behavior of carbon columns 

when exposed to ambient conditions. However, 

when the carbon column was relatively new and 

the NMHC concentrations were high, the method 

was reasonably accurate. 

EPA REFERENCE METHOD 

The EPA reference method for NMHC, which 

was promulgated in 1971, involves gas 

chromatographic separation of CH 4 from total 

hydrocarbons in an air sample followed by FID of 

both CH, and total hydrocarbons. 106 The NMHC 

value is obtained by subtraction of the two 

measurements. In a 1974 survey, some 160 users 

of this method were identified. 76 

Several studies have been conducted to 

estimate the quality of ambient air data being 

obtained with this method. One study 76involved 

the analysis of synthetic hydrocarbon mixtures in 

compressed air cylinders by 16 different users of 

the reference method. The NMHC concentrations 

tested were 0.23 and 2.90 ppm. The results of this 

study are given in Table 7-4 and indicate the 

percent error from the known concentrations. 

TABLE 7-4. PERCENT DIFFERENCE FROM KNOWN 

CONCENTRATIONS OF NONMETHANE 

HYDROCARBONS OBTAINED BY SIXTEEN USERS 

Known % difference 

concentration, 

PPm 100 50-100 20-50 10-20 0-10 

023 6 4 3 2 1 

290 2 -- 3 2 9 

The results show that at the level of the NAAQS, 

0.24 ppm carbon, most of the measurements were 

in error by 50 to 100 percent. At 2.90 ppm, most of 

the measurements were in error by only 0 to 20 

percent. Thus the higher the concentration tested, 

the better the accuracy. 

The overriding causes of the inaccuracies were 

the inability of the instrumentation to measurethe 

low levels of NMHC, the complexity of the 

instrumentation, and the inability of the average 

user to identify and correct problems. 

Another study 57 involved monitoring the same 

ambient air with five different commercial FID 

instruments operated by skilled professionals. The 

results show that different analyzer pairs agreed 

with 0.1 to 0.5 ppm carbon. Although these 

differences represent only 1 to 5 percent of the fullscale (0 to 10 ppm) range of the instruments and 

are normal errors for ambient monitoring, they are 

obviously very large relative to the NAAQS of 0.24 

ppm carbon. (The 0- to 10-ppm range is necessary 

to include all ambient values.) Thus even under 

127 
optimum operating conditions, agreement 

between instruments is poor at low 

concentrations. This result is not surprising when 

one realizes that the instrumentation is not 

optimized for measurement at these low levels. 

Several studies on the performance of ambient 

hydrocarbon monitors have been published.°s ,7,,e ,,s7 

In a recent EPA-sponsored study, 35the EPA reference method was subjected to a comprehensive evaluation, includ ing testing of si x commercial instruments. Results showed, in general, poor 

performance of the commercial instruments, the 

major problems being wide differences in response to different NMHC species and discrepancies apparently related to ambient water vapor 

variation. 

HEAT OF COMBUSTION METHOD 

A different approach to measurement of 

nonmethane hydrocarbons was developed in 

1973. 75This technique utilizes the fact that CHa 

has a higher heat of combustion than other 

hydrocarbons. One portion of the air sample 

passes through a catalyst bed where all 

hydrocarbons, except CH4 , are combusted. This 

CH,-only stream passes to one FID. The other 

portion of the sample passes directly to a second 

FID for a total hydrocarbon measurement. By 

simultaneous processing of the signals from the 

two FID's and by subtraction of the CH,-only value 

from the total hydrocarbon val ue, the NMHC val ue 

can be obtained. This technique has several 

advantages over the reference method. It is 

simpler to use, it produces continuous NMHC 

values, and the instrument system can maintain its 

own zero. However, most of the shortcomings 

attributed to the EPA reference method also apply 

to this technique. 

Measurement of Individual Hydrocarbons 

GAS CHROMATOGRAPHY 

Gas chromatography (GC) is the most effective 

method for determining the concentration of 

individual hydrocarbons that make up the 

complicated hydrocarbon mixture such as is found 

in auto exhaust and the ambient atmosphere. With 

FID, the method is sensitive down to the ppb range. 

GC methods in general involve the separation of a 

complex mixture into individual compounds. This 

separation is achieved using both capillary (liquid 

phase coated on the inner surface of the column) 

and analytical columns. The latter may contain 

either a solid polymeric adsorbent (gas-solid 

chromatography) or an inert support coated with a 

liquid (gas-liquid chromatography). An inert gas 

(carrier gas) continuously flows through the GC 

column. When a complex sample is injected onto 

the GC column, the carrier gas carries the sample 

through the column. Separation of the mixture 

occurs as the result of the different propensities of 

the respective components for interacting with the 

column substrate. The net result is the separation 

of a complex mixture into a number of individual 

components. The degree of separation depends on 

column length, carrier gas flow rate, temperature, 

and a variety of other parameters. The column 

support is selected from numerous available 

materials, depending on the types of components 

that make up the sample mixture. 

GC techniques have been used to investigate the 

hydrocarbon composition of both urban and rural 

atmospheres. z,47,50,78In urban atmospheres, 

hydrocarbons generally exist at levels high enough 

to permit the collection of samples without 

concentration. Samples can be collected in inert, 

flexible bags and transported to a central 

laboratory for GC analysis. Problems often arise 

with this sampling technique because of 

hydrocarbon losses resulting from adsorption on 

the walls of the bags, contamination of bags, and 

reactions that occur after the sample has been 

collected. Since the hydrocarbon components in 

rural ambient atmospheres are typically found in 

ppb concentrations, cryogenictrapping techniques 

for large air samples are required. Quantitative 

measurements of the GC peaks can be made with 

integrator and computer interfacing. Quantitative 

evaluation of the individual peaks can be made 

without standardization of each compound peak 

analyzed. Computation of each component 

concentration can be made by using an average 

per-carbon factor determined by known 

concentrations of the identified components. 25 

In recent years, the development of highresolution capillary and support-coated, open 

tubular columns combined with wide-range 

temperature programming from subambient to , 

elevated temperatures have provided better 

separation of the complex ambient hydrocarbon 

mixture. The complexity of the ambient air mixture, 

however, still prevents complete resolution of the 

air sample into all of its components. To determine 

the purity of the GC peaks and to obtain 

information for the identification of unknown 

peaks, a combination of GC with either infrared (IR) 

128 
or mass spectrometry, (MS) can be used. These 

approaches, however, require both large sample 

concentration and highly trained personnel. 

GC - CHEMILUMINESCENCE DETECTOR 

A procedure has been developed that permits 

detection of unsaturated hydrocarbons (e.g., 

ethylene, propylene, and terpenes) using 

separation with a gas chromatograph and analysis 

with a chemiluminescence detector. 56'88The 

unsaturated compound of interest reacts with an 

ozone stream to produce light in the region of 400 

A. Chromatographic separation makes the 

technique specific for each compound. Sensitivity 

for this method is in the ppb range.ee 

INFRARED SPECTROMETRIC TECHNIQUES 

Recent advances in long-path IR techniques 

using Fourier-transform spectroscopy (FS) have 

resulted in an increase in sensitivity (10 ppb) for 

measurement of selected hydrocarbons such as 

ethylene, propylene, methane, formaldehyde, and 

PAN. Whereas previous IR techniques required a 

concentration step to measure ambient levels of 

hydrocarbons, the FS approach allows for-direct 

measurement at ow pollutant concentrations. 33 

The system has been used successfully in 

atmospheric studi-s as well as in characterization 

of photochemica reactions. 34The size and 

complexity of th .~ system, however, limits its 

usefulness for ro: tine air monitoring. 

Measurement of Reactive Hydrocarbons 

Hydrocarbons eliffer greatly in the ability to 

produce photoch.,mical smog. For example, CH a 

and acetylene cari be considered unreactive, and 

ethylene and n-butane, reactive hydrocarbons. 

However, n-butane concentrations several fold 

higher than ethylene concentrations are required 

to produce similar rates of smog formation. There 

is accordingly a need for a measurement method 

that gives an indication of total hydrocarbon 

reactivity (i.e., a measurement that gives the sum 

of the concentrations of each reactive hydrocarbon 

species multiplied by a reactivity factor). Fontijn et 

a1. 30have recently developed a chemiluminescence method that appears to satisfy this need. 

This method is based on the difference between 

the light emission intensities at 308.9 and 312.2 

nm that result from the reaction between the 

hydrocarbon sample and oxygen atoms under low 

total pressure (1 torr) conditions. A limit of 

sensitivity of 0.05 ppm ethylene-equivalent 

hydrocarbon and a linear response to individual 

hydrocarbons up to at least 3000 ppm have been 

obtained. The response to hydrocarbon mixtures 

appears to be additive, and interferences from CO, 

CO2, S02, CH 4, C21-1 2and NOXin concentrations 

typical of those in auto exhaust were found to be 

negligible. Such an instrument response obviously 

measures the reactivity of the hydrocarbons with 

oxygen atoms. Such reactivity, in turn, is a 

measure—although a crude one—of the sample's 

ability to produce oxidants. 

Calibration 

Calibration at regular intervals is, of course, 

required for all analytical methods for measuring 

air pollutants. Calibration techniques and the 

required frequency of calibration vary for different 

pollutants. The preferred protie:iure consists of 

passing known concentrations of the pollutant in 

air into the measuring system. This dynamic 

procedure calibrates not only the detector 

response, but also the inlet system to the detector. 

Calibration gases in steel or aluminum cyfinders 

are commonly used to calibrate hydrocarbon analyzers. Cylinder gases may be diluted with clean, 

dry air to give the desired concentration range. Dry 

air with a hydrocarbon concentration that does not 

exceed 0.1 ppm is needed for dilution and for 

providing zero gas for the instrument. Calibration 

gases and zero gas are available commercially, and 

some standard gases, such as propane in air, are 

available from the National Bureau of Standards as 

standard reference materials. AII commercial 

mixtures should be referenced against a standard 

gas whenever possible. The air used for 

instrument zeroing purposes should contain the 

normal constituents of clean air— that is, 02 at 20 

percent, N2at 79 percent, CO2 at 320 ppm, andthe 

normal levels of inert gases such as argon (Ar), 

helium (He), neon (Ne), and nitrous oxide (N20). 

Permeation tubes can also be used to generate 

known concentrations of certain hydrocarbons 

such as butane, which can be condensed at 

moderate pressures. The gas trapped inside the 

permeation tube will diffuse through the tube wall 

at a rate dependent on the surface area and the 

temperature of the tube. 52,s8 The permeation rate 

of the tube can be determined gravimetrically by 

holding the tube at a constant temperature 

(±0.1 °C) and measuring weight loss with time. The 

calculated permeation rate remains constant for 

properly prepared tubes. Because the permeation 

rates of different hydrocarbons are significantly 

129 
different, only one hydrocarbon can be used in a 

given permeation tube. 

Another dynamic calibration technique involves 

the addition of a measured amount of pollutant to a 

known, fixed volume of air in a large vessel and 

then drawing tiie atmosphere into the analyzer. ss 

The addition may be made by syringe injection or 

by the crushing of a weighted glass ampule 

containing the pollutant. Rigid vessels or plastic 

bags, which have the advantage of collapsing as 

the sample is withdrawn, may also be used. Bags 

must be made of an inert plastic to avoid changes 

in concentration through absorption or reaction 

with the walls of the bag. The bags must also be 

checked for permeation rates of the compounds 

being used, since permeation can result in loss of 

sample or, in some cases, contamination of the 

sample as a result of bag permeation by ambient 

hydrocarbons. The above techniques are preferred 

for more reactive hydrocarbons that do not have 

sufficient stability to be stored in cylinders. 

MEASUREMENT OF NITROGEN OXIDES 

The NOx involved in photochemical oxidant 

formation are NO and NO2. Since oxidant control 

regulations and practices to date have been based 

on unilateral control of the hydrocarbon precursor, 

interest in the NOX factor was only peripheral and 

of research nature. The recent findings, however, 

on the need to consider the NO x factor in 

formulating oxidant control strategies have raised 

questions regarding adequacy of the existing 

analytical methodsforambientNOxmeasurement. 

Since the primary needs insofar as the oxidant 

problem is concerned are short-term (hourly) NOx 

concentration data for urban atmospheres and 

short-term (hourly) data for rural atmospheres, 

analytical methods used for oxidant-related 

applications must be capable of short-term 

sampling and analysis and interference-free 

response, and they must be sensitive. This 

discussion will thus be limited to continuous 

methods for measuring NO 2 and NO. 

Measurement of NOz 

CHEMILUMINESCENCE METHODS (EPA 

REFERENCE METHODS) 

On December 1, 1976, EPA promulgated a new 

measurement principle and calibration procedures 

for reference methods for measuring NO2. 105 The 

measurement principle and calibration procedures 

are described in Appendix F of 40 CFR Part 50. The 

measurement principle is based on the gas-phase 

reaction of 03 and NO. Atmospheric concentrations of NO2 are measured indirectly by 

photometrically measuring the light intensity (at 

wavelengths greater than 600 nm), resulting from 

the chemiluminescent reaction of NO with 

03•29.54,99 NOz is first quantitatively reduced to 

NO 13 '42 '99 by means of a converter. N0, which 

commonly exists in ambient air together with NO2, 

passes through the converter unchanged, causing 

a resulting total NOX concentration equal to NO + 

NO2. A sample of the input air is also measured 

without having passed through the converter. This 

latter NO measurement is subtracted from the 

former measurement (NO + NOz) to yield the final 

NOz measurement. The NO and NO + NO2 

measurements may be made concurrently with 

dual systems or cyclically with the same system. 

Two calibration procedures are prescribed in 

Appendix F of 40 CFR Part 50. One is a gas-phase 

titration procedure referenced to an NO-innitrogen standard. The other calibration procedure 

is referenced to an NO permeation device. Both 

of these standards can be obtained from the 

National Bureau of Standards as standard 

reference materials. Chemiluminescence 

NO/NO X /NO2 analyzers will respond to other 

nitrogen-containing compounds such as PAN, 

which might be reduced to NO in the thermal 

converter. 107 Atmospheric concentrations of these 

potential interferences are generally low relative 

to NO2, and valid NO2 measurements may be 

obtained. 

GRIESS-SALTZMAN METHODS 

Before the development of chemiluminescence 

analyzers, most NO2 data were collected using 

methods based on variations of the GriessSaltzman83 methodology. These methods are 

based on the specific reaction of the nitrite ion 

(NO2) with diazotizing-coupling reagents to form a 

deeply colored azo dye. The NO2 in the ambient air 

is converted to nitrite ion on contact with an 

absorbing solution. As applied to continuous 

analyzers, 84 the absorbing solution contains the 

diazotizing-coupling reagents, and the absorbance 

of the azo dye is measured continuously with a 

flowing photometer cell. The absorbance of the azo 

dye solution is directly proportional to the 

concentration of NO2 absorbed. 

For ordinary atmospheres, interferences have 

been claimed to be of negligibfe importance. The 

method is commonly calibrated with standard 

nitrite solutions, assuming 0.72 mole of nitrite to 

i[cZi 
be equivalent to 1 mole of NO2. This latter 

assumption has been at issue. 86 In addition, there 

are indications of an ozone interference problem. e 

For all practical purposes, this method has been 

replaced with the chemiluminescence method. 

Measurement of NO 

Before the advent of the chemiluminescence 

method, NO measurements were made almost 

exclusively by contacting the air sample with a 

solid or liquid oxidant and measuring resulting NO2 

by conventional azo dye colorimetric procedures. ae,as Currently, the chemiluminescence 

method is believed to be unquestionably superior 

to all methods available. Thus, for example, 

relative to the continuous Griess-Saltzman, the 

chemiluminescence method is more accurate 

because it can be calibrated more accurately with 

standard NO mixtures, and also because it is 

subject to practically no interferences from other 

vapors. The speed of response of c hemiluminescence-NO instruments is typical ly only a 

few seconds, and their sensitivity is about 5 

ppb. Overall, such instruments are practical, 

reliable, and suitable for field use. 

SUMMARY 

The chemiluminescence method, based on the 

gas-phase reaction of 03 with ethylene, was 

adopted by EPA as the reference method and is 

now being used extensively. Several techniques 

using commercial analyzers have been designated 

as reference methods under the EPA ambient air 

monitoring reference and equivalent methods 

regulations. Data indicate that the performance of 

these analyzers is better than that specified by the 

EPA regulations. Continuous analyzers based on 

gas-solid chemiluminescence and UV photometry 

have been developed, and techniques using such 

analyzers have been designated as equivalent 

methods. 

The methods for measuring total oxidants are 

based on the oxidation of KI and the electrochemical or colorimetric detection of 1 2 . Nitrogen 

dioxide causes a positive interference, and S02 

results in negative interference. Serlous problems 

arise, however, with methods for correcting for 

S02 and NO2 interferences. 

Extensive studies in recent years have shown 

the varlous KI calibration procedures for oxidantor 

03 analyzers to be deficient. These methods suffer 

from systematic, accuracy-related errors as well as 

from random, precision-related errors. EPA 

intends to study and evaluate several new 

calibration procedures and to amend Appendix D of 

40 CFR Part 50 to revise the 1-percent NBKI 

calibration procedure or replace it with one or more 

of several alternatives under consideration. The 

alternative procedures under consideration are: (1) 

GPT with excess N0; (2) UV photometry; (3) GPT 

with excess 03; and (4) boric acid KI. 

Analysis of the data indicates that oxidant-by-Kl 

measurements of oxidant levels are generally 

comparable or slightly higher than levels of ozone 

as measured by ozone-specific techniques. 

However, most oxidant/03 comparison studies 

suffer from the imprecision of the oxidant methods 

and from the lack of data regarding levels of 

compounds known to interfere with the KI method. 

Commercial instruments for ambient total 

NMHC monitoring have been tested extensively 

and found to be inaccurate at levels approaching 

the 0.24-ppm C air quality standard. At present, 

ambient hydrocarbons can be accurately 

measured only by sophisticated gas chromatography. Routine methods are, however, under 

development. 

On December 1, 1976, EPA promulgated a new 

measurement principle and calibratlon procedure 

for measuring NO2. The measurement principle is 

based on the gas-phase chemiluminescent 

reaction of 03 and NO. Two calibration procedures 

are prescribed. One is a GPT procedure referenced 

to an NO-irl-nitrogen standard. The other 

procedure is referenced to an NO2 permeation 

device. Before the development of chemiluminescence analyses, most NO2 data were 

collected using methods based on variations of the 

Griess-Saltzman _ methodology. For all practical 

purposes, this method has been replaced with the 

chemiluminescence method. 

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Control Association, Denver, Colo., June 9-13, 1974. Monitoring Air Quality. ASTM Special Technical 
Publication 555, American Society for Testing and 

Materials, Philadelphia, Pa , June 1974. 

98 Stevens, R K, T A Clark, C. E. Decker, and L. F. Ballard. 

Field performance characteristics of advanced monitors 

for oxides of nitrogen, ozone, sulfur dioxide, carbon 

monoxide, methane, and nonmethane hydrocarbons. 

Presented at the 65th Annual Meeting, Air Pollution 

Control Association, Miami, Florida, June 18-22, 1972. 

99 Stevens, R K, and J. A Hodgeson. Applications of 

chemiluminescent reactions to the measurement of air 

pollutants. Anal Chem 45.443A-447A, 1973 

100 Stevens, R. K., J. A. Hodgeson, L F Ballard, and C. E. 

Decker Ratio of sulfur dioxide to total gaseous sulfur 

compounds and ozone to total oxidants in the Los 

Angeles atmosphere—an instrument evaluation study. 

/n Determination of AirQuality. G. Mamantov and W. D. 

Shults, eds Plenum Publishing Co., NewYork, 1972. pp 

83-108 

101 Tokiwa, Y, S Twiss, E R. de Vera, and P. K. Mueller 

Atmospheric ozone determination by amperometry and 

colorimetry. /n. Determination of Air Quality, G 

Mamantov and W D Shults, eds. Plenum Publishing 

Co , New York, 1972 pp 109-130. 

102 U S Environmental Protection Agency Ambient air 

monitoring reference and equivalent methods. Fed 

Regist 40.7042-7070, February 18, 1975. 

103 U.S Environmental Protection Agency. Measurement 

of photochemical oxidants in the atmosphere. 

Calibration of reference methods Fed Regist. 

41 - 44049-44057, October 6, 1976. 

104 U S Environmental Protection Agency. National 

primary and secondary air quality standards Fed. 

Regist. 36 8186-8201, April 30, 1971. 

105 U S Environmental Protection Agency. Nrtrogen dioxide 

measurement principle and calibration procedure Fed. 

Regist. 41 ~ 52686-52695, December 1, 1976, 

106 U S Environmental Protection Agency. Reference 

method for determination of hydrocarbons corrected for 

methane In: Code of Federal Regulations Title 40. Part 

50 11 Appendix E. U S. Government Printing Office, 

Washington, D.C, July 1, 1975 pp. 21-27. 

107 W iner, A. M., J W. Peters, J P. Smith, andJ N. Pitts, Jr 

Response of commercial chemiluminescent NO-NOz 

analyzers to other nitrogen-containing compounds. 

Environ Sci Technol 81118-1121, 1974. 

108 Zafonte, L, W Long, and J N Pitts, Jr Evaluation of an 

ozone photometer for ambient ozone measurements. 

Anal Chem 46 1872-1874, 1974 

135 
8. TOXICOLOGICAL APPRAISAL OF 

PHOTOCHEMICAL OXIDANTS 

INTRODUCTION 

Photochemical oxidants such as ozone and 

peroxyacylnitrates are gases that exert their toxic 

effects by entering the body through inhalation. If 

present in sufficient concentrations, they are 

capable of causing death to various organisms. At 

sublethal concentrations, they may alter, impair, or 

otherwise interfere with physiological processes. 

Alterations in pulmonary function and in 

mechanical properties of the lungs are among the 

effects that result from inhalation of these 

compounds. Other effects include morphological 

changes in the lungs, increased susceptibility to 

infectious respiratory disease, and biochemical 

alterations in the lungs and in other organs. Since 

there is a scientific consensus that concentrations 

above 1960 /ig/m 3 (1 ppm) ozone are very 

hazardous to health, generally only research 

conducted at or below this concentration will be 

described here. 

The toxicological effects of ozone and two major 

pollutant groups, oxidants (mixtures of substances 

produced by photochemical reactions) and 

peroxyacylnitrates, are discussed in this chapter. 

Each compound or group is treated separately. 

EFFECTS OF OZONE ON EXPERIMENTAL 

ANIMALS 

Respiratory Tract Transport and Absorption 

NASOPHARYNGEALUPTAKE 

The extent to which air pollutants can directly 

affect the lung depends largely on the amounts of 

pollutant and reaction products that penetrate to 

the lower airways. Nasopharyngeal removal of 

ozone lessens the insult to the lung and must be 

accounted for when estimating ozone concentrations reponsible for observed pulmonary 

effects. Experimental estimates of nasopharyngeal 

ozone removal determine the appropriate 

boundary conditions when using convective/ 

diffusion equations to model ozonetransport in the 

lower airways. 

Vaughn et a1. 200 exposed the isolated upper 

airways of beagle dogs to ozone at a continuous 

flow of 3.9 I/min and collected the gas just below 

the larynx in a plastic (Mylar) bag. Concentrations 

below 784 Ng/m 3 (0.4 ppm) yielded essentially 

100-percent uptake. However, Yokoyama and 

Frank215 observed 60- to 70- percent uptake of 

ozone by the upper airways in similar studies on 

beagles where Teflon tubing was used. When 

these investigators repeated the procedure of 

Vaughn et a1., 200 they found that some ozone was 

lost because of adsorption on the bag wall. 

Nasal uptake significantly exceeded (pG0.01) 

orat uptake at both flow rates (3.5 and 35 I/min) 

used in the Yokoyama and Frank 215 studies. The 

overall uptake coefficient for the nose increases 

with air flow rate. This latter point was shown by 

Aharonson et al.,' who demonstrated the necessity for expressing retention data on the basis of 

the average uptake coefficient when comparing 

uptake at different flow rates. 

The decomposition of ozone in the nasopharynx 

of acutely versus chronically exposed beagle dogs 

was studied by Moorman et a1. 139 Dogs chronically 

exposed (18 months) to 1960 to 5880/jg/m 3 (1 to 3 

ppm) ozone, using various daily exposure 

regimens, were shown to have significantly higher 

mean tracheal concentrations of ozone than 

animals tested after 1 day of exposure to the 

corresponding regimens. These investigators 

postulated that the differences were likely to be 

due to physiochemical alterations of the mucosal 

lining in the chronically exposed animals. 

When dogs were chronically exposed to 1960 

Ng/m 3 (1 ppm), those exposed for 8 hr/day had 

significantly lower tracheal values than those 

continuously exposed. However, the average 

concentration for the acute exposure was not 

different from that of the 8 hr/day chronic 

exposure group (19.6 vs 44.1 Ng/m 3 , 0.01 vs 0.023 

136 
ppm). If one takes into account the sensitivity of the 

Mast ozone meter used to measure the responses, 

this latter difference would not represent a 

significant difference in treatment unlessthe Mast 

ozone meter had been modified. Moorman et a1. 139 

did not state what modifications, if any, were 

performed. Nevertheless, in view of the small 

difference observed with exposure to 1960 Ng/m 3 

(1.0 ppm), it is likely that chronic exposureto lower 

levels would not result in tracheal ozone concentrations significantly greater than those 

observed with acute exposure. 

Nasopharyngeal removal of ozone in rabbits of 

both sexes and in male guinea pigs has been 

studied by Miller 134 over a concentration range of 

196 to 3920 μg/m 3 (0.1 to 2.0 ppm). The trac#leal 

ozone concentration in these species was 

markedly similar and was linearly related to the 

chamber concentration of ozone drawn 

undirectionally through the isolated upper 

airways. Regression analyses showed that ozone 

removal in the nasopharyngeal region is 

approximately 50 percent in both species. No 

difference in ozone removal was observed 

between male and female rabbits. 

TRACHEOBRONCHIAL UPTAKE 

Lower airway removal of ozone from inspired air 

was measured by Yokoyama and Frank 215 in dogs 

that were mechanically ventilated through a 

tracheal cannula. Two ranges of ozone concentration were studied: (1) 1372 to 1666 pg/m 3 

(0.7 to 0.85 ppm) and (2) 392 to 784 pg/m 3 (0.2 to 

0.4 ppm). The rate of uptake was found to vary 

between 80 and 87 percent when the tidal volume 

was kept constant and the respiratory pump was 

operated at 20 to 30 cycles/min. This estimate of 

uptake applies to the lung as a whole and does not 

indicate the uptake of ozone by individual airway 

generations. 

A major goal of environmental toxicological 

studies on animals involves the eventual 

extrapolation of the results to man. In addressing 

the likelihood that the animals studied mimic the 

human response, estimation of the effective dose 

delivered to the target organ is required. Also, 

differences between man and experimental 

animals in the ratio of effective dose to exposure 

concentration must be considered. Extensive 

lower airway morphometric data on human 

beings, 206 guinea pigs, rabbits, and rats," I I and the 

technical inability of obtaining local lower airway 

ozone uptake data make mathematical modeling 

the method of choice forexamining ozone uptake 

in the deep lung. 

The mathematical model of lower airway ozone 

uptake by McJilton et a1., 125 although widely cited, 

has never been formally published. However, the 

major features of the McJilton et al. model have 

been described in some detail, and model results 

for absorption of ozone in each generation of the 

human tracheobronchial tree have been 

presented.' 55 Since nonreactivity of ozone with the 

mucous layer was assumed, the model of McJilton 

et al. is really more useful for estimating lower 

airway uptake of water soluble and relatively water 

insoluble gases that are nonreactive with the 

mucous layer than it is for estimating the uptake of 

ozone. 

The problem of treating chemical reactions of 

ozone with various components of mucus has been 

included in the mathematical model of transport 

and removal of ozone developed by Miller. 134 These 

reactions were shown to be characterized by an 

instantaneous reaction regime. Three cases, 

which are a function of the lumen ozone 

concentration, were used to characterize the 

removal of ozone from an airway. As did the model 

of McJilton et a1., 125 Miller included the effects on 

gas transport of convection, axial diffusion, and 

radial diffusion, although the distance-time grid 

mesh used was 5-fold smaller than that used by 

McJilton et al. Also, Miller treated the effects of 

both molecular diffusion and eddy diffusivity on 

axial diffusion, rather than including only 

molecular diffusion. 

Miller et a1.t 36 modeled tracheobronchial uptake 

of ozone in the lungs of guinea pigs and rabbits, as 

well as man. The predicted pulmonary ozone dose 

curves obtained indicate that a general similarity 

exists between these species in the shape of the 

dose curves. Independent of the inhaled tracheal 

concentration of ozone, the respiratory bronchioles are predicted to receive the maximum dose 

of ozone, a result that is in good agreement with 

experimental findings in various animal 

species. 50,190,191 

The model predicts uptake of ozone by respiratory airway tissue for all tracheal concentrations studied (62.5 to 4000 Ng/ m 3 , or 0.03 to 

2.04 ppm). However, penetration of ozone to the 

tissue in airways lined by mucus is not predicted 

for inhaled tracheal concentrations less than 125 

pg/m3 (0.06 ppm) in man and 62.5 pg/m 3 (0.03 

ppm) in guinea pigs and rabbits. As the inhaled 

tracheal concentration is increased from these low 

137 
levels, the tissue deposition pattern of ozone in the 

conducting airways becomes smoother, increases 

in magnitude, and includes more airways. Alveolar 

ozone doses decline sharply from the maximum 

values predicted for the respiratory bronchioles. 

As the tracheal ozone concentration decreases 

from approximately 100Ng/m 3 (0.05 ppm),there is 

a more gradual decline in the respiratory 

bronchiolar dose curve for guinea pigs and rabbits 

than there is in the curve for man. However, for any 

given tracheal concentration greater than 100 

Ng/m 3 (0.05 ppm), the predicted respiratory 

bronchiolar dose for rabbits is 80 percent of that for 

man and twice that for guinea pigs. With tidal 

volumes corresponding to mild exercise, a 2.4-fold 

increase in ozone dose to the respiratory 

bronchioles of man is predicted. This dosage 

increase correlates with pulmonary function 

effects observed with exposure of human subjects 

to ozone while exercising. 10 

Mortality 

Mittler et a1. 137 have determined the LDso for 

ozone in a variety of laboratory animals. The LDso of 

a toxic substance is defined as that dose expected 

to kill 50 percent of a population of experimental 

animals. For common laboratory animals such as 

mice, rats, guinea pigs, and cats, 3-hr exposures of 

>41,160Ng/m3 (21 ppm) are required to reach the 

LDso. Mice treated with selected antioxidants can 

be partially protected against mortality from high 

dose ozone exposures. 132,159,174,175 Concentration 

and length of exposure are notthe only factors thatdetermine toxicity. Stokinger cited other factors 

that influence the response to a specific level of 

ozone. 194 These include age, temperature, 

exercise, dosage rate, respiratory infection, and 

reducing agents. 

In addition to these factors, Skillen 189 confirmed 

the observation of Fairchild et a1. 63 of a variation in 

the effect of continuous ozone exposure to 11,800 

ug/m3 (6 ppm) on rats with varying thyroid status. 

The average survival times of these rats were as 

follows: More than 10 hr for those rats with 

reduced thyroid function, 6.7 hr for rats with 

unaltered thyroid activity, and 2.2 hr for rats with 

stimulated thyroid function. 

Pulmonary Effects 

HOST DEFENSE MECHANISMS 

The adverse effects of a numberof air pollutants, 

including ozone, on pulmonary defense 

mechanisms against infectious disease have been 

studied. This section will describe how low concentrations of ozone result in an enhancement of 

mortality in animals exposed to bacterial aerosols. 

This increased susceptibilty to pneumonia is 

ascribed primarily to dysfunction of the primary 

defense cells of the lungs, the alveolar 

macrophages. 

Interaction with Infectious Agents —The effects of 

a number of pollutants on a host challenged with 

infe_ctious microorganisms have been reviewed. 3s." 

Briefly, mice are exposed either to ozone or 

filtered clean air. At various time periods, all of the 

animals are challenged with an aerosol of viable 

microorganisms, and the accumulated mortality 

over a 15-day observation period in clean air is 

reported. The concentrations of poliutants used 

alone (i.e., without infectious agents) caused no 

deaths. 

Coffin et a1. 35 exposed mice to different concentrations of ozone ranging from 137 to 981 

Ng/m 3 (0.07 to 0.5 ppm). The 3-hr exposures were 

followed immediately by bacterial aerosol 

exposure (Streptococcuspyogenes, Group C). With 

the exception of the lowest ozone concentration, 

137 ug/m3 (0.07 ppm), each concentration was 

tested once (40 mice/concentration). It was 

reported that ? 157 Ng/m3 (0.08 ppm) ozone 

resulted in a significant (p <0.05) enhancement of 

mortality of at least 23 percent. As the 

concentration of ozone was increased up to 1019 

Ng/m3 (0.52 ppm), there was a trend toward 

increased mortality. 

Ehrlich et a1. 54 conducted studies using the same 

microorganism as Coffin et a1., 35 but with different 

strains of mice. Gas concentrations were 

monitored by the chemiluminescence method. A 

single 3-hr exposureto 196/jg/m 3 (0.1 ppm) ozone 

caused a significant (p < 0.05) increase in 

mortality. 

UsingCD-1 mice and S. pyogenes, Miller et al.135 

compared the effects of a 3-hr exposure to ozone at 

196 pg/m3 (0.1 ppm) in which the bacterial aerosol 

was administered either immediately, 2, 4, or 6 hr 

after cessation of the ozone exposure. In each 

replicate experiment, 20 mice per group were 

used, and ozone was monitored continuously by 

chemiluminescence. For these post-exposure 

challenges, only the 2 hr time resulted in a 

significant (p < 0.05) increase in mortality (6.7 

percent) over controls. However, when the animals 

were infected with Streptococci during the ozone 

exposure, a significant (p < 0.01) increase in 

138 
mortality of 21 percent was observed. When this 

latter experimental regimen was used, exposure to 

157 Ng/m3(0.08 ppm) ozone resulted in a 

significant (p < 0.05) increase in mortality of 5.4 

perce nt. 

The differences in results among these studies 

may have been due to a variation in the sensitivity 

of inethod of ozone monitoring, a difference in 

mouse strain, changes in the pathogenicity of the 

bacteria, or differences in sample size. 

The interactions of other environmental stresses 

(cold and other pollutants) using the infectivity 

model have also been examined. Using S. 

pyogenes as the infectious agent, Coffin and 

Blommer34showed that animals preexposed to 

cold (6 1 to 9°C, or 43 1 to 48 ° F) for 3 hr had a 

greater mortality after a 3-hr exposure to 1372 to 

1764 Ng/m3(0.7 to 0.9 ppm) than did animals 

exposed to ozone only. 

The effects of exposures to mixtures of NO2 and 

ozone were examined by Ehrlich et a1. 54using the 

infectivity model. Significant (p < 0.05) increases 

in mortality occurred when mice were exposed to 

concentrations at or above 3926Ng/m 3(2 ppm) 

NO2 and 98 Ng/m 3(0.05 ppm) ozone for 3 hr before 

challenges with aerosols of Streptococcus. 

Although not statistically tested, the effect of the 

exposure to the combination appeared to be 

additive (i.e., the increases in mortality were 

approximately equivalent to the sum of those 

induced by the exposure to each individual 

pollutant. In addition, the animals exposed to the 

mixture show a reduced rate of bacterial clearance 

from the lung. 

Gardner et a1. 80examined the effects of 

sequentialexposureto196/.rg/m 3 (0.1 ppm)ozone 

for 3 hr and 0.9 mg sulfuric acid (H2SO4)/m 3(0.3 

Nm) for 2 hr using CD-1 mice. The bacterial aerosol 

was administered at the end of the pollutant 

exposure. When the ozone preceeded the H2SO4 

exposure, there was a significant increase in 

mortality (p < 0.05), which was additive. 

The results derived from studies utilizing the 

infectivity model indicate its sensitivity for 

detecting biological effects at low pollutant 

concentrations and its response to modifications in 

technique (i.e., using different mouse strains or 

varying the time of bacterial challenge). The model 

is supported by experimental evidence (discussed 

in the following section and reviewed in reference 

24) that shows that pollutants, albeit at different 

concentrations, that cause an enhancement of 

mortality in the infectivity system also cause 

reductions in essential host defense systems, such 

as pulmonary bactericidal capability, the 

functioning of the alveolar macrophage, and the 

cytological and biochemical integrity of the 

alveolar macrophage. 

Coffin and Blommer34examined the mechanism 

of action of the infection following pollutant 

exposure. In these studies, the number of bacteria 

in the lung and the presence of bacteria in the 

blood was followed at various time periods. Mice 

wereexposedto1960Ng/m3 (1 ppm)ozonefor3hr 

before a bacterial aerosol. Bacterial invasion of the 

blood began 2 days after ozone exposure. 

Additional research 90has shown that exposure to 

ozone concentrations greater than 780 Ng/m 3(0.4 

ppm) results in lower deposition rz:tes of inhaled 

Streptococcus. Nevertheless, the bacteria that are 

deposited multiply, so that shortly after exposure, 

there are more bacteria in the ozone-exposed 

lungs than in the lungs of control animals. Again, it 

was hypothesized that this oxidant gas adversely 

affected pulmonary defense systems other than 

mucociliary clearance. 

Goldstein et al.'3'89exposed miceto an aerosol of 

32P-labeled Staphylococcus aureus either after a 

17-hr exposure to ozone or before a 4-hr exposure. 

Concentrations of ozone were 1180, 1370, 1570, 

or 1960 /ag/m 3(0.6, 0.7, 0.8, or 1 ppm), or higher. 

The mechanical clearance and bactericidal 

capabilities of the lung were then measured 4 to 5 

hr after bacterial exposure. Exposure for 17 hr 

before infection caused a significant (p < 0.05) 

reduction in bactericidal activity beginning at 1960 

/ag/m 3(1 ppm). When mice were exposed to ozone 

for 4 hr after being infected, there was a significant 

decrease in bactericidal activity for each ozone 

exposure level. The lowest level of ineasurable 

effect was 1 180 Ng/m3(0.6 ppm). With increasing 

ozone concentration, there was a progressive 

decrease in bactericidal activity. The investigators 

proposed that because mucociliary clearance was 

unaffected by subsequent ozone exposure, the 

bactericidal effect was due to dysfunction of 

another type of pulmonary defense, most probably 

the alveolar macrophage. Other workers 203found 

that exposure to 980 pg/m 3(0.5 ppm) of ozone, 16 

hr/day for 7 months had no effect on the 

mechanical clearance of polystyrene and iron 

particles from rabbit lungs. In the guinea pigs 

exposed to the same concentration for 16 hr/day 

for 2 months, there was only a small reduction in 

bacterial clearance. 

Warshauer et a1. 203demonstrated that a 

139 
deficiency of vitamin E augmented the adverse 

effect of ozone at 1374 /ag/m 3 (0.7 ppm)on murine 

pulmonary bactericidal capacity only after a 

prolonged exposure (7 days). Identical 

hypovitaminosis failed to influence pulmonary 

bactericidal activity in rats exposed for only 4 hr to 

980 to 1960 ug/m 3 (0.5 to 1.0 ppm) of ozone. 

The effect of pollutant combinations on the 

bactericidal function of the lung has also been 

examined.84 Some mice received an intratracheal 

injection of 10 mg of silica, and others received 

latex. Seventy days iater, the animals were 

infected with 32 P-labeled Staphylococcus aureus 

and exposed to either 4 hr of 785 /ag/m3 (0.4 ppm) 

ozone or to clean air. Both the silicotic and latexinjected (control) mice had similarly reduced levels 

(12 percent) of bactericidal activity after breathing 

ozone (p < 0.05), when compared to their ozoneexposed counterparts. Silicosis itself did not inhibit 

the pulmonary bactericidal response. Goldstein et 

al. 91 conducted a similar study in which mice were 

exposed to ozone/NO2 combinations: From 196 to 

790 Ng/m3 (0.1 to 0.4 ppm) ozone, and from 3760 

to 13,720 Ng/m 3 (2 to 7.3 ppm) NO2 either for 17 hr 

before infection or for 4 hr after infection. The 

lungs were capable of functioning well until the 

higher pollutant level was reached. Physical 

clearance was not affected at either level. The 

demonstrated injuries were those that would be 

expected from each individual oxidant. 

Fairchild 62 found that mice exposed for 1 hr to 

1770 Ng/m 3 (0.9 ppm) ozone exhibited a 70- 

percent increase in respiratory deposition of 

vesicular stomatitis virus (p < 0.005) occurring in 

the nasal cavity rather than in the lung. Also, the 

minute ventilation was reduced (p < 0.05) by a 

maxim um of 30 percent at the end of the exposure. 

Fifteen minutes later, the minute volume 

increased but remained lower than that of the 

controls. 

An ozone concentration of 1177 /ag/m 3 (0.6 

ppm) for 3 hr caused an inhibition of replication of 

influenza virus (A2/Japan, 305/57) deposited in 

the nasal cavities of mice. In contrast, a slight 

increase in growth of vesicular stomatitis virus 

was seen in the noses of mice exposed to 1767 

Ng/m 3 (0.9 ppm) ozone for 3 hr. 61 

Laboratory-induced parasitic infection (Plasmodium berghel) of mice was also exacerbated by 

exposure to 1686 Ng/m 3 (0.86 ppm) ozone for 8 

hr/day, 5 days/week for 6 months. 162 

Alveolar Macrophages — In most of the foregoing 

studies, the authors recognized the possibility that 

damage to the alveolar macrophages (AM) was 

responsible primarily for the enhanced infectivity 

and reduced bactericidal response. Recent 

investigations have furthei advanced this 

hypothesis. When rabbits were exposed to 980 

Ng/m 3 (0.5 ppm) or 1313 Ng/m3 (0.67 ppm) for 3 hr, 

there was a significant reduction (p <0.001 ) in the 

number of bacteria phagocytized by AM. 3s ,sa 

Because phagocytosis begins with particle 

attachment to the cell membrane, increased 

fragility of the AM could play a role. Rabbits 

exposed to 980 Ng/m 3 (0.5 ppm) for 8 hr/day for 7 

days exhibited a trend toward increased 

membrane fragility of AM, although lipid 

peroxidation was undetectable at this level. 48 

The AM within the lung reside within a liquid 

layer. Gardner76 demonstrated that the protective 

components of this layer are inactivated by a 2.5-hr 

exposure to 196 pg/m3 (0.1 ppm) ozone. When 

normal or ozone-exposed AM were placed in fluid 

lavaged from exposed rabbits, they showed more 

lysis (10 percent over controls). A similar effect 

was seen when normal AM were placed in the 

protective fluid that had been exposed in vitro to 

ozone at 196 Ng/m3 (0.1 ppm) or 1960 Ng/m 3 (1 

ppm) for 30 min. 

Goldstein et a1. 85 studied the effect of a 2-hr 

ozone exposure on the ability of AM to be 

agglutinated by concanavalin A, a parameter 

reflecting membrane organization. A decrease in 

agglutination of rat AM was found after exposure 

to 980 or 1960 Ng/m 3 (0.5 or 1.0 ppm). A decrease 

in concanavalin A agglutinability of trypsinized red 

blood cells obtained from rats exposed for 2 hr to 

1960 pg/m 3 (1 ppm) was also noted. Hadley et a1. 94 

investigated AM membrane receptors from rabbits 

exposed to 980 Ng/m 3 (0.5 ppm) ozone for 3 hr. 

Following ozone exposure, lectin treated AM have 

increased rosette formation (p < 0.05) with rabbit 

red blood cells. The authors hypothesized that the 

ozone-induced response indicates alterations of 

macrophage membrane receptors for the wheat 

germ agglutinin that may lead to changes in the 

recognitive ability of the cell. 

Hurst et a1.t 06 showed thatthe acid hydrolases of 

AM lysosomes are significantly reduced after 

rabbits are exposed for 3 hr to either 490 Ng/m 3 

(0.25 ppm) or 980 /jg/m3 (0.5 ppm) of ozone. 

Greatest reductions (25 percent and 40 percent, 

respectively) were seen in the lysozyme activity. 

Acid phosphatase and Q-glucuronidase activities 

were also affected. Since these enzymes are 

involved in intracellular degradation of bacteria, 

140 
their reduced activities could contribute to poor 

macrophage functioning and, consequently, to 

enhanced mortality from bacterial invasion. 

Similar enzymatic reductions were observed in AM 

exposed in tissue culture. 105 The effects of ozone 

on host defenses were also studied by means of 

unilateral lung exposures of rabbits. 3 Three hours 

of ozone exposure was found to decrease cellular 

viability, depress various intracellular enzymes, 

and increase the number of pulmonary 

polymorphonuclear leukocytes. The effects were 

dose-related, beginning at 980 Ng/m 3 (0.5 ppm). 

The responses were fou nd to be specific to the lung 

that breathed ozone rather than any generalized 

systemic response. 

In vitro techniques have also been employed to 

study AM function and biochemistry after ozone 

exposure. Weissbecker et a1. 207 established doseresponse curves for the effect of ozone on the 

viability of AM, with effects being seen at 118 

/Ig/m3 (0.06 ppm). Richmond 13 studied the in vitro 

phagocytic activity of AM using radioisotopelabeled bacteria. Exposure of adhered AM to 

ambient air or'to 1570 Ng/m 3 (0.8 ppm) ozone 

resulted in little difference in uptake of 32 P by 

Staphylococcus albus. The exposed AM engulfed 

fewer bacteria than controls. The concentration of 

ozone was not-measured either during or following 

the 2-hr exposure. 

Evidence that ozone may be inhibitory to 

interferon (an antiviral substance) synthesis was 

studied by Ibrahim et a1. 123 Mice were exposed for 

14 or 21 days to 1570 /jg/m 3 (0.8 ppm) ozone. At 

the end of the exposure periods, some mice were 

removed to ambient air for recovery studies. 

Tracheal explants and AM from the exposed mice 

were cultured. The data indicate that for the first 

10 days of ozone exposure, no effect was observed 

on the capacity of the tracheal epithetial cells to 

produce interferon. However, starting on the 11 th 

day, there was a continual decrease in interferon 

production. In the recovery studies, it was found 

that 10 days after the mice were moved to clean 

air, the epithelial cells began to produce a small 

amount of interferon. Complete recovery occurred 

24 days after removal to clean air. The authors 

reason that the results could be due to a decreased 

synthesis of interferon or an inhibition of 

interferon release from the tissues. No effect on 

the capacity of AM to produce interferon was seen 

after 21 days of exposure. 

Immunology — Matsumura 123 exposed albuminsensitized guinea pigs to 1960 Ng/m 3 (1.0 ppm) 

ozone and found no increases in anaphylactic 

attacks after subsequent antigen inhalation. In a 

further study, Matsumura et a1. 124 found that 

guinea pigs that received a 1-hr pretreatment with 

1960 Ng/m 3 (1 ppm) ozone had no anaphylactic 

responses to inhaled acetylcholine, a bronchoconstrictor agent, after a later exposure to 

3930 pg/m3 (2.0 ppm) ozone. 

In an attempt to define a mechanism for the 

edemagenic effect of ozone, Easton and Murphy 52 

noted that ozone-exposed guinea pigs appeared to 

be more susceptible to the toxic action of 

histamine, a vasoactive substance released bY 

certain cells in allergic reactions. It was observed 

that pre-exposure to 9800 /jg/m 3 (5.0 ppm) ozone 

for 2 hr followed by a histamine challenge of 0.9 to 

1.4 mg/kg body weight (injected 1.5 to 2.0 hr after 

the end of exposure) resulted in increased 

mortality compared with an air-exposed control 

group. Autopsy of the dead animals indicated that 

members of both groups died of acute 

bronchoconstriction. The increased susceptibility 

to histamine was detectable for 12 hr after the 

termination of exposure to ozone. The minimum 

concentration of ozone that produced an increase 

in mortality was 980 to 1960 Ng/m 3 (0.5 to 1.0 

ppm), one-twentieth of that required to produce 

death from pulmonary edema resulting from ozone 

alone. Since there was no significant difference in 

lung water content between the two groups, it was 

concluded that pulmonary edema did not 

contribute to the increased susceptibility. 

Increased mortality was found to occur only when 

exposure to ozone took place before challenge with 

histamine and not when guinea pigs were injected 

with histamine before exposure. 

BIOCHEMISTRY 

The actual mechanism of the toxicity of ozone at 

the subcellular level is unclear. The following 

theories have been advanced about the 

biochemical damage caused by ozone: (a) 

Nonspecific stress with the release of histamine, 

(b) oxidation of sulfhydryl groups or their 

precursors, (c) oxidation of polyunsaturated lipids 

contained mainly in cell membranes, (d) formation 

of toxic compounds (ozonides) through reaction 

with polyunsaturated lipid, (e) formation of free 

radicals, and (f) injury mediated by a pharmacologic action (i.e., via a neurohormonal 

mechanism). These mechanisms have been 

discussed in several reviews. 39,129,130,154,188 

141 
Amino Acids and Proteins — The susceptibility of 

aqueous soiutions of amino acids to oxidation in 

vitro from ozone exposure was ranked by Mudd et 

a1. 140 From high to low susceptibility, the ranking is 

as follows: Cysteine, methionine, tryptophan, 

tyrosine, histidine, cystine, and phenylalanine. 

Other amino acids were unaffected. Sulfhydryl 

compounds were found to the be most susceptible 

to oxidation. In addition, when avidin was exposed 

to ozone, its ability to bind to biotin was lost, 

presumably because of oxidation of tryptophan 

residues. In vitro ozone exposure 169 to formic acid 

solutions of amino acids was found to have the 

following decreasing order of reactivity: 

Tryptophan, methionine, cystine, tyrosine. Other 

amino acids were not tested. 

Protein synthesis of rat lung tissue is a4tered by 

continuous exposure to 1570 Ng/m 3 (0.8 ppm) 

ozone, as described by Mustafa et a1. 149 After 1 day 

of exposure, there was no difference in the in vitro 

incorporation of labeled amino acids into the lung 

slices. However, 35- and 84-percent increases in 

incorporation were observed after 2 and 3 days of 

exposure, respectively. Throughout the remainder 

of the study (up to 7 days), the level remained 

elevated and unchanged. When in vivo amino acid 

incorporation procedures were used, there was a 

50-percent decrease in incorporation after 1 day of 

exposure. On days 2 and 3, there were increases of 

60 percent and 100 percent over control. A plateau 

was reached on day 3 that extended to day 7. U nder 

the in vivo conditions, no radioactive incorporation 

of amino acids occurred in the AM obtainable b.y 

lavage. Similar studies conducted in the presence 

of puromyc;in (an inhibitor of protein synthesis) 

showed that the increase in amino acid 

incorporation observed in vitro and in vivo for the 

ozone-exposed animals was reflected in an 

increase in protein synthesis. 

The influence of ozone on lung prolyl 

hydroxylase (an enzyme thoughtto be rate-limiting 

in collagen synthesis) and the product of its 

reaction, hydroxyproline, was studied by Hussain 

et aV. 108 Rp* -; were exposed continuously to either 

390, 980, or 1570 /jg/m3 (0.2, 0.5, or 0.8 ppm) 

ozone. At the end of a 7-day exposure to the lowest 

ozone concentration, no significant changes in 

prolyl hydroxylase activity were found. However, 

by 7 days there were statistically significant 

increases of 150 and 200 percent in the enzyme 

activity of lungs from animals exposed to 980 or 

1570 Ng/m 3 (0.5 or 0.8 ppm) ozone, respectively. 

For the 980 Ng/m3 (0.5 ppm) ozone treatment 

group, the increased activity of prolyl hydroxylase 

had partiaily returned to normal by 30 days, but it 

was still elevated (p <0.05) over the controls. After 

60 days of exposure to 980pg/m 3 (0.5 ppm) ozone, 

this enzyme activity was not significantly different 

from control. When prolyl hydroxylase activity and 

hydroxyproline levels were determined in the 

groups receiving 1 570 ,Ug/m 3 (0.8 ppm) for 7 days, 

it was found that enzyme activitywas elevated (p < 

0.05) beginning atday 1. Hydroxyproline levels had 

increased (p < 0.05) by day 3. Experiments were 

also performed in which measurements were 

made on animals allowed to recover in air 

following a 7-day continuous exposure to 1570 

/ag/m 3 (0.8 ppm) ozone. Prolyl hydroxylase activity 

returned to control values after 12 to 13 days of 

recovery However, hydroxyproline levels remained 

constantly elevated over 28 days of recovery. 

A similar investigation by Hussain et a1. 107 was 

conducted in which rats were exposed 

continuousiy to 1570 Ng/m 3 (0.8 ppm) ozone for 7 

days. Results were generally similar to those 

reported for 1570 Ng/m3 (0.8 ppm) in the above 

mentioned study, 108 so that only additional 

information will be described here. The rates of 

collagen and noncollagenous protein synthesis 

increased over the 7-day exposure period. 

Collagen synthesis was greater than noncollagenous protein synthesis, particularly on days 

1 through 4. There was a net accumulation oftotal 

lung collagen (p < 0.05) by day 3, which remained 

constantly elevated over the 7 days, reflecting the 

increased collagen synthesis. 

Lung tissue ground substance may include 

hyaluronic acid, chondroitin sulfuric acids A, B, 

and C, heparin, keratosulfate, and the proteins 

collagen and elastin. In one experiment, Buell et 

a1. 23 used four litter-mate rabbits. Two were 

exposed to 1960 Ng/m 3 (1 ppm) ozone for 1 hr, one 

of which was sacrificed immediately after 

exposure and the second, 24 hr later. Anotherwas 

killed immediatelyafterexposureto9800/jg/m 3 (5 

ppm) for 1 hr. The fourth rabbit was used as a 

control. After enzyme hydrolysis of the protein 

fraction of the lung tissue, the presence of carbonyl 

compounds (e.g., aldehydes and ketones) was 

determined. The carbonyl compounds were 

identified spectrophotometrically as the corresponding dinitrophenyl-hydrazones. The data 

from animals sacrificed immediately after 

exposure were similartothose obtained 24 hr after 

exposure. It was hypothesized that these carbonyl 

compounds might cross-link collagen or elastin, 

142 
leading to structural changes in lung tissue. 

Last et al. 1 e studied in vitro mucus glycoprotein 

secretion by tracheal explants from rats exposed to 

390 or 1570 Ng/m 3(0.2 or 0.8 ppm) ozone for 8 or 

24 hr/day for periods of 2 to 90 days. Significant 

ozone-concentration-related decreases in glycoprotein secretion were observed. The depression 

of secretion at days 2 to 3 could be reversed by the 

administration of indomethacin or hydrocortisone 

during exposure. 

Lipids — Many investigators postulate that lipid 

peroxidation is an important toxic mechanism in 

ozone injury. These ideas are presented in 

reviews39,129 that describe the propensity of ozone to 

react with the ethylene groups of unsaturated fatty 

acids. This reaction can lead to free radical 

formation, which in the presence of molecular 

oxygen leads to the peroxidation of the 

unsaturated fatty acid by formation of fatty acid 

lipoperoxides. Alterations found in erythrocytes 

following ozone exposure are often cited as 

evidence for these concepts. 82,86,87,732 (For a more 

complete discussion of effects on erythrocytes, see 

Chapter 9.) 

Buell et a1. 22suggested that the interaction of 

ozone and water results in the fomation of atomicor radical-oxygen and molecular oxygen, whereas 

Alder and Hillz postulated the formation of a variety 

of radicals. Although high-energy sources such as 

X-irradiation undoubtedly decompose water into a 

variety of free radicals, it has not been shown that 

ozone can form more than one. 

That free radicals may be involved in ozone 

toxicity is suggested indirectly by the work of 

Mustafa et a1. 15 ' The influence of ozone on 

superoxide dismutase (SOD) activity of the lung 

was investigated. SOD is an inducible enzyme that 

catalyzes the dismutation of superoxide radical, 

thereby preventing oxidant toxicity that may be 

consequent to this radical. Rats were exposed to 

390, 980, or 1570 /ag/m 3(0.2, 0.5, or 0.8 ppm) 

ozone for 7 days. While it is not stated explicitly, it 

can be assumed from the abstract that exposure 

was continuous. SOD activity increased by 17 

percent, 26 percent, and 38 percent after exposu re 

to 390, 980, and 1570/jg/m 3(0.2, 0.5, or 0.8 ppm), 

respectively. At the highest ozone r:oncentration, 

the location of the SOD activity was determined, 

and it was found that exposure resulted in a 38- 

percent increase in the cytosolic fraction and a 46- 

percent increase in the mitochondrial fraction. 

Using a different exposure mode, rats were 

exposed stepwise to 1570 /ig/m 3(0.8 ppm) for 72 

hr, to 2940 Ng/m 3(1.5 ppm) for 24 hr, and finally to 

5890 pg/m3(3 ppm) for 8 hr. Following treatment, 

SOD activity increased (as ozone concentration 

increased) by 15 percent, 25 percent, and 50 

percent in the cytosol and 50 percent, 67 percent, 

and 118 percent in the mitochondria, respectively. 

The authors suggest that the increase in SOD 

activity represents adaptive changes in the lung 

that might reduce oxidant toxicity. 

Pryor et al.' 1 ' and Pryor 10exposed pure samples 

of polyunsaturated fatty acids (methyl linoleate 

and methyl linolenate) to 0 to 2940 Ng/m 3(0 to 1.5 

ppm ozone) in vitro and followQd the formation of 

peroxides, conjugated dienes, and thiobarbituricacid-reactive material as a fu nction of time. Ozone 

shortened the induction period for auto-oxidation, 

but did not significantly affect the rate of product 

formation after the induction period. As the 

concentration of ozone was raised from 0 to 2940 

pg/m 3(0 to 1 5 ppm) during the induction period, 

there were greatly increased rates of peroxide 

formation, a slightly increased rate of conjugated 

diene formation, and no significant change in the 

rate of production of thiobarbituric-acid- reactive 

material. When vitamin E was added, the induction 

period was lengthened, but the rate of product 

formation during the auto-oxidation phase was 

unchanged. The authors hypothesized that most of 

the ozone-induced in vivo alterations occur during 

the induction period of lipid auto-oxidation. 

Roehm et al."',16studied the oxidation of 

polyunsaturated lipids in vitro by exposing samples 

of pure methyl esters of fatty acids to 2940 Ng/m 3 

(1.5 ppm) ozone and 2820/_Ig/m 3(1.5 ppm) NOz. At 

equivalent concentrations of these two oxidants, 

ozone produced the greatest changes. Methyl 

linoleate was completely reacted by ozone to yield 

stable ozonides. These researchers hypothesized 

that ozone acts by direct addition of ozone across 

the fatty acid double bond, and this agreeswith the 

mechanism proposed by Criegee 41concerning the 

primary mechanism for ozonolysis. 

Other investigators have studied the effects of 

ozonides in vitro and in vivo. Menzel et a1. 133 

injected intradermally 10 picograms to 10 /ig of 

fatty acid ozonides (from oleic, linoleic, linolenic, 

and arachidonic acids) into animals and found 

increased vascular permeability of the capillaries, 

as measured by extravascularly located, 

pontamine-blue-bound serum proteins. This 

reaction was blocked by simultaneous antihistamine injection or by prior treatment with 

compound 48/80 (a substance that can deplete 

143 
histamine stores . It therefore appeared that 

histamine was involved in the toxicity of the 

ozonides (but histamine release could be 

secondary and not primary). The same series of 

experiments also showed that the ozonide caused 

peroxidation of isolated microsomes and 

mitochondria. There were also indications of 

oxidation of erythrocyte membranes. Cortesi and 

Privett 40also prepared a methyl linoleate ozonide 

and administered it to rats by intravenous injection 

or by oral dosage. This treatment was lethal as a 

result of acute lung edema. Also, significant 

changes occurred in the fatty acid composition of 

serum and lung lipids. 

To investigate some of the possible effects of 

ozone on membrane lipids, Teige et a1. 196exposed 

phosphatidyl choline liposomes containing 

trapped glucose and human erythrocytes to ozone 

in vitro (3 Nmoles ozone/min). Phosphatidyl 

choline is a phospholipid commonly found in cell 

membranes. Ozone exposure caused a leakage of 

glucose from the liposomes Liposomes exposed to 

ozone were more active than ozone alone in 

causing lysis of red blood cells. Hydrogen peroxide 

was found not to be responsible for this effect. 

Chow and Tappe1 32observed an increased 

formation of malonaldehyde (a product of lipid 

peroxidation) in the lungs of rats following 

continuous exposure to 1370 Ng/m 3(0.7 ppm) for 

5 days or 1570 Ng/m3(0.8 ppm) for 7 days. The 

formation of malonaldehyde, along with the ozoneinduced increased activities of glutathione 

peroxidase and glucose-6-phosphate dehydrogenase (G-6-PD), was partially inhibited as a 

logarithmic function of dietary a-tocopherol 

(vitamin E) from 0 to 1500 Ng/kg. Mustafa et a1. 148 

found no lipid peroxidation (as determined by assay 

for thiobarbiturate-reacting materials and conjugated dienes) in the lung homogenate of rats 

exposed to 3920 ug/m 3(2 ppm) ozone for 8 hr. 

Roehm et al."''15continuously exposed rats to 

1960 pg/m3(1.0 ppm) ozone, which eventually 

resulted in 100-percent mortality due to 

pulmonary edema. Fifty percent of the atocopherol-depleted group died (LTso) after 8 2 

days of continuous exposure, while the vitaminsupplemented rats exhibited an LT so of 18.5 days. 

When Fletcher and Tappe1 68studied the 

continuous effects on rats of ozone from exposure 

to 1570 /_Ig/m 3(0.8 ppm) or higher concentrations 

for 7 days, they too found that a-tocopherol 

protected the animals from severe toxicity 

(mortality) and weight change. At low levels, the 

vitamin E protection against lung lipid peroxidation 

was a reciprocal function of the logarithm of 

dietary a-tocopherol. Rats maintained on vitaminE-supplemented diets and exposed to 1560 /jg/m 3 

(0.8 ppm) ozone continuously for 7 days were also 

partially protected from alteration in 6- 

phosphogluconate dehydrogenase (6-P-GD), 6- 

phosphogluconate (6-PG), and malic enzyme. 

Later investigations by Roehm et a1. 15showed that 

rats continuously exposed to 1960 Ng/m 3(1 ppm) 

ozone for 9 days showed a ~ ignificantly shorter 

LT50 and greater symptoms of respiratory distress 

when they were depleted of vitamin E. After 6 

weeks of exposure to 980 Ng/m 3(0.5 ppm) ozone, 

pulmonary edema and higher mortalities were 

noted in animals with diets depleted in atocopherol. Also, their lung weights were different 

from those of the a-tocopherol-supplemented 

groups. After 6 weeks of ozone treatment, 

significant changes were seen in the fatty acid 

composition of total lung lipid. The most extensive 

change was an increase in arachidonic acid in both 

diet groups (p <0.01), but the increase was higher 

in the vitamin-E-depleted rats (p < 0.05). This 

effect occurred late in the exposure, and it was 

associated with the onset of pulmonary edema and 

death. Unlike the lung tissue lipids, the fatty acids 

from endobronchial saline lavage were little 

affected by ozone or vitamin E. In both exposures, 

the onset of the edema was associated with 

elevated levels of arachidonic acid and 

docosahexenoic acid (22:6) (p < 0.05). These two 

compounds are important constituents of cell 

membranes, so membranes could be the site of 

ozone damage. 

Similar results were obtained by Menzel et a1. 132 

who exposed rats continuously to ozone. After 3 

days of exposure to 2078 /jg/m 3(1.6 ppm), linoleic 

and linolenic acid concentrations of lavage lipids 

were reduced and remained reduced over 17 days 

of exposure. Lung tissue lipids were also altered in 

rats ex;losed for 9 days to 1960 Ng/m 3(1 ppm) and 

maintained on diets either supplemented with or 

deficient in vitamin E. The greatest change was an 

increase in arachidonic acid that occurred to a 

greater extent in the animals with vitamin E 

deficiency. There were also decreases in linolenic 

acid in both diet groups; however, supplemental 

vitamin E partially retarded this change. Oleic, 

stearic, and palmitic acids also were decreased, 

but only in the vitamin-E-deficient group. Similar 

measurements were made on rats exposed 

continuously for 6 weeks to 980 /ag/m 3(0.5 ppm) 

144 
ozone. Under these conditions, the greatest 

changes after ozone exposure were a decrease in 

oleic acid (particularly in the vitamin-E-deficient 

group), a decrease in linolenic acid in the vitaminE-deficient rats, an increase in palmitic acid in the 

vitamin-E-deficient group, and an increase in the 

arachidonic acid, particularly in the vitamin-Edeficient animals. Sixty-five days of exposure to 

980 Ng/m3 ozone also caused a slight decrease 

(which appears not to be statistically significant) in 

lung tissue sulfhydryl content. From day 18 to 65 of 

a continuous exposure to an unspecified ozone 

concentration (presumably 980pg/m 3 , or0.5 ppm) 

there was a decrease in serum-reduced glutathione in both diet groups. 

Menzel et a1. 13 ' also showed that a short 

exposure of perfused rat lungs to 5880 /ag/m 3 (3 

ppm) decreased the enzymatic conversion of 

arachidonic acid to prostaglandins in such a way 

as to suggest an uncompetitive inhibition of 

prostaglandin synthetase by ozone. If this 

response occurs in vivo at lower concentrations of 

ozone, it would be possible that this could be the 

mechanism responsible for the ozone-induced 

increase in arachi(lonic acid seen in the previously 

discussed studies t32,"5 

Kyei-Aboagye et al."' also studied pulmonary 

lipids. Rabbits ex )osed to 1960 Ng/m3 (1 ppm) 

ozone for 4 hr sh-wed a reduced incorporation of 

3 1-1-oleate into leci hin (p =0.02). Pulmonary lavage 

from these anima s revealed increased activity of 

radiolabeled lecitnins. The authors observed that 

ozone may affect the lung by decreasing lecithin 

formation while ;imultaneously stimulating the 

release of surfac ant lecithins. The formation of 

pulmonary phospholipid was investigated by Seto 

et a1. 186 When rabbits were exposed to 980 and 

1960 /jg/m 3 (0.5 and 1 ppm) ozone for 1 to 2 

weeks, the amount of 14C taken into sphingomyelin, lecithin, phosphatidyl inositol plus 

phosphatidyl serine, and phosphatidyl ethanolamine was significantly reduced. The same 

researchers studied these phenomena further. 187 

Under continuous exposure to 980 Ng/m 3 (0.5 

ppm) ozone for up to 2 weeks, rabbit lu ngs showed 

decreased incorporation of 14C into lecithin until 3 

hr post exposure, when this parameter returned to 

normal. The reduction in phospholipid formation 

was more pronounced after 2 weeks of exposure 

rather than 1 week of exposure. An exposure to 

1960 /jg/m 3 (1 ppm) for 1 hr resulted in a 

decreased synthesis of sphingomyelin, lecithin, 

phosphatidyl inositol, phosphatidyl serine, and 

phosphatidyl ethanolamine. 

Even though the lipid composition of pulmonary 

wash fluid can be altered by ozone exposure, it 

would appear that the surface-tension-lowering 

properties of this fluid (which influence pulmonary 

function) are relatively unaltered. Gardner et al.a' 

and Huber et a1. 103 reported that exposure of 

rabbits to 19,600 Ng/m 3 (10 ppm) and 9800 Ng/m 3 

(5 ppm), respectively, did not destroy the surface 

activity of pulmonary wash fluid. However, 

Mendenhall and Stokinger 127 exposed saline 

washings obtained from the lungs of mice exp ~ sed 

to 9800 to 15,700 Ng/m 3 (5 to 8 ppm) ozone and 

noted rapid increases in the film pressure (the 

force opposing surface tensions). The authors 

suggested that if analogous changes weretooccur 

in vivo, the consequence would be an increase in 

the distensibility of the lungs, a situation proposed 

to be conducive to the development of emphysema. 

This effect was not confirmed in another study,e in 

which saline washings from the lungs of dogs 

were exposed in vitro to similar concentrations of 

ozone. 

Sulfhydryl Compounds and Pyridine Nucleotides 

— A number of intracellular compounds are active 

in cellular redox reactions and as such can 

constitute an antioxidant defense system. Many of 

the effects of ozone on this system have been 

reviewed. 136,149 Much of the research with ozone 

has centered on the reduced pyridine nucleotides, namely, reduced nicotinamide adenine 

dinucleotide (NADH) and reduced nicotinamide 

adenine dinucleotide phosphate (NADPH), and on 

sulfhydryl compounds, particularly reduced 

glutatttione (GSH) and related enzymes. 128 The 

relationship of these compounds to antioxidant 

activity has been described as follows: 

(--G-6-P—y--~NADP`~GSH—r—[O] 

G-6- PD I GSH GSH 

HMP shunt reductase peroxidase 

6-PG .f- 4NADPH—LGSSG "H2O 

+ 

H + 

(G-6-P = glucose-6-phosphate; 6-PG = 6- 

phosphogluconate; G-6-PD = glucose-6- 

phosphate dehydrogenase; HMP shunt - hexose 

monophosphate shunt; NADP+ = nicotinamide 

adenine dinucleotide phosphate; NADPH = 

reduced NADP; GSH = reduced glutathione; GSSG 

= oxidized glutathione; [0] = oxidizing moiety [i.e., 

hydrogen peroxide, free radical, lipid peroxide]; 

145 
GSH peroxidase = glutathione peroxidase; and 

GSH reductase = glutathione reductase.) 

A number of researchers 128 ' '4','53 have shown 

that ozonization of aqueous solutions of NADH and 

NADPH results in their oxidation. Menze1t 28 found 

that after oxidation (0.032 to 0.057 /imole Oa/min 

x 3 hr), NADH and NADPH were still biologically 

active as coenzymes. However, Nasr et a1. 153 

reported that ozone (33 ppm, 1000 ml/min, 50 

min) destroyed NADPH but had no effect on 

NADP + . In vitro exposure 14 ' to 0.1 to 6 Nmoles 

ozone oxidized NADH, but it had no effect on 

nicotinamide adenine dinucleotide (NAD). Similar 

results were not found in vivo 153 when rats were 

exposed to 64,780 Ng/m3 (33 ppm) ozone for 1 hr. 

The NADPH/NADP +ratio of the tracheal 

epithelium was not significantly altered. 

I n vitro ozone exposu re' 26 (0.032 to 0.057 /imole 

Os/min x 3 hr) was also able to oxidize aqueous 

solutions of a number of biologically active 

reducing substances (cysteine, GSH, and 

thioglycolic acid). This treatment inactivated 

papain and glyceraldehyde 3-phosphate dehydrogenase and oxidized GSH and GSSG to nonbiologically reducible forms. 

The role of sulfur-containing compounds in 

ozone toxicity is partially illustrated by the work of 

Fairchild et a1. 64 Inhalation of a variety of sulfur 

compounds (1-hexamethiol, methanethiol, 

dimethyl disulfide, di-tert-butyl disulfide, benzene 

thiol, and hydrogen sulfide) partially protected 

mice from the lethal effects of a 4-hr exposure to 

8000 to 12,000 Ng/m 3 (4.1 to 6.1 ppm) ozone. The 

functional unit of the sulfur units appeared to be 

-SHor SS-,or both, but not-S-, as dimethyl-sulfide 

and thiophene were not effective. 64 

The content of nonprotein sulfhydryls (NPSH) (a 

major source of cellular reducing substances), 

GSH, and GSSG of lung homogenate from ozoneexposed rats was determined by DeLucia et a1. 45 

The NPSH level was not significantly affected by 

exposure to 1570 Ng/m 3 (0.8 ppm) for up to 24 hr, 

to 2940 /.Ig/m 3 (1.5 ppm) for up to 8 hr, or to 3920 

/ag/m 3 (2 ppm) for up to 4 hr. When the animals 

were exposed to this higher concentration for 6 

and 8 hr, however, there was a decrease (p <0.01) 

in NPSH. GSH, which represents about 90 percent 

of the lung NPSH, was significantly reduced at 

7850 pg/m 3 (4 ppm) ozone for 6 hr, and GSSG 

remained unchanged under these conditions. 

Further experimentation suggested that mixed 

disulfides were transiently formed that reacted 

with other sulfhydryl groups of lung tissue. 

Analysis also indicated that GSH appeared to be 

the only NPSH bound to pulmonary tissue proteins 

via a mixed disulfide linkage. In an earlier study, 

DeLucia et a1. 44 found no changes in sulfhydryl 

levels in lung homogenates of rats continuously 

exposed (10 days) to 1570 Ng/m 3 (0.8 ppm) ozone. 

However, there was a 20-percent decrease (p < 

0.05) in cytochrome C reductase activity and a 32- 

percent increase (p < 0.05) in G-6-PD activity. 

The effects of dietary a-tocopherol on enzyme 

systems and lipid peroxidation within the lungs of 

rats exposed continuously to 1370 Ng/m3 (0.7 

ppm) for 5 days or 1570 Ng/m 3 (0.8 ppm) for 7 days 

were explored by Chow and Tappe1. 32 The 

increased (p <0.05)formation of malonaldehyde (a 

product of lipid peroxidation) and the activities of 

GSH peroxidase and G-6-PD (see preceding 

section on lipids) were partially inhibited as a 

logarithmic function of dietary a-tocopherol (from 

0 to 1 500 mg/kg). The increased (p<0.05) activity 

of GSH reductase was not affected by the level of 

dietary vitamin E. In addition, the activity of GSH 

peroxidase and concentration of malonaldehyde 

were linearly related (p< 0.001). The authors 

suggest that this represents an apparent 

compensation mechanism in that, with increased 

levels of lipid peroxides, there is a corresponding 

increase in the activity of GSH peroxidase, which 

in turn increases lipid peroxide catabolism. 

The effect of acute (4-hr) and chronic (4-hr/day, 

up to 30 days) exposure of mice to ozone on lung 

GSH and vitamin C content was examined by 

Fukase et a1. 7475 Immediately following the acute 

exposure to 16,100 pg/m 3 (8.2 ppm) ozone, there 

was a decrease (p <0.05) in GSH content. At 7850 

Ng/m 3 (4 ppm) ozone, there were no changes 

immediately after exposure. But 2 days later, GSH 

content increased (p < 0.1) and remained elevated 

for several days. Acute exposures to various ozone 

concentrations between 2350 and 16,1100 Ng/m 3 

(1.2 and 8.2 ppm) resulted in a decrease (p <0.05) 

in vitamin C content of the lung. Conversely, 

chronic exposures for 30 days to 390, 980, and 

1960 pg/m 3 (0.2, 0.5, and 1.0 ppm) ozone resulted 

in a progressive increase in GSH and vitamin C 

content as the ozone concentration and length of 

exposure (up to 30 days) increased. After 7 days of 

exposure to 980 or 1960 /ag/m 3 (0.5 or 1.0 ppm) 

ozone, there were increases (p <0.05) in G-6-PD, 

GSH reductase, and GSH peroxidase. The administration of vitamin C was found to retard partially 

(p< 0.05) the ozone-induced (1960 Ng/m 3 , 4 

hr/day, 7 davs) increase in G-6-PD. 

146 
Chow and Tappel 31 studied the effects of a 7-day 

continuous in vivo exposure to 1570 /ag/m 3 (0.8 

ppm) ozone on hex03e monophosphate shunt and 

glycolytic enzymes of lung homogenates of rats 

maintained with and without supplemental dietary 

a-tocopherol. The vitamin E had no effect on the 

enzyme activities in air-control animals. Ozone 

caused increases (p < 0.01) in G-6-PD and 6- 

phosphogluconate dehydrogenase (6-P-GD) 

activities in the lungs of animals from both diet 

groups, although the increase was less (p < 0.05) 

in those rats that received supplemental vitamin E. 

Malic enzyme activitywas also increasedfollowing 

ozone exposure in the normal (p < 0.05) and the 

supplemented (p < 0.1) diet groups, but the 

increase was less (p <0.05) in the supplemented 

vitamin E group. Neither ozone nor a-tocopherol 

supplementation altered the activity of soluble 

malic dehydrogenase. The enzymes that regulate 

glycolysis—phosphofructokinase and pyruvate 

kinase—had increased activities following ozone 

exposure and were not affected by vitamin E in the 

levels administered. Ozone exposure resulted in 

increases in aldolase activity (p< 0.1) in the 

dietary-supplemented animals, but not in the 

normal diet group (p < 0.1) compared to air 

controls. The differences between the supplemented and normal diet groups receiving 

ozone were not significant.Lactate dehydrogenase 

(LDH) activity increased in both diet groups following ozoneezposure (p< 0.001 ), a lthough_the 

increase was less (p< 0.1) in the supplemental 

diet group. 

To determine the influence of the duration of 

ozone exposure on some of these ozonP-induced 

responses, rats maintained on normal diets were 

exposed continuously to 1470 Ng/m 3 (0.75 ppm) 

ozone. 31 The activities of GSH peroxidase, GSH 

reductase, G-6-PD, 6-P-GD, and pyruvate kinase 

were decreased after 1 day of exposure. 

Thereafter, they increased until day 10. By day 30, 

all enzyme activities except for GSH peroxidase 

and GSH reductase had decreased from their 10- 

day values but were still increased over control 

values. GSH reductase exhibited a very slight 

decrease between days 10 and 30. GSH 

peroxidase continued to increase over this time 

period. The authors hypothesized that an 

increased rate of glycolysis and hexose 

monophosphate shunt activity is an adaptive 

response to the increased need for reductive 

detoxification of ozone-induced lipid peroxidation. 

Dungworth et a1.50 exposed monkeys to ozone for 

8 hr/day for 7 days. Six rhesus monkeys received 

1570 Ng/m3 (0.8 ppm), and six were exposed to 

980 /jg/m3 (0.5 ppm). Bonnet monkeys (2 to 4 per 

exposure group) were exposed to either 980Pg/m 3 

(0.5 ppm), 690 Ng/m 3 (0.35 ppm), or 390 ,ug/m 3 

(0.2 ppm). In the lungs of ozone-exposed monkeys, 

there were increased activities of GSH peroxidase, 

GSH reductase, G-6-PD, NADPH-cytochrome-C 

reductase, succinate oxidase, acid phosphatase, 

and /3-N-acetyl-glucosaminidase. Linear regression analysis indicated that there was a 

significant (p < 0.05) correlation between ozone 

concentration and increase in enzyme activity in 

both rhesus and Bonnet monkeys. Morphological 

investigations of the same animals (see later 

section on morphology studies) showed the 

presence of a lesion at the level of the respiratory 

bronchiole and increased numbers of Type 2 cells. 

Chow et a1. 28 exposed rats to 390, 980, or 1570 

/jg/m3 (0.2, 0.5, or 0.8 ppm) ozone continuously (8 

days) or intermittently (8 hr/day X 7 days) before 

biochemical assays of lung homogenates. For the 

continuous exposure to the two higher ozone 

concentrations, activities of GSH peroxidase, GSH 

reductase, and G-6-PD were increased (p < 0.05) 

wer controls. At the lower ozone concentration, 

there was an increase (p <0.05) in the activities of 

GSH peroxidase and GSH reductase. Linear 

regression analysis indicated that there was a 

linear increase in all 3 enzyme activities as the 

concentration of ozone was increased (p <0.001). 

Similar results were obtained for the intermittent 

exposure groups. No statistical comparisons of the 

intermittent and continuous exposure groups were 

made. The authors suggest that the increase in 

enzyme activity is in response to the need for 

reduction of ozone-induced lipid peroxides. 

Similar measurements were made by Mustafa 

and Lee150 of the lungs of rats and monkeys 

exposed to various concentrations of ozone. Lung 

homogenates of rats exposed continuously for 7 

days to 1 570 Ng/m3 (0.8 ppm) were examined. On 

the first day, the activities of microsomal NADPHcytochrome-C reductase and cytosolic G-6-PD 

activities were slightly depressed, but by day 2 they 

were elevated, reaching a plateau at days 3 to 4. By 

day 7, NADPH-cytochrome-C reductase had 

increased by 42 percent (p <0.001), and G-6-PD by 

67 percent (p < 0.001). Similar increases were 

found in 02 consumption and mitochondrialsuccinate-cytochrome-C reductase (see the 

following section on mitochondrial enzyme 

activities). 

147 
The influences of intermittent (8 hr/day) and 

continuous exposure for 7 days were compared as 

part of the same investigation by Mustafa and Lee. 150 

Exposures were to 390, 980, or 1570,Ug/m 3 (0.2, 

0.5, or 0.8 ppm) ozone. Specific data were not 

given for NADPH-cytochrome-C reductase or G-6- 

PD; however, the authors stated that these enzyme 

activities increased in a manner similar to 

succinate oxidase activity (see the following 

section on mitochondrial enzyme activities). Thus 

it would seem that rats exhibited the greatest 

significant increase, with effects being observed at 

390 /ag/m3 (0.2 ppm), while these enzyme 

activities in rhesus monkeys only increased 

significantly (p < 0.05) after exposure to 1570 

/jg/m3 (0.8 ppm). Bonnet monkeys exhibited a 

significant (p < 0.05) increase in these enzyme 

activities at 690 Ng/m 3 (0.35 ppm). 

Biochemical assays of the lungs of rats and 

rhesus monkeys were also made by Chow et al. 3o 

Assays were made following a 7-day exposure (8 

hr/day) to 980 pg/m3 (0.5 ppm) ozone. In rat lung 

homogenates, there were 20- to 26-percent 

increases (p < 0.05) in the activities of GSH 

peroxidase, GSH reductase, and G-6-PD. GSH was 

also significantly elevated by 22 percent. Though 

increases in all these parameters occurred in 

monkeys (n=12), the increases (which ranged from 

10 to 15 percent) were smaller in magnitude as 

compared to the rats, and they were not 

statistically significant because of relatively large 

variations. Similar measurements were made on 

the erythrocytes of these animals, but no 

significant changes were observed. 

The effects of intermittent (8 hr/day) and 

continuous ozone exposures for 7 days on rats 

were compared by Schwartz et a1. 184 Ozone 

exposures were to 392, 980, or 1568 Ug/m 3 (0.2, 

0.5, or 0.8 ppm). Biochemical changes were 

compared to morphologic alterations. The latter 

are discussed in more detail in a later section on 

morphology studies. The activities of G-6-PD and 

NADPH-cytochrome-C reductase in cellular 

oxygen utilization (succinate oxidase activity)were 

increased in an ozone-concentration-dependent 

fashion following exposure. The increases in the 

continuous exposure groups were only slightly 

greater than in the intermittently exposed animals. 

Concurrent morphologic studies also showed little 

difference between continuous and intermittent 

exposure. Therefore it would appear the recovery 

did not occur during the clean air period of the 

intermittent exposure. 

Chow et a1. 29 examined the biochemical 

responses of lung homogenates of ozone-exposed 

rats during recovery and re-exposure. AII ozone 

exposures were continuous (3 days) to 1568 

/μg/m 3 (0.8 ppm). The activities of GSH peroxidase, 

GSH reductase, and G-6-PD were significantly 

(p< 0.01) increased by 25, 18, and 46 percent, 

respectively, immediately after the initial 3-day 

exposure. There was also an 85-percent increase 

(p < 0.001) in protein synthesis and a 24-percent 

increase (p < 0.001) in nonprotein sulfhydryl 

(NPSH) content at this time. These biochemical 

changes began to revert toward control values 

after a 2-day holding period in clean air. Recovery 

continued and completely reached control values 9 

days after exposure cessation. No further changes 

were found up to 30 days after ozone exposure 

ended. The ozone-exposed rats were re-exposed to 

ozone (1568 /jg/m 3 , or 0.8 ppm, continuouslyfor 3 

days) at various times during the recovery period 

(day 6, when recovery was incomplete, and days 

13 and 27). Following this re-exposure, values 

from all biochemical measurements increased to 

approximately the same levels as found with the 

initial ozone exposure, thereby indicating that no 

adaptation to ozone occurred. 

The effects of ozone tolerance on many of these 

enzyme systems were investigated by Chow. 27 To 

develop tolerance, rats were exposed to 0 or 1490 

Ng/m3 (0.76 ppm) ozone for 3 days. The ozone 

treatment resulted in increased activities of GSH 

peroxidase, GSH reductase, and G-6-PD, and in 

GSH levels that returned to normal approximately 

7 days after recovery in air. After 8 days of recovery 

in clean air, some animals were exposed to 7840 

Ng/m3 (4 ppm) ozone for 8 hr Lung homogenates 

were assayed 16 hr later. Fifty percent of the nonpre-exposed (i.e., nontolerant) rats died following 

the 7840 Ng/m3 (4 ppm) exposure, but only 1 of 7 of 

the tolerant group died. The lungs of the tolerant 

and nontolerant animals exposed to the high ozone 

dose exhibited an increase in protein content, 

decreased (p < 0.05) activities of GSH peroxidase, 

GSH reductase, and G-6-PD, and a decrease in 

GSH levels. However, the lungs of tolerant rats had 

significantly greater (p < 0.05) enzyme activities 

and higher GSH levels compared to nontolerant 

animals. When the animals were allowed to 

recover for 9 days before the 7840 /~g/m3 (4 ppm) 

challenge, there were no differences between the 

tolerant and nontolerant groups. In a similar study, 

rats that were 10 days younger were pre-exposed 

for 3 days to 1568 ug/m 3 (0.8 ppm) before an 8-hr 

148 
challenge with 7644 /jg/m3 43.9 ppm) ozone. 

Allowing an 1 1-day recovery period between the 

two exposures resulted in findings similar to those 

for the 8-day recovery. The authors suggest that 

the tolerance observed might render the animals 

more resistant to peroxidative, ozone-induced 

damage. 

Mitochondrial Enzyme Activities — Mustafa"' 

demonstrated alterations in lung mitochondrial 

oxygen consumption in lung homogenates of rats 

exposed to 5880 Ng/m 3 (3 ppm) ozone for 4 hr and 

then placed in air for several days. Oxidation of 

succinate was decreased (p < 0.05) immediately 

a#ter exposure and remained so during the next 12 

hr. The rate of oxidation reached control values by 

24 hr and then increased and peaked (p < 0.001), 

relative to control, between 72 and 96 hr. Oxygen 

consumption then began to return to normal 

values and was not significantly different from 

control by day 21. These observations made with 

succinate are similar to those made using 2- 

oxyglutarate, glycerol-1 -phosphate, and ascorbate-Wurster's blue as substrates, except that 

the magnitude of the changes was different. 

Succinate-cytochrome-C reductase activity was 

greater in the exposed lungs after recovery for 2 to 

4 days. When the mitochondrial fraction of the 

lungs was examined, generally similar changes in 

Oz consumPlion were observed. The increase in 

oxidation was found up to day 7 of recovery, but not 

after days 14 and 21 of recovery. To elucidate the 

reasons for the observed alterations in oxidative 

activity, other experiments were performed. The 

cytochrome content of mitochondria (on a permilligram-of-protein basis) was not significantly 

different in the exposed animals when examined 

after 2, 3, and 4 days of recovery. However, the 

mitochondrial population of the exposed animals 

increased and was significantly higher (p< 0.01 ) 

after 48 hr of recovery. After 7 days, the population 

began to decline. Concurrent transmission 

electron microscopic observations indicated that 

there appeared to be no increase in number of 

mitochondria within the cells of the exposed 

animals' lungs, but the number of Type 2 cells, 

which contain numerous mitochondria, had 

increased by 50 to 100 percent after ozone 

exposure, and succinate-02 consumption of these 

cells was unchenged (on a per-milligram-ofprotein basis). , 

In contrast to the inhibitory effects of acute 

exposures to high concentrations of ozone, lowlevel, chronic exposures result in ari increase of 

lung oxidative metabolism. Mustafa et a1. 144 

studied mitochondrial oxygen consumption in rats 

exposed conti nuously to 1 568 /_Ig/m 3 (0.8 ppm) for 

10 to 20 days. They found a 45-percent increase 

(p<0.02) in oxygen utilization bythe 20th day of the 

experiment. There was also a 20- to 30-percent 

increase in the oxidation of 2-oxyglutarate and 

glycerol-l-phosphate. After 10 days of exposure, 

there- was a simultaneous increase (threefold) 

(p<0.01) in the number of Type 2 alveolar cells that 

are rich in mitochondria, so perhaps the increase in 

OZ comsumption was due to proliferation of these 

cells. After 7 days of exposure to 392, 980, or 1568 

/jg/m3 (0.2, 0.5, or 0.8 ppm) ozone, there were 

increases (p < 0.05) in Oz consumption of 17, 30, 

and 40 percent, respectively. 

The effects of various modes of ozone exposure 

on 02 consumption of lung tissue were 

investigated by Mustafa and Lee. 150 In the first 

experiment, rats were exposed to 1568 Pg/m 3 (0.8 

ppm) continuously for 1 to 30 days. The rates of 

oxygen consumption for oxidation of 2- 

oxyglutarate, succinate, and glycerol-1-phosphate 

were slightly reduced in lung homogenate at day 1, 

but began to increase thereafter. The increased 

(p< 0.001) rate of 02 consumption reached a peak 

at day 4 and plateaued over the remainder of the 

exposure (up to 30 days). The oxidation of 

succinate was increased more than the other two 

substrates. During a 7-day continuous exposure to 

this ozone concentration (1568 Ng/m3 or 0.8 ppm), 

there was an initial decrease (day 1) and a 

subsequent increase (day 2) in the activity of 

mitochondrial-succinate-cytochrome-C reductase 

that plateaued between days 3 and 7. By day 7, the 

increased activity was 55 percent above control 

(p<0.001). Similar results were found for 

microsomal NADPH-cytochrome-C reductase and 

G-6-PD (see preceding section on . sulfhydryl 

compounds and pyridine nucleotides). 

As part of the same study, 150 the effects of 

continuous and intermittent(8 hr/day) exposure of 

rats for 7 days were compared a: the end of the 

exposure. Exposures were to 392, 980, or 1568 

Ng/m3 (0.2, 0.5, or 0.8 ppm) ozone. The increases 

in 02 consumption (using succinate as a substrate) 

and succinate-cytochrome-C reductase activity 

were all significant (p < 0.05) and fairly proportional to the ozone concentration. At the lower 

ozone concentration, the increase in enzyme 

activity was slightly greater in the intermittent 

exposure group. However, the reverse occurred at 

the two higher concentrations. The differences in 

149 
the data from the two modes of exposure (i.e., 

intermittent, versus continuous) were not significant. Similar concentration-related responses 

occurred for NADPH-cytochrome-C reductase and 

G-6-PD (see preceding section on sulfhydryl 

compounds and pyridine nucleotides). Monkeys 

were exposed intermittently to various 

concentrations of ozone, and after 7 days, enzyme 

activities of lung tissue were made. Rhesus 

monkeys (n=24) showed elevations in succinate 

oxidase activity of 12 percent (not statistically 

significant) at 980 Ng/m3 (0.5 ppm) and of 24 

percent (p < 0.05) at 1568 Ng/m3 (0.8 ppm). 

Greater increases were observed in Bonnet 

monkeys (n=13): 13 percent (not statistically 

significant), 22 percent (p< 0.05), and 30 percent 

(p < 0.02), for 392, 686, and 1568 Pg/m 3 (0.02, 

0.35, and 0.8 ppm), respectively. However, greater 

increases were observed in the rats for the 

corresponding ozone concentrations. Similar 

species differences with respect to ozone 

concentration were found for NADPHcytochrome-C reductase and G-6-PD. After 7 days 

of exposure of the rats, there were significant 

(p< 0.05) increases in NADPH-cytochrome-C reductase and G-6-PD that were related to ozone 

concentration. Though there was less increase in 

the intermittent group, there was no statistically 

significant difference between intermittent and 

continuous exposure. Similar results were 

observed for succinate oxidase and succinatecytochrome-C reductase (see preceding section on 

sulfhydryl compounds and pyridine nucleotides). 

As part of the same study, Mustafa and Lee' so 

also examined the effect of vitamin E on the effect 

of ozone on succinate-dependent 02 consumption 

of lung homogenate. Five weeks before ozone 

exposure, rats were fed diets with either 66 ppm or 

11 ppm of vitamin E. The authors state that 66 ppm 

vitamin E is approximately twice the recommended 

daily allowance, and that 11 ppm vitamin E is the 

average concentration in American diets. The 

animals were then exposed continuously for 7 

days to either 196 or 392 Pg/m3 (0.1 or 0.2 ppm) 

ozone before assaysThe vitamin E-supplemented 

group (66 ppm) exhibited an increase in succinate 

oxidase activity of 3 percent (not significant) and 

18 percent (p < 0.05) at 196 and 392 Ng/m3 (0.1 

and 0.2 ppm) ozone, respectively. Those animals 

that received 11 ppm vitamin E had greater 

increases in succinate oxidase activity, namely a 

25-percent (p < 0.02) and a 38-percent (p < 0.01) 

increase for 196 and 392 Ng/m 3 (0.1 and 0.2 ppm) 

ozone, respectively. Vitamin E did not cause any 

significant differences in succinate oxidase activity 

of control animals. Mustafa and Lee 150 primarily 

attribute the increases in these enzyme activities 

to a concomitant increase of Type 2 cells (see the 

later section on morphology studies), which are 

rich in mitochondria and exhibit high metabolic 

activity. 

The effects of recovery from and re-exposure to 

ozone on 02 consumption of lung was investigated 

by Chow et a1. 29 Rats exposed continuously to 1568 

,ug/m3 (0.8 ppm) ozone for 3 days exhibited a 48- 

percent increase (p < 0.001) in the rate of mitochondrial succinate oxidation. After the animals 

recovered for 2 days in filtered air, thisvalue began 

to return to normal and reached control values 9 

days after the initial exposure ceased. When the 

rats were re-exposed to the same ozone 

concentration (3 days, continuous) on days 6, 13, 

and 27 of recovery, the rate of mitochondrial 

succinate oxidation again increased to levels 

similar to those observed for the intial ozone 

exposure. Similar effects were observed for GSH 

peroxidase, GSH reductase, and G-6-PD (see 

preceding section on sulfhydryl compounds and 

pyridine nucleotides). So again the data support 

the inference that adaptation to these ozoneinduced responses did not occur. 

Other Biochemical Alterations — In a review, 

Mustafa et a1. 149 present the resdits of a study on 

the effects of ozone on glucose metabolism in the 

;ung. Rats exposed to 1568 Ng/m 3 (0.8 ppm) ozone 

continuously for 4 days exhibited a 59 percent 

(p<0.02) increasein the rate of glucose consumption. In addition, the rates of pyruvate and lactate 

production both increased 43 percent (p < 0.02), 

but the absolute amount of lactate produced (22.2 

,umoles/hr per lung) was greater than the amount 

of pyruvate produced (3.7 μmol es/hr per lung). 

This review149 also describes an effect of ozone 

on monoamine oxidase (MAO), an enzyme that 

catalyzes the metabolic degradation of biological 

amines. Acute exposure (8 hr) to 3920 Ng/m 3 (2 

ppm) ozone caused a 30- to 40-percent (p < 0.05) 

decrease in MAO activity of lung homogenate, 

mitochondria, and microsomes. However, a 7-day 

continuous exposure to 1568 Ng/m3 (0.8 ppm) 

resulted in a 20- to 35-percent (p < 0.05) increase 

of MAO activity. 

Other microsomal enzymes, namely mixed 

function oxidases like cytochrome Paso (cyt. P450) 

150 
can be affected by ozone. Goldstein et al. B8 found a 

decrease (p < 0.01) in iung microsomal cyt. P450 

levels immediately or 1, 2, 3, or 5 days after rabbits 

were exposed to 1960/ag/m 3 (1 ppm) ozone for 90 

min. The data for up to 45 days post exposure were 

fitted to a parabolic curve with a significant 

(p<0.001) multiple correlation coefficient. The 

greatest depression of cyt. Paso occurred at 3.6 

days after ozone exposure. Liver cyt. Paso levels 

from the ozone-exposed rabbits were not 

significantly different from control immediately or 

1 day post exposure. In vitro exposure (1960 

Pg/m3 , or 1 ppm, for 90 min) of lung homogenate 

resulted in a 52-percent decrease in microsomal 

cyt. PoSO levels. Lung microsomal fractions similarly treated exhibited a 68-percent decrease in 

cyt. Pa5o• 

A cyt.-Paeo-dependent mixed-function oxidase 

(benzpyrene hydroxylase) was also examined for 

ozone susceptibility. Palmer et al. made 

measurements of both the lung parenchyma' fi ' 

and tracheobronchial mucosa 160 of Syrian golden 

hamsters exposed to 1470 /.Ig/m 3 (0.75 ppm) 

ozone for 3 hr. The lung tissue itself had a 33- 

percent reduction in the activity of benzpyrene 

hydroxylase, whereas the tracheobronchial 

mucosa exhibited a 53-percent drop immediately 

after exposure. The mucosal enzymatic activity had 

recovered by 24 hr after ozone exposure. 

Lysosomes (cellular organelles containing a 

variety of enzymes) are also affected by ozone 

exposure, as several researchers have shown. For 

example, rats exposed to 1568 /ag/m 3 (0.8 ppm) 

ozone continuously for 8 days showed significant 

increases in lysozyme activity in lung homogenate 

and plasma over the level of lysozyme activity in 

rats exposed in the same manner to 0, 392, or 980 

/lg/m3 (0, 0.2, or 0.5 ppm) ozone. When animals 

were exposed to the same ozone concentrations 

intermittently (8 hr/day for 7 days), there were no 

significant changes in pulmonary lysozyme 

act,vity. 28 In another study, 46 rats were continuously exposed to 1372 Ng/m3 (0.7 ppm) ozone 

for 5 days or 1568 Ng/ m 3 (0.8 ppm) for 7 days, and 

the activities of various lysosomal hydrolases were 

measured in whole lung homogenates and found 

to increase significantly (p < 0.05). The authors 

attributed this response to an infiltration of 

phagocytic cells (which have a high concentration 

of lysosomes) into the lung in response to ozone. 

The higher enzymatic levels also possibly reflect 

greater cell membrane lability. The authors 

hypothesized that the increase in protease and 

peptidase activities could lead to chronic 

obstructive pulmonary disease. 46 Athough these 

data are contrary to that of Hurst et al.'o5,1os (see 

the alveolar macrophage section), the authors 

state that the difference was probably because 

Hurst used isolated cells (alveolar macrophages), 

whereas they used whole lung tissue. Damage to 

lysosomal membranes was also proposed by 

others after histo- and cyto-chemical studies of the 

effects of 1372 to 1568 Ng/m3 (0.7 to 0.8 ppm) 

ozone administered continuously for 7 days. 25 

These researchers observed increased acid 

phosphatase activity and no changes in the Pglucuronidase activity in alveolar macrophages of 

rats. The terminal airway epithelium and adjacent 

structures also exhibited increased acid 

phosphatase activity. This particular enzyme had a 

nonvacuolar, as well as an intracellular distribution, indicating lysosomal membrane damage. 

In another publication, the same authorszs 

examined similarly exposed rats for enzyme 

activities. In areas of the bronchiolar epithelium 

that were infiltrated by mononuclear cells, there 

was a lower NADH- and NADPH-diaphorase 

activity and an increased ATPase activity. 

However, intra-alveolar septa in the centriacinar 

region had increased diaphorase, LDH, ATPase 

and cytochrome oxidase activities. These 

increases were also seen in septa that were not 

thickened or infiltrated with increased numbers of 

cells. It was proposed that these enzymatic 

changes are part of protective-adaptive 

mechanisms that operate mainly in the 

centriacinar region of the lung. 

MORPHOLOGY STUDIES 

Scheel et a1. 18 ' provided histopathologic 

evidence of injury caused by a single acute 

exposure to 1960 or 6272 Ng/m 3 (1.0 or 3.2 ppm) 

ozone for 4 hr in mice and by repeated intermittent 

exposures of 1 5,680 to 88,200%Ig/m 3 (8 to 45 ppm) 

ozone for 1 hr in rabbits. Pulmonary edema was not 

observed in mice sacrificed immediately after 

exposure to 1960 Ug/m3 (1 ppm) ozone, but 

moderately engorged capillaries containing an 

excess of leukocytes were visible. Mice examined 

20 hr after exposure showed mild edema and 

migration of leukocytes into the alveolar spaces. 

Superficial desquamation of the epithelium in the 

bronchi and bronchioles was also observed. 

Inhalation of 6272 Ng/m 3 (3.2 ppm) ozone 

produced grossly visible edema. The perivascular 

lymphatic vessels were distended and filled with 

151 
edema fluid and precipitate. Hyperemia, 

mobilization of leukocytes, and varying degrees of 

extravasation of red cells into the tissues 

accompanied the edema. Sheets of desquamated 

bronchiolar epithelial cells were seen in the 

lumina. 

Pulmonary lesions observed in cats exposed to 

510, 980, and 1960 /ag/m 3 (0.26, 0.5, and 1 ppm) 

ozone for 4 to 6 hr indicated that desquamation of 

the ciliated epithelium was apparently doserelated. 15 '

16 Other ultrastructural changes were 

cytoplasmic vacuolizations of the ciliated cells that 

occurred in airways predominantly 0.8 to 1.7 mm 

in diameter. At the same sites, condensed 

mitochondria with abnormal cristae appeared. In 

the same reports, 15 '' s swelling and desquamation 

of Type 1 alveolar cells, swelling and breakage of 

capillary endothelium, and erythrocyte lysiswithin 

the interalveolar capillaries were seen. 

Mice (18- to 20-month-old males) were exposed 

for 6 hr to 980 Ng/m 3 (0.5 ppm), 2160 /Jg/m3 (1.2 

ppm), and higher levels of ozone and then were 

given injections of tritiated thymidine that labeled 

alveolar cells undergoing DNA synthesis. 59 

Inhibition of DNA synthesis occurred at all ozone 

levels to a similar extent, thus representing 

maximum inhibition. This depression was seen up 

to 24 hr after the ozone-exposed mice were 

transferred to clean air and did not return 

completely to normal until 72 hr later. 59 

Evans et a1.57,513,60 studied the kinetics of alveolar 

cell division in rats exposed continuously for 8 days 

to 686 or 980 /ag/m 3 (0.35 or 0.5 ppm) ozone. Cell. 

proliferation increased to a maximum at 2 days and 

began to decrease toward normal by the fourth 

day. The principal dividing cell observed was the 

Type 2 celf. This process is known to be a 

mechanism for replacing damaged Type 1 cells. 

After the fourth day, no further tissue damage or 

increase in proliferation occurred, suggesting that 

the tissue had become tolerant to that particular 

concentration of ozone. To evaluate the extent of 

this possible tolerance, after 4 days of exposure to 

686 Ng/m3 (0.35 ppm), the ozone concentration 

was elevated to 980 or 1372 /Jg/m3 (0.5 or 0.7 

ppm) for up to 4 days. Under these conditions, 

morphological damage increased, indicating that 

tolerance did not occur. However, in rats exposed 

initially for 4 days to 980 Ng/m 3 (0.5 ppm) and reexposed for 4 days to 1470 or 1960 Ng/m 3 (0.75 or 

1 ppm), some tolerance was evident. Note that 

studies with young and old mice exposed to ozone 

have shown a decrease in cell proliferation. ss '' so 

This result may be due to age, species, or the ozone 

concentration used in the studies. 

From the studies of Stephens et a1. 190 conducted 

with rats, it also appears that the Type 1 cells are 

the alveolar epithelial cells most sensitive to low 

levels of ozone, 980 /Ig/m 3 (0.5 ppm) for 2 hr. The 

earliest change noted was a swelling of the 

mitochondria of these cells, particularly those 

located in the first two or three alveoli immediately 

beyond the terminal bronchiolar epithelium. This 

was followed by more severe alterations, which led 

to leaving the basement lamina devoid of an 

epithelial covering. Type 2 cells were resistant to 

the ozone treatment, and after 4 to 6 hr of 

exposure, showed signs of spreading over the 

injured area. _ 

Evans et a1. 58 examined renewal of the terminal 

bronchiolar epithelium of rats at various time 

periods after a 24-hr exposure to 1372 pg/m 3 (0.7 

ppm). One hour after conclusion of the exposure, 

almost all proliferating cells were nonciliated; 

however, by 4 days, only approximately 76 percent of the proliferating cells were nonciliated, the 

remainder being ciliated. At 15 days, approximately the same relationship was observed. These 

events as well as other observations led the 

authors to the conclusion that nonciliated cells 

divide after ozone exposure and form new ciliated 

and nonciliated cells. In this manner, the 

nonciliated cells were thought to act as progenitor 

cells that participate in the recovery of the 

damaged terminal bronchiolar epithelium. 

Morphologic observations made by Dungworth 

and coworkers, 49 '

50 indicate that the rat and 

Bonnet monkey (Macaca radiata) are approximately equal in susceptibilityto short-term effects 

of ozone. Mild but significant lesions were caused 

in both species by exposure to 392 Ng/m 3 (0.2 ppm) 

for 8 hr/day for 7 days. The authors stated that 

detectable morphological ' effects in the rat 

occurred at levels as low as 196 Ig/m3 (0.1 ppm). 

In both species, the lesion occurred at the junction 

of the small airways and the gaseous exchange 

region. In rats, the prominent features were 

accumulation of macrophages, replacement of 

necrotic Type 1 epithelial cells with Type 2 cells, 

and damage to ciliated and nonciliated Clara cells. 

The principal site of damage was the alveolar duct. 

In monkeys, the prominent ozone-induced injury 

was limited to the small airways. At 392 Ng/m 3 

(0.2 ppm), the lesion was observed at the proximal 

portion of the respiratory bronchioles. As 

concentrations of ozone were increased up to 

152 
1568 /Jg/m3 (0.8 ppm), the seveMty of the lesion 

increased, and the damage extended distally to 

involve the proximal portions of the alveolar duct. 

Mellick and coworkers 126 tound similar but 

more pronounced effects when rhesus monkeys (3 

to 5 years of age) were exposed to 980 to 1568 

Ng/m3 (0.5 and 0.8 ppm) ozone, 8 hr/day for 7 

days. In these experiments, the respiratory 

bronchioles were the most severely damaged, and 

more distal parenchymal regions were unaffected. 

Major effects were hyperplasia and hypertrophy of 

the nonciliated bronchiolar epithelial cells and the 

accumulation of macrophages intraluminally. In 

mice, continuous exposure to 980 Ng/m 3 (0.5 ppm) 

ozone caused nodular hyperplasia of Clara cells 

after 7 days of exposure. 

Similar findings were reported by Schwartz' es 

and Schwartz et al., 1B4 who exposed rats to 392, 

980, or 1568 Ng/ m 3 (0.2, 0.5 or 0.8 ppm) ozone for 

8 or 24 hr/day for 1 week. Changes observed 

within the proximal alveoli included infiltration of 

inflammatory cells and swelling and necrosis of 

Type 1 cells. In the terminal bronchiole, the 

changes reported were shortened cilia, clustering 

of basal bodies in ciliated cells suggesting ciliogenesis, and reduction in height or loss of 

cytoplasmic luminal projection of the-Clara cells. 

Effects were-seen at ozone concentrations as low 

as 392 Ng/m3 (0.2 ppm). A dose-dependent 

pulmonary response to the three levels of ozone 

was evident. No differences were observed in 

morphologic characteristics of the lesions 

between rats exposed continuously and those 

exposed intermittently for 8 hr/day. 

Using electron microscopy, Bils" studied the 

lungs of mice of different ages (4 days or 1 to 2 

months) exposed to 1176 to 2548 /ag/ m 3 (0. 6 to 1.3 

ppm) ozone for 6 to 7 hr/day for 1 to 2 days and 

noted swelling of the alveolar epithelial lining cells 

without intra-alveolar edema. Swelling of 

endothelial cells and occasional breaks in the 

basement membrane were seen. The younger 

mice exposed for 2 days were the most sensitive, 

although these observations are contrary to the 

demonstrations of the limited sensitivity of 

newborn rats exposed from birth to NO2. 71 ' 121 

Brummer et a1. 21 used scanning electron 

microscopy (SEM) to examine centriacinar regions 

of the lung and to count the influx of cells within 

the lumina in order to evaluate the cellular 

response during ozone exposure. Continuous 

exposure to 981 or 1570pg/m 3 (0.5 or0.8 ppm) for 

7 days resulted in an 18-fold increase in 

inflammatory cells within the lumina of proximal 

alveoli. 

Sato et a1. 1S0 studied the effects of 588 /ag/m 3 

(0.3 ppm) ozone (3 hr/day for 16 days) on the 

morphologic features of the conducting airways 

and alveoli of rats using SEM. Observation of the 

luminal surface of the bronchi, bronchioles, and 

terminal bronchioles of the exposed animals 

showed cilia that were swollen and adhered to one 

another. Small, smooth-surfaced round bodies 

were observed mainly around the tips of the cilia. 

The ciliated areas of the lobar bronchi and proximal 

bronchioles were covered with a pseudomembrane. Clara cells were more prominent and 

greater in size in all rats exposed to ozone. The 

surface of the alveolar ducts and alveolar walls 

showed scattered areas of cytoplasmic swelling 

and attachment of round bodies throughout the 

parenchyma. Alveolar pores were distorted and 

smaller in size than the contro{ groups. The Type 1 

cells, as others have shown, appeared to be most 

vulnerable to ozone. These studies and others 126 

also showed that the vitamin-E-deficient rats were 

more sensitive to ozone than rats fed a diet 

supplemented with vitamin E. 

Stokinger et a1. 195 reported that chronic 

bronchitis, bronchiolitis, and emphysematous and 

fibrotic changes develop in the lung tissues of 

mice, rats, hamsters, and guinea pigs exposed 6 

hr/day, 5 days/week for 14.5 months to a 

concentration slightly above 1960 Ng/m 3 (1 ppm) 

ozone. 

Rats exposed for 3 to 5 months to 1568 Pg/m 3 

(0.8 ppm) ozone develop a disease that resembles 

emphysema, and they finally die of respiratory 

failure. 192 Ozone results in a greater response of 

fibroblasts in the lesion, thickening of the alveolar 

septae, and an increase in number of alveolar 

macrophages in the proximal alveoli. 

Dogs were exposed to 1960 Ng/m 3 (1 ppm) 

ozone for 8 hr daily for 18 months. 72 The resulting 

damage appeared roughly proportional to the time 

and concentration of the ozone exposure. The 

number of alveolar macrophages increased, 

fibrous elements were deposited, and the small 

airway lumina were reduced by a thickening of the 

terminal airways and respiratory bronchiolar 

walls. The peribronchiolar area contained 

excessive numbers of lymphocytes and plasma 

cells, and squamous metaplasia of the columnar 

and cuboidal epithelium developed. 

Another long-term experiment was undertaken 

by Freeman et a1. 70 in which rats were 

153 
continuously breathing ozone at either 1058 or 

1725 Ng/m 3(0.54 or 0.88 ppm) for periods of up to 

6 months. When the animals were exposed at the 

lower ozone level for 2 hr, no immediate significant 

histological changes were seen; but after 24 hr, 

epithelial hypertrophy was found between the 

distal portions of the terminal bronchioles and the 

alveolar ducts. The peribronchiolar alveolar area 

contained amorphous material resembling 

necrotic cells. After 48 hr of exposure, the 

hypertrophy of the epithelium of the alveolar ducts 

was in sharp contrast to the controls, and 

numerous mitotic figures were seen in the 

terminal bronchiolar and proximal alveolar 

epithelium. The interstitial tissue in this area 

contained some cells with pyknotic nuclei. 

Macrophages were prominent. Fibroblasts 

appeared to be present beneath the ductal 

epithelium, and the respiratory bronchiolar 

epithelium had deposits of connective tissue 

elements. Histochemical examination suggested a 

change in the collagen. Additional rats were 

studied at 6 days, 8 days, 3 weeks, and 6 months, 

and progressive changes occurred in the airway 

epithelium. Metaplasia of cuboidal epithelium was 

seen, which continued to be replaced by 

connective tissue. However, the terminal 

bronchioles appeared more normal after 3 weeks 

of ozone and remained so for the rest of the 

exposure period. Even with this partial recovery, 

the deposition of connective tissue interrupted the 

continuity of the small airways with their proximal 

a Iveoli 

When the rats were exposed to 1725 /Jg/m 3 

(0.88 ppm) ozone, epithelial injury was seen in 4 

hr. The morphological aiterations found at the 

lower concentration were present in these rats 

also, but they were more extensive and occurred 

earlier. Furthermore, after 48 hr of ozone, the 

bronchiolar epithelium was often metaplastic. By 

day 3, there was an onset of early fibrosis, which 

constricted some terminal airways. After 6 days, 

adenoma-like structures containing large 

numbers of macrophages were more prevalent. 

Fibrosis had extended into the termi,nal 

bronchiales. After 3 months of exposure to 1725 

μg/m3(0.88 ppm) ozone, emphysema-like lesions 

had developed. This study also included a group of 

animals exposed to both 1692 Ng/m3(0.9 ppm) 

NOz and 1764 /Ig/m 3(0.9 ppm) ozone, and another 

group that received 4900Ng/m3(2.5 ppm) NOz and 

490 Ng/m3(0.25 ppm) ozone. They, too, were 

examined for pathological changes. However, the 

authors found no synergism because ozone 

appeared to be largely responsible for the 

alterations seen at these concentrations. 70 

Investigations by others have supported 

previously discussed data and, in some cases, have 

added more information. P'an et a1. 162exposed 

rabbits to 784 pg/m 3(0.4 ppm) ozone for 6 hr a day, 

5 days a week for 10 months. The a uthors observed 

both emphysematous and vascular lesions in the 

lungs. The small pulmonary arteries were thicker 

than in controls because of the increased size of 

the tunica media vasorum, which in some 

instances appeared to be a resuit of tissue edema 

or muscular hyperplasia. 

The possibility that daily ozone exposure might 

increase the incidence of tumors has also been 

studied. Stokinger 193reported that acceleration of 

lung tumorigenesis (adenoma) in a strain of mice 

susceptible to such tumors occurred from daily 

ozone exposures to about 196011g/m 3(1 ppm). At 

15 months, a tumor incidence of 85 percent was 

found in the ozone-exposed, as against 38 percent 

in the control mice. The average number of tumors 

per exposed mouse was 1.9 compared with 1.5 in 

the controls. Experimental details were not given. 

Kotin and coworkers 14 ' 16studied the 

experimental induction of pulmonary adenomas in 

Strain A mice (which are prone to develop 

pulmonary adenomas) and in C-57 black mice 

exposed for 52 weeks to an atmosphere of 

ozonized gasoline. The concentration of oxidants 

varied from 1 to 3.8 ppm. The concentration of 

other pollutants present was not reported. A 

significantly greater incidence of tumors occurred 

in the exposed than in the control mice. There was . 

no significant difference in tumor incidence 

between males and females. The respiratory 

epithelium of the mice revealed significant 

hyperplastic and metaplastic responses. 

Nettesheim et a1. 157 investigated the effect of ozonized gasoline on tumor production in hamsters. 

The ozone concentration was 2353 Pg/m 3(1.2 

ppm) in excess of that which reacted with the 

gasoline. The resulting hydrocarbon mixture was 

40 to 45 ppm methane equivalents. Animals were 

exposed 6 hr/day, 5 days/week for life to ozonized 

gasoline, tc ferric oxide (Fe203), or to both. Some of 

the groups also received injections of the 

carcinogen, diethylnitrosamine (DEN). The 

tumorigenicity of DEN was enhanced by FezOs,but 

not by the ozonized gasoline. The ozonized 

gasoline, alone or in combination with FezOs, did 

not appear to be carcinogenic. When the data for 

154 
the groups of ozonized gasoline plus DEN and 

ozonized gasoline plus Fe203 were compared with 

data for DEN and Fe203 control groups, and were 

analyzed under the assumption that the tumors of 

the bronchi and lungs were lethal, there was a 

reduction (p < 0.05) in tumor incidence in the 

groups receiving ozonized gasoline. 

PULMONARY FUNCTION 

Scheel et a1. 18 ' exposed 75 rats to 3920Ng/m3 (2 

ppm) ozone for 3 hr and then measured their 

oxygen uptake, tidal volume, and frequency of 

breathing. The rats were examined at intervals 

over a period of 960 hr after exposure. The lungs 

were excised and weighed before and after drying. 

It was found that the water content of the lungs 

increased during the post-exposure period, the 

increase reaching a maximum after 12 hr. These 

authors expressed pulmonary edema in terms of 

water in the lung per kilogram of body weight 

instead of per unit of dry-lung weight. Since no 

data are given on body weight, the changes in 

lung-water content must be interpreted with 

caution. A decrease in minute ventilation (the 

volume of air breathed per minute), tidal volume 

(volume per breath), and oxygen uptake occurred 

immediately after exposure and reached minimum 

recorded values 8 hr after exposure. At 20 hr after 

exposure, all measurements had returned to their 

initial values. The early fall in minute ventilation 

and oxygen uptake could have reflected a decrease 

in activity (metabolic rate) secondary to acute 

injury of tissue and the development of pulmonary 

edema. The simultaneous increase in minute 

ventilation and decrease in oxygen consumption 

after 40 hr suggests that delayed impairment may 

have occurred. 

Murphy et a1. 146 exposed guinea pigs to 666 to 

2646 Ng/m3 (0.34 to 1.35 ppm) ozone for a period 

of 2 hr. Measurements of respiratory function 

were made before, during, and after exposure. It 

was observed that respiratory rates increased 

while tidal volumes decreased during exposure to 

all concentrations. The maximum changes were 

different (p < 0.05) from pre-exposure control 

values for each concentration. Generally, as the 

concentration of ozone was increased, the 

magnitude of the response increased, and the 

response occurred sooner. After a maximum 

response was reached, the effects tended to 

remain constantfor the rest of the exposure period. 

Values tended to return to pre-exposure control 

levels when the animals were returned to clean 

air. In a later study by Easton and Murphy, 154 

guinea pigs were exposed to 9800 to 13,720 

/Jg/m 3 (5 to 7 ppm) ozone for 2 hr. Measurements 

of flow resistance, frequency of breathing, tidal 

volume, and lung compliance were made before, 

during, and after exposure. A threefold increase in 

flow resistance occurred during exposure and 

reached a maximum after 1 hr, a condition that 

may reflect narrowing of airways (predominantly 

in the region of large-to-medium-sized bronchi) or 

smaller lung volumes. There was a 50-percent 

increase in frequency of breathing and a small 

decrease in tidal volume. Lung compliance (a 

measurement of distensibility) was reduced 50 

percent. AII measurements returned to preexposure levels within 60 to 90 min after 

termination of exposure. 

In another investigation, 212 the right lung of 

rabbits was exposed to 1960 ug/m 3 (1 ppm) ozone 

for 3 hr. The left deflated lung was used as a control 

after the air pressure was returned to normal. The 

exposed lungs of rabbits sacrificed 1 and 3 days 

after exposure had reduced vital capacities. Those 

studied 7 days post exposure were not significantly 

reduced. Yokoyama21 studied the ventilatory 

functions of guinea pigs before, during, and after a 

2-hr exposure to 980 Ng/m3 (0.5 ppm) ozone. The 

following results were noted: Air flow resistance 

increased by 113 percent (p < 0.05), frequency of 

respiration increased (p <0.05), and tidal volumes 

decreased. Yokoyama 214 also investigated the 

pulmonary function of rabbits exposed to 1960 or 

3920 pg/m3 (1 or 2 ppm) for 6 hr/day for 3 to 4 

days. At the higher ozone concentrations, there 

were increases in residual volume/total lung 

capacity, functional residual capacity/total lung 

capacity, total lung resistance, and a decrease in 

chestwall resistance. For 1960Pg/m3 (1 ppm),the 

changes were similar, but fewer than at the higher 

concentration. At 1960 ,ug/m 3 (1 ppm), the flow 

volume curve was not different from control. 

When cats were exposed to 510, 980, and 1960 

Ng/m3 (0.26, 0.5 and 1 ppm) ozone for 2 to 6.5 hr, 

pulmonary flow resistance increased with 

increasing ozone levels. The lower ozone 

concentration produced alterations in fewer 

animals. As the length of the exposure increased 

from 0 to 240 min, there was a trend toward an 

exponential increase in resistance. Dynamic 

compliance (Ca Y„) and diffusing capacity for carbon 

monoxide (DLco) (a measure of gaseous diffusion 

across the alveoli into the blood) decreased fess 

frequently and less markedly than the alteration in 

155 
pulmonary resistance. Greatest reductions in Cdyn 

and DLco were observed at the higher ozone 

concentration (1960 Ng/m 3 , or 1 ppm). There were 

no changes in vital capacity. Alveolar stability was 

atso unchanged, as illustrated bythe shapesofthe 

volume-pressure curves during deflation for 

exposed and control animals. Pathological reports 

on similarly treated animals indicated severe 

injury to the bronchial and bronchiolar epithelium, 

Type 1 alveolar cells, and interalveolar capillaries. 

This probably contributed to the depression of 

diffusing capacity. No evidence of intra-alveolar 

edema was seen. The authors suggest that acute 

ozone exposure affected airway caliber more than 

either the transfer of CO across the alveolarcapillary membrane or alveolar surface forces. 2oa 

Bartlett et a1. 9 exposed young rats (3 to 4 weeks 

old) continuously for 30 days to 392 Ng/m 3 (0.2 

ppm) ozone. No changes in respiratory frequency 

occurred. Morphometric analysis indicated that 

the numbers of alveoli were unchanged, but the 

average lung volume increased by 16 percent 

(p< 0.02) following ozone exposure.The increases 

(p< 0.05) in meancord length and alveolar surface 

area of ozone-exposed animals reflect 

overdistension of the lung. Overdistension is also 

illustrated by the lower (p <0.05)transpulmonary 

pressure that occurred in both air- and saline-filled 

lungs, which indicated that a decrease in tissue 

elasticity rather than alterations of surface 

tension, was responsible for the results. Using 

light microscopy, no morphological changes were 

evident. At higher concentrations of ozone, 

investigators216 found no significant changes of 

the pulmonary pressure/vofume relationship or 

the ratio of collagen to elastin in the lungs of rats 

exposed to 880 pg/m3 (0.45 ppm) ozone for 6 

hr/day for 6 to 7 weeks 

Exposure to 1960 /ag/m 3 (1 ppm) ozone for 3 hr, 

using the unilateral lung technique, in which only 

one lung is exposed to ozone, resulted in a loss of 

elasticity in rabbit lungs immediately after 

exposure (p <0.05) and 3 days later (p <0.05). 2 ' 3 

By day 14, the lung had recovered, suggesting that 

edema, present in the exposed lung on days 1 

through 3(p < 0.05), could have been responsible. 

EDEMAGENESIS AND TOLERANCE 

Data from many sources reviewed by Coffin and 

Gardner37 indicate that brief exposure to ozone 

may elicit edema and an acute inflammatory 

response in the lungs of many species. It is striking 

at higher levels of exposure and diminishes with 

descending concentrations of the gas. Thus no 

evidence of edema was noted in mice exposed to 

1960 /ag/m3 (1 ppm) ozone for 4 hr, whereas 

exposure to this concentration for 2 hr resulted in 

very slight edema when a gravimetric measurement of lung water was employed. 18 ''' 94 These 

investigators 16 '' 94 detected evidence of edema in 

rats after exposure to 3920 Ng/m3 (2 ppm) ozone 

for 3 hr. Exposures at the high level of 6272ug/m 3 

(3.2 ppm) ozone quickly produced gross evidence of 

edema in mice. 

It is generally believed that gross edema is 

probably not elicited in any species exposed to 

ambient concentrations of ozone. More refined 

methods for the detection of possible edema were 

developed by Alpert et a1., 5 greatly increasing the 

sensitivity of the measurement. They injected 732 1- 

serum albumin into rats and recovered pulmonary 

fluid 6 hr later by lung lavage, which was then 

tested for radioactivity. Radioactivity in the fluid 

would be indicative of fluid flux across pulmonary 

membrane barriers, and an increase over controls 

would represent possible edema. After 6 hr of 

exposure to 490 Ng/m 3 (0.25 ppm) ozone, there 

was no significant effect; but to 980 Ng/m3 (0.5 

ppm), there was increased recovery of 132 1 (two 

times that of controls) (p< 0.001). Simultaneous 

studies using lung wet weight/dry weight ratios 

showed an effect only with 4900 /ug/m 3 (2.5 ppm) 

ozone (p < 0.01). 

Another report 102 indicates that a 5-hr exposure 

to lower levels of ozone caused increased permeability of the alveolar-capillary membrane in mice 

as measured by recovery of radiolabeled albumin 

in the lavage fluid. However, because the objective 

of the study was to measure the ozone hazard in 

UV isolation units, the mice were exposed to 

varying concentrations of ozone (an average of 196 

Ng/m3 , or 0.1 ppm) under conditions that could be 

called uncontrolled relative to typical studies of 

ozone toxicology. 

Frank et a1. 69 exposed the right lung of rabbits to 

4312 and 23,716 pg/m3 (2.2 to 12.1 ppm) ozone 

for 3 hr, the left lung having been collapsed before 

exposure. When edema occurred in the right lung, 

changes in surfactant (a substance that lowers 

surface tension in the lung, helping to make 

normal breathing possible) behavior were 

observed in the left lung of some animals. No such 

changes were observed in the absence of edema in 

the right lung. These results suggest that ozone is 

not only capable of inducing chemical changes in 

exposed lungs, but also that the products of such 

156 
changes are capable of producing deleterious 

effects or compensatory responses in nonexposed 

lungs. 

Ozone has been found to induce tolerance, 

which can be described as the acquired capacity of 

a pretreated host to exhibit a lesser response to a 

challenge than would be observed in a comparable 

but nontreated host. Using the radiolabeled 

albumin technique, Alpert et a1. 5 examined the role 

of inethylprednisoline (a corticosteroid with potent 

anti-inflammatory properties) on edema and 

tolerance to edema in rats. They found that it 

increased susceptibility to edema production 

following exposure to low levels of ozone. 

However, when animals received the steroid 

befofe exposure to 490 Ng/m' (0.25 ppm) ozone, 

they became tolerant to a subsequent ozone 

challengewith 1960Ng/m 3 (1 ppm)48 hr later(i.e., 

edema was not produced). Untreated rats did not 

become tolerant. 

Other work was undertaken to ascertain the 

mechanisms and extensiveness of tolerance. In 

one such study, the left lungs of Flemish Giant 

rabbits were catheterized and exposed to 980 

Ng/m3 (0.5 ppm) ozone for 3 hr. The right lung 

inspired clean air. This was followed by an 18-hr 

latent period, after which- the whole animal was 

challenged with 43,120 μg/m 3 (22 ppm) for 3 hr. 

The pre-exposed left lung exhibited tolerance to 

pulmonary edema (p < 0.001), and the right lung 

did not, indicating that tolerance is a localized, 

rather than a systemic, effect. 4 

Similar methods were used by Gardner et a1., 78 

who pre-exposed the left lung to 980 or 1960 

pg/m3 (0.5 or 1 ppm) ozone for 3 hr, and 18 hr later 

exposed the whole animal to either 5880 Ug/m3 (3 

ppm) or 43,1120 /ag/m3 (22 ppm) ozone for 3 hr. The 

right and left lungs were then examined 

separately. Again, it was found that pulmonary 

edema was prevented only in the pre-exposed lung 

(p < 0.001). Also, the 980 ug/m 3 (0.5 ppm) ozone 

produced greater tolerance than did the 1960- 

/jg/m3 (1 ppm) ozone pre-exposure. The same 

authors had demonstrated that ozone exposures 

resulted in an influx of polymorphonuclear 

leukocytes (PMN) into the lung, while the total 

number of alveolar macrophages remained the 

same. Therefore, the effect of ozone pre-exposure 

on this parameter was studied. The tolerant preexposed lung had th2 same total number of 

alveolar macrophages as the nontolerant lung, as 

well as a higher number of PMN This 

demonstrated that the prior exposure induced 

further chemotaxis of PMN but had no effect on 

alveolar macrophages. Macrophage enzyme 

activities (lysozyme and ~ -glucuronidase) were 

reduced in response to ozone, and pre-exposure 

failed to influence the action of ozone on these 

enzymes. These investigations iridicated that the 

extent of tolerance depends on the biological 

endpoint and is more effective against pulmonary 

edema than against other health effects. 

Using the infectivity model, which measuresthe 

accumulated mortality of mice exposed to 

pollutants and aerosols of Streptococcus 

pyogenes, Gardner and Graham" investigated 

ozone tolerance. Some animals received two 3-hr 

exposures to the same concentration of ozone, 

with a 24-hr interval between the exposures. 

Other mice received only one 3-hr exposure to 

ozone. The bacterial aerosol was administered 

immediately after the last ozone exposure. At 196 

/ag/m3 (0.1 ppm), there was only a slight difference 

in mortality between the mice receiving 2 and 1 

exposures to ozone. As the concentration was 

increased, up to 1960 Ng/m3 (1 ppm), there was 

greater protection in those animals pre-exposed 

(i.e., the mortality was less in those mice receiving 

ozone twice, as compared to animals exposed 

once). However, excess mortality occurred 

irrespective of the number of ozone exposures, 

indicating that complete tolerance was not 

evident. The partial tolerance to infectivity that 

occurred at higher ozone concentrations was 

probably due to inhibition of edema, and not to 

tolerance to an ozone effect on alveolar 

macrophages. That ozone-induced damage to 

alveolar macrophages cannot be completely 

prevented by prior ozone exposure has been 

demonstrated by Gardner et a1. 93 

Evans et a1. 5s,so measured tolerance by studying 

the kinetics of alveolar cell division in rats during a 

period of exposure to an elevated ozone 

concentration (980 or 1372 Ng/m3 , or 0.5 or 0.7 

ppm, up to 4 days) that followed initial exposure at 

a lower concentration (686 Pg/m 3 , or 0.35 ppm for 

4 days). Tolerance in this case was the ability of 

Type 1 cells to withstand re-exposure, and any 

increase in the numbers of Type 2 cells would 

indicate a lack of tolerance. These studies showed 

that tolerance to the initial concentration of ozone 

did not ensure total protection against re-exposure 

to higher concentrations (see section on 

morphology studies for more complete discussion). 

Note that when mice were exposed to 1960 

Ng/m3 (1 ppm) ozone for 1 hr and then X-irradiated 

157 
with 800 R 10 days later, 60 percent of the animals 

survived, whereas all previously non-ozoneexposed mice died. This tolerance lasted 30 days or 

more. 99 

The mechanism for development of tolerance to 

ozone-induced edema is not well understood, but 

the thymus may play a role. In a study by Gregory et 

a1., 93 male mice thymectomized at birth were 

unable to develop tolerance to a 2-hr exposure of 

39,200 Ng/m3 (20 ppm) ozone when they had been 

pre-exposed to 588 Ng/m3 (0.3 ppm) of ozone for 1 

hr (p G 0.01). 93 Sham-operated animals exhibited 

tolerance under the same oxidant conditions. 

Contrary to these studies, Thompson 198 found that 

thymectomizing the animals had no effect on 

tolerance. 

Biochemical responses in lungs of ozonetolerant rats were studied by Chow 27 and Chow et 

a1. 29 (see section on sulfhydryl compounds and 

pyridine nucleotides, and earlier section on 

mitochondrial enzyme activities for complete 

description). The lungs of tolerant animals showed 

relatively less injury and maintained significantly 

higher activities of glutathione peroxidase, 

glutathione reductase, and glucose-6-phosphate 

dehydrogenase, and higher levels of reduced 

glutathione. The author speculatesthatthis higher 

activity in the lungs of tolerant animals may render 

them more resistant to peroxidation damage 

induced by ozone. However, with respect to the 

mitochondrial oxidation of succinate, re-exposure 

after a recovery period resulted in alterations in 

enzymatic activity similar to those observed after 

initial exposures. 

Dixon and Mountain47 concluded that edemagenesis in mice exposed to ozone probably 

involves the release of histamine and other 

endogenous products such as slow-reacting 

substances, but they found that lung histamine 

content did not parallel tolerance and that 

tolerance was not affected by histamine 

antagonists or liberators. Their conclusion was 

that histamine per se had no function in 

development of tolerance to ozone. 

Extrapulmo%dry Effects 

HEMATOLOGICAL AND SERUM CHEMISTRY 

CHANGES 

Some of the studies to be described here have 

also been conducted with human blood and are 

discussed in Chapter 9. 

Brinkman et a1. 20 have shown that inhalation of 

392 to 490 Ng/m3 (0 20 to 0.25 ppm) ozone over 

periods of 30 to 60 min by mice, rats, rabbits, and 

man increased the rate of sphering of red cells in 

vitro, with the cells losing their characteristic 

biconcave shape more rapidly when the diluted 

blood is subsequently exposed to X-radiation. 

These changes were greatest after 1 hr and 

approached control values 6 hr after exposure 

ended. 

Menzel et a1. 132 investigated the effects of ozone 

on erythrocyte hemolysis. Rats maintained on 

diets either deficient in or supplemented with 

vitamin E were continuously exposed to 980 

/Jg/m3 (0.5 ppm) ozone, and their red blood cells 

were subjected to dialuric acid hemolysis to 

estimate plasma tocopherol. After 23 days, the 

erythrocytes from 60 percent of the rats depleted of 

vitamin E and exposed to ozone showed hemolysis. 

This response did not occur in the vitamin-Edepleted, air-exposed control animals until 36 

days. Those animals supplemented with vitamin E 

did not show hemolysis, regardless of exposure. 

These data are believed to illustrate that ozone 

accelerates the depletion of tocopherol reserves. 

Ross et al."' examined erythrocytes of rabbits 

exposed for 4 hr to 1960 or 5880 Ng/m 3 (1 or 3 

ppm) ozone. There was no significant effect, 

immediate or delayed, on parameters that reflect 

oxygen delivery by the red cell; i.e., oxyhemoglobin 

affinity, heme-oxygen binding site interaction, and 

2, 3-diphosphoglycerate concentration. 

Other studies 182 were conducted in which mice 

breathed 1686 Ng/m3 (0.86 ppm) ozone for 8 

hr/day, 5 days/week for 6 months, after which the 

animals were infected with Plasmodium berghei (a 

sporozoan, of the same family as the malaria 

organisms, that parasitizes the red blood cells of 

certain mammals). Up to the 6th week of exposure, 

there was a significant increase in resistance of 

the erythrocytes to acid hemolysis. 182 Other 

investigators observed increased resistance to 

hemolysis in mice exposed to 1960 Ng/m3 (1 ppm) 

ozone for 30 min. 138 

Ozone may not only affect the unsaturated fatty 

acids of cell membranes, but it may also damage 

acetylcholinesterase (AChE), an enzyme bound to 

red cell membranes. This was studied 163 after in 

vitro exposure of AChE derived from bovine 

erythrocytes. The enzymatic activity was inhibited 

after exposure to ? 588 Ng/m 3 (0.3 ppm). Eglites3 

reported that whole blood cholinesterase of rats 

decreased by the middle of the third month of a 93- 

day continuous exposure to 110 Ng/m3 (0.056 

ppm), but returned to normal 12 days after 

158 
exposure ended. The method of ozone measurement was not specified. 

Chow et a1. 30 found no statistically significant 

changes in the level of GSH or the activities of GSH 

peroxidase, GSH reductase, and G-6-PD in the 

erythrocytes of rhesus monkeys or rats exposed to 

0.980 Ng/m3 (0.5 ppm) ozone for 8 hr/day for 7 

days. However, inthe lungsoftherats, increases(p 

< 0.05) of GSH and these enzyme activities were 

observed (see earlier section on sulfhydryl 

compounds and pyridine nucleotides). 

Leukocytes also have been investigated. High 

concentrations of ozone (> 2500 Ng/m 3 , or > 12.8 

ppm for 2 hr) can increase the neutrophil: 

lymphocyte ratio of circulating blood of rabbits. 

However, exposure to 3920 or 2940 Ng/m 3 (2 or 

1.5 ppm) ozone for 5 hr did not change this ratio." 

P'an and Jegier 164 observed serum protein 

changes in rabbits exposed to 784 or 1960Ng/m 3 

(0.4 or 1.0 ppm) ozone for 6 hr/day, 5 days/week 

for 10 months. Exposure to the lower ozone 

concentration resulted in a small progressive 

decrease of serum albumin (16 percent by day 

210). Gamma globulin varied within ± 10 percent 

of control values over the first 90 days, but 

increased thereafter and was 45 percent above 

control after 210 days of exposure to 780 Pg/m 3 

(0.4 ppm) ozone. At the same ozone concentration, 

there was a slight decrease (approximately 8 to 10 

percent from controls) of a and /3 globulin over the 

first 30 days of exposure; /3 globulin then increased 

to control levels for the remainder of the 

experiment. However, the a globulin of the 

exposed animals continued to increase, reaching 

78 percent above controls at 210 days of exposure. 

Similar types of changes were observed at the 

1960 Ng/m3 (1 ppm) exposure for 190 days, at 

which time a and y globulin had increased by 46 

percent and 48 percent, respectively, and albumin 

had decreased by 11 percent. No significant 

changes were observed in total serum protein 

concentrations of either of the exposure groups. 

To determine whether ozone can cause preemphysematous changes in the lungs of small 

animals by destroying serum antitryptic factors, 

P'an arid Jegier 165 undertook to examine the sera 

of rabbits exposed to 784 Ng/m 3 (0.4 ppm) ozone 

for 6 hr/day, 5 days/week for 6 months. Except for 

an increase in the serum trypsin inhibitor capacity 

on the first day of ozone exposure, no significant 

changes were found. A slow but steady rise in 

§erum protein esterase was found also after 

rabbits were exposed to 784 pg/m 3 (0.4 ppm) for 6 

hr/day, 5 days/week for 10 months."o For 10 

months, rabbits were exposed to 784 Ng/m 3 (0.4 

ppm) ozone, and the concentration of serum 

trypsin protein esterase tripled by the end of 

exposure. This rise may be related to the observed 

thickening of small pulmonary arteries.' ss 

Numerous other changes have been observed in 

the blood of ozone-exposed animals. Veninga"s 2°2 

work, in which rabbits were exposed for 60 min to 

392 Ng/m3 (0.2 ppm) ozone, showed a small but 

significant drop in total blood serotonin 

immediately after termination of exposure. This 

reduction was probably due to a loss of plateletbound amine because there was no measurable 

free circulating plasma serotonin. Investigation of 

plasma Iysozyme28 activity showed that rats 

continuously exposed to 1568 /_Ig/m 3 (0.8 ppm) 

ozone over 29 days had increased (p < 0.001) 

enzyme activity by the third day of exposure. The 

lysozyme activity remained elevated on day 10and 

day 29. In another study, mice exposed to 392 

Ng/m3 (0.2 ppm) ozone for 2 hr exhibited an 

increase in serum glutamic-pyruvic transaminase 

(SGPT), indicating enhanced fat deposition in the 

liver as well as an increase in hepatic ascorbic acid. 

There was no change in blood catalase, a strong 

reducing agent. 20' 

CHROMOSOMES 

There have been numerous studies designed to 

provide information on the possible role of ozone 

as a mutagenic agent. A number of investigators 42,43 95.96.97 185 have used the microorganism, 

Escherichia cofi, as the indicator system for ozoneinduced specific modifications of the genetic 

material. Fetner 65 has demonstrated the capability 

of ozone to produce chromosome breaks in the root 

meristem cells of the broad bean, Vicia faba. The 

same author66 reports a significant delay in mitosis 

when living neuroblasts of the grasshopper, 

Chortophaga viridifaciata, are exposed to ozone. 

No effect was detected until the embryos were 

exposed to an ozone atmosphere present in a 

closed system with a solution of 3500 to 4500 pg 

ozone/liter. These effects were reversible. The 

effects of ozone-treated seawater on the oyster 

has also indicated the presence of fragmented 

nuclei, indicating chromosome breaks. 122 

Zelac et a1. 217 exposed female Chinese hamsters 

to 470 /ig/m 3 (0.24 ppm) ozone for 5 hr and then 

examined circulating blood lymphocytes for 

chromosome damage. Ozone-induced chromosomal breaks (p < 0.05) and aberrations were still 

159 
present 6 and 15 days post exposure to ozone. The 

authors suggest the possibility of long-term effects 

from these cellular alterations. Expanding these 

studies, Zelac et a1. 218 calculated that the 

exposure-adjusted break frequency was 1.67 x 10-3 

breaks/cells (ppm/min). When they combined 

ozone (392 Ng/m3 , or 0.2 ppm, for 5 hr) with 

radiation exposure (230 rads delivered in 5 hr), the 

two agents simultaneously exhibited > 70 percent 

of the total number of breaks anticipated, 

assuming the actions of two agents were additive. 

Gooch et al. 92 studied the cytogenetic effects of 

ozone in three systems: Chinese hamster bone 

marrow, mouse peripheral leukocytes and mouse 

primary spermatocytes. The hamsters were 

exposed to 451 Ng/m3 (0.23 ppm) for 5 hr or 

10,192 Ng/m 3 (5.2 ppm) for 6 hr. The mice were 

exposed to 294 ug/m 3 (0.15 ppm) and 412 Ng/m 3 

(0.21 ppm) for 5 hr, or 1940pg/m 3 (0.99 ppm)for 2 

hr. The data tended to disagree with those of Zelac 

et al. 21,218 in that no appreciable increase in 

frequency of ozone-induced chromosome-type 

aberrations was observed. Other researchers 19 

exposed cell cultures of embryonic chick 

fibroblasts (total flask vol. of 160 ml) to 10to 100/al 

ozone/ml for 30 min. These celts exhibited major 

but nonspecific alterations in both interphase and 

mitotic cells at the margins and top layers of the 

cultures. Several hours post exposure, abnormal 

bi- and poly-nucleated reconstructed cells were 

present. A few cells had chromosome bridges in 

anaphase and telophase together with nuclear 

fragments that resembled X-ray-induced damage. 

Fetner 67 exposed human cell cultures in vitro to 

ozone (8.0 ppm by weight of ozone in 02 for 5 and 

10 min). This investigation demonstrated that 

ozone is capable of producing chromatid breakage 

in the KB human cell line. 

A review article by Veninga, 202 which includes 

some of his own research, presents evidence for 

the radiomimetic properties of ozone. C-57 black 

mice were treated with 392 ug/m 3 (0.2 ppm) ozone 

for 7 hr/day, 5 days/week during gestation and 

then for the first 3 weeks of life. Unlimited incisor 

growth was found in 0.9 percent of the normal 

newborn mice, whereas ozone-exposed animals 

had an incidence of 5.4 percent. In the same 

species, neonatal death rose from 9 to 34 percent 

after exposure. In addition, blepharophimosis in 

another strain of normal mice occurred in 0.6 

percent of control animals and in 9.6 percent of the 

ozone groups. Similar but less dramatic results 

were seen in C-57 black mice in which the rate of 

blepharophimosis rose from 4.5 to 9.2 percent. In 

another study by the same researcher, 201 

binucleated lymphocytes doubled in number in 

murine blood after exposure to 392 Ng/m 3 (0.2 

ppm) for 2 hr (p = 0.005). The action of ozone in 

changing the adsorption spectra of nucleic acids 33 

and in altering the pyrimidine bases of E. coli 

nucleic acids 168 may be an indication of a 

chromosomal effect. 

CENTRAL NERVOUS SYSTEM-S AND 

BEHAVIORAL EFFECTS 

Several studies have shown tne effects of ozone 

on behavior patterns in animals. 

Various responses of mice exposed for 30 min to 

various concentrations of ozone from 1176 to 

16,660 /jg/m3 (0.6 to 8.5 ppm) were studied.' 67 At 

1 176 Ng/m3 (0.6 ppm), mice began attempting to 

move away from the ozone. This avoidance 

response was more definite at 2156 Ng/m 3 (1.1 

ppm) ozone, and it became more pronounced as 

the ozone concentration increased. In addition, as 

ozone concentration increased, activity decreased. 

After a 20-min exposure to 2156 Ng/m3 (1.1 ppm), 

the animals appeared confused. Other researchers12," 3 exposed rats to 98, 196, 392, 980, 

and 1960 Ng/m 3 (0.05, 0.1, 0.2, 0.5, and 1 ppm) 

ozone and found that the greater the concentration 

of gas, the greater the depression in gross motor 

activity (p < 0.05). Although not specified in the 

paper, it would appear that a significant response 

did not occur at the lowest concentration tested. In 

addition, the pollutant-exposed animals had 

prolonged periods of inactivity. The precise time of 

the ozone exposures that were related to the 

observations was not given, but it appeared to be 

less than 45 min. In another series of 

experiments, 12 subhuman primates exhibited an 

elevation of both simple and choice reaction time 

in atmospheres of 980 /jg/m 3 (0.5 ppm) ozone after 

only a 30-min pre-exposure to this concentration. 

When Fletcher and Tappe1 68 continuously exposed 

rats to 1960 ,ug/m 3 (1 ppm) for 7 days to ozone, 

they found an 84-percent reduction in voluntary 

activity (p < 0.001). Rats exposed to 110 pg/m3 

(0.056 ppm) ozone for 93 days exhibited no change 

in behavior or chronaxial muscle ratios. 53 

Xintaris et a1. 210 found a depression of the 

evoked response to flash in the specific visual 

cortex and in the superior colliculus of rats in 

reponse to exposures of 980 to 1 960 /ag/m 3 (0.5 to 

1 ppm) ozone Tor 1 hr. He suggested that such 

changes reflect a possible morphological or 

160 
functional change in the central 'nervous system. 

Bokina et a1. 19reported on animals (species not 

identified) that were initially exposed to (time not 

given) 3920 to 5880 Ng/m 3(2 to 3 ppm) ozone and 

then subsequently exposed (time not given) to 30 

Ng/m 3(0.015 ppm). When this exposure was 

combined with a rhythmic, light stimulus, 

paroxysmal activity in the olfactory analyzer 

structures was provoked. Evoked potential of the 

optic cortex was also investigated 19during a 1.5- 

month continuous exposure to 50 /jg/m 3(0.026 

ppm) ozone. The following observations were 

made: A decrease in the amplitude of the primary 

response of the evoked potential, a slow negative 

wave, and a decrease in the duration of•the slow 

negative wave. The authors suggest that this 

represents a deterioration of the cortical 

processes. The method of ozone monitoring was 

not given. 

EXTRAPULMONARY MORPHOLOGY 

Atwall and Wilson,' using light and electron 

microscopy, found histological and ultrastructural 

changes in the parathyroid glands of rabbits after 

4- to 8-hr exposures to 1470 Ng/m 3(0.75 ppm) 

ozone. The major changes found in exposed 

animals were jarge numbers of secretion granules, 

hyperplasia of the chief cells, proliferation and 

hypertrophy of the rough endoplasmic reticulum, 

free ribosomes and mitochondria, lipid bodies, and 

an accumulaton o'r secretion granules of the chief 

cells inside the va-cular endothelium of the blood 

stream. Alteration ; were observed 18 and 22 hr 

after exposure, bu by 66 hr, the cells had normal 

appearances. The authors hypothesize that this 

damage could lea+l to alteration of parathormone 

production and surage. 

Brinkman et a! 20exposed adult mice to 390 

Ng/m3(0.2 ppm) ozone 5 hr/day for 3 weeks. 

Structural changes in the cell membranes and 

nuclei of myocardial muscle fibers were produced 

that were reversible about 1 month following 

exposure. The physiological implications of these 

changes were not discussed. 

MISCELLANEOUS EFFECTS 

Gardner et al. 7 e exposed mice to 1960Ng/m 3 (1 

ppm) ozone for 3 hr/day up to 7 days. Immediately 

after exposure, the animals were injected with 

sodium pentobarbitaL and the induction time for 

sleep and the actual sleeping time were 

determined. The induction time was not affected 

by ozone; however, sleeping time was altered. 

After the second ozone exposure, there was a 13- 

min prolongation in sleeping time (p< 0.05), 

whereas the increase was 9.2 min (p <0.05) after 

3 days of ozone treatment. No significant changes 

were evident after a single exposure or after four or 

more successive daily exposures. After seven daily 

exposures to 1960 Ng/m 3(1 ppm) ozone, the 

concentration was increased to 9800 Ug/m 3(5 

ppm) for 3 hr. This increased the sleeping time by 

59.5 min (p <0.001) and was taken to indicate that 

tolerance did not occur. The authors hypothesized 

that these effects may reflect alterations in 

cytochrome Paso(cyt. Paso), a microsomal enzyme(a 

mixed function oxidase) that oxidizes pentobarbital. Goldstein and Balchum 83investigatet'the 

possible role of this enzyme in ozone-induced 

toxicity. They found that injections of phenobarbital (an inducer of cyt. Paso) decreased (p = 

0.05) the survival times of rats exposed to a lethal 

ozone concentration (157,680 /jg/m 3 , or 8 ppm), 

whereas treatment with allylisopropylaceta-mide 

(which destroys cyt. Paso) increased the survival 

time of ozone-exposed animals. Goldstein et a1. 88 

also showed that there was a decrease (p<0.01) in 

lung microsomal cyt. P450 levels immediately, or 1, 

2, 3, or 5 days after rabbits were exposed to 1960 

Ng/m 3(1 ppm) ozone for 90 min. (See earlier 

section on other biochemical alterations.) Liver cyt. 

Paso levels of the ozone-exposed rabbits were not 

significantly different from control immediately or 

1 day post exposure. 

The effects of ozone on pulmonary arterial 

pressure were investigated in 31 dogs exposed to 

1960 pg/m3(1 ppm) for 17 months for varying 

hours each day. 14Three dogs developed 

pulmonary arterial hypertension, and 9 dogs had 

excessive systolic pressure. Because there was no 

proportional relationship between pulmonary 

arterial hypertension and oxidant exposure, it was 

suggested that the results seen were due to 

genetic susceptibility. 

Roth and Tansy18exposed rats to 490 /jg/m 3 

(0.25 ppm) ozone for 2 hr and found no differences 

in gastric secreto-motor activities, although a 

temporary effect was present at higher levels. 

Trams et a1. 199found no lipid peroxidation in 

brain tissue of dogs chronically (8 to 24 hr/day) 

exposed to 1960 pg/m 3(1 ppm) ozone for 18 

months. Monoamine oxidase activity was 

increased (p < 0.05) in animals exposed for 8 to 16 

hr/day, but it was decreased in those dogs exposed 

for 24/hr day. Catechol-o-methyltransferase 

activity was decreased (p < 0.05) for all periods of 

161 
exposure. There were no significant changes in 5- 

nucleotidase, acetylcholinesterase, and ATPase 

activities or in the levels of catecholamines. 

The functional state of the adrenal cortex was 

investigated by Eglite.53 Rats were exposed to 110 

Ng/m 3 (0.056 ppm) continuously for 93 days. After 

6 weeks, the levels of urinary 17-ketosteroids were 

elevated and remained elevated during the course 

of the experiment. The ascorbic acid content of the 

adrenal decreased during exposure, but returned 

to normal levels 15 days after ozone exposure 

ceased. The method of ozone measurement wa^ 

not specified. 

Quantitative analyses of urinary constituents of 

rats exposed to ozone ranging from 1568 to 2940 

/ag/m 3 (0.8 to 1.5 ppm) 5 days/week for 18 weeks 

were made by Hathaway and Terrill. 98 The urine of 

the exposed animals had lower (p < 0.05) titratable 

acidity on days 91, 98, and 112, and a higher 

(p<0.05) pH on days 98 and 112, but not day 91. On 

various days (days 3 to 84), there were no 

significant changes in urinary creatinine, creatine, 

uric acid/creatinine, and amino acid nitrogen/creatinine. For the first 53 days of the study, 

caging arrangements partially hampered the 

animals' ability to obtain food, and this may have 

influenced the results. 

There are suggestive data that exposure to ozone 

may accelerate the aging process. Bjorksten and 

Andrews 13 and Bjorksten 12 have presented the 

concept that aging may be due to irreversible 

cross-linking between macromolecules, principally proteins and nucleic acids. They included 

aldehydes in their list of active cross-linking 

agents. Aldehydes are potential cross-linking 

agents and may be produced in the lung by ozone 

exposure. 

Stokinger 194 reported accelerated or premature 

aging in rabbits after 1 year of weekly 1-hr 

exposures to ozone (no concentration given). His 

evidence included premature calcification of the 

sternocostal cartilage, appearance and coarseness 

of the pelage (hairy system of the body), severe 

depletion of body fat, and general signs of 

senescence, such as dull corneas and sagging 

conjunctivae. -It has been suggested that the 

radiomimetic properties of ozone are implicated in 

the effects on aging. 

Summary and Conclusions 

Animal toxicological studies in conjunction with 

human clinical and epidemiological studies serve 

to provide information on the health effects of 

ozone. Investigations with animals are valuable in 

that they both support and extend the information 

derived from other experimental approaches. For 

example, with animals it is possible to use longterm exposures, controlled pollutant mixtures, and 

invasive measurement techniques that cannot be 

employed with humans because of ethical 

considerations. A major area of concern in animal 

studies involves the validity of extrapolating the 

results to man. Since many physiological 

mechanisms are common to animals and man, it 

can be hypothesized that if ozone causes a 

particular health effect in several animal species, it 

is likely to cause similar effects in exposed 

humans. But at this time, it is not possible to 

predict the concentration of ozone that would be 

responsible. 

Interpretation of animal study results regarding 

the severity of the effect and its implication to 

human health is also difficult. Exposure to ozone 

results in an array of effects that vary from 

relatively small changes observed at low 

concentrations after short-term exposure, to gross 

alterations (including death) with higher concentrations and longer exposure times. A 

statistically significant change observed after 

exposure to ozone may be of unknown 

physiological significance. However, it could be 

hypothesized that any detectable deviation from 

normal is potentially undesirable. 

With the foregoing as background, the results of 

the animal studies can be summarized. The weight 

of the data from numerous laboratories indicates 

that exposure to ozone results in alterations of host 

defense mechanisms, pulmonary morphology, and 

pulmonary function; biochemical changes; and 

effects on circulating blood cells and sera. In mice, 

a 3-hr exposure to concentrations of ozone as low 

as 157 Ug/m 3 (0.08 ppm) results in a 

concentration-related increase in susceptibility to 

infectious respiratory disease, as measured by an 

increase in mortality from laboratory-induced 

pneumonia. Other studies employing this model 

system indicated that the presence of other 

pollutants (nitrogen dioxide and sulfuric acid) 

would have additive effects with ozone. 

Investigations of host defense mechanisms have 

indicated that a 2.5- to 4-hr exposure of ozone 

depresses pulmonary bactericidal activity (1176 

/jg/m3 , or 0.6 ppm) and causes increased lability of 

functional and biochemical alterations of alveolar 

macrophages (196 to 980 pg/m 3 , or 0.1 to 0.5 

ppm), which are primarily responsibte for 

maintaining sterility of the deep lung. 

162 
Numerous investigations in a variety of animal 

species have shown that exposure to 196 to 1568 

/jg/m3 (0.1 to 0.8 ppm) ozone from a few hours to 

several days alters the activity of several enzymes 

and other biochemical constituents (proteins and 

lipids) in the lungs. At the 196-Ng ozone/m 3 (0.1- 

ppm) concentration, a 7-day continuous exposure 

of rats maintained on a vitamin E level typical of 

that in the standard American diet caused an 

increase in oxygen consumption of pulmonary 

tissue. A similar effect was not noted in vitamin-Esupplemented rats until the concentration was 

increased to 392 ,ug/m 3 (0.2 ppm). Additional 

research has also shown thatvitamin E can protect 

the host from the adverse effects of ozone. In a 

comparative study, rats were affected (increased 

02 consumption of pulmonary tissue) by a lower 

concentration (392 pg/m3 , or 0.2 ppm) of ozone 

than monkeys (686 /Ug/m3 , or 0.35 ppm) following 

a 7-day intermittent exposure. The activities of 

other enzymes (e.g., glucose-6-phosphate 

dehydrogenase, glutathione reductase, and 

glutathione peroxidase) and concentrations of 

glutathione also increase following ozone 

exposure to levels equal to or greater than 392 

pg/m3 (0.2 ppm) for several days (typical 

experiments were for 7 days, but in some studies, 

effects were noted earlier). Since these enzyme 

systems can detoxify oxidizing substances such as 

ozone and its reaction products, these changes are 

interpreted as representing an increased 

protection against ozone. Thus the increased 

enzymatic activity might represent a reaction to 

potential toxicity, rather than a toxic response 

itself. 

Many of the biochemical effects of ozone have 

been attributed to concomitant morphological 

alterations of the lung. Concentrations of ozone 

equal to or greater than 392 ug/m3 (0.2 ppm) can 

lead to an increase in the number of Type 2 cells 

that replace Type 1 cells in both rats and monkeys. 

Since Type 2 cells are rich in mitochondria and 

have higher metabolic activity, this situation would 

lead to increased activity of several enzyme 

systems in the lung. In monkeys, the predominant 

injury is located at the respiratory bronchiole (8 

hr/day for 7 days). With increasing concentrations 

of ozone, the extent of the damage expands 

distally. In rats, which do not have respiratory 

bronchioles, the principal site of damage was the 

alveolar duct. The lesion generally reaches a peak 

in 3 to 5 days (after continuous or intermittent 

exposure), and then progressively diminishes, 

even during continuing ozone exposure. The 

meaning of these changes is not immediately 

apparent, but it has been suggested that the 

alterations are part of an adaptive response. 

Morphological alterations caused by ozone can be 

quite extensive and involve areas of the lung other 

than the area of the respiratory bronchiole and 

alveolar duct. For example, a 3-month continuous 

exposure to 1725 Ng/m3 (0.88 ppm) can produce 

emphysema-like structures in rats. Intermittent 

exposure (6 hr/day, 5 days/weekfor 10 months)to 

984 Pg/m3 (0.4 ppm) can produce emphysematous-like lesions in rabbits. 

Alterations in pulmonary function have been 

observed in animals following short-term 

exposures equal to or greater than 510 Ng/m 3 

(0.26 ppm) ozone. Pulmonary flow resistance (a 

measure of airway diameter) and respiratory rates 

increased, and tidal volume decreased as the 

concentration increased. At a higher concentration (1960 Ng/m 3 , or 1 ppm), compliance (a 

measure of lung distensibility) and carbonmonoxide-diffusing capacity (a measure of 

alveolar gas exchange) decreased. Young rats 

continuously exposed (30 days) to 392 Ng/m 3 (0.2 

ppm) were also affected, as indicated by increased 

lung volumes and other changes that were 

interpreted as a decrease in lung tissue elasticity. 

Sensitive measurements of small airway disease, 

such as those made in humans, are very difficult to 

perform in small animals because of the size and 

voluntary maneuvers of the subject that are 

required. Therefore it would be expected that many 

of the slight-to- moderate morphological 

alterations typically seen in animals would not be 

detected by pulmonary function measurements. 

The health effects of ozone are affected by other 

environmental factors such as dietary levels of 

vitamin E and the presence of other pollutants that 

have already been mentioned. The potential of 

ozone to modify the transformation of other 

environmental contaminants or drugs is suggested 

by the results of several studies that show that 1.5- 

to 3-hr exposures to 1470 to 1960 /_Ig/m 3 (0.75 to 

1.0 ppm) ozone decrease the concentration of 

mixed-function oxidases of pulmonary tissue. In 

another experiment, a 2-day exposure (3 hr/day)to 

1960 ,ug/m 3 (1 ppm) ozone was interpreted as 

having a similar effect, perhaps on the liver. Lower 

concentrationswere nottested. Nonetheless, such 

data would lead to the inference that by lowering 

the concentration of mixed-function oxidases that 

either detoxify or activate chemical compounds 

163 
(depending on the compound), ozone would 

influence the toxicity of other environmental 

chemicals that are substrates for this enzyme 

system. The net result depends on whether the 

toxicity of the chemical would be enhanced or 

decreased by mixed-function oxidase activity. 

A considerable number of research studies have 

addressed tolerance to ozone, a phenomenon by 

which a prior dose of ozone will protect an animal 

from a later higher (or equivalent) dose of ozone. 

Though such work is interesting, its relevance to 

the protection of health is difficult to assess, since 

concentrations of ozone found to induce tolerance 

also elicit alterations in biological endpoints. In 

addition, tolerance is only highly efficient against 

edema and results in partial or no protection 

against some of the alterations in pulmonary biochemistry, morphology, and host defense 

mechanisms against infectious pulmonary 

disease. 

In some studies of host-defense mechanisms, 

biochemistry, and morphology, concentrationresponse relationships were investigated. As the 

concentration of ozone was increased, the effect 

also increased. Also, in most cases in which 

different exposure modes were compared, there 

were no significant differences between 

intermittent (7 to 8 hr/day) and continuous 

exposure. From such information, it can be 

postulated that insufficient recovery occurs during 

the clean-air period of the intermittent exposure 

mode. 

The persistence of the health effects caused by 

ozone has only been measured in a few studies and 

varies considerably. Some pulmonary biochemical 

alterations exhibit a plateau or continue to 

increase during exposure and then subside 

immediately or a few days following cessation of 

exposure Other enzyme activities remain elevated 

a few weeks after exposure. The typical 

morphological lesion (in which Type 2 cells replace 

Type 1 cells) reverts toward normal during ozone 

exposure. However, more severe pathological 

effects such as emphysema would remain 

throughout the life of the animal. 

Though most ozone toxicological studies have 

focused on the lung, systemic effects have also 

been observed. Extrapulmonary effects might be a 

result of neurohormonal mechanisms initiated by 

ozone or of the toxic action of the reaction products 

of ozone affecting blood components as they pass 

through the capillaries surrounding the alveoli; or 

these reaction products could possibly enter the 

circulation, exerting effects at distant target sites. 

Also conceivable is that ozone itself could cross the 

alveoli and affect blooa components, though such 

an event is unlikely, since mathematical 

predictions estimate that only a miniscule dose 

would reach the level of the alveoli. Whatever the 

reason(s), extrapulmonary effects have been noted 

at concentrations as low as 392 Ng/m 3 (0.2 ppm) 

for a 30-min exposure. 

Numerous alterations in erythrocytes and in the 

sera have been observed following ozone 

exposure. Increased lysis -of red blood cells of 

exposed (980 Ng/m 3 , or 0.5 ppm for 23 days, 

continuous) vitamin-E-deficient, animals has been 

reported. An enzyme bound to red cpll membranes 

is also affected by ozone. Serum protein changes 

have also been shown to occur in animals exposed 

to ozone levels between 392 and 1568 Ng/m 3 (0.2 

and 0.8 ppm). Levels of albumin, globulins, and 

serum enzymes were altered after a 6- to 10- 

month intermittent exposure to 784 Ng/m3 (0.4 

ppm). Exposure to 392 /Jg/m 3 (0.2 ppm) for 1 hr 

reduced total blood serotonin, and a 3-week 

intermittent exposure to this ozone level increased 

serum glutamine pyruvic transaminase. 

The influence of ozone on chromosomes has 

also been investigated and is the subject of some 

controversy. In one study, Chinese hamsters 

exposed to 392 Ng/m3 (0.2 ppm) ozone for 5 hr 

exhibited an increased number of chromosomal 

breaks in circulating lymphocytes, which were 

detectable up to 15 days following the end of the 

ozone exposure. Another investigation using 

approximately the same ozone exposure failed to 

demonstrate any chromosomal aberrations in 

Chinese hamster bone marrow, mouse peripheral 

leukocytes, and mouse primary spermatocytes. A 

number of investigations have shown that 

bacteria, plant cells, oyster cells, and chick 

fibroblasts exposed to ozone in vitro exhibited 

chromosomal alterations. Because of these 

conflicting data, no definitive conclusions can be 

drawn at present regarding the effects of ozone on 

chromosomes. Even if the work with circulating 

lymphocytes were replicated in the future, the 

biological significance of the findings (beyond that 

of indicating systemic chromosomal damage from 

an environmental agent) would be difficult to 

assess Lymphocytes are considered to be a 

terminal cell; but for proper immune functioning, 

they must divide and form an additional line of 

cells Consequently, immune functioning could be 

affected by ozone. However, a potential danger to 

164 
human health—that of chomosomal aberrations of 

germ cells (i.e., ova or sperm)—has not been 

directly observed. In spite of the conflicting results 

of ozone with chromosomes, mutagenic effects 

have been observed. The offspring of mice exposed 

for 7 hr/day, 5 days/week to 392 Ng/m 3(0.2 ppm) 

during gestation and the first 3 weeks of life 

exhibited increased neonatal deaths and 

mutagenic effects such as increased incisor 

growth and blepharophimosis (a narrowing of the 

slit between the eyelids). 

A number of other extrapulmonary effects have 

also been reported. Structural changes have been 

found in mouse heart musclefollowing a 3-week(5 

hr/day) exposure to 392 /jg/m 3(0.2 ppm) and in 

the parathyroid glands of rabbits after a 4- to 8-hr 

exposure to 1470 Ng/m 3(0.75 ppm). Short-term (1 

hr or less) exposures of greater than or equal to 

980 /jg/m3(0.5 ppm) have caused alterations in 

behavior and in responses of the central nervous 

system (i.e., decreased activity and depression of 

evoked reponse to flash). 

Review of the literature of the health effects of 

ozone provides strong evidence that in animals, a 

large variety of pulmonary and extrapulmonary 

alterations - are produced after a short-term 

exposure to concentrations between 392 and 980 

Ng/m3(0.2 and 0.5 ppm). Pulmonary biochemical 

alterations and an increased susceptibility to 

infectious disease have been observed at levels 

between 157 and 392 /jg/m 3(0.08 and 0.02 ppm). 

A prudent conclusion from the animal toxicological 

data is that humans exposed to ozone may 

experience similar effects, but it is not possible to 

predict precisely the severity of the effects or the 

concentrations at which they may occur in man. 

EFFECTS OF PHOTOCHEMICAL OXIDANTS 

ON EXPERIMENTAL ANIMALS 

Experimental Data 

Investigations have been conducted of the 

potential biological actions of a complex photochemical reaction mixture produced by irradiating 

mixtures of air and auto exhaust under laboratory 

conditions that simulated real driving patterns and 

solar irradiation.' oo,1o1,1oa,1a2.+44 The effects of both 

nonirradiated and irradiated exhaust mixtures 

were studieri. Clearly, irradiation of the air-exhaust 

mixture led to the formation of photochemical 

reaction products that were biologically more 

active. The relative proportions of the suspect 

biologically active chemical species varied with the 

total concentration of exhaust gases in the 

irradiated mixture and with the duration of 

irradiation. 142,144Single-inhalation exposure 

studies lasting a few hours demonstrated that 

irradiation of exhaust mixtures led to greater 

effects on respiratory mechanics (increased flow 

resistance and tidal volume and decreased 

breath7ng frequency) in guinea pigs, greater 

reduction in voluntary running activity of mice, 

increased susceptibility to infection, and slightly 

greater carboxyhemoglobin formation in rats, 

compared with animals exposed to the same total 

concentration of exhaust gases that were not 

irradiated. The concentration of total oxidant as 

expressed by ozone in these experiments ranged 

between 588 and 1568Ng/m3 (0.30and0.80ppm) 

in the irradiated-exhaust mixtures. Only a trace or 

no oxidant was detected in the unirradiated 

exhaust. The irritant aldehydes, formaldehyde and 

acrolein, were also present in higher 

concentrations (0.39 to 2.42 ppm and 0.09 to 0.2 

ppm, respectively) in the irradiated atmospheres. 

Formaldehyde concentrations were between 0.12 

ppm and 0.38 ppm, and acrolein ranged from 0.02 

to 0.07 ppm in the unirradiated exhaust chamber. 

The effects that were noted were reversible within 

a few hours when the animals returned to clean 

air. The effects in animals exposed to the 

irradiated-exhaust mixture are not necessarily 

uniquely characteristic of ozone, but most of them 

could have been produced by ozone. 

Murphy et a1. 142,' 4°found that the nature of 

changes in respiratory mechanics in guinea pigs 

exposed to irradiated exhaust varied according to 

the ratio of oxidant to aldehyde concentrations 

(formaldehyde and acrolein were measured), and 

this ratio in turn varied with the duration of 

irradiation of the air-exhaust mixture. Thus when 

the oxidant:aldehyde ratio was low, the guinea pig 

respiration pattern resembled that reported for 

animals exposed to irritants such as formaldehyde 

and acroleins,143and was characterized by increased pulmonaryflow resistance, increasedtidal 

volume, and decreased frequency of breathing. 

Increasing the ratio resulted in a shift inthe pattern 

of respiration toward that produced by deep-lung 

irritants (e.g., ozone and nitrogen dioxide' a6), 

namely decreased tidal volume and increased 

frequency, although the increased flow resistance 

typical of the aldehyde effect persisted. This 

interactive effect of an oxidant-aldehyde mixture 

could be reproduced by a simple mixture of ozone 

and acrolein. 12 

165 
TABLE 8-1. PULMONARY EFFECTS OF OZONE: HOST DEFENSE MECHANISMS 

Ozone, 

pg/rn' 

Ozone, 

ppm 

Length of 

exposure Observed effecqs) Species References 

1960 1 17 hr before Decrease in bacterial pulmonary depo- Mice Goldstein et al 90 

bacteria sttton, decrease tn bactertctdal 

activity 

1960 1 3 hr Bacteria observed in the blood Mice Cofftn and Gardnerss 

sooner and with tncreased frequency 

1764 OS 1-4 hr Increased nasal, but not lung, deposi- Mice Fairchild6 '•s2 

tion and growth of vtrus Decreased 

mtnute venttlation 

1568 0.8 11 days Decreased production of tnterferon bv Mice Ibrahtm et a1 109 

tracheal epitheltal cells 

1372- 0 7- 3 hr Increased mortality of mtce pre-exposed Mice Coffin and Blommer 34 

1764 0.9 over those animals not so treated 

Aerosols of S pyogenes received by 

all animals immedtately after 03 

exposure 

1372 07 7 days Defictency of vitamtn E further Rats Warshauer et al 203 

reduced bactertctdal acttvity after 

7 days 

1176 0 6 4 hr after No effect on bacterial deposition Mtce Goldstetn et al 8990 

bacterta and mucoctltary clearance 

Decreased bacterictdal acttvity 

980 0 5 3 hr Decreased enzyme activtty Rabbtts Alpert et al 3 

in alveolar macrophages, increase 

in number of pulmonary 

polymorphonuclear leukocytes 

(appears to be Itnearly related to 

dose) 

980 0.5 16 hr/day x No effect on clearance of polystyrene Rabbits Frtberg et al 73 

7 months and iron parttcles 

980 0.5 3 hr Increased fragility of alveolar Rabbtts Dowell et al 48 

macrophages 

980 0.5 2 hr Decrease in aggluttnation of alveolar Rats Goldstein et a1. 85 

macrophage, indicattng membrane 

alterattons 

980 0 5 3 hr Increased red blood cell rosette Rabbtts Hadley et al 94 

formatton by lectin-treated alveolar 

macrophages 

980 0.5 3 hr Reductton in phagocytosis of alveolar Rabbits Coffin and Gardner 36 

macrophage 

785 04 3 hr before Lower deposition, but subsequently Mice Coffin and Gardner's 

bacterta a higher number of bacteria present 

due to reproduction. 

784 0.4 4 hr Bactericidal acttvity tnhtbtted by 03, Mtce Goldstetn et al 84 

but no role played by an tnduced 

silicotic conditton 

784 0.5 17 hr before Phystcal clearance not affected, Mtce Goldstein et al 91 

bacterta or 4 hr but bacterictdal activtty affected 

after bacterta No synergtsm noted wtth NOP 

490 0.25 3 hr Lysozyme, acid phosphatase, and P- Rabbtts Hurst et al tos 

glucuronidase activities of alveolar 

macrophagesreduced 

196 0.1 2.5 hr tn vtvo Lung protecttve factor parttally Rabbtrs Gardner 76 

or 30 mtn inactivated (Appears to be 

tn vttro dose-related ) 

196 0.1 3 hr Increased mortaltty when S pyogenes Mice Ehrltch et al 54 

aerosol challenge received immediately after exposure Additive effect 

from simultaneous exposure to 

?3760 ,ag/m 3 (2 ppm) NO2 and 

?98 pg/m 3 (0 05 ppm) 03 

157 0.08 3 hr Stgniftcant increase tn mortality of Mtce Miller et a1 135 

196 0.1 mice exposed to aerosols of S. 

pyogenes durtng ozone exposure 

157 0.08 3 hr Increased mortality in mice chal- Mice Cofftn et a1. 35 

lenged with aerosols of S pyogenes 

immediately after exposure 

166 
TABLE 8-2. PULMONARY EFFECTS OF OZONE: BIOCHEMISTRY 

Ozone, Ozone, Length of 

pg/m 3 ppm exposure Observed effect(s) Species Reference 

1960 1 1 hr Carbonyl compounds found Rabbits Buell et a1. 23 

1960 1 Continuous 50% of vitamin-E-depleted group Rats Roehm et a1. 14 

died in 8 2 days, 50% of vitamin-Esupplemented group died in 18 5 

days 

1960 1 90 min Decreased lung microsomal Rabbits Goldstein et al ss 

cytochrome P450 levels after 1,2,3, or 

5 days The greater depression at 3 6 

days following exposure. 

1568 0.8 Continuous Decreased protein synthesis, day 1, Rats Mustafa et al 149 

7 days increased protein synthesis, days 2 

and 3 (remained elevated and 

unchanged) 

1568 0 8 Continuous Increased rates of collagen and non- Rats Hussain et a1. 107 

7 days collagenous protein synthesis 

1568 0 8 Continuous Increase in protein synthesis, non- Rats Chow et al 29 

3 days protein sulfhydryl content and activities of GSH peroxidase, GSH 

reductase and G-6-PD Complete 

recovery 9 days after exposure 

ceased Increased rate of 

mitochondrial succinate oxidation 

returning to normal levels 9 days 

after the original exposure ceased 

1568 0.8 Continuous Increased rates of 02 consumption, Rats Mustafa and Lee 150 

1-30 days reaching a peak at day 4 and 

remaining at a plateau for the 

remainder of the 30 days Most 

increase in the oxidation of succinate 

Also an initial decrease (day 1 ) and a 

subsequent increase (day 2) in the 

activity of succinate-cytochrome-C 

reductase activity which plateaued 

between days 3 and 7 

1568 0.8 Continuous Increased rate of glucose consumption, Rats Mustafa et a1 149 

4-7 days pyruvate and lactate production after 

4 days of exposure Increased MAO 

activity after 7 days of exposure 

1568 0.8 7 days Increased activities of hexose mono- Rats Chow and Tappel 31 

phosphate shunt and glycolytic 

enzymes of lung 

1568 08 10 days Decreased cytochrome-C-reductase Rats Delucia et al.°4 '45 

1960 1 activity, increased G-6-PD activity, 

no change in sulfhydryl levels 

1470 075 3 hr Reduction in activity of benzpyrene Hamsters Palmer et al.'so., s , 

hydroxylase in both tracheobronchial 

mucosa and lung parenchyma. 

1470 0.75 Continuous Decreased activfties of GSH peroxidase, Rats Chow and Tappel 31 

30 days GSH reductase, G-6-PD, 6-P-GD, and 

pyruvate kinase on day 1 Thereafter, 

increase in most of these enzyme 

activities until day 10, at which time, 

beginning of a slight decrease At day 

30, still elevated over control 

1372 07 Continuous Increased formation of malonaldehyde Rats Chow and Tappe1 32 

1568 08 7 days Activities of GSH peroxidase and 

G-6-PD partially inhibited as a 

logarithmic function of dietary 

vitamin E Increased activity of GSH 

reductase not affected by vitamin E 

1372 07 Continuous Increase in lysosomal hydrolases in RatE Castleman et al Zs.zs 

1568 08 5 days homogenates and tissue sections Dillard et al 46 

7 days Increase in protease and peptidase 

seen along with other enzymatic 

changes Increased activity of acid 

phosphatase in alveolar macrophages, terminal airway, epithelium, 

and adjacentstructures 

167 
TABLE 8-2. PULMONARY EFFECTS OF OZONE: BIOCHEMISTRY (cont'd). 

Ozone, 

pg/ m' 

Ozone, 

ppm 

Length of 

exposure Observed effect(s) Species Reference 

980 05 Continuous Alterations of lung tissue lipids Rats Menzel et a1. 132 

1960 1 9 days Greatest change an increase in 

arachidonic acid, which occurred to a 

greater extent in vitamin-E-deficient 

rats. Decreases in linolenic, oleic, 

stearic, and palmitic acid 

980 05 4 hr Release of surfactant lecithins and Rabbits Kyei-Aboagye et al 117 

Continuous decreased lecithin formation Setp et al 1ee 

1960 1 1-2 weeks 

980 05 Continuous Vitamin E acts as an anttoxtdant and Rats Fletcher and Tappel 68 

1960 1 9 days protects against some ozone altera- Roehm et al 111

' 15 

tions (mortality, high increases Shakman 788 

tn arachtdonic acid content, and Menzel et a1 132 

lipid peroxidation). 

980 05 8 hr/day Greater increases in the activities Rats, Chow et al 30 

7 days of GSH peroxidase, GSH reductase, monkeys 

and G-6-PD exhibited by rats Only 

slight increases by monkeys in these 

enzyme activities. 

980 05 8 hr/day Increased succinate oxidase activity Monkeys Mustafa and Lee 150 

1568 08 7 days Increases not significant at lower 

concentrations 

980 05 Continuous Increased prolyl hydroxylase activity Rats Hussain et al 108 

1568 08 7 days No change at lower concentrattons 

At 1568 Ng/m3 , partial return of 

activity to normal after a 30-day 

recovery, but stttl elevated Increased 

hydroxyproline after 3 days of 

exposure to 1568 Ng/m', remaining 

elevated after 28 days of recovery 

392 02 8 hr/day Increased activities of GSH peroxidase, Monkeys Dungworth et al. 50 

686 035 7 days GSH reduptase, G-6-PD, NADPH- Mustafa and Lee'so 

980 05 cytochrome-C reductase, succinate 

1568 08 oxidase, acid phosphatase, and B-Nacetyl-glucosaminidase Asignificant 

correlation found between ozone 

concentration and increased enzyme 

activities 

392 0.2 Continuous For the continuous exposure to the Rats Chow et al 18 

980 05 (7-8 days) two higherconcentrations, increased Mustafa and Lee 150 

1568 08 or intermtttent activities GSH peroxidase, GSH 

(8 hr/day reductase, and G-6-PD At the lower 

for 7 days) concentration (continuous), increased 

activities of GSH peroxidase and GSH 

reductase A linear increase in all 

three enzyme activities as the concentration of ozone was increased 

Increased 02 consumption (using 

succinate-cytochrome-C reductase 

activity fairly proportional to ozone 

concentration Similar results 

obtained for intermtttent exposure 

groups 

168 
TABLE B-2 PULMONARY EFFECTS OF OZONE: BIOCHEMISTRY (cont'd). 

Ozone, 

yg/m 

Ozone, 

ppm 

Length of 

exposure Observed effect(s) Species Reference 

392 0.2 Continuous Increased activities of NADPH- Rats Mustafa and Lee 150 

980 05 7 days cytochrome-C reductase and G-6-PD 

1568 08 

392 02 Continuous Activitfes of G-6-PD and NADPH- Rats Schwartz et al 184 

980 05 Intermittent cytochrome-C reductase and 

1568 08 (8 hr/day) succinate oxidase increased in an 

7 days ozone -dose-dependentfashion 

following exposure No significant 

differences found between the 

intermittent and continuous exposure 

groups 

-392 02 Continuous At the higher concentration Increase Rats Mustafa et a1 14e '' 87 

1568 08 10-20 days in the lung mitochondrial ozone 

7 days consumption in oxidation of 2- 

oxyglutarate and glycerol-1 -phosphate and the number of Type 2 

alveolar cells that are rich in 

mitochondria At the lower concentration Increase in Oz 

consumptfon. 

392 0.2 8 hr/day or Decreased glycoprotein secretion by Rats Last et al 18 

1568 0.8 continuous tracheal explants 

2-90 days 

392 0.2 Continuous Increased superoxide dismutase Rats Mustafa et a1 15 ' 

980 05 7 days activity as ozone concentration 

1568 08 increased 

392 0.2 Continuous Tncreased lysozyme actfvities at 1568 Rats Chow et al 28 

980 '0 5 (8 days) /!g/m' (continuous) No significant 

1568 0 8 intermittent changes following intermittent 

(8 hr/day, exposure. 

7 days) 

196 0.1 Continuous Significant increase in succinate Rats Mustafa and Lee'so 

392 02 7 days oxidase activity at 196 Ng/m 3 in 

those animals maintafned on 11 ppm 

vitamin E Increased succinate 

oxidase activity only at 392 /lg/m 3 for 

those rats receiving 66 ppm vitamin 

E 

AII the functional effects observed in shortduration experiments with laboratory-produced 

photochemical smog mixtures could have been 

due to ozone alone if one considers total oxidant 

concentraion of the mixture equivalent to ozone 

concentration. One possible exception was the 

increase in respiratory flow resistance in guinea 

pigs, which is more characteristic of an irritant 

aldehyde. The increase in respiratory frequency in 

guinea pigs is most probably due to the oxidant (or 

ozone) content of the mixture. 

Comparison of the concentrations for equal 

effectiveness in decreasing the spontaneous 

running activity in mice also suggests that this 

action of the mixture may be largely due to oxidant. 

Likewise, the oxidant content of irradiated auto 

exhaust appears to explain adequately the 

increase in susceptibility to respiratory infection in 

mice exposed to the mixture. These concluslons 

must be qualified, since the possibility exists that 

other chemical species, such as free hydroxyl 

radicals, which were not measured, might also 

have produced a similar effect. IVevertheless, it is 

reasonable to conclude that many of the effects 

produced by exposures to complex photochemical 

oxidant mixtures are due to ozone. 

Hueter et a1. 104 exposed animals to irradiated 

automobile exhaust for periods of 6 weeks to 23 

months. The concentrations were cycled to 

simulate daily pollution concentrations in urban 

citie&. Daily peak concentrations of carbon 

monoxide of 20, 50, 60, and 100 ppm were 

169 
TABLE 8-3. PULMONARY EFFECTS OF OZONE: MORPHOLOGY 

Ozone, Ozone, Length of 

pg/m 3 ppm exposure Observed effect(s) Species References 

1960- 1-026 4-6 hr Loss of ciliated eptthelium, damage Cats Boatman et a1 15, ' 6 

510 to ciliated cells and mitochondria 

in some airways, swelling and desquamation of Type 1 alveolar cells, 

and swelling and breakage of interalveolar capillaries Apparently 

dose-related. 

1960 1 8 hr/day Damage roughly proportional to time Dogs Freeman et al 72 

and dose of exposure, fibrous 

elements deposited, lumina of small 

airways reduced, metaplasia of 

columnar and cuboidal epithelium. 

1568 08 Continuous Thickening of alveolar septa and Rats Stephens et al 192 

3-5 months increase in number of alveolar 

macrophages Emphysematous and 

fibrotic changes. 

1058 054 Continuous Malor site of injury at the lunction Rats Freeman et al 7 O 

1725 088 6 months of the respiratory bronchiole and the 

alveolar duct A multitude of alterations observed at the lower 

concentration. After 3 weeks, 

terminal bronchioles seemed to 

return to normal appearance In 

general, at the higher concentrations, 

pathological changes similar but 

more extensive and occurred earlier 

After 3 months, emphysema-like 

structures seen. 

1176 06 6-7 hr/day Younger mice more sensitivethan older Mice Bils" 

1-2 days animals Swelling of epithelial 

alveolar lining cells and endothelium 

cells. Occasional breaks in basement 

membrane 

980 05 8 hr/day Lesions in centriacinar region, hyper- Rhesus Mellick et al. 126 

1568 08 7 days plasia of nonciliated epithelial monkeys, 

cells and intraluminal accumulation mice 

of macrophages. Replacement of 

Type 1 with Type 2 cells 

980 05 6 hr Lowered rates of DNA synthesis in Aging Evans et al 59 

alveolar cells. mice 

980 05 2,4,6,8 or Accumulation of inflammatory cells in Rats Brummer et al 21 

1568 08 24 hr/day centriacinar region of lung 

for 7 days 

784 0.4 6 hr/day Emphysematous and vascular-type Rabbits P'an et a1. 762 

5 days/week lesions observed in the lung, and 

10 months small pulmonary arteries thicker. 

686- 0 35- Continuous Type 1 cells replaced by Type 2 Rats Evans et al 57 

980 05 8 days alveolar cells. No further tissue 

damage after 4th day 

588 03 3 hr/day Presence of hemispheric extrusions of Rats Sato et a1. 180 

16 days cilia, and small round bodies on 

surface of airways. Changes in 

Clara cells. 

392 02 2 hr Type 1 cells replaced by Type 2 Rats Stephens et al.tso 

alveolar cells after 24 hr Evans et al. ea,eo 

392, 02, 8 hr/day Pulmonary lesions occurring in Rhesus Mellick et al 126 

686 035 for 7 days respiratory bronchioles Hyperplasia and Dungworth49 

980, 05, and hypertrophy of bronchiolar Bonnet Schwartz 183 

1568 08 epithelium. Increase in Type 2 cells monkeys, Schwartz et a1. 184 

Damage to ciliated and Clara cells. rats, mice 

Rats and monkeys equally 

susceptible 

170 
established in four sets of exposure chambers. 

There was considerable loss of ozone and nitrogen 

dioxide on chamber walls, cages, and anlmal fur, 

so the concentrations of chemically reactive gases 

to which the animals were actually exposed 

probably ranged from about 78 to 392 Ng/m3 (0.04 

to 0.2 ppm) for ozone and about 280 to 940 pg/m 3 

(0.15 to 0.5 ppm) for nitrogen dioxide. Interpretation of these studies is difficult because of 

loss of contaminants on the chamber surface. No 

significant treatment effects were observed when 

pulmonary flow resistance, tidal volume, 

respiratory frequency, and oxygen consumption 

were measured in guinea pigs, mice, or rats at 16- 

week Intervals during the chronic exposures to 

exhaust. Exhaust-exposed mice showed a 

decrease in running activityfor the firstfewweeks 

of exposure but then recovered to attain control 

levels. Decreases in mouse fertillty rate and infant 

survival rate occurred in the exhaust chambers. 

This effect was confirmed in a second 

experiment. 19 Also, there was an increase in the 

rate of spontaneous pulmonary infection in exhaust-exposed animals. There were no significant 

effects of exhaust exposure on mortality, 

histopathology, growth rate, or hematologic 

indices. 

Wayne and Chambers205 reviewed studies on 

experimental animals exposed throughout their 

lifetimes to ambient Los Angeles atmosphere. 

Control animals were kept in rooms that were 

ventilated wlth special filters that removed most of 

the ambient air pollutants. The following maximal 

peak concentratlons were recorded (ranges of the 

four exposure stations are given): 29 to 72 ppm CO, 

50 to 121 pphm NO, 49 to 73 pphm NO2, and 46 to 

82 pphm oxidant. No clear evidence of chronic 

injury from the ambient air pollution was observed. 

However, there was suggestive evidence from 

pulmonary function tests, electron-microscopic 

examinations, and the incidence of pulmonary 

adenomas that aged animals had been adversely 

affected by ambient smog and that some reversible 

changes in pulmonary function of guinea pigs 

were noted during periods of peak air pollution. 

Increased 17-ketosteroid excretion suggested that 

breathing polluted ambient air was stressful for 

guinea pigs. The reported effects were marginal, 

and some of them may have been due to variations 

in temperature and humidity. 

Beagles were exposed 12o,20o to various pollutant 

mlxes for 16 hr/day, 7 days/week for 61 months, 

and measurements of cardiovascular parameters 

and pulmonary function were made periodically. 

TABLE 8-4. PULMONARY EFFECTS OF OZONE: PULMONARY FUNCTION 

Ozone, Ozone, Length of 

/g/rn' ppm exposure Observed effect(s) Species References 

1960 1 3 hr 1-3 days post exposure, reduced Rabbits Yokoyama 2 ' zz' 3 

vital capacity, 7 days post exposure, 

vital capacity reduced only slightly 

A decrease in lung elasticity back to 

near normal conditions 3 days post 

exposure 

1960 1 6 hr/day Increased residual volume/total lung Rabbits Yokoyama 274 

3-4 days capacity, functional residual 

capacity/total lung capacity, andtotal 

lung resistance; decreased chest wall 

resistance No change in flow volume 

curves 

882 045 6 hr/day No change in pulmonary pressure- Rats Yokoyama and 

6 days/week volume relationship or ratio of Ichikawa 216 

6-7 weeks collagen to elastin 

510 026 2 hr Increased pulmonary flow resistance Cats Watanabe et al 204 

980 05 6 5 hr with increasing 0 3 levels. Vital 

1960 1 0 capacity not affected. Reduced 

diffusion capacity shown by some 

cats 

980 0 5 2 hr Increased air current resistance Guinea Yokoyama 21 

and frequency of respiration, pigs 

decreased tidal volume 

392 0 2 Continuous Increase in lung volume and alveolar Young Bartlett et a1. 9 

30 days dimensions and a reduction in lung rats 

elasticity 

666- 034- 2 hr Increased respiratory frequency and Guinea Murphy et a1 146 

2646 1 35 decreased tidal volume pigs 

171 
TABLE 8-5. PULMONARY EFFECTS OF OZONE: EDEMA AND TOLERANCE 

Ozone, Ozone, Length of 

Ozone, Ozone, Vg/m 3 ppm exposure 

Ng/m' ppm Length after after after 

pre- pre- of pre- latent latent latent 

exposure exposure exposure period period period Observed effecqs) Species Reference 

490 025 6 hr 1966 1 6 hr No tolerance to edema Rats Alpert et al 5 

unless pretreated with 

methylprednlsolone. 

588 03 1 hr 39,200 20 2 hr Tolerance not developed Mice Gregory et al 93 

by thymectomlzed 

anlmals, but developed by 

sham-operated anlmals. 

588 0.3 3 hr 588 0.3 3 hr 20% lower mortality for Mlce Coffln and 

pre-exposed mlce than Gardner 37 

mice recelving only one 

03 dose. Partlal tolerance probably due to 

Inhlbitlon of edemagenesis. 

588- 0 3- 4 days 980, 0 5,0 7, 1,2,4 Lack of total protectlon Rats Evans et al 57 

980 05 1372, 10 days indicated by increased 

1960 numbers of Type 2 cells 

980 05 6 hr Edema as measured by re- Rats Alpert et al 5 

covery of 132 1 In pulmonary 

lavage fluld. 

980 05 3 hr 43,120 22 3 hr Using unilateral lung Rabbits Alpert et a1. 4 

exposure technlque, 

tolerance to edema a local 

effect and seen only In the 

pre-exposed lung. 

980 0.5 3 hr 5880 or 3 and 3 hr Using unllateral lung Rabbits Gardner et a1. 79 

43,120 22 exposuretechnlque, 

tolerance developed only 

to pulmonary edema. No 

tolerance to the.chemotaxls of polymorphonuclear leukocytes or 

decreased lysosomal 

hydrolase enzyme 

activlty. 

1470 075 3 days 7840 40 8 hr A smaller decrease in actl- Rats Chow27 

vltltles of glutathione 

peroxldase, glutathione 

reductase, glucose-6- 

phosphate dehydrogenase and levels of reduced glutathione In 

lungs of tolerant anlmals 

as compound to 

nontolerant anlmals. 

1960 1 1 hr All anlmals X-Irradlated Mlce Hattori et al 99 

to 800 R. 60% of 03-preexposed mlce survlved. 

100% of controls died. 

1960 1 1 hr 3920 2 1 hr Tolerance to allergic Gulnea Matsumura 

response to Inhaled plgs et a) 124 

acetylcholl ne. 

172 
Treatment groups are shown in Table 8-10. There 

were no specific abnormalities in cardiovascular 

function attributable to air pollution exposure 

during the exposure period. Pulmonary function 

measurements of the beagles were made after 

18, 200 36, 120 and 61 120 months of exposure. After 

18 months, there were no differences in CO 

diffusing capacity(DLco), dynamic lung compliance 

(CLdyn), or total expiratory pulmonary resistance. 

After 36 months of exposure, no statistically 

significant effects were observed, although there 

was an increased frequency of abnormal 

measurements in those animals (Group 7) 

receiving nitrogen oxides. By 61 months, more 

changes were evident, but only those related to 

oxidant exposure will be described here. Dogs 

exposed to irradiated auto exhaust (Group 3) had a 

higher (p < 0.05) mean single breath nitrogen 

washout than controi animals. When the data 

were analyzed differently based on the number of 

animals showing alterations, it was found that 

more animals of groups 3 and 6 had higher (p < 

0.0001) total expiratory resistances than the 

comparable control animals in groups 1 and 4. 

Pulmonary biochemical measurements, made 

by Orthoefer et a1. 15e on these dogs after a 2 1/2-year 

TABLE B-6. EXTRAPULMONARY EFFECTS OF OZONE: HEMATOLOGY AND SERUM CHEMISTR Y 

Ozone, Ozone, Length of 

pg/m' ppm exposure Observed effecqsl Species Reference 

1960 1 30 min Increased resistance to erythrocyte Mice Mizoguchi et a1 13 e 

hemolysis. 

1960 1 30 min Increased resistance to erythrocyte Mice Christensen and Giese 33 

hemolysis. 

1686 0.86 8 hr/day Increased infestation and mortality Mice Schlipkoter and Bruch 182 

5 days/week after infection with P berghei. 

6 months Increased acid resistance of 

erythrocytes. 

1568 0.8 Continuous Increased lysozyme activity by day 3 Rats Chow et a1. 28 

29 days 

980 0.5 Continuous Increased hemolysis of erythrocytes Rats Menzel et a1 13 z 

23 days of animals depleted of vitamin E No 

such change when rats received 

vitamin E supplements. 

980 0.5 8 hr/day No change in level of GSH or activities Monkeys, Chow et al 30 

7 days of GSH peroxidase, GSH reductase, rats 

or G-6-PD in erythrocytes. 

784 0.4 6 hr/day Decreased serum albumin concen- Rabbits P'an and Jegier 1 fi4 

1

5 days/week tration; increased concentration of 

10 months a and y globulins, not much change in 

,6 globulin; no change tn total serum 

proteins. 

784 0.4 6 hr/day No change fn serum trypsin Inhibttor Rabbits P'an and Jegier' 65 

5 days/week capacity. 

6 months 

784 04 6 hr/day Increase in serum protein esterase. Rabbits Jegier 10 

5 days/week 

10 months 

784 0.4 10 months Increase in serum protein esterase Rabbits P'an and Jegier 166 

392 0.2 8 hr/day Increase in serum glutamic pyruvic Murine Veninga 201 

5 days/week transaminase, and hepatic ascorbic 

3 weeks acid. No change in blood catalase 

392 0.2 60 min Small decrease In total blood Rabbits Veninga 2°2 

serotinin. 

392 0.2 2 hr Binucleated lymphocytes in Murine Veningaz°z 

blood doubled in number 

after exposure. 

392 0.2 5 hr Circulating blood lymphocytes had Hamsters Zelac et al z"z'B 

chromosome breaks up to 2 weeks 

post 03. Additive effect with radiation 

exposure. 

294 0.15 5 hr No increase in chromosomal aber- Mice, Gooch et a1. 92 

451 0.23 5 hr rations. hamsters 

1960 1.00 2 hr 

110 0056 93 days Decrease in whole blood Rats Eglrte 53 

cholinesterase, which returned to 

normal 12 days after exposure 

ceased. 

173 
TABLE 8-7. EXTRAPULMONARY EFFECTS OF OZONE: CENTRAL NERVOUS SYSTEM AND BEHAVIOR 

Ozone, Ozone, Length of 

pg/m3 ppm exposure Observed effect(s) Species Reference 

1960 1 Continuous Reduction in voluntary activity Rats Fletcher et al.se 

7 days 

1176 0.6 30 min Avoidance response to 03. Mice Peterson et a1. 167 

980- 0.5-1 .1 hr Depression of evoked response to Rats Xintaras et a1.210 

1960 flash 

980 0.5 30 min Elevation of simple and choice re- Subhuman Reynolds and Chaffee 12 

active time. primates 

118 006 — Depression of gross motor activity Rats Konigsberg and Bachman 13 

as 03 concentration increased. 

110 0 056 Continuous No behavior change No change in Rats Eglite53 

93 days chronaxial ratios in muscles 

TABLE 8-8. EXTRAPULMONARY EFFECTS OF OZONE: MORPHOLOGY 

Ozone, Ozone, Length of 

Ng/m' ppm exposure Observed effect(s) Species Reference 

1470 0.75 4-8 hr Morphological alterations of Rabbits Atwal and Wilson 7 

parathyroid gland These changes 

reverted to normal 66 hr after 

exposure. 

392 0.2 5 hr/day Structural changes in cell mem- Mice Brinkman et al 20 

3 weeks branes and nuclei of myocardial 

muscle fibers that were reversible 

about 1 month following exposure. 

TABLE 8-9. EXTRAPULMONARY EFFECTS OF OZONE: MISCELLANEOUS 

Ozone, 

Ng/m' 

Ozone, 

ppm 

Length of 

exposure Observed effect(s) Species Reference 

1960 1 3 hr/day After 2 or 3 days of exposure, mice Mice Gardner et a1. 78 

up to 7 slept longer after injections of 

days sodium pentobarbital. 

1960 1 90 min No change in liver cytochrome P 450 Rabbits Goldstein et a1. 88 

level 

1960 1 7- to 24- In brain tissue, decreased COMT and Dogs Trams et a1. 199 

hr/day altered MAO activity, no lipid 

18 months peroxidation and no change in 

catecholamine levels, 5- 

nucleotidase, acetylcholinesterase, 

or ATPase 

1568 0.8 5 days/week Lower titratable acidity in urine Rats Hathaway and Terril1 98 

18 weeks on days 91, 98 and 112, and a higher 

pH on days 98 and 112 No change in 

urinary creatinine, creatine, uric 

acid/creatinine or amino acid 

nitrogen/creatinine. 

490 0.25 2 hr No differences in gastric secreto- Rats Roth and Tansy 178 

motor activity 

392 02 7 hr/day Increased incidence of blepharo- Mice Veninga201 

5_.iys/week phimosis and unlimited incisor 

during growth 

gestation and 

3 weeks 

after birth 

110 0 056 Continuous Increased levels of urinary 17- Rats Eglite53 

93 days ketosteroids that remained elevated 

after exposure. Decreased ascorbic 

acid content of adrenal gland, which 

returned to normal levels 15 days 

after exposure ceased. 

174 
recovery period, showed no significant changes in 

collagen:protein ratios. However, prolyl 

hydroxylase (thought to be the rate-limiting 

enzyme in collagen synthesis) levels were elevated 

(p < 0.05) most in the lungs of animals exposed to 

irradiated exhaust (Group 3). 158 

Emik et a1.56 exposed various species of 

laboratory animals (mice, rats, and rabbits) to 

ambient California air for 2.5 years. The average 

ambient concentrations were 0.057 ppm oxidant, 

1.7 ppm CO3 2.4 ppm hydrocarbons (as carbon), 

0.019 ppm NO2, 0.015 ppm NO, and 4.2 ppb PAN. 

The following results were obtained: Reduced 

pulmonary alkaline phosphatase in rats, reduced 

serum glutamic oxaloacetic transaminase in 

rabbits, increased pneumonitis in mice, increased 

mortality in male mice but not in female mice, 

reduced body weights in mice, and decreased 

running activity of male mice. When aging guinea 

pigs (24 months old) that lived in smog for 2 years 

were allowed to recover for 6 weeks in clean, 

filtered air and then exposed to 980 Pg/m3 (0.5 

ppm) ozone for 10 min, they had a smaller increase 

in lung resistance following ozone exposure than 

animals that lived in clean air before the same 

ozone exposure. The authors suggest that a 

possible adaptation occurred. Pulmonary tumors 

were found in the lungs of some mice, but there 

was no significant induction of lung adenomas in 

the two strains of mice exposed to ambient, smogcontaining air. They state further that the 

exposure was probably near the threshold of 

effect, and therefore measurement of differences 

induced by smog was difficult. 

The spontaneous activity of mice was reduced 

when the mice were exposed to smog ozone + 

gasoline vapor for 24 hr. Decreases (p <0.05) were 

observed at 980 Ng/m3 (0.05 ppm) ozone. A 

simultaneous measurement of 1.69 ppm oxidant 

was made. As the concentrations of ozone and 

oxidant were increased (3650Ng/m 3 , or 1.86 ppm 

ozone and 6.26 ppm oxidant), greater decreases in 

spontaneous activity were observed. 18 Emik and 

Plata 55 made a similar study of mice exposed 

continuously either to filtered air or to ambient air 

(oxidant from 0.062 to 0.239 ppm; NO2 from 0.03 

to 0.07 ppm; total hydrocarbons from 2.7 to 4.4 

ppm) for 13 months. Animals exposed to the 

ambient air had decreased running activity 

compared to controls over the course of the study. 

The differences in activity were strongly related to 

oxidant for weekly intervals. High temperature and 

age were related to decreased activity in both 

groups. 

Kotin and Thomas 16 exposed mice of both sexes 

continuously for 19 weeks to smog (formed by 

reacting gasoline with ozone, average of 1.25 ppm 

oxidant); natural urban atmosphere (fluctuated, 

highest reading recorded was 0.4 ppm oxidant); or 

clean, filtered air. Females held in the smog 

chamber had a decrease in conception rate (p = 

0.02). The significant difference in litter rate in the 

smog-exposed animals was primarily attributed to 

an effect on the females. The survival rate of the 

newborns was also decreased (p <0.01) when the 

parents were exposed to smog. Those animals in 

the smog chamber also had lower (p < 0.05) 

average litter sizes. 

TABLE 8-10. ATMOSPHERIC MEAN CONCENTRATIONS AND THEIR STANDARD DEVIATIONS ADMINISTERED 

FROM 8 a.m. TO MIDNIGHT EACH DAY 

Group Atmosphere CO HC (as CH,) NO z 

Pollutant,mg/m' 

NO O. (as Oal soz H zSO a 

1 Control alr — — 

2 Nonlrradlated 112 1±1 1 5 18 0±2.9 0 09±0 04 1 78±0 52 — 

auto exhaust 

3 Irradlated auto 108 6±22 5 15 6±4 0 1 77±0 68 0 23±0 36 0 39±0 18 — — 

exhaust 

4 S02 + H2SO4 — — 1 10±0 57 0.09±0.04 

5 Nonlrradlated 1 13.1 ±15 9 17 9±2 8 0.09±0 06 1 86±50 54 — 1 27±0 61 0 09±0.04 

auto exhaust 

+ SOz + H2SO4 

6 Irradlated auto 109 0±22.8 15 6±3 9 1 68±0 68 0.23±0.36 0 39±0 16 1 10±0 56 0 1 1±0 04 

exhaust + S02 

+ H2SOe 

7 Nltrogenoxldes — — 121±022 0 31±0 08 — — — 

8 N Itrogen oxldes 0 27±0 62 2 05±0.26 — — — 

175 
Nakajima et a1. 152 studied histopathologic 

changes in the lungs of mice that were exposed to 

irradiated auto exhaust and oxidant-fortified 

exhaust-gas mixtures for 2 to 3 hr/day, 5 

days/week for a month. Histopathologic changes 

resembling tracheitis and bronchial pneumonia 

were observed in mice exposed to atmospheres 

containing oxidant at 0.1 to 0.5 ppm. In those 

exposed to atmospheres containing 0.1 to 0.15 

ppm, the changes were minimal, the main finding 

being irregular arrangement of the epithelial cells 

of the relatively thick bronchioles. 

Summary 

Animal toxicologlcal studies have investigated 

the biological response of laboratory animals to 

sample atmospheres of photochemical reaction 

mixtures. Long-term exposure of various species 

of animalsto ambientCalifornia atmospheres have 

produced changes In pulmonary functional 

measurements in the guinea pig (980 /jg/m 3 , or 

0.5 ppm) and a number of biochemical and 

pathological effects in mice, rats, and rabbits. 

Exposure to irradiated auto exhaust containing 

oxldant levels ranging from 0.2 to 1.0 ppm also 

produced numerous changes in experimental 

animals. In mice, an increase in susceptibility to 

infection and a decrease in spontaneous running 

activity, infant survival rate, and fertility were 

reported in exhaust-exposed animals. In guinea 

pigs, the following changes were observed: 

Increased tidal volume, increased minute volume, 

increased flow resistance, and a decreased 

frequency of breathing after short-term exposure 

to irradiated auto exhaust. Dogs exhibited several 

alterations in normal pulmonary function 

capabilities. 

Note that experimental exposure to irradiated 

auto exhaust usually involves variable concentrations of carbon monoxide, hydrocarbons, 

and nitrogen oxides, as well as oxidants. The 

studies of the effects of oxidants on animals are 

summarized in tabular form in Table 8-11. 

TABLE 8-11. EFFECTS OF OXIDANTS ON ANIMALS 

Pollutant 

concentrauon 

Length of 

eaposure Observed effect(s) Species Reference 

03 (980 Ng/m 3 , 24 hr Decreased spontaneous running Mice Boche and Qullllgan'a 

0 5 ppm) and activlty 

gasollne vapor 

(oxldant 1 69 ppm) 

03 and gasollne Contlnuous Decreased conceptlon rate, Iltter Mlce Kotln and Thomas 16 

(oxldant 1 25 ppm) 19 weeks rate, and newborn survlval. 

Irradlated auto 2-3 hr/day Tracheltls and bronchlal pneumonla Mlce Nakajima et a1 152 

exhaust (oxldant, 5 days/week for 

0 1-0 5 ppm) 1 month 

Oxldant, 0 062- Contlnuous Decreased spontaneous running Mlce Emlk and Plata 55 

0 239 ppm, NOz 13 months activlty 

0 03-0 07 ppm, 

hydrocarbons, 

2 7-4 4 ppm 

Oxldant, 0 057 Contlnuous Reduced pulmonary alkallne phos- Mlce, Emlk et al ss 

ppm, CO3 1 7 2 5 years phatase (rats), reduced serum rats, 

ppm, hydro- glutamlc oxaloacetic transaminase rabblts 

carbons, 2 4 ppm, (rabblts), Increased pneumonitls 

NO2, 0019 ppm, (mlce), Increased mortallty (male 

NO, 0 015 ppm, mlce), reduced body welghts 

PAN, 4 2 ppb (mlce), decreased running activlty 

(male mlce), no slgnlflcant Inductlon 

of lung adenomas (mlce) 

7 exposure groups 16 hr/day, No changes In cardlovascular Beagles Vaughan et al.zoo 

(see Table 8-10), 7 days/weeks parameters attrlbutable to Lewls et a1 120 

varlous for 68 months pollutants, alteratlons In pulmonary 

mlxtures of CO, functlon 

hydrocarbons, NO2, 

NO, Os, S02, H2SO4, 

and Irradlated and 

nonlrradlated auto 

exhaust 

176 
EFFECTS OF PEROXYACETYLNITRATE ON 

EXPERIMENTAL ANIMALS 

Experimental Data 

To determine the effects of PAN on acute 

respiratory infections, Thomas et a1. 197 exposed 

mice to PAN for 2 or 3 hr and then to aerosols of 

Streptococcus pyogenes (Group C). The data 

indicate that a 3-hr exposure to 26,000Ng/m 3 (5.2 

ppm) PAN resulted in an increased (p < 0.05) 

incidence of fatal pulmonary infection. 

Campbell et a1. 24 exposed mice to PAN, 485,000 

to 725,000 /~g/m3 (97 to 145 ppm) as measured at 

the chamber outlet, for 2 hr at 80°F (270C). The 

studies demonstrated that most mice exposed to 

550,000Ng/m3 (1 10 ppm) or more PAN died within 

a month, and mice exposed to higher 

concentrations died earlier. Median lethal 

exposures characteristically produced a delayed 

mortality pattern, with most deaths occurring 

during the second and third weeks after exposure. 

Mortality was greater among older than among 

younger mice. It was greater at higher 

temperatures, but was not influenced appreciably 

by changes in relative humidity. 

Dungworth et a1. 51 exposed mice to 75,000 

μg/m3 (15 F pm) PAN for 6 hr/day, 5 days/weekfor 

26 weeks. Exposed animals showed a 28;percent 

reduction i,, i body weight (p < 0.001) and a 26- 

percent inc , ease in lung=heart weight (p <0.001). 

Histologic,il examination revealed chronic 

hyperplast ~ : bronchitis and proliferative peribronchiolitis. Bronchi developed various degrees 

of epithE'ial hyperplasia, and sometimes 

metaplasia. Approximately 50 percent of the lungs 

had foci of •;quamous metaplasia in the trachea or 

major bronchi. The most noteworthy feature of the 

hyperplastic bronchial response was the tendency 

for acinar structures to form within the bronchial 

walls. In the bronchial epithelium, cilia were 

frequently absent, and there was a severe 

reduction in mucus-secreting cells. There was no 

evidence of the accumulation of perivascular and 

peribronchiolar lymphocytes and plasma cells. The 

most conspicuous bronchiolar alteration was 

bronchiolectasis. Peribronchiolar epithelial 

hyperplasia or metaplasia was often accompanied 

by cellular accumulations, principally of 

monocytes. Some alveoli had increased numbers 

of Type 2 cells and nuclei (probably of Type 1 cells). 

There was also some dilatation of alveolar ducts 

and breakdown of walls in peribronchiolar regions, 

usually in association with epithelial hyperplasia. 

Summary 

Short-term exposures to PAN in excess of 

26,000 Ng/m 3 (5.2 ppm) have been found to result 

in increased mortality of mice challenged with 

aerosols of viable bacteria.Longer-term exposures 

to 75,000 Ng/m3 (15 ppm) resulted in pulmonary 

morphological alterations. 

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25 703, 1969. 

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37T329-334, 1976 

165. P'an, A Y S, and Z Jegier The serum trypsin inhibitor 

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23 215-219, 1971 

166 P'an, A. Y. S., and Z. Jegier Trypsin protein esterase in 

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Environ. Health 24 233-236, 1972 

167 Peterson, D.C., and H. L Andrews The role of ozone in 

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169 Previero, A, A Signor, and S Bezzi Tryptophan 

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204 687-688, 1964 

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171 Pryor, W A., J.P Stanley, E. Blair, and G B. Cullen 

Autoxidation of polyunsaturated fatty acids Part I. Effect 

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210, 1976 

172 Reynolds, R W, and R R Chaffee Studies on the 

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23.142-148, 1971. 

177 Ross, B K, M P Hlastala, and R Frank On the lack of 

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Environ Health (in press) 

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J Air Pollut Control Assoc 22 706-709, 1972 

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180. Sato, S, M Kawakami, S Maeda, and T Takishima 

Scanning electron microscopy of the lungs of vitamin-Edeficient rats exposed to low concentration of ozone 

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181 Scheel, L D, 0 J Dobrogorski, J T Mountain, J L 

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182 Schlipkoter, H, and J Bruch Functional and 

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184 Schwartz, L. W., D. L Dungworth, M G Mustafa, B K. 

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185 Scott, D B. M, and E C Lesher. Effect of ozone on 

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187 Seto, K, M. Kawakami, M Takeshima, M Kon, K. 

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Seibutsugaku 87 57-60, 1973 

188 Shakman, R Nutritional influences on the toxicity of 

environmental pollutants Arch Environ Health 

28105-113, 1974. 

189 Skillen, R G Progress Report—Research Contract No 

50. State of California, Department of Public Health, 

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190 Stephens, R J, M F Sloan, M J Evans, and G. 

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23, 1974 

191 Stephens, R J, M F Sloan, M J Evans, and G 

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Amer J Pathol 74 31-58, 1973 

192 Stephens, R J, M. F Sloan, and D G Groth Effectsof 

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Environ Health Persp 16 178-179, 1976. 

193 Stokinger, H E Effects of air pollution on animals. /n. Air 

Pollution Volume I A C Stern, ed. Academic Press, 

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194 Stokinger, H E Ozone toxicology A Review of research 

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195 Stokinger, H E., W D Wagner, and 0. L J Dobrogorski. 

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196 Teige, B, T T McManus, and J. B. Mudd Reaction of 

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12153-171, 1974 

197 Thomas, G, J D Fenters, and R. Ehrlich Effect of 

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Bacterial Infection Quarterly Report IITRI Report 

L6075-12, IIT Research Institute, Chicago, III , February 

1977 

198 Thompson, G E Experimental acute pulmonary edema' 

in the rat Effect of Bordetella pertussis vaccine on 

ozone mortality Arch Environ Health 23 1 54-1 60, 

1971 

199 Trams, E G, C J Lauter, E A B Brown, and 0 Young 

Cerebral cortical metabolism after chronic exposure to 

03 Arch Environ Health 24 1 53-1 59, 1972 

200 Vaughan, T R, Jr, , L F Jennelle, and T R Lewis Longterm exposure to low levels of air pollutants. Effects on 

pulmonary function inthebeagle Arch Environ Health 

19 45-50, 1969 

201 Veninga, T S Ozone induced alterations in murine 

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Air Congress, Washington, D C, December 6-11, 1970 

Paper MB-15E 

202 Veninga, T Toxicity of ozone in comparison with 

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1967 

203 Warshauer, D, E Goldstein, P D Hoeprich, and W 

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204. Watanabe, S., R Frank, and E Yokoyama. Acute effects 

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205. Wayne, L. G., and L A. Chambers. Biological effects of 

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207 Weissbecker, L., R. D Carpenter, P. C. Luchsinger, and 

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1969. 

208 Werthamen, S, P D Penha, and L. Amaral. Pulmonary 

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209 White, A, P. Handler, and E. L Smith, eds. Principals of 

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4 325-342. 1971 

183 
9. CLINICAL APPRAISAL OF THE EFFECTS OF OXIDANTS 

OCCUPATIONAL AND ACCIDENTAL EXPOSURES TO OZONE 

Schonbein, 55 the discoverer of ozone, was 

probably the first person occupationally exposed to 

this gas. His description in 1851 of subjective 

symptoms and basic characteristics of ozone was 

very complete. Dadlez" in 1928 found that 2940 

Ng/m 3 (1.5 ppm) ozone rendered the atmosphere 

intolerable. He cites an investigation by D'Arsonval 

who found that 780 pg/m 3 (0.4 ppm) ozone in the 

atmosphere produced symptoms of discomfort and 

irritation within about 30 min. after exposure 

began. In 1931, Flury and Zernik 14 described the 

following symptoms as being characteristic of 

increasing exposure to ozone: 920 Ng/m3 (0.47 

ppm) causes distinct irritation of mucous 

membranes, and 1840 /jg/m 3 (0.94 ppm) causes 

sleepiness in 1 hr; at higher concentrations, ozone 

causes increased pulse rate, sleepiness, and 

prolonged headache. Ozone exposure may also 

result in dyspnea (difficult breathing) and 

pulmonary edema. 

Kleinfeld et a1. 44 and Kleinfeld 43 reported several 

cases of severe ozone intoxication in welders using 

a consumable electrode technique, which was 

new at that time (1957). Three plants were 

investigated, and in all cases, the ozone 

concentration was monitored at the breathing 

zone of the consumable electrode machine. In the 

first plant, an ozone concentration of 490 /jg/m 3 

(0.25 ppm) was found. The workers had no 

complaints, and clinical findings were 

noncontributory. In the second plant, the ozone 

concentration ranged from 590 to 1570/jg/m 3 (0.3 

to 0.8 ppm). Two of the four welders complained of 

chest constriction and throat irritation. Clinical 

examination disclosed no abnormalities. In the 

third welding plant, the ozone concentration was 

17,990 Ng/m 3 (9.2 ppm). Also, a trichloroethylene 

degreaser was located about 50 ft from the 

welding area. Concentrations of nickel carbonyl 

and nitrogen oxides were found to be negligible, 

and tests for phosgene in the welding area were 

negative. The authors gave case histories of three 

workers (although there were others) who also 

complained of severe headaches, throat irritation, 

and lassitude. One of the cited patients developed 

severe dyspnea and substernal oppression and, on 

admission to a hospital, was found to be in 

pulmonary edema. Chest X-rays showed diffuse 

peribronchial infiltration consistent with 

peribronchial pneumonia. The patient made a slow 

recovery over a 2-week period but still complained 

of fatigue and exertional dyspnea after 9 months. 

The other two workers had similar but less severe 

symptoms. 

Challen et a1. 10 performed a similar clinical and 

environmental survey. Ozone concentrations of 

1570 to 3330 Ng/m 3 (0.8 to 1.7 ppm) were found. 

Eleven of 14 workers who were directly involved in 

welding complained of respiratory symptoms. No 

further symptoms were reported when ozone 

concentrations were reduced to 390 Ng/m 3 (0.2 

ppm). The results of this study, however, were 

complicated by the fact that concentrations of 

trichloroethylene upto 1275 Ng/m 3 (0.638 ppm) 

were also present. 

In 1965, Kelly and Gi11 38 reported a case of 

severe,'accidental ozone poisoning in which the 

worker could have been exposed to concentrations 

as high as 21,950 Ng/m 3 (11.2 ppm) for up to 120 

min. The symptoms he developed were so severe 

that he almost lost consciousness. He perspired, 

coughed continuously, and had a decrease in blood 

pressure that was accompanied by a weak and 

accelerated pulse. Administration of oxygen 

relieved his symptoms rather quickly, and 48 hr 

after the incident, he was completely 

asymptomatic. 

Young et a1. 61 made the first study of pulmonary 

function changes in workers exposed to ozone. 

They studied seven men, all smokers, who were 

engaged in argon-shielded electric arc welding. 

The concentration of ozone in the welding shop 

was estimated by the rubber cracking technique 

and found to be 390 to 590 Ng/m 3 (0.2 to 0.3 ppm). 

184 
The following measurements of pulmonary 

function were made: Vital capacity (VC), functional 

residual capacity (FRC), maximal midexpiratory 

ftow rate (FEF 25 to 75), 0.75-second forced 

expiratory volume (FEV075), and carbon monoxide 

diffusing capacity (DLco) at rest and at exercise. No 

convincing evidence was found that functional 

impairment developed in association with longterm exposu re to 390 to 590 Ng/ m 3 (0.2 to 0.3 ppm) 

ozone in these seven smokers. 

The available data on occupational exposures of 

humans to ozone are summarized in Table 

10,11 ,14,38,43,44,61 

9-1. 

TABLE 9-1. SUMMARY OF AVAILABLE DATA ON OCCUPATIONAL EXPOSURE OF HUMANS TO OZONE'o,ii,t4,3e,43,44,s 

Ozone, 

pg/fn' 

Ozone, 

ppm Sublective complaints 

Clinical findings 

attributed to ozone 

Measurements 

of pulmonary 

function Other comments Reference 

490 0.25 None None None Klelnfeld 

et al 44 

590- 0 3- Chest constrlctlon None None Klelnfeld 

1570 0.8 and throat Irritatlon et al 44 

In 2 to 4 subjects. 

17,990 9.2 Severe headaches, None Negllglble nlckel Klelnfeld 

(peak (peak throat Irritatlon, carbonyl and et al 44 

concen- concen- and lassltude In oxldes of nitro- Klelnfeld43 

tration) tration) 7 or 8 subjects. gen. Trlchloroethylene deCough, choking, By X-ray, molted None greaser located 

dyspnea, and densltles In both 50 ft from 

substernal oppres- lungs, clearing welding area 

slon In 3 of 8 after 9 days. Tests for 

subjects phosgene, negative 

Very severe head- -Severe pulmonary None 

ache. dyspnea. edema. By X-ray 

Substernal oppres- perlbronchlal Inslon in 1 of 8 filtratlon conslssubjects. tent wlth perlbronchlal pneumonla. 

390 0 2 None None Challen 

et a1 10 

1570- 0.8- Dry mouth and throat, None None Concentratlon Challen 

3330 1 7 Irritatlon of nose of trlchloro- et a1. 10 

and eyes, detectlon ethylene up to 238 

of disagreeable smell ppm found 

In 11 of 14 subjects. 

390- 0.2- Detectlon of Irritating None VC decreased AII decreases In Young etal 

590 0.3 odor, soreness of eyes In 3 of 7 pulmonary funcand dryness of mouth, subjects FRC tion measurements 

throat, and trachea In 1 decreased In 2 of were small. AII 

of 7 subjects. 7 subjects DLco subjects were 

decreased In 1 of smokers 

7 subjects 

780 0.4 Discomfort and Irrl- None None Dadlez" 

tatlon In about 30 min (D'Arsonval) 

920 0.47 Dlstlnct Irrltatlon of None None Flury and 

mucous membranes Zernik 14 

1,840 094 Coughing, Irrltatlon, None None Flury and 

and exhaustlon, wlthln Zernik 14 

1'/2 hr. 

5,900 30 Sleepiness wlthln None None Flury and 

1 hr. Zernik 14 

21,950 11 2 Profuse persplratlon, None None Severe symptoms Kelly and 

continual coughing; almost caused G111 38 

decreased blood pres- subject to lose 

stare; weak, accelerated consclousness 

pulse. 

fEM 
CONTROLLED STUDIES OF HUMAN HEALTH 

EFFECTS 

Studies conducted before 1970 may be 

summarized as follows. 

Under experimental conditions, repeated 

exposure of humans to ozone produced the 

following effects: 

1. No apparent effects on pulmonaryfunction 

were observed at concentrations up to 390 

pg/m 3(0.2 ppm)for 3 hr/day, 6 days/ week 

for 12 weeks.s 

2. The threshold level at which nasal and 

throat irritation will occur appears to be 

about 590 pg/m 3(0.3 ppm).s' 

3. Concentrations of 980 Ng/m 3(0.5 ppm) 

have caused a 20-percent decrease in the 

1-sec forced expiratory volume (FEV,) 

observed after 8 weeks of intermittent 

exposure (3 hr/day, 6 days/week); this 

change returned to normal during the postexposure period of 6 weeks.s 

In Table 9-2 s,zo,zs,s,,ss,so the results of 

experimental appraisal of short-term exposures to 

ozone are shown as follows. 

1. Some subjects have shown small but 

statistically significant increases in airway 

resistanceafterl hrof(presumablyresting) 

exposure to 200 /tg/m 3(0.10 ppm) ozone. 20 

However, the significance of this finding is 

unclear, since increases in resistance were 

small, and since the same subjects showed 

smaller, nonsignificant increases in 

resistance after exposure to 780 Ng/m 3 

(0.4 ppm) ozone than they had shown after 

exposure to 200 /ag/m 3(0.1 ppm). 

2. Concentrations of 200 to 780 Ng/m3(0.1 to 

0.4 ppm) for 1 hr have been shown to 

increase airway resistance (Raw) slightly, 

but adequate information for this 

concentration range is lacking. 20 

3. Exposure to a concentration of 1960Ng/m 3 

(1.0 ppm) for periods of 1 to 2 hr produced 

changes in pulmonary function. These 

were increased airway resistance, 

decreased vital capacity, decreased carbon 

monoxide diffusing capacity, and 

decreased forced expiratory volume. 20 

4. One individual was unable to tolerate 

concentrations of 1960 to 5880 Ng/m 3(1.0 

to 3.0 ppm) over a period of about 2 hr. 

Extreme fatigue and lack of coordination 

were experienced. 25 

5. Concentrations of about 17,640Ng/m 3(9.0 

ppm) produced severe pulmonary edema 

and possible acute bronchiolitis. 36 

Details of selected controlled human studies 

reported after 1970 are discussed below. 

Bates et a{.3° measured significant changes in 

lung function: A decrease (a) in maximal flow rate 

at 50 percent of the vital capacity (FEF 50 percent) 

and (b) in maximal transpulmonary pressure 

(PstTLC); and an increase in total pulmonary 

resistance (RL) in 10 normal male subjects aged 23 

to 53 years (including two smokers) exposed to 

pure ozone at 1470 /ag/m 3(0.75 ppm) for 2 hr. Two 

of the three subjects who exercised intermittently 

at twice the resting volume showed accentuated 

effects. In a separate study by Hazucha et a1. 35on 

the effects of short-term exposure, significant 

decreases in forced vital capacity (FVC), maximal 

midexpiratory flow rates, FEF 25 to 75 percent, 

FEV,, and FEF 50 percent, and increases in closing 

capacity (CC) and residual volume (RV) were found 

in 12 normal young males (including six smokers) 

exposed to pure ozone at 1470 and 730 Ng/m 3 

(0.75 and 0.37 ppm) for 2 hr during alternating rest 

and exercise periods. The higher concentration 

affected smokers more than nonsmokers, whereas 

at the lower concentration, the reverse wasfound. 

In these two studies, most subjects complained of 

cough, chesttightness, and substernal soreness. A 

few also had pharyngitis, dyspnea, and wheezing. 

In another study, Z ' 32 all mean dynamic lung 

function parameters in 10 nonsmokers and 10 

smokers showed a progressive decrease with 

continuation of exposure, returning close to preexposure levels after 2 hr of recovery(Figure 9-1). 32 

Average minute ventilation changed only slightly 

during the exposure, although the frequency of 

breathing increased, and the tidal volume 

decreased steadily with the duration of exposure 

(Figure 9-2). 

Bates and Hazucha 2and Hazucha and Bates 33 

reported a marked decrease in pulmonaryfunction 

among healthy subjects performing light exercise 

while exposed to 730 μg/m3(0.37 ppm) of ozone 

and 1000 ug/m 3(0.37 ppm) of sulfur dioxide for 2 

hr. Throat irritation, coughing, and chest pain were 

also experienced. These effects, as well as the 

decrease in lung function, occurred after exposure 

to the mixture for periods as short as one-half to 1 

hr and persisted for several hours aftertermination 

of the exposure. Ozone concentrations were 

measured by a Mast meter with CrOs scrubber for 

SOz removal, and SOz levels were monitored with 

a conductimetric analyzer. To investigate further 

186 
the possible interactive effects of S02 + 03 and the 

mechanism of interaction, Bell et a1. 5 initiated a 

series of controlled human-exposure studies. The 

studies of Bell et al. suggest less severe acute 

toxicity of mixtures of (730 Ng/m3 ) 0.37 ppm ozone 

and (1000 Ng/m 3 ) 0.37 ppm S02 than Bates and 

Hazucha had previously observed. There are 

several possible explanations: (1) The Los Angeles 

residents had undergone biological adaptation to 

chronlc pollutant exposure; (2) the Montreal 

subjects used in the experiment were not as 

reactive to the S02 + 03 mixture when tested in Los 

Angeles as when tested in Montreal, possibly 

because of significantly higher concentrations of 

the sulfur compounds in the respirable aerosols 

that can form in the Montreal chamber. The 

background air in the Rancho Los Amigos studies 

was highly purified, whereas the sulfur aerosol 

concentration in the Montreal chamber during the 

mixed-gas exposures was similar to 2-hr sulfate 

aerosol concentrations during the worst pollution 

episodes in urban areas. The effects observed in 

the Montreal chamber probably more nearly 

parallel the health effects that might result during 

TABLE 9-2. SUMMARY OF DATA ON HUMAN EXNtRIMENTAL EXPOSURE TO OZONE BEFORE 19706,20.25,31,36,60 

Ozone, Ozone, Length of No and sex Subjective Measurements of Other 

Ng/m' ppm exposure of subjects complaints pulmonary function comments Reference 

9,800- 5-10 Not avallable 3 male Drowslness, 

19,600 headache 

2,940- 1 5-2 2 hr 1 male CNS depresslon, 

3,920 lack of coordlnatlon, chest paln, 

cough for 2 days, 

tlredness for 

2 weeks 

390 0 2 3 hr/day 6 male None 

6 days/week 

for 12 weeks 

980 0 5 3 hr/day 6 male No Irrltating 

6 days/week symptoms, but 

for 12 weeks could detect 

ozone by smell 

1,180- 0 6-0 8 2 hr 10 male Substernal sore1,570 1 female ness and tracheal 

Irrltatlon 6 to 12 hr 

after exposure, 

dlsappearing wlthIn 12 to 24 hr In 

10/11 subjects 

None 

VC Decreased 13%, 

returned to normal 

In 22 hr FEVso. 

Decreased 16 8% 

after 22 hr MBC 

Decreased very 

sllghtly a 

VC No change 

FEV,o No change 

VC Sllght but not 

slgnlflcant decrease toward end 

of 12 weeks 

Returned to normal 

wlthln 6 weeks after 

exposure 

DLco Meandecrease 

of 25%(11/11 

subjects) VC Mean 

decrease of 104'0, 

whlch was slgnlflcant (10/10 

subjects) FEVo 7s x 

40 Mean decrease 

of 10%, whlch was 

slgnlflcant 

(10/10 subjects). 

FEF 25-75 Mean 

decrease of 15%, 

whlch was not slgnlflcant Mlxing 

efflclency No 

change (2/2 subjects) 

Alrway reslstance 

Sllght Increase, but 

wlthln normal Ilmlts 

Dynamlc compllance No change 

(2/2 subjects) 

Measurement of Os Jordan and 

probably Inaccurate Carlson 36 

Grlswold 

et al 25 

0 66 upper resplr- Bennetfi 

atory Infectlons/ 

person In 12 weeks, 

Cf control group 

had 0 95 In the 

same perlod. 0 80 

upper resplratory 

Infectlons/person 

In 12 weeks 

0 80 upper resplratory Infectlons/ 

person In 12 weeks 

Young etal 60 

Young etal 60 

187 
TABLE 9-2. (cont'd). SUMMARY OF DATA ON HUMAN EXPERIMENTAL EXPOSURE TO OZONE BEFORE 

1 9706,20,25,31,36,60 

Ozone, Ozone, Length of No and sex Subtective Measurements of Other 

pg/m' ppm exposure of subjects complaints pulmonary function comments Reference 

Up to Up to 10 to 30 11 Headache, short- VC Mean decrease Only 5/11 subjects Hallett 31 

7,800 40 min ness of breath, of 16.5% (4/8 tolerated dose for 

lasting more than subjects showed full 30 min 

1 hr decrease > 10%) Wlde varlatlons In 

FEV, o• Mean DLco. 

decrease of 20% 

(5/8 subjects 

showed decrease 

> 10%. FEF 25-75: 

Mean decrease of 

10.5% (5/6 subjects 

showed a decrease) 

MBC Mean 

decrease of 12% 

(5/8 subjects 

showed a decrease) 

DLco. Decrease of 20 

to 50% In 7/11 

subjects; Increase 

of 10% to 50% In 

4/11 subjects. 

200 01 1 hr 4 male Alrway reslstance One subject Goldsmlth 

Mean Increase of had history of and Nadel 20 

3.3% at 0 hr after asthma and exexposure (1/4 sub- perlenced hejects showed an In- moptysls 2 days 

crease of 45%). after 1 ppm. 

780 04 1 hr 4 male Odor Alrway resfstance Goldsmlth 

Mean Increase of and Nadel 20 

3.5% at 0 hr after 

exposure; (1 /4 

subjects showed an 

Increase of 60%), 

mean Increase of 

12 5% 1 hr after 

exposure). 

1,180 0 6 1 hr 4 male Odor Alrway resistance 

Mean Increase of 

5 8% at 0 hr after 

exposure (1/4 

subjects showed an 

Increase of 75%); 

mean Increase of 

5% 1 hr after 

exposure. 

1,960 1 0 1 hr 4 male Throat Irrltatlon Alrway reslstance 

and cough Mean Increase of 

19 3% at 0 hr after 

exposure (3/4 

subjects showed an 

an Increase of > 

20%); mean 

Increase of 5% 1 hr 

after exposure 

'MBC = maximum breathing capacity 

smog episodes in regions with high oxidant and 

sulfur pollution than do the effects observed in the 

Rancho Los Amigos chamber. 

Studies by Hackney et al 26,28,30 used basically 

the same rest or intermittent exercise protocol as 

that developed in the Montreal laboratory. To 

simulate summer exposure in the Los Angeles 

southern coastal basin, the additional stress of 

heat (31 0C, or 88°F at 35 percent relative humidity) 

was included, and the same subjects were exposed 

several times to either ozone or mixtures of ozone 

with other pollutants. Careful attention was given 

to environmental control, pollutant monitoring and 

generation, and subject selection. Four male 

188 
subjects, aged 36 to 49 years and judged by 

subjective criteria to have normally reactive 

airways (i.e., with no history of cough, chest 

discomfort, or wheezing), completed this protocol. 

As assessed by clinical response and measures of 

respiratory, cardiac, and metabolic functional 

change, no obvious effects were noted after 

exposure for 4 to 5 hr to 980 /ig/m 3 (0.5 ppm) 

ozone, to a combination of 0.5 ppm ozone and 560 

Ng/m 3 (0.3 ppm) nitrogen dioxide, or to a mixture of 

0.5 ppm ozone, 0.3 ppm nitrogen dioxide, and 35 

Ng/m 3 (30 ppm) carbon monoxide. A point of 

interest is that in a group of unreactive subjects, 

the same investigators observed substantial 

decrements in lung function after only 2 hr of 

exposure to 980 μg/m3 (0.5 ppm) ozone and 

intermittent light exercise. Another group of four, 

aged 29 to 41 years, who had previously 

experienced clinical bronchospasms and were 

judged by subjective criteria to have hyper-reactive 

airways, developed clinical discomfort and were 

unable to complete the protocol. Exposed to ozone 

at 980 jug/m3 (0.5 ppm) for 4 to 5 hr, this group 

developed marked changes in pulmonary 

mechanics and gas distribution. 

In later experiments, some effects were found 

after exposure of the same group of subjects to 

ozone at 730 pg/m 3 (0.37 ppm), but not after 

exposure at 490 /ag/m 3 (0.25 ppm). A third group of 

seven subjects, aged 22 to 36 years and judged to 

have normally reactive airways, showed only 

minimal effects on the first day of exposure when 

exposed to ozone at 980 /jg/m 3 (0.5 ppm) for 2 hr; 

however, five of the seven showed signiflcant 

effects on a second exposure day. A fourth group of 

seven subjects, aged 22 to 41 years (three hyperreactors and four normals) were exposed for' 2 

hr/day on 2 successive days in 3 consecutive 

weeks to 490ug/m3 (0.25 ppm) ozone, a mixture of 

490 /jg/m3 (0.25 ppm) ozone and 560 pg/m3 (0.3 

ppm) nitrogen dioxide, or a mixture of 490 Ng/m 3 

(0.25 ppm) ozone, 560 Ng/m 3 (0.3 ppm) nitrogen 

dioxide, and 35 mg/m 3 (30ppm)carbon monoxide. 

These subjects showed no obvious effects. A fifth 

LEGEND 

_ FEFinax PEAK EXPIRATORY FLOW 

•••••• FVC 

---FE VI 

~ -FEF 25-75%-MEAN EXPIRATORY FLOW DURING 

MIDDLE HALF OF FVC 

-••-FEF 509,1 INSTANTANEOUS EXPIRATORY FLOW 

AT 50% OF FVC 

90 

J ao[ ''\. •4 

~ `4` r''t4, •~ 

 . ► .... 

 .... ....-4.+ ~•"'r'"'.wn 

~ ,....:~ ~.~ 

I Z 80 

O •• ~. •_ 

ii'~... .r* ~ 

t ~f•--• • ~~ . . 

./ •I—~ ..~

. 

U 

U. 

O 

\' 

.` 

22 7 0 ~• 

• ~ 

/• NOTE: Mean values for individual 

~ tests at 30 minute intervals are 

•\• I '•• expressed as a percentage of the 

control (100%) value. 

60 Full recovery was not achieved 

15-min EXERCISE PERIODS I for any of the tested parameters 

✓ 

within the 2-hour recovery 

I period. 

•5 1•0 1-5 2•0 2•5 3•0 3•5 4•0 

EXPOSURE - - -d RECOVERY 

TIME, hours 

Figure 9-1. Changeswith time in dynamic lungfunction tests in nonsmokers during a 2-hr exposure to 0.75 ppm ozone and 

during recovery. 32 

189 
group of five subjects, aged 27 to 41 years, was 

exposed to 730 Ng/m3 (0.37 ppm) ozone for 2 hr. 

No important changes with exposure were found 

in most physiologic measures. The experimental 

design in all these studies does not permit 

statistical analysis of the combined data; therefore, 

no firm conclusions can be drawn concerning 

dose-response relationships. 

15 

14 

Z 

0 13 H 

Q 

J 12 

F La 

W ~ 11— 

> 

LU 10 

~ z_ 9 

2 8 

1s 

W 

F- 15 a 

}.~ 1a 

MN 0«13 

E ,a 12 

N T 

W 11 jI ~ 

10 

i 

1 

I 

I 

i 

~ 

~ 

~ 

I 1 

1.4 

1•3 

~ 1•2 

d 

= 1•1 

ui 

2 1•0 

D 

p 0.9 

> 

Q 0.8 

O 

~ 0.7 

0.6 

N=10 

0 0•5 1•0 1•5 2•0 2•5 3•0 3•5 4•0 

rE EXPOSURE a} .4 1 RECOVERY—10 

TIME, hours 

Figure 9-2. Changes with time of minute ventilation, 'respiratory rate, and tidal volume in ozone-exposure (0.75) 

and subsequent recovery period in exercising nonsmokers. 32 (Note: Heavy bars on the abscissa mark 15-min periods of 

light exercise.) 

190 
In studies by Kerr et a1., 39 10 smokers and 10 

nonsmokers, aged 21 to 60 years, were exposed to 

ozone at 980 pg/m 3 (0.5 ppm) for 6 hr in an 

environmental chamber. During this period, they 

engaged in two 1 5-min medium exercise sessions 

(100 watts) on a bicycle ergometer. Subjects who 

experienced typical symptoms were, in general, 

the ones who developed objective evidence of 

decreased pulmonary function. The most 

significant changes from control values for the 

group as a whole (20 subjects) after ozone 

exposure were observed in several pulmonary 

function tests—specific airway conductance 

(SGaw), pulmonary resistance (RL), and FVC. No 

significant change was observed with respect to 

diffusing capacity (DLco), static lung compliance 

(Cst), or the various tests derived from the singlebreath nitrogen elimination rate. When the 

smokers were considered as a separate group, no 

significant decrease in pulmonary function was 

observed. The group of nonsmokers considered 

separately showed a significant decrease in 

dynamic compliance as well as in those 

parameters noted for all 20 subjects considered 

together. Prolonged exposure of four subjects to 

0.5 ppm for 10 hr further decreased specific airway 

conductance. 

Folinsbee et al. 17 tested the response of 28 

subjects after ozone exposure to three stages of 

ergometer exercise with loads adjusted to 45, 60 

and 75 percent of maximal aerobic power. The 

subjects were exposed to ozone at 730, 980, or 

1470,ug/m3 (0.37, 0.50, or 0.75 ppm) for 2 hr, at 

rest or while exercising intermittently. Subjects 

had 15 min of rest alternated with 15 min of 

exercise at a workload sufficient to increase 

ventilation by a factor of 2.5. At submaximal 

exercise, neither oxygen consumption nor minute 

ventilation was significantly altered after ozone 

exposure at any concentration. The primary 

response was an alteration of exercise ventilatory 

pattern. An increase in breathing rate(r=0.98)and 

a decrease in tidal volume (r=0.91) correlated well 

with the dose of ozone, calculated as the volume of 

ozone inspired during exposure. It was concluded 

that through its irritant properties, ozone modified 

normal ventilatory response to exercise and that 

this effect was dose-dependent. 

In a second study, Folinsbee and associates 16 

assessed the effect of exposure to 1470 Ng/m 3 

(0.75 ppm) ozone on the cardiac and pulmonary 

function of maximally exercising, healthy young 

adult males. During 2-hr exposures, subjects 

alternately rested for 15 min and lightly exercised 

for 15 min at a workload of about 50 watts. In 

random order, each subject also underwent a 2-hr 

control exposure tofiltered air. At the conclusion of 

all exposures, subjects exercised maximally until 

exhausted. Values of the following parameters, 

measured during maximal exercise, were 

significantly lowerafter ozone exposure than after 

filtered air exposure: Maximum work load attained, 

heart rate, minute volume, tidal volume, and 

oxygen uptake. Respiratoryfrequency and the ratio 

of tidal volume to FVC during maximal exercise did 

not differ sigriificantly following ozone versus 

filtered air exposures. The authors concluded that 

the decrease in maximal exercise performance 

after ozone exposure probably stemmed from 

respiratory rather than cardiac factors. In their 

minds, the most likely mechanism underlying the 

observed results is the stimulation by ozone of 

irritant receptors in the lung. Such stimulation in 

turn produces restriction of inspiratory reserve 

volume, reduction of tidal vol ume during maximum 

exercise and a modest increase in airway 

resistance. 

A more specific study of airway irritability was 

conducted by Golden et a1. 19 They showed that 

after a 2-hr exposure to 1180 /ag/m 3 (0.6 ppm) 

ozone, bronchial reactivity (as assessed by 

response to histamine challenge) increased. 

Seven days following the exposure, bronchial 

sensitivity was still elevated, and in some subjects, 

hyperirritability persisted for up to 3 weeks. The 

authors believe that ozone damaged the airway 

epithelium and sensitized bronchial irritant 

receptors. 

DeLucia and Adams 12 studied the effects of 

graded exercise on lung function and blood 

biochemistry irt six men after 1 hr of exposure to 

290 Ng/m 3 (0.15 ppm) and 590 /ag/m 3 (0.30 ppm) 

of ozone via a mouthpiece. The workloads were 25 

percent, 45 percent, and 65 percent of each 

individual's maximum oxygen uptake (V02 max). 

Ventilation volume and V02 were unaffected by 

even the most severe exposure/exercise 

protocols. However, most subjects demonstrated 

signs of toxicity (symptoms such as congestion, 

wheezing, and headache) during the most 

stressful protocols. In addition, vital capacity, 

forced expiratory volume at 1 sec, and 

midmaximum flow rate decreased significantly 

after inhalation for 1 hr of 590%ig/ m 3 (0.30 ppm) at 

65 percent V02 max. Discernible, though not 

statistically significant, changes in respiratory 

191 
pattern were also observed after exposure to 290 

/ig/m 3(0.15 ppm) ozone and exercise at 65 percent 

V02 max. This study emphasizes the importance of 

actually quantifying the dose rather than mereiy 

defining the exposure Ievel, as well as quantifying 

the differential effects that may result from mouth 

breathing compared to nose breathing. 

The combined effects of different levels of 

exercise, heat stress, and ozone on lung function of 

14 males were studied by Folinsbee et a1. 15 

Subjects were exposed to 980 Ng; m 3(0.5 ppm) 

ozone for 2-hr periods under four environmental 

conditions: (1) 25°C (77 1 F), 45 percent RH; (2) 

31 °C (88 1 F), 35 percent RH; (3) 35°C (95 1 F), 40 

percent RH; and (4) 40°C (104 1 F), 50 percent RH. 

One30-min exercise period (40 percent of V02 max) 

was included in every 2-hr exposure run. The 

results of this study show that besides well 

established physical factors such as concentration 

of ozone, duration of exposure, and intensity of 

exercise, the extent of lung functional response 

will depend also on timing of exercise into the 

exposure period, lapse time between end of 

exercise and testing period, relative humidity, and 

ambient air temperature 

Silverman et a1., 56using the Montreal exposure 

protocol (intermittent exercise, 730 Ng/m 3[0.37 

ppm] or 1470 Ng/m 3[0.75 ppm] ozone for 2 hr), 

basically confirmed the results obtained previously 

by Hackney et al.ZS,2s,so and Bates and Hazucha. 2 ' 19 

Moreover, they showed a high linear correlation 

between the effective dose of ozone (calculated as 

concentration times the relative volume of 

ventilation) and percent changes in lung function 

measurements (r = 0.70 to 0.95). The reported data 

indicate that for a given effective dose, exposure to 

a high concentration for a short time is more 

effective than a longer exposure to a lower 

concentration. 

Knelson et a1. 45exposed 22 male volunteers, 

aged 19 to 27, to ozone for up to 4 hr at 780/ag/m 3 

(0 4 ppm). Subjects were sedentary during 

exposure except for two 15-min exercise periods 

on a bicycle ergometer at 700 kg-m/min exercise 

that about doubled the heart rate and quadrupled 

the minute ventilation. After 2 hr of ozone exposure, there was a significant change (pG 0.05) in 

FVC, midmaximal expiratory flow (MMEF), and 

airway resistance (Raw). Several other measures 

(FEV,, V5o, and V25 ) were lower after 2 hr of 

exposure, but the statistical significance was 

borderline. However, after 4 hr of exposure, all 

flow measures were significantly decreased, 

compared with controls. After4 hr, Raw increased, 

FVC decreased further, and FEV, decreased 

significantly. Residual volume, functional residual 

capacity, and total lung capacity (TLC) did not 

change as a result of the ozone exposure. Ketcham 

et a1., 40employing the same laboratory facilities as 

the previous investigators, also demonstrated 

significant deterioration of pulmonary function in 

30 subjects. The average FEF 25 to 75 percent, 

which is the most sensitive test, decreased by 

almost 30 percent from the control value after 2 hr 

of exposure to 1 180 Ng/m 3(0.6 ppm) ozone. AII 

other dynamic tests were also decreased 

significantly. These changes were accompanied by 

increased RV and FRC and slightly decreased TLC. 

Kagawa and Toyama 37have reported on the 

results of limited studies involving four normal 

male subjects exercising while exposed to ozone at 

1760 Ng/m3(0.9 ppm) for 5 min. A significant 

decrease in SGaw was found during exposure and 

after 5 min of recovery. 

Von Nieding et a1. 59studied the effects of 196 

Ng/m 3(0.1 ppm) of ozone for 2 hr in 12 healthy 

males aged 24 to 38 years. Arterial oxygen tension 

(Pa o ) decreased significantly by 7 mm Hg from a 

mean of 84.6 ± 1.3 mm Hgto77.6±1.9(pG0.01) 

and returned to the initial level at the end of the 1- 

hr post-exposure period (84.3 ± 1.8 mm Hg). The 

alveolar-arterial gradient(AaDp, ) increased with 

decreasing Pao, (p <0.01). Airway resistance was 

significantly higher at the end of the 2-hr exposure 

than at the start. The subjects' airway resistance 

had not returned to normal 1 hr after exposure. 

Thoracic gas volume (TGV) did not change in the 

course of the experiment. Limitations in this study 

include the use of nonstandard measurement of 

flow resistance (Rt) and the use of arterialized 

capillary blood for Pp, measurement. Hence, until 

confirmed, these studies must be interpreted with 

caution. 

Several investigators have reported apparent 

adaptation to pulmonary effects of ozone on 

repeated or chronic exposure. A discussion of 

these studies, along with a recent controlled 

exposure experiment, has been reported by 

Hackney et a1. 29Six men with respiratory hyperreactivity were exposed to 980 pg/m 3(0.5 ppm) 

ozone for 2 hr each day during 4 successive days. 

One subject showed little measurable response. 

The other five subjects showed decrements in lung 

function (generally on exposure days 1 to 3) that 

were largely reversed on day 4. These results 

suggest that some humans do not continue to 

192 
experience the same decrerpents in lung function 

after repeated exposures Wozone. It is not known 

whether adaptation to other adverse effects of 

ozone exposure occurs. 

Hackney and associates 27 also compared the 

response to ozone exposure of four southern 

Californians with that of four Canadians,whose 

cumulative ambient ozone exposure appeared to 

have been less than that of the Californians. In 

Hackney's southern California laboratory, all eight 

subjects underwent 2 hr of exposureto730Ng/m 3 

(0.37 ppm) ozone and intermittent light exercise. 

The investigators observed no statistically 

significant changes in lung function. However, the 

Canadians showed discernible post-exposure 

decrements in most lung function parameters 

measured, whereas the Californians did not. The 

Canadians also showed statistically significant 

changes inin vitroerythrocyte fragility, erythrocyte 

acetylcholinesterase activity, and serum vitamin E 

level. Among Californians, erythrocyte acetylcholinesterase activity was the only blood 

parameter showing post-exposure changes. Tothe 

investigators, adaptation of southern Californians 

to the effects of ozone exposure was the most 

plausible explanation for the observed results. 

Hovrever, selective migration of ozone-sensitive 

pec :)le away from southern California could not be 

wholly ruled out. 

I , a similar 4-day, 2-hr exposure protocol, 

Mc iler et a1.52 exposed six subjects to 730 Ng/m 3 

(0."7 ppm) ozone. Although conventional tests did 

not reveal any functional abnormalities, more 

sensitive nitrogen-clearance measurements 

shrwed that in hyper-reactive subjects, the 

spE.cific distribution of ventilation had been 

a It. red. 

Linn et a1.46 studied the effects of ozone 

exposure on symptomatology, respiratory 

physiology, and blood biochemistry in 22 

physician-diagnosed asthmatic subjects (20 males 

and two females) living in the Los Angeles area. 

Persons with marked respiratory disability were 

excluded from study. Study participants varied in 

age from 19 to 59 years and covered a clinical 

range from slight wheezing to marked abnormality 

in forced expiratory performance. All but six used 

medication regulary. 

Each subject was studied at the same time of day 

on 3 successive days in the Rancho Los Amigos 

exposure chamber. At the beginning of each day's 

study, baseiine lung function measurements were 

obtained with subjects breathing purified air. 

Following this, subjects exercised lightly and 

rested over alternate 15-min periods for 2 hr. 

Exercise work loads were chosen to double each 

subject's resting minute ventilation (light 

exercise). In all studies, temperature and relative 

humidity were controlled to 31 ± 1°C and 35 ± 4 

percent, respectively. Subjects were instructed to 

take oral medications on their regular schedules 

but to refrain from using inhaled bronchodilators 

during each 3-day study period. 

On the first day, subjects were exposed only to 

purified air. On the second day, they were exposed 

to just enough ozone to permit detection of its odor 

at the beginning of the exercis- -rest period, and to 

purified air for the rest of the period. On the third 

day, they were exposed to 0.20 to 0.25 ppm ozone 

throughout the period. At the end of each day's 

study period, the lung function tests of the subjects 

were repeated, their symptoms were assessed, 

and they were bled for measurement of 

hematologic and biochemical parameters. 

To quantitate the effect of the 3-day study 

protocol on the parameters measured, the 

investigators repeated the entire protocol, with no 

ozone exposure, using a subsample of 14 persons 

(12 men and the 2 women) from the original group 

of subjects. On the average, subjects underwent 

the 3-day control study 10 months after the 

original study (range 1 to 23 months). 

In all data analyses, the mean results of the 

whole group or the subsample were compared 

across different days of study. Noformal attemptto 

identify or characterize unusually sensitive 

individuals was reported. 

In the whole group of 22 subjects, the within-day 

difference between pre- and post-exposure lung 

function measurements differed significantly 

between the oxidant-exposure day and any other 

day for only one of nine measured parameters. This 

was total lung capacity (TLC), whose mean value 

increased by 0.06 liter on the odor-sham day and 

decreased by 0.10 liter on the oxidant-exposure 

day (p G 0.05). In the subsample of 14 subjects, no 

statistically significant differences in lung function 

between the ozone-exposure day and any other 

day of the first 3-day protocol was observed. For 

this group, between-day differences in lung 

function were slightly larger during the second 3- 

day (control) protocol than in the first. 

For the whole group, th3 mean symptom score 

was higher (but not significantly so) on the ozoneexposure day than on the other 2 days, and it was 

virtually identical on the other 2 days. For the 

193 
subsample in the first 3-day (exposure) protocol, 

the mean symptom score was also highest by a 

small margin on the ozone-exposure day. 

However, the highest daily score in the subsample 

occurred during the 3-day control protocol. 

Ozone exposure was more strongly associated 

with blood biochemical changes than with 

symptoms or lung function changes. For thewhole 

group, mean values of the following parameters 

differed significantly(pG0.05)between the ozoneexposure day and at least one of the other 2 days 

(directions of difference on the ozone-exposure 

day are given in parentheses): total hemoglobin 

(lower), red cell fragility in H2O2 (higher), reduced 

glutathione (higher than odor-sham days, lower 

than clean-air days), acetylcholinesterase (lower), 

glucose-6-phosphate dehydrogenase(higher), and 

lactate dehydrogenase (higher). In the subsample 

of subjects in the 3-day exposure protocol, the 

same types of significant differences between 

ozone-exposure days and other days were 

observed, with the exception that no ozone-related 

difference in reduced glutathione occurred. In the 

3-day control protocol, the only biochemical 

parameter showing significant differences 

between days was acetylcholinesterase. 

The results of this study suggest that, in a 

reasonably representative sample of adult 

asthmatics, short-term exposure to realistic ozone 

levels (0.20 to 0.25 ppm) produces no measurable 

adverse effect on lung function. On the other ha nd, 

the results suggest a moderate tendency toward 

increased symptom frequency in asthmatics atthe 

ozone level used, and they strongly suggest that 

ozone at this level can alter certain biochemical 

and hematologic parameters. 

The changes that Linn et a1. 46 have associated 

most confidently with ozone exposure are changes 

of the least certain clinical significance. Since 

most of the observed biochemical and hematologic 

effects relate directly or indirectly to the oxygencarrying capacity of the blood, they might be 

unusually important in groups, such as 

asthmatics, with compromised pulmonary 

function. Also, as the authors mention, these 

findings raise the possibility that asthmatics may 

react biochemically at lower ozone concentrations 

than do normal persons. However, the observed 

changes were small when compared tothe normal 

inter-individual variability of the parameters 

measured, and they were considerably smaller 

than would occur with obvious clinical disease. 

Thus the question as to whether these changes 

represent harmful effects in asthmatics remains 

open. 

As mentioned, Linn et a1. 46 reported only group 

mean results Thus their findings do not touch on 

the question of whether certain individual 

asthmatics may be particularly sensitive or 

resistant to ozone concentrations of 0.20 to 0.25 

ppm Finally, their findings do not allow inference 

as to what the effects of ozone might be in 

childhood asthma. 

The effects of sequential exposures separated by 

1 day to 2 months, in combination with different 

concentrations of ozone, have been investigated by 

Hazucha et a1. 34 The 2-hr ozone exposure protocol 

for 16 subjects, divided into four groups, was as 

follows: 

1. Group A. 780 /ag/m 3 (0.4 ppm), 1- to 2- 

month delay, 390 ug/m 3 (0.2 ppm), 1-day 

delay, 780 Ng/m3 (0.4 ppm) ozone; 

2. Group B: 390 pg/m 3 (0.2 ppm), 1-day 

delay, 780 /Ig/m 3 (0.4 ppm), 1- to 2-month 

delay, 780 Ng/m3 (0.4 ppm); 

3. Group C: 1 180 Ng/m 3 (0.6 ppm), 1- to 2- 

month delay, 390 /ag/m3 (0.2 ppm), 3-day 

delay, 1 180 ,ug/m3 (0.6 ppm); 

4. Group D: 1 180 Ng/m3 (0.6 ppm), 1- to 2- 

month delay, 780 pg/m 3 (0.4 ppm), 3-day 

delay, 1180 Ng/m 3 (0.6 ppm). 

From all four groups, only group D showed clear 

signs of adaptation (i.e., response to the third 

challenge exposure was less marked than a 

response observed earlier after exposure to the 

same concentration). Although the size of the 

groups was small, the results obtained indicate 

that the extent of changes induced by the 

challenge exposure depend primarily on the ozone 

concentration during pre-exposures and the time 

interval between preconditioning and challenge 

exposures. 

In most reported studies,3,12,16,26,32,35,45,56 an 

association between symptoms and changes in 

lung function was usually found. Ozone-induced 

defects in function were not usually found in the 

absence of definite symptoms of ozone-induced 

respiratory irritation. 

The newer experimental studies described 

above2,12,1',19'32,35,37,39,56 show that significant 

adverse changes in lung function occur in humans 

at ozone concentrations of 725 /jg/m 3 (0.37 ppm) 

and higher. Some limited studies show evidence of 

human health effects of exposure to pure ozone at 

concentrations as low as 490 ug/m 3 (0.25 ppm) 

(see Figure 9-3). 211 ' 32 The prelimininary findings of 

194 
Von Nieding et a1. 59 suggest decrements in lung 

function at 196 pg/m3 (0.1 ppm) exposure for 2 hr. 

Hematology 

Although the toxic effects of oxygen on red blood 

cells (RBC) have been known for a long time, it was 

not until recently that injurious effects of a much 

stronger oxidant, ozone, have been investigated. 

Initial studies concerning ozone toxicity on RBC in 

animals showed that ozone and oxygen share a 

great number of pharmacological and toxicological 

features. The striking similarity between the 

toxicity of these two gases has attracted 

considerable interest among both researchers and 

clinicians and an increasing number of articles, 

including a review,411 have been published on this 

problem. 

lN VITRO STUDIES 

The RBC constituent most sensitive to ozone 

damage seems to be the membrane. The increased 

breakdown of unsaturated fatty acids i n the red cell 

membrane was observed after exposure to 780 

Ng/m3 (0.4 ppm) ozone for 2 hr. The degree of 

unsaturation of the acids was positively correlated 

with the extent of lipid peroxidation.' The same 

intensity of exposure significantly reduced 

acetylcholinesterase activity and decreased 

neuraminic acid levels in cell membranes. Subsequent incubation of the exposed cells in plasma 

resulted in complement-mediated RBC membrane 

dai-rlage as measured by acid, sucrose, and insulin 

hemolysis tests. Since such a reaction is 

characteristic of RBC In paroxysmal nocturnal 

hemoglobinuria (PNH) disorder, Goldstein et al. 

hypothesized that the ozone-induced changes in 

the red cell membrane have produced PNH-like 

RBC's. 2 ''22 In addition, a recent study from the 

same laboratory showed that exposure of RBC 

under similar experimental conditions also caused 

a loss of native protein (tryptophan)fluorescence in 

the cell membrane.21 With regard to the above 

studies, it can be argued that the concentration of 

ozone used was unrealistically high, but serious 

disturbances in cell chemistry caused by such 

concentrations can be detected much more easily 

than the subtle changes induced by lower levels. 

Increased sophistication and sensitivity of various 

tests have allowed considerable reduction of ozone 

concentrations in hemotological studies. Recently, 

Kindya and Chan 42 demonstrated that 3-min 

exposure of 1.0- mi sample of erythrocyte membrane fragments to 12 mmol ozone significantly 

decreased ouabaine-sensitive adenosine 

10.0 

0.0 

Y 

C 

~ ~ 

a 

> 

U. -10.0 

Z 

W 

0 

Z 

Q 

_ v 

20.0 

-30.0 

~ 18 ~ LOS ANGELES 

(Hackney) 

3 

12 15 

~ 

MONTREAL 

(Hazuchal 

3 

I

= ONE STD. ERROR 

12 

0 0.2 0.4 0.6 0.8 

OZONE CONCENTRATION (BY NEUTRAL BUFFERED KI METHOD), ppm 

Figure 9-3. Dose-response curves for Los Angeles and Montreal subjects. 32 '28 

195 
triphosphatase (ATPase) activity. Since this 

enzyme plays a major role in maintaining 

intactness of erythrocytes, the investigators postulated that such inactivation of the activated ATPase 

in the cell membrane may lead to increased 

osmotic fragility and sphering of RBC. It is of 

interest to note that both cysteine and ascorbic 

acid, when added to the red cell membrane 

fragments before exposure, afforded protection to 

the ATPase against ozone. 

In recent years, a number of compounds have 

been studied as to their antioxidant effects on 

various enzyme systems. Goldstein and Levine 23 

demonstrated that p-aminobenzoic acid inhibited 

the ozone-induced loss of activity of acetycholinesterase in red cell membranes. Menzel et 

a1. 50 showed that addition of vitamin E (atocopherol) or d-a-tocopheryl acetate prevented 

formation of Heinz bodies formed in RBC by 

ozonides, which are potent indicators of lipid 

peroxidation in cellular membranes.49 

lN VIVO STUDI ES 

Brinkman and Lamberts' were the first to report 

that inhalation of ozone interfered with oxygen 

exchange in the capillaries of skin. In a later study, 

Brinkman et a1. 6 demonstrated potentiation of 

erythrocyte sphering in subjects exposed to 490 

,ug/m 3 (0.25 ppm) ozone for periods of 30 to 60 

min. More than 10 years later, Buckley et a1. 9 

employed a comprehensive battery of biochemical 

tests to investigate the toxic effect of ozone to RBC 

of subjects exposed to 980 Ng/m3 (0.5 ppm) ozone 

for 2 3/a hr. The observed changes were similar to 

the effects reported previously in either animal or 

human blood in vitrostudies. They demonstrated a 

significant increase in RBC fragility. Lactate 

dehydrogenase (LDH) and glucose-6-phosphate 

dehydrogenase (G-6-PD) enzyme activities were 

increased, while acetylcholinesterase activity and 

reduced glutathione (GSH) were depressed. Cell 

membrane glutathione reductase (GSSRase) 

showed no change in activities, whereas serum 

GSSRase activities were decreased. The postexposure level of serum vitamin E was significantly 

higher as was lipid peroxidation. Clearly these 

results indicate that ozone or its by-products can 

induce changes across the alveolo-capillary 

barrier. 

Although the presented data display a spectrum 

of ozone interference with biochemical 

mechanisms, the physiological significance of all 

these studies remains to ba established. To 

evaluate clinical implicationsoftheozone-induced 

cellular damage, quantitative studies at realistic 

concentrations are needed. 

Mutagenesis 

The work described in the section on chromosomes in Chapter 8 of this document prompted 

investigators to evaluate the potential for ozone to 

cause chromosomal aberrations. MPrz et a1. 51 

reported results from six men exposed to 980 

Ng/m 3 (0.5 ppm) ozone, two of them for 6 hr and 

the other four for 10 hr. Blood was obtained from 

the first two subjects before and immediately after 

exposure. The other four subjects had blood drawn 

before exposure, immediately after, and then at 2 

and 6 weeks following exposure. The lymphocytes 

were cultured and prepared for chromosomal 

analysis following standard procedures. No true 

chromosomal-type abnormalities were observed 

except for one instance in one individual. However, 

there were lesions that the authors interpreted as 

achromatic, unrepaired single-strand breaks, and 

chromatid deletions. Although such aberrations 

were seen in some of the pre-exposure 

preparations, the authors reported an increased 

frequency of abnormalities 2 weeks postexposure, with reversion to lower frequency 6 

weeks post-exposure. 

Because of the observations of Merz et a1., 51 EPA 

conducted a study to evaluate the potential human 

mutagenic effects of ozone in a more rigorous 

fashion. Thirty nonsmoking, normal, young male 

volunteers breathed ozone at 780 Ng/m 3 (0.4 ppm) 

during 4 hr in a controlled-environment laboratory. 58 The cytogenic results of this study have 

been reported by McKenzie et a1. 47 Blood was 

drawn from the subjects before exposure, 

immediately following exposure, and at 3 days, 2 

weeks, and 4 weeks after exposure. Lymphocytes 

were cultured for 48 hr, and slides were prepared 

in the usual way, with 100 metaphase spreads per 

subject per treatment scored for chromosomal 

aberrations. A total of 13,000 human lymphocytes 

were cytogenetically analyzed in this study. Cells 

with suspected aberrations were photographed, 

destained, restained with banding procedure, and 

photographed again to identify the specific 

chromosomes and regions involved. The data from 

this experiment consist essentially of five 

measurements on each subject over the period of 1 

month. Thus the appropriate statistical analysis of 

variance for reported measurements was done on 

the raw data and on appropriately aresintransformed observations. There was no 

significantdifference in any of the observationsfor 

196 
the respective blood sampling times. The authors 

conclude that there is no detectable human 

cytogenetic effect related to exposure to ozone 

under the conditions of this experiment. 

These findings are in contrast to those reported 

by other investigators. The in vitro and animal 

studies discussed in the section on chromosomes 

in Chapter 8 of this document used either 

extremely high ozone doses or inadequate 

controls. The study of Merz et a1. 51 used higher 

ozone concentrations and much longer exposures 

than that of McKenzie et al." Also, the small 

number of subjects in the Merz et al. study did not 

permit the rlgorous statistical analysis of the 

McKenzie et al. study. Clearly, additional 

evaluation of the human mutagenic potential of 

ozone is needed, and such research is now in 

progress. Evidence nowavailable, however, fails to 

demonstrate any mtitagenlc effect of ozone in 

humans when exposure schedules are used that 

are representative of such exposures of the 

population at large as might actually occur in urban 

areas. 

Controlled Studies of Human Health Effects of 

Peroxyacetylinitrate 

Experiments conducted on a group of male 

college students averaging 21 years of age have 

suggested that exposure to PAN results in 

increased oxygen uptake during exercise 

compared to uptake during breathing of clean air.s' 

This report, however, did not adequately describe 

the experimental design or the statistical analysis. 

Subjects were exposed to 1485 Ng/m 3 (0.3 ppm) 

PAN by breathing through the mouth (nose clamps 

were used) for 5 min while at rest. Then the 

subjects were immediately engaged in 5 min of 

exercise on a bicycle ergometer. Both air 

containing PAN and air free of PAN were used. 

Expiration velocity was reduced after exercise. The 

changes could reflect an increase in the effort 

needed in breathing as a result of the exercise or 

an increase in airway resistance. 

In a series of studies of the effects of PAN and 

carbon monoxide on healthy young and middleaged males during treadmill work in an exposure 

chamber, Raven and coworkers found no changes 

in maximum aerobic power when the subjects 

were exposed to .1337 /jg/m 3 (0.27 ppm) 

PAN.13,sssa,sassso When the subjects worked at a 

level requiring 35 percent of maximum oxygen 

consumption for 3.5 out of 4 hr of continuous 

exposure to 1188 /jg/m3 (0.24 ppm) PAN, no 

significant changes were observed in the 

metabolic, cardlovascular, or thermoregulatory 

responses.'a A small (4 to 7 percent) but significant,'a reduction In standing FVC was observed in 

the younger group of subjects. 18 

SUMMARY 

Convincing new information on the health 

effects of oxidant exposure has emerged from 

controlled studies on humans, from which tentative dose-response curves have been constructed. The new data show statistically significant reduced pulmonary functicn in healthy 

smokers and nonsmokers at ozone concentrations 

at and above 730 Ng/m3 (0.37 ppm) for 2-hr 

exposures. However, a recent study by Von 

Nieding et a1. 59 showed some effect at as low a 

concentration of ozone as 0.1 ppm for 2 hr. Some 

studies suggest that mixtures of sulfur dioxide and 

ozone at a concentration of 0.37 ppm are more 

active physiologically than would be expected from 

the behavlor of the gases acting separately. Wlde 

variation in response among different individuals 

is a general finding in studies of oxidants, as well 

as other pollutants. Undesirable health effects of 

oxidant air pollution exposure are increased by 

exercise and, as judged by informal surveys, many 

people apparently limit strenuous exercise 

voluntarily when oxidant pollution is high. 

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199 
10. EPIDEMIOLOGIC APPRAtSAL OF PHOTOCHEMICAL OXIDANTS 

INTRODUCTION 

A review is presented in this chapter of the 

evidence gathered to date in the epidemiologic 

studies of whether or not ozone and other photochemical substances exert deleterious effects on 

human health. Every effort has been made to 

describe study designs and investigative methods 

thoroughly so that readers with either a technical 

or nontechnical background may judge both the 

reliability of findings presented and the degree to 

which observed effects may be attributed specifically to photochemical air pollution. 

This chapter consists of four sections. The first 

deafs with effects of short-term (generally less 

than 1 week) exposures to photochemical air 

pollutants. In many studies of short-term exposures, pollutant concentrations have been 

measured on the same day, or even in the same 

hour, as the health indices to which they have been 

compared. The second section deals with effects of 

long-term exposures to photochemical air 

pollutants. The health data for most of these 

studies have been collected at one point in time. 

Thus, even though certain health impairments 

have been associated with long-term pollutant 

exposures, it has generally not been possible to 

state the duration of exposure that may have 

produced those impairments. 

The sections of this chapter dealing with shortterm and long-term exposures have been divided 

into subsections in which studies of similar effects 

are reviewed. Following each subsection is a 

discussion that assesses the reliability of current 

evidence and identifies the areas of uncertainty 

requiring future research. Experimental studies, 

which give some indication of physiological 

mechanisms underlying findings of epidemiologic 

studies, are discussed where practicable. The 

degree to which observed epidemiologic findings 

may be attributed specificallyto photochemical air 

pollution or to individual components of this broad 

class is also assessed. Finally, an effort is made to 

identify specific pollutant concentrations and the 

duration of exposure necessary to promote the 

observed effects. 

Following the sections on short-term and longterm exposures, a brief assessment of the attitudes 

of laymen and physicians toward oxidant pollution 

will be presented. Finally, the available 

epidemiologic evidence related to oxidant pollution 

will be summarized. 

EFFECTS OF SHORT-TERM PHOTOCHEMICAL OXIDANT EXPOSURES 

To identify the acute health effects of 

photochemical oxidant pollution, observations of 

the same populations of communities are made 

during periods of both high- and low-level 

pollution. Changes in health-related indices are 

compared with short-term pollutant concentrations measured as 24-hr averages, hourly 

maxima, or instantaneous peak concentrations. 

Daily Mortality in Relation to Variations in 

Oxidant Levels 

MORTALITY AMONG RESIDENTS AGED 65 

YEARS AND OVER 

Over a 3-year period from 1954 to 1957, the 

California State Health Department conducted a 

study of the relationship between daily 

concentrations of photochemical oxidants and 

daily mortality among residents of Los Angeles 

County ages 65 years and over. 6'''eDuring these 

years, photochemical oxidant concentrations in 

Los Angeles County were generally measured by 

the potassium iodide (KI) method. Ozone 

concentrations were generally measured by visual 

assessment of rubber cracking. Both methods 

were calibrated with unbuffered 2-percent KI 

solution. The number of deaths per day was related 

to two indices—maximum dailytemperature atthe 

downtown weather bureau, and oxidant 

concentrations from August through November 

1954 and from July through November 1955. 

200 
Data collected over these periods of time are 

summarized in Table 10-1 and Figure 10-1. 

Examination of the table and figure reveals a 

pronounced effect of the September 1955 heat 

wave on mortality. The fig ure reveals no consistent 

association between mortality and high oxidant 

concentrations in the absence of unusually high 

temperatures. 

TABLE 10-1. AVERAGE NUMBER OF DEATHS PER DAY RESULTING FROM CARDIAC AND RESPIRATORY CAUSES 

AMONG RESIDENTS OF LOSANGELES COUNTY, AGED 65 AND OVER, AS RELATED TO OXIDANTCONCENTRATIONS 

AND MAXIMUM DAILY TEMPERATURE BY MONTH, 1954-55 

Temperature readings _ 

100 -15 0 C 160 -200 C 21 0 -260 C 27o-31oC 32°-37°C 

Totals (50°-59°F) (60°-69°F) (70°-79°F) (80°-89°F) (90°-99°F) - '-38°C( °100°F) _ 

Average Average Average Average Average Average Average 

Concentration, Number number Number number Number number Number number Number number Number number Number number 

ppm of days of deaths of days of deaths of lays of deaths of days of deaths of days of deaths of days of deaths of days of de aths 

August 1954 

Low (00-0 24) 8 299 4 282 4 31 5 

Medlum (0 25-0 49) 22 32.2 7 301 12 31 8 3 390 

Hlgh (0.50+) 1 320 1 320 

September 1954 

Low (00-0 24) 1 260 1 260 

Medlum (0.25-0.49) 25 321 5 296 16 35 1 4 360 

Hlgh (0 50+) 4 333 4 333 

October 1954 

Low (00-0 24) 9 394 1 31.0 6 382 2 475 

Medlum (0 25-0 49) 14 371 1 430 10 360 2 395 1 370 

Hlgh (0 50+) 8 363 3 367 5 360 

November-1954 

Low (00-0.24) 16 38.6 1 39.0 5 360 4 420 6 386 

Medlum (0.25-0.49) 14 379 4 368 5 348 5 41 8 

Hlgh (0.50+)' 

July 1955 

Low (00-0 24) 4 350 1 280 3 37.3 

Medlum (0.25-0.49) 11 34.8 5 344 6 35.2 

Hlgh (0 50+) 2 420 1 420 1 420 

No readtngs 14 375 10 387 4 345 

August 1955 

Low (00-0 24) 5 368 4 355 1 420 

Medlum (0 25-0 49) 16 384 16 384 

Htgh (0 50+) 4 372 4 372 

No readings 6 378 4 385 2 365 

September 1955 

Low (00-0 24) 5 290 1 330 3 27.3 1 300 

Medlum (0 25-0.49) 13 61.5 4 308 3 43.7 1 520 5 988 

Hlgh (0 50+) 7 503 1 320 1 280 3 407 2 850 

No readings 5 348 4 332 1 41 0 

Mean 

Low (00-0 24) 48 U33 5' 1 39.0 7 333 19 31 6 20 367 1 420 

W35.5 

Medlum (0 25-0 49) 115 U39 1 5 399 36 326 60 379 9 41 0 5 988 

W37 9 

Hlgh (0 50+) 26 U38 5 6 357 15 353 3 407 2 850 

W40 0 

No readings 25 U36 7 14 360 8 36.5 3 388 

W37 0 

Total days 1 12 75 103 15 8 

Total deaths 

Unwelghted 39.0 36.6 34.0 36.6 402 753 

Welghted 390 361 33.2 372 40.5 88.3 

'U = unweighted, W = wetghted 

201 
Table 10-1 contains too few data to yield any 

conclus:ve trends. However, examination of the 

table's marginal means suggests that the effect of 

temperature on death rates, at least during the 

months considered, is smallest in the comfortable 

temperature range of 21 1 to 26°C (701 to 79°F). 

Such examination also suggests a positive 

association between oxidant exposure and 

mortality in this temperature range. Examination 

in Table 10-1 of overall mean death rates by 

pollution exposure category also suggests such an 

association. 

It must be emphaslzed that Table 10-1 does not 

reveal a convincing relationship between oxidant 

exposure and daily mortality. Indeed, the table 

contains far too few data to warrant conclusions of 

any kind, except perhaps that the effect of 

unseasonable temperatures on mortality is large 

enough to obscure any effectthat oxidant pollution 

may have. However, Table 10-1 also arouses 

interest in the hypothesis that any effect that 

oxidant might exert on mortality may be most 

apparent at times when temperatures are 

seasonal and comfortable. As yet, this hypothesis 

has not been adequately tested. 

MORTALITY AND HEAT WAVES 

In the LosAngeles Basin, high temperatures and 

elevated oxidant concentrations tend to occur 

simultaneously. The question thus arises whether 

oxidant exposure augments the effect of 

temperature on mortality rates. Oechsli and 

Buechley41 considered this question briefly in a 

study of the effect on mortality of three Los 

Angeles heat waves occurring in 1939, 1955, and 

1963. Daily mortality during these heat waves was 

compared with daily mortality occurring 

immediately before and after each heat wave and 

with mortality during the same season in 1947, 

when no heat wave occurred. 

Statistically significant increases in mortality 

rates were observed during each heat wave, 

particularly among elderly persons. However, 

there was no apparent difference between the 

effects of the 1939 and 1955 heat waves on 

mortality rates. Quite probably, considerably less 

photochemical oxidant pollution accompanied the 

1939 heat wave than that of 1955. (Oxidant 

concentrations were not routinely measured in 

1939.) The comparison of the two heat waves thus 

320 

300 

280 

260 

240 

> 220 

m 

~ 200 0 

c 

y 180 

2 

Q 160 

p 140 

120 

100 

80 

60 

40 

T = SMOG ALERT DAYS 

TEMPERATURE 

50 U 0 

40 UJ 

30 ~ 

Q 

20 oC 

w 

10 CL 

W 

0 ~ 

DEATHS 

7 14 

[-0- JULY - +t--AUG.-44f SEPT.- }t- OCT.--- 1 t--NOV.- ~ 

TIME, days 

Figure 10-1. Comparison of deaths of personsaged 65years and over, and maximum daily temperatures, Los Angeles 

County, July 1 to November 30, 1955. 6,7e 

202 
suggests that high photochemical oxidant 

concentrations do not notably augment the effect 

of high temperatures on mortality. On the other 

hand, it must be remembered that Oechsli and 

Buechley did not statistically determine whether a 

relationship between mortality and oxidant 

exposure existed. 

MORTALITY OF NURSING HOME RESIDENTS 

The California State Health Department also 

made an effort to determine whether patients in 

Los Angeles nursing homes, many of whom are 

chronically ill, experienced increased mortality 

during or just after days of high oxidant 

concentratlons. 6 '''8 Deaths and transfer to 

hospitals among residents of 16 Los Angeles 

nursing homes having a total of 358 beds were 

recorded for 1954. An unusually large number of 

patients died following a particularly heavy 

episode of smog during 1 week of the study period. 

During the same week, however, the number of 

residents transferred to hospitals did not appear to 

be unusually high. Neither the number of deaths 

nor the number of transfers to hospitals was 

elevated during a high-smog period about a month 

earlier than the one mentioned above. 

Measurements of pollutant concentrations were 

not reported. 

A larger study of the nursing home population 

was conducted from July through December 1955, 

during which all nursing homes in Los Angeles 

County containing 25 or more bedswere surveyed. 

Daily mortality rates were reported from 92 homes 

with a total of 3826 beds. Daily mortality, the 

corresponding maximum daily temperature, and 

the occurrence of smog-alert days, with ozone 

concentrations of 590/jg/m3 (0.30 ppm) or higher, 

are shown in Figure 10-2. The heat wave in late 

August and early September, during which several 

smog-alert days occurred, showed a striking ef`ect 

on mortality. At no other time could a relationship between daily mortality and smog-alert days 

be discerned. 

50 

TEMPERATURE 1 =DAYS OF OFFICIAL ALERTS, 

OZON E ? 0.30 ppm 

40 

40 

~ 

x 

~ 

a 

W 

~ 30 

w 

~ 

O 

x 

~ 

Z 

~ 20 

~ 

Z 

10 

DEATHS 

U 

0 

Nl 

w 

a: 

~ 

~ 

Q 

cc 

W 

a 

~ 

w 

H 

} J_ Q 

~ 

~ 

7 

X 

1Q Q 

~ 

0 

1 5 10 15 20 25 30 4 9 14 19 24 29 3 8 13 18 23 28 3 8 1318 23 28 2 7 12 17 22 27 2 7 12 17 22 27 31 

1-t-- JULY -- I-*--- AUG. ---10 1-4-- SEPT. ►T-0 OCT. 0- 1 -0 NOV. —10 1t DEC. —10-1 

TIME, days 

Figure 10-2. Comparison of nursing home deaths, maximum daily temperature, and smog-alert days in Los Angeles 

County, July through December 1955. 678 

203 
30 30 

V 

E 

L y 20 

Fz 

a 

X 10 

O 

w25 a: 

~ 

F 

a 

~ 

~ 20 

w 

H 

15 

TWO-COMMUNITY STUDY 

Massey et a1. 33 compared daily mortality in two 

areas of Los Angeles County selected to be similar 

in temperature but different in air pollution levels. 

The investigators constructed two synthetic 

communities, one of intermediate pollution and 

one of high pollution, containing a combined 

population of 944,391 persons. The pollutant 

variables used in data analysis were the daily 

maximum and mean oxidant levels, as measured 

by the potassium iodide (KI) method and sulfur 

dioxide and carbon monoxide concentrations. 

Intercommunity differences in temperature were 

also considered. The mean number of daily deaths 

in the intermediate pollution area was subtracted 

from the mean number of deaths in the high 

pollution area, and the differences were related by 

multiple correlation and regression to differences 

in pollution concentrations. No significant 

correlations between differences in mortality and 

differences in pollutant levels were observed. 

Mean daily death rates per 100,000were 3.18 and 

3.06, respectively, in the intermediate- and highpollution communities. 

MORTALITY RESULTING FROM CARDIAC AND 

RESPIRATORY DISEASES 

Hechter and Goldsmith 22 analyzed the effect of 

pollutant concentrationson average daily mortality 

from cardiac and respiratory diseases in Los 

Angeles County for the years 1956 through 1958. 

During these years, photochemical oxidant 

concentrations were measured in Los Angeles 

County by the KI method, using an unbuffered 2- 

percent KI solutionasthecalibration reagent. Daily 

mortality, (averaged within each month of the 

study)fluctuated between-1.0 and 1.3 per 100,000 

population. These fluctuations were approximately 

180 degrees (6 months) out of phase with 

fluctuations in oxidant and temperaure values and 

approximately in phase with maximum carbon 

monoxide concentrations (Figure 10-3). To remove 

the effect of season of year, the authors fitted 

Fourier curves to the data. The residual variations 

from these fitted curves for each of the variables 

were presumed to be independent of season. The 

relationship between pollution or temperature on 

one day with the value of the same variable on the 

preceding or following days was also accounted for 

E 

a 

ui 

O 

X 

O 

z 

O 

2 

z 

O 0o 

~ 

Q 

~ 

ok~ 

n 

> 1.4 

O ° 

~ o ao 

~o y o 1.2 

w~ c[ ° c 

OW 

Q Q 1.0 

Q X 

OF 

oc a 

v o 0.8 

[-*1956 -s -IE 1957 ' ~ 1958'N-j 

YEAR 

1~-1956 -110+011- 1957 -0}* 1958 - { 

YEAR 

Figure 10-3. Comparison of maximum concentrations of oxidant and carbon monoxide, maximum 

temperature, and daily death rate for cardiac and respiratory causes, Los iAngeles County, 1956-58. 22 

204 
in the analysis. When residuals from the fitted 

curves were thus analyzed, no significant 

correlations between pollutants and mortality for 

cardiorespiratory diseases were found. Neither 

were there sig nificant correlations when a 1- to 4- 

day lag between exposure and mortality was 

applied. 

Mills36correlated daily cardiac and respiratory 

mortality in Los Angeles with corresponding daily 

maximum oxidant concentrations for the following 

periods: 1947 through 1949; August 17, 1953, 

through December 31, 1954; and January 1 

through September 30, 1955, excluding the severe 

heat wave of September 1 through 4. To correct for 

possible seasonal effects on mortality, Mills 

compared mean daily death rates on low-smog 

days to mean rates on higher-smog days occurring 

within the same month. 

For 1947-49, mortality data were related to the 

Stanford Research Institute's smog index, 56,57,58 

which was based on meteorologic conditions, not 

on air pollution measurements. (Coefficients of 

correlation between the smog index and maximum 

ozone measurements, supplied bythe U. S. Rubber 

Co., ranged from 0.08 to 0.949. AII were 

statistically significant at a= 0.05.) For 1953-55, 

mortality data appear to have been related to daily 

maximum total oxidant measurements supplied by 

Dr. A. J. Haagen-Smit of the California lnstitute of 

Technology. These measurements were 

presumably made with the phenolphthalein 

method. 

In all periods, Mills 36observed a consistent 

positive relationship between daily mortality and 

daily maximum ozone or oxidant concentration. 

This relationship held for persons under age 65 as 

well as for older persons. On the average, daily 

death rates in 1947-49 were about 7 percent 

higher when the smog index was six through nine 

(corresponding to maximum ozone concentrations 

of about 0.36 to 0.37 ppm) than when the smog 

index was zero through five. In the same period, 

daily death rates when the smog index was 10 or 

above (corresponding to maximum ozone concentrations of at least 0.42 ppm) averaged 12 percent 

higher than when the smog index was zero through 

five. For 1953-55, the mean daily death rate when 

maximum total oxidant exceeded 0.2 ppm averaged about 5 percent higher then when maximum 

total oxidant vvas below 0.2 ppm. Mills, 36like the 

California Department of Health, 6,7,8 performed an 

analysis of death rates in Los Angeles nursing 

homes during the second half of 1955. Unlike the 

California Department of Health, Mills applied a 

seasonal correction factor to death rates within 

each month of this period. Mills' analysis suggested a continuous increase in daily death rates with 

increasing daily maximum oxidant concentrations 

above 0.2 ppm. Corrected daily death rates ranged 

from 4.72 when daily maximum oxidant was below 

0.2 ppm, to 6.23 when maximum oxidant was 0.8 

ppm or above The correlation between seasonally 

corrected death rate and maximum oxidant was 

0.206 (p = 0.01). 

In a separate report, Mills 35stated that more 

than 334 deaths in Los Angeles during 1954 were 

associated with daily oxidant or ozone maxima 

above 0.2 ppm. 

The California Department of Health has 

specifically questioned Mills' findings. In CleanAir 

ForCalifornia, s '''8 the Departmentexplainsthatthe 

Stanford Research Institute's smog index, by 

which Mills classified mortality data for 1947-49, 

was developed as a prediction device and not as a 

measurement of air pollution. The Department 

also states that the abandonment of the smog 

index by the Institute indicated that it was not 

satisfactory in either respect. They add that Mills' 

manner of selecting smog-free days to be used for 

comparison may not have been entirely 

satisfactory. 

The California Department of Health also applied 

the essential details of Mills' analytical procedure 

to LosAngeles Countycardiac and respirator death 

rates during August-November 1954. 6'

7

'8Results 

of the California analysis are shown in Table 10-2. 

Comparison of mortality rates on smoggy and 

smog-free days within each of the months shown 

reveals no effect of oxidant pollution on mortality. 

Thus, as stated in references, 6 '''8and the Breslow 

and Goldsmith's report, 4analyses performed in 

California did not support Mills' conclusion that 

334 deaths in Los Angeles during 1954 were 

associated with oxidant levels above 0.2 ppm. 

Interpretation of the results summarized in 

Table 10-2 is clouded because references 6 '

7

' edo 

not contain an explanation of criteria used to differentiate smoggy from smog-free days. Also, the 

temperatures on the two types of days cannot be 

ascertained from three references. However, that 

Mills and the California Department of Health have 

interpreted Los Angeles mortality data differently 

is undeniable. 

DISCUSSION OF MORTALITY STUDIES 

As yet, no convincing association between daily 

205 
mortality and daily oxidant concentrations in Los 

Angeles has been shown. Mills has certainly 

described a positive association between mortality 

and oxidants. However, because the smog index 

used for much of his analysis appearsto have been 

inaccurate, and because investigators in California 

have observed no oxidant-mortality association in 

data used by Mills himself, the vigor wlth which 

Mills" conclusions can be advanced must be 

considerably restricted. However, careful examination of available studies raises the 

interesting question as to whether oxidants might 

affect mortality at times when temperatures are 

comfortable and seasonal. To date, most efforts to 

determine whether oxidants affect mortality have 

focused on high-smog periods. During such 

periods, temperatures also tend to be high and may 

thus obscure or eliminate any effect of oxidants on 

mortality. The data In Table 10-1, which are 

apparently the only extant cross-tabulation of 

mortality by pollution and temperature, suggest 

that the effect of oxidant on mortality may be 

strongest or most readily detectable, when 

temperatures are seasonal. Indeed, it is plausible 

that oxidants would noticeably affect mortality at 

no other times. 

Thus whether oxidants affect daily mortality has 

not been conclusively resolved. Recent advances 

in statistical analysis of mortality data, coupled 

with the accumulation of such data over the two 

decades since most oxidant-mortality studies were 

performed in Los Angeles, should enable 

investigators to clarify this issue considerably over 

the next several years. 

Hospital Admissions in Relation to Oxidant 

Levels 

ADMISSIONS TO LOS ANGELES COUNTY 

HOSPITAL, 1954 

The California State Health Department 

examined several categories of admissions to Los 

Angeles County Hospital from August through 

November 1954. 6,78 These categories were 

asthma, other respiratory conditions, and cardiac 

conditions. Total admissions, the number of 

persons with acute conditions in all units, and the 

number who died were tabulated. A formal 

statistical analysis does not appear in clean-airfor-California reports. 6, ''8 However, visual 

inspection of these data reveals no consistent 

relationship between admissions and high smog 

perlods. 

Brant and Hi11 2' 3 studied 9- to 90-year-old 

patients with respiratory or cardiovascular 

diagnoses who were admitted to or discharged 

from LosAngeles County Hospital betweenAugust 

and December 1954. Patients were considered 

only if they had resided for at least 3 years in an 

area within 13 km (8 miles) of downtown Los 

Angeles. Although the method of selecting 

patients for the study was not described, the 

selection process yielded 246 cardiovascular 

admissions and 122 respiratory admissions. Daily 

average total oxldant concentrations between 6 

a.m. and 1 p.m., as measured about 1.6km(1 mile) 

from the hospital, were the only indices of air 

pollution employed in statistical analyses. Multiple 

regression analyses were used to relate hospital 

admissions to atmospheric and meteorological 

variables. Calculations included regressions of 

hospital admissions as late as 4 weeks after the 

occurrence of a given set of environmental 

measurements, which included total oxidant, 

temperature, and relative humidity. Brantobtained 

a positive partial correlation coefficient of 0.982 

between the total oxidant level and the number of 

respiratory and cardiovascular admissions 

occurring 4 weeks later. However, the correlations 

between total oxidants and admissions during the 

same week and 2 weeks later were, respectively, -0.986 and -0.870. 

Although Brant's findings are interesting, they 

must be regarded as inconclusive forfour reasons. 

First, it is difficult to rationalize why hospital 

admissions should be more dependent on oxidant 

TABLE 10-2. COMPARISON OF RESPIRATORYaAND CARDIAC °DEATHS DURING SMOG AND SMOG-FREE PERIODS 

OCCURRING IN LOS ANGELES COUNTY, AUG UST-NOVEMBER 19546 '

7

' 8 

Total Total 

deaths, deaths, 

selected Daily selected Daily 

Smog periods _c_aus_es_ average Smog-free periods causes average 

September 21-24 181 46 September 12-15 191 48 

October 15-20 294 49 October 1-6 303 50 

November 24-28 235 47 November 16-20 244 49 

a

Respiratoiy tuberculosis (001-008), pneumonia, all forms (490-493) Sixth revision, international list numbers 

°Diseases of the heart (410-443) Sixth revision, international hst numbers 

206 
levels 4 weeks before than on more recent levels. 

Second, the partial correlation coefficients 

between cardiovascular admissions and total 

oxidant concentrations during both the week of the 

admissions and 2 weeks before were very highly 

negative. Third, as far as we can determine, Brant 

did not examine the variables used in his statistical 

models for autocorrelation. Fourth, no indices of 

pollution other than oxidant concentrations were 

considered. 

HOSPITAL ADMISSIONS THROUGHOUT THE 

CITY OF LOS ANGELES 

In two studies, Sterling et al. ss,so assessed the 

influence of air pollution exposures on persons 

admitted to hospitals with more than 100 beds in 

the city of Los Angeles. Only patients who were 

members of Blue Cross were considered. 

Discharge diagnoses were assigned to one of three 

categories—highly relevant, relevant, and 

irrelevant—which reflected the presumptive 

susceptibility of the diagnoses to air pollution 

exposure. Included in the "highly relevant" 

category were allergic disorders, inflammations of 

the eye, and acute upper and lower respiratory 

infections. Included in the "relevant" category 

were cardiovascular diseases and other 

respiratory diseases. AII other conditions were 

included in the "irrelevent" category. The authors 

corrected both number of admissions and pollution 

exposure measurements for day-of-week effects. 

Nine pollution indices, including oxidant, ozone, 

carbon monoxide, sulfur dioxide, nitrogen dioxide, 

nitric oxide, and particulate matter, were 

considered in Sterling's analysis. Air pollution 

measurements were obtained from the Los 

Angeles County Air Pollution Control District. For 

each pollutant, the exposure index used in 

statistical analyses was the average of the 

maximum and minimum concentrations for each 

day of the study. 

In Sterling's first study, 59air pollution indices 

were correlated with the number of hospital 

admissions occurring on the same day in each 

diagnostic category. In all, 223 days between 

March and October 1961 were considered. 

Correlation coefficients oetween admissions for 

highly relevant diseases and all nine pollution 

indices measured were all statistically significant 

at a= 0.05. AII but one correlation (that with sulfur 

dioxide) were significant at a= 0.01. The 

magnitude of these correlation coefficients ranged 

from 0.16 (for sulfur dioxide)to0.25 (for particulate 

matter). Correlations between relevant diseases 

and pollution were significant for oxidant, ozone, 

and sulfur dioxide. For all relevant diseases, the 

highest correlations were observed with ozone 

(0.27), sulfur dioxide (0.27), and oxidant (0.25). For 

all pollutants except sulfur dioxide, correlations 

between irrelevent diseases and pollution were 

negative or not significant. Coefficients of 

correlation between temperature or relative 

humidity and admissionswere not significant in ali 

disease categories. 

In the second study performed by Sterling et 

a1., 60tength of stay in the hospital was correlated 

with air pollution and meteorologic variables over 

the same time period, as in the first study. The 

absolute value of correlation coefficients was 

usually less than 0.1 and never exceeded 0.169. 

Despite their diminutive values, coefficients of 

correlation between length of stay and all pollution 

indices were statistically significant at a= 0.05 for 

the irrelevent diseases and for all disease 

categories combined. AII correlations between 

pollution indices and length of stay for irrelevant 

diseases and all disease groupings combined were 

positive, except that for ozone concentration. The 

only pollutants consistently and significantly 

positively correlated with length of stay for 

relevant disease categories were sulfur dioxide, 

nitrogen dioxide, and total oxides of nitrogen. 

Coefficients of correlation between humidity and 

temperature and length of stay in all disease 

categories were negative and significant at a= 

0 01 . This finding with respect to temperature 

contrasts with the findings of several of the 

mortality studies cited above. 

DISCUSSION OF STUDIES OF HOSPI'TAL 

ADMISSIONS 

Studies of the relationship of short-term oxidant 

exposures to hospital admissions have yielded 

mixed results Even studies in which a positive 

association between exposures and admissions 

has been observed must be considered 

inconclusive. As mentioned above, it is difficult to 

rationalize Brant's observation of a strong 

association between pollutant levels in 1 week and 

hospital admissions 4 weeks later, in the face of 

highly negative associations in the intervening 

weeks Also, in the light of Sterling's studies, one 

must wonder whether Brant, if he had chosen to 

calculate them, would not have obtained 

correlation coefficients between admissions and 

207 
pollutants other than oxidants that were 

comparable to those calculated for oxidants. 

Thus even if the association between short-term 

exposures and hospital admissions observed in 

Los Angeles proves to be valid, available evidence 

in this field will not support the incrimination of 

certain pollutants and the exoneration of others. 

Also, available evidence gives no indication of 

pollutant concentrations at which hospital 

admission rates might be expected to increase. 

Furthermore, since no studies relating oxidant 

concentrations to hospital admission rates have 

been performed outside of Los Angeles, it is 

impossible at present to say whether oxidants 

influence admissions in other areas. 

Aggravation of Existing Respiratory Diseases by 

Oxidant Pollution 

AGGRAVATION OF ASTHMA 

As a result of reports by physicians that 

asthmatic attacks are frequently associated with 

high-smog periods, Schoettlin and Landau 53 

undertook a study to determine whether such a 

phenomenon indeed takes place. Five physicians 

selected 157 patients, 137 of whom participated in 

the study AII resided and worked in the Pasadena 

area Fifty-four of the patients were younger than 

age 15. Most had had asthma for at least 5 years. 

Daily records of the time of onset and severity of 

asthma attacks were maintained by the patients 

between September 3 and December 9, 1956. 

The Schoettlin and Landau study, as published, 

does not mention pollution measurement methods 

or averaging times used in data analysis. In Air 

Quality Criteria for Photochemical Oxidants, 39 it is 

assumed that oxidant levels in this study were 

daily instantaneous peak values as measured by 

the phenolphthalein method. Errata to the 

document were issued indicating that oxidant 

levels in this study were, in fact, determined by the 

KI method and not the phenolphthalein 

method.' s,ao,a7 

Since publication of Air Quality Criteria for 

Photochemical Oxidants 39 (AP-63) in 1970, a 

considerable effort has been made to determine 

with certainty the measurement methods and 

averaging times used in the Schoettlin and Landau 

study Consultations with the authors have 

established that daily asthma attack rates were 

correlated with daily maximum hourly average 

oxidant levels, not with instantaneous peak levels 

These consultations have also confirmed that 

oxidant measurements were indeed obtained from 

the Los Angeles County Air Pollution Control 

District, and from no other source. Careful 

examination of Air Pollution Control District 

records has further established that the District 

used only the potassium iodide method for 

measuring oxidant levels in Pasadena over the 

course of the Schoettlin and Landau study. Thus in 

the discussion to follow, Schoettlin and Landau are 

presumed to have used daily maximum hourly 

average oxidant concentrations, as measured by 

the potassium iodide method. In the discussion to 

follow, we also assumed that oxidant levels 

reported in this study correspond to daily 

maximum hourly levels and not to instantaneous 

peak levels, recognizing the error that might result 

if readings had corresponded to the latter. 

In the Schoettlin and Landau study, the greatest 

number of asthma attacks occurred between 

midnight and 6 a.m., whereas the maximum 

oxidant levels were recorded between 10 a.m. and 

4 p.m. Of the 3435 attacks reported, fewer than 5 

percent were consciously associated with smog by 

the patients. No severe attacks were consciously 

associated with smog. One-third of the attacks 

consciously associated with smog were reported 

by a single patient. The correlation coefficient 

between daily attacks and the concurrent 

maximum oxidant reading was 0.37. The addition 

of other variables to the analysis did not 

significantly alter these results. Lagged 

correlations between oxidant concentration and 

the number of patients having attacks 6, 12, 18, 

and 24 hr later were generally lower than 

concurrent correlations. There was no significant 

difference between the average number of 

subjects having attacks on days above the median 

maximum hourly oxidant level of 250Ng/m 3 (0.13 

ppm) ozone and the average number of patients 

having attacks on days when levels were below the 

median However, the mean number of patients 

having attacks on days when daily maximum 

hourly ozidant levels exceeded 490 Ng/m 3 (0.25 

ppm) was significantly higher than on days when 

the daily maximum hourly oxidant level fell below 

this level. The authors suggested that this finding 

might indicate a threshold level for oxidants above 

which a physiologic response could be observed. 

Also, attack rates on days in which plant damage 

occurred were significantly higher than on days 

without plant damage. Specific oxidant levels 

associated with plant damage were not reported in 

this study, however The effect of oxidant on 

fZiY.3 
asthma attack rates was most pronounced among 

persons who had lived in the area for 10 years or 

more. The data were examined further to see 

whether a small number of the subjects might be 

responsible for the observed correlation. The 

authors identified eight individuals (6 percent of 

the total panel) whose attacks corresponded most 

often to days on which plant damage occurred. 

Seven of these eight people were females. No 

other common characteristic could be discerned. 

AGGRAVATION OF EMPHYSEMA AND CHRONIC 

BRONCHITIS 

Several studies have been conducted to 

determine whether air pollution aggravates the 

condition of subjects suffering from chronic 

bronchitis and emphysema. 

Motley et a1. 38 reported a study of the lung 

function of 66 volunteers, 47 of whom had 

pulmonary emphysema. Before testing, subjects 

spent differing amounts of time in rooms from 

which oxidants had been removed by activated 

charcoal fi!ters. Twenty-one subjects stayed in the 

filtered rooms for periods of 2 to 4 hr, 20 subjects 

for periods of 18 to 20 hr, and 25 subjects for 

pericds of 40 to 90 hr. The study was performed 

over 3 3 1/2-year period in the late 1950"s. Air quality 

mea , curements were provided by the Los Angeles 

Cou ity Air Pollution Control District. On the days 

of t is study, maximum oxidant concentrations 

(pre , umably outdoors) between 9 a.m. and 2 p.m., 

calclilated as ozone, ranged from 390 to 1040 

/tg/m 3 (0.20 to 0.53 ppm) at monitoring stations 

sevr: ral kilometers from the chamber. Maximum 

conc entrations of other pollutants fell into the 

foIIC Ni ng ranges: Oxide of nitrogen, 0.2 to 0.6 ppm; 

sulfur dioxide, 0.05 to 0.25 ppm; and carbon 

monoxide, 5 to 27 ppm. Air was classified as 

smoggy when there was definite odor of ozone, 

reduced visibility, eye irritation, and the prediction 

of smog by the Los Angeles Air Pollution Control 

District. The investigators measured vital capacity, 

3-sec forced expiratory volume (FEV 3.0), and 

maximal breathing capacity. Residual volume and 

air distribution measurements were also recorded. 

An improvement in lung function, particularly a 

decrease in the residual lung volume, was 

observed in emphysematous subjects who had 

entered the filtered roomson smoggydaysand had 

remained in them for 40 or more hr. No significant 

changes in lung-volume measurements were 

observed when normal subjects breathed filtered 

air. No significant changes were observed when 

emphysematous subjects entered the chamber on 

nonsmoggy days. The smoking habits of subjects 

are not discussed in the report, but variations in 

these might have influenced the results, 

particularly if smokers were not allowed to smoke 

while in filtered rooms. The methods of analysis 

used in this study did not allow the effects of 

individual pollutants to be separated from one 

another. 

At Los Angeles County Hospital, Remmers and 

Balchum45 utilized a room with an air-conditioning 

system and a filter that could be used at the 

discretion of the investigators o remove photochemical oxidants, ozone, nitrogen oxides, and a 

portion of particulate matter from ambient air. 

Studies were conducted between July 1964 and 

February 1965. Analyses of total oxidant by the 

buffered KI method and ofnitrogen dioxide by the 

Saltzman method were performed five times daily. 

Subjects performed lung-function tests one or 

more times daily while they lived in the room. In 

general, they spent 1 week in unfiltered air, a 

second week in filtered air, and a third week in 

unfiltered air. Throughout the study, air conditioning was adjusted to maintain a room 

temperature of 22 1 ± 1.4 °C (72 1 ± 2.5°F) and a 

relative humidity of 50 ± 5 percent. 

Among other tests, determinations of airway 

resistance, carbon monoxide diffusing capacity, 

capillary oxygen tension, and oxygen consumption were performed while subjects were 

resting. Several of these determinations were 

repeated after subjects exercised. 

Only four subjects were considered in the 

Remmers and Balchum report. AII four had chronic 

lung disease. Two of them were considered to have 

relatively advanced emphysema but the other two 

were deemed to have only moderate pulmonary 

impairment. Smoking habits of subjects were not 

mentioned in the report of this study. 

Beneficial effects of air filtration in studies of 

resting patients were most pronounced in the pair 

with only moderate pulmonary impairment. In this 

pair, airway resistance was about 20 percent lower 

during exposuretofiltered airthan to unfiltered air. 

A simultaneous increase in the speed of nitrogen 

washout also occurred in this pair. These changes 

were statistically significant at a= 0.10 

The beneficial effects of air filtration in studies of 

exercising patients were slightly more pronounced 

in patients with advanced emphysema than in 

those with only moderate impairment. In all four 

209 
patients, post-exercise oxygen consumption 

decreased significantly during exposure to filtered 

air. Capillary oxygen tension increased 

simultaneously in all four patients. Changes in 

oxygen tension were statistically significant only in 

patients with advanced emphysema. During 

studies of exercising patients, the mean oxidant 

concentration (calculated as ozone) was about 255 

Ng/m3 (0.13 ppm) when air was not filtered, and 

about 40 Ng/m 3 (0.02 ppm) when air was filtered. 

For several reasons, the Remmers and Balchum 

study must be regarded as inconclusive. First, and 

probably most important, this report does not 

consider variations in the smoking habits of 

subjects. It has become quite clear that subjects 

were not allowed to smoke while breathing filtered 

air, but they were allowed to leave the study room 

and smoke, if desired, during their 2 weeks of 

exposure to ambient air. 43 Variation in smoking 

habits may thus have explained a major part of the 

physiologic difference observed between subjects 

exposed to filtered air and those exposed to 

ambient air. 

Second, the ambient air to which subjects were 

exposed contained not only oxidants but other 

substances as well. Thus, even if the observed 

changes in lung function were attributable to air 

pollution, they might also be attributable, at least in 

part, to these other substances. Third, Remmers 

and Balchum appear to have analyzed data for only 

a very small number of subjects. 

Though their report45 considered only four 

patients, Remmers and Balchum collected data 

from 15 patients, most of them with relatively 

severe emphysema. Nine of these patients were 

smokers, five were non-smokers, and one stopped 

smoking when the study began. Patients generally 

spent about 1 week in unfiltered air, then a second 

week in filtered air, and finally a third week in 

unfiltered air. Analysis of the study of all 15 

patients was performed for inclusion in the 

document, Air Quality Criteria for Photochemical 

Oxidants. 39 Results of that analysis are presented 

in Table 10-3, which shows coefficients of 

correlation between daily values of oxygen 

consumption and airway resistance (both 

measured under conditions of rest and exercise, 

with corresponding daily oxidantvalues measured 

in the morning and the afternoon). Each 

correlation coefficient was converted to a"t" 

statistic. The "t" statistics were then summed 

within pollution - test - specific categories. The 

investigators then derived a"z" statistic for each 

categorybydividingthe sumof"t"statisticsbythe 

sum's variance. The "z" statistics are presented in 

the last line of Table 10-3. 

Using these methods, the authors observed a 

positive relationship, significant at a= 0.01, 

between oxidant concentration and oxygen 

consumption during rest and exercise They also 

observed a generally positive relationship, 

significant at a= 0.001, between oxidant concentration and airway resistance measured at rest. 

As Table 10-3 shows, the relationship between 

airway resistance and afternoon oxidant 

concentrations was more consistently positive 

than that between resistance and morning concentrations. 

In a published report of the study just described, 

Ury and Hexter 62 mention that each subject 

underwent a daily battery of 20 pulmonary 

function tests. The authors also mention that 

concentrations of three pollutants—oxidants, 

nitrogen dioxide, and nitric oxide—were measured. Though it is not explicitly stated, a distinct 

implication of the Ury and Hexter report is that 

oxidant levels were more strongly correlated with 

pulmonary function test results than were levels of 

either nitrogen oxide or nitric oxide. Of the 20 tests 

performed, only airway resistance is considered in 

this report. Thus the degree of correlation between 

pollution exposure and results of other tests 

cannot be determined, though the report implies 

that the other tests were not as strongly correlated 

with pollution exposure as was airway resistance. 

Finally, Ury and Hexter performed separate 

analyses for smokers and non-smokers. In 

smokers, the relationship between airway 

resistance and afternoon oxidant exposure, as 

tested by "z" statistic derived as described above, 

was significant at a= 0.002. In nonsmokers, the 

relationship was significant at a= 0.001 

In the Ury and Hexter report, unlike that of 

Remmers and Balchum, smokers are clearly 

separated from nonsmokers. That summed "z" 

statistics were more highly significant for 

nonsmokers tends to corroborate the conclusion of 

Remmers and Balchum, at least with respect to 

airway resistance. However, these findings must 

still be interpreted with some caution, since, as Ury 

and Hexter note, correlations between airway 

resistance and pollution exposure were significant 

at a= 0.05 in only one-third of the individual 

subjects. 

The relative effects of smoking and pollution on 

oxygen consumption are left largely unexplained. 

210 
The follow[ng average correlat[ons between 

pollution exposure and oxygen consumpt[on were 

computed from Table 10-3: 

NonSmokers smokers 

Resting patlents, 

a.m. oxidants . . . . . . . . . . . 0.331 0.034 

Resting patients, 

p.m. oxidants ........... 0.231 0.175 

Exercis[ng patients, 

p.m. oxidants ........... 0.292 0.055 

That average correlat[ons are cons[stently 

higher for smokers than for nonsmokers suggests 

that variat[ons [n smok[ng habits contributed at 

least part[y to observed changes in oxygen 

consumpt[on. 

Rokaw and Massey 50 conducted a prel[m[nary 

study of the effects of environmental var[ables on 

pulmonary funct[on [n a group of 31 patients [n a 

chronic disease hospital in Los Angeles over a 

per[od of 18 months. A group of normal sub]ects 

was stud[ed concurrently. AII of the pat[ents had 

chron[c, nontuberculous respriatory diseases 

(predominant[y pulmonary emphysema). Each 

subject underwent a ser[es of pu[monary function 

tests four times weekly. In addition, function 

res[dual capacity by the hellum method was 

determined monthly. Air pollut[on measurements 

were obtained from a stat[on about 0.4 km (0 25 

m[le) upwind from the hospital. Concentrations of 

oxidant and ox[dant precursor were measured by 

the KI method. Concentrations of ozone were also 

measured, but the method of ineasurement was 

not reported. Statist[cal methods were employed to 

detect associations between changes [n 

pulmonary function and a[r pollut[on levels. The 

authors noted no cons[stent pattern of response to 

ep[sodes of h[gh pollution exposure, though in 6 of 

31 patients, coeff[c[ents of correlatlon between 

daily pollution levels and corresponding 

pulmonary funct[on were high enough to be 

termed "interesting." During the Rokaw and 

Massey study, 50 the mean odx[dant concentration 

was 120 Ng/m 3 (0 06 ppm), with a max]mum of 

820 Ng/m 3 (0.42 ppm). These concentrations are 

quite moderate for the Los Ange[es Basin and may 

well have been too low to promote any effect on 

lung funct[on. 

TABLE 10-3. CORRELATION OF MORNING AND EARLY AFTERNOON OXIDANT LEVELS 

WITH OXYGEN CONSUMPTION AND AIRWAY RESISTANCE OF 15 PATIENTS 

WITH CHRONIC RESPIRATORY DISEASE 45 

Patient s 

number 

and 

smoking 

history a 

Number ot 

observations 

Oxygen Airway 

consump- resistion tance 

Maximum 

breathing 

capacity 

lites/min 

 Ob_s_er_ved correlation coefPficients 

Oxygen consum_ption °_ Airway resistance` 

Resting Exercising Resting 

a m oxidants p m oxidants p m oxidants a m oxidants° p m oxidants" 

102 S 11 17 0 282 0 405 0 774 -0 379 -0 313 

[103 NS] 14 14 0 123 0 210 0 251 0 717 0 567 

[104 NS] 14 14 -0 313 0 007 0 258 0 638 0 641 

106 S 17 17 884 0 473 0 579 0 521 -0 361 0 146 

[107 S] 17 17 884 0 473 0 579 0 521 -0 361 0 146 

[108 S] 18 18 994 0 489 0 448 0 409 -0 378 0 656 

1 10 S 14 16 69 1 0 255 -0 136 -0 172 0 431 0 124 

[1 1 1 NS] 15 17 11770 434 0 092 -0 459 0 251 0 354 

[1 12 S] 15 15 529 0 413 0209 -0 348 0 339 0 433 

[1 13 NS] 12 12 181 5 -0 107 0 222 0 088 0 034 0 006 

[1 14 S] 13 13 65 3 -0 114 -0 158 -0 120 -0 161 0.058 

[1 15 S] 14 14 26.3 0.423 0 290 0 130 0 217 0 557 

[1 16 SS] 14 15 96 1 0 288 -0 094 0 751 0 715 0 460 

1117 S] 15 15 386 0 189 0 456 0 609 

[1 18 NS] 15 15 374 0 345 0 138 0 453 

z'"r 2991 9 2 761 9 2 8379 3 621" 4 976" 

'Smoking history S= smoker, NS = nonsmoker, SS = stopped smoking when study began Rrackets indicate patients who were tested during the same penod 

°The first two correlations are with resting oxygen, which was measured around 11 a m, the third correlation is with exercise oxygen consurnption, which was measured 

arorIld 3 p m 

`Airway resistance is measured while resting Values given are averages of four measurements made throughout the day 

° a m oxidant was measured around 9 30 a m 

` p m oxidant measured around 1 30 p m 

' z-valueswerefoundbyconvertingtheindividualcorrelationstotvalues,usingtherelationshipt,=r,[(n,-2) (1-r,2)11 2thensummingthetvaluesoverallpatients,thesums 

have variance V(Ft)= 1[In,-21i1n,-41] The z values shown are the ratio of 7(t,)'[F]n,-21, (n,-4)1, which is approximately N(0,1) 

9Significant at the 0 Ol level 

"Significant at the 0 001 level 

om 
The analyses presented in Rokaw's report are 

quite preliminary in nature. To the best of our 

knowledge, a thorough analysis of Rokaw's data 

has not yet appeared in the scientific literature 

Shoettlin 52 studied the effects of community air 

pollution, occupational exposure to air pollution, 

and smoking among Armed Forces veterans living 

in the Domiciliary Unit and Chronic DiseaseAnnex 

of the Los Angeles Veterans Administration 

Center Day-to-day variations in the physical 

status of inen with chronic respiratory disease 

were studied in relation to changes in 

environmental conditions in the coastal area of the 

Los Angeles Basin. Two groups of inen were 

selected for study. One of them consisted of 200 

men with clinically determined chronic respiratory 

disease The second group consisted of 200 

asymptomatic men, matched on age and smoking 

history with the first group. Case-control pairs of 

men were studied weekly by means of repeated 

pulmonary function tests and responses to a 

respiratory symptom questionnaire. The study was 

performed between mid-August and midDecember 1958. 

An air pollution monitoring station was set up at 

the site. Concentrations of total oxidant and 

oxidant precursor were measured by the KI 

met hod 

Multiple regression analysis showed no 

statistically significant effect of air pollution on 

respiratory function or symptoms. However, air 

pollutant measurements consistently explained 

more variation in symptom frequency and 

objective findings in the diseased group than in the 

control group. In this study, the statistical effect of 

maximal oxidant precursorondependentvariables 

was slightly stronger than the effects of other 

pollution variables measured 

Peters44 examined pulmonary function in 

shipyard workers (welders, pipecoverers, and 

pipefitters) exposed to a variety of pollutants including metal fumes, asbestos, nitrogen oxides, 

and ozone. The mean concentration of ozone to 

which welders were exposed was 0.10 ppm (range 

0.01 to 0 36 ppm); the mean concentration of 

nitrogen dioxide was 0.04 ppm (range 0.01 to 0.08 

ppm). The results of the study supported the 

hypotheses (1 ) that chronic exposure to oxides of 

nitrogen and ozone among welders favors development of obstructive lung disease, perhaps in 

association with elastic recoil and increased 

residual volume, and (2) that chronic exposure to 

asbestos among pipecoverers promotes the 

development of restrictive lung disease (decreased 

total lung capacity). The pulmonary function of 

these groups was consistently less robust than 

that in pipefitters engaged in new ship construction who had minimal or no exposure to 

asbestos or welding fumes. These data suggest 

that chronic exposure to ozone or nitrogen oxides 

may contribute to the development of chronic lung 

disease. However, since welders were exposed to 

metal fumes and some asbestos as well as ozone 

and nitrogen oxides, the data do not allow a 

specific inference as to what the primary toxicant 

might have been. 

DISCUSSION OF STUDIES OF AGGRAVATION OF 

EXISTING RESPIRATORY DISEASE 

Available evidence tentatively suggests an 

association between exposure to ambient 

pollution in Los Angeles and both increased 

frequency of asthma attacks and decrements in 

pulmonary function among those with chronic 

lung disease. Studies published to date suggest 

that a maximum hourly oxidant concentration of 

0.25 ppm may be sufficient to promote an increase 

in the proportion of asthamatics having attacks. 

It must be noted clearly, however, that no study 

suggesting an association between oxidant 

exposure and exacerbations of chronic respiratory 

disease is without serious limitations. In studies 

performed to date, variations in the smoking habits 

of subjects have not been adequately considered. 

Also, investigators have tended to consider oxidant 

to the exclusion of other pollutants present in the 

air. It is possible that pollutants other than oxidant, 

acting singly or in combination with oxidant 

components, may have accounted at least partly 

for observed effects. Substantial further research 

in which covariates are appropriately treated and 

in which all pollutants present are considered 

must clearly be performed before the acute effects 

of photochemical oxidant pollution on persons 

with existing respiratory disease are fully understood. 

Effects of Oxidants on the Promotion of 

Symptoms and Illness in Healthy Populations 

SYMPTOM REPORTING AMONG STUDENT 

NURSES IN LOS ANGELES 

Hammer et al'a examined symptom reporting in 

student nurses in relation to photochemical 

oxidant exposure. Freshman students at two 

nursing schools in Los Angeles were invited to 

212 
participate In a prospective study of viral 

resplratory disease To minimize blas, nelther 

faculty nor students were informed that effects of 

air pollutlon were of major Interest.Airqualitywas 

measured at monitoring stations located 1.5 to 3.0 

km (0.9 to 2 mlles) from both hospitals. Oxldant 

concentrations were measured by the KI method. 

Daily symptom diaries, whlch were collected each 

week, included questions related to headache, eye 

discomfort, cough, and chest discomfort. 

Symptoms were graded mild, moderate, or severe. 

Symptom reporting covered the period October 

1961 through June 1964. A dally average of 61 

students particlpated 

Patterns of symptom reporting from both schools 

were similar and were pooled in all analyses. AII 

three grades of symptoms were considered 

posltive reponses, although the occurrence of 

moderate or severe symptoms was rare 

Simultaneous daily measurements of oxidants, 

carbon monoxide, nitric oxide, nitrogen dloxide, 

sulfur dioxide, and maximum daily temperature 

were avallable on more than 90 percent of the 868 

days In this study. 

Results of the study are presented in Table 10-4. 

Simple headache frequency rose slightly at and 

above oxidant concentrations of 0.25-0.29 ppm. 

The frequency of simple eye dlscomfort, however, 

Increased as daily maxlmum hourly photochemlcal 

oxidant levels exceeded 294 to 372 Ng/m3 (0.15 to 

0.19 ppm). Simple rates of cough remained 

relatfvely constant untll the maximum hourly 

oxidant reached 588 to 764 pg/m 3 (0.30 to 0 39 

ppm), at whlch level the rate began to increase 

fairly steeply. The simple rate of chest discomfort 

began to rlse at an oxldant concentration of about 

0.25 to 0.29 ppm 

The authors also computed adjusted symptom 

rates by excluding days In whlch student nurses 

reported a fever. For all symptoms except 

headache, the relatlonship of adjusted symptom 

rates to oxldant exposures was slmllar to that of 

slmple rates. Temperature-fever adjusted headache rates increased slightly at daily maximum 

hourly oxidant levels of 0 15-0.19 ppm and increased more steeply as oxidant levels reached 

588 to 764 /,Ig/m 3 (0.30 to 0.39 ppm). 

Symptom frequencies In thls study were more 

closely related to photochemical oxidants than to 

carbon monoxlde, nitrogen dloxide, or daily 

minimum temperature Oxidant concentratlons at 

which rates of eye discomfort were observed to 

increase were comparable to those observed in 

other published studles. Oxidant concentrations at 

which cough and chest discomfort rates were 

observed to increase were quite similar to ozone 

concentratlons observed to produce Impairment of 

pulmonary function and respiratory Irritation in 

Bates' experimental studies of humans.' In these 

experimental studies, healthy males performing 

Intermlttent light exercise were exposed to 725 

/_Ig/m 3 (0 37 ppm) ozone for 2 hr. The tolerance to 

the effects of photochemical oxidants of healthy 

young adults like the student nurses studied by 

Hammer et al. may be different from that of other 

populatlon segments like the aged, the very young, 

the ill, and the pregnant. 

The results of Hammer's study' $ arouse interest as 

to what the effects of photochemlcal oxidants on 

these other population segments might be 

TABLE 10-4. RELATIONSHIP OF AVERAGE DAILY SIMPLE AND ADJUSTED aPERCENTAGE OF STUDENT NURSES 

REPORT TO PHOTOCHEMICAL OXIDANT LEVELS FOR 868 DAYS, 1VOVEMBER 1961 THROUGH MAY 1964 t8 

Daily maximum Number Average number Average daily percent of symptoms reported 

hourly oxidant of of nurses Headache Eye discomfort _ Cough Chest discomfort 

level, ppm ° days reporting daily Simple Adjusted Simple Adtusted Simple Adlusted Simple Adlusted 

<004 229 64 165 105 86 50 127 91 35 18 

005 - 008 184 59 163 107 9.2 54 134 99 36 1 8 

009 35 58 160 106 90 56 133 102 32 1 9 

010 - 0.14 176 62 156 1 1 0 8.6 5.9 11.9 9.4 34 1 8 

015 - 019 144 58 15.7 11.4 10.0 69 123 97 37 1 7 

020 - 024 63 60 156 11 6 122 9.2 11.6 9.1 31 1 6 

025 - 029 25 60 167 11 5 149 11 2 124 96 3.6 20 

030 - 039 9 67 169 134 21 1 178 152 11.7 41 23 

0.40 - 0.50 3 53 168 150 350 31 8 193 169 70 5.8 

Overall average 61 16.1 109 9.6 6.3 126 9.5 3 5 1 8 

eAll days on which the system was reported along with "feverish," "chilly," or "temperature" are eacluded 

° I ppm = 1960 pg/m 3 

213 
EFFECTS OF OXIDANTS ON NEW ILLNESS IN 

COLLEGE STUDENTS 

Durham 12 reported a study of the short-term 

effects of air pollution on the health of students at 

seven California universities—five in the Los 

Angeles area, and two in the San Francisco Bay 

Area The Los Angeles area generally experiences 

higher pollution concentrations than the BayArea 

AII seven universities participating in Durham's 

study were located within 8 km (5 miles) of a 

weather station and a pollution monitoring station. 

Nine indices of weather and eight indices of 

pollution were considered. The method by which 

oxidant concentrations were measured was not 

reported, although presumably the method was KI, 

at least in the Los Angeles area 

Health data were collected during the 1970-71 

school year. Each time a student visited the 

student health service with a health-related 

complaint a sheet requesting demographic 

information, smoking habits, and physician's 

diagnosis was completed. Diagnoses were 

assigned to 1 of 14 categories, including eye 

irritation, respiratory and allergic diagnoses, and 

gastroenteritis (a diagnosis not expected to be 

related to pollution exposure). Only first visits with 

individual illnesses were included in data analysis 

About 22 percent of collected data sheets showed 

no physician's diagnoses. In all, 11,659 sheets 

with first-visit respiratory diagnoses were 

received. 

For each school, the author computed 

coefficients of correlation between levels of 

pollution and weather variables on 1 day and 

proportions of new illness on the same day and on 

days up through 7 days later 

In general, correlations of pollution with 

bronchitis were greatest when lagged 5 or 6 days; 

correlations of pollution with combined respiratory 

disease were greatest when lagged zero to 3 days; 

and correlations with asthma, eye irritation, 

headache, and hay fever were greatest when 

lagged zero days or 1 day. 

Between 20 and 25 percent of pollution/ 

respiratory illness correlations were statistically 

significant at a= 0.05, whereas only 5 percent of 

pollution/gastroenteritis correlations were 

significant The illnesses most strongly associated 

with pollution were, in descending order, 

pharyngitis, bronchitis, tonsillitis, colds, and sore 

throat. The pollutant variables most strongly 

associated with illness in general were, in 

descending order, peak oxidant, mean sulfur 

dioxide, mean nitrogen dioxide, and mean nitric 

oxide. Stronger associations between pollution 

and illness were generally observed in the Los 

Angeles area than in the Bay Area The authors 

attributed this finding to the difference in pollution 

exposure between the two areas, although 

pollution measurements in the two areas were not 

compared in the report 

In a separate a nalysis, the days of the study were 

separated into high- and low-pollution days for 

each school in the Los Angeles area. Highpollution days were defined as days on which 

concentrations of at least half the measured 

pollutants exceeded their means by at least 0.25 

standard deviation. Days on which concentrations 

of at least half the measured pollutants we.e less 

than 0.25 standard deviation below their means 

were assigned to the low-pollution category For 

each school, the authors calculated ratios of upper 

respiratory illness rates occurring on or following 

high-pollution days to illness rates occurring on or 

following low-pollution days. At the University of 

California, Irvine, which consistently experienced 

lower pollution levels than any other school in the 

Los Angeles area, this ratio was very close to 1.0 

for all lag periods from zero through 7 days 

between the occurrence of pollution and the onset 

of symptoms. At the University of Southern 

California (USC), which experienced the highest 

pollution levels of any school, this ratio was larger 

than that observed at Irvine for all lag periods 

except zero days. On the average, the ratio at USC 

.exceeded the ratio at Irvine by 16.7 percent. The 

largest interschool difference in ratios, about 50 

percent, occurred at a lag period of 6 days The 

methods of analysis used in this study did not 

permit inferences as to the lowest oxidant levels 

necessary to promote increased illness rates. 

OXIDANTS AND ELEMENTARY SCHOOL 

ABSENTEEISM 

Wayne and Wehrle64 examined the effects of 

oxidant air pollution on respiratory illness among 

children as measured by absentee rates from 

elementary school. Absentee data were collected 

from two elementary schools in Los Angeles 

throughout the 1962-63 school year. Reasons for 

absences were intially obtained from parents and 

were classified into various categories by teachers. 

Air pollution measurements were supplied by the 

Los Angeles Air Pollution Control District. Oxidant 

concentrations were measured by the KI method. 

Measurements for school 1, located in east 

214 
downtown Los Angeles, were made at a station 

located within 3 km (2 miles) of that school. Air 

quality data for school 2 were monitored at a 

station within 3 km (2 miles) of the school during 

the initial 3 months of study and at a station 6.5 km 

(4.5 miles) from the school for the remainder of the 

study. During this study, daily oxidant 

concentration averaged from 10 a.m. to 3 p.m. 

ranged from nearly zero to about 0.23 ppm. This 

concentration exceeded 0.20 ppm on 6(1.8 

percent) of a possible 336 days. Oxidant was the 

only pollutant considered in this study. 

Absence rates in both schools were highest 

during the winter season, when levels of oxidants 

were generally lowest. No consistent association 

was observed between weekly mean oxidant 

levels and weekly absence rates for respiratory 

disease. The highest absence rates were reported 

on Mondays and Fridays at both schools; in 

contrast, oxidant levels were consistently higher 

during midweek periods. In a further analysis, 

correlations were computed between uncorrected 

daily absence rates and same-day average oxidant 

concentrations between 10 a.m. and 3 p.m. In a 

second analysis, absence rates corrected for dayof-week effect were correlated with same-day 10 

a.m. to 3 p.m. oxidant concentrations and with 

corresponding concentrations occurring 1 day 

before. Results from the two schools were kept 

separate in all analyses. No analysis revealed a 

positive association between oxidant concentration and absence rates. 

EFFECT OF PHOTOCHEMICAL OXIDANTS ON 

SYMPTOM RATES IN JAPANESE ELEMENTARY 

SCHOOLCHILDREN 

Shimizu55 discussed the effects of photochemical smog exposures on symptom reporting 

rates at two junior high schools in Osaka, Japan, 

which will be designated schools A and B. At 

school A, an unusually high number of students 

complained of symptoms on 3 days in the fall of 

1972 (September 13, 21, and 22). An unusually 

high number of eighth graders at school B 

complained of symptoms on October 3, 1972. At 

each school, symptom questionnaires were 

distributed on the day or the day after the unusual 

complaint rates occurred. The questionnaires 

inquired about the presence of nine symptoms, 

including eye irritation, respiratory discomfort, 

cough, dizziness, nausea, and numbness of the 

extrem ities. 

At school A, questionnaires appear to have been 

distributed to all students. However, they were 

collected only from students who reported the 

presence of at least one symptom. Faced with 

uncertainty as to the appropriate denominator, the 

author selected the total enrollment of school A, 

(1313 students) as the basis for calculation of 

symptom rates. 

Maximum concentrations of pollutants 

measured at a station near school A(Station P) on 

September 13 were as follows: 

Pol I uta nt: ppm 

Oxidant (3 p.m.) .. . . . . . . .0.14 

Nitric oxide (2 p.m.) .. . . .0.17 

Nitrogen dioxide (2 p.m.) .0.12 

Sulfur oxide (1 p.m.) ..... 0.6 

The maximum temperature, 29.4°C (85 1 F), was 

recorded at 11 a.m. At another nearby station 

(Station 0), a maximum oxidant concentration of 

0.19 ppm was recorded between 2 and 3 p.m. Only 

Station 0, which measured only oxidant, was 

operating on September 21 and 22. Atthis station, 

the maximum oxidant concentration on September 

21 was 0.17 ppm, recorded at 1 p. m. On 

September .22, the maximum oxidant 

concentration was 0.11 ppm, recorded at 12 noon. 

Aerometric measurement methods were not 

reported. 

At school A, a total of 263 students (20.0 

percent) reported at least one symptom on 

September 13. Corresponding totals on September 

21 and 22 were, respectively, 133 (10.1 percent) 

and 72 (5.5 percent). 

It is of interest that on September 13, the rate of 

symptom reporting in physical education classes 

increased as concentrations of oxidants, NO, and 

NO2 increased. Physical education classes were 

conducted outdoors. The average rate of symptom 

reporting among students not having physical 

education classes that day and students having 

class in the morning was 7.5 percent. The highest 

rate of symptom reporting, 50.9 percent, was 

observed in the class which met between 1 and 2 

p.m. Peak levels of NO and NO2 were recorded 

during this hour. As mentioned, the peak level of 

sulfur oxide had been recorded at 1 p.m. In the 

class that met 1 hr later, when peak levels of 

oxidant were recorded, the rate of symptom 

reporting dropped slightly to 45 percent. On 

September 21 and 22, when both oxidant 

concentrations and symptom rates were 

somewhat lower than on September 13, symptom 

215 
rates were distributed randomly among physical 

education classes. Unfortunately, concentrations 

of pollutants other than oxidant were not 

measured on these two days. 

The author noted that on September 13, notonly 

the rate of symptom reporting but also the 

distribution of symptoms changed with physical 

education class. Among students not having 

physical education class or having it in the 

morning, 94.6 percent of students with symptoms 

reported eye irritation. Only 37.5 percent of these 

students complained of sore throat, and 19.6 

percent complained of coughing. In the physical 

education class meeting between 1 and 2 p.m., 

however, only 50 percent of students with 

symptoms reported eye irritation, while 81.0 

percent reported sore throat, 60.7 percent reported 

coughing, and 59.5 percent reported chest 

discomfort. These findings suggested tothe author 

that the components of photochemical pollution 

that promote eye irritation may be different from 

those that promote respiratory symptoms. 

At school A, the majority of students with 

symptoms on September 21 and 22 complained of 

eye irritation. 

At school B, as mentioned, an unusually high 

number of eighth-grade students complained of 

symptoms on October 3, 1972. At two nearby 

stations, maximum oxidant concentrations of 0.09 

and 0.07 ppm were recorded on that day. No 

mention of other pollutant concentrations was 

made in Shimizu's report. Of 248 students 

surveyed, 152 (61.3 percent) reported some type of 

symptom. The pattern of symptom reporting atthis 

school was somewhat different from either pattern 

observed at school A. At school B, 53.5 percent of 

males and 71.7 percent of the females surveyed 

reported symptoms, whereas at school A there had 

been little difference in symptom rates between 

the sexes. In school B, higher percentages of 

students with symptoms than in school A reported 

such nervous-system-related symptoms as 

headache, dizziness, nausea, and numbnessofthe 

extremities (which can result from hyperventilation).These symptoms, like chest discomfort 

occurred morefrequently in femalesthan in males. 

In school B, only 21.7 percent of students with 

symptoms reported eye irritation. 

Shimizu's findings arouse interestastowhether 

the components of photochemical air pollution that 

promote nervous-system-related symptoms like 

those described above are differentfrom eitherthe 

components that promote eye irritation or those 

that promote respiratory symptoms. As yet, 

however, these findings are far from conclusive, 

particularly since pollutants other than oxidants 

were in the ambient air during this study. 

Makino and Mizoguchi 32 reported a study, 

performed over the year July 1972 to June 1973, 

of the influence of air pollution exposures on rates 

of symptom reporting in students. This study 

included 854 students, of whom 110 were in 

kindergarten, 327 were in elementary school, 335 

were in junior high school, and 82 were in senior 

'high school. AII students attended schools in the 

northern part of Tokyo. Each day they completed a 

questionnaire inquiring about the presence of 17 

symptoms, including eye irritation, irritation of the 

upper respiratory tract, cough, phlegm production, 

fatigue, headache, and fever. Daily rates of 

symptom reporting were correlated with same-day 

pollution concentrations. We believe that the 

pollution concentrations used in statistical 

analyses were daily maximum hourly 

concentrations, but this is not clearly stated in the 

report. Measured pollutants included oxidant, 

nitric oxide, nitrogen dioxide, sulfur dioxide, and 

micro-particulates. Measurement methods were 

not reported. Daily maximum hourly daytime 

temperature and minimum hourly daytime 

humidity were also considered. 

The data were analyzed in several different 

ways. In the first analysis, rates of symptom 

reporting on two days of high pollution, one in July 

and one in August, were computed. On the first 

day, maximum hourly concentrations of oxidant, 

nitrogen dioxide, nitric oxide, and sulfur dioxide 

were, respectively, as follows: 0.17, 0.10, 0.10, 

and 0.03 ppm. On the second day, maximum 

hourly concentrations of OX, NO2, NO, and S02 

were, respectively, as follows: 0.21, 0.07, 0.09, 

and 0.14 ppm. On both days, rates of nearly all 

symptoms were higher than corresponding 

monthly average rates. The elevation in rates was 

most marked for eye irritation, which an average of 

10.7 percent of students reported on the two highpollution days, versus an average of 1.6 percent in 

the months of July and August. Rates of sore 

throats (average of 4.0 percent on high-pollution 

days versus 0.65 percent in corresponding 

months) and headache (2.9 vs. 1.0 percent) were 

also elevated noticeably. 

In the next analysis, individual environmental 

measurements were correlated with same-day 

symptom rates within each month of the study. Of 

105 oxidant/symptom correlations, 37 (35 

216 
percent) were significant at a= 0.05. Of these, 14 

(13 percent) were significant at a= 0.001. Of 98 

S02 symptom correlations, 22 (22 percent) were 

significant at a= 0.05, and 10 (10 percent) were 

significant at 0.001. Of 105 NO2/symptom 

correlations, 22 (21 percent) were significant at a 

= 0.05, and none were significant at a= 0.01. Of 

116 temperature/symptom correlations, 19 (16 

percent) were significant at a= 0.05. Only 5(6 

percent) of 88 NO/symptom correlations were 

significant at a= 0.05. The directions of these 

correlations were not presented. 

When these types of correlations were 

computed over the whole year of study, 6(46 

percent) of 13 oxidant/symptom correlations were 

significant at a= 0.01. AII coefficients were 

positive. The association between oxidant 

exposure and symptom rate was most marked for 

dyspnea (for which the oxidant/symptom 

correlation was 0.653) and for eye irritation, 

lacrimation, and sore throat. For each of these 

latter three symptoms, the oxidant/symptom 

correlation was 0.621 (p < 0.001). No yearly 

symptom/pollution correlations were significant 

at a= 0.05 for S02, NO2, or NO. Seven of 13 (54 

percent) _yearly temperature/symptom correlations were significant at a=0.05. AII seven were 

positive. Coefficients of correlation between 

oxidant concentrations and symptoms were 

generally larger than those between temperature 

and symptoms. 

In another analysis, pairs of environmental 

variables were correlated with same-day rates of 

symptom reporting. Correlations between oxidant/NO2 and symptom rates were significant 

at a= 0.05 in 9 of 13 cases (69 percent). 

Correlations between oxidant/S02 and symptom 

rates were significant in 7 of 13 cases(54 percent), 

as were correlations between oxidant/temperature and symptom rates. Environmental variable 

pairs that did notcontain oxidantwere significantly 

correlated with symptoms less often and less 

strongly than those that contained oxidant. 

In another analysis, the authors compared 

symptom rates on days when the maximum hourly 

oxidant level exceeded 0.10 ppm to rates on days 

when it did not. Such comparisons are shown for 

six symptoms in Figure 10-4. As the figure shows, 

symptom rates, particularly rates of eye irritation 

and sore throat, were quite consistently elevated 

on the higher-oxidant days. The report does not 

clearly state why the months of January through 

April 1973 are missing from the line showing 

symptom rates on higher-oxidant days in Figure 

10-4. It is probably safe to surmise, however, that 

since these are winter or early spring months, they 

contained very few days on which the oxidant 

concentrations exceeded 0 10 ppm. 

Mizoguchi et a1. 37 investigated the effects of 

short-term air pollution exposure on 515 students 

in a junior high school in southeasternTokyo. Over 

a 2-month period between May and July 1974, 

these students completed a daily questionnaire 

inquiring about the presence of 17 symptoms of 

the respiratory and other systems. Air pollution 

measurements were made on the school grounds. 

Oxidants were measured each hour by the KI 

method; ozone was measured by (presumably 

ethylene)chemiluminescence; and nitric oxide and 

nitrogen dioxide were measured by the Saltzman 

method. Concentrations of eight other pollutants 

were also measured. The maximum hourlyoxidant 

level observed during this study was 0.23 ppm. No 

frequency distribution of pollutant concentrations 

was presented. 

In still another analysis, Makino and Mizoguchi 

compared symptom rates on days when the 

oxidant concentration exceeded 0.15 ppm to rates 

on days when oxidant concentration did not 

achieve 0.10 ppm. Results of this comparison are 

shown in Figure 10-5. As expected from the results 

of other analyses of these data, increases in 

symptom rates on the higher-oxidant days were 

most marked for eye irritation, sore throat, 

headache, and coughing. 

Three types of statistical analyses were 

performed on data gathered from all students. In 

the first type, a simple correlation analysis, daily 

maximum hourly measurements of each pollutant, 

were correlated with the proportion of students 

reporting each symptom on the same day the 

pollution measurements were made. Correlation 

coefficients statistically significant at a= 0.001 (r>_ 

0.5) were computed between oxidant 

concentrations and 5 of 17 symptoms, including 

eye irritation, shortness of breath, sore throat, 

headache, and blurred vision. Positive coefficients 

significant at a= 0.01 (r > 0.35) were computed 

between oxidant concentrations and seven other 

symptoms. Ozone was found to correlate 

significantly at a=0.001 with three symptoms(eye 

irritation, shortness of breath, and sore throat) and 

at a= 0.01 with seven other symptoms. Sulfur 

dioxide, like oxidant, was found to correlate 

significantly with 12 of 17 symptoms at the 0.01 

level. Suspended particulate matter correlated 

217 
slgnlflcantly wlth 13 symptoms. Daily minimum 

relative humidity correlated negatively and 

significantly with 15 symptoms. No correlations of 

pollutants with other pollutants and with 

meteorologic variables were presented. 

In the second analysis, daily proportions of each 

individual symptom were correlated multiply with 

pairs of same-day measurements of environmental variables (The report was unclear as to 

whether all possible environmental-variable pairs 

or only selected pairs were considered.) Six such 

pairs were correlated significantly at a= 0.001 (r? 

0.6) with both eye irritation and shortness of 

breath. Oxidant was a member of all 12 of these 

pairs Seven pairs, of which six contained oxidant, 

were correlated signiflcantly with sore throat. Five 

pairs correlated significantly with hoarsness, but 

only one of them contained oxidant. None of the 

pairs of environmental variables that correlated 

significantly with symptom rates contained ozone, 

but whether ozone was included in any of the 

tested pairs is not clear. 

The third analysis was a principal components 

analysis. Three environmental principal 

components were derived. The first was loaded 

heavily for oxidant, ozone, and sulfur dioxide; the 

second was loaded heavily for most pollutants 

except oxldant and ozone (the second also included 

OXIDANT CONCENTRATION 

> 0.10 ppm 

~~~~ <0.10ppm 

EYE IRRITATION 

2.0 

c 

1.5 

d U 

61 a 1 

W 1.01 

N ~ 

Q ~ 

CC. ~ 

0.5 

~ 

✓ 

0 

8 10 12 2 4 6 8 10 12 2 4 6 8 10 12 2 4 6 

2.0 72-1-IE-73—loIs--72-0 4- 73--1•Is-72-1 F73-- I 

111 

DYPSNEA I' HEADACHE 

L STRANGE ODOR 

c m 

u 

a 1.0~ I: 

Lu 

0.5 

8 10 12 2 4 6 8 10 12 2 4 6 8 10 12 2 4 6 

TIME, month and year 

Figure 10-4. Monthly changes in symptom and complaint rates with daily maximum 

hourly oxidant content above and below 0.10 ppm. 32 

218 
sulfur dioxide ; and thethlydwas loaded heavllyfor 

temperature and carbon monoxide. Nearly all 

symptoms, particularly such irritation symptoms 

as eye irritation, sore throat, hoarsness, cough, 

and phlegm, were associated strongly with the first 

principal component. No symptoms were strongly 

associated with either of the other two 

components. 

From the overall study sample, the authors 

selected a group of 74 students with allergic 

tendencies and a group of 47 with orthostatic 

dysregulation (O.D.). In the report, the author 

stated that O.D. is not the same entity as 

orthostatic hypotension, though he did not define 

the condition further. O.D. appears to be a 

condition of unusually intense reactivity to stress. 

Over the entire study period, the group with O.D. 

reported noticeably but not significantly hlgher 

rates of cough, headache, and sneezing than either 

of the allergic group or the students as a whole. 

Symptom rates in the allergic group were generally 

higher than in the students as a whole, but not as 

markedly as In the group with O.D. On a day when 

maximum hourly oxidant achieved a concentration 

of 0.23 ppm, rates of symptom reporting increased 

in all groups. Increases in symptom rates were 

largest in the O.D. group, particularly for eye 

irritation, cough, and headache. Again, symptom 

rates in the allerglc group were intermediate 

between the students as a whole and the group 

with O.D. In this report, the author mentions 

(though does not reference) a concurrent 

investigation in whlch no effect of air pollutior 

exposure on pulmonary function was observed. 

This finding is consistent with the hypothesis that 

subjective symptoms may sometlmes reflect 

pollution exposures more accurately than 

objective parameters. 

The Japanese Environment Agency conducted a 

large survey of student health in 1975. Results 

were drawn from schools in seven prefectures 

throughout the country. A preliminary analysis of 

these results has been reported. 21 The period 

covered by this survey is not clearly stated, but it 

Figure 10-5. Comparison of various symptom and complaint , rates on days when 

oxidant concentrations were over 0.15 ppm and below 0.10 ppm. 32 

219 
appears to have been about 180 days. The majority 

of students included in the survey were in junior 

high school, although students in elementary and 

senior high school were also included. 

Unfortunately, the report of the survey often 

presents numbers of people reporting illness, but 

not rates of illness. Rates cannot be computed 

since the report does not present the total number 

of persons included in the survey. Also, the report 

does not present the methods used to generate 

aerometric data, so its findings are quite difficult 

to compare with findings made in the United States. 

The primary survey tool was a symptom 

questionnaire (in some prefectures selfadministered, and in others interviewer-administered) that was completed by students who 

complained of symptoms at school. It must be 

remembered that this survey was based primarily 

on students who voluntarily reported sXrriptoms. 

No systematic effort was made todetermine either 

the extent of nonresponse or ~he effects that 

nonresponse bias may have exerted on the results. 

Thus, as the authors acknowledge, the majority of 

findings of this survey, though interesting and 

suggestive, must be considered preliminary and 

inconclusive. 

The most common symptom reported was eye 

irritation which, on the average, constituted about 

36 percent of all symptoms reported. About 30 

percent of all symptoms reported were general 

symptoms, including numbness in the extremities, 

headache, dizziness, nausea, and lethargy. 

Irritation of the nose and throat constituted about 

20 percent of all reported symptoms. Respiratory 

symptoms, including cough, chest pain, and 

phlegm production, also accounted for about 20 

percent of all reported symptoms. 

In Saitama prefecture, 10 schools containing 

7440 students were included in the survey. On 

days when the oxidant concentration never 

exceeded 0.15 ppm, an average of only 0.052 

percent of students reported smog-related 

symptoms. On days with oxidant concentrations of 

at least 0 15 ppm "ut less than 0 25 ppm, this 

percentage rose to 0.48 percent. On two days 

when oxidant concentrations were at least 0.25 

ppm, an average of 16.4 percent of students 

reported symptoms. A similar (though less strictly 

designed) survey conducted in Kanagawa 

prefecture apparently yielded similar results. In 

one elementary school, 140 of 1510 students (9 

percent) complained of smog-related symptoms on 

one afternoon when the following pollution 

measurements were made at a nearby monitoring 

station: oxidant, 0.253 ppm; nitrogen dioxide, 

0.018 ppm; and oxides of sulfur, 0.042 ppm. (This 

is the only instance in the report in which 

measurements of pollutants other than oxidants 

are presented.) Eleven students reporting feelings 

of choking and numbness in the extremities were 

taken by ambulance to a nearby hospital. Detailed 

family and personal histories were obtained from 

five hospitalized students. Of these, all had positive 

personal histories of allergic conditions, and four 

had positive family histories. 

DISCUSSION OF OXIDANT EFFECTS ON 

PROMOTION OF SYMPTOMS AND ILLNESS IN 

HEALTHY POPULATIONS 

A consistent positive association between 

oxidant concentrations and rates of new illness 

and symptoms has been observed both in the 

United States and in Japan. The Hammer et al. 

study of student nursest 8 suggests that rates of 

chest discomfort and cough begin to increase at 

maximum hourly oxidant concentrations of 0.25 to 

0.29 ppm and 0.30 to 0.39 ppm, respectively. As 

mentioned, this finding is qu ite consistent with the 

results of the human experimental studies by 

Bates et al., in which decrements in pulmonary 

function and respiratory irritation have occurred at 

an ozone level of 0.37 ppm. Recent Japanese 

studies suggest that cough, chest discomfort, and 

other symptoms may occur in school children at 

oxidant concentrations between 0.10 and 0.15 

ppm. 

The consistency between Hammer's epidemiologic observations and Bates' experimental 

findings suggests that ozone alone may well 

account for some of the symptoms associated with 

oxidant exposures in epidemiologic studies. 

However, it appears quite clearthat ozone does not 

account for al1 the symptoms observed in the field. 

(Indeed, that ozone does not produce the eye 

irritation so often associated with photochemical 

oxidants has been quite well established.) Results 

of the Japanese studies cited above (in which 

correlations between total oxidant and symptom 

reporting rates were larger and more consistently 

significant than ozone/symptom correlations) 

bring nonozone components of photochemical 

pollution under suspicion. 

As mentioned, Shimizu 55 observed that the 

majority of students reporting symptoms in the 

morning of a high-pollution day complained of eye 

irritation. By the afternoon of the same day, when 

220 
ozone concentrations had risen above morning 

levels, the majority of students with symptoms 

complained of respiratory discomfort. This 

observation, coupled with the findings of Bates and 

Hammer, appears to favor the hypothesis that 

certain oxidants other than ozone, though perhaps 

including ozone precursors, produced the eye 

irritation experienced in the morning, and that 

ozone was an important contributor to the 

respiratory irritation experienced in the afternoon. 

On the basis of findings presented here, it 

appears that lower levels of oxidant pollution affect 

Japanese subjects more than American subjects. 

One or both of the following factors may explain 

this disparity. First, the components of Japanese 

oxidant pollution may be different from 

corresponding components in the United States. 

For example, high sulfur oxide levels appear to 

accompany high oxidant levels more frequently in 

Japan than in the United States (e.g., LosAngeles). 

Second, occurrences of elevated pollution appear 

to receive considerably more publicity in Japan 

than United States. This publicity may influence 

symptom, reporting. For these reasons, the results 

of Japanese and American studies should be 

compared with caution, particularly in view of the 

apparent discrepancy between the Japanese 

studies and the Wayne and Wehrle study of 

absenteeism.sa 

The Durham study 12 and the Japanese studies 

cited above arouse interest as to whether 

photochemical oxidant pollution predisposeS 

young populations to the development of increased 

rates of chronic respiratory disease in adulthood. 

Unfortunately, the relationship between acute 

illness or symptoms in childhood and chronic 

respiratory illness in adulthood is not at all clearly 

characterized as yet. Until it has been 

characterized, the question as to whether 

transient irritative symptoms constitute a bona fide 

impairment of health must remain open. 

Impairment of Performance Associated with 

Oxidant Pollution 

ATHLETIC PERFORMANCE 

Wayne et a1. 65 have studied the athletic 

performance of student cross-country track 

runners in 21 competitive meets at a high school in 

Los Angeles County from 1959 to 1964. 

Aerometric data were supplied by the Los Angeles 

County Air Pollution Control District. Oxidant 

measurements for the hour of the race, and for 1, 

2, and 3 hr before the race were related to the 

percentage of athletes who did not improve their 

running times from the previous meet. Oxides of 

nitrogen, carbon monoxide, particulates, 

temperature, relative humidity, wind velocity, and 

wind direction were also considered, but they bore 

less relationship to performance than did oxidant. 

Evidently, correlations between performance and 

sulfur dioxide were not computed. 

The authors observed a significant positive 

relationship between hourly oxidant levels and the 

percentage of team members whose performance 

failed to improve from the previous home meet. 

This relationship is shown in Figure 10-6. As the 

figure shows, the proportion of runners failing to 

improve their times rose as concentrations of 

oxidant in the hour before the race increased over a 

range of 60 to 590 Ng/m 3 (0.03 to 0.30 ppm). 

However, convincing linear relationships between 

oxidant concentration and performance could not 

be discerned within individual portions of this 

concentration range. For both 1959-61 and 1962- 

64, the coefficient of correlations between oxidant 

concentration and percentage of runners failing to 

improve their times was 0.945. As the interval 

between the time of oxidant measurement and the 

race increased, corresponding correlation 

coefficients decreased. 

The results of this study strongly suggest an 

effect of some component of the pollution 

measured as oxidant on team performance. 

Speculating as to possible mechanisms underlying 

the observed association, Wayne et al. cited the 

possibility that some component of photochemical 

smog might elevate the body's demand for oxygen 

during exercise. They also felt that breathing 

photochemical air pollutants might produce 

increased airway resistance or might lead to 

discomfort, which might in turn limit the runners' 

motivation. 

In an analysis performed at the University of 

North Carolina, Herman 23 also investigated the 

effects of air pollution on performance of crosscountry runners. In his analysis, Herman used the 

same data that Wayne et a1. 65 had used from the 

cross-country seasons of 1959-64 as well as data 

from the seasons of 1966-68. The dependent 

variable in Herman's analysis was the average 

speed attained in each meet by each runner who 

participated in all home meets in a given season, 

corrected both for the runner's average speed over 

the season and for the teams'average speed over 

the season. This differed from the dependent 

221 
variable used by Wayne, which was the 

percentage of runners who had failed to improve 

their times from the previous meet. 

Herman constructed regression models that 

incorporated all data from 1959-68 and that 

employed the following as independent variabies: 

hourly air pollution measurements, the individual 

running seasons, the number of days since the first 

home meet of the season, the square of this 

number of days, the maximum daily temperature, 

and the square of this temperature. Stepwise 

regressions in which pollution measurements 

were entered into the model both before and after 

temperature variables were performed. In both 

cases, an inverse association between running 

speed and oxidant measured in the hour before the 

meet (significant at a= 0.0001) was observed. 

Little association between running speed andtotal 

suspended particulates, carbon monoxide, and 

oxides of nitrogen was observed. 

Folinsbee and his associates 14 '15 have conducted two experimental studies that suggest a 

mechanism underlying Wayne and Wehrle's 

epidemiologic observations. These studies are 

described in detail in the preceding chapter. In the 

flrst study, healthy young adults (20 males and 8 

females, 18 nonsmokers and 10 smokers) were 

assigned to one of six exposure groups. Two 

groups of healthy young adults received a 2 hr 

exposure to 0.37 ppm ozone; two other groups 

were exposed to 0.50 ppm; and two others were 

exposed to 0.75 ppm. At each exposure level, one 

group rested throughout exposure, and the other 

underwent alternating 15-min periods of rest and 

exercise. Each of the six groups was also subjected 

to a mock exposure while adhering to its experimental protocol during actual exposure. Atthe end 

of all exposures and mock exposures, all subjects 

underwent a submaximal exerclse test. 

Respiratory frequency significantly increased 

over control values after intermittent exercise at all 

exposure levels and with resting exposures to 0.75 

ppm ozone. Tidal volume decreased significantly 

after intermittent exercise at the 0.50- and 0.75- 

ppm exposure levels. Forced vital capacity decreased significantly after intermittent exercise at 

0.50 ppm ozone, and after both rest and exercise at 

0.75 ppm. Maximum expiratory flow rate at 50 

percent of vital capacity decreased significantly 

after intermittent exercise at all three exposure 

levels. Many subjects reported common symptoms 

of ozone exposure, including sore throat and 

80 

c 

(D 

o. 

4i 

J 

z 

~ 60 

Y 

~ 

Y 

11 

1 

7 

L 

Q 40 

L 

r 

~ 

L 

7 

L 

~ a 

n 

Y 20 

L 

n 

Z 

L 

z 

i 

i! 

O % 

/ 

— Q — 1959-1961 / 

/ 

/ 

-- O-- 1962-1964 ~ Q 

/ 

r= 0.945 FOR BOTH LINES // O 

O * 

O 

/ 

/ 

/ O 

/ 

/ 

/ 

O / 

/ Q 

/ 

/ 

O / 0 Q~ 

/0 

o//O QQ 

/ o , 

0 L 

0 0.10 0.20 0.30 

OXIDANT CONCENTRATION 1 hour BEFORE EVENT, ppm 

Figure 10-6. Relationship between oxidant concentration in the hour before an 

athletic event and percentage of the team failing to improve running time. 65 

222 
cough. Symptom severity increased with exposure 

level and exercise. No significant changes in 

minute volume or in oxygen uptake were observed 

after the submaximal exercise tests employed in 

this study. 

The authors believed that because of the speed 

with which they developed, the observed physiologic changes were due to reflex bronchoconstriction mediated by irritant receptors and 

perhaps by Hering-Breuer (stretch) receptors in the 

lung. 

In the second study of Folinsbee et a1., 14 healthy 

young adult males were exposed to 0.75 ppm 

ozone for 2 hr. During exposure, subjects 

alternately rested for 15 min and lightly exercised 

for 15 min. In random order, each subject also 

underwent a 2-hr control exposure to filtered air. 

At the conclusion of all exposures, subjects 

exercised until exhausted. 

Values of the following parameters, measured 

during maximal exercise, were significantly lower 

after ozone exposure than after filtered air 

exposure: maximum work load attained, heart rate, 

minute voliime, tidal volume, and oxygen uptake. 

The authors believed that the most likely 

mechanism underlying the results observed was 

that ozone produced stimulation of irritant 

receF tors in the lung, which in turn produces 

restri.;tion of inspiratory reserve volume, reduction 

of mr ximal tidal volume, and a modest increase in 

airw; y resistance. 

In the light of Folinsbee's results, it is quite 

conct !ivable that on days of high oxidant exposure, 

ozone irritated the respiratory systems of crosscour, ry runners sufficiently to restrict inspiratory 

capa :ity and to reduce tidal volume. These 

chan les might in turn have prevented the runners 

from taking up enough oxygen to sustain the work 

loads they might have sustained cn lowerexposure days. (In this case, the work load 

sustainable by the runners would be inversely 

proportional to running time.) 

Folinsbee's work 75 also suggests that a healthy 

person exercising submaximally and exposed to 

ozone levels near the highest ambient 

concentrations ever achieved in Los Angeles is 

able to maintain a normal rate of oxygen uptake, 

even in the face of changes in respiratory pattern 

and spirometric parameters. Thus, the decrements 

in running time observed by Wayne in crosscountry runners might not have been seen, or 

might not have been as evident, in shorterdistance runners. Of course, neither the research 

of Folinsbee nor of Wayne allows conclusions as to 

the effects of ozone on oxygen uptake in the ill 

when they are exercising submaximally. 

Folinsbee's work has practical significance 

beyond these interesting physiological 

considerations. In epidemiologic studies, 

decrements in health and performance have been 

quite commonly associated with elevated 

concentrations of photochemical oxidants as a 

class. However, the extent to which such 

decrements might be related specifically to ozone 

exposure has usually been obscure. Though 

Folinsbee's studies do not rigorously prove that 

ozone exposure caused the c creased running 

times that Wayne observed, they do suggest a 

plausible mechanism by which ozone alone might 

have produced the decreased times. 

AUTOMOBILE ACCIDENTS 

To examine the possibility that oxidant pollution 

may impair performance, Ury performed a study61 

of the association of automobile accidents with 

days of elevated hourly oxidant levels. Oxidant 

levels supplied by the Los Angeles Air Follution 

Control District were measured at the District's 

downtown station. Ury applied two nonparametric analyses, a sign test and a Kendall's tau, to 

data for each daylight hour of each weekday in the 

3-month period from August through October for 

both 1963 and 1965. Ninety sets of data covering 9 

hr daily and 5 days weekly were available for 

testing. The sign-test results of each set were 

obtained by taking successive pairs of weeks (first 

week compared with second; third week compared 

with fourth, etc ) and scoring a plus (+) if the week 

with the higher oxidant had more accidents for that 

set, a minus (-) if it had fewer, and a tie if the 

accident frequencies or the oxidant levels were 

equal (Table 10-5). 

AII accidents involving driving under the 

influence of alcohol, narcotics, mechanical 

failures, and spillage on the roadway were 

excluded from analysis, as were accidents occurring in rain, drizzle, or fog. The author does not 

state the fraction of total accidents included in 

these categories, though it may well have been 

quite large. 

In both analyses, photochemical oxidant 

concentrations correlated positively with the 

frequency of motor vehicle accidents. The sign test 

yielded a descriptive two-sided significance level 

of 4 percent. Kendall's tau yielded a level of 5 

223 
percent. In a further analysis, the author compared 

accident rates on days when hourly oxidant levels 

exceeded 0.15 ppm to rates on days when levels 

did not achieve 0.10 ppm. Accident rates were 

elevated on the higher-pollution days. A Wilcoxon 

two-sample test yielded a two-slded significance 

level of 0.07. In this study, oxidant was the only 

pollutant whose relationship to auto accidents was 

considered. 

TABLE 10-5. SIGN-TEST DATA FOR TESTING THE 

ASSOCIATION OF OXIDANT LEVELS WITH ACCIDENTS 

IN LOS ANGELES, AUGUST THROUGH OCTOBER, 

1963 and 1965 61 

Weekday Year Plusa Minus' Tie a 

Monday 1963 22 17 6 

1965 18 18 12 

Tuesday 1963 26 11 7 

1965 23 19 9 

Wednesday 1963 20 15 8 

1965 26 18 10 

Thursday 1963 26 12 11 

1965 31 16 5 

Frlday 1963 27 18 8 

1965 26 19 7 

Total 1963 121 73 40° 

Total 1965 124 90 43` 

Grand total 245 163 83 

aNumbers of accidents during pairs of hours at the same time of dayon thesame 

day of week, one week apart, were compared When the number of accidents 

during the hour with higher oxidant concentration was higher than during the 

lower-oxidant hour, a+1 was assigned When the number of accidents in the 

higher-oxidant hour was lower, a-1 was assigned Ties occurred when the 

number of accidents during the 2 hr was identical 

°Significantly positive at a = 0 001 excluding ties, a = 0 01 including ties 

`Signihcantly positive at a= 0 05, including or excluding ties 

Ury et al. also reported an extension 63 of the 

study clted above, 61 in which the effects of both 

oxidant and carbon monoxide concentrations on 

motor vehlcle accident frequency In Los Angeles 

were Investigated The investigators assessed the 

effects of oxidants over the summers of 1963 and 

1965 (the same two periods that had been 

considered in the original study), and they 

assessed the effects of carbon monoxide over the 

same two periods and over the winter months of 

1964-65 and 1965-66 as well. The same methods 

of data reduction were used in both studies. In the 

follow-up study, the sign test was used to correlate 

the frequency of accidents with mean pollutant 

concentrations during the hour of the accident and 

during each of the 3 hr preceding it. 

In Ury's second study, 63 none of the 90 individual 

sets of comparisons speciflcforday, hour, andyear 

yielded a statistically slgnificant difference 

between the number of positives and negatives 

recorded. This is hardly surprising, since no set 

contained more than six comparisons. However, 

the degree of significance In the relationship 

between accident frequency and the oxidant 

concentration during the hour of the accident was 

greaterthan in the original study.Thisdiscrepancy . 

between studies arose from a systematic error in 

data coding, which was discovered between the 

initial and followup studies. With respect to time of 

day, the strongest relationships between oxidant 

concentration and accident frequency were noted 

at 9 a.m., 10 a m., and 12 noon. This finding raises 

the question of whether accident frequency is 

more strongly associated with an ozone precursor 

than with ozone itself. With respect to day of week, 

the strongest relatlonships were noted on Tuesday 

and Thursday. No consistent relationship between 

accident frequency and lagged oxidant 

concentrations was observed. No relationship 

between carbon monoxide concentration and 

accident frequency was observed in any of the 

perlods considered. 

Ury et a1. 63 present a discussion of variables that 

might have confounded the observed association 

between oxidant concentration and accident 

frequency. It is quite unlikely that inaccuracies in 

accident reporting or pollutant measurements 

could have been large enough to influence study 

results appreciably. Disparitles between pollution 

concentration at accident sites and monitoring 

sites would have been fairly well absorbed by the 

statistical methods employed. The study design 

either negated or minimized effects of hour of day, 

day of week, and weather. Finally, the lack of 

associatlon between carbon monoxide 

concentration and accident frequency argues 

against an effect of varying traffic density on the 

results observed. However, the degree to which 

carbon monoxide measurements actually reflected 

traffic density must remain open to questlon, since 

aerometric information was taken only from a 

single statlon. 

Possibly other pollutants, particularly nitrogen 

and sulfur oxides, may have confounded the 

observed association between oxidant 

concentration and accident frequency. However, it 

is unlikely that such other pollutants could have 

accounted for the bulk of the observed effect, since 

their concentrations tend to be lower in slammer 

than in winter. 

Ury et al. do not speculate as to a mechanism 

underlying the observed association between 

224 
oxidant concentration and accident frequency. 

Conceivably, reduced visual activity, which has 

been observed by Lagerwerff 26 in humans after a 

3-hr inhatation of 392-980 Ng/m 3 (0.2 to 0.5 ppm) 

ozone, was partly responsible for the observed 

results. Increased eye irritation9 46,4e,49,54 Or 

reduced visibility during smoggy periods may also 

have been partly responsible. 

VENTI LATORY PERFORMANCE IN SOUTHERN CALIFORNIA 

The ventilatory performance (measured by the 

Wright Peak Flow Meter) of two groups of thirdgrade children living in the Los Angeles Basin was 

assessed twice monthly for 11 months by 

McMillan et a1. 34 One group of 50 children resided 

in an area exposed to seasonally high photochemical oxidant concentrations. The other group 

of 28 children lived in a less polluted area. 

Aerometric data were obtained from the Los 

Angeles County Air Pollution Control District. 

During the 11 months of the study, no correlations 

between short-term changes in photochemical 

oxidant pollution and ventilatory performance 

were observed. Persistently higher ventilatory 

performance results were obtained from the 

children residing in the more polluted of the two 

communities 

The results of this study are difficult to interpret 

because the two groups of children tested were 

different in several respects. The children with 

lower ventilatory performance reported upper 

respiratory symptoms three times more frequently 

than the children with higher performance. Also, 

the majority of children in the less polluted 

community were from a single ethnic group, 

whereas children in the other community were 

ethnically heterogeneous. As closely as we can 

determine, no statistical adjustment of the data for 

ethnic differences was made. Furthermore, as 

noted by the authors, nitrogen dioxide levels were 

consistently lowest during the winter in the city 

with elevated oxidant exposures. It is conceivable 

`hat the effects of nitrogen dioxide on the study 

results may have offset thuse of oxidant. Finally, 

differences in oxidant exposure in the two towns 

appear not to have been substantial. During the 

days of this study, the mean daily oxidant 

concentration in the low-oxidant city was 0.088 

ppm. The corresponding mean in the high-oxidant 

city was 0.114 ppm. 

PULMONARY FUNCTION IN ARIZONA 

Lebowitz et af. 27 reported a study of the 

combined effects of air pollution and weather on 

the ventilatory function of exercising children, 

adolescents, and adults in Tucson, Arizona. The 

study was conducted in the spring and summer of 

one year. 

Ventilatory function tests inciuded the forced 

vital capacity (FVC) and 1-sec forced expiratory 

volume (FEV). Tests were administered to four 

groups of persons living in Tucson. Two of these 

groups consisted of elementary-school-age 

children. Since no oxidant measurements during 

studies of these groups are mentioned in the 

report, results of these studies will not be 

presented here. 

The third group consisted of 10 white adults of 

both sexes, aged 22 to 32 years, who walked or ran 

5 km (3 miles) along major roads in Tucson during 

the morning or afternoon of one Saturday in 

summer. Members of this group appear to have 

been tested before and after exercising. 

The fourth group consisted of nine white 

adolescents of both sexes, aged 16 to 18 years, 

who participated in a 32 km (20-mile)walkthrough 

major roads in Tucson one Saturday in spring. 

Members of this group were tested before and 

after the walk. 

Aerometric measurements were obtained from 

the Pima County Air Pollution Control District and 

the Arizona State Health Department. Stations 

used in the studies of adults and adolescents wzre 

at least 5 km (3 miles) away from testing sites. 

Among adults who performed the 5-km (3-mile) 

walk or run in the morning, no significant 

differences between ventilatory function values 

before and after exercise were observed During 

the morning, the average temperature was 28°C 

(83 0 F), the relative humidity was 43 percent, and 

the concentrations of suspended particulate 

matter and oxidantswere, respectively, 104Ng/m 3 

and 0.01 ppm. Among adults who performed the 

walk or run in the afternoon, post-exercise 

decreases in ventilatory function of less than 5 

percent were observed. These decreases were not 

statistically significant, and they disappeared 

within 30 min after exercise. However, they were 

evidently larger than changes in ventilatory 

function among those who had exercised in the 

morning. During the afternoon, the average 

temperature was 34°C (941 F), the relative 

humidity was 23 percent, and the concentrations 

of suspended particulate matter and oxidant were, 

225 
respectively, 89 /Ug/m 3 and 0.03 ppm On this day, 

the suspended sulfate level was estimated to have 

been less than 2.5 Ng/m 3 . 

Among the nine adolescents who completed the 

32-km (20-mile) walk in the spring, consistent and 

statistically significant post-exercise decreases in 

ventilatory function were observed. Average 

values of FVC before and after exercise were, 

respectively, 3.6 and 3.0 liters. Corresponding 

average values of FEV, were 3.0 and 2.7 liters. On 

the day of the 32-km (20-mile) walk, the 

temperature ranged from 15 1 C to 31 °C (59°F to 

881 F), the average humidity was 30.5 percent, the 

average suspended particulate concentration was 

133.7 ug/m3 , the average sulfate concentration 

was 3.7 Mg/m3 , and hourly peak oxidant 

concentrations increased with time from 0 01 to 

0.12 ppm. The 32-km (20-mile) walk ended about 2 

p.m., which is usually near the hour of daily 

maximal oxidant concentration in Los Angeles. 

Whether this is also true of Tucson is not stated in 

the report. 

Since oxidant levels appear to have been higher 

during the 32-km (20-mile) adolescent walk than 

during the 5-km (3-mile) adult walk or run, and 

since statistically significant post-exercise 

decreases in lung function were observed in the 

adolescents but not in the adults, it is conceivable 

that hourly maximum oxidant concentrations 

somewhere between 0.03 and 0.12 ppm may 

affect the ventilatory function of exercising 

humans, if exercise is sufficiently strenuous or 

sustained. However, the Lebowitz study does not 

provide a rigorous test of this hypothesis, since 

adolescents and adults underwent different 

exercise regimens and since the aerometric 

measurements employed were made at least 5 km 

(3 miles) from the study site. 

Lebowitz et a1 27 suggest five hypothetical 

mechanisms by which pollution might produce 

decreased ventilatory function: (a) an irritant effect 

of pollution on the upper airways, (b) bronchial 

constriction irr response to irritation, (c) increase in 

flow-resistance in the upper airways and possibly 

in the lower airways, (d) decreases in lung 

compliance and lung recoil, and (e) transient 

edema of the alveoli. 

Note that two factors other than oxidant 

exposure may have influenced the outcome of the 

studies of adolescents and adults. First, fairly 

substantial levels of suspended particulate matter 

were present along with oxidants on the days 

when these studies were conducted. This fact 

raises the possibility that particulates alone or in 

combination with oxidants may have affected 

ventilatory function. Second, the decline in 

ventilatory function was greater after a 32-km (20- 

mile) walk than after a 5-km (3-mile) walk or run. 

The 32-km (20-mile) walk may well have been 

more demandi ng for adolescents than the 5-km (3- 

mile) walk or run for adults, even though the adults 

were somewhat older. Thusthe results might have 

been observed even in the absence of pollution 

exposure These two factors considerably restrict 

the vigor with which the hypotheses stated in the 

previous paragraph can be advanced 

EFFECTS OF OXIDANT ON PULMONARY 

FUNCTION IN JAPAN 

Kagawa and Toyama 24 reported a study of the 

effects of environmental factors on the pulmonary 

function of 21 children, all aged 11 years, at an 

elementary school in Toyko, Japan. The study 

sample appears to have been quite evenly divided 

by sex Pulmonary function tests were 

administered once a week for 29 weeks between 

June and December 1972. Tests were generally 

performed between 1 and 3 p.m. Six physiologic 

variables were measured. total airway resistance 

(Raw), specific conductance (Gaw/Vtg), maximal 

expiratory flow at 50 and 25 percent vital capacity 

left to be expired (respectively, Vso and V25 ), forced 

vital capacity (FVC), and a pulmonary gas 

distribution index (GDI) based on the single-breath 

nitrogen elimination rate following a full 

inspiration of pure oxygen. 

Aerometric measurements were made on top of 

the children's three-story school. The following 

measurement methods were used: For oxidant, 

neutral buffered potassium iodide and coulometric 

methods; for ozone (03), ethylene chemiluminescence; for hydrocarbons (HC), hydrogen flame 

ionization; for nitric oxide (NO) and nitrogen 

dioxide (NOz), Saltzman method; for sulfur dioxide 

(S02), conductimetric method; and for suspended 

particulate matter (SPM), a light scattering 

method. Temperature and relative humidity were 

also measured. 

During this study, hourly average concentrations of oxidant ranged from about 0.03 to 

about 0.17 ppm, and hourly average 

concentrations of ozone ranged from about0.01 to 

about 0.15 ppm. Over this period, the maximum 

hourly concentrations of NO, NO2, and SOz were 

about 0.08, 0.23, and 0.05 ppm, respectively. The 

226 
maximum hourly average concentration of 

particulate matter was about 350 /jg/m 3 . 

Simple correlation coefficients were computed 

between pulmonary function test results over the 

29 weeks of study and mean pollutant 

concentrations (1 ) between 1 and 3 p.m. on the day 

of testing, (2) between 12 noon and 1 p.m. on the 

same day, (3) between 1 p.m. on the day before 

testing and 1 p.m. on the testing day. Correlations 

between temperature and humidity (averaged over 

the same periods) and pulmonary function test 

results were also computed. A summary of 

correlation coefficients significant at a= 0.05 is 

presented in Table 10-6. As the table shows, 

pulmonary function test results were significantly 

correlated with temperature far more oftenthan 

with any other environmental factor. Temperature 

was also correlated positively and significantly 

with ozone, and negatively and significantly with 

NO and suspended particulate matter (SPM). 

Significant correlations between temperature and 

Raw, Vso, V25, and GDI were consistently positive. 

The degree and consistency of correlation of 

temperature with V5o and V25 were particularly 

striking. Significant correlations of temperature 

with Gaw/Vtg and wlth FVC were consistently 

negative. 

The degree of correlation between pollutant 

concentrations and pulmonary function test 

results was generally greater with concentrations 

during testing (1 to 3 p.m.) than during either of the 

two previous perfods. AII significant correlations 

between pollutant concentrations and test results 

bore the sign that would be expected if pollution 

TABLE 10-6. NUMBER OF SUBJECTS FOR WHOM CORRELATION COEFFICIENTS BETWEEN ENVIRONMENTAL 

AND RESPIRATORY FUNCTION MEASUREMENTS ARE SIGNIFICANT AT P< 0.05, JAPAN, 1972 1'24 

Physiologic variables 

V max V max Gas ~ 

Environmental at at distribution 

variables Raw Gaw/Vtg 5_0 1% FVC 25_%_FVC index _ FVC 

Oxldant D° 1(0 53)° 0 0 0 0 1(-0 45) 

1 ° 1(0 49) 1(-0 56) 0 0 0 1(-0 44) 

24e 2(0 65--0 63) 0 1(-0 71) 1(-0 60) 0 0 

03 D 5(0 80--0 45) 5(-0 66---0 48) 1(-0 62) 1(-0 66) 2(0 56--0 48) 3(-0 69 ---0 48) 

1 2(0 66--0 63) 2(-0 68---0 52) 0 0 0 4(-0 62--0 46) 

24 3(0.62---0 45) 3(-0 59-0 45) 0 0 0 2(-0 44) 

Hydro- D 1(0 59) 2(-0 51---0 44) 1(-0 50) 0 4(0 76-0 56) 4(-0 63-0 46) 

carbon 1 2(0 53--0 48) 1(-0 57) 2(-0 74-0 56) 1(-0 59) 1(0 55) 5(-0 70--0 44) 

24 0 0 0 0 0 0 

NO D 0 0 8(-0.56---0 47) 10(-0 60--0 47) 0 0 

1 0 0 4(-0.56---0 49) 7(-0 71 ---0 45) 0 0 

24 1(0 69) 1(-0 70) 4(-0 50~-0 44) 7(-0 64--0 47) 0 0 

NO2 D 0 0 2(-0 51---0 44) 1(-0 58) 0 0 

1 0 0 3(-0 56---0 44) 2(-0 68 --0 47) 0 0 

24 0 0 0 0 0 0 

SOz D 2(0 47) 1(-0 50) 0 1(-0 76) 6(0 55--0 47) 0 

1 1(0 54) 2(-0 53--0 45) 1(-0 47) 1(-0 75) 1(0 52) 0 

24 0 0 0 0 0 3(-0 59---0 44) 

SPM D 0 0 1(-0 45) 1(-0 44) 0 0 

1 0 0 0 1(-0 46) 0 0 

24 1(0 58) 0 0 0 0 0 

Tempera- D 12(0 72--0 46) 9(-0 76---0 52) 19(0 82-0 56) 17(0 81- 0 46) 3(0 56-0 45) 5(-0 75---0 47) 

ture 1 13(0 72--0 44) 10(-0 75---0 44) 19(0 83-0 55) 13(0 81 --0 44) 4(0 58-0 44) 6(-0 77--0 47) 

24 14(0 73--0 48) 9(-0 79---0 45) 19(0 90-0 58) 19(0 82-0 58) 4(0 61--0 46) 5(-0 75---0 55) 

Relative D 0 0 0 1(0 50) 0 0 

humldlty 1 0 0 1(0 46) 1(0 55) 1(0 44) 0 

24 2(0 53--0 45) 3(-0 54---0 46) 15(0 68-0 44) 12(0 74--0 46) 3(0 55-0 48) 4(-0 74-0 51) 

'Total of 21 children 

°D, During measuwement of respiratory function 

`Numbers in parentheses are the range of their correlation coefficients 

° One hour before measurement of respiratory function 

e 24, Average of hourly values during 24 hr before measurement of respiratory function 

227 
indeed exerted a deleterious effect on pulmonary 

function. The pollutants most frequentlycorrelated 

significantly with test results were (in descending 

order) NO, ozone, HC, and S02. A point of interest is 

that oxidant and NOz were only infrequently 

correlated with test results. In about 25 percent of 

subjects, the ozone concentration during testing 

was significantly correlated with Raw, Gaw/Vtg, 

and FVC. Concentrations of S02 were not 

significantly correlated with pulmonary function 

parameters as frequently as were concentrations 

of ozone. However, S02 concentrations tended to 

correlate significantly with the same parameters 

as ozone Nitric oxide and NO2, unlike ozone and 

SOz, tended to correlate significantly with Vso and 

V25. On the basis of these findings, the authors 

suggested that ozone and SOz may exert effects 

primarily in the upper airways, while the nitrogen 

oxides may exert effects primarily in the lower 

a irways. 

Kagawa and Toyama 24 also presented the 

individual significant correlations between 

pulmonary and pollution concentrations between 

1 and 3 p.m. on the testing day. Such correlations 

were unusually frequent in three of the 21 

students. 

In further analysis, the authors statistically 

corrected for the effects of temperature by 

computing partial corretations between pollution 

concentrations (presumably between 1 and 3 p.m.) 

and pulmonary function test results. This analysis 

greatly reduced the number of significanf 

correlations between pollution and pulmonary 

function. However, significant partial correlations 

of ozone concentration with Raw were observed in 

three subjects. Significant partial correlations of 

ozone with Gaw/Vtg and with V50 or V25 were 

observed in one subject each. The pattern of 

significant partial correlation between S02 and 

pulmonary function remained very similar to that 

between ozone and pufmonary function. After the 

partial correlation analyses, only one significant 

correlation of nitrogen oxrdes with Vso or V25 

remained. 

Kagawa and his associates continued to collect 

pulmonary function data from the students 

described above. Results obtained from November 

1972 to October 1973 have been presented by 

Kagawa et al in a separate report. 25 In Kagawa's 

origirial study, temperature was observed to exert 

a consistent effect on pulmonary funciion To deal 

with this effect, the investigators divided the study 

into a low-temperature season lasting from 

November 1972 to March 1973, and a hightemperature season lasting from April to October 

1973. Data were collected on 19 days in the lowtemperature season and on 30 days in the hightemperature season. Data from 19 students (10 

males and nine females) were analyzed. 

As in the first study, simple correlations between 

levels of environmental factors and pulmonary 

function test results were cornputed. The period 

over which levels of environmental factors were 

averaged is not clearly stated in the second study. 

However, we believe that these levels were 

averaged over the 2 hr between 12 noon a nd 2 p. m. 

on the day of pulmonary function testing. In the 

analysis of the second study, the investigators 

considered the environmental and pulmonary 

function variables that had yielded an appreciable 

number of significant correlations in the first 

study. The environmental variables considered 

were temperature, ozone, NO, NO2, [NO + NO21, 

SOz, and SPM. Oxidant was not considered. The 

pulmonary function variables considered were 

Raw, Gaw/Vtg, Vso, and V25. 

During this study, hourly averaged ozone 

concentrations ranged from about 0.01 to about 

0.30 ppm. The maximum hourly average 

concentrations of NO, NO2, and SOz were about 

0.18, 0.30, and 0.16 ppm, respectively. The 

maximum hourly average concentration of 

suspended particulate matter was about 450 

Ng/m 3 . 

In the high- and low-temperature seasonspecific analyses, temperature was consistently 

positively correlated with Raw, Vso and Vzs , and 

negatively correlated with Gaw/Vtg. However, 

when data for one full year were analyzed, 

temperature was negatively associated with Raw 

in 17 of 19 subjects. Thus it appeared that the 

effect of temperature on Raw might be quite 

heavily dependent of the selection of the study 

period. 

The results of this second study were somewhat 

similar to those of the first with respect to ozone. 

Concentrations of ozone were generally positively 

correlated with Raw and negatively correlated with 

Gaw/Vtg in both the high- and low-temperature 

seasons. Interestingly, this was more consistently 

true during the low-temperature season than 

during the high-temperature season, when 

measured ozone concentrations were highest 

During the low-temperature season, 8 of the 19 

ozone-Raw correlations and 7 of 19 ozoneGaw/Vtg corretations were significant at a= 0.05. 

228 
When partial correlation analysis, which 

statistically removed the effects of temperature, 

was performed, five ozone - Raw correlation 

coefficients retained statistical significance. Thus 

it appeared that the apparent effect of ozone on 

Raw during the low-temperature season would not 

have been due to temperature alone. In the hightemperature season, only 1 of 38 correlations of 

ozone with Raw or Gaw/Vtg was significant. 

Simple correlations suggested little detrimental 

effect of ozone on V50 or V25 in either season. 

However, after a partial correlation analysis that 

incorporated temperature, the number of 

significant negative correlations between ozone 

and V50 increased from one to five. This result is 

difficult to square with results of Kagawa's first 

study,24 in which correction for temperature 

considerably reduced the number of significant 

correlations between pollution and pulmonary 

function. 

As in Kagawa's first study, concentrations of NO 

were significantly correlated (negatively) with V50 

and V2e considerably more consistently than with 

Raw or Gaw/Vtg. However, concentrations of NO2 

were significantly correlated (positively) with Raw 

and (negatively) with Gaw/Vtg more consistentiy 

than with -Vso or V25 . Significant correlations of 

NO2 with Raw and Gaw/Vtg occurred only during 

the high-temperature season. Few significant 

correlations between S02 concentrations and 

pulmonary function parameters were observed. 

During the low-temperature season, concentrations of SPM were generally correlated 

negatively with Raw and positively with Gaw/Vtg. 

During the high-temperature season, the direction 

of these correlations was generally reversed. In 

both seasons, SPM concentrations were generally 

negatively correlated with both Vso and V25. These 

results suggest quite strongly that the calculated 

effects of pollution on pulmonary function, as with 

temperature, may depend quite heavily on the 

selection of study period. 

Among the 19 students in Kagawa's second 

study, 5 showed significant correlations both 

between pulmonary function and at least three 

environmental factors, and between 

environmental factors and measures of airway 

resistance (Raw or Gaw/Vtg) as well as maximal 

flow ( V50 or V25). Thus the second study, like the 

first, suggests tha't some segments of the healthy 

population may be more susceptible to pollution 

exposure than others. 

Three interesting considerations emerge from 

the results of Kagawa's studies. First, the results 

disclose an association between ozone (but not 

oxidant) and decrements in pulmonary function. 

Second, even within the healthy population, 

certain groups may be more sensitive than others 

to the effects of air pollution exposure. The results 

of several studies already described in this chapter 

are consistent with the same hypothesis. One 

might hypothesize further that such sensitive 

groups may be at unusually high risk of developing 

chronic illness after years or decades of elevated 

pollution exposure. No studies have as yet 

specifically addressed this hypothesis. Third, 

statistical techniques currently available do not 

appear fully equal to the task of separating the 

health effects of pollutants from temperature or 

from each other. Available statistical techniques 

tend to focus the attention on individual 

environmental factors as separate entities. In 

reality, however, the effects of an individual 

pollutant may be dependent both on the presence 

of other pollutants and combinations of climatic 

factors. Statistical separation of the effects of 

individual components of existing environmental 

conditions may therefore yield a misleading 

description of the true situation. It is hoped that 

future advances in statistical methodology will 

enable investigators to characterize interactions of 

environmental factors more completely than is 

possible at present. 

DISCUSSION OF THE EFFECTS OF OXIDANTS ON 

PERFORMANCE 

The studies reported by Wayne et a1. 65 and by 

Ury61 suggest that photochemical oxidant pollution 

can impair performance of tasks as different as 

competitive running and automobile operation. As 

mentioned in the Wayne et al. study, the proportion 

of runners failing to improve their times increased 

quite consistently (r = 0.945) with increasingly 

hourly oxidant exposures over a range of 60 to 590 

Ng/m 3 (0.03 to 0.30 ppm). However, within 

individual portions of the oxidant concentration 

range, unequivocal linear relationship between 

oxidant exposure and performance could not be 

discerned. 

Findings of Folinsbee's experimental studies of 

ozone exposures 14 '' 5 suggest that on high-oxidant 

days, air pollutants may have restricted the 

mechanical ventilatory function of the runners 

observed by Wayne et al. to the point where these 

229 
runnerv were no longer able to take up enough 

oxygen to support optimum performance at 

maxrmum exertion. Folinsbee's findings further 

suggest that ozone alone may have accounted for 

the results observed by Wayne et al. This 

suggestion remains open to question, since 

Folinsbee's exposure concentration of ozone, 0.75 

ppm, was considerably higher than most oxidant 

concentrations observed in the Wayne et al. study. 

Studies of ambient oxidant exposure and 

pulmonary function have yielded mixed results. 

McMillan's study 34 showed no association 

between either short-term or long-term oxidant 

exposure and impairment of pulmonary function in 

children. However, this study is difficult to 

rnterpret, since pulmonary function tests were 

performed at rather wide intervals (twice per 

month) and since the children in the high- and lowpollution communities were ethnically dissimilar. 

The findings of Lebowitz 27 and Kagawa et al. 2a,zs 

in contrast to those of McMillan, 34 suggest that 

oxidant pollution may contribute to decrernents in 

pulmonary function. The results of Lebowitz, like 

those of Folinsbee, are consistent with the 

hypothesis that the degree to which oxidants affect 

pulmonary function is positively related to the level 

of exercise undergone by the subjects. Clearly, 

though, the Lebowitz study must be interpreted 

cautiously, since its design did not allow for 

separation of the effects of environmental and 

meteorologic factors. 

The results of Kagawa et a1. 24,25 suggest that 

short-term exposure to oxidant air pollution may 

affect the large airways more than the small ones. 

A point of interest is that Kagawa observed 

stronger correlations of pulmonary function with 

ozone than with oxidant. Conceivably, the 

mechanism underlying Kagawa's observations is 

similar to that underlying Folinsbee's. In any case, 

the results of Kagawa et al., like those of Wayne et 

al., enhance confidence that ambient ozone alone 

exerts effects on humans, whatever the effects of 

other photochemrcal substances may be. 

Whether transient decrements in pulmonary 

function constitute a clean-cut hazard to health is 

not yet known. Recent evidence suggests that 

childhood infection, often accompanied by 

rmparrment of pulmonary function, may 

predispose subjects to chronic respiratory disease 

later in life. 28 However, the degree to which 

pollution-associated impairment promotes such 

an outcome has not yet been determined. 

Eye Irritation In Relation to Variations in Oxidant 

Levels 

PANEL STUDIES 

No symptom has been associated with ambient 

photochemical pollution more frequently or 

consistently than eye irrrtation. In an effort to 

determine the types and concentrations of 

pollutants responsible for eye irritation, 

investigators have studied a variety of individuals 

in the Los Angeles area. Studies conducted in 

1954, 1955, and 1956, reported by Renzetti and 

Gobran46 of the Air Pollution Foundation, San 

Marino, California, were among the first studies in 

this field. 

The first part of the Renzetti and Gobran study 

was conducted from August through November 

1954. 46 In this study, several panels of observers 

were asked to report eye irritation on Tuesdays and 

Fridays. Later, panelrsts were asked to report only 

on those days for which eye-irritating levels of 

pollution had been predicted. Thrs latter study 

design may have introduced bias into observed 

results. In general, the observers were office and 

factory workers. One of the panels consisted of a 

group of scientists of the California lnstitute of 

Technology. The eye-irritation data were 

compared with instantaneous values of oxidant 

concentrations as measured by potassium iodide 

recorders. 

Data from the 1954 study46 are summarized in 

Figure 10-7 and in Tables 10-7 and 10-8. These 

data strongly suggest that the degree of eye 

irritation increases as the oxidant level increases 

over a range from nearly zero to about 0.45 ppm. 

From Figure 10-7, it is impossible to discern a 

discrete threshold oxidant concentration below 

which no eye irritation occurs. In Table 10-8, data 

from a panel of scientists are summarized. The 

table suggests that oxidant was not the only 

environmental variable statistically associated 

with eye irritation in Los Angeles in 1954, 

although oxidant explained a higher proportion of 

the variation in eye irritation than any of the other 

variables measured. Data from the panel of 

scientists yielded the greatest number of 

significant correlations between eye irritation and 

environmental variables other than oxidant. 

The second part of the study46 was conducted 

from August through November 1955. In Figure 

10-8, a regression line relating maximum eye 

230 
irritation in a panel of scientists to maximum 

oxidant concentration is presented. The 

relationship between eye irritation and oxidant 

concentration is qualitatively similar to that 

observed in 1954 in that eye irritation increased as 

the oxldant level increased, and in that a discrete 

oxldant threshold concentration could not be 

clearly discerned. 

From the data provided by the Air Pollution 

Foundation studles, 46 linear mathematical 

relationships between maximum oxidant values 

and mean maximum eye-irritation values were 

derived. The data from these studies demonstrated 

increasing eye irritation wlth increasing 

concentrations of oxidant pollutlon over the range 

of Instantaneous values from 100 to 880 Ng/m 3 

(0.05 to 0.45 ppm), although no clear threshold 

level for this effect was apparent (Figure 10-7). 

Other studies on eye irritation have been 

performed, including one in which a panel of 

employees of the Los Angeles Air Pol lution Control 

Dlstrict was queried during the period 1955-58." 

A group of environmental sanitation workers in the 

San Francisco Bay Area was also studied during 

thls same period. These panels demonstrated a 

tendency to experience increasing occurrence of 

eye irritation wlth increasing oxidant levels. As in 

all such studies, there were some individuals who 

reported eye irritation even when there was no 

oxidant present. 

TABLE 10-7. CORRELATION OF EYE IRRITATION WITH 

SIMULTANEOUS OXIDANT CONCENTRATIONS, 

IN ORDER OF DECREASING EYE IRRITATION SCORE, 

FOR A NUMBER OF STATIONS IN THE 

LOS ANGELES AREA, 195446 

Averege Average Variation in eye 

eye oxidant irritation score Number 

irrita- concen- explained by of daily 

tion tration, oxidantconcen- observascore ppm tration (r') Station tions 

26.2 0.13 0.88 5 25 

220 0.10 0.68 8 29 

21 9 0.21 0.76 4La 24 

21 3 0.11 006 2 30 

182 0.15 056 3 67 

13.0 0.17 0.65 4E' 66 

188 014 0.18 11 344 

a L = panel of laymen in Pasadena, California, E= pa nel of scientists at the California 

Institute of Technology in Pasadena 

A large study of student nurses, conducted by 

Hammer et al.,'g has been described previously. As 

mentioned, rates of eye irritation in this study 

increased wlth daily maximum hourly oxidant 

levels in and above the range of 294 to 372 /jg/m 3 

(0.15 to 0.19 ppm). 

EVALUATION OF FILTERS FOR REMOVING IRRITANTS FROM POLLUTED AIR 

A study was conducted by Richardson and 

Middleton 48,49 to evaluate the sensory 

effectiveness of alr filter media for removing eye 

irritants from polluted air. Eye irritation in two 

40 

~ 

. ~ : 

i 

/ 

/ • ......y~ ,. i 

~/ ••• •• ~ ~ ' ~i 

i' 

o•'~ ~i 

~ •• 

, 

STATION 3 

------ STATION 4E a 

.~ 

••••••••••• STATION 4L a 

---- STATION 5 

~ •••••••• STATION 8 

ALL STATIONS 

D 10 20 30 40 5a 

OXIDANT CONCENTRATIONS, pphm 

a "E"=panel of scienttsts at the California lnstitute of Technology. 

L=panel of laymen in Pasadena, California. For both "E" and "L" panels, 

aerometric measurements from station 4 were used. 

Figure 10-7. Regression curves relating eye irritation scores and simultaneous oxidant concentrations from a number 

of stations in the Los Angeles area, 1954. 46 

30 

20 

10 

231 
groups of 20 female telephone company employees, similar with respect to age and job 

characteristics and employed in identical adjacent 

rooms, was evaluated over 123 workdays from 

May to November 1956. Active and dummy filter 

units were switched periodically between the two 

rooms so that the groups were alternately exposed 

to test and control conditions. The sensory 

response of the subjects was measured daily at 11 

a.m. by means of a questionnaire; simultaneous 

measurements of oxidants, particulate matter, and 

nitrogen dioxide were obtained within each of the 

two rooms and immediately outside the building. 

The differences in eye irrltation between the 

activated-carbon filtered and nonfiltered test 

situations were in all cases highly significant 

(Table 10-9). A statistically significant correlation 

between eye irritatlon and oxidant concentrations 

occurred in the nonfiltered room (Tabte 10-10). The 

scatter diagram of results (Figure 10-9) suggests 

that the severity of eye irritation begins to increase 

above a simultaneous oxidant concentration of 

about 200 ug/ m 3 (0.10 ppm) as measured by the KI 

method. 

Nitrogen dioxide concentrations were reduced 

by the activated carbon filters during their early 

use but, after a period of time, nitrogen dioxide 

concentrations in the filtered atmosphere increased. No significant correlations between eye 

irritation and nitrogen dioxide levels were 

observed, nor were significant correlations found 

between eye Irritation and concentrations of 

particulate matter. 

TABLE 10-8. CORRELATION BETWEEN EYE IRRITATION 

AND SIMULTANEOUS ENVIRONMENTAL 

MEASUREMENTS, AS JUDGED BY A PANEL OF 

SCIENTISTS, 195446 

Variance in eye 

irrntation score 

Environ- explained by Average eye 

mental environmental Average value irritation Number of 

variables variable (r ~ ) of variable score observations 

Oxldant 065 0 17 ppm 1 30 66 

1\10, 007 0 20 ppm 131 51 

CO 0.53 0 27 ppm 142 47 

Hydrocarbons 039 0 17 ppm 140 53 

Vlslblllty 017 1 2 mlles 13.3 56 

Partlculates 053 21 1 Coh 137 26 

units 

Aldehydes 048 0 19 ppm 140 18 

PHOTOCHEMICAL OXIDANT AND EYE 

IRRITATION IN LOCATIONS OTHER THAN 

CALIFORNIA 

Oxidant measurements at levels posslbly 

associated with eye irritation have been reported 

from a number of cities other than Los Angeles. 

Circumstantial evidence of increased eye irritation 

has been reported in Washington, D.C., Denver, 

New York City, and St. Louis. An epidemiologic 

study of eye irritation and other health indiceswas 

carried out by Cassell et a1. 9 on a population living 

on the lower East Side in Manhattan. In this study, 

families reported the presence or absence of 

symptoms, including eye irritation, each week. In 

October 1963 (a period of increased pollution) the 

y 40 

FZ 

Z :) 

O > 30 

H cc Q Q F_—cc H 

cc op 20 ¢ cc 

w Q 

> Z_ 

ww 10 

cc 

O 

fii 

0 

• • 

• 

• • • 

• 

•O•• • • 

o 

• 

• • • 

• • • • 

• •~ • 

• 

n 10 20 30 40 50 60 70 SO 9r 

MAXIMUM OXIDANT CONCENTRATION, pphm 

Figure 10-8. Variation of inean maximum eye irritation, as judged by a panel of scientists, with maximum oxidant 

concentrations, Pasadena, August-November 1955. 

232 
frequency of new reports of eye irrltation Increased 

from about 2 to nearly 5 percent of the population. 

However, Cassell's study design did not allow the 

effects of individual pollutants to be separated 

from each other. 

In the Makino and Mizoguchl study of Japanese 

students, cited above, 32 the daily frequency of eye 

irritation regressed on corresponding daily 

(presumably maxlmum hourly) oxidant concentratlon for each of the 12 months of study. 

Regresslon lines that yielded significant 

associations between Irrltation rate are presented 

'in Figure 10-10 As the flgure shows, the rate of 

eye Irritation rose most qufckly wlth increasing 

oxidant levels during July. The data for that month 

predicted that 10 percent of students would 

complain of eye Irritation when the oxidant level 

was about 0.18 ppm, and that 15 percent of 

students would slmllarly complain when the level 

was about 0.26 ppm. On the other hand, data for 

December predicted that only about 3.5 percent of 

students would complain of eye irritation when the 

oxldant level was about 0.26 ppm. Statlstically 

significant associations between oxidant 

concentration and eye irritation rates occurred 

more frequently in summer and autumn than in 

winter and spring. 

Shimizu et a1. 54 reported a combined 

epidemiologic, clinical, and toxicologic study of the 

effects of photochemical smog on the eyes of 

humans and rabbits. In the epidemlologic portion 

of the study, all 515 students at a junior high 

school In Tokyo were requested to complete a 

symptom questionnaire each day over the 61 -day 

period between May 20 and July 19, 1974. The 

questlonnalre inqulred about the presence of 17 

symptoms, including eye irrftation, eye paln, 

hyperemia of the eye, lacrimation, blurred vlsion, 

and a variety of resplratory and constitutional 

symptoms. 

TABLE 10-9. EFFECT OF FILTER ON SENSORY IRRITATION AND CHEMICAL MEASUREMENTS49 

_ Test condition 

Eye 

irritation 

index' 

Oxidants, 

pphm ° 

NOz, 

pphm 

0.032`Activated carbon filter 

Mean, nonfiltered room 1 99 9.8 1 5 

Mean, filtered room 101 049 041 

Difference between means 098 94 1 1 

Probability that the difference could have 

occurred by chance <0 01 «0 01 «0 01 

0 016 Activated carbon filter 

Mean, nonfiltered room 1.95 84 34 

Mean, filtered room 141 1 8 1 6 

Difference between means 1 54 6.7 1 8 

Probability that the difference could have 

occurred by chance <0 01 «0.01 «0.01 

0 075 Acttvated carbon filter 

Mean, nonfiltered room 545 13.9 27 

Mean, filtered room 2.35 4.9 57 

Difference between means 3109 O 30 

Probability that the difference could have 

occurred by chance <0 05 <0 01 ` 

0 0030 Activated carbon filter 

Mean, nonfiltered room 235 73 47 

Mean, ftltered room 1 19 36 49 

Difference between means 1 16 37 02 

Probability that the difference could have 

occurred by chance <0 01 <0.01 ° 

Particulate filter 

Mean, nonfiltered room 2.13 5.7 63 

Mean, filtered room 1 91 34 5.5 

Difference lietween means 0.22 2.3 03 

Probability that the difference could have 

occurred by chance ° <0 01 <0.02 

'An eye irritation index of 3 corresponds to barely noticeable irritation, an index of 7 corresponds to moderate irritation, an index of 11 corresponds to severe irritation 

°Measured by the KI method 

`Refers to detention time in seconds 

°Difference not significant 

233 
During the 61 days of the epidemiologic study, 

the weather appears to have been humid and 

rather cool, with maximum temperatures rarely 

exceeding 30°C. The oxidant level exceeded 0.15 

ppm on only 5 days, and the highest oxidant level 

recorded during the study was 0 23 ppm. Though 

averaging times were not specified in the report, 

these levels appear to have been maximum 

instantaneous levels. Levels of S02 as well as 

oxidant were presented in the report. The methods 

used to measure oxldant and S02 concentrations 

were not mentioned. 

Symptom rates averaged over the 5 days when 

oxidant concentrations exceeded 0.15 ppm were 

compared to corresponding rates averaged over all 

days of the study. The percentages of students 

reporting eye symptoms on the high-oxidant days 

and on all study days, respectively, were as 

follows: eye irritation, 8.0 and 2.4 percent; eye 

pain, 3 3 and 1.9 percent; blurred vision, 1.4 and 

1.1 percent; lacrimation, 1.4 and 0.5 percent; and 

hyperemia of the eyes, 0.6 and 0.5 percent. 

Differences between high-oxidant days and all 

study days in eye irritation and lacrimation were 

statistically significant at a= 0.05. Incidentally, a 

significantly hlgher mean percentage of students 

also reported sore throat (2.6 versus 1.1 percent) 

and dyspnea (2.5 versus 1.9 percent) on the highoxidant days than on all study days Thesefindings 

are quite consistent with the findings of Makino 

and Mizoguchi 32and Mizoguchi et a1. 37 

TABLE 10-10. PEARSON PRODUCT MOMENT CORRELATION OF COEFFICIENTS BETWEEN EYE IRRITATION AND 

ENVIRONMENTAL FACTORS IN A NONFILTERED ROOM 49 

Item _ _ Factor Correlation 

Irrltatlon vs Oxldants concentratlon, by phenolphtaleln method 081 

Irrltatlon vs Oxldants concentratlons, by KI method 031 

Irrltatlon vs NO2 concentratlons 005 

Irrltatlon vs Particulate 015 

Irrltatlon vs Temperature 049 

Irrltatlon vs Relative humldlty -0 24 

Temperature vs Relative humldlty -0 38 

Temperature vs Oxldants concentratlon, by KI method 029 

Oxldants 

concentratlon, 

by phenolphtaleln method vs Oxldants concentratlon, by KI method 088 

N O2 concentratlons vs Oxldants concentratlon, by KI method -0.15 

18 

16 

1=0.5770 K1 -/323 

"MODERATE" IRRITATION 

-- -- -- --- -------- 

----------- 

NOTICEABLE" IRRITATION 

-------------- ---------- 

0 5 10 15 20 25 30 35 40 

OXIDANT CONCENTRATION, pphm 

Figure 10-9. Mean index of eye irritation versus oxidant concentration. 49 

O 14 

F 

Q 

~ 12 

~ 11 

w10 

U. 

~ 

w 

O 8 

X 

w 7 

O 

Z_ 6 

Z 

Q 

w q 

2 

3 

2 

0 

234 
Data presented in the Shimizu et al. report 5 a 

suggest that the highest concentrations of both 

oxidant and S02 tended to occur on the same days. 

Concentrations of S02 and oxidant appear to have 

been of generally similar magnitudes. Thus we do 

not belleve it is justlfiable to attribute solely to 

oxidant the differences between high- and lowoxidant days In symptom rates observed in this 

study. It is conceivable that the presence of S02 or 

other sulfur oxide compounds may have been a 

necessary factor in the production of these 

symptoms. 

In the clinical portion of the Shimizu et al. 

study, 54 the eyes on 41 seventh graders and 41 

eighth graders were examined on three sets of 2 

consecutive days—one set in May, one in July, and 

one in October 1974. On the first day of each set, 

elther the seventh or eighth graders were tested. 

On the next day, the remaining grade was tested. 

The second day of the 2-day set in July happened to 

be one of the epidemiologic study days on which 

the oxidant concentration exceeded 0.15 ppm. On 

each of the 6 days of the clinical study, subjects 

were given a physlcal examinatlon of the eye, the 

volume and pH of tear fluid were measured, and 

the amount and activity of tear lysozyme were 

determined. On the hlgh-oxidant day in July, four 

(10.0 percent) of 40 students reported symptoms of 

eye Irritation. (This flgure is consistent with the 8.0 

percent of all students reporting eye irritation on 

days with oxidant levels exceeding 0.15 ppm.) On 

the other 5 days of clinical examinations, an 

average of 1.2 students, or about 3 percent of 

students examined, reported such symptoms. On 

the second day of the July clinical examinations, 

the mean pH of the eighth-graders" tear fluid was 

significantly lower (about 0.1 pH unit lower) than it 

had been in the seventh graders tested the day 

before. On the other two sets of days, when 

between-days differences in oxidant concentrations were smaller than in July, no 

significant between-days difference in lacrimal pH 

was observed. We believe that thisfinding, though 

suggestive, must be interpreted cautiously, 

because different subjects were tested on the 2 

days of each set of days. The authors observed no 

significant pollution-related differences in lacrimal 

volume or in the volume or activity of tear lysozyme 

secreted. However, a slight shift in the pattern of 

lysozyme activity was noted on the high-oxidant 

day. The significance of this shift is as yet 

uncertain. 

The toxicologic portion of the Shimizu et al. 

study54 had two facets. In the first, the eyes of four 

men and two women aged 20 to 40 years were 

exposed to 0.5 percent (5000 ppm) acrolein gas. In 

most subjects, smarting of the eyes developed 

within 3 min. In others, however, no unusual 

sensation was noted. 

•• ••• ••• 

SEPT. * AUG. 

30 JULV 

of 090 

DEC. OCT. * 

20 • 

APR. 

• 

MAY SIGNIFICANTAT: 

••• 0.1% 

•• 1 % 

• 5 % 

10 

*The regression lines for September and October 

are nearly identical. 

0 n 5 10 1s 20 

SYMPTOM AND COMPLAINT RATE, percent 

Figure 10-10. Monthly regression lines between oxidant levels and eye irritation (symptom no. 1).3 2 

E r a 

a 

vi 

H z Q _d 

X O 

235 
In the second facet of the Shimizu et al. 

toxicologic study, 54six rabbits were exposed to 10 

ppm acrolein gas for up to 2 hr. One eye of each of 

two rabbits was kept closed throughout the 

exposure. After 1 hr of exposure, 3 of 10 eyes had 

developed spotty, fluorescent stainable, white 

corneal lesions. After 2 hr of exposure, this type of 

corneal lesion covered approximately the entire 

area of the pupil in all the experimental eyes. The 

authors did not describe the reversibility of these 

lesions. This type of lesion did not develop in the 

two closed eyes. 

DISCUSSION OF PHOTOCHEMICAL OXIDANTS 

AND EYE IRRITATION 

In the Los Angeles area and in Japan, strong and 

consistent associations between photochemical 

oxidant exposures and both the frequency and 

severity of eye irritation have been observed. In 

most studies performed to date, the rate of subjects 

reporting eye irritation has been higher at oxidant 

concentrations above 0.15 ppm than at lower 

concentrations. Hammer observed the frequency 

of eye irritation to increase at maximum hourly 

oxidant concentrations in the range of 294 to 372 

pg/m 3(0.15 to 0.19 ppm). Recent Japanese 

studies, especiallythatofMakinoandMizoguchi, 3 z 

suggest that eye irritation may begin to occur even 

at (presumably maximum hourly) oxidant 

concentrations of 0.10 ppm or below. 

As yet, the components of photochemical 

pollution specifically responsible for eye irrita.tion 

have not been identified in epidemiologic studies. 

Such identification must await refinements in 

available aerometric technology. Experimental 

studies indicate that ozone, which is the principal 

contributor to total oxidant concentration, is not 

itself an eye irritant at ambient levels. However, 

the possibility remains that ozone in the ambient 

atmosphere may interact with other substances 

(which need not necessarily be a part of the 

photochemical pollutant complex) to produce eye 

irritation. 

Constituents of the photochemical oxidant 

complex that have been shown to be eye irritants 

include peroxyacetylnitrate, peroxybenzoylnitrate, 

acrolein, and formaldehyde. The broad range of 

actual and potential eye irritants in photochemical 

smog render it possible, even likely, that different 

pollutants or blends of pollutants account for eye 

irritation in different places, or in the same place at 

different times. This hypothesis can be tested only 

by further epidemiologic study of pollution-related 

eye irritation in a variety of locations. 

The strong and consistent association observed 

between short-term photochemical oxidant 

exposure and eye irritation arouses interest as to 

what the effects of such long-term exposures on 

ocular structure and function might be. This 

concern is heightened by the demonstration by 

Shimizu et a1. 54of opaque corneal lesions in rabbits 

resulting from as little as 1 hr of exposure to 

acrolein. Little epidemiologic effort has as yet been 

devoted to detecting the-ocular effects of chronic 

ambient oxidant exposures. It is quite conceivable 

that such effects have not yet become apparent, 

since no city in the United States has experienced 

consistently elevated oxidant concentrations for 

more than 30 years or so. Overall conclusions as to 

the impact of photochemical oxidant exposures on 

the human eye must await a thorough, systematic 

investigation of chronic exposures. 

EFFECTS OF CHRONIC PHOTOCHEMICAL 

OXIDANT EXPOSURES 

Introduction 

Knowledge of the effects of long-term photochemical oxidant exposure is still distressingly 

limited. In most studies to date that have assessed 

such effects, health data have been collected at 

one point in time in areas whose long-term 

pollution exposures are expected to have differed. 

Studies of this design are termed cross-sectional. 

In carefully planned cross-sectional studies, study 

populations are selected to be as similar as 

possible with respect to all characteristics except 

pollution exposure, lest nonpollution variables 

interfere with comparisons made among 

populations. In environmental epidemiology, 

nonpollution variables of particular importance 

include cigarette smoking habits, occupational 

exposure to respiratory irritants, socioeconomic 

status, and climate. 

For two reasons, cross-sectional studies of the 

effects of long-term pollution exposures must be 

interpreted cautiously. First, it is virtually never 

possible to study populations similar in all 

characteristics except their pollution exposure. 

Indeed, there is little question that not all the 

variables complicating comparisons of populations 

with different pollution exposures have as yet even 

been identified, let alone controlled in field studies. 

Second, even when health effects conform to 

pollution exposure gradients, the investigator, 

since he has made health measurements at only 

236 
one point in time, is usually unsure as to the 

duration or concentration of {exposure that may 

have been necessary to produce the observed 

effects. 

Existing studies must be replicated, or as nearly 

replicated as possible, before the effects of chronic 

oxidant exposures can be confidently described. 

Full characterization of such effects wlll require 

carefully designed and patiently conducted 

prospective studies. As will be seen, these 

conditions have not yet been fulfilled. 

Mortality in Areas of High- and Low-Oxidant 

Qollution 

LUNG CANCER MORTALITY 

It is known that active organic carcinogens are 

found in polluted atmospheres 51 and that ozone, in 

concentrations above those found in ambient air, 

has radiomimetic properties. 13 However it is not 

yet established whether ambient concentrations of 

organic carcinogens or ozone are sufficient to 

promote the development of cancer in humans. 

Buell et a1. 5 reported a prospective study of lung 

cancer among 69,160 members of the California 

Division of the American Legion. This number 

represented about 50 percent of all eligible 

individuals. Since military person>7el must meet 

certain standards,of health, the American Legion 

may under-represent the population with respect 

to the prevalence of chronic disease. However, it 

may over-represent the population with respect to 

cigarette smoking. The cooperating subjects 

reported by postal questionnaire their residence, 

occupation, and smoking histories. Identifying data 

for each individual were maintained on a roster 

against which the death certificates were checked 

for the 5-year period 1958-62. It thus became 

possible to carry out a reasonably economical 

longitudinal study comparing the major 

metropolitan areas of California with respect to 

mortality due to lung cancer and other conditions. 

A total of 336,571 man-years of observation was 

included in the report. 

As shown in Table 10-1 1, long-term residents of 

Los Angeles County had slightly lower age- and 

smoking-adjusted lung cancer ratesthan residents 

of the San Francisco Bay Area counties and San 

Diego County. These urban groups had higher 

rates than the population residing in the rest of the 

state. The relative risk of lung cancer for heavy 

smokers (more than one pack a day) was greater in 

Los Angeles County than in other areas of 

California (Table 10-12). For nonsmokers, the rate 

in the two metropolitan groups was substantially 

greater than in the rest of the state. The San 

Francisco/San Diego rates, however, were higher 

than those in Los Angeles. 

For three reasons, the Buell et al. study must be 

considered inconclusive. First, the rate of 

questionnaire return, though impossible to 

determine precisely, probably did not exceed 60 

percent. Thus it is quite conceivable that undetected selective factors may have influenced the 

published results. Second, if chronic oxidant 

exposures produce lung cancer, the latent period 

between the first exposure and tumor 

development may have exceeded the maximum 

observation period possible in this study. This 

maximum period was only about 15 years, 

between the late 1940's, when Los Angeles first 

experienced elevated photochemical pollution 

levels, and 1962. Third, Buell et al. did not relate 

mortality rates to actual pollution measurements. 

CHRONIC RESPIRATORY DISEASE MORTALITY 

Mahoney reported a preliminary study31 in 

which respiratory disease mortality rates in Los 

TABLE 10-11. TOTAL LUNG CANCER MORTALITY IN AN AMERICAN LEGION STUDY POPULATION 

CALIFORNIA, 1958-625 

San Francisco 

Los Angeles Bay Area and AII other 

County San Diego Counties Calif counties 

Mortality Total Mortality Total Mortality Total 

Item rate' deaths rate' deaths ratea deaths 

Age-adjusted ° 959 n/a 1045 n/a 753 n/a 

Age- and smokingadjusted 954 n/a 102.0 n/a 755 n/a 

Resldency:° 

At least 10 years 96.6 79 1063 58 199 69 

Less than 10 years 76.7 27 69.1 13 685 30 

Unknown 1234 12 215.3 10 652 6 

°Deaths per 100,000 man-years 

°Age-adlusted by the direct method to the total study population 

`Age- and smoking-adlusted 

237 
Angeles during 1961 were related to wind-flow 

patterns in the city. In the Los Angeles Basin, the 

prevailing wind blows in a southwesterly direction 

from the Pacific Ocean. Mahoney constructed five 

concentric zones within the Basin (Zones 1 

through 5), each about 10 km (6 miles) wide and 

each inland and downwind from the last. He then 

computed respiratory death rates separately for 

each zone. Death rates were computed by dfviding 

the number of deaths in 1961 by the population in 

the zone as determined by the 1960 census. Zonal 

populations ranged from 36,312 in Zone 5, the 

most downwind and inland zone, to 574,512 in 

Zone 3. AII death rates were adjusted, by the 

indirect method, for age, sex, and income level. AII 

persons in each zone were assumed to have the 

median income for that zone. Only whites were 

considered in the analysis. Variables such as 

smoking, migration within the city, and variation 

among zones in population densfty were not 

considered. 

Adjusted respiratory death rates per 100,000 in 

Zones 1 through 5, respectively, were as follows: 

53, 51, 58, 66, and 1 1 1. This finding is consistent 

with the hypothesis that photochemical air 

pollution influences mortality rates, since pollution 

levels are generally higher in leeward areas of Los 

Angeles than in windward areas. However, as the 

author mentions, other factors such as 

temperature and humidity are also intimately 

associated with wind-flow pattern. The relative 

contribution to mortality rates of these factors, 

pollution, and demographic and behavioral 

variables not considered could not be determined 

from Mahoney's report. Also, no pollution 

measurements were presented to document the 

degree to which pollution levels increased with 

increasing distance from the ocean. Thus as the 

author himself observed, this report must be 

consldered inconclusive, suggestive as it is of an 

effect of pollution on mortality. 

Rates of mortality resulting from chronic respiratory diseases other than lung cancer were 

briefly considered in the Buell et al. study. 5 These 

rates were somewhat higher in Los Angeles than 

in San Francisco and San Diego Counties among 

persons residing for 10 or more years in their 

respective counties, but the rates were highest in 

the other less urbanized counties (Table 10-13). 

Interpretation of these observations is clouded by 

several factors: (1) The possibility that oxidant 

pollution may induce chronic respiratory disease 

only after a long latent period, (2) the lack of actual 

air pollution measurements, and (3) the lack of 

control for possible differences in socioeconomic 

level among the areas compared. Winkelstein et 

a1. 66,67 have observed a strong effect of 

socioeconomic level on chronic respiratory disease 

mortality. (In these reports, interarea differences in 

socioeconomic level may have been minimized by 

the fact that only American Legion members were 

studied.) 

DISCUSSION OF CHRONIC PHOTOCHEMICAL 

POLLUTION EXPOSURES AND MORTALITY 

Buell et a1. 5 observed no consistent association 

between long-term oxidant exposure and lung 

cancer mortality in California. Mahoney 3 ' reported 

higher total respiratory disease mortality rates in 

inland, downwind sections of Los Angeles than in 

coastal, upwind sections. In Los Angeles, oxidant 

concentrations tend to be higher inland than in 

coastal areas. Socioeconomic, demographic, and 

behavioral variables were not fuily controlled in 

either study. Neither were mortality rates related 

TABLE 10-12. LUNG CANCER DEATHS AND RELATIVE RISKS PER 100,000 MAN-YEARS IN AN 

AMERICAN LEGION STUDY POPULATION, BY EXTENT OF CIGARETTE SMOKING AND RESIDENCE, 

CALIFORNIA, 1958-625 

Los Angeles S F Bay Area and AII other 

Dady cigarette smoking, 

County San Diego Counties _ counties ° 

lifetime Relative Relative Relative 

hi• ,,rv' Rate risk Rate risk Rate risk 

None 281 2.5 439 39 1 1 2 1.0 

Less than one'pack 636 5 7 77.1 69 6.10 54 

About one pack 1260 11 3 1345 120 1249 11 2 

More than one pack 241 3 21 5 2260 202 1375 123 

Ratlo 

More than one pac k 

none 36 5 1 12.3 

aAge-adlusted by the direct method to the total study population 

°Nonsmokers m all other counties taken as unit risk 

238 
to actual pollution measurements. Thus both of 

them must be considered as inconclusive. 

In view of the long latent periods known to be 

involved in the development of many cancers and 

chronic diseases, it may be that effects of 

photochemical oxidant exposures on mortality 

rates and other health indices have not yet become 

apparent. Considerable further study, in which the 

effects of socioeconomic and demographic 

variables are carefully considered, is required 

before the true relationship of photochemical 

pollution to mortality rates can be conclusively 

defined. 

General Morbidity in Areas of High- and LowOxidant Pollution 

STATE OF CALIFORNIA HEALTH SURVEY 

In 1954, weekly surveys of new illness and 

injury were conducted throughout California by 

the State Department of Public Health.6,7e 

Sampling units consisted of homes selected to be 

representative of all homes in the state. Weekly 

rates of illness and injury in Los Angeles County 

were compared to those in the rest of the state 

during the 17 weeks from August 2 through 

November 29, 1954. Combined weekly incidence 

of colds, asthma attacks, hay fever, and other 

respiratory conditions in persons of all ages are 

presented in Figure 10-11. As the figure shows, 

there was little difference between Los Angeles 

County and the rest of Californla in average rates of 

these illnesses over the study period. The high 

peaks of incidence in October are quite likely 

reflections of the recent beginning of the academic 

year, though this is not stated in the report. 

In Figure 10-12, weekly Incidences of all illness 

and injury in persons aged 65 and over are 

presented. As the figure shows, the average 

weekly incidence of illness and injury was about 

10.4 percent in Los Angeles County and about 7.0 

percent in the rest of the state. This finding 

suggests that long-term exposures to 

photochemical oxidants may promote increased 

susceptibility to illness in the elderly. However, the 

finding must be considered inconclusive, sincethe 

investigators did not adjust for differences 

between Los Angeles and the rest of California in 

such factors as population density, ethnic characteristics, and socioeconomic level. 

In Figures 10-11 and 10-12, three high-smog 

periods in Los Angeles County are noted. Criterla 

for selection of these periods were not presented in 

the report. Aerometric data collected during this 

study in Los Angeles City and Pasadena suggest 

that during these high-smog periods, maximum 

concentrations of suspended particulates, 

airborne lead, and carbon monoxide were 

generally unusually high. However, maximum 

concentrations of oxidant and nitrogen dioxide do 

not appear to have been unusally high during these 

periods. In 3ny event, weekly incidences of illness 

in Los Angeles County do not generally appear to 

have risen appreciably during these periods. 

In May and June 1956, another adult health 

survey was undertaken throughout the state of 

California. 19 '20 One goal of this survey was to 

determine the prevalence of various conditions In 

different areas of the state. A probability sample of 

3545 households, selected to be representative of 

all households in the state in the ratio of 1 to 1155 

was selected. Populations in service camps and 

other institutions were not sampled. A questionnaire was administered by personal interview 

to one adult in each sample household. After 

weighting for the rlumber of adults in each household, the total study sample consisted of 6939 

persons. In thls phase of the survey, care was 

taken not to lead subjects toward attributing thelr 

illnesses to air pollution. 

Study results were distributed by area of the 

respondent's residence. In Table 10-14 are presented the proportions of respondents reporting 

TABLE 10-13. TOTAL CHRONIC RESPIRATORY DISEASE MORTALITY IN AN AMERICAN LEGION STUDY POPULATION, 

CALIFORNIA, 1958-625 

San Franscisco Bay 

Los Angeles Area and San Diego AII other 

County Counties countues 

Mortahty Total Mortality Total Mortality Total 

Residency rate ° deaths rate° deaths rate ° deaths 

10 years 33.4 31 283 15 456 40 

Less than 10 years 41 2 14 456 8 41 3 17 

Unknown 1391 12 598 3 397 4 

Total 467 57 340 26 444 61 

aAge- and smoking-adtusted by the direct method to the total study population 

°Per 100,000 man-years 

239 
various respiratory conditions in three counties in 

the Los Angeles/San Diego area, nine counties in 

the San Francisco Bay Area, and the remainder of 

the state. As the table shows, the proportion of 

respondents reporting cough, nose complalnts, 

and throat complaints was higher in the Los 

Angeles/San Diego area than elsewhere in the 

state. The proportion of respondents reporting hay 

fever was lowest in the Los Angeles/San Diego 

area. Differences among areas in the proportion of 

respondents reporting the other conditions listed 

were slight. 

75 

LOS ANGELES COUNTY 

CALIFORNIA LESS 

LOS ANGELES COUNTY 

50 ~ =HIGH SMOG PERIODS /^ 

~ 

25 .000, ~ 

~ ~ \ ~ 

V 

\ ~ 

n 

8 15 22 29 5 12 19 26 3 10 17 24 31 7 14 21 29 

r----AUG. I~-4—SEPT. OCT. TE NOV.----N 

WEEK ENDING 

Figurel0-11. Combined weekly incidence rates of selected conditions (colds, hay fever, asthma, and other respiratory 

conditions) in persons of all ages, Los Angeles County and the remainder of California, August 7 to November 28, 

1954. s," 

3. 

10 

N 

Z 

O Vl 

cc 

W 

a 

0 0 

cc 

w 

a 

w 

~ 

Q 

cc 

~ — — ~ ~ LOS ANGELES COUNTY 

10 CALIFORNIA LESS 

LOS ANGELES CGUNTY 

ZO ~ =HIGH SMOG PERIODS 

10 

 r 

2s -15 ZZ cy a 14 1v co .o .v 11 c" a. i 1y c. co 

It--- AUG. -- ~t— SEPT. -- l -0-- OCT. --0 1 -1--- NOV. ~ 

WEEK ENDING 

Figure 10-12. Weekly incidence rates of illness and injuryfor persons aged 65 and over in 

Los Angeles County and the remainder of California, August 2 to November 28, 1954. 6 '''e 

H 

Z 

O 

y 

cc 

W 

a 

0 0 

~ 

cc w 

c. 

y 

W 

H 

Q 

2 

240 
Another goal of this su rvey was to determine the 

degree to which subjects attributed exacerbations 

of respiratory conditions to air pollution. Figure 10- 

13 presents the proportions of respondents in Los 

Angeles County and the San Francisco Bay Area 

attributing exacerbation of respiratory conditions 

to air pollution and other factors. As the figure 

shows, the proportion of respondents attributing 

exacerbation of each condition to air pollution was 

higher in Los Angelesthan in San Francisco. For all 

conditions but bronchitis, intercity differences 

were quite marked. Clearly, it cannot be concluded 

that air pollution in Los Angeles caused all the 

exacerbations that respondents attributed to it. 

However, the findings presented in Figures 10-13 

at least indicate that Los Angeles residents 

considered local air pollution a hazard to health. 

A panel consisting of all persons at least 30 

years of age who appeared likely to have chronic 

respiratory disease was selected from the 1956 

general population survey described above. 

Specifically, the panel was selected on the basis of 

having reported chronic or repeated attacks of 

bronchitis, asthma, or coughing in 1956. In 

selecting the panel, the aid of a chronic respiratory 

disease spbcialist and of other medical consultants 

was enlistFd: The initial panel consisted of 1070 

persons. ' he panel was interviewed on four 

occasions- -twice in 1957, and once each in 1958 

and 1959 Of the 1070 persons in the original 

panel, 524 were interviewed all four times. 

Results of the panel study were reported by 

HausknecF t. 19 Of the general population sample of 

3545 adul's interviewed in 1956 (representing a 

wefghted .:ample of 6939 persons), 41 percent 

lived in three counties in the Los Angeles/San 

Diego area, 27 percent lived in nine San Francisco 

Bay Area counties, and 32 percent lived in the 

remainder of the state. Of the 524 panelists 

completing all four interviews in 1957-59, 48 

percent lived in the Los Angeles/San Diego area, 

25 percent lived in the San Francisco Bay Area, 

and 27 percent lived in the remainder of the state. 

Since all persons throughout the state having 

reported evidence of chronic respiratory disease 

were selected for the panel, this finding suggests 

that rates of chronic respiratory disease were 

disproportionately high in the Los Angeles/San 

Diego area. Though it is not clearly S,ated in the 

report, proportional distributions of bronchitis, 

asthma, and cough appear to have been very 

similar in the Los Angeles/San Diego area and in 

the rest of the state, excluding the Bay Area. In the 

Bay Area, the proportions of panelists with 

bronchitis, asthma, and coughing appear to have 

been, respectively, lower than, similar to, and 

higher than corresponding proportions in panelists 

elsewhere in the state. The logical consequence of 

these finding is that, among the general 

population, rates of bronchitis and asthma in the 

Los Angeles/San Diego area appear to have been 

higher than efsewhere in the state. Rates of cough 

in the Los Angeles/San Diego area seem to have 

been higher than in the rest of the state (excluding 

the Bay Area), and they may or may not have been 

higher than in the Bay Area. 

Three factors substantially cioud the 

interpretation of Hausknecht's findings. First, 

many rates necessaryto confirm logical inferences 

are not presented in the report. Second, over half of 

the original chronic respiratory disease panel did 

not complete all four interviews. Illness rates 

among these nonrespondents are not presented. 

Third, statistical adjustments are not made for 

TABLE 10-14. SELECTED RESPIRATORY CONDITIONS REPORTED BY GENERAL POPULATION SAMPLE, 

CALIFORNIA, MAY 1956 19 

Los Angeles, Orange, 

and San Francisco Bay 

Condiuons Cahfornia San Diego Counttes Area Counties' Rest of state 

reported Frequency Percent° Frequency Percent Frequency Percent Frequency Percent 

Bronchltls 309 4 156 5 71 4 82 5 

Asthma 188 3 104 3 45 2 39 2 

Cough 1341 19 746 22 323 17 272 17 

Slnus 1202 17 576 17 302 16 324 20 

Hayfever 695 10 265 8 221 12 209 13 

Nose complalnts 751 11 445 13 186 10 120 7 

Throat complalnts 848 12 505 15 192 10 151 9 

Number of persons 

Intervlewed 6939° 100 3450 100 1846 100 1643 100 

aSan Francisco, Alameda, Contra Costa, San Mateo, Santa Clara, Marin, Napa, Solano, and Sonoma Counties 

° Percentages will not add to 100 because of reports of multiple conditions or of none of the conditions listed 

`The number of persons interviewed personally was 3545 After weighting for the number of adults in sample households, this figure represented a total sample of 6939 

241 
possible Interarea differences in the distribution of 

important covariates (most notably, cigarette 

smoking habits). 

CHRONIC RESPIRATORY DISEASE SURVEY OF 

TELEPHONE WORKERS 

Deane et al." and Goldsmith and Deane" used 

standardized repsiratory illness survey techniques 

to compare respiratory symptom rates in outdoor 

telephone company workers in Los Angeles and 

San Francisco. No aerometric data were presented 

In these reports. In the older group (aged 50 to 59 

years), respiratory symptoms were more frequent 

in the populatlon of Los Angeles than in that of San 

Franclsco. Persistent cough and phlegm were 

reported by 31 .4 percent of the group aged 50 to 59 

years in Los Angeles, compared with 14.3 percent 

in San Francisco. This difference could not be 

explalned by differences In smoking habits, since 

In both age groups, proportions of smokers were 

higher in San Franclscothan in Los Angeles. There 

were no substantial intercity differences In the 

AIR POLLUTION OTHER FACTORS,a,b 

CONDITION 

51 49 

ASTHMA 

6 94 

50 50 

NOSE 

COMPLAINTS 10 90 

TH ROAT 44 56 

COMPLAINTS 5 95 

q1 59 

SINUS TROUBLE 

9 91 

30 70 

HAY FEVER 

10 90 

22 78 

BRONCHITIS 

11 89 

~ LOSANGELESCOUNTY 

~SAN FRANCISCO BAY AREA 

a lncludes the "don't know" responses. 

b includes specific foods, overeating, working too hard, 

not getting enough sleep, emotional upsets, smoking, 

and the presence of other conditions. 

WORSENING EFFECTS, percent 

Figure 10-13. Percentage of respondents in Los Angeles County and San Francisco Bay Area 

attributing exacerbation of respiratory conditions to air pollution and other factors, 1956. 20 

242 
results of pulmonary function tests. In the younger 

group (aged 40 to 49 years), the frequencies of 

respiratory symptoms werequite similar in thetwo 

cities. 

A point of interest is that rates of persistent 

cough and persistent phlegm in San Francisco 

were higher in the younger age group than in the 

older. The proportion of San Francisco smokers 

was also higher in the younger age group, which 

may partly explain this finding. However, this is 

probably not the full explanation, since the 

younger group also had a higher proportion of 

smokers in Los Angeles, where symptom rates 

increased with age. The authors suggested that a 

lost-to-study factor might have been operating in 

the older group in San Francisco. Deane and 

Goldsmith drew no conclusion as to the effect of 

chronic oxidant exposures on respiratory symptom 

rates. 

Questions regarding eye irritation were also 

asked by Deane and Goldsmith. The group aged 40 

to 49 years in San Francisco reported eye irritation 

about 10 percent of the time, and the group aged 

50 to 59 reported it about 4 percent of the time The 

corresponding figures in Los Angeles were 30 and 

29 percent, respectively. Perhaps more important 

is the fact that more than 50 percent of those in 

both age groups in San Francisco had never 

experienced eye irritation, whereas the 

corresponding figure for Los Angeles was less 

than 10 percent. 

OXIDANTS AND EPIDEMIC INFLUENZA 

Pearlman et a1. 42 studied whether chronic 

exposure to photochemical oxidants affects 

susceptibility to influenza infection. These 

investigators performed a retrospective study 

during 1968 and 1969 among 3500 elementary 

school children residing in five southern California 

communities. Seven to eight hundred second-, 

fourth-, and sixth-grade students from uppermiddle-class socioeconomic areas in each city 

participated. Selection of these communities was 

based on historical differences in oxidant 

exposure, although no difference in exposure was 

present before or during the epidemic. Pasadena 

and Riverside were chosen as the high-oxidant 

cities, Garden Grove as an intermediate city, and 

San Diego and Santa Barbara as low-oxidant 

cities. Seasonal peak mean daily maximum hourly 

oxidant levels recorded in each city from August to 

October during 1964-67 were, respectively, 451, 

368, 235, 157, and 176 Ng/m3 (0.23, 0 19, 0.12, 

0.08, and 0.09 ppm). Concentrations of pollutants 

other than oxidant in the study cities were not 

presented in the report. 

The incidence and duration of influenza-like 

illnesses between November 1968 and January 

1969 were determined by administration of a 

questionnaire to the parents of the subjects during 

March 1969. Parents were asked whether their 

chifdren had had influenza. If so, the length of 

illness and presence or absence of fever, coryza, 

and myalgia were also ascertained. Occurrence of 

an influenza-like illness was defined as a febrile 

illness accompanied by coryza and/or myalgia. 

During April 1969, finger-prick blood specimens 

were obtained from these children for subsequent 

titration by hemagglutination inhibition (HI) 

against A2 /Hong Kong influenza and by 

complement fixation against type A soluble 

antigen. Complement fixation established a 

hemoglobin HI titer of at least 1:32 as indicative of 

recent infection with A2 /Hong Kong influenza. 

In the questionnaire survey, 72 8 percent of the 

children reported illness, 35 4 percent reported 

febrile illness, and 21.5 percent reported 

influenza-like illness. Intercity morbidity did not 

consistently reflect differences in chronic oxidant 

exposure. A high- and a low-exposure city 

(Pasadena and San Diego) reported the greatest 

degree of febrile illness. Pasadena and Santa 

Barbara, high- and low-exposure cities, 

respectively, reported the most influenza-like 

illness. Adjustment for age and sex differences by 

probit analysis did not reveal any significant 

differences in morbidity rates among cities. 

Overall, 24.6 percent of children tested were 

found to have HI titers greater than or equal to 

1:32. The percentage of children with significant 

titers rose from 10.3 percent among those with no 

illness, to 28.9 percent among those with any 

illness, to 39.5 percent in those with febrile illness, 

and to 45.6 percent among those with an 

influenza-like illness The frequency of positive 

titers among febrile and influenza-like illness 

categories in the two high-exposure cities was 

lower than that in the two low-exposure cities. This 

difference was statistically significant. Although 

the two high-pollution cities studied, Pasadena 

and Riverside, reported higher subclinical illness 

rates (elevated titers without illness) than the low 

pollution cities, the differences were not 

statistically significant. 

Thus Pearlman's study did not demonstrate a 

positive association between chronic oxidant 

243 
exposure and influenza-like illness In animal 

studies, however, increased morbidity has 

resulted from acute oxidant exposures. 

Confirmation of Pearlman's results must await 

studies in cities exhibiting clear-cut differences in 

both acute and chronic oxidant concentrations. 

Chronic Oxidant Exposure and Pulmonary 

Function 

SURVEY OF INSURANCE COMPANY WORKERS 

Linn et a1. 29 reported a study in which pulmonary 

function and respiratory symptom rates in indoor 

insurance company workers in Los Angeles were 

compared to those in workers for the same 

company in San Francisco. Respiratory symptom 

questionnaires based on the standard 

questionnaire of the National Heart and Lung 

Institute were administered to all subjects. 

Pulmonary function tests included the forced vital 

capacity (FVC), the 1-sec forced expiratory volume 

(FEV,), maximal expiratory flow at 50 percent and 

25 percent of vital capacity ( Vso and V25), closing 

volume, and slope of the single-breath N 2alveolar 

plateau (AN2) Questionnaires were adm:nistered 

in April 1973, and pulmonary function tests were 

performed in August 1973 In one analysis, sexspecific intercity comparisons of pulmonary 

function test results were adjusted for age and 

height. In another analysis, city, smoking, and citysmoking interaction were employed as 

independent variables. In all, 441 workers in San 

Francisco and 206 workers in Los Angeles 

participated in this study. 

The proportions of participating males and 

females were very similar in the two cities, as were 

the mean heights and weights of inen and women. 

However, the study sample in San Francisco was 

somewhat older than that in Los Angeles. In San 

Francisco, 57 percentof the sample was at Ieast40 

years of age, in Los Angeles, the corresponding 

proportion was 48 percent. Also, higher 

proportions of both men and women were current 

smokers in San Francisco (45 percent and 30 

percent, respectively) than in Los Angeles (35 

percent and 19 percent, respectively). Furthermore, the Los Angeles sample contained a higher 

proportion of Latin Americans than that in San 

Francisco, whereas the San Francisco sample 

contained a higher proportion of Asiatics than that 

in Los Angeles. 

Air pollutant concentrations in the two cities had 

been measured from 1969 to 1972 at central-city 

monitoring stations. Over this period, the median 

oxidant concentration in Los Angeles, expressed 

according to the post-1974 California standard 

ultravioletcalibration method, was 0.07 ppm, and 

the concentration exceeded on 10 percent of days 

was 0.15 ppm. Corresponding concentrations in 

San Francisco were 0.02 and 0.03 ppm, 

respectively. Concentrations of nitrogen dioxide, 

carbon monoxide, and total suspended 

particulates were also higfier in Los Angeles than 

in San Francisco. Median concentrations of sulf ur 

dioxide appearto have -been very similar in thetwo 

cities. Temperature was generally higher and 

rainfall lower in Los Angeles than in San 

Francisco, although relative htimidity in summer 

appears to have been slightly higher in Los 

Angeles. 

Sex-specific pulmonary function test results 

were very similar in the two cities for all tests 

performed except the AN2in women, which wzs 

higher in San Francisco than in Los Angeles to a 

degree approaching statistical significance (p = 

0.06). (Elevations in the ON2, in the absence of 

other perturbations in pulmonary function, are 

thought to reflect early obstruction of small 

airways.) Cigarette smoking was found to have a 

significant deleterious effect on several indices 

of pulmonary function in males, and one index 

(ANz ) in females. 

Nonpersistent coughing during bad weather at 

times of day other than the first thing in the 

morning was reported by 30 percent of women in 

Los Angeles and by 14 percent of women in San 

Francisco Nonpersistent phlegm production 

under the same circumstances was reported by 23 

percent of women in Los Angeles and by 11 

percent of women in San Francisco. Respondents 

had been instructed that high-smog episodes 

could be considered periods of bad weather. 

Among women, intercity differences in rates of 

nonpersistent cough and phlegm were significant 

at a = 0.01 

The results of this study did not reveal a 

consistent association between chronic 

photochemical oxidant exposure and impairment 

of respiratory health, though they suggested an 

association between oxidant exposure and nonpersistent respiratory symptoms in women. In an 

interesting discussion, the authors gave several 

alternative explanations for their findings. First, 

the effects of acute oxidant exposures may be 

wholly reversible. Second, oxidant concentrations 

in Los Angeles may have been offset by other 

244 
adverse environmental factors such as cold and 

dampness in San Francisco. Third, oxidant 

exposures in Los Angeles may actually promote 

the development of chronic lung disease, but the 

difference in exposure between Los Angeles and 

San Francisco may not have been great enough to 

show such an effect. 

STUDY OF SEVENTH DAY ADVENTISTS 

Cohen et a1. 10 examined the effects of oxidant air 

pollution on pulmonary function in nonsmoking 

adults. Seventh Day Adventists were chosen for 

study, since few of them smoke, and they 

constituted a readily accessible population that 

was interested in health. The San Gabriel Valley in 

California was selected as the high-pollution area, 

and the San Diego area was chosen as a lowpollution area. 

The study population in each area consisted of 

white English-speaking adults aged 45 to 

64 who had not smoked in the last 20 years and 

who had a lifetime history of smoking less than one 

pack per year. Data were collected in January 

1970. Each participant was interviewed by a 

physician and underwent tests ol ventilatory 

function, including the 1-sec expiratory volume 

(FEV,) and the forced vital capacity (FVC). Study 

participants were also requested to complete a 

respiratory questionnaire that' was a modified 

combination of the British Medical Research 

Council respiratory questionnaire and the London 

School of Hygiene cardiovascular questionnaire. 

Aerometric data were obtained from the National 

Air Pollution Control Administration, which made 

measurements during September 1969 and 

January 1970. Daily oxidant measurements for 

January 1970 were also obtained from the Los 

Angeles County and San Diego County Air 

Pollution Control Districts. In addition, historical 

records from the Air Pollution Control Districts of 

these two counties were reviewed to obtain an 

estimate of chronic exposures. 

Average daily maximum hourly oxidant levels in 

the San Gabriel Valley and in San Diegoduring the 

month of study were 235 and 137 Ng/m3 (0.12 

ppm and 0.07 ppm), respectively. Measurements 

of total suspended particulates, respirable 

particulates, and sulfur dioxide were essentially 

equivalent in both areas during the time of study. 

From 1963 through 1967, both areas experienced 

similar arithmetic mean oxidant concentrations 

(0.047 ppm in the San Gabriel Valley and 0.038 

ppm in San Diego). However, over the same period, 

the mean of daily maximum hourly oxidant 

concentrations in the San Gabriel Valley (0.144 

ppm) was nearly twice as high as the corresponding mean of 0.074 ppm in San Diego. Also, 

the proportion of days in this period on which daily 

maximum hourly oxidant concentrations in the San 

Gabriel Valley exceeded 0.15 ppm (44.8 percent of 

days) was about seven times higher than the 

corresponding proportion of days (6.1 percent) in 

San Diego. Average concentrations of other 

pollutants (carbon monoxide, nitric oxide, nitrogen 

dioxide, hydrocarbons, sulfur dioxide, and 

particulates) during 1963-67 were genarally higher in the San Gabriel Valley than in San Diego. 

The prevalence of respiratory symptoms did not 

differ significantly between the two areas. 

Prevalence rates generally were considerably 

lower than those observed in most other studies. 

Similarly, no significant differences were found in 

measurements of pulmonary function between 

areas, and all measurements were within expected normal values. 

Thus Cohen et a1. 10 demonstrated no significant 

difference in symptom rates or pulmonary function 

between the San Gabriel Valley and San Diego. 

Interpretation of this study is clouded by the 

similarity of annual average exposure levels 

between the two areas. Clarification of the 

question of whether ambient oxidant exposure 

affects pulmonary function and respiratory 

symptom rates must await studies in areas having 

unequivocally different acute and chronic 

exposure levels. 

DISCUSSION OF CHRONIC OXIDANT 

EXPOSURES AND PULMONARY FUNCTION 

As yet, no association between chronic ambient 

oxidant exposure and pulmonary function has 

been observed. However, as with other indices of 

chronic exposure, very few studies investigating 

such a relationship have yet been performed. 

Furthermore, those that have been performed are 

limited in their import, because oxidant exposures 

for the test population cannot be known with 

certainty and because complicati ng effects of other 

personal and community environmental factors 

cannot be reliably evaluated. 

We have been unable to find any studies of longterm exposure effects on the pulmonary function 

of those whose health is impaired, Also, no 

prospective studies have yet been undertaken to 

determine whether chronic exposures promote 

declines in the pulmonaryfunction of once-healthy 

245 
Individuals. Finally, effects of long-term oxidant 

exposure on pulmonary function, as on other 

Indices of chronic exposure, may only now be 

starting to become evident. 

ATTITUDES OF LAYMEN AND PHYSICIANS 

TOWARD OXIDANT AIR POLLUTION 

State of California General Health Survey 

At the end of each interview in the general 

health survey undertaken in Callfornia in 1956 and 

prevlously described, 20direct questions concerning the effects of air pollution were asked. 

Seventy-five percent of the whole surveyed 

populatlon in Los Angeles County was bothered by 

air pollutlon, in contrast to 24 percent in the San 

Francisco Bay Area and 22 percent In the rest of 

the state. Corresponding proportions among the 

working populatlon were, respectively, 80, 29, and 

27 percent (Table 10-15). Thirty-two percent of 

native-born Californians were bothered by air 

pollution, and 39 percent of those moving to 

California were so bothered. Of those who were 

bothered by air pollution, 17 percent in Los 

Angeles considered moving because of it, in 

contrast to 4 percent in San Francisco and 12 

percent in the rest of the state. Of the same total 

number, 9 percent in Los Angeles considered 

changing jobs because of alr pollutlon, in contrast 

to 3 percent in both San Francisco and the rest of 

the state. About 20 percent of the state residents 

who had moved out of a polluted area reported that 

pollution had some influence on thely decision to 

move; 4 percent gave air pollutlon as thelr sole 

reason for moving. Among those who moved from 

California communities because of air pollution, 

75 percent had moved out of Los Angeles County, 8 

percent had moved out of the San Francisco Bay 

Area, and 17 percent had moved out of other areas 

of the state. Air pollution was given as the reason 

for 13 percent of the moves from Los Angeles 

County since 1947. In other areas of the state, the 

proportlon of moves attributed to air pollutlon was 

1 percent or less. 

Eye irritation was the most frequently reported 

effect of air ~ pollution. In some instances, thls 

symptom was accompanied by nasal irrltation 

(Table 10-1 6). In metropolitan areas, 80 percent of 

respondents bothered by air poklution complained 

of aye irritatlon. In nonmetropolitan areas, the 

corresponding proportion was 29 percent. 

Before air pollutlon was speclflcally mentloned 

by interviewers, respondents were asked several 

questions about satisfaction with the communitles 

in which they Ilved. About 21 percent of all 

respondents In Los Angeles County expressed 

dlssatisfaction with the communities In whlch they 

lived, as compared to 18 percent in both the Bay 

area and the rest of the state. A far greater 

proportion of dissatisfied Los Angeles residents 

(32 percent) voluntarlly attrlbuted their 

dlssatlsfaction to air pollution than dld resldents of 

the San Franclsco Bay Area (1 percent) or those in 

the rest of the state (6 percent). 

TABLE 10-15. PERCENT OF SURVEY RESPONSE OF 

GENERAL AND WORKING POPULATION BOTHERED 

BY AIR POLLUTION, BY MAJOR GEOGRAPHIC 

AREAS IN CALIFORNIA, MAY 1956 20 

Responses California 

Los 

Angeles 

County 

San 

Francisco 

Bay Area 

Rest 

of 

state 

General population sample 6393 2892 1846 2210 

% Not bothered by 

air pollution a 55 24 76 78 

% Bothered by air 

pollution 

Either at home 

or work 45 75 24 22 

Both at home 

and at work 14 27 4 4 

At home only 24 39 14 13 

At work only 7 8 6 5 

Total % at home 38 66 18 17 

Total % at work 21 35 10 9 

Working population sample 3732 1577 1028 1127 

% Not bothered by 

air pollution 51 20 71 73 

% Bothered by air 

pollution 

Either at home 

or work 49 80 29 27 

Both at home 

and at work 25 49 7 9 

At home only 12 16 11 8 

At work only 12 15 11 10 

Total % at home 37 66 18 17 

Total % at work 38 65 18 18 

a Percents are rounded independently 

Survey of Los Angeles Physicians 

A survey of Los Angeles physicians was 

conducted jolntly by the Los Angeles County 

Medical Associatlon and Tuberculosis and Health 

Association in December 1960. 30 A sample 

representing about one in 16 of those physicians 

reglstered to practice In the county during 1958 

was drawn, resulting in a sample of 526 from a 

total of 9228 physicians. A pretested questionnaire was mailed with a letter signed by the 

246 
chalrman of the air pollution subcommittee. A 

follow-up was also mailed, and telephone calls 

were made to the offices of those physicians who 

had not responded. 

Of the questionnaires mailed, 350 were returned. Of those, 307 (58 percent of the original 

sample of 526) were completed and tabulated. The 

words '"air pollution" did not appear in the 

questionnaire, although bias could have been 

introduced by the fact that the chairman of the air 

pollution subcommittee attached a letter to the 

questionnaire. Seventy-seven percent of the 

physicians who returned completed questionnaires believed that air pollution adversely 

affected the health of their patients. Two-thirds of 

the responding physicians felt that air pollution 

was a factor adversely affecting chronic 

respiratory disease. One-third of the physicians 

had advised one or more of their patients to leave 

the Los Angeles area for health reasons; air 

pollution was a factor mentioned in two-thirds of 

these instances. By extrapolation from the sample, 

assuming it to be representative, it was estimated 

that physicians had advlsed more than 10,000 

patients to move. It was reported that 

approximately 25 percent of the patients had done 

so. Nearly one-third of the physlcians had 

themselves considered moving from the Los 

Angeles area because of air pollution. Among 

other environmental factors mentioned as 

deleterious to health were overcrowding and 

traffic congestlon, but these factors were not 

mentioned nearly as often as air pollution. 

Discussion cf Attitudes of Respondents and 

Physicians Toward Oxidant Air Pollution 

The studies summarized in this section (10.4) 

were subjective in nature and did not yield 

scientifically confirmed informatlon about rates of 

illness or functional Impairment associated with 

oxidant pollution. However, the results presented 

here are interesting in that they demonstrate 

considerable concern, on the part of laymen and 

physicians alike, about the effects of such 

pollution. 

SUMMARY OF EPIDEMIOLOGIC APPRAISAL 

OF PHOTOCHEMICAL OXIDANTS 

In this summary, a brief discussion of findings in 

the preceding three sections of this chapter will be 

presented (Effects of Short-Term Photochemical 

Oxidant Exposures, Effects of Chronic Photochemical Oxidant Exposures, and Attitudes of 

Respondents and Physicians Toward Oxidant Air 

Pollution). The discussion of each section will 

begin wlth the health Indices that can be most 

confidently associated wlth ambient oxidant 

exposures and will work toward those indices for 

whlch little association with such exposures has 

been shown. Directions for future research will 

also be identified. 

TABLE 10-16. AIR POLLUTION EFFECTS REPORTED IN GENERAL POPULATION SURVEY, BY TYPE OF COMMUNITY 

AND BY MAJOR GEOGRAPHIC AREAS IN CALIFOfiNIA, MAY 1956 20 

Item 

Total 

Cahfornia 

At 

home 

At 

work 

Los 

Angeles 

County 

At At 

home work 

San 

Francisco 

Bay Area 

At 

home 

At 

work 

At 

home 

Rest 

of 

state 

At 

work 

General population sample 6939 3732 2392 1577 1846 1028 2201 1127 

Respondents bothered 

by air pollution 2616 1410 1904 1012 326 190 386 208 

% Bothered by air pollution 38 37 66 64 18 18 17 19 

% Persons bothered 

Air pollution effects cited 

Eyes, effects 75 76 89 88 38 39 41 51 

Eye irritation 44 46 54 53 17 18 22 30 

Eye and nasal irritation 23 24 26 27 15 14 14 19 

Eye irritation and annoying 5 3 6 4 4 3 3 2 

Eye, nasal irritation and annoying 3 3 3 4 2 4 1 - 

Nasal irritation, eye not mentioned 10 9 5 4 22 23 22 21 

Nasal irritation 8 8 4 3 19 19 18 21 

Nasal irritation and annoying 2 1 1 1 3 4 4 - 

Annoying only 5 7 2 3 17 26 10 8 

Other effects only 5 2 2 1 5 5 17 4 

No effects reported 5 6 2 4 18 7 10 16 

Total % 100 1 00 100 100 100 100 100 100 

247 
Effects of Short-Term Photochemical Oxidant 

Exposures 

The health index most frequently and consistently associated with short-term exposures to 

ambient photochemical oxidants is eye irritation. 

AII available evidence suggests that ozone alone is 

not an eye irritant at ambient concentrations. 

However, the possibility that ozone may interact 

with other substances to produce eye irritants 

remains open. In American studies, daily 

maximum hourly oxidant concentrations above 

which the rates and severity of eye irritation have 

been observed to increase have ranged from about 

200 pg/m3 (0.1 ppm) to about 294 Ng/m 3 (0.15 

ppm). RecentJapanese studies raisethe possibility 

that even lower oxidant concentrations may 

promote eye irritation under certain conditions. 

The consistency of the association between shortterm exposures and eye irritation arouses interest 

as to what the ocular effects of long-term 

exposures might be. Until careful studies of longterm exposure effects on the eye have been 

performed, the question of whether transient 

instances of eye irritation constitute bona fide 

impairments of health must remain open. 

Short-term photochemical oxidant exposures 

have been quite consistently associated with 

decrements in human performance. Wayne et al. 65 

have observed the proportion of high school crosscountry runners failing to improve their running 

times to increase as hourly oxidant concentrations 

increased from about 59 to 590 Ng/m 3 (0.03 to 

0.30 ppm). However, in the range of 0.03 to 0.10 

ppm oxidant, no consistent linear relationship 

between oxidant concentration and performance 

could be detected. Folinsbee's experimental 

studies suggest that on high-oxidant days, the 

irritant effect of pollutants may have restricted the 

runners' mechanical lung function sufficiently to 

prevent them from taking up enough oxygen to 

support the performance level of which they were 

potentially capable. The studies of Folinsbee et 

a1. 14 ' 15 suggest further that ozone alone may have 

been responsible for this effect. 

Ury et a1. 63 have reported a statistically 

significant positive association between hourly 

oxidant levels and automobile accident frequency 

in Los Angeles. The study design employed by Ury 

did not allow dose-response relationships to be 

developed. Reduced visual acuity, reduced 

visibility, and eye irritation may all be contributing 

factors to Ury's findings. 

The observations of Lebowitz et a1. 27 suggest 

that the degree to which photochemical oxidants 

affect pulmonary function may depend quite 

heavily on the subject's level of exercise. This 

observation is quite consistent with the 

experimental findings of Bates' and Folinsbee et 

a1. 14,15 It must be noted that too few pollution 

measurements were reported by Lebowitz to 

support a dose-response relationship. Also, the 

Lebowitz et al. study desigri did not permit oxidant 

effects to be separated from the effects of other 

pollutants and of ineteorologic'factors. 

Kagawa and Toyama 24 ' 25 observed that 

impairment of pulmonary function in Japanese 

schoolchildren was more strongly associated with 

exposure to ozone than to total oxidants. This 

observation enhances confidence that ozone alone 

may be responsible for decrements in pulmonary 

function, no matter what the effects of other 

pollutants may be. Kagawa also observed larger 

correlations of ozone concentration with indices 

thought to reflect large airway function (airway 

resistance and specific conductance) than with 

indices thought to reflect small airway function 

(instantaneous flow at 25 and 50 percent of vital 

capacity). The Kagawa and Toyama study design 

did not allow dose-response relationships to be 

inferred. 

Several investigators have noted associations 

between short-term oxidant concentrations and 

the frequency of respiratory a nd other symptoms in 

healthy people. In their large study of student 

nurses, Hammer et a1. 18 observed simple 

frequencies of cough and chest discomfort and the 

adjusted frequency of headache to increase with 

daily maximum hourly oxidant concentrations in 

and above the range of 588 to 764 /ig/m 3 (0.30 to 

0.39 ppm). Japanese investigators have observed 

the frequencies of several symptoms in 

schoolchildren, including sore throat, headache, 

cough, and dyspnea, to be higher on days when 

maximum hourly oxidant concentration equalled 

or exceeded 0.15 ppm than on days when 

corresponding concentrations were below 0.10 

ppm. In Japanese studies, symptom frequencies 

have generally been more strongly associated with 

total oxidant concentrations than with ozone 

concentrations. Results of Japanese studies also 

suggest that people with allergic tendencies and 

orthostatic dysregulation are more susceptible to 

short-term photochemical oxidant exposure than 

are other segments of the population 

Japanese studies have generally shown 

oxidant- or ozone-associated effects at lower 

248 
measured oxidant or ozone concentrations than 

American studies. The consistent difference 

between Japanese and American findings raises 

several questions, including whether the 

components of oxidant pollution in Japan are 

different from those in Los Angeles, or, indeed, 

from those in any U.S. location. It is possible, for 

instance, that oxidants in Japan are accompanied 

by higher su!fur oxide levels than in the United 

States. In any case, the Japanese results cited in 

this chapter underscore the point that 

epidemio!ogic results gathered in one area can be 

generalized to other areas only with the greatest 

caution. The Japanese resu!ts also demonstrate 

the need to gather comprehensive data in U.S. 

locations other than Los Angeles. 

As yet, it is not possible to judge confidently 

whether transient symptoms, irritation, or 

decrements in pu!monaryfunctionconstitutebona 

fide impairments of health. As with eye irritation, 

confident judgement must await studies of the 

cumulative effect of many of these minor insults 

occurring over long periods of time. 

Short-term photochemical oxidant, exposures 

have also bqen associated with aggravation of 

existing disease, though not as reliably as with the 

production of symptoms and minor illness in the 

healthy. Schoettlin and Landau 53observed a 

significantly higher rate of asthma attacks on days 

when the (presumably maximum hourly) oxidant 

concentration exceeded 0.25 ppm than on days 

when it did not. The resu!ts of Schoettlin and 

Landau a!so suggested that a portion of the 

asthmatic popu!ation might be particularly 

susceptible to oxidants. 

Motley et a1. 38 , Remmers and Balchum, 45and 

Ury and Hexter 62have all observed a beneficial 

effect of air filtration on the lung function of 

patients with chronic respiratory disease. In 

studies reported bythese investigators, changes in 

pulmonary function appear to have been more 

strongly correlated with changes in oxidant 

concentrations than with changes in nitric oxide or 

nitrogen oxide concentrations. However, these 

studies do not support confident estimates of doseresponse relationships. Also, these studies are 

open to fairly serious methodologic questions. 

Studies of the re!ationship between short-term 

oxidant exposures and hospital admissions have 

yielded mixed results. Although Brant and Hi11 2' 3 

and Sterlin et al. s9,so g have observed positive 

associations between exposures and admissions, 

their observations must as yet be considered 

inconclusive for at least three reasons. First, these 

investigators have not ruled out an association 

between nonoxidant pollutants and admissions 

that might be just as strong as that between 

oxidant and admissions. Second, the Brant and Hill 

observation of high positive correlations between 

oxidant concentrations and admissions 4 weeks 

later is difficu!t to rationalize pathophysiologically, 

particu!arly in view of the negative correlations 

occurring in the intervening time. Third, coefficients of correlation between oxidant 

concentration and same-day admissions have nof 

exceeded the relative!y small va!ue of 0.27 (r 2 = 

0.073). 

As yet, no convincing association has been 

shown between short-term oxidant exposures and 

rates of mortality resulting from any cause. The 

positive association observed by Mills 36may yet 

prove to be valid. However, the vigor with which his 

conclusions can be advanced is considerably 

limited by the reana!ysis by Breslow and 

Goldsmith' of a considerable portion of the data 

used by Mills, in which no association between 

oxidants and mortality was observed. 

Interpretation of mortality studies to date has 

been hampered by limitations in statistical 

methodo!ogy. It has not yet proven possible to 

separate fully the effects on mortality of oxidants, 

other pollutants, and meteorologic factors, most 

notably temperature. Future improvements in 

statistical methodology may allow these factors to 

be separated more clearly than they can be at 

present. Future biomedical research should also 

enhance knowledge of the combined effects of 

pollution and meteorologic factors. Only with such 

advances can the true relationships of oxidants to 

mortality be determined. 

Effects of Chronic Photochemical Oxidant 

Exposures 

The effects on human health of long-term 

photochemical oxidant exposures have not been 

characterized nearly as completely as those of 

short-term exposures. When impairments in 

health have been associated with long-term 

exposures, it has not yet proven possible to 

determine the level or duration of exposure 

necessary to promote the impairments, since most 

studies of long-term exposure effects have been 

cross-sectional in design, not longitudinal. Also, 

studies of long-term exposure effects, whether or 

not they have revealed associations between 

exposure and hea!th impairment, have often been 

249 
rather Ilmlted wlth respect to methods of data 

collectlon or analysls. Furthermore, slnce no 

American city has experlenced elevated oxldant 

levels over more than about 30 years, consistent 

effects of long-term exposures concelvably have 

gone undetected before the present tlme, no 

matter how carefully studles were designed and 

conducted. 

Several studles suggest a tenuous assoclatlon 

between long-term oxldant exposures and chronlc 

respiratory morbidity. Deane and Goldsmith" have 

observed higher rates of perslstent cough and 

phlegm In Los Angeles telephone workers aged 50 

through 59 years than in comparable workers in 

San Franclsco. Hausknecht has reported that a 

disproportlonate number of chronic respiratory 

dlsease patients, randomly selected from the 

whole state of Callfornia, lived In the Los Angeles 

area. Llnn has observed hlgher rates of nonpersistent cough and phlegm In women Ilving In 

Los Angeles than In San Francisco, a finding that 

would reflect an effect of oxldant on chronlc or 

acute respiratory morbidlty However, the flndings 

of these studles are not clear wlth respect to the 

existence of an assoclatlon between oxldant exposure and chronlc respiratory dlsease. Nor do the 

findings allow confident Inference astothe level or 

duratlon of oxldant exposure necessaryto promote 

increased rates of chronlc resplratory illness. 

Buell et a1. 5 observed no conslstent assoclation 

between long-term oxldant exposure and lung 

cancer mortallty in Californla. Mahoney 31 has 

reported hlgher total resplratory dlsease mortality 

rates In Inland, downwlnd sectlons of Los Angeles 

than In coastal, upwind sectlons. However, 

Ilmitatlons In statlstical control for Important 

covarlates and a lack of actual pollutlon 

measurements render the results of both studles 

inconcluslve. 

In vlew of the long post-exposure latent periods 

known to be involved In the development of cancer 

and other chronlc dlseases, it Is qulte concelvable 

that an Influence of chronlc oxldant exposure on 

mortality could go undetected untll now or 

sometime In the future Studles conducted 

carefully over the next decade or so may well 

provide the most useful Informatlon concerning 

the relatlonshlp of chronic oxidant exposure to 

mortallty. 

As yet, no associatlon between chronic oxidant 

exposure and acute Illness has been shown. Asfar 

as we are aware, the Pearlman et al study 42 Is the 

only one available In thls fleld 

Llnn et a1. 29 and Cohen et a1. 10 have reported 

epldemiologlc studies of chronic oxidant 

exposures and pulmonary function. In neither 

study has an association between such exposure 

and pulmonary functlon been observed. However, 

Interpretatlon of these results Is Ilmlted by 

Imperfect matching of high- and low-exposure 

populatlons, Incomplete knowledge of actual 

exposure levels, and the relative absence of 

indlviduals Ilkely to be at hlgh risk in the study 

populations (e.g., those with clear-cut chronic 

respiratory dlsease). 

Attitudes of Laymen and Physicians Toward 

Oxidant Air Pollution 

Studies of community attltudes toward oxidant 

pollution do not yield sclentlfically confirmed 

information regarding the effect of oxidant 

pollution on illness rates and physiologic function. 

However, these results are Interesting in that they 

demonstrate considerable community concern 

about the effect that oxidant pollutlon may be 

exerting on the public health 

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ozone on the human lung /n Proceedings of the 

Conference on Health Effects of Air Pollutants, prepared 

for the U S Senate, Committee on Public Works 

Government Printing Office, Washington, D C, 1973 pp 

507-540 

2 Brant, J W. A Human cardiovascular diseases and 

atmospheric air pollution in Los Angetes, California lnt 

J Air Water Pollut 9 219-231 , 1965 

3 Brant, J W A, and S R G Hill Human respiratory 

diseases and atmospheric air pollution in Los Angeles, 

California lnt J Air Water Pollut 8259-277, 1964 

4 Breslow, L, and J Goldsmith Health effects of air 

pollution Am J Public Health 48 91 3-91 7, 1958 

5 Buell, P, J E Dunn, Jr , and L Breslow Cancer of the 

lung and Los Angeles-type air pollution Prospective 

study Cancer (Philadelphia) 20 2139-2147, 1967 

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for California lnitial Report of the Air Pollution Study 

Project State of California, Department of Public Health, 

San Francisco, Calif , March 1955 

7 California State Department of Public Health Clean Air 

for California Second Report State of California, 

Department of Public Health, Berkeley, Calif , March 

1956 

8 California State Department of Public Health Report III A 

Progress Report of California's Fight Against Air 

Pollution State of California, Department of Public 

Health, Berkeley, Calif , February 1957 

9 Cassell, E J, J R McCarroll, W Ingram, and D Wolter 

Health and the urban environment Air pollution and 

family illness III Two acute air pollution episodes in New 

250 
York City. Health effects Arch Environ Health 10 367- children and adolescents Am Rev Respir Dis 109. 262- 

369, 1965 273, 1974 

10 Cohen, C A, A R Hudson, J L. Clausen, and J H 28 Leeder, S R Role of infection in the cause and course of 

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11 Deane, M., J R Goldsmith, and D Tuma Respiratory J. V Patterson, C A Mulry, and J F Coyle Respiratory 

conditions in outside workers Report on outside plant function and symptoms in urban office workers in 

telephone workers in San Francisco and Los Angeles relation to oxidant air pollution exposure Am Rev 

Arch Enrivon Health 10 323-331 , 1965 Respir Dis 1 14 477-483, 1976 

12 Durham, W H Air pollution and student health Arch 30 Los Angeles County Medical Association Physicians 

Environ Health 28 241-254, 1974 Environmental Health Survey A Poll of Med+cal Opinion 

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human cell cultures Nature (London) 194 793-794, Health Associations, Los Angeles, Calif , May 1961 

1962 31 Mahoney, L E, Jr Wir,d flow and respiratory mortality in 

14 Folinsbee, L J, F Silverman, and R J. Shepard Los Angeles. Arch Environ. Health 22 344-347, 1971 

Decrease of maximum work performance following 32 Makino, K, and I. Mizoguchi Symptoms caused by 

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Exercise Physiol 42 531-536, 1977 430, 1975 

15 Folinsbee, L J, F Silverman, and R J Shepard Exercise 33 Massey, F J, Jr , E Landau, and M Deane Air Pollution 

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38996-1001, 1975 Presented at the Joint Meeting of the American 

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Barth, Director, Bureau of Criteria and Standards, New York, December 27, 1961 

National Air Pollution Control Administration, July 20, 34 McMillan, R S, D H Wiseman, B Hanes, and P F 

1970 Wehrle Effects of oxidant air pollution on peak expiratory 

17 Goldsmith, J R, and M Deane Outdoor workers in the flow rates in Los Angeles schoolchildren Arch Environ 

United States and Europe Milbank Mem Fund Q 43 Health 18 94-99, 1969 

107-116, 1965 35 Mills, C A Do smogs threaten community health? 

18 Hammer, D I, V Hasselbald, B Portnoy, and P F Cincinnati J Med 38 259, 1957 

Wehrle The Los Angeles student nurse study Daily 36 MiIIs,C A Respiratory and cardiac deaths in Los Angeles 

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Health, Berkeley, Calif , 1960 38 Motley, H L, R H Smart, and C I Leftwich Effect of 

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Athletic Performance M S thesis, University of North 1970 

Carolina, Chapel Hill, N C, 1972 40 National Air Pollution Control Administration Errata for 

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Its effects on respiratory function of elementary school Publication No AP-63, U S Department of Health, 

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25 Kagawa, J, T Toyama, and M Nakaza Pulmonary Washington, D C, March 1970 p 2 

function tests in children exposed to air pollution /n 41 Oechsli, F W, and R W Buechley Excess mortality 

Clinical Implications of Air Pollution Research A J associated with three Los Angeles hot spells Environ 

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Inc , Acton, Mass , 1976 pp 305-320 42 Pearlman, M E, J F Finklea, C M Shy, J Van Bruggen, 

26 Lagerwerff, J M Prolonged ozone inhalation and its and V A Newill Chronic oxidant exposure and epidemic 

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1963 43 Personal communication from 0 J Balchum to R E 

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Misiaszek, M Staniec, and D Van Wyck The effect of air 44 Peters, J M., R L H Murphy, B G Ferris, W A Burgess, 

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251 
63 Ury, H K., N M. Perkins, and J R Goldsmith Motor 

vehicle accidents and vehicular pollution in Los Angeles 

Arch Environ Health 25 314-322, 1972 

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school absenteeism Arch Environ Health 19 315-322, 

1969 

65 Wayne, W S, P F Wehrle, and R E Carroll Oxidant air 

pollution and athletic performance J Am Med Assoc 

199 901-904, 1967 

66 Winkelstein, W., Jr, , S Kantor, E W Davis, C S Maneri, 

and W E Mosher The relationship of air pollution and 

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particulates Arch Environ Health 14 162-171, 1967 

67 Winkelstein, W, Jr , S Kantor, E W Davis, C S Maneri, 

and W E Mosher The relationship of air pollution and 

economic status to total mortality and selected 

respiratory system mortality in men II Oxides of sulfur 

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Arch Environ Health 26 28-31 1973 

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urban air pollution upon respiratory function of 

emphysematous patients Presented at 58th Annual 

Meeting, Air Pollution Control Association, Toronto, 

Canada, June 21, 1965 

46 Renzetti, N A, and V Gobran Studies of Eye Irritation 

Due to Los Angeles Smog 1954-1956 Air Pollution 

Foundation, San Marino, Calif, , July 1, 1957 

47 Renzetti, N A, and H G Marcus, eds An Aerometric 

Survey of the Los Angeles Basin August-November, 

1954 Report No 9, Air Pollution Foundation, Los 

Angeles, Calif , July 1, 1955 

48 Richardson, N A, and W C Middleton Evaluation of 

filters for removing irri[ants from polluted air Heat 

Piping Air Cond 30 147-154, 1958 

49 Richardson, N A, and W C Middleton Evaluation of 

Filters for Removing Irritants from Polluted Air Report 

No 57-43, University of California, Department of 

Engineering, Los Angeles, Calif , June 1957 

50 Rokaw, S N, and F Massey Air pollution and chronic 

respiratory disease Am Rev Respir Dis 86 703-704, 

1962 

51 Sawicki, E Airborne carcinogens and aliied compounds 

Arch Environ Health 14 46-53, 1967 

52 Schoettlin, C E The health effect of air pollution on 

elderly males Am Rev Respir Dis 86 878-897, 1962 

53 Schoettlin, C E, and E Landau Air pollution and 

asthmatic attacks in the Los Angeles area Public Health 

Rep 76 545-548, 1961 

54 Shimizu, K, M Harada, and M Miyata Effects of 

photochemical smog on the human eye Rinsho Ganka 

30 407-418, 1976 

55 Shimizu, T Classification of subjective symptoms of 

junior high school students affectedby photochemicalair 

pollution Taiki Osen Kenkyu 9 734-741, 1975 

56 Stanford Research Institute The Smog Problem in Los 

Angeles County An Interim Report on Smog Research. 

Western Oil and Gas Association, Committee on Smoke 

and Fumes, Los Angeles, Calif, , 1948 

57 Stanford Research Institute The Smog Problem in Los 

Angeles County Second Interim Report on Studies to 

Determine the Nature and Sources of the Smog Western 

Oil and Gas Association, Comm+ttee on Smoke and 

Fumes, Los Angeles, Calif, , 1949 

58 Stanford Research Institute The Smog Problem in Los 

Angeles County Third Interim Report on Studies to 

Determine the Nature and Sources of the Smog Western 

Oil and Gas Association, Committee on Smoke and 

Fumes, Los Angeles, Calif , 1951 

59 Sterling, T D, J J Phair, S V Pollack, D A Schurnsky, 

and I DeGroot Urban morbidity and air pollution A first 

report Arch Environ Health 13 158-170, 1966 

60 Sterling, T D, S V Pollack, and J H Phair Urban 

hospital morbidity and air pollution A second report 

Arch Environ Health 15 362-374, 1967 

61 Ury, H K Photochemical air pollution and automobile 

accidents in Los Angeles Arch Environ Health 17 334- 

342, 1968 

62 Ury, H K, and A C Hexter Relating photochemical 

pollution to human physiological reactions under 

controlled conditions Arch Environ Health 18 473-480, 

1969 

252 
11. EFFECTS OF PHOTOCHEMICAL OXIDANTS ON 

VEGETATION AND CERTAIN MICROORGANISMS 

INTRODUCTION 

Injury to terrestrial vegetation was one of the 

earliest manifestations of photochemical oxidant 

2,8,9,21z2,24,100,144,160,199,200,201,203,212,216, air pollution. 

217,219,220,238,263,266,273,274,300,314 Investigations by 

Middleton et a1. 203 in 1944 described smoginduced injury to leafy vegetables, ornamentals, 

and field crops in a small area of Los Angeles 

County. By 1950, such injury was observed over a 

large portion of southern California and the San 

Francisco Bay Area. 199 Plant injury caused by 

photochemical oxidants now occurs commonly in 

most, if not all, of the metropolitan areas of the 

United - States. With increasiRg frequency, 

photochemical oxidants are associated with injury 

to vegetation in rural areasfar removedfrom urban 

complexes. - 

Analysis of the photochemical oxidant air 

pollution complex has resulted in the isolation of 

three specific phytotoxic components: ozone, 

nitrogen dioxide, and peroxyacylnitrates. The 

peroxyacylnitrates are the most phytotoxic of the 

known photochemical oxidants. A homologous 

series of compounds, they include 

peroxyacetylnitrate (PAN), peroxypropionylnitrate 

(PPN), peroxybutyrylnitrate (PBN), peroxyisobutyrylnitrate (P, soBN), and peroxybenzoylnitrate 

(PBzN). The degree of phytotoxicity of these 

compounds increases with the increase in their 

molecular weight: PAN<PPN<P, soBN<PBN (PBzN 

has not been tested). 2 ' 2 '2 ' 7 '3°° Because PPN and 

PBN are not usually detected in the atmosphere, 

PAN is the only member of the series that has 

received attention. Discussion of the 

peroxyacetylnitrates will therefore be restricted to 

PAN. The phytotoxic characteristics of nitrogen 

dioxide will be discussed in a separate document. 

Consideration of the specific effects of ozone and 

PAN will be limited to laboratory and controlled 

field exposures, since quantitative effects of these 

compounds cannot be easily differentiated in the 

ambient environment. The term "oxidant" will 

therefore be used exclusively when discussing 

ambient air photochemical oxidant exposures that 

contain variable combinations of PAN, 03, NO2, 

and, in most cases, additional phytotoxicants. 100, 

116,133,217 Ozone, the most prevalent photochemical 

oxidant, has received the greatest amount of study, 

and its effects on vegetation are best understood. 

The first studies calling attention to ozone as a 

pollutant affecting crops were the studies of 

Richards et a1. 250 using grapes, and Heggestad and 

Middleton 125 on tobacco. 

Interactions of the oxidant mixtures and other 

atmospheric contaminants may produce 

synergistic effects in many plant species '0,68,191,216, 

217,236,245,269,286 and antagonistic effects on 

others. '46,292,293 Increasing attention is now being 

focused on these effects. Sensitive vascular plants 

are useful biological indicators of photochemical 

21,22,44,116,120,149,197-199,201,202,204,212,216, air pollution. 

217,219,220,221 ,238,255,266,300,301 

The limited knowledge relating to the direct 

effects of photochemical oxidants on nonvascular 

plants and microorganisms is also discussed in 

this chapter. Although some mosses and lichens 

may be useful as biological indicators of sulfur 

compounds, there is no evidence indicating that 

these nonvascular plants are highly sensitive to 

photochemical oxidants. 

VASCULAR PLANT RESPONSE TO 

PHOTOCHEMICAL OXIDANTS 

The effects of photochemical oxidants on 

vascular plants can be envisioned as occurring at 

several response levels, from the molecular to the 

organismal (Figure 1 1-1), depending on the 

concentration of pollutant, length of exposures, 

and elapsed time between the exposure and the 

observation of the effects. The earliest effects 

include an increase in cell membrane 

permeability, a decrease in carbon dioxide fixation, 

253 
and a stimulation of stress-+nduced ethylene 

production. 13.283,z9° These subtle cellular changes 

are followed by both Inactivation and/or activatlon 

of specific enzymes, alteration in metabolite pools, 

and modlfied metabollte translocation. 283,2e6z95 

Biochemical changes in individual plants are 

ultimately expressed in visible follar injury, 

premature senescence and Increased leaf 

abscisslon, reduced plant vigor and growth, and 

death. In the final analysis, biochemical 

modifications on an individual level are manifested 

by changes in plant communities and, ultlmately, 

in whole ecosystems.2 "'2s3 These changes 

occurring In stressed systems can ultimately be 

measured in socioeconomlc impacts. The 

sequence of topics In this chapter describing 

photochemical oxidant effects on vascular plants is 

based on the logical hierarchlcal ordering of plant 

response depicted In Figure 1 1-1 . The complexities 

of the entire subject are apparent in the sections on 

dose response and factors affecting plant 

response. 

Physiological Processes 

In vascular plants, foliage is the prlmary receptor 

of photochemical pollutants. For photochemical 

oxidants to produce an effect in plants, they must 

come into contact wlth the leaf, pass through the 

stomata, and dissolve in the aqueous layer coating 

the cell walls. 2' ° ' Z83 Since stomata arethe princlpal 

entry sites for ozone and PAN into plant leaves, 

stomatal closure presents a physical barrier to the 

entrance of oxidants and effectively protects the 

plant from injury. 785 Several studies suggest that 

oxidants may cause stomatal closure. 'a4,,so,,ao,24s 

In one study, stomatal closure was associated wlth 

a genetic trait in onlon wherein the stomata of 

sensitive plants did not close in response to 

ozone. 78 Dean65 related the differences in ozone 

sensitivlty between two tobacco cultivars to 

differences in stomatal density. Evans and Ting 82 

found that maximum sensitivity of bean primary 

leaves was not associated with differences in 

stomatal number or leaf resistance to gas transfer. 

The effect of azone and PAN on stomatal opening 

depends on both environmental and genetic 

factors. 

Ozone can modify amino acids, proteins, 

unsaturated fatty acids, and sulfhydryl residues 13 

located in cellular membranes. The initial effect of 

oxidants is to increase the leakage of water and 

ions, such as K + (potassium ion), from ce11s. In 

addition, ozone can induce the production of 

stress-induced ethylene.' 50,2e3z94 The amount of 

ethylene produced in response to ozone stress is 

proportlonal to ozone concentration or duration of 

CHANGES IN PLANT COMMUNITIES AND 

ECOSYSTEMS 

REDUCED PLANT GROWTH 

REDUCED PLANT YIELD 

ALTERED PRODUCT QUALITY 

LOSS OF PLANT VIGOR 

ALTERED ENZYME ACTIVITIES 

ALTERED METABOLIC POOLS 

ALTERED TRANSLOCATION 

REDUCED PHOTOSYNTHESIS 

INCREASED MEMBRANE PERMEABILITY 

PRODUCTION OF STRESS ETHYLENE 

BIOCHEMICAL AND CELLULAR 

CHANGES 

Figure 11-1. Sequence of ozone-induced responses. 282 

254 
exposure. 294 Plants sensitive to ozone produce 

more stress ethylene than less sensitive plants. 

Ethylene production is induced before the 

appearance of visible injury and frequently occurs 

without visible injury. 

Todd 296 and Todd and Probst 298 also measured 

the effects of ozone at 7840 /jg/m 3 (4 ppm) for 40 

min on photosynthesis and found that the 

development of symptoms was associated with an 

inhibition of carbon dioxide fixation. This effect 

was also confirmed by Macdowall,"' who reported 

that the inhibition of photosynthesis was greater 

than that which could be accounted for 6y 

chlorophyll destruction alone. Hill and Littlefield 130 

associated decreased net photosynthesis caused 

by ozone (at 0.60 ppm for 1 hr) with both decreased 

stomatal opening and decreased transpiration. 

These studies have generally shown that net 

photosynthesis can be reduced without the 

association of visible injury. 

The photosynthetic rate is an important indicator 

of plant vigor. In.ponderosa pine, a reduction in this 

rate may occur at a low dose of ozone without 

causing visible symptoms. Miller et a1. 210 found 

that a daily 9-hr exposure to ozone at 294 Ng/m 3 

(0.15 ppm) reduced apparent photosynthetic rates 

by 10 percent after 30 days, without typical ozone 

symptoms. Botkin et a1. 23 found that a threshold 

ozone dose for suppression of net photosynthesis 

in eastern white pine was a 4-hr exposure to 980 

pg/m 3 (0.50 ppm). 

Ozone, in addition to inhibiting photosynthesis, 

alters the way in which the products of 

photosynthesis are distributed within plants. 

Results of studies in which alfalfa and ponderosa 

pine were exposed to low levels of ozone for a 

growing season indicated that sugars were 

retained in the foliage and were not translocated to 

the roots. 2 ' s ' 295 The resulting reduction of 

carbohydrates in the roots could reduce nitrogen 

fixation and plant growth. 93,2so 

The vital physiological process of nitrogen 

fixation may be a key factor in the impact of 

photochemical oxidants on the plant 

community/ecosystem complex. Ozone is known 

to suppress nodulation in the rootsof 

soybean' s 'z's 'zsa and ladino clover. 2 '' SS Blum and 

Tingey'$ found no direct effect of ozone on 

Rhizobium or on nodule formation. They attributed 

the decrease in nodule number and nitrogen 

fixation to the reduction in the available energy in 

the root tissues. Studies of the chronic exposure (7 

hr per day) of alfalfa to 98 pg/m 3 (0.05 ppm) Os by 

Tingey283 and Neely et a1. 218 show that the total 

amount of fixed nitrogen was depressed by 40 

percent. Weber 307 found that the effect of ozone 

and a mixture of ozone and sulfur dioxide on 

soybean resulted in suppression of nitrogen 

fixation by 50 percent. Suppression of atmospheric 

nitrogen fixation by root nodules could affect total 

biomass and agricultural yield, especially in areas 

of high oxidant pollution and low soil nitrogen. 

Kochhar 156 also reported an inhibition of plant 

growth and nodulation of Trifolium repens (clover) 

when plants were treatedwith root exudates taken 

from fescue grass that had been exposed to ozone. 

If these responses are of widespread occurrence, 

the competitive ability of plant species could be 

modified with a resulting change in plant diversity 

and a possible decrease in productivity. 

The acute responses of plants to ozone and PAN 

result from disruption of normal cell structure and 

processes. The initial response results in cellular 

disorganization. Water and salts are lost from the 

cell interior; then plasmolysis results and cell 

death normally occurs. However, depending on 

dose and environmental conditions, membrane 

permeability may be restored and cell recovery 

occurs. The extent of recovery depends on the 

severity of the external stresses and on the ability 

of the cells to repair themselves. As indicated 

previously, the biochemical and physiological 

effects of ozone on plants are better understood 

than those of PAN. 

Visible Symptoms 

Visible symptoms are commonly used in 

characterizing the response of vegetation to a 

variety of stresses, including air pollution. 30 ' 

Different types of stress induce similar symptoms, 

thus causing difficulty in diagnosis. The visible 

symptoms resulting from oxidant injury to plants 

can be classified as belonging to two general 

categories—acute and chronic injury. Acute injury 

is usually manifested by cell destruction. Necrotic 

symptoms of acute injury are sometimes 

characteristic of a given oxidant. These patterns, at 

the least, demonstrate the effect of a chemical 

toxicant. Acute injury usually appears within 24 hr 

after exposure and is associated with short 

exposures (hours) to a specific oxidant or pollutant 

mixtures at relatively high concentrations. Chronic 

injury, whether mild or severe, is usually 

associated with long-term or multiple exposures to 

low concentrations of oxidants. Disruption of 

normal cellular activityoccurs, leadingtochlorosis 

255 
or other pigment or color change. Cell death may 

eventually result. Chronic oxidant injury patterns 

may be confused with symptoms resulting from 

normal senescence and biotic pathogens, 

including insects, nutritional disorders, or other 

environmental stresses. These patterns may 

appear as premature leaf senescence. 

Bobrov, 19 '

2° ' 2 ''22 Bystrom et a1., 37 and Glater et 

a1.96 conducted the earliest studies of microscopic 

changes and developmental patterns resulting 

from simulated smog and ambient pollution. These 

workers first suggested thatthe initial effects were 

due to cell membrane injury. They described 

developmental patterns and showed that leaves 

near maximal expansion were most sensitive and 

that sensitivity was related to stomatal function, 

volume of intercellular spaces, and the extent of 

suberization of inesophyll cells. Other workers 

have since substantiated their studies. 192,2'6,2a,,ze6 

Although ozone and PAN are considered to be 

the two primary phytotoxic oxidants in the 

photochemical complex, the response of plants to 

simulated polluted atmospheric conditions 

suggests the existence of other ambient phytotoxic 

oxidants. 96 The symptoms associated with many of 

these reactant mixtures are closely related to those 

caused by ozone and PAN. 15,"8 In some tests, 

however, the reactant mixtures used wouid not 

have produced either ozone or PAN. In other cases, 

the pattern of injury on sensitive test plants or age 

of tissue affected suggested the presence of one or 

more pollutants other than ozone or PAN Plant 

injury symptoms observed in the field often 

resemble those reported from controlled 

exposures to ozone or PAN, but the response 

pattern in some cases is sufficiently different that 

accurate field diagnosis isdifficult. Brennan et al. 3 o 

correlated development of oxidant symptoms with 

aldehyde concentrations in New Jersey and 

suggested that aldehyde may be a major phytotoxic 

component of the photochemical oxidant complex. 

The symptoms observed were probably not ir, 

response to the aldehydes, but rather to a 

compound or group of compounds present under 

the same conditions as the aldehyde 132 The 

concentration of the compound or group of 

compounds was probably directly related to the 

concentration of the aldehydes 

OZONE 

The four general types of lesions found on plant 

leaves as a result of ozone injury are described in 

detail in Recognition of Air Pollution lnjury to 

Vegetation: A Pictorial Atlas. 129 These are 

pigmentation (stippling), bleaching, foliar 

chlorosis, and bifacial necrosis. AII exceptthe last 

type of symptom occur primarily on the upper 

surface of the leaf. 

1. Pigmentation (stippling). The palisade• 

mesophyll cells of injured leaves take on 

brown, black, red, or purple colorations. 

The injury is evident primarily on the upper 

leaf surface. On many deciduous trees, 

shrubs, and some herbaceous plants, the 

accumulation of pigments in the dying cells 

results in small dot-like lesions. 

2. Bleaching(fleck). Bleached or unpigmented 

lesions usually occur on upper leaf 

surfaces following collapse of the palisade 

cells and sometimes of the epidermal cells. 

Individual lesions are usually small and 

irregular in shape but may coalesce and 

become large, frequently resulting in 

slightly sunken areas on the upper leaf 

surface in certain herbaceous species. 

3. Foliar chlorosis. Chlorotic areas usually 

occur on the upper surfaces of leaves, often 

coalescing to present a mottled 

appearance. Pine needles and grasses that 

do not possess differentiated mesophyll 

tissue may develop the chlorotic mottling 

on either leaf surface. 

4. Bifacial necrosis. Bifacial necrosis results 

when the tissues connecting the upper and 

lower leaf surface are killed. The coloration 

of the tissue in the lesions may range from 

ivory to orange or brownish-red. Upper and 

lower surfaces often are drawn together, 

forming a thin, papery lesion. 

The two classic symptoms (fleck and stippling) 

are more widely associated with the response of 

dicotyledonous plants to ozone than are other 

symptoms. Many plants (e.g., pinto bean, 

cucumber, tomato, soybean, and sycamore) may 

have the entire upper surface covered with a 

bleached appearance as a result of ozone 

exposure, with no observable injury on the lower 

surface. On closer examination, the bleached area 

is seen to be made up of many small groups of 

palisade cells that are dead and contain no 

pigmant. In other plants or under different 

conditions, the palisade cells mayaccumulatedark 

alkaloid pigments (stipple) coincidentally with cell 

death After exposure to higher ozone 

concentrations or after longer periods of exposure, 

injury extends to the spongy cells, producing 

256 
bifacial necrosis. Plants exposed to a high 

concentration of ozone or to a high concentration 

of ambient pollution during a pollution episode 

usually develop dark, watersoaked areas in the leaf. 

within a few hours. Leaves may show partial 

recovery, or these areas mayform light-tan bifacial 

necrotic lesions within 24 to 48 hr. Individual 

lesions may be small, but groups of them can 

extend and affect a considerable portion of the leaf. 

In monocotyledonous plants (grasses or cereals) 

and in some nonmonocotyledonous plants there is 

no division of inesophyll tissue, and injury usually 

appears as a bifacial fleck. 21 

The foregoing discussion is not descriptive of 

' effects noted in coniferous trees such as white 

pine. Two classic oxidant (ozone) syndromes of 

pine, one in the eastern and the other in the 

western United States, have been described. 

Ozone is probably the cause of emergence tipburn 

in white pine (white pine needle dieback). 15 The 

injury is characterized as a tip dieback of newly 

elongating needles and occurs throughout the 

range of eastern white pine. Affected trees are 

found at random in a stand, and symptoms develop 

in discrete episodes in successive years. 21 

Primar, f roots of affected trees often die after 

repeat- ,d needle injury. Costonis and Sinclair 48 

reportecf silvery or chlorotic flecks, chlorotic 

mottlir g, and tip necrosis of needles as a result of 

ozone ;xposure. 

Chlo -otic decline, a needle injury of ponderosa 

pine, v ,as first noticed in 1953 and was related to 

oxidant air pollution by 1961. 234 Chlorotic decline 

was c ~ iaracterized by a progressive reduction in 

termir 31 and diameter growth of the tree; only the 

currer t season's needles were retained. Yellow 

mottling and a reduction in the number and size of 

the remaining needles were noted. Eventually the 

tree died. The chlorotic decline was not associated 

with stresses other than ozone. 235 

PAN 

The injury symptoms for the various peroxyacyl 

compounds are similar and cannot be 

distinguished. The characteristic symptoms are 

glazing, silvering, or bronzing of the lower surface 

of the leaves of plants such as spinach, garden 

beets, romaine lettuce, and chard. Symptoms on 

endive and turnip appear as a bleaching of the 

lower leaf surface that often develops into lighttan 

necrotic areas. In some instances, upper leaf 

surfaces may also be affected.216'217 '238 '272 

Microscopic examination of 6ffected areas 

reveals a collapse of spongy mesophyll cells with a 

subsequent development of large intercellular air 

pockets, especially near the stomata. The air 

pockets give the leaves the glazed appearance. 2 ' 2 ' 

217,238 

Young expanding leaves are normally more 

sensitive to PAN than mature leaves. Leaves of 

plants such as grasses, tobacco, and petunia, 

which do not mature uniformly, may show leaf 

banding where injury is related to a sensitive 

region of the expanding leaf. Successive exposure 

to PAN may result in the formation of multiple 

ba nds. 2o,238 

PAN symptoms are slow to deve' -)p and maytake 

up to 72 hr for full development. A complete 

description of PAN injury to plants was written by 

Taylor and MacLean. 272 

Growth and Yield 

Photochemical cx;dants, including ozone and 

PAN, suppress growth and yield in many plant 

species. Although growth and yield effects are 

normally associated with visible injury, oxidants 

can inhibit growth with little or no injury. The basis 

for this variability is not understood, but probably it 

is associated with the genetic composition of 

plants, environmental condition, and pollutant 

combination and dose. 

Attempts have been made to associate visible 

injury with other indices of plant response. Todd 

and Arnold 297 compared visible injury with 

biomass production and chlorophyll content of 

pinto bean exposed to a synthetic oxidant (ozone 

plus hexene). They noted a logarithmic 

relationship between injury and the two response 

parameters and suggested that leaf injury was not 

a reliable index for estimating growth losses. A 

group of Canadian workers 3 '7 used physiological 

measurements exclusively to monitor the effects 

of acute ozone (oxidant) exposures. Because of the 

subjective nature of injury measurements and the 

often apparent poor correlation with growth 

responses, growth or physiological parameters are 

often evaluated directly. 

AMBIENT AIR STUDIES 

Since the first observations of oxidant injury by 

Middleton et a1., 203 there has been a continuing 

flow of reports mentioning the effects of oxidants 

on vegetation. The majority of these reports 

associate ozone or oxidant injury symptoms with 

episodes of given levels of oxidant or ozone. Engle 

et a1. 80 in Wisconsin, Laurence et a1. 167 and Kohut 

et a1. 759 in Minnesota, Gardner 91 in South Dakota, 

Weaver and Jackson306 and Haast 01 in Ontario, 

257 
Rich et a1. 247 in Connecticut, Daines et a1. 54 in New 

Jersey, Brasher et a1. 25 in Delaware, Skellyetal.z 59 

In Virginia, Reinert et a1. 243 In Ohio, Tingey and 

HiII 299 in Utah, and Oshima et a1., 232 Cobb and 

Stark,43 and Mlller and Millecan 209 in Californla all 

noted plant effects from ambient oxldant. Haas'o' 

found that the rate of growth during oxldant 

exposure influenced the symptom severity, that 

the stage of growth determined the dose requlred 

to produce injury effects, and that the physical 

conditlons within a field could cause variable plant 

responses to oxidant. 

Cobb and Stark43 and Mlller and Millecan209 

reported the severe effects of ambient oxidant on 

ponderosa pine in the San Bernardino Mountalns. 

The results of quantitative studies are reported In 

Chapter 12. Skelly et a1. 259 assoclated postemergence tipburn of eastern whlte pine with high 

levels of ambient oxidant. 

Greenhouses with filtered and nonfiltered air or 

field chamber studles have been used to determine 

the effects of amblent pollutants on growth and 

yield of selected crops. Reductlons in yield and 

biomass were some of the observed effects noted. 

Summary data from selected studies are shown in 

Table 1 1-1 . Thompson and Taylor 280 summarized 

several years of detailed fleld chamber studies, 

during which lemon and orange trees were 

exposed to many pollutant combinations. The 

inhibiting effects of the pollutant on frult size and 

number and on total yields were noted in these 

studies. The results of these studies provided the 

basis for the projected 50-percent reductions In 

citrus yields from the Los Angeles Basin as a result 

of photochemlcal oxidants. Thompson and Katz 279 

showed that some of the effects noted on the citrus 

trees were probably related to concentrations of 

PAN in the ambient air. Thompson and 

coworkers, 277 ' 278 using charcoal-filtered and 

unfiltered chambers to determine effects of 

ambient oxidants on grapes, found nominal yield 

effects in the first year and 50 to 60 percent 

reduction during the next 2 years. The year to year 

dlfferences were attrlbuted to the effects of 

oxidants on floral initiation the year before the flrst 

year study. A slmilar response may be expected for 

plants that initiate floral structures in the season 

prevlous to experlmental treatments. A wax 

emulsion spray on the leaves gave a 20-percent 

Increase in yield over unsprayed plants, 

suggesting that selected protectants may be useful 

in protecting grapes grown in areas of high oxidant 

concentration. 

TABLE 11-1. EFFECTS OF OXIDANTS (OZONE) IN AMBIENT AIR ON GROWTH, YIELD, AND 

FOLIAR INJURY IN SELECTED PLANTS a 

Plant response 

Plant Oxidant concen- Duratron of (reduction frorn control 

specres tratron, ppm exposure listed as °„) Reference 

Lemon >0 10 Over growtng season 32, yleld 280 

52, yleld (leaf drop and other effects) 

Orange >0 10 148 hr/month avg from March- 54,yleld 280 

Oct , 254 hr/month avg from (other reductlons found) 

July-Sept 

Grape, cultivar ?0 25 Often over May-September 12, yleld (flrst year) 277 

growing season 61, yteld (second year) 278 

(Increased sugar content) 

47, yleld (thlyd year) 275 

Corn, sweet 0 20-0 35 Hourly maxlmum for 3 to 4 days 67, Injury (10 cultivars, 5 unmarketable) 38 

before Injury 18, Injury (13 cultivars) 

1, Injury (11 cultivars) 

Bean, whlte >0 08 9 hr (Bronze color, necrotic stlpple, premature 306 

absclsslon) 

Tobacco, cultivar 0 02-0 03 6 to 8 hr (Mlnlmal Injury) 119 

Bel W3 

Tobacco, cultivar >0.05 Often over growing 22 (fresh wt), top 108 

Bel W3 season 27 (fresh wt), root 

Cotton, cultivar Amblent Over growing season 7-20, Ilnt + seed (3 locatlons, 1972) 33 

Acula 5-29, Ilnt + seed (3 locatlons, 1973) 

Potato, 4 >_0 05 326 to 533 hr (2 years) 34-50, yleld (2 years for 2 cultivars) 122 

cultivars b 20-26, yleld ( 1 year for 2 cultivars) 

Potato, cultivar 015 3 consecutive days 95, Inlury (leaf area covered) 25 

Halg 

aTable taken from Ref 217 

° Greenhouse studres 

258 
Other experimental studies noted the effects of 

ambient air levels of oxidant on cotton, potato, and 

tobacco yields. In the San Joaquin Valley, 

California, a 5- to 29-percent reduction in lint and 

seed was noted over a 2-year period when cotton 

was grown in charcoal-filtered vs unfiltered field 

chambers. 33 Heggestad 122 reported the results of a 

3-year study comparing the growth of four potato 

cultivars in greenhouses with charcoal-filtered 

and unfiltered ambient air. Yields of sensitive 

cultivars were suppressed as much as 50 percent 

by ambient oxidants. Heagle et a1., 108 using opentop field chambers, reported preliminary results 

indicating a reduction in leaf yields of a sensitive 

tobacco cultivar when plants grown in ambient air 

and nonfiltered chambers were compared with 

plants grown in chambers with charcoal filters. 

The results of the research discussed in this 

section indicate that oxidants in the ambient air 

decrease plant growth and yield. Injury symptoms 

resulting from oxidant exposure have been noted 

on a nationwide basis. The most severe effects are 

found in California in the San Bernardino 

Mountains and the Los Angeles Basin. 

CONTROLLED CHAMBER STUDIES 

To define the effects of oxidants on plant growth 

and yields more accurately, many workers have 

used controlled additions of ozone to determine the 

effects of acute or chronic exposures on a variety of 

growth parameters. Although the results of the 

effects of ambient oxidants on vegetation may not 

be directly comparable with the results obtained in 

the controlled exposure studies discussed in the 

following sections, reduced yields and similar 

oxidant symptoms are common results. Most of the 

results discussed are from exposures in 

greenhouses and controlled environmental 

chambers, but several are from studies using 

exposure chambers placed over field plantings 

Short-Term Exposures — Adedipe and 

associates 3 reported reduced biomass and floral 

production in four bedding plants and reduced 

biomass in two radish cultivars' from acute ozone 

exposures (Table 1 1-2). They reported no effects 

on marigold, celosia, impatiens, and salvia 

cultivars, even at the high concentration of 0.80 

ppm for a 2- hrexposure. Research involving radish 

has included the effects of exposure temperatures 

on the growth response to ozone.' One cultivar 

reacted to ozone in the same way regardless of 

temperature variation, but the response of the 

second cultivar was influenced by temperature. 

Tingey et a1. 285 exposed radish at 7, 14, or 21 days 

of age and all combinations of these ages to ozone 

at 785 Ng/m3 (0.40 ppm) for 1.5 hr. For a single 

exposure, the greatest effect on root growth was 

noted on the 14-day-old cultivar; for double 

exposures, the greatest root growth effect 

occurred with the 7- and 14-day-old cultivars. 

However, the greatest reduction of root growth 

occurred with triple exposures of 7-, 14-, and 21- 

day-old cultivars. The reductions in root growth 

from the multiple ozone exposures were equal to 

the additive effects of three single exposures. It 

was concluded that root growth reductions 

resulted from the preferential use of 

photosynthate for foliar growth. Inhibition in the 

rate of root growth remained during the second 

week after exposure. Tingey and Blum 284 reported 

that when soybean plants were exposed to 1468 

Ng/m 3 (0.75 ppm) of ozone for 1 hr, root growth 

was consistently reduced more than top growth 

and, in addition, there was a reduction in nodule 

weight and number. Evans87 exposed the middle 

leaflet of the first trifoliate leaf of pinto bean to 

various ozone concentrations. The results 

indicated a differential growth response in various 

leaf positions. A reduction in eaflet expansion was 

noted after a 12-hr treatment with 98 ug/m 3 (0.05 

ppm) ozone. The foregoing discussion represents 

only a few of the representative examples 

regarding the effects of acute ozone exposure on 

plant growth. 

Long-Term Exposures — Experimental long-term 

exposures of various crops as well as ornamental 

and native plants to ozone have resulted in a 

reduction in growth and/or yield. Harward and 

Treshow105 exposed 14 species representative of 

the aspen plant community to ambient air 

containing ozone concentrations of 98 to 137 

pg/m 3 (0.05 to 0.07 ppm) and to ozone at 290 and 

588 pg/m3 (0 15 and 0 30 ppm) for 3 hr/day, 5 

days/week, and tocharcoal-filtered airthroughout 

the growing season. In all species, foliar injurywas 

seen at the highest pollution concentration (Table 

1 1-3). There was considerable variability in the 

responses, and only six species formed seed, 

however, in most cases, growth was reduced and 

most species were sensitive Price andTreshowz 3 g 

found major biomass reductions in six grass and 

two tree species exposed for 4 hr/day to ozone at 

290 to 647 Ng/m 3 (0.15 to 0.33 ppm) over a 

growing season. They also found reduced 

reproduction and a loss of some reproductive 

components. These effects on growth and 

259 
reproduction coutd result In subtle shlfts in 

community composltion after several years of 

ozone exposure. Taylor et a1. 271 reported a 52- 

percent reduction in the fresh weight of avocado 

seedlings exposed to a synthetic smog (ozone plus 

hexene) for 280 hr. Tingey et a1. 293 found that the 

growth of two soybean cultivars (Hood and Dare) 

was inhibited by intermlttent exposure to ozone at 

196 μg/m3 (0.10 ppm) for 3 weeks. A decrease in 

both root and top growth occurred. Similar 

results287 were noted with radish, except that 

growth was inhibited at 98 Ng/m3 (0.05 ppm). The 

reduced growth noted in the aforementioned 

studies occurred even though there were very few 

visible symptoms of plant injury. 

A 30-percent reductlon in wheat yleld occurred 

when at anthesls, wheat was exposed to ozone at 

392 ,ug/m 3 (0.2 ppm) 4 hr/day for 7 days. 156 

Oshfma et a1. 231 reported a reductlon in tomato 

yleld at 686 μg/m 3 (0.35 ppm) over an exposure 

perlod of 97 hr. Signlficant injury occurred at both 

392 and 686 μg/m 3 (0.20 and 0.35 ppm) ozone. 

Plants exposed to the low ozone concentration 

tolerated a considerable amount of defoliatlon and 

a significant decrease In blomass wlthout a corresponding reduction in yield. A signiflcant reduction in yleld, however, was recordeC from 

plants in the higher (686 μg/m 3 , or 0.35 ppm) 

ozone exposure where a greater decrease in biomass was observed. This yield reduction was 

caused by a lower fruit set and subsequentlyfewer 

harvested fruit. Oshima suggested an injury 

tolerance threshold for tomato below which no 

reduction in yield would occur In an eariler study, 

Oshima 229 reported a decrease in kernel weight of 

sweet corn exposed to ozone for 4 percent of the 

growing period at concentrations of 392 or 686 

/jg/m 3 (0 20 or 0.35 ppm). The reduced weight was 

TABLE 11-2. EFFECTS OF ACUTE EXPOSURE O NGROWTH AND YIELD OF SELECTED PLANTS a 

--_ ---- _-----_-_----- -~ - - Plant response 

Plant Ozone concen- Exposure (reduction from control 

species tration, ppm time, hr listed as ol° Reference 

Begonla, cultivar 010 2 5, avg of 3 growth responses shoot wt, flower wt, 3 

Whlte Tausendschon flower no 

020 2 10, avg of same responses 

040 2 19, avg of same responses 

080 2 38, avg of same responses 

Petunla, cultivar 010 2 9, avg of same responses 3 

Caprl 020 2 11, avg of same responses 

040 2 21, avg of same responses 

080 2 31, avg of same responses 

Coleus, cultivar 010 2 2, avg of same responses 3 

Scarlet Ralnbow 020 2 - 17, avg of same responses 

040 2 24, avg of same responses 

080 2 39, avg of same responses 

Snapdragon, cultivar 010 2 0, avg of same responses 3 

Floral Carpet, mlxture 020 2 6, avg of same responses 

040 2 8, avg of same responses 

080 2 16, avg of same responses 

Radlsh, cultivar 025 3 36, top dry wt (Cavaller) 7 

Cavaller, Cherry Belle 38, root dry wt (Cherry Belle) 

Radlsh 040 1 5(1)` 37, root dry wt 285 

1 5(2)` 63, root dry wt 

1 5(3)` 75, root dry wt 

Cucumber, cultivar 100 1 19, top dry wt (1 % Injury) 226 

Ohlo Mosalc 1.00 4 37, top dry wt (18% Injury) 

Potato, cultivar 1 00 4 0, tuber dry wt (no Injury) 226 

Norland 1 00 4(3)° 30, tuber dry wt (Injury severe) 

Tomato, cultivar 050 1 15, plant dry wt (grown In molst soll) 153 

Flreball 1 00 1 20, plant dry wt (grown In molst soll) 

Tomato, cultivar 050 1 15, Increase In plant dry wt (grown In dry soll) 153 

Flreball 1 00 1 25, Increase In plant dry wt (grown In dry soll) 

Onlon, cultivar 020 24 0, effect 226 

Spartan Era 1 00 1 19, plant dry wt (no Injury) 

1 00 4 49, plant dry wt 

Tobacco, cultivar 030 2 48, chlorophyll content 4 

Bel W3 

"Taken from Ref 217 

° Unless otherwise noted 

`Number of exposures in parentheses 

260 
associated with a shriveled-ear condition (kernels) 

that might be related to the effects of ozone on 

pollen development. 

Craker49 reported a reduction in the weight of 

petunia flowers after plants were exposed to ozone 

for 53 days at 98 to 137 Ng/m 3 (0.05 to 0.07 ppm); 

however, an increase in the weight of petunia 

flower52 was found when exposure to three 

different concentrations of ozone was for 7 days. 

Carnations (80 plants)continuouslyexposed for38 

days to 98 to 196 /ig/m 3 (0.05 to 0.10 ppm) 

produced a single deformed flower, while the 

controls had 24 normal flowers. 84 Poinsettia bract 

area was decreased by 39 percent after a 50-day 

exposure (6 hr/day) to ozone at 196 to 235 Ng/m 3 

(0.10 to 0.12 ppm). 52 

Heagle and associates 110 found a reduction in 

yield of sweet corn and soybean 109 after exposure 

to ozone at 196 /jg/m3 (0.10 ppm) for 6 hr/day 

administered over much of the growing season. 

These exposures were carried out in field 

chambers set up over soybean and corn plots in the 

field. They suggest that a threshold for measurable 

effects vn these crops would lie between ozone 

(oxidant) 'concentrations of 98 and 196 /jg/m3 

(0.05 and 0.10 ppm)for 6 hr/day if exposures were 

continued throughout most of the growing season. 

These concentratfon values resemble growingseason averages found fn the eastern United 

States. 

In one of the few examples of chronic ozone 

studies involving forest tree species, Wilhour and 

Neely310 exposed eight species of conifers to 200 

Ng/m 3 (0.10 ppm) of 03 for 6 hr/day, 7 days/week, 

for 18 continuous weeks. Significant growth 

reduction (given as percent reduction from control) 

was observed in root length (12 percent), dry 

weight (DW) of stem (21 percent), and DW of root 

(26 percent) of ponderosa pine (Pinus ponderosa 

Laws), and in western white pine (P. monticola 

Dougl.) in DW of foliage (13 percent) and DW of 

stem (9 percent). Biweekly harvests of ponderosa 

pine (exposed as above) throughout a 20-week 

study period showed highly significant growth 

reductions in root DW (26 percent). A trend of 

increased growth differences associated with 

increased length of exposureto ozone was evident. 

Bennett et a1. 12 found experimental evidence for 

stimulation of growth at low concentrations of 

ozone. They exposed bean (cultivar Pure Gold 

Wax), barley (cultivar Brock), and smartweed to 

ozone at 59 /_Ig/m3 (0.03 ppm) and found instances 

of significant growth increases. The concept needs 

further,study in light of the current concern over 

"normal" background ozone concentrations. 

A number of significant investigations have 

been conducted that demonstrate the response of 

vegetation to long-term exposure of relatively low 

ozone concentrations. The results of these chronic 

ozone studies are summarized in Table 1 1-4. The 

results of such experiments suggest that overall 

effects on agriculture production could be 

extensive, depending on the sensitivity of the 

cultivars used. 

To illustrate the relationship between ozone 

concentration, duration of exposure, and effects on 

foliage, growth, or yield, the data from Table 1 1-4 

have been graphed (Figure 1 1-2). Each pofnt on the 

graph represents a combination of concentration 

and time at which a significant reduction in 

growth, yield, or photosynthesis occurred. The 

dashed line is an indicator ofthe level belowwhich 

TABLE 11-3. EFFECTS OF OZONE ON SELECTED UNDERSTORY SPECIES FROM AN ASPEN COMMUNITYa 

Plant 

species 

Foliar 

Ambient 

air° 

inlury, % of 

290 pg/m' 

(0 15 ppm) 

Plant response at drfferent ozone concentratwrr:° 

control Plant wt, % of control 

588 pg/m' Ambient 290 pg/m 3 588 pg/ml 

(0 30 ppm) air° (0 15 ppm) f0 30 ppm) 

Ambient 

air° 

Seed wt, % of control 

290 pg/m' 

(0 15 ppm) 

588 pgim' 

(0 30 ppm) 

Chenopodium album L 0 35 40 103 71 ` 83 87 99 87 

C fremontif L 10 35 90 71 98 32 102 96 94 

Descurainia sp 0 15 55 179 ° 77 56° 

Geramum fremontu, L Torr 

ex A Gray 7 50 90 93 94 53° 

Lepidium virginicum L 50 100 100 121 72 31 ` 94 69 47` 

Madfa glomerata 40 100 100 112 38` 13` 79 74 18 

Polygonum aviculare L 30 95 95 271 186` 29° 127 43 50 

P. douglasa Greene 5 35 95 87 29° 5` 93 84 3` 

'Table from Ref 217 

°Exposures were 3 hr/day, 5 days/week through growing season 

`Significant eftect 

°Ambient air = 98 to 137 pg/m' (005 to 007 ppm) 

261 
TABLE 11-4. EFFECTS OF LONG-TERM, CONTROLLED OZONE EXPOSURES ON GROWTH, YIELD, 

AND FOLIAR INJURY TO SELECTED PLANTSa 

Plant 

species 

Fig 1+-2 

Nos 

Ozone concentration, 

pg/m' (pprn) Exposure time, hr 

Plant response, percent 

reduction from control Reference 

Lemna, duckweed 1 196 (0 10) 5/day, 14 days 100, flowering, 36, flowering 86 

(1 wk after exposure completed) 

50, frond doubling rate 

Carnatton 2 98-177 (0 05-0 09) 24/day, 90 days 50, flowering (reduced vegetative 83 

growth) 

Geranlum 3 137-196 (0 07-0 10) 9 5/day, 90 days 50, flowering (shorter flower 83 

lasting tlme, reduced vegetative 

growth) 

Petunla 4 98-137 (0 05-0 07) 24/day, 53 days 30, flower fresh wt 49 

Polnsettla 5 196-235 (0 10-0 12) 6/day, 5 days/week, 39, bract slze 52 

10 weeks 

Radlsh 6 98 (0 05) 8/day, 5 days/week, 54, root fresh wt 287 

5 weeks 20, leaf fresh wt 

98 (0 05) 8/day, 5 days/week 63, root fresh wt 

(mlxture of 03 and S02 22, leaf fresh wt 

for same perlods) 

Beet, garden 7 392 (0 20) 3/day, 38 days 50, top dry wt 223 

Bean, cultivar 8 255 (0 13) 8/day, 28 days 79, top fresh wt 182 

Plnto 73, root fresh wt 

70, helght 

Bean, cultivar 9 290 (0 1 5) 2/day, 63 days 33, plant dry wt, 46, pod fresh wt 139 

Plnto 10 490 (0 25) 2/day, 63 days 95, plant dry wt, 99, pod fresh wt 

11 686 (0 35) 2/day, 63 days 97, plant dry wt, 100, pod fresh wt 

Bean, cultivar 12 290 (0 15) 2/day, 14 days 8, leaf dry wt 175 

Plnto 

13 290 (0 15) 3/day, 14 days 8, leaf dry wt 

14 290 (0 15) 4/day, 14 days 23, leaf dry wt (Data avallable on 

whole plants, roots, 

leaves, Injury, and 

15 290 (0 15) 6/day, 14 days 49, leaf dry wt 3 levels of soll 

molsture stress) 

16 440 (0 225) 2/day, 14 days 44, leaf dry wt 

Bean, cultivar 17 440 (0 225) 4/day, 14 days 68, leaf dry wt (Data avallable on 175 

Plnto whole plants, roots, 

18 588 (0 30) 1/day, 14 days 40, leaf dry wt leaves, tnjury, and 

3 levels of soll 

19 588 (0 30) 3/day, 14 days 76, leaf dry wt motsture stress) 

Tomato 20 392 (0 20) 2 5/day, 3 days/week 1, yteld, 32, top dry wt, 11 , 231 

14 weeks root dry wt 

21 686 (0 35) 2 5/day, 3 days/week, 45, yleld, 72, top dry wt, 59, 

14 weeks root dry wt 

Corn, sweet, 22 392 (0 20) 3/day, 3 days/week 13, kernel dry wt, 20, top dry wt, 229 

cultivar Golden tlll harvest 24, root dry wt 

Jubllee 

23 686 (0.35) 3/day, 3 days/week 20, kernel dry wt, 48, top dry wt, 

ttll harvest 54, root dry wt 

Wheat, cultivar 24 392 (0 20) 4/day, 7 days 30, yleld 156 

Arthur 71 (anthesls) 

Soybean 25 98 (0 05) 8/day, 5 days/week 13, follar Injury 293 

3 weeks 

8/day, 5 days/week 16, follar Injury 

(mlxture of 03 and SOz 20, root dry wt 

for same perlods) 

Soybean 26 196 (0 10) 8/day, 5 days/week 21, top dry wt 

3 weeks 9, root dry wt 

Alfalfa 27 196 (0 10) 2/day, 21 days 16, top dry wt 138 

28 290 (0 15) 2/day, 21 days 26, top dry wt 

29 390 (0 20) 2/day, 21 days 39, top dry wt 

Grass, brome 30 290-647 4/day, 5 days/week 83, blomass 239 

(0 15-0 33) (varled) growing season 

Alfalfa` 31 196 (0 10) 6/day, 70 days 4, top dry wt, harvest 1 218 

20, top dry wt, harvest 2 

50, top dry wt, harvest 3 

Alfalfa` 32 98 (0 05) 7/day, 68 days 30, top dry wt, harvest 1 218 

50, top dry wt, harvest 2 

262 
TABLE 11-4. EFFECTS OF LONG-TERM, CONTROLLED OZONE EXPOSURES ON GROWTH, YIELD, 

AND FOLIAR INJURY TO SELECTED PLANTS ° (cont'd). 

Plant 

species 

Fig 11-2 

Nos ° 

Ozone concentration, 

pg/m , (ppm) Exposure time hr 

Plant response, percent 

reduction from control Reference 

Alfalfa 33 98 (0 05) 8/day, 5 days/week 18, top dry wt 290 

12 weeks 

Plne, eastern 34 196 (0.10) 4/day, 5 days/week 3, needle mottle 69 

whlte 4 weeks (mlxture of 03 (over 2-3 days cf exposure) 

and S02 for same perlods) 16, needle mottle 

Plne, ponderosa 35 290 (0 15) 9/day, 10 days 4, photosynthesls 210 

36 290 (0 15) 9/day, 20 days 25, photosynthesls 

Plne, ponderosa 37 290 (0.15) 9/day, 30 days 25, photosynthesls 210 

38 290 (0 15) 9/day, 60 days 34, photosynthesls 

39 588 (0 30) 9/day, 10 days 12, photosynthesls 

40 588 (0 30) 9/day, 20 days 50, photosynthesls 

41 588 (0.30) 9/day, 30 days 72, photosynthesls 

42 880 (0 45) 9/day, 30 days 85, photosynthesls 

Poplar, yellow 43 588 (0 30) 8/day, 5 days/week 82, leaf drop, 0, helght 147 

13 weeks 

Maple, sllver 44 588 (0.30) 8/day, 5 days/week, 50, leaf drop, 78, helght 147 

13 weeks 

Ash, whlte 45 588 (0 30) 8/day, 5 days/week 66, leaf drop; 0, helght 147 

13 weeks 

Sycamore 46 588 (0 30) 8/day, 5 days/week 0, leaf drop; 22, helght 147 

13 weeks 

Maple, sugar 47 588 (0 30) 8/day, 5 days/week 28, leaf drop; 64, helght 147 

13 weeks 

Corn, sweet, 48 98 (0.05) 6/day, 64 days 9, kernel dry wt, 14, Injury 110 

cultivar Golden (12, avg 4 yleld responses) 

M Idget` 

49 196 (0 10) 6/day, 64 days 45, 25, 35 for same responses 

Plne, ponderosa` 50 196 (0 10) 6/day, 126 davs 12, root length 310 

21, stem dry wt, 26, root dry wt 

Plne, western 51 196 (0 10) 6/day, 126 days 13, follage dry wt 310 

whlte° 9, stem dry wt 

Soybean, cultivar 52 98 (0 05) 6/day, 133 days 3, seed yleld, 22, plant fresh wt, 109 

Dare` 19, Injury, defollation, no reduction 

In growth or yleld 

53 196 (0 10) 6/day, 133 days 55, 65, 37 for same responses 

Poplar, hybrld 54 290 (0 15) 8/day, 5 days/week 50, shoot dry wt, 56, leaf dry vJt, 148 

6 weeks 47, root dry wt 

aModified irom Ref 217 

°Numbers in this column are keyed to numbers in Fig 11-2 

`Studiesconductedunderfieldconditions,exceptthatplantswereenclosedtoensurecontrolledpollutantdoses Plantsgrown under conditions making them more sensitive 

significant effects probably do not occur. In 

general, as the length of exposure increases up to 

15 days, the average ozone concentration must be 

decreased to prevent growth effects. Beyond 15 

days, if the average concentration of ozone 

exceeds 98 /ag/m3 (0.05 ppm), significant growth 

and yield effects could occur. 

Quality - A limited number of studies have 

investigated the effects of ozone on crop quality. 

Thompson and his co-workers 277'278 compared the 

quality of grape juice made from grapes harvested 

from plants grown for two seasons in either 

ambient air oxidants or in carbon-filtered air. 

Sugar content of the grapes grown in ambient air 

was reduced 13 to 17 percent, but the 

concentration of organic acids showed no 

detectable trends. FreyS9 reported a 5-percent 

decrease in lipids arld a 21-percent increase in 

amino acids in seeds from soybeans exposed to 

ozone. Exposure of alfalfa to 98 /ag/m 3 (0.05 ppm) 

or to 196 Ng/m3 (0.10 ppm) ozone increased the 

levels of protein and amino acids, had no effect on 

carbohydrates or lignin, and decreased /3 carotene 

per unit weight of tissue. 218 The protein increase 

per unit weight of tissue is of no practical 

significance, because the ozone exposure 

produced a reduction in growth that resulted in a 

decrease in total production of protein. 

DOSE-RESPONSE RELATIONSHIPS 

An understanding of dose-response 

relationships is important for a basic 

understanding of the mechanism of oxidant effects 

on plants. Ideally this relationship could be 

263 
a 

c. 

Z 

O 

H 

Q 

Z 0.1 

w 

u 

Z 

O 

U 

w 

Z 

O 

N 

O 

0.01 

expressed by a set of standard equations that 

would relate plant response to pollutant 

concentration and duration of exposure and would 

also incorporate the effects of all other factors that 

control the responses of plants. Development of 

such equations requires a data base sufficient to 

relate a given dose (concentration of pollutant 

times duration of exposure) of oxidant (e.g., ozone 

or PAN) to some meaningful plant effect. Such 

equations are not yet available; however, 

discussions of the relationship of time, 

concentration, and response have been 

published."''14 

Limiting Values — The concept of limiting values 

may be used to define the boundary between doses 

of a pollutant that are likely to cause measurable 

injury to an organism and those that are not likely 

to cause injury.' 45Jacobson 745used this concept to 

estimate limiting values for the exposure of trees, 

shrubs, and agrlcultural cropsto ozone and PAN. In 

estimating limiting values, several factors were 

taken into consideration. These were: (1) Of the 

known effects on vegetation, which were the most 

1.0 

important? (2) What kinds of data should be 

included—data from the field, where ambient 

pollutant concentrations were monitored, or from 

the results of experimental fumigations with 

controlled dosages of the pollutant? (3) Which 

model should be used to estimate limlting values? 

Alteration of biochemical or physiological 

processes, reductions in growth or yield, or foliar 

lesions are effects on vegetation that can be 

consldered. However, most of the published data 

discussing dose-response relationships use visible 

foliar injury as the index of response. 

Consequently, Jacobson 145 in estimating limiting 

values, used the dose-response data for visible 

follar Injury on the assumption that preventlon of 

foliar injury would also prevent other adverse 

effects. In addition, inderiving limiting values, only 

data from experimental investigations in which 

both concentration and duration of exposures 

were monitored or controlled were used. More 

than 200 studies were surveyed to obtain the data. 

The concentratlon-time model developed by 

Jacobson for summarizing the dose-response 

relationships for effects of oxidants on vegetation 

47 • 

210 110 

~ 440 19d18 !45 046 048-52 

~ ~10 

\~24 16C1017 031 70020 

c 

15 30 59 

40 • ?0014 ~1 • 0, 4243009 

~\ 12, 13 4T7 08 50 33 

\ \ 1 p1111126p029 5440 55, 56 00 58 

~ 39 30 

\ 2• 

\ 4• 

25~ 6 57 

---~ ----38 ~~~34 -- ~ ------ 

53 

EXPOSURE, hr/day 

• < 1.99 

O 2 TO 3.99 

O 4 TO 5.99 

0 > 6 

NOS. = REF. NOS. ON TABLE 11-4 

6 8 10 20 40 60 80 100 200 400 

EXPOSURE PERIOD, days 

Figure 11-2. Relation between ozone concentration, foliar injury, and a reduction in plant growth or yield (see Table 

1 1-4). 

264 
is similar to the one used by McCune 169 for 

fluorides and by Larsen and Heck 166 for ozone and 

S02. In the model, foliar injury is expressed as a 

function of the concentration of ozone or PAN and 

the logarithm of the duration of exposure. 

Limiting Values for the Effects of Ozone — A 

single coordinate point for each published study 

was used in developing the limiting values in 

Figures 1 1-3 and 1 1-4. The single point represents 

the iowest concentration and duration of exposure 

in the published study that resulted in foliar 

symptoms. The data points used to develop the 

limiting values that will protect vegetation against 

oxidant-induced foliar injury are not necessarily 

threshold values. Since these points are based on 

available published research data (more than 100 

studies), the shortcomings that were prese-1t inthe 

experiments will be reflected in the derived points 

(e.g., shortcomings in calibration and 

measurement techniques and the use of 

subjective methods to determine foliar injury). 

Woody Trees and Shrubs. The limiting values for 

the effects of ozone on trees and shrubs (Figure 1 1- 

3) are based on a single coordinate corresponding 

to the lowest concentration of ozone and duration 

of exposure that produced foliar injury on woody 

plants. The data used to establish the coordinates 

came from 18 studies.l3 '14,17,47,56,57,60,126,131,152,158, 

161,168,171,211,250,253,311 The shaded area in Figure 1 1- 

3 depicts the range of uncertainty and referstothe 

range, as given in the reports, of the lowest doses 

of ozone observed to cause foliar injury. Doses of 

ozone abovP and to the right of the shaded area are 

likely to cause foliar injury to susceptible woody 

plant species. There is little likelihoodthatdosesof 

ozone below and to the left of the shaded area will 

cause foliar injury. 

AgriculturalCrops. More data (over 100 studies) on 

dose-response relationships for agricultural crops 

are available than for any other class of vegetation. 

A wide range of uncertainty exists for the limiting 

values as given in Figure 11-4 because of the 

variability in plant response. In addition, the 

limiting values (shaded area, Figure 1 1-4) overlap 

the range of ozone concentrations producing 5 

percent injury to crops as reported by Heck and 

Tingey 12 ' (Figure 1 1-5, Tables 1 1-5 and 1 1-6), and 

the response threshold for ozone effects on plants, 

published by the National Research Council of 

Canada,z 38 corresponds closely to the lower curve 

in Figure 1 1-4. Doses of ozone above and to the 

right of the shaded area in Figure 1 1-4 will probably cause foliar injury in susceptible agricultural 

0.4 

E 

a 

a 

Z 

O 

H 

Q 

¢ 

H 

Z 

W 

U 

0 0.2 

U 

w 

Z 

O 

N 

O 

RANGE OF UNCERTAINTY FOR LIMITING VALUES FOR 

SUSCEPTIBLE SPECIES TREES AND SHRUBS 

800 ME 

0) 

i 

Z O_ 

FQ 

~ 

H 

z 

w 

fU 

Z 

O 

400 L) 

W Z O N O 

0.1 0.5 

DURATION OF EXPOSURE, hours 

Figure 11-3. Limiting values for foliar injury to trees and 

shrubs by ozone. 145 

265 
crops Doses below and to the left of the shaded 

area are unlikely to cause foliar injury. The doseresponse data used in establishing the limiting 

values in Figure 1 1-4 were obtained from many 

sou rces98,117,1 74,238 (see also author citations, Table 

1 1-2) The data available at present are not 

sufficient to determine if the curves in Figure 1 1-4 

become parallel to the horizontal axis or, if at 

durations of 8 hr or more, they approach the axis 

asymptotically. The inaccuracies in measurements 

make the interpretation of results of repeated or 

long-duration exposures difficult, and limiting 

values of ozone concentrations below 100 Ng/m 3 

(0 05 ppm) are not useful. 145 

Limiting Values for the Effects of PAN — The 

limiting valuesfor PAN are represented by the solid 

line in Figure 1 1-6. Appreciable risk of foliar injury 

to susceptible species of vegetation will occur 

above and to the right of the limiting values A low 

risk of foliar injury exists below and to the left of the 

limiting values. The limited information base for 

the effects of PAN makes it impossible to estimate 

a range of uncertainty at present. 

CONCLUSIONS 

Based on the data available, the limiting values 

for the effects of ozone on trees and shrubs range 

from 400 to 1000 /ig/m 3(0.2 to 0.5 ppm) for a 

duration of 1 hr, 200 to 500 /jg/m3(0.1 to 0.25 

ppm)for 2 hr, and 120to 340Ng/m 3 (0.06to0.153 

ppm) for 4 hr. For agricultural crops, the ranges for 

limiting values are 400 to 800 Ng/m 3(0.2 to 0.41 

ppm)for0.5 hr, 200to500Ng/m 3 (0.1 to0.25ppm) 

for 1 hr, and 75 to 180pg/m 3(0.04to0.09 ppm)for 

4 hr. 145These values are similar to those of Heck 

and Tingey 12 ''21for sensitive vegetation. These 

were: 400/ig/m 3(0.2 ppm)for 1 hr, 200Ng/m 3(0.1 

ppm) for 2 hr, and 98 /jg/m3(0.05 ppm) for 4 hr. 

Limiting values for oxidant exposures longer than 

4 hr are not significant because of inaccuracies in 

measuring low concentrations. 

The Ilmlting values for the effects of PAN on 

agricultural plants are. 1000 Ng/m 3(0.2 ppm) for 

0.5 hr, 500 Ng/m 3(0.1 ppm) for 1 hr, and 175 

Ng/m 3(0.035 ppm) for 4 hr. The absence of data 

distinguishing the effects of PAN on woody plants 

or agricultural crops makes the separation of the 

data impossible. 

ECONOMIC ASSESSMENT 

This discussion will bring into focus our present 

understanding of the economic effects of oxidant 

air pollution on vegetation. Heck and Brandt"' 

presented in depth the problems inherent in 

~ 

~ 

E 

a 

a 

Z 

O 

H 

Q 

~ 

F 

z 

w 

U 

Z 

O 

U 

w 

z 

O 

N 

O 

0.4 

0.3 

0.2 

I I I 

RANGE OF UNCERTAINTY FOR, 

SUSCEPTIBLE SPECIES 

LIMITING VALUES FOR 

AGRICULTURAL CROPS 

800 

M 

E 

rn 

Y 

Z 

O 

H 

Q 

~ 

H 

400 w 

U Z 

O 

U 

W 

Z 

O N 

O 

0.1 0.5 

DURATION OF EXPOSURE. hours 

Figure 11 -4. Limiting values for foliar injury to agricultural 

crops by ozone. 145 

266 
E a 

a 

Z O 

H Q 

a: 

~ z 

w 

u 

z 

O 

u 

w 

z 

O 

N O 

1.0 

0.9 

0.8 

0.7 

0.6 

0.5 

0.4 

0.3 

0.2 

0.1 

making an economic evaluation of the response of 

plants to air pollutants, including ozone and other 

oxidants. They used the distinction between injury 

and damage proposed by German workers. 98 /njury 

is defined as any indentifiable and measurable 

response of a plant to air pollution; damage is any 

measurable adverse effect on the desired or 

intended use of the plant. Hence, before an effect 

on a plant can be evaluated in terms of economics, 

the plant must have been altered either 

quantitatively or qualitatively in such a way as to 

reduce its use value. In this context, visible 

symptoms or transient changes in physiologic 

responses may not result in an economic loss. For 

example, leaf necrosls in soybean is injury; to be 

classified as damage, the injury must affect bean 

yield. In contrast, an oxidant episode that bronzes 

the leaves of romaine lettuce may not affect 

biomass, but it will affect use and may result in 

complete economic loss. Similarly, ornamental 

plants, whose major use value depends on 

appearance, may be both injured and damaged. 

Emergence tipburn of eastern white pine 75 and 

other physiogenic diseases of white pine are 

associated with air pollution throughout the 

natural range of the species. Insular stands 

containing ponderosa pine are frequently injured 

in the Southwest. The significance of the 

physiogenic diseases is not understood because 

only sensitive genotypes are affected. The disease 

occurs randomly in the forest, and its most obvious 

effect is the gradual elimination of genotypes that 

may have otherwise superior silvicultural 

characteristics. This could be a serious loss to 

future tree improvement efforts, and similar 

effects may be occurring in other forest species. 

Economic considerations have not been addressed 

in any reasonable way. 

Oshlma and his coworkers z2 ''228 ' 23o have 

developed a methodology for evaluating and 

reporting economic crop losses that involves 

continuous air monitoring, chamber exposures, 

and monitoring plant species. Oshima has 

attempted to weld these parameters into a 

comprehensive method of determining yield 

reductions. Several species have been 

investigated, but the procedure has not been fully 

clarified. No economic analyses of the yield 

reductions were presented. This type of approach 

should be investigated further. 

Any attempt to assess oxidant damage to 

agricultural crops requires judgement by a 

~. 

~ . 

0 1 2 3 4 5 6 7 8 

TIME, hours 

Figure 11-5. Ozone concentrations versus duration of exposure required to produce a 5 % response in three different plant susceptibility groupings. The curves were generated by developing 95% confidence limits around the 

equations for "all plants" in each susceptibility grouping from Table 11-5. Curves: a=sensitive plants, b=intermediate 

plants, c=resistant plants. 21 

TIME 

CONCENTRATION, ppm 

SENSITIVE INTERMEDIATE RESISTANT 

0.5 0.431 ± 0.044 0.637 ± 0.043 0.772 ± 0.070 

1.0 0.218 ± 0.023 0.347 ± 0.020 0.494 ± 0.028 

2.0 0.111 *- 0.020 0.202 ± 0.017 0.355 ± 0.023 

4.0 0.058 ± 0.022 0.129 ± 0.019 0.286 ± 0,026 

8.0 0.031 ± 0.023 0.093 0.251 ~ 0.034 

267 
competent investlgator. Landau and Brandt 165 

suggest that the accuracy of crop surveys is 

directly related to the number of subjective 

decisions requlred in data collection. The first 

surveys were conducted in California 2o3,204 and 

were used, with a general survey of conditions on 

the east coast, to develop some of the early 

economic loss estimates of $8 to $10 million in 

California and $18 million on the east coast. 21 ' 

These estimateswere raised to $500 mlllion on the 

basis of'Increased awareness of pollution effects 

and increased recognition of additional sensitive 

specfes. However, all early estimates were 

subjective, with no substantlal backup data. 

Since 1969, a number of states have instituted 

an intenslve training program for county 

agricultural agents and have made detailed reports 

of crop Injury and damage67,164,18s,2o5,214,236 (Table 

1 1-7). The flrst such report came from 

Pennsylvania 164 in 1969 and gave an estimate of a 

$9.6 million loss to agronomic commodities from 

oxldant pollutants. Thls survey included dlrect and 

some indirect costs. Similar surveys have been 

conducted in New England, 214 New Jersey,

236,237 

and California. 205 These surveys considered yield 

reductions on the basis of injury and made no 

direct assessments of growth or yield, although 

subjective estimates of damage were obtained. 

Pell and Brennan 237 presented a well developed 

thesis on the rationale for differences in estimating 

losses to agriculture in NewJersey between 1971 

and 1972. This subject wasdlscussed in relation to 

the overall problem of , assessing agricultural 

losses. 

A study was initiated in 1969 11 by Stanford 

Research Institute (SRI) to develop an empirical 

model for assessing damage to vegetation. This 

program made use of laboratory and field data from 

controlled exposures of various crops and of 

chemical data from simulated reaction chambers 

so that estimates of ozone and other oxida nts could 

be made on the basis of concentrations of primary 

pollutants. Hydrocarbon was chosen as the basic 

pollutant from which to develop the model for 

TABLE 11-5. CONCENTRATION, TIME, AND RESPONSE EQUATIONS FOR THREE SUSCEPTIBILITY GROUPS AND FOR 

- -- - - - 

SELECTED PLANTS OR PLANT TYPES WITH RESPECT TO OZONE a 

-- - — - -- - -- — --- ---- 

Threshold Mean valuese 

Plants IC-Ao ~ A,I ' A 1 TI ° Rz 

concentra tion, ppm `= N. data 

points 

Conc (C) 

ppm 

Time (T), 

hr 

Respon~ se (1), Dose, 

ppm Ihr 

1 hr 4 hr 8 hr 

Sensltive 

AII plants -0 0152 + 0 00401 + 0 213/T 057 022 006 003 471 029 1 74 454 0 503 

Grasses -0 0565 + 0 00481 + 0 291 /T 074 026 004 001 71 037 1 66 509 0 608 

Legumes 00452 + 0 00361 + 0 172/T. 046 024 0 1 1 009 100 034 1 42 401 0 480 

Tomato -0 0823 + 0 00431 + 0 243/T 050 018 None None 20 0 31 1 50 56 5 0 491 

Oat -0 0427 + 0 00511 + 0 273/T 076 026 005 002 30 037 1 66 402 0 61 1 

Bean -0 0090 + 0 00301 + 0 164/T 0 58 017 005 0 03 62 030 1 23 472 0 370 

Tobacco 00245 + 0 00341 + 0 137 /T 052 018 008 0 06 197 023 1 90 38 9 0 448 

Intermedlate 

AII plants 00244 + 0 00651 + 0 290/T 074 035 013 0 09 373 037 1 67 270 0 625 

Vegetables -0 0079 + 0 00641 + 0 263/T 079 029 009 0 06 25 0 41 1 29 335 0 532 

Grasses 00107 + 0 00591 + 0 292/T 0 82 033 0 11 009 68 039 1 61 31 0 0 625 

Legumes 00116 + 0 00741 + 0 329/T 0 81 0.38 013 0 09 104 040 1 59 250 0 642 

Perennlal 00748 + 0 00701 + 0 237/T 077 035 017 014 27 0.36 1 91 229 0 687 

Clover -0 0099 + 0 00711 + 0 268/T 0 95 029 009 006 24 028 213 230 0 595 

Wheat -0 0036 + 0 0081 1+ 0 302/T 088 034 0 1 1 008 15 047 1 25 289 0 508 

Tobacco 00631 + 0 00871 + 0 152/T 078 026 014 013 59 0 28 1 99 157 0 551 

Reslstant 

AII ptants 01689 + 0 00951 + 0 278/T 0 51 050 027 025 291 045 1 55 106 0 696 

Legumes 00890 + 0 01081 + 0 304/T 082 045 022 018 36 030 1 89 122 0 722 

Grasses 01906 + 0 01 171 + 0 263/T 055 0 51 0 31 020 13 045 1 47 6 5 0 655 

Vegetables 0 1979 + 0 01261 + 0 107/T 070 038 029 0 20 16 055 1 50 178 0 819 

Woody plants 02312 + 0 00611 + 0 208/T 045 047 0 31 0.30 46 039 250 7 8 0 905 

Cucumber 01505 + 0 01411 + 0 106/T 0 83 033 025 023 18 041 1 41 133 0 581 

Chrysanthemum 02060 + 0 00521 + 0 256/T 040 049 030 027 45 039 2 17 126 0 847 

T Equations were developed lrom exposures lunited in time (0 5 to 8 hr, except for 2 to 12 hr points in the sensitive group) and denote acute responses of the plants 

Concentrations range from 0 05 to J 99 (1 0) ppm and responses from 0 to 99 110010-0 of contuol Reference 217 

° C is ozone concentration in ppm I is percent inlury T is time in hours, and Ao , A,, and Az are constants (partial regression coefficients) that are specific for pollutant plant 

species or group of species and environmental conditions used 

`Multuple correlation coefficient squared, which represents the percent variation ezplained by the model 

° For 5°o response in 1- 4- and 8-hr periods 

`From the computer analysis 

268 
prediction of expected oxidant values and, 

therefore, effects on various crops. From the 

oxidant value, injury and damage for specific crops 

were calculated for over 100 statistical reporting 

areas in the United States. The report used many 

subjective assumptions and was related primarily 

to visible injury symptoms. On the basis of the SRI 

model, the 1969 estimated loss to vegetation from 

oxidants in the United States was approximately 

$125 million. According to the National Research 

Council, 217 if the increase in crop values are 

considered and if it is assumed that oxidant 

concentrations have not been signlficantly 

reduced during the last few years, the loss in 1974 

from oxidants could approach $300 million as 

based on the SRI report. 

A summary of estimates derived from various 

surveys and assessment techniques is shown in 

Table 1 1-7. These values are suggestive at best. As 

with all values developed for agricultural losses, 

these have been directed at losses to the 

producer—not the consumer. 

Whereas a reduction in production may actually 

increase the aggregate farm income and produce 

serious income distribution problems, the 

consequent reduction In marketable surplus would 

cause a significant rise in the cost to consumers 

0.24 

~ 

a 0.16 

a 

Z 

O 

H 

Q 

¢ 

H 

Z ut 

U 

Z 

v 0.08 

Z 

Q 

a 

LIMITING VALUES 

OL 

0.1 0.5 

because of the inelastic consumer demand for 

most agricultural crops. Thus at the consumer 

level, losses based on farm prices are not 

appropriate and are likely to be conservative. 

Because of percentage markups and fixed 

wholesale and retail marketing costs, the cost to 

the consumer of agricultural losses could be twice 

as great as that observed at the farm level. 

TABLE 11-6. OZONE CONCENTRATIONS FOR SHORTTERM EXPOSURES THAT PRODUCE 5 OR 20 PERCENT 

INJURY TO VEGETATION GROWN UNDER 

SEN SITIVE CONDITIONS a 

Ozone concentrations that may produce 5% or 20% inlury, ppm ° 

Exposure 

time, hr Sensitive plants Intermediate plants Resistant plants 

05 035-050 055-070 ?070(085) 

(0 45 - 0 60) (0 65 - 0 85) 

10 015 -025 025-040 >_040(055) 

(0 20 - 0 35) (0 35 - 0 55) 

20 009-015 015-025 >030(040) 

(0 12 - 0 25) (0 25 - 0 35) 

40 004-009 010-015 ?025(035) 

(0 10 - 0 15) (0 15 - 0 30) 

80 002 - 0 04 0 07 - 0 12 >0 20 (0 30) 

(0 06 - 0 12) (0 15 - 0 25) 

~ Data developed from analysis of acute responses shown in Table 11 -5 and Fig ure 

11-5 Reference 217 

° 1 ppm = 1960 pgi m' 

1200 

M 

E 

rn 

800 ~ Z 

O 

F 

Q 

¢ 

Z 

w 

~ Z 

O 

U 

400 Z 

Q 

a 

0 

~ 

0 

5 

0 

0 

DURATION OF EXPOSURE, hours 

Figure 11-6. Dose-response relationships and limiting values for foliar injury to vegetation by peroxyacetylnitrate (PAN). 105 

269 
TABLE 11-7. ESTIMATES OF ECONOMIC LOSSES TO CROPS AND VEGETATION IN THE UNITED STATES 

ATTRIBUTABLE TO OXIDANT AIR POLLUTION a21 

Estimated 

Area and year loss, $10' Comments Reference 

Untted States 1963 $ 65,000 First approximation for commerctal crops (SRI) 11 

121,400 Revised SRI report to tnclude ornamentals 11 

California 1963 33,700 Revised SRI report 11 

1970 17,500 Does not tnclude ornamentals or indirect costs 205 

Pennsylvania 1963 6,300 Revised SRI report 11 

1969 9,600 Pa survey, includes tndirect costs 164 

1970 60 Pa survey, as above 163 

New Jersey 1971 960 N J survey of a limited number of crops, based on 87 

vtstble tnjury 

1972 60 N J asabove 236 

New England 1971 1,100 Mass survey, primarily crops and ornamentals 214 

'Some of variation reflects methodology, other reflects differences in plant susceptibihty and pollution over years 

Factors Affecting Plant Response 

The response of plants to ozone, PAN, or any 

envlronmental stress is conditloned by complex, 

interacting internal and external factors. These 

include cllmatic and edaphlc factors, interactions 

among atmospheric pollutants, genetic variability 

(both between and within species) of plants, the 

growth and physiologic age of susceptible plant 

tissue, and interaction of the plants with a variety 

of pathogens. A conceptualization of the 

interacting factors involved in air pollution effects 

on vegetation Is shown In Figure 1 1-7. 

GENETIC FACTORS 

Resistance to ozone and PAN varies among 

specles of a given genus and among cultivars 

within a glven species. Variatlons in response are 

functions of genetic variability and environmental 

stresses as they affect morphologlcal, 

physiological, and biochemical characteristics. In 

native populations and in breeding experiments, 

both ozone and PAN may act as stresses 

Influencing selective pressure. Variations In 

species response to ozone and PAN are well 

do c u me nte d .

12s,12s,150,, 6a,270,302,312 

A number of papers discussing the variation in 

response of cultivars within specles have been 

published.123-125,250 The research of Brennan et 

a1. 31 indicated `'1at cultivars of oats and potato 

responded differently to ozone. Heck 174 

summarized the variatlon in response of cultivars 

wlthin several plant species, whlle Reinert 241 

compiled a compendium of papers that discussed 

the response of cultivars of horticultural crops to 

ozone, PAN, and other pollutants. Variations inthe 

responses of cultivars within three species have 

been studied Intensively to determine their 

sensitivity to ozone. They are: petunia, 25,40,a5 

tomato, 41 '42 and tobacco. 34sss7,,s2-,s5 

Additlonal studles discussing cultivar responses 

to ozone are available for bean, 58 begonia, 3 

morning glory, 215 chrysanthemum, 2 '' 155 

poinsettia, 183 spinach, 184 Iettuce, 244 radish, 244 

turfgrasses, 26 forage Iegumes, 32 alfalfa, 141 

safflower, 143 soybean, 142,209 '291 small grains (oat, 

rye, wheat, barley), 242 and English holly. 28 Petunia 

has been studied with regard to both auto exhaust 

and PAN, 85 and the effects of PAN alone on both 

petunia and chrysanthemum have been 

studied. 71313 Most of these studies reported the 

results of acute exposures, which may or may not 

be related to resultsfrom chronic exposures. Foliar 

injury was generally used as a measure of 

response. It is not known whether rankings 

according to foliar injury relate to loss in economic 

yield. 

Hanson 103 published a list of 160 woody species 

that were sensitive or tolerant to oxidants, based 

on observations made at the Los Angeles State and 

County Arboretum. A number of recent 

investigations have considered susceptibility of 

1 4,17 ,47,55 -5 7,60,1 26,1-07 ,206,310 tree species to ozone. A 

Ilmited number of studies discuss selection of 

resistant individuals within native tree 

s pec I es.14,60,210,253 

Two studies have explored the mechanism of 

genetic resistance to ozone. Engle" and Eng1e and 

Gableman79 found thatozone sensitivity in onion is 

probably controlled by a single gene pair, with 

dominance of the resistant gene. In resistant 

plants, the membrane of the guard cells was more 

sensitive to ozone; when exposed to ozone, it lost 

its differential permeability, thus causing stomatal 

closure. This did not occur in the guard cells of the 

sensitive cultivar, and thus the stomata remained 

open. Taylor267 crossed the sensitive BeI W3 

tobacco with a resistant line and found that the F, 

generation was of intermediate sensitivity. The F2 

270 
generation segregated into 40 percent resistant, 

10 percent sensitive, and 50 percent intermediate. 

He suggested that sensistivity was controlled by at 

least two genes. Resistance mechanisms to air 

pollutants are poorly understood, and further 

studies are needed. 

A study using Arabidopsis thaliana was 

conducted to determine the potential mutagenic 

effects of ozone. 35 This plant completes its life 

cycle in about 35 days. Many generations may 

therefore be grown within a relatively short period 

of time. Plants were exposed to acute doses of 

ozone for 6 hr/day,3 days/week, throughout the 

life cycle. Seeds were collected from control and 

exposed plants and planted for seven generations. 

Seed production and biomasswere reducedwithin 

a specific generation, but none of the factors 

studied were transmitted to subsequent 

generations. The results showed that for this 

particular species, the concentrations of ozone 

used produced no mutagenic effects. 

The aforementioned studies suggest that a 

spectrum of genotypes exists that varies in 

susceptibility to oxidants, and that environmental 

factors are important in conditioning a plant's 

susceptibility to pollutants. The degree to which 

environmental modification can control the 

response of sensitive genotypes to ozone may be 

less pronounced if specific biochemical or 

physiological mechanisms involved in plant 

response to pollutants have weak interactions with 

the environment. 

PHYSIOLOGICAL AGE 

The physiological age of a plant is an important 

factor in modifying plant sensitivity. Young, rapidly 

expanding leaves are most sensitive to PAN 

injury.Z°'238 Ozone, in contrast, affects more 

POLLUTANT 

CONCENTRATION 

NUMBER OF ' DOSE DURATION OF 

EXPOSURES EACH EXPOSURE 

CLIMATIC FACTORS~ 

BIOTIC FACTORS 

EDAPHIC FACTORS PLANT 

-------'I'-RECEPTOR 

GENETIC 

COMPOSITION 

STAGE 

OF 

DEVELOPMENT 

MECHANISM OF ACTION 

EFFECTS 

Figure 11-7. Conceptual model of factors involved in air pollution effects on vegetation (modified from van Haut and 

Stratmann). 302 

271 
mature tissue. Maximum sensitivity is found when 

cotton leaves are approximately 70 percent 

expanded, 287red maple 90 percent, 299and soybean 

60 to 80 percent. 286 In tobacco, maximum 

sensitivity occurs just after full leaf expansion. 116 

Davis55a nd Davis and Wood 60found that the age 

of Virginia pine needles influenced their response 

to a 4-hr exposure to ozone at 490 Ng/m3(0.25 

ppm). Generally, cotyledons were more sensitive 

than primary needles, which in turn were more 

sensitive than secondary needles. Secondary 

needles of seedlings were approximately as 

sensitive as those of 3-year-old trees. The 

cotyledons and secondary needles became 

resistant after 16 and 18 weeks of age, 

respectively, whereas the primary needles 

remained sensitive beyond 18 weeks. Berry 13 

reported that Virginia, shortleaf, loblolly, and slash 

pines at 2 to 6 weeks from seed were most 

sensitive when exposed to ozone at 490 Ng/m 3 

(0.25 ppm) for 2-hr. 

Hanson et a1. 104reported increased tolerance in 

petunia cultivars to ozone as they approached the 

flowering stage. This was true for both ozonesensitive and tolerant cultivars, with the latter 

being the more strongly influenced. They 

suggested that bud development resulted in the 

production of diffusible substances that moved 

down the plant and acted as a protectant. 

Generally, studies have shown that plants are 

most sensitive to ozone at a physiologic age 

associated with full leaf expansion. Sensitivity is 

also associated with functional stomata, 

intercellular spaces, and rate of cutin formation on 

cell walls 20Plants generally are more sensitive to 

oxidants during stages of rapid growth and less 

sensitive as leaves mature. When oxidant episodes 

occur throughout the growing season, the older 

leaves, weakened during their stage of maximal 

physiologic growth, senesce prematurely. 

CLIMATIC CONDITIONS 

Plant response to ozone and PAN may be altered 

by climatic conditions before, during, and after 

exposure. 14Plants may be sensitized by a given 

set of conditions after 1 to 5 days. 

Conditions before and during exposure are 

critical, and those after exposure may be 

important. The responses of plants to ozone and 

PAN under varied climatic conditions were studied 

primarily under laboratory and greenhouse 

conditions. Field observations have often 

substantiated these results Most studies have 

involved individual environmental factors and one 

or two response measures, including usually the 

evaluation of injury. Several investigations have 

dealt with the interactions of environmental 

factors. Information sufficient to make 

generalizations regarding plant response to 

oxidants exists, but there is much uncertainty 

because of the small number of species studied 

and the lack of information on the interactions of 

the environmental factors evaluated. 

Light Quality — The quality of light affects the 

growth and development of plants and plays a role 

in determining the response of plants such as pinto 

bean to PAN.7273 Injury to pinto bean from PAN 

was maximal when exposed to 420 and 480 nm 

and less than half at 640 nm. The response was 

apparently associated with changes in carotenoid 

pigments. Shinohara et a1. 258reported the effect of 

light q uality on the response of tobacco (H-mutant) 

exposed to 785 Ng/m 3(0.40 ppm) ozone for 30 min. 

The least injury occurred in far red light, followed 

by blue, green, and white, with the greatest effect 

in the red spectrum. 

Photoperiod — Physiological control over some 

aspects of plant development is exerted by a 

specific light period based on a 24-hr cycle. 

Research has shown that plants are more sensitive 

to ambient oxidants and ozone when grown under 

an 8-hr photoperiod compared to either a 12- or 

16-hr photoperiod. 19,'

as,,7s 

Light Intensity — The intensity of light affects 

many physiological processes within plants and is 

known to affect the response of plants to oxidants. 

Studies have been reported on the effects of light 

intensity before, during, and after exposure to 

oxidants. 

Dugger et a1. 73found a direct correlation 

between the sensitivity of pinto bean to PAN and 

increasing light intensity. Pinto bean required light 

before, during, and after a PAN exposure for injury 

to occur. 72 ' 73This was not true of response to 

ozone, although some light period was necessary. 

Generally, plants are more sensitive to ozone 

when grown under a short photoperiod at low-light 

intensities. This was demonstrated with pinto 

bean 74 ' 19and tobacco.'4' "9' 258 

Temperature — The response of plants to ozone 

varies with temperature. The effect of temperature 

on plant sensistivity to ozone varies with plant 

species, and thus no constant pattern of response 

is discernible. Some plants (radish'' 225 ) were more 

sensitive to ozone if grown under cool conditions, 

272 
and others (snap bean, 5soybean, 75BeI W3 

tobacco ,

193

' 257 Virginia pine, 55 '5s and white ash 309 

were more sensitive if grown under warm 

conditions. Pinto bean 73was sensitive to ozone 

regardless of temperature. Macdowell 16found 

that a low day or high night temperature increased 

the susceptibility of White Gold tobacco to ozone. 

Juhren et a1. 149used eight combinations of day and 

night growth temperatures with Poa annua and 

then exposed these plants to ambient oxidants for 

a day. The sensitivity varied with plant age and was 

greatest at the 26 1to 20°C day/night 

temperatures. Both high and low temperatures 

during growth could, in certain plants, produce 

physiological changes that are associated with 

stress resistance and thus protect the plant from 

air pollutant stress. Difficulties arise in 

interpreting the results of environmental studies 

conducted under greenhouse conditions. 

Relative Humidity — Davis 55and Davis and 

Wood59found an increase in sensitivity of Virginia 

pine to ozone at high humidityduring exposure, but 

they reported no effects from post-exposure 

changes in humidity. Otto and Daines 233 found 

similar results for pinto bean and tobacco exposed 

over a wide humidity range and at - several ozone 

concentr•itions. They did not study growth or postexposure conditions. The studies of Dunning and 

Heck74chowed a significant increase in the 

responsf of pinto bean, but not of tobacco, when 

humidity was increased during ozone exposure. 

Pinto be, n grown at 60-percent relative humidity 

was moi e sensitive to ozone when compared to 

plants qrown at 80-percent humidity. The 

responsf-of tobacco to ozone was unaffected by 

humidit ~, differences during exposure; however, its 

sensitivity was conditioned by the humidity before 

exposure. Sensitivity of tobacco decreased with an 

increase in humidity. Response of pinto bean was 

unaffected by humidity when grown under a light 

intensity of 4000 ft-c (43,060 Ix), but it was 

increased with an increased humidity (80 percent) 

and a decrease in light intensity levels of 2000 ft-c 

(21,530 Ix) during growth." Table 11-8 

summarizes some of these results. 

Carbon Dioxide — Stomatal opening isdecreased 

by high carbon dioxide levels and may affect plant 

sensitivity to oxidants. Heck and Dunning"g 

reported a decrease in sensitivity of tobacco to 

ozone if the tobacco was exposed to elevated 

carbon dioxide concentrations of 500 ppm 

immediately before and during exposure to ozone 

(22 percent injury with added carbon dioxide, and 

66 percent injury without). 

METEOROLOGICAL PARAMETERS 

Canadian workers using an ambient oxidant 

dose have correlated variations in meteorological 

parameters with plant injury. 19' 213A correlation 

was discovered when an empirical relationship 

involving evapo-transpiration (the coefficient of 

evaporation) was developed and used to modifythe 

dose information This empirical relationship has 

been used on a limited basis to predict damaging 

oxidant concentrations from monitored 

meteorologic conditions. 

Linzon 12'"3also noted plant injury that was 

associated with changes in meteorological 

conditions. He reported needle blight symptoms on 

white pine subsequent to several days of wet 

weather followed by a continuous sunny period. 

Symptoms were observed severa I ti mes d uring the 

1957-64 growing seasons at Chalk River, Ontario. 

However, the time of occurrence did not correlate 

well with peak oxidant concentrations. 

Skelly et a1. 259associated post-emergence acute 

tipburn on white pine growing at three different 

sites along the Blue Ridge Parkway with higr 

oxidant during the summers of 1975 and 1976. 

The two episodes were associated with 

meteorological conditions that resulted in the 

transport of oxidant or oxidant precursors from 

many miles away. The episode of July 1975 

resulted because of a low-pressure system 

(Hurricane Amy) that was off the Atlantic Coast in 

the vicinity of New York and a high-pressure 

system from Canada that became stationary over 

the Great Lakes. The circulation of air around a 

low-pressure system is counter clockwise, and it is 

clockwise around a high-pressure system. This 

pattern forced air from the northeast south into 

Virginia. The movement of the high-pressure 

system into Virginia permitted further oxidant 

synthesis. The June 5-1 2, 1976, episode resulted 

because of windsfrom the northeast on June 5 and 

6 and a stationary high-pressure system that 

continued through June 12. As a result of the air 

movement, oxidant levels in July 1975 and again 

in June 1976 exceeded 160 Ng/m 3(0.08 ppm). In 

July 1975, needle injury was associated with a 1- 

day episode, and from June 5-13, 1976, the three 

sites exceeded 160,ug/m 3(0.08 ppm) for 110, 186, 

and 122 consecutive hours, respectively. 

A widely held belief is that vegetation growing in 

the humid eastern United States would be severely 

273 
injured if oxldant concentrations r'eached the daily 

peak concentrations of 390 to 780 Ng/m 3 (0.20 to 

0.40 ppm) commonly experienced in the less 

humid sections of southern California. An air 

pollution episode that occurred on July 27-30, 

1970, in the Washington, D.C., area (as well as 

those decribed above by Skelly et a1. 259 ) is 

indicative of what may happen. During thls 4-day 

period, the peak oxidant concentrations ranged 

from 220 to 400 Ng/m 3 (0.14 to 0.22 ppm) and 

were accompanled by a low concentration of sulfur 

dioxide (0.04 ppm). Oxidant injury was observed on 

31 tree, 15 shrub, and 18 herbaceous species in an 

area of about 187 km 2 (72 mlles2 ). Increased 

emissions of the precursors associated with 

oxldant fomatlon could result In repeated 

occurrences of acute injury or even chronic injury 

to eastern vegetation. 5 

Such factors as windspeed and atmospheric 

pressure appear to play little or no role In affecting 

plant sensitivlty to oxidant pollutants. Air 

movement would be expected to play a role under 

ambient conditions because of Its known effect on 

air boundary layers of leaves, but it probably has 

little effect in chamber work unless wind velocities 

are greater than 1.6 km/hr (1 mph). 29 '" 2 '' 28 

EDAPHIC CONDITION 

Khatamian et a1. 153 reported that tomato plants 

grown under water stress, whlch did not in Itself 

cause a reductlon In growth, were more tolerant of 

ozone injury. The effects of soil moisture on the 

response of selected plants to ozone are presented 

in Table 1 1-9. Markowski and Grzesiak 186 founti 

that bean and barley grown under drought 

condltions were protected from ozone Injury. 

Several field studles 67,26a,3o4 showed that there 

was a close posltive correlatlon between soll 

moisture and oxidant injury to several cultivars of 

tobacco. Fleld observations generally suggest that 

TABLE 11-8. RESPONSE OF PLANTS TO OZONE, AS CONDITIONED BY HUMIDITY DURING GROWTH AND EXPOSURE 

Ozone 

Plant concenlralion, Growth or Response, 

species ppm, hr Notes " exposure ° % injury (% RH)` Reference 

Plne, Vtrglnfa 0 25, 4 Control condltlons, (60) (85) 59 

3-year seedlings Exposure 4 25 

Growth 50 58 

0 25, 4 Juvenlle Exposure 1 35 

Bean, cultivar 040, 1 Control condltlons, (45) (60) (75) (90) 233 

Plnto, and PP, 8 hr Growth 

Tobacco, cultivar 45% EH 36 39 41 31 

Bel W3, averaged 90% EH 73 67 81 80 

Control condltlons, Exposure 41 53 70 81 

PP, 8 hr, 75% GH 

Bean, cultivar 040, 1 Control condltlons, (60) (80) 74 

Plnto PP, 8 hr, 2,000 Growth 66 78 

ft-c (21,529 Ix) Exposure 52 67 

control condttlons, 

PP, 8 hr 

Tobacco, 040, 1 Control condltlons, Growth 42 36 74 

cultivar Bel Ws PP, 8 hr, (2,000 ft-c 

(21,529 Ix) control Exposure 33 36 

condltlons, PP, 8 hr 

Tobacco, 030, 1 5 Control condltlons, (26) (51) (95) 233 

cultivar Bel W3 31 °C Exposure 9 39 50 

Bean, cultivar 020, 1 5 Control condltlons, Exposure 0 0 55 233 

Plnto 31 °C 

Ash, whlte 0 25, 4 Control condltlons, (60) (80) 309 

1-yr seedlings Growth 33 46 

Exposure 38 41 

Post-exposure 36 41 

e PP = photoperiod, GH = humidity during growth, EH = humidity during exposure, ft-c = foot candle 

°Time of humidity treatment 

`Humidity values are in parentheses 

274 
sensltive plants may become resistant under 

drought conditions. Rich and Turner249 found rapld 

stomatal closure In pinto bean during a 30-min 

exposure to ozone at 392 to 490 Ng/m 3 (0.20 to 

0.25 ppm) if plants were grown under a soil 

moisture stress; however, closure was slower 

under optimal ' water availability. They also 

reported rapid stomatal closure In pinto bean and 

Bel Ws tobacco if the plants were conditioned and 

exposed to ozone at a relative humidity of 37 

percent; however, a similar reponse was notfound 

at a relative humidity of 73 percent. This evidence 

suggests that ozone may induce more rapld 

closure of stomata when plants are already under 

some type of water stress. 

Starkey265 found that the foliage of bean that 

was sensitive to subacute concentrations of PAN 

was also injured by drought following PAN 

exposure. Plants resistant to PAN were not injured 

similarly by drought following PAN exposure. 

Salinity and low soll moisture have been shown 

to increase the resistance of plants to ambient 

oxidants. 139,,3s,175,222,223 Sallnity, however, 

suppresses plant growth so that the protective 

effect Is offset. The protective effect against ozone 

Is enhanced with increasing salinity. 34 

The interaction of soil fertility and the response 

of plants to oxldant is not well understood. 

Nitrogen nutrition has received some attention. 

Menser and Street, 196 in anamblentoxidantstudy, 

reported an increase in tobacco fleck with 

increasing applications of soil nitrogen. This 

response was also found in spinach exposed to 

ozone. 34 Leone et a1. 170 reported that 

concentratlons of nitrogen optimal for growth 

resulted in tobacco being most sensltive to ozone, 

whereas either higher or lower nitrogen 

appllcatlons Increased resistance. The opposite 

was reported for White Gold tobacco, in whlch the 

optimal nitrogen concentration for growth gave the 

greatest resistance to ozone. 16 Ormrod et a1. 225 

found that concentrations of nitrogen had no effect 

on growth of radish exposed to ozone. It is apparent 

that the nitrogen concentrations and other 

experlmental conditlons used in these studies 

were not sufficlently critical for an evaluation of 

nitrogen-oxidant interactions. 

Several studies have explored the importance of 

phosphorus In modlfying the sensitivityof plantsto 

oxldant. Rlpaldi and Brennan 252 reported an 

increase in phosphoruswithin leaves of pintobean 

after exposure to ozone. Leone and Brennan 769 

reported Increases in ozone injury and in 

phosphorus content of tomato leaves with 

increasing applications of phosphorus. Brewer et 

a1. 34 found an Interaction between potassium and 

phosphorus in the response of spinach to ozone. 

They reported that at low phosphorus content, an 

increase in potassium tends to increase injury, but 

at high concentrations of phosphorus, the Increase 

in potasslum tends to inhiblt injury. Dunning et 

a1. 75 found that pinto bean and soybean were more 

TABLE 11-9. EFFECTS OF SOIL MOISTURE ON RESPONSE OF SELECTED PLANTS TO OXIDANT STRESS217 

---- --- --- --- -- — ------ 

Response, percent reduction frorn control 

Oxidant concentration Moisture conditions' 

Plant species ppm, hr Type of response high to low Reference 

Tobacco, cultivar Amblent oxldant Irrlgated Normal 196 

Catterton % Injury 29 11 

Tomato, cultivar 90% turgld 80% turgld 

Flreball 1 00, 1 5 % red In chlorophyll 54 10 6 

1 00, 1 0 % red In chlorophyll 67 24 153 

050, 1 0 % red In chlorophyll 36 +3 153 

1 00, 1 0 % red leaf dry wt 48 +40 153 

Beet, garden -40 kPa -440 kPa -840 kPa 223 

Control % red In dry wt of 0 24 68 

020, 3(dally for 38 days) storage root from 40 52 69 

nonsallne controt 

Bean, cultivar 

Plnto Control 

0 15, 2/day (63 days) 

0 25, 2/day (63 days) 

Control 

0 15, 2/day (63 days) 

0 25, 2/day (63 days) 

-40 kPa -200 kPa -400kPa 139 

% red In shoot dry 0 18 78 

wt from nonsallne 27 42 87 

control 93 91 88 

% reductlon In root 0 25 65 

dry wt from nonsallne 25 28 78 

control 91 89 79 

aSpecial soil rnoisture conditions are underlined kPa = kilopascals fbars x 10 2 ) 

275 
sensitive to ozone at low potassium 

concentratlons. Adedipe et a1. 5 reported that low 

sulfur concentrations increased the response of 

Blue Lake snapbeans to ozone. Mcllvenn et al. 190 

reported increased Injury with increasing 

concentratlons of zinc in the soil. Sofl nutritlon 

probabfy plays an important role in the responseof 

plants to pollutants only in cases of nutrient 

imbalances, although total nutrient salts could 

affect response under some conditions. In soils 

with balanced fertilizer regimes, plants with 

similar genotypes would probably respond fairly 

uniformly to oxldant stress. The responses of 

plants to ozone stress when grown under various 

nutrient reglmes are summarized in Table 1 1-10. 

POLLUTANT INTERACTIONS 

Oxidants are components of a complex mixture 

of gases in the atmosphere, many of which may be 

phytotoxic. Except for ambient air studies and 

studies simulating photochemical oxidants, there 

have been few investigations of the effects of 

pollutant combinations on vegetation. 

Ozone and sulfur dioxide mixtures are of special 

interest, owing to their widespread co-occurrence 

and to the possibility of a greater than additive 

TABLE 11-10. EFFECTS OF VARIOUS NUTRIENTS ON RESPONSE OF SELECTED PLANTS 

TO OZONE (OXIDANT) STRESS 217 

Oxrdant Response, °!o reduction from control 

concentration nutrdional levels' _ 

Plant species ppm, hr Type of response Element ---- ow to ~i'igTi— Reference 

Tobacco, cultivar 0 35, 48 01 05 10 5 0° 176 

Whlte Gold % Injury Nltrogen 21 16 4 22 

Tobacco, cultivar Amblent 60 Ib/acre 90 120 196 

Catterton oxldant o/o Injury Nltrogen 29 20 11 

Tomato, cultivar 0 18, 4 28 mg/Ilter 280 560 1120 170 

Rutgers % Intury Nltrogen 20 40 40 20 

Spinach, cultivar 025, 10 ppm 30 ppm 90 ppm 34 

Vlroflay 3 daY % Injury Nltrogen 3 18 22 

Radlsh, cultivar 025,4 60 mg/Ilter 300 mg/Ilter 225 

Cavaller %growthreductlon Nltrogen 50 55 

Tomato, cultivar 1 5 ppm 15 5 ppm 62 ppm 170 

Rutgers 0 15, 3 % Infury Phosphorus 0 0 40 

025, 3 % Inlury Phosphorus 20 40 60 

030, 3 % Injury Phosphorus 20 60 60 

Spinach, cultivar 0 25, % Injury Phosphorus 20 ppm 150 ppm 

Vlrofla 

y 

9/day 

3 days 5 ppm K 14 13 

40 ppm K 25 9 

Radlsh, cultivar 0 25, 4 30 mg/Ilter 150 mg/Ilter 

Cavaller % growth reductlon Phosphorus 35 43 

Bean, cultivar 050, 1 3 mg/Ilte r 32 mg/Ilter 

Blue Lake 2 day °/n chlorophyll Sulfur 55 11 

2 days reductlon 

Soybean, cultivar 8 doses 

Dare (acute) % Injury Potasslum 

Bean, cultivar 8 doses 

Plnto (acute) °/n lnjury Potasslum 

`Nutrit ~ onal values are underltned and show a nurnber of different units 

° Relative to a full-strength nutnent solution 

276 

105 mg/Ilter 710 mg/Ilter 

40 23 

26 18 

34 

225 

5 

75 

75 
effect on vegetation.t 91Most studles of the effects 

of ozone on vegetatlon have been directed 

primarlly to understanding the responses of 

varlous plant species or cultivars to a single alr 

pollutant and the manner In which these 

responses are modified by environmental factors. 

However, In the field, vegetation Is always exposed 

slmultaneously to several air pollutants. When the 

effect produced by exposure to a combination of 

pollutants results in a greater effect than exposure 

to a single pollutant, the effects are synergistic. 

Antagonlsm is the opposite reaction. The effect 

level resulting from exposure to the combined 

pollutants is less than the sum of the Injury 

produced by exposure to the indlvidual pollutants. 

If the effect level resulting from exposure to the 

combined pollutants is not signiflcantly different 

from the sum of the levels of the effects from 

Individual exposures, no Interaction has occurred 

and the follar response to the combined pollutants 

Is additive. Menser and Heggestad In 1966 19 ' first 

reported that exposure of the sensitive Bel Ws 

tobacco to mixtures of sulfur dioxide (1310ug/m 3 

or 0.50 ppm) and ozone (59 Ng/m 3or 0.03 ppm) for 

2 or 4 hr caused foliar Injury of 23 to 48 percent, 

whereas the same concentratlons of the individual 

gases produced no injury. The synergistic 

interactlon between ozone and sulfur dioxlde 

deplcted In the above study stimulated plant 

sclentists to begln research on pollutant 

combinatlons. Middleton et a1., 202working with 

ratios of sulfur dioxide to ozone of 4:1 to 6:1, did not 

observe an Increase in injury, although theyfound 

that at 4:1 , ozone appeared to interfere wlth the 

expected sulfur dioxide injury. Macdowall and 

Cole 1e reported that the two-gas combination 

lowered the threshold concentrations for injury of 

tobacco (cultivar Whlte Gold) by sulfur dioxide but 

not the threshold for ozone Injury. Injury from 

ozone alone was first noted at a dose of 98 Ng/m 3 

(0.05 ppm) for 1 hr. From S02 alone, injury was 

noted at 260 /ag/m3(0 1 ppm). And when the two 

gases were combined, Injury was noted at the end 

of 1.5 hr. Macdowall et a1. 19defined thethreshold 

in terms of dose when they reported the threshold 

at 20 pphm-hr (392Ng-hr/m 3 , or 0.20 pphm-hr). 

This has not appeared to be true in some other 

reports. 19 ''292Symptoms observed when sulfur 

dloxide was below the threshold for S02 injury for 

the speciflc plant are similar to those reported for 

ozone. 

Tingey et a1. 292 exposed 11 species of plants to 

different ratios of sulfur dioxlde and ozone 

mixtures. Plants were exposed to either 98 or 196 

Ng/m 3(0.05 or 0.1 ppm) ozone and to 260, 660, or 

1310 Ng/m 3(0.1, 0.25, or 0.5 ppm) sulfur dioxide 

for 4 hr. There was no general trend observed in 

the manner in which the ratios of pollutant 

concentrations caused follar injury. Additive, 

greater than additive, and less than additive 

responses were noted (Table 1 1-1 1). Menser et 

a1., 194 '' 95Grosso et a1., 97and Hodges et al. 134 

determined the response of several Nicotiana 

speciesandvarlous N. tabaccumcultivarstosulfur 

dioxide and ozone mixtures. They found that ozone 

and sulfur dloxide acted synerglstically and 

produced ozone-type symptoms on all cultivars of 

Maryland tobacco. When plants were fumigated for 

4 hr wlth 60 to 70 pg/m 3(0.03 to 0.035 ppm) ozone 

alone or with 115 to 130 /jg/m3(0.045 to 0.05 

ppm) with S02 alone, no injury was observed. 

However, when the gases were combined and the 

plants were exposed for the same length of tlme, 

the result was leaf injury ranging from 5 to 15 

percent. Jacobson and Colavit0146found that 

sulfur dioxide at 79 /jg/m3(0.04 ppm) decreased 

the sensitivlty of bean to ozone and increased that 

of tobacco during a 4-hr exposure. 

TABLE 11-11. SUMMARY EFFECTS OF SULFUR DIOXIDE 

AND OZONE MIXTURES ON FOLIAR INJURY292 

Response at concentration ratio, S_0 2/03, ppma _ 

Plant spe c ies 0 50/0 05 0 50/0 1 _0 0 _1_ 0/0 10 0 25 ; 0_ 10__ 

Alfalfa - + + + 

Broccoll + 0 + 0 

Cabbage 0 + 0 0 

Radlsh 0 + + + 

Tomato 0 0 - 0 

Tobacco, Bel W3 + + 0 + 

+= greater than additive, 0= additive, -= less than additive 

Dlfferentlal susceptibility of Indlvidual clones of 

eastern white pines to ozone and sulfur dioxlde 

was shown by Berry and Heggestad 16and 

Costonis. 46When Dochinger et a1. 70determined 

that chlorotic dwarf could be caused by an 

Interaction of ozone and sulfur dioxide, they used a 

chlorotic-dwarf-susceptible clone to eliminate the 

genotype variable. Houston 140tested the response 

of tolerant and susceptible clones of eastern white 

pine (on the basis of symptom expression under 

ambient condltions) to ozone or sulfur dioxlde. 

Injury caused by sulfur dioxlde or sulfur dloxlde 

wlth ozone correlated well with the earlier fleld 

responses, but ozone alone did not produce a 

consistent response. Dochinger et a1. 70and 

Houston 140found that the S02-03 mlxture 

277 
increased the amount of injury, but Costonis 47 

reported less injury from the mixture than froni 

sulfur dioxide alone. Both Costonis and Houston 

reported effects from sulfur dioxide and its mixture 

with ozone at concentrations of both gases well 

below those reported by others. It is possible that 

they used ultra-sensitive clonal materials 

Whatever the reason, this work needs verification. 

Applegate and Durrant 10 also reported injury to 

peanut at sulfur dioxide/ozone concentrations and 

ozone concentrations well below those reported 

for other plants. Their work also requires 

substantiation. In the latter two cases, the 

concentrations reported are close to the detection 

limits of the gas-measuring instruments used. 

Tingey et a1. 287 found an additive inhibition oftop 

growth of radish and a less-than-additive 

inhibition of root growth after exposure to sulfur 

dioxide-ozone mixtures. Tingey and Reinert 290 and 

Tingey et a1. 293 exposed soybean, tobacco, and 

alfalfa to mixtures of sulfur dioxide and ozone and 

reported a greater-than-additive inhibition of root 

growth of soybean, an additive inhibition for 

tobacco, and a less-than-additive inhibition for 

alfalfa. Heagle et a1. 109 reported a greater-thanadditive effect on growth and yield in soybean 

grown under field conditions in a mixture of these 

gases, but the differences between the mixture 

and the ozone treatments were not significant. 

Weber 307 reported a reduction in the growth of 

leaves, stems, and roots of soybeans and an 

increase in leaf abscission as influenced by a 

mixture of ozone and sulfur dioxide. These 

changes were similar to those caused by ozone 

alone. 

Combinations of other pollutants with ozone, 

PAN, or both may be important, but they have 

received little study. Matsushima 187 reported 

additive foliar effects on pinto bean and tomato 

from a mixture of sulfur dioxide and PAN and a 

less-than-additive effect on tomato from mixtures 

of ozone and nitrogen dioxide. Fujiwara 90 reported 

a greater-than-additive effect on pea from a 

mixture of ozone and nitrogen dioxide. Kress's' 

and Kohut 157 studied the response of hybrid poplar 

to ozone-PAN mixtures. Kress used sequential 

exposures and found a greater-than-additive effect 

after most exposures. After others, he reported 

mixed c- esponses. Kohut used simultaneous 

exposure and found all three types of responses in 

replications of the study. The reasons for these 

variations are unclear. 

Fujiwara90 and Reinert et a1. 242 have reviewed 

the subject of pollutant interaction. Reinert et a1.z 42 

tabulated some of the studies dealing with 

pollutant interaction. This information is presented 

in Tables 1 1-12 and 1 1-13. 

Studies of pollutant interactions are preliminary. 

It is still not possible to define adequately the 

potential impact of pollutant combinations on the 

production of quality food, feed, and fiber. Plant 

species are known to respond differently to 

combinations of pollutants, and the responses can 

be additive, greater than additive, or less than 

additive. The variation in cultivar or species 

response or the variation in the response of plants 

grown or exposed under a variety of enviromental 

stresses is still not understood. 

POLLUTANT-PARASITE INTERACTIONS 

Infection by biotic pathogens has been shown to 

be a factor in the response of vegetation to oxida nts 

(primarily ozone). Such responses have been 

studied from several perspectives since Yarwood 

and Middleton314 accidentally found that rustinfected bean leaves were less sensitive to 

photochemical oxidants. A number of investigators 

have studied the protection from ozone injury 

afforded to plants with active infections. Others 

have noted that ozone injury increases the 

sensitivity of plants to infection. Some 

investigators have studied the effects of ozone on 

pathogens, and several have found no interacting 

effects. Other studies have involved bacteria, 

fungi, viruses, insects, and nematodes. Stark et 

a1. 264 and Miller et a1. 207 in California reported that 

oxidant (ozone) injury to ponderosa pine 

predisposed the trees to subsequent invasion by 

pine bark beetles. The beetles increase the rate of 

tree decline and may be the final cause of tree 

mortality43 (Chapter 12). It is possible that oxidant 

stress in other parts of the country contributes to 

insect infestation in the forest areas (e.g., the Blue 

Ridge Parkway, Va. 259 ). Weber308 has shown that 

ozone and mixtures of ozone with sulfur dioxide 

(0.25 ppm, 4 hr/day) can cause a decrease in the 

populations of several species of nematodes 

parasitizing roots of soybean or leaves of begonia. 

These types of interactions may be of significance 

in areas of the country with significant oxidant 

pollution problems. In general, it is felt that the 

interacting effects resulting in modification of 

pathogens are due to changes in the host 

physiology and not to direct effects on the 

pathogen. Heagle 106 has reviewed pollutantparasite interactions and has also discussed the 

278 
direct effects of pollutants on pathogens 

themselves. 

OTHER FACTORS 

Heagle and Heck"' found that Bel W3 tobacco 

was predisposed to oxidant injury by previous 

exposure to ambient pollutants. Macdowa11 16 

reported the same results when the first and 

second exposures were to low oxidant levels. 

Antagonism was noted when both exposures were 

to high doses. 

Although there has been considerable interest 

in understanding how various factors affect the 

response of plants to pesticides, especially 

herbicides, very little has been done with the 

effects of interaction between pesticides and air 

pollutants. Hodgson and associates 135- ' 3

' first 

showed an effect of ozone on the metabolism of 

herbicides. They found that ozone inhibited the 

dealkylation of atrazine in corn and altered the 

pathway of diphenamid metabolism in tomato. The 

changes could be beneficial if oxidants increase 

pesticide degradation, or harmful if oxidants stop 

the biologlc breakdown at a toxic intermediate or 

retard the degradation process. Carney et a1. 39 

reported that the herbicide pebulate in 

combination with ozone caused a greater-thanadditive effect on White Gold tobacco and that 

TABLE 11-12. FOLIAR RESPONSE OF SELECTED PLANTS TO SULFUR DIOXIDE AND OZONE MIXTURES 26 

Plant 

species 

Concentration 

ratio, SOz/03, 

pam 

Exposure 

duration, 

hr 

Foliar 

infury, 

% 

Response to 

mixturea Reference 

Bean, garden 1 70/0 19 05 24 + 187 

Bean, Ilma 0 25/0 05 4 0 0 292 

Broccoll 0.50/0 05 4 17 + 292 

Cabbage 1 00/0 10 4 28 0 292 

Tomato 0 10/0 10 4 10 - 292 

Radlsh 0 50/0 10 4 50 + 292 

Alfalfa 0 50/0.10 4 60 + 292 

Eastern whlte pine 0 025/0 05 6 26 + 140 

Tobacco, cultivar 

Bel W3 0 25/0 03 4 41 + 191 

Tobacco, cultivar 

Bel W3 0.50/0 10 4 88 + 292 

Tobacco, Md 

(6 cultivars) 0.50/0.10 2 20 + 195 

— - — 

,- greater than additive, 0- 

---- - - 

additive, -= less than additive 

------- -- — - — --- ---- -------- -- 

TABLE 11-13. GROWTH RESPONSE OF SELECTED PLANTS TO SULFUR DIOXIDE AND OZONE MIXTURES 26 

Plant 

species 

Concentration 

ratio, SOz/Oa, 

ppm 

Exposure 

duration, 

hr 

Plantresponse, 

% reduction 

from control' 

Response 

to 

mixture ° Reference 

Radish 0 05/O 05 8/day, 5 1 O TDW 0 287 

days/week, 55 RDW - 

5 weeks 

Radlsh 0 45/0.45 4 16 TDW 0 242 

70 RDW 0 

Alfalfa 0 05/0 05 8/day, 5 18 TDW - 242 

days/week, 24 RDW - 

12 weeks 

Soybean 0 05/0 05 7/day, 5 24 RFW + 293 

days/week, 

3 weeks 

Soybean 0.10/0 10 7/day, 5 72 TFW 0 109 

days/week 63 seed wt 0 

untll harvest 

Tobacco 0 05/0 05 7/day, 5 32 RDW 0 242 

days/week, 49 RDW 0 

4 weeks 

'TDW = top dry wt, RDW = root dry weight, RFW = root fresh weight, TFW = top fresh weight 

°+ = greater than additive, 0= additive, -= less than additive , 

279 
chloramben did the same with Delhi 34 tobacco. 

They reported a less-than-additive response of 

both tobacco cultivars to the combination of 

benefin and ozone. These and other herbicides 

acted independently of ozone exposure on tomato 

and white bean. Ordin et a1. 124found that Avena 

coleoptile growth was less inhibited by PAN when 

2,4-D was used in amounts giving optimal growth. 

These interactions with herbicides need additional 

investigation to determine whether the responses 

noted are of general importance. Research needs 

to be directed at possible interactions between 

atmospheric pesticides (vapors or fine particles) 

and oxidant air pollutants. 

Another interaction has recently been reported 

between cadmium applied to soil and ozone 

exposure of cress. 53If cadmium potentiates the 

ozone response of cress, possibly other heavy 

metals can cause a similar interactive response. 

RESPONSES OF MOSSES, FERNS, AND 

MICROORGANISMS 

Mosses, ferns, and lichens have not been 

extensively studied to determine ozone and 

oxidant effects. Comeau and LeBlanc 45found that 

a 4-hr exposure of Funaria hygrometrica to ozone 

at 490 to 1960 Ng/m3(0.25 to 1.00 ppm) 

stimulated the regenerative capacity of the moss 

leaves. This did not occur with 6- and 8-hr 

exposures. Glater 95reported oxidant injury to 

several species of fern growing in the Los Angeles 

area. Initially, tan colored lesions appeared near 

the smaller veins, but in no special pattern. Later, 

the entire leaf became necrotic. Symptom 

development and sensitivity of leaves were 

different from those noted in more highly evolved 

plants. AII leaves appeared to be equally sensitive, 

except for the growing tip and the youngest 

uncoiling leaves Occasionally, a young plant was 

killed 

Lichenologists have long used the presence and 

abundance of lichen species to map the biologic 

impact of large urban and industrial areas.$$ 

Though early workers considered changes in the 

presence and abundance of these organisms to be 

related to such factors as temperature and 

humidity, more recently, most researchers have 

tended to relate changes in lichen population more 

to industrial air pollution than to other 

environmental changes There is strong indication 

that both the presence and the abundance of 

certain lichen species are correlated with sulfur 

dioxide concentrations in urban and industrial 

areas. However, littfe is known about the direct 

effects of ozone or other oxidants on lichen 

morphology or physiology. Ozone or some of the 

other oxidants may have an adverse ecological 

impact on lichens 

Ozone in high concentrations has been used in a 

variety of applications for the control and 

suppression of fungi and bacteria. These 

applications have included food protection, 

drinking-water purification,99and treatment of 

sewage. 154 '' 88The germicidal effectiveness 

depends on concentration, relative -humidity, and 

the specific organism. In many cases, even a 

concentration of 5880 to 9800 ug/m 3(3 to 5 ppm) 

was not sufficient to kiil some bacteria. Burleson et 

a1. 36showed inactivation of several viruses and 

bacteria after ozone exposure, and a greater 

inactivation with simultaneous sonication. 

Zobnina and Morkovina 315related the tolerance of 

a carotinoid strain of Mycobacterium carothenum 

with the presence of the pigment. 

Large doses of ozone may inhibit growth and 

sporulation of fungi on fruit, although most fungi 

tested were resistant to ozone. Spalding 262 

reported that ozone acted as a surface biocide. 

Above 980 Ng/m3(0.5 ppm), ozone inhibited 

surface growth of fungi on strawberry and peach. 

Ridley and Sims 251extended the shelf-life of 

strawberry and peach by exposing them to ozone, 

but stated no concentrations. Ozone at 1960 to 

3720 ug/m3(1 to 2 ppm) for 1 to 2 hr/day 

controlled the surface growth of fungi and 

sporulation on apple, reduced offensive odors, and 

decreased the ripening rate. 261Watson3 o5 found 

that ozone at 785 to 3920 pg/m 3(0.4 to 2.0 ppm) 

acted as surface fungicide on fruit. Fungal growth 

within the fruit was not affected. Sporulation and 

some control of decay by PemcilJium digitatum and 

P. italicum were noted in open storage boxes of 

lemon and orange exposed to ozone at 1960pg/m 3 

(1 ppm). 51Ozone was more effective than a 

fungicide dip in controlling Botrytis bud rot of 

gladiolus, but no concentrations were given.'$' In 

general, researchers have suggested that rather 

large dosages of ozone are required to protect 

storage fruits from fungal infection. These 

concentrations may be so high as to preclude the 

use of ozone in storage facilities. The ability of 

ozone to reduce spore germination in fungi 

apparently depends on species, spore morphology, 

moisture, and substrate. 106Single-celled spores 

and those with thin cell walls are most sensitive 

Wet spores are more sensitive than dry spores. 

280 
Hibben 127 found ozone toxic to moist fungus 

spores of some species, even at concentrations of 

200 Ng/m3 (0.1 ppm). Exposure to 980 and 1960 

Ng /m 3 (0.5 and 1.0 ppm) reduced or prevented 

germination of spores of all species tested. Ozone 

at 200 Ng/m 3 (0.1 ppm) for 4 hr or at 1960/jg/m 3 

(1.0 ppm, for 2 hr stopped apical cell division of 

conidiophores of Alternaria solani and caused 

collapse of the apical cell wall. 248 

Heagle 106 has reviewed the effects of ozone on 

fungus growth, sporulation, and germination. 

Ozone may inhibit colony growth on artificial 

media, but it rarely causes death, even at high 

concentrations Differences in species 

susceptibility are known. In several fungi, 

exposure to ozone at 196 or 785 Ng/m 3 (0.10 or 

0.40 ppm) for 4 hr caused a 10- to 25-fold increase 

in sporutation. 106 Heagle 107 alsr) reported the 

effects on three obligate parasitic fungi of low 

exposures to ozone. Germination of spores was not 

affected in any of these studies. Kuss 162 grew 30 

representative fungi on agar and found that spore 

production in some species was increased after 

exposure to ozone. 

Rabotnova et a1. 240 exposed two species of yeast 

to ozone: Candida lipolytica was sensitive, and C. 

auilliermondii was resistant. The biocidal activity 

of ozone was determined under various cultural 

conditions with air streams of about 294,000 to 

10,780,000 Ng/m 3 (150 or 5500 ppm) (v/v for 10 

to 30 min). Ozone was an effective biocide under 

most conditions. Its effectiveness increased with 

decreasing pH of the culture medium. Kanoh 15 ' 

found that exposure to ozone at 58,800 Ng/m 3 (30 

ppm) for 30 min increased oxygen uptake in slime 

mold homogenate from Physarum polycephalum. 

Ozone also increased succinoxidase activity and 

inhibited part of glycolysis. Effects of ozone on 

Euglena gracilis that were reported by de Koning 

and Jegier61-64 included reduction of net 

photosynthesis, increase in respiration, and 

effects on pyridine nucleotide reduction and 

phosphorylation. They also reported that the 

reduction of net photosynthesis was a logarithmic 

function of ozone concentration in 1-hr exposures. 

These investigators also found a 5-percent 

reduction in oxygen evolution after a 1-hr exposure 

to 980 Ng/m 3 (0.5 ppm) ozone bubbled into 5 ml of 

solution and an additive effect with a mixture of 

sulfur dioxide and ozone. 63 Verkroost3o 3 carried out 

a detailed study of the effects of ozone on 

Scenedesmus obtusiusculus, Chod. witFi special 

concern over the effects on photosynthesis and 

respiration. A major weakness in this study was 

the use of an air stream containing ozone at 

58,800 /ag/m3 (150 ppm). The report suggested 

that the primary site of ozone action is the 

membrane structure, which produces changes in 

photosynthesis and respiration. 

Giese and Christiensen 94 found that protozoa in 

hanging drop suspensions exposed to 

approximately 8 percent ozone in ozonized water 

were killed within a period of 4 m in (Colpidium) to a 

maximum of 64 min (Tillina). 

Haines 102 reported that ozone at 4 ppm retarded 

the growth of Escherichia coli, whereas 19,600 

Ng/m 3 (10 ppm) prevented growth. Scott and , 

Lesherz 54 found that approximately 2 x 10' 

molecules of ozone per bacteri um killed 50 percent 

of the cells of E. coli and that the primary effect 

was on the cell membrane. Elford and van den 

Ende 76 reported that ozone at 390 Ng/m3 (0.2 ppm) 

had a lethal effect on some bacteria deposited from 

aerosol mists on various surfaces. Relative 

humidity is an important factor, particularly when 

ozone concentration is low. They found little death 

at a humidity below 45 percent at ozone 

concentrations of 1960/jg/m 3 (1 ppm), as opposed 

to a 90-percent kill in 30 minutes at 40 Ng/m 3 

(0.025 ppm) ozone with a humidity of around 70 

percent. A 5-min exposure of Bacillus cereus to 

ozone at 0.12 mg/liter was the minimal lethal 

dose, whereas 0.10 mg/liter was effective for B. 

megaterium and E. coli. 62Spores of the Bacillus sp. 

were killed by ozone at 2.29 mg/liter. In most of the 

research studying the effects of ozone on lower 

organisms, ozone has been used as a germicide or 

as part of an attempt to understand the 

interactions of pollutants and pathogens on higher 

plant response. 

SUMMARY 

Oxidant injury to vegetation was first identified 

in 1944 in the Los Angeles Basin. Our 

understanding of oxidant effects and of the 

widespread nature of their occurrence has 

increased steadily since then. Although the major 

phytotoxic components of the photochemical 

oxidant compiex are ozone and peroxyacetyl nitrate 

(PAN), some data suggest that other 

phytotoxicants are also present. The 

peroxyacylnitrates are the most phytotoxic of the 

known photochemical oxidants; however, the 

ubiquitous nature of ozone and its association with 

widespread injury to vegetation make it the most 

281 
important phytotoxic component of the 

photochemical oxidant complex 

The effects of photochemical oxidants on 

vascular plants can be envisioned as occurring at 

several levels, ranging from the subcellular to the 

organismal, depending on the concentration and 

duration of exposure to the pollutant, and on the 

elapsed time after exposure that effects are 

observed. 

The earliest effect is an increase in cell 

membrane permeability. Cellular and biochemical 

changes are ultimately expressed on the 

organismic level in visible foliar injury, increased 

leaf drop, reduced plant vigor, reduced plant 

growth, and death. In the final analysis, 

biochemical modifications on an individual plant 

level are manifested by changes in plant 

communities and then in whole ecosystems. 

Leaf stomata are the principal plant entry sites 

for ozone and PAN. Oxidants affect such 

physiologic processes as photosynthesis, 

respiration, transpiration, stomatal opening, 

metabolic pools, biochemical pathways, and 

enzyme systems. 

Visible injury is identifiable as pigmented, 

chlorotic, or necrotic foliar patterns Metabolic 

cellular disturbances can occur without visible 

injury and may be reversible However, mostofthe 

growth effects reported until recently were 

associated with visible injury. 

Classic ozone injury is demonstrated by the 

upper-surface leaf fleck on tobacco and the leaf 

stipple of grape. Many plants show an uppersurface response with no associated injury to the 

lower surface of leaves However, in 

monocotyledonous plants such as grasses or 

cereals, and some nonmonocotyledonous plants, 

the mesophyll tissue is not divided, and bifacial 

necrotic spotting (flecking) is a common symptom 

of ozone injury. 

Coniferous trees exhibit different symptoms. 

Ozone is probably the cause of emergence tipburn 

in eastern white pine (white pine needle dieback) 

and chlorotic decline, a needle injury of ponderosa 

pine. 

Classic PAN injury appears as a glaze followed 

by bronzing of the lower leaf surface of many 

plants Complete collapse of leaf tissue can occur if 

concentrations are sufficiently high. Early leaf 

senescence and abscission usually follow the 

chronic response symptoms. Chronic injury 

patterns generally are not characteristic and may 

be confused with symptoms caused by biotic 

diseases, insect infestation, nutritional disorders, 

or other environmental stresses. 

A great deal of research has been done to define 

the effects of oxidants on plant growth and yield 

more accurately Studies comparing the growth of 

plants in filtered and nonfiltered field chambers 

using oxidants in the ambient air have reported up 

to 50-percent decreases in citrus yield (orange and 

lemon); 10 to 15 percent supression in grape yield 

in the first year, and 50 to 60 percent reduction 

over the following 2 years; and a 5 to 29 percent 

decrease in yield of cotton lint and seed in 

California Losses of 50 percent in some sensitive 

potato, tobacco, and soybean cultivars have been 

reported in the eastern United States. It is apparent 

that oxidants in the ambient air reduce yields of 

many sensitive plant cultivars. 

Experimental chambers with controlled 

environments have been used to study both shortterm and long-term effects of exposure to ozone 

(Tables 1 1-2 and 1 1-4). Multiple acute exposures 

(785 pg/m 3 , or 0.40 ppm) of radishes for 1.5 hr 

resulted in reductions in root growth. The 

reductions in root growth from the multiple ozone 

exposures were equal to the additive effects of 

three single exposures. When soybean plants 

were exposed to 1468 Ng/m 3 (0.75 ppm) ozone for 

1 hr, root growth was consistently reduced more 

than top growth. There was also a reduction in 

nodule weight and number The greater reduction 

of root growth than top growth is related to the 

transport of photosynthate. Ozone also affects the 

process of nitrogen fixation in clover, soybean, and 

pinto bean through reduction in nodule number, 

but neither nodule size nor efficiency of nitrogen 

fixation is influenced. The effect of ozone on the 

nitrogen fixation process in legumes, if 

widespread, could have a major impact on plant 

communities and affect fertilizer requirements. 

There are indications that the effect of ozone on 

nodulation may be related to carbohydrate supply 

in host plants. 

Experimental long-term exposures of a variety of 

crops as well as ornamental and native plants to 

ozone have resulted in a reduction in growth 

and/or yield. Throughout a growing season, 14 

species representative of the aspen plant community were exposed to ambient air (98 to 137 μg/m 3 

ozone, or 0.05 and 0.07 ppm) and to ozone (290 and 

588μg/m 3 or 0.15 and 0.30 ppm) for 3 hr/day, 5 

days/week, and to charcoal-filtered air. Foliar 

injury to all species resulted at the highest pollution 

concentration. The growth of two soybean cultivars 

282 
(Hood and Dare) was inhibited by intermittent 

exposure to ozone at 196μg/m3 (0.10 ppm) for 3 

weeks. Growth of both root and top was decreased. 

Similar results were noted with radish, except that 

a lower concentration (98 μg/m 3 or 0.05 ppm) 

inhibited growth. In the aforementioned studies, 

the reduced growth occurred even though there 

were very few visible symptoms of plant injury. 

A reduction of 30 percent in the yield of wheat 

occurred when, at anthesis, wheat was exposed to 

ozone at 392 μg/m 3 (0.2 ppm), 4 hr/day for 7 days. 

A significant reduction in the yield of tomato was 

noted when plants were experimentally treated 

with ozone at 686 μg/m 3 (0.35 ppm). Lower fruit 

set and fewer harvested fruit caused the reduction. 

Chronic exposures to ozone at 98 to 290 μg/m 3 

(0.05 to 0.15 ppm) for 4 to 6 hr/day produced 

reductions in yield in soybean and corn grown 

under field conditions. The threshold for measurable effects for ozone appears to be between 98 

and 196 μg/m 3 (0.05 to 0.10 ppm) for sensitive 

plant cultivars. This is well within the range of 

ozone levels monitored in the eastern United 

States Growth or flowering effects were reported 

for carnation, geranium, radish, and pinto bean 

grown in greenhouse chambers exposed to ozone 

at 98 to 294 μg/m 3 (0 05 to 0.15 ppm) for 2 to 24 

hr/day 

The two most critical factors in determining plant 

response to air pollution are duration of exposure 

and concentration of pollutants. These two factors 

describe exposure dose. In determining the response of vegetation to oxidants, concentration is 

more important than time. Any given dose presented to a plant in a short period of time lias a 

greater effect than the same dose applied over a 

longer period 

The concept of limiting values was used by 

Jacobson to define the boundary between doses of 

a pollutant that are likely to cause measurable 

foliar injury to vegetation and those that are not. 

Foliar injury was used as the index of plant response. The ranges for limiting values for effects of 

ozone are. 

1 . Trees and shrubs. 

400 to 1 000 Ng/m 3 (0.2 to 0.51 ppm) for 1 

hr 

200 to 500 ,Ug/m 3 (0.1 to 0.251 ppm) for 2 

hr 

120 to 340 Ng/m 3 (0.06 to 0.17 ppm) for 4 

hr 

2. Agricultural crops: 

400 to 800 Ng/m 3 (0.2 to 0.41 ppm) for 0.5 

hr 

200 to 500 Ng/m 3 (0.1 to 0.251 ppm) for 1 

hr 

75 to 180 /ag/m3 (0.04 to 0.09 ppm) for 4 hr 

The range of limiting values for PAN is: 

1000 Ng/m 3 (0.2 ppm) for 0.5 hr 

500 Ng/m 3 (0.1 ppm) for 1 hr 

175 Ng/m 3 (0.035 ppm) for 4 hr 

Doses of ozone or PAN greater than the upper 

limiting values are likely to cause foliar injury. 

The data points used to determine the limiting 

values listed above are not necessarily threshold 

values but were based on available published 

research data. More than 200 studies were 

surveyed. Any limitations that were present in the 

experimental techniq'Ctes used in the studies are 

expressed in the data points. Another constraint of 

the PAN data is the limited number of studies. 

Plant sensitivity to ozone and PAN is conditioned 

by many factors. Genetic diversity in sensitivity to 

ozone between species and cultivars within a 

species is well documented. Variants in sensitivity 

to ozone within a natural species are well known 

for several pine species, including white, loblolly, 

and ponderosa. Plant sensitivity to oxidants can be 

changed by both climatic and edaphic factors. A 

change in environmental conditions can initiate a 

change in sensitivity at once, but it will be 3 to 5 

days before the response of the plant is totally 

modified. Plants generally are more sensitive to 

ozone when grown under short photoperiods, 

medium light conditions, medium temperature, 

high humidity, and high soil moisture. Injury from 

PAN may increase with increasing light intensity. 

Conditions during exposure and growth affect the 

response of plants to oxidants in similar ways. In 

general, environmental conditions optimum for 

plant growth tend to increase the sensitivity to 

ozone. At the time of exposure, factors that 

increase water stress tend to make plants more 

tolerant to ozone. Soil moisture is probably the 

most important environmental factor that affects 

plant response to oxidants during the normal 

growing season. Physiologic age affects the 

response of the leaf to oxidants. Young leaf tissue 

is most sensitive to PAN, whereas newly 

expanding and maturing tissue is most sensitive to 

ozone. Light is required for plant tissue to respond 

to PAN; a similar light requirement is not needed 

for plants to respond to ozone. 

The majority of effects observed, such as 

suppression of root growth, mineral uptake, and 

nitrogen fixation, apparently result from a 

283 
suppression in photosynthesls and modlfications 

in photosynthate dlstribution. This suppression In 

metabolic reserves ultimately slows plant growth 

and renders the plant more sensitive to other 

stresses. Physiologlcal changes can provlde a 

sensitive means of monitoring the health and vlgor 

of the plant with or without visual injury. Ozone 

affects pollen germinatlon in some specles and 

may affect yield through incomplete polllnation of 

flowers. Investigations wlth Arabidopsis thaliana 

showed no mutagenic effects from ozone over 

seven generatlons. 

Mixtures of pollutants can cause effects below 

the levels caused by either gas alone; however, 

there Is some dlsagreement concerning ozone 

Interactions with other gases. Ratios of gas 

mixtures, intermittent exposures, sequential 

exposures to pollutants, and predisposition by one 

pollutant to the effects of a second pollutant may 

be important in nature, but insufficient knowledge 

Is available to elucidate the effects. 

The response of plants to oxldants may be 

conditioned by the presence or absence of biotic 

pathogens. Depending on the plant and the 

pathogen, oxidants may cause more or less injury 

to a given specles. Oxidant injury to ponderosa 

pine predlsposes the trees to later invasion by bark 

beetles. Ozone and ozone-sulfur dioxide mlxtures 

can decrease the populatlon of some plantparasitic nematodes. Variable plant responses 

have been noted when herbicldes were used in the 

presence of high oxidant concentrations. 

Little research on the effects of oxldants on 

ferns, nonvascular green plants, and 

microorganisms has been reported. Lichens and 

mosses are responslve to acid gases, but there is 

no definite evidence that they respond to oxidants. 

Ferns may be especially sensitive, but thelr Injury 

response Is different from that of higher vascular 

plants. Growth and sporulation of fungl on 

surfaces are usually, but not always, affected. 

Ozone from 0.1 to several milligrams per liter of 

solutlon is requlred to kill many mlcroorganisms in 

Ilquid media. Most work with microorganisms has 

been done to study the effectiveness of ozone as a 

biocide in the storage of vegetation or treatment of 

water or sewage supplies. 

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23, 1975 ozone, ozonated hexene-1 and ambient air of 

106 Heagle, A S Interactions between air pollutants and metropolitan areas Int J Air Water Pollut 8.1-10, 

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1973 124. Heggestad, H E, and H A Menser Leaf spot-sensitive 

107 Heagle, A. S Response of three obligate parasites to tobacco strain Bel W-3, a biological indicator of the air 

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108 Heagle, A. S, D. E Body, and W W Heck An open-top 125 Heggestad, H E, and J T Middleton Ozone in high 

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109 Heagle,A S,D E Body,andG E Neely Injuryandyield 126 Hibben, C R Ozone toxic;ty to sugar maple. 

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sulfur dioxide in the field Phytopathology 64 132-136, 127 Hibben, C R Sensitivity of fungal spores to sulphur 

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112 Heagle, A S, W W Heck, and D. Body Ozone injury to Informative Report No 1, Air Pollution Control 

plants as influenced by air velocity during exposure Association, Pittsburgh, Pa , 1970 pp B1 -B22 

Phytopathology 61 1209-1212, 1971 130. Hill, A C, and N Littlefield Ozone Effect on apparent 

113 Heath, R L Ozone. /n Response of Plants to Air photosynthesis, rate of transpiration, and stomatal 

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Press, Inc , N Y, 1975 pp 23-55 131 Hill, A C, M R. Pack, M Treshow, R J Downs, and L G 

114 Heck, W. W Factors influencing expression of oxidant Transtrum Plant injury induced by ozone 

damage to plants Annu Rev. Phytopathol 6 165-188, Phytopathology 51 356-363, 1961 

1968 132 Hindawi, I J.,andA P Altshuller Plantdamagecaused 

115 Heck, W. W Plant injury induced by photochemical by irradiation of aldehydes Science 146.540-542, 

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116 Heck, W. W The use of plants as indicators of air bean and petunia leaves exposed to irradiated auto 

nollution. Air Water Pollut 10 99-11 1, 1966 exhaust Phytopathology 55 27-30, 1965 

117 Heck, W W, and C S Brandt Effects on vegetation 134 Hodges, G H, H A Menser, Jr, , and W B Ogden 

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Academic Press, Inc , N Y., 1978 pp 157-229 135. Hodgson, R H Alteration of triazine metabolism by 

118 Heck, W. W, R H Daines, and I J Hindawi Other ozone Paper No 28, presented at the Weed Science 

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138 Hoffman, G J, E V Mass, and S L Rawlins Salinity- Exposure to Ozone and PAN CAES Publication No 288- 

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139 Hoffman, G J, E V Mass, and S L Rawlins Salinity- 158 Kohut, R. J The Interaction of 03 and PAN on Hybrid 

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140 Houston, D A Response of selected Pinus strobus L Environmental Studies, University Park, Pa., 1975. 

clones to fumigations with sulfur dioxide and ozone 159 Kohut, R J, S. V Krupa, and F. Russo An open-topfield 

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141 Howell, R K, T E Devine, and C H Hanson Resistance soybean yields Proc. Am Phytopathol Soc 4 25, 1977. 

of selected alfalfa strains to ozone Crop Sci 11.114- 160 Koritz, H G,and F W Went The physiological action of 

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142 Howell, R K, and D F Kremer Ozone injury,to soybean studies Plant Physiol 28 50-62, 1953 

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143 Howell, R K, and C A Thomas Relative tolerances of Exposure to Ozone and PAN CAES,Publication No 259- 

twelve safflower cultivars to ozone Plant Dis Rep 56 272, Pennsylvania State University, Center for Air 

195-197, 1972 Environment Studies, University Park, Pa , 1972 

144 Hull, H H, and F W Went Life processes of plants as 162 Kuss, F R The Effect of Ozone on Fungus Sporulation 

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128 vegetation in Pennsylvania CAES Publication No 209- 

145 Jacobson, J S The effects of photochemical oxidants 71, Pennsylvania State University, Center for Air 

on vegetation /n Ozone und Begleitsubstanzen im Environment Studies, University Park, Pa 1971 

photochemischen Smog VDI Ber (270) 163-173, 1977 164 Lacasse, N L, and T C Weidensaul A cooperative 

146 Jacobson, J S and L J Colavito The combined effect of extension-based system of assessing air pollution 

sulfur dioxide and ozone on bean and tobacco plants. damage to vegetation. Organization, results and 

Environ Exp Bot 16 277-285, 1976 recommendations for future surveys fn Proceedings of 

147 Jensen, K F Response of nine forest tree species to the Second International Clean Air Congress. H. M 

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148 Jensen, K F, and L S Dochinger Responses of hybrid 165. Landau, E., and C S Brandt The use of surveys to 

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149 Juhren, M, W Noble, and F W Went The 166 Larsen, R I, and W W Heck An air quality data 

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150 Kadota, M, and K Ohta Ozone sensitivity of Japanese transport of ozone and ozone precursors Proc Am 

plant species in summer, with special reference to a Phytopathol Soc. 4.31, 1977 

tentative sensitivity grade list for applying tofield survey 168 Ledbetter, M C, P W Zimmerman, and A E Hitchcock 

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151 Kanoh, F Ozone reaction on slime mold Tokyo Toritsu Contrib Boyce Thompson Inst 20 275-282, 1959 

Eisei Kenyusho Kenkyu Nempo 24 337-342, 1972 169 Leone, I A, and E Brennan Ozone toxicity in tomato as 

152 Karnosky, D F Threshold levels for foliar injury to modified by phosphorus nutrition Phytopathology 

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J For Res 6 166-169, 1976 170 LEone, I. A, E Brennan, and R H Daines Effect of 

153 Khatamian, H, N 0 Adedipe, and D P Ormrod Soil- nitrogen nutrition on the response of tobacco to ozone in 

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154 Kinman, R N Water and wastewater disinfection with 171 Linzon, S N Ozone damage and semimature-tissue 

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155 Klingaman, G L, and C B Link Reduction in air 172 Linzon, S N Semimature-tissue Needle Blight of 

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156 Kochhar, M Phytotoxic and Competitive Effects of Tall the possible cause and origin of white pine needle 

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175 Maas, E. V., G J Hoffman, S. L Rawlins, and G Ogata 

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177 Macdowall, F D H Stages of ozone damage to 

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178 Macdowall, F D H, and A F W Cole Threshold and 

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179 Macdowall, F D H, E I Mukammal, and A F W. Cole 

Direct correlation of air-polluting ozone and tobacco 

weather fleck Can J Plant Sci 44 410-417, 1964 

180 MacKnight, M L The Effect of Ozone on Stomatal 

Aperture and Transpiration M A thesis, University of 

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181 Magie, R 0 Controlling gladiolus botrytis bud rot with 

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182 Manning, W J, W A Feder, P M. Papia, and I Perkins 

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183 Manning, W J, W A Feder,andl.Perkins Responseof 

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184 Manning, W J, W A Feder, and I Perkins Sensitivity 

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185 Mansfield, T/ The role of stomata in determining the 

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186 Markowski, A and S Grzesiak Influence of sulphur 

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187 Matsushima, J On composite harm to plants by 

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188 McCarthy, J J, and C H Smith. A review of ozone and 

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189 McCune, D C On the Establishment of Air Quality 

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3, American Petroleum Institute, N Y, 1969 

190 Mcllvenn, W D, R A Spotts, and D D. Davis The 

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191 Menser, H A, and H E Heggestad Ozone and sulfur 

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192 Menser, H A, H E Heggestad, and 0 E Street. 

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193 Menser, H A, H E Heggestad, 0 E Street, and R N 

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194 Menser, H A, Jr , and G H Hodges Effects of air 

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195 Menser, H A, Jr, , G H Hodges, and C G McKee 

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196 Menser, H A, Jr , and 0 E Street Effects of air 

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197 Middleton, J T Photochemical air pollution damage ~ to 

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198 Middleton,J T Responseof plants to air pollution J Air 

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199 Middleton, J. T., A S Crafts, R F Brewer, and 0 C 

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200 Middleton, J T, E F Darley, and R F Brewer Damage 

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201 Middleton, J T., J B Kendrick, Jr , and E F Darley Air 

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203 Middleton, J T, J B Kendrick, Jr., and H W Schwalm 

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204 Middleton, J T, and A 0 Paulus The identificat on and 

distribution of air pollutants through plant reponse 

AMA Arch Ind Health 14 526-532, 1956 

205 Millecan, A A A Survey and Assessment of Air 

Pollution Damage to California Vegetation in 1970 

APTD-0694, U S Environmental Protection Agency, Air 

Pollution Control Office, Research Triangle Park, N C, 

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206 Miller, P R Susceptibility to ozone of selected western 

(US) conifers For Abstr 36(4) 2095, 1975 

207 Miller, P R, F W Cobb, Jr , and E Zavarin 

Photochemical oxidant injury and bark beetle 

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III Effect of injury upon oleoresin composition, phloem 

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208. MiIler, V L, R K Howell, and B E Caldwell Relative 

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209 Miller, P R, and A A Millecan Extent of oxidant air 

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210 Miller, P R, J R Parmeter, Jr , B H Flick and C W 

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211 Miller,P R,andS Rich Ozone damage on apples Plant 

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212 Mudd, J B, and T T Kozlowski, eds Responses of Ozone Dosage-Crop Loss Conversion Function State of 

Plants to Air Pollution Academic Press, Inc , N Y, 1975 California, Department of Food and Agriculture, 

213 Mukammal, E I Ozone as a cause of tobacco injury Sacramento, Calif , June 1974 

Agric Meteorol 2 145-165, 1965 229 Oshima, R J Effect of ozone on a commercial sweet 

214 Naegele, J A, W A Feder, and C J Brandt corn variety Plant Dis Rep 57 719-723, 1973 

Assessment of Air Pollution Damage to Vegetation in 230 Oshima, R.J., M P Poe, P K Braegelmann, D W 

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215 Nakamura, H, and S Matsunaka Indicator plantsforair Control Assoc 26 861-865, 1976 

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photochemical oxidants Varietal difference and effect Baldwin Effect of ozone on a commercial variety of 

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43 517-522, 1974 232 Oshima, R, 0 C Taylor, and E A Cardiff Possible new 

216 NationalAir Pollution Control Administration Effectsof toxicant indicated in severe air pollution episode in 

photochemical oxidants on vegetation and certain South Coast Basin Calif Agric 28 12-13, 1974 

microorganisms /n Air Quality Criteria for 233 Otto, H W, and R H Daines Plant intury by air 

Photochemical Oxidants NAPCA Publication No AP- pollutants Influence of humidity on stomatal and plant 

63, U S. Department of Health, Education, and Welfare, response to ozone Science 163 1 209-1 210, 1969 

Public Health Service, Washington, D C, March 1970 234 Parmeter, J R, Jr , R V Bega, and T Neff A chlorotic 

pp 6-1 - 6-23 dechne of ponderosa pine in southern California Plant 

217 National Research Council Ozone and Other Dis Rep 46 269-273, 1962 

Photochemical Oxidants Washington, D C, National 235 Parmeter, J R, Jr , and P R Miller Studies relating to 

Academy of Sciences, 1977 pp 437-585 the cause of decline and death of ponderosa pine in 

218 Neely, G E, D T Tingey, and R G Wilhour Effects of southern California Plant Dis Rep 52 707-71 1, 1968 

ozone and sulfur dioxide singly and in combination on 236 Pell, E J 1972 Survey and Assessment of Air Pollution 

yield, quality and N-fixation of alfalfa /n International Damage to Vegetation in New Jersey EPA-R5-73-022, 

Conference on Photochemical Oxidant Pollution and Its U S Environmental Protection Agency, Research 

Control. Proceedings Volume II B Dimitriades, ed Triangle Park, N C, June 1973 

EPA-600/3-77-001b, US Environmental Protection 237 Pell, E J, and E Brennan Economic impact of air 

Agency, Research Triangle Park, N C, January 1977 pollution on vegetation in New Jersey and an 

pp 663-673 interpretation of its annual variabtlity Environ Pollut 

219 Noble, W Air pollution effects Pattern of damage 8 23-33, 1975 

produced on vegetation by smog J Agric Food Chem 238 Photochemical Air Pollution Formation, Transport, and 

3 330-332, 1955 Effects Environmental Secretariat Publication No 

220 Noble,W Smog damage to plants Lasca Leaves 15 2-4, NRCC 14096, National Research Council of Canada, 

1965 Associate Committee on Scientific Criteria for 

221 Noble, W M, and L A Wright Air pollution with Environmental Quality, Ottawa, Canada, 1975 

relation to agronomic crops 11 A bio-assay approach to 239 Price, H, and M Treshow Effects of ozone on the 

the study of air pollution Agron J 50 551 -553, 1958 growth and reproduction of grasses /n Proceedings of 

222 Oertli, J J Effect of salinity on susceptibility 'of the International Clean Air Conference Clean Air 

sunflower plants to smog Soil Sci 87 249-251, 1959 Conference, National Science Centre, Victoria, 

223 Ogata, G, and E V Maas Interactive effects of salinity Australia, 1972 pp 275-280 

and ozone on growth and yield of garden beet J 240 Rabotnova, I L, V S Somov, T S Bobkova, I V 

Environ Qual 2 518-520, 1973 Zlochevskaya, L N Checkunova, I F Knyazeva, and S 1 

224 Ordin, L, M J Garber, and J I Kindinger Effect of 2,4- Belen 'Kii Toxic action of ozone on yeasts as a function 

dichlorophenoxy acetic acid on growth and on /3-glucan of some components and pH of the medium Vestn 

synthetases of peroxyacetyl nitrate pretreated Avena Mosk Univ Biol Pochvoved 26 47-51, 1971 

coleoptile sections Physiol Plant 26 17-23, 1972 241 Reinert, R A Monitoring, detecting, and effects of air 

225 Ormrod, D P, N 0 Adedipe, and G Hofstra Ozone pollutants on horticultural crops Sensitivity of genera 

effects on growth of radish plants as influenced by and species Hort Sci 10 495-500, 1975 

nitrogen and phosphorus nutrition and by temperature 242 Reinert, R A, A S Heagle, and W W Heck Plant 

Plant Soil 38437-439, 1973 responses to pollutant combinations /n Responses of 

226 Ormrod, D P, N 0 Adedipe, and G Hofstra Responses Plants to Air Pollution B Mudd andT T Kozlowski, eds 

of cucumber, onion, and potato cultivars to ozone Can Academic Press, Inc , N Y, 1975 pp 159-177 

J Plant Sci 51 283-288, 1971 243 Reinert, R A, A S Heagle, J R Miller, and W R 

227 Oshima, R J Development of a System for Evaluating Geckeler Field studies of air pollution injury to 

and Reporting Economic Crop Losses Caused by Air vegetation in Cincinnati, Ohio Plant Dis Rep 54 8-11, 

Pollution in California l Quality Study State of 1970 

California, Department of Food and Agriculture, 244 Reinert, R A, D T Tingey, and H B Carter Ozone 

Sacramento, Calif , July 1973- induced foliar injury in lettuce and radish cultivars J 

228 Oshima, R J Development of a System for Evaluating Am Soc Hort Sci 97 711-714, 1972 

and Reporting Economic Crop Losses Caused by Air 245 Reinert, R A, D T Tingey, W W Heck, and C Wickliff 

Pollution in California lI Yield Study IIA Prototype Tobacco growth influenced by concentrations of sulfur 

290 
dioxide and ozone Agron Abstr 61 34, 1969 263 Stanford Research Institute The Smog Probletn in Los 

246 Reinert, R A, D T Tingey, and C E Koons The early Angeles County A Report by Stanford Research 

growth of soybean as influenced byozone stress Agron Institute on the Nature and Causes of Smog Western 

Abstr 63 148, 1971 Oil and Gas Association, Los Angeles, Calif January 

247 Rich, S, G S Taylor, and H Tomlinson Cropdamaging 1954 

periods of ambient ozone in Connecticut Plant Dis Rep 264 Stark, R W, P R Miller, F W Cobb, Jr, , D L Wood, and 

53 969-973, 1969 J R Parmeter, Jr Photochemical oxidant intury and 

248 Rich, S., and H Tomlinson Effects of ozone on bark beetle (Coleoptera Scolytidae) infestation of 

conidiophores and conidia of Alternaria solani ponderosa pine I Incidence of bark beetle infestation in 

Phytopathology 58 444-446, 1968 injured trees Hilgardia 39 121-126, 1968 

249 Rich, S, and N C Turner Importance of moisture on 265 Starkey, T D The Influence of Peroxyacetyl Nitrate on 

stomatal behavior of plants subtected to ozone J Air Bean (Phaseolus vulgaris L) Subtected to PostPollut Control Assoc 22 718-721, 1972 Exposure Water Stress CAES Publication No 400-75, 

250 Richards, B L, J T Middleton, and W B Hewitt Air Pennsylvania State University, Center for Air 

pollution with relation to agronomic crops V Oxidant Environment Studies, University Park, Pa , 1975 

stipple of grape Agron J 50 559-561, 1958 266 Stephens, E R, E F Darley, 0 C Taylor, and W E 

251 Ridley, J D, and E T Sims, Jr Preliminary Scott Photochemical reaction products in air pollution 

Investigations on the Use of Ozone to Extend the Shelf- Int J Air Water Poliut 4 79-100, 1961 

Life and Maintain the Market Quality of Peaches and 267 Taylor, G S Ozone intury on Bel W-3 tobacco controlled 

Strawberries South Carolina Agricultural Experiment by at least two genes Phytopathology 58 1069, 1968 

Station Research Series No 70, Clemson University, 268 Taylor, G S, H G DeRoo, and P E Waggoner Moisture 

Clemson, S C, January 1966 and fleck of tobacco Tob Sci 4 62-68, 1960 

252 Ripaldi, C P, and E Brennan Effect of ozone on 269 Taylor,0 C Effects of oxidantair pollutants J Occupat 

phosphorus levels of pinto bean stems and foliage Med 10(2) 485-492, September 1968 

Phytopathology 63 206, 1973 270 Taylor, 0 C Importance of peroxyacetyl nitrate (PAN)as 

253 Santamour, F S, Jr Air pollution studies on Plantanus a phytotoxic air poilutant J Air Pollut Control Assoc 

and American elm seedlings Plant Dis Rep 53 482- 19 347-351, 1969 

484, 1969 271 Taylor, 0 C, E A Cardiff, J D Mersereau, and J T 

254 Scott, D B M, and E C Lesher Effect of ozone on Middleton Effect of air-borne reaction products of 

survival and permeability of Escherichia coli J ozoneand 1 -n-hexene vapor (synthetic smog) on growth 

Bacteriol 85 567-576, 1963 of avocado seedlings Proc Am Soc Hort Sci 71 320- 

255 Seidman, G, I J Hindawi, and W W Heck 325, 1958 

Environmental conditions affecting the use of plants as 272 Taylor, 0 C, and D C MacLean Nitrogen oxides and 

indicators of air pollution J Air Pollut Control Assoc the peroxyacyl nitrates /n Recognition of Air Pollution 

15 168-170, 1965 Intury to Vegetation A Pictorial Atlas J S Jacobson 

256 Shannon, J G, and C L Mulchi Ozone damage to and A C Hill, eds Informative Report No 1, Air 

wheat varieties at anthesis Crop Sci 14 335-337, Pollution Control Association, Pittsburgh, Pa , 1970 pp 

1974 E1-E14 

257 Shinohara, T, S Kuroda, T Kitamura, and K Kunisawa 273 Thomas, M D Effects of air pollution on plants Air 

Studies on weather fleck on tobacco leaves VI Effects Pollution Worid Health Organization Monograph Series 

of temperature on the fleck inlury induced by air-borne No 46, Columbia University Press, NewYork, 1961 pp 

oxidants Okayama Tabako Shikenlo Hokoku 33 51-54, 233-278 

1973 274 Thomas, M D, R H Hendricks, and G R Hill Some 

258 Shinohara, T, Y Yamamoto, H Kitano, and M Fukuda impurities in the air and their effects on plants /n Air 

Interactions of light and ozone inlury in tobacco Nippon Pollution Proceedings of the United States Technical 

Sakumotsu Gakkai Kili 43 433-438, 1974 Conference on Air Pollution McGraw-Hill, Inc , N Y, 

259 Skelly, J M, C F Croghan and E M Hayes Oxidant 1952 pp 41 -47 

levels in remote mountainous areas of southwestern 275 Thompson, C R Personal communications Cited in 

Virginia and their effects on native white pine (Pinas Ozone and Other Photochemical Oxidants National 

strobus L) ln International Conference on Academyof Sciences, Washington, D C, 1977 pp 464- 

Photochemical Oxidant Pollution and its Control 465 

Proceedings Volume II B Dimitriades, ed EPA-600/3- 276 Thompson, W W, W M Dugger, Jr, , and R L Palmer 

77-001b, U S Environmental Protection Agency, Effects of ozone on the fine structure of the palisade 

Research Triangle Park, N C, January 1977 pp 61 1- parencY yma cells of bean leaves Can J Bot 44 1 677- 

620 1682, 1966 

260 Smith, D, and J P Silva Use of carbohydrate and 277 Thompson, C R, E Hensel, and G Kats Effects of 

nitrogen root reserves in the regrowth of alfalfa from photochemical air pollutants on Zinfandel grapes Hort 

greenhouse experiments under hght and dark Sci 4 222-224, 1969 

conditions Crop Sci 9 464-467, 1969 278 Thompson, C R, and G Kats Antioxidants reduce 

261 Smock, R M, and R D Watson Ozone in apple storage grape yield reductions from photochemical smog Calif 

Refrig Eng 42 97-101, 1941 Agric 24 12-13, 1970 

262 Spalding, D H Appearance and decay of strawberries, 279 Thompson, C R, and G Kats Eftects of ambient 

peaches, and lettuce treated with ozone U S Dept concentrations of peroxyacetyl nitrate on navel orange 

Agric Mark Res Rep (756) 1-11 , 1966 trees Environ Sci Technol 9 35-38, 1975 

291 
280 Thompson, C R, and 0 C Taylor Effects of air with ozonated hexene or ozone gas Physiol Plant 

poilutants on growth, leaf drop, fruit drop, and yield of 16 57-65, 1963 

citrus trees Environ Sci Technol 3 934-940, 1969 299 Townsend, A M, and L S Dochinger Relationship of 

281 Ting, I P., andW M Dugger,Jr Factors affecting ozone seed source and developmental stage to the ozone 

sensitivity and susceptibility of cotton plants J Air tolerance of Acer rubrum seedlings Atmos Environ 

Pollut Control Assoc 18 810-813, 1968 8 957-964, 1974 

282 Tingey, D T LettertoJ H B Garner,Criteria and Special 300 Treshow, M Environment and Plant Response 

Studies Office, HERL, U S Environmental Protection McGraw-Hill, Inc New York, 1970 

Agency, Research Triangle Park, N C, October 1976 301 Treshow, M Evaluation of vegetation injury as an air 

283 Tingey, D T Ozone induced alterations in plant growth pollution criteria J Air Pollut Control Assoc 15 266- 

and metabolism /n International Conference on 269, 1965 

Photochemical Oxidant Pollution and Its Control 302 van Haut, H, and H Stratmann Experimental Proceedings Volumell B Dimitriades,ed EPA-600/3- 

77-001b, US Environmental Protection Agency, 

investigations of the effectof nitrogen dioxide on plants 

Research Triangle Park, N C, January 1977 pp 601- 

Schriftenr LIB Landesanst Immissions 

609 

Bodenutzungsschutz Landes Nordheim Westfalen 

(F) 50-70, 1967 

284 Tingey, D T, and U Blum Effects of ozone on soybean 303 Verkroost, M. The effect of oione on photosynt,iesis and 

nodules J Environ Qual 2 341 -342, 1973 respiration of Scenedesmus obtusiusculus Chod with a 

285 Tingey, D T, J A Dunning, and G M Jividen Radish general discussion of effects of air pollutants in plants 

root growth reduced by acute ozone exposures /n Meded Landouwhogesch Wageningen 74 1-78, 

Proceedings of the Third International Clean Air 1974 

Congress Vereins Deutscher Ingenieur, Kommission 304 Walker, E K, and L S Vickery Infiuence of sprinkler 

Reinhaltungder Luft, Dusseldorf, 1973 pp A154-A156 irrigation on the incidence of weather fleck on flue286, Tingey, D T, R C Fites, and C Wickliff Foliar sensitivity cured tobacco in Ontario Can J Plant Sci 41 281 -287, 

of soybeans to ozone as related to several leaf 1961 

parameters Environ Pollut 4 183-192, 1973 305 Watson, R D Ozone as a Fungicide Ph D thesis, 287 Tingey, D T, W W Heck, and R A Reinert Effectof low Cornell University, Ithaca,N Y, 1942 

concentrations of ozone and sulfur dioxide on foliage, 

growth and yield of radish J Am Soc Hort Sci 306 Weaver, G M, and H 0 Jackson Relationship 

96 369-371 1971 between bronzing in wh te beans and phytotoxic levels 

288 Tingey,D T,W W Heck,andR A Reinert Reductionof of atmospheric ozone in Ontario Can. J Plant Sci 

radish yields by low concentrations of ozone and sulfur 48 561-568, 1968 

dioxide Hort Sci 4 189, 1969 307 Weber, D E Interactions of Plant-Parasitic Nematodes 

289 Tingey, D T, and A C Hill The occurrence of and Ozone and Sulfur Dioxide with Soybean and 

photochemicai phytotoxicants in the Salt Lake Valley Begonia Ph D thesis, North Carolina State University, 

Proc Utah Acad Sci Arts Lett 44 387-395, 1967 Raleigh, N C, 1976 

290 Tingey, D T, and R A Reinert The effect of ozone and 308 Weber, D-- The effects of ozone on plant-parasitic 

sulfur dioxide singly and in combination on plant nematodes and certain plant-microorganism 

growth Environ Pollut 9117-126, 1975 interaction /n International Conference on 

291 Tingey, D T, R A Reinert, and H B Carter Soybean Photochemical Oxidant Pollut on and Its Control 

cultivars. Acute foiiar response to ozone Crop Sci Proceedings Volume II B Dimitriades, ed EPA-600/3- 

12 268-270, 1962 77-001 b, U S Environmental Protection Agency, 

292 Tingey, D T, R A Reinert, J A Dunning, and W W Research Triangle Park, N C, January 1977 pp 621- 

Heck Foliar injury responses of eleven plant speciesto 631 

ozone/sulfur dioxide mixtures Atmos Environ 7 201 - 

309 Wilhour, R G The Influence of Ozone on White Ash 

208, 1973 CAES Publication No 188-71, Pennsylvania State 

293 Tingey, D T, R A Reinert, C W ickliff, and W W Heck University, Center for Air Environment Studies, 

Chronic ozone or sulfur dioxide exposures, or both, University Park, Pa , 1971 

affect the early vegetative growth of soybeans Can. J 310 Wilhour, R G, and G E Neely Growth response of 

Plant Sci 53 875-879, 1973 conifer seedlings to low ozone concentrations /n 

294 Tingey, D T, C Standley, and R W Field Stress International Conference on Photochemical Oxidant 

ethylene envolution A measure of ozone effects on Pollution and Its Controi Proceedings Volume II B 

plants Atmos Environ 10969-974, 1976 Dimitriades, ed EPA-600/3-77-001b, U S 

295 Tingey, D T, R G Wilhour, and C Standley The effect Environmental Protection Agency, Research Triangle 

of chronic ozone exposures on the metabolite contentof Park, N C, January 1977 pp 635-645 

ponderosa pine seedlings For Sci 22 234-241, 1976 311 Wood, F A, and J B Coppolino The influence ofozone 

296 Todd, G W Effect of ozone and ozonated 1-hexene on on deciduous forest tree species Mitt Forst 

respiration and photosynthesis of leaves Plant Physiol Bundesversuchsanst, Wien 97 233-253, 1972 

33 416-420, 1958 312 Wood, F A, and J B Coppolino The influence of ozone 

297 Todd, G W, and W N Arnold An evaluation of inethods on selected woody ornamentais Phytopathology 

used to determine inlury to plant leaves by air 61 133, 1971 

pollutants Bot Gaz (Chicago) 123 1 51-1 54, 1961 313 Wood, F A, and D B Drummond Response of eight 

298 Todd,G W,andB Probst Changesintranspirationand cultivars of chrysanthemum to peroxyacetyl nitrate 

photosynthetic rates of various leaves during treatment Phytopathology 64 897-898, 1974 

292 
314 Yarwood, C E, and J T Middleton Smog inlury and 

rust infection Plant Physiol 29 393-395, 1954 

315 Zobnina, V P, and E A Morkovina Effect of ozone on 

survival of carotinoid strain of Mycobacterium 

carothenum and its white mutant obtained with 

nitrosoguanidine Microbiology (Engl Transl ) 4079- 

81. 1971 

293 
12. ECOSYSTEMS 

INTRODUCTION 

The preceding chapters have dealt with the 

formation and chemistry of ozone and other 

oxidants and with the effects of oxidant/ozone on 

human health and on experimental plants and 

animals. In this chapter, the effects of oxidantpollutant stress on slmple and complex 

communities are discussed to illustrate that 

plants, animals, man, and the environment are 

interconnected and that the relatlonships between 

them are profoundly complex. 

Plants, animals, and mlcroorganisms usually do 

not live alone, but exist as populations. Populations 

live together and interact as communities. 

Commmunities, because of the interactions of 

their populations and of the individuals that 

constitute them, respond to pollutant stress 

differently from individuals. Man is an integral part 

of these communities, and as such, he is directly 

involved in the complex ecological Interactions 

that occur withln the communities and the 

ecosystem of which he is a part. 

The stresses placed on the communitles and the 

ecosystems in which they exist can be farreaching, since the changes that occur may be 

irreversible. For example, it has been suggested 

that the arid lands of India are the result of 

defoliation and elimination of vegetation that 

induced local climatic changes not conducive to 

the reestablishment of the original vegetation. 10 

An ecosystem (e.g., the planet Earth, a forest, a 

pond, an old field, or a fallen log) is a major 

ecological unit made up of living (biotic) and 

physical (ablotic) components through which the 

cycling of energy and nutrients occurs (Table 12- 

1). A structural relationship exists among the 

various components. The biotic units are linked 

together by functional interdependence, and the 

ablotic units make up all ofthe physical factors and 

chemical substances that interact with the biotic 

units. The processes occurring within the biotic 

and abiotic units and the interactions among them 

are subject to environmental influences. 9 

TABLE 12-1. COMPOSITION OF ECOSYSTEMS 

Component Description 

Biotic (biological) 

Individuals Plants, an mals (man), and microorganisms These are either producers, 

consumers, or decomposers 

Producers Green plants 

Consumers Herbivores, carnivores 

Decomposers Macroorganisms (mites, earthworms, 

millipedes, and slugs) and microorganisms (bacteria and fungi) 

Populations Groups of similar and related 

organisms 

Communities Interacting populations linked together 

by their responses to a common 

environment 

Abiotic (physical) 

Energy Radiation, light, temperature, and heat 

flow. 

Water Liquid, ice, etc 

Atmosphere Gases and wind 

Fire Combustion 

Topography Surface features 

Geological Soil, a complex system Nutrients. 

substratum 

Ecosystems tend to change with time, and 

sequential changes In the types of populations 

within a community are usually recognizable. 

Adaptation, adjustment, and evolution are 

constantly taking place as the biotic component, 

the populations, and the communities of living 

organisms interact with the abiotic component in 

the environment. The interaction and exchange of 

energy and nutrients over time result in sequential 

or, in some cases, cyclic or telescoped changes in 

populatlons and communities. The sequential 

replacement of one population by another in a 

continual serles, going from pioneer (first and less 

diversified) populationsto so-called climax(mature 

and more dlversified) communities, is termed 

11 succession." 9 Climax communities are 

structurally complex and more or less stable, and 

they are held in a steady state through the 

operation of a particular combination of blotic and 

abiotic factors. Man is often a factor, as for 

294 
example, when his grazing cattle maintain a 

pasture.s The disturbance or destruction of a 

climax community or ecosystem results in its being 

returned to a simpler stage."' 7z Existing studies 

indicate that changes occurring within 

ecosystems, in response to pollution or other 

disturbances, follow definite patterns that are 

similar even in different ecosystems. It istherefore 

possible to predict broadly the basic biotic 

responses to the disturbance of an ecosystem. zz,ss, ~o- ~ z These responses to disturbances 

are: 

1. Reduction in standing crop. 

2. Inhibition of growth or reduction in 

productivity. 

3. Differential kill (removal of sensitive 

organisms at the species and subspecies 

level). 

4. Food chain disruption. 

5. Successlonal setback. 

6. Changes in nutrient cycling rates. 

Organisms vary in their ability to withstand 

environmental changes. The ability of a population 

to withstand injury from polluted air, weather 

extremes, herbicides, or other disturbances 

depends on its range of tolerance—that is, the 

range of variation within whlch it can survive and 

function. The range of tolerance (also termed the 

"law of tolerance," Figure 12-1), differs because of 

inter- and intraspecific variations in susceptibility 

to injury by polluted air or other disturbances. 50 

The highly specialized populations (those with a 

narrow range of tolerance or adaptability) are 

either reduced in number or eliminated. 

Diversity and structure are most changed by 

pollution as a result of the elimination of sensitive 

species of flora and fauna and the selective 

removal of the larger overstory plants in favor of 

plants of small stature. 71 '72 The result is a shift from 

the complex forest community to the less complex, 

hardy shrub and herb communities. The opening of 

the forest canopy changes the environmental 

stresses on the forest floor, causing differential 

survival and, consequently, changed gene 

frequencles In subcanopy species. 

Associated with the reduction in diversity and 

structure is a shortening of food chains, a 

reduction in the total nutrient inventory, and a 

return to a simpler and less stable successional 

stage."'7z Jn addition, the pollutants act as 

predisposing agents, and an increase in the activity 

of insect pests and certain diseases occurs. 48'" It 

ZONE OF 

INTOLERANCE 

TOLERANCERANGE 

I ZONE OF 

ZONEOF ZONEOF INTOLERANCE 

PHYSIOLOGICAL RANGE OF OPTIMUM PHYSIOLOGICAL 

STRESS STRESS 

ORGANISMS 

INFREQUENT 

~ ~ 

'~ ~1i~, 

ORGANISMS 

INFREQUENT 

1 ~ ir 3 

ORGANISMS `" '— —~— -- ORGANISMS 

ABSENT GREATEST ABSENT 

ABUNDANCE 

Figure 12-1. Law of tolerance. 50 

295 
should be emphasized that ecosystems are usually 

subjected to a nu mber of stresses at the same ti me, 

not just to a single perturbation. 

Ecosystems are usually evaluated by modern 

man solely on the basis of their economic value to 

him. This economic value, in turn, depends on the 

extent to which man can manipulate the 

ecosystem for his own purpose. This singlepurpose point of view makes it dlfficult to explain 

the many benefits of a natural ecosystem to man"s 

welfare in terms of the conventional cost-benefit 

analysls. Gosselink et a1. 24 have, however, placed a 

value on a tidal marsh by assigning monetary 

values to the multiple contributions to man's 

welfare such as fish nurseries, food suppliers, and 

waste treatment functions of the marsh. They 

estimate the total social values to range from 

$50,000 to S80,000/acre. 

Westman 67 also evaluated the benefits of 

natural ecosystems by estimating the monetary 

costs associated with the loss of the free services 

(absorption of air pollution, regulation of global 

climate and radiation balance, and soil binding) 

provlded by the ecosystems. Westman estimated 

that the oxldant damage to the San Bernardino 

National Forest could result In a cost of $27 million 

per year(1973 dollars) for sedlment removal alone 

because of erosion as long as the forest remained 

in the early stages of succession. 

Estimates of the dollar values of such items as 

clean air and water, untamed wildllfe, .and 

wilderness (once regarded as priceless) are 

attempts to rationalize the activitles of 

civillzation. 67 When environmental decisions are 

made based on the cost of damaged ecosystems, it 

is usually assumed that the path chosen will be 

that which is most socially beneficial, as indicated 

by costs compared to beneflts. As Westman 67 

points out, certain corollaries accompany the 

assumption that decisions maximizing the benefit. 

cost ratios simultaneously optimize social equity 

and utility. These corollaries are - 

(1) The human species has the exclusive right to use and 

manipulate nature for its own purposes (2) Monetary 

units are sociaily acceptable as meansto equate the value 

of natural resources destroyed and those developed. (3) 

The value of services lost during the interval before the 

replacement or substitution of the usurped resource has 

occurred is included in the cost of the damaged resource 

(4) The amount of compensation in monetary units 

accurately reflects the full value of the loss to each loser in 

the transaction (5) The value of the item to future 

generations has been judged and included in an accurate 

way in the total value (6) The benefits of development 

accrue to the same sectors of society, and in the same 

proportions, as the sectors on whom the costs are levied, 

or acceptable compensation has been transferred Each of 

these assumptions, and others not listed, can and have 

been challenged 67 

In the case of corollary 4, for example, the losses 

incurred include species other than man, butthese 

losses are seldom, if ever, compensated. Also, the 

public at large is not usually consulted to 

determine whether the dollar compensation is 

adequate and acceptable. Frequently, there is no 

direct compensation. Corollary 5 can never be 

fulfilled because It is impoSsible to determine 

accurately the value to future generations. 

Evaluating the contribution of functioning 

natural ecosystems to human welfare is a very 

complex task and usually involves weighing both 

economic and human social values. However, 

because natural ecosystems are life support 

systems, their values should not be quantified in 

economic terms. 

With the passage of time, man has destroyed 

many of the naturally occurring ecosystems of 

which he was a part and has replaced them with 

simplified ecosystems wholly dependent on his 

care and protection and requlring a large input of 

energy. 5 o 

Man favors the simple, unstable and synthetic 

ecosystems, because when they are extensively 

managed and subsidized by the use of fossil fuels, 

they are highly productive. Productivity is the rate 

at which energy is stored by the photosynthetic 

activity of green plants. 9 ' 50 Young and successional ecosystems are more productive 

because they add biomass (accumulate energy) 

each year. An agricultural ecosystem 

(agroecosystem) is an example of such a slmplified 

ecosystem. Urban ecosystems, with their 

cultivated trees, shrubs, grasses, and flowers, are 

also examples of ecosystems simplified by man. 

The structural simplicity of these ecosystems (in 

many cases monocultures) makes them less 

resistant to environmental and disease stresses or 

to perturbations such as oxidant pollution. The 

greater diversity of a mature ecosystem retards the 

disruption of normal structure and function caused 

by any type of perturbation. For example, a forest 

ecosystem in which the communities are 

composed of many species would show less 

immediate damage by stress than successional 

stages having only a few species. Even greater 

damage would be anticipated in an agroecosystem, which may be considered the simplest 

of successional stages since often only a single 

producer species Is present. 

296 
GENERAL RESPONSES OF NATURAL AND 

AGROECOSYSTEMS TO STRE'SS BY 

OXIDANTS 

Agroecosystems 

Photochemical oxidant air pollutants have been 

recognized as a type of chronic pollution problem 

only during the last 20 to 25 years. The problem 

was first recognized in southern California, where 

it perhaps has had its greatest impact. Citrus 

groves and vineyards in the inland valleys of 

southern California are prime examples of stress to 

agroecosystems caused by chronic exposure to 

oxidants. 

Studies were initiated in 1960 on lemon and 

navel orange trees 58and in 1968 on wine grapes to 

determine the economic losses caused by oxidant 

pollutants. Both studies were conducted under 

field conditions for several years. The lemon and 

orange tree studies provided only a small amount 

of data that may be interpreted in an agroecosystem context because they were highly 

oriented toward the primary producer components,5a-so and no effort was made to examine 

the effects of oxidants on consumer components 

and decomposer organisms. The studies indicated 

that oxidant stress reduced water use and 

photosynthesis, increased leaf and fruit drop, and 

resulted in a severe reduction in the yield of 

marketable fruit. AII of these effects occurred 

without the development of plainly visible leaf 

symptoms. None of the above studies managed to 

distinguish the different effects of ozone and 

peroxyacetylnitrate (PAN) or its homologues in the 

photochemical oxidant mixtures; however, inferences drawn from these data suggest probable 

impact on the various components of these 

agroecosystems, particularly on the levels of 

consumer and decomposer populations. 

Accelerated leaf drop may influence the development of insect pests such as aphids, scale 

insects, and red citrus mites. Higher concentrations of amino acids or free sugars in injured 

leaves before abscission could result in an 

increase in pest populations or a diminution if 

leaves fall too rapidly. Leaf and fruit drop would 

provide an increased substrate for populations of 

decomposer organisms at the soil surface. 

Natural Ecosystems 

Natural ecosystems in California and in the 

Appalachian Mountains in the eastern United 

States have also suffered from oxidant pollution. 

THE APPALACHIAN MOUNTAINS 

In the eastern United States, a disease called 

emergence tipburn, found in eastern white pine, 

was related to ozone by Berry and Ripperton. 5The 

disease is characterized by bands of necrosis 

initiated in the semimature tissue of elongating 

needles and spreading to the needle tip. 

Under forest conditions, the affected trees occur 

randomly in the stand, and the same trees are 

injured repeatedly in a single season or in 

successive years. 4Only sensitive genotypes are 

affected, and these are gradually eliminated. 

Eastern white pine either forms pure stands or 

occurs in mixtures with other species in 

abandoned fields. Under these conditions, it is an 

important pioneertree. 65 1n established stands, it is 

a major component of 4 forest types and an 

associate in 14 other types and inhabits a range 

extending over 7 million acres, from the Lake 

States to the Appalachian Mountains. 65Berry4in 

1961 reported that post-emergence tipburn occurs 

throughout the natural range of this species. There 

is also evidence of a slow decline in tree vigor 

caused by the deterioration of feeder rootlets. 

Skelly et a1. 49in 1975 and 1976 also noted postemergence acute tipburn on white pine growing at 

three different sites along the Blue Ridge Parkway. 

High concentrations of ozone in the forested 

areas of the eastern United States cause severe 

injury to eastern white pine 3.as,ss and other forest 

species. Berry3reported levels of oxidant as high as 

230 /jg/m 3(0.12 ppm) at a mountaintop 

monitoring station inJune 1962. An air monitoring 

network operated by Virginia Polytechnic Institute 

and State University at three locations (the Blue 

Ridge Mountains, the Shenandoah Valley, and the 

southern Appalachians) recorded total oxidant 

peaks as high as 250 pg/m 3(0.13 ppm) during 

early July 1975, along with 43 hr of exposure at 

concentrations of 160 ug/m 3(0.08 ppm) or higher 

for 9 days. 22In June 1976, oxidant levels exceeded 

160 /ag/m3(0.08 ppm). After these episodes, 

significant increases in oxidant injury were 

observed (particularly in the Blue Ridge 

Mountains) involving three categories of eastern 

white pine: Those previously without symptoms, 

those with chlorotic mottle, and those exhibiting 

chlorotic dwarf symptoms. Such incidences 

suggest the need for more comprehensive studies 

of oxidant (and sulfur dioxide) effects in forests of 

the eastern United States. 

The oxidant peaks mentioned above were 

related to oxidant transport from urban areas to the 

297 
northeast (see Chapter 11, section on meteorological parameters). 

Studies by Davis and Wood' 5 suggest that other 

conifer species, in particular, Virginia pine and jack 

pine, may be more sensitive to ozone than eastern 

white pine. In addition, there is a synergistic 

interaction between low concentrations of ozone 

and sulfur dioxide that is the cause of the chlorotic 

dwarf disease of eastern white pine. 16 A study by 

Ellertsen et a1. 19 showed 10 percent mortality 

between 1956 and 1965 in dominant and codominant eastern white pines near an 

industrialized area that included several hundred 

square miles on the Cumberland Plateau. The 

combined effects of ozone and sulfur dioxide were 

considered responsible for the tree decline. 

Because eastern white pine represented only 5 

percent of the total wood volume available for 

harvest, the economic impact was slight. There 

was no effort to interpret pollutant effects in an 

ecosystem context. In the long run, the broader 

question to be addressed regards the effects of 

pollutant stress on all major ecosystem 

components, primarily on producers, consumers, 

and decomposers. An analysis of the multiple 

effects of oxidants on eastern forest ecosystems 

will present a much more adequate picture of the 

effects pollution is having on these forests. 

The studies to delineate the effects of oxidant 

episodes in the Appalachian Mountains are 

continuing. 

CALIFORNIA 

In southern California, the coastal chaparral 

ecosystem, dominated by chamise and manzanita 

or by woodla nd species ( including the live oaks and 

big cone spruce), and the coniferous forest 

ecosystems have received severe exposure. The 

desert ecosystems in the vicinity of mountain 

passes connecting the coastal and desert regions 

have also undoubtedly been expo5ed. 

Injury has been well documented only in the 

mixed-conifer forest ecosystem of the San 

Bernardino Mountains. Early symptoms of injury in 

conifer species were reported in a number of 

California national forests in 1970. 36 In the 

southern Sierra Nevada, Forest Service surveys 

made in 1974 69 have detected increased injury in 

ponderosa pine at many locations in the Sequoia 

National Forest, Sequoia National Park, and Kings 

Canyon National Park since 1970. Specific stands 

of mixed con ifer forest on the western slopes of the 

southern Sierra Nevada now appear to be affected 

by oxidants from the San Joaquin Valley. 35 The 

potential loss of timber growth in this area alone is 

a very serious prospect. 

A project is now underway ss,5s to determine in 

detail the effects of oxidant air pollutants on a 

mixed conifer forest ecosystem in southern 

California. The planning documents and early 

results from this study as described in the NAS 

document, Ozone and Other Photochemical 

Oxidants, 38 constitute the major source of 

information found in the remainder of this chapter. 

ORIGIN OF INJURIOUS CONCENTRATIONS 

OF OZONE AND OXIDANTS 

Advection from Urban Centers to Remote Areas 

in Southern California 

Descriptions of the vertical and horizontal 

distributions of photochemical smog in the Los 

Angeles Basin (southern coastal air basin) during 

typical summer days have been provided by 

Blumenthal et a1., 6 Edinger," Edinger et a1., 78 and 

Miller et a1. 34 Important observations to be drawn 

from their reports are the interactions of basin and 

mountain topography and local meteorology in 

determining the transport and concentrations of 

oxidant air pollutants in relation to elevational 

zones of vegetation. 

The marine temperature inversion layer that 

frequently forms above the heavily urbanized Los 

Angeles metropolitan area often extends inland as 

far as 144 km (90 miles), depending on season and 

time of day. Surface heating of air under the 

inversion increases with distance eastward in the 

basin and often disrupts the inversion by midmorning at its eastern edge. The northern rim of 

the basin is formed by the San Gabriel and San 

Bernardino Mountains, interrupted only by the 

Cajon Pass about 88 km (55 miles) inland (see 

Figure 12-2). The marine temperature inversion 

layer encounters the mountain slopes, usually 

below 1200 m(4000 ft). In the morning, the 

temperature inversion often remains intact at this 

juncture, and air pollutants are confined beneath 

it. Studies by Edinger" and Edinger et al.'a have 

described how the heated mountain slopes act to 

vent oxidant air pollutants over the crest of the 

mountains and cause the injection of pollutants 

into the stable inversion Iayer horizontally away 

from the slope. Oxidant concentrations within the 

inversion are not uniform, but occur in multiple 

layers and strong vertical gradients. In some cases, 

the inversion may serve as a reservoir for oxidants, 

298 
principally ozone, which may arrive at downwind 

locations along the mountain slopes relatively 

undiluted because of a lack of vertical mixing 

within the inversion layer and a lack of contact with 

ozone-destroying material generated at the 

ground. The important result of the trapping of 

oxidant In these layers is its prolonged contact with 

hlgh terrain at night. 

The most important effect of the interaction of 

pollutant and inversion layer at the heateci 

mountaln slope Is the vertical venting of oxidants 

over the mountain crest by upslope flow. A 

gradlent of oxidant concentrations or doses is 

established across distinct vegetation zones 

ordered along an elevatlonal gradient, i.e., the 

chaparral and conifer forest ecosystems that 

occupy the slopes and mountain terrain beyond the 

crest, respectively. The altitudinal sequence of 

these ecosystems is illustrated in Figure 12-3. 

According to Horton, 26 the chaparral zone is 

subdivided, from lower to higher elevations, into 

three subzones called the chamise, manzanita, 

and woodland chaparral; the mixed conifer forest 

occupies the mountain crest. 

The daytime changes in oxidant concentrations 

at several stations (A, B, C, and D in Figure 12-2) 

along the southern slope a nd at the crest of the San 

Bernardino Mountains is illustrated in Figure 12-4. 

In the late afternoon, the highest concentrations,in 

th i s profile were at 900 to 1200 m(3000 to 4000 ft) 

and adjacent to the mountain slope. The oxidant 

was not always confined belowthe inversion layer, 

but it was present in the inversion layer and above 

the mountain crest. 18 An instrumented aircraft 

measured concentrations of oxidant ranging from 

100 to 200 /ag/m 3 (0.05 to 0.11 ppm) as high as 

2432 m(8000 ft) approximately 1033 m(3400 ft) 

above the ridge crest during several flights at noon 

and at4 p.m. At these times, downwind diffusion of 

oxidant beyond the crest, on the basis of 

measurements taken on aircraft flights 

approximately 150 m(500 ft) above the terrain, 

suggested only slight dilution in the first 10 km (6 

miles) north of the crest. 18 Observations on other 

days34 suggested a 50- to 60-percent reduction in 

oxidant 10 km (6 miles) north of the crest. There 

was no ground station at this point for comparison 

with the aircraft measurements at either time. 

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San Gobriel Volley ~ cable •••••••• ~ '%i~?o: 

• ~ ~ 

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Beaumont o 

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~ o . . . corono oi 

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• 9y"-- ~~ •7 Elsinore ~ 

 3 

5,000-9,000 

000 • 5,000 0 

I,

,

000-3,000 S 

0 10 20 MILES BELOW 1,000 

Figure 12-2. Major topographic features of the Los Angeles Basin with inland valleys and mountains. Station locations: A. 

Highland; B, City Creek; C, Mud Flat; D, Rim Forest. Aircraft flight paths for the study area are also shown. 1 e 

299 
Total oxidant, temperature, and vapor-pressure 

gradient were measured continuously during 16 

days in July and August at the mountain slope and 

crest stations (A, B, C, and D, in Figure 12-2). 

Figure 12-5 shows that the time of the daily peak 

oxidant concentration was progressively later at 

stations of higher elevation. Temperatures and 

vapor-pressure gradients were also progessively 

lower at higher elevations at the time of oxidant 

peak. The duration of oxidant concentrations exceeding 200 Ng/m 3 (0.10 ppm) was 9, 13, 9 and 8 

hr/day going from lower to higher stations. The 

longer duration at City Creek (elevation 817 m, or 

2680 ft) probably coincides with the zone where 

the inversion layer most often contacts the 

mountain slope. The oxidant concentrations rarely 

decreased below 98 Ng/m 3 (0.05 ppm) at night on 

the slope of the mountain crest, whereas they 

usually decayed to near zero at the basin station 

(Highland). 

The vegetation zones along the slope and at the 

crest are subjected to oxidant exposure differently. 

Even though the lower chaparral receives longer 

exposure, the peak concentrations coincide more 

closely with the maximal evaporative stress for the 

day. There is some support for the hypothesis that 

plant stomata would be closed during this period 

and that pollutant uptake would thus be lower. 

There is, in fact, very little visible injury to the 

species in this zone; however, chaparral is more 

sclerophyllous and therefore less likely to show 

visible injury. In contrast, the daily oxidant peak 

oCcurs well after the maximum temperature and 

vapor-pressure gradients have occurred in the 

conifer forest at the mountain crest, where oxidant 

injury to plant species is severe. These suggestions 

of possible microclimatic control of the sensitivity 

of these native species to ozone form a working 

hypothesis that needs further investigation. 

2745 

2135 

12 d ~ d 

E 

1..: 1525 

2 

O_ 

W 

2 

915 

305 

CHAMISE CONIFEROUS 

FOREST 

CHAPARRAL 

RIM 

" FOREST jROCK 

~ CAMP 

1 

~ MUD FLAT 

I DEEP 

CITY ~CREEK CREEK 

~ I — N —i 

1 

REDLANDS HIGHLAND 

n a 8 12 16 20 24 28 39 36 

90 

70 

w 

0 

50 1-: 

2 

c7 

_ W 

30 

10 

DISTANCE, kilometers 

Figure 12-3. Altitudinal sequence of ecosystems in the San Bernardino Mountains. 34 

300 
San Joaquin Valley and Adjacent Sierra Nevada development may cause adverse oxidant conMountains centratlons. 

Field surveys36,69 have confirmed oxidant injury 

to ponderosa pine and associated species at 

numerous locations in the Sierra Nevada foothills 

east and southeast of Fresno. Oxidant measurements at ground stations and by instrumented 

aircraft show late-afternoon peaks of transported 

oxidant on the western slopes of the Sierras. 

Limited measurements by instrumented aircraft 

sugQest the development of a layer of oxidant 

approaching the forested mountain slopes 

between 610 and 1829 m(2000 and 6000 ft) 

during the late afternoon. 35 A very weak inversion 

or isothermal layer may serve as a reservoir of 

oxidant, which is advected to the mountain slope in 

the southern coastal air basin, as suggested by 

Edinger." 

Considerable concern has been registered about 

air quality in the Lake Tahoe Basin, where local 

Seasonal and Daily Variations of Injurious 

Concentrations—Synoptic Weather Patterns 

Associated with Episodes of High Pollution 

McCutchan and Schroeder 30 classified 145 days 

during May through September 1970 with respect 

to pollution and meteorology on the basis of data 

collected on the southern slopes of the Sari 

Bernardino Mountains. Five general weather 

patterns were described, along with the associated 

synoptic patterns at the surface and at 500 

millibars (mb) (Table 12-2) An analysis of eight 

meteorologic variables was used to classify days 

during May through September into the five 

general categories. Of 123 days classified by 

stepwise discriminant analysis, 10, 13,44, 23, and 

24 were placed in classes 1 through 5, 

respectively; the remaining 9 days could not be 

6 

4 

2 

0900 June 19,1970 

1.000 ft 

6 

4 

2 

0 

05 /

0-0.10 ppm 

t s'%l — 0.10-0.20 

~ 0.20-0.30 

-- 0.30-0.40 

~ABOVE 0.40 

Deep 

Creek 

A S a0'tg 

Redlands 

– ~ -- TEMPERATURE INVERSION BASE 

TERRAIN PROFILE 

Figure 12-4. Daytime changes in oxidant concentrations along a west-to-east transect in the southern coastal air 

basin, including the slopes of the San Bernardino Mountains (see Figure 12-2). Reprinted with permission from Edinger 

et a1. 18 

301 
24 = 

E 

E 

1- 

z 

LU 

18 p 

Q 

~ 

c~ 

w 

¢ 

12 v=i 

fA 

w 

cc 

a 

m 

O 

a 

6 ~ 

0 

0 3 6 9 12 15 18 21 

TIME, hours 

Figure 12-5. The relationship of time of occurrence of the daily peak oxidant concentration to temperature and vaporpressure gradients in an elevational sequence (see Figures 12-1 and 12-2) on the slopes of the San Bernardino Mountains, 

July-August 1969. 36 

0.40 100 30 

0.35 95 VPG 

T 

CITY CREEK 817 m 24 = 

0.30 90 E E 

E a ~ LL Z 

a 0.25 °w 85 Ox ~~ - ~~ ' 18 C 

Z ~ i ~ ~ • aoc 

o ~ X 0.20 a 80 ~\ W 

O w 

Q g / ~ 12 ~ 

O

0.15 ~ 75 ~ \\ ~ 

~ / . a 

I `~ 

cc 

0.10 70 ~ ~~ O 

6 > 

0.05 65 

0 0 

0 3 6 9 12 15 18 21 

TIME, hours 

Figure 12-5 (continued). The relationship of time of occurrence of the daily peak oxidant concentration to temperature and 

vapor-pressure gradients in an elevational sequence (see Figures 12-1 and 12-2) on the slopes of the San Bernardino 

Mountains, July-August 1969. 34 

302 

0.35 

0.30 

E 

a 

a 

~.: 0.25 

Z 

Q 

0 

X 0.20 

O 

J 

FQ- 0.15 

O 

H 

0.10 

0.05 

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95 

90 

U. 

° 85 ui 

cc 

~ 

~ 

Q 80 

¢ 

w 

a 

W 75 

70 

65 + \ ` 

HIGHLAND 442 m 

/ 

/ 

/ 

i 

i 

i 

/ 

~ 

/ 

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T VPG 

.- ~ 

i ~ 

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cc= 

y E g W 

az 

~ W 

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0.30 

E 

a 0.25 

H 

z 

_p 0.20 

X 

O 

J 

~ 0.15 

O H 

0.10 

0.05 

0 

95 MUD FLAT 1110 m 

T 

90 ^ ~ 

VPG ~I ~ 

U. / \ 

0W 85 ` 

~ 

Q 80 / w O ~ ` \ a x ~ 

/ \ 

w 75 

/ ~ \ 

70 

/ 

65 ,~ ,~ ~~ •_. \ 

0 3 6 9 12 15 18 21 

TIME, hours 

rn 24 S 

E 

E 

F 

Z 

W 

18 Q 

~ 

(~ 

W 

o: 

~ 

12 

W 

d: 

a 

¢ 

O 

a 

6 Q > 

0 

Figure 12-5 (continued). The relationship of time of occurrence of the daily peak oxidant concentration to temperature and 

vapor-pressure gradients in an elevational sequence (see Figures 12-1 and 12-2) on the slopes of the San Bernardino 

Mountains, July-August 1969. 34 

a 

E 

5 

0 

RIM FOREST 1725 m 

N 

~ 180 S 

~ 

N 

° 160 SSE 

~ 

O 

140 SE tU W 

> 

80 VPG J 

LL 

O 

ui 

? 75 

Q ' \ 

a 70 

w TEMP 

~ 65 ~ -• - - ~-- ~ 

i~ OX 

_ ~ 

0 3 6 9 12 15 7t3 21 

TIME, hours 

Figure 12-5 (continued). The relationship of time of occurrence of the daily peak oxidant concentration to temperature and 

vapor-pressure gradients in an elevational sequence (see Figures 12-1 and 12-2) on the slopes of the San Bernardino 

Mountains, July-August 1969. 34 

303 
placed clearly in any of the five classes. The oxidant 

concentrations associated wlth these classes were 

Class 1, low; Class 2, low and high; Class 3, high; 

Class 4, moderately high; and Class 5, low. In this 

sample, the sum of days in classes 2 and 3(57 

days) suggests that about 46 percent of the sample 

days had high concentrations of oxidant air 

pollutants. 

Class 2 and 3 days are both characterized by high 

pressure (a 500-mb ridge over the area). 

Descriptions of the synoptic weather patterns 

(contained in the U.S. Forest Service California Fire 

Weather Severity, 10-Day Summaries) for May 

through August 1972-74 were compared with 

episodes of severe oxidant concentratlon at Rim 

Forest and nearby Sky Forest. For the purposes of 

thls comparison, synoptic patterns were reviewed 

for all days having a maxlmum hourly 

concentration of 646 Ng/m3 (0.33 ppm) or higher. 

In all cases, the persistent 500-mb hlgh pressure 

over the area was the most common synoptic 

feature. For 8 quallfying days in 1972, the mean of 

the maximum hourly concentrations was 724 

Ng/m3 (0.37 ppm); for 16 days in 1973, it was 803 

/ig/m 3 (0.41 ppm); and for 46 days in 1974, it was 

744 pg/m3 (0.38 ppm). The highest hourly 

concentratlon obtalned at that time was 1176 

μg/m 3 (0.60 ppm) on June 28, 1974. 

During episodes of severe oxidant pollution, the 

weather is generally very hot (85° to 100° F, or 

about 29° to 38°C). The relative humidity may be 

elther low or moderately high on class 2 and 3 

days, depending on the behavlor of the marine 

layer. The small difference in the means of maximum hourly concentrations on high-pollution days 

in 1972 through 1974 suggests that heavy primary 

pollutant emission continues in spite of current 

control strategies. 

Annual Trends of Total Oxidant Concentrations 

at a San Bernardino Station and the Nearby City 

of San Bernardino 

Since 1968, total oxidant concentrations have 

been measured contlnuously with a Mast ozone 

meter (calibrated by the California Air Resources 

Board method) from May through September at 

Rim Forest/Sky Forest. 34 The fall, winter, and early 

spring months have generally been omitted until 

recently, because synoptic patterns are usually not 

conducive to oxidant accumulation and transport. 

For example, average maximum hourly oxidant 

concentrations from October through March 1973 

and 1974 stayed below 196 frg/m 3 (0.10 ppm); 

those for March were 196 to 294 Ng/m 3 (0.10 to 

0.15 ppm). 34 The main data collection period 

coincldes with the growing season and thus 

permits a reasonable estimate of the total annual 

dose of oxidant air pollutant received by 

vegetation. 

In documentation of oxidant concentration 

trends during the 1968 to mid-1 976 period at Rim 

Forest/Sky Forest, the accumulated dose Is 

expressed as the sum of all hourly values (in 

Ng/m 3 ), including concentrations for each month 

separately, June through September (the main 

part of the growing season) (Flgure 12-6). These 

TABLE 12-2. DESCRIPTIONS OF METEOROLOGIC PATTERNS FOR FIVE CLASSES OF 

SPRING AND SUMMER DAYS IN SOUTHERN CALIFORNIA a 

Class General weather 

Associated synoptic pattern 

At surface At 500 mb 

Oxidant 

concentration 

1 Hot, dry contlnental alr Large hlgh pressure over Strong northerly wlnds over Low 

throughout the day Great Basln area wlth trough east of 

(Santa Ana) the area 

2 Relatively dry forenoon, Hlgh pressure over Great Subtroplcal closed hlgh over Low and hlgh 

modlfled marine atr In Bastn and thermal trough area 

afternoon, very hot over desert 

(heat wave) 

3 Molst, modlfled marine alr, Thermal trough over desert Rldge over area Hlgh 

hot In afternoon 

4 Molst, modlfled marine alr, Thermal trough over desert Trough over area Moderately hlgh 

warm In afternoon 

5 Cool, molst, deep marine Synoptic low over desert Deep trough or closed low Low 

alr throughout the day over area 

'Modiffied from Reference 38 

304 
doses exclude background concentrations (those 

less than or equal to 59 Ng/m3 , or0.03 ppm). 23 The 

percentage of valid data reAcovered, as well as the 

total possible hours for which data could be 

obtained for each month, June through September, is also indicated. The absence of some 

data, ranging up to 17.8 percent in 1970, but 

averaging 8.3 percent during the 7 years, 

represents a margin of error that cannot at present 

be adjusted with any certainty. The total number of 

hours with concentrations of 160 Ng/m 3 (0.08 

ppm) or more during June through Septemberwas 

never less than 1300 hours during each of the first 

7 years. Recent predictions suggest that oxidant 

doses will either increase annually or oscillate 

around the mean of the present high levels unless 

dramatic improvements occur. 33 

Data from the downtown San Bernardino station 

operated by the County Air Pollution Control 

District (APCD) are available back to 1963. The 

colorimetric potassium iodide method used to 

measure total oxidants was calibrated according to 

the method of the California Air Resources Board. 

A positive correction factor of 1.22 was used to 

adjust mountain data for the decreased air 

pre,,,sure at the higher elevation. 

The data from the Rim Forest/Sky Forest station 

were compared with published data from the San 

Bernardino County APCD. The number of hours 

with concentrations exceeding 392 /jg/m 3 (0.20 

ppm) during July, August, and September 1969 

through 1974 were comoared (Figure 12-7). For 

1963 through 1968, data are shown only from the 

San Bernardino APCD. A large part of the year-toyear differences at the same station and between 

stations can be attributed to differences in synoptic 

and mesoscale (local) meteorologic patterns. For 

example, the increases in 1972, 1973, and 1974 at 

Rim Forest/Sky Forest are as :)ciated with 6, 16, 

and 46 days, respectively, when a persistent 500- 

mb ridge occurred overtheSouthwest, particularly 

southern California. The difference between 

stations in the same year is probably influenced 

most by inversion height. Lower inversions 

partially restrain transport upslope to shorter 

periods each day. Higher inversions would have 

the opposite effect and also allow the greater air 

volume below to dilute the oxidants. The index for 

comparison chosen in Figure 12-7 (i.e., hours > 

392 Ng/m 3 ) would be sensitiveto inversion height. 

The 3-year moving averages for each station tend 

to remove some of the variation resulting from 

5. 0 — 

PERCENT OF TOTAL. OF .• 

0 82 94 86 85 100 100 

_ , ~~ 

MOVING AVERAGE `.w 

' , 9q 

. 

~ \ ~ ~~ \ 

. 

, , 

0 

\ 

~ \ 

\ 

79: ~ ~ ~ ~ 

\ 

•i•i•~•~ ~i•i•i•i ~ ~ 

i•••••i 

. 

2.0- i • \ \ 

\ 

~ ~ `~ 

~ " ~ ~ 

•i•i•i` ••~ 

••••••~ 

~~i • • •••••~ ~ ~•~•••~ ••••••~ ~ , ,••i•i•~ ~~•~•~•~ •••••~ ~~~ ► ~ ~ ~ 

.~~•~~~ ••• ~ ~•❖~~ i•i•i•i•~ i•~•i ••Q•i •••O•~ 

~ \ ~~ i•i•i•i~ ~ ••~ • ~ 

♦ 

i ~ • ~ ~ ► , , i ~ ~ ...-.-. ► ~ .-•.•.. 

, :•-❖•~ ~~•~•~•! .•?'0'~i~ ~~••••~ 

, ~'i' •••• ~~ 

0 

0 

® •~ ~

JUNE 'i•~'i ~ 

 

\ SEPTEMBER 

Figure 12-6. Monthly summation of total oxidant concentration data at Rim Forest/Sky Forest, San Bernardino Mountains, 

California, June through September, 1968-75. 33 

305 
Z O 

H 

Q 

¢ 

H 

2 

W 

U 

Z O u 

H 

Z 

~ p E O z J N 

F M OLL ~O _ H ~ 

N 

d: 

~ 

O 

2 

400 

300 

200 

100 

0 

meteorology. In terms of numbers of hours with 

oxidant equal to or exceeding 392 Ng/m 3 , the 

moving average between 1970 and 1973 at Rim 

Forest/Sky Forest has increased from 175 to 290 

hr. The increased oxidant concentrations at both 

these stations are the reverse of those in upwind, 

urban Los Angeles County, where increased 

emmission of NO X tends to shift the chemical 

equilibrium to the left, toward the ozone 

precursors. The most recent data 13 firmly indicate 

that oxidant concentrations will either increase 

annually or continue to oscillate around the mean 

of present high concentrations in the foreseeable 

future at these distant locations. 

Robinson's tropospheric ozone cycle 13 describing rural upwind, urban, and rural downwind 

variations in concentration can be easily 

demonstrated in the Los Angeles and connected 

inland basins. The effects on both natural 

ecosystems and agroecosystems also can be 

demonstrated. For example, oxidant measurements were made during August 1972 at six 

oxidant stations (Costa Mesa, La Habra, Corona, 

Riverside, City Creek, and Rim Forest) extending in 

a line northeastward from the coast to the 

mountains. These measurements show low doses 

at the coast, increasing to a maximum on the 

chaparral-covered mountains and decreasing 

beyond the mountain crest (Figure 12-8). In Figure 

12-8, the oxidant dose is indicated by the dashed 

line. A crude estimate of the relative economic 

value of ecosystems encountered along this 

transect is expressed in a very general way by the 

solid line and the nomenclature on the abscissa. 

Finally, the relative complexity of the ecosystems 

involved is shown below the abscissa. This 

conceptualization emphasizes the enormously 

greater dosage received by the natural ecosystems 

during thls month. This pattern of dosages is very 

typical of June, July, and August, but the offshore 

flow typified by the Santa Ana winds may reverse 

the situation in September or October. Susceptible 

crops growing on the coastal plain may be 

seriously damaged. 

In general, the permanent vegetation constituting natural ecosystems receives much 

greater chronic exposure than the short-lived, 

hlgher-value vegetation constituting the agroecosystems of the coastal plain. The latter can be 

subjected to injurious doses, but in intermittent, 

short-term fumigations. Each situation has 

measurable economic and aesthetic effects, but on 

different time scales. The simple agroecosystem 

has little resiliency to pollutant stress; losses are 

immediate and may be catastrophic. The complex 

natural ecosystem is initially more resistant to 

SAN BERNARDINO APCD (DOWNTOWN) El 99 400 

RIM FOREST/SICY FOREST ~ 

JULY, AUGUST, SEPTEMBER PERCENT DATA AVAILABLE RF/SF 

3- year MOV ING AVERAGES: 98 78 93 91 96 

300 

APCD ~--- ~ 

R F/SF • * 

200 

i 

~ 

i~ 

100 

r' 

1963 1964 1965 1966 1967 1968 1969 1970 1971 1972 1973 1974 

Figure 12-7. Number of hours of total oxidant, July through September, greater than or equal to 392 Ng/m 3 (0.20 ppm) at the 

downtown San Bernardino County Air Pollution Control District Station, 1963-74, and Rim Forest/Sky Forest, 1968-74. 33 

306 
pollutant stress, but the longer chronlc exposures 

cause the disruption of both structure and function 

in the system. The damage may not be reversible. 

INVESTIGATING THE EFFECTS OF OXIDANT 

STRESS ON ECOSYSTEMS 

Ecosystem Modeling 

Ecosystems are very complex and extremely 

difficult to understand. An approach to 

understanding these complexities is to describe 

them in mathematical terms. However, before 

mathematical shorthand can be used, the 

components to be studied must be defined and 

their interactions and relationshlps with one 

another identified. To understand the stresses 

placed on ecosystems by perturbations such as 

ozone-oxidant alr pollution, those elements that 

could be particularly vulnerable to pollutants must 

also be identlfied. The mathematical and computer 

capability for modeling ecosystems exists, but 

ecological science does not yet possess sufflcient 

understanding of all of the interactions at the 

ecosystem level 2 Therefore, slmulation models of 

forest ecosystems are extremely scarce. 68 

Modeling of the conlferous forest biome is 

discussed by Overton, 41 and modeling of the 

eastern forest biome is treated by O'Neill. 40 The 

usual modeling approach Is to select speciflc 

processes such as energy flow and nutrient 

cycling. These processes are a result of the 

structural interrelationships existing among the 

various components (soll, water, nutrients, 

producers, consumers, and decomposers). 48 

Energy and nutrients may enter or leave an 

ecosystem by a variety of pathways. These 

processes may be described mathematically, and a 

model may be developed that is an approximatlon 

of the real world. This model may then be used to 

make predictions about the ecosystem. Computer 

programs for solving the equatlons explaining 

interactions of the ecosystem components already 

exist. Once the model Is running smoothly on the 

computer, it is possible to Impose varlous 

experimental conditions (e.g., clear cutting or 

selective cutting) and observe the effects on 

specific processes such as energy or nutrientflow. 

Sensltivity analysis can then be performed to 

determine which transfer coefficients are most 

sensitive to stress and how much stress Is requlred 

to cause deterioration of the ecosystem. 

- 

CITY CREEK 

~ ~ 

NOTE: OXIDANT DOSES, WHiCH ARE REAL 

~ i ~% 

, 

DATA, DEFINE THE POLLUTANT CONCEN- 

~ ~~` TRATION GRADIENT FROM COAST TO INTERIOR. 

~ RIM FOREST 

/ / ` J 

i 

s, 

% % 

Q 

/ / `~ W Z W 

W ~ 

~ 

% ~ 

% , RIVERSIDE J ~ G 

J Q 

mQ y Z 

~_px -

/ w ~ W Q a J ` F- W Z W~ Z O 

~ a 

 Q 

W 

CC 

~/ Q `\ ~~ uJ U. 

i cc o[ U , 

I W J 

O 

lL 

J ~ 

D 0 

i~ LL w Q W U U. COSTA MESA 

V O Q ~ %9 CORONA 

a Z 

y v ' LA HABRA 

w ~` 

~ 

__ `• 

~ CLIMAX WOODY PERENNIAL IRRIGATED LOW HIGH COASTAL 

O VEGETATION SHRUBS GRASSES PASTURE VALUE VALUE LANDS 

a AND WEEDS CROPS CROPS 

VEGETATIVE COMPOSITION SIMPLE AGROECOSYSTEMS bo 

COMPLEX NATURAL ECOSYSTEMS 

Figure 12-8. Hypothetical relationships of oxidant dose, natural ecosystems, agroecosystems, and the relative values of their 

vegetation components along a transect of southern coastal air basin of California. 3 e 

r 

x 

E 

O. a 

N 

n 

0) 

~ 

~ Q 

W 

C7 

N 

O 

~ 

FZ 

Q 

X 

O 

307 
No models dealing with oxidant stress on 

communities or ecosystems exist; however, 

models do exist that deal in general terms 

with disturbance, ' sensitivity, 8,20,27,44 a n d 

stability8 '

2°z ''4° at community and ecosystem 

levels. Forest succession has been described by 

Schugart et al. 47 and Botkin and Miller. 7 The area 

occupied per biotic unit over time is very important 

for defining and predicting long-term successional 

changes in plant communities as a result of 

pollutant stress. In view of the trend of increasing 

oxidant concentrations downwind from urban 

areas, 6 a much more precise understanding of 

chronic effects on both natural ecosystems and 

agroecosystems is required Descriptive and 

predictive models dealing with the responses of 

biologic systems can provide the best input to the 

decision models needed for standard setting, land 

use planning, and resource management. 

Modeling the Effects of Oxidant Stress on a 

Western Mixed Conifer Forest Ecosystem 

The recent history of the mixed conifer forest of 

the San Bernardino Mountains has been 

analyzed. 55 The analysis was conducted by nearly a 

dozen coinvestigators representing many 

disciplines. 56 This analysis included an initial 

inventory of ecosystem components and 

processes, as indicated in Figures 12-9 through 

12-13. The inventory emphasizes ponderosa and 

Jeffrey pines, the most dominant species in the 

climax community, and is stratified according to 

organizational level• Organism or tree (Figures 12- 

9 and 12-10), community or stand (Figure 12-11 

and 1 2-1 2), and, finally, a time-oriented analysis of 

plant succession in the aggregation of relatively 

distinct communities or stands that collectively 

make up the mixed conifer forest ecosystem 

(Figure 12-13). These figures present in 

diagrammatic form the complexity of ecosystem 

interactions at each level of biological 

organization. Only the interactions considered to 

be the most important ones guiding the course of 

plant succession in the several forest plant 

communities now constituting the mixed conifer 

forest have been selected by project investigators 

for immediate investigation. 57 In the case of each 

interaction, it is important to decide the time 

frequency at which the selected variables will be 

measured (i.e., hourly, weekly, or annually) 

Because this project is the most active effort to 

date directed toward understanding the effects of 

ozone and other oxidants on a natural ecosystem, 

most of the remainder of this chapter is a 

discussion of its findings. 

Effects on Primary Producers (Green Plants) 

The ozone dose responses of both herbaceous 

and woody plants and the specific effects on the 

photosynthetic activity (principally in controlled 

short-term exposures) are discussed in Chapter 

1 1. The aim of this section isto evaluate the effects 

of the chronic exposure of vegetation in natural 

ecosystems tototal oxidants(more than 90 percent 

ozone) under field conditions or simulated field 

conditions. The effects of Ghronic exposure on 

agroecosystems are also discussed to a limited 

extent in Chapter 11 . 

Smith 51 has suggested three classes of 

ecosystem response to air pollutants: Those in 

which vegetation and soils serve only as asink for 

pollutants, with no visible vegetation injury; those 

in which some species, or sensitive individuals 

within species, are injured and are more subjectto 

other stresses; and those in which high dosages 

cause acute morbidity or mortality of some species. 

Although these classes are convenient for 

discussion, they are not clearly separated in space 

in most situations. More often, these classes of 

response occur along a gradient of decreasing 

pollutant exposure, as in the San Bernardino 

Mountains. 

EXTENT AND INTENSITY OF INJURY TO 

OVERSTORY TREES IN THE SAN BERNARDINO 

NATIONAL FOREST 

Wert65 used aerial photography to determine the 

extent of oxidant injury to ponderosa and Jeffrey 

pines in diameter classes larger than 30 cm. Injury 

was categorized as heavy, moderate, light, or 

negligible, and it generally decreased with 

distance from the source area. Of the 64,380 ha 

(160,950 acres) of ponderosa-Jeffrey type within 

the forest boundaries, 18,492 ha (46,230 acres) 

had heavy damage, 21,568 ha (53,920 acres) had 

moderate damage, and 24,320 ha (60,800 acres) 

had light or negligible damage. An estimated 

1,298,000 trees were affected. Of these, 82 

percent were moderately affected, 15 percent 

were severely affected, and 3 percent had died. 

The term "ponderosa-Jeffrey type" is a general 

term that includes a mosaic of five subtypes 

described by McBride on the basis of species 

dominance. 38 These subtypes are: Ponderosa pine 

308 
forest, ponderosa pine/whlte fir forest, ponderosa 

pine/Jeffrey pine forest, Jeffrey pine forest, and 

Jeffrey pine/white flr forest. The injury by oxidant 

air pollutants is most intense in the Jeffrey pine 

types. In the fleld plots of these various types, as a 

result of oxidant air pollution, the average area 

covered by shrubs is only 3.8 percent in the 

ponderosa types, but 26 percent in theJeffrey pine 

types. 36 

Later studies32,55,5s have expressed the amount 

of injury to ponderosa and Jeffrey pines and 

associated tree species in permanent study plots 

as a numerical score. The range of scores Is 

subdivided Into seven categories, ranging from 

dead to no visible symptoms. 32 

In 1974, all tree species at 19 permanent study 

plots were scored individually by binocular 

Inspection. T he data can be obtalned from conifers 

early in the fall, but the most important deciduous 

species, black oak, was evaluated during the period 

from August 28 to 31 to prevent confusion of 

oxidant-injury symptoms with natural autumn 

senescence of leaves. The injury to black oak on 

August 31, 1974, at several representative study 

sites, and the June-August accumulated dose at 

nearby monitoring stations are shown in relation 

to the topographic projection of the San 

Bernardino Mountains in Figure 12-14. 28 Lower 

scores mean greater injury. The darkened portlon` 

of the bar representing oak injury is for leaf 

2 OXIDANT 

F3 

AIR 

~ POLLUTANTS ~ 

1~ MAMMALS 

CLIMATE 

CONE 

INSECTS 

4 

SOIL 

MICRO— 

ARTHROPODS 

5 17 

6 7 8 9 10 11 Iz 13 14 16 

BARK 

BEETLES 

19 

18 

NATURAL 20 

ENEMIES OF 

BARK BEETLES 

21 

25 ~,f26 

SOI L 

PATHOGENS 

28 

24 

22 WOODPECKERS 2-j 

AND OTHER 

NON— 

HOLE NESTING 

PATHOGENIC 

BIRDS 

FUNGI 

TREE 

23 

Figure 12-9. Organism-level interactions in a mixed conifer forest. 56 

e11Z:] 
1. Competition for food supply 

2. Direct effect of ozone on small-mammal physiology 

3. Climatic control of oxidant concentration in forest 

4. Direct effect of ozone in soil microarthropods 

5. Effect of precipitation and temperature on soil moisture and soil temperature 

6. Insect damage to developing cones 

7. Damage by small mammals to developing cones and importance of cone crop as animal 

food supply 

8. Direct effect of ozone on physiology of cavity-nesting birds 

9. Role of fruiting bodies of nonpathogenic fungi in nutrition of small animals 

10. Direct effect of ozone on tree physiology 

11. Role of fruiting bodies of pathogens in nutrition of small animals 

12. Direct effect of ozone on nonpathogenic fungi 

13. Effect of temperature and evaporative stress on tree growth 

14. Direct effect of ozone on pathogenic fungi 

15. Interaction of nonpathogenic fungi and soil microarthropods 

16. Interaction of pathogenic fungi and soil microarthropods 

17. Effect of soil microarthropods on litter reduction 

18. Impact of predation and parasitism on bark beetles 

19. Predation of bark beetles by woodpeckers 

20. Effect of bark beetles on tree mortality and vigor and effect of phloem thickness 

and moisture on bark beetles 

21. Effect of phloem moisture and thickness on natural enemies of bark beetles 

22. Influence of woodpeckers on rate of parasitism 

23. Effect of nonpatfiogenic fungi on tree growth 

24. Effect of pathogens on tree vigor and mortality 

25. Effect of soil moisture and soil temperature on tree growth 

26. Effect of soil moisture and temperature on occurrence of nonpathogenic fungi 

27. Interaction of pathogenic and nonpathogenic fungi 

28. Effect of soil moisture and temperature on occurrence of pathogenic fungi 

Figure 12-9 (continued). Organism-level interactions in a mixed conifer forest. 56Types of interactions. 

chlorotic mottle and interveinal necrosis. A score 

of 8 means no injury. The remal ning portion of the 

score is the sum of scores for leaf complement, leaf 

size, and twig mortality (not shown separately). 

These data suggestthat oak shows no visible injury 

where the accumulated June-August dose does 

not exceed about 2.5 x 1 05 /jg/m 3times hours from 

about Snow Valley eastward. 

The distribution of ponderosa and Jeffrey pines 

into various injury classes with respect to the 

dlstance of the study site along the gradient of 

oxidant dose (June-September) is illustrated above 

the topographic projection in Figure 12-15. 28It is 

important to realize that the 1974 distribution into 

injury classes is also a product of earller years, 

when the oxldant concentrations were not always 

as high as in 1974 (see Figure 12-6). The trend 

toward greater numbers in the very slight injury 

(29 to 35) and no visible Injury (36 and greater) 

categories is quite evident in the eastern plots 

receiving lower doses-for example, Holcomb 

Valley. The assumption has been made that 

ponderosa and Jeffrey pine respond similarly to 

oxidant. Ponderosa pine is replaced by Jeffrey pine 

in the natural stands east of Camp 0'ongo, and 

they intermix at Barton Flats. The valldity of this 

assumption can be partially verlfied by examining 

the distributions of the two species into injury 

classes at Barton Flats(Figure 1 2-1 5). 28 These data 

Indicate reasonable similarity at a common site; 

but the influence of other environmental variables 

that change continuously along the oxidant 

gradlent (such as soll moisture availablity, 

temperature, and humidlty) must be examined 

more intensively to understand the degree to 

whlch they influence oxidant susceptibility (see 

Flgures 12-9 throughl2-13). 

OXIDANT DAMAGE TO CONIFER SPECIES IN THE 

19 MAJOR STUDY PLOTS FROM 1973 TO 1974 

The first evaluation of oxidant injury to all tree 

species in the new study plots was completed in 

September and October 1973. The second 

evaluation in 1974 offered the first opportunity to 

compare increases In tree injury and mortality. In 

Table 12-3, the plots are arranged in the order of 

severe injury (flrst) to no visible injury (last), 

according to the 1974 average injury score for all 

ponderosa or Jeffrey pines In each plot. Of the 12 

plots categorized as severe and moderate, all but 6 

showed injury significantly increased (lower 

scores), with a probabillty of 0.05. Among the six 

310 
remaining plots where injury was classified as and two decreases (one slgnificant and one 

slight, very slight, or not vislble, there were three insignificant), all at a probability of 0.05. 

signlficant increases, one inslgnificant increase, 

OXIDANT 

CLIMATE 

AIR 

POLLUTANTS 

10b 

10a 

13 

A FOILAGE 

PHOTOSYNTHESIS 

AND 

~ RESPIRATION 

C 

SOIL 

MOISTURE 

/ 

BARK BEETLES 

20c 

t 

SOIL 

MINERALS 

CONE 

INSECTS 

6 

7a 

(: 

SMALL 

MAMMA LS 

7b 

e7 

WATER 

UPTAKE MINERAL 

AND E NUTRITION 

TRANSPIRATION 

CARBOHYDRATE 

POOL 

20b F H i . G \ 

BARK 

WOOD 

TEXTURE CONES 

THICKNESS 

PHLOEM THICKNESS 

PHLOEM MOISTURE STEMS ROOTS 

RESIN QUALITY 

RESIN QUANTITY SEEDS 

23a 

24a 

NON24b PATHOGENS PATHOGENIC 23b 

FUNGI 

Figure 12-10. Tree-level interactions in a mixed conifer forest ecosystem (a = direct influence of external factors on trees; b and 

c= influence of tree condition on external factors). sfi 

311 
A. Relationship between net photosynthesis, foliage age, and foliage retention 

B. Effect of plant moisture stress on net photosynthesis 

C. Relationship between mineral uptake and net photosynthesis 

D. Relationship between net photosynthesis and carbohydrate storage 

E. Relationship between water uptake and mineral nutrition 

F. Relationship between carbohydrate storage and bark characteristics 

G. Relationship between carbohydrate storage and wood production 

H. Relationship between carbohydrate storage and cone production 

I. Relationship between cone crop and seed crop 

6. Cone insect damage to developing cones 

7a. Small-mammal damage to developing cones 

7b. Small-mammal predation of seeds 

10a. Effect of ozone on photosynthesis and respiration 

10b. Effect of ozone on needle retention13. Effect of temperature, light intensity, and evaporative stress on photosynthesis 

and respiration 

20a. Effect of bark beetles on water uptake and transpiration, and relationships of 

tree moisture stress to bark beetle attack 

20b. Effect of bark beetles on tree carbohydrate concentration and relationships of 

carbohydrate concentration to bark beetle population in trees 

20c. Relationship between bark beetle characteristics and bark beetle attack and 

population 

21. Relationship between bark characteristics and natural enemies of bark beetles 

23a. Relationship between root characteristics and mycorrhizal-forming nonpathogenic fungi 

23b. Effect of nonpathogenic fungi on mineral uptake 

24a. Effect of pathogens on tree carbohydrate concentration and relationship of 

carbohydrate concentrations to pathogen attack 

24b. Effect of pathogens on water uptake and transpiration 

24c. Relationship between stem and root characteristics and pathogen attack 

25a. Effect of soil moisture and temperature on water uptake and transpiration 

25b. Effect of soil mineral concentration and temperature on mineral nutrition of tree 

Figure 12-10. Tree-level interactions in a mixed-coniferforestecosystem. 56 

Tree mortality among ponderosa and Jeffrey 

pines was about the same In 1973 and 1974. The 

greatest mortallty was in the permanent study 

plots listed as recelving moderate Injury. Possibly 

the populations In these plots still retain greater 

numbers of the more susceptible genotypes. In 

prevlous years, tree mortality rates for ponderosa 

or Jeffrey pines in the stands suffering moderate to 

severe injury were 8 and 10 percent from 1968 to 

1972, 55 8 percent from 1969 to 1971, 32 and 24 

percent from 1966 to 1969. 12 The death of 

weakened trees is usually due to the pine bark 

beetle. 53 Mortality has not been observed in tree 

species other than ponderosa and Jeffrey pine. 

Two 2-ha (5-acre) control plots in the vlcinity of 

Barton Flats in the San Bernardino Natlonal Forest 

provlde data for the longest observed period of tree 

decllne, 1952 to 1972. 65 These plots are located in 

the Jeffrey pines, where trees with a dlameter 

breast height (dbh) of 30.5 cm (12 in.) or greater 

were measured and their vigor described by 

judging the rlsk or probability that they would be 

susceptible to attack and kill by bark beetles 

(Dendroctonus sp). Risk classes 1 and 2 indlcate 

low-risk trees that would definitely be preserved if 

trees were being marked for a tlmber sale. Classes 

3 and 4 are high-rlsk trees that would be marked 

for removaf in a timber sale. In Tabfe 12-4, the 

changes In merchantable volume in board feet (bd 

ft) in all four classes are recorded for two control 

plots In 1952, 1963, and 1972. The increase in 

volume of trees in the hlgh-rlsk category since 

1952 is astounding, whereas the decreases in 

volume of low-rlsk trees and total plot volume are 

very large. The decrease in total voVume is due to 

one-by-one removal of bark-beetle-killed trees in 

the plots as Indlcated by the Increase in number of 

snags and stumps; It is also posslbly due to 

suppressed radlal growth. 

Information avallable from the study of the 

ponderosa pine subtype suggests that the biomass 

productlon of overstory species is dlminished In 

proportlon to the oxidant dose recelved. Parmeter 

et a1. 43 observed decreases in the height of 

312 
ponderosa pine that showed injury symptoms. 

Injured trees did not respond with greater growth 

during years with more favorable soil moisture 

content; but uninjured trees (often side by side 

with injured trees) did increase in height during 

these years. In another study 38 of two populations 

(one ranging in age from 52 to 71 years and the 

other from 20 to 39 years) of dominant ponderosa 

pine stands, the influence of the LosAngeles smog 

was noted. The width of growth rings before 1940 

was compared with those after 1940. After the 

influence of precipitation on growth was 

evaluated, a difference of 0.20 cm in average 

annual growth was attributable to oxidant air 

pollution injury. 

OXIDANT 

AIR 

POLLUTANT 

2 

~ 

SMALL 

MAMMALS 

1 

CONE 

INSECTS 

4 

7 

BARK 5 6 

BEETLES 

8 

14 l~~ 

CLIMATE 

\SO I L 

3 

t

MICROARTHROPODS 

11 

\ 13 

10 9 12 

, . ~ 

I SOIL 

18 

NATURAL 

ENEMIES 

OF BAR K 

BEETLES 

15 \ 

19 

WOOD- 

\ 

PECKERS 

AND OTHER 

HOLE NESTING 

BIRDS 

20 

~ 1~ PATHOGENS 

PLANTS 

NON— Y2 

PATHOGENIC 

FUNGI 

Figure 12-11. Community-level interactions in a mixed-conifer forest ecosystem. s6 

313 
1. Competition between woodpeckers and smalt 

mammals 

2. Climate control of oxidant concentration in different 

forest communities 

3. Effect of precipitation and temperature on soil 

moisture and soil temperature in different forest 

communities 

4. Predation of bark beetles by woodpeckers in different 

forest communities 

5. Effect of cone crop abundance on cone insect 

populations in different forest communities 

6. Effect of cone crop abundance on small-mammal 

populations in difterent forest communities 

7. Fruiting bodies of nonpathogenic fungi as food for 

small mammals in different forest communities 

8. Smog-caused mortality and morbidity in different 

forest communities 

9. Fruiting bodies of pathogens as food for small 

mammals in different forest communities 

10. Effect of temperature and evaporative stress on 

species composition in different forest communities 

11. Relationship between soil characteristics and 

population density of burrowing sma11 mammals in 

different communities 

12. Relationship between plants and microarthropod 

population 

13. Relationship between soil characteristics and 

microarthropod population 

14. Bark beetle mortality caused by natural enemies in 

different forest communities 

15. Effect of bark beetles on tree mortality and vigor in 

different forest communities 

16. Relationship between soil characteristics and forest 

community composition and growth 

17. Relationship between soil characteristics and species 

distribution and behavior of nonpathogenic fungi 

18. Relationship between soil characteristics and species 

distribution and behavior of pathogens 

19. Influence of forest community type on populations 

of natural enemies of bark beetles 

20. Woodpecker distribution and density in different forest 

communities 

21. Effect of pathogens on tree vigor and mortality in 

different forest communities 

22. Relationship between nonpathogenic fungi and 

forest community composition and growth 

Figure 12-11 . Community-level interactions in a mixed- conifer forest ecosystem. s6 

The growth suppression of ponderosa pine 

saplings has been demonstrated experimentally by 

Thompson. 58 Trees grown in a plastic-covered 

greenhouse and provided with charcoal-filtered air 

(after an initial lag in the growth of shoots and 

branches in the first years of the experiment) 

showed dramatically increased growth when 

compared to trees grown in ambient air outside or 

trees grown in a greenhouse with unfiltered air 

(Figure 12-16) 28 Understory ponderosa pines 

appear to be more susceptible to oxidant than 

larger-sized trees 12 The probable effect of tree 

mortality on stand composition, based on the 

present species and size-class composition, is 

shown in Table 1 2-5. The incense cedar and sugar 

pine are the most tolerant to oxidant; however, the 

sugar pine is present only in very low numbers.The 

accelerated mortality of ponderosa pines has 

particular significance in this ecosystem because it 

is the dominant member of the climax community 

The direct effects of ozone on plant species 

constituting the shrub layer in the conifer forest 

are not yet sufficiently understood to permit any 

conclusions to be drawn. Initial field observations 

suggest that at least 10 species are obviously 

injured by total oxidant in areas receiving high 

dosages These areas have been subject to 

exposure for at least 20 years, so some species or 

subspecies of annual plants may have been 

completely eliminated. 

In a series of experiments, Treshow and 

Stewart 64 fumigated native plants growing under 

natural fie{d conditions. The ozone concentrations 

required to Injure the more prevalent species in the 

grassland-oak and aspen-conifer communities 

during 2-hr exposures to 290, 490, 588, and 785 

Ng/m 3 (0 15, 0.25, 0 30, and 0 40 ppm) ozone were 

determined. Seventy common plant species 

indigenous to the plant communities were 

fumigated. Of these, 5 species were injured at 290 

Ng/m 3 (0 15 ppm), and 20 species at 490 Ng/m 3 

(0.25 ppm). These species included grasses, 

perennial forbs, and trees, and they were 

distributed over all vegetation zones (seeTable 12- 

6). The sensitivity of aspen in the aspen-conifer 

community was considered of great significance. 

Not only is it dominant, but its presence is vitai to 

the integrity of the community. The shade of the 

aspen is required by the seedlings of the white fir 

(Abies concolor) and some other species of plants 

for growth. In the aspen forest of the Wasatch 

Mountains, where this study was conducted, 64 the 

tree canopy acted as an effective filter. When 

ozone concentrations of 1770 ug/m 3 (0.9 ppm) 

were measured in the canopy and in clearings, the 

concentrations under the canopy were only 196 

314 
Ng/m 3 (0.1 ppm). It was also noted thatthough one possible imbalances in community stability are 

exposure to 290 /jg/m3 (0.15 ppm) appeared to readily apparent if these plant communities 

produce no effect, repeated exposures could injure received dosages similar to those typical in the San 

both growth and reproduction.The implicationsfor Bernardino Mountains. 

BARK CLIMATE BARK PATHOGENS 

BEETLES BEETLES 

OXIDANT 

AIR SOIL 

POLLUTANTS 

NON CONE 

PATHOGENS PATHOGENIC INSECTS 

FUNGI 

t0a 

so 168 15a 

15b 22a 

NATURAL 21a 5 

ENEMIES OF 

BARK 21b 

BEETLES 

19 ABUNDANCE 68 SMALL 

OFCONES MAMMALS 

A AND SEEDS 

PLANT 

NON COMPETITION 

PATHOGENIC 

FUNGI E 

D 

22c B C 

WOODLIVING TREES SPECIES SNAGS 20 PECKERS 

SOIL AND OTHER 

MICRO— 12b CAVITY NESTING 

ARTHROPODS BIRDS 

SPECIES DENSITY SPECIES 

10b 

DENSITY FREQUENCY DENSITY 

22b 16b 

CLIMATE SIZE FREQUENCY SIZE 

PATTERN COVER PATTERN 

Sb 

AGE PATTERN AGE 

SOIL / sb COVER 

6c 

OXIDANT 

AIR SMALL 

POLLUTANTS MAMMALS 

Figure 12-12. Stand-level interactions in a mixed conifer forest ecosystem (a = direct influence of external factors on trees in 

stand; b and c= influence of stand condition on nonpathogenic fungi)5 6 

315 
A. Effect of plant competition on abundance of cone and seeds 

B. Effect of plant competition on characteristics of living trees 

C. Effect of plant competition on characteristics of shrubs 

D. Effect of plant competition on characteristics of herbs 

E. Effect of plant competition on tree mortality 

5. Abundance of cones and seeds and predation by cone insects 

6a. Abundance of cones and small-mammal predation of cones 

6b. Characteristics of forest stands and small-mammal populations 

6c. Influence of shrub and herb layer vegetation on small-mammal populations 

Ba. Smogcaused mortality and morbidity in different tree species with forest 

stands 

gb. Influence of stand conditions on concentration of oxidants 

10a. Influence of temperature and evaporative stress on stand structure and 

composition 

12b. Influence of stand condition bn temperature and evaporative stress 

15a. Influence of barkbeetle caused tree mortality on stand condition 

15b. Influence of stand condition on bark beetle population 

16a. Influence of soil moisture and temperature on stand characteristics 

16b. Influence of stand condition on soil characteristics 

19, Influence of stand condition on population dynamics of natural enemies 

of bark beetles 

20. Relationship between smog occurrence and woodpecker population 

21a. Influence of pathogencaused mortality on stand condition 

21b. Influence of stand condition on pathogen population 

22a. Influence of mycorrhiza fungi 

22b. Influence of snags (and downed trees) on nonpathogenic fungi 

22c. Influence of stand condition on nonpathogenic fungi 

Figure 12-12 (continued). Stand-level interactions in a mixed conifer forest ecosystem. 56 

EFFECTS ON REPRODUCTION 

The effect of ozone injury on herbaceous plant 

reproduction has been mentloned earlier in this 

chapter and In Chapter 11. Seed production by 

annuals Is influenced mainly by the environmental 

condltions of the current year, but perennlal woody 

plants, particularly conlfers, are erratic geed 

producers. Factors affecting cone production 

Include age, vigor, seasonal temperature, and soil 

molsture Z ' 

Decrease in tree vigor may decrease or totally 

eliminate cone production or result in a decrease in 

the size, weight, and germination of the seed 

produced. 45.46 

Frult and seeds make up the largest part of the 

dlet of most of the common small mammals on the 

study sites, particularly the deer mouse (Peromyscus sp.), harvest mouse (Reithrodontomys), 

chlpmunk (Eutamias), ground squirrel 

(Callospermophilus), and western gray squirrel 

(Sciurus griseus anthonyi). The graysquirrel is an 

excellent example of the interactions withln this 

forest and of the potential effects of oxldant air 

pollution. It Is abundant throughout the mixedconifer-type forest, depending specifically on the 

pines and oaks for most of its food, cover, and nest 

sites. This squirrel eats or stores a major portion of 

the pine and oak seed crops each year. On some 

yellow pine trees in the study plots, gray squirrels 

cut more than 2000 cones per tree. During periods 

of low seed production because of dlminished tree 

vigor, squirrels converge on the few remalning 

vigorous ponderosa pines and consume about half 

the seed crop before it matures and reaches the 

ground. In the areas severely affected by ozone 

(oxidant), squirrels return to the same trees year 

after. year. After the seed reaches the ground, other 

small vertebrates, such as mice, seek It out. The 

habit of preferential seed use by small vertebrates, 

when considered additively with ozone Injury, 

could seriously reduce the regeneration potential 

of ponderosa pine. 

Thus tree squlrrels are a major souce of loss of 

seeds from the ponderosa, Jeffrey, and sugar 

pines, and of black oak acorns. Vertebrates, then, 

can have a major effect on the reproductlon of 

these species, particularly because the gray 

squirrel is only one of numerous species in this 

forest that feed on conifer seeds and acorns 

Removal of the dominant specles In a specific 

community can have a profound effect on reproduction of other species. Mention has already 

been made of the effect of the disappeara nce of the 

aspens from the aspen-conlfer communitles. The 

316 
CLIMATE FIRE 

OXIDANT SOIL 

AIR CHARACTER— 

POLLUTANTS ISTICS 

1 2 3 4 

COMMUNITY COMMUNITY 

STRUCTURE 10 STRUCTURE 

NO. 1 NO. 2 

5 6 7 8 9 

INSECTS PATHOGENS LOGGING 

MAMMALS I I PEOPLE 

IMPACT 

1. Oxidant modification of community structure 

2. Climate modification of community structure 

3. Fire modification of community structure 

4. Soil characteristics and their influence on community 

structure 

B. Insect modification of community structure 

6. Mammal modification of community structure 

7. Pathogen modification of community structure 

8. People impact on community structure 

9. Logging modification of community structure 

10. Predictive capability through integration of submodels 

for items 1-9 

Figure 12-13. Community-succession interactions in a mixed conifer forest ecosystem. 56 

317 
Figure 12-14. Topographic projection, San Bernardino Mountains, with comparison of oxidant injury to black oaks at major 

study sites, August 31, 1974, with accumulated total oxidant dose for June-August measured at nearby monitoring 

stations.28 

Figure 12-15. Topographic projection, San Bernardino Mountains, showing how ponderosa pines (PP) and Jeffrey pines (JP) 

in major study sites are distributed in six injury classes according to seasonal dose of total oxidant. 28 

318 
reproduction of white fir is reduced or ellminated, 

since the shade required by whlte fir seedlings is 

no longer present.64 Other shade-tolerant species 

are also affected. 

Changes in such physical factors as light, temperature (particularly maximums and minimums), 

relative humidlty, and wind speed for forest 

communitles subject to structural alteration by 

mortallty of susceptible species could change the 

suitability of some sites for growth, reproductlon; 

and reestablishment of survivor species. Some of 

the possible secondary effects are only speculative 

until more data are gathered. 32 

EFFECTS ON CONSUMER POPULATIONS 

Vertebrate Populations 

The effects of oxidant air pollutants on •dertebrates can be separated into direct and indirect 

categories. Direct effects include clinical and 

pathological alteration of tissues as a result of 

TABLE 12-3. CHANGES IN OXIDANT INJURY SCORES AND MORTALITY RATES OF PONDEROSA AND JEFFREY 

PINES AT 18 MAJOR STUDY PLOTS, 1973-74 38 

Tree Average intury Mortality Accumulated 

density, a score° rate, % mortality, % 

Plot Species 1973 1973 1974 1973 1974 1974 Infury description 

Schnelder Creek JP 28 12.4 11 7 00 0.0 00 Severe 

Camp O'ongo PP 90 15.1 12 9° 0.0 0.0 0.0 

Sky Forest PP 144 133 137 08 0.8 1 6 

University Conf Center PP 309 15.5 15.6 00 1 5 1 5 Moderate 

Breezy Polnt PP 236 163 160 27 2.7 5.5 

Camp Palvlka PP 217 171 164 00 31 3 1 

Dogwood A PP 168 19.9 16.5b 1 2 0.0 1 2 

Tunnel Two Rldge PP 122 195 16 7b 00 14 1.4 

Camp Angeles PP 112 25.6 16 8b 00 1.5 1.5 

Barton Flats PP 200 21 4 18 7 6 37 37 7.4 

Barton Flats JP 124 21 0 19 7° 3.6 36 73 

Snow Valley 2 JP 129 22 1 19.7° 0.0 1.0 1.0 

Green Valley Creek JP 43 21 8 20 5b 0.0 1 5 1.5 

Camp Oceola JP 192 21 7 22 8° 08 72 80 Sllght 

Bluff Lake JP 186 294 31 8° 0.0 00 0.0 Very slight 

N E Green Valley JP 120 33 1 32 1 00 0.0 00 

Heart Bar JP 130 440 39.2° 0.0 09 09 No vlslble symptoms 

Sand Canyon JP 56 41.3 47 3° 00 00 0.0 

Holcomb Valley JP 193 464 477 0 0 00 00 

aNumber of trees per hectare 

°Difference significant at probabdrty of 005 (comparisons valid only between years at a single plot) 

TABLE 12-4. CHANGES OFTIMBER VOLUMEAND PERCENTAGE OF TOTAL JEFFREY PINESa AT BARTON FLATS INTHE 

SAN BERNARDINO NATIONAL FOREST3e 

1952 1963 1972 

Timber Percentage Timber Percentage Timber Percentage 

Risk classes volume, bd it of trees volume, bd it of trees volume, bd it of trees 

Control plot 1(JCA Camp, Hlghvvay 38) 

Total, all classes 73,040 100 63,530 100 52,730 100 

Rlsks 1 and 2 58,520 87 38,700 73 23,780 55 

Rlsk 3 6,740 7 14,630 13 14,140 16 

Rlsk 4 7,780 5 10,200 7 14,810 20 

Snags and current stumps ° 1 1 11 7 13 8 

Control plot 2(Camp Oceola Road) 

Total, all classes 120,130 100 112,660 100 112,930 100 

Rlsks 1 and 2 110,830 93 98,080 82 45,670 32 

Rlsk 3 5,990 3 10,170 6 37,420 30 

Rlsk 4 3,310 2 4,410 6 29,840 28 

Snags and current stumps ° 3 2 13 6 18 10 

'In four insect risk classes at two control plots ezcluded from sanitation salvage logging between 1952 and 1972 38 

°Accumulation during 10-year period Data obtained from the Supervisor's Office, San Bernardino National Forest 

319 
exposure to ambient air. Indirect effects resuft 

from alterations in numbers or distribution of the 

plant and animal population exposed to ambient 

air. For example, if air pollution eliminates or 

decreases the quantity of a susceptible plant 

species, the food chain of the consumers that feed 

on it may break down. The result could be a simpler 

and less stable ecosystem, with fewer numbers 

and species of plants and animals. 

The clinical and pathological effects of oxidant 

air pollutants on domesticated vertebrates have 

been studied in the laboratory. No major references to studies of these effects on free-ranging 

native species seem to exist. The possible 

Interactions of vertebrates, determined by 

extrapolation from laboratory studies, are shown 

in Figures 12-11 through 12-13 for the San 

Bernardino Mountain ecosystem. 

When changes occur in one part of an 

ecosystem, the intimate nature of the interrelationships results in changes in many other 

parts. Any factor that causes change in one 

component of a system potentially affects all 

subsystems of that ecosystem. The most important 

indirect effects of oxidant air pollutants on 

vertebrates are those resulting in changes in the 

habitat. Foremost among these effects are those 

on the vegetation and the successional patterns of 

ANNUAL GROWTH OF BRANCHES, UPPER HALF OF SAPLINGS 

TERMINAL SHOOT GROWTH 

1 - AMBIENT AIR OUTSIDE ~ 

2 - AMBIENT AIR HOUSE 

3- FILTERED AIR HOUSE T 

32 

30 

28 

26 

~ 24 

= 22 

t- 20 

Z 18 

~ 16 

14 

12 

10 

8 

6 

4 

1 2 3 1 2 3 1 2 3 1 2 3 1 2 3 

1969 1970 1971 1972 1973 

32 

30 

28 

E 26 c+ 24 

2 22 

~ 20 

Z 18 

w 

-~ 16 

14 

12 

10 

8 

6 

4 

FIRST ORDER BRANCH GROWTH 

1 - AMBIENT AIR OUTSIDE 

2- AMBIENT AIR HOUSE 

3 - FILTERED AIR HOUSE 

1 2 3 1 2 3 1 2 3 1 2 3 1 2 3 

1969 1970 1971 1972 1973 

Figure 12-16. Annual growth of the terminal shoot (upper) 

and first-order branches (lower) in upper half of ponderosa 

pine saplings maintained in filtered or unfiltered (ambient) 

air greenhouses, or in outside ambient air (1968-73). 28 

320 
the plant community. Because of the high degree 

of interrelationship and interaction of the 

vegetation, the fauna, and the inorganic matrix of 

an ecosystem, effects of air pollution on the 

vegetatfon potentially can result in changes 

throughout the ecosystem. Damage to vegetation 

is probably the most important effect of chronic, 

low-concentration air pollution on wildlife. 

Ponderosa pine, Jeffrey pine, and black oak are all 

susceptible to injury, and these are the most 

important trees wlthin the forest as providers of 

food and habitat for wildlife. A similar selectivity by 

species doubtless occurs within the shrub and 

herb layers of the vegetation. The long-term effects 

will be (1 ) reduced production of fruits and seeds 

and (2) elimination of the sensitive plant species 

and a consequent reduction in the diversity of the 

vegetation. These effects will in turn lead to a 

reduction in the abundance and diversity of 

vertebrate fauna (in the numbers of pine-seedeating squirrels, for example). 

Likewise, Woodwell's prediction 71 of enhancement of the activity of insect pests and some 

disease agents (which has been demonstrated in 

this forest) could lead to an Increase in vertebrate 

species that feed on invertebrates or utilize dead 

p'ants for cove'r. Birds would be the most likely to 

increase, as would (to a smaller extent) such small 

rrammals as deer mice, which are partially 

ir sectivorous. 

IABLE 12-5. TREE SPECIES AND SIZE COMPOSITION IN 

: STUDY AFiEAe AFFECTED BY OXIDANT AIR POLLUTION38 

Ponderosa Incense White Sugar 

ree size and class pine cedar fir pine 

Understory, 

number/acre 

Seedlings (up to 

3 00 ft tall) 1057 2381 1043 302 

Saplings (more than 

3 01 ft tall, less 

than 3 99 In dbh) 3 33 57 10 

Poles (4 00 to 11 99 

In dbh) 21 12 38 3 

As % of total 22.2 48.6 22.8 63 

Overstory, 

number/acre 

Standing (12 00 to 

23 99 In dbh) 18 

Veteran (24 In dbh 

and larger) 12 

As % of total 496 22.7 19.7 8.0 

aTrees within a 575-acre study area, San Bernardino National Forest, Calif 

The indirect effects of ozone through modification of the availability of food for insects, 

particularly in a conifer forest ecosystem, has 

recelved some i nvestlgatio n.52'53 The weakenf ng of 

ponderosa pines by chronic exposure to ozone 

makes them more vulnerable to successful 

infestation by pine bark beetles (Dendroctonus 

brevicomis and D. ponderosae). Figure 12-17 

shows a positive relationship between degree of 

tree injury and frequency of bark beetle infestation 

and the relative frequency of attack by the two 

species of bark beetles. 52 The relationship (see 

Ffgures 12-10 through 12-1'1)betweentree health 

and brood productivity and the population 

dynamics of bark beetles and thelr insect 

associates in infested trees is under 

investigation. 38,56 Pine bark beetles have been a 

constant threat to ponderosa pines in the San 

Bernardino !:lountains for many years, since 

before the inception of oxidant air pollutlon 

injury. 54 Bark beetles are a key element in 

accelerating the modification of stand structure. 

Plant Parasites and Symbionts 

Ozone injury to needles of eastern white pine 

increased infection byLophodermium pinastri and 

Aureobasidium pullulans. 14 These results suggest 

that leaf tissue of many species may become 

susceptible to fungi that are normally saprophytes 

but become parasites when circumstances permft. 

Another way that oxidant air pollution could 

affect thls ecosystem is through an alteration in 

forest molsture. Elimination of vegetation cover 

allows the exposed soil to dry more rapidly, which 

would affect soil-burrowing and soil-inhabiting 

vertebrates. Also, the lower moisture content 

could reduce or inhlblt fruiting-body formatlon of 

fleshy fungi. These fleshy fungi are an important 

food source for tree squirrels and make up a third 

or more of thefr diet in some seasons. A reduction 

in this food source would doubtless result In an 

even greater utilization of conlfer seeds and 

acorns, thus reducing further the reproductive 

capability of these 'trees and eventually Ilmiting 

future food supplies for the squirrel population. 

Beneficial mycorrhizal fungi infect the small 

feeder roots of trees and other plants. The resulting 

relationship is symbiotic and involves an intimate 

exchange of minerals and essential metabolites. 

The hosttree benefitsthrough increased efficiency 

of nutrient uptakefrom the soil. Any interruptlon or 

imbalance of the exchange of materials between 

the host root tissue and the fungus mantle 

321 
surrounding It can have deleterious effects on the 

fungus and the host. Such stresses as air pollution 

injury to the host undoubtedly disrupt this 

balance. 25 The feeder rootlet system of ponderosa 

pines In the San Bernardfno Mountains and those 

of eastern white pine have shown marked 

deterioration involving a decrease in numbers of 

mycorrhizal rootlets and thelr replacement by 

saprophytic fungi that decay the small rootlets. 43 

Root-infecting fungi such as Armillaria mellea 

and Formes annosus are generally more virulent 

pathogens when they encounter trees already 

weakened by other stresses. This observatlon has 

been made mostly in Europe, where sulfur dioxide 

was the principal pollutant. 

EFFECTS ON DECOMPOSERS 

Although some of the solar energy fixed by 

producer plants Is released by the respiration of 

these plants and of animals, much of it is stored in 

dead organic matter untll released by decomposer 

organisms at rates that vary greatly with place, 

season, and kind of organic matter. Generally, onethird or more of the energy and carbon fixed 

annually in the forests is contributed to the forest 

floor as litter (mostly leaves). 42 Because litter Is 

generally related to the quantlty of photosynthetic 

tlssue In the ecosystem, it is a useful Index of 

ecosystem productivity. 

TABLE 12-6. INJURY THRESHOLDS FOR 2-HOUR EXPOSURES TO OZONE 64 

Species 

Injury threshold 

(ppm ozone 

for 2 hr) Species 

Injury threshold 

(ppm ozone 

for 2 hr) 

Grassland-oak community specles Perennlal forbs 

Allium acuminatum Hook 25 

Trees and shrubs Angehca pinnata S Wats. under 25 

Acer grandidentatum Nutt over 40 Aster engelmanm (Eat.) A Gray 15 

Acer negundo L over .25 Carex siccata Dewey 30 

Artemesia tridentata Nutt. 40 Cichorium intybus L. 25 

Mahonfa repens G. Don over .40 Cirsium arvense (L ) Scop under 40 

Potentilfa fruticosa L. .30 Epilobium angustifolium L 30 

Quercus gambehi Nutt. .25 Epifobfum watsom Barbey 30 

Toxicodendron radicans (L.) Kuntze over 30 Eriogonum herachoides Nutt 30 

Fragaria ovalis (Lehm.) Rydb 30 

Perennlal forbs Gentiana amarella L over 15 

Achillea milfefolium L. over 30 Geranium fremontii Torr. under 40 

Ambrosia psilostachya DC over 40 Geramum richardsonu Flsch & Traut 15 

Calochortus nuttalfii Torr over 40 Juncus sp over 25 

Cirsium arvense (L.) Scop. 40 Lathyrus lanzwertn Kell over .25 

Conium maculatum L over 25 Lathyrus pauciflorus Fern 25 

Hedysarum boreafe Nutt .15 Mertensia arizomca Greene 30 

Hebanthus anuus L over .30 Mimulus guttatus DC over 25 

Medocagp satova L. 25 Mimulus moschatus Dougl under 40 

Rumex crispus L. 25 Mitelfa stenopetala Plper over .30 

Urtica gracilis Alt 30 Osmorhiza occidentalis Torr 25 

Vicia americana Muhl over 40 Phacelia heterophylfa Pursh under .25 

Po%momum folrosissimum A G ray 30 

Grasses Rudbeckia occidentalis Nutt 30 

Bromus brizaeformis Flsh. & Mey. .30 Saxifraga arguta D Don under 30 

Bromus tectorum L 15 Senecio serra Hook. 15 

Poa pratensis L. 25 Taraxacum officinale Wlggers over 25 

Thalictrum fendferi Engelm over 25 

Aspen and conlfer community specles. Veromca anagaNis-aquatica L 25 

Victa americana Muhl over 25 

Trees and shrubs Viofa adunca Sm over 30 

Abtes concolor (Gord & Glend.) Llndl .25 

Amelanchier alnifolia Nutt. .20 Annual forbs 

Pachystima myrsinites (Pursh) Raf. over .30 Chenopodium fremontu Wats. under .25 

Popufus tremuloides Mlchx. 15 Callomia linearis Nutt under .25 

Rtbes hudsomanum Rlchards. 30 Descurainia californica (Gray) 0 E Schuls 25 

Rosa woodsii Llndl over 30 Galium bifoAum Wats. over 30 

Sambucus melanocarpa A. Gray over .25 Gayophytum racemosum T & G 30 

Symphoricarpos vaccimotders Rydb. .30 Polygonum douglasii Greene over .25 

Perennlal forbs Grasses. 

Actaeu arguta Nutt. 25 Agropyron camnum (L.) Beauv over 25 

Agastache urticifolia (Benth.) Kuntze 20 Bromus carinatus Hook & Arn under 25 

322 
One of the predicted effects of pollutants on 

ecosystems suggested by Woodwell" is a 

reduction in the standing crop of organic matter, 

which would lead to a reduction in nutrient 

elements held within the living system. The 

evidence discussed earlier deflnitely shows that 

primary production is much lower In an ozonestressed conifer forest ecosystem. This result 

would be anticipated in all natural ecosystems or 

agroecosystems under similar stress. 

The reservoir of energy and mineral nutrients 

represented by litter is a very important resource in 

natural ecosystems with closed nutrient cycles. 

The growth of new green plant tissue depends on 

the slow release of nutrients by decomposer 

organisms. In agroecosystems geared for high 

production, litter is often removed or burned, and 

fertilizer is added to the soil; the nutrient cycle is 

open and subsidized. 

In a conifer forest, litter production and 

decomposition release about 80 percent of the 

total minerals in the biomass of the stand; the 

remainder is retained in the living parts of the 

tree. 31 Standing dead material is not considered 

litter. 

In terrestrial ecosystems, most decomposers 

occupy the mantle of litter on the surface layers of 

the soil, where they supply the necessary recycling 

mechanisms to convert dead plant or animal 

material into humus and eventually into minerals, 

gases, and water. Small animals, arthropods, 

fungi, and bacteria exist as a complex in intricate 

500 

TOTAL NUMBER OF TREES 

400 TREES KILLED BY BARK 

W BEETLES 

W 

~ 300 

LL 

O 

~ z 2°° n 

,UO 

4,.2% 

3.5% 7.0% 

[~~

d 

0 

HEALTHY LIGHT MODERATE SEVERE 

INJURY INJURY INJURY 

SMOG INJURY RATING 

food chains in which they feed on dead material 

and on one another as well, ultimately releasing 

the mineral nutrients needed by the producer 

populations. Without the decomposers, some 

essential elements (such as calcium, phosphorus, 

and magnesium) would concentrate in the litter 

until the supply in the soil was depleted. Growth of 

green plants would then be seriously limited. 

It is not known whether ozone, PAN, or other 

oxidants could have any direct influence on 

decomposer organisms other than fungi (see 

Chapter 1 1, section on responses of mosses, ferns, 

and microorganisms) in the litter layer. But there 

does appear to be a rapid flux of ozone to soil 

surfaces. The ozone flux to some kinds of surfaces 

constituting ecosystems (e.g., vegetation, soil, and 

water) has been determined by Aldaz,l who 

expressed the flux as molecules/cmz-sec X 10. The 

relativefluxes intodifferentsurfaces, assuming an 

ozone concentration of 40 Ug/m3 , were: Fresh 

water, 0.5; snow, 0.9; grass, 1.1 ; sand or dry grass, 

5; and juniper bush, 10. Furthermore, it wasfound 

that bare soil destroyed about 75 percent more 

ozone when dry than when moist. The 

determination of ozone flux to surfaces may be a 

far more realistic measure of dose to living 

organisms than atmospheric concentration of 

ozone, according to Munn. 37 

In summary, it is anticipated that decreasing 

litter production by green plants experiencing 

pollutant stress would result in a similar reduction 

in the inventory of nutrient elements held within 

60 r 

D. ponderosae ONLY 

O 50 

w 

J 

J 

D. brevicomis ONLY 

Y 

y 40 ATTACKED BY BOTH 

w SPECIES 

S 

~ 30 

U. 

0 

. 

0 ' 

HEALTHY LIGHT MODERATE SEVERE 

INJURY INJURY INJURY 

SMOG INJURY RATING 

Figure 12-17. Relationship of degree of oxidant injury in ponderosa pines with bark beetle attack (teft) and number of trees 

killed by western pine beetle, mountain pine beetle, or both species (right). 46 

323 
the system, owing to the interruption of nutrient 

cycling pathways and mechanisms of nutrient 

conservation. 71' 72 

Overall, it can be seen that subtle and simple 

initial changes may radiate and magnify 

throughout all trophic levels of the ecosystem. 

Restoration of the system may be impossible. 

SUMMARY 

Plants, animals, and microorganisms usuallydo 

not live alone but exist as populations Populations 

live together and interact as communities. 

Communities, because of the interactions of their 

populations and of the individuals that constitute 

them, respond to pollutant stress differently from 

individuals. Man is an integral part of these 

communities, and as such, he is directly involved in 

the complex ecological interactions that occur 

within the communities and the ecosystem of 

which he is a part. 

The stresses placed on the communities and the 

ecosystems in which they exist can be farreaching, since the changes that occur may be 

irreversible. For example, it has been suggested 

that the arid lands of India are the result of 

defoliation and elimination of vegetation that 

induced local climatic changes not conducive to 

the reestablishment of the original vegetation 

An ecosystem (e.g , the planet Earth, a forest, a 

pond, an old field, or a fallen log) is a major 

ecological unit made up of living (biotic) and 

physical (abiotic) components through which the 

cyciing of energy and nutrients occurs. A 

structured relationship exists among the various 

components. The biotic units are linked together by 

functional interdependence, and the abiotic units 

rnake up all of the physical factors and chemical 

substances that interact with the biotic units. The 

processes occurring within the biotic and abiotic 

units and the interactions among them can be 

influenced by the environment 

Ecosystems tend to change with time. Adaptation, adjustment, and evolution are constantly 

taking place as the biotic component, the 

populations, and the communities of living 

organisms interact with the abiotic component in 

the environment. Recognizable sequential 

changes occur With time, populations and 

communities may replace one another This 

sequential change, termed "succession," may 

result in climax cornmunities The latter, which are 

structurally complex and more or less stable, are 

held in a steady state through the operation of a 

particular combination of biotic and abiotic factors. 

The disturbance or destruction of a climax 

community or ecosystem results in a return to a 

simpler stage. Existing studies indicate that 

changes occurring within ecosystems in response 

to pollution or other disturbances follow definite 

patterns that are similar even, in different 

ecosystems. The basic biotic responses to the 

disturbance of an ecosystem can thus be broadly 

predicted. 

Diversity and structure are most changed by 

pollution as a result of the elimination of sensitive 

species of flora and fauna and the selective 

removal of the larger overstory plants in favor of 

plants of small stature. The result is a shift from the 

complex forest community to the less complex, 

hardy shrub and herb communities.The opening of 

the forest canopy changes the environmental 

stresses on the forest floor, causing differential 

survival and, consequently, changed gene 

frequencies in subcanopy species. Associated with 

the reduction in diversity and structure is a 

shortening of food chains, a reduction in the total 

nutrient inventory, and a return to a simpler and 

less stable successional stage. 

It should be emphasized that ecosystems are 

usually subjected to a number of stresses at the 

same time, not just to a single perturbation (e.g., 

oxidant). 

The effects of oxidants on the San Bernardino 

Forest graphically demonstrate the changes that 

occur in natural ecosystems, as discussed earlier. 

The San Bernardino Forest has been undergoing 

oxidant stress as a result of long-range transport 

from Los Angeles, 224 km (140 miles) away, since 

the early 1940"s. Losses of ponderosa and Jeffrey 

pines, the overstory vegetation, have increased 

dramatically as pollutant levels have risen. Black 

oak has also suffered oxidant injury. An alteration 

in the composition of both plant and animal 

populations has resulted because of the death of 

the ponderosa and Jeffrey pines. 

The interaction of pollutant and inversion layers 

at the heated mountain slope results in the vertical 

venting of oxidants over the mountain crest by upslope flow. 

Oxidant concentrations ranging from 100 to 200 

/_Ig/m 3 (0.05 to 0.10 ppm) at altitudes as high as 

2432 m(8000 ft), approximately 1033 m(3400 ft) 

above the mountain crest, were measured by 

aircraft 

The total oxidant concentrations have been 

measured continuously from May through 

3 :1a 
September since 1968 at the Rim Forest/Sky 

Forest monitoring station. During each of the first 7 

years of monitoring, between June and 

September, the total number of hours with 

concentrations of 1 60 ,ug/m3 (0.08 ppm) or more of 

ozone was never less than 1300 hours. The 

number of hours wherein the total oxidant 

concentration was 390/jg/m 3 (0.20 ppm) or higher 

increased from fewer than 100 in 1969 to nearly 

400 in 1974. It is not uncommon to observe 

momentary oxidant peaks as high as 1 180 Ng/m 3 

(0.60 ppm). The duration of oxidant concentrations 

exceeding 200 pg/m 3 (0.10 ppm) was 9, 13, 9, and 

8_ hr/day going from the lower to the higher 

altitude stations. 

The most recent data firmly indicate that oxidant 

concentrations will either increase annually or 

oscillate around the mean of present high 

concentrations in the foreseeable future. 

The transport of the urban plume from the coast 

northeastward to the mountains can be readily 

demonstrated. Because of this transport, the 

permanent vegetation constituting natural 

ecosystems receives a large chronic exposure, and 

the short-lived, higher-value vegetation constituting the agroecosystem of the Los Angeles 

coastal plain is subjected to injurious doses in 

intermittent, short-term fumigations. Each situtation has measurable economic and aesthetic 

effects, but on different time scales. The singlespecies argricultural ecotogic system (the 

agroecosystem) has little resilience to pollutant 

stress; losses are sometimes immediate and 

occasionally catastrophic. The complex natural 

ecosystem is initially more resistant to pollutant 

stress, but the longer chronic exposures cause 

disruption of both structure and function in the 

system that may be irreversible. 

Oxidant injury to the mixed conifer stands of the 

San Bernardino Mountains beginning in the early 

1940's, as indicated above, is well advanced. A 

similar problem is developing in the forests of the 

southern Sierra Nevada. Both areas show direct 

and indirect effects on all subsystems of the forest 

ecosystem—producers, consumers, and decomposers. 

In summary. 

1. Ozone injury has limited the growth and 

caused the death of ponderosa and Jeffrey 

pines. An estimated 1,298,000 trees have 

been affected. Decrease in cone production 

has resulted in a decrease in reproduction. 

Black oak has also suffered injury from 

ozone. 

2. Reduction in fruits and seeds that make up 

the diet of most of the common small 

mammals influences the populations of 

these organisms. 

3. Essential processes, such as recycling of 

nutrients, may be disrupted, causing a 

limitation in the growth of vegetation. 

4. Death of the predominant vegetation has 

caused an alteration in the species 

composition and a change in the wildlife 

habitat. 

The San Bernardino Mountain study illustrates 

the complexity of the problems caused by 

environmental pollution. The changes that have 

occurred in this mountain ecosystem as a result of 

oxidant transport have already influenced the 

importance and value of this natural resource to 

the residents of southern California. 67 

The injury to the eastern white pine in the 

Appalachian Mountains resulting from oxidant 

transport from the urban northeast has begun a 

similar sequential change that could degrade this 

important recreational area. Total oxidant peaks as 

high as 220 Ng/m 3 (0.11 ppm) were recorded for 

July 1975. Concentrations exceeding 160 Ng/m 3 

(0.08 ppm) were measured in June 1976. These 

episodes resulted in significant increases in 

oxidant injury to three categories of eastern white 

pine in the Blue Ridge Mountains. 

Evaluating the contribution of functioning 

natural ecosystems to human welfare is a complex 

task and usually involves weighing both economic 

and social values. However, because natural 

ecosystems are life support systems, their value 

should not be quantified in economic terms. 

With the passage of time, man has destroyed 

many of the naturally occurring ecosystems of 

which he was a part and has replaced them with 

simplified ecosystems wholly dependent on his 

care and protection and requiring a large input of 

energy. 5 o 

Man favors the simple, unstable and synthetic 

ecosystems, because when they are extensively 

managed and subsidized by the use of fossil fuels, 

they are highly productive. An agricultural 

ecosystem (agroecosystem) is an example of such 

a simplified ecosystem. The effects of oxidants on 

agroecosystems have been under study for more 

than 20 years. The study of effects on natural 

ecosystems is much more recent. 

Plants grown in agroecosystems are largely 

325 
annuals and can be replaced when they are 

susceptible to pollutant stress. Natural ecosystems 

remain in place year after year. Manmade 

pollutants are undoing relationships developed 

within these ecosystems over millions of years. 

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36 Miller, P R, and A A Millecan Extent of oxidant air Background and Proposed Systems Study of the San 

pollution damage to some pines and other conifers in Bernardino Mountain Area EPA-R3-73-043a, U S 

California Plant Dis Rep 55 555-559, 1971 Environmental Protection Agency, Washington, D C, 

37. Munn, R E Biometeorological Methods Academic 1973 

Press, Inc, N Y 1970 55 Taylor, 0 C Oxidant Air Pollutant Effects on a Western 

38 National Research Council Ozone and other Coniferous Forest Ecosystem Task C Study Site 

PhotochemicalOxidants National Academy of Sciences, Selection and On-site Collection of Background 

Washington, D C, 1977 pp 586-642 Information EPA-R3-73-043B, U S Environmental 

39 Odum, E P Summary /n Ecological Effects of Nuclear Protection Agency, Corvallis, Ore , February 1973 

War G M Woodwell, ed BNL 917 (C-43), Brookhaven 56 Taylor, 0 C Oxidant Air Pollutant Effects on a Western 

National Laboratory, Upton, N Y, 1965 pp 69-72 Coniferous Forest Ecosystem Task D University of 

40 0'Neill, R V Modeling in the eastern deciduous forest California, Statewide Air Pollution Research Center, 

biome /n Systems Analysis and Simulation Ecology Riverside, Calif , July 1974 

Volume III B C Patten, ed Academic Press, N Y, 1975 57 Taylor, 0 C, and P R Miller Modeling and oxidant air 

pp 49-72• pollutantimpactonaforestecosystem Calif AirEnviron 

41 Overton, W S The ecosystem modeling approach in the 4 1-3, 1973 

coniferous forest biome /n Systems Analysis and 58 Thompson, C R Effects of air pollutants on lemons and 

Simulation Ecology Volumelll B C Patten,ed Academic navel oranges Calif Agric 22 2-3, 1968 

Press, N Y, 1975 pp 117-138 59 Thompson, C R, and G Kats Antioxidants reduce grape 

42 Ovington, J D Dry-matter production by Pinus sylvestris yield reductions from photochemical smog Calif Agric 

L Ann Bot (London) 21 287-314, 1957 24 12-13, 1970 

43 Parmeter, J R, Jr , R V Bega, and T Neff A chlorotic 60 Thompson, C. R., G Kats, and E Hensel Effects of 

decline of ponderosa pine in southern California Plant ambient levels of ozone on navel oranges Environ Sci 

Dis Rep 46 269-273, 1962 Technol 6:1014-1016, 1972. 

44 Patten, B C The relation between sensitivity and stability 61 Thompson, C.R., and 0 C Taylor Effects of air pollutants 

/n Ecosystem Analysis and Prediction S A Levin, ed on growth, leaf drop, fruit drop, and yield of citrus trees 

Society for Industrial and Applied Mathematics, Environ Sci Technol 3 934-940, 1969 

Philadelphia, Pa , 1976 pp 141 -143 62 Thompson, C R, 0 C Taylor, and B L Richards Effects 

45 Pelz, E Untersuchungen uber die Fruktification of photochemical smog on lemons and navel oranges 

rauchgeschadigter Fichtenbestande Arch Forstwes. Calif Agric.24 10-11, 1970 

12 1066-1077, 1963 63 Thompson C R, 0 C Taylor, M D Thomas, and J 0 Ivie 

46 Scheffer, T C, and G G Hedgecock Injury to Effects of a ir pollutants on apparent photosynthesis and 

northwestern trees by sulfur dioxide from smelters U S water use by citrus trees Environ Sci Technol 1 644- 

Dept Agric Tech Bull (1117) 1-49, 1955 650, 1967 

47 Shugart, H H, Jr, ,T R Crow, and J M Hett Forest 64 Treshow, M, and D Stewart Ozone sensitivity of plants 

succession models A rationale and methodology for in natural communities Biol Conserv 5 209-214, 1973 

modeling forest succession over large regions For Sci 65 U S Forest Service Silvicultural systems for the major 

19 203-212, 1973 forest types of the United States U S Department of 

48 Sinclair, W A Poliuted air Potent new select ve force in Agriculture, Agric Handb (445) 1-1 14, 1973 

forests J For 67 305-309, 1969 66 Wert, S L A system for using remote sensing techniques 

49 Skelly, J M, C F Croghan, and E M Hayes Oxidant to detect and evaluate air pollution effects on forest 

levels in remote mountainous areas of southwestern stands /n. Proceedings of the 6th International 

Virginia and their effects on native white pine (Pinus Symposium on Remote Sensing of the Environment 

strobus L). ln International Conference on University of Michigan, Ann Arbor, Mich 1969 pp 1169- 

Photochemical Oxidant Pollution and Its Control 1178 

Proceedings Volume II B Dimitriades, ed EPA-600/3- 67 Westman, W E How much are nature's services worth? 

77-001 b, U S Environmental Protection Agency, Science 197 960-964, 1977 

Research Triangle Park, N.0 , January 1977 pp 611- 68 Wiegert, R G Simulation models of ecosystems Annu 

620 Rev Ecol Syst 6 31 1-338, 1975 

327 
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damage to the forests of the Sierra Nevada Mountains of 

California. J Air Pollut Control Assoc 27 230-234, 

1977 

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terrestrial ecosystems Science 138 572-577, 1962 

71 Woodwell, G M Effects of pollution on the structure and 

physiology of ecosystems Science 168 429-433, 1970 

72 Woodwell, G M The ecological effects of radiation Sci 

Am 208 40-49, 1963 

328 
13. EFFECTS OF OZONE ON MATERIAl.S 

INTRODUCTION 

Ozone is a major causative factor in the overall 

Aeterioration of many different types of organic 

materials. In fact, certain polymeric materials are 

more sensitive to ozone attack than are humans or 

animals. The magnitude of ozone damage, 

however, is difficult to assess because it is only one 

of the many photochemical oxidants in the 

atmosphere that contribute to the weathering of 

materiais. Nevertheless, researchers have shown 

that ozone does accelerate the deterioriation of 

several classes of material, including elastomers 

(rubber), textile dyes and fibers, and certain types 

of paints. Also, a National Academy of Sciences 

report28 goes into detail to show that the damage 

observed in most laboratory controlled 

experiments is caused by ozone rather than some 

other unmeasured oxidizing species. 

That same document postulates that in urban 

atmospheres, other oxidizing species may be more 

damaging than ozone. It was assumed that the 

relative reaction rates of various oxidizing species 

with trans-2-butene (a gas) are the same for 

reactions with solid surfaces. This assumption did 

not consider that at ambient levels, reactions with 

surfaces will most likely be diffusion-controlled 

rather than activation-energy-controlled. Thistype 

of rate -controlling mechanism depends on the 

concentration gradient at the surface, which is 

roughly proportional to the ambient concentration. 

Ozone is the most abundant of the active oxidants. 

MECHANISMS OF OZONE ATTACK 

Ozone is so chemically active that, when 

concentrated, handling it becomes a problem 

because of its effect on ordinary materials. In 

general, materials of organic origin are affected 

deleteriously by concentrated ozone. 9 Bailey' has 

thoroughly reviewed the literature from 1939 to 

1957 for reactions of ozone with a host of organic 

compounds, and he describes the reaction 

mechanisms in detail. Although it is incorrect to 

assume that all of these reactions would occvr at 

atmospheric concentrations of ozone, it is possible 

that many of these reaction mechanisms would be 

operant. 

Many polymers are sensitive to atmospheric 

concentrations of ozone, 22 resulting in the 

occurrence of chain-scissioning or cross-linking or 

both. These reactions are related to the prevalence 

of double bonds in the polymer structure. Chainscissioning results in a reduction in average 

molecular weight and in decreased tensile 

strength. Cross-linking increases the rigidity of 

some polymers, thus increasing brittleness and 

reducing elasticity. 

Effects On Elastomers 

OZONE CRACKING 

The cracking of stressed natural rubber exposed 

to outdoor environments has been a troublesome 

materials problem for many years. At first, most 

rubber technologists believed that sunlight was 

the major cause of this phenomenon. However, 

several investigators, mainly Williams 39 and Van 

Rossem et a1., 38 concluded that cracking was due 

to atmospheric ozone rather than sunlight, but the 

relative importance of ozone was not immediatety 

recognized. Not until the 1940's did the research of 

Norton, 30 and especially that of Newton, 29 and 

Crabtree et a1., 10 '" suggest that free radicals, 

produced by the catalyzed photolysis of volatile 

peroxides present in smog, may also contribute to 

rubber cracking. 

Cracking is related to the chemical structure of 

rubber compounds and their elastic properties. 

Vulnerable elastomers are those containing many 

double bonds. An example of a chemical 

mechanism may be written: 28 

329 
/ o \ 

0 0 

03 +-C ~ C -~ C C - 

I I I I 

H H H H 

--C`-0-0- + 0=C - 

I I 

H H (13-1) 

The zwitterion and aldehydic group may combine 

to form a more brittle oxidized structure: 

0 

—C; —O—O- + 0=C–%C/ \C~ 

I 1 H \ /I 

H H 0-O 

H 

(13-2) 

The most vulnerable compounds are natural 

rubber and synthetic polymers of styrenebutadiene, polybutadiene, and polyisoprene. 

These elastomers account for about 75 percent of 

the annual production value in the United States. 

Except for natural rubber, the major use for 

these elastomers is in tires. Butyl, halogenated 

butyl, polychloroprene, vinyl-modified nitrilebutadiene, and carboxylated nitrile elastomer.s 

have some ozone resistance but required special 

formulation for optimum performance. Synthetic 

elastomers with saturated chemical structures 

such as silicones, ethylenepropylenes, 

chlorosulfated polyethylenes, polyacrylates, and 

fluorocarbons have inherent ozone resistance. 

These latter special-application materials, 

however, are relatively expensive and account for 

only a small fraction of the market on a weight 

basis. 

Tensile stress is necessary to produce ozone 

cracking in sensitive elastomers. The resulting 

cracks develop at right angles to the direction of 

stress. Elastomers in a relaxed state can be 

exposed for long periods of time to relatively high 

c;oncentrations of ozone without developing 

cracks. Crabtree and Malm 1 z reported that cracks 

will develop in sensitive elastomerswhen strained 

as little as 2 to 3 percent and exposed to 

atmospheres containing only 20 /_Ig/m 3 (0.01 ppm) 

ozone. As strain is increased to 100 percent plus, 

the number of cracks increases from a few deep 

cuts to numerous shallow ones. At still higher 

strain, small cracks are so numerous that the 

surface simply presents a frosted appearance, and 

damage from deep cracks is negfigible. 

Bradley and Haagen-Smit' summarized the 

factors that influence the action of ozone on 

elastomers. These include (1) the nature of the 

elastomeric compound, (2) degree of stress, (3) 

concentration of ozone, (4) time of exposure, (5) 

rate of the ozone contacting the elastomer, and (6) 

temperature. Furthermore, cracking may be 

divided into two main phases: crack formation and 

crack growth. Scientists have proposed several 

theories to explain ozone cracking, but the exact 

mechanism is still not clear. Braden and Gent 6 

explained the strong dependence of crack growth 

on nominal tensile stress in terms of the Griffith 

theory of fracture mechanism. Fracture mechanics 

alone only partially explain observed relationships 

between number and size of cracks as a function of 

strain. Crack growth rate is also ozoneconcentration dependent, which suggests that the 

rate of diffusion of ozone to the root of a crack is the 

rate-controlling factor. 

More recently, Devries and Simonson 13 have 

applied the Griffith theory on a molecular scale. 

The energy required for crack growth is extracted 

from the elastic strain energy in the elastomer and 

is expressed in terms of the energy to rupture 

bonds and the number of bonds broken. They 

indirectly determined the cracking rates 

experimentally by measuring the number of 

resulting free radicals with a highly sensitive 

electron spin resonance (ESR) technique. Their 

observations were consistent with both theory and 

the results of previous damage studies. 

ANTIOZONANTS 

Fisher 17 and Mueller and Stickney27 discussed 

the use of antiozonant additives to protect 

elastomers from ozone degradation. First 

developed in 1955, antiozonants are organic 

compounds, generally secondary aromatic amines 

and phenols. They are incorporated into 

elastomeric formulations during mixing and tend 

to migrate to the surfaces of parts after 

vulcanizing, where theyform a film that chemically 

reacts with atmospheric ozone before it contacts 

the elastomer. These protective films are effective 

even when elastomers are stretched or flexed. 

Although widely used in such elastomeric 

products as tires, conveyer belts, automotive parts, 

and cable insulation, antiozonants have 

330 
limitations. They are expensive and add to the cost 

of finished products. For example, the addition of 

1.5 percent antiozonants to automobile tires 

Increases the cost by as much as $0.50 per tire. 

Furthermore, during product usage, antiozonants 

provide only temporary protection against ozone 

damage because they react with ozone and are 

inactivated. Contact with oils, gasoline, and other 

chemicals may also remove them by extraction. 

The amount of antiozonant necessary for 

effective control increases with the anticipated 

concentration of atmospheric ozone. Although 

undocumented, several sources have told EPA 

scientists that tire manufacturers roughly double 

the amount of antiozonant added to rubber used in 

tires sold in California. Despite preventive 

measures, however, ozone cracking of sensitive 

elastomeric products still remains a major 

problem. 

DOSE-RESPONSE DATA 

In reviewing dose-response data, one must keep 

in mind the many factors that affect the rate of 

attack by ozone on vulnerable elastomers. 

Furthermore, methods of reporting effects data 

vary from one research to another and thus further 

complicate comparison. For example, an effect 

may be expressed as time requlred to initiate either 

microcracks or visible cracks, or it may be 

expressed as crackdepth or crackgrowth rate. 

Much of the documented research on ozoneelastomer effects has been conducted at ozone 

concentrations considerably higher than those 

normally found in polluted environments. This has 

been intentional in order to accelerate reaction 

rates. However, some investigators have carried 

out research at lower ozone concentrations. 

Bradley and Haagen-Smit' evaluated a natural 

rubber formulation (Table 13-1) for susceptibility to 

ozone cracking. Strlps were strained 

approximately 100 percent by bending. When 

exposed in a 13-mni-diameterglasstubeto40,000 

mg/m3 (2 percent or 20,000 ppm) ozone in air at a 

flow rate of 1 5 I/min, these specimens cracked 

instantaneously and broke completely within 1 

sec; however, when they were exposed to various 

lower concentrations of ozone, different time 

periods were required for cracks to develop (Table 

13-2). (Ozone levels were measured bythe neutral 

KI method.) Based on these data, the initiation of 

cracks is controlled by the dose of ozone 

(concentration x time). The mean and estimated 

standard deviation of the dose for this particular 

experiment is a product of 1.32 ± 0.03 ppm X 

minutes. 

TABLE 13-1 . FORMULATION OF HIGHLY 

OZONE—SENSITIVE NATURAL RUBBER 8 

Ingredients Parts by weight % by weight 

Rubber 100 35.91 

Tire reclaim 125 44.88 

SRF Black 33 11.85 

Sterlc acld 1.5 054 

Plne tar 84 3.02 

Zlnc oxlde 47 1.69 

Mercaptobenzothlazole 08 0.29 

Dlphenylguanldlne 01 0.03 

Sulfur 5 1.79 

'Cured 40 min at 310,050 N/m' (45 psi) steam pressure 

TABLE 13-2. EFFECT OF OZONE ON NATURAL RUBBER a 

Ozone concentration Time-to first sign of crack at 

pg/m3 ppm 4x magnification, min 

40 0.02 65 

500 025 5 

900 045 3 

'See Table 13-1 for formulation, strained 100 percent 

Meyer and Sommer 25 exposed thin 

polybutadiene specimens, under constant load, to 

room air for which the average concentrations of 

ozone had been measured by the neutral KI 

method. Specimens exposed In the summer 

months to average ozone concentrations of about 

96 pg/m 3 (0.048 ppm) failed by breaking into two 

separate parts after 150 to 250 hr. In the fall, at 

average ozone concentrations of 84 Ng/m 3 (0.042 

ppm), specimensfailed between 400 and 500 hr. In 

the winter, at average ozone concentrations of 48 

/_Ig/m 3 (0.024 ppm), failures occurred between 500 

and 700 hr. These data show the strong 

dependence of . cracking rate on average 

concentrations of ozone. It takes much longer for 

complete failures to occur than it does to initlate 

cracks. The mean and estimated standard 

devlation of the dose required to cause 100 percent 

complete failures in these specimens were 996 ± 

270 ppm x minutes. 

Edwards and Storey 16 determined the effects of 

ozone on elastomeric formulations (Table 13-3) 

containing various amounts of antiozonants and 

elther a styrene-butadiene rubber (SBR) polymer 

that had been polymerized at elevated 

temperatures ( rr hot" SBR) or one polymerized at 

room temperatures ("cold" SBR). The basic polymers were used in tire sidewall formulations. The 

investlgators exposed test specimens under strain 

(100 percent) to ozone concentrations (measured 

by the neutral KI method) of 490 ± 100 Ng/m 3 

331 
(0.25 ± 0.05 ppm) at 49°C (120 0 F). Table 13-4 

shows the calculated rate of cracking for the 

various formulations. The results provided 

evidence that the hot SBR polymer is inherently 

superior in resistance to attack by ozone, and 

increasing amounts of antiozonants produced 

significant reductions in the rate of cracking and 

thus increased the dose necessary to initiate 

visible cracks. The function is exponential: 

Dose (ppm x minutes) = a e bZ (13-3) 

where z is percent antiozonant. Regressions on 

these data show that b Is essentially the same for 

the two formulations (1.5) and that the a values are 

17.3 and 9.8, respectively, for the hot and cold 

SBR. The dose would have to be three orders of 

magnitude greater for cracks to grow to 2.54 mm. 

To prevent failure of 5-mm-thick sidewalls 

exposed under 100 percent strain at 49°C (120 0 F) 

to 100 Ng/m3 ozone for 3 years (781,840 ppm x 

minutes), an estimated 0.56 percent and 0.94 

percent of antiozonant in the hot and cold SBR 

would be needed, respectively. 

TABLE 13-3. TIRE SIDEWALL FORMULATION 16 

Ingredients Parts by wetght 

Polymer (hot or cold SBR a ) 100 

Ctrcosol 2 XH 10 

FEF black 30 

SRF black 10 

Zinc oxlde 3 

Sterlc acld 2 

Antlozonant (Santoflex AW) Varlable 

Crystex 2 

aSBR is styrene-butadiene rubber polymenzed either at high or room temperature 

TABLE 13-4. EFFECTS OF OZONE ON SIDEWALL 

FORMULATIONS CONTAINING VARIOUS 

ANTIOZONANT CONCENTRATIONS 

Antiozonant Rate of crackmg _ Time to first 

concentration, μm/hr tn /hr s+gn of crack, 

Polymer % x 10 -' mm, _ 

Hot SBR 0 234 092 65 

032 1 75 069 87 

063 089 035 170 

1 25 033 013 460 

Cold SBR 0 401 1 58 38 

032 216 085 71 

063 1 45 057 105 

1 25 061 024 250 

~ Added to enable comparison with data in Table 13-2 First 

sign of crack was assumed to be 2 54 Nm (1 x 10 ' in ) crack 

depth, visible at 4x magnification Data are not found tn the 

paper by Edwards et al 11 

Hofmann and Miller 21 found that the behavior of 

rubber exposed to ozone under laboratory 

conditions correlated well wfth the service 

behavior of tlres In localities where atmospheric 

ozone concentrations were high. The relative 

susceptibility of different formulations of white 

sidewall rubber remained the same, whether 

exposed under laboratory conditions to as much as 

1000 /jg/m3 (0.5 ppm) ozone, or In the ambient air 

of the Los Angeles areas. The rate of cracking is 

thus a function of ozone concentration. 

In a factorial-design, controlled-environment 

experiment, Haynie et a1. 79 exposed several 

classes of materials to realistic levels of pollutants 

and climatic factors. White sidewall speclmens 

from a top-quality steel-belted radial tire were 

exposed (strained at 10 and 20 percent) for up to 

1000 hr. The level of ozone was a statistically 

significant factor in the rate of cracking of the 

white sidewall rubber. The average results with 

respect to strain and ozone level are given in Table 

13-5. 

TABLE 13-5. CRACKING RATES OF WHITE SIDEWALL 

TIRE SPECIMENS 19 

Ozone conc , Mean cracking rate ± S D,' 

pg/m3 (ppm) Strain, % mm/yr 

160 (0 08) 10 1036 % 776 

20 11 70 % 7 22 

1000(05) 10 1980%964 

20 24.09 % 6 24 

'S D= esttmated standard devtatuon of the mean 

Cracking rates are not directly proportional to 

ozone concentrations for these two levels. A 

coefficient for estimating crack depth based on the 

lower concentration is 34.5 ± 4 8 mm/ppm-year. 

This indlcates it would take 3 years to crack a 5-mm 

sidewail exposed to 100 /lg/m 3 (0.05 ppm). This 

does not include the time requiredforthe resulting 

exposed tire cord to fail. 

For this particular premium tire, one would 

expect the tread to wear out before sidewall failure 

from ozone damage occurred. However, the casing 

would have questlonable value for retreading. 

ECONOMICS 

As the tread wear on passenger car tires 

improves, more or better antiozonants will have to 

be added to sidewall rubber formulations to 

prevent cracking from becoming the limiting factor 

in tire life. Thus part of the cost of premium tires 

will be the result of increased protection against 

atmospherlc ozone. 

Mueller and SticlCney, 27 on the basis of a rubber 

industry survey, assessed the economic Impact of 

332 
air pollution on elastomeric products in the United 

States. They estimated the loss at the consumer 

level to be $500 million annually. About $170 

million of this total was associated with various 

means of protection, including antiozonants and 

special polymers. The remaining $330 million was 

associated with premature failure of rubber 

products. (See Reference 28 for a more complete 

description of technique and costs.)The respective 

annual per capita costs in 1970 are $0.85 and 

$1 .65. If more were spent on preventive measures, 

there would be less cost for failures. The 

relationship between dose to initiate cracks and 

antiozonant level suggests that for a fixed dose in 

1970, failure costs (Y) would be related to 

preventive costs (X) by the relationship 

Y = 5.9 e-' 5X (13-4) 

The total cost is the sum of X and Y. By 

differentiating with respect to (X) and setting it 

equal to zero, the optimum total cost in 1970 is 

calculated to be $2.12. This value is $0.38 less per 

person than was estimated. 

By reducing ambient levels of ozone, it is 

possible to establish some new optimization of 

preventive and failure costs. Assuming that a 

population-weighted national annual average for 

ozone was 65 Ng/m3in 1970, the optimum per 

capita cost as a function of average ozone 

concentration in the ambient is: 

Cost = 0.66 (In 03 1) (13-5) 

when Os concentration is pg/m 3annual average. 

Because it is unlikely that consumers will 

optimize present prices with anticipated use life, 

these costs serve as a minimum estimate. A cost 

function with a 25-percent error range is 

Cost = $0.88 (1 ± 0.25) x(In 03 1) (13-6) 

This relationship suggests that if the national 

annual average concentration of ozone were 

lowered from 65 Ng/m3to 50Ng/m3there could be 

a savings in elastomer damage and damage 

prevention costs of from 37 to 61 million dollars. 

Comparably, lowering the annual average from 

100 /jg/m3to 50 Ng/m 3for 6.9 million people in 

the Los Angeles Standard Metropolitan Statistical 

Area (SMSA) could save from 2.0 to 3.3 million 

dollars. 

Effects on Textiles 

Both fibers and dyes can be damaged by ozone; 

however the fading of dyes is a more signi.ficant 

factor than the loss of fiber strength. 

DYE FADING 

Although atmospheric nitrogen oxides were 

identified during the early 1900's as an important 

cause of color fading in certain textile dyes, mainly 

disperse dyes on acetate fabrics, it was not until 

the mid-1950's that the research of Salvin and 

Walker 32showed the effects of atmospheric ozone. 

This discovery came about as a result of field 

testing acetate fabrics containing newly 

synthesized blue disperse dyes. Previous 

laboratory exposures of these dyes had shown 

them to be highly resistant to fading by nitrogen 

oxides. Field testing was carried out to determine if 

the performance of these new dyes was as good in 

actual use as in laboratory tests. 

The researchers exposed fabrics dyed with one 

of the new blue dyes (as a color component) in 

homes located in areas known to have either low or 

relatively high levels of nitrogen oxides. At the lownitrogen-oxides sites, they found that fading for 

many of the fabrics equaled, and in some cases 

exceeded, the fading observed at the highernitrogen-oxides site. Much of the observed fading 

was characterized by a bleached, washed-out 

appearance rather than the famil iar reddening that 

nitrogen oxides produce in most sensitive dyes. 

This anomalous behavior suggested that some 

other oxidizing agent was responsible and was 

present at all exposure locations. 

To describe this fading phenomenon, the 

investigators coined a new term, "0-fading." 

Follow-up laboratory investigations and general 

observations showed atmospheric ozone to be 

responsible. Ozone concentrations of 200 Ng/m 3 

(0.10 ppm) produced marked fading in most of the 

blue disperse dyes and in some of the reds and 

yellows. 

The discovery of the 0-fading was useful in 

explaining much of the anomalous fading of 

certain dyed fabrics observed during subsequent 

lightfastness testing and service exposure trials 

reported by Schmitt. 3a,as Other types of dyes 

besides the disperse dyes showed abnormal 

fading. Furthermore, the results of the service 

trials emphasized the importance of relative 

humidity, suggesting that the increased moisture 

content of fibers such as cotton promoted and 

accelerated the absorption and reaction of 

pollutants with vulnerable dyes. They also alerted 

the textile industry to the possibility of potential 

consumer complaints. Such complaints began to 

appear in the early 1960's and concerned mainly 

333 
two distinctly different textile materials— 

polyester-cotton/permanent press fabrics, and 

nylon carpet. 

Salvin 31 reported that the fading of polyestercotton/permanent press fabrics was first noted on 

the folds and edges of slacks stored in warehouses 

or on the stock shelves of retail outlets. Some 

garments faded after storage in warehouses for as 

few as 10 days. Incidents occurred in various 

locations including California, Texas, and 

Tennessee. Because of the volume of garments 

involved, some producers suffered heavy 

economic losses. Fading was marked by a loss in 

blue along with a slight increase in red, suggesting 

that ozone and, to a lesser degree, nitrogen oxides 

may have been the active fading agents, since 

sunlight was obviously not a factor. This 

conclusion did not seem reasonable, however, 

because the cotton was dyed with vat dyes and the 

polyester with disperse dyes, and both dye-fiber 

systems are generally resistant to fading by 

common air pollutants. Furthermore, fading 

occurred only on fabrics that had been made into 

finished products and then cured to set the 

permanent press resin Fading had not been 

observed during the temporary storage of dyed 

fabrics either before or after treatment with 

permanent press resins (before curing). 

However, after a thorough investigation, 

including extensive laboratory tests, researchers 

found ozone to be the major fading agent, with 

nitrogen oxides also capable of causing fading, but 

to a lesser extent. The fading mechanism, which is 

unique and compiex, takes place as a result of the 

curing operation and involves the disperse dyes on 

the polyester fibers rather than the vat dyes on the 

cotton. During curing, some disperse dyes partially 

migrate to the permanent press finish, which is a 

combination of reactant resin, catafysts, softeners, 

and nonionic wetting agents. The disperse dyes 

migrate to the solubilizing agents (nonionic 

surfactants and softeners) in the finish and are 

then in a medium in which fading by air 

contaminants can easily occur. Softeners are an 

especially good medium for absorbing gases 

The choice of catalyst used in the finish plays an 

important role, as the migration of disperse dyes 

increases significantly when magnesiurn chloride 

is used as a catalyst rather than zinc nitrate. 

Magnesium chloride is capable of forming 

complexes with certain anthraquinone disperse 

dyes (blues and reds), and these complexes are 

soluble in the resin finish Therefore, as Dorset 15 

pointed out, to eliminate this fading problem, 

textile processors must carefully select materials 

that make up the permanent press finish and/or 

replace vulnerable dyes with those that resist 

migration. 

According toSalvin, 31 thefading of nyloncarpets 

originated mainly in the warm humid areas from 

Texas to Florida and, as a result, became known as 

"Gulf Coast fading." In one case, nylon carpeting 

in a Texas apartment complex showed visible 

fading only 30 days after installation. A few similar 

incidents were also noted along the east coast and 

in the Los Angeles area. Fading occurred on 

carpets manufactured from both nylon 77 and 

nylon 6 fibers. Disperse dyes were used because 

many possess easy leveling properties necessary 

to avoid dye streaks. Fading took place largely on 

those carpets dyed with Disperse Blue 3 as one of 

the color components. Avocado, a tertiary-dyed, 

dull green shade, was a particularly sensitive color. 

The fading of this color was characterized primarily 

by loss in blue, which caused the green color to 

turn gradually to a dull orange shade. 

Investigators eliminated sunlight as a primary 

cause of fading, since the phenomenon occurred in 

rooms where light intensity was low. Exposure of 

carpet samples to standard test methods for ozone 

also failed to duplicate the color change. Since 

fading complaints occurred in humid 

environments, and since previous lightfastness 

testing and service trials had established that 

conditions of high relative humidity promoted 

fading of certain dyes by ozone, the investigators 

next exposed carpet samples to ozone in the 

presence of high relative humidity (85 to 90 

percent). Under these conditions, pronounced 

fading took place on those samples containing 

Disperse Blue 3, and the fading was similar to the 

color changes observed in homes along the Gulf 

Coast. Later experiments established that the 

relative humidity must be somewhat above 65 

percent for pronounced ozone fading to occur. The 

fading problem may be prevented by using dyes 

that are more ozone resistant and by using nylon 

fibers that have been modified (by dry-heat 

texturing) to decrease the accessibility and 

diffusion rate of ozone. 

Complaints were also received from consumers 

about faded drapery and upholstery fabrics. 

Salvin31 reported that the combination of ozone 

and high humidity causes pronounced fading of 

certain dyes on cotton and rayon fabrics. 

334 
Beloin3' 4 investigated the effects of air pollution 

on various dyed textiles by conducting both field 

and controlled-environment laboratory studies. 

The field study consisted of exposing a wide range 

of dyed fabric in light-tight cabinets located at four 

urban and four rural (control) sites that were 

nearby and had similar characteristics except for 

air pollution. These sites represented a cross 

section of various types of pollution (urban sites) 

and climates. The study was carried out over a 2- 

year period, with eight consecutive 3-month 

seasonal exposures. 

Color change data, along with air pollution and 

weather measurements, were statistically 

analyzed in an effort to identify the factors that 

caused fading. Beloin found that about two-thirds 

of the fabrics studied showed appreciable fading. 

Most of these fabrics faded significantly more at 

urban sites than at the rural sites, and the amount 

of fading varied among metropolitan areas and 

among seasons. Air pollution was assumed to 

account for most of the environmental differences 

between the urban and the corresponding rural 

control sites. Analysis suggested that the 

pollutants measured (NO2, ozone, and SOz) 

appeared to be those most responsible for fading. 

Generally it was impossible to separate the effects 

of individual pollutants because they were 

confounded with the effects of other pollutants. 

The controlled-environment laboratory study 

was designed to assess the effects of common air 

pollutants, temperature, and relative humidity on 

the colorfastness of 30 dyed fabrics selected from 

those exposed during the field study. Fabric 

samples were exposed to two concentrations of 

ozone: 100 Ng/m3 (0.05 ppm) and 1000 /ag/m 3 

(0.50 ppm). Ozone concentrations were 

continuousiy measured by coulometric (Mast) 

analyzers. As might be expected, under similar 

exposure conditions, high ozone levels produced 

significant fading in more fabric samples than did 

low levels. Low levels, nevertheless, produced 

visible fading in about one-third of the sensitive 

fabrics—an important finding since the low levels 

were similar to those frequently found in 

metropolitan areas. The study also demonstrated 

that high relative humidity (90 percent) and, to a 

lesser extent, high temperature (32°C or 90°F) are 

significant factors in promoting and accelerating 

ozone-induced fading, thus confirming what 

investigators observed during previous service 

trials. The amount of ozone fading as a function of 

time was dependent on such factors as color and 

type of dye, fiber substrate, and environmental 

conditions. 

Haynie et a1. 19 and Upham et a1. 37 exposed three 

moderate-to-high-volume-usage drapery fabrics 

to combinations of controlled-environment 

conditions to determine both direct and synergistic 

effects of gaseous pollutants. There were no 

statistically significant direct or synergistic effects 

of ozone on the fading of any of the dyes after 

exposures of 1000 hr to ozone up to 1000 pg/m 3 . 

Relative humidity was a significant fading factor 

for all three fabrics, and nitrogen dioxide faded one 

of the fabrics. Fading as a function of time was 

consistent with the theoretical relationship: 

DE = AE m(1-e--at) ( 13-7) 

where DER, represents the maximum fade or 

complete dye destruction, t is time, and a is a 

constant containing the effects of environmental 

variables. 

An unacceptable level of fading is subjective and 

varies considerably with individuals. A percentage 

of useful life lost depends only on the ozone level, 

because other factors, including subjective 

unacceptable I.evels of fading, cancel out. This 

relationship is: 

Percentage life lost = (a' -ao) 100 (13-8) 

a, 

where ao is the exponential coefficient for clean 

air, and a, is the value with some level of pollution. 

These functions should be applicable to ozone 

fading as well as NOz fading. 

Haylock and Rusht 8 studied ozone fading of 

anthraquinone dyes on nylon fibers in controlled 

environments. Olive I and Olive II dyes on nylon 6 

carpets yarn was exposed to 400 Ng/m3 and 1800 

pg/m 3 ozone at 40°C (104°F) and 90 percent 

relative humidity. The same materials were 

exposed to 400 /!g/m 3 ozone at 40°C (104 0 F) and 

70 percent and 80 percent relative humidity. C.I. 

Disperse Blue 3 and C.I. Disperse Blue 7 on nylon 6 

were exposed to 400 Ng/m 3 , 1000 Ng/m 3 , and 

2000 Ng/m 3 ozone at 40°C (104 1 F) and 90 percent 

relative humidity. They were also exposed at 50°C 

(122°F) and 30 percent relative humidity to 400 

Ng/m3 ozone. 

The fading curves were highly consistent with 

the theoretical relationship of equation 13-7. 

Regression equations on the Haylock and RushI$ 

data can account for 99 percent of the variability. 

With these data, coefficients were calculated for 

three of the dyes that were significantly affected by 

335 
different ozone levels. Linear regressions of these 

coefficients with respect to ozone were then 

calculated. For the exposures at 40°C (104 0 F) and 

90 percent refative humidity, the results are as 

fol lows: 

Olive I: 

a= 0.381 + 3.65 X 10-5 03 (13-9) 

Olive II: 

a= 0.00107 + 1.18 x 10-5 03 (13-10) 

C.I. Disperse Blue 7: 

a= 0.0212 + 5.35 x 10-6 03 (13-11) 

where a is reciprocal hours, and 03 is in Ng/m 3 . 

Assuming that the relative effect of ozone with 

respect to other fading mechanisms remains the 

same at normal temperatures and relative 

humidities, these relationships convert to the 

fol lowi ng. 

Olive I: 

Percent life lost = 0.09603 

1 + 0.00096 03 (13-12) 

Olive II: 

Percent life lost= 1.1 03 

1 + 0.011 03 (13-13) 

C.I. Disperse Blue 7: 

Percent life lost = 0.02503 

1 + 0.00025 03 (13-14) 

These functions curve only slightly when ozone is 

below 100 pg/m 3 . Thus the costs of early 

replacements can be assumed to be directly 

proportional to ozone levels. 

FIBERS 

Because cellulose fibers are vulnerable to 

oxidation, atmospheric ozone is a potential cause 

of degradation. With this in mind, Bogaty et a1. 5 

carried out experiments to study the possible role 

of ozone in the deterioration of cotton textiles. They 

exposed samples of duck and print cloth to air 

containing between 40 and 120 Ng/m 3 (0.02 and 

0.06 ppm) ozone (measured by the neutral KI 

method at room temperature and in the absence of 

light). Samples were exposed both dry and wet; the 

moisture content of the wet samples was never 

less than 50 percent. The researchers used 

changes in fluidity values to assess degradation. 

Fluidity (reciprocal of viscosity) is an indirect 

measure of the average molecular weight of 

polymer. Such reductions reflect changes in 

tensile strength and other physical properties. 

After the cloth samples were exposed for 50 

days, fluidity values increased for the cotton 

samples that were moist during exposure, butthey 

did not appreciably change for the samples that 

remained dry during exposure. Fluidity values for 

control samples that were kept moist but not 

exposed to ozone showed little change. These 

results indicate that ozone caused virtually all the 

degradation. In addition to increased fluidity, the 

moist samples experienced a 20-percent loss in 

tensile strength after exposure to ozone. Similar 

fabrics were also exposed to higher levels of ozone, 

resulting in a greater increase in the'degradation 

(fluidity) of the moist samples. The overall study 

showed that low levels will degrade cotton fabrics 

if they are sufficiently moist. The mechanism of 

ozone attack appears to be primarily due to its 

increased solubility in water, since at room 

temperature, ozone is considerably more soluble in 

water than is air. 

The investigators estimated that the laboratory 

exposure conditions (50 days, high moisture and 

ozone) were equivalent to 500 days of exposure 

under field conditions. They concluded that 

ambient levels of ozone, while capable of 

damaging moist cotton fabrics, produce 

deterioration that was slight compared with that 

from other elements of weathering such as 

sunlight, heat, alternate wetting and drying, and 

micro-organisms. 

Morris26 also studied the effects of ozone on 

cotton. Samples of a special print cloth were 

exposed in the absence of light to 1000Ng/m 3 (0.5 

ppm) ozone (coulometric method, Mast analyzer) 

for 50 days in a chamber maintained at 21 °C (70°F) 

and 72 percent relative humidity. No appreciable 

effect on breaking strength or fluidity was found. 

Apparently, the moisture content of the cotton (9 

percent) was not high enough to produce the 

degradation that Bogaxy measured in wet cotton 

samples, even though the concentration of ozone 

was considerably higher (about 10 times). 

The laboratory study of Kerr et a1. 23 examined the 

effect of periodic washing on the tendering of 

cotton fabrics exposed to ozone. They exposed 

samples of print cloth, dyed with C.I. Vat Blue 29, in 

a chamber to a continuous supply of clean air with 

known levels of ozone added. The concentration of 

ozone (coulometric method, Mast ana{yzer) 

averaged 1500 ,ug/m 3 (0.75 ppm), and samples 

were exposed at room temperature in the absence 

of light. The investigators did not measure relative 

humidity, although they attempted to increase the 

336 
humidity by placing a pan of water on the chamber 

floor. At 3-day intervals, the cotton samples were 

removed from the chamber. Half of them were 

machine-washed, and the other half were soaked 

in water for 1 min. AII samples were passed 

through a hand wringer to remove excess water 

before they were returned to the chamber for 

further exposure. Control samples were kept in a 

light-tight box maintained at 21 °C (70°F) and 65 

percent relative humidity, and they were given the 

same washing and soaking treatment. 

After an exposure period of 60 days, which 

included 20 washing and soaking treatments, the 

change in strength of the control fabrics was not 

significant. By comparison, the fabrics exposed to 

ozone changed significantly; the loss in strength 

for the washed fabrics was 18 percent, and for the 

soaked fabrics, 9 percent. The investigators 

attributed these losses to ozone. 

Since Morris26 found no degradation under 

exposure conditions similar to those used by Kerr, 

the washing and soaking treatment would appear 

to affect in some way the sensitivity of the fabrics 

to ozone. Nevertheless, when one attempts to 

equate Kerr's findings with actual conditions 

encountered by ,consumers, the degradation 

seems minimal in view of the fact that average 

levels of ozone under field conditions are less than 

10 percent of the levels used in the laboratory 

exposure. 

In laboratory studies, Zeronian et al.ao 

simultaneously exposed modacrylic (Dynel), 

acrylic (Orion), nylon 66, and polyester (Dacron) 

fabrics to artificial sunlight (xenon arc) and 

charcoal-filtered clean air contaminated with 400 

/jg/m3 (0.2 ppm) ozone (analytical method not 

given) at 48°C (118°F) and 39 percent relative 

humidity. During exposure, the fabric samples 

were sprayed with water for 18 min every 2 hr. 

Ozone damage was measured by comparing these 

samples with fabrics exposed to the same 

environmental conditions but without ozone. After 

exposure for 7 days, the investigators found that 

ozone did not affect the modacrylic and polyester 

fibers; but it did seem to affect the acrylic and nylon 

fibers slightly. 

ECONOMICS 

Barrett and Wadde11 2 used data from an 

unpublished contract report by Salvin to estimate 

the national cost of ozone fading at approximately 

$80 million/year. These costs were associated 

with the fading of acetates/triacetates, nylon 

carpets,and permanent press fabrics. Salvin 

produced his estimates from costs of preventive 

measures as well as loss-of-use life based on an 

Industry survey. Preventive measures included 

more expensive dyes and manufacturing 

procedures, research, and quality control testing. 

The estimated totals for preventive and failure 

costs were $43 and $37 million, respectively. On a 

per capita basis, these respective annual costs are 

$0.22 and $0.18. 

Because there was a lackofdose- responsedata, 

Barrett and Waddellz did not attempt to establish 

an economic damage function based on these 

estimates. One can be postulated assuming an 

analogy with elastomer economic damage costs. 

For elastomers, an estimate of the amount of 

damage saved by preventive measures is 5 times 

the cost of those measures An analogous 

relationship between damage costs (Y) and 

preventive cost (X) is: 

Y = 1 .28e-asx (13-15) 

It follows, using the same procedures as with 

elastomers, that a reasonable economic damage 

function with 50 percent error is: 

Cost = $0.22 (1 ± 0.5) (1 n 03 - 0.74) (13-16) 

over the range of ozone concentrations greater 

than 5.7 /_Ig/m 3 . 

This relationship suggests that from $6.2 to 

$18.6 million could be saved annually by lowering 

the national annual average ozone concentration 

from 65 to 50,ug/m 3 . 

Effects on Paints 

DAMAGE FUNCTION 

Campbell et al.$ have conducted laboratory 

research and field studies indicating that ozone 

may damage palnt. The technique used to assess 

damage, erosion measurements (weight loss 

converted to thickness loss), proved to be the most 

meaningful. Erosion, or the gradual weathering of 

the surface of paint film, is the normal mechanism 

of failure that limits the service life of well 

formulated and properly applied exterlor coatings. 

The researchers selected five exterior coatings 

from four commercially important paint types: 

house paints (oil and acrylic latex), coil coating* 

finishes (urea-alkyd), automotive refinishes 

(nitrocellulose/acrylic), and industrial 

maintenance coatings (alkyd). 

'Cod coating is a factory-apphed coating to a coil of sheet metal 

337 
Panels coated with the dffferent exterior paints 

were exposed to controlled-environment 

conditions, including clean air (control), clean air 

containing 200 /jg/m 3 (0.1 ppm) ozone, and clean 

air containing 2000Ng/m 3 (1.0 ppm)ozone. Ozone 

concentrations were measured using the buffered 

KI method. The exposure chamber operated on a 2 

hr light-dew cycle consisting of 1 hr of xenon light, 

70 percent relative humidity, and a black panel 

temperature of 66°C (151 °F), followed by 1 hr of 

darkness at 100 percent relatfve humidity of 49°C 

(1201 F), during which time moisture condensed on 

the coated panels. One group of panels was 

exposed to simulated sunllght while a like group of 

panels was shaded during the exposures. 

Erosion measurements were made after 

exposure periods of 0, 400, 700, and 1000 hours. 

Erosion rates for each paint type and exposure 

condition were then caiculated from the erosion 

results. Zero-hour results, however, were 

excluded from these calculations because erosion 

rates during the 0- to 400-hr period were greater 

than during the remaining exposure (400 to 1000 

hr). The researchers concluded that this was 

primarily caused by removal of water soluble 

materials and that materials subsequently eroded 

consisted mainly of binder and pigment. 

Generally, exposures to 2000 /_Ig/m 3 (1 ppm) 

ozone produced statistically significant increases 

in erosion rates compared to clean air (zero 

pollution) conditions. Erosion rate increases, 

however, varied considerably among pafnt types. 

Oil-based house paint experienced the largest 

erosion rate increase; industrial maintenance 

paint, a moderate increase; and latex and coil 

coatings and automotive refinishes the smallest 

increases. As would be expected, unshaded panels 

eroded more (degradation by sunlight)than shaded 

panels. Because of considerable data variabil+ty, 

exposures to 200 Ng/m 3 (0.1 ppm) ozone generally 

did not produce statistically significant erosion rate 

increases over clean air exposures. 

Table 13-6 gives regression coefficlents for the 

effects of ozone baspd on the data of Campbell et 

a1.8 Because the rdte of ozone damage is controlled 

by the rate of ozone transport to the paint rather 

than activation energy for reaction, these 

coefficients should be applicable to lower ambient 

temperatures. 

AII of the coefficients are positive, and half are 

statistically significant. The largest coefficients 

were determined on data with the greatest 

variance. Consequently, they are not statistically 

signiflcant, although the effects they represent 

could be real. 

Field exposures were conducted in Leeds, 

N.Dak., Valparaiso, Ind., Chicago, Ill., and Los 

Angeles, Calif. These locations, respectively, 

represent clean, moderate-S02, high-S02, and 

high-ozone environments. 

Panels of the five different coatings were 

mounted at an angle of 85 1 from the horizontal to 

represent normal exposure conditions of house 

siding. Half of the panels were mounted facing 

south, and half facing north. Panels were 

evaluated after 0, 3, 7, and 14 months of exposure. 

As with the laboratory data, the zero-month results 

were not used In calculating erosion rates. 

TABLE 13-6. PAINT EROSION RATE COEFFICIENTS 

FOR THE EFFECTS OF OZ0f11E IN 

LABORATORY-CONTROLLED ENVIRONMENTS 36 

Mean and estimated S D of erosion rate 

coefficients for ozone, pm/yr per pg/m 3 

Shaded Unshaded 

Automottve 0 00216 ±0 00043a 0 00325 ± 0 00026' 

Latex 0.00099 ± 0 00074 0.00214 ± 0.00007' 

Industrlal 

malntenance 0.01073 ±0 01473 0 01098 ± 0.01774 

Coll coating 0 00129 ± 0 00207 0.00752 ± 0 00176 e 

011 house Dalnt 0.00812 ±0.00378 a 0.02726 ± 0.01894 

aCoefficient significantly greater than zero at 0 95 probabdity level 

The erosion rates for Leeds and Los Angeles are 

presented in Table 13-7. With the exception of the 

north-facing automotive coating, all of the erosion 

rates are signlficantly higher in Los Angeles than 

in Leeds. The latex, coil coating, and oil house paint 

contain fillers that are susceptible to SOz attack. 

The automotfve and industrial maintenance 

coatings do not contain fillers. Thus, many of the 

differences in erosion rates between Leeds and 

Los Angeles for the filler-containing paints could 

be caused by differences in S02 levels. The 

observed dffferences in the automobile and 

industrial maintenance coatinas could be 

attributed primarily to higher ozone levels in Los 

Angeles. For example, using the laboratoryobtained coefficients, ozone differences of 85 to 

111 Mg/m3 can account for the erosion rate 

difference between Leeds and Los Angeles. Ozone 

levels were not measured, but an average 

difference of 40 to 60 pg/m 3 ozone is consistent 

with reported air pollutfon data. Also, average 

differences in temperature and other pollutants 

would be expected to contribute to the higher 

erosion rates in Los Angeles. 

338 
TAB LE 13-7. PAINT EROS I O N RATES AT FIELD EXPOSURE SITES 

Mean and estimated S D of erosion rates, Nm/year 

Panel facinq north Panel facing south 

Leeds Los Leeds Los 

Automotive 0 305 ± 0.076 0.305 ± 0 046 0.305 ± 0.107 0 610 ± 0 031 

Latex 0 305 ± 0.046 0 914 ± 0 137 0.305 ± 0.076 0 914 ± 0.351 

Industrial maint 0.914 ± 0 198 1 829 ± 0 213 1 219 ± 0.366 2 438 ± 0.320 

Coll coating 0 610 ± 0.091 3.088 ± 0 351 0 610 ± 0 122 3 658 ± 0 381 

011 house palnt 0.305 ± 0.137 3.962 ± 0 945 0 610 ± 0.213 4.877 ± 0.793 

In laboratory-controlled environments, Spence 

et a1. 36 studied the direct and synergistic effects of 

gaseous pollutants on commonly used exterior 

paints. Useful data were obtained on a vinyl coil 

coating, an acrylic coil coating, and an oil-base 

house paint. The oil-base house paint contained a 

calcium carbonate filler that was strongly attacked 

by S02 and moisture. The magnitude and 

variability in this effect masked any possible 

observed effect of ozone. Statistically significant 

effects of ozone were observed for the vinyl coil 

coating and the acrylic coil coating. There was a 

positive interaction effect between ozone and 

relative humidity on the vinyl coil coating, and a 

positive direct ozone effect on the erosion rate of 

the acrylic coil coating. Both of these coatings are 

very durable, which is why they were selected for 

factory application to aluminum siding material. 

Coatings as thin as 20 Nm should last more tha n 20 

yea rs. 

The vinyl coil coating was not affected by ozone 

at an input relative humidity of 50 percent, but it 

was at 90 percent. At the high relative humidity, 

the multiple regression coefficient for ozone was 

0.00166 Nm/year X(pg/m 3 ). The average erosfon 

rate in clean air was 1.3 Nm/year. 

A linear regression for the acrylic coil coating 

data gives. 

Erosion rate = 0.159 + 0.000714 03 (13-17) 

where erosion rate is /im/year and 03 is Ng/m 3 . 

Although the ozone effect on this coating is 

statistically signlficant, it has no practical 

significance because the erosfon rate Is so slow. At 

an average annual 03 level of 100 /jg/m 3 , this 

regression predicts that a 20-pm-thick coating 

would last over 80 years. 

ECONOMICS 

Most of the laboratory-observed effects of ozone 

on paint have little practical slgnlficance because 

their relative contrlbutions to reducing useful life 

at ambient concentrations are so small. Ozone 

damage to some industrial maintenance paints 

and vinyl coil coatings could possibly produce 

economic losses. 

Estimates of damage functions for the two 

affected coatings can be obtained by extrapolating 

the laboratory data to expected ambient 

conditions. The result for the industrial 

maintenance paint is: 

Erosion rate = 1+ 0.01 03 ± 0.3 (13-18) 

where erosion rate is mm/year, 03 ispg/m 3 , and 

±0.3 is the estimated standard deviation. 

Similarly, the result for the vinyl coil coating is: 

Erosion rate = 1+ 0.001 03 ± 0.4 (13-19) 

If erosion rate controls paint life, a percent life 

lost as a function of ozone concentration can be 

calculated. With estimates of the existing amounts 

of exposed palnted surfaces and repainting costs, 

economic loss functions can be postulated. 

Paint industry statistics are reported annually by 

Charles H. Kline and Co., Inc. 24 Estimated 

shipments of all Industrial maintenance coatings 

in 1974 were 55 million gal. Alkyds that do not 

contain fillers probably account for 25 percent of 

those sales. Assuming a coverage of 300 ftz/gal at 

50.40/ft2 and half exterior exposure, the annual 

per capita repainting cbsts are estimated at $3.83. 

Conslderable labor is involved in surface 

preparation and application of industrial 

maintenance paints. 14 

Coil-coated aluminum and glavanized steel have 

experienced a growth rate In shipments of 

approximately 13 percent from 1962 to 1974. 24 

Seventy percent of these shipments are used in 

exterior applications. It is estimated from these 

production flgures that 290 ft 2 /person of all coil 

coatings are exposed to exterior ambient 

conditions. If 40 percent are vinyl coatings and 

repainting costs are 50.25/ft 2 , the per capita 

repaintfng costs for exposed susceptible coatings 

are $29. At a 23-year life expectancy, the annual 

cost is $ 1 .26. 

The fraction of paint life lost as a function of 

ozone concentration tlmes the annual per capita 

339 
repainting costs of affected paints gives an annual 

economic loss function. For industrlal 

malntenance paints: 

Annual per capita costs = 0.0383 03 (13-20) 

1 + 0.01 03 

And for the vinyl coatings: 

Annual per capita costs = 0.00126 03 (13-21) 

1 + 0.001 03 

Industrial maintenance costs are indlrectly paid 

by the public in hlgher prices for products and 

services. These costs are considered a nontaxable 

cost of doing business on which profit margins and 

markups are partially based. These difficult-toquantlfy factors were not included in the per capita 

cost estimates as a function of ozone level. Losttax 

revenues and markups could add conslderably to 

the cost of ozone damage. Preventive maintenance 

is a nonproductive consumption of energy, labor, 

and materials that could be redirected to improve 

quality of Ilfe. 

Effects on Other Materials 

In a revlew of the effects of photochemical smog 

on materlals, Sanderson 33 included possible 

effects on plastic tract recorders and asphalt. 

Because the effects were observed in laboratory 

tests at extremely high ozone levels (200,000 

pg/m 3 and 104,000 pg/m3 , respectively), they 

should have no practical signlflcance at amblent 

levels. 

Haynle and Upham20 reported a possible 

beneficial effect of photochemical oxldants on the 

corrosion behavior of steel. Their study used a 

nonlinear multiple regression technlque to 

evaluate corrosion data as a function of field 

envlronmental condltions. Laboratory studies 19 did 

not show any statistically significant effect of 

ozone on steel corrosion. Some unmeasuredfactor 

that was covariant with photochemical oxidants 

could have caused the beneflcial effect that was 

observed in the field studles. 

SUMMARY 

Although many organlc materials have been 

shown to be susceptible to ozone attack, only 

damage to certain paints, elastomers, and dyes 

represents signlficant economic loss. Measures to 

prevent ozone damage to elastomers and dyes are 

a major cost. In contrast, the paint Industry has not 

recognized the economic significance of posslble 

ozone damage, and costs to prevent such attack 

are not identifiable. 

Figure 13-1 graphically presents a summary of 

the estimated total annual per caplta cost of ozone 

damage and preventive measures as a function of 

annual average concentration. The low and hlgh 

estimates are based on data error and lack of 

confidence in many of the assumptlons that were 

necessarily made. 

This figure predicts that considerable savings 

from reduced damage to materials will be reallzed 

as the annual average ozone levels are decreased. 

This economic benefit is in addition to improved 

health, agriculture, visibility, and ecology, andthus 

it adds to the total quallty of life. 

Ozone materlals damage as an Indivldual 

problem can be solved more cost effectively by 

developing, identifying, and buying ozoneresistant materials. This approach has the distinct 

advantage of being applicable below natural 

background levels of ozone because, in general, 

there are no threshold limits to material damage. 

10 

9 

G 0 

1- fA B 

O 

U 

w 

c7 7 

a ~ 

o s 

a 

¢ 5 

W 

a 

~ 4 

a Ju 3 

~ 

W 

J 2 

a 

~ 

Z 

Z 1 a 

10 20 30 40 50 60 70 80 90 100 

ANNUALAVERAGEOZONECONCENTRATION,μg/m' 

Figure 13-1. Effect of annual average ozone concentration 

on added costs resulting from damage to materials and 

preventive measures. 

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compounds Chem Rev 58 925-1010, 1958 

2 Barrett, L. B. and T E Waddell Cost of Air Pollution 

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Protection Agency, Research Triangle Park, N C, 

February 1973 pp 23-25 

3 Beloin, N J Fading of dyed fabrics by air pollutants A 

chamber study Text Chem Color 5 128-133, 1973 

HIGH ESTIMATE 

BEST ESTIMATE 

LOW ESTIMATE 

340 
4. Beloin, N J. A field study. Fading of dyed fabrics by air 

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5 Bogaty,H,K S Campbell,andW.D.Appel.Theoxidation 

of cellulose by ozone in small concentrations Text. Res J 

22 81-83, 1952. 

6 Braden, M, and A N. Gent The attack of ozone on 

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7 Bradley, C. E., and A J. Haagen-Smit The application of 

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Chem Technol 24 750-755, 1951. 

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Paint Technol 46 59-71, 1974 

9 Cloyd, D R, and W. J Murphy. Technology Survey 

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D C , September 1965 

10 Crabtree, J, and B S Biggs. Cracking of stressed rubber 

by free radicals J Polym. Sci 11.280-281, 1953. 

11 Crabtree, J, and A R. Kemp Accelerated ozone 

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14 Dillon, C P The economic advantage of deferred topcoat 

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18 Haylock, J.0 , and J.L Rush Studies on the ozone fading 

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8, 1976 

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pollutants on corrosion behavior of steels Mater Prot 

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