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/m 3 (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

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

. . . . . . . . . . . . . .. 

### . . . . . . . . . . . . . . . . . . . .
.. .. 

### 1 SOURCES AND SINKS OF OXIDANTS

. 

### .... ...... . . . . . . .. 

### . . 

### ... . 

### 1 OXIDANT PRECURSORS

........ . 

### .... . . . . .
.. 

### . .

.. 

### . .
.. 

### . .

.. 

### . 

### .... 2 RELATIONSHIPS BETWEEN AMBIENT OXIDANT AND PRECURSOR EMISSIONS

................................................. 3MEASUREMENT 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

............................................. 

### 65AMBIENT 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/O s 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 Co j unty 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
Br 2

B 

### scat oC

14c CAMP
CARB
C1'C3
C1'C4 C2+

C2H2
C4+

C4,5 C4-C6 C5-C10 C6H5
C6H5C002NO2 CC

Cdyn 

### CH(CH 3 )CHQ
CH2CHCH0
CH 2 CH 2
CH2C0 CH2O
CH 3
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

cm 3 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)
C s t 

### 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 ft 2 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
H 2 C0 Formaldehyde; also HCHO and CH2O
H z 0 Water
H z Oz Hydrogen peroxide H 2 S 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 K H 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

m 2 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 N z 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

90 

### Sr 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
V 25 Maximum expiratory flow rate at 25% of VC
V 50 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/m 3 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. Theyconsist 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/m 3 (0.3 ppm). In rural areas, peak concentrations are lower but often exceed the 1-hr National Ambient Air Quality Standard of 160 pg/m 3 (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, themechanisms 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 reactionwith 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
55 0 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 ruralareas. Based on the evidence of stratospheretroposphere interchange, the annual averagestratospheric contribution to ozone concentrations at ground level is estimated to be 43 to 98 Ng/m 3 (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/m 3 (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, thecomposition 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 manmadesources, with natural sources probably contributing more on a global scale. Natural and anthropogenic sources are, however, generally segregated geographically, so that anthropogenicemissions 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 underconsideration. 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 accuratelymeasured 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 maysignal 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 secondgroup of unreactive subjects, the same investigators observed substantial decrements in lung function after only 2 hr of exposure to 980 μg/m 3 (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 inairway resistance, as measured by plethysmography, were observed in two of four healthy subjects immediately after a 1-hr exposure to 200 ug/m 3 (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/m 3 (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 investigatorsdid 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/m 3 (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/m 3 (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/m 3 (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/m 3

(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/m 3 ,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 2 3 /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 anincreased 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/m 3 (0.5 ppm) ozone and intermittent light
exercise for 2 3

/a 

### hr. Following a 2-hr exposure to 730Ng/m 3 (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/m 3 (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 haveyielded 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 0.2ppm 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/m 3 , or 0.54 ppm ozone continuous for 3months). 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/m 3 (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/m 3 (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/m 3 (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 OXIDANTSON 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 leafstipple of grape. Many plants show an uppersurface response with no associated injury to thelower 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 ofplants 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 controlledenvironments 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 temporaldistribution was nota significantfactor. When soybean plants were exposed to 1468 /jg/m 3 (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/m 3 (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/m 3 (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/m 3 (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/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 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/m 3 (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 mixturescan 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 onferns, 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 beenundergoing 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 theverticalventing 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/m 3 (0.08 ppm) or more was
never less than 1300. The number of hours in
which the total oxidant concentration was 390 Ng/m 3 (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/m 3 (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 asfish 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, andclimate. 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 areassociated 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 theother 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 anthropogenicsources 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 inwhich 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/m 3 (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/m 3 294 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

oftTABLE 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 sites a 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 onabsolute 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., 1968 21

' 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/m 3 = 1 ppb as PAN

NETABLE 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 1130 24 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.. 1973 21

' 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 areasor 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

22TABLE 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 Freonsor 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 lowerthan 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 thirdconceivable 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 resultlargely 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 ofatmospheric 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

a

+6% `.

+89% BASINWIDE HC EMISSION CHANGE: 18%

BASINWIDE NO X EMISSION 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 2 5 9 ~ 0. Q w O L / \

' O 20 % / ~O

o ' ~ O z 15 -

~ 0 .1

y 30

w z O Oa ° m 25 - 

# rnwv a 20 ` ~ /~ 

# — `

~ P--0\\ 

### 20 a ~ 7 b~

~ 

### OO 15 1 0

, ` 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

2514

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
process 18,3 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, NO X , 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

27A 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 ItsControl 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 onphotochemical 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 ViewpointsPart III The Issue of Stratospheric Ozone Intrusion EPA600/3-77-115, U S Environmental Protection Agency, Research Triangle Park, N C, December 1977

26 National Air Pollution Control Administration. Air Quality
Criteria for Photochemical Oxidants. NAPCA Publication No AP-63, U S Department of Health, Education, and Welfare, Public Health Service, Washington, D. C, March
1970 27 National Research Council. Ozone and Other Photochemical Oxidants National Academy of Sciences, Washington, D C , 1977 28 Office of Air Quality and Planning Standards Monitoring and Air Quality Trends Report, 1972 EPA-450/1 -73- 004, U S Environmental Protection Agency, Research Triangle Park, N C, December 1973 29 Office of Air Quality and Planning Standards Monitoring and Air Quality Trends Report, 1973 EPA-450/1-74- 007, U S Environmental Protection Agency, Research Triangle Park, N C, October 1974 30 Office of Air Quality and Planning Standards Monitoring and Air Quality Trends Report, 1974 EPA-450/1-76- 001, U S Environmental Protection Agency, Research Triangle Park, N C, February 1976
31 Office of Air Qualityand Planning Standards NationalAir Quality and Emission Trends Report, 1975 EPA-450/1- 76-002, U S Environmental Protection Agency, Research Triangle Park, N C, November 1976 32 Office of Air Quality Planning and Standards The National Air Monitoring Program Air Quality andEmissions Trends Annual Report Volumes I and II EPA450/1-73-001a and b, U S Environmental Protection Agency, Research Triangle Park, N C, August 1973 33 Rasmussen, R A Surface ozone observations in rural and remote areas J Occup Med 18 346-350, 1976

28 36

37

38

39

40

41

42

43

44

45

46 Ripperton, L A, and J J. B Worth Chemical and Environmental Factors Affecting Ozone Concentration in the Lower Atmosphere Environmental Science and Engineering Publication No 234, University of North Carolina, Chapel Hill, N C., 1969. R+pperton, L A, J J B. Worth, F M. Vukovich, and C. E Decker Research Triangle Institute studiesof highozone
concentrations in nonurban areas. /n International
Conference on Photochemical Oxidant Pollution and ItsControl Proceedings Volume I B Dimitriades, ed EPA600/3-77-001a, U S. Environmental ProtectionAgency, 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
purposes /n Speciality Conference on Ozone/
Oxidants—Interactions with the Total Environment Air Pollutton Control Association, Pittsburgh, Pa., March 1976 pp 3-13 Russell, P A(ed ) Denver Air Pollution Study-1973 Proceedings of a Symposium Volume I. EPA-600/9-76- 007a, U S. Environmental Protection Agency, Research Triangle Park, N C., June 1976 Russell, P A (ed ) Denver Air Pollution Study - 1973 Proceedings of a Symposium Volume II EPA-600/9-77- 001, U S Environmental Protection Agency, Research Triangle Park, N C, February 1977 Seizinger, D E, and B Dimitriades Oxygenates in exhaust from simple hydrocarbon fuels J Air Pollut Control Assoc 22 47-51, 1972 Spicer, C W, J L Gemma, D. W Joseph, P S 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 Trijonis, J Empirical Relationships BetweenAtmospheric Nitrogen Dioxide and Its Precursors EPA600/3-78-018, U S Environmental Protection Agency, Research Triangle Park, N C, February 1978 Trilonis, J C, T K Peng, G J McRae, and L Lees Emissions and Air Quality Trends in the South Coast Air Basin EQL Memorandum No. 16, California lnstitute of Technology, Pasadena, Calif , January 1976 Westberg, H, K Allwine, E Robinson, and P Zimmerman Light Hydrocarbon and Oxidant Transport Studies in Ohio-1974. EPA-600/3-78-007, U.S Environmental Protection Agency, Research Triangle Park, N C, January 1978 White, W H., and P T Roberts The nature and origins of visibility-reducing aerosols in Los Angeles Presented at 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 Council, Inc , New York, April 15, 1974 Wolff, G T, P J Lioy, G D Wight, R F Meyers, and R. T Cederwall An investigation of long-range transport of
ozone across the midwestern and eastern United States

/n International Conference on Photochemical Oxidant Pollution and Its Control. Proceedings Volume I. BDimitriades, ed EPA-600/3-77-001a, U S Environmental Protection Agency, Research Triangle Park, 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 pollutantsthat 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 theinformation 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 reactionmechanisms, 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 OC FN \ o \ °+° \ E

~~ .

~

O , O S O ~ON~

F ~ O QP

IRftAOIATION TINIEFigure 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 equation 2a



### [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 NO 2 (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 ofan 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). 93 Sources 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

aOE (' A g ) CH s =CHCH(O z H)CH E



# ~ CH g CHO z +



# ~ 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

0 3



# d ° o

CH e CH-CHCH $



# ~ CH,CH(U)CH(O,)C

EHO*

]



# ~ CH 3 CH (U)O + 0 2 

## O : NO

CH 3 CO s + HO Z CH E CHO* + NO x

CH, +OE CH 3 C0 + RH 

# 1 °E

~ 0 1 CH, O, CH 3 C061 NO
NO ~ CH 3 CO E + NO, 4 NO E 

# ~ AS BEFORE CH 3 0 + NO a



# ~ O, CH 3 COO Z NO 2 =PAN CO,

CH = O + HO, NO 3 CH 2 O*

*



# ~ R NO CH, ONO = CO

CH 

# ~ ONO* CHO + RH 

# 1 O, 

# F

c— 

# ~ + 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 O z ~ O 2

CH S CH=CHCH,b A CH s CHOHCH(O = )CH 3



### O 1

— 

### O 

# ~NO

I I CH 3 CHOHCH(6)CH 3 + NO z 

### CH 3 CHCHCH 1

p = CH 3 CH H + CH 

# ~ CHO* 

# O ~ O Oa 

# I I 

# ~ CH e CH(O = )OH CH s 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

CH g CH10 CHO + CH=O* CHaO'

CH 3 CH0* + tHO



# ~ pa \ *, 03 CO + Hb s HCOb y

NO i IVO

HCOO z NO i HCb s + NO =

HONO = + F0

1 H •-I F O . 

# 1 ~ O =

HO : t N0



### CH, O + NO X NO



# ~ 02 NO . 

# ~ CH 3 0NO z 

### CH~ 

### O* + HO ~ 

### CH a ONO*

CH a CO + H z 0 -4 HO

1 AS BEFORE

CO a , CO 

### PAN CH 2 O CH y ONO y
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 extremelytemperature 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) wasidentified 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 evidence 33,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 effects 96 associated with particulate sulfates. Though it is beyond the scope of thisdocument 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 SO x

. 

### 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) F o rml c acl d, 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 + M e 40 RO2NO2 Ozonldes, 03-olefin 03 + olefln + M a 7 Ketene, CH2C0 03 + olefln 88 Nltrous acld, HONO OH + NO 8,32 Pernitrlc acld, H0 2 NO2 NOz + HOz + M a 50,79,95 Pernitrous acld, HOzNO NO + H02 + M a 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, arethose 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

INTRODUCTIONThe 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 processinvolving 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

35TABLE 4-4. SECONDARY ORGANIC AEROSOLS 2

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

36TABLE 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 inwinter (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

3716 14
12 10

.° 16 Figure 4-4. Isopleths (m x 10 2 ) of inean summer afternoon mixing heights. 65

38g---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.°°

39DATA 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 76

compiled 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; 73,18 changes 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,

4050"

45

40 °

35

30 °

25 ° 105 ° 100 ° 95 ° 90 ° 85 ° 80 ° 75 ° 70 ° 65 ° 60

2 1 

## 1 1 3 1 3 {

2 1

~ 

## 3

5

s 4 3 3 q 5 8I 0 ~ \
4 i
3 ]
7 6 3 3 4 6 /11 2

3 1 31 ~ / 7 +

i 8 9 1 0 2
1 I 

### r

4 ~ ~ n,

\ "

~ / 1 i '

B 9 1 4

10 3 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 {r l

l

, ^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

r 2.0
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 -- CH 3 + 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-NO x 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. 78Since 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 PETERSON 100 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



### 42TABLE 4-7. CALCULATED VALUES OF NO2 PHOTODISSOCIATION RATE CONSTANT a 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 0114 0 025
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

—

a ln 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 (10.0 0 to 15.6 0 C), oxidant yields were lower than those in the summer (80 0 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 (16.7 0 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 areconducive 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 farfrom 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 themost 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 foroxidant/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 airstream 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 metropolitanDade 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 notoccur 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. 38A 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 receivedconsiderable 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 Coast 38 and Midwest S6 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 night 15 and the Sunday-weekday effect 13,24,4s,ao,,s5 ) Thus downward intrusion, from layers aloft, of transported anthropogenicoxidant/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 significantadvance 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/ozoneconcentrations 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, theevidence 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 oftropopause level, and (4) mesoscale and smallscale eddy transport. Each of these mechanisms ischaracterized 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, themost 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 10 20 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/m 2 •sec. During the winter period, however, when the strongest cross-tropopause fluxes occur, this ozone flux could be 0.4 x 10

- ' g/m 2 • 

### sec. From this stratospheric mass flux (0.4 x 10

- ' g/m 2 • 

### 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/m 3 (0.017 ppm)."' Superimposed on the background concentration caused by the MMC process, there is an ozoneincrement 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

90 

### Sr-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/m 3 (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 Rosaepisode occurred. Attmannspacher and Hartmannsgruber 9 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/m 3 (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 90 Sr 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/m 3 (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 10 10 molecules/cm 2 • 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 byLamb" and Attmannspacher and Hartmannsgruber 9 (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/m 3 (0.022 to 0.035 ppm). 90 Such background levels vary with season and latitude because the stratospheric ozone reservoir also varies withseason 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/m 3 (0.022 to 0.035 ppm) constitutes a representative tropospheric ozone level (of stratospheric origin) for 35 1 to 50 0 N latitudes. Mohnen also concluded that TF events may lead to ozone concentrations at ground level as high as 30 Ng/m 3 (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 ozoneformation 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 48 0 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/m 3 (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 WhitefaceMountain 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/m 3 (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 suggestsan anthropogenic-influences explanation. However, in this case, such an explanation alone is not

510.070

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 ofcyclogenetic 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 ozonemeasurements 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
Reiter 13 and about 60 /jg/m 3 (0.03 ppm) by
Mohnen 90 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 Mohnen 90 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/m 3 (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 meansthat 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 ruledout 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 troposphere1?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 NO x 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 survivetransport 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. investigators 90 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 ruralatmospheres 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
Penkett 47 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 oforganic 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 Hidy 63 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. Bothprocesses 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 theevidence 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/m 3 (0.03 ppm). There are also more recentdata obtained at Whiteface Mountain, New York, suggesting a maximum 24-hr concentration of 72 /Ig/m 3 (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.



### REFERENCES FOR CHAPTER 4

1 Aldaz, L Flux measurements of atmospheric ozone over land and water J Geophys Res 74 6943-6946, 1969 2 Allwine, K J, and H Westberg Potential Impact of Coai-Fired Power Plants on Ground Level Ozone Concentrations in Wisconsin Final Report—Wisconsin Public Service Commission Contract No 8110, Washington State University, Pullman, Wash , 1977 3 Altshuller, A P Evaluation of oxidant results at CAMP sites in the United States J Air Pollut Control Assoc 25 19-24, 1975 4 Altshuller, A P, and J J Bufalini Photochemical aspects of air pollution A review Environ Sci Technol 5 39-64, 1971 5 Altshuller, A P, and J J Bufalini Photochemical aspects of air pollution A review Photochem Photobiol. 4 97-146, 19656 Altshuller, A P, and S P McPherson Spectrophotometric analysis of aldehydes in the LosAngeles atmosphere J Air Pollut Control Assoc 13 109-111,
19637. Atkinson, R., B. J. Finlayson, and J. N. Pitts, Jr. Photoionization mass spectrometer studies of gas phase ozone-olefin reactions. J Am. Chem. Soc. 95:7592-7599, 1973.
8. Atkinson, R., D. A. Hansen, and J. N. Pitts, Jr. Rate
constants for the reaction of OH radicalswith H z and NO (M = AR and N2). J. Chem Phys. 62:3284-3288, 1975.
9. Attmannspacher, W., and R. Hartmannsgruber. On extremely high values of ozone near the ground. Pure Appl. Geophys. 106-108.1091-1096, 1973.
10. Bach, W. D., Jr. Investigation of Ozone and Ozone
Precursor Concentrations in Nonurban Locations in the Eastern United States. Phase II, Meteorological Analyses. EPA-450/3-74-034a, U.S. Environmental Protection Agency, Research Triangle Park, N.C., February 1975.
11. Bach, W. D., Jr., J. E. Sickles, 11, R. Denyszyn, and W. C. Eaton. Chemical and meteorological analysis of themesoscale variability of ozone concentrations over a sixday period. /n: International Conference on
Photochemical Oxidant Pollution and Its Control. Proceedings. Volume 1. B Dimitriades, ed EPA-600/3- 77-001 a, U.S. Environmental Protection Agency, Research Triangle Park, N.C., January 1977. pp. 197-
210.
12. Bell, G. B. Meteorological Conditions During Oxidant Episodes in Coastal San Diego County in October and November, 1959. State of California, Department of Public Health, Sacramento, Calif., 1960.
13. Bruntz, S. M., W. S. Cleveland, T. E. Graedel, B. Kleiner, and J. L. Warner. Ozone concentrations in New Jersey and New York: Statistical association with related variables. Science 186:257-259, 1974.
14. Bufalini, J. J., B. W. Gay, Jr., and K. L. Brubaker. Hydrogen peroxide formation from formaldehyde photooxidation and its presence in urban atmospheres. Environ. Sci. Technol. 6:816-821, 1972.
15. Bufalini, J. J, T. A. Walter, and M. Bufalini. Ozone formation potentials of organic compounds. Environ. Sci. Technol. 10:908-912, 1976. 16 Calvert, J G. Modes of formation of the salts of sulfur and nitrogen in an N0.-S02-hydrocarbon-polluted atmosphere. In: Conference on Atmospheric Salts and Gases of Sulfur and Nitrogen in Association with
Photochemical Oxidant. Volume II. Reference Documents. T. T. Crocker, ed. California Air Resources Board Contract No 3-197, University of California, Irvine, Calif., January 1974. Chapter VIII. 17 Calvert, J. G Review and anatysis. /n: International Conference on Oxidants, 1976-Analysis of Evidenceand Viewpoints. Part II. The Issue of Reactivity. EPA600/3-77-114, U.S. Environmental Protection Agency, Research Triangle Park, N.C., October 1977. pp. 5-34.
18. Caivert, J. G. Test of the theory of ozone generation in Los Angeles atmosphere. Environ. Sci. Technoi. f 0.248-256, 1976. 19. Calvert, J. G., and R. D. McQuigg. The computer
simulation of the rates and mechanisms of photochemical smog formation. /n: Proceedings of the Symposium on Chemical Kinetics Data for the Upper and Lower Atmosphere. Int. J. Chem. Kinet. Symp. (1).113-154, 1975.
20. Castleman, A W., Jr., R. E. Davis, H. R. Munkelwitz, I. N. Tang, and W. P. Wood. Kinetics of association reactions pertaining to H2SO4 aerosol formation. /n: Proceedings of the Symposium on Chemical Kinetics Data for the Upper and Lower Atmosphere. Int. J. Chem. Kinet. Symp. (1):629-640, 1975.
21. Chameides, W., and J. C. G. Walker. A photochemical theory of tropospheric ozone. J. Geophys. Res. 78:8751- 8760, 1973.
22. Chatfield, R., and H. Harrison. Ozone in the remote troposphere: Higher levels? /n: Specialty Conference On: Ozone/ Oxida nts-Interactions with the Total Environment. Air Pollution Control Association, Pittsburgh, Pa., 1976. pp. 77-83.
23. Chatfield, R and R. A. RasmUssen. An assessment of the continental lower tropospheric ozone budget. /n: Internationat' Conference on Photochemical Oxidant Pollution and Its Control. Proceedings. Volume I. B. Dimitriades, ed. EPA-600/3-77-001a, U.S. Environrlaental Protection Agency, Research Triangle Park, N.0 , January 1977. pp. 121-136.

24. Cleveland, W. S., T. E. Graedei, B. Kleiner, and J. L. Warner. Sunday and workday variations in photochemical air pollutants in New Jersey and New York. Science 186.1037-1038, 1974.
25. Cleveland, W. S., R. Guarino, B. Kleiner, J. E. McRae, and J. L. Warner. The analysis of the ozone problem in
the northeast United States. /n: Specialty Conference On: Ozone/ Oxida nts-Interactions with the Total Environment. Air. Pollut. Control Association, Pittsburgh, Pa., 1976. pp 109-120.

26. Coffey, P. E., and W. N. Stasiuk. Evidence of atmospheric transport of ozone into urban areas. Environ. Sci. Technol. 9:59-62, 1975. 27, Coffey, P. E., and W. N. Stasiuk. Urban ozone: Its local and extraregional components. Presented at the 79th Annual National Meeting, American Institute of Chemical Engineers, Houston, Texas, March 1975. Paper No.60C.
28. Coffey, P. E., W. N. Stasiuk, and V. Mohnen. Ozone in
rural and urban areas of New York State. /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. pp. 89-96.
29. Coffey, P. E., and H. Westberg International Conference on Oxidants, 1976-Analysis of Evidence and Viewpoints. Part IV. The Issue of Natural Organic Emissions. EPA-600/3-77-116, U.S. Environmental
Protection Agency, Research Triangle Park, N.C.,
October 1977.
30. Cox, R. A, A E. J. Eggleton, R G Derwent, J. E. Lovelock, and D. H. Pack Long-range transport of photochemical oxidant in northwestern Europe. Nature (London) 225(55404).118-121, 1975,
31 Cox, R. A., and R. G. Derwent Kinetics of the reaction of HOz with nitric oxide and nitrogen dioxide. J. Photochem. 4.139-153, 1975.
32. Cox, R. A., R. G. Derwent, and P M. Holt Relative rate
constants for the reactions of OH radicals with HZ, CH4, CO, NO, and HONO at atmospheric pressure and 296K. J. Chem. Soc. FaradayTrans. 1. 72:2031-2043, 1976.

33. Cox, R. A, R. G. Derwent, and A. J L. Hutton. The significance of peroxynitric acid in atmospheric chemistry of the nitrogen oxidPC. Nature (London) 270:328-329, 1977.

5934.

35.

36.

37.

38.

39.

40.

41.

42.

43

44.

45.

46.

47.

48.

60 Cox, R. A., and M. J. Roffey. Thermal decomposition of Conference on Photochemical Oxidant Pollution and Its peroxyacetyl nitrate in the presence of nitric oxide. Control. Proceedings Volume I. B. Dimitriades, ed. EPAEnviron Sci. Technol. 11:900-906, 1977. 600/3-77-001 b, U.S Environmental Protection Crutzen, P. J. Photochemical reaction initiated by and Agency, Research Triangle Park, N C, January 1977. influencing ozone in unpolluted tropospheric air Tellus. pp 745-751 26:47-56, 1974. 49. Graedel, T. E, L. A. Farrow, and T. A. Weber. The Crutzen, P. J., and J. Fishman. Average concentrations influence of aerosols on the chemistry of the of hydroxyl radicals in the troposphere and the budgets troposphere. /n. Proceedings of the Symposium on of inethane, carbon monoxide, molecular hydrogen, and Chemical Kinetics Data for the Upper and Lower 1,1,1-trichloroethane. Geophys. Res Lett. 4•321-324, Atmosphere. Int J. Chem. Kinet. Symp. (1).581-594,
1977 1975. Darnall, K. R., W. P. L. Carter, A. M. Winer, A. C. Lloyd, 50. Graham, R. A., A. M. Winer, and J. N. Pitts, Jr. andJ.N.Pitts,Jr.ImportanceofROz+NOinalkylnitrate Temperature dependence of the unimolecular formation from C4-C6 alkane photooxidations under decomposition of pernitric acid and its atmospheric
simulated atmospheric conditions J. Phys. Chem. implications. Chem. Phys. Lett 51.215-220, 1977 80:1948-1950, 1976. 51. Greenfelt, P. Ozone episodes on the Swedish west Decker, C. E., L. A. Ripperton, J J. B. Worth, F. M. coast. !n• International Conference on Photochemical Vukovich, W. D Bach, J B. Tommerdahl, F. Smith, and Oxidant Pollution and Its Control. Proceedings Volume D. E. Wagoner. Formation and Transport of Oxidants I. B. Dimitriades, ed. EPA-600/3-77-001a, U.S. Along the Gulf Coast and in Northern U.S. EPA-450/3- Environmental Protection Agency, Research Triangle 76-033, U.S. Environmental Protection Agency, Park, N.C., January 1977 pp. 329-337 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, Bach. Ambient Monitoring Aloft of Ozone and N0,-photooxidation, and ozonalysis. In. Proceedings of Precursors in the Vicinity and Downwind of a Major City. the Symposium on Chemical Kinetics Data for the Upper EPA-450/3-77-009, U.S Environmental Protection and Lower Atmosphere. Int. J. Chem Kinet. Symp. Agency, Research Triangle Park, N.C., January 1977 (1):183-195, 1975. Demerlian, K. L, J. A Kerr, and J. G. Calvert. The 53. Guidance for Air Quality Monitoring Network Design
mechanisms of photochemical smog formation. and Instrument Siting. Guideline No 1 2-012, U.S Environ. Sci Technol 4:1-262, 1974. Environmental Protection Agency, Research Triangle Dimitriades,

- B. Oxidant control strategy:' Recent Park, N.C., 1975. developments: /n: Intgrnational Conference on 54. Haagen-Smit, A J. Chemistry and physiology of Los
Photochemical Oxidant Pollution and Its Control. Angeles smog. Ind Eng. Chem. 44.1342-1346, 1952. Proceedings Volume II. B. Dimitriades, ed. EPA-600/3- 55. Hanst, P. L., W. E. Wilson, Jr., R. K. Patterson, B W Gay, 77-001 b, U.S. Environmental Protection Agency, Jr., L. W. Chaney, and C. S. Burton A spectroscopic Research Triangle Park, N.C., January 1977. pp. 1143- study of Pasadena smog. !n: Abstracts of Papers: 167th
1154. National Meeting American Chemical Society. Dimitriades, B. Oxidant/Oa air quality benefits from American Chemical Society, Washington, D C., 1974. "emission substitution." !n. Specialty Conference On: Abstract ENVT 056. Hydrocarbon Control Feasibility - Its Impact on Air 56. Harvey, R. B., D. H Stedman, and W Chameides. Quality. Air Pollution Control Association, Pittsburgh, Determination of the absolute rate of solar photolysis of Pa., 1977. pp. 111-121. NOz J. Air Poliut. Control Assoc. 27•663-666, 1977 Dimitriades, B., and A. P Altshuller. International 57. Hathorn, J. W., 111, and H. M Walker. A"Texas size"
conference on oxidant problems: Analysis of the ozone episode tracked to its source. /n: International evidence and viewpoints presented. Part I Definition of Conference on Photochemical Oxidant Pollution and Its 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 Dobbins, R. A., J. L Nolan, J. P Okolowicz, and A J. Agency, Research Triangle Park, N.C., January 1977,
Gilbert. Meteorological factors controlling photo- pp.353-380. chemical pollutants in southeastern New England.!n: 58. Heicklen, J., K. Westberg, and N Cohen. The conversion
International Conference on Photochemical Oxidant of NO to NOz in Polluted Atmospheres. CAES Pollution and Its Control. Proceedings Volume I. B. Publication No. 115-69, Pennsylvania State University, Dimitriades, ed. EPA-600/3-77-001 a, U.S. Center for Air Environment Studies, University Park, Environmental Protection Agency, Research Triangle Pa., 1969. Park, N.C., January 1977. pp. 109-118 59. Hendry, D. G, and R. A. Kenley Gas-phase free radical Elkus, B., and K. R. Wilson. Photochemical oxidant: reactions of peroxyacetyl nitrate. Presented atthe 173rd Weekday-weekend differences. Draft. 1976. National Meeting, American Chemical Society, New Fankhauser, R K Ozone levels in the vicinity of 33 Orleans, Louisianna, March 21-25, 1977
cities. J. Air Pollut. Control Assoc. 26

- 771-777, 1976, 60. Hendry, D. G., and R. A. Kenley. Generation of peroxy Garland, J A, and S A. Peiikett. Absorption of peroxyl radicals from peroxynitrates (R02NO2). Decomposition acetyl nitrate and ozone by natural surfaces. Atmos. of peracyl nitrates. J Am. Chem. Soc 99:3198-3199,
Environ. 10 1127-1131, 1976 1977. Gay, B. W., Jr., and R. R. Arnts. The chemistry of 61 Hester, N. E., R. B. Evans, F. G Johnson, and E. L. naturally emitted hydrocarbons. In. Internat+onal Martinez. Airborne measurements of primary andPhotochemical 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. 145-
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 Pollutant Removal. Draft Final Report. U.S. Environmental Protection Agency Contract No. 68-02- 2216, Systems Applications, Inc., San Rafael, Calif., March 1977. pp. 67-120.
62. Korshover, J. Climatology of stagnating anticyclones east of the Rocky Mountains, 1936-1975. NOAA Technical Memorandum ERLARL-55, U.S. Department of Commerce, National Oceanic and Atmospheric Administration, Washington, D.C., July 1975.
63. Lamb, R. G. A case study of stratospheric ozone affecting ground-level oxidant concentrations. J. Appl. Meteorol. 16:780-794, 1977.78 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,
and J. H. Shaw. The kinetics and mechanism of the H02- NO2 reactions: The significance of peroxynitric acid formation in photochemical smog. Chem. Phys. Lett. 48:528-535, 1977.
80. Levitt, S. B, and D. P. Chock. Weekday-weekend pollutant studies of the Los Angeles Basin. J Air Pollut. Control Assoc. 26:1091-1092, 1976.
81. Levy, H., 11. Photochemistry of the lower troposphere. Planet. Space Sci. 20:919-935, 1972.

82. Lonneman, W. A. Ozone and hydrocarbon measurements in recent oxidant transport studies. /n
International Conference on Photochemical Oxidant Pollution and Its Control. Proceedings. Volume 1. B.Dimitriades, ed. EPA-600/3-77-001a, U.S. Environmental Protection Agency, Research Triangle Park, N.C., January 1977. pp. 211-223.
83. Lonneman, W. A., R. L. Seila, and S. A. Meeks. Preliminary results of hydrocarbon and other pollutant measurements taken during the 1975 northeast oxidant transport study. /n: Proceedings of Symposium on 1975 Northeast Oxidant Transport Study. EPA-600/3-77- 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 Findings. EPA-450/3-77-022a, U.S. Environmental Protection Agency, Research Triangle Park, N.C., September 1977.
85. Lyons, W. A., and H. S. Cole. Photochemical oxidant transport: Mesoscale lake breeze and synoptic-scale aspects. J Appl. Meteorol. 15:733-743, 1976.
86. Marks, J. E., and J. L. Herman. Mesoscale transportation of ozone: An episode, August 18, 1974. /n. Specialty Conference On: Ozone/Oxidants- .
Interactions with the Total Environment. Air Pollution. Control Association, Pittsburgh, Pa., 1976. pp 293-302.
87. Martinez, E. L., and E. L. Meyer, Jr. Urban-nonurban ozone gradients and their significance. /n: Special 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- 77-001 a, U.S Environmental Protection Agency, Research Triangle Park, N.C., January 1977. pp. 259-
274.
62. Heuss, J. M., and W. A. Glasson. Hydrocarbon reactivity and eye irrritation. Environ. Sci. Technol. 2:1109-11 16,
1968.
63. Hidy, G M. Removal processes of gaseous and particulate pollutants. /n: Chemistry in the Lower Atmosphere S. I. Rasool, ed. Plenum Press, New York,
1973.
64. Hill, A. C. Vegetation. A sink for atmospheric pollutants. J Air Pollut. Control Assoc. 21:341-346, 1971.

65. Holzworth, G. C. Mixing Heights, Wind Speeds, and Potential for Urban Air Pollution Throughout the Contiguous United States. Office of Air Programs Publication No. AP-101, U.S. Environmental Protection Agency, Research Triangle Park, N.C., January 1972.
66 Huffman, G. D., G. W. Haering, R. C. Bourke, P. P. Cook,
and M. P. Sillars. Ozone observations in and around a midwestern metropolitan area. /n: International
Conference on Photochemical Oxidant Pollution and ItsControl. Proceedings. Volume I. B. Dimitriades, ed. EPA600/3-77-001 a, U.S. Environmental Protection 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 ItsControl. 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, and P 0. Warner. Direct NOz photolysis rate monitor. 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 Evidenceand 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 onTotal 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.

621 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-

6377-001a, 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 Aerial investigation of the ozone plume phenomenon. J. Air Pollut. Control Assoc. 27•460-463, 1977.
147. Zafonte, L., P. L. Rieger, and J. R. Holmes. Nitrogen dioxide photolysis in the Los Angeles atmosphere. Environ. Sci. Technol 11.483-487, 1977.

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 thecomposition 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) otheremissions, 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 n tane

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 considerablemeasurement 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 aconsequence 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 10 Q 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



### 68TABLE 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 areas 82 but not in others. 80

Figure 5-3 shows such a downward trend for the Los Angeles atmosphere. 40 The 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 beobserved. 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 ambientconcentration, and by the disproportionate influence of a single emission source on measurements made at an improperly located measurement station.

69z



## m V Cc E Q a 

## V 0Z O

W Q 

### z ~ QZ Lu 

### w V

Z C 0 .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 ruraland 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 6 e

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 wasinvariably evidence of anthropogenic contamination. 50

' 72



### Finally, 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, earlymeasurements of the NO2 background concentration showed levels generally below 5 ppb aa,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."' 72

Furthermore, 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 aregeographically 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

71TABLE 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. 65 b 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 70 b 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) 63 b 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 69 b 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. 62 b 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 63 b 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 68 b 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, 62 b 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. 63 b 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. 65 b 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 67 b 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 68 b 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 72 b 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. 69 b 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 72 b 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

73TABLE 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 70 b 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.

74TABLE 5-6. NITRIC OXIDE CONCENTRATI014 e 1N 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

75TABLE 5-7. NITROGEN DIOXIDE CONCENTRATION a 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

7650

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 BIOMASS 80

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 1972 63 1972 83 1973 83 1974 8 ] 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. 83

Information 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.

77TABLE 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 berecognized 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 10 14 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 organicsubstances, including ethylene, isoprene, apinene, and a variety of other terpenes. Rasmussen 68 and Rasmussen and Went 70 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

79Moblle 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 SOURCESAs 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 generationautomobiles. 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 ofexhaust 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 Se izinger 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 a range, 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.

82TABLE 5-15. 1974 NATIONWIDE ESTIMATES OF NITROGEN OXIDE SOURCES AND EMISSIONS 63

Source category Emission, 10 6 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 naturalsources 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 specificchemical-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 Altshuller 3 and presented in terms of a reactivity classification of hydrocarbons and aldehydes, asshown 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 Glasson 37 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 Mlller 4 e 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.

84TABLE 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 1Primary 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

85TABLE 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 Acetylene a 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 parafflns a 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 Ethers a 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 measuredsystemically 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 recently 29 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, becausethey 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 Weinstock 20 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 beenmeasured 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, reportedusually 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, becausethe 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.

REFERENCES FOR CHAPTER 5

1. Abeles, F. B., L. E. Craker, L. E. Forrence, and G. R. Leather. Fate of air pollutants: Removal of ethylene, " sulfur dioxide, and nitrogen dioxide by soil. Science. 173:914-916, 1971.
2. Air Pollution Control Office. Air Quality Criteria for Nitrogen Oxides. APCO Publication No. AP-84, U.S. Environmental Protection Agency, Washington, U.C., January 1971.
3. Altshuller, A. P. An evaluation of techniques for the determination of the photochemical reactivity of organic emissions. J. Air Pollut. Control Assoc. 16:257-260,
1966.
4. Altshuller, A. P Hydrocarbons and carbon oxides. In: Air Pollution. Volume III. Measuring, Monitoring, and Surveillance of Air Pollution. A. C. Stern, ed. Academic Press, Inc., New York, 1976. pp. 183-21 1
5. Altshuiler, A. P. Natural sources of gaseous pollutants in the atrnosphere. Tellus 10:479-492, 1958.
6. Altshuller, A. P. Reactivity of organic substances in atmospheric photo-oxidation reactions. Int. J. Air Water Pollut. 10:713-733, 1966.
7. Altshuller, A. P., and J. J. Bufalini. Photochemical aspects of air pollution: A review. Environ. Sci. Technol. 5.•39-64, 1971.
8. Altshuller, A. P., and S. P. McPherson. Spectrophotometric analysis of aldehydes in the Los Angeles atmosphere. J. Air Pollut. Control Assoc. 13:109-111,
1963.
9. Altshuller, A. P., S. L. Kopczynski, D. Wilson, W. A. Lonneman, and F. D. Sutterfield. Photochemical reactivities of n-butane and other paraffinic hydrocarbons. J. Air Pollut. Control Assoc. 19:787-790,
1969.
10. Altshuller, A. P., G. C. Ortman, and B. E. Saltzman. Continuous monitoring of inethane and other hydrocarbons in urban atmospheres J. Air Pollut. Control Assoc. 16:87-91, 1966.
11. Ashby, H. A., R. C. Stahman, B. H. Eccleston, and R. W,
Hurn. Vehicle emissions-summer to winter. SAE Tech. Pap. No. 741053, Society of Automotive Engineers, Inc., Warrendale, Pa., 1974.
12. Black, F. M. The impact of emissions control technology on passenger car hydrocarbon emission rates and patterns. /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.C., January 1977. pp. 1053-1067.
13. Black, F. M., and R. L. Bradow. Patterns of hydrocarbon emissions from 1975 production cars. SAE Tech. Pap. N o. 750681, Society of Automotive Engineers, Inc., Warrendale, Pa., 1975. 14, Black, F. M., and L. Hish. Automotive hydrocarbon emission patterns and the measurement of nonmethane hydrocarbon emission rates. SAE Tech. Pap No. 770144, Society of Automotive Engineers, Inc., Warrendale, Pa.,
1977.
15. Brunelle, M. F., J. E. Dickinson, and W. J. Hamming. Effectiveness of Organic Solvents in Photochemical Smog Formation. County of Los Angeles, Air Pollution Control District, Los Angeles, Calif., July 1966
16. California Air Resources Board. Ten Year Summary of California Air Quality Data, 1963-1972. State of California, Air Resources Board, Sacramento, Calif,

, January 1974.
17. Calvert, J G., and H. E Jeffries.lnternational Conferer ce on Oxidants, 1976-Analysis of Evidence and Viewpoints. Part II. The Issue of Reactivity. EPA-600/3- 77-114, U.S. Environmental Protection Agency, Research Triangle Park, N.C., October 1977.
18. Caragay, A. B., J. T. Funkhauser, D. A Dendall, G. Leonardos, and P. L Levins. Identification of diesel exhaust odor species. 1. Hydrocarbons: Oily-kerosene odor complex. Anal. Chem. 1978. (ln press).
19. Cavanagh, L. A., C. F. Schadt, and E Robinson Atmospheric hydrocarbons and carbon monoxide measurements at Point Barrow, Alaska. Environ Sci Technol. 3:251-257, 1969
20. Chang, T. Y., and B. Weinstock. Net ozone formation in rural atmospheres. /n: International Conference on
Photochemical Oxidant Pollution and Its Control. Proceedings. Vol. I. B. Dimitriades, ed. EPA-600/3-77- 001a, U.S. Environmental Protection Agency, Research Triangle Park, N.C., January 1977. pp. 451-465
21. Chase, J. O., and R. W Hurn. Measuring gaseous emissions from an aircraft turbine engine SAE Tech. Pap. No. 700249, Society of Automotive Engineers, Inc., Warrendale, Pa., 1970.
22. Committee on Challenges of Modern Society. Air Quality Criteria for Nitrogen Oxides. NATO/CCMS Document No 15, North Atlantic Treaty Organization, Brussels, Belgium, June 1973.
23. Committee on Challenges of Modern Society. Air Quality
Criteria for Photochemical Oxidants and Related Hydrocarbons. NATO/CCMS Publication No 29, North Atlantic Treaty Organization, Brussels, Belgium, February 1974.
24. Community Air Monitoring Program Data National
Aerometric Data Bank. U.S. Environmental Protection Agency, Research Triangle Park, N.0
25. Dimitriades, B. Oxidant/0 3 quality benefits from "emission substitution." /n Specialty Conference On: Hydrocarbon Control Feasibdity: Its I mpact on Air Qual ity. Air Pollution Control Association, Pittsburgh, Pa., 1977. pp• 111-121.
26. Dimitriades, B. Photochemical Oxidants in the Ambient Air of the United States. EPA-600/3-76-017, U.S. Environmental Protection Agency, Research Triangle Park, N.C., February 1976.
27. Dimitriades, B. Proceedings of the Solvent Reactivity Conference. EPA-650/3-75-010, U S. Environmental Protection Agency, Research Triangle Park, N.C., November 1974.
28. Dimitriades, B., and A. P. Altshuller. /n.• International

89Conference on Oxidant Problems. Analysis of the Evidence and Viewpoints Presented Part I. Definition of Key Issues J Air Pollut Control Assoc 27•299-307,
1977 29 Dimitriades, B, and S B Joshi Application of reactivity
criteria in oxidant-related emission control in the USA. /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 , 1977 pp 705-71 1 30 Dimitriades, B., C J Raible, and C. A. Wilson. Interpretation of Gas Chromatographic Spectra in Routine Analysis of Exhaust Hydrocarbons Report of Investigation RI 7700, U S Department of the Interior, Bureau of Mines, Washington, D.C, 1972.
31 Dimitriades, B., G. P Sturm, Jr , T C Wesson, and F D. Sutterfield. Development and Utility of Reactivlty Scales from Smog Chamber Data Report of Investigation RI 8023, U.S. Department of the Interior, Bureau of Mines, Washington, D.0 , March 1975 32 Dimitriades,B,andT C Wesson Reactivities of Exhaust Aldehydes Report of Investigation RI 7527, U S Department of the Interior, Bureau of Mines, Washington, D C, May 1971. 33. Ehhalt, D H. Methane in the atmosphere J. Air Pollut. Control Assoc. 17:518-519, 1967 34 Fracchia, M F, F J. Schuette, and P K Mueller. A method for sampling and determination of organic carbonyl compounds in automobile exhaust. Environ Sci. Technol 1:915-922, 1967 35. Glasson, W A, and P H Wendschuh Multi-day irradiation of N0.-organic mixtures. /n: International Conference on Photochemical Oxidant Pollution and ItsControl Proceedings Vol II. B. Dimitriades, ed. EPA600/3-77-0016, U.S. Environmental Protection Agency, Research Triangle Park, N C, January 1977. pp 677-
685 36 Heuss, J. Smog chamber simulation of the Los Ang8les atmosphere. /n Scientific Seminar on Automotive Pollutants. U S Environmental Protection Agency, Research Triangle Park, N C, 1975. 37 Heuss, J. M, and W. A Glasson. Hydrocarbon reactivity and eye irritation. Environ. Sci. Technol. 2:1109-1116,
1968. 38 Heywood, J B, and M. K. Martin Aggregate emissions from the automotive population. SAE Tech. Pap. No. 740536 Society of Automotive Engineers, Inc., Warrendale, Pa , 1974 39 Hurn, R W, and W F Marshall Techniques for diesel emissions measurements SAE Trans. 77 (sect.2) 1492- 1501, 1971 40 Kinosian, J R., and J Paskind Hydrocarbon, Oxides of Nitrogen and OxidantTrends in the South Coast Air Basin 1963-1972. State of California, Air Resources Board, Sacramento, Calif., June 1973 41 Ivanov, V P, and G A Yakobson Exchange of metabolites in plants via aerial organics Soviet Plant Physiol (Engl Transl ) 12:351-356, 1965. 42 Jeffries, H. E., R. Kamens, D. L. Fox, and B. Dimitriades. Outdoor smog chamber studies. Effect of diurnal light, dilution, and continuous emission on oxidant precursor relationships /n. International Conference on Photochemical Oxidant Pollution and Its Control. Proceedings Vol I B Dimltriades, ed., EPA-600/3-77- 001b, U.S. Environmental Protection Agency, Research Triangle Park, N.C., January 1977. 43 Junge, C. E. Recent investigations in air chemistry Tellus. 8:127-139, 1956.
44. Kopczynski, S. L., R L Kuntz, and J J Bufalini Reactivities of complex hydrocarbon mixtures. Environ Sci. Technol. 9.648-653, 1975.
45. Kopczynski, S. L, W. A. Lonneman, T. Winfield, and R Seila. Gaseous pollutants in St. Louis and other cities. J Air Pollut Control Assoc. 25.•251-255, 1975.
46. Koyama, T. Gaseous metabolism in lake sediments and paddy soils and the production of atmospheric methane and hydrogen. J. Geophys. Res. 68:3971-3973, 1963
47. Laity, J L, I. G. Burstain, and B. R. Appel Photochemical smog and the atmospheric reactions of solvents. S hel I O il Company Paper No. P-1957, Presented at the National American Chemical Society Meeting, Washington, D.C., September 12-17, 1971. 48 Levy, A., and S. E. Miller Paint IndustrySmog Chamber 3. Final Technical Report on the Role of Solvents in Photochemical Smog Formation National Paint, Varnish, and Lacquer Association, Inc., Washington, D C, 1970.
49. Lodge, J. P., Jr, , and J. B. Pate. Atmospheric gases and particulates in Panama. Science 153:408-410, 1966
50. Lonneman, W. A. Ozone and hydrocarbon measurements in recent oxidant transport studies /n: International Conference on Photochemical Oxidant Pollution and ItsControl. Proceedings. Vol. I. B. Dimitriades, ed EPA600/3-77-001 a, U.S Environmental Protection Agency, Research Triangle Park, N.C., January 1977 pp 21 1-
223.
51. Lonneman, W. A., S L Kopczynski, P. E. Darley, and F D Sutterfield. Hydrocarbon composition of urban air pollutlon. Environ Sci. Technol 8.•229-236, 1974
52. Manufacturing Chemists Association, Inc., and Public Health Service. Atmospheric Emissions from Nitric Acid Manufacturing Processes. Public Health Service Publication No. 999-AP-27, U.S. Department of Health, Education and Welfare, Public Health Service, National Center for Air Pollution Control, Cincinnati, Ohio, 1966. 53. Mayrsohn, H., and J H Crabtree. Source Reconciliation 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.

90No 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

91Environmental Protection Agency, Ann Arbor, Mich , February 1974. 88 Wilson, K. W, and G. J Doyle Investigation ofPhotochemical 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

INTRODUCTIONThis 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/NOxrelationship(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 usefulto 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-effectrelationships 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 derivingthe 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 O x /HC/NO x 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 pointi 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/ozonecontrol 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 andthe 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 notsupported 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 attention 5s,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. Thislatter 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 conduciveto 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 0 30

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/NO x = 12

SMOG CHAMBER DATA NO x = 0.4 ppm

AEROMETRIC DATA (UPPER LIMIT CU

0.10 SMOG CHAMBER DATA HC/NO x = 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, providedby 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 ofemissions 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 NO x 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, weightedaccording 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 ofCalifornia, 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, theinvestigators 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 25 a 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)

0 1 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



### 9935



### '6(3.0)

512.3)

1.5)

3(0.8) 35

E 30 t a a Z
2 25 H Q ¢ Z
v 20 Z O UFQ 15 

## G_ X

0



### X 10 Q 

# ~ E
a 30

Z O H a 25 ¢ H 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. 54 developed 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 54 is 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 atmosphericdispersion 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 smogchamber 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

102E— 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 andn-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 theagreement 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 theconstant slope line ab corresponding to a NMHCto-NO x 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 appearsusually 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 tests 51 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 thataffect 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 toequation 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 K H 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 tothelevel of detail of the treatment of both meteorological and chemical processes. From a meteorological point of view, the basicdistinction lies inthe level of spatial resolution of the model. Socalled grid models are based on the solution ofequation 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 hasbeen 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 beendevoted 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 ofoxidant 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

LIRAQ H ' 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

DIFKIN e,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
model e 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

LIRAQ a 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

Bell a 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 theproperties 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 inpu 

### t uncer tainti 

### eswere estimated by Seinfeld 51 (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. Seinfelddid 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 deviationsarising 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 andchemical 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 tothe 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 1974 41,45 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 1973 31 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

113Triangle 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
197628 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

11458. 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. TheIssue 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 Oscontrol 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, statisticalconsiderations 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 reactionsthat 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 analyzersbased 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/m 3 (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 obtainedby 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. Theprecision 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 reagentproduces 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 predominantly03 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 EQ UIVALENT METHODS

Designation number Identification and source
EQOA-0777-023 Phtltps PW9771 0 3 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, C at 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 2 is 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 2

is 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 z and the triiodide ion (T s ), 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 Cr0 3 scrubber rriay cause new interferences by partially oxidizing the nitric oxide (NO) and hydrogen sulfide (H2S) possibly present in the sample to NO 2

and 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 incertain 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 severelycriticized 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 1 2 /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 developother 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 103 a 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 hasbeen 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 surrogatespecies. 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 withepidemiological 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 standardshould 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-O s 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-O s 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 readingsconsistently lower than those of a chemilu

### minescence ozone detector by a factor of three. The coulometric instruments were operated usingfactory 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 Jensen 21 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 Inugami 69 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
Neal 64 ' 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 •

r r

• ~ ~ ~

~ ~ ~• ~ 

## •%

. . *

•e ~►

~ •

. ;`

. i ~ i

. . . • ii.Y.•V.i i.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 Seversreflect 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

0.4 i 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 }


### m 0.5 w Z N 0.4 O
0.3

0.2

0.1 •S

1.0

0.9



### E 0.8

O, a 0.7 H Q 0.6

~ m 0.5


## w

~ 0.4

N 

### O 0.3

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 theatmosphere 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. SincePAN 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 atconcentrations 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 (100ml) 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 knownconcentrations 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 atechnique 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 bygas 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 theambient 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. 4 In 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 76 involved 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 thesedifferences 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 ,, s 7 In a recent EPA-sponsored study, 35the EPA reference method was subject 

### ed to a comprehensive evaluation, includ 

### ing testing of si x commercial instruments. Results showed, in general, poor performance of the commercial instruments, themajor 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. 75 This 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 CH 4 , 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,47,50,78 In 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. 25In 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 ' 88 The 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. 34 The 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 2 and NO X in 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 cyfindersare 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, N 2

at 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 NO 2 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-phasetitration 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 usingmethods based on variations of the GriessSaltzman 83 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 NO2by 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
vapor 

### s. The speed o f response 

### of c hemiluminescence-NO instruments is t 

### ypical 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 arebased 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 accuratelymeasured 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 permeationdevice. 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.



### REFERENCES FOR CHAPTER 7

1. Air Pollution Control Office Air Quality Criteria for Nitrogen Oxides. APCO Publication No AP-84, U S Environmental Protection Agency, Washington, D C, January 1971 2 Altshuller, A P, W A Lonneman, F D Sutterfield, and S. L Kopczynski Hydrocarbon composition of the atmosphere of the Los Angeles Basin — 1967 Environ Sci. Technol. 5 1009-1016, 1971 3 Altshuller, A P, G C Ortman, B E Saltzman, and R E Neligan Continuous monitoring of inethane and other hydrocarbons in urban atmospheres J Air Pollut ControlAssoc 1687-91, 1966 4. Andreatch, A J, and R Feinland Continuous trace hydrocarbon analysis by flame ionization Anal Chem 32 1021-1024, 1960 5 Appel, B R A new and more sensitive procedure for

131analysis of peroxybenzoyl nitrate J. Air Pollut. Control Assoc 23 1 042-1 044, 1973.
6. Ballard, L F, J. B. Tommerdahl, C. E. Decker, T. M Royal, and L K Matus. Field Evaluation of New Air Pollution Monitoring Systems: St. Louis Study, Phase 1. Interim Report Contract No EPA 70-101, U.S. Environmental Protection Agency, Research Triangle Institute, Research Triangle Park, N.C., 1971.
7. Ballard, L F., J. B. Tommerdahl, C. E. Decker, T. M Royal, and D R. Nifong. Field Evaluation of New Air Pollution Monitoring Systems - The Los Angeles Study. APTD-0775, U S. Environmental Protection Agency, Research Triangle Park, N C., April 1971 8 Baumgardner, R E, T A Clark, and R. K Stevens. Comparison of instrumental methods to measure nitrogen dioxide. Environ Sci Technol. 9:67-69, 1975. 9 Beard, M E, J H. Margeson, and E C. Ellis. Evaluation
of 1% Neutral Buffered Potassium lodide Procedure for Calibration of Ozone Monitors. EPA-600/4-77-005, U S Environmental Protection Agency, Research Triangle Park, N C., January 1977. 10 Becker, K H, U Schurath, and H Seitz Ozone-olefin reactions in the gas phase. 1 Rate constants and activation energies Int J Chem. Kinet 6:725-739,
1974
11 Bocek, P, J Novak, and J Janak Effect of pressure on the performance of the flame ionization detector J Chromatogr. 48 431-436, 1969. 12 Bowman, L D, and R. F. Horak Acontinuous ultraviolet ozone photometer Air Qual. Instrum.2•305-315, 1974 13 Breitenbach, L P, and M Shelef Development of a method for the analysis of NO2 and NH 3 by NOmeasuring instruments. J. Air Pollut Control Assoc. 23.128-131, 1973. 14 Burton, C S, P.J Bekowies, R I Pollack, and P Connell. Oxidant/Ozone Ambient Measurement Methods: An Assessment and Evaluation EF76-111 R, Systems Applications, Inc , San Rafael, Calif., August 10, 1976
15 California Air Resources Board Differences in ARB and LA-APCD oxidant readings Calif. Air Resour. Board Bull 5 1, 1974
16 California Air Resources Board Ozone data Calif. Air Qual Data 6 2-39, January-March 1974.17 Carroll, H, B Dimitriades, and R. M. Ray. A Chemiluminescent Detector for Ozone Measurement Report of Investigation RI 7650 U S Department of the Interior, Bureau of Mines, Washington, D.C. 1972. 18 Clark, T A., R. E. Baumgardner, R. K Stevens, and K. J Krost Evaluation of new ozone monitoring instruments by measuring in non-urban atmospheres /n. Instrumentation for Monitoring Air Quality ASTM Special Technical Publication 555, American Society for Testing and Materials, Philadelphia, Pa , 1974. pp. 101-
111 19 Clements, J. B Summary Report Workshop on OzoneMeasurement by Potassium lodide Method EPA650/4-75-007, U S Environmental Protection Agency, Research Triangle Park, N.C., February 1975 20 Darley, E. F, K A Kettner, and E. R Stephens Analysis of peroxyacetyl nitrates by gas chromatography with electron capture detection Anal Chem 35 589-591,
1963 21 Davis, D R, and R E Jensen Low level ozone and weather systems /n. Specialty Conference On Ozone/Oxidants-Interactions with the Total Environment. Air Pollution Control Association, Philadelphia, Pa., 1976 pp 242-251.
22. Decker, C.E., T.M. Royal, J.B. Tommerdahl, and L K Matus. Field Evaluation of NewAir Pollution Monitoring Systems: St. Louis Study, Phase II Interim Report. U S Environmental Protection Agency Contract No EPA 70- 101, Research Triangle Institute, Research Triangle Park, N.C., 1971
23. DeMore, W. B., and 0 Raper. Hartley band extinction coefficients of ozone in the gas phase and in liquid nitrogen, carbon monoxide, and argon. J. Phys. Chem. 68:412-414, 1964.
24. DeMore, W. B., J C. Romanovsky, M. Feldstein, W. J Hamming, P K Mueller Interagency comparison of
iodometric methods for ozone determination. /n: Calibration in Air Monitoring. ASTM Special

- "echnical Publication 598, American Society for Testing and Materials, Philadelphia, Pa , 1976. pp. 131-143.
25. Dietz, W. A. Response factors for gas chromatographic analyses J Gas Chromatogr. 5:68-71, 1967
26. Dimitriades, B., and A. P Altshuller International Conference on Oxidant Problems• Analysis of the Evidence and Viewpoints Presented. Part I. Definition of Key Issues. J. Air Pollut Control Assoc. 27 299-307,
1977. 27 Flamm, D. L Analysis of ozone at low concentrations
with boric acid buffered KI Environ Sci. Technol. 11•978-983, 1977. 28 Folmer, 0 F, Jr., and D. J Haase. A statistical study of gas chromatographic systems employing flame
ionization detectors. Anal Chim Acta. 48

- 63-78, 1969. 29 Fontiln, A., A. J. Sabadell, and R. J Ronco. Homogeneous chemiluminescent measurement of nitric oxide with ozone implications for selective monitoring of gaseous pollutants Anal Chem 42:575- 579, 1970.30 Fontijn, A, H N Volitrauer, and R Ellison. Chemiluminescent Reactive Hydrocarbon Analyzer for Mobile Sources. EPA-650/2-75-069, U S Environmental Protection Agency, Research Triangle Park, N.0 , June 1975. 31 Grant, D W, and A. Clarke A systematic study of the quantitative effects of instrument control on analytical precision inflame ionization gas chromatography. Anal Chem 43 1951-1957, 1971 32 Griggs, M Absorption coefficients of ozone in the ultraviolet and visible regions J. Chem Phys 49 857- 859, 1968 33 Hanst, P L, A S. Lefohn, and B. W. Gay, Jr. Detection of atmospheric pollutants at parts-per-billion levels by infrared spectroscopy. Appl. Spectrosc 27188-198,
1973. 34. Hanst, P L, W E. Wilson, R K. Patterson, B. W Gay, Jr., L. W. Chaney, and C S. Burton A Spectroscopic Study of California Smog. EPA-650/4-75-006, U S Environmental Protection Agency, Research Triangle Park, N C, February 1975 35 Harrison, J W, M L Timmons, R. B. Denyszyn, and C. E.
Decker Evaluation of the EPA Reference Method forMeasurement of Nonmethane Hydrocarbons, EPA600/4-77-033, U S Environmental Protection Agency, Research Triangle Park, N C, June 1977 36 Hearn, A G The absorption of ozone in the ultra-violet

132and visible regions of the spectrum. Proc Phys. Soc. Conference on Methods in Air Pollution Studies (London) 78:932-940, 1961 Regional Workshops on Quality Assurance, California 37. Hersh, P., and R. Deuringer. Galvanic monitoring of State University, Long Beach, Calif, January 14-15, ozone in air Anal. Chem. 35.897-899, 1963 1976, and Sacramento, Cal!f

, January 20-21, 1976 38 Heuss, J M., and W. A. Glasson Hydrocarbon reactivity 52. Lucero, D. J. Performance characteristics of permeation and eye irritation Environ Sci. Technol 2,1109-1116, tubes. Anal. Chem. 43•1744-1749, 1971 1968. 53. MacPhee, R. D, J E Higuchi, and F K V Leh

39 Hodgeson, J. A. Ozone. Sampling analysis and methods Comparison of oxidant measurement methods,

evaluation Presented at the 15th Conference on ultraviolet photometry, and moisture effects /n MethodsinAirPoliutionStudies,RegionalWorkshopon Specialty Conference On. Ozone/Oxidants— Quality Assurance, California State University, Long Interactions with the Total Environment Air Pollution Beach, Calif., January 14-15, 1976, and Sacramento, ControlAssociation, Pittsburgh, Pa

, 1976. pp. 166-179 Calif, January 20-21, 1976. 54. Martin, B E., J A Hodgeson, and R K Stevens

40 Hodgeson, J. A. Review of analytical methods for Detection of nitric oxide chemiluminescence at atmospheric oxidant measurements Int. J Environ. atmospheric pressure Prepr. Pap Natl Meet Div
Anal. Chem. 2 113-132, 1972. Environ Chem. Am. Chem. Soc 12 182, 1972.

41 Hodg;;son, J A, C B. Bennett, H. L. Kelly, and B. A.
Mitchell Ozone measurements by iodometry, 55 Mast, G. M, and H E Saunders Research and ultraviolet photometry and gas-phase titration development of the instrumentation of ozone sensing Presented at the American Society for Testing Materials ISA Trans. 1:325-328, 1962. (ASTM) Symposium on Calibration in Air Monitoring, 56 McClenny, W A, B. E Martin, R. E Baumgardner, Jr,

, R University of Colorado, Boulder, Colo

, August 5-7, K. Stevens, and A. E. 0'Keeffe. Detection of vinyl
1975. chloride and related compounds using a gas 42 Hodgeson, J A., K. A. Rehme, B. E. Martin, and R. K. chromatographic chemiluminescence technique.
Stevens Measurements for atmospheric oxides of Environ Sci. Technol. 10.810-813, 1976. nitrogen and ammonia by chemiluminescence 57 McElroy, F. F, and V L Thompson Hydrocarbon Presented at 65th Annual Meeting, Air Pollution Control Measurement Discrepancies Among Various Analyzers Association, Miami Beach, Fla

, June 18-22, 1972. Using Flame-lonization Detectors. EPA-600/4-75-010,
43. Inn, E. C Y., and Y. Tanaka Absorption coefficient of U S Environmental Protection Agency, Research ozone in the ultraviolet and visible regions. J. Opt. Sco Triangle Park, N.C., September 1975 Am. 43•870-873, 1953 58. McKee, H. C, R. E. Childers, a nd V. B. Parr. Col laborative
44. Intersociety Committee Tentative Method of Analysis Study of Reference Method for Measurement of for Peroxyacetylnitrate (PAN) in the Atmosphere in Photochemical Oxidants in the Atmosphere (OzoneMethodsofSamplingandAnalysis.Amer.PublicHealth Ethylene Chemiluminescent Method). EPA-650/4-75- Assoc Washington, D C, 1972. pp. 215-219 016, U.S. Environmental Protection Agency, Research
45 Izumikawa, H., M. Hayafuku, K. Nakano, K. Asakino, and Triangle Park, N.C., February 1975 T Ohira Continuous determination and quantification 59 Meiler, G. M., and H. Nieboer Determination of of atmospheric PAN Tokyo-to Kogia Kenkyusho Nenpo peroxybenzoyl nitrate (PB,N) in ambient air /n. Ozon 4.41-49, 1973 und Begleitungssubstanzen im photochemischen
46. Kaplan, H. Plumbing problems—gases for 6800 smog. VID Ber. (270):55-56, 1977. hydrocarbon analyzers /n Instrumentation for 60. National Air Pollution Control Administration. Air Monitoring Air Quality ASTM Special Technical Quality Criteria for Photochemical Oxidants NAPCA Publication 555, American Society for Testing and Publication No. AP-63, U.S. Department of Health, Materials, Philadelphia, Pa

, 1974. pp. 85-87. Education, and Welfare, Public Health Service, 47 Kopczynski, S L, W A Lonneman, T Winfield, and R Washington, D C, March 1970 Seila Gaseous pollutants in St. Louis and other cities J 61. National Air Pollution Control Administration Air Air Pollut Control Assoc 25 251-255, 1975 Quality Criteria for Hydrocarbons NAPCA Publication 48. Kothny, E. L, W A Cook, B Dimitriades, E. F. Ferrand, No. AP-64, U S Department of Health, Education, and C. A Johnson, L. Levin, P. W McDaniel, and B. E Welfare, Public Health Service, Washington, D C, Saltzman Tentative method of analysis of nitric oxide March 1970. content of the atmosphere Health Lab. Sci. 971-74, 62. National Research Council. Analytical Studies for the 1972 U.S. Environmental Protection Agency Vol IV 49 Levaggi, D, E. L Kothny, T Belsky, E. DeVera, and P. K. Environmental Monitoring National Academy of Mueller Quantitative analysis of nitric oxide in Sciences, Washington, D C, 1977.
presence of nitrogen dioxide at atmospheric 63. National Research Council Ozone and Other concentrations. Environ. Sci Technol. 8:348-350, Photochemical Oxidants National Academy of 1974 Sciences, Washington, D.C., 1977
50. Lonneman, W. A., S. L. Kopczynski, P. E. Darley, and F 64 Neal, R., and R. K. Severs Simultaneous D. Sutterfield. Hydrocarbon composition of urban air chemiluminescent and KI oxidant measurements in pollution. Environ. Sci Technol. 8 229-236, 1974 Houston, Texas, 1975. /n.• Specialty Conference on. 51. Los Angeles County Air Pollution Control District and Ozone/Oxidants—Interactions with the Total California Air Resources Board A study of the effect of Environment. Air Pollution Control Association, atmospheric humidity on analytical oxidant Pittsburgh, Pa., 1976 pp. 180-188.
measurement methods Presented at the 15th 65. Nederbragt, G W., A Van der Horst, and J Van Duijn

13366.

67

68.

69.

70.

71

72.

73.

74.

75.

76.

77.

78

79.

80

81.

134 Rapid ozone determination near an accelerator Nature 82 Saenz, 0., Jr., C A. Boldt, Jr

, and D S Tarazi (London) 206:87, 1965. Measurement of Non-Methane Hydrocarbons APTDNelson, G. 0. Controlled Test Atmospheres—Principles 0905, U S Environmental Protection Agency, and Tachniques. Ann Arbor, Mich., Ann Arbor Science Cincinnati, Ohio, June 1971 Publishers, Inc. 1971 83 Saltzman, B E. Colorimetric microdetermination of Office of Air Quality Planning and Standards. Standing nitrogen dioxide in the atmosphere Anal. Chem. Air Monitoring Work Group. Air Monitoring Strategyfor 26 1 949-1 955, 1954 Implementation Plans. EPA-450/2-77-010 U.S. 84. Saltzman, B E Modified nitrogen dioxide reagentforair Environmental Protection Agency, Research Triangle analyzers. Anal Chem 32 135, 1960. Park, N.C., June 1977. 85. Saltzman, B. E., W. A. Cook, B Dimitriades, E. L Kothny, O'Keeffe, A. E., and G. C. Ortman. Primary standardsfor L. Levin, D. W. McDaniel, and J. H. Smith Tentative trace gas analysis. Anal Chem. 38 760-763, 1966. method for continuous monitoring of atmospheric Okita, T, and M. Inugami. Measurement of ozone by oxidant with amperometric instruments /n Methods of
chemiluminescent methods. Koshu Eiseiin Kenkyu Air Sampling and Analysis American Public Health Hokoku 20.207-211, 1971. Association, Washington, D C, 1972 pp 341-350. Ortman, G. C. Monitoring methane in atmosphere with 86 Scaringelli, F P, E Rosenberg, and K A Rehme. a flame ionization detector. Anal. Chem. 38:644-656, Comparison of permeation devices and nitrite ion as
1966. standards for the colorimetric determination of nitrogen Ortman, G. C., and V. L. Thompson. Performance of dioxide. Environ. Sci Technol 4 924-929, 1970 hydrocarbon monitortng instrumentatton. !n: 87 Scott,W.E,E R Stephens,P L H anst, and R. C. Doerr
Instrumentation for Monitoring Air Quality. ASTM Further developments in the chemistry of the Special Technical Publication 555, American Societyfor atmosphere. Proc. Amer Pet Inst Sect. 3 37.171-183, Testing and Materials, Philadelphia, Pa., 1974. pp.74- 1957
84 88. Seila, R L GC-chemiluminescence method for the Ott, W. Development of criteria for citing air monitoring analysis of ambient terpenes /n: International stations. J. Air Pollut. Control Assoc 27 543-547, 1977. Conference on Photochemical Oxidant Pollution and Its Paur, R. J., R. E. Baumgardner, W. A. McClenny, and R. Control. Proceedings Vol I B Dimitriades, ed U S
K.Stevens.Statusofinethodforthecalibrationofozone Environmental Protection Agency, Research Triangle monitors. Prepr Pap. Natl Meet. Div, Environ. Chem. J Park, N.0

, January 1977 pp 41-50. Am Chem. Soc 16.185-188, 1976 89. Severs, R. K. Simultaneous total oxidant and Pitts, J. N, Jr

, H. Fuhr, J S. Gaffney, and J. W. Peters. chemiluminescent ozone measurements in ambient air Chemiluminescent reactions of pe roxyacetyl nitrate and J. Air Pollut Control Assoc 25 394-396, 1975 ozone with triethylamine. Possible atmospheric monitor 90 Severs, R K., R. M. Neal, and T D Downs Time as a for peroxyacetylnitrate. Environ. Sci Technol. 7•550- factor in atmospheric sampling. J Am Ind Hyg Assoc 552, 1973. 38.134-141, 1977 Poli, A A., and T. L. Zinn. A new continuous monitor for 91. Smith, R G., R J. Bryan, M Feldstein, B. Levadie, F A
methane and non-methane hydrocarbons. Anal. Miller, and E. R Stephens Tentative method of analysis Instrum. 11:135-142, 1973. for peroxyacetylnitrate (PAN) in the atmosphere. /n Reckner, L. R. Survey of Users of EPA-Reference Methods of Air Sampling andAnalysis American Public
Method for Measurement of Non-Methane Health Association, Washington, D C, 1972 pp 215- Hydrocarbons in Ambient Air EPA-650/4-75-008, U.S 219 Environmental Protection Agency, Research Triangle 92. Stedman, D H, E E. Darby, F Stuhl, and H. Niki Park, N.C., December 1974. Analysis of ozone and nitric oxide by a Regener, V. H. Measurement of atmospheric ozone with chemiluminescent method in laboratory and
the chemiluminescent method J. Geophys. Res. atmospheric studies of photochemical smog J Air 69.3795-3800, 1964. Pollut. Control Assoc. 22 260-263, 1972 Regener, V H On a sensitive method for the recording 93. Stephens, E R, P L Hanst, R C. Doerr, and W E Scott of atmospheric ozone. J. Geophys Res. 65:3975-3977, Reactions of nitrogen dioxide and organic compounds in
1960. air. Ind Eng Chem 48 1498-1504, 1956 Rehme, K. A., B. E. Martin, and J A Hodgeson. 94. Stephens, E R, and M A. Price Analysis of an
Tentative Method for Calibration of Nitric Oxide, important air pollutant peroxyacetylnitrate J Chem Nitrogen Dioxide, and Ozone Analyzers by Gas Phase Educ 50 351-354, 1973
Titration EPA-R2-73-246, U.S. Environmental 95 Stephens, E R, W. E Scott, P L. Hanst, and R C Doerr. Protection Agency, Research Triangte Park, N.C., March Recent developments in the study of the organic

1974. chemistry of the atmosphere J Air Poll. Control Assoc
Research Triangle Institute Investigation of Rural 6

- 159-164, 1956 Oxidant Levels as Related to Urban Hydrocarbon Control 96 Sternberg, J. C, W S. Gallaway, a nd D T L Jones The Strategies. EPA-450/3-75-036, U.S. Environmental mechanism of response of flame ionization detectors. Protection Agency, Research Triangle Park, N.C., March /n.Gaschromatography N Brenner,J E Callen,andM.

1975. D Weiss, eds. Academic Press, New York, 1962 pp Richardson, R. L. Performance of ambient hydrocarbon 231 -267 monitors in the Texas continuous monitoring network. 97. Stevens, D. W. Obtaining reliable performance from Presented at the 67th Annual Meeting, Air Pollution hydrocarbon analyzers. /n. Instrumentation for Control Association, Denver, Colo., June 9-13, 1974. Monitoring Air Quality. ASTM Special TechnicalPublication 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-NO z 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 beaccounted 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 Frank 215 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 byAharonson 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 lowerlevels 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 atracheal 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 trachealconcentration 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/m 3 (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/m 3 (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 Concentrationand 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/m 3 (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 beenstudied. 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/m 3 (0.07 ppm), each concentration was tested once (40 mice/concentration). It was reported that ? 157 Ng/m 3 (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/m 3 (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/m 3 (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/m 3

(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
Blommer 34

showed 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/m 3

(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. 54 using 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. 80

examined 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 Blommer 34 examined 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/m 3 (1 ppm)ozonefor3hr
before a bacterial aerosol. Bacterial invasion of the blood began 2 days after ozone exposure.
Additional research 90 has 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

' 89



### exposed miceto an aerosol of

32 

### P-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/m 3 (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 203 found 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. 203 demonstrated 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/m 3 (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 breathingozone (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/m 3 (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/m 3 (0.67 ppm) for 3 hr, there was a significant reduction (p <0.001 ) in the number of bacteria phagocytized by AM. 3 s , 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. Gardner 76 demonstrated that the protective components of this layer are inactivated by a 2.5-hr exposure to 196 pg/m 3 (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/m 3 (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/m 3 (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/m 3 (0.06 ppm). Richmond 13 studied the in vitrophagocytic 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 anaphylacticresponses to inhaled acetylcholine, a bronchoconstrictor agent, after a later exposure to 3930 pg/m 3 (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 freeradicals, 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/m 3 (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/m 3 (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/m 3 (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 wereidentified 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. Significantozone-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
reviews 39,129 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. 22

suggested that the interaction ofozone 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/m 3

(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 10 exposed 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 ofperoxides, 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."' ,16 studied 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 41 concerning 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. Thisreaction 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 40

also 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. 196 exposed 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 32 observed 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/m 3 (0.8 ppm) for 7 days. Theformation of malonaldehyde, along with the ozoneinduced increased activities of glutathioneperoxidase 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 assayfor 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."'' 15

continuously exposed rats to 1960 pg/m 3

(1.0 ppm) ozone, which eventually resulted in 100-percent mortality due topulmonary edema. Fifty percent of the atocopherol-depleted group died (LTso) after 8 2days of continuous exposure, while the vitaminsupplemented rats exhibited an LT so of 18.5 days. When Fletcher and Tappe1 68 studied 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 ofdietary 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. 15 showed that rats continuously exposed to 1960 Ng/m 3 (1 ppm) ozone for 9 days showed a

~ 

### ignificantly shorter
LT 50 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 werenoted 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-deficientgroup), 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 thearachidonic acid, particularly in the vitamin-Edeficient animals. Sixty-five days of exposure to 980 Ng/m 3 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/m 3 (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 14 C taken into sphingomyelin, lecithin, phosphatidyl inositol plusphosphatidyl serine, and phosphatidyl ethanol

### amine 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 14 C 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- I PD 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/m 3 (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 inactivatedpapain 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/m 3 (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 aircontrols. The differences between the supplemented and normal diet groups receiving ozone were not significant.Lactate dehydrogenase(LDH) activity increased in both diet groups followin 

### g ozone ezposure (p< 0. 

### 001 ), a 

### lth ough_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/m 3 (0.8 ppm), and six were exposed to 980 /jg/m 3 (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/m 3 (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 Lee 150 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/m 3 (0.8 ppm) were examined. Onthe 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/m 3 (0.2 ppm), while these enzyme activities in rhesus monkeys only increased significantly (p < 0.05) after exposure to 1570 /jg/m 3 (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/m 3 (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/m 3 (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/m 3 (4 ppm) ozone for 8 hr Lung homogenateswere assayed 16 hr later. Fifty percent of the nonpre-exposed (i.e., nontolerant) rats died following the 7840 Ng/m 3 (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/m 3 (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/m 3 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. Thecytochrome 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 thesecells was unchenged (on a per-milligram-ofprotein basis). , In contrast to the inhibitory effects of acuteexposures 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 O Z comsumption was due to proliferation of these cells. After 7 days of exposure to 392, 980, or 1568 /jg/m 3 (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/m 3 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/m 3 (0.2, 0.5, or 0.8 ppm) ozone. The increases in 02 consumption (using succinate as a substrate) and succinate-cytochrome-C reductase activitywere 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/m 3 (0.5 ppm) and of 24 percent (p < 0.05) at 1568 Ng/m 3 (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 ozoneconcentration 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 wereobserved 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/m 3 (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/m 3 (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/m 3 (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 supportthe 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) increas 

### e in 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 μm 

### ol es/hr per lung). This review

149 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/m 3 (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/m 3 , or 1 ppm, for 90 min) of lung homogenate resulted in a 52-percent decrease in microsomal cyt. PoSOlevels. 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/m 3 (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/m 3 (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/m 3 (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 anonvacuolar, 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/m 3 (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 ofthe 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/m 3 (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/m 3 (0.35 ppm), the ozone concentration was elevated to 980 or 1372 /Jg/m 3 (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, theremainder 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/m 3 (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/m 3 (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/m 3 (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, clusteringof 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/m 3 (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 proximalbronchioles 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/m 3 (0.88 ppm) ozone, emphysema-like lesions had developed. This study also included a group of animals exposed to both 1692 Ng/m 3 (0.9 ppm) NOz and 1764 /Ig/m 3 (0.9 ppm) ozone, and another group that received 4900Ng/m 3 (2.5 ppm) NOz and 490 Ng/m 3

(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. 162 exposed 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 193 reported 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

' 16 

### studied 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/m 3 (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/m 3 (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 50percent. 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. Yokoyama 21 studied the ventilatory functions of guinea pigs before, during, and after a 2-hr exposure to 980 Ng/m 3 (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/m 3 (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/m 3 (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/m 3 (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 Cd y n



### 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 thaneither 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 in 

### crea sed 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, investigators 216 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/m 3 (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
Gardner 37 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/m 3 (1 ppm) ozone for 4 hr, whereas exposure to this concentration for 2 hr resulted invery 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/m 3 (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/m 3 (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 exposureto 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/m 3 , 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/m 3 (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/m 3 (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/m 3 (0.5 or 1 ppm) ozone for 3 hr, and 18 hr later exposed the whole animal to either 5880 Ug/m 3 (3 ppm) or 43,1120 /ag/m 3 (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/m 3 (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-exposureon 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/m 3 (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/m 3 (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/m 3 , 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/m 3 (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/m 3 (20 ppm) ozone when they had been pre-exposed to 588 Ng/m 3 (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 Mountain 47 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/m 3 (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/m 3 (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/m 3 (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/m 3 (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). Eglite s3
reported that whole blood cholinesterase of rats decreased by the middle of the third month of a 93- day continuous exposure to 110 Ng/m 3 (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/m 3 (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/m 3 (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/m 3 (0.2 ppm) ozone, showed a small but significant drop in total blood serotonin immediately after termination of exposure. Thisreduction was probably due to a loss of plateletbound amine because there was no measurable free circulating plasma serotonin. Investigation of plasma Iysozyme 28 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/m 3 (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 ozoneas 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 author 66 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 forchromosome 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/m 3 , 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/m 3 (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/m 3 (0.6 to 8.5 ppm) were studied.' 67 At 1 176 Ng/m 3 (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 researchers 12, " 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. 19

reported 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 19 during 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! 20

exposed adult mice to 390 Ng/m 3 (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(amixed function oxidase) that oxidizes pentobarbital. Goldstein and Balchum 83 investigatet'the possible role of this enzyme in ozone-inducedtoxicity. 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. P4 5 0 

### 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/m 3

(1 ppm) for 17 months for varying hours each day. 14 Three 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 Tansy 18

exposed 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. 199

found 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 irreversiblecross-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. Forexample, 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 grossalterations (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/m 3 , 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/m 3 (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 pulmonarytissue. 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/m 3 , or 0.2 ppm) of ozone than monkeys (686 /Ug/m 3 , 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/m 3 (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/m 3 (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/m 3 (0.88 ppm) can produce emphysema-like structures in rats. Intermittent exposure (6 hr/day, 5 days/weekfor 10 months)to 984 Pg/m 3 (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 theconcentration increased. At a higher concentration (1960 Ng/m 3 , or 1 ppm), compliance (ameasure 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 protectionagainst 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/m 3 (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/m 3 (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/m 3

(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/m 3 (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 thepotential 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. 142,144

Single-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/m 3 (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 acrolein s,143

and 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

165TABLE 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 Fairchild 6 '• 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 54aerosol 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

166TABLE 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. 14died 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 acidphosphatase in alveolar macrophages, terminal airway, epithelium, and adjacentstructures

167TABLE 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/m 3

, 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 allthree enzyme activities as the concentration of ozone was increased
Increased 0 2

consumption (using succinate-cytochrome-C reductase activity fairly proportional to ozone
concentration Similar results obtained for intermtttent exposure
groups

168TABLE 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

169TABLE 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 mitochondriain 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 thealveolar 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 Dungworth 49 980, 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/m 3 (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 therate 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 Chambers 205 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

171TABLE 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 one03 dose. Partlal tolerance probably due toInhlbitlon 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. Notolerance 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 Chow 27 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 99to 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 effecqs l 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 fi 4

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.

173TABLE 8-7. EXTRAPULMONARY EFFECTS OF OZONE: CENTRAL NERVOUS SYSTEM AND BEHAVIOR

Ozone, Ozone, Length of pg/m 3 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 Eglite 53 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 Veninga 201 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 Eglite 53 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/m 3 (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 inthe 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/m 3 (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 so z H z SO 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 irradiatedauto 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/m 3 (97 to 145 ppm) as measured at the chamber outlet, for 2 hr at 80°F (27 0 C). The studies demonstrated that most mice exposed to 550,000Ng/m 3 (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/m 3 (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/m 3 (15 ppm) resulted in pulmonary morphological alterations.

REFERENCES FOR CHAPTER 8

1. Aharonson, E F, H Menkes, G Gurtner, D L. Swift, and D. F Proctor Effect of respiratory airflow iate on removal of soluble vapors by the nose J Appl. Physiol. 37:654-657, 1974 2 Alder, M G, and G. R Hill. The kinetics and mechanism of hydroxide ion catalyzed ozone decomposition in aqueous solution J Am. Chem. Soc 72.1884-1886, 1950 3 Alpert, S M., D E Gardner, D J Hurst, T R Lewis, and D. L Coffin Effects of exposure to ozone on defensive
mechanisms of the lu.ic y J Appl. Physiol. 31 •247-252,
1971. 4. Alpert, S M, and T. R Lewis Ozone tolerance studies utilizing unilateral lung exposure J. Appl Physiol. 31•243-246, 1971. 5 Alpert, S M., B B Schwartz, S D. Lee, and T. R. Lewis Alveolar protein accumulation A sensitive indicator of low level oxidant toxicity. Arch. Intern Med 128 69-73, 1971 6 Amdur, M. 0. The effect of aerosols on the response to irritant gases. /n: Inhaled Particles and Vapours C N Davies, ed. Pergamon Press, NewYork, 1961. pp. 281- 294. 7 Atwall, 0 S, andT Wilson Parathyroid gland changes following ozone inhalation. A morphologic study. Arch.
Environ. Health 28

- 91-100, 1974 8. Avery, M. E., and S. I. Said. Surface phenomena in lung in health and disease Medicine (Baltimore) 44 503- 526, 1965 9 Bartlett, D., Jr., C. S. Faulkner, and K Cook. Effect of chronic ozone exposure on lung elasticity in young rats J. Appl Physiol. 37.92-96, 1974. 10. Bates, D. V., G M Bell, C D. Burnham, M. Hazucha, J. Mantha, L D. Pengelly, and F Silverman Short term effects of ozone on the lung. J. Appl. Physiol 32 176- 181, 1972.
11 BiIs,R F Ultrastructural alterationsof alveolar tissue of mice. III Ozone. Arch Environ. Health 20 468-480,
1970. 12. Bjorksten, J. Aging, primary mechanism Gerontologia 8 179-192, 1`963. 13. Bjorksten, J, and F. Andrews. Chemical mechanisms underlying the biological mechanisms of the aging process. J. Am Geriatr Soc. 12.627-631, 1964. 14. Block, W N., F J Miller, and T R Lewis Pulmonary Hypertension in Dogs Exposed to Ozone. U S. Environmental Protection Agency, Cincinnati, Ohio, 1971 15. Boatman, E S, and R Frank. Acute effects of ozone on cats" lungs. II. Sfructural. Paper presented at the American Industrial Hygiene Assoc. Conference, San Francisco, 1972.

17716 Boatman, E S, S Sato, and R Frank Acute effects of ozone on cats' lungs.11. Structural Am Rev Respir Dis
110 157-169, 1974
17 Bobb, G A, and E J Fairchild, II Neutrophil-tolymphocyte ratio as indicator of ozone exposure Toxicol Appl Pharmacol 11 558-564, 1967 18 Boche, R D, and J J Quilligan, Jr Effects of synthetic smog on spontaneous activity of mice Science
131 1733-1734, 1960 19 Bokina, A I., N D Eksler, A D Semenenko, and R V Merkur'yeva. Investigation of the mechanism of action of atmospheric pollutants on the central nervous system and comparative evaluation of inethods of study Environ Health Persp 13 37-42, 1976 20 Brinkman, R, H B Lamberts, and T S Veninga Radiomimetic toxicity of ozonized air Lancet 1 133- 136, 1964 21 Brummer, M E G., L W Schwartz, and N K McQuillen A quantitative study of lung damage by scanning electronmicroscopy Inflammatory cell response to high ambient levels of ozone /n Scanning Electron Microscopy/1977 Vol II Proceedings of the Workshop on Biomedical Application—SEM and General Organ Systems IIT Research Institute, Chicago, III , March 1977 pp 513-518. 22 Buell, G. C, E Jeung, and W Fenninger Chemical changes in respiratory tissue following ozone exposure Presented at the Third Technical Meeting, West Coast Section, Air Pollution Control Association, Monterey, Calif., September 19-26, 1963 23 Buell, G C, Y Tokiwa, and P K Mueller Potential crosslinking agents in lung tissue Formation and isolation after in vivo exposure to ozone Arch. Environ
Health 10 213-219, 1969 24 Campbell, K I, G L Clarke, L. 0 Emik, and R. L Plata The atmospheric contaminant peroxyacetylnitrate Acute inhalation toxicity in mice Arch Environ Health 15 739-744, 196725 Castleman, W L, D L Dungworth, and W S Tyler Cytochemically detected alterations of lung acid phosphatase reactivity followang ozone exposur2 Lab Invest 29 310-319, 1973 26 Castleman, W L., D L Dungworth, and W S Tyler Histochemically detected enzymatic alterations in rat lung exposed to ozone Exp Mol Pathol 19 402-421,
197327 Chow, C K Biochemical responses in lungs of ozonetolerant rats Nature (London) 260 721-722, 1976. 28 Chow, C. K, C J. Dillard, and A L Tappel Glutathione peroxidase system and lysozyme in rats exposed to ozone or nitrogen dioxide Environ Res 7 311 -31 9,
1974 29 Chow, C K, M Z. Hussain, C E Cross, D L Dungworth, and M. G. Mustafa Effect of low levels of ozone on rat lungs I Biochemical responses during recovery and reexposure Exp Mol Pathol 25 182-188, 1976 30 Chow, C K, M G Mustafa, C E Cross, and B K Tarkington. Effects of ozone exposure on the lungs and the erythrocytes of rats and monkeys Relative biochemical changes Environ Physiol Biochem 5 142-146, 1975
31 Chow, C K.,andA L Tappel Activitiesofpentoseshunt and glycolytic enzymes in lungs of ozone-exposed rats Arch Environ Health 27 205-108, 1973

178 32. Chow, C. K., and A L Tappel. An enzymatic protective mechanism against lipid peroxidation damage to lungs of ozone-exposed rats Lipids 7 518-524, 1972 33 Christensen, E, and A C Giese Changes in adsorption spectra of nucleic acids and their derivatives following their exposure to ozone and ultraviolet irradiation Arch Biochem Biophys 51 208-216, 1954 34 Coffin, D L, and E J Blommer Alteration of the pathogenic role of streptococci group C in mice conferred by previous exposure to ozone /n Aerobiology Academic Press, Inc., New York, 1970. pp.
54-61 35 Coffin, D L, E J Blommer, D E Gardner, and R Holzman Effect of air pollution on alteration of susceptibility to pulmonary infections /n Proceedings of the 3rd Annual Conference on Atmospheric Contaminants in Confined Spaces AMRL-TR-67-200,Aerospace Medical Research Laboratories, WrightPatterson Air Force Base, Dayton, Ohio, 1968 pp 71-
80
36 Coffin, D L, and D E Gardner Interaction of biological agents and chemical air pollutants Ann Occup Hyg 15 219-235, 1972 37 Coffin, D L, and D E Gardner The role of tolerance in protection of the lung against secondary insults. /n Erstes internationales der Werksartz Symposium der chemischen Industrie Medichem, Ludwigshafen, W Ger , July 1972 pp 344-364 38 Coffin, D L, D E Gardner, R S Holzman, and F J Wolock Influence of ozone on pulmonary cells Arch Environ Health 16 633-636, 1968
39 Committee on the Challenges of Modern Society Air Quality Criteria for Photochemical Oxidantsand Related Hydrocarbons, NATO/CCMS Publication No 29, North Atlantic Treaty Organization, Brussels, Belgium, February 1974 40 Cortesi, R, and 0 S Privett Toxicity of fatty ozonides and peroxides Lipids 7 715-721 , 1972
41 Criegee, R Course of ozonization of unsaturated compounds Rec Chem Progr 18 1 11-120, 1957
42 Davis, I Microbiologic Studies with Ozone Mutagenesis of ozone for Escherichia coli Document No 61-60 U S Air Force, School of Aerospace Medicine, Aerospace Medical Center, Brooks Air Force Base, Tex , June 1961 43 Davis, I Microbiologic Studies with Ozone MutagenesisofOzonefromEscherichiaco/i ReportNo 61-60, US Air Force, Aerospace Medical Center, School of Aerospace Medicine, Brooks Air Force Base, Tex , June 1961 44 DeLucia, A J, P M Hogue, M G Mustafa, and C E Cross Ozone interaction with rodent lung Effect on sulfhydryls and sulfhydryl-containing enzyme activities
J Lab Clin Med 80 559-566, 1973 45 DeLucia, A J, M G Mustafa, M Z Hussain, and C E Cross Ozone interaction with rodent lung III Oxidation of reduced glutathione and formation of mixed disulfides between protein and nonprotein sulfhydryls J Clin Invest 55 794-802, 1975
46 Dillard, C J, N Urribarri, K Reddy, B Fletcher, S Taylor, B DeLumen, S Langberg, and A L Tappel.Increased lysosomal enzymes in lungs of ozoneexposed rats Arch Environ Health 25 426-431, 197247 Dixon, J R., and J. T. Mountain. Role of histamine and related substances in development of tolerance to edemagenic gases. Toxicol Appl. Pharmacol. 7 756- 766, 1965. 48. Dowell, A. R, L. A Lohrbauer, D. Hurst, and S. D. Lee. Rabbit alveolar macrophage damage caused by in vivo

03 inhalation. Arch. Environ. Health21.121-127, 1970.
49. Dungworth,D L. Short-term effects of ozone on lungs of rats, mice, and monkeys Environ. Health Persp. 16

- 179, 1976. 50 Dungworth, D L., W. L. Castleman, C. K. Chow, P. W Mellick, M. G. Mustafa, B. Tarkington, and W. S. Tyler. Effect of ambient levels of ozone on monkeys. Fed. Proc Fed. Am. Soc. Exp. Biol 34 1 670-1 674, 1975. 51. Dungworth, D. L., G L Clarke, and R L. Plata.Pulmonary lesions produced in A-strain mice by longterm exposure to peroxyacetylnitrate Am Rev Respir. Dis 99 565-574, 1969. 52 Easton, R. E, and S D. Murphy Experimental ozone pre-exposure and histamine. Effect on the acutetoxicity and respiratory function effects of histamine in guinea pigs Arch. Environ. Health 15

- 160-166, 1967. 53 Eglite, M E A contribution to the hygienic assessment of atmospheric ozone. Hyg Sanit. 33 18-23, 1968. 54 Ehrlich, R., J. C Findlay, J. D. Fenters, and D. E. Gardner Health effects of short-term inhalation of nitrogen dioxide and ozone mixtures Environ Res 14 223-231, 1977 55 Emik, L 0, and R L Plata Depression of running activity in mice by exposure to polluted air Arch Environ Health 18: 574-579, 1969 56 Emik, L 0., R L Plata, K. I. Campbell, and G. L. Clarke Biological effects of urban air pollution Riverside summary Arch. Environ. Health 23.335-342, 1971 57 Evans, M J, L V Johnson, R J Stephens, and G. Freeman Cell renewal in the lungs of rats exposed to low levels of ozone Exp. Mol. Pathol. 24:70-83, 1976. 58 Evans, M J, L V Johnson, R J. Stephens, and G. Freeman Renewal of the terminal bronchiolar epithelium in the rat following exposure to NO2 or 03. Lab Invest 35•246-257, 1976. 59 Evans, M J, W Mayr, R F. Bils, and C G Loosli Effects of ozone on cell renewal in pulmonary alveoli of aging mice Arch Environ Health 22 450-453, 1971 60. Evans, M J, R J. Stephens, and G Freeman Renewal of pulmonary epithelium following oxidant injury. /n Lung Cells in Disease A Bonhuys, ed Elsevier, New York, 1976 pp 165-178.

61 Fairchild, G A Effects of ozone and sulfur dioxide on virus growth in mice. Arch. Environ Health 32.28-33, 1977. 62 Fairchild, G A Ozone effect on respiratorydeposition of vesicular stomatitis virus aerosols. Amer Rev Respir Dis 109 446-449, 1974. 63 Fairchild, E J, S L Graham, M. Hite, R Killens, and L D Scheel Changes in thyroid 1 13 ' activity in ozonetolerant and ozone-susceptible rats Toxicol Appl. Pharmacol 6 607-613, 1964
64 Fairchild, E.J., II, S D Murphy, and H. E. Stokinger Protection by sulfur compounds against the air pollutants ozone and nitrogen dioxide Science 130 861-862, 1959 65. Fetner, R H Chromosome breakage in Vicia faba by ozone Nature (London) 181 504-505, 1958 66 Fetner, R.H Mitotic Inhibition Induced in Grasshopper Neuroblasts by Exposure to Ozone SAM-TDM-63-39, U.S Air Force, School of Aerospace Medicine, Aerospace Medical Center, Brooks Air Force Base, Tex , June 1963 67. Fetner, R H. Ozone-induced chromosome breakage in human cell culture. Nature (London) 194 793-794,
1962 68 Fletcher, B L., and A. L. Tappel Protective effects of dietary alphatocopherol in rats exposed to toxic levelsof ozone and nitrogen dioxide Environ. Res 6:165-175,
1973. 69 Frank, N. R, J. D. Brain, and D E Sherry Unilateral lung exposure to ozone. Fed Proc. Fed Am Soc Exp. Biol 27•279, 1968 70 Freeman, G, L T Juhos, N.J. Furiosi, R Mussenden, R J Stephens, and M. J Evans Pathology of pulmonary disease from exposure to interdependent ambient gases (NO2 and 03). Arch Environ Health 29 203-210, 1974

71. Freeman, G, L Juhos, N J Furiosi, W. Powell, and R Mussenden Criteria from animals exposed to known concentrations of nitrogen dioxide and ozone, with potential used in epidemiology /n Proceedings International Symposium on Recent Advances in the Assessment of Health Effects of Environmental Pollution. Volume II EUR 5360, Commission of European Communities, Luxembourg, 1975
72. Freeman, G, R. J. Stephens, D L. Coffin, and J F Stara. Changes in dogs' lungs after long-term exposure to ozone Arch Environ Health 29 209-216, 1973 73 Friberg, L, B Holman, and R Rylander Animal lung reactions after inhalation of lead and ozone Environ Physiol Biochem 2 170-178, 1972.
74. Fukase, 0, K Isomura, and H. Watanabe Effect of ozone on glutathione in vivo Taiki Osen Kenkyu 10.58- 62, 1975
75. Fukase, 0, K. Isomura, and H Watanabe Effect of ozone on vitamin C in vivo Taiki Osen Kenkyu 10.63-66, 1975 76 Gardner, D E Environmental Influences of Living Alveolar Macrophages. Ph D thesis, University of Cincinnati, Cincinnati, Ohio, 1971
77. Gardner, D E, and J A Graham Increased pulmonary disease mediated through altered bacterial defenses /n Pulmonary Macrophage and Epithelial Cells C L Sanders, R P Schneider, G E. Dagle, and H. A Ragan, eds ERDA Symposium Series 43, U S Energy Research and Development Administration, Washington, D C, September 1977 pp 1-21
78. Gardner, D E, J W Illing, F J Miller, and D L. Coffin The effect of ozone on pentobarbital sleeping time in mice Res Commun Chem Pathol Pharmacol 9 689- 700, 1974 79 Gardner, D E., T R Lewis, S M Alpert, D J Hurst, and D L Coffin The role of tolerance in pulmonary defense mechanisms Arch Environ Health 25 432-438, 1972

80. Gardner, D E, F J Miller, J W Illing, and J M Kirtz Increased infectivity with exposure to ozone and sulfuric acid Toxicol Lett 1 59-64, 1977
81. Gardner, D E, E. A Pfitzer, R T Christian, and D L Coffin Loss of protective factor for alveolar macrophages when exposed to ozone Arch.lntern Med 127 1078-1084, 1971

17982 Goldstein, D B, and 0 J Balchum Effects of ozone on lipid peroxidation in the red blood cell. Proc Soc Exp Biol Med 126 356-358, 1967 83 Goldstein, B. D., and 0 J Balchum Modification of thrresponse of rats to lethal levels of ozone by enzymeinducing agents Toxicol Appl Pharmacol 27.330-335, 1974 84 Goldstein, E, M C Eagle, and P. Hoeprich. Influence of ozone on pulmonary defense mechanisms of silicotic mice Arch Environ Health 24:444-448, 1972 85 Goldstein, B. D, S J. Hamburger, G. W. Falk, and M. A. Amoruso Effect of ozone and nitrogen dioxide on the agglutination of rat alveolar macrophages by concanavalin A Life Sci 21.1637-1644, 1977. 86 Goldstein,B D,C.Lodi,C Collinson, and 0 J.Balchum Ozone and lipid peroxidation Arch. Environ Health 18 631-635, 1969. 87 Goldstein, B D, B Pearson, C. Lodi, R E. Buckley, and 0 J Balchum The effect of ozone on mouse blood in vivo Arch Environ Health 16 648-650, 1968. 88 Goldstein, B D, S Solomon, B S. Pasternack, and D R Bickers. Decrease in rabbit lung microsomal cytochrome P-450 levels following ozone exposure Res Commun Chem Pathol. Pharmacol 10 759-762, 1975 89 Goldstein, E, W S Tyler, P D Hoeprich, and C. Eagle. Adverse influence of ozone on pulmonary bactericidal activity of murine lung Nature (London) 229

- 262-263, 1971 90 Goldstein, E., W S Tyler, D Hoeprich, and C. Eagle. Ozone and the antibacterial defense mechanismsof the murine lung Arch Intern Med 128 1099-1102, 1971. 91 Goldstein, E, M A Warshauer, W Lippert, and B. Tarkington 03 and NO2 exposure Murine pulmonary defense mechanisms Arch Environ. Health 28•85-90, 1974 92 Gooch, P C, D A Creasia, and J G Brewen The cytogenetic effect of ozone Inhalation and in vitro exposures Environ Res 12.188-195, 1976 93 Gregory, A R, L A Ripperton, and B Miller Effect of neonatal thymectomy on the development of ozone tolerance in mice J Am. Ind. Hyg. Assoc 28.278-283, 1967 94 Hadley, J G, D E Gardner, D L Coffin, and D B. Menzel Enhanced binding of autologous red cells to the macrophage plasma membrane as a sensitive indicator of pollutant damage /n Pulmonary Macrophage and Epithelial Cells C L Sanders, R. P. Schneider, G E. Dagle, and H A Ragan, eds ERDA Symposium Series 43, U S Research and Development Administration, Washington, D C, 1977 pp 66-77 95 Hamelin, C, and Y S Chung Characterization of mucoid mutants of Escherichia coli K-12 isolated after exposure to ozone J Bacteriol 122 19-24, 1975 96 Hamelin, C, and Y S Chung Rapid test for assay of ozone sensitivity in Escherichia coli Mol Gen Genet
145 191-194, 1976 97 Hamelin, C, and Y S Chung. Resistance a I'ozone chez
Escherichia coli II. Relations avec certains mecanismes de reparation de I'ADN Mol Gen Genet 129 177-184, 1974 98 Hathaway, J A, and R E Terrill Metabolic effects of chronic ozone exposure on rats. J Am Ind Hyg Assoc. 23 392-395, 1962 99 Hattori, K, N Kato, M. Kinoshita, S Kinoshita, and T Sunada Protective effect of ozone in mice against whole-body X-irradiation. Nature (London) 198•1220, 1963 100 Hinners, R G. Engineering the chronic exposure of animals to laboratory produced automobile exhaust. J Air Pollut. Control Assoc. 12.527-530, 1962 101 Hinners, R. G Laboratory produced automobile exhaust facility Biomed Sci. Instrum. 1 53-58, 1963. 102. Holt, P. G., and A. Nulsen. Ozone hazard in UV isolation units. J Occup. Med 17.186-188, 1975

103. Huber, G. L., R J Mason, M. LaForce, N. J. Spencer, D E. Gardner, and D. L. Coffin Alterations in the lung following the administration of ozone. Arch Intern. Med. 128

- 81-87, 1971 104 Hueter, F. G, G L Contner, K A Busch, and R G Hinners Biological effects of atmospheres contaminated by auto exh3ust. Arch. Environ Health 12 553-560, 1966 105 Hurst, D J, and D L Coffin Ozone effect on lysosomal hydrolases of alveolar macrophages in vitro. Arch. Intern Med 127.1059-1063, 1971 106 Hurst, D J, D E Gardner, and D. L. Coffin. Effect of 03 on acid hydrolases of the pulmonary a;reolar macrophage Res J Reticuloendothel Soc 8 288-300, 1970 107 Hussain, M Z, C E Cross, M G Mustafa, and R S. Bhatnagar Hydroxyproline contents and prolyl hydroxylase activities in lungs of rats exposed to low levels of ozone Life Sci 18•897-904, 1976 108 Hussain, M. Z., M G. Mustafa, C K Chow, and C. E Cross. Ozone-induced increase of lung proline hydroxylase activity and hydroxy-proline content Chest 691Suppl 2 .273-275, 1976. 109 Ibrahim, A L., Y C Zee, and J W Osebold The effects of ozone on the respiratory epithelium and alveolar macrophages of mice I Interferon product on Proc Soc Exp. Biol Med 152 483-488, 1976 110 Jegier, Z Ozone as an air pollutant. Can. J. Public Health 64.161-166, 1973 111. Kliment, V Similarity and dimensional analysis, evaluation of aerosol deposition in the lungs of laboratory animals and man Folia Morphol. (Prague) 21 59-64, 1973 112 Konigsberg, A S. A study of the Measurement of Ozone and Some Effects of Ozone and Nitrogen Oxides on the Activity of Rats Ph D thesis, Syracuse University, Syracuse, N.Y., 1969 113 Konigsberg, A S, and C Bachman. Ozonized atmosphere and gross motor activity of rats. Int J Biometeorol 14.261-266, 1970 114 Kotin, P, and H L Falk II The experimental induction of pulmonary tumors in strain-A mice after exposure to atmosphere of ozonized gasoline Cancer(Philadelphia) 9:910-917, 1956 115 Kotin, P., H L Falk, and C J McCammon III The experimental induction of pulmonary tumors and changes in respiratory epithelium in C57BL mice following exposure to ozonized gasoline Cancer (Philadelphia) 11.473-481, 1958 116 Kotin, P, and M Thomas Effect of air contaminants on reproduction and offspring survival in mice AMA Arch Ind Health 16 41 1-41 3. 1957

180117 Kyei-Aboagye, K., M Hazucha, I Wyszogrodski, D Rubinstein, and M E. Avery The effect of ozone exposure in vivo on the appearance of lung tissue lipids in the endobronchial lavage ot rabbits Biochem Biophys Res Commun 54 907-913, 1973 118. Last, J. A, M Jennings, and C. E. Cross. Mucus g!ycoprotein secretion by tracheal explants from rats exposed to ozone Fed. Proc Fed Am Soc Exp Biol 36.413, 1977 119 Lewis, T. R., F G Hueter, and K. A Busch. Irradiated automobile exhaust• Its effects on the reproduction of mice Arch Environ Health 15:26-35, 1967. 120. Lewis, T R., W. J Moorman, Y. Y. Yang, andJ. F Stara Long-term exposure to auto exhaust and other pollutant mixtures. Effects on pulmonary function in the beagle Arch Environ Health 29

- 102-106, 1974
121 Lunan, K D, P Short, D. Negi, and R J Stephens Glucose-6-phosphate dehydrogenase response of postnatal lungs to NO2 and 03. /n Pulmonary Macrophage and Epithelial Cells C. L. Sanders, R. P. 3chneider, G E Dagle, and H A Ragan, eds ERDA Symposium Series 43, U S Energy Research and Development Administration, Washington, D.C., 1977 122 Maclean, S. A., A C Longwell, and W. J Blogoslawski. Effects of ozone-treated seawater on the spawned, fertilized, miotic, and cleaving eggs of the commercial American oyster Mutat. Res 21.283-285, 1973 123 Matsumura, Y. The effects of ozone, nitrogen dioxide, and su!fur dioxide on the experimentally induced allergic respiratory disorder in guinea pigs. I The effect on sensitization with albumin through the airway. Amer. Rev Respir Dis 102.430-437, 1970.
124. Matsumura, Y, K Mizuno, T Miyamoto, T Suzuki, and Y Oshima The effects of ozone, nitrogen dioxide, and su!fur dioxide on experimentally induced allergic respiratory disorder in guinea pigs IV Effects on respiratory sensitivity to inha!ed acetylcholine. Amer Rev Respir Dis. 105.262-267, 1972
125. McJilton, C. E., J Thielke, and R Frank. Ozone uptake model for the respiratory system J Am. Ind. Hyg. Assoc 33 20, 1972 126 Mellick, P W, D L. Dungworth, L W Schwartz, and W S. Tyler Short-term morpho!ogic effects of high ambient levels of ozone on lungs of rhesus monkeys. Lab Invest 36 82-90, 1977. 127 Mendenhall, R. M., and H E. Stokinger. Films from lung washings as a mechanism model for lung injury by ozone J Appl Physiol 17 28-32, 1962. 128 Menzel, D B Oxidation of biologically active reducing substances by ozone Arch Environ. Health 23 149- 153, 1971 129 Menzel, D B. The ro!e of free radicals in the toxicity of air pollutants (nitrogen oxides and ozone). /n Free Radicals in Biology Volume II W A Pryor, ed. Academic Press, Inc., New York, 1976 pp 181-202. 130 Menzel, D B Toxicity of ozone, oxygen, and radiation Annu. Rev. Pharmacol 10•379-394, 1970.
131. Menzel, D. B., W G Anderson, M B Abou-Donia. Ozone exposure modifies prostag!andin biosynthesis in perfused rat lungs. Res. Commun. Chem. Pathol Pharmacol 15

- 135-147, 1976. 132. Menzel, D B., J. N Roehm, and S D Lee Vitamin E. The bio!ogical and environmental antioxidant J. Agric. Food Chem 20 481-486 ; 1972. 133 Menzel, D B., R. Slaughter, D Donovan, and A Bryant Fatty acid ozonides as the toxic agents on ozone inhalation Pharmacologist 15 239, 1973. 134 Miller, F J A Mathematical Model of Transport and Removal of Ozone in Mammalian Lungs. Ph D. thesis, North Carolina State University, Raleigh, N C, 1977 135 Miller, F J, J W. Illing, and D E Gardner Effect of urban ozone levels on laboratory-induced respiratory infections. Toxicol Lett. 2 163-169, 1978

136 Miller, F. J., D. B. Menzel, and D L. Coffin. Similarity between man and laboratory animals in regional pu!monary deposition of ozone. Environ. Res 17 84- 101, 1978. 137 Mittler, S, D. Hendrick, M King, andA Gaynor Toxicity of ozone 1. Acutetoxicity Ind Med Surg 25.301 -306, 1956 138 Mizcguchi, I, M Osawa, Y Sato, K Makino, and H. Yagyu Studies on erythrocyte and photochemical smog Part I Effects of air pollutants on erythrocyte resistance.. Taiki Osen Kenkyu 8 414, 1973
139 Moorman, W J, J. J Chmiel, J F Stara, and T R Lewis. Comparative decomposition of ozone in the nasopharynx of beagles. Acute vs chronic exposure Arch Environ Health 26.153-155, 1973

140. Mudd, J. B, R Leavitt, A Ongun, and T T. McManus Reaction of ozone with amino acids and proteins Atmos Environ 3•669-681, 1969

141. Mudd, J B., F. Leh, and T T. McManus Reaction of ozone with nicotinamide and its derivatives. Arch Biochem Biophys 161 •408-419, 1974.
142. Murphy, S. D. A review of effects on animals of exposure to auto exhaust and some of its components J Air Pollut. Control Assoc 14 303-308, 1964 143 Murphy, S. D., D. A. Klingshine, and C E Ulrich Respiratory response of guinea pigs during acro!ein inhalation and its modification by drugs J Pharmacol Exp. Ther. 141.79-83, 1963 144 Murphy, S D., J. K. Leng, C E Ulrich, and H V Davis Effects on animals of exposure to auto exhaust Arch Environ Health 7.60-70, 1963 145. Murphy, S D, and C E. Ulrich Multi-animaltestsystem for measuring effects of irritant gases and vapors on respiratory function of guinea pigs J Am. Ind Hyg Assoc. 25.28-36, 1964 146 Murphy, S. D, C. E Ulrich, S. H Frankowitz, and C Xintaris Altered function in anima!s inhaling low concentrations of ozone and nitrogen dioxide J Am Ind Hyg Assoc. 25 246-253, 1964 147. Mustafa, M G Augmentation of mitochondrial oxidative metabolism in lung tissue during recovery of anima!s from acute ozone exposure Arch Biochem Biophys 165 531-538, 1974. 148. Mustafa, M. G, A. J. DeLucia, G K York, C Arth, and C E Cross Ozone interaction with rodent lung II. Effects on oxygen consumption of mitochondria. J. Lab Clin. Med. 82.357-365, 1973. 149. Mustafa,M.G,A.B Hacker,J J Ospital,M Z Hussain, and S. D. Lee Biochemical effects of environmental oxidant pol!utants in animal lungs. /n• Biochemical Effects of Environmental Pollutants S. D. Lee, ed Ann Arbor Science Publishers, Ann Arbor, Mich., 1977 pp. 59-96

181150. Mustafa, M G, and S D Lee Pulmonary biochemical alterations resulting from ozone exposure Ann Occup Hyg. 19 17-26, 1976 151 Mustafa, M G, S M Macres, B K Tarkington, C K Chow, and M Z Hussain Lung superoxide dismutase (SOD). Stimulation by low-level ozone exposure Clin Res. 23 138A, 1975 152 Nakalima, T, S Kusumoto, Y Tsubota, E Yonekawa, R Yoshida, K Motomiya, K Ito, G. Ide, and H Otsu Histopathological changes in the respiratory organs of mice exposed to photochemical oxidants and automobile exhaust gas Osaka-furitsu Koshu Eisei Kenkyusho Kenkyu Hokoku Rodo Eisei Hen (10) 35-42,
1972 153. Nasr, A N.M , B D. Dinman, and I A Bernstein Nonparticulate air pollutants ll Effect of ozone inhalation on nadide phosphate levels in tracheal mucosa Arch Environ. Health 22 545-550, 1971
154 National Air Pollution Control Administration Air Quality Criteria for Photochemical Oxidants NAPCA Publication No. AP-63, U S Department of Health, Education, and Welfare, Public Health Service, Washington, D C, March 1970
155 National Research Council Ozone and Other Photochemical Oxidants National Academy of Sciences, Washington, D C, 1977 pp 306-312 156 National Research Council Toxicology /n Ozone and Other Photochemical Oxidants. National Academy of Sciences, Washington, D C, 1977 pp 323-387 157 Nettesheim, P, D A Creasia, and T J Mitchell Carcinogenic and cocarcinogenic effects of inhaled synthetic smog and ferric oxide particles J Nat Cancer Inst 55 1 59-1 66, 1975
158 Orthoefer, J G, R S Bhatnagar, A Rahman, Y Y Yang, S D. Lee, and J F Stara Collagen and prolyl hydroxylase levels in lungs of beagles exposed to air pollutants. Environ Res 12 299-305, 1976 159. Pagnotto, L D, and S S. Epstein Protection by antioxidants against ozone toxicity in mice Experientia 25 703, 1969. 160 Palmer, M S, R. W Exley, and D L Coffin Influence of pollutant gases on benzpyrene hydroxylase activity Arch Environ Health 25.439-442, 1972.
161. Palmer, M S, D H Swanson, and D L Coffin. Effect of

03 on benzpyrene hydroxylase activity in the Syrian golden hamster Cancer Res 31.730-733, 1971
162. P'an, A, J Beland, and Z Jegier Ozone-induced arterial lesions. Arch Environ Health 24:229-232,
1972. 163 P'an, A. Y S, and Z. Jegier The effect of sulfur dioxide and ozone on acetylcholinesterase Arch Environ Health 21 498-501, 1970
164. P'an, A Y. S, and Z. Jegier Serum protein changes during exposure to ozone J Am Ind Hyg Assoc. 37T329-334, 1976
165. P'an, A Y S, and Z Jegier The serum trypsin inhibitor capacity during orone exposure Arch Environ Health 23 215-219, 1971 166 P'an, A. Y. S., and Z. Jegier Trypsin protein esterase in relation to ozone-induced vascular damage Arch Environ. Health 24 233-236, 1972 167 Peterson, D.C., and H. L Andrews The role of ozone in
radiation avoidance in the mouse Radiat Res 19

- 331- 336, 1963. 168. Prat, R., C Nofre, and A Cier Effects of sodium hypochlorite, ozone, and ionizing radiations on pyrimidine constituents of Escherichia coli Ann Inst
Pasteur 114 595-607, 1968 169 Previero, A, A Signor, and S Bezzi Tryptophan modification in polypeptide chains Nature (London) 204 687-688, 1964 170 Pryor, W A Free radical reactions in biology Initiation of lipid autoxidation by ozone and nitrogen dioxide Environ Health Persp 16 180-181, 1976
171 Pryor, W A., J.P Stanley, E. Blair, and G B. Cullen Autoxidation of polyunsaturated fatty acids Part I. Effect of ozone on the autoxidation of neat methyl Iinoleate and methyl linolenate Arch Environ Health 31 201- 210, 1976 172 Reynolds, R W, and R R Chaffee Studies on the
combined effects of ozone and a hot environment on reaction time in subhuman primates In Project Clean Air Volume 2 California University, Research Project S-6, Santa Barbara, Calif , 1970
173 Richmond, V L In vitro hydrolase and phagocytic activity of alveolar macrophages J Lab Clin. Med. 83.757-767, 1974 174 Roehm, J, J G Hadley, and D. B Menzel Antioxidants vs. lung disease Arch 1-itern Med. 128

- 88-93, 1971. 175. Roehm, J, J G. Hadley, and D B Menzel Influence of vitamin E on the lung fatty acids of rats exposed to
ozone Arch Environ Health 24

- 237-242, 1972 176 Roehm, J. N., J G Hadley, and D B Menzel. Oxidation of unsaturated fatty acids by ozone and nitrogen dioxide
A common mechanism of action Arch Environ. Health 23.142-148, 1971. 177 Ross, B K, M P Hlastala, and R Frank On the lack of effect of ozone on hemoglobin-oxygen affinity Arch Environ Health (in press) 178 Roth, R. P., and M F Tansy Effects of gaseous air pollutants on gastric secreto-motor activities in the rat J Air Pollut Control Assoc 22 706-709, 1972
179. Sachsenmaier, W, W Siebs, and T Tan Effects of
ozone on mouse ascites tumor cells and on chick
fibroblasts in tissue culture Z Krebsforsch 67.113- 126, 1965
180. Sato, S, M Kawakami, S Maeda, and T TakishimaScanning electron microscopy of the lungs of vitamin-Edeficient rats exposed to low concentration of ozone Am Rev Respir Dis. 113

- 809-821, 1976 181 Scheel, L D, 0 J Dobrogorski, J T Mountain, J L Svirbely, and H E Stokinger Phys+ologic, biochemical, immunologic, and pathologic changes following ozone exposure J Appl Physiol 14 67-80, 1959 182 Schlipkoter, H, and J Bruch Functional and morphological alterations caused by exposure to ozone. Zentralbl Bakteriol Parasitenkd.lnfektionskr Hyg Abt. 1 Orig Reihe B 156 486-499, 1973 183 Schwartz, L W Comparison of the effects of ozone and oxygen on lungs of rats Environ Health Persp 16.179- 180, 1976 184 Schwartz, L. W., D. L Dungworth, M G Mustafa, B K. Tarkington, and W S Tyler Pulmonary responseof rats to ambient levels of ozone Effects of 7-day intermittent or continuous exposure Lab Invest 34.565-578, 1976 185 Scott, D B. M, and E C Lesher. Effect of ozone on survival and permeability of Escherrchia cob J
Bacteriol 85 567-576, 1963

182186 Seto, K, M Kawakami, K Sugita, M Shishido, M. Yamaji, and T. Tsuda, Influence of inhalation of ozone and nitrogen dioxide on the formation of phospholipids on the lung. Igaku to Seibutsugaku 86 317-320, 1973. 187 Seto, K, M. Kawakami, M Takeshima, M Kon, K. Sugita, and M. Shishido Influence of short period exposure to ozone and nitrogen dioxide on the formation of phospholipids in the lungs of rabbits Igaku to 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, Berkeley, Calif., April 17, 1961 190 Stephens, R J, M F Sloan, M J Evans, and G. Freeman Alveolar Type 1 cell response to exposure to 0.5 ppm 03 for short periods Exp Mol Pathol 20 1 1- 23, 1974 191 Stephens, R J, M F Sloan, M J Evans, and G Freeman Early response of lung to low levels of ozone. Amer J Pathol 74 31-58, 1973 192 Stephens, R J, M. F Sloan, and D G Groth Effectsof long-term, low-level exposure of NO2 or 03 on rat lungs. 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, Inc , New York, 1962 pp. 282-334 194 Stokinger, H E Ozone toxicology A Review of research and industrial experience, 1954-1964 Arch Environ Health 10.719-731, 1965 195 Stokinger, H E., W D Wagner, and 0. L J Dobrogorski. Ozone toxicity studies III. Chronic injury to lungs of animals following exposure at a low level AMA Arch Ind Health 16 514-522, 1957. 196 Teige, B, T T McManus, and J. B. Mudd Reaction of ozone with phosphatidylcholine liposomes and the lytic effect of products on red blood cells Chem Phys Lipids 12153-171, 1974 197 Thomas, G, J D Fenters, and R. Ehrlich Effect of Exposu re to PAN and Ozone on Susceptibility to Chronic 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 bloodandliver Presentedatthe2ndlnternationalClean Air Congress, Washington, D C, December 6-11, 1970 Paper MB-15E 202 Veninga, T Toxicity of ozone in comparison with ionizing radiation Strahlentherapie 134 469-477,
1967 203 Warshauer, D, E Goldstein, P D Hoeprich, and W Lippert Effect of vitamin E and ozone on the pulmonary antibacterial defense mechanisms. J. Lab Clin. Med.
83

- 228-240, 1974
204. Watanabe, S., R Frank, and E Yokoyama. Acute effects of ozone on lungs of cats. Amer. J Rev Respir Dis. 1081141-1151, 1973
205. Wayne, L. G., and L A. Chambers. Biological effects of urban air pollution V A study of effects of Los Angeles atmosphere on laboratory rodents Arch. Environ. Health 16.871-885, 1968.
206. Weibel, E R. Morphometry of the Human Lung. Academic Press, Inc , New York, 1963. 207 Weissbecker, L., R. D Carpenter, P. C. Luchsinger, and T. S Osdene In vitro alveolar macrophage viability. Effect of gases Arch. Environ. Health 18

- 756-759,
1969. 208 Werthamen, S, P D Penha, and L. Amaral. Pulmonary lesions induced by chronic exposure to ozone. Arch. Environ Health 29 164-166, 1974. 209 White, A, P. Handler, and E. L Smith, eds. Principals of Biochemistry Fifth Edition, McGraw-Hill Book Co., New York, 1973. pp 409, 873. 210 Xintaras, C, B. L Johnson, C E. Ulrich, R. E. Terrill, and M F. Sobecki Application of the evoked response technique in air pollution toxicology. Toxicol. Appl
Pharmacol 877-87, 1966. 211 Yokoyama, E. A comparison of the effects of S02, NOz, and 03 on pulmonary ventilation. Guinea pig exposure experiments. Sangyo Igaku 11:563-568, 1969. 212. Yokoyama,E The effects of low concentrations of ozone on the lung pressure of rabbits and rats Presented at the 46th Annual Meeting, Japan Society of Industrial Hygiene, April 1973. Paper 223. 213 Yokoyama, E The effects of 03 on lung function /n: Proceedings of the Science Lecture Meeting on Air Pollution Caused by Photochemical Reaction Japan Society of Air Pollution, Tokyo, March 1972 pp 123-
143. 214 Yokoyama, E On the maximal expiratory flow volume curve of rabbit lung exposed to ozone Dihon Kyobu Shikkan Gakkai Zasshi 12 (Suppl ) 2, 1974. 215 Yokoyama, E, and R. Frank Respiratory uptake of ozone in dogs Arch Environ. Health 25• 132-138, 1972.
216. Yokoyama, E., and I. Ichikawa. Study on the biological effects of atmospheric pollutants (FY 1972-1975). /n: Research Report for Funds of the Environmental Agency in 1974 Institute of Public Health, Department of Industrial Health, Tokyo, 1974 pp 16-1 to 16-6.
217. Zelac, R. E., H. L. Cromroy, W E Bolch, Jr, , B. G Dunavant, and H A Bevis. Inhaled ozone asa mutagen. I. Chromosome aberrations induced in Chinese hamster lymphocytes. Environ Res 4•262-282, 1971. 218 Zelac, R. E, H. L Cromroy, W E. Bolch, Jr, , B. G. Dunavant, and H A. Bevis. Inhaled ozoneasa mutagen. II Effect on the frequency of chromosome aberrations observed in irradiated Chinese hamsters Environ. Res.
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/m 3 (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- Klelnfeld 43 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.

fE M

### 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); thischange 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/m 3 (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. 35 on 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 withcontinuation 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 2 and Hazucha and Bates 33 reported a marked decrease in pulmonaryfunction among healthy subjects performing light exercise while exposed to 730 μg/m 3 (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/m 3 ) 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 1970 6,20.25,31,36,60

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 notslgnlflcant 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 Nochange (2/2 subjects) Alrway reslstance Sllght Increase, but wlthln normal IlmltsDynamlc 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 weeks0 80 upper resplratory Infectlons/ person In 12 weeks

Young etal 60

Young etal 60

187TABLE 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 0 C, 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/m 3 (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 j ug/m 3 (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 ofseven 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/m 3 (0.25 ppm) ozone, a mixture of 490 /jg/m 3 (0.25 ppm) ozone and 560 pg/m 3 (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 V I

~ -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/m 3 (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 j 

# I ~ 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 (DL c o), 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/m 3

(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., 56

using 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. 45

exposed 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 

# V 25 ) 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., 40 employing 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 37 have reported on the results of limited studies involving four normal male subjects exercising while exposed to ozone at 1760 Ng/m 3

(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. 59 studied 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. 29

Six 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 Elevel. 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 scorewas 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 parametersdiffered 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 hematologiceffects 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/m 3 (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/m 3 (0.4 ppm);
3. Group C: 1 180 Ng/m 3 (0.6 ppm), 1- to 2- month delay, 390 /ag/m 3 (0.2 ppm), 3-day delay, 1 180 ,ug/m 3 (0.6 ppm);
4. Group D: 1 180 Ng/m 3 (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/m 3 (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/m 3 (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 decreasedneuraminic 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-minexposure 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 maintainingintactness 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 inhibitedthe 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/m 3 (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 serumGSSRase 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 increasedfrequency 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 onthe 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 andcarbon 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/m 3 (0.24 ppm) PAN, no significant changes were observed in the metabolic, cardlovascular, or thermoregulatoryresponses.'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 fromcontrolled 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/m 3 (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.

REFERENCES FOR CHAPTER 9

1. Balchum 0. J., J. S O'Brien, and B D Goldstein Ozone and unsaturated fatty acids Arch Environ Health22 32- 34, 1971 2 Bates, D. V, and M. Hazucha. The short-term effects of 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 U S Government Printing Office, Washington, D C, 1973 pp 507-540. 3 Bates, D. V, G M. Bell, C D Burnham, M Hazucha, J Mantha, L D Pengelly, and F Silverman Short-term effects of ozone on the lung J Appl Physiol 32 176-181, 1972 4 Bates, D. V, G M Bell, C D Burnham, M Hazucha, J Mantha, L D. Pengelly, and F Silverman Problems in studies of human exposure to air pollutants Can Med Assoc J. 103 833-837, 1970 5 Bell, K A, W S Linn, M Hazucha, J D Hackney, and D V Bates. Respiratory effects of exposure to ozone plus sulfur dioxide in southern Californians and eastern Canadians. J. Am. Ind Hyg Assoc. 38 696-706, 1977 6. Bennett, G Ozone contamination of high altitude aircraft cabins Aerosp Med 33 969-973, 1962
7. Brinkman, R., and H. B Lamberts Ozone as a possible radiomimetic gas. Nature (London) 181 1202-1203, 1958

19710

11.

12

13

14

15

16

17.

18

19

20.

21.

22.

23.

24.

25

26. Brinkman, R, H. B. Lamberts, and T. S. Vening. Design consideratlons Arch Environ Health 30 373- Radiomimetic toxicity of ozonized air Lancet 1 133-136, 378, 1975 1964. 27 Hackney, J D, W S Linn, S K Karuza, R D Buckley, D Buckley, R D, J D Hackney, K Clark, and C Posin C Law, D V. Bates, M Hazucha, L D Pengelly, and F Ozone and human blood Arch. Environ Health3040-43, Silverman Effects of ozone exposure in Canadians and 1975• Southern Californians Evidence for adaptation? Arch Challen, P. J. R, D E Hickish, and J Bedford An Environ Health 32 110-116, 1977 investigation of some health hazards in an inert-gas 28 Hackney, J D, W S Linn, D C Law, S K Karuza, H tungsten-arc welding shop Br J Ind Med 15 276-282, Greenberg, R D Buckley, and E E Pedersen. 1958 Experimental studies on human health effects of air Dadlez, M. J. Ozone formed by ultraviolet rays. Q. J pollutants. III. Two-hour exposure to ozone alone and in Pharm. 1 99-100, 1928 combination with other pollutant gases Arch Environ DeLucia, A. J., and W C Adams. Effects of 03 inhalation Health 30 385-390, 1975 during exercise on pulmonary function and blood 29. Hackney, J. D, W S Linn, J G Mohler, and C R Collier. biochemistry J Appl Physiol. Respirat Environ Adaptation to short-term respiratory effects of ozone in Exercise Physiol 43 75-81, 1977 men exposed repeatedly J Appl Physiol Respirat Drinkwater, B. L., P. B. Raven, S M Horvath, J A Gliner, Environ Exercise Physiol 43.82-85, 1977 R 0. Ruhling, N. W. Bolduan, and S Taguchl. Air 30 Hackney, J D, W S Linn, J G. Mohler, E. E Pedersen, P pollution, exercise, and health stress Arch Environ. Breisacher, and A Russo Experimental studies on Health 28.177-181, 1974 human health effects of air pollutants II Four-hour Flury, F., and F Zernik Ozone /n. Schadliche Gase, exposure to ozor•.e alone and in combination with other Dampfe, Nebel, Rauch und Staubarten. Julius Springer, pollutant gases Arch Environ Health 30 379-384, Berlin, 1931 pp 115-116 1975 Folinsbee, L J, S M Horvath, P B Raven, J. F Bedi, A. R 31 Hallett, W Y Effect of ozone and cigarette smoke on lung Morton, B. L. Drinkwater, N. W. Bolduan,andJ A Gliner. function. Arch. Environ. Health 10 295-302, 1965. Influence of exercise and heat stress on pulmonary 32. Hazucha, M. Effects of ozone and sulfur dioxide on function during ozone exposure J Appl. Physiol pulmonary function in man Ph D Thesis, McGill Respirat. Environ. Exercise Physiol 43 409-413, 1977 University, Montreal, Canada, 1973 Folinsbee, L. J., F. Silverman, and R. J. Shephard. 33. Hazucha, M, and D V Bates Combined effect of ozone Decrease of maximum work performance following and sulfur dioxide on human pulmonaryfunction Nature exposure. J Appl Physiol - Respirat Environ. Exercise 25750-51, 1975. Physiol. 42 531-536, 1977 34 Hazucha, M, C Parent, and D. V Bates Development of Folinsbee, L. J, F. Silverman, and R J. Shephard ozone tolerance in man. /n. International Conference on Exercise responses following ozone exposure J. Appl. Photochemical Oxidant Pollution and Its Control Physiol 38:996-1001, 1975. Proceedings Vol. I. B Dimitriades, ed EPA-600/3-77- Gliner, J. A., P. B. Raven, S M Horvath, B L. Drinkwater, 001 a, U S Environmental Protection Agency, Research and J C. Sutton Man's physiologic response to long- Triangle Park, N C., January 1977 pp 527-541 term work during thermal and pollutant stress. J. Appl 35 Hazucha, M, F Silverman, C Parent, S Field, and D V Physiol. 39.628-632, 1975 Bates. Pulmonary function in man after short-term Golden, J A, J. A Nadel, and H A Boushey Bronchial exposure to ozone. Arch Environ Health 27 183-188, hyper-irritability in healthy subjects after exposure to 1973. ozone. Am. Rev Respir Dis 118 287-294, 1978 36 Jordan, E O, and A J Carlson Ozone Its bacGoldsmith, J. R., and J. Nadel Experimental exposure of teriological, physiologic and deodorizing action J Am human subjects to ozone J. Air Pollut Control Assoc Med Assoc 61•1007-1012, 1913 19 329-330, 1969 37 Kagawa, J, and T Toyama Effects of ozone and brief Goldstein, B. D. Production of paroxysmal nocturnal exercise on specific airway conductance in man Arch haemoglobinuria-like red cells by reducing andoxidizing Environ. Health 30 36-39, 1975 agents Br. J. Haematol 26:49-58, 1974. 38 Kelly, F J, and W E Gill Ozone poisoning Arch Goldstein, B. D., L. Y Lai, and R. Cuzzi-Spada Environ. Health 10.517-519, 1965. Potentiation of complement-dependent membrane 39. Kerr, H D, T J Kulle, M L Mclhany, and P Swidersky damage by ozone. Arch Environ Health 28 40-42, 1974 Effects of ozone on pulmonary function in normal Goldstein, B D, and M R. Levin p-Aminobenzoicaciaas sublects An environmental-chamber study Am Rev a protective agent in ozone toxicity. Arch Environ Health Respir Dis 1 11 763-773, 1975 24•243-247, 1972 40 Ketcham, B, S Lassiter, E D Haak, Jr

, and J H Goldstein, B. D., and E M. McDonagh. Effect of ozone on Knelson Effects of ozone plus moderate exercise on cell membrane protein fluorescence. I. In vitro studies pulmonary function in healthy young men /n. utilizing the red cell membrane. Environ. Res.9.179-186, International Conference on Photochemical Oxidant
1975. Pollution and Its Control Proceedings Vol I B Griswold, S. M, L A Chambers, and H. L Motley Report Dimitriades, ed EPA-600/3-77-001 a, U.S. Environof a case of exposure to high ozone concentrationsfor two mental Protection Agency, Research Triangle Park, N.0

, hours. AMA Arch Ind Health 15 108-1 10, 1957. January 1977 pp 495-504 Hackney, J. D., W. S Linn, R D Buckley, E E Pedersen, 41 Ketcham, G, S Lassiter, E D Haak, Jr

, and J. H. S. K Karuza, D C Law, and D. A. Fischer. Experimental Knelson. Ozone exposure impairs pulmonary function in studies on human health effects of air pollutants. I. healthy young men Clin. Res. 25 37A, 1977

198Exposure System for Controlled Ozone Atmospheres. EPA-600/1-77-048, U.S Environmental Protection Agency, Research Triangle Park, N C, October 1977
59. Von Nieding, G., M. Wagner, H. Lollgen, and H. Krekeler Zur akuten Wi-kung von Ozon auf die Lungenfunktion des
menschen /n• Ozon und Begleitsubstanzen im photochemichen Smog. VDI Ber. (270)

- 123-129, 1977.
60. Young, W. A., D B Shaw, and D. V. Bates. Effect of low concentrations of ozone on pulmonaryfunction in man. J. Appl Physiol 19.765-768, 1964.
61. Young, W. A., D. B. Shaw, and D V. Bates. Pulmonary function tn welders exposed to ozone. Arch. Environ. Health 7 337-340, 1963 42 Kindya, R J, and P C Chan Effect of ozone on erythrocyte membrane adenos-ne triphosphatase Biochim. Biophys. Acta 429 608-615, 1976 43 Kleinfeld, M Acute pulmonary edema of chemical origin Arch Environ Health 10 942-946, 1965 44 Kleinfeld, M., C Giel, and I R. Tabershaw Health hazards associated with inert-gas-shielded metal arc welding AMA Arch Ind Health 15 27-31, 1957. 45 Knelson, J H, M L Peterson, G. M. Goldstein, D E. Gardner, and C G Hayes Health effects of oxidant exposures A research progress report /n Report on UCARB Conference "Technical Basesfor Control Strategies
of Photochemical Oxidant. Current Status and Priorities in Research " University of Caifornia, Statewide Air Pollution Research Center, Riverside, Calif., May 1976. pp 15-50 46 Linn, W S, R D Buckley, C. E. Spier, R. L. Blessey, M. P. Jones, D A Fischer, and J D Hackney. Health effects of ozone exposure in asthmatics Am Rev. Respir. Dis 117 835-843, 1978 47 McKenzie, W H, J. H Knelson, N. J. Rummo, and D. E. House Cytogenetic effects of inhaled ozone in man Mutat Res 48 95-102, 1977 48 Menzel, D B Toxicity of ozone, oxygen, and radiation. Annu Rev Pharmacol 10 379-394,1970 49 Menzel, D B, R. J Slaughter, A M Bryant, and H 0. Jauregui. Heinz bodies formed in erythrocytes by fatty
acid ozonides and ozone Arch. Environ Health 30 296- 301, 1975 50 Menzel, D B, R J Slaughter, A M Bryant, and H 0 Jauregui Prevention of ozonide-induced Heinz bodies in human erythrocytes by vitamin E Arch Environ Health 30 234-236, 1975 51 Merz, T, M A Bender, H D Kerr, and T J Kulle
Observations of aberrations in chromosomes of lymphocytes from human subjects exposed to ozone at a concentration of 0 5 ppm for 6 and 10 hr Mutat Res
31.299-302 1975 52 Mohler, J G, J P Butler, J D Hackney, C R Collier, D C Law, and W S Linn Redistribution of specific ventilation in humans exposed to ozone. A new nitrogen model Am Rev Respir. Dis 113.227, 1976 53 Raven, P B, B L Drinkwater, S M Horvath, R. 0 Ruhling, J A Gliner, J C Sutton, and N W Bolduan Age, smoking habits, heat stress, and their interactive effects with carbon monoxide and peroxyacetyl nitrate on man's aerobic power Int J Biometeorol 18 222-232,
1974 54 Raven, P B, B L Drinkwater, R 0 Ruhling, N W Bolduan, S Taguchi, J A Gliner, and S M Horvath Effect of carbon monoxide and peroxyacetyl nitrate on man's maximum aerobic capacity J Appl Physiol 36 288-293, 1974 55 Schonbein, C F On some secondary physiological effects produced by atmospheric electricity Med Chir Trans 34 205-220, 1851 56 Silverman, F, L J Folinsbee, J Barnard, and R JShephard Pulmonary function changes in ozoneinteraction of concentration and ventilation J Appl Physiol 41 859-864, 1976 57 Smith, L E Peroxyacetyl nitrate inhalation Cardiorespiratory effects Arch Environ Health 10 161- 164, 1965 58. Strong, A A, R Penley, and J H Knelson Human

199

# 10. EPIDEMIOLOGIC APPRAtSAL OF PHOTOCHEMICAL OXIDANTS

INTRODUCTION
A review is presented in this chapter of the evidence gathered to date in the epidemiologicstudies 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 towhich 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 airpollutants. 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 arecompared 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 ''' e During 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



### _ 10 0 -15 0 C 16 0 -20 0 C 21 0 -26 0 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 (70 1 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 Buechley 41 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/m 3 (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. ---1 0 1-4-- SEPT.► T-0 OCT. 0- 1 -0 NOV. —1 0 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
F

## z a 

# X 10

O 

### w 25 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 and3.06, 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 -11 0 +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.

Mills 36 correlated 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 36 observed 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 orabove (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 whenmaximum total oxidant exceeded 0.2 ppm averaged about 5 percent higher then when maximum total oxidant vvas below 0.2 ppm. Mills, 36 like 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 withineach 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 35 stated 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

' 8 

### Results 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

''' 8 

### and the Breslow and Goldsmith's report, 4 analyses 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

' e 

### donot 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 beconsiderably 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 thesame week and 2 weeks later were, respective

### ly, -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 RESPIRATORY a AND CARDIAC ° DEATHS DURING SMOG AND SMOG-FREE PERIODS OCCURRING IN LOS ANGELES COUNTY, AU G UST-NOVEMBER 1954 6

' 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, 59 air 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., 60 tength 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
Balchum 45 utilized a room with an air-conditioning system and a filter that could be used at thediscretion 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 inunfiltered 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/m 3 (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 report 45 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 positivethan 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 1177 0 434 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 2 837 9 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)

9 Significant 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 wasperformed 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
Peters 44 examined pulmonary function in shipyard workers (welders, pipecoverers, andpipefitters) 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 ofnitrogen 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 thanthat 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 personswith 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/m 3 (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 ofslmple rates. Temperature-fever adjusted headache rates increased slightly at daily maximumhourly 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 a PERCENTAGE 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

e All 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 foreach 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 Wehrle 64 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 asecond 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 apositive association between oxidant concentration and absence rates.

EFFECT OF PHOTOCHEMICAL OXIDANTS ON
SYMPTOM RATES IN JAPANESE ELEMENTARY SCHOOLCHILDREN

Shimizu 55 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 numbnessoftheextremities (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 of10.7 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 (54percent) _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 ofsymptom 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 withpairs 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 symptomquestionnaire (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 theeffects 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 subjectedto 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 Q

Q / 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 speedwith 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 workloads 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 decrementsin running time observed by Wayne in crosscountry runners might not have been seen, ormight 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 study 61
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'sdowntown 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 wereexcluded 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 Plus a 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

a Numbers 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 theWright 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 residedin 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 (94 1 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
88 1 F), the average humidity was 30.5 percent, the average suspended particulate concentration was 133.7 ug/m 3 , the average sulfate concentration was 3.7 Mg/m 3 , 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 V 25 ), 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 V 25 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) 24 e 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 6 8- 0 44) 12(0 74--0 46) 3(0 55-0 48) 4(-0 7 4 -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 V 5 0 

### 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 October1973. 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 V zs , 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 nothave 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 V 50 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 V 25 . 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 V 25 ). 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 Ury 61 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 permonth) 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
Gobran 46 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 study 46 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 study 46 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, 1954 46

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 4L a 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 dioxideconcentrations 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, 1954 46

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 47Hydrocarbons 039 0 17 ppm 140 53 Vlslblllty 017 1 2 mlles 13.3 56Partlculates 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 40FZ Z :) O > 30 

### H cc Q Q 

### F_

— 

### cc H cc op 20 

### ¢ cc w Q > Z_

w w 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 MEASUREMENTS 49

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 310 9 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 32 and 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



### w 10

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 tooxidant 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, whenbetween-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. study 54 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, 54 six 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. 54

of 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 60percent. 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 study 31 in which respiratory disease mortality rates in Los

TABLE 10-11. TOTAL LUNG CANCER MORTALITY IN AN AMERICAN LEGION STUDY POPULATION CALIFORNIA, 1958-62 5

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 rate a deaths Age-adjusted ° 959 n/a 1045 n/a 753 n/aAge- 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, 1958-62 5

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

a Age-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 insuch 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 andother institutions were not sampled. A questionnaire was administered by personal interview to one adult in each sample household. Afterweighting 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 therespondent'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, 1958-62 5

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

a Age- 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

a San 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/m 3 (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 A 2 /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 A 2 /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 2 alveolar plateau (AN2) Questionnaires were adm:nistered in April 1973, and pulmonary function tests wereperformed in August 1973 In one analysis, sexspecific intercity comparisons of pulmonary function test results were adjusted for age andheight. 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 (35percent 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 AN 2 in 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 (AN z ) 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 anassociation 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/m 3 (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 (0.144ppm) 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, andparticulates) 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 betweenareas, 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
stateGeneral 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 atotal 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 thephysicians 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 PhotochemicalOxidant 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
Tot al % 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/m 3 (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-termexposures 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. 65have 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 53 observed 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, 45 and Ury and Hexter 62 have 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, thesestudies 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 have observed

g 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 correlationsoccurring 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 36 may 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 Angelesarea. 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



### REFERENCES FOR CHAPTER 10

1 Bates, D V, and M Hazucha The short-term effects of 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 6 California State Department of Public Health Clean Air 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

250York 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 Knelson Respiratory symptoms spirometry, and oxidant chronic bronchitis and emphysema J Infect. Dis. 131 air pollution in nonsmoking adults Amer Rev Respir 731-742, 1975
Dis 105 251-261, 1972 29 Linn, W S, J D. Hackney, E E Pedersen, P Breisacher,
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
13 Fetner, R H Ozone-induced chromosome breakage in County of Los Angeles, Medical and Tuberculosis and
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

ozone exposure J Appl Physiol Respirat Environ photochemical smog Nihon Koshu Eisei Zasshi 22 421- 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 responses following ozone exposure J Appl. Physiol and mortality in two areas of Los Angeles County 38996-1001, 1975 Presented at the Joint Meeting of the American
16 Goldsmith, J R Personal communication to Delbert S Statistical Association and the Biometric Society(ENAR), 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 symptom reporting and photochemical oxidants Arch smogs Am J Med Sci 233379-386, 1957 Environ Health 28 255-260, 1974 37 Mizoguchi, I, K Makino, S Kudou, and R Mikami Onthe 19 Hausknecht, R Experiences of a respiratory disease Relationship of Subjective Symptoms to Photochemical panel selected from a representative sample of the adult Oxidant /n International Conference on Photochemical population Am Rev Respir Dis. 86 858-866, 1962 Oxidant Pollution and Its Control Proceedings Vol I B 20 Hausknecht, R, and L Breslow Air Pollution Effects Dimitriades, ed EPA-600/3-77-001a, U S Reported by California Residents from the California Environmental Protection Agency, Research Triangle Health Survey State of California, Department of Public Park, N C, January 1977 pp 477-494 Health, Berkeley, Calif

, 1960 38 Motley, H L, R H Smart, and C I Leftwich Effect of 21 Air Quality Bureau Health Hazards of Photochemical Aor polluted Los Angeles air (SMOG) on lung volume Pollution (The Results of a Survey of Health Hazards of ineasurements J Am Med Assoc 171 1469-1477, Photochemical Air Pollution in 1975) Environment 1959 Agency, Tokyo, Japan, March 1976 39 National Air Pollution Control Admin+stration Air Quality 22 Hechter, H H,andJ R Goldsmith Airpollutionanddaily Criteria for Photochemical Oxidants NAPCA Publication mortality Am J Med Sci 241 581 -588, 1961 No AP-63, U S Department of Health, Education, and 23 Herman, D R The Effect of Oxidant Air Pollution on Welfare, Public Health Service, Washington, D C, March Athletic Performance M S thesis, University of North 1970 Carolina, Chapel Hill, N C, 1972 40 National Air Pollution Control Administration Errata for 24 Kagawa, J, and T Toyama Photochemical air pollution Air Quality Criteria for Photochemical Oxidants NAPCA Its effects on respiratory function of elementary school Publication No AP-63, U S Department of Health, children Arch Environ Health 30 117-122, 1975 Education, and Welfare, Public Health Service, 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 Finkel and W C Duel, eds Publishing Sciences Group, Res 3 277-284, 1970 (1b) 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 effects on visual parameters .Aerosp Med 34 479-486, influenza Environ Res 4 129-140, 1971
1963 43 Personal communication from 0 J Balchum to R E
27 Lebowitz, M D, P Bendheim, G Cristea, D Markowitz, J Carroll 1967 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, pollution and weather on lung function in exercising M V Ranadive, and H P Pendergrass Pulmonary

25163 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 64 Wayne, W S., and P F Wehrle Oxidant air pollution and 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 economic status to total mortality and selected respiratory system mortality in men I Suspended 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 Arch Environ Health 16401-405, March 1968 function in shipyard welders An epidemiologic study
Arch Environ Health 26 28-31 1973 45 Remmers, J E, and O J Balchum Effects of Los Angeles 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, so BN), and peroxybenzoylnitrate (PBzN). The degree of phytotoxicity of these compounds increases with the increase in their molecular weight: PAN<PPN<P, so BN<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 Dean 65 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 Tingey 283 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 Jackson 306 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 Stark 43

and Mlller and Millecan 209 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

a Table 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/m 3

(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. Evans 87 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
Treshow 105 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/m 3

(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/m 3 (0.10 ppm) for 3 weeks. A decrease in both root and top growth occurred. Similar results 287 were noted with radish, except that growth was inhibited at 98 Ng/m 3 (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 anda 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 N GROWTH 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 W 3

"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.
Craker 49 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
flower 52 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/m 3 (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/m 3 (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 Neely 310 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/m 3 (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 COMMUNITY a

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)

261TABLE 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

262TABLE 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

a Modified 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/m 3 (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. FreyS 9 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/m 3 (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.' 45

Jacobson 745

used 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 4 T

7 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 theright 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 M E

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/m 3 (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. 145 These values are similar to those of Heck and Tingey 12 '' 21 for 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/m 3 (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 damage 67,164,18s,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 values e

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 11001 0 -0 of contuol Reference 217

° C is ozone concentration in ppm I is percent inlury T is time in hours, and A o
, A,, and A z 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 SI T IV E CO NDITIONS 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

269TABLE 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
Gableman 79 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. Taylor 267 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, 287 red maple 90 percent, 299 and soybean 60 to 80 percent. 286 In tobacco, maximum sensitivity occurs just after full leaf expansion. 116 Davis 55 a nd Davis and Wood 60 found that the age of Virginia pine needles influenced their response to a 4-hr exposure to ozone at 490 Ng/m 3 (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. 104 reported increased tolerance in petunia cultivars to ozone as they approached theflowering 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 20 Plants 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. 14 Plants 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. 258 reported 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. 73 found 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

' 73 

### This 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

' 19 

### and 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, 5 soybean, 75 BeI W3

tobacco

, 193 ' 257 

### Virginia pine, 55 ' 5s and white ash 309 were more sensitive if grown under warm
conditions. Pinto bean 73 was sensitive to ozone regardless of temperature. Macdowell 16 found that a low day or high night temperature increased the susceptibility of White Gold tobacco to ozone.
Juhren et a1. 149

used 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 1 to 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 55 and Davis and
Wood 59 found 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 ozoneconcentr•itions. They did not study growth or postexposure conditions. The studies of Dunning and
Heck 74 chowed 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 ' 213 A 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 '" 3

also 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. 259

associated 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 mlles 2 ). 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 W s 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 W 3 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 Turner 249 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 W s 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. Starkey 265

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 STRESS 217

---- --- --- --- -- — ------ 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

a Special 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/Ilte r
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 91 Most 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 W s tobacco to mixtures of sulfur dioxide (1310ug/m 3 or 0.50 ppm) and ozone (59 Ng/m 3 or 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., 202 working 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 1 e 

### 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/m 3 (0 1 ppm). And when the two gases were combined, Injury was noted at the end of 1.5 hr. Macdowall et a1. 19 defined 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 '' 292



### Symptoms 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 '' 95



### Grosso et a1., 97 and 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/m 3 (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 Colavit0 146 found that sulfur dioxide at 79 /jg/m 3 (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 INJURY 292

Response at concentration ratio, S_0 2/03, ppm a

_ 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 16 and Costonis. 46

When Dochinger et a1. 70 determined 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 140 tested 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. 70 and
Houston 140

found 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. Fujiwara 90 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 Middleton 314 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 mortality 43 (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 ). Weber 308 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 incombination 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
mixture a 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 cultivar s) 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. 124 found 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. 53 If 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 45 found that a 4-hr exposure of Funaria hygrometrica to ozone at 490 to 1960 Ng/m 3 (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 95 reported 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, 99 and treatment of
sewage. 154

'' 88



### The 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. 36 showed inactivation of several viruses and bacteria after ozone exposure, and a greater inactivation with simultaneous sonication.
Zobnina and Morkovina 315 related 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/m 3 (0.5 ppm), ozone inhibited surface growth of fungi on strawberry and peach. Ridley and Sims 251 extended the shelf-life of strawberry and peach by exposing them to ozone,
but stated no concentrations. Ozone at 1960 to 3720 ug/m 3

(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. 261 Watson 3 o 5 

### 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). 51 Ozone 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. 106 Single-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/m 3 (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 Jegier 61-64 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 Verkroost 3 o 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/m 3 (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/m 3 (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. 62 Spores 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 leafstipple 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 controlledenvironments 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, 14species 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/m 3 (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 factorsdescribe exposure dose. In determining the response of vegetation to oxidants, concentration ismore 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/m 3 (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 mlxturescan 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.



### REFERENCES FOR CHAPTER 11

1 Abeles, A L, and F B Abeles Biochemical pathway of stress-induced ethylene Plant Physiol 50 496-498,
1972 2 Adams, D F The effects of air pollution on plant life A review AMA Arch Ind Health 14 199-245, 1956 3. Adedipe, N. 0., R E Barrett, and D P Ormrod Phytotoxicity and growth responses of ornamental bedding plants to ozone and sulfur dioxide J Am Soc Hort Sci 97 341-345, 1972 4 Adedipe, N. 0., R. A. Fletcher, and D. P Ormrod. Ozone lesions in relation to senescence of attached and detached leaves of tobacco Atmos Environ 7 357-361,
1973. 5 Adedipe, N. 0, G. Hofstra, and D P Ormrod Effects of sulfur nutrition on phytotoxicity and growth responses of bean plants to ozone Can J Bot 50 1789-1793,
1972.
6. Adedipe, N. O., H. Khatamian, and D P Ormrod Stomatal regulation of ozone phytotoxicity in tomato Z Pflanzenphysiol 68 323-328, 1973

7. Adedipe, N 0., and D P Ormrod Ozone-inducedgrowth suppression in radish plants in relation to preand post-fumigation temperatures. Z Pflanzen Physiol 71 •281-287, 1974.
8. Atr Pollution Control Board. Technical and Administrative Report on Air Pollution Control in Los Angeles County, 1949-1950 County of Los Angeles, Air Pollution Control District, Los Angeles, Calif , 1950 9 Air Pollution Control Board Second Technical and Administrative Report on Air Pollution Control in Los Angeles County, 1950-1951 County of Los Angeles, Air Pollution Control District, Los Angeles, Calif , 1951 10 Applegate, H. G., and L C Durrant Synergistic action of ozone-sulfur dioxide on peanuts Environ Sci Technol 3 759-760, 1969
11 Benedict, H. M, C J. Miller, and R E Olson Economic Impact of Air Pollutants on Plants in the United States APTD-0953, U S. Environmental Protection Agency, Research Triangle Park, N C, November 1971 12 Bennett, J. P, H M Resh, and V C Runeckles Apparent stimulations of plant growth by air pollutants Can J Bot. 52 35-42, 1974 13 Berry, C R Age of pine seedlings with primary needles affects sensitivity to ozone and sulfur dioxide Phytopathology 64 207-209, 1974 14 Berry, C R. Relative sensitivity of red, jack, and white pine seedlings to ozone and sulfur dioxide Phytopathology 61 231-232, 1971 15. Berry, C R White pine emergence tipburn, a physiogenic disturbance U S For Serv Southeast For Exp. Stn. Stn Pap (130) 1-8, 1961 16 Berry, C. R, and H E Heggestad Air Pollution
Detectives /n Yearbook of Agriculture 1968 Science for Better Living U S Government Printing Office, Washington, D C, 1968 pp 142-146 17 Berry, C R, and L A. Ripperton. Ozone as possible cause of white pine emergence tipburn Phytopathology 53 552-557, 1963 18 Blum, U., and D T Tingey A study of the potential ways by which ozone could reduce root growth and nodulation of soybean Atmos Environ 11 737-739,
1977 19 Bobrov, R A. Cork formation in table beet leaves (Beta vulgaris) in response to smog /n Proceedings of the Third National Air Pollution Symposium National Air Pollution Symposium, Los Angeles, Calif , 1955 pp
199 -206 20 Bobrov, R. A The anatomical effects of air pollution on plants !n Proceedings of the Second National Air

284Pollution Symposium National Air Pollution Symposium, Los Angeles, Calif , 1952 pp 129-134 21 Bobrov, R. A The effect of smog on the anatomy of oats leaves. Phytopathology 42 558-563, 1952 22 Bobrov, R. A The leaf structure of Poa annua with observations of its smog sensitivity in Los Angeles County Am J. Bot 42.467-474, 1955 23 Botkin, D. B, W. H. Smith, R W. Carlson, andT L Smith Effects of ozone on white pine saplings Variation in inhibition and recovery of net photosynthesis. Environ Pollut 3.273-289, 1972. 24 Brandt,C S,andW W Heck Effects of air pollutants on vegetation /n Air Pollution Volume I. Air Pollution and Its Effects Second Edition. A C. Stern, ed Academic Press, Inc., New York, 1968 pp 401 -443. 25 Brasher, E P, D J. Fieldhouse, and M Sasser Ozone infury in potato variety trials Plant Dis. Rep 57 542- 544, 1973 26 Brennan, E., and P M. Halisky Response of turfgrass cultivars to ozone and sulfur dioxide in the atmosphere Phytopathology 60 1544-1546, 1970. 27 Brennan, E, and I A Leone Chrysanthemum response to sulfur dioxide and ozone Plant Dis. Rep 56 85-87,
1972 28 Brennan, E, and I A Leone. The response of English holly selections to ozone and sulfur dioxide. Holly Lett 37 6-7, 1970 29 Brennan, E, and I A Leone The response of plants to sulfur dioxide or ozone-polluted air supplied at varying flow rates Phytopathology 58 1 661-1 664, 1968 30 Brennan, E. G, I A. Leone, and R. H Daines Atmospheric aldehydes related to petunia leaf damage Science 143 818-820, 1964 31 Brennan, E, I A Leone, and R. H. Daines The importance of variety in ozone plant damage. Plant Dis. Rep 48 923-924, 1964 32 Brennan, E, I. A. Leone, and P M Halisky Response of forage legumes to ozone fumigations Phytopathology
59

- 1458-1459, 1969 33 Brewer, R. F, and G. Ferry Effects of air pollution on cotton in the San Joaquin Valley. Calif Agric. 28:6-7, 1974 34 Brewer, R. F., F. B. Guillemet, and R. K. Creveling. Influence of NPK fertilization on incidence and severity of oxidant injury to mangels and spinach. Soil Sci. 92 298-301, 1961 35 Bruton, V. C Environmental influences on the growth of Arabidopsis thaliana Ph D thesis, North Carolina State University, Raleigh, N C, 1974. 36 Burleson, G R, T M. Murray, and M. Pollard Inactivation of viruses and bacteria by ozone, with and without sonication. Appl. Microbiol. 29:340-344, 1975 37 Bystrom, B G, R B Glater, F. M Scott, and E S. C Bowler Leaf surface of Beta vu/garis-electron microscope study Bot. Gaz (Chicago) 129133-138,
1968 38 Cameron, J W, H Johnson, Jr, , O C Taylor, and H W Otto Differential susceptibility of sweet corn hybrids to field injury by air pollution Hort. Sci. 5•217-219, 1970. 39 Carney, A W, G R Stephenson, D. P. Ormrod, and G C Ashton Ozone-herbicide interactions in crop plants Weed Sci 21.508-511, 1973. 40 Cathey, H M, and H E. Heggestad. Reduction of ozone damage to Petunia hybrvda Vilm. by use of growthregulating chemicals and tolerant cultivars J Am Soc Hort Sci 97 695-700, 1972
41 Clayberg, C D Evaluation of tomato varieties for resistance to ozone Conn Agric Exp Stn New Haven Circ (246) 1-11, 1972 42 Clayberg, C D Screening tomatoes for ozone resistance Hort Sci 6 396-397, 1971 43 Cobb, F W, Jr , and R W Stark Decline and mortalityof smog-injured ponderosa pine J For 68147-149,
1970 44 Cole, G A Air pollution with relation to agronomic crops III Vegetation survey methods in air pollution studies Agron J 50 553-555, 1958 45 Comeau, G, and F LeBlanc Influence de I'ozone et de I'anhydride sulfureaux sur la regeneration des feuilles
de Funana hygrometrica HEDW Nat Can (Que 198 347-358, 1971 46 Costonis, A C Acute foliar injury of eastern white pine induced by sulfur dioxide and ozone. Phytopathology 60 994-999, 1970 47 Costonis, A. C Injury to eastern white pine by sulfur
dioxide and ozone alone and in mixture Eur J For Pathol 3 50-55, 1973 48 Costonis, A C, and W A Sinclair Relationships of atmospheric ozone to needle blight of eastern white pine Phytopathology 59 1 566-1 574, 1969 49 Craker, L E Decline and recovery of petunia flower development from ozone stress Hort Sci 7 484, 1972 50 Craker, L E Ethylene production from ozone-injured plants Environ Pollut 1 299-304, 1971. 51 Craker, L E Influence of ozone on RNA and protein
content of Lemna minor L Environ Pollut 3 319-323,
1972 52 Craker, L E, and W A Feder Development of the inflorescence in petunia, geranium, and poinsettia under ozone stress Hort. Sci 7.59-60, 1972 53 Czuba, M, and D P Ormrod Effects of cadmium and zinc on ozone-induced phytotoxicity in cress and lettuce Can J. Bot 52.645-649, 1974 54 Daines, R H, I A Leone, and E Brennan Air pollution as it affects agriculture in New Jersey N J Agric Exp Stn Bull (794) 1-14, 1960 55 Davis, D. D The Influence of Ozone on Conifers Ph D thesis, Pennsylvania State University, University Park, Pa., 1970 56 Davis, D D, and J B Coppolino. Relationship between age and ozone sensitivity of current needles of ponderosa pine Plant Dis. Rep 58 660-663, 1974 57 Davis, D D, and J B Coppolino Relative ozone susceptibility of selected woody ornamentals Hort Sci 9.537-539, 1974. 58 Davis, D D, and L Kress. The relative susceptibility of ten bean varieties to ozone Plant Dis Rep 58 14-16, 1974 59 Davis, D D, and F A Wood The influence of environmental factors on the sensitivity of Virginia pine to ozone Phytopathology 63 371-376, 1973 60 Davis, D D, and F A Wood The relative susceptibility of eighteen coniferous species to ozone Phytopathol3gy 62 14-19, 1972 61 de Koning, H W, and Z Jegier A study of the effects of ozone and sulfur dioxide on the photosynthesis and

285respiration of Euglena gracilis Atmos Environ 2 321- 326, 1968 62 de Koning, H W, and Z Jegier Effect of ozone on pyridine nucleotide reduction and phosphorylation of Euglena gracdis Arch Environ Health 18 913-916, 1969 63 de Koning, H W, and Z Jegier Effects of sulfur dioxide and ozone on Euglena gracilis Atmos Environ 4 357- 361, 1970 64 de Koning, H W, and Z Jegier Quantitative relation between ozone concentration and reduction of photosynthesis of Euglena gracihs Atmos Environ 2 615-616, 196865 Dean, C E Stomata density and size as related to ozoneinducedweatherfleckintobacco CropSci 12547-548,
1972
66 Dean, C E Weather fleck on Florida shadegrown tobacco. Tob Sci 7 41-45, 1963 67 Dean, C E, and D R Davis Ozone and soil moisture in relation to the occurrence of weather fleck on Florida cigar-wrapper tobacco in 1966 Plant Dis Rep 51 72- 75, 1967. 68 Dochinger, L S The impact of air pollution on eastern white pine The chlorotic dwarf disease J Air Pollut Control Assoc 18 814-816, 1968 69. Dochinger, L S, and C E Seliskar Air pollution and the chlorotic dwarf disease of eastern white•pine For Sci 16 46-55, 1970 70 Dochinger, L S, F W Bender, F L Fox, and W. W Heck Chlorotic dwarf of eastern white pine caused by an ozone and sulphur dioxide interaction. Nature (London) 225 476, 1970 71 Drummond, D B The effect of peroxyacetyl nitrate on petunia (Petunia hybrida Vilm I CAES Publication No 260-72, Center for Air Environment Studies, Pennsylvania State University, University Park, Pa ,
June 1972 72 Dugger, W M, Jr, , 0 C Taylor, W H Klein, and W Shropshire, Jr Action spectrum of peroxyacetyl nitrate damage to bean plants Nature (London) 198 75-76,
1963. 73 Dugger, W.M. Jr, , 0 C Taylor, C R Thompson, and E Cardiff The etfect of light on predisposing plants to ozone and PAN damage J Air Pollut Control Assoc 13 423-428, 1963 74 Dunning, J A, and W W Heck Response of pinto bean and tobacco to ozone as conditioned by light intensity and/or humidity Environ Sci Technol. 7 824-826,
1973 75. Dunning, J. A, W W Heck, and D T Tingey Foliar sensitivity of pinto bean and soybean to ozone as affected by temperature, potassium nutrition and ozone dose Water Air Soil Pollut 3 305-313, 1974 76 Elford, W. J..od J van den Ende An investigation of the merits of ozone as an aerial disinfectant J Hyg 42 240-265, 1942 77 Engle, R L Reaction of Onion, Allium cepa L, and Pinto Bean, Phaseolus vulgaris L, to Ozone. Ph D thesis, University of Wisconsin, Madison, Wis., 1966 78 Engle, R L, and W H Gabelman Inheritance and mechanism for resistance to ozone damage in onion, ANium cepa L. Proc Am Soc Hort Sci 89 423-430,
1966 79 Engle, R L, and W H Gabelman The effects of low

286 levels of ozone on pinto beans, Phaseolus vulgaris L Proc Am Soc Hort Sci 91 304-309, 1967 80 Engle, R L, W H Gabelman, and R R Romanowski, Jr Tipburn, an ozone incited response in onion, Allium cepa L Proc Am Soc Hort Sci 86 468-474, 1965 81 Evans, L S Bean leaf growth response to moderate ozone levels Environ Pollut 4 17-26, 1973 82 Evans, L S, and I P Ting Ozone sensitivity of leaves Relationship to leaf water content, gas transfer resistance, and anatomical characteristics Am. J Bot
61 592-597, 1974 83 Feder, W A Plant response to chronic exposure of low levels of oxidant-type air pollution Environ Pollut 1 73- 79, 1970 84 Feder, W A, and F J Campbell Influence of low levels of ozone on flowering of carnations Phytopathology 58 1038-1039, 1968. 85 Feder, W A, F L Fox, W W Heck, and F J Campbell Varietal responses of petunia to several air pollutants Plant Dis Rep 53.506-510, 1969 86 Feder, W A, and F Sullivan Ozone. Depression of frond multiplication and floral production in duckweed Science 165 1373-1374, 1969

87 Feliciano, A 1971 Survey and Assessment of AirPollution Damage to Vegetation in New Jersey EPAR5-72-010, U S Environmental Protection Agency, Research Triangle Park, N C, October 1972. 88 Ferry, B W., M S Baddeley, a nd D. L. Hawksworth, eds Air Pollution and Lichens Athlone Press, London, 1973. pp 39-88, 109-123. 89 Frey, J E The Effects of Ozone on the Synthesis and Storage of Nutrients in Soybean Seeds Ph D thesis, University of Northern Colorado, Greeley, Colo., 1972

90 Fujiwara, T Damage to plants caused by complex pollution of the atmosphere Shokubutsu Boeki 27.233- 236, 1973 91. Gardner, W S Ozone infury to tobacco plants in South Dakota Plant Dis Rep 57 106-110, 1973 92 Gentile, A G, W A Feder, R E. Young, and Z Santner Susceptibility of Lycopersicon spp to ozone intury J Am Soc Hort Sci 96 94-96, 1971. 93. Gibson, A H Limitation to dinitrogen fixation by legumes /n Nitrogen Fixation W. E Nexton and C J Nyman, eds Washington State Univ Press, Pullmab, Wash 1976 pp 400-428 94 Giese, A C, and E Christensen. Effects of ozone on organisms Physiol Zool.27•101-115, 1954 95 Glater,R A B Smog damage to ferns in the Los Angeles area Phytopathology 46.696-698, 1956 96 Glater, R B., R A Solberg, and F M Scott A developmental study of the leaves of Nicotiana glutinosa as related to their smog-sensitivity Am. J Bot 49 954-970, 1962 97 Grosso, J J, H A Menser, Jr , G. H Hodges, and H. H McKinney Effects of air pollutants on Nicotiana cultivars and species used for virus studies Phytopathology 61:945-950, 1971. 98. Guderian, R., H van Haut, and H. Stratmann Probleme der Erfassung und Beurteilung von Wirkungen gasformiger Luftverunreinigungen auf die Vegetation Z. Pflanzenkr Pflanzenpathol Pflanzenschutz 67.257- 264, 1960 99 Guinarch, P Three years of ozone sterilization of waterin Paris. /n Ozone Chemistry and Technology. Adv 119 Heck, W W., and J. A Dunning The effects of ozone on Chem. Ser. 21.416-429, 1957. tobacco and pinto bean as conditioned by several
100. Haagen-Smit, A J Chemistry and physiology of Los ecological factors. J. Air Pollut Control Assoc 17.112- Angeles smog. Ind Eng. Chem. 44 1342-1346, 1952 114, 1967
101. Haas, J. H Relation of crop maturity and physiology to 120. Heck, W W, F. L Fox, C S Brandt, and J A. Dunning air pollution incited bronzing of Phaseolus vulgaris Tobacco, A Sensitive Monitor for Photochemical Air Phytopathology 60:407-410, 1970. Pollution NAPCA Publication No AP-55, U S.
102 Haines, R. B. Effect of pure ozone on bacteria ln Report Department of Health, Education and Welfare, Public of the Food Investigation Board for the Year 1935 His Health Service, National Air Pollution Control Majesty's Stationery Office, London, 1936. pp. 30-31. Administration, Cincinnati, Ohio, June 1969
103 Hanson, G P. Relative air pollution sensitivity of some 121 Heck, W W., and D. T. Tingey Ozone TimeLos Angeles Arboretum plants Lasca Leaves22 86-89, concentration model to predict acute foliar infury /n.
1972 Proceedings of the Second International Clean Air
104 Hanson, G. P, L. Thorne, and D H Addis Ozone Congress H M Englur,d and W T Beery, eds sensitivity of Petunia hybrida Vilm. as related to Academic Press, Inc., N.Y., 1971 pp 249-255. physiological age J Am. Soc. Hort. Sci. 100 188-190, 122 Heggestad, H E. Photochemical air pollution injury to
1975 potatoes in the Atlantic coastal states Am Potato J
105. Harward, M, and M. Treshow Impact of ozone on the 50 315-328, 1973. growth and reproduction of understory plants in the 123. Heggestad, H E, F R Burleson, J T Middleton, and E aspen zone of western U.S A. Environ. Conserv. 2 17- F. Darley Leaf injury on tobacco varieties resulting from 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, plant parasites. Annu. Rev Phytopathol 11 365-388, 1964
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

ozone Environ Pollut 9.91-95, 1975. pollutant ozone Phytopathology 52.735, 1962.
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 field chamber to assess the impact of air pollution on concentrations as cause of tobacco leaf infury Science plants. J Environ. Qual 2 365-368, 1973 129 208-210, 1959.
109 Heagle,A S,D E Body,andG E Neely Injuryandyield 126 Hibben, C R Ozone toxic;ty to sugar maple. responses of soybean to chronic doses of ozone and Phytopathology 59.1423-1428, 1969 sulfur dioxide in the field Phytopathology 64 132-136, 127 Hibben, C R Sensitivity of fungal spores to sulphur
1974. dioxide and ozone. Phytopathology 56.880-881, 1966
110. Heagle, A. S., D. E. Body, and E. K Pounds. Effect of 128. Hill, A.C. A special purpose plant environmental ozone on yield of sweet corn Phytopathology 62 683- chamber for air pollution studies J Air Pollut Control 687, 1972 Assoc 17 743-748, 1967.

1 1 1 Heagle, A S, and W. W Heck. Predisposition of tobacco 129 Hill, A C, H. E. Heggestad, and S N Linzon. Ozone /n to oxidant air pollution injury by previous exposure to Recognition of Air Pollution Infury to Vegetation. A oxidants Environ Pollut 7 247-252, 1974 Pictorial Atlas J S Jacobson and A. C. Hill, eds

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 Pollution. J B Mudd and T T Kozlowski, eds Academic closure in plants Environ Sci Technol 3 52-56, 1969 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,
reaction products of propylene-nitrogen dioxide 1964
mixtures J Air Pollut Control Assoc. 14.255-261, 133. Hindawi, I J., J. A. Dunning, and C. S. Brandt.
1964. Morphological and microscopical changes in tobacco,
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 Native, crops, forests /n Air Pollution Volume II The Susceptibility of Wisconsin Havana tobacco cultivars to
Effects of Air Pollution Third edition A C Stern, ed air pollutants Agron J 63107-111, 1971 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 phytotoxic pollutants /n Recognition of Air Pollution Society of America, Montreal, Quebec, February 3, Injury to Vegetation A Pictorial Atlas J S Jacobson 1970
and A C Hill, eds Informative Report No. 1, Air 136 Hodgson, R H, K E Dusbabek,_and B L Hoffer. Pollution Control Association, Pittsburgh, Pa

, 1970 pp Diphenamid metabolism in tomato Time course of an
F1 -F24 ozone fumigation effect Weed Sci 22 205-210, 1974

287137 Hodgson, R H, D S Frear, H R Swanson, and L A Rhizoctonia solam. Ph.D thesis, North Carolina State Regan. Alteration of diphenamid metabolism in tomato University, Raleigh, N C., 1974. by ozone Weed Sci 21 542-549, 1973 157 Kohut, R J Response of Hybrid Poplar to Simultaneous 138 Hoffman, G J, E V Mass, and S L Rawlins Salinity- Exposure to Ozone and PAN CAES Publication No 288-

ozone interactive effects on alfalfa yield and water 72, Pennsylvania State University, Center for Air relations J Environ Qual 4 326-331, 1975 Environment Studies, University Park, Pa

, 1972. 139 Hoffman, G J, E V Mass, and S L Rawlins Salinity- 158 Kohut, R. J The Interaction of 03 and PAN on Hybrid ozone interactive effects on yield and water relations of Poplar and Pinto Bean CAES Publication No 428-76, pinto bean J Environ Qual 2 148-152, 1973 Pennsylvania State University, Center for 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 Can J For Res 4 65-68, 1974 chamber study to evaluate the effects of pollutants on
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 115, 1971 smog on plants I Initial growth and transpiration
142 Howell, R K, and D F Kremer Ozone injury,to soybean studies Plant Physiol 28 50-62, 1953 cotyledonary leaves J Environ Qual 1 94-97, 1972. 161 Kress, L W Response of Hybrid Poplar to Sequential
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 affected by air pollution /n Proceedings of the Second M S thesis, University of New Hampshire, Durham, National Air Pollution Symposium National Air N.H

, 1950 Pollution Symposium, Pasadena, Calif,

, 1952 pp 122- 163 Lacasse, N L Assessment of air pollution damage to
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 chronic ozone fumigation Plant Dis Rep 57 914-917, Englund and W T Beery, eds Academic Press, Inc

, 1973. N,Y„ 1971, pp, 132-136.
148 Jensen, K F, and L S Dochinger Responses of hybrid 165. Landau, E., and C S Brandt The use of surveys to poplar cuttings to chronic and acute levels of ozone estimate air pollution damage to agriculture Environ Environ Pollut 6 289-295, 1974 Res 3 54-61, 1970
149 Juhren, M, W Noble, and F W Went The 166 Larsen, R I, and W W Heck An air quality data
standardization of Poa annua as an indicator of smog analysis system for interrelating effects, standards, and
concentrations 1 Effects of temperature, photoperiod, needed source reductions Part 3 Vegetation injury J and light intensity during growth of test plants Plant Air Pollut Control Assoc 26 325-333, 1976 Physiol 32 576-586, 1957 167 Laurence, J. A, F A Wood, and S V Krupa Possible
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 on ozone injury Taiki Osen Kenkyu 7 19-26

, 1972 The histopathological effect of ozone on plant foliage
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 Populus tremufoides by sulfur dioxide and ozone Can 60 1 521-1 524, 1970
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 plant-water aspects of ozone phytoxicity in tomato the atmosphere J Air Pollut Control Assoc 16 191- plants Plant Soil 38 531-541, 1973 196, 1966
154 Kinman, R N Water and wastewater disinfection with 171 Linzon, S N Ozone damage and semimature-tissue
ozone. A critical review Crit Rev Environ Control needle blight of eastern white pine Can J Bot 5 141-152, 1975 45 2047-2060, 1967
155 Klingaman, G L, and C B Link Reduction in air 172 Linzon, S N Semimature-tissue Needle Blight of pollution inlury to foliage of Chrysanthemum Eastern White Pine and Local Weather Information

morifolium Ramata using tolerant cultivars and Report 0-X-1, Canada Department of Forestry, Ontario chemical protectants J Am Soc Hort Sci 100 173- Region, Sault Ste Marie, Ont

, Canada, August 1965 175, 1975 173 Linzon, S N, The development of foliar symptoms and
156 Kochhar, M Phytotoxic and Competitive Effects of Tall the possible cause and origin of white pine needle Fescue on Ladino Clover as Modified by Ozone and/or blight Can J Bot 38 1 53-1 61, 1960

288174 Linzon, S N, W W. Heck, anti F. D. H. Macdowall Effects of photochemical oxidants on vegetation. /n Photochemical Air Pollution Formation, Transport and Effects Environmental Secretariat Publication No. NRCC 14096, National Research Council of Canada, Associate Committee on Scientific Criteria for Environmental Quality, Ottawa, Canada, 1975 175 Maas, E. V., G J Hoffman, S. L Rawlins, and G Ogata Salinity-ozone interactions on pinto bean Integrated response to ozone concentration and duration J Environ Qual. 2.400-404, 1973. 176 Macdowall, F D H Predisposition of tobacco to ozone damage Can J. Plant Sci 45 1-12, 1965 177 Macdowall, F D H Stages of ozone damage to respiration of tobacco leaves Can J Bot 43:419-427,
1965 178 Macdowall, F D H, and A F W Cole Threshold and synergistic damage to tobacco by ozone and sulfur dioxide Atmos Environ 5 553-559, 1971 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 Utah, Salt Lake City, Utah, 1968
181 Magie, R 0 Controlling gladiolus botrytis bud rot with ozone gas Proc Fla State Hort Soc 73 373-375, 1960 182 Manning, W J, W A Feder, P M. Papia, and I Perkins Influence of foliar ozone injury on root development and root surface fungi of pinto bean plants Environ Pollut 1 305-312, 1971 183 Manning, W J, W A Feder,andl.Perkins Responseof poinsottia cult jars to several concentrations of ozone Plant Dis Rep 57.774-775, 1973 184 Manning, W J, W A Feder, and I Perkins Sensitivity of spinach.cul

, ivars to ozone Plant Dis Rep 56 832- 833, 1972 185 Mansfield, T/ The role of stomata in determining the responses of F lants to air pollutants Comment Plant Sci 2 1 1-20, i 973 186 Markowski, A and S Grzesiak Influence of sulphur dioxide and c, one on vegetation of bean and barley plants under .lifferent soil moisture conditions. Bull Acad Pol Sci Ser Sci Biol 22.875-887, 1975 187 Matsushima, J On composite harm to plants by sulfurous acid gas and oxidant Sangyo Kogai 7 218- 224, 1971 188 McCarthy, J J, and C H Smith. A review of ozone and its application to domestic wastewater treatment J Am Water Works Assoc 66 718-725, 1974 189 McCune, D C On the Establishment of Air Quality Criteria with Reference to the Effects of Atmospheric Fluorine on Vegetation Air Quality Monograph No 69- 3, American Petroleum Institute, N Y, 1969 190 Mcllvenn, W D, R A Spotts, and D D. Davis The influence of soil zinc on nodulation, mycorrhizae, and ozone-sensitivityofpintobean Phytopathology65645- 647, 1975 191 Menser, H A, and H E Heggestad Ozone and sulfur dioxide synergism In)ury to tobacco plants. Science
153 424-425, 1966 192 Menser, H A, H E Heggestad, and 0 E Street. Response of plants to air pollutants II Effects of ozone concentration and leaf maturity on in)ury to Nicotiana tabacum Phytopathology 53 1 304-1 308, 1963 193 Menser, H A, H E Heggestad, 0 E Street, and R N Jeffrey Response of plants to air pollutants I Effects of ozone on tobacco plants preconditioned by light and temperature Plant Physiol 38 605-609, 1963 194 Menser, H A, Jr , and G H Hodges Effects of air pollutants on burley tobacco cultivars Agron J 62265- 269, 1970 195 Menser, H A, Jr, , G H Hodges, and C G McKee Effects of air pollution on Maryland (Type 32)tobacco J Environ Qual 2.253-258, 1973
196 Menser, H A, Jr , and 0 E Street Effects of air pollution, nitrogen levels, supplemental irrigation, and plant spacing on weather fleck and leaf losses of Maryland tobacco Tobacco 155 1 92-1 96, 1962
197 Middleton, J T Photochemical air pollution damage

~ to leaves Annu Rev Plant Physiol 12 431-448, 1961 198 Middleton,J T Responseof plants to air pollution J Air Pollut Control Assoc 6 1-4, 1956 199 Middleton, J. T., A S Crafts, R F Brewer, and 0 C Taylor Plant damage byair pollution Calif Agric 10 9- 12, 1956 200 Middleton, J T, E F Darley, and R F Brewer Damage to vegetation from polluted atmospheres J Air Pollut Control Assoc 8 9-15, 1958
201 Middleton, J T., J B Kendrick, Jr , and E F Darley Air pollution injury to crops Calif Agric 7 11-12, 1953
202 Middleton, J T, J B Kendrick, Jr , and E F Darley Airborne oxidants as plant-damaging agents /n Proceedings of the Third National Air Pollution Symposium National Air Pollution Symposium, Los Angeles, Calif , 1955 pp 191-198 203 Middleton, J T, J B Kendrick, Jr., and H W Schwalm In)ury to herbaceous plants by smog or air pollution Plant Dis Rep 34 254-252, 1950 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,
June 1971 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 (Coleoptera Scolytidae) infestation of ponderosa pine III Effect of injury upon oleoresin composition, phloem carbohydrates, and phloem pH Hilgardia 39 135-140,
1968 208. MiIler, V L, R K Howell, and B E Caldwell Relative sensitivity of soybean genotypes to ozone and sulfur dioxide J Environ Qual 3 35-37, 1974 209 Miller, P R, and A A Millecan Extent of oxidant air pollution damage to some pines and other conifers in California Plant Dis Rep 55 555-559, 1971 210 Miller, P R, J R Parmeter, Jr , B H Flick and C W Martinez Ozone dosage response of ponderosa pine seedlings J Air Pollut Control Assoc 19 435-438,
1969
211 Miller,P R,andS Rich Ozone damage on apples Plant Dis Rep 52 730-731, 1968

289212 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 New England July 1971 - July 1972 Final Report EPA- Baldwin, and V Van Way Ozone dosage-crop loss R5-72-009, U S Environmental Protection Agency, function for alfalfa A standardized method for Research Triangle Park, N.C., August 1972 assessing crop losses from air pollutants J Air Pollut 215 Nakamura, H, and S Matsunaka Indicator plantsforair Control Assoc 26 861-865, 1976 pollutants (1 ) Susceptibility of morning glory to 231 Oshima, R J, 0 C Taylor, P K Braegelmann, and D W photochemical oxidants Varietal difference and effect Baldwin Effect of ozone on a commercial variety of of environmental factors Nippon SakumotsuGakkai Kiji tomato J Environ Qual 4 463-464, 1975 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

290dioxide 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

291280 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

292314 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 andanimals. 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 theecosystems 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 bioticresponses 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 

### INTOLERANCE ZONEOF ZONEOF 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 theecosystem 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 greaterdamage 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 58 and 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 amountof data that may be interpreted in an agroecosystem context because they were highlyoriented 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 thephotochemical 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, scaleinsects, 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. 5 The 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. 4 Only 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. 65 Berry 4 in 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. 49

in 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. Berry 3

reported 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. 22

In June 1976, oxidant levels exceeded 160 /ag/m 3

(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 thebasin 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 days 34 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.

~~ ,/7 •

- ~ .,POimtlale ~~^' ~—~'.~, \ .~S~J ~ ~ t. • 1, ~~• ~ .

(~ ~'

✓ •'--

~ .^ °aer

~ .'

~ - ✓ - ~ ' '

~ . -. ~ ~ ' ~ ~ Victorv,lleo x ~ •~•~

.

.. ... . ` ~ ..-_ Soled?E —
~ y ~ r 'W ~ • ,

f •• Pase

... . .. . . ~ . , ~^ ~ . ~ ..•

.

~ r: ,

~ >, `t

. l •.~~

`~.. ~ `,•

. ._. ~ 1. • . G ,

, ~ ,,.. ~ .rT . J,esper,a ° .I I / .. ; ; ' . . .•. ':.
~ A N 6

~ •,,,,G , .Ar

~ a R I E ir
~ '^' ,yb •. Y • • ,

. SanFernando („ y ~ ,o:x ^ /E t' M-0uNr4 \

~ IDeep ~/ ~ .~~ 'M • '. Pass` -, , •

~ •'t

~ / Y.3 ~! ~ N 5 T ' ~ Creek/ ..«./' . •v.~~ 4-1 FI ~ colon
~

• '~ ~, ~ ( j f 1-., '

~ c Pass 4 v i

. . _. ./ ( ✓ J - ~.~ ~ ~ ? 1 '+ ~S ~. ~ l ~ .S 4 ! '`

.. ~ ,., y

.

FemondoVolley

~ `

., . F

~ . .. - :'

~ _ -....: 1
- ~t~~•C o q .v N p f 7.l 

### ~ 1 ~ ?r ✓ J \ L~ >

Po o sodeno •../'... J

. . ~~1f~~~F~: M

~ 5 '

, . ~ • ~ . ~ Rwlto-Mlro -

. . L'

~ ..'

~ - M. San Gobriel Volley
~ cable ••••••••

~ '%i

~ ?o:

• ~ ~ - . . . . . . . . ~ . / j,
~ i \ 7

•• ~ 5r~

~ I Monte ' •

~ .,.. ... . - 1 ' 't o

~ • Redlands

~

Sanfa Monlca

~ o 9° Riverslde Beaumont o

~ B a r

. .

~ o
. . . corono oi

f

~

. , p

~ _'t

~~ • Feet above sea level

, ~ •~• ~ ~" N •: ABOVE9,000

• 9 y"

-- ~~ •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 oxidantpeak. 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 surveys 36,69 have confirmed oxidant injury to ponderosa pine and associated species at numerous locations in the Sierra Nevada foothillseast 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 a 0 '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



### 30124 =
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 ~ ~ • o a c 

## 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
F Q - 0.15 O H

0.10

0.05

0 95

90

U. ° 85 ui cc

~

~ Q 80 ¢
w a
W 75

70

65 + \ ` HIGHLAND 442 m

/ /

/ i i i /

~ /

~ T VPG

.- ~ i ~ / ~ /

.`

\ \

0 ` x `

\

~ \ `N G 

# z_

~

~. O 

### H U lu

>



### 0.2C

E
a 0.15 F z Q

~ 

### 0.10 

### X O

J



### ~ 0.05
O H

0 

### 15

12 cc= 

# y E g W

az ~ W 6 013

Q ~ 3 >a

0 0.35

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/m 3 (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/m 3 (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/m 3 (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/m 3 , or0.03 ppm). 23 The percentage of valid data re A covered, as well as the total possible hours for which data could beobtained 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 theSan 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

_ , ~~

M O V ING AVERAG 

### E `.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 •••O•

~ 

# ••Q•i

~ 

## \

~~ 

## 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

305Z 

### 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 bedemonstrated. 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
m Q y Z

~ 

# - _px

/ 

# w ~ W Q 

## a J 

# F- W Z W~ Z O 

# `

~ a Q W CC ~/ Q `\ ~~ uJ U. 

## i cc U 

## , o[ I W 

### J O
l 

### L 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 stability 8

' 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

Wert 65 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 studies 32,55,5s 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 2 0 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. 56 Types 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 3 times 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. 28 It 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 NUTRITIONTRANSPIRATION

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



### 311A. 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 MICROt ARTHROPODS

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

3131. 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/m 3 (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

315A. 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 specificcommunity 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

316CLIMATE 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

317Figure 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 16.5 b 1 2 0.0 1 2 Tunnel Two Rldge PP 122 195 16 7 b 00 14 1.4 Camp Angeles PP 112 25.6 16 8 b 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 5 b 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

a Number 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 PINES a AT BARTON FLATS INTHE SAN BERNARDINO NATIONAL FOREST 3 e

195 2 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 havebeen 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 anecosystem, 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 ofvertebrate 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 AFiEA e AFFECTED BY OXIDANT AIR POLLUTION 38

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

a Trees 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 thatprimary 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/m 3 , 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 theecosystems 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 environmentEcosystems 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 verticalventing 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/m 3 (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, andthe short-lived, higher-value vegetation constituting the agroecosystem of the Los Angeles coastal pla

in is subjected to injurious doses inintermittent, short-term fumigations. Each situtation has measurable economic and aestheticeffects, 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 forestecosystem—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.



### REFERENCES FOR CHAPTER 12

1 Aldaz, L Flux measurement of atmospheric ozone over land and water. /n Studies of Atmospheric Ozone Section III AFCRL-69-0138, U S Air Force, Cambridge Research Laboratories, Bedford, Mass , March 1969. 2. Auerbach, S. I, R. L. Burgess, andR V 0'NeiIl.The biome programss Evaluating an experiment Science 195 902- 904, 1977. 3 Berry, C. R Differences in concentrations of surface oxidant between valley and mountaintop conditions in the southern Appalachians J Air Pollut Control Assoc 14.•238-239, 19644 Berry, C R White pine emergence tipburn, a physiogenic disturbance U.S For Serv Southeast For Exp. Stn. Stn Pap (130).1-8, 1961 5 Berry, C. R, and L A Ripperton Ozone, a possible cause of white pine emergence tipburn Phytopathology 53.552-557, 1963 6. Blumenthal, D. L, W H White, R. L Peace, and T B Smith Determination of the Feasibility of the Long-range Transport of OzoneorOzone Precursors EPA-450/3-74- 061, U.S. Environmental Protection Agency, Research Triangle Park, N.C., November 1974. 7 Botkin, D B, and R. S. Miller Complex ecosystems. Models and predictions Am. Sci 62.448-453, 1974 8 Botkin, D B, and M J Sobel. The complexity of ecosystem stability /n. Ecosystem Analysis and Prediction. S. A. Levin, ed Society for Industrial and Applied Mathematics, Philadelphia, Pa , 1976 pp 144- 150 9. Boughey, A S Fundamental Ecology Intex Educational Publishers, Scranton, Pa., 1971 pp 1-50 10. Bryson, R. A, and W. M Wendland Climate effects of atmospheric pollution /n. Global Effects ofEnvironmental Pollution S F Singer, ed SpringerVerlag, N.Y , 1970 pp 130-138
11. California Air Resources Board. Air Quality in the Tahoe Basin, Summer 1973 State of California, Air Resources Board, Sacramento, Calif , March 1974.
12. Cobb, F W, Jr., and R W Stark. Decline and mortality of smog-injured ponderosa pine J For.68 147-149, 1970
13. Corn, M, R. W. Dunlap, L.A. Goldmuntz, and L. H. Rogers. Photochemical oxidants - Sources, sinks, and strategies. J. Air Pollut. Control Assoc. 25:16-18, 1975.
14. Costonis, A C The Relationships of Ozone, Lophoderrimium pinastri and Pullulana to Needle Blight of Eastern White Pine. Ph D. thesis, Cornell University, Ithaca, N.Y , 1968. 15 Davis, D. D, and F A. Wood The relative susceptibility of eighteen coniferous species to ozone Phytopathology 62:14-19, 1972 16 Dochinger, L S, F W Bender, F L Fox, and W W Heck Chlorotic dwarf of eastern white pine caused by an ozone and sulphur dioxide interaction. Nature (London) 225:476, 1970 17 Edinger, J G. Vertical distribution of photochemical smog in Los Angeles basin Environ Sci Technol 7.247-252, 1973 18 Edinger, J. G, M H McCutchan, P R Miller, B C Ryan, M J Schroeder, and J V. Behar Penetration and duration of oxidant air pollution in the south coast air basin of California J Air Pollut Control Assoc 22 882- 886, 1972 19 Ellertsen, B W, C J Powell, and C L Massey Reporton study of diseased white pine in Tennessee Mitt Forst Bundesversuchsanst. Wien 97 195-208, 1972 20 Estberg, G N, and B C Patton The relation between sensitivityand persistence under small perturbations /n. Ecosystem Analysis and Prediction S A Levin, ed Society for Industrial and Applied Mathematics, Philadelphia , Pa , 1976 pp 151-154
21 Fowells, H. A., and G H Schubert. Natural reproduction in certain cutover pine-fir stands of California J For 49 192-196, 1951 22 Garrett, A Compositional changes of ecosystem during chronic gamma irradiation /n Symposium on Radioecology CONF-670503, D J Nelson and F C Evans, eds U S Atomic Energy Commission, Oak Ridge, Tenn 1969 pp.99-109 23 Glona,H R.,G Bradburn,R F Reinisch,J.N Pitts,Jr,J. V Behar, and L Zafonte Airborne survey of major air basins in California J Air Pollut. Control Assoc 24 645- 652, 1974 24. Gosselink,J G,E P Odum,andR M PopeTheValueof the Tidal Marsh LSU-SG-74-03, Louisiana State University, Center for Wetland Resources, Baton Rouge, La , 1974 25. Hacskaylo, E The Torrey symposium on current aspects of fungal development IV Dependence of mycorrhizal fungi on hosts Bull Torrey Bot Club 100 217-223, 1973. 26 Horton, J S Vegetation types of the San Bernardino Mountains Forest Service Technical Paper No 44, U S Department of Agriculture, 1960 29 pp. 27. Innis, G Stability, sensitivity, resilience, persistence. What is of interest? /n• Ecosystem Analysis and Prediction. S A Levin, ed Society for Industrial and Applied Mathematics, Philadelphia, Pa , 1976. pp 131- 140. 28 Kickert, R. N, P R Miller, 0 C Taylor, J R. McBride, J. Barbieri, R Arkley, F Cobb, Jr , D Dahlsten, W. W Wilcox, J Wenz, J. R Parmeter, Jr, , R F. Luck, and M White. Photochemical Air Pollutant Effects on MixedConifer Forest Ecosystems A Progress Report. EPA600/3-77-058, U S. Environmental Protection Agency, Corvallis,Ore , May 1977 29. Levin, S. A., and R. T. Paine The role of disturbance in models of community structure /n.Ecosystem Analysis and Prediction. S A Levin, ed. Society for Industrial and Applied Mathematics, Philadephia, Pa., 1976 pp. 56-76 30 McCutchan, M. H, and M. J. Schroeder Classification of meteorological patterns in southern California by discriminant analysis J Appl Meteorol 12.571 -577,
1973 31 Mdlar, C. S Decomposition of coniferous leaf litter /n Biology of Plant Litter Decomposition Volume 1 C H Dickinson and G. J. F Pugh, eds. Academic Press, Inc., N.Y., 1974. pp 105-128 32. Miller, P L Oxidant-induced community change in a mixed conifer forest. Adv. Chem. Ser. (122) 101 -1 17,

3261973 50 Smith, R. L. Ecologyand Field Biology 2nd Ed Harperand
33 Miller, P R, and M J Elderman, eds Photochemical Row, N Y, 1974 pp 30-85, 170 Oxidant Air Pollutant Effects on a Mixed Conifer Forest 51 Smith, W H, Air pollution—effects on the structure and Ecosystem A Progress Report 1976 EPA-600/3-77- function of the temperate forest ecosystem Environ 104, U S Environmental Protection Agency, Corvallis, Pollut 6 1 1 1-129, 1974 Ore., September 1977 52 Stark, R W, and F W Cobb, Jr Smog injury, root
34 Miller, P R, M H McCutchan, and B C Ryan. Influence diseases, and bark beetle damage in ponderosa pine
of climate and topography on oxidant air pollution Calif Agric 23 13-15, 1969 concentrations that damage conifer forests in southern 53 Stark, R W, P R Miller, F W Cobb, Jr

, D L Wood, and California Mitt Forst Bundesversuchsanst Wien J R Parmeter, Jr Photochemical oxidant injury and bark 97 585-607, 1972 beetle (Coleoptera Scolytidae) infestation of ponderosa
35. Miller,P R,M H McCutchan, and H P Milligan Oxidant pine I Incidence of bark beetle infestation in injured air pollution in the central valley, Sierra Nevada foothills, trees Hilgardia 39 121 -1 26, 1968 and Mineral King Valley of California Atmos Environ. 54 Taylor, 0 C Oxidant Air Pollutant Effects on a Western 6 623-633, 1972. Coniferous Forest Ecosystem Task B Report Historical
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

32769 Williams, W T, M Brady, and S C Willison Air pollution damage to the forests of the Sierra Nevada Mountains of California. J Air Pollut Control Assoc 27 230-234,
1977 70 Woodwell, G M Effects of ionizing radiation on 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 report 28 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 prevalenceof 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 naturalrubber 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, halogenatedbutyl, 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 ofstrain. 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 Stickney 27 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/m 3 (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/m 3 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 temperat 

### ures ("c old" 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/m 3 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

a SBR 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/m 3 (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/m 3 (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/m 3 in 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 3 annual 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/m 3 to 50Ng/m 3

there 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/m 3

to 50 Ng/m 3

for 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 32

showed 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 orrelatively high levels of nitrogen oxides. At the lownitrogen-oxides sites, they found that fading for many of the fabrics equaled, and in some casesexceeded, 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.
Salvin 31 reported that the combination of ozone and high humidity causes pronounced fading of certain dyes on cotton and rayon fabrics.

334

### Beloin 3

' 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/m 3 (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 

### DE R , 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/m 3 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/m 3 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.

Morris 26 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 Morris 26 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/m 3 (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 (120 1 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 00043 a 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

a Coefficient 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 LosAngeles. For example, using the laboratoryobtained coefficients, ozone differences of 85 to 111 Mg/m 3 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.

338TA B LE 13- 7. PAINT ER OS 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/ft 2 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 andmarkups 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/m 3 , respectively), they should have no practical signlflcance at amblent
levels. Haynle and Upham 20 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 bydeveloping, 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.



### REFERENCES FOR CHAPTER 13

1 Bailey, P S The reactions of ozone with organic compounds Chem Rev 58 925-1010, 1958
2 Barrett, L. B. and T E Waddell Cost of Air Pollution Damage—A Status Report AP-85, U S Environmental Protection Agency, Research Triangle Park, 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



### 3404. Beloin, N J. A field study. Fading of dyed fabrics by air pollution Text Chem. Color. 4 77-82, 1972. 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 stretchedrubbervulcanizates I Therateofcutgrowth.11. Conditions for cut growth. J Appl Polym Sci 3 90-93, 100-106, 1960 7 Bradley, C. E., and A J. Haagen-Smit The application of rubber in the quantitative determination of ozone Rubber Chem Technol 24 750-755, 1951. 8. Campbell, G G, G G Schurr, D. E Slawikowski, and J W Spence Assessing air pollution damage to coatings. J. Paint Technol 46 59-71, 1974 9 Cloyd, D R, and W. J Murphy. Technology Survey Handling Hazardous Materials NASA SP-5032, National Aeronaut cs and Space Administration, Washington, 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 weathering test for rubber Ind Eng. Chem Anal Ed.
18 769-774, 1946 12 Crabtree, J, and F S Malm Deterioration of rubberfrom use and with age /n Engineering Uses of Rubber. A T McPherson and A. Klemin, eds Reinhold Publishing Corp , N Y, 1956. pp 140-170 13 Devries, K L., and E R Simonson Section 2 Ozone and elastomers /n Ozone Chemistry Technology. A Review of the Literature. 1961-1974. J. S. Murphy and J. R Orr, eds. Franklin Institute Press, Philadelphia, Pa , 1975 pp 257-294 14 Dillon, C P The economic advantage of deferred topcoat zinc-base painting systems. (,Vlater. Perform. 1329-31, 1975 15 Dorset,B C M Pollution and fading fabrics. Text Manuf 99 27-29, 31, 1972. 16 Edwards, D C., and E B Storey. A quantitative ozone test for small specimens Chem. Can. 11:34-38, 1959. 17. Fisher, H L Antioxidation and antiozonation. /n• Chemistry of Natural and Synthetic Rubbers. Reinhold Publishing Corp , N Y, 1957 pp 49-55. 18 Haylock, J.0 , and J.L Rush Studies on the ozone fading of anthraquinone dyes on nylon fibers Tex Res J 46 1- 8, 1976 19 Haynie, F H, J W. Spence, and J. B Upham. Effects of Gaseous Pollutants on Materials—A Chamber Study EPA-600/3-76-015, U.S. Environmental Protection Agency, Research Triangle Park, N C., February 1976. 20. Haynie, F. H., and J. B. Upham. Effects of atmospheric pollutants on corrosion behavior of steels Mater Prot Perform. 10 18-21, 1971 21 Hofmann, C M, and R L Miller. Resistanceof passenger tires to atmospheric exposure J. Mater. 4•31-43, 1969 22 Jellinek, H. H. G. Fundamental degradation processes relevant to outdoor exposure of polymers /n Weatherability of Plastic Materials. Appl Polym Symp (4) 41-59, 1967 23 Kerr, N, M A Morris, and S H. Zeronian The effect of ozone and laundering on a vat-dyed cotton fabric Am. Dyest. Rep. 58.34-36, 1969. 24 The Kline Guide to the Paint Industry 1975. Charles H. Kline and Co , Inc., Fairfield, N J., 1975. 25. Meyer, D A, and J G Sommer The Development of Weather and Aging Resistant Pneumatic Tires and Mechanical Rubber Goods Final Technical Report Dayton Rubber Co, Dayton, Ohio, June 1957 26 Morris,M.A Effect of weathering on cotton fabrics Calif Agric Exp Stn Bull (823).1-29, 1966 27 Mueller,W.J.,andP.B Stickney ASurveyandEconomic Assessment of the Effects of Air Pollution on Elastomers NAPCA Contract No CPA-22-69-146, Battelle Memorial Inslitute, Columbus, Ohio, June 1970 28 National Research Council Ozone and Other Photochemical Oxidants National Academy of Sciences, Washington, D C., 1977 29 Newton, R G Mechanism of exposure-cracking of rubber (With a review of the influence of ozone ) J. Rubber Res 14 27-62, 1945 30 Norton, F J Action of ozone on rubbt, RubberAge(N Y) 47 87-90, 1940 31 Salvin, V S. Ozone fading of dyes Text Chem Color 1.245-251 , 1969 32 Salvin, V. S, and R A Walker Service fading of disperse dyestuffs by chemical agents other than the oxides of nitrogen Text Res J. 24 571-585, 1955 33. Sanderson, H P The effect of photochemical smog on materials /n Photochemical Air Pollution Formation, Transport and Effects Environmental Secretariat Publication No. NRCC 14096, National Research Council of Canada, Associate Committee on Scientific Criteria for Environmental Quality, Ottawa, Canada, 1975 pp 71- 87. 34 Schmitt,C H. A. Daylight fastness testing by the Langley System. Ani Dyest Rep 51:664-675, 1962 35 Schmitt, C H. A. Lightfastness of dyestuffs on textiles Am Dyest Rep 49 974-980, 1960 36 Spence, J W., F. H Haynie and J B Upham Effects of gaseous pollutants on paints A chamber study. J Paint Technol 47 57-63, 1975 37. Upham, J B, F H. Haynie, and J. W Spence. Fading of selected drapery fabrics by air pollutants J. Air Pollut Control Assoc 26 790-792, 1976. 38. Van Rossem, A, and H W Talem The appearance of atmospheric cracks in stretched rubber Kautschuk 7 79- 86, 115-117, 1931. 39. Williams,l Oxidation of rubber exposed to light Ind Eng Chem 18 367-369, 1926 40 Zeronian, S. H, K W Alger, and S. T Omaye Reaction of fabrics made from synthetic fibers to air contaminated with nitrogen dioxide, ozone, or sulfur dioxide /n• Proceedings of the Second International Clean Air Congress H M Englund and W T Berry, eds Academic Press, I nc , N Y, 1971 pp 468-476

341

o U S GOVERNMENT PRINTING OFFICE:1979 659-545