United States Environmental Criteria and 

Environmental Protection Assessment Office 

Agency Research Triangle Park, NC 27711 

EPA-600/8-84-020aF 

August1986 

• • 

EPA-600/8-84-020aF 

August 1986 

Air Quality Criteria 

for Ozone and Other 

Ph®tochemical Oxidants 

Volume I of V 

Environmental Criteria and Assessment Office 

Office of Nealth and Environmental Assessment 

Office of Research and Development 

U.S. Environmental Protection Agency 

Research Triangie Park, N.C. 27711 
DISCLAIMER 

This document has been reviewed in accordance with U.S. Environmental 

Protection Agency policy and approved for publication. Mention of trade names 

or commerical products does not constitute endorsement or recommendation for 

use. 

ii 
ABSTRACT 

Scientific information is presented and evaluated relative to the health 

and welfare effects associated wi'th exposure to ozone and other photochemical 

oxidants. Although it is not intended as a complete and detailed literature 

review, the document covers pertinent literature through early 1986. 

Data on heaith and welfare effects are emphasized, but additional information is provided for understanding the nature of the oxidant pollution problem and for evaluating the reliability of effects data as well as their 

relevance to potentiai exposures to ozone and other oxidants at concentrations 

occurring in ambient air. Information is presented on the following exposurerelated topics: nature, source, measurement, and concentrations of precursors 

to ozone and other photochemical oxidants; the formation of ozone and other 

photochemical oxidants and their transport once formed; the properties, chemistry, and measurement of ozone and other photochemical oxidants; and the 

concentrations of ozone and other photochemical oxidants that are typically 

found in ambient air. 

The specific areas addressed by chapters on health and welfare effects 

are the toxicological appraisal of effects of ozone and other oxidants; effects 

observed in controlled human exposures; effects observed in field and epidemiological studies; effects on vegetation seen in field and controlled exposures; 

effects on natural and agroecosystems; and effects on nonbiological materials 

observed in field and chamber studies. 

iii 
AIR QUALITY CRITERIA FOR OZONE 

AND OTHER PHOTOCHEMICAL OXIDANTS 

Page 

VOLUME I 

Chapter 1. Summary and Conclusions ............................... 1-1 

VOLUME II 

Chapter 2. Introduction .......................................... 2-1 

Chapter 3. Properties, Chemistry, and Transport of Ozone and 

Other Photochemical Oxidants and Their Precursors ..... 3-1 

Chapter 4. Sampling and Measurement of Ozone and Other 

Photochemical Oxidants and Their Precursors ........... 4-1 

Chapter 5. Concentrations of Ozone and Other Photochemical 

Oxidants in Ambient Air ............................... 5-1 

VOLUME III 

Chapter 6. Effects of Ozone and Other Photochemical Oxidants 

on Vegetation ......................................... 6-1 

Chapter 7. Effects of Ozone on Natural.Ecosystems and Their 

Components .............................. .. .......... 7-1 

Chapter 8. Effects of Ozone and Other Photochemical Oxidants 

on Nonbiological Materials ............................ 8-1 

VOLUME IV 

Chapter 9. Toxicological Effects of Ozone and Other 

Photochemical Oxidants ................................ 9-1 

VOLUME V 

Chapter 10. Controlled Human Studies of the Effects of Ozone 

and Other Photochemical Oxidants ...................... 10-1 

Chapter 11. Field and Epidemiological Studies of the Effects 

of Ozone and Other Photochemical Oxidants ............. 11-1 

Chapter 12. Evaluation of Health Effects Data for Ozone and 

Other Photochemical Oxidants .......................... 12-1 

iv 
TABLE OF CONTENTS 

Pa e 

LIST OF TABLES ...................................................... ix 

LIST OF FIGURES ..................................................... x 

LIST OF ABBREVIATIONS ....................................... ..... xi 

AUTHORS, CONTRIBUTORS, AND REVIEWERS ................................ xv 

1. SUMMARY AND CONCLUSIONS ............................ .... ...... 171 

1.1 INTRODUCTION ...................................... l-1 

1.2 PROPERTIES, CHEMISTRY, AND TRANSPORT OF OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS AND THEIR PftECURSORS .............. 1-3 

1.2.1 Descriptions and Properties of Ozone and Other 

Photochemical Oxidants ........................... 1-3 

1.2.2 Nature of Precursors to Ozone and Other 

Photochemical Oxidants ........................... 1-4 

1.2.3 Atmospheric Reactions of Ozone and Other Oxidants 

Inciuding Their Role in Aerosol Formation ........ 1-5 

1.2.3.1 Formation and Transformation of Ozone 

and Other Photochemical Oxidants ....... 1-6 

1.2..3.2 Atmospheric Chemical Processes 

Involving Ozone ....... .. .. ..... 1-7 

1.2:3.3 Atmospheric Reactions of PAN, ~ H2O2 ; 

and HCOOH ............. ............... 1-8 

1.2.4 Meteorological and Climatological Processes ...... 17,9 

1.2.4.1 Atmospheric Mixing ...................... 1-9 

1.2.4.2 Wind Speed and Direction .. .. ...... .. i-11 

1.2.4.3 Effects of Sunlight and Temperature .... 1-11 

1.2.4.4 Transport of Ozone and Other Oxidants 

and Their Precursors .................. 1-12 

14.4.5 Stratospheri.c-Trbpospheric Ozone 

Exchange ....... ......:..... ... ... 1-13 

1.2.4.6 Stratospheric Ozone at Ground Level ~ .... ~ 1-14 

1.2.4:7 . Background Ozone from Photochemical 

Reactions .................. .......... 1-15 

1.2.5 Sources, Emissions, and Concentrations of 

Precursors to Ozone and Other Photochemical 

Oxidants ......................................... 1-16 

1.2.5.1 Sources and Emissions of Precursors .... 1-16 

1.2.5.2 Representative Concentrations in 

Ambient Air ............................ 1-17 

1.2.6 Source-Receptor (Oxidant-Precursor) Models ....... 1-19 

1.2.6.1 Trajectory Models ...................... 1-19 

1.2.6.2 Fixed-Grid Mode7s ...................... 1-20 

1.2.6.3 Box Models ............................. 1-20 

1.2.6.4 Validation and Sensitivity Analyses 

for Dynamic Models ..................... 1-20 

1.3 SAMPLING AND MEASUREMENT OF OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS AND THEIR PRECURSORS .............. 1-21 

1.3.1 Sampling and Measurement of Ozone and Other 

Photochemical Oxidants ........................... 1-21 

m 
1.4 

1.5 

TABLE OF CONTENTS 

(continued) 

Page 

1.3.1.1 Quality Assurance and Sampling ......... 1-21 

1.3.1.2 Measurement Methods for Total Oxidants 

and Ozone .............................. 1-22 

1.3.1.3 Calibration Methods .................... 1-24 

1.3.1.4 Relationships of Total Oxidants and 

Ozone Measurements ..................... 1-26 

1.3.1.5 Methods for Sampling and Analysis of 

Peroxyacetyl Nitrate and Its 

Homologues ............................. 1-27 

1.3.1.6 Methods for Sampling and Analysis of 

Hydrogen Peroxide ...................... 1-30 

1.3.2 Measurement of Precursors to Ozone and Other 

Photochemical Oxidants ........................... 1-32 

1.3.2.1 Nonmethane Organic Compounds ........... 1-32 

1.3.2.2 Nitrogen Oxides .. ...... .......... 1-34 

CONCENTRATIONS OF OZONE AND OTHER PHOTOCHEMICAL 

OXIDANTS IN AMBIENT AIR .................................. 1-36 

1.4.1 Ozone Concentrations in Urban Areas .............. 1-36 

1.4.2 Trends in Nationwide Ozone Concentrations ........ 1-39 

1.4.3 Ozone Concentration•s in Nonurban Areas ........... 1-41 

1.4.4 Diurnal and Seasonal Patterns in Ozone 

Concentrations ..................... ............. 1-44 

1.4.5 Spatial Patterns in Ozone Concentrations ......... 1-46 

1.4.5.1 Urban-Nonurban Differences in Ozone 

Concentrations ......................... 1-46 

1.4.5.2 Geographic, Vertical, and Altitudinal 

Variations in Ozone Concentrations ..... 1-47 

1.4.5.3 Other Spatial Variations in Ozone 

Concentrations ......................... 1-50 

1.4.6 Concentrations and Patterns of Other 

Photochemical Oxidants ........................... 1-51 

1.4.6.1 Concentrations ......................... 1-51 

1.4.6.2 Patterns ............................... 1-52 

1.4.7 Relationship Between Ozone and Other 

Photochemical Oxidants .............:............. 1-53 

EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS 

ON VEGETATION ....................... 1-55 

1.5.1 Limiting Values of Plant Response to Ozone ....... 1-56 

1.5.2 Methods for Determining Ozone Yield Losses ....... 1-58 

1.5.3 Estimates of Ozone-Induced Yield Loss ............ 1-60 

1.5.3.1 Yield Loss: Determination by 

Regression Fnalysis .................... 1-61 

1.5.3.2 Yield Loss: Determination from 

Discrete Treatment ..................... 1-67 

1.5.3.3 Yield Loss: Determination with 

Chemical Protectants ....... .......... 1-67 

1.5.3.4 Yield Loss: Determination from 

Ambient Exposures ...................... 1-69 

1.5.3.5 Yield Loss Summary ..................... 1-69 

vi 
TABLE OF CONTENTS 

(continued) 

Page 

1.5.4 Effects on Crop Quality .......................... 1-72 

1.5.5 Statistics Used to Characterize Ozone Exposures .. 1-72 

1.5.6 Relationship Between Yield Loss and Foliar 

.Injury ........................................... 1-75 

1.5.7 Physiological Basis of Yield Reductions .......... 1-75 

1.5.8 Factors Affecting Plant Response to Ozone ........ 1-76 

1.5.8.1 Environmental Conditions ............... 1-77 

1.5.8.2 Interaction with Plant Diseases ........ 1-78 

1.5.8.3 Interaction of Ozone with Other 

Air Pollutants ......................... 1-78 

1.5.9 Economic Assessment of Effects of Ozone on 

Agriculture ...................... .. .............. 1-79 

1.5.10 Effects of Peroxyacetyl Nitrate on ~ Vegetation .... 1-90 

1.5.10.1 Factors Affecting Plant Response to 

PAN..................................... 1-90 

1.5.10.2 Limiting Values of Plant Response .. .. 1-90 

1.5.10.3 Effects of PAN on Piant Yield .......... 1-91 

1.6 EFFECTS OF OZONE ON NATURAL ECOSYSTEMS AND THEIR 

COMPONENTS .............................................. 1-91 

1.6.1 Responses of Ecosystems to Ozone Stress .......... 1-91 

1.6.2 Effects of Ozone on Producers .................... 1-92 

1.6.3 Effects of Ozone on Other Ecosystem Components 

and on Ecosystem Interactions ..... . ............... 1-94 

1.6.4 Effects of Ozone on Specific Ecosystems .......... 1-95 

1.6.5 Economic Valuation of Ecosystems ................. 1-97 

1.7 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON 

NONBIOLOGICAL MATERIALS .................................. 1-98 

1.8 TOXICOLOGICAL EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL 

OXIDANTS ................................................. 1-103 

1.8.1 Introduction ..................................... 1-103 

1.8.2 Regional Ddsimetry in the Respiratory Tract ...... 1-104 

1.8.3 Effects of Ozone on the Respiratory Tract ........ 1-107 

1.8.3.1 Morphological Effects ................ 1-107 

1.8.3.2 Pulmonary Function ..................... 1-110 

1.8.3.3 Biochemical Effects .................... 1-116 

1.8.3.4 Host Defense Mechanisms ................ 1-122 

1.8.3.5 Tolerance .............................. 1-127 

1.8.4 Extrapulmonary Effects of Ozone .................. 1-131 

1.8.4.1 Centrai Nervous System and Behavioral 

Effects ................................ 1-131 

1.8.4.2 Cardiovascular Effects ................. 1-132 

1.8.4.3 Hematological and Serum Chemistry 

Effects ................................ 1-132 

1.8.4.4 Cytogenetic and Teratogenic Effects .... 1-134 

1.8.4.5 Other Extrapulmonary Effects ........... 1-135 

1.8.5 Interaction of Ozone with Other Pollutants ....... 1-136 

1.8.6 Effects of Other Photochemical Oxidants .......... 1-136 

1.9 CONTROLLED HUMAN STUDIES OF THE EFFECTS OF OZONE AND 

OTHER PHOTOCHEMICAL OXIDANTS ............................. 1-142 

vii 
TABLE OF CONTENTS 

(continued) 

Page 

1.10 FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF 

OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ................... 1-151 

1.11 EVALUATION OF HEALTH EFFECTS DATA FOR OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS ........................... ..... 1-156 

1.11.1 Health Effects in the General Human Population ... 1-156 

1.11.2 Health Effects in Individuals with 

Preexisting Disease .............................. 1-162 

1.11.3 Extrapolation of Effects Observed in Animals 

to Human Populations ............................. 1-163 

1.11.4 Health Effects of Other Photochemical Oxidants 

and Pollutant Mixtures ........................... 1-164 

1.11.5 Identification of Potentially At-Risk 

Groups........................................... 1-164 

1.12 REFERENCES ............................................... 1-166 

viii 
LIST OF TABLES 

Table page 

1-1 Summary of ozone monitoring techniques ......................... 1-23 

1-2 Ozone calibration techniques ................................... 1-25 

1-3 Second-highest ozone concentrations among daily maximum 1-hr 

values in 1983 in Standard Metropolitan Statistical Areas 

with populations >1 million, given by census divisions and 

regions........................................................ 1-37 

1-4 Ozone concentrations for short-term exposures that 

produce 5 or 20 percent injury to vegetation grown under 

sensitive conditions ........................................... 1-57 

1-5 Summary of ozone concentrations predicted to cause 10 percent 

and 30 percent yield losses and summary of yield losses 

predicted to occur at 7-hr seasonal mean ozone concentrations 

of 0.04 and 0.06 ppm ........................................... 1-64 

1-6 Ozone concentrations at which significant yield losses have 

been noted for a variety of plant species exposed under 

various experimental conditions ................................ 1-68 

1-7 Effects of ozone on crop yield as determined by the use 

of chemical protectants ........................................ 1-70 

1-8 Effects of ambient oxidants on yield of selected crops ......... 1-71 

1-9 Summary of estimates of regional economic consequences of 

ozone pollution ................................................ 1-81 

1-10 Summary of estimates of national economic consequences of 

ozone pollution ................................................ 1-73 

1-11 Summary table: Morphological effects of ozone in 

experimental animals ........................................... 1-112 

1-12 Summary table: Effects on pulmonary function of short-term 

exposures to ozone in experimental animals ..................... 1-116 

1-13 Summary table: Effects on pulmonary function of long-term 

exposures to ozone in experimental animals ..................... 1-118 

1-14 Summary table: Biochemical changes in experimental animals 

exposed to ozone ............................................... 1-124 

1-15 Summary table: Effects of ozone on host defense mechanisms 

in experimental animals ........................................ 1-129 

1-16 Summary table: Extrapulmonary effects of ozone in 

experimental animals ........................................... 1-138 

1-17 Summary table: Interaction of ozone with other pollutants 

in experimental animals ........................................ 1-140 

1-18 Summary table: Controlled human exposure to ozone ............. 1-143 

1-19 Summary table: Acute effects of ozone and other photochemical 

oxidants in field studies with a mobiie laboratory ............. 1-152 

ix 
LIST OF FIGURES 

Figure Page 

1-1 National trend in composite average of the second highest 

value among daily maximum 1-hour ozone concentrations at 

selected groups of sites, 1975 through 1983 ..................... 1-40 

1-2 Distributions of the three highest 1-hour ozone concentrations 

at valid sites (906 station-years) aggregated for 3 years 

(1979, 1980, and 1981) and the highest ozone concentrations 

at NAPBN sites aggregated for those years (24 station-years) .... 1-42 

1-3 Relationship between ozone concentration, exposure duration, 

and a reduction in plant growth or yield ....................... 1-59 

1-4 Examples of the effects of ozone on the yield of soybean 

and wheat cultivars ............................................. 1-62 

1-5 Examples of the effects of ozone on the yield of cotton, 

tomato, and turnip ............. ... .......................... 1-63 

1-6 Number and percentage of 37 crop species or cultivars 

predicted to show a 10 percent yield loss at various ranges 

of 7-hr seasonal mean ozone concentrations ...................... 1-66 

1-7 Summary of morphological effects in experimental animals 

exposed to ozone ................................................ 1-111 

1-8 Summary of effects of short-term ozone exposures on pulmonary 

function in experimental animals ................................ 1-115 

1-9 Summary of effects of long-term ozone exposures on pulmonary 

function in experimental animals ................................ 1-117 

1-10 Summary of biochemical changes in experimental animals 

exposed to ozone ................................................ 1-123 

1-11 Summary of effects of ozone.on host defense mechanisms in 

experimental animals ............................................ 1-128 

1-12 Summary of extrapulmonary effects of ozone in experimental 

animals......................................................... 1-137 

1-13 Summary of effects in experimental animals exposed to 

ozone combined with other pollutants ............................ 1-139 

1-14 Group mean decrements in 1-sec forced expiratory volume 

during 2-hr ozone exposures with different levels of 

intermittent exercise ........................................... 1-158 

x 
LIST OF ABBREVIATIONS 

AChE acetylcholinesterase 

avg average 

BAKI boric acid buf.fered potassium iodide 

Be ( 7Be) beryllium (radioactive isotope of beryllium) 

C carbon, concentration 

°C degrees Celsius 

CA chromotropic acid 

CC closing capacity 

CH3 C(0)O 2 acetylperoxy radical 

cm centimeter 

CNS central nervous system 

CO carbon monoxide 

CO2 carbon dioxide 

COLD chronic obstructive lung disease 

conc., concn. concentration 

CV closing volume 

dba diameter at breast height 

DNPH 2,4-dinitrophenylhydrazine 

ECD electron-capture detector 

EDU ethylenediurea 

EKMA Empirical Kinetic Modeling Approach 

FEF forced expiratory flow 

Fe2 (SO 4 ) 3 ferric sulfate 

FEV forced expiratory volume 

FEV1 forced expiratory volume in 1 sec 

FID flame ionization detector 

fR respiratory frequency 

FTIR Fourier-transform infrared 

FVC forced vital capacity 

G-6-PD glucose-6-phosphate dehydrogenase 

GC gas chromatography 

GPT gas-phase titration 

xi 
LIST OF ABBREVIATIONS 

(continued) 

GSH glutathione 

HC hydrocarbon(s) 

HCOOH formic acid 

HNO3 nitric acid 

HN04 peroxynitric acid ' 

HO hydroxy 

H02 hydroperoxy 

HONO nitrous acid 

HPLC high-pressure liquid chromatograpy; high-performance 

liquid chromatography 

HPPA 3-(p-hydroxyphenyl)propionic acid 

hr hour(s) 

hr/day hours per day 

HRP horseradish peroxidase 

H2O2 hydrogen peroxide 

H2SO4 sulfuric acid 

I impact 

I iodide ion 

IC inspiratory capacity 

I/0 ratio of indoor to.outdoor ozone concentrations 

IR infrared 

KI03 potassium iodate 

km kilometer 

LAAPCD Los Angeles Air Pollution Control District : 

LCV leuco crystal violet 

LDH lactate deyhydrogenase 

L/min liters per minute : 

M molar 

m meter(s)_. 

MBTH 3-methyl-2-benzothiazolinone hydrazone 

mi mile(s) 

xii 
LIST OF ABBREVIATIONS 

(continued) 

NADPH nicotinamide adenine dinucleotide phosphate 

NAPBN National Air Pollution Background Network 

NBKI neutral buffered potassium iodide 

(NH4 ) 2SO4 ammonium sulfate 

NF National Forest 

mm nanometer(s) 

NMHC nonmethane hydrocarbons 

NMOC nonmethane organic compounds 

N0 nitric oxide 

NO 2 nitrogen dioxide 

NO3 nitrogen trioxide 

NOx nitrogen oxides 

ON2 nitrogen washout 

NPSH non-protein sulfhydryls 

NR natural rubber 

N20 nitrous oxide 

OH hydroxyl group (or radical) 

0 2 oxygen 

0 3 ozone 

OZIPP Ozone Isopleth Plotting Package 

PAN peroxyacetyl nitrate 

PA0 2 alveolar partial pressure of oxygen 

PBzN peroxybenzoyl nitrate 

PEFR peak expiratory flow rate 

pH negative log of H ion concentration 

PPN peroxypropionyl nitrate 

ppb parts per bill.ion 

ppm parts per million 

rad radiation absorbed dose 

RBC red blood cell 

RV residual volume 

xiii 
LIST OF ABBREVIATIONS 

(continued) . 

SaOZ arterial oxygen saturation 

SAROAD Storage and Retrieval of Aerometric Data 

SBR styrene-butadiene rubber 

sec second(s) 

SGaw specific airway conductance 

SNAAQS Secondary Nationa7 Ambient Air Quality Standards 

S02 sulfur dioxide 

SO4 sulfate 

SOx sulfur oxide(s) 

SRaw specific airway resistance 

SRM Standard Reference Material 

SURE Sulfate Regional Experiment Sites 

T time, temperature 

TF tropopause-folding events 

Tg/yr teragrams per year 

TGS-ANSA triethanolamine, guaiacol(o-methoxyphenol), sodium 

metabisulfite; and 8-anilino-l-naphthalene sulfonic acid 

TLC total lung capacity 

TSH thyroid stimulating hormone 

pg/m3 microgram(s) per cubic meter 

Nm/hr micrometer(s) per hour 

UV ultraviolet 

VT tidal volume 

VE minute ventilation; expired volume per minute 

VOC volatile organic compounds 

ZnSO4 zinc sulfate 

r 

xiv 
AUTHORS, CONTRIBUTORS, AND REVIEWERS 

Authors: 

Dr. Richard M. Adams 

Department of Agricultural and Resource Economics 

Oregon State University 

Corvaliis, OR 97331 

Dr. Donald E. Gardner 

Northrop Services, I.nc. 

Environmental Sciences 

P. 0. Box 12313 

Research Triangle Park, NC 27709 

Dr. J. H. B. Garner 

Environmental Criteria and Assessment Office 

MD-52 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. Judith A. Graham 

Health Effects Research Laboratory 

MD-51 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. Milan J. Hazucha 

School of Medicine 

Center for Environmental Health and Medical Sciences 

University of North Carolina 

Chapel Hill, NC 27514 

Dr. Jimmie A. Hodgeson 

U.S. Environmental Protection Agency 

Environmental Monitoring Systems Laboratory 

26 West St. Clair 

Cincinnati, OH 45268 

Mr. Michael W. Holdren 

Battelie, Columbus Laboratories 

505 King Avenue 

Columbus, OH 43201 

Dr. Donald H. Horstman 

Health Effects Research Laboratory 

MD-58 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

xv 
Authors (continued): 

Mr. James M. Kawecki 

TRC Environmental Consultants, Inc. 

2001 Wisconsin Avenue, N.W. 

Suite 261 

Washington, DC 20007 

Dr. Jan G. Laarman 

Department of Forestry 

North Carolina State University 

Raleigh, NC 27607 

Mr. Thomas B. McMullen 

Environmental Criteria and Assessment Office 

MD-52 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. Daniel B. Menzel 

Laboratory of Environmental Toxicology and Pharmacology 

Duke University Medical Center 

P. 0. Box 3813 

Durham, NC 27710 

Mr. James A. Raub 

Environmental Criteria and Assessment Office 

MD-52 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Ms. Beverly E. Tilton 

Environmental Criteria and Assessment Office 

MD-52 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. David T. Tingey 

Environmental Research Laboratory 

200 SW 35th Street 

Corvallis, OR 97330 

Dr. Halvor Westberg 

Director, Laboratory for Atmospheric Research, 

and Professor, Civil and Environmental Engineering 

Washington State University 

Pullman, WA 99164-2730 

Dr. Arthur M. Winer 

Assistant Director _ 

Statewide Air Pollution Research Center 

University of California 

Riverside, CA 92521 

xvi 
Contributing Authors: 

Dr. Robert Frank 

Department of Environmental Health Sciences , 

Johns Hopkins School of Hygiene and Public Health 

615 N. Wo1fe Street 

Baltimore, MD 21205 

Dr. Michael D. Lebowitz 

Department of Internal Medicine 

College of Medicine 

University of Arizona 

Tucson, AZ 85724 

Dr. Harold G. Richter 

Office of Air Quality Planning and Standards 

Monitoring and Data Analysis Division 

MD-14 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Mr. Elmer Robinson 

Director, Mauna Loa Observatory 

National Oceanic and Atmospheric Administration 

(NOAA/CMCO) 

P.O. Box 275 

Hilo, HI 96720 

xvii 
SCIENCE ADVISORY BOARD 

CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE 

The substance of this document was reviewed by the C1ean Air Scientific 

Advisory Committee of the Science Advisory Board in public sessions. 

SUBCOMMITTEE ON OZONE 

Chairman 

Dr. Morton Lippmann 

Professor 

Department of Environmental Medicine. 

= New York University Medical Center 

f Tuxedo, New York 10987 

Members 

Dr. Mary 0. Amdur Dr. Robert Frank 

Senior Research Scientist Professor of Environmental Health 

Energy Laboratory Sciences 

Massachusetts Institute of Technology Johns Hopkins School of Hygiene 

Cambridge, Massachusetts 02139 and Public Health 

615 N. Wolfe Street 

Dr. Eileen G. Brennan Baltimore, Maryland 21205 

Professor 

Department of Plant Pathology Professor A. Myrick Freeman II 

Martin Hall, Room 213, Lipman Drive Department of Economics 

Cook College-NJAES Bowdoin College 

Rutgers University Brunswick, Maine 04011 

New Brunswick, New Jersey 08903 

Dr. Edward D. Crandall 

Professor of Medicine 

School of Medicine 

Cornell University 

New York, New York 10021 

Dr. James D. Crapo 

Associate Professor of Medicine 

Chief, Division of Allergy, Critical 

Care and Respiratory Medicine 

Duke University Medical Center 

Durham, North Carolina 27710 

Dr. Ronald J. Hall 

Senior Research Scientist and Leader 

Aquatic and Terrestrial Ecosystems 

Section 

Ontario Ministry of the Environment 

Dorset Research Center 

Dorset, Ontario 

Canada POAlEO 

Dr. Jay S. Jacobson 

Plant Physiologist 

Boyce Thompson Institute 

Tower Road 

Ithaca, New York 14853 

xviii 
Dr. Warren B. Johnson 

Director, Atmospheric Science Center 

SRI International 

333 Ravenswood Avenue 

Menlo Park, California 94025 

Dr. Jane Q. Koenig 

Research Associate Professor 

Department of Environmental Health 

University of Washington 

Seattle, Washington 98195 

Dr. Paul Kotin 

Adjunct Professor of Pathology 

University of Colorado Medical School 

4505 S. Yosemite, #339 

Denver, Colorado 80237 

Dr. Timothy Larson 

Associate Professor 

Environmental Engineering and 

Science Program 

Department of Civil Engineering 

University of Washington 

Seattle, Washington 98195 

Professor M. Granger Morgan 

Head, Department of Engineering 

and Public Policy 

Carnegie-Mellon University 

Pittsburgh, Pennsylvania 15253 

Dr. D. Warner North 

Principal 

Decision Focus Inc., Los Altos 

Office Center, Suite 200 

4984 E1 Camino Real 

Los Altos, California 94022 

Dr. Robert D. Rowe 

Vice President, Environmental and 

Resource Economics 

Energy and Resources Consultants, Inc 

207 Canyon Boulevard 

Boulder, Colorado 80302 

Dr. George Taylor 

Environmental Sciences Division 

P.O. Box X 

Oak Ridge National Laboratory 

Oak Ridge, Tennessee 37831 

Dr. Michael Treshow 

Professor 

Department of Biology 

University of Utah 

Salt Lake City, Utah 84112 

Dr. Mark J. Utell 

Co-Director, Pulmonary Disease Unit 

Associate Professor of Medicine and 

Toxicology in Radiation Biology 

and Biophysics 

University of Rochester Medical 

Center 

Rochester, New York 14642 

Dr. James H. Ware 

Associate Professor 

Harvard School of Public Health 

Department of Biostatistics 

677 Huntington Avenue 

Boston, Massachusetts 02115 

Dr. Jerry Wesolowski 

Air and Industrial Hygiene Laboratory 

California Department of Health 

2151 Berkeley Way 

Berkeley, California 94704 

Dr. James L. Whittenberger 

Director, University of California 

Southern Occupational Heaith Center 

Professor and Chair, Department of 

Community and Environmental Medicine 

California College of Medicine 

University of California - Irvine 

19772 MacArthur Boulevard 

Irvine, California 92717 

Dr. George T. Wolff 

Senior Staff Research Scientist 

General Motors Research Labs 

Environmental Science Department 

Warren, Michigan 48090 

xix 
PROJECT TEAM FOR DEVELOPMENT 

OF 

Air Quality Criteria for Ozone and Other Photochemical Oxidants 

Ms. Beverly E. Tilton, Project Manager 

and Coordinator for Chapters 1 through 5, Volumes I and II 

Environmental Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Mr. Norman E. Childs 

Environmental Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. J. H. B. Garner 

Coordinator for Chapters 7 and 8, Volume III 

Environmental Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Mr. Thnmas B. McMullen 

Environmantal Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Mr. James A. Raub 

Coordinator for Chapters 9 through 12, Volumes IV and V 

Environmental Criteria and Assessment Office (MD-52) 

U.S. Environmental Protection Agency 

Research Triangle Park, NC 27711 

Dr. David T. Tingey 

Coordinator for Chapter 6, Volume III 

Environmental Research Laboratory 

U.S. Environmental Protection Agency 

200 S.W. 35th Street 

Corvallis, OR 97330 

xx 
1. SUMMARY AND CONCLUSIONS 

1.1 INTRODUCTION 

This document is a revision of Air Quality Criteria for Ozone and Other 

Photochemical Oxidants, published in 1978 (U.S. Environmental Protection 

Agency, 1978). Its purpose is' to provide the scientific basis for the derivation of National Ambient Air Quaiity Standards (NAAQS) by consolidating'and 

assessing knowledge regarding the origin and distribution of, ozone and other 

photochemical oxidants and the effects of these pollutants on humans, experimental animals, vegetation, terrestrial ecosystems, and nonbiological materials. 

Because the indirect contributions of the photochemical oxidants to visibility 

degradation, climatic changes, and acidic deposition cannot, at present be 

quantified, these atmospheric effects and phenomena are not addressed in this 

document. They have been addressed, however, in other, recent air quality 

criteria documents (U.S. Environmental Protection Agency, 1982a,b). 

Research has established that photochemicai oxidants in ambient air 

consist mainly of ozone, peroxyacetyl nitrate,,and nitr.ogen dioxide, and of 

considerably lesser amounts of other peroxyacyl nitrates; hydrogen peroxide, 

alkyl 'hydroperoxides, nitric and nitrous acids, and formic acid. Other,oxidants 

suspected to occur in ambient air but only in trace amounts inc7ude peracids 

and ozonides. Only data on ozone, peroxyacyl ni.trates,,;hydrogen peroxide, and 

formic acid are examined in this document. Coverage has been limited to these 

photochemical oxidants on the basis of available information on effects, 

ambient air concentrations, or both. Of these`oxidants; only ozone,and.peroxyacetyl nitrate have been studied at concentrations having relevance for potential 

exposures of human populations or of vegetation, ecosystems, or nonbiological 

materials. Although by definition a photochemical oxidant, nitrogen dioxide 

is not included among the oxidants discussed in this document. Separate 

criteria documents are issued for oxides of nitrogen, and the second document 

in that series, completed in 1982, presented information on nitrosamines and 

inorganic nitrogen acids, as well as the oxides of nitrogen (U.S. Environmental. 

Protection Agency, 1982a). 

This document presents a review and evaluation of relevant literature on 

ozone and other photochemical oxidants published through early 1986. The 

document is not intended as a complete literature review, however; but is 

1-1 
intended, rather, to present current data of probable consequence for the 

derivation of national ambient air quality standards for protecting public 

health and welfare. The scientific information selected for review and comment 

in the text generally came from the more recent literature, with emphasis on 

studies conducted at or near pollutant concentrations found in ambient air. 

6enerally, only published material that has undergone scientific peer review 

has been included. In the interest of admitting new and important information, 

however, some material not published in the open literature but meeting other 

standards of scientific reporting may have been included. In addition, the 

studies reviewed in the health- and welfare-related chapters met other selection 

criteria, including the appropriate use and satisfaction of sta -tistical tests. 

In the early chapters of this document, an overview is presented of the 

nature, origins, and distribution in ambient air of those organic and inorganic 

compounds that serve as precursors to ozone and other photochemical oxidants. 

The currently available measurement techniques for these precursors are briefly 

evaluated, inasmuch as the assessment of the occurrence of the precursors 

depends up«r, their accurate measurement. Similarly, an overview is presented 

of the chemical and physical processes in the atmosphere by which precursors 

give rise to the production of ozone and other photochemical oxidants. In 

addition, the properties of ozone and other photochemical oxidants are presented 

as background for understanding information presented in the chapters on 

health and welfare effects. Likewise, techniques for the measurement of 

ozone, total oxidants, and individual oxidant species other than ozone are 

evaluated, since the significance of aerometric and exposure data on these 

pollutants is dependent upon the accuracy and specificity of the analytical 

techniques used. Typical concentrations of the respective oxidants are presented to permit assessment of potential exposures of human populations and 

other receptors. 

Remaining chapters of the document contain the actual air quality criteria; 

that is, quantitative and qualitative information that describes the nature of 

the health and welfare effects attributable to ozone and other photochemical 

oxidants and the concentrations at which these pollutants are thought to 

produce the observed effects. 

Neither techniques nor strategies for the abatement of photochemical 

oxidants are reviewed in this document. Technology for controlling the emissions 

of nitrogen oxides and of volatile organic compounds is discussed in documents 

1-2 
issued by the Office of Air Quality Planning and Standards (OAQPS) of the U.S. 

Environmental Protection Agency (e.g., U.S. Environmental Protection Agency, 

1978b, 1983). Likewise, research findings and issues germane to the scientific 

basis for control strategies are addressed in numerous documents issued by 

OAQPS and by the Office of Research and Development. 

In addition, certain issues of direct relevance to standard-setting are 

not explicitly addressed in this document, but are addressed instead in 

documentation prepared by OAQPS as part of its regulatory analyses. Such 

analyses include: (1) discussion of what constitutes an "adverse effect," 

that is, the effect or effects the NAAQS are intended to protect against; (2) 

assessment of risk; and (3) discussion of factors to be considered in providing 

an adequate margin of safety. While scientific data contribute significantly 

to decisions regarding these three issues, their resolution cannot be achieved 

solely on the basis of experimentally acquired information. Final decisions 

on items (1) and (3) are made by the Administrator of the U.S. Environmental 

Protection Agency. 

The legislative basis for the development and issuance of the air quality 

criteria and related information presented in this document is found 'in 

Sections 108 and 109 of the Clean Air Act (U.S.C., 1982). 

1.2 PROPERTIES, CHEMISTRY, AND TRANSPORT OF OZONE AND OTHER PHOTOCHEMICAL 

OXIDANTS AND THEIR PRECURSORS 

1.2.1 Descriptions and Properties of Ozone and Other Photochemical Oxidants 

Ozone (03 ) and other photochemical oxidants occurring at low concentrations in ambient air, such as peroxyacetyl nitrate (PAN), hydrogen peroxide 

(H2O2 ), and formic acid (HCOOH), are characterized chiefly by their ability to 

remove electrons from, or. to share electrons with, other'molecules or ions 

(i.e., oxidation). The capability of a chemical species for oxidizing or 

reducing other chemical species is termed "redox potential" (positive or 

negative standard potential) and is expressed in volts. A reactive allotrope 

of oxygen that is only about one-tenth as soluble as oxygen in water, ozone 

has a standard potential of +2.07 volts in aqueous systems for the redox pair, 

03/H20 (Weast, 1977). Hydrogen peroxide, which is highly soluble in water and 

other polar solvents, has a standard potential of +1.776 in the redox pair, 

H 2O 2/H20 (Weast, 1977). No standard potential for peroxyacetyl nitrate in 

neutral or buffered aqueous systems, such as those that occur in biological 

1-3 
systems, appears in the literature. In acidic solution (pH 5 to 6), PAN 

hydrolyzes fairly rapidly (Lee et al., 1983; Holdren et al., 1984); in alkaline 

solution it decomposes with the production of nitrite ion and molecular oxygen 

(Stephens, 1967; Nicksic et al., 1967). An important property.of PAN, especially in the laboratory, is its thermal instability. Its explosiveness dictates its synthesis for experimental and calibration purposes by experienced 

personnel only. 

Formic acid is formed as a stable product in photochemical air pollution. 

It has the structure of both an acid and an aldehyde and in concentrated form 

is a pungent-smelling, highly corrosive liquid. 

The toxic effects of oxidants are attributable to their oxidizing ability. Their oxidizing properties also form the basis of several measurement 

techniques for 03 and PAN. The calibration of ozone and PAN measurements, 

however, is achieved via their spectra in the ultraviolet and infrared regions, 

respectively. A11 three pollutants of most concern in this document (0 3 , PAN, 

and H2O2 ) must be generated in situ for the calibration of ineasurement techniques. For ozone and H2O 2 , generation of calibration gases is reasonably 

straightforward. 

1.2.2 Nature of Precursors to Ozone and Other Photochemical Oxidants 

Photochemical oxidants are products of atmospheric reactions involving 

volatile organic compounds (VOC) and oxides of nitrogen (NOx ), as well as 

hydroxyl (OH) and other radicals, oxygen, and sunlight (see, e.g., Demerjian 

et al., 1974; National Research Council, 1977; U.S. Environmental Protection 

Agency, 1978; Atkinson, 1985). The oxidants are largely secondary pollutants 

formed in the atmosphere from their precursors by processes that are a complex, 

non-linear function of precursor emis'sions and meteorological factors. 

The properties of organic compounds that are most relevant to their role 

as precursors to ozone and other oxidants are their volatility, which governs 

their emissions into the atmosphere; and their chemical reactivity, which 

determines their lifetime in the atmosphere. Although vapor-phase hydrocarbons (compounds of carbon and hydrogen only) are the predominant organic 

compounds in ambient air that serve as precursors to photochemical oxidants, 

other volatile organic compounds are also photochemically reactive in those 

atmospheric processes that give rise to oxidants. In particular, halogenated 

organics (e.g., haloalkenes) that participate in photochemical reactions are 

1-4 
present in ambient air, although at lower concentrations than the hydrocarbons. 

They are oxidized through the same initial step involved in the oxidation of 

the hydrocarbons; that is, attack by hydroxyl radicals. Alkenes, haloalkenes, 

and aliphatic aldehydes are, as classes, among the most reactive organic , compounds found in ambient air (e.g., Altshuller and Bufalini, 1971; Darnall 

et al., 1976; Pitts et al., 1977; U.S. Environmental Protection Agency, 1978, 

and references therein). Alkenes and haloalkenes are unique among VOC in 

ambient air in that they are susceptible both to attack by OH radicals (OH) 

and by ozone (Niki et al., 1983). Methane, halomethanes, and certain haioethenes are of negligible reactivity in ambient air and have been classed as 

unreactive by the U.S. Environmental Protection Agency (1980a,b). Since methane 

is considered only negligibly reactive in ambient air, the volatile organic 

compounds of importance as oxidant precursors are usually referred to as 

nonmethane hydrocarbons (NMHC) or, more properly, as nonmethane organic 

compounds (NMOC). 

The oxides of nitrogen that are important as precursors to ozone and 

other photochemical oxidants are nitrogen dioxide (NO 2 ) and nitric oxide (NO). 

Nitrogen dioxide is itself an oxidant that produces deleterious effects, which 

are the subject of a separate criteria document (U.S. Environmental Protection 

Agency, 1982). Nitrogen dioxide is an important precursor (1) because its 

photolysis in ambient air leads to the formation of oxygen atoms that combine 

with molecular oxygen to form ozone; and (2) because it reacts with acetylperoxy radicais to form peroxyacetyl nitrate, a phytotoxicant and a lachrymator. Although ubiquitous, nitrous oxide (N 20) is unimportant in the production 

of oxidants in ambient air because it is virtually inert in the troposphere. 

1.2.3 Atmospheric Reactio.ns of Ozone and Other Oxidants Including Their Role 

in Aerosol Formation 

The chemistry of the polluted atmosphere is exceedingly complex, but an 

understanding of the basic phenomena is not difficult to acquire. Three 

processes occur: the emission of precprsors to ozone from predominantly 

manmade sources; photochemical reactions that take place during the dispersion and transport of these precursors; and scavenging processes that reduce 

the concentrations of both 0 3 and precursors along the trajectory. 

The specific atmospheric reactions of ozone and of other photochemical 

oxidants such as peroxyacetyl nitrate and hydrogen peroxide are becoming 

1-5 
increasingly well-characterized. The reactions of these species result in 

products and processes that may have significant environmental and health- and 

welfare-related implications, including effects on biological systems, nonbiological materials, and such phenomena as visibility degradation and acidification of cloud and rain water. 

1.2.3.1 Formation and Transformation of Ozone and Other Photochemical Oxidants. In the troposphere, ozone is formed through the d.issociation of NO 2 by 

sunlight to yield an oxygen atom, which then reacts with molecular oxygen (0 2 ) 

to produce an 0 3 molecule. If it is present, NO can react rapidly with 0 3 to 

form NO 2 and an 0 2 molecule. In the absence of competing reactions, a steadystate or equilibrium concentration of 03 is soon established between 0 3 , NO2 , 

and NO (National Research Council, 1977). The injection of organic compounds 

into the atmosphere upsets the equilibrium and allows the ozone to accumulate 

at higher than steady-state concentrations. The length of the induction 

period before the accumulation of 0 3 begins depends heavily on the initial 

NO/NO2 and NMOC/NOx ratios (National Research Council, 1977). 

The major role played by organic compounds in smog reactions is attributable to the hydroxyl radical (OH), since it reacts with essentially all organic 

compounds (e.g., Atkinson, 1985; Herron and Huie, 1977, 1978; Dodge and Arnts, 

1979; Niki et a1., 1981). Aldehydes, which are constituents of automobile 

exhaust as well as decomposition products of most atmospheric photochemical 

reactions involving hydrocarbons, and nitrous acid (HONO), are important 

sources of OH radicals, as is 03 itself. Other free radicals, such as hydroand alkylperoxy radicals and the nitrate (NO 3 ) radical play important roles in 

photochemical air pollution. 

The presence of organic compounds, oxides of nitrogen, and sun.light does 

not mean that the photochemical reactions will continue indefinitely. Termination reactions gradually remove NO2 from the reaction mixtures, such that 

the photochemical cycles slowly come to an end unless fresh NO and NO 2 emissions are injected into the atmosphere. Compounds containing nitrogen, such 

as PAN, nitric acid (HNO 3 ), and peroxynitric acid (HN0 4 ), as well as organic 

and inorganic nitrates, are formed in these termination reactions. 

Recent studies on the photooxidation of organic compounds under simulated 

atmospheric conditions have been reasonably successful. The rate constants 

for the reaction of OH radicals with a large number of organic compounds have 

been measured (e.g., Atkinson et al., 1979; Atkinson et al., 1985). The 

1-6 
mechanisms of the reactions of paraffinic compounds are fairly well under- 

.stood, as are those of olefinic compounds, at least for the smaller compounds. 

Photooxidation reactions of the aromatic compounds, however, are poorly understood. 

In the presence of NO x , natural hydrocarbons (i.e., those organic compounds emitted from vegetation) can also undergo photooxidation reactions to 

yield 03 , although most naturally emitted hydrocarbons are olefins and are 

scavengers as well as producers of 0 3 (e.g., Lloyd et ai., 1983;.Atkinson 

et ai., 1979; Kamens° et al., 1982; Killus and Whitten, 1984; Atkinson and 

Carter, 1984). 

1.2.3.2 Atmospheric Chemical Processes Involving Ozone. Ozone can react with 

organic compounds in the boundary layer of the troposphere (Atkinson and 

Carter, 1984). It is important to recognize, however, that organics undergo 

competing reactions with OH radicals in the daytime (Atkinson et al., 1979; 

Atkinson, 1985) and, in certa.incases, with NO 3 radicals during the night 

(Japar and Niki, 1975; Carter et al., 1981a; Atkinson et al., 1984a,b,c,d,e; 

Winer et al., 1984), as weli as photolysis, in the case of aldehydes and other 

oxygenated organics. Only for organics whose ozone reaction rate constants 

are greater than —10 -21 cm3 molecule-1 sec-1 can consumption by ozone be 

considered to be atmospherically important (Atkinson and Carter, 1984). 

Ozone reacts rapidly with the acyclic mono-, di-, and tri - alkenes and 

with cyclic alkenes. The rate constants for these reactions range from —10 -18 

to —10-14 cm3 molecule-1 sec-1 (Atkinson and Carter,.1984), corresponding to 

atmospheric lifetimes ranging from a few minutes for the more reactive cyclic 

alkenes, such as the monoterpenes, to several days. In polluted atmospheres, 

a significant portion of .the consumption of the more reactive alkenes will 

occur via reaction with ozone rather than with OH radicals, especially in the 

afternoons during photochemicai oxidant episodes. Reactions between ozone and 

alkenes can result in aerosol formation (National Research Council, 1977; 

Schuetzle and Rasmussen, 1978), with alkenes of higher carbon numbers the 

chief contributors. 

Because of their respective rate constants, neither alkanes (Atkinson and 

Carter, 1984) nor alkynes (Atkin.son and-Aschmann, 1984) are expected to react 

with ozone in the atmosphere, since competing reactions with OH radicals have 

higher rate constants (Atkinson et al., 1979; Atkinson, 1985). 

1-7 
The aromatics react with ozone, but quite slowly (Atkinson and Carter, 

1984), such that their reactions with ozone are expected to be unimportant in 

the atmosphere. Cresols are more reactive toward ozone than the aromatic 

hydrocarbons (Atkinson and Carter, 1984), but their reactions with OH radicals 

(Atkinson, 1985) or NO 3 radicals (Carter et al., 1981a; Atkinson et al., 

1984d) predominate. 

For oxygen-containing organic compounds, especially those without carboncarbon double bonds, reactions with ozone are slow. For carbonyls and ethers 

(other than ketene) that contain unsaturated carbon-carbon bonds, however,: 

much faster reactions are observed (Atkinsbn and Carter, 1984). 

Certain reactions of ozone other than its reactions with organic compounds are important in the atmosphere. Ozone reacts rapidly with NO to form 

NO 2 , and subsequently with NO 2 to produce the nitrate (NO 3 ) radical and an 

oxygen molecule. Photolysis of ozone can be a significant pathway for the 

formation of OH radicals, particularly in polluted atmospheres when ozone 

concentrations are at their peak. 

Ozone may play a role in the oxidation of S0 2 to H 2SO4 , both indirectly 

in the gas phase (via formation of OH radicals and Criegee biradicals) and 

directly in aqueous droplets. 

1.2.3.3Atmospheric Reactions of PAN, H,0 „ and HCOOH . Because PAN is in 

equilibrium with acetyl peroxy radical.s and NO 2 , any process that leads to the 

removal of either of these species will lead to the decomposition of PAN. One 

such process is the reaction of NO with acetyl peroxy radicals. This can 

lead, however, to the formation of OH radicals. Thus, PAN remaining overnight 

from an episode on the previous day can react with NO emitted from morning 

traffic to produce OH radicals (Cox and Roffey,.1977; Carter et al., 1981b) 

that will enhance smog formation.on that day.(e.g., Tuazon et al.., 1981). In 

the absence of significant NO,concentrations, and in,regions of moderate to 

1 ower temperatures xPAN wi 11 pers i st_ei n the atm,osphere (Wal l i ngton et al ., 

1984; Aikin et al., 1983) and.contr.ibute to the long-range transport of NO x . 

Although hydrogen.,peroxide,,formed-in. the„gas ; phase from the reactions of 

hydroperoxyl radicals plays .a role,=in HO X chemistry i: n th.eltroposphere, and 

especially in the stratosphere .(Crutzen . ;and.Fishman, 1977; Cox and Burrows, 

1979), its major importance arises from its high solubility in water. The 

latter ensures that a . large fraction of gaseous H2O 2wi; l1 be . taken " up in 

aqueous droplets. Over the past decade, evidence has accumulated that H 2O 2 

E~=~ 
dissolved in cloud, fog, and rainwater may play an important, and, in acidic 

droplets (i.e., pH <5), even a dominant role in the oxidation of S0 2 to H2SO4 

(e.g., Hoffman and Edwards, 1975; Martin and Damschen, 1981; Chameides and 

Davis, 1982; Calvert and Stockwell, 1983, 1984; Schwartz, 1984). Hydrogen 

peroxide may also play a role in the oxidation of NO 2 dissolved in aqueous 

droplets, although relevant data are limited and additional research is required 

(see, e.g., Gertler et al., 1984). Substantial uncertainties remain concerning 

the quantitative role of H 2O2 in acidification of aqueous particles and droplets 

(Riehards et al., 1983). 

Because it can be scavenged rapidly into water droplets, formic acid can 

potentially function as an oxidant in cloud water and rain water. Thus, HCOOH 

is an example of a compound that is a non-oxidant or weak oxidant in the gas 

phase but that is transformed upon incorporation in aqueous solutions into an 

effective oxidizer of S(IV). Although much uncertainty remaihs concerning the 

quantitative role of HCOOH and the higher organic acids, they.potentially piay 

a minor but still significant role in the acidification of rain. 

1.2.4 Meteorological and Climatological Processes 

Meteorological and climatological processes are important in determining 

the extent to which precursors to ozone and other photochemical oxidants can 

accumulate, and thereby the concentrations of ozone and other oxidants that 

can result. The meteorological factors most important in the formation and 

transport of ozone and other photochemical oxidants in the lower troposphere 

are: (1) degree of atmospheric stability; (2) wind speed and direction; 

(3) intensity and wavelength of sunlight; and.(4) synoptic weather conditions. 

These factors are in turn dependent upon or interrelated with geographic, 

seasonal, and other climatological factors. 

Incursions of ozone-from the stratosphere are an additional source of the 

ozone f.ound in the lower troposphere. The physical and meteorological mechanisms 

by which ozone is brought into the troposphere from the stratosphere are 

important in determining the resulting ground-level concentrations, ground-level 

locations impacted,rand the seasonality of incursions of stratospheric ozone, 

1.2.4.1 Atmospheric Mixing. The concentration of a pollutant in ambient air 

depends significantly on the degree of atmospheric mixing that occurs from the 

time the pollutant or its precursors are emitted and the arrival of the pollutant at the receptor. The rate at which atmospheric mixin'g proceeds and the 

1-9 
extent of the final dilution depends on the amount of turbulent mixing that 

occurs and on wind speed and direction. Atmospheric stability is one of the 

chief determinants of turbulent mixing since pollutants do'not spread rapidly 

within stable layers nor do they mix upward through stable layers to higher 

altitudes. 

Temperature inversions, in which the temperature increases with increasing 

altitude, represent the most stable atmospheric conditions. Surface inversions (base at ground level) and elevated inversions (the entire layer is 

above the surface) are both common (Hosler, 1961; Holzworth, 1964) and both 

can occur simultaneously at the same location. Surface inversions show a 

diurnal pattern, forming at night in the absence of so.lar radiation but breaking up by about mid-morning as the result of surface heating by the sun (Hosler, 

1961; Slade, 1968). Elevated inversions can persist throughout the day and 

pollutants can be trapped between the ground surface and the base of the 

inversion. The persistence of elevated inversions is a major meteorological 

factor contributing to high pollutant concentrations and photochemical smog 

conditions along the California coast (Hosler, 1961; Holzworth, 1964; Robinson, 

1952). In coastal areas generally, such as the New England coast (Hosler, 

1961) and along the Great Lakes (Lyons and Olsson, 1972), increased atmospheric 

stability (and diminished mixing) occurs in summer and fall as the result of 

the temperature differential between the water and the land mass. 

The depth of the layer in which turbulent mixing can occur (i.e., the 

"mixing height") shows geographical dependence. Summer morning mixing heights 

are usually >300 m in the United States except for the Great Basin (part of 

Oregon, Idaho, Utah, Arizona, and most of Nevada), where the mixing height is 

N200 m(Holzworth, 1972). By mid-morning, mixing heights increase markedly 

such that only a few coastal areas have mixing heights <1000 m. 

Summer afternoon mixing heights are generally an indication of the potential for recurring photochemical oxidant problems. Photochemical smog problems 

in the United States are somewhat unexpected since the lowest afternoon mixing 

height is —600 m(Holzworth, 1972). Elevated inversions having bases <500 m 

(i.e., low-level inversions) occur in the United States, however, with the 

following frequencies: 90 percent on the California coast; >20 percent on the 

Atlantic coast (New Jersey to Maine); >5 percent along the Great Lakes; and 5 

to 10 percent from Louisiana to Arkansas and eastward to about Atlanta, Georgia. 

For most areas of the United States, though, the persistence through the 

1-10 
afternoon of low-level stable layers is a rare event, occurring on <1 day in 

20 (Holzworth and Fisher, 1979). 

1.2.4.2 Wind Speed and Direction. For areas in which mixing heights are not 

restrictive, wind speed and, in some cases, wind direction are major determinants of pollution potential. Since strong winds dilute precursors to ozone 

and other photochemical oxidants, a location may have good ventilation despite 

the occurrence of persistent inversions (e.g.,'San Francisco). Conversely, 

1 i ght wi nds can resul t i n hi gh oxi dant 1 evel s even i f the mi xi ng 1 ayer i s 

deep. 

The frequency of weak winds, then, is important in oxidant formation. In 

industrialized, inland areas east of the Mississippi River, surface inversions 

in the morning coupled with wind speeds <2.5 m/sec (<6 mi/hr) occur with a 

frequency >50 percent (Holzworth and Fisher, 1979). These surface inversions 

break up by afternoon, however, permitting dispersion. 

The effects of wind speed and direction include the amount of dilution 

occurring in the source areas, as well as along the.trajectory foliowed by an 

urban or source-area plume. Regions having steady prevailing winds, such that 

a given air parcel can pass over a number of significant source areas, can - 

develop significant levels of pollutants even in the absence of weather patterns 

that iead to the stagnation type of air pollution episodes. The Northeast 

states are highly susceptibie to pollutant plume transport effects, although 

some notable stagnation episodes have also affected this area (e.g., - Lynn 

et al., 1964). Along the Pacific Coast, especially along the coast of 

California, coastal winds and a persistent low inversion layer contribute to 

major pollutant buildups in urban source areas and downwind along the urban 

plume trajectory (Robinson, 1952; Neiburger et al., 1961). 

1.2.4.3 Effects of Sunlight and'Temperature. The effects of sunlight on 

photochemical oxidant formation, aside from the role of solar radiation in 

meteorological processes, are related to its intensity and its spectral distribution. Intensity varies diurnally, seasonally, and iaith latitude, but the 

effect of iatitude is strong only in the winter. Experimental studies have 

verified the effects on oxidant formation of light intensity (Peterson, 1976; 

Demerjian et al., 1980) and its diurnal variations (Jeffries et al., 1975; 

1976), as well as on the overall photooxidation process (Jaffee et al., 1974; 

Winer et al., 1979). 

1-11 
A correlation between high oxidant concentrations and warm, above-normal 

temperatures has been demonstrated generally (Bach, 1975; Wolff and Lioy, 

1978) and for specific locations, e.g., St. Louis (Shreffler and Evans, 1982). 

Coincident meteorology appears to be the cause of the observed correlation. 

Certain synoptic weather conditions are favorable both for the occurrence of 

higher temperatures and for the formation of ozone and other oxidants, so that 

temperature is often used to forecast the potential for high oxidant concentrations (e.g., Wolff and Lioy, 1978; Shreffler and Evans, 1982). Data from 

smog chamber studies show an effect of temperature on ozone formation (e.g., 

Carter et al. , 1979; Countess et al ., 1981), but the effect i s thought to 

result from the volatilization and reaction of chamber wall contaminants as 

the temperature is increased. 

1.2.4.4 Transport of Ozone and Other Oxidants and Their Precursors. The 

levels of ozone and other oxidants that will occur at a given receptor site 

downwind of a precursor source area depend upon many interrelated factors, 

which include but are not restricted to: (1) the concentrations of respective 

precursors leaving the source area; (2) induction time; (3) turbulent mixing; 

(4) wind speed and wind direction; (5) scavenging during transport; (6) injection of new emissions from source areas in the trajectory of the air mass; 

and (7) local and synoptic weather conditions. 

Ozone and other photochemical oxidants can be transported hundreds of 

miles from the place of origin of their precursors, as documented by the 

numerous studies on transport phenomena that were described in the 1978 criteria document for ozone and other photochemical oxidants (U.S. Environmental 

Protection Agency, 1978). In that document, transport phenomena were classified into three categories, depending upon transport distance: urban-scale, 

mesoscale, and synoptic-scale. In urban-scale transport, maximum concentrations of 0 3 are produced about 20 miles or so (and about 2 to 3 hours) downwind from the major pollutant source areas. In mesoscale transport, 0 3 has 

been observed up to 200 miles downwind from the sources of its precursors. 

Synoptic-scale transport is associated with large-scale, high-pressure air 

masses that may extend over and persist for many hundreds of miles. 

Urban-scale transport has been identified as a significant, characteristic feature of the oxidant problem in the Los Angeles Basin (Tiao et al., 

1975), as well as in San Franciso, New York, Houston, Phoenix, and St. Louis 

(e.g., Altshuller, 1975; Coffey and Stasiuk, 1975; Shreffler and Evans, 1982; 

1-12 
Wolff et al., 1977a). Simpie advection of a photochemically reactive air 

mass, local wind patterns, and diurnal wind cycles appear to be the main 

factors involved in urban-scale transport. 

Mesoscale transport is in many respects an extension of urban-scale 

transport and is characterized by the development of urban plumes. Bell 

documented cases in 1959 in which precursors from the Los Angeles Basin and 

the resultant oxidant plume were transported over the coastal Pacific Ocean, 

producing elevated oxidant concentrations in San Diego County the next day 

(Bell, 1960). Similar scales of transport have been reported by Cleveland 

et al. (1976a,b) for the New York-Connecticut area; by Wolff and coworkers and 

others (Wolff et al., 1977a,b; Wolff and Lioy, 1978; Clark and Clarke, 1982; 

Clarke et al., 1982; Vaughan et al., 1982) for the Washington, DC-Boston 

corridor; and by Westberg and coworkers for the Chicago-Great Lakes area 

(Sexton and Westberg, 1980; Westberg et al., 1981). These and other studies 

have demonstrated that ozone-oxidant plumes from major urban areas can extend 

downwind about 100 to 200 miles and can have widths of tens of miles (Sexton, 

1982), frequently up to half the length of the plume. 

Synoptic-scale transport is characterized by the general and widespread 

occurrence of elevated oxidants and precursors on a regional or air-mass scale 

as the result of certain favorable weather conditions, notably, slow-moving, 

well-developed high-pressure, or anti-cyclonic, systems characterized by weak 

winds and limited vertical mixing (Korshover, 1967; 1975). The size of the 

region that can be affected has been described by Wolff and coworkers, who 

reported the occurrence of haze and elevated ozone levels in an area extending 

from the Midwest to the Gulf Coast (Wolff et al., 1982) and the occurrence of 

elevated ozone concentrations extending in a virtual "ozone river" from the 

Gulf Coast to New England that affected anywhere from a few hundred square 

miles to a thousand square miles during a 1-week period in July 1977 (Wolff 

and Lioy, 1980). 

1.2.4.5 Stratospheric-Tropospheric Ozone Exchange. The fact that ozone is 

formed in the stratosphere, mixed downward, and incorporated into the troposphere, where it forms a more or less uniformly mixed background concentration, has been known in various degrees of detail for many years (Junge, 

1963). It is widely accepted that the long-term average tropospheric background concentration of about 30 ppb to 50 ppb results primarily, though not 

1-13 
exclusively, from the transfer of stratospheric ozone into the upper troposphere, followed by subsequent dispersion throughout the troposphere (e.g., 

Kelly et al., 1982). 

The exchange of ozone between the stratosphere and the troposphere in the 

middle latitudes occurs to a major extent in events called "tropopause folds" 

(TF) (Reiter, 1963; Reiter and Mahlman, 1965; Danielsen, 1968; Reiter, 1975; 

Danielsen and Mohnen, 1977; Danielsen, 1980), in which the polar jet stream 

plays a major role. From recent studies, Johnson and Viezee (1981) proposed 

four types or mechanisms of TF injection and concluded that two of these, both 

of which are consistent with theory, could cause substantial effects in terms 

of high ozone concentrations at ground level. They concluded, in addition, 

that all low-pressure trough systems may induce TF events and cause the' transtropopause movement of ozone-rich air into the troposphere (Johnson and Viezee, 

1981). 

1.2.4.6Stratospheric Ozone at Ground Level . From a detailed review of 

studies on background tropospheric ozone, Viezee and Singh (1982) concluded 

that the stratosphere is a major but not the sole source of background ozone 

in the unpolluted troposphere, a conclusion reached by other investigators as 

well (e.g., Kelly et al., 1982). The stratospheric ozone reservoir shows a 

strong seasonal cycle that is reflected at ground-level. At some stations 

that monitor background ozone levels, average spring background levels may be 

as high as 80 ppb, with average fall levels ranging from 20 to 40 ppb (e.g., 

Singh et al., 1977; Mohnen, 1977; U.S. Environmental Protection Agency, 1978). 

Viezee and Singh (1982) and Viezee et al. (1983) concluded that relatively 

high ozone concentrations can occur for short periods of time (minutes to a 

few hours) over local areas as a result of stratospheric intrusions. 

A number of investigators have attempted to quantify the amount of the 

surface ozone that can be attributed to stratospheric sources. The method 

most commonly used i s based on the assumpti on that beryl 1 i um-7 ( 7 Be) i s a 

unique tracer for air parcels of stratospheric origin. Calculated correlations 

between surface ozone and 7Be show, however, that their relationship is highly , variable (e.g., Kelly et al., 1982; Ferman and Monson ; 1978; Johnson and 

Viezee, 1981; Husain et al., 1977). Singh et al. (1980) and Viezee and Singh 

(1982) have pointed out problems with using this technique to quantify the 

contribution of stratospheric ozone to surface ozone. Singh et al. (1980) 

1-14 
concluded that "the experimental technique involving a 7Be/0 3 ratio to estimate the daily stratospheric component of ground-level 0 3 is unverified and 

considered to be inadequate for air quality applications" (p. 1009). This 

group of investigators have suggested, however, that 7Be may be used, under 

appropriate meteorological conditions, as a qualitative tracer for air masses 

of stratospheric origin (Johnson and Viezee, 1981; Viezee et al., 1979). 

Other methods used to attempt to quantify the stratospheric component of 

surface ozone include aircraft observations of TF events coupled with calculations of downward ozone flux, and examination of surface ozone data records. 

From such data, Viezee et al. (1983) concluded that direct ground-level contributions from stratospheric ozone are infrequent (<1 percent of the time), 

short-lived, and associated with ozone concentrations <0.1 ppm. 

Notwithstanding difficulties with quantifying its contribution to surface 

ozone, however, stratospheric ozone is clearly present in atmospheric surface 

layers, and the meteorological mechanisms responsible have been described by a 

number of investigators (e.g., Danielsen, 1968; Wolff et al., 1979; Johnson 

and Viezee, 1981). 

1.2.4.7Background Ozone from Photochemical Reactions . Whereas stratospheric 

ozone is thought by many investigators to be the dominant contributor to 

background leveis of ozone, as discussed above, other investigators have 

concluded that as much as two-thirds of the annual average background concentrations may resuit from photochemical reactions. For example, Altshuller 

(1986), in a recent review article, has concluded that photochemically generated 

ozone should equal or exceed the stratospheric contribution at lower-elevation 

remote locations; and that photochemically generated ozone from manmade emissions 

probably constitutes most of the ozone measured at more polluted rural locations 

during the warmest months of the year. His conclusions were based, in part, 

on an analysis of global circulation (e.g., Levy et al., 1985) and photochemical 

modeling studies (e.g., Fishman and Seiler, 1983; Fishman and Carney, 1984; 

Fishman et al., 1985; Dignon and Hameed, 1985). In these modeling studies, 

the photochemical contribution to background ozone levels was estimated to 

range from —15 ppb (long-term) to —80 ppb (summertime), depending on the level 

of NO emissions assumed. 

x 

Studies on the role of NO x in nonurban ozone photochemistry have shown 

that ozone formation at many. of the locations is not NO x-limited, but depends 

on VOC reactions, as well (e.g., Martinez and Singh, 1979; Kelly et al., 1984; 

1-15 
Liu et al., 1984). Background NO xconcentrations at most remote, clean locations range from <0.05 ppb upward. Mean concentrations of NO xat nonurban 

locations in the United States east of the Rocky Mountains range from —1 ppb 

to 10 ppb (Altshuller, 1986; see also Section 1.2.5.2.4 and Chapter 3). These 

background concentrations of NO xare higher than previously thought (see, 

e. g. , Si ngh et al ., 1980; Kel ly et al ., 1984, regardi ng gl obal model s and 

assumed reservoirs of NOX). 

The contributions of biogenic VOC to background ozone, although a matter 

of controversy in recent years, appear not to be significant under most atmospheric conditions, since ambient air concentrations of biogenic VOC are quite 

low, even at rural sites (Altshuller, 1983). 

Thus, photochemistry and stratospheric intrusions are both regarded as 

contributing to background ozone concentrations, but the apportionment of 

background to respective sources remains a matter of investigation. 

1.2.5 Sources, Emissions, and Concentrations of Precursors to Ozone and Other 

Photochemical Oxidants 

As noted earlier, photochemical production of ozone depends both on the 

presence of precursors, volatile organic compounds (VOCs) and nitrogen oxides 

(NOx ), emitted by manmade and by natural sources; and on suitable conditions 

of sunlight, temperature, and other meteorological factors. Because of the 

intervening requirement for meteorological conditions conducive to the photochemical generation of ozone, emission inventories are not as direct predictors of ambient concentrations of secondary pollutants such as ozone and other 

oxidants as they are for primary pollutants. 

1.2.5.1 Sources and Emissions of Precursors. Emissions of manmade VOCs 

(excluding several relatively unreactive compounds such as methane) in the 

United States have been estimated at 19.9 Tg/yr for 1983 (U.S. Environmental 

Protection Agency, 1984). Retrospective estimates show that manmade VOC 

emissions rose from about 18.5 Tg/yr in 1940 to about 27.1 Tg/yr in 1970 (U.S. 

Environmental Protection Agency, 1986). An examination of trends in manmade 

VOC emissions for 1970 through 1983 shows that the annual emission rate for 

manmade VOCs decreased some 26 percent during this period. The main sources 

nationwide are industrial processes, which emit a wide variety of VOCs, such 

as chemical solvents; and transportation, which includes the emission of VOCs 

in gasoline vapor as well as in gasoline combustion products. Estimates of 

1-16 
biogenic emissions of organic compounds in the United States are highly 

inferential but data suggest that the yearly rate is the same order of magnitude as manmade emissions. Most of the biogenic emissions actually occur 

during the growing season, however, and the kinds of compounds emitted are 

different from those arising from manmade sources. 

Emissions of manmade NO xin the United States were estimated at 19.4 Tg/yr 

for 1983. Retrospective estimates show that manmade NOxemissions rose from 

about 6.8 Tg/yr in 1940 to about 18.1 Tg/yr in 1970 (U.S. Environmental Protection Agency, 1986). Annual emissions of manmade NO xwere some 12 percent 

higher in 1983 than in 1970, but the rate leveled off in the late 1970s and 

exhibited a small decline from about 1980 through 1982 (U.S. Environmental 

Protection Agency, 1984). The increase over the period 1970 through 1983 had 

two main causes: (1) increased fuel combustion in stationary sources such as 

power plants; and (2) increased fuel combustion in highway motor vehicles, as 

the result of the increase in vehicle miles driven. Total vehicle miles 

driven increased by 42 percent over the 14 years in question. 

Estimated biogenic NO xemissions are based on uncertain extrapolations 

from very limited studies, but appear to be about an order of magnitude less 

than manmade NOxemissions. 

1.2.5.2 Representative Concentrations in Ambient Air. 

1.2.5.2.1 Hydrocarbons in urban areas. Most of the available ambient air 

data on the concentrations of nonmethane hydrocarbons (NMHC) in urban areas 

have been obtained during the 6:00 to 9:00 a.m. period. Since hydrocarbon 

emissions are at their peak during that period of the day, and since atmospheric 

dispersion is limited that early in the morning, NMHC concentrations measured 

then generally reflect maximum diurnal levels. Representative data for urban 

areas show mean NMHC concentrations between 0.4 and 0.9 ppm. 

The hydrocarbon composition of urban atmospheres is dominated by species 

in the C 2to C10molecular-weight range. The paraffinic hydrocarbons (alkanes) 

are most prominent, followed by aromatics and alkenes. Based on speciation 

data obtained in a number of urban areas, alkanes generaliy constitute 50 to 

60 percent of the hydrocarbon burden in ambient air, aromatics 20 to 30 percent, 

with alkenes and acetylene making up the remaining 5 to 15 percent (Sexton and 

Westberg, 1984). 

1.2.5.2.2 Hydrocarbons in nonurban areas. Rural nonmethane hydrocarbon 

concentrations are usually one to two orders of magnitude lower than those 

1-17 
measured in urban areas (Ferman, 1981; Sexton and Westberg, 1984). In samples 

from sites carefully selected to guarantee their rural character, total NMHC 

concentrations ranged from 0.006 to 0.150 ppm C(e.g., Cronn, 1982; Seila, 

1981; Holdren et al., 1979). Concentrations of individual species seldom 

exceeded 0.010 ppm C. The bulk of species present in rural areas are alkanes; 

ethane, propane, n-butane, iso-pentane, and n-pentane are most abundant. 

Ethylene and propene are sometimes present at <0.001 ppm C, and toluene is 

usually present at —0.001 ppm C. Monoterpene concentrations are usually 

<0.020 ppm C. During the summer months, isoprene concentrations as high as 

0.150 ppm C have been measured (Ferman, 1981). The maximum concentrations of 

isoprene usually encountered, however, are in the range of 0.030 to 0.040 

ppm C. 

1.2.5.2.3 Nitrogen oxides in urban areas. Concentrations of NO x , like hydrocarbon concentrations, tend to peak in urban areas during the early morning, 

when atmospheric dispersion is limited and automobile traffic is dense. Most 

NOX is emitted as nitric oxide (NO), but the NO is rapidly converted to NO 2 , 

initially by thermal oxidation and subsequently by ozone and peroxy radicals 

produced in atmospheric photochemical reactions. The relative concentrations 

of NO versus NO2fluctuate day-to-day, depending on diurnal and day-to-day 

fluctuations in ozone levels and photochemical activity. 

Urban NOxconcentrations during the 6:00 to 9:00 a.m. period in 10 cities 

ranged from 0.05 to 0.15 ppm in studies done in the last 5 to 7 years (e.g., 

Westberg and Lamb, 1983; Richter, 1983; Eaton et al., 1979), although concentrations two to three times higher occur in cities such as Los Angeles. 

Concurrent NMHC measurements for these 10 cities showed that NMHC/NO xratios 

ranged from 5 to 16. 

1.2.5.2.4 Nitrogen oxides in nonurban areas. Concentrations of NO xin clean 

remote environments are usually <0.5 ppb (Logan, 1983). In exceptionally 

clean air, NOxconcentrations as low as 0.015 ppb have been recorded (Bollinger 

et al., 1982). Concentrations of NO xat nonurban sites in the northeastern 

United States appear to be higher than NO xconcentrations in the west by a 

factor of ten (Mueller and Hidy, 1983). From the limited amount of data 

available, NOxconcentrations in unpopulated nonurban areas in the west average 

<1 ppb; but in nonurban northeastern areas average NO xcan exceed 10 ppb. 

1-18 
1.2.6 Source-Receptor (Oxidant-Precursor) Models 

In order to apply knowledge of the atmospheric chemistry of precursors, 

and of ozone and other photochemical oxidants, during their dispersion and 

transport, models describing these phenomena have been developed in a variety 

of forms over the past 15 years. Most of these models relate the rates of 

precursor emissions from mobile and stationary sources, or precursor atmaspheric concentrations, to the resulting ambient concentrations of secondary 

pollutants that impact receptors at downwind sites. For this reason they have 

been described as source-receptor models. 

Current air quality, or source-receptor, models can be classified as 

either statistical or computational-dynamic. Statistical models are generally 

based on a statistical analysis of historical air quality data, and are not 

explicitly concerned with atmospheric chemistry or meteorology. An example of 

statistical models is the linear rollback concept. 

Computational, or dynamic, models attempt to describe mathematically the 

atmospheric chemicai and physical processes influencing air pollution formation and impacts. Examples of computational models include trajectory and 

fixed-grid airshed models. Two phenomenologically different approaches have 

been employed in dynamic models with respect to - the coordinate systems chosen. 

A coordinate system fixed with respect to the earth is termed Euierian, while 

in Lagrangian models the reference frame moves with the air parcel whose 

behavior is being simulated. 

1.2.6.1 Trajectory Models. In trajectory models, a moving-coordinate system 

describes pollutant transport as influenced by local meteorological conditions. 

Trajectory models provide dynamic descriptions of atmospheric source-receptor 

relationships that are simpler and less expensive to derive than those obtained 

from fixed-cell models. 

The simpiest form of, trajectory model is the empirical kinetic modeling 

approach (EKMA). This approach was developed from earl.ier efforts (Dimitriades, 

1972) to use smog chamber data.to develop graphical relationships between 

morning NMOC and NO xlevels and afternoon.maximum concentrations of ozone. In 

applying EKMA, the Ozone Isopleth Plotting Package (OZIPP) (Whitten and Hogo, 

1978) is used to generate ozone isoplet.hs at.various levels of sophistication 

corresponding to "standard" EKMA, "city-specific" EKMA, or the simplified 

trajectory model (F.R., 1979). The EKMA isopleths generated are used to 

determine the relative degree of control of precursor emissions needed to 

achieve a given percentage reduction in ozone. 

1-19 
The use of EKMA in ozone abatement programs is relatively widespread. It 

is therefore worth noting the general control implications of EKMA isopleths. 

For areas with high levels of morning precursor emissions and meteorology 

conducive to oxidant formation, such as Los Angeles, for example, EKMA isopleths 

predict that (1) at high NMOC/NOxconcentration ratios, reductions in NOxwill 

decrease ozone formation; (2) at moderate NMOC/NO xratios, reductions in NMOC 

and NOxwill decrease ozone formation; and (3) at very low NMOC/NO xratios, 

increases in NOxwill inhibit ozone formation. These predictions cannot'be 

assumed to apply to a11 urban areas, or even to all high-oxidant urban areas, 

since the shape of the EKMA isopleths is a function of numerous factors, many 

of which are location-specific. For discussions of the specific assumptions 

employed in EKMA and the underlying chemistry and meteorology, the primary 

literature should be consulted (e.g., Dimitriades, 1970, 1972, 1977a,b; Dodge, 

1977a,b; Whitten and Hogo, 1977; U.S. Environmental Protection Agency, 1977, 

1978; Whitten, 1983). Likewise, the primary literature should be consulted 

for additional data and discussions on the respective effects on ozone formation of controlling NMHC and NO x(e.g., Liu and Grisinger, 1981; Chock et al., 

1981; Kelly, 1985; Kelly et al., 1986; Glasson and Tuesday, 1970; Dimitriades, 

1970, 1972, 1977a,b). 

1.2.6.2 Fixed-Grid Models. Fixed-grid models, also called regional airshed 

models, are based on two- or three-dimensional arrays of grid cells and are 

the most sophisticated source-receptor models presently available. Such 

models are computationally complex and require the most extensive set of input 

data; but they also provide the most realistic treatment of the various processes 

involved in photochemical air pollution formation. 

1.2.6.3 Box Models. Box models (Hanna, 1973; Demerjian and Schere, 1979; 

Derwent and Hov, 1980) are the simplest of dynamic,models. ~ They treat the 

atmosphere as a single cell, bounded by the mixing layer, having an area on 

the order of 100 square miles. 

1.2.6.4 Validation and Sensitivity Analyses for Dynamic Models. All presently available source-receptor models require a degree of simplifying assump- 

° tions to deal with practical limitations imposed by existing computer capabilities, time and cost constraints, or lack of knowledge concerning inputs such 

as boundary conditions, emissions, or detailed reaction mechanisms. The 

reliability and applicability of any particular model therefore depends upon 

its specific limitations, data requirements, and degree of validation against 

1-20 
experimental data from ambient air measurements or environmental chamber runs. 

Reliabiiity and applicability also depend on the quality of the chemical 

kinetics mechanisms used to define the 0 3-HC-NOx relationship. 

Attempts are made to validate model predictions by comparing them with 

real observations; and operating parameters are often varied to determine the 

sensitivity of the model to respective parameter changes (Gelinas and Vajk, 

1979). In addition, the extent of agreement between the results from two 

simulations can be tested. In this way, completely different models may be 

compared, or an internal component, such as the chemical kinetics mechanisms, 

may be substituted and the model run again to ascertain the effect of such 

substitutions. 

1.3 SAMPLING AND MEASUREMENT OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS AND 

THEIR PRECURSORS 

1.3.1 Sampling and Measurement of Ozone and Other Photochemical Oxidants 

The analysis of ozone and other, related atmospheric oxidants includes 

requirements for representative sampling, specific and sensitive measurement 

methodologies, methods for the generation of standard samples, absolute methods 

for the calibration of these standards, and procedures by which to provide 

quality assurance for the whole measurement process. In this summary, recommended procedures are given for all of these analytical steps. Because of the 

large existing data base that employed measurements for "total oxidants," 

non-specific iodometric techniques are discussed and compared to current 

specific 0 3 measurements. 

1.3.1.1 Quality Assurance and Sampling. A quality assurance program is 

employed by the U.S. Environmental Protection Agency for assessing the accuracy 

and precision of monitoring data and for maintaining and improving.the quality 

of ambient air data. Procedures and operational details have been prescribed 

in each of the following areas: selection of analytical methods and instrumentation (i.e., reference and equivalent methods}; method specifications for 

gaseous standards; methods for primary and secondary (transfer standards) 

calibration; instrumental zero and span check requirements, including frequency 

of checks, multiple-point calibration procedures, and preventive and remedial 

maintenance requirements; procedures for air pollution episode monitoring; 

methods for recording and validating data; and information on documenting 

- 1=21 
quality control (U.S. Environmental Protection Agency, 1977b). Design criteria 

for 03 monitoring stations, to help ensure the quality of aerometric data, 

have been established (U.S. Environmental Protection Agency, 1977a; National 

Research Council, 1977). 

1.3.1.2 Measurement Methods for Total Oxidants and Ozone. Techniques for the 

continuous monitoring of total oxidants and 0 3 in ambient air are summarized 

in Table 1-1. The earliest methods used for routinely monitoring oxidants in 

the atmosphere were based on iodometry. When atmospheric oxidants are absorbed 

in potassium iodide (KI) reagent, the iodine produced, 

0 3 + 3I + H20 -> I 3 + 02 + 20H 

is measured by ultraviolet absorption in colorimetric instruments and by 

amperometric means in electrochemical instruments. The term "tatal oxidants" 

is of historical significance only and should not be construed to mean that 

such measurements yield a sum of the concentrations of the oxidants in the 

atmosphere. The various oxidants in the atmosphere react to yield iodine at 

different rates and with different stoichiometries. Only ozone reacts immediately to give a quantitative yield of iodine. As discussed below, the total 

oxidants measurement correlates fairly well with the specific measurement of 

ozone, except during periods when significant nitrogen dioxide (NO2 ) and 

sulfur dioxide (S0 2 ) interferences are present. The major problem with the 

total oxidants measurement was the effect of these interferences. Total 

oxidants instruments have now been replaced by specific ozone monitors in all 

aerometric networks and in most research laboratories. Biases among and 

between total oxidants and ozone methods are still important, however, for 

evaluating existing data on health and welfare effects levels where concentrations were measured by total oxidants methods. 

The reference method promulgated by EPA for compliance monitoring for 

ozone is the chemiluminescence technique based on the gas-phase ozone-ethylene 

reaction (F.R., 1971). The technique is specific for ozone, the response is a 

linear function of concentration, detection limits of 0.001 to 0.005 ppm are 

readily obtained, and response times are 30 seconds or less. Prescribed 

methods of testing and prescribed performance specifications that a commercial 

analyzer must meet in order to be designated as a reference method, or an 

equivalent method have been published by EPA (F.R., 1975). An analyzer may be 

1-22 
d U 

C 

m 

L 

d 

w 

ai 

o: 

N 

w 

~ 

O' 

H 

Z 

S 

CJ 

LtJ 

H 

ca 

z 

Ce 

d 

F~- 

Z 

d 

m 

W 

Z 

d 

AJ 

d 

LL_ 

0 

>- 

ae 

~ 

~ 

~ 

tn 

r-i 

~ 

W 

J 

m 

Q 

F- 

~ 

G1 

U 

C 

L i 

o d 

•,'7 4- 

ro s 

z 4-) 

c 

ro 

N 

aU_ 

N 

C aQ 00 

n ai 

tn 

N ^ 

E 

~ 

~ • E 

E ~ 

7 c 

E O_ • C +; 

r U 

~ w 

+~ N 

'O 

a 

N 

C 

0 

n 

tn 

N 

0: 

~ 

C 

N 

af ~ O 

N 

~ 

I G1 

i 

G • U 

~ • L 

I a 

N 

n 

Ol 

rl 

~ 

Y 

ro 

L 

0 

S 

v 

c 

ro 

C ~ O 

E 

3 

o 

m 

U 

E 

c 

d 

+1 LP7 

ro N 

L 

4.) 4-) 

ro 

a

Ln

i t~ 

rL 

~ uo 

N(n 

n.n 

~ ro 

~ 

M 

LO 

Ol 

rl 

~ 

N ^ 

r Q1 

C v 

4J 

m • 

~ ro ro +j ai 

c 

ro ro 

E 3 

r O 

J H 

~ 

H 

Y 

~ 

O 

ri 

— 

~IiO 

00 

N r1 +

v 

 ~ 

~ 

N N 00 

z Ln 

O 

U1 

4-) 

~ 

c 

.~ 

If'1 

O 

4~ 

M 

E 

n 

n 

d 

rl 

O 

0 

(n 

a-) 

C 

r- ~ o 

ro v 

.4~ •.- 

I- O 

a-~ 

ro 

Y 'O 00 

aQ 

(3) 

 l0 

N 

v72 oa n 

U 

IJl }7 

7 N 

O E 

o .r 

C L 

~ o 

c o 

U V 

M 

n 

O — — C1 

l0 N tn rl 

01 (p tD v 

rl ~ 01 

vN ~ +O 

~ F\ N 

L V Q1 (L) 40- GJ r-i rt O 

r• 'O O ~

C • +~ 2 

a r• ar 

ro ro ~ 

cN ++ mro 

roc OL w 

rtfco ~L c 

a~ 3 s ai 

3+)•r al > 

Gl Vi G1 

i ro O O +) 

m S F- Z N 

~ 

~ 

2

00 

t 

+ ~

0 r-I 

v v 

 m 

GJ 

N N C 

0 0 0 

z cn z 

V1 

V 

c 

a 

~ aU

i 

o U) 

C 

0 

• E M 

rl V 

E E 

n CL. 

O U') 

ri O 

0 0 

0 0 

U 

Na 

+J U 

C N 

r• ro a 

ro w 

41 7 r I 

f- O O 

iJ 

m 

d 

~~ II j, N 

O S t f0 

~Q .0 n W a~ ~I 

ai 

U 

ro C 

u ai 

U 

•E 

~ n 

d N 

N L C 

7 U 

O O 

•E 

o s o 

C +~ 

U +1 N E 

G r N 

O N L 

U U 

1-23 

O 

~ n 

ct C~ lD rl 

~ ro 

rn 41 

rl a~ ~.. 

c 

i o 

N N 

c ar 

Of•O 

ar o 

C S 

' a 

' C 

O 

z 

.~ 

4J 

v 

0 

c 

v 

N 

c 

0 

V 

d 

~ 

rl 

O 

V M 

' E 

l7. 

E 

n d. 

a 

r-I Ln 

O O 

0 0 

'o 0 

V U 

W W • U • U 

N Ol ~ n n 

y ' N 

dJ 

O O 

m 

N 

C 

• E ~ 0 

V (7 

O I C 

.0 O 

~ z 

a~ 

U l 

c 

ai 

U 

N 

N 4- ~ 

C y L 

r_ 4,1 

• E i O G1 

> O 

~ 

• E L O 

N 4J a 

U d 

1 

I- +1 O 

rl .0 O 

I i-) L 

I L N 

ro •r t 

m ar •r 

aL Ln tn 

a) vu H ~ 

s o 

~ 

o n . 

N C O 

G1 O GJ 

p.,' • 4•i 

+~ u 

s a0d 

L n 

Q +) X 

G N 

•

ro ro 

r u G1 

C C •O 

L O 

~ u ro 

.r L E ro d O 

U L N 

v G 

L. 

Op• 

~ o io m ~ E L 

> 

 s 

L O CU 

~ •r 

w ro +-) 

O 

'n 4-~ . s. H o 

ar n • 

t7 cm E G n~n 

C O O E r n 

~ •i 

L O ^ Q) 

iJ +J L 

G •r C 

- C G! OJ 

O tn >.. 

M E a~ •r 

4 M o `° ~ a ° 

41 +> t0 

G C 16 

43) N ~ i0- E a. O a ro to> v> > as rtr ai E •

c 

 s-. +O

i 

I L ~ V 'O 

O O L 41 V- L GJ cn 

E O 

a c 

Q1 •r C Gl +~ C p 

L 

.0 

 R7 

O Gl +> 

n +J n v> 

G7 i C 7 L o o E 

na 

C y L n 

Gl L ro L 

dU C/ 

.a C O +~ 

ro a >, w 

L L 

d 4J 

aE > U N 

N ro•rr- +3 C1 O ^ 

M ~roa~i 

4- L ^ C. 

i.) Z. ~ cn 

c a a~ ai ai +J aD 

c aEi ~ E m 

O U C uni N c d• c 

a~ r (a J) 

 o 

L C U N •r 

O w 4J ro ~ 0 L 

4- C 01.0 C 

Of •r L Gl 

II ~ -Nou 

V1tN C 

lL Q Z m U 

16 -0 U 
designated as a reference method if it is based on the same principle as the 

reference method and meets performance specifications. An acceptable equivalent method must meet the prescribed performance specifications and also show 

a consistent relation with the reference method. 

The designated equivalent methods are based on either the gas-solid 

chemiluminescence procedure or the ultraviolet absorption procedure (Table 

1-1). The first designated equivalent method was based on ultraviolet absorption by ozone of the mercury 254 nm emission line. The measurement is in 

principle an absolute one, in that the ozone concentration can be computed 

from the measured transmission signal since the absorption coefficient and 

pathlength are accurately known. In the gas-solid chemiluminescence analyzer, 

the reaction between ozone and Rhodamine-B adsorbed on activated silica produces chemiluminescence, the intensity of which is directly proportional to 

ozone concentration. 

1.3.1.3Calibration Methods . A11 the analyzers discussed above must be 

calibrated periodically with ozonized air streams, in which the ozone concentration has been determined by some absolute technique. This includes the 

ultraviolet (UV) absorption analyzer, which, when used for continuous ambient 

monitoring, may experience ozone losses in the inlet system because of contamination. 

A primary ozone calibration system consists of a clean air source, ozone 

generator, sampling manifold, and means for measuring absolute ozone concentration. The ozone generator most often used is a photolytic source employing a 

mercury lamp that irradiates a quartz tube through which clean air flows at a 

controlled rate (Hodgeson et al., 1972). Once the output of the generator has 

been calibrated by a primary reference method, it may be used to calibrate 0 3 

transfer standards, which are portable generators, instruments, or other 

devices used to calibrate analyzers in the field. Reference calibration 

procedures that have been used for total oxidants and ozqne-specific analyzers 

in the United States are summarized in Table 1-2. 

The original reference calibration procedure promulgated by EPA was the 

1 percent neutral buffered potassium iodide (NBKI) method (F.R., 1971). This 

technique was employed in most of the United States, with the exception of 

California. The California Air Resources Board (CARB) (1976) and the Los 

Angeles Air Pollution Control District (LAAPCD) employed different versions of 

iodometric techniques. Procedural details of the calibration methods are 

1-24 
I 'a 

~ 

Q1 

O 

U') 

r-i 0 

0 

+I 

O 

M 

O 

r-i 

~ 

c 

a~ 

G1 L 

n 

1 

~ ^ 

C~ 01 Ql 

G1 r-i 

U O1C75.- 

a vrna 

L Lri C 

cu 

4F() v 

 to 

d i-) 

L L r L N 

L N C N 40- 

E L +~ ~ m 

L n r n L 

a ¢ I4-) 4J 

C N C 

N }.1 N 

L 4-) L 

n N n 

Ql M 

r 1~ Q I , 

Q -i W ri 

+-3 o 

m •r 

N ~ 

~ •r N N 

a c +~ E 

nC •X r N L o E m 

N 13'f U n Z 

rt NC S O O 

OI•r .~.~ LO L 

MS - O ~ 4- Z 

(L) 

U 

C 

a~ 

L 

f11 4-. 

-a S- 

^ 

S C 

O L 

U a . c 

L m N 

4-) 

~ Cf 

z 

N L 

L +~ 

~O E 

4- O 

O 4-) 

~ O 

_ 

aJ 

U 

C 

d 

L 

C1 

4- 

L L 

~ 

i y 

E O 

L Q a 

U') 

n 

rn 

r•i 

O ~ 

a •r 

Q +) 

J 7 

~ 

o_ 

~ 

v 

N O 

N•- 

L m aL 

N •r 

C.s ~ 

m 

0 

0 

+I 

O 

O 

r-I 

0) 

r L 

C GJ 

L U 

¢ a 

01 

~ 

cn 

ri 

L!'f 

Q Ia. 01 

W rI 

~ 

M 

O 

H 

Y N 

a O 

L •r 

m +-) 

ro O 

N N 

S-. 

N 

~ 4- 7 

a 

a 

• U 

ro 

LO 

~ ~ 11 

Y L 

a~ ~On n 

Y 

¢ 

m 

2 

0) U 

C 

CJ 

L 

C1 

4- i O 

L 

U 

Y 

m 

z 

m 

cN 

W 

0 

z

aLU

s 

CU 

F-- 

Z 

0 

F- 

¢ 

d' 

m 

J 

¢ 

U 

W 

Z 

O 

N 

0 

N 

r-I 

m 

H 

> ~ ~ 

~ o 0 

-o 0 0 

ro ~ +I +I 

m M N 'IN 

G1 U U N C C 

°La N GLOJ 

7 4- 4- CL 

L L S. O. L 

Lv L a 

m U m U 

E L E i 

L O. L Q 

a a 

C 

O 

r N 

1 ~ N lD 

LO 

I~l 

N ro rn t

cn

-i 

•C a ri ~ 

m a ri m •r 

I LT C Q 1~ 

'. i. m G. 01 Q C 

O W r-1 U 7 

v 4-) 

ro m 

o 

"mQ G7 X Ol ~ r 

C a O a 

m m m 

a ~~ ~~ 

L 

O 

C C C N 

E o~ u0i p~ ~ 

i N ro 43) n 

[i C w 

L S-. 

~ w 4•- 4- 

o n 

iJ dJ Cb i-) OO C ci3 m 

C1 C lD L lD 

ami Y O II ~ o II 

3~ nn ~ an 

aY 

O m 

~ z 

N aQ 

N 

c 0 E 

O i•) 

L 7 

-G 4- O 

QI N 

L C N 

7 • O) C 

a C N v m a 

O p L ~ 

4-) L N 

~ N L 

o c°1i m v 

v ro 

C N N N 

a 

4-- 

G7 

+-) 

1 w 

O L O O 

r ~ 

N 

UJ 

> i C 

O 

N 

iP N 4J 

ro L a m 

y 

co 

+~ ro N n N N 

s• E o r O N 4.1 N L > 

i •O + 0.~ S.O. ~ o 

a°i " w ~ 

L c <u 

n +J m 4-) 

C N N 

+J a (U Q1 ~ 

C rI 

a) n aa , ro 

N a N C N 

7 a 7 O 7 

C N 

C O O1 p 41 O a Q7 ro O O ro L c x + ~ 

N N L 

L > U a 

47 N C ~ 

N N +J m L 

+1 C N a 

> 

r y }t 

r a ~- • L .: L 

"a 

a 

C 

~ rn 

~ I~ 

o 

tn 

Q1 Q 

-roa ~ 

+~ O rl 

1~ A O r ON N Q! L }I 

GJ U al r 7 

i O C > W r 

U O 7: N 

m •C a 1 • L 4- lD 

O_ O OJ 1- Q 4F m i--~ U 01 U N L 

an 

O ri a L a 

+J C O ~ .n i.~ Nro ro 

m 1N N d a 

L a O1 C 

~ ar ro o +1 • ro 

a v c t m LO fj 

O .G O 4-1 +) r- t, N 

~ ~ o m E ai ri ~. ro al +J al ~ 

E C N L N +~ •• a 

U N •Y f C C r- a 

ar a a r m c 

•L L L C1 L N 

d ani 40- v 40- 

a N 0/ ~ i O O O1 

O i•~ N . ro N Ql ¢, }1 L 

s rn L ~ o ai • L m a-1 m N L r > y y v +J to m _N o 7 r0 

c 

4J m ai 

O C d a >>CO > 07 L 

N • m 4- +J •F~ 01 O S- Ua N +.) N GJ ri L O GJ m L Q E -P n U 

U a) • al O E O U E C •14 O N O L N C O O O L r ri n 

L O L C 4- 

,n o N 

C t L C ~i a L L 

~ I--• o_ O ~ W 

ro m U a N 4- O) 

1-25 
summarized in Table 1-2. A number of studies conducted between 1974 and 1978 

revealed several deficiencies with KI methods, the most notable of which were 

poor precision or interlaboratory comparability and a positive bias of NBKI 

measurements relative to simultaneous absolute UV absorption measurements. 

The positive bias observed is peculiar to the use of phosphate buffer in the 

NBKI techniques. The bias was not observed in the unbuffered LAAPCD method 

(which nevertheless suffered from poor precision), nor in the 1 percent EPA KI 

method without phosphate buffer (Hodgeson et al., 1977), nor in a KI procedure 

that used boric acid as buffer (Flamm, 1977). A summary of resu1ts of these 

prior studies was presented in the previous criteria document (U.S. Environmental Protection Agency, 1978) and in a review by Burton et al. (1976). 

Correction factors for converting NBKI calibration data to a UV photometry 

basis are given in Table 1-2 and discussed in Chapter 4(Section 4.2.4.2.1). 

Subsequently, EPA evaluated four alternative reference calibration procedures and selected UV photometry on the basis of superior accuracy and precision 

and simplicity of use (Rehme et al., 1981). In 1979 regulations were amended 

to specify UV photometry as the reference calibration procedure (F.R., 1979). 

Laboratory photometers used as reference systems for absolute 0 3 measurements 

have been described by DeMore and Patapoff (1976) and Bass et al. (1977). 

These laboratory photometers contain long path cells (1 to 5 m) and 

employ sophisticated digital techniques for making effective double beam 

measurements of small absorbancies at low ozone concentrations. A primary 

standard UV photometer is one that meets the requirements and specifications 

given in the revised ozone calibration procedures (F.R., 1979e). Since these 

are currently available in only a few laboratories, EPA has allowed the use of 

transfer standards, which are devices or methods that can be calibrated against 

a primary standard and transferred to another location for calibration of 0 3 

analyzers. Examples of transfer standards that have been used are commercial 

03 photometers, calibrated generators, and gas-phase titration (GPT) apparatus. 

Guidelines on transfer standards have been published by EPA (McElroy, 1979). 

1.3.1.4• Relationships of Total Oxidants and Ozone Measurements. The temporal 

and quantitative relationship, between simultaneous total oxidants and ozone 

measurements has been examined in this chapter because of the existence of a 

data base obtained by total oxidants measurements. Such a comparison is complicated by the relative scarcity of simultaneous data, the presence of both 

positive (NO 2 ) and negative (S0 2 ) interferences in total oxidants measurements 

1-26 
of ambient air, and the change in the basis of calibration. In particular, 

the presence of NO2 and S02 interferences prevent the establishment of a 

definite quantitative relationship between ozone and oxidants data. Nevertheless, some interesting conciusions can be drawn and are summarized below. 

Studies concluded in the early to mid - 1970s were reviewed in the previous 

criteria document (U.S. Environmental Protection Agency, 1978). Averaged data 

showed fairly good qualitative and quantitative agreement between diurnal 

variations of total oxidants and ozone. For example, uncorrected monthly 

averaged data from Los Angeles and St. Louis showed distinct morning and 

evening peaks resulting from NO 2 interference (Stevens et al., 1972a,b). The 

most recent comparison in the literature involved simultaneous ozone and total 

oxidant measurements in the Los Angeles basin by the California Air Resources 

Board (1978) i n 1974, 1976, and 1978. The maximum hourly data pai rs were 

correlated (Chock et al., 1982) and yielded the following regression equation 

for 1978, in which a large number (927) of data pairs were available: 

Oxidant (ppm) = 0.870 0 3 + 0.005 

(Correlation coefficient = 0.92) (1-2) 

The oxidant data were uncorrected for NO 2 and S0 2 interferences, and on individual days maximum oxidant averages were both higher than and lower than ozone 

averages. 

In,summary, specific ozone measurements agr.eefairly well with total oxidants corrected for NO 2 and S02 interferences,.and in such corrected totai 

oxidants measurements ozone is the dominant contributor. Indeed; it is difficult to discern the presence of other oxidants in corrected total oxidant 

data. Without corrections there can be major temporal discrepancies between 

ozone and oxidants data, which are primarily a result of oxidizing and reducing 

interferences with KI measurements. As a result of these interferences, on 

any given day the total oxidant values may be higher than or lower than simul- '. 

taneous ozone data. The measurement of ozone is a more reliable indicator 

than total oxidant measurements of oxidant air quality. 

1.3.1.5 Methods for Sampling and Anal sis of Peroxyacetyl Nitrate and Its 

Homologues. Only two analytical techniques have been used to obtain significant data on ambient peroxyacetyl nitrate (PAN) concentrations. These are gas 

chromatography with electron capture detection (GC-ECD) and long-path Fourier 

1-27 
transform infrared (FTIR) spectrometry. Atmospheric data on PAN concentrations 

have been obtained predominantly by GC-ECD because of its relative simplicity 

and superior sensitivity. These techniques have been described in this chapter 

along with attendant methods of sampling, PAN generation, absolute analysis, 

and calibration. 

By far the most widely used technique for the quantitative determination 

of ppb concentrations of PAN and its homologues is GC-ECD (Darley et al., 

1963; Stephens, 1969). With carbowax or SE30 as a stationary phase, PAN, 

peroxypropionyl nitrate (PPN), peroxybenzoyl nitrate (PBzN), and other homologues (e.g., peroxybutyryl nitrate) are readily separated from components such 

as air, water, and other atmospheric compounds, as well as ethyl nitrate, 

methyl nitrate, and other contaminants that are present in synthetic mixtures. 

Electron-capture detection provides sensitivities in the ppb and sub-ppb 

ranges. Typically, manual air samples are collected in 50- to 200-m1 ungreased 

glass syringes and purged through the gas-sampling valve. Continuous analyses 

are performed by pumping ambient air through a gas sampling loop of an automatic valve, which periodically injects the sample onto the column. Samples 

collected from the atmosphere should be analyzed as soon as possible because 

PAN and its homologues undergo thermal decomposition in the gas phase and at 

the surface of containers. The recent work of Singh and Salas (1983a,b) on 

the measurement of PAN in the free (unpolluted) troposphere (see Chapter 5) is 

illustrative of current capabilities for measuring low concentrations. A 

minimum detection limit of 0.010 ppb was obtained. 

The literature contains conflicting reports on the effects of variable 

relative humidity on PAN measurements by GC-ECD. If a moisture effect is 

suspected in a PAN analysis, the bulk of this evidence suggests that humidification of PAN calibration samples (to a range approximating the humidity of 

the samples being analyzed) would be advisable. 

Conventional long-path infrared spectroscopy and Fourier-transform infrared spectroscopy (FTIR) have been used to detect and measure atmospheric 

PAN. Sensitivity is enhanced by the use of FTIR. The most frequently used IR 

bands have been assigned and the absorptivities reported in the literature 

(Stephens, 1964; Bruckmann and Willner, 1983; Holdren and Spicer, 1984) permit 

the quantitative analysis of PAN without calibration standards. The absorptivity of the 990 cm-1 band of PBzN, a higher homologue of PAN, has been reported 

by Stephens (1969). Tuazon et al. (1978) describes an FTIR system operable at 

1- 28 
pathlengths up to 2 km for ambient measurements of PAN and _other trace constituents. This system employed an eight-mirror multiple reflection cell with a 

22.5-m base path. Tuazon et al. (1981b) reported maximum PAN concentrations 

ranging from 6 to 37 ppb over a 5-day smog episode in Claremont, CA. Hanst et 

al. (1982) made measurements with a 1260-m folded optical path system during a 

2-day smog episode in Los Angeles in 1980. An upper limit of 1 ppb of PBzN 

was placed, and the maximum PAN concentration observed was 15 ppb. The large 

internal surface area of the White cells may serve to promote the decomposition 

or irreversible adsorption of reactive trace species such as PAN. High volume 

sampling rates and inert i-nternal-surface materials are used to minimize these 

effects. 

Because of the thermal instability of dilute PAN samples and the explosive 

nature of liquefied PAN, calibration samples - are not commercially avail-able; 

and must be prepared. Earlier methods used to synthesize PAN have been summarized by Stephens (1969). The photolysis of alkyl nitrites in oxygen was the 

most commonly used procedure and.may still be used by some investigators. As 

described by Stephens et al. (1965), the liquefied crude mixture obtained at 

the outlet of the photolysis chamber is purified by preparative-scale GC. 

[CAUTION: Both the liquid crude mixture and the purified PAN samples are 

violent1y explosive and should be handled behind explosion shields using 

plastic fu11-face protection, gloves, and a leather coat at all times.] The 

pure PAN is usually diluted to about 1000 ppm in cylinders pressurized with 

nitrogen to 100 psig and stored at reduced temperatures, <15°C. 

Gay et al. (1976) have used the photolysis of chlorine: aldehyde: nitrogen 

dioxide mixtures in air or oxygen for the preparation of PAN and a number of 

its homologues at high yields. This procedure has been utilized in a portable 

PAN generator that can be used for the calibration of GC-ECD instruments in 

the field (Grosjean, 1983; Grosjean et al., 1984). 

Several investigators have recently reported on a condensed-phase synthesis 

of PAN by nitration of peracetic acid in a hydrocarbon solvent. High yields 

are produced of a pure product free of other aikyl nitrates (Hendry and Kenley, 

1977; Kravetz et al., 1980; Nieisen et al., 1982; Holdren and Spicer, 1984). 

After the nitration is complete, the hydrocarbon fraction containing PAN 

concentrati.ons of 2 to 4 mg/ml can be stored at -20°C for periods longer than 

a year (Holdren and Spicer, 1984). 

1-29 
The most direct method for absolute analysis of these PAN samples is by 

infrared absorption, using the IR absorptivities mentioned earlier. Conventional IR instruments and 10-cm gas cells can analyze gas standards of concentrations >35 ppm.. Liquid microcells can be used for the analysis of PAN in 

isooctane solutions. The alkaline hydrolysis of PAN to acetate ion and nitrite 

ion in quantitative yield (Nicksic et al., 1967) provides a means independent 

of infrared for the quantitative analysis of PAN. Following hydrolysis, 

nitrite ion may be quantitatively analyzed by the Saltzman.colorimetric procedure (Stephens, 1969). The favored procedures now use ion chromatography to 

analyze for nitrite (Nielsen et al., 1982) or acetate (Grosjean, 1983; Grosjean 

et al., 1984) ions. Another calibration procedure has been proposed that is 

based on the thermal decomposition of PAN in the presence of excess and measured 

NO concentrations (Lonneman et al., 1982). The acetylperoxy radical, CH 3C(0)02 , 

and its decomposition products rapidly oxidize nitric oxide (NO) to NO2 with a 

stoichiometry that has been experimentally determined. 

1.3.1.6 Methods for Sampling and Analysis of Hydroqen Peroxide. Hydrogen 

peroxide (H2O2 ) is significant in photochemical smog as a chain terminator; as 

an index of the hydroperoxyl radical (H02 ) concentration (Bufalini and Brubaker, 

1969; Demerjian et al., 1974); and as a reactant in the aqueous-phase oxidation 

of S02 to 504-2 and in the acidification of rain (Penkett et a1.,.1979; Dasgupta, 

1980a,b; Martin and Damschen, 1981; Overton and.Durham, 1982). 

One of the major problems, however, in assessing the role of atmospheric 

H2O2 has been a lack of adequate measurement methodology. Earlier measurements 

(Gay and Bufalini, 1972a,b; Bufalini et al., 1972; Kok et a1., 1978a,b) reporting 

H2O2 concentrations of 0.01 to 0.18 ppm are now believed to be far too high, 

and to be the result of artifact H2O2 formation from reactions of ,absorbed 03 

(Zika and Saltzman, 1982; Heikes et a1., 1982; Heikes, 1984). Maximum tropospheric H2O2 concentrations predicted by.modeling calculations (Chameides and 

Tan, 1981; Logan et al., 1981) and observed in recent field studi, es (Das et 

al., 1983) are on the order of 1 ppb. 

Almost all of the methods used for the measurement of atmospheric H 2O 2 

have used aqueous traps for sampling. Atmospheric 0 3 , however, which is also 

absorbed at concentrations much higher than H 2O 2 , reacts in the bulk aqueous 

phase and at surfaces to produce H202 and thus is a serious interference (Zika 

and Saltzman, 1982; Heikes et al., 1982; Heikes, 1984). The removal of absorbed 

03 by purging immediately after sample collection may remove or s.ubstantially 

1-30 : .- 
reduce this interference (Zika and Saltzman, 1982; Das et al., 1983). Another 

problem identified with aqueous sampling is that other atmospheric species (in 

particular, S02 ) may interfere with the generation of H 2O2 in aqueous traps" 

and also react with collected H 2O 2 to reduce the apparent concentration measured 

(Heikes et al., 1982). 

Of the techniques that have been used for the mea'surement of aqueous and 

gas-phase H 2O2 , only the chemiluminescence and enzyme-catalyzed methods are 

summarized below. The other techniques are now believed to have inadequate 

sensitivity and specificity for the atmospheric concentrations actually present. 

In addition, the use of a tunable diode infrared laser source should eliminate 

the problem associated with nearby water bands, and this method is currently 

under investigation for atmospheric measurements (unpublished work in progress, 

Schiff, 1985). + 

Hydrogen peroxide in the atmosphere may be detected at low concentrations 

by the chemiluminescence obtained from copper(II)-catalyzed oxidaton of luminol 

(5-amino-2,3-dihydro-1,4-phthalazinedione) by H 2O2 (Armstrong and Humphreys, 

1965; Kok et al., 1978a,b). This technique as initially employed suffered the 

interferences from 0 3 and S02 discussed above for aqueous traps. Das et al. 

(1982) employed a static version of the method of Kok et al. (1978a) to measure 

H20 2 concentrations in the 0.01 to 1 ppb range. In addition, samples were 

purged with argon immediately after collection to eliminate, reportedly, the, 

03 interference. Recently, a modified chemiluminescence method has been 

reported which used hemin, a blood component, as a catalyst for the luminolbased H2O 2 oxidation (Yoshizumi et al., 1984). 

The most promising chemical approach employs the catalytic activity of 

the enzyme horseradish peroxidase (HRP) on the oxidation of organic substratesby H2O2 . The production or decay of the fluorescence intensity of the-substrate 

or reaction product is measured as it is oxidized by H2O 2 , catalyzed by HRP. 

Some of the more widely used substrates have been scopoletin (6-methoxy-7- 

hydroxyl,2-benzopyrone) (Andreae, 1955; Perschke and Broda, 1961); 3-(p-hydroxyphenyl)propionic acid (HPPA) (Zaitsu and Okhura, 1980);.and leuco crystal 

violet (LCV) (Mottola et al., 1970). 

The decrease in the fluorescence"i`ntensity of scopoietin is measured as a 

function of H°0 concentration. Detection limits have been reported to be 

quite low (10?1~ M). The chief disadvantage of this approach is'that the 

concentration , of H2O2 must be within a narrow range to obtain an accurately 

1-31 
measureable decrease in fluorescence. Oxidation of LCV produces intensely 

colored crystal violet, which has a molar absorption coefficient of 10 5 M-1 ` 

cm 1 at the analytical wavelength, 596 nm. The detection limit reported was 

10-8 M in 5 cm cells. Two quite similar hydrogen donor'substrates have been 

used. Zaitsu and Okhura (1980) employed 3-(p-hydroxyphenyl) propionic acid 

and more recently the p-hydroxyphenyl acetic acid homologue is being used 

(Kunen et al., 1983; Dasgupta and Hwang, 1985). The measurement of the fluorescence intensity of the product dimer provides a quite sensitive means for the 

assay of H2O2 . 

As with 03 , H2O 2 calibration standards are not commercially available and 

are usually prepared at the time of use. The most convenient method for preparing aqueous samples containing micromolar concentrations of H 2O 2 is simply 

the serial dilution of commercial grade 30 percent H2O 2 (Fisher Ana'lytical' 

Reagent). Techniques for the convenient generation of gas-phase standards are 

not available. A technique often used for generating ppm concentrations of 

H2O2 in air involves the injection of microliter quantities of 30 percent H 2O2 

solution into a metered stream of air that flows into a Teflon bag. Aqueous 

and gas-phase samples are then standardized by conventional iodometric procedures (Allen et al., 1952; Cohen et al., 1967). 

1.3.2 Measurement of Precursors to Ozone and Other Photochemical Oxidants 

1.3.2.1 Nonmethane Organic Compounds. Numerous analytical methods have been 

employed to determine nonmethane organic compounds (NMOC) in ambient air. 

Measurement methods for the organic species may be .grouped according to three 

major classifications: nonmethane hydrocarbons, aldehydes, and other oxygenated 

compounds. 

Nonmethane hydrocarbons have been determined primarily by methods that 

employ a flame ionization detector (FID) as the sensing element. Early methods 

for the measurement of total nonmethane hydrocarbons did not provide for 

speciation of the complex mixture of organics in ambient air. The`se methods, 

still in use for analysis of total nonmethane organic compounds, are essentially 

organic carbon analyzers, since the response of the FID detector i& essentially 

proportional to the number of carbon atoms present in the organic , molecule 

(Sevcik, 1975). Carbon atoms bound, however, to oxygen, nitrogen; or halogens 

give reduced relative responses (Dietz, 1967). The FID detectorqehas been 

utilized both as a stand-alone continuous detection system (non'=speciation 

1-32 
analyzers have indicated an overall poor performance of the commercial instruments when calibration or ambient mixtures containing nonmethane organic 

compounds (NMOC) concentrations less than 1 ppm C were analyzed (e.g., Reckner, 

1974; McElroy and Thompson, 1975; Sexton et al., 1982). The major problems 

associated with the non-speciation analyzers have been summarized in a recent 

technical assistance document published by the U.S. Environmental Protection 

Agency (1981). The document also presents ways to reduce some of the existing 

problems. 

Because of the above deficiencies, other approaches to the measurement of 

nonmethane hydrocarbons are currently under development. The use of gas 

chromatography coupled to an FID isystem circumvents many of the problems 

associated with continuous non-speciation analyzers. This method, however, 

requires sample preconcentration because the organic components are present at 

part-per-billion (ppb) levels or lower in ambient air. The two main preconcentration techniques in present use are cryogenic collection and the use of 

solid adsorbents (McClenny et al., 1984; Jayanty et al., 1982; Westberg 

et al., 1980; Ogle et al., 1982). The preferred preconcentration method for 

obtaining speciated data is cryogenic collection. Speciation methods involving 

cryogenic preconcentration have also been compared with continuous nonspeciation 

analyzers (e.g., Richter, 1983). Results indicate poor correlation between 

methods at ambient concentrations below 1 part-per-million carbon (ppm C). 

Aldehydes, which are both primary and secondary pollutants in ambient 

air, are detected by total NMOC and NMHC speciation methods but can not be 

quantitatively determined by those methods. Primary measurement techniques 

for aldehydes include the chromotropic acid (CA) method for formaldehyde 

(Altshuller and McPherson, 1963; Johnson et al., 1981), the 3-methyl-2-benzothiazolene (MBTH) technique for total aldehydes (e.g., Sawicki et al., 1961; 

Hauser and Cummins, 1964), Fourier-transform infrared (FTIR) spectroscopy 

(e.g., Hanst et al., 1982; Tuazon et al., 1978, 1980, 1981a), and high-performance liquid.chromatography employing_2,4-dinitrophenyl-hydrazine derivatization (HPLC-DNPH) for aldehyde speciation (e.g., Lipari and Swarin, 1982; Kuntz 

et al., 1980). The CA and MBTH methods utilize wet chemical procedures and 

spectrophotometric detection. Interferences from other compounds have been 

reported for both techniques. The FTIR method offers good specificity and 

direct in situ analysis of ambient air. These advantages are offset, however, 

by the relatively high cost and lack of portability of the instrumentation. 

1-33 
On the other hand, the HPLC-DNPH method not only offers good specificity but 

can also be easily transported to field sites. A few intercomparison studies 

of the above methods have been conducted and considerable differences in 

measured concentrations were found. The data base is still quite limited at 

present, however, and further intercomparisons are needed. 

Literature reports describing the vapor-phase organic composition of 

ambient air indicate that the major fraction of material consists of unsubstituted hydrocarbons and aldehydes. With the exception of formic acid, other 

oxygenated species are seldom reported. The lack of oxygenated hydrocarbon 

data is somewhat surprising since significant quantities of these species are 

emitted into the atmosphere by solvent-related industries and since at least 

some oxygenated species appear to be emitted by vegetation. In addition to 

direct emissions, it is also expected that photochemical reactions of hydrocarbons with oxides of nitrogen, 03 , and hydroxyl radicals will produce significant quantities of oxygenated species. Difficulties during sample collection 

and analysis may account for the apparent lack of data. Attempts have been 

made to decrease adsorption by deactivating the reactive surface or by modifying 

the compound of interest (Osman et al., 1979; Westberg et al., 1980). Additional 

research efforts should focus on this area. 

1.3.2.2 Nitrogen Oxides . Aside from the essentially unreactive nitrous oxide 

(N20), only two oxides of nitrogen occur in ambient air at appreciable concentrations: nitric oxide (NO) and nitrogen dioxide (NO2 ). Both compounds, 

together designated as NOx , participate in the cyclic reactions in the atmosphere 

that lead to the formation of ozone. Other minor reactive oxides of nitrogen 

in ambient air include peroxyacyl nitrates, nitrogen trioxide, dinitrogen 

pentoxide, and peroxynitric acid. 

The preferred means (Federal Reference Method) of ineasuring NO and NO Z is' 

the chemiluminescence method (F.R., 1976). The measurement principle is the 

gas-phase chemiluminescent reaction of 0 3 and NO (Fontijn et al., 1970). 

While NO is determined directly in this fashion, NO 2 is detected indirectly by 

first reducing or thermally decomposing the gas quantitatively to NO with a 

converter. The reaction of NO and 0 3 forms excited NO 2 molecules that release 

light energy that is proportional to the NO concentration. Although the NO 

chemiluminescence is interference-free, other nitrogen compounds do interfere 

when directed through the NO 2 converter. The magnitude of these interferences 

is dependent upon the type of converter used (Winer et al., 1974; Joshi and 

1-34 
Bufalini, 1978). The detection limit of commerciai chemiluminescence instruments for NO 2 measurement is 2.5 pg/m3 (0.002 ppm) (Katz, 1976). 

Development of an instrument based on the chemiluminescent reaction of 

NO 2 with luminol (5-amino-2, 3-dihydro-1, 4-phthalazine dione) has been reported 

by Maeda et al. (1980). Wendel et al. (1983) have reported modifications of 

this luminol-based method in which better response time and less interference 

from 0 3 have been achieved. 

Other acceptable methods for measuring ambient NO 2 levels, including two 

methods designated as equivalent methods, are the Lyshkow-modified Griess-. 

Saltzman method, the instrumental colorimetric Griess-Saltzman method, ,the 

triethanolamine method, the sodium arsenite method, and the TGS-ANSA method 

[TGS-ANSA = triethanoiamine, guaiacol (o-methoxyphenol), sodium metabisulfite, 

and 8-aniiino-l-naphthalene sulfonic acid]. The sodium arsenite method and 

the TGS-ANSA method were designated as equivalent methods in 1977. For descriptions of these methods, the reader is referred to the EPA criteria document 

for nitrogen oxides (U.S. Environmental Protection Agency, 1982). 1Jhile some 

of these methods measure the species of interest directly, others require 

oxidation, reduction, or thermal decomposition of the sample, or separation 

from interferences, before measurement. None of these other techniques, 

however, is widely used to monitor air quality. 

Careful adherence to specified calibration procedures is essential for 

obtaining accurate NOx measurements. The U.S. Environmental Protection Agency 

(1975) has issued a technical assistance document that describes in detail the 

two acceptable calibration methods for NO x : (1) the use of standard reference 

materials (SRMs) and (2) gas-phase titration (GPT) of NO with 0 3 . The SRM for 

NO i s a cyl i nder of compressed NO i n N2 ; the mi xture i s both accurate and 

stable (Hughes, 1975). The SRM for NO 2 is the NO 2 permeation tube (0'Keeffe 

and Ortman, 1966; Scaringelli et al., 1970). The gas-phase titration, described 

by Rehme et al. (1974), is based upon the bimolecular reaction of NO with 0 3 , 

to form NO 2plus 02 . The U.S. Environmental Protection Agency (1975) recommends 

the combined use of GPT plus SRM procedures, using one technique to check the 

other. 

1-35 
1.4 CONCENTRATIONS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN AMBIENT AIR 

In the context of this document, the concentrations of ozone and other , 

photochemical oxidants found in ambient air are important for: (1) assessing 

potential exposures of human and other receptors; (2) determining the range of 

ambient air concentrations of ozone and other photochemical oxidants relative 

to demonstrated "effects levels" (Chapters 6-12); (3) determining indooroutdoor gradients for exposure analyses; (4) assessing whether the concentrations of oxidants other than ozone, singly, collectively, or in combination 

with ozone, are cause for concern; and (5) evaluating the adequacy of ozone as 

a control surrogate for other photochemical oxidants, if concentrations of the 

other oxidants are cause for concern given the effects and the "effects levels" 

of those oxidants. 

1.4.1 Ozone Concentrations in Urban Areas 

In Table 1-3, 1983 ozone concentrations for Standard Metropolitan Statistical Areas (SMSAs) having populations > 1 million are given by geographic 

area, demarcated according to United States Census divisions and regions (U.S. 

Department of Commerce, 1982). The second-highest concentrations among daily 

maximum 1-hour values measured in 1983 in the 38 SMSAs having populations of 

at least 1 million ranged from 0.10 ppm in the Ft. Lauderdale, Florida; Philadelphia, Pennsylvania; and Seattle, Washington, areas to 0.37 ppm in the Los 

Angeles-Long Beach, California, area. The second-highest value among daily 

maximum 1-hour ozone concentrations for 35 of the 38 SMSAs in Table 1-3 

equaled or exceeded 0.12 ppm. The data clearly show, as well, that the 

highest 1-hour ozone concentrations in the United States occurred in the 

northeast (New England and Middle Atlantic states), in the Gulf Coast area 

(West South Central states), and on the west coast (Pacific states). Secondhighest daily maximum 1-hour concentrations in 1983 in the SMSAs within each 

of these three areas averaged 0.16, 0.17, and 0.21 ppm, respe,ctively. It 

should be emphasized that these three areas of the United States are subject 

to those meteorological and climatological factors that are conducive to local 

oxidant formation, or transport, or both. It should also be emphasized that 9 

of the 16 SMSAs in the country with populations > 2 million are located in 

these areas. 

1-36 
TABLE 1-3. SECOND-HIGHEST OZONE CONCENTRATIONS AMONG DAILY MAXIMUM 1-hr 

VALUES IN 1983 IN STANDARD METROPOLITAN STATISTICAL AREAS WITH POPULATIONS 

> 1 MILLION, GIVEN BY CENSUS DIVISIONS AND REGIONS a 

SMSA Second-highest 

Division population, 1983 03 

and region SMSA millions concn., ppm 

Northeast 

New England Boston, MA >2 0.18 

Middle Atlantic Buffalo, NY 1 to <2. 0.12 

Nassau-Suffolk, NY >2 0.17 

Newark, NJ 1 to <2 0.25 

New York, NY/NJ >2 0.19 

Philadelphia, PA/NJ >2 0.10 

Pittsburgh, PA >2 0.14 

South 

South Atlantic Atlanta, GA >2 0.17 

Baltimore, MD >2 0.19 

Ft. Lauderdale-Hollywood, FL 1 to <2 0.10 

Miami, FL 1 to <2 0.12 

Tampa-St. Petersburg, FL 1 to <2 0.14 

Washington, DC/MD/VA >2 0.17 

South 

West South 

Central Dallas-Ft. Worth, TX >2 0.16 , 

Houston, TX >2 0.28 

New Orleans, LA 1 to <2 0.12` 

San Antonio, TX 1 to <2 0.12 , 

North Central 

East North 

Central Chicago, IL >2 0.17 

Detroit, MI >2 0.17 

Cleveland, OH 1 to <2 0.15 

Cincinnati, OH/KY/IN 1 to <2 0.15 - ~ 

Milwaukee, WI 1 to <2 0.18 

Indianapolis, IN 1 to <2 0.14 

Columbus, OH 1 to <2 0.12 

West North 

Central St. Louis, MO/IL >2 0.18 ' 

Minneapolis-St. Paul, MN/WI >2 0.13 

Kansas City, MO/KS 1 to <2 0.13 

1-37 
TABLE 1-3 (cont'd). SECOND-HIGHEST OZONE CONCENTRATIONS AMONG DAILY MAXIMUM 

1-hr VALUES IN 1983 IN STANDARD METROPOLITAN STATISTICAL AREAS 

WITH > 1 MILLION, GIVEN BY CENSUS DIVISIONS AND REGIONS a 

SMSA Second-highest 

Division population, 1983 03 

and region SMSA millions concn., ppm 

West 

Mountain Denver-Boulder, CO 1 to <2 0.14 

Phoenix, AZ 1 to <2 0.16 

Pacific Los Angeles-Long Beach, CA >2 0.37 

San Francisco-Oakland, CA >2 0.17 

Anaheim-Santa AnaGarden Grove, CA 1 to <2 0.28 

San Diego, CA 1 to <2 0.20 

Seattle-Everett, WA 1 to <2 0.10 

Riverside-San Bernardino- 1 to <2 0.34 

Ontario, CA 

San Jose, CA 1 to <2 0.16 

Portland, OR/WA 1 to <2 0.12 

Sacramento, CA 1 to <2 0.15 

aStandard Metropolitan Statistical Areas and geographic divisions and regions 

as defined by Statistical Abstract of the United States (U.S. Department of 

Commerce, 1982). 

Source: U.S. Environmental Protection Agency (1984). 

Emissions of manmade oxidant precursors are usually correlated with 

population, especially emissions from area source categories such as transportation and residential heating (Chapter 3). Accordingly, when grouped by 

population, the 80 largest SMSAs had the following median values for their 

collective second-highest daily maximum 1-hour ozone concentrations in 1983: 

populations > 2 million, 0.17 ppm 0 3 ; populations of 1 to 2 million, 0.14 ppm 

03 ; and populations of 0.5 to 1 million, 0.13 ppm 0 3 . As noted above, however, 

coincident meteorology favorable for oxidant formation undoubtediy contributes 

to the apparent correlation between population and ozone levels. 

Among all stations reporting valid ozone data (> 75 percent of possible 

hourly values per year) in 1979, 1980, and 1981 (collectively, 906 stationyears) in the United States, the median second-highest 1-hour ozone value was 

0.12 ppm, and 5 percent of the stations reported second-highest 1-hour values 

> 0.28 ppm. 

1-38 
A pattern of concern in assessing responses to ozone in human populations 

and in vegetation is the occurrence of repeated or prolonged. multiday periods' 

when the ozone concentrations in ambient air are in the.range of.those known 

to elicit responses (see Chapters 10 and 12). In addition, the number of days 

of respite between such multiple-day periods of high ozone is of possible 

consequence. Data show that repeated, consecutive-day exposures to_or resp'ites 

from specified concentrations are location-specific. At a site in Dallas; 

Texas, for example, daily maximum 1-hour concentrations were > 0.06 ppm for`' ` 

2 to 7 days in a row 37 times in a 3-year period (1979 through 1981).. A con= 

centrati on of >0.18 ppm was recorded at that si te on only 2 si ngl e days , 

however, and no multiple-day recurrences of that concentration or greater'were 

recorded over the 3-year period. At a site in Pasadena, California, daily 

maximum 1-hour concentrations >0.18 ppm recurred on 2 to 7 consecutive days 

33 times in that same 3-year period (1979 through 1981) and*occurred, as well, 

on 21 separate days. These and other data demonstrate the occurrence in some 

urban areas of multiple-day potential exposures to relatively high concentrations of ozone. 

1.4.2. Trends in Nationwide Ozone Concentrations 

Trends in ozone concentrations nationwide are important for.estimating.,. 

potential exposures in the future of human populations and other receptors,'`as 

well as for examining the effectiveness of abatement.programs. The.determina=: 

tion of nationwide trends requires the application of statistical tests to 

comparable, representative, multiyear aerometric data. The der:ivation.'of 

recent trends in ozone concentrations, and the interpretation of.those.trends°:, 

is complicated by two potentially significant factors that have affected°,z. 

aerometri c data si nce 1979: (1) the promul gati on by EPA. i n 1979 of a'new s 

calibration procedure for ozone monitoring (see Chapter 4);.,and.(2) the introduction by EPA of a quality-assurance:program ,that has resulted in.improved•, :; 

data-quality audits. The effects of these factors on ozone concentration ,:: , measurements are superimposed on the effects on concentrations of any chan.ges ~ , 

in meteorology or in precursor emission rates that may have occurred over the< ~ 

same time span. 

The nationwide trends in ozone conce.ntrations for a 9-year period, 1975- 

through 1983,.are shown in Figure 1-1 (U. S. Environmental ; Protection Agency ; °i 

1984). The data given are trends as gauged by the composite.average of.the 

1-39. 
0.18 

~.~ 

/ 

tk

~ 

CA (27 Stations) 

, 

1 ~ 

0 NAMS STATIONS (62) 

I INTERVALS 

95% CONFIDENCE l ; ~ 

O ALL STATIONS (176) ;1 ` / 

; 95% CONFIDENCE 

s.INTERVALS :0.13 

p CALIFORNIA STATIONS (27) 

0 ALL STATIONS EXCEPT 

CALIFORNIA (149) 

1975 1976 1977 1978 1979 1980 1981 '1982 1983 

YEAR 

Figure 1-1. National trend in composite average of the second highest value 

among daily maximum 1-hour ozone concentrations at selected groups of 

sites, 1975 through 1983. 

Source: U.S. Environmental Protection Agency (1984). 

0.17 

n. 

c. 

2 

O 

Q 

cc 

~ 

Z 

w 

v 

z 

O 

U 

W 

Z 

O 

N 

O 

10N ~ 

0.15 

0.14 

0.12 

1-40 
second-highest value among daily maximum 1-hour ozone concentrations. Data 

from four subsets of monitoring stations, most of them urban stations, are 

given: (1) California stations only; (2) all stations except those in 

California; (3) all stations including those in California; and (4) all 

National Air Monitoring Stations (NAMS), which report data directly to EPA. 

Only stations reporting > 75 percent of possible hourly values in the respective 

years are represented in the data. 

For the entire 9-year period, 1975 through 1983, all subsets of monitoring 

stations show a decline in the composite second-highest daily maximum 1-hour 

ozone concentration. Between 1979, when the new, more accurate calibration 

procedure was promulgated, and 1982, a small decline of 9 to 10 percent in 

nationwide ozone concentrations occurred. From 1982 to 1983, however, concentrations increased by about 10 percent in California, by about 14 percent _ 

outside California, and by about 12 percent nationwide (all states). Recently 

published data for 1984 from a somewhat smaller number of sites (163) (U.S. 

Environmental Protection Agency, 1986) show a decrease in nationwide ozone 

concentrations from 1983 to 1984, with 1984 levels approximating those recorded 

in 1981. The portion of the apparent decline in ozone nationwide from 1975 

through 1984 that is attributable to the calibration change of 1979 cannot be . 

determined by simply applying a correction factor to all data, since not all 

monitoring stations began using the UV calibration procedure in the same year. 

Figure 1-2 shows the nationwide frequency distributions of the first-, 

second-, and third-highest 1 - hour 03 concentrations at predominantly urban 

stations aggregated for 1979, 1980, and 1981, as well as the highest 1-hour 0 3 

concentration at site of the National Air Pollution Background Network (NAPBN) 

aggregated for the same 3 years. As shown by Figure 1-2, 50 percent of the 

second-highest 1-hour values from non-NAPBN sites in this 3-year period were 

0.12 ppm or less and about 10 percent were equal to or greater than 0.20 ppm. 

At the NAPBN sites, the collective 3-year distribution (1979 through 1981) is 

such that about 6 percent of the values are less than 0.10 ppm and fewer than 

20 percent are higher than 0.12 ppm. 

1.4.3. Ozone Concentrations in Nonurban Areas 

Few nonurban areas have been routinely monitored for ozone concentrations. 

Consequently, the aerometric data base for nonurban areas is considerably less 

substantial than for urban areas. Data are available, however, from two 

1-41 
~ 

c 

c 

c 

r 

c 

u 

c 

~ 

N 

tn 

O 

~ 

~ 

.Y 

0 

~ 

0 

e 

~ 

0 

W 

2 

LM 

ca 

01 

oa 

cq 

~ 

oa 

~1 

~ ~ 

at 

O 

~ 

~ (0 

O 

~ 

o) 

~ 

` 

d 

\ 

ao 

oi a+ 

•*—• y 

y = 

\ ~ " ON 

O 

\~ cn 

m a *- y ^ > 

W y L ~ 

> O N 

c0 J 

ui 

~ ~ N 

\~\ ~ vi~ a) cc 

~ 

aa 

\' ~ ~ o ~ >, 

\\. ® L ~ N O 00 

00 = O • Ln cc .c co *, 

Cl) 

~ `•\ ° ~ 

W U y '~ d ~ v QD 

y ~ 

a~ ° ® y 

CM c) +•~ Q 

a ~• N O 

O 

= y y ` 

~ L L ~C tm + 0 +W (n Z ` • a' ~ ~ +r 

,••, O 

W C7 

• 

W "Y ~ L ~ ,~j a' 

~ ~ O .

0 

 y ~C 

C7 C 

N 

~ 

C7 

C_7 

~ • 

'd m C 

' • N 

~ 

0- 

O m 

 m E 

C CbDZ 0 

o y~ Oy LLJ 

c cn 

~ 'A 

tV d c6 

L 

O v 0 O O 

_ W O 

o It N 0 V) 

~ C• ~9 M N N r ~ G C O C C G G 

wdd 'NOI Lda1N30N00 3NOZ0 

!n O ° 

O 

O 

1-42 
special-purpose networks, the National Air Pollution Background Network (NAPBN) 

and the Sulfate Regional Experiment network (SURE). Data on maximum 1-hour 

concentrations and arithmetic mean 1-hour concentrations reveal that maximum 

1-hour concentrations at nonurban sites classified as rural (SURE study, 

Martinez and Singh, 1979; NAPBN studies, Evans et al., 1983) can sometimes . 

exceed the concentrations observed at sites classified as suburban (SURE. . 

study, Martinez and Singh, 1979). For example, maximum 1-hour ozone concentrations measured in 1980 at Kisatchie National Forest (NF), Louisiana; Custer 

NF, Montana; and Green Mt. NF, Vermont, were 0.105, 0.070, and 0.115 ppm, 

respectively. Arithmetic mean 1-hour concentrations for 1980 were 0.028, " 

0.037, and 0.032 ppm at the respective sites. For four nonurban (rural) sites 

in the SURE study, maximum 1-hour ozone concentrations were 0.106, 0.107, 

0.117, and 0.153; and mean 1-hour concentrations ranged from 0.021 to 0.035 

ppm. At the five nonurban (suburban) sites of.the SURE study, maximum concentrations were 0.077, 0.099, 0.099, 0.080, and 0.118 ppm, respectively. The 

mean 1- hour concentrations at those sites were 0.023, 0.030, 0.025, 0.020,.and 

0.025 ppm, respectively. 

Ranges of concentrations and the maximum 1-hour concentrations at some of 

the NAPBN and SURE sites show the probable influence of ozone transported from 

urban areas. In one documented case, for example, a 1-hour peak ozone concentration of 0.125 ppm at an NAPBN site in Mark Twain National Forest, Missouri, 

was measured during passage of an air mass whose trajectory was calculated to 

have included Detroit, Cincinnati, and Louisville in the preceding hours 

(Evans et ai., 1983). 

The second-highest concentration among all the daily maximum 1-hour 

concentrations measured at the NAPBN sites appear to be about one-half the 

corresponding concentrations measured at urban sites in the same years. No 

trend in concentrations at these NAPBN sites is discernible in the data record 

for 1979 through 1983. 

These data corroborate the conclusion given in the 1978 criteria document 

(U.S. Environmental Protection Agency, 1978) regarding urban-nonurban and 

urban-suburban gradients; i.e., nonurban areas may sometimes sustain higher 

peak ozone concentrations than those found in urban areas. 

1-43 
1.4.4. Diurnal and Seasonal Patterns in Ozone Concentrations 

Since the photochemical reactions of precursors that result in ozone formation are driven by sunlight, as weli as by emissions, the patterns of ozone 

occurrence in ambient air depend on daily and seasonal variations in sunlight 

intensity. The typical diurnal pattern of ozone in ambient air has a minimum 

ozone level around sunrise (near zero in most urban areas), increasing through 

the morning to a peak concentration in early afternoon, and decreasing toward 

minimal levels again in the evening. The 1978 criteria document ascribed the 

daily ozone pattern to three simuitaneous processes: (1) downwaH transport of 

ozone from layers aloft; (2) destruction of ozone through contact with surfaces 

and through reaction with nitric oxide (NO) at ground level; and (3) in situ 

photochemical production of ozone (U.S. Environmental Protection Agency, 1978; 

Coffey et al., 1977; Mohnen, 1977; Reiter, 1977). Obviously, meteorology is 

a controlling factor; if strong winds disperse the precursors or heavy clouds 

intercept the sunlight, high ozone levels will not develop. Another important 

variation on the basic diurnal pattern appears in some localities as a secondary 

peak in addition to the early afternoon peak. This secondary peak may occur 

any time from midafternoon to the middle of the night and is attributed to 

ozone transported from upwind areas where high ozone levels have occurred 

earlier in the day. Secondary peak concentrations can be higher than concentrations resulting from the photochemical reactions of locally emitted precursors 

(Martinez and Singh, 1979). At one nonurban site in Massachusetts (August 

1977), for example, primary peak concentrations of about 0.11, 0.14, and 0.14 

occurred at noon, from noon to about 4:00 p.m., and at noon, respectively, on 

3 successive days of high ozone levels (Martinez and Singh, 1979). Secondary 

peaks at the same site for those same 3 days were about 0.150, 0.157, and 

0.130 ppm at about 6:00 p.m., 8:00 p.m., and 8:00 p.m., respectively (Martinez 

and Singh, 1979). 

Because weather patterns, ambient temperatures, and the intensity and 

wavelengths of sunlight all play important roles in oxidant formation, strong 

seasonal as well as diurnal patterns exist. The highest ozone levels generally 

occur in the spring and summer (second and third quarters), when sunlight 

reaching the lower troposphere is most intense and stagnant meteorological 

conditions augment the potential for ozone formation and accumulation. Average 

summer afternoon levels can be from 150 to 250 percent of the average winter 

afternoon levels. Minor variations in the smog season occur with'location, 

1-44 
however. In addition, it is possible for the maximum and second-highest 

1-hour ozone concentration to occur outside the two quarters of highest average 

ozone concentrations. Exceptions to seasonal patterns are potentially important 

considerations with regard.tothe protection of crops from ozone damage, 

especially since respective crops have different growing seasons in terms of 

length, time of year, and areas of the country in which they are grown. 

In addition to the seasonal meteorological conditions that obtain in the 

lower troposphere, stratospheric-tropospheric exchange mechanisms exist that 

produce relatively frequent but sporadic, short-term incursions into the 

troposphere of stratospheric ozone (see Chapter 3). Such incursions show a 

seasonal pattern, usually occurring in late winter or early spring. 

Percentile distributions, by season of the year, of concentration data 

from all eight NAPBN sites show that the arithmetic mean 1-hour concentration 

(averaged over a minimum of 3 years of data at each site, for 1977 through 

1983) was higher in the second quarter of the year (April, May, June) at seven 

of the eight stations; and was only negligibly lower than the third-quarter 

value at the eighth station. The maximum 1-hour concentrations at respective 

sites, aggregated over 3 to 6 years, depending on the data record for each 

site, ranged from 0.050 ppm at Custer NF, MT (in the fourth quarter) to 

0.155 ppm at Mark Twain NF, MO (in the third quarter). The second-highest 

1-hour concentration among maximum daily 1-hour values ranged from 0.050 ppm 

at Custer NF, MT (in the fourth quarter), to 0.150 ppm at Mark Twain NF, MO 

(i n the thi rd quarter). The data al so show that 99 percent of the 1-hour 

concentrations measured were well below 0.12 ppm, even in the second quarter 

of the year, when incursions of stratospheric ozone are expected to affect, 

at ieast to some degree,.the concentrations measured at these stations. 

Excursions above 0.12 ppm were recorded in 1979 and 1980 at NAPBN sites; but 

none were recorded in 1981 (Evans et al., 1983; Lefohn, 1984). 

Because of the diurnal patterns of ozone, averaging across longer-term 

periods such as a month, a season, or longer masks the occurrence of peak 

concentrations (see, e.g., Lefohn and Benedict, 1985). This is an obvious and 

familiar statistical phenomenon. It is pointed out, however, because it has 

direct relevance to the protection of public heaith and welfare. Averaging 

times must correspond to, or be related in a consistent manner to, the pattern 

of exposure that elicits untoward responses. 

1-45 
1.4.5 Spatial Patterns in Ozone Concentrations 

In addition to temporal variations, both macro- and microscale spatial 

variations in ozone concentrations occur that have relevance ranging from 

important to- inconsequential for exposure assessments. Differences in concentrations or patterns of occurrence, or both, are known to exist, for example, 

between urban and nonurban areas, between indoor and outdoor air, within large 

metropolises, and between lower and higher elevations. The more important 

variations are summarized below. 

1.4.5.1 Urban-Nonurban Differences in Ozone Concentrations. Ozone concentrations differ between urban and rural, between urban and remote, and even 

between rural and remote sites, as discussed in part in the preceding section 

on temporal variations. The variations with area and type of site are variations °.th in the tiroing and the magnitude of the peak concentrations, and, in 

the case of transported ozone, are related to the temporal variations between 

uMban and nonurban areas discussed above. Data from urban, suburban, rural, 

e ~ id remote sites (see, e.g., SAROAD, 1985a-f; Martinez and Singh, 1979; Lefohn, 

1 984 Evans, 1985; respectively) corroborate the conclusion drawn in the 1978 

t , it ~_ria document (U.S. Environmental Protection Agency, 1978) that ozone 

:,_nre,trations can sometimes be higher in some suburban or even rural areas 

ow ~ wind of urban plumes than in the urban areas themselves; and, furthermore, 

at }aigher concentrations can persist longer in rural and remote areas, 

arge!v° because of the absence of nitric oxide (NO) for chemical scavenging. 

onurban areas downwind of urban plumes, peak concentrations can 

ur, as the result of transport, at virtually any hour of the day or night, 

dF e tiding upon many factors, such as the strength of the emission source, 

i°md,ti..;on time, scavenging, and wind speed (travel time) and other meteorological 

tac°,o-s. The dependence of the timing of peak exposures upon these transportreiated factors is well-known and is illustrated here by two studies. Evans 

e ~ , a'i'. (1983) calculated multiday trajectories for air parcels reaching a 

rionurban sites in the Mark Twain National F,orest, Missouri, during an episode. 

Four separate trajectories, all of which passed over the Ohio River Valley and 

the Great Lakes region, impacted the forest site at different times in a 

24-hottr period (in which the maximum 1-hour concentration measured was 0.125 

ppm). Subsequently, regional cloud cover and rains produced shi`fts in air 

flow and also reduced the potential for ozone formation, alleviating the 

impact at the site. Kelly et al. (1986) showed in the Detroit area that peak 

1-46 
ozone concentrations occurred at distances of 10 to 70 km (ca. 6 to 43 mi) 

north-northeast of the urban center. Consequently, it wouid be possible for 

peak ozone concentrations to occur in the iate afternoon or early evening in 

nonurban areas downwind of Detroit. Kelly et al. (1986) also found that 

concentrations diminished again beyond 70 km (ca. 43 mi) downwind of the urban 

center. Thus, as illustrated by these and similar data, beyond the distance 

traversed in the time required for maximum ozone formation in an urban plume, 

ozone concentrations will decrease (unless fresh emissions are injected into 

the plume) as the rate of ozone formation decreases, the plume disperses, 

surface deposition or other scavenging occurs, and meteorological conditions 

intervene. 

It is not surprising, therefore, that in rural areas lying beyond the 

point of maximum ozone formation, for a given set of conditions, peak concentrations are lower and average diurnal profiles are flatter than in urban and 

near-urban areas (see, e.g., SAROAD, 1985b-f, for rural and remote sites). In 

remote areas beyond the influence of urban plumes, average peak concentrations 

will be still lower and average diurnal profiles still flatter (see e.g., 

Evans, 1985). Exceptions to these generalizations occur, of course, because 

of the complex interactions of topography, meteorology, and photochemistry. 

Such temporal and spatial differences between ozone concentrations in 

urban versus nonurban areas are important considerations for accurately assessing 

actual and potential exposures for human populations and for vegetation in 

nonurban areas, especiaily since the aerometric data for nonurban areas are 

far from abundant. 

1.4.5.2 Geographic, Vertical, and Altitudinal Variations in Ozone Concentrations. 

Although of interest and concern when estimating global ozone budgets, demonstrated variations in ozone concentrations with latitude and the lesser variations 

with longitude have little practical significance for assessing exposure 

within the contiguous United States. The effects on ozone concentrations of 

latitude and longitude within the contiguous states are minor, and are reflected 

in the aerometric data bases. Of more importance, ozone concentrations are 

known to increase with increasing height above the surface of the earth. 

Conversely, they may be viewed as decreasing with proximity to the surface of 

the earth, since the earth's surface acts as a sink for ozone (see, e.g., 

Seiler and Fishman, 1981; Galbally and Roy, 1980; Oltmans, 1981, cited in 

Logan et al., 1981). The most pertinent vertical and altitudinal gradients in 

1-47 1 
ozone concentrations are: (1) increases in concentration with height above 

the surface of the ground (regardless of altitude); (2) increases in concentration with altitude; and (3) variations in concentrations with elevation in 

mountainous areas, attributable to transport and overnight conservation of 

ozone aloft, nocturnal inversions, trapping inversions, upslope flows, and 

other, often location-specific interactions between topography, meteorology, 

and photochemistry. 

The importance of monitoring concentrations at the proper height above 

the surface of the ground has been known for a long time, and EPA guidance on 

the placement of monitoring instruments (see Chapter 4) is predicated on the 

existence of a vertical gradient as ozone is depleted by reaction with groundlevel emissions of NO or by deposition on reactive surfaces such as vegetation. 

Data illustrative of the near-surface: gradient, were.reported.byPratt et al. 

(1983), who measured ozone concentrations at two separate heights (3 and 9 or 

6 and 9 meters) above the ground at three rural, vegetated sites. Although 

the maximum mean difference between 3 and 9 meters was 3 ppb, this difference 

was similar to the mean difference between sites at the same height. Given 

the height of some vegetation canopies, especially forests, even such small 

differences over a spread of 6 meters should probably be taken into consideration when interpreting reported dose-response functions. 

The gradual increase in ozone concentrations with altitude has been 

documented by a number of workers (see e.g., Viezee et al., 1979; Seiler and 

Fishman, 1981; Oltmans, 1981, as cited in Logan et al., 1981). There is a 

general increase in concentration with altitude, but as described by Seiler 

and Fishman (1981) and Oltmans (1981; cited in Logan et al., 1981), for example, 

two relatively pronounced gradients exist, one between the surface of the 

earth and 2 km (ca. 1 mi) and one even more pronounced between 8 and 12 km 

(ca. 5 and 7.5 mi). 

Tncreases in concentrations with altitude could potentially be of some 

consequence for passengers and airline personnel on high-altitude flights in 

the absence of adequate ventilation-filtration systems (see Chapter 11). 

Variations with height above the surface and with elevation, in mountainous 

areas, however, should be taken into account to ensure the accurate assessment 

of exposures and the accurate derivation of dose-response functions, especially 

for forests and other vegetation. 

1-48 
Variations in ozone concentrations with elevation, not always consistent 

or predictable, have been reported by researchers investigating the effects of 

ozone on the mixed-conifer forest ecosystem of the San Bernardino Mountains of 

California. Measurements taken at four monitoring stations at four different 

elevations showed that peak ozone concentrations occurred progressively later 

in the day at progressively higher elevations (Miller et al., 1972). Ozone 

concentrations >0.10 ppm occurred for average durations of 9, 13, 9, and 

8 hr/day at the four respective stations, going from lower to higher elevations. 

The occurrence for 13 hr/d4y of concentrations >0.10 ppm at the station at 

817 m(2860 ft) was probably the result of contact of that zone of the mountainside with the inversion layer (U.S. Environmental Protection Agency, 1978). 

Nighttime concentrations rarely decreased below 0.05 ppm at the mountain crest; 

whereas at the lowest elevation, the basin station at 442 m(1459 ft), the 

nighttime concentration usually decayed to near zero. Trapping inversions 

were major contributors to the elevational gradients observed in this study, 

which was conducted in the 1970s. Oxidant concentrations within the inversion 

were found not to be uniform but to occur in multiple layers and strong vertical 

gradients. The important result of the trapping of oxidants in the inversion 

layers was the prolonged contact of high terrain with oxidants at night (U.S. 

Environmental Protection Agency, 1978). 

In a more recent report, Wolff et al. (1986) described measurements made 

in July 1975 at three separate elevations at High Point Mountain in northeastern 

New Jersey. The daily ozone maxima were similar at different elevations. At 

night, however, ozone concentrations were nearly zero in the valley but increased 

with elevation on the mountainside. Greater cumulative doses (number of hours 

at >0.08 ppm) were sustained at the higher elevations, 300 and 500 m, respectively (ca. 990 and 1650 ft, respectively). Wolff et al. (1986) related this 

phenomenon to the depth of the nocturnal inversion layer and the contact with 

the mountainside of ozone conserved aloft at night. 

These concentration gradients with increased elevation are important for 

accurately describing concentrations at which injury or damage to vegetation, 

especially forests, may occur. Researchers investigating the effects of ozone 

on forest ecosystems have seldom measured nighttime ozone concentrations 

because the stomates of most species are thought to be closed at night, thus 

preventing the internal flux of ozone that produces injury or damage (see 

Chapter 6). If stomates remain even partially open at night, however, the 

1-49 
possible occurrence of nighttime peak concentrations of ozone, the occurrence 

of multiple peaks in a 24-hour period, or the persistence of elevated concentrations that do not decay to near zero overnight should not be overlooked. 

Furthermore, the lack of NO for nighttime scavenging in nonurban areas and the 

persistence of ozone overnight at higher elevations will result in the presence 

of relatively higher concentrations in such areas at sunrise when the stomates 

open and photosynthesis begins. This possibility requires that exposure 

assessments, in the absence of sufficient aerometric data for forests and 

other vegetated areas, take such factors into consideration. 

1.4.5.3 Other Spatial Variations in Ozone Concentrations. Other spatial variations are important for exposure assessments for human populations. Indooroutdoor gradients in ozone concentrations are known to occur even in buildings 

or vehicles ventilated by fresh air rather than air conditioning (e.g., Sabersky 

et al., 1973; Thompson et al., 1973; Peterson and Sabersky, 1975). Ozone reacts 

with surfaces inside buildings, so that decay may occur fai'rly rapidly, depending 

upon the nature of interior surfaces and furnishings (e.g., Davies et al., 1984; 

Contant et al., 1985). Ratios of indoor-to-outdoor (I/0) ozone concentrations 

are quite variable, however, since cooling and ventilation systems, air infiltration or exchange rates, interior air circulation rates, and the composition 

of interior surfaces all affect indoor ozone concentrations. Ratios (I/0, 

expressed as percentages) in the literature thus vary from 100 percent in a 

non-air-conditioned residence (Contant et al., 1985); to 80 ± 10 percent 

(Sabersl4Y et al., 1973) in an air-conditioned office building (but with 100 percent outside air intake); to 10 to 25 percent in air-conditioned residences 

(Berk et al., 1981); and to as low as near zero in air-conditione -d residences 

(Stock et al., 1983; Contant et al., 1985). 

On a larger scale, within-city variations in ozone concentrations can 

occur, even though ozone is a"regional" pollutant. Data show, for example, 

relatively homogeneous ozone concentrations in New Haven, Connecticut (SAROAD, 

1985a), a moderately large city that is downwind of a reasonably well-mixed 

urban plume (Wolff et al., 1975; Cleveland et al.; 1976a,b). In a large 

metropolis, however, appreciable gradients in ozone concentrations can exist 

from one side of the city to the other, as demonstrated for New York Ci.ty 

(Smith, 1981), and for Detroit (Kelly et al., 1986). Such gradients should be 

taken into consideration, where possible, in exposure assessments. 

1-50 
1.4.6 Concentrations and Patterns of Other Photochemical Oxidants 

1.4.6.1 Concentrations. No aerometric data are routinely obtained by Federal, 

state, or local air pollution agencies for any photochemical oxidants other 

than nitrogen dioxide and ozone. The concentrations presented in this document 

for non-ozone oxidants were all obtained in special field investigations. The 

limitations in the number of locations and areas of the country represented in 

the information presented simply reflect the relative paucity of data in the 

published literature. 

The four non-ozone photochemical oxidants for which at least minimal 

concentration data are available are formic acid, peroxyacetyl nitrate (PAN), 

peroxypropi'onyl nitrate (PPN), and hydrogen peroxide (H2O2 ). Peroxybenzoyl 

nitrate has not been clearly identified in ambient air in the United States. 

The highest concentrations of PAN reported in the older literature, 1960 

through the present, were those found in the Los Angeles area: 70 ppb (1960), 

214 ppb (1965); and 68 ppb (1968) (Renzetti and Bryan, 1961; Mayrsohn and 

Brooks, 1965; Lonneman et al., 1976; respectively). 

The highest concentrations of PAN measured and reported in urban areas in 

the past 5 years were 42 ppb at Riverside, California, in 1980 (Temple and 

Tayior, 1983) and 47 ppb at Claremont, California, also in 1980 (Grosjean 

1981). These are clearly the maximum concentrations of PAN reported for 

California and for the entire country in this period. Other maximum PAN 

concentrations measured in the last decade in the Los Angeles Basin have been 

in the range of 11 to 37 ppb. Average concentrations of PAN in the Los Angeles 

Basin in the past 5 years have ranged from 4 to 13 ppb (Tuazon et al., 1981a; 

Grosjean, 1983; respectiveiy). The only pubiished study covering urban PAN 

concentrations outside California in the past 5 years is that of Lewis et al. 

(1983) for New Brunswick, New Jersey, in which the average PAN concentration 

was 0.5 ppb and the maximum was 11 ppb during September 1978 through May 1980. 

Studies outside California from the early 1970s through 1978 showed average 

PAN concentrations ranging from 0.4 ppb in Houston, Texas, in 1976 (Westberg 

et al., 1978) to 6.3 ppb in St. Louis, Missouri, in 1973 (Lonneman et al., 

1976). Maximum PAN concentrations outside California for the same period 

ranged from 10 ppb in Dayton, Ohio, in 1974 (Spicer et al., 1976) to 25 ppb in 

St. Louis (Lonneman et al., 1976). 

The highest PPN concentration reported in studies over the period 1963 

through the present was 6 ppb in Riverside, California (Darley et al., 1963). 

1- 51 
The next highest reported PPN concentration was 5 ppb at St. Louis, Missouri, 

in 1973 (Lonneman et al., 1976). Among more recent data, maximum PPN concentrations at respective sites ranged from 0.07 ppb in Pittsburgh, Pennsylvania, in 

1981 (Singh et al., 1982) to 3.1 ppb at Staten Island, New York (Singh et al., 

1982). California concentrations fell within this range. Average PPN concentrations at the respective sites for the more recent data ranged from 0.05 ppb at 

Denver and Pittsburgh to 0.7 ppb •at Los Angeles in 1979 (Singh et al., 1981). 

Altshuller (1983) has succinctly summarized the nonurban concentrations 

of PAN and PPN by pointing out that they overlap the lower end of the range of 

urban concentrations at sites outside California. At remote locations, PAN 

and PPN concentrations are lower than even the lowest of the urban concentrations by a factor of 3 to 4. 

The concentrations of H 2O2 reported in the literature to date must be 

regarded as inaccurate since ozone is now thought to be an interference in all 

methods used to date except FTIR (Chapter 4). Measurements by FTIR, the most 

specific and accurate method now available, have not demonstrated unambiguously 

the presence of H 2O2 in ambient air, even in the high-oxidant atmosphere of the 

Los Angeles area. (The limit of detection for a 1-km-pathlength FTIR system 

is around 0.04 ppm.) 

Recent data indicate the presence in urban atmospheres of only trace 

amounts of formic acid: < 15 ppb, measured by FTIR (Tuazon et al., 1981b). 

Estimates in the earlier literature (1950s) of 600 to 700 ppb of formic'acid 

in smoggy atmospheres were erroneous because of faulty measurement methodology 

(Hanst et al., 1982). 

1.4.6.2Patterns . The patterns of formic acid (HCOOH), PAN, PPN, and H 2O 2 

may be summarized fairly succinctly. Qualitatively, diurnal patterns are 

similar to those of ozone, with peak concentrations of each of these occurring 

in close proximity to the time of the ozone peak. The correspondence in time 

of day is not exact, but is close. As demonstrated by the work of Tuazon 

et al. (1981b), ozone concentrations return to baseline levels somewhat faster 

than the concentrations of PAN, HCOOH, or H2O 2 (PPN was not measured). 

Seasonally, winter concentrations (third and fourth quarters) of PAN are 

lower than summer concentrations (second and third quarters). The percentage 

of PAN concentrations (PAN/0 3 x 100) relative to ozone, however, is higher in 

winter than in summer. Data are not readily available on the seasonal patterns 

of the other non-ozone oxidants. 

1-52 
Indoor-outdoor data on .PAN are limited to one report (Thompson et al., 

1973), which confirms the pattern to be expected from the known chemistry of 

PAN; that i s, i t pers i sts 1 onger i ndoors than ozone. Data are 1 acki ng on 

indoor-outdoor ratios for the other non-ozone oxidants. 

1.4.7 Relationship Between Ozone and Other Photochemical Oxidants 

The relationship between ozone concentrations and the concentrations of 

PAN, PPN, H

2

02 , and HCOOH is important only if these non-ozone oxidants are 

shown to produce potentially adverse health or welfare effects, singly, in 

combination with each other, or in various combinations with ozone at concentrations correponding to those found in ambient air. If only ozone is shown to 

produce adverse health or welfare effects in the concentration ranges of 

concern, then only ozone must be controlled. If any or all of these other 

four oxidants are shown to produce potentiaily adverse health or welfare 

effects, at or near levels found in ambient air, then such oxidants will also 

have to be controlled. Since ozone and all four of the other oxidants arise 

from reactions among the same organic and inorganic precursors, an obvious 

question is whether the. control of ozone will aiso resuit in the control of 

the other four oxidants. 

Cdntrolled- exposure studies on these non-ozone oxidants have employed 

concentrations much higher than those found in ambient air (see Chapters 9 and 

10). Because PAN may have contributed, however, to the eye irritation symptoms 

reported in earlier epidemiological -studies, and because PAN is the most 

abundant of these non-ozone oxidants, the relationship between ozone and PAN 

concentrations in ambient air remains of interest. 

The patterns of PAN and ozone concentrations are not quantitatively 

similar but do show qualitative similarities for most locations at which both 

pollutants have been measured in the same study. That a quantitative, monotonic 

relationship between ozone and PAN is lacking, however, is shown by the range 

of PAN-to-ozone ratios, expressed as percentages, between iocations and at the 

same location, as reported in the review of Altshuller (1983). 

Certain other information bears out the lack of a.monotonic relationship 

between PAN,.and ozone. Not only are PAN-ozone relationships not consistent 

between different urban areas, but they are not consistent in urban versus 

nonurban areas, in summer versus winter, in indoor versus outdoor environments, 

or even, as the data show, in location, timing, or magnitude of diurnal peak 

1- 53 
concentrations within the same city. Data obtained in Houston by Jorgen 

et al. (1978), for example, show variations in peak concentrations of PAN and 

in relationships to ozone concentrations of those peaks among three separate 

monitoring sites. Temple and Taylor (1983) have showh that PAN concentrations 

ar® a greater percentage of ozone concentrations in winter than in the remainder 

of the year in California. Lonneman et al. (1976) demonstrated that PAN, 

absolutely and as a percentage .of ozone, is considerably lower in nonurban 

than in urban areas. Thompson et al. (1973), in what is apparently the only 

published report on indoor concentrations of PAN, showed that PAN persists 

longer than ozone indoors. (This is to be expected from its enhanced stability 

at cooler-than-ambient temperatures such as found in air-conditioned buildings.) 

Tuazon et al. (1981b) demonstrated that PAN persists in ambient air longer 

than ozone, its persistence paralleling that of nitric acid, at least in the 

locality studied (Claremont, CA). Reactivity data presented in the 1978 

criteria document for ozone and other photochemical oxidants indicated that 

all precursors that give rise to PAN also give rise to ozone. The data also 

showed, however, that not all precursors giving rise to ozone also give rise 

to PAN, and that not all that give rise to both are equally reactive toward 

both, with some precursors preferentially giving rise, on the basis of units 

of product per unit of reactant, to more of one product than the other (U.S. 

Environmental Protection Agency, 1978). 

In the review cited earlier, Altshuller (1983) examined the relationships 

between ozone and a variety of other smog components, including PAN, PPN, 

H2O2 , HCOOH, aldehydes, aerosols, and nitric acid. He concluded that "the 

ambient air measurements indicate that ozone may serve directionally, but 

cannot be expected to serve quantitatively, as a surrogate for the other 

products" (Altshuller, 1983). It must be emphasized that the issue Altshuller 

examined was whether ozone could serve as an abatement surrogate for all 

photochemical products, not just the subset of non-ozone oxidants of concern 

in this document. Nevertheless, a review of the data presented indicates that 

his conclusion is applicable to the non-ozone oxidants examined in this document. 

1-54 
1.5 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON VEGETATION 

Foliar injury on vegetation is one of the earliest and most obvious 

manifestations of 03 injury. The effects of 0 3 are not limited to visible 

injury, however. Impacts can range from reduced plant growth and decreased 

yield, to changes in crop quality and alterations in susceptibility to abiotic 

and biotic stresses. The plant foliage is the primary site of 0 3 effects, 

although significant secondary effects, including reduced growth (both roots 

and foliage) and yield, can occur. 

Ozone exerts a phytotoxic effect only if a sufficient amount reaches the 

sensitive cellular sites within the leaf. The 0 3 diffuses from the ambient 

ai r i nto the 1 eaf through the stomata, whi ch can exert some control on 0 3 

uptake, to the active sites within the leaf. Ozone injury will not occur if 

(1) the rate of 0 3 uptake is low enough that the'plant can detoxify or metabolize 03 or its metabolites; or (2) the plant is able to repair or compensate 

for the effects (Tingey and Taylor, 1982). This is analogous to the plant 

response to S0 2 (Thomas et al., 1950). Cellular disturbances that are not 

repaired or compensated are ultimately expressed as visible injury to the leaf 

or as secondary effects that can be expressed as reduced root growth, or 

reduced yield of fruits or seeds, or both. 

Plant growth and yield are the end products of a series of biochemical 

and physiological processes related to uptake, assimilation, biosynthesis, and 

translocation. Sunlight drives the processes that convert carbon dioxide into 

the organic compounds (assimilation) necessary for plant growth and development. 

In addition to nutrients supplied through photosynthesis, the'plant must 

extract from the soil the essential mineral nutrients and water for plant 

growth. Plant organs convert these raw materials into a wide array of compounds 

required for plant growth and yield. A disruption or reduction in the rates 

of uptake, assimilation, or subsequent biochemical reactions will be reflected 

in reduced plant growth and yield. Ozone would be expected to reduce plant 

growth or yield if (1) it directly impacted the plant process that was limiting 

plant growth; or (2) it impacted another step sufficiently so that it becomes 

the step limiting plant growth (Tingey, 1977). Conversely, 0 3 will not limit 

plant growth if the process impacted by 0 3 is not or does not become ratelimiting. This implies that not all effects of 0 3 on plants are reflected in 

growth or yield reductions. These conditions also suggest that there are 

combinations of 0 3 concentration and exposure duration that the plant can 

1-55 
experience that will not result in visible injury or reduced plant growth and 

yield. Indeed, numerous studies have demonstrated combinations of concentration 

and time that did not cause a significant effect on the plant growth or yield. 

Ozone induces a diverse range of effects on plants and plant communities. 

These effects are usually classified as either injury or damage. Injury 

encompasses all plant reactions such as reversible changes in plant metabolism 

(e.g., altered photosynthesis), leaf necrosis, altered plant quality, or 

reduced growth that does not impair yield or the intended use of the plant 

(Guderian, 1977). In contrast, damage or yield loss includes all effects that 

reduce or impair the intended use or the value of the plant. Thus, for example, 

visible foliar injury to ornamental plants, detrimental responses in native 

species, and reductions in fruit and grain production are all considered 

damage or yield loss. Although foliar injury is not always classified as damage, 

its occurrence is an indication that phytotoxic concentrations of 03 are present. 

The occurrence of injury indicates that additional studies should be conducted 

i n areas where vegetati on shows fol i ar i n j ury to assess the ri s k of 0 3 to 

vegetation and to determine if the intended use or value of the p1ants is being 

impaired. 

1.5.1 Limiting_Values of plant Response to Ozone 

Several approaches have been used to estimate the 0 3 concentrations and 

exposure durations that induce foliar injury. Most of these studies used 

short-term exposures (less than 1 day) and measured visible injury as the 

response variable. One method for estimating the 03 concentrations and exposure 

durations that would induce specific amounts of visible injury involves exposing 

plants to a range of 0 3 concentrations and exposure durations, and then evaluating the data by regression analysis (Heck and Tingey, 1971). The data obtained 

by this method for several species are summarized in Table 1-4 to illustrate 

the range of concentrations required to induce foliar injury (5% and 20%) on 

sensitive, intermediate, and less sensitive species. 

An alternative method for estimating the 0 3 concentrations and exposure 

durations that induce foliar injury is the use of the limiting-value approach 

(Jacobson, 1977). The limiting-value method, which was developed from a 

review of the literature, identified the lowest concentration and exposure 

duration reported to cause visible injury on various plant species. The 

analysis was based on more than 100 studies of agricultural crops and 18 

1-56 
TABLE 1-4. OZONE CONCENTRATIONS FOR SHORT-TERM 

EXPOSURES THAT PRODUCE 5 OR 20 PERCENT INJURY TO VEGETATION 

GROWN UNDER SENSITIVE CONDITIONS a 

(ppm) 

Ozone concentrations that may produce 5% (20%) injury: 

Exposure Less 

time, hr Sensitive plants Intermediate plants sensitive plants 

0.5 0.35 - 0.50 

(0.45 - 0.60) 

1.0 0.15 - 0.25 

(0.20 - 0.35) 

2.0 0.09 - 0.15 

(0.12 - 0.25) 

4.0 0.04 - 0.09 

(0.10 - 0.15) 

8.0 0.02 - 0.04 

0.55 - 0.70 

(0.65 - 0.85) 

0.25 - 0.40 

(0.35 - 0.55) 

0.15 - 0.25 

(0.25 - 0.35) 

0.10 - 0.15 

(0.15 - 0.30) 

0.07 - 0.12 

>0.70 (0.85) 

>0.40 (0.55) 

>0.30 (0.40) 

?0.25 (0.35) 

>0.20 (0.30) 

aThe concentrations in parenthesis are for the 20% injury level. 

Source: U.S. Environmental Protection Agency (1978). 

studies of tree species. The analysis yielded the following range of concentrations and exposure durations that were likely to induce foliar injury (U.S. 

Environmental Protection Agency, 1978): 

1. Agricultural crops: 

a. 0.20 to 0.41 ppm for 0.5 hr. 

b. 0.10 to 0.25 ppm for 1.0 hr. 

c. 0.04 to 0.09 ppm for 4.0 hr. 

2. Trees and shrubs: 

a. 0.20 to 0.51 ppm for 1.0 hr. 

b. 0.10 to 0.25 ppm for 2.0 hr. 

C. 0.06 to 0.17 ppm for 4.0 hr. 

It should be emphasized that both methods described above can estimate 

concentrations and exposure durations that might induce visible injury, but 

that neither method can predict impacts of 0 3 on crop yield or intended use. 

The concept of limiting values also was used to estimate the 0 3 concentrations and exposure durations that could potentially reduce plant growth and 

yield (U.S. Environmental Protection Agency, 1978). The data were analyzed 

1-57 
and plotted in a manner similar to the approach used by Jacobson (1977) 

(Figure 1-3). In Figure 1-3 the line bounds mean 0 3 concentrations and 

exposure durations below which effects on plant growth and yield were not 

detected. This graphical analysis used data from both greenhouse and field 

studies and indicated that the lower limit for reduced plant performance was a 

mean 03 concentration of 0.05 ppm for several hours per day for exposure 

periods greater than 16 days. At 10 days the 03 response threshold increased 

to about 0.10 ppm, and to about 0.30 ppm at 6 days. , 

1.5.2 Methods for Determining Ozone Yield Losses 

Diverse experimental procedures have been used'to study the effects of 0 3 

on plants, ranging from studies done under highly controlled conditions, to 

exposures in open-top chambers, and to field exposures without chambers. In 

general, the more controlled conditions•are most appropriate for investigating 

specific responses and for providing the scientific basis for interpreting and 

extrapolating results. These systems are powerful tools for adding to an 

understanding of the biological effects of air pollutants. To assess, however, 

the impact of 03 on plant yield and to provide data for economic assessments, 

deviations from the typical environment in which the plant is grown should be 

minimized. For field crops, this implies that the studies should be.conducted 

in the fi'eld, but for crops that are typically grown in glass houses, the 

studies should be conducted under glass-house conditions. 

To improve estimates of yield loss in the field, the National Crop Loss 

Assessment Network (NCLAN) was initiated by EPA in'1980 to estimate the magnitude 

of crop losses caused by 0 3 (Heck et al., 1982). The primary objectives of 

NCLAN were: 

1. To define the relationships between yields of major agricultural 

crops and 0 3 exposure as required to provide data necessary for 

economic assessments and the development of National Ambient 

Air Quality Standards; 

2. To assess the national economic consequences resulting from the 

exposure of major agricultural crops to 03 ; 

3. To advance understandng of the cause and effect relationships that 

determine crop responses to pollutant exposures. 

1-58 
0.01 L 

4 

470 

21 ❑ 11 ❑ 

\ 44 • 19 ®18 ® 45 0 46 • 48-52 

\ 

13O

10 

'024 

160017 ~ 31 70C]20 

~ 1514 30 59 

400 ~ ~ ~ * 42 43 0 ❑ 9 

\\ 12143 26 41 08 50 33 

\ 1 a ® 29 5400 55,5600 58 

\ 39 3 ~ 

~ 20 

 i-®- .- 4 S 57 2510 - 38 ~ 34 - --. - - -- -- 

53 

EXPOSURE, hr/day 

A < 1.99 

❑ 2 TO 3.99 

O 4 T0 5.99 

~ >6 

NOS. = REF. NOS. ON TABLE 11-4 

6 8 10 20 40 60 80 100 200 

EXPOSURE PERIOD, days 

Figure 1-3. Relationship between ozone concentration, 

exposure duration, and reduction in plant growth or yie6d (see 

Table 6-18; also U.S. EPA, 1978). 

Source: U.S. Environmental Protection Agency (1978). 

1.0 

a 

a 

z 

O 

Q 

~ 

H 

z 

w 

U 

Z 

O 

U 

W 

z 

O 

N 

O 

0.1 

400 

1-59 
In the NCLAN studies, the cultural conditions used approximated typical 

agronomic practices, and open-top field exposure chambers were used to minimize 

perturbations to the plant environment during the exposure. The studies have 

attempted to use a range of realistic 03 concentrations and sufficient replication to permit the development of exposure-response models. In the NCLAN 

studies, plants were exposed to a range of 0 3 concentrations. Chambers were 

supplied with either charcoal-filtered air (control), ambient air, or ambient 

air supplemented with 0 3 to provide concentrations three or four levels greater 

than ambient. Consequently, the 0 3 exposures were coupled to the ambient 0 3 

level; days with the highest ambient 0 3 were also the same days when the 

highest concentrations occurred in a specific treatment in a chamber. As the 

ambient 0 3 varied from day-to-day, the base to which additional 0 3 was added 

also varied. This coupling of the 0 3 exposures to the ambient environment 

means that high 03 concentrations occurred in the chambers when the environmental and air chemistry conditions, in the ambient air, were conducive for 

producing elevated ambient 03 levels. The plant response data have been 

analyzed using regression approaches. The exposures were typically characterized by a 7-hr (9:00 a.m. to 4:00 p.m.) seasonal mean 0 3 concentration. This 

is the time period when 0 3 was added to the exposure chambers. 

1.5.3 Estimates of Ozone-Induced Yield Loss 

Yield loss is defined as an impairment or decrease in the intended use of 

the plant. Included in the concept of yield loss are reductions in aesthetic 

values, the occurrence of foliar injury (changes in plant appearance), and 

losses in terms of weight, number, or size of the plant part that is harvested. 

Yield loss may also include changes in physical appearance, chemical composition, or ability to withstand storage; which collectively are traits called 

crop quality. Losses in aesthetic values.are difficult to quantify. For 

example, because of its aesthetic value, the loss of or adverse effect on a 

specimen plant in a landscape planting may result in a greater economic loss 

than that incurred by the same impact on a plant of the same species growing 

as a part of natural plant community. Foliar in.jury symptoms may decrease the 

value of ornamental plants with or without concomitant growth reductions. 

Similarly, foliar injury on crops in which the foliage is the marketable plant 

part (e.g., spinach, lettuce, cabbage) can substantially reduce marketability 

and thus can constitute yield loss. Attainment of the li'miting values for 

1-60 
ozone previously discussed in this section should be sufficient to prevent 

foliar injury and thereby reduce this type of yield loss. Most studies of the 

relationship between yield loss and ozone concentration have focused on yields 

as measured by weight of the marketable plant organ, and that kind of yield 

loss will be the primary focus of this section. 

Studies have been conducted, frequently using open-top field exposure 

chambers, to estimate the impact of 03 on the yield of various crop species. 

These studies can be grouped into two types, depending on the experimental 

design and statistical methods used to anaiyze the data: (1) studies that 

developed predictive equations relating 0 3 exposure to plant response, and (2) 

studies that compared discrete treatment levels to a control. The advantage 

of the regression approach is that exposure-response models can be used to 

interpolate results between treatment levels. 

When the regression approach was used to estimate yield loss, 0 3 was 

added to either charcoal-filtered or ambient air to create a range of 0 3 

concentrations. In summarizing the data, 0 3-induced yield loss was derived 

from a comparison of the performance of the plants in charcoal -filtered air, 

although other reference concentrati.ons have been used. Various regression 

techniques have been used to derive exposure-response functions. The use of 

regression approaches permits the estimation of the 0 3 impact on plant yield 

over the range of concentrations, not just at the treatment means as is the 

case with analysis of variance methods. 

1.5.3.1 Yield.Loss: Determination by Regression Analysis. Examples of the 

relationship between 0 3 concentration and plant yield are shown in Figures 

1-4 and 1-5. These cultivars and species were selected because they also 

illustrated the type of year-to-year variation in plant response to ozone that 

may occur. The derived regression equations can be used to determine the 

concentrations that would be predicted to cause a specific yield loss or to 

estimate the predicted yield loss that would result from a specifc 0 3 concentration. Both approaches have been used to summarize the data on crop responses 

to 03 using the Weibull function (Rawlings and Cure, 1985). As an example of 

response, the 0 3 concentrations that would be predicted to cause a 10 or 30 

percent yield loss have been estimated (Table 1-5). A brief review of the 

data in this table indicates that for some species mean yield reductions of 10 

percent were predicted when the 7-hr seasonal mean 0 3 concentration exceeded 

0.04 to 0.05 ppm. Concentrations of 0.028 to 0.033 ppm were predicted to 

1-61 
)ARGONNE,

HEAT (ABE) 

(C)

A 

82 AND 1983 

 O 

0 

1982(0) 

y = 5236'(01/0.153)2.272 

1983(A) 

Y = 5873'(O3/0.108)14.4 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 

03 CONCENTRATION, ppm 

6000 

5000 

~ 

t 

\ 

~ 4000 

C -1 w 

} 

O 

w 

y 3000 

2000 

6000 6000 

6000 

~ 

~ 

~ 4000 

~ 

~ 

_W } 0 

LU 3000 

m 

2000 

SOYBEAN (DAVIS) 

(A) RALEIGH, 1981 AND 1982 

A A 1992(s) 

y = 4931'(O~/0128)2.144 

rS 

O 

A 

1981(0) 

y = 5593- (03/0,128)0.872 

5000 

~ 

t 

04000 Y 

~ W } 

~ 

W 3000 

w 

2000 

(B ~A BE TSYILLE, MD! 1981 AND 1982 

f~ 

1000 1000 1 1 1 1 1 1 1 .J 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 

03 CONCENTRATION, ppm 

6000 WHEAT (ARTHUR 71) 

(p) . ARGONNE,1982 AND 1983 

5000 ~ 

O 

~ 

i " \ 

Y 4000 

C J 

W 

} 

0 

w 

y 3000 

1982(o) 

y= 4613'(03/0. 146)2 •58 

2000 - 1983 (A) 

I y = 5210"(03/0. 148) 3.781 

1000 1000 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 

03 C01110ENTRATION, ppm 03 CONCENTRATION, ppm 

Figure 1-4. Examples of the effects of ozone on the yield of soybean and wheat 

cultivars. The 03 concentrations are expressed as 7-hr seasonal mean concentrations. 

The cultivars were selected as examples of 0 3 effects and of year-to-year variations in 

ptant response to 0 3 . 

Source: Soybean data from Heck et al. (1984); wheat data from Kress et al. (1985). 

1-62 
6000 

5500 

5000 

a 

= 4500 

~ 

~ 4000 

O 

LU 

N 3500 

O 

Z 

Q 

z 3000 

J 

(A) COTTON (SJ•2) 

&. SHAFTER. CA. 1981 AND 1982 

1981(0) I 

y = 654003/0.199)1 •228 I 

~~~~ 

34 

33 

32 

31 

« 30 0 

a 

Y 29 

~ 28 

s 

N 

W 

ac 27 

LL 

26 

2500 

2000 

1500 

1982(A) I 

y = 6872'(O3/0.088)

2.1 

i i i i 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16 0.18 0.2 

03 CONCENTRATION, ppm 

25 1 

1982(A) 

24

y = 32.3-(O3/0.Q82)3.05 

~ 

23 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16 

03 CONCENTRATfON, ppm 

16 

15 

14 

13 

12 

e 11 

m 

c. 

co 10 

~ g 

y 8 

W 

U. 7 

H 

O 6 

O 

s 5 

4 

3 

2 

~ 

0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16 

03 CONCENTRATION, ppm 

Figure 1-5. Examples of the effects of ozone on the yield of cotton, tomato, and 

turnip. The 0 3 concentrations are expressed as 7-hr seasona( mean concentrations. 

The species were se{ected as examples of 0 3 effects and of year-to-year variations in 

plant response to 03 . 

Source: Cotton and tomato data from Heck et al. (1984); turnip data from Heagle et 

al. (1985). 

1-63 
TABLE 1-5. SUMMARY OF OZONE CONCENTRATIONS PREDICTED TO CAUSE 

10 PERCENT AND 30 PERCENT YIELD LOSSES AND SUMMARY OF YIELD LOSSES PREDICTiD 

TO OCCUR AT 7-hr SEASONAL MEAN OZONE CONCENTRATIONS OF 0.40 and 0.06 ppm 

03 concentrations, ppm, Percent yield losses predicted 

predicted to cause to occur at 7-hr seasonal 

ield losses of: mean 03 concentration of: 

Species 4 ppm 0.06 ppm 

Lequme crops 

Soybean, Corsoy 0.048 0.082 6.4 16.6 

Soybean, Davis (81) 0.038 0.071 11.5 24.1 

Soybean, Davis (CA-82) 0.048 0.081 6.4 16.5 

Soybean, Davis (PA-82) 0.059 0.081 2.0 10.4 

Soybean, Essex 0.048 0.099 7.2 14.3 

Soybean, Forrest 0.076 0.118 1.7 5.3 

Soybean, Williams 0.039 0.093 10.4 18.1 

Soybean, Hodgson 0.032 0.066 15.4 18.4 

Bean, Kidney 0.033 0.063 14.9 28 

Peanut, NC-6 0.046 0.073 6.4 19.4 

Grain crops 

Wheat, Abe 0.059 0.095 3.3 10.4 

Wheat, Arthur 71 0.056 0.094 4.1 11.7 

Wheat, Roland 0.039 0.067• 10.3 24.5 

Wheat, Vona 0.028 0.041 28.8 51.2 

Wheat, Blueboy II 0.088 0.127 0.5 2.8 

Wheat, Coker 47-27 0.064 0.107 2.2 8.4 

Wheat, Holly 0.099 0.127 0.0 0.9 

Wheat, Oasis 0.093 0.135 0.4 2.4 

Corn, PAG 397 0.095 0.126 0.3 1.5 

Corn, Pioneer 3780 0.075 0.111 1.4' 5.1 

Corn, Coker 16 0.133 0.175 0.0 0.3 

Sorghum, DeKalb-28 0.108 0.186 0.0 2.7 

Barley, Poco 0.121 0.161 0.0 0.5 

Fiber crops 

Cotton, Acala SJ-2 (81) 0.044 0.096 8.3, 16.2 

Cotton, Acala SJ-2 (82) 0.032 0.055 16.1 ` 35.1 

Cotton, Stoneville 0.047 0.075 4.6 16.2 

Horticultural crops 

Tomato, Murrieta (81)• 0.079 0.108 0.8 3.7 

Tomato, Murrieta (82) 0.040 0.059 10.3 .31.2 

Lettuce, Empire 0.053 0.075 0.0 16.8 

Spinach, America 0.046 0.082 6.8 17.2 

Spinach, Hybrid 0.043 0.082 2.6 9.2 

Spinach, Viroflay 0.048 0.080 6.0 16.7 

Spinach, Winter Bloom 0.049 0.080 5.8 16.5 

Turnip, Just Right 0.043 0.064 7.7 24.9 

Turnip, Pur Top W. G. 0.040 0.064 10.1 26.5 

Turnip, Shogoin 0.036 0.060 13.0 29.7 

Turnip, Tokyo Cross 0.053 0.072 3.3 15.6 

aThe yield losses are derived from Weibull equations and are based on the control 

yields in charcoal-filtered air. 

Source: Derived from Heck et al. (1984). 

1-64 
cause a 10 percent yield loss in Vona wheat, kidney bean, and Hodgson soybean. 

At a 7-hr seasonal mean 03 concentration of 0.04 ppm, mean yield reductions 

ranged from zero percent in sorghum, barley, and a corn cultivar to a high of 

28.8 percent in Vona wheat. 

A histogram of the 7-hr seasonal mean 0 3 concentrations predicted to 

cause a 10 percent yi el d 1 oss (Tabl e 1-5) i s gi ven i n Fi gure 1-6 to help 

illustrate the range of concentrations and their relative frequency of occurrence. The data i n Fi gure 1-6 are based on 37 speci es or cul ti var yi el dresponse functions developed from studies in open-top fieid exposure chambers. 

Approximately 57 percent of the species or cultivars were predicted to exhibit 

10 percent yield reductions at 7-hr seasonal mean concentrations below 0.05 

ppm. Thirty-five percent of plant types were predicted to display a 10 percent 

yield loss at 7-hr mean concentrations between 0.04 and 0.05 ppm. Seven-hr 

seasonal mean concentrations in excess of 0.08 ppm were required to cause a 10 

percent yield loss in almost 19 percent of the species or cultivars. The data 

indicate that approximately.11 percent of the species or cultivars would 

display a 10 percent loss at 7-hr seasonal mean concentrations below 0.035 

ppm, suggesting that these plant types are very sensitive to 0 3 - induced yield 

losses. 

A review of the data in Table 1-5 indicates that the grain crops were 

apparently generally less sensitive than the other crops to 0 3 . Mean yield 

reductions at 0.04 ppm were predicted to be less than 5 percent for all the 

species and cultivars tested except for the Roland and Vona wheat cultivars. 

The data also demonstrate that sensitivity differences within a species may be 

as large as differences between species. For example, at 0.04 ppm 03 , estimated 

yield losses ranged from 2 to 15 percent in soybean and from 0 to 28 percent 

in wheat. In addition to differences in sensitivity among species and cultivars, 

the data in Figures 1-4 and 1-5 illustrate year-to-year variations in plant 

response to 03 . 

Several exposure-response models, ranging from simple linear to complex 

nonlinear models, have been used to describe the reiationship between plant 

yield and 03 exposure. When exposure-response models are used, it is important 

for the fitted equations not to show systematic deviation from the data points 

and for the coefficient of determination (R2 ) to be high. Although linear 

regression equations have been used to estimate yield loss, there appear to be 

systematic deviations from the data for some species and cultivars even though 

1-65 
10 

9 

m 21.6% 

.° E 8 

c O 18.9% 

Vi 7 Q» O 

> 

1-- 6 

M 13.5% 13.5% 

CU cc 

O 

5 

10.8% 10.8% ~ ~ 10.8% 

w 4 

W 

a. 

~ 

3 

a 

0 

n~ 2 

v 

1 

0 

<0.035 0.040-0.044 0.050-0.059 >0.080 

0.035-0.039 0.045-0:049 0.060-0.079 

7-hr SEASONAL MEAN 

OZONE CONCENTRATIONS, pprn 

Figure 1-6. Number and percentage of 37 crop species or cultivars predicted to 

show a 10 percent yield loss at various ranges of 7-hr seasonal mean ozone 

concentrations. Concentration ranges and 10% yield loss data are derived from 

Table 1-5. Data represent 12 separate crop species; circled numbers represent 

separate species for each concentration range. 

1-66 
the equations have moderate-to-high coefficients of determination (R 2 ). . 

Plateau-linear or polynomial equations appear to fit the data better. More 

recently, a Weibull model has been used to estimate percentage yield loss 

(Heck et al., 1983). The Weibull model yields a curvilinear response line 

that seems to provide a reasonable fit to the data. Based on available data, 

it is recommended that curvilinear exposure-response functions- be used to 

describe and analyze plant response to 0 3 . 

1.5.3.2 Yield Loss: Determination from Discrete Treatments. In addition to 

the use of regression approaches in some studies, various other approaches 

have been used to investigate the effects of 0 3 on crop yield. These studies 

were designed to test whether specific 0 3 treatments were different from the 

control rather than to develop exposure-response ~ equations. In general, these 

data were analyzed using analysis of variance. To summarize the data from 

studies that used discrete treatments, the lowest 0 3 concentration that significantly reduced yield was determined from analyses done by the authors (Table 

1-6). The lowest concentration reported to reduce yield was frequently the 

lowest concentration used in the study; hence it was not always possible to 

estimate a no-effect exposure concentration. In general, the data indicate 

that 0 3 concentrations of 0.10 ppm (frequentiy the lowest concentration used 

i n the studi es) for a few hours per day for several days to several weeks 

generally caused significant yield reductions. Although it appears from this 

analysis that a higher 0 3 concentration was required to cause an effect than 

was estimated from the regression studies, it should be noted that the concentrations derived from the regression studies were based on a 10 percent yield 

loss, whiie in studies using analysis of variance (Table 1-6) the 0.10 ppm 

concentration frequently induced mean yield , losses of 10 to 50 percent. 

1.5.3.3 Yield Loss: Determination with Chemical Protectants. Chemicai 

protectants (antioxidants) have been used to estimate the impact of ambient 0 3 

on crop yield. In these studies, some plots were treated with the chemical 

and others were not. Yield loss was determined by comparing the yield in the 

plots treated with the chemical to the yield in untreated plots. When chemicai 

protectants are used, care must be used in interpreting the data because the 

chemical itself may alter plant growth. The chemical may not be ef.fective 

against all concentrations of all pollutants in the study area, which would 

result in an underestimation of yield loss. With an understanding of these 

limitations, however, researchers have concluded that chemical protectants are 

NQ:~l 
rn ~ 

o, 

..Zr 14- oo o, ~... ,~ .... .. 

, ~, .,....r... 

0101 01 Q1 1~ I - 1 - I - I - "ON NNNNN 

r-I ri r--I Q1 Q1 Q1 Q1 Q1 C 00 CL' 00 W N 00 td) O ~ v M Ql ~ ~ N rl rl. rl 1-1 r-i d On 01 01 Q1 Q1 Q1 

~ (~ 00 ct• N 1r I - Qn I , ~ v ~ ~~ v) r-i rl r-i r-I r--I rl rl- rnrnr.tl- r , 'orn rnt , rrn c c.~ ~.......... 

(-_rlriN0101 L OrlO r4Qlrr-1 O >>_a _a_a_a 3 d Ql v ~ Op r-I rl U L v Op v rl d v LA O a aaaaa U r-I Gl v v r E Q1 u.G U) N N N N F- r 

C v . r-I 7 L tn r-I . d • N O1 N C1 O1 d 

N • ~ • •~ f O C0 ai • E Z Z Z Z z Z ~~ "O (3) (3)N al a) N L • f0 f0 r r M (O RJ r ro ro r-1 r-I C-lC -~ L Y Y Y Y 

4-0- ~Od~~l•~ r C C ~ 

rotn Cn tnt!'1NN 

~ ro O1 +~ roU +~ C C C C C CQ1Q1 

O) O1 Gl t0 •FJ +) r-I rtl R7 '0 (0 N+-) V a) Rf (o Rf ro t0 ro rl rl L"O "O 'O "Q 'O 'O 

o: 1= 4•) ai a) .. c (L) c .... ai C c c c c c 

t'C6 cco c~i N d ro o Q rod ~ ro `°n. s~- ~ 7 

ro 

7~~ 

ro ro ro ro ro 

c c c 

G r~-•' v-E- vEi E 01 ~1 •E c•II d-% r C•E. aii •O c .0 .0.0 L.0 ~~ L v~i 0 v~i vNi vNi u~i v~i 

w CJ 4- i 7 t0 ro.0 (O N ro C.0 "O G1 • r.FJ 4-> U d 41 U1 p) v N 

•~ Ol O O r 41 N tn L O O d G1 U1 N"O N r- m fCf O L L L f-. f-. S-. 

?tn Z S S m S S O tN Q O 4_ m O LL. 3 3 3 3 3 0-0- O Y Y Y Y Y Y 

O 

W F~- W t-/ 

CC C1 

Z C 

> C0.7 •r 

S J ~f0 O 

N F-Q- +i•~ O 

W Z C E I rl 

NW C) p. 000100000tl700 N ~LL~O~ 00 tPfO ~•t.[) ~~ ~CY~ O~.L70 ~~ 

N~ C C. rl rl O ri r-I ri N N N N N ri N O N N rl r-1 O rl O r-I rl N O r-I r-I r•i r-I ~ -I 

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . J ~ v O O O O O O O O O O O O O O O O O O O O O O O O O O O O O O 

O x 

co W W O 

~-• tn 

F- O 

Q 41 

C) Q 

N 

U. a ~ 

Z W C 'p L •N ' 

(7C Or 4•J4•1 L .CL•r-L L L tLL i-r Z ' r- O iJ C C iJ i-)+) d 4J 4J U+) +J +J L +•> •i-) ~ F•) ~ 1-) +) 

=o Ln~ .+-~i 3 rtrrtr 3 •+ ~ 0 333 +~ 33L0 333+J 33333 U ~ u a 3 0 0• 3+) O o.o O 0 3 O o o O 3 a p. p. L r i >> >> r O+~ 3 L L Rf L a L O L a L L i 

~ LLJ N ~ U i\\ N Cla •F~ L i 4- C 3 a G1 01 O) L Q7 L 07 L O G1 O 

So L L Z~- sa.~ 3 3 ~ •~~ Cf 3 'O ~ w L L 'v s~. +~ +>ro+) ~ +) O ++ ~ +3 4-++ 3 3 n- V- •O 'C •C 4•) 4- rtf t. 4J L O N N 'O L.0 N L+3L+) .0 L L.0 

o'c -a -a +) L (D 

•7 a

) 3 3 E Orn Crn r O~ O C~ L cA ro a) c'n - a~ 

F- W '- O. f1 G. O Ol G) L d O O-G .O . O O G) E • • • O• af • d~ • • •r. 

00 O.0 GI Gl Rf N O+•> > L•r O +~ d N GJ ^ O L d•r N O OJ N O 

tn •F 3+J +3tN IN tN Gl tn i V7 +) q- V- C 4- 4- N}J t S M.0 Vl L 41 L4-) L t t 

? ui u1 M L ^ M OC7 r-ItO00t.P)t17MOM0 ~ Q1Na•O ~ rl ^ OpMrI0O01_ ^ 01 f_d•Cl N 6-4 ~ t1') e-1 N NLf') et r--I M M d• N r-I tD I- N ~ .C) N Ol r-1 ri t L2"1 t.f) M 01 ~ N rl N rl r-1 

Z Z W d uf _1 a 

GO.3 Ll.. 3 3 rl M ~ ; 

wO Oc ~n a0 ri ,-i ~D ~ .,tD 

O Y tn '^ N w rt 3 3 3tn cD +J (n >, a Y u) \ a N \ u, N \ \ a > >, ro (n i ) ro 3 (n ~n ~ n ~n in in 

aa~n u~ ~o a~n wtn ro a)cr 

>, >, 

roa 

rtf 'o L t0 ~ n N 4- t0 a 'o E -~ G 'O '% io 'v -0 70 l0 d •D ZJ M 'Q •Q N V'O N U O tD N O•a 3 1 Q L O ri M c!• CO > rl C N rl OJ 00 t.f) e-I 00 00 00 - a0 Op Op rl N i~ N lt'f LLO rl l0 M t- M Cl M N O ro ri N N L1'f lD N _ N aCV N N.N 

-~ ~ O 

m 

n ~a >, a a >> >, a a a >; >, >, x - 

W 

rt! fv m ro ro ~a f0 ro ro to 

\\\\\\\ a \\ -0 \\ 

~0 to v f0 i•~ 

i 

ro N ro ro•a v ro(d co 

L 

rtr ro ca ro ro 

\ R7\\ \\ i\\\ \\\\\ L L i L L L i i L O L L L i L L i L L L L L L L i L L L L • LL.C.0 L L t L.0 L t N t.0 L L L L L L L L.0 L L L L L t 

(~ N'ct'lDIOIOM'ctMNM ~ MtONNeZ•40-•IDtD CCIOrN-IrN-ICOOOlO lD tDID ID t0 . 

1A IM L Cw N L f.. d 1A GJ C t0 ro •e- f6 > •p.•r- d 

U 5- O C C C d rnr L L c ca 3 ° c o o a L s t m c 

cnroai u

vi cco.~coi o ro oc ~ n °O OCCO OE~ ror`"o o E v- 4-• i O m .c o L c+:~ v, •,- i i ai r i -p -v ro u ro m 3 4J r- r O C N+) •FJ •FJ t!f +1 d O c0 7 C N Gl C O t CO •r- •- E•r U+J G) C O i C f0 fQ +J •r L Gl GJ R1 •e- +3 R7 C. 4-3 C N O 'a i.) •- r U S- L L 

R7 4- 4- cn ~ >1 Gl O1 G) 'II N+3 G. +•~ L r DI C N O. L+•~ d L L"O N tl~f Q1 r N r Cf 

e~ e- r- fG r0 O 3 3•C rtJ GJ O N O f0 O N O U1 O•r- O a a G) E 3 L L'i- 7 

d ¢QC..JtNtNtl13=DOG- dUC.)C> m D_3 -IdG.SS d'Q N 3 C73 cn 

1-68 

~ 
an objective method of assessing the effects of 0 3 on crop yield, especially 

in conjunction with other methods. Results of several studies with chemical 

protectants showed decreased crop yield from exposure to ambient oxidants 

(Tabie 1-7). Crop yields were reduced 18 to 41 perecent when the ambient 

oxidant concentration exceeded 0.08 ppm for 5 to 18 days over the growing 

season of the crop. 

1.5.3.4 Yield Loss: Determination from Ambient Exposures. A number of 

research studies have demonstrated that ambient 0 3 concentrations in a number 

of locations in the United States are sufficently high to impair plant yield. 

Of studies to determine the impact of ambient oxidants (primarily 0 3 ) on plant 

yield, most have compared the yield differences between plants grown in ambient 

air and those grown in charcoal-filtered air. Early research documented that 

ambient oxidants reduced the yield and quality of citrus, grape, tobacco, 

cotton, and.potato (U.S. Environmental Protection Agency, 1978). Subsequent 

studies substantiated the impacts of ambient oxidants on plant yieid (Table 

1-8). Over several years, bean yields varied from a 5 percent increase to a 

22 percent decrease in response to 0 3 concentrations in excess of 0.06 ppm 

(Heggestad and Bennett, 1981). 

Studies conducted on eastern white pine in the southern Appalachian 

mountains showed that ambient 0 3 may have reduced the,radial growth of sensitive 

individuals as much as 30 to 50 percent annually over the.last 15 to- 20 years 

(Mann et al ., 1980) . Fi el d studi es i n the San Bernardi no Nati onal Forest 

showed that during the last 30 years ambient 0 3 may have reduced height growth 

of ponderosa pine by as much as 25 percent, radial growth by 37 percent,. and 

the total wood volume produced by 84 percent (Miller et al., 1982). Calculations of biomass in these studies were based, however, on apparent reductions 

in radial growth without standardization of radial growth data with respect to 

tree age. 

1.5.3.5 Yield Loss Summary. Several general conclusions can be drawn from 

the various approaches used to estimate crop yield loss: The data from t.he 

comparisons of crop yield in charcoal-filtered and unfi.ltered air (ambient 

exposures) clearly show that,ambient levels of 0 3 are sufficiently elevated in 

several parts of the country to impair the growth and yield of plants. The 

data from the chemical protectant studies support and extend this conclusion 

to other plant species. Both approaches indicate that the effects occur at 

low mean concentrations, with only a few 03 occurrences greater than 0.08 ppm. 

1-69 
f~T N 

H 

Z 

C1 ¢ J {--• 

W U 

l--1 W >" F" 

CD 

a a: 

C) 936 

U _J 

Q 

Z U 

O I--I 

~ 

w w 

zx 

O U 

O tL 

LL Q O `LLJ FN— 

U W 

tW tzW >- 

m 

t~ 

°w 

~ z 

~ 

W ~ 

J W 

mr ¢ W 

H cm 

N 

¢ 

d 

u 

C 

N i. 

d 

4- 

O 

~ 

CJ 

L 

~ 

N 

O E 

O. Q 

X 0- 

N 

c 

m 

r r 

i-)O 

V S- ~ 4-) 

'II C 

L V 

't7 4- 

r O 

N 

•r aQ 

r I

M 

O 

~ 

c 

N 

d S- >) 

•r Q1 it) v p 

41 O u p• uI C {-) 

N C O rtt C 

ro r E rt1 

OO O f— m 

O 

U i-) +) 

rt1 td co 

L +-) +-) 

O O O 

1-- a a 

>1 

-0 ~a 4-) 

:3 r 

+-) 3 

O 

C UJ L 

fii .{-) 1 

a1 cu E 

L i Q 

N i-) 

L • O 

{.] r ln 1-'I 

-i-) E C ~ 

0- O rt1 

-C7 

-o 

N C r d C 

X.a ~t~0 ~ 

N 4-- N IO 

O .F 

(.0 . d v~ = T3 W N f0 •r "O iJ S fO W •r a c 3 a 

TT •r 

a ~ a~ v4-) 

b~ L 3 0 ~ 

•r (U +) "0 O •E C1R! Mftt 

•r O CL Or 

4-) iJ •r d-) •r .vc •E b ~ ro a~ 4-) U) 

a ~ E O 

L O O L C tn 

i-) ~ t~ i~ rO 

L ~ 

cn 

r N U) lA 

s- O 

O Nr fClr 

"Q C O N 

-°~ ~ e + a ~ 

t0 •r L C N U! ~ 3 ~ u +) 

. ~ a > a~ 

v d UI O L 

~ I\ In 4-3 4-) 

3m 3 ~ ~ ~ 

tn C U -n 

N O N tn 

r r •r }) (d 

U Iti 4--) O 3 >> 

N U i- r 

a.-N :3 ci >a v 

tn N 

- O "O > 

N r 7 • r 

N Ln f-- td i-> +-) 

L c U tf) U 

4- ) •r 'O •r O 

C r E Lo O.. 

r C N N •r lA 

r (d •r .0 L 4J 

M cd¢ ~ U U ~ 

.-. 

m 03 p- ~ 

r- 00 

.-. ... -a .. .. 

ct O r . 

M 

L 

v~

r~-i 4-) i E 

O

OD

i 

v v! O tn ri 

4- N 

O 'O ul a N 

r = C r 00 

Rf fIf 00 "O Ol r 

'CS C r-I rC 

•1-~ C N 'C3 fU v 

GI Rf 

U R1 S- N 

Qf L r f0 fq 

C U TA U1 tn tA N 

•r N l!I r M N ,C 

C Rf (0 L1 ' O N L 

C .IC o) E IA u) Rl 

Rf 7 QJ N •r •r r 

, 

~ OO 00 CJ 

I w 

+> >a 

:3 R7 O s o 

Lti a sU)

, 

~, E Oo s 

•1-~ ~- ~ "C ul Z7 L ~A 'C3 ~ ~ L tn 

4-3 > ~ N i-) r-1 M i-) d- ~ OtD +-3 

O.G 

Ln 

L N ~ O ~ 4- O ~ L E 4-- O 

O s- +

-) c c E c O E c4

-) Q O E 

4- L C O O 

O_ O Q. U 

O M r M 0) r M I OO rl_ E 00 OO OO 00 co 00 c OO rtf 

ON O d O S- O+-) i- O•r O+) i 

O 4- N O V- O> O-1-> > O 7 O+> > 

A O M n O A O A v O A -0 A 

1--' O 

d- M M N ~ M N ~ 

1- 70 
0 

~ C L 

O +-) 

C 

a +-) O 

r- V V 

~ N O 

r p E 

>- N O 

L L 

4- 

C 

0 

4-) 

ro 

L 

7 

a 

a 

i 

3 

O 

d 

X 

W 

C 

O 

4•.) ro 

L 

cl++ E 

O C t1 i 

G7 tz I 

V 

C 

O 

U 

N 

d 

O 

tr 

U 

0 

w 

FU 

W 

J 

L.LI 

cn 

ti 

O 

fl 

J 

W 

H } 

Z 

0 

N 

FZ Q 0 

H 

x 

O 

F-~ 

Z 

W 

m 

~ 

Q 

1.L 

O 

cn 

H 

CJ 

W , 

L.L 

l.L 

W 

I W 

r-I 

W 

J 

m 

¢ 

I-- 

~ 

C1 . 0 

N 

O U,

+-) 

C 

ro 

a 

ar 

V 

C 

N 

L 

C! 

4- 

Gf 

tL' 

C ~ 

oa 

r o 

m w 

o4- 

J O 

r. 

~ .. . 

r` .. r o 

rn a,--+ r oo 

~ c 00 r- ai rn 

a.. ro rn ro 3 r+ 4-) +) 

C rl O v N N 

10 L a ~ a.•> 2 ' d RJ G1 GJ _N C 

C "O •F) i• ) , ••• t!f O ~ 

ro•r tn +J in RS 

N N OJN r 01 d.' Gl M IZ lD 

UL O)G 3Q1a V O~

l O N 

t6 U N GJ O r-i C 

M:N ZOO 2 ~ 10 

ro 

Y a a Rf f0 C 

L C C 

o m Io •c •c 

i 

o 

} 4- 

a~ ns /o io 

Z ~ E :> i U 

U) 3 > 4n > v > V) ; 3 

a r oro• oro oro c L v~ wc E -0 E wo E s v~ 

V- Gl +-) rO.O /0 O /0 O cn 41 

i 3 GJ L 

+-) 4- +~ r- ~ r- ~ r-.O i 4 3 a co ro ro v- 

•i O 'C N O C O C O C L IO 

4- p. O M dJ 7 •F) 7 +-) 7 'f6 Gl r-L 

^+•~ ^L ^S.. O ^i O I 

3 co M N r1 N CM ~ N ~ N ~ 01 N I 

E E E E a E v~ O~ ~ a~ E O) E - v+ ~ ro ro o ro a ro rz 

E i 

i N OJO dO NO' N 

O C O C C O S L C > ~ O > o >o 

O O O N O+•~ 4-~ -~ O 3 •I rtf • ro• rtJ • E - G7 CO L l0 L O IL . O) Q1 N Q1 00 3 O OJ L 4- +) ~ N~ d>> OJ O +J Cf ~ +J ri C GJ O cC /0 1•0 rt1 I ~ ro 1 ~ .. 

./0 I 16 I d I N O> L a E'C E a E tD ^ N 

L 

a) 

L 

a) 

iT 

/o 

~ 1 '••~ O Z~R 

Ln c 

41 \ • 41 \ • 41 

s E+J L E+) L E+) 

> E > E L E L 41 L N E L O. L G..O n. s E tD 

10 (0 OJ L E+ ) N•^ V Q. tC N ro N /0 Gl L . I ' 

/0 /0 > IQ /0 -0 N C O_ 00 tN 00 tN 00 cN Q_ >> - >> >> 10 V- /0 r• E L O O I O I O 1 4- 

rtf O [6 O O O N 41 V 00 ^ O 3 

a0 a0 00 O E+-) E O Q1 • O•• ri ••• O•'7 ' 

E - - O O O.E v 1 , 0 LOoO L000 

01 l0 M lD Q1 rl L N 7 L O Ql r-1 IZ 01 r•-I IZ 01 rl Q O~D 01 rl i Q1 M v M Cp ~ tN U1 +) A rI ri Q ri v Q t,C) 

N O r\ rn 

O O 

O O 

I 

r i f

I

in I~ - N N r-1 L27 

M ri cY r-i ~ I- tf•) t.f) U7 M 00 OO 

O O O O O O O O O O O 

O O O O O O O O O (M O 

v — n n n 

w in 

L J Y y 

~ >_ m s"'- ro ,v .

~ to r a) a) 

> +> > U tn V 

,••a .. ~ r~ +~ (a 

tD C U tV r- Y VJ > 

OC) 

L v00 V >O- u i ~ .. ¢ 

a~ m ~ ro c ro ~ 

M s c L tV V 

J N ro L pf O C L 

d a N O C Gl _ U R7 t0 

O i C fq r N C C 

{.) •r N + ) O G) +~ L N •N O O IvLL. c c.wrn a ro m aim ~ m v N Q N N U ~ LL N v v 

1-71 
Growth and yield data from the previous criteria document (U.S. Environmental 

Protection Agency, 1978), shown in Figure 1-3, indicate that effects on 

growth and yield of several plant species occurred when the mean 0 3 concentration (for 4 to 6 hr/day) exceeded 0.05 ppm for at least 2 wk. The data from 

the regression studies, conducted to develop exposure-response functions for 

estimating yield loss, indicated that at least 50 percent of the species/cultivars tested were predicted to display a 10 percent yield loss at 7-hr seasonal 

mean 03 concentrations of 0.05 ppm or less. Most of the data from the discrete 

treatment studies did not use levels low enough to support these values directly. 

The magnitude of yield losses reported at 0.10 ppm, however, indicate that 

maintenance of a substantially lower concentration than 0.10 ppm is needed to 

prevent 0 3 effects, although a specific value cannot be derived from the 

discrete treatment studies. 

1.5.4Effects on Crop Quality 

Based on results of the few studies that have been conducted, 0 3 can 

reduce crop quality in addition to reducing the total yield of the crop. 

Quality is a general term that includes many features of the crop, such as 

nutritional composition, appearance, taste, and ability to withstand storage 

and shipment. Examples of 0 3-induced alterations in quality are decreased oil 

in soybean seeds (Howell and Rose, 1980; Kress and Miller, 1983); decreased 

R-carotene, vitamin C, and carbohydrates in alfalfa (Thompson et al., 1976b; 

Neely et al., 1977); and increased reducing sugars that are associated with 

undesirable darkening when potatoes are used to make potato chips (Pell et 

al., 1980). 

1.5.5Statistics Used to Characterize Ozone Exposures 

The characterization and representation of plant exposures to 0 3 has 

been, and continues to be a major problem. Research has not yet clearly 

identified which components of the pollutant exposure cause the plant response. 

Most studies have characterized the exposure by the use of inean 0 3 concentrations, although various averaging times have been used. Some studies have 

also used cumulative 0 3 dose. The difficulty of selecting an appropriate 

statistic to characterize plant exposure has been summarized by Heagle and 

Heck (1980). Ambient and experimental 0 3 exposures have been presented as 

1-72 
seasonal, monthly, weekly, or daily means; peak hourly means; number of hours 

above a selected concentration; or the number of hours above selected concentration intervals. None of these statistics adequately characterize the 

relationships among 0 3 concentration, exposure duration, interval between 

exposures, and plant response. The-use of a mean concentration (with long 

averaging times) (1) implies that all concentrations of 0 3 are equally effective in causing piant responses and (2) minimizes the contributions of the 

peak concentrations to the resonse. The mean treats low-level, iong-term 

exposures the same as high-concentration, short-term ones. Thus, the use of a 

long-term mean concentration ignores the importance of peak concentrations; to 

ignore the peaks is inconsistent with the literature. 

The total ozone dose (concentration muitiplied by time) has been used to 

describe plant exposure; however, it suffers from the same problem as the 

mean. The total dose is simply the summation of the ppm-hr over the study 

period, which also treats all concentrations as being equally effective. 

Several investigators have attempted to give greater importance to peak 0 3 

concentrations. For example, Oshima et al. (1977a,b) and Lefohn and Benedict 

(1982) have summed only the ppm-hr of exposure greater than some preselected . 

value. Larsen et al. (1983) have introduced the concept of "impact" to describe 

the effects of 0 3 and S0 2 on soybeans. The "impact (I)" is calculated similarly 

to total dose, except the concentration is raised to an exponent greater than 

one (I = Cw X T); this method of calculation effectively gives greater weight 

to the higher concentrations. More recently, Larsen and Heck (1984) have 

suggested the term "effective mean" to describe an approach in which greater 

importance is given to higher concentrations. The "effective mean" is defined 

as the average hourly impact raised to an exponent and divided by the duration. 

Several lines of evidence suggest that higher concentrations should be 

regarded as having the greater influence in determining the impact of 0 3 on 

vegetation. Studies have shown that plants can tolerate some combinations of 

exposure duration and concentration without exhibiting foliar injury or effects 

on growth or yield, illustrating that not all concentrations are equaily 

effective in causing a response. From the toxicological perspective, it is 

the peaks or concentrations above some level that are most likely to have an 

impact. Effects occur on vegetation when the amount of pollutant that the 

plant has absorbed exceeds the ability of the organism to repair or compensate 

for the impact. 

1-73 
Studies with beans and tobacco (Heck et al., 1966) showed that a dose 

(concentration times time) distributed over a short period induced more injury 

than did the same dose distributed over a longer period. Tobacco studies 

showed that the 0 3 concentration was substantially more important than exposure 

duration in causing foliar injury (Tonneijck, 1984). In beans, foliar injury 

occurred when the internal 0 3 flux exceeded 115 pmoles/m 2 in 1 hr (Bennett, 

1979). A single 3-hr exposure, however, at approximately half the concentration 

(0.27 compared with 0.49 ppm) required a 64 percent greater internal flux of 

03 to produce the same amount of foliar injury as the 1-hr exposure required. 

More recently, Amiro et al. (1984) showed that higher concentrations were more 

important than low concentrations in causing injury. Their study also suggested 

the existence'of a biochemical injury threshold (i.e., the 0 3 uptake rates 

that plants can experience without incurring visible foliar injury). The 

greater importance of concentration compared to exposure duration has also 

been reported by other authors (e.g., Heck and Tingey, 1971; Henderson and 

Reinert, 1979; Reinert and Nelson, 1979). 

Studies with soybean (Johnston and Heag1e, 1982), tobacco (Heagle and 

Heck, 1974), and bean (Runeckles and Rosen, 1977) showed that plants exposed 

to a low level of 0 3 for a few days became more sensitive to subsequent 0 3 

exposures. In studies with tobacco, Mukammal (1965) showed that a high 0 3 

concentration on one day caused substantial injury, whereas an equal or higher 

concentration on the second day caused only slight injury. Using stress 

ethylene as an indicator of 0 3 effects, Stan and Schicker (1982) showed that a 

series of successive short exposures was more injurious,to plants than a 

continuous exposure at the same 0 3 concentration for the same total exposure 

period. Walmsley et al. (1980) continuously exposed radishes to 0 3 for several 

weeks and found that the plants acquired some 0 3 tolerance. The acquired 

tolerance displayed two components: (1) the exposed plants developed new 

leaves faster than the controls, and (2) there was a progressive decrease in 

sensitivity of the new leaves to 0 3 . The newer leaves also displayed a slower 

rate of senescence. The observations by Elkiey and Ormrod (1981) that the 0 3 

uptake decreased during a 3-day study period may provide an explanation for 

the results with radish. 

Not only are concentration and time important but the dynamic nature of 

the 03 exposure is also important; i.e. whether the exposure is at a constant 

or variable concent°ration. Musselman et al. (1983) recently showed that 

constant concentrations of 0 3 caused the same types of plant responses as 

1-74 
variable concentrations at equivalent doses. - Constant concentrations, however, 

had less effect on plant growth responses than variable concentrations at 

similar doses. Exposures of radishes to ambient 0 3 in open-top exposure 

chambers showed that significant yield reductions occurred when the maximum 0 3 

concentration exceeded 0.06 ppm at least 10 percent of the days when the crop 

was growing (Ashmore, 1984). Initial studies have compared the response of 

alfalfa to daily peak and episodic 0 3 exposure profiles that gave the equivaient 

total 0 3 dose over the growing season (Hogsett et al., 1985). Alfalfa yield 

was reduced to a greater extent in the episodic than in the daily peak exposure. 

This study also illustrates the problem with the 7-hr seasonal mean concentration; i.e., it does not properly account for the peak concentrations. The 

plants that displayed the greater growth reduction (in the episodic exposure) 

were exposed to a significantly lower 7-hr seasonal mean concentration. 

Studies with S02 also showed that plants exposed to variable concentrations 

exhibited a greater plant response than those exposed to a constant concentration (McLaughlin et al., 1979; Male et al., 1983). 

1.5.6 Relationship Between Yield Loss and Foliar Injury 

Because plant growth and production depend on photosynthetically functional 

leaves, various studies have been conducted to determine the association 

between foliar injury and yield for species in which the foliage is not part 

of the yield. Some research has demonstrated significant yield loss with 

little or no foiiar injury (e.g., Tingey et al., 1971; Tingey and Reinert, 

1975; Kress and Skelly, 1982; Feder and Campbell, 1968; Adedipe et al., 1972). 

Other studies showed that significant foliar injury was not always associated 

with yield ioss (Heagle et al., 1974; Oshima et al., 1975). The relative 

sensitivities of two potato cultivars were reversed when judged by foliar 

injury versus yield reductions (Pell et ai., 1980). In field corn, foliar 

injury occurred at a lower 0 3 concentration than yield reductions; but as the 

0 3 concentration increased, yield was reduced to a greater extent than foliar 

injury was increased (Heagle et al., 1979a). In wheat, foliar injury was not 

a good predictor of 03-induced yield reductions (Heagle et al., 1979b). 

1.5.7 Physiological Basis of Yield Reductions 

As discussed earlier in this summary, plant growth is the summation of a 

series of biochemical and physiological processes related to iaptake, assimilation, biosynthesis, and translocation. An impairment in these processes may 

iead to reduced plant yield if the process is limiting. 

1-75 
For plant growth to occur, plants must assimilate CO 2 and convert it into 

organic substances; an inhibition in carbon assimilation may be reflected in 

plant growth or yield. In several species 0 3 (at 0.05 ppm and higher) inhibited 

photosynthesis, as measured by gas-exchange (e.g., U.S. Environmental Protection 

Agency, 1978; Coyne and Bingham, 1978; Black et al., 1982; Bennett and Hill, 

1974; Yang et al., 1983). Biochemical studies showed that 0 3 (0.12 ppm for 2 

hr) inhibited an enzyme that catalyzes the assimilation of CO 2 (Pell and 

Pearson, 1983). 

Ozone, in addition to decreasing the total amount of CO2 that is assimilated, alters that pattern by which the reduced amount of assimilate is partitioned throughout the plant. There is generally less photosynthate translocated to the roots and to the reproductive organs (e.g., Tingey et al., 1971; 

Jacobson, 1982; Oshima et al., 1978, 1979; Bennett et al., 1979). This reduces 

root size and marketable yield as well as rendering the plant more sensitive 

to injury from environmental stresses. Another consequence of reduced root 

growth and altered carbon allocation is an impairment of symbiotic nitrogen 

fixation (U.S. Environmental Protection Agency, 1978; Ensing and Hofstra, 

1982). 

The reproductive capacity (flowering and seed set) is reduced by 0 3 in 

ornamental plants, soybean, corn, wheat, and other plants (Adedipe et al., 

1972; Feder and Campbell, 1968; Heagle et al., 1972, 1974; Shannon and Mulchi, 

1974). These data suggest that 03 impairs the fertilization process in plants. 

This suggestion has been confirmed in tobacco and corn studies using low 

concentrations of 0 3 (0.05 to 0.10 ppm) for a.few hours (Feder, 1968; Mumford 

et al., 1972). 

Ozone both in the field and in chamber studies stimulates premature 

senescence and leaf drop (Menser and Street, 1962; Heagle et al., 1974; 

Heggestad, 1973; Pell et al.; 1980; Hofstra et al., 1978). In part, the 

03-induced yield reducti,on has been attributed.to premature senescence. The 

premature leaf drop decreases the amount of photosynthate tbat a leaf can 

contribute to plant growth. 

1.5.8 Factors Affecting Plant Response to Ozone 

Numerous factors influence the type and magnitude of plant response to 

03 . Most studies of the factors influencing plant response have. been limited 

to effects on foliar injury; however, some studies have measured yield and 

1-76 
some have researched the physiological basis for the influences. The parameters studied include environmental factors, biological factors, and interactions with other air pollutants. 

1.5.8.1 Environmental Conditions. Environmental conditions before and during 

plant exposure are more influentiai than post-exposure conditions in determining 

the magnitude of the plant response. The influence of environmental factors 

has been studied primarily under controlled conditions, but field observations 

have substantiated the results. Most studies have evaluated the influence of 

only a single environmental factor and have relied primarily upon foliar 

injury as the plant response measure. Some generalizations of the influence 

of environmental factors can be made: 

1. Light conditions that are conducive to stomatal opening appear to 

enhance 0 3 injury (U.S. Environmental Protection Agency, 1978). 

Light is required to induce stomatal opening, which permits the 

plant to absorb pollutants. 

2. No consistent pattern relating plant response to temperature has 

been observed (U.S. Environmental Protection Agency, 1978). Plants 

do not appear to be as sensitive at extremely high or low temperatures, however, as they are under more moderate conditions. 

3. Plant.injury tends to increase with increasing relative humidity 

(U.S. Environmental Protection Agency, 1978). The relative humidity 

effect appears to be related to stomatal aperture, which tends to 

increase with increasing relative humidity. McLaughlin and Taylor 

(1981) demonstrated that plants absorb significantly more 0 3 at high 

humidity than at low humidity. It is generally accepted that plants 

in the eastern United States are injured by lower concentrations of 

0 3 .than their counterparts in California; this phenomenon has been 

attributed to differences in humidity (U.S. Environmental Protection 

Agency,..1978). 

4. As soil moisture decreases, plant water stress increases and there 

is a reduction in plant sensitivity to 03 (U.S. Environmental Protection Agency, 1978). The reduced 03 sensitivity is apparently related 

to stomatal closure, which reduces 0 3 uptake (U.S. Environmental 

Protection Agency, 1978; Olszyk and Tibbitts, 1981; Tingey et al., 

1982). Water stress does not confer a permanent tolerance to 0 3 ; 

1-77 
once the water stress has been alleviated, the plants regain their 

sensitivity to 0 3 (Tingey et al., 1982). 

1.5.8.2 Interaction with Plant Diseases. Ozone can affect the development of 

disease in plant populations. Laboratory evi'dence suggests that 0 3 (at ambient 

concentrations or greater for 4 hr or more) inhibits infection by pathogens 

and subsequent disease development (Laurence, 1981; Heagle, 1982; U.S. Environmental Protection Agency, 1978). Increases, however, in diseases from "stress 

pathogens" have been noted. For example, plants exposed to 0 3 were more 

readily injured by Botrytis than plants not exposed to 0 3 (Manning et al., 

1970a,b; Wukasch and Hofstra, 1977a,b; Bisessar, 1982). Both field and laboratory studies have confirmed that the roots and cut stumps of 0 3-injured ponderosa 

and Jeffrey pines are more readily colonized by a root rot (Heterobasidion 

annosus). The degree of infection was correlated with the foliar injury 

(James et al ., 1980; Mi 11 er et al ., 1982). Studi es i n the San Bernardi no 

National Forest showed that 0 3-injured trees were predisposed to attack by 

bark beetles and that fewer bark beetles were required to kill an 0 3-injured 

tree (Miller et al., 1982). 

1.5.8.3 Interaction of Ozone with Other Air Pollutants. The report of Menser 

and Heggestad (1966) provided the initial impetus for studying the interaction 

of 03 with S02 . They showed that Bel W-3 tobacco plants exposed to 0 3 (0.03 

ppm) or S02 (0.24 to 0.28 ppm) were uninjured but that substantial foliar 

injury resulted when the plants were exposed to both gases simultaneously. 

Subsequent studies have confirmed and extended the observation that combinations 

of 03 and S02 may cause more visible injury than expected based on the injury 

from the individual gases. This injury enhancement (synergism) is most common 

at low concentrations of each gas and also when the amount of foliar injury 

induced by each gas, individually, is small. At higher concentrations or when 

extensive injury occurs; the effects of the individual gases tend to be less 

than additive (antagonistic). In addition to foliar injury, the effects of 

pollutant combinations have also been investigated in relation to other plant 

effects, and these have been discussed in several reviews and numerous individual 

reports (e.g., Reinert et al., 1975; Ormrod, 1982; jacobson and Colavito, 1976; 

Heagle and Johnston, 1979; Olszyk and Tibbitts, 1981; Flagler and Youngner, 

1982; Foster et al., 1983; Heggestad and Bennett, 1981; Heagle et al., 1983a). 

1-78 
Field studies have investigated the influence of S0 2 on plant response to 

0 3 at ambient and higher concentrations in several plant species: soybean 

(Heagle et al., 1983b; Reich and Amundson, 1984), beans (Oshima, 1978; Heggestad 

and Bennett, 1981), and potatoes (Foster et al., 1983). In these studies, 0 3 

altered plant yield but S02 had no significant effect and did not interact 

with 03 to reduce plant yield uniess the S0 2 exposure concentrations and 

frequency of occurrence were much greater than the concentrations and frequencies of occurrence typically found in the ambient air in the.United States. 

The applicability of the yield results from pollutant combination studies 

to ambient conditions is not known. An analysis of ambient air monitoring 

data for instances of co-occurrence of 0 3 and S0 2 indicated that at sites 

where the two pollutants were monitored, they both were present for ten or 

fewer periods during,the growing season (Lefohn and Tingey, 1984). Cooccurrence was defined as the simultaneous occurrence of hourly averaged 

concentrations of 0.05 ppm or greater for both pollutants. At this time, it 

appears that most of the studies of the effects on pollutant combinations (0 3 

and S02 ) on plant yield have used a longer exposure duration and a higher 

frequency of pollutant co-occurrence than are found in the ambient air. 

Only a few studies have investigated the effects.of 0 3 when combined with 

pollutants other than S0 2 , and no clear trend is available. Preliminary 

studies using three-pollutant mixtures (0 3 , 502 , NO2 ) showed that the additions 

of S02 and NO2 (at low concentrations) caused a greater growth reduction than 

03 alone. 

1.5.9 Economic Assessment of Effects of Ozone on Agriculture 

Evidence from the plant science literature clearly demonstrates that 0 3 

at ambient levels will reduce yields of some crops (see Chapter 6, Section 

6.4.3.2.2). In, view of the importance of U.S. agriculture to both 'domestic 

and world consumption of food and fiber, such reductions in crop yields could 

adversely affect human weifare. The plausibility of this premise has resulted 

in numerous attempts to assess, in monetary terms, the losses from ambient 03 

or the benef.its of 03 control to agriculture. Many of these assessments have 

been performed since publication of the 1978 0 3 criteria document (U.S. 

Environmental Protection Agency, 1978). The utility of these post-1978 

studies in regulatory decision-making can be evaluated in terms of how well 

the requisite biological, aerometric, and economic inputs conform to specific 

criteria, as discussed in Section 6.5 of Chapter 6. 

1-79 
While a complete discussion of the criteria for evaluating economic 

~ 

assessments is not appropriate here, it is instructive to highlight certain 

key issues. First, the evidence on crop response to 0 3 should reflect how 

crop yields will respond under actual field conditions. Second, the air 

quality data used to frame current or hypothetical effects of 03 on crops 

should represent the actual exposures sustained by crops in each production 

area. Finally, the assessment methodology into which such data are entered 

should (1) capture the economic behavior of producers and consumers as they 

adjust to changes in crop yields and prices that may accompany changes in 0 3 

air quality; and (2) ideally, should accurately reflect institutional considerations, such as regulatory programs, that may result in market distortions. 

The assessments of 0 3 damages to agricu.lture found in the literature 

display a range of procedures for calculating economic losses, from simple 

monetary calculation procedures to more complex economic assessment methodologies. The simple procedures calculate monetary effects by multiplying 

predicted yield or production changes resulting from exposure to 03 by an 

assumed constant crop price, thus failing to recognize possible crop price 

changes arising from yield changes as well as not accounting for the processes 

underlying economic response. Conversely, a rigorous economic assessment will 

provide estimates of the benefits of air pollution control that account for 

producer-consumer decision-making processes, associated market adjustments, 

and perhaps some measure of distributional consequences between affected 

parties. It is important to distinugish between those studies based on naive 

or simple models and those based on correct procedures, since the naive procedure may be badly biased, leading to potentially incorrect policy decisions. 

Most of the post-1978 economic assessments focus on 0 3 effects in specific 

regions, primarily California and the Corn Belt (Illinois, Indiana, Iowa, 

Ohio, and Missouri). This regional emphasis may be attributed to the relative 

abundance of data on crop response and air quality for selected regions, as 

well as the national importance of these agricultural regions. Economic 

estimates for selected regions are presented in Table 1-9. In addition to 

reporting the monetary loss or benefit estimates derived from each assessment, 

this table provides some evaluation of the adequacy of the plant science, 

aerometric, and economic data, and assumptions used in each assessment. 

Adequacy as defined here does not mean that the estimates are free of error; 

rather, it implies that the estimates are based on the most defensible biologic, 

I C :Ti 
0 H 

H 

~ 

0 

CL 

W 

Z O 

N 

O 

O 

w 

CU 

Z 

W 

~ 

O 

LU 

Z 

O 

c~ 

f 

O 

LU

O 

U 

J 

Q 

O 

cm LU 

0 V)

}WE 

F 

W 

O 

>- 

z 

¢ 

~ 

f 

N 

rn 

~ 

w 

Q F•-• 

E' t C ' m 

7 +1 N m •r 

N- N` m~ G/ 3 a7cat m N a u ul E o mN0 E 

a al ~mr =m =n..a~i 

m N N ro/~ 7 i y}1 n ' p L U t0 +~ CO7 c L ro^ a r- w N c 0. 

d nU Gl Q1 Lr• roa N 7 LCf L L LNL - t)p N L i 7 N ri i•~ m•r .r 

ro .O O +~ a 7 7 II m ~ N L d C~^ n O E X G7 01 +~ N N Cn E E U rl C ro c m O 

E Cl U n c•r C p0.• N v p O) U ro . . 

E E• GJ N aa u i0 r o C) c E•r L N= a N E u r •r c c 

tt o +~ o c 3 C7 7 N C•r e•aa/r ia' uao cNO No aa mo O +•t o ro i .F.1 c c+1 > N u c 10 a-+ > N•r •r E u u u•r a/ o al ^ a/ o v v > aui °u °.°1 0l ln a°'i m w U N.G u~0 Gl .0 4- N c 4- 0! Gl = O L C 4- N L G) L. U 4- 4- = N G! 4F GJ e- m . p al d~ M E L at o O al •r m a/ c L ro L o r• c E N o o 3++ .o i r.c 3 u +~ u•r ~ a u at u +1 +t o 

a o e a/ cm o°u~ c o.~ e c aci °o e ai N~vo N 

Q O Of O 7 Gl a O a O ro N C O~ N 7 N c C U n+) r- ri C c L o m L u a 7•01t- ro O U~ 6m1 s o~~~ V o 0 

uLV- = ro c o am+~ u a/r a uL urn c o u W U O N v m; L rl N W ro a U N W U ro rl •r .I..t m 

al a 

o OI 1 c a a o Ol m E t C 

a c o ^o r al o m N L .N C L r-•r •N n > E U C ~ G1m•E ~~ Y O m i-t 0! +1 Na•r N a L L+~ 7 r- U m W c E E m GJ u~ Co a c N m a u m.L] t a ro o C U•r L GI 4/ = m•r y c a i •E N 7 c o 

•i m O C C U ~ C m L •• d O E r- N O L r E U.C. t- U C m U 0. U• G! p. E L a..1 O a N r• y m+•t I, = O a C O Gl > a 61 G. U L U a a N•r~a . U Q•r L c o roL at•r•r c ow E +1 ~.- > E O E O a L 3 rl O~ N O~ U 0^0 N 

^ m U W = O C O'C CO C. C •.•.t.l 7 r Ql ro U C7 E•r y y C c! U a m V- CJ u7 d N L m r-1 m N•r }i }1 L O lD +1 •r y +•t Q1 N E 4•1 L U C E m N m ^ U(~ m E N T N t0 r•I G/ i•t m m/~•C N•r O O 7 7 L r- U 0, O> 7 O O r- d E L. N 7 r• N C+j C C C• O a Gl •r rl Q C G. 0.>•r E O~ IT•r pp p/ U L +1 O Gl c ro II E a O7 O E 0. i+~ O C••-•~ Gl E 01 L N U U a G! 7 O O C G a U O 7 7 N S.. Oa a•r ~ W Q ITv E c m•r Q d U N U O! Y- v- m Q N v nV- +t 

N N N t m L t U 01 N t E ro m s. N . a t Z 

'Q t0 7 7 tA E_ E t N 7 E L i t 0.~ +3 •1- O/ O N N r• N Gl • Q 1 a O•- Cf ~ O 7 Gl C O. O m C C w U N m m L r- C C y~ J C+.) O 7 r L i O a~ O N N> O C1 i r i i+t L y 7 m•r O ro CJ m m G. U Rf • ro Y- U•r L • O m U C•L O O N•L • 7 O•r 7 L N C • a X c m a N C. N i 0. r y}.t W y O m O~ N L ro m O d+/ E 

+~ u ro alNOCVC ro N•r ro— aJ L. o p ^ro c ox=T a. U++ c~•N aNOlupt w Gl •r r• c - tp L•r CI m pf o c E m m 7 U+.~ m•r ... m 4- i-t E m o+J •r L o i E C..7 3 c ••• C.H c ~..~ o G! L a a i va at d o N oav- ol v•^a++•rL E o o v m•r d N a o L 3 ai 

i N 3 N m 0. +~ N +.t N G1 C a~ m . ri N E ~•t L a L+~ +1 i > L. O L 

m E 7 3 G! N N• r~ _Ta N L ro C i O rO N 0.t0 Ol . m• O N U 7 N m 0.w T~ y y 7 O 7 E f- ri O C a N 7¢ a+t 7J p N t U O O• N> O Ol C O i iJ N C IT•r N +1 O O E L. G1 6 L•r N a O iJ L. L tb •.- i - N m• . n U i • 7 U O O 61 O m N C L O O L m i~ N m RI C O O p_ L U p• +~ N a Cl +~ X X O O O d r•r a GJ N Of G! O 1~ • L•r O•r a•r p O r i X N I ro L•r X •L ¢ Q E ro al al 4- vL ~- U a•~ ¢ L E m U 9- vn ~F Q m N ¢ c m E u n.w ro Il- 0! m d y 

U r 

w•1 L r Gl i tU O C 7 OJ VI w N ro 41 41 O a•r,•r t a n c+~ ro ++ = N c T a r- oo m rn a to = 61 L•r a o u Y 

ro•mo J ro iJ ~ °1 c aui >' a! c¢ 7 o Q. •~, o N C. E 3 J tn W a ai 

^m N > C N o 41 IC•1 }f E~ 1~ ~ z a~ a 7 4- L O U O U Ol . N m W o Gl ~ C 5- L N E N N G1 c 0.•^^> ^ 7 4- C O C 003 7 U O N N i0 C G! 4- O 4- O L Q1 • G7 +J t' O +> a n4- rf N•L +.t i m 01 G m G! G/ m Gl N y N {.> ~rl . 7 N+1+J +~ daL N^ N Qv N N O'• C m m m i G7 m G N 7 c C1 N Gl O E a 7 > O O c O• ro a Y d N a n•r tTy1 •r O n O m U a N m N}1 T y N L L N•r y 

a' tiSp E.°- H s aNi m Q E•OO+L.I L o ro 

N ~ c 00 ^ ~ y r ~ L. 

+•t t0 1, GJ L 4- N n C1 v+J E O v L 

~G! o c r~-1 ''i c 

C L O c~ . l.f) U n al+1•r c w r N M vr N no i us4-o.~ m o.a ro m p N 

m U E In - M'-' E o I~ i 0000 Ln O't- '~Y O ri O i~ O M C° C1 c O V} 64 a Nf a lL 4- }t ty •r O rl • 

¢ T 

N i m 3 ^ N m i ^ o m ^ ro o ui N•r 1 N+/ ~ N•f.l L a 61 N N •• nr- r>~ = m 7 = c+1 -m U m ^ ^ o N O O L O E N O Gl uf O U 4- N •• C Cl +~ Gl L U ^ 7 O/ •r O E r• +t O.O C c•r U RI O U U N m — C+t a Cl m ^ m >= m m f•. m 7 i.t i.t N O 61 U Gl O C r- >~ E m m d O L+3 O m O. L n . •• N .. Ql yi •. ^ N G! o m L ~ O I!1 •• 0! Cl ^ N N> m GI n •• r- •• }1 y CJ c ^ +i L U O C • 0. G/ m W U O T T c N .0 c N m O N 7+J O N O Df Z T = L G! L O C ^; m C i-1 L 3+•t m iJ -0b~ L. c i m+J U r• y ~..t E O 01 m C L O 1J +J +J N U m a L 4- +J L r• .t.t ~•.- U a N Ol m m ^ O O G7 L. C G) r• y M m O/ O L C•r C ri L u u'~ O. U a 01 p m L m.- rl a u U OI o L m 

a c c mo m ro•~ m ro io m ~^ m 

c i d • ^ i •L ~G1 • ^ L •L ~ L L . 

L T NN.cw OlNL4•0- ~+t..1 CO40- 

4 ~ mrn ~r otrn ~r aa Eao+J•r cao++•r •3~r 

a) 41V1 QvN U JvH U Sv(,roj 

1-81 
2 

O_ 

f-- 

~ J 

J 

O 

a 

W 

Z 

O 

N 

O 

UO 

N 

W 

LLJ

U 

2 

O 

W 

N 

2 

O 

U 

t..1 

~ 

b 

~ 

b 

W 

Q 

2 

O 

~•r 

C:J 

W 

C 

lL. 

O 

N 

W 

H 

N 

W 

lL 

0 

r 

Q: 

~ 

~ 

N 

n 

~ 

Y 

c 

0 

u 

v 

Ol 

r•1 

W 

~I 

m 

Q ~ ". 

d 

a ~ 

C! L r 

L L 4- M 

i~ 1•1•~ r C O O 

N a ~ L•~ 'O C .{.~ 'p O O 

m C iJ iJ L m 

N m C U N m 

C N I C N OO 

Gl 7 O C m C+~ r C Lp 

V 7 O 7 v'O O) 

G/ •- Cl U'O C C 

N r ~. i N r U N O ~O 

G) n n. Ul N 7>•~ tq 

N 

f-nN ai • - m•r 

7 L m dJ L. E dJ 41 

L L 3r Nv a rn 

n 7•II •H Cl N G! r y 4-• 

41 

c 

N 7 U C n N G! 

m N C! aQ n 61 E 

GJ N C N> N G.' L. O 

f.. ro a ~ ro +~ 

67 

E 

~l N Of O i•~ E O. 

6 U N C tP) O C d 

U N C r- N 

N•r - ~ L • N r.1..~ 

E 

O 

•'•' m•.- r•I G7 

N •E a L m • L M 00 

G7 E N N M U N•~ m••'• . 

+J O L 01 O N r a 4- 

U a•~ O +~ O L. v O 

u C CO N ~ n 1 ~ 

ro C G! N 'O 4J E N GI 

E O E=— > m N c 

~O 

ai o ~ ~1 u•oo 

V- U Q1 Tv L C 

u cro -o a~ o ar 

~•.1 0! N nW C r E i a 

C V- Gf rl r L Cl m V- N C i O1 m i U 

O G7 Ol • - L O 

C Gl C N 4- i•~ • 

N C O 7 1-1 M O m C 

~ V N v N O 4- 

d•~ V•r .0 •r- O O E ~ u N - E^ 

r- N ~ - i•~ N}> •C n N C 

~ 

v 

•E 

}t N•~ 01 n L 

N m L . c n ro oolcaimo•- o 

• E G1 O N C t0 C 7 n+J o 

orn imma~ O C 

o ro Of u Ol C7 rl m 

C C E G7 L L•r- m V' 7 r 

o m 7 u L u a o N r- . U L 3 C U C G1 • d•~ 

w U i•~ •r N•r- E O N 

V L N 7 7 C E O • N•.- 

W U v'O U•r m dJ o L E 

'a I 

ai 1 O) E 

C m L Nr m C 

m 

Y 

~ 

•N 

L n~ i~ L.L C! N C 

U C! U N 

m T ^ 

~ ro 

r c r 4- d N y N N 

•E d m O r L V n•O > 

a> 

O O)U V- N •r N C.O nd N 

c • v c a -1 d E c N•- 

N 

'D 

E 

m r 

O N+J O1 L O N L N 7 1 

U L ro V r C T= E 

O 

E 

N m G! m E o Ql }~ O a L d N t0 

ai E i•r n r m+++~ c 

m u 

•^4..1 /~ 

G7 G! a 

.• N L ~ V N"O m 4- m C O 

N Gl •1-> OI ~ c G1 N 7 L Cl •rN• 

C€ 

b1 ^ 

m r~ ro 

+> +~ m c r o 

ro m u Gl C+•+ m 

O O 

r•• C 

O+1 ~' 

G'•r Op 

7 E E u r i>> 4/ N c.- 

O• •r m E -- O ( / +•~ •r •r O 7 O) 

+1 O N ~ Ql G! +•~ ro L 00 > f-. 'O +1 '•", N'O 

cx U 

E W 

b O ri 

QSv 

•O N T i O1 Ql d O C m O'O L O 

¢ G! a 07mr1r n•.-i-~ +J m+~ E 

7 

m 1 L C N N O L 

~ m 

o C1 Of N •C c Of i N 7 

O. i> U GJ O C W '0 G/ L 

ro"O N N 

4..1 .1..~ y N N 1 C i~ X El m CN • m L L d•~ 

O} r 

n 4- __T m•I•~ i-~ _ E Of di 

m•O 

m 

61 U U[.7 L Q O •N 

d' N L N C G/ m ~ FJ 

U O m L b m • N m Cl N O 

X Ul C 7 O C1 a N C O] N r •O 

+J u 

m• 

F- Tm o+J 3 m o,c 

•- G7 3 ~ U N C m 

ai rno o. o.¢ rnrn -ro o m>,ro N ar 

m N L N L O C C Ol N L i i~ 

~ a~ N CJ . 7 C+~ L i~ •L U •L •r N C 61 O L N Q -Nd •L •b 7 N C! > d-~ r•M ~ a 

r d 

m E 

tp r'O 0 .2 N Cl m O i O E 

7 Ol .0 •r O L•O 4- 7+J O N 

m•~ N d-> m C N O•

_ 

 'O L N m ro N O r 

7 r 'O •r i•3 L O/ 7 T 10 •L 

U O 

.- L 

O' 67 d-~ i-~ E n r O•.- •O m 

d f.. N GJ m r- N C Ol v 

O' L C C E•r ]G U VI O f.. 7 r+.~ E d-~ 

U1 L L m N G7 O C O ro 00 .0 Of m m L N 

i•~ Cf o 7 G7 O) L C O r m N O L L 

N+J ro+-•~+•~ QtU ~ E n m 

'O O 1 d+J L L O`~ i Cl Ol 1 61 C L O• 

Q 4-1~ E N ro 4- Ea nE rri I_ ro+l C•O 

• L 

U 

4- • ••'O •O C - O N 07 C r C 

nN ro . •10 O VC 

O m 

O m +~ m E O 

L a r N 4J O/ 'D Gl 

"O N 

C 41 N ' 

~ 

+1 ro 

U m O m i C7 N t

N i~ ~ 'O N Gl }1 

O L"O .{, C 

'O •.- T r ro o 

ro v 

~ 

v c c v m N 

E o C7 z L a C c 

~ a E n 

d ro M•r-'r N - 

QI 

m N 

O•r E ¢ ++ O•r 

N i~ •r m-1 G! G. 

E ~+-~ G! •T L L N L 

> C 

W O 

u L a-1 U L i N N 

i C 67 m Z O G/ d n 

O O GJ 

M 4- ~ F • 

n 

N 

O=1 n'O 4- 3i o 

4-4- X E L. 

O c• ~ N ~ 

rZN 41 O ' 

~ ar al 67 sT 0 ai n+°'+ ".-+ ci av ¢J m m ~ 

i•~ 

.}J N.0 m V- N O m f.. Cl 

ro C Y'O C L Cl m N 

i~ N U ri E 4J 

III C Z 1 i~ 3 N 

C 

m 

7 o O C N O U O r Qnn o c.o L.,- ro 7 O O N cc.Ew o E d 

C. 

Ol N u o N O) L E+~ 

'D N C d L. d C 7•~ ro 

U/ N o 01 •ri O .O 

~ N i rl 'O i O 

Q L O ul U G.' •.- N N L Q i ~ v m 4- E 

N O 

i~ C N OO 

V- r 

I~ O C L 

r°I •- m 

Ol 

,-+ 

(ioc -Irnv- cLO 

N L•1 •.••• 

wco .•v= 

rOl o 

c~. 

~ N 

a C r O'O G/ O L•O v f.. 

O r 

r U•~ 

1-) C G! L. 7 

G7 L 4..1 N b 

m . m r 

lo E 

owcn a rn c ro t~ ~ mmoarn 

Io r 

t oo 

c O K vl• •O 'O u E ~ -1 1.4 •o 

C 

G 

N U7 

d N 

d GT7 N •• InQ iC L L O C 7 Cf •N 'O ~ C 

10 U m L. O L O C O m 

tn 

a 

a L+J 01 ^ n - rtl 

m i•~ 5-T L V 

p . Yf 

i 

0 f - u o oro ^ OJ N 

~•~ m u N L ai 3 au ~n c 

U C C 4•• L O O 

C C.- N-C N 7rY iJ 

n~C 

m G! m C C v- u) •N 4- m m 

i ~ F m i m m N V- E C) 

L a m 

U T G/ N o. io a u rn rn n w ~ 3 M ~ 3 

v 

C C 

m o c 

m 

ct rn m :1 c•~ v +~ 

u a 

ci 

v~ c 

+J•..m L 

c 

m ^al 

Qf 

i6f 'o 

al .. O>~ o 

a~ a`ro ~ a~ ~ 

~ m 

ro m 

4- 7 301 Cr•- E c .. Id U Ql i 

m+- 

1' N 

o r•i m m m 

Cvn1 ~jU 

'O u rl o 

Qfvu 

1-02 
vro C a+ 

m m 

~ 

m 

~ u 

ro •r 

O L 

Y r y 

ro E 

U O 

0 

C 

~ 

H 

07 

c 

O 

C 

ul 

L 

4J 

C 

~ 

U 

~O 

C 

0 

4J 

~ 

Q 

m ~u 

C E 

O O 

C 

N N 

G!L N a9 m 01 

ro •O O G! > 

L 7 C r L•C- u o •r cu N a+ 

•r +.+ooarro 

a.+ m •r co > er 

CL+J 

01 

 G! L 

01 a~ u rt .- U

Lo 

L d n C r G/ 

O.•r L 01 W r• O1 

O7 4-r1 •r /O C 

L tn E 41 L 

N GN L ro C U 

.i~ - CO Gml L ~ L 

ro N T d o 0 

'r GE L! o L n 

4 

l 

Y EL Y- U•r- N N 

EI 'O07 G) t 4). 

d~ N L~ Cf O 

L C L 0 — r L H•~-m a-3 s a 

L 

N E 

O1 

a ~ 

N r 41 N 

L d NL C ~ N C 

U O ~ C 1+~ L v01 ~ O U 

7 E L O•r • t0 a1 N f 

a 0! •r- V- ~ L~•I d N 

O U 041 O N N O.v '0 N 

aE m ~ ao o L ni ~ aui o oi o m u w- 

+, C Y- L- +) +J O 01 C VmU Or• L C C Y ~ TT O 

01 Gl N m ( ! 7 7 ~ •s+4 — 

iJ 

•••

1J 7 ~ 4h 4-O) N U O'O 

m N C 4J N GJ m C C 

7 r•r c ro GI G! N 07 m 

O' 61N ro 4- N N 7 C N E 

N> C N N•~ m L N C/ 

'D 01 O Y- C.0 .0 ~ L O o•Q Q.- u o o ~ - f- m u w- v.. 

N N 

mC I m m 2+•~ 

a-~ m L ro C O aQ m 

E u0i N ~. w E vOi 4J

o Jci E 

IA m m00 T C /1 Uf CI O) U Z N 

~ •~ •O Ql r ro L. O•r N m O! L 41 

QI ~ Q v O N T Ol N N d m ~ O/ 

m~~ra~o"~ii~m~>o~3c th 

7 O/ L G. C L tp N'a .- C o 

O' O7 V m O/ •r- GI t- O CI i•r O G 

N•r C/ C.) U r• > Q1 a L.L u N N 

'O L N U X r- o r4 x 7 1 ro-r y 

Q Y 7 E CI ~••~ u v W N 1

, 

 4- L L. 

N 

N 

L< d 

G! U U C 

W- m C •r y 

v- • .. o r N lA v ~ v •i. a~ ai ar 

N a. O. L 

10 1-0 • 

X 

r m 

7 O w W 

~ C7 N •r L N 

L II +J ~ 

L i t0 C7 U 

N u Ol 3 G7 Vm 7 U N> 4- 

E O N0 O G/ 

L N /~ L 

01 O. ~ 07 N OJ 

~ c° r- E 9v 

V07 01 > u r• u N 

tq U 0/ ••- m m 

L Cw 

1 N O 

OC o i c v u0i T•'y- ayi .->-•' 

U N 7 L ~ C m O O._T C OQ. 

O ~Vl U~C/ N• Cl i 7 mL 1A 

L •N ~ . C~ ro m N m UC 

J c a a ro N u o a G7 •r 

O G O L L r O Ol U 

••• U 7 i U -•L L L•r N 

N N U C L ro U 

N r• 'O O•r C a4- 

m G! r• L G! •r Cd G7 4 1 = V m U i•~i~ U4- • NL 

m U U C N•r N G! N 

d E O Gl •r 7 m .0 G/ L 

~ U •Ol L d O ~ U NL G O 

~ •E L YO-• O. G U Gro) +O

•i U.,VL0/ 7 N 

N E r• m i•O a7 

•o u C m O~ u N•.- 

O L +~ •N O ~ L .- 

••• N N O•6 GI f0 

0/ ro ro v- o •.. O)~ m i•+ C 

t

y,

0 ~ vOi 0! •i E E ~~ aii tU0 r G! 

7 G1 L dl m . L T 3 L O) L 

Q L G/ O O. a O r- m 41 3 

N 7> N O i•! C N L i N 

•O N•r O L th C•r O C U O

CL 

C•1 ~ ;-° axi ~ : .°: v ~ ~ ++ .°.l N axi 

V 

N r• N 

~ N N O•r 

2QI m L 7 •T C 

~n J O/ O C EO O N O d r 

N U L U G) L 1' a.1 L r• 

0 2 ro G/ E c0 V c m r+ 

L• N•r V- c r G 

U++ N L m • E E 

N y E C! r•• 0 10 O O 

C C N O O. m ~ C d u L 

GI•r C L. X 7 a~ O+J VL m O Y- G! 

t 

 7•r m ~ 

3m w o c m c rt n ~ N C1 O d O •- L c m 

ro d Lt0 v O • ~ C L~~ 

=Y •-E v a) 14 uz 

O'U ro•r Tmr u 01Q 

V.0 m ai ro tp •.O- O L V- t

j

J 

Q u•o aD •OV Tu m az 

~ 

N C V- .- 

EO O t0 

O N w- 1- 

v 

O 4- K^ r~-1 

N+~ 

O 

O~ LO.- 0/ N m O O~l ' 

1 r- U•r O) 7•r r•1 

C tn c L 

J 

~ w 

O W 

min c ai o 

O: fR ro 0,+1 - 

~ 

G 

a 

~ 

cv L C 

N 

O ~O 

u 

n 

O 

i 

N 

N C 

U C m 

O 0/ +; 

L L t0 

u oL en N 3 

• O 

C C 

0! Cl 4J 

u G/ 

C L 

01 N 

~ •r 

L T ~ C 

GI •O 

4-7 

•- OO •r 

6J Q1 - 

GI i-~ 

1' N 

••-9ri r- $ v 1•-i 

1-83 

N 

G7 ~ 

o m .91 4E r•• N +~ 

Y •~~ N m 

CU~ 0!•r+i 

LO CO .~ O~o 

UJ r01-I Ol 

• 

4- r` 

TvO O m 

A-1 LO N N C 

ro II C Gl r Cl 

7 CIm N N E 

O'~ N C Gl •r 

y •rc O .0 L 

'C > G! G iJ Ci 

C L i G7 T X 

~••~ O.Q L N CI 

~ 

N 

7 O N O O 

N L 67 O 1~ 

m~ GN~ O'O C7N 

O! C N O N C! L i¢ 

E Gl ~ O•r IV m . 

N O r• L O•r • t0 N 

N C/ 61 +J r• N X 1- L 

N i N L. a t0 Gl O 01 m 

O G 7 Gl t0 = uf L ri .- 

7 o O^1 c o n c o 

vs m > v w ~ -+¢r• +o•rv 

c 

L •a 

O C u •e 

• N • 

N C 

O N +; 

i L m 

UO L 

M N 3 

L ro a 

a~ > 

OI ~C 

GI ONO O vC- O)Ol.r N 

m e1 L /IS 

D.vOm 
N Ol Y ^ C O 

L O O L 7 

d C N t!'i C V1 •r U 

y•r 7.0 N O •r 

L 4-a U N M d 

7 O O O iH Of 4- E r 

N L L O r- C O N ' . Co d r.+J aa m 1 ,ar 

• aN•+ E C 0,0 aCi fi0 cLi a~ fN0 .n f>C 

C 

Gl 

7+j Ol 

+~ i O E•N N N i C L N 

E U 1 N 7 L a U C' N 

E 

O 

d d-~ C/ N ro G! 

d•ro C 

V- L C N i~ U 61 .0 Of•r 

d Gl 

4- +1 

U 4- O C iII O 7•r ~ 

OJ t•r N a T N4F 

d r . a - • N . 

f0 

N'E G! d O a i. O 

U L C L 4- C G/ +1 O 

C 

O 

r 4- L 16 C dH ro U i•~ 

E O O 7 r 

N C 

O 

•i 

~ 

O ~F NM R7 ro a 7 

O E N aC O C O L N 

E 

41 +~ 

a 

'O 

U L G) Gl •r N O N d L N 

Gl d O•r N•r Gl N 

L 

Y •C 

¢ s~ c>~ Tcr ccro^ 

ai m r• c r- c v 

O 

c E 

L C L W C•r•r•r L 

N•i 

f- •r U O f E f -P ro d O O 

Z a c 

~ N L F- ci ro U 

~ 

-1 

•oN u 

•N iJ 

•E 

a L 

G1 3 

Od +%+ a E 10 

Oc +°~ m c 

W 

ro 

a 

c•r O 

ro iYE U a 

r 

N 

Z 

N G/ 

E N O d N 

cu 

a O4-Ol CO 

d 

N

co 

t~E d 

O a 

O 

U > L • 

C•r a•r L N 

E L 

ro 

LL. E O E 7! N•r Gl ++ 

O O> C 7 N 

tn O i 

w 

roN U 

c€ 

d-~ O

•L. t U ro 

ro c~ aiai > ar ~ 

U O O 7 Gl a L r L L 

W +1 O Ol G! GI E a N ~ L , 

w 

~

w ¢F ro u E

~i -

.c ~ 

tN N 

>,c 

1 c0 iJ ro 

U ro G1 d d-~ N C o E N 

ra 

C.7 

a ro 

C+~ 

i i 7 r L Gl • 

~ 0 . L. N C 

1--i 

f 

f0 ro 

a 

L L O N L U 4- +~ Of CO W O N ~ O N IA 7 G/ O ~ 0 

0_ O 

E 

O 

Z 

ro . 4••~ U 

•ro +JO w Q1 N t0 N r i i CO rl E ~ O~ E O N 

• 

+~ 

~0 

o ro• -a m ro 3 ~ o. v> > ^ L 

U 

W 

a ~ 

r N 

Gl +~ +~ •O N X i N N ro 

f~0 +T1 +%1 w CN ~~tl i0 OU i Cf T 

+1 

•• N 

J 

Q 

ro E 

U O 

7•r N a N L L T• 67 ro 

O'.- C Ol O Gl O/ i-~ L L i 

L U 

d C 

Z 

C 

r L 

•N G1 

G! ~ O L. C 1~ d> C•r N a~ d 7 

a O O•r Ol X Gl Ol R1 •r •r > O 

L . O 

41 U 

H 

W 

Q 

U 

Q O' 4- E ri W N p1 a i~ d~0 L ro 

L• O 

G.' 

V.. G! 

^ N L r y 

~ y 

O 

O 

C 

~ ~ .0 ~ 0 N G1 M d~ 

> N•L L U N O N 

O L i•> 

L f0 f0 

i r L 

N 

W 

H 

O~O 

r i.~ 

dJ ro 

O r- N N G1 r C d-~ 7 O 

C G1 d ~ t •C O C C C O C 

c a X ro U O) O d G1 •r T O•r •r 

d•r C! 

ro C 

4- > d 

O C1 a L C S.. N E a L L ~ > O ro 07 

rZ•~ r=- Cl Y E 07 M N ~ U L O i a 

d N•r 10d a L U N Y ~Op •~ L ^ O 

C/ T O 

N ~ 

W 

> C 

W O O N a L O+~ •r > U C T O N N 

L i-~ 

4- C a 

li d N •^ r- ~ r- E o a ai ro o u- 3 rtf d Gl L .O O a w d O O 41 ai a d L N 

O 61 

i 

i-~ d a• N N N N C N a N` 

ro O C7 TL N 

. •r d N G! •r y C 

i L. 7 

ro 7 

}. 

D: iJ 

O i+1 i+> O N d O 

~ O L N L•r ~ 

O•U~ O r• O r- a N L N 7 3C 

U C 

N d 

~ 

C 

ro 

G7 E(O 7 G7 U G) a G! N 

a N•r +.~ E dr• CI.- L O v ~ 

Cl N d 

•~-~ L 

E 

~ G. 

ro>+j c O O U a a ro Gl Of d E O 

C•r N d L L C C C a~ •r 0! X•r i 

cO N 

E a N 

tn ~-•• +J d E'r- U•r ro ro N T L Gl +J O y E L 

_ aN 07 a iJ G! i C ro 

ro i-f 

dJ 

c 

O 

Y- r 0

7 O C 

N r 

10 O 

G/ a 

iJ C 

O Cl 

+> •r L 

U 

v 

C L O 

Gl +..~ •r 

E 

v O 

N d•~ 7^ 

L ro a.G 

C1 LO 01 ~ L U 00 

rl rtl U•E 

O ~ t0 WO- i r~-1 - 

uw c o us ~ 

nv 

-J C 

Q > oii 

C 

~ c ro 

t0 a•r d 

E+~ O ro iJ 

4- C d•> 

i0 ro7.G C 

N C C) 

O u G•Y . V- ••U O a O/ L- U 

N 

d f0 L Y O 

O • +J 

G1 i ~ S i O C 

O 

L 

• u0

,0 

N N G/ a 

Gl r C7 

L O7 

U d•• O> OJ 

O ++ +1 ai . ~ . 

U r N 

a •r ro 

L roro•r •r d 

V y41 r- E O 

61 L 

c+1 +1 . 

L OGl •r L 

3 d.a r U 

r y tE a ' 9- E d 01 •00 s0. N a a 

C C 

_ c~ m •r 

N ro 

f0 O ~ 0 ro • N .O 

ro 

v a°fi a ° u r~ ai ~ 

c L. 

G7 

•- O 

c/~ N 

ro Cl c G! 

7O•r 

Q) •O N CO c GJ O ~ N 

0. 7 

6! +1 z w 

C 01 C 

m..E Cl r-i •r 

a•r • i d 

Q L Y d ro a 

1-84 

~ 
aerometric, or economic information and models currently available in the 

literature. The estimates can then be ranked relative to the strength of 

these data and assumptions. Of the eight regional studies reviewed, most have 

adequate economic models, but only four are judged adequate across all input 

categories. Further, most regional studies abstract from the interdependencies 

that exist between regions, which limits their utility in evaluating secondary 

national ambient air quality standards (SNAAQS). 

National-level studies can overcome this limitation of regional analyses 

by accounting for economic linkages between groups and regions. A proper 

accounting for these linkages, however, requires additional data and more 

complex models, and frequently poses more difficult analytical problems. 

Thus, detailed national assessments tend to be more costly to perform. As a 

result, there are fewer assessments of pollution effects at the national than 

at the regional ievel. Six national-level assessments performed since the 

last criteria document was published in 1978 are reported in Table 1-10. Of 

these, two used the simple "price times quantity" approach to quantify dollar 

effects. Four used more defensible economic approaches. As with Table 1-9, 

an evaluation of the adequacy of critical plant science, aerometric, and 

economic data is presented, along with the estimates of benefits or damages. 

As is evident from the evaluation, most of the national studies reviewed 

here suffer from either plant science and aerometric data problems, incomplete 

economic models, or both. As a result of these limitations, decision-makers 

should be cautious in using these estimates to evaluate the efficiency of 

alternative SNAAQS. Two of the studies, however, are judged to be much more 

adequate in terms of the three critical areas of data inputs. Together, they 

provide reasonably comprehensive estimates of the economic consequences of 

changes in ambient air 0 3 levels on agriculture. 

In the first of these studies, Kopp et al. (1984) measured the national 

economi c effects of changes i n ambi ent ai r 0 3 1 evel s on the producti on of 

corn, soybeans, cotton, wheat, and peanuts. In addition to accounting for 

price effects on producers and consumers, the assessment methodology used is 

notable in that it placed emphasis on developing producer-level responses to 

0 3-induced yield changes (from NCLAN data) in 200 production regions. The 

results of the Kopp et al. (1984) study indicated that a reduction in 0 3 from 

1978 regional ambient levels to a seasonal 7-hr average of approximately 0.04 

ppm would result in a$1.2 billion net benefit in 1978 dollars. Conversely, 

1-85 
~ 

~ 

1-1 o ro 

eMt~ ~ c m • 

^ 

, c 

• 

r i U 

O.JO iJ ri 

d O_ u N ~ N 

d O 

•Q E N 

L T• c o ~0 L d•> d 7 N 

~ Nri = a~Qi •r o ~ ++ w aui 7 c m 

N 

44 

L d m c•O 

O.0 O -- d d 

W N d4- 

t d 4- 

N o N 

m U d M 

GC1 ~~ V- C mL L ~ A md E C 7 p 

~ 

N CI o d 9- o m O) >f 

C1' N d 

r C 

d • O.•r 

u 

• r C N O O.•1-~ 

• •O N O/ C 

d•O L d C L d 

tN •r d> 

d U L+~ d 

+- N L 

m d 7 d 

r• 

a~1 d m O E 

10 d ~ N•r /~ ~ 

+1 7 m r• 

ro•O •r E 

E C1 N 07 

• c C 

m € u c•r N ri u E o 3•r L ++ m s. m 

C 41r X m L I~ G 

N d N'O~>r'~~ 

• L +1 d 

41 

 gQ 

N.0 d t 

d U= U 

O Nd'7 

d-) d 6Ni ^ O U C C L 

•O 

d +» v m 

L•r m N d • •L L•r . ~ L •E L a~ 

17 m F~ L a~ d m 1•~ N rl O_ 

4 ~ 7 •d0•.N-• M m r c E~ t 

r 7 OOp1 f•.r-~ O L"O +J 

C u U. ~--• 7 d u CI U U v 40-. O W i~ m • 3 

O m d ^ I 4- 

c ~ T . = ++aNi V cIO o ~ rn N 

N ~auiNn~ ~ a ~ i x uTT T i 

o m 

M 4 1 

d L a N.O 

10 d o G 

N O. u 

ro d•r 

+~ O."O u u 7 

V N•^N ~ C 7 N

m

. 

p-• IO d FJ •O m C N O U L c'O t•r N O+~ E •O N 

~ 

J 

v>ddcorn dxo. 

E d 

mooN o.•r oo d++ 

E E•r C ~ N+~ N C L N E U 

J •

m C i~ m•r r-i +~ 

O m L d-~ U T m G. d > O C d C d O O. d d 

O d C Z r• U U C m r N~ O •O C m U m L m i U N T 4" 

~ 

O d 2 

W 

p 

E 

••• U O)•O •r E O 

d. c o d•r 

•^N U 

d01 

C d V O O' N O C d 

o d a Gl cU ++C G.O 

2 +~ r• M. f- U N +~ rl 0p +~ •O m TJ C•r N d 

C m u m d U>f d••r N L m — 1 - d m L O E c d . d•^ d-~ 

N 

o 

N 

c ~ 

7•O L d d 

C• O i~ a T O. L u 

7 Ol 

O• .ri 

~ O d E d . m E N N i•O m 

ro o- u 'O N b•> d 7 d O) 

O o d E u•r +~ 7 7 d 7 d O U d d N ~ r• r• r- d 

{L 

O 

C 

1•~ O 

Lf m+~ c O_ N•O 

m U LLr• 7 O m O ~ 

•O ro N 

m d 

O'V •O •r p. > U 7 C G d d L 

d m O E O i•r •n m L> V O) 

N E~ H •E ~ E U U ~ O_ 

C i-~ N 

~ -r d 7 a 

~ C i O L O L•CI L 7 d O OI 

Q•r p• C u u O. m u N r- E m 

W 

U 

7 

N 

tm 

C 

w ro d tN0 a0 •Of •O 

~ 

d 1 ~ tO 

N> •C1 L 1~ i I, •r d 

N Ct ^ m 

Q N 

p• •O m o d ~ d O Q1 7'O i Z r• 1 01 L•r d O d O 

W 

Vf 

C 41 

m m 

Z7 N O U> r• 'O d w rl 

O i- C•r m C U 1 

N d d Q ro C rl ]L r m 

O L t.J L d Q i•~ 

O> CC if 1•~ 

0.7 d Q•r C L 

C ~ N 7 L C m C ct C. 7 f.. +~ U~ U L T a ro 01 .- T N N•r L 

6 m d•r •O C14- d O U d >+1~ 

•r Y L 3-~ Ql 

X N L m Z 1' C O a m•O 

d m 1 L O ~ 

rl a 1 M ~ F OI .O 1~ f3 i•1 U 

m 

~ N C C ~ •r 

ro SI T o•r d +~ L C 3 T o rl d I~ f- u •O d G •-o V o C d 

V ~ L 7 d m Q. T N m m i~ m m d i~ •- E ^ L N d L Q d d • +~ r• . 

41 

d 

~•+ O' S. 3 N r C+~ Z d 00 J m'O 

d O d L O m E d L O 

C i~ d 1 d+~ C+.~ 7 C 

3 d N GIi~ ~ C O m ~ K 

d•~ +~ +~ 07 L m m d 

¢ m c m C O r c CA 

(O E •D N r• L d O.'O € O m E Y O•r O a d m m d•r E d Q 7 d E•r ~..~ N O m 

p 

U O 

L 

m m m L ~ N C L+~ O L.0 i 

C d L O C d M L d ro L. G7 m d 

C L L C L•r +~ •r U N 

Y T Of d m d a m+J O 

O'•r •r 01•r C N L 

d a}1 •r C ro m d 

W i~ ¢ 

.~ 

~••~ E d U 7 L O V- Q C 4- Ca J 0_ C m•r > L > E i N L O 

~ E L m iJ m ro+J d O_+J 

•O E N L O L d> 

Q m d]G E iJ N ro 

J U d U 

~ 4- C E L • N c I C E M n. 

O O O O 7 1 C O •O 1 C N L. Op 'O E N i O L O O- ' 

~ 

C 

C. L'O d-~ d O f- N d O C O 

Vi V- ,- m L•r t O. N+- m C 

d O 1 I~ d O. 

tn 4- •r +J C1 E O. 

d O• O'D 

N V- +3 4- d ~~ C 

6J O m d d L I-~ i~ U O ro N • O ~ E U rl 4- 7 7 U i.~-~ d O O 

i.1 

4.1 m 

L•O •r d C U N L L•O a M N C N 

~ d Ti•> >> C.0 d O U d O r d 

m N L d O N tn 

N+~ d O C N N 

m C L 7 C E 

N+> > m N d 7 O+~ 

4. 

p 

m•O 

7 

•O > •r N 7+~ S. lL lM d • 

tn ~ 9- O 7 O 7 L C m E+J 

m W4F d N m O 

•N •O N d d r 

r m tL d m•r N U 

•N 'O C d a N 4- 7 

d 

N 

N L a N rl m•r L 2 C 

d V- d d O . d d O. ~ 

T c L i; d'II o 

^

m d o m +> > c 

T r E E m O -O 

'O .- m O 

~0 LL~J > c T'O O L o N L O. N 0I L N N'O O N•r d N d d ro 4- C r• rl N c c fL 

C d 00 C d O ro o a 1~ 

4T` 

W O 

O. 

• 4~ Ct7 G O X O. C m N C d N U 

- C N Ql O V- d O•r O) O lL rl 

C C d-1 G d a r• O . O 

m O U•r 07 T m•r Ol •r G7C0 

'O 

H 

N 

d 

d O•r C ri O_ L C N C•r d 

41 •r N•r N•O d U•r d m+~ O O u 

d G r• C d M+~ 'Q +~ 

•^ N 7 m u O C C m 

T rl C Ql +~ r 

•^ 1 •O m rl C ro r- 

~•-• L m+~ d O d d Y m N L U 00 C d d LJ.. C.0 C 7 7 L d M"O d.0 ro i ro • 

N 

W d•~ 

~ m L N 1.~ L+> > X E m U 7 01 4- m 

G• €+~ d m U•r d OI •O r~ O•r 

iJ L •r U d i•~ O O+~ 

m i G U L C 

+~ O C_+1 U C aJ N 

m m m d N C N C 

C O7 L C v- i'O E m N L O ~ d 7 Z 'i7 'O d d O) d O Z E•O d d N O 

tL m •O O T~ O d•r L r L d-~ 'O O. O'Q O d r• ~ F •r L Y U O•Q O ; d U O•r 

p m V® N ~ •r N•1• d J GO i-~ d+> > C L. O) ~ 'O L d L d G! L E d J N+~ d 4- a U U C 

} 

4M. 

r ~ m N C N d ro ~ Y N} O E•O U Q Z r7 E}•O m d a U Q Z ~ -1 d} a r• U m L 

4: 

p N 

O 

Oi ~ ~ 

N d O C C rl 

a) 

O 

C L O 

d A~ •r v/~ C/~ C/~ 

1••1 a C r• N r N •r N 

°u•~ ~ ro 

v L 

m a r~ r or N ~ 

J C p H► rf O M O N O 

07 C M• •O L') 'O W'D 

H ¢ N 

V-m. .. ~•p •• C O 

•r N - m u 

^ m+J 

+~ 7 

L d 

o d 

ip r• G1 c N d U . 10 

~ 

• a ^ u L 

N 

4- o c•r m d a m•O 

r U L 4- d O Ta C 

c d +1 

L.0 • N 

c T7 t 

L- C O+•~ 

n. muo a+- oom o3N;a oro3 

L .. L UC m i~

•1 N i/ U ^ ~ U L U ^ H' N i-~ 

C.1 N a ^ m E O •• VI .. N C d U 

[3, d • O. E L d 

o-o~+~r ~ u o 

N G. m r• N 

nro d ar ++ 

N C m C 

am c> ro c 

L N m d -L m+J +1 O d G•r r• O O d O•r d O 

U i•~ a d N Of C m m 

d L 3 T a~ L•r E d 

L a i~ m C 

U T•O r• m 

L a d-~ i~ a •1•~ 

u T+> r• >> d-~ 

r a+•o~ H~ E o C. M voi u cOi tOA u 

~

i a u v t o voi 3 st 

V~ 

m 03 

4n 

;o 

41 

•p ya 

c 

y d~ C N N Y 

~ 'oo' rcn v s° 

gzv Nv QU 

1-86 

m 
Z 

O 

~ --i 

~ --• 

~ 

O 

a 

z 

N 

O 

O 

w 

Z 

Lu 

~ 

0 

Lu 

N 

Z O 

U 

P-1 

f 

Z 

O 

U 

W 

Q 

o_ 

I-- 

Q 

O 

tNil 

Q 

F 

W 

O 

} 

Q 

f 

f 

N 

aft 

41 

O 

v 

r~-I i 

rt 

w 

m 

F41 

E 

E 

u 

ro 

0 

II 

v 

¢ 

m ju 

OI 

O 

i~

m 

4~ ro 

m 'o 

7 O 

m N 

> c 

W O 

O_ 

C 

ar aa 

.c >(V . N L 

C N 

4- ~ 

"O • N 

Y 0) 

N C 0 

E L 

o 

N +~ 

L r 

++ c 

C E 

O O 

'O C 

N 

N L 

m

ro u 

ar 3 

m C 

V) 

Gl N 

+~ m m a ~ 

E L 

4 m 

N 

O L 

N 7 

i 

+J O 

L ~ 

41 m 

1-3 

N m 

N ~ 

C 

E ~ 

r ...i m 

^ S.. 

41 

C 

N 

L U 

G! C 

L O 

m u 

L M 

O 

W 

I L ro i 

i a •r a 

4- > CCi 

O m m 

d T O 

L + 4J 

m a~ 

L L 7 

m ~ 

U C 

N G1 

+1 r m 

E 0 N 

+1 E .c 

N 

N 'O +1 

C m 

Gl m L 

L +~ 

+~ C 

m ++ ~ .. 

L m 'O.0 

4Ji U Co 

C O O Ol 

m F L ri 

G! C av E •r 

+~ U O r 

c 

N C roN 

O U aY 

'O 0! L U 

G! i ~ 2 

L O C 

N r CI 

C' ^ Gl 

U N 

-cj •r o 

4L1 1 dJ 

4- E d C. G/ N L O 

a L N 

v m•r 

n m 

m N .G 

TU •r +~ 

U•r mN 

m OI C Gl 

7 O 

O 

'O 

Q p Y a 

m a 

. L 

~ L C 

co 0) LO 

r-i L N 

v L 

C O1 ^ 

i •r •r .G N • 

U r G! 71 • O 

O 7 U+1 N a 

i N C m fPr N 

U N N E v N 

i L•r L 

C N 'O N +1 U 

m C C N m•r 

N O m N E N 

E y N N+> i 

m u 41 O N'O 

O C N r N m 

~ O U 'G O' C 

N r y O 

m S- rE+~ S.. •r 

ro L o L o+J 

C O V- U 

E C N 

d: 

O a C 

m • U d ~ 7 

tn J>> G! • 4- 

+.T ai 

N ^ r N 

L E 

O/ ro/~ • N N•r o Em 

u

¢`co o r ~~m+~ umio 

O N r~•1 c N E U- E ~ 

L m v ro 0)•r m'O O U 

aN L+~ m N >L 4- 7 

G! E C1 ro L. Ol O) a Y-- 

1

4

"~4 Umf U ~ N u ~ V C a 

7 o d •r ~..~ .- •r C 

O' ••• L N C E U G! +~ ro 

O7 U a•r O Of • 

•o v ai E C T 3 d E 

m•O 'O U m O 4- N N L 

1 C O C X X C.i d C Gl •r O 

E m CJ G! Gl L•r L N4F 

C m +•1 

`6v 

+1 U 

ro •r 

~ 

41 

m E 

~ L U~ +Gl . Q 

L 

U 

'O U 

C 

NL Ol 

N 40-}. 3.. ~ N•~ Sm

~ ++c v 

N.i•~ ..n r O G! 7 

r m N Gl •07+~ Q 

•N 'O 00 ~ > C N m 

mr• 3 c ~ ++ m 

m•r 0) m c• ^ro N L 

^ T O E•~ u N N 6m1 

~ O L N E'Q O O ~ 

m i•~ N m Gl L. •r r• 

O'Q O c O Lm U L E 

OJ J C) m N aQ C•i-~ L 

V U Ol.0 Q) t!'1 t+l 7 O O 

Q Z rf U rl N O L.L L YN 

•r O~ 

4F• r Ql 

G7 O C ri C i O 

01 a~ •r C ~ 

•--• U •r m 

~ a 

C O tR N O 

c s4 0 

Q 

i C! 

+13 U L C 

^ m 1-- .L m 

C 61 S. aJ 

0 3 • 4- ^ C 

U^ O N O N+1 

NC Y m+1 T 7/ 

O. m o> O o L 

O 

(1)U•r 

 U N; 

U T•O~"O L~ 

O C ~ C O C 

~ N m U m V-- m 

r 

d ~ 

N ~• 

E N m Ol 

Q v 

L CJ E VOL m V- 0Y7 41 w+J X O G! 

L N Ol N 

4j 7 N C ~ 7 = 

Olr r m•r ~ N c aa> > ro a 

L > N •r C • 

•L 7 d d •1-~ L 

~ N r 'O •r y N 

N 7 N L C 

m U o'7 r• C +~ O 

y•r0 U N 

E O'O•~ N ~ +,O 

~ o E O t N ai 

U 7 N+J N L r• 

C dN r y~ Q1 

~ C ro m O E C O 

~ •r N r m E 

N •r C +~ E 

~ G1 7 N O N G! 61 

ro'a 4~ 

f0 L, m m G1 G7 

C L m C 

•-r U > m •r }1 41 •r 

G1 C \ a a 

E S- 0+1 UOn O U N L vOi 

d L U V 7 •0) a 61 7 

U U u N T d L•r U ra 

O O L L r ro ct 3 C O 7 

C L a~ 7 U O L N 

0!1 ^ Gl N N m'O •r a 

U N N L d d G) +~ L 

Gl V- r 3 O_ D7 61 C m d G/ 

O d O C+> L•rr N E 'oi mroonaim3 

~ d-~ E E N U Gl ~ O L ~ C 

m N 3 C C N U'O a~ O 

~ •r r• C O .O O1 +~ C N U 

N C> L m C! ~~ O E O ~ 

• O L i N O C 

Q U r• 4-

O 

L

N 

 T+J N U'O +~ m 

N L 

m C1 N 

Y E 

OlU (t ~ C 

EO O L O 

m L Q -~r coN 

N U 40 1. m 

O 01 Ol O) 

• ••'O C ri ri N 

O7 

7N 0-• •rC- O'9co m 3 

'D 'Q 1-4+> i ~ L 

Q Q v O/ .D Cf 

G! N YO- SO- L. ~0,-1 ~ 3 

N C L v y GJ Gl 

O O O7 L 4- +> E Gl V 

NN 'oa~"~a c iv'~ cro 

r aJ L N d a•r N ro'O 

•N L L N 41 .0 m•r C 

T'o 41 o o.c r o

EO r• n~ 

i0 r• o +~ a) E N 

c ai ap -O a) a c> o 

m•r OlL N OJ Gl U EcL 

T ~ r~ N m 3 ^ +~ a 

O1 NL } y•O ~..1 m C 

rt ~ 4- m L.Oa VOiO

ao 

7 Z E 7 C d • 

O'Q m N•r N Ol m i O 

C! J+J Cp m U a 

,a U m QlN GJ C vJ OJ C 

Q Z'O 4 N E N O L'Rf r00 

~ 

Ol 

rl 

•r yl 

N r 

ri o 

N 

OL 7 

a U C 

-m ++aai 

C C1 a 

L L 7 F 

O 3 O S O Y 

U t.O,i 

N C N m X 

O. m C+> > ar 

O d O 7 •r 

L -0+~ C 4~ a 

U T+~ m r O 

O O 0l7 5-

tn N U a U U 

0 

4J 

61 ;~ 

0.00 

Onr

Cn

-1 

Y v 

C L 01 

OI F- V- C 

O •r 

V Gl F~ C7 

d L N . d U O 

+ O 7 C O Gl 

m v- o c r• v 

E n.•r m 4- c 

+1 C 7 C! L N 

N ro N L m(1) c 

OU L T N Gl C ~ 

N•r y •p 41 a.~ O i•~ 

7 a•1 U 'Q m a a 

N 7'O 3 E N E 

CL E O m UZ i N 

:3 

v i '0 d _T ~ aNi c A 

LL • r N U •r ~ 

Cl i-~ N m•r •r N C 

z.n N o To m 

N Y•r r• C C m 

C L L+1m O m+j 

O O m m C U L m 

U 4- E C m N U'O 

/ 4- 

N E O 

O O m L N C N C 

E a w U C r m N 

E m O Gl E 3 m r 

U O V- Ol •r 'O N C'O 

r U O O7 O V Cl O N 

O O N O i EVcL0 O) 7 

c 3 ar ~ r- c 

0 

• 

O+~ •r C m m N L N d 

U L N O C G1 +J 'O 

OO N G! }1 ~ N C aJ ••- E 

~ y mE'a c G. u Gii N ~O 

ro N•• _ o o c T c 

7•r N L m L'D 6! r• O 

Q N•F1 N a l.1 07 a•r 

~ O N ~ d tA C 4- ~ O 7 Iy0 

Q U C r• A[) m O}4~ N C 

O 

N 00 mrnL 

r♦ rn 

E L O 

m O i N 

N 4-L O 

•., a.,l +J O. 

N 7 t0 L 

iJ d n d 

o• > o ai o a ao 

•II~ C Ol 

Q m ro ri 

N G1 L 

N N U 

7 O~ N E~ C Gml 

N uni o Of L w mL 

r N i 04- OC O 

N L.0 N O 4- 

>> .i•.1 L N c7•r 

m a O U 01~ U u0i 

ca~ aoac+~ =m 

m•rmr ro 0.0 ai 

U ~ L U 

41 O 0 } +1E aQ r VOi 

7Z

4-

. m cF3Y O 

0•Q m M r•

G7 

 O t.[) a 

GlJ d•~ 00w00 BN Vl 

~ v rorn aio+ c ar 

Q Z'O r1 L rl m m i 

CD 

00 

cn 

ri 

C ~ 

•r N 

v ro 

n rri o 

^c C m 

OG1 L L 61 

C r• O L O G 

T ^ m 0.4- Q•rC-O4 °-" o 

d N •• i-1 'O G/ m V- L N 

i fC0 t

4J

tl 7 vOi X 01 O GY OI O- L 

m C7 C1 Z 7 N 3 L O 

m T3 Nac ~;~ 

N N ^ E m i m E 4J C 

a O ^ o L•r y L O i•~ c 

L C+J 01.1•~ L r• ~ y.t m 

U L+1 L r• U L i. ij G! 'O 

l0 U U N U d d tOif t,0.7 3 m 

~ 

~ 

N CY 

Q ~ 

,a 7000 

N C Q1 m ri 

O N 

+1E L mmai 

7 V Y o- ¢ u 

6! O 

'O N i 

Q m U 

c 

U 

'D 

N 

IMA 
an increase in 0 3 to an assumed ambient concentration of 0.08 ppm (seasonal 

7-hr average) across all regions produced a net loss of approximately $3.0 

billion. 

The second study, by Adams et al. (1984b), is a component of the NCLAN 

program. The results were derived from an economic model of the U.S. agricultural sector that includes individual farm models for 55 production regions 

integrated with national supply-and-demand relationships for a range of crop 

and livestock activities. Using NCLAN data, the analysis examined yield 

changes for six major crops (corn, soybeans, wheat, cotton, grain, sorghum, 

and barley) that together account for over 75 percent of U.S. crop acreage. 

The estimated annual benefits (in 1980 dollars) from 0 3 adjustments are substantial, but make up a relatively small percentage of total agricultural 

output (about 4 percent). Specifically, in this analysis, a 25 percent reduction in ozone from 1980 ambient levels resulted in benefits of $1.7 billion. 

A 25 percent increase in ozone resulted in an annual loss (negative benefit) 

of $2.363 billion. When adjusted for differences in years and crop coverages, 

these estimates are quite close to the Kopp et al. (1984) benefit estimates. 

While the estimates from both Kopp et al. (1984) and Adams et al. (1984b) 

were derived from conceptually sound economic models and from the most defensible plant science and aerometric data currently available, there are several 

sources of uncertainty. These include the issue of exposure dynamics (7-hr 

per day exposures from the NCLAN experiments versus longer exposure periods, 

such as 12-hr exposures), and the lack of environmental interactions, particularly 03-moisture stress interactions, in many of the response experiments. 

Also, the 0 3 data in both studies are based on a limited set of the monitoring 

sites in the SAROAD system of EPA, mainly sites in urban and suburban areas. 

While the spatial interpolation process used for obtaining 0 3 concentration 

data (Kriging) results in a fairly close correspondence between predicted and 

actual 03 levels at selected validation points, validation requires more 

monitoring sites in rural areas. The economic models, with their large number 

of variables, and parameters, and the underlying data used to derive these 

values, contain potential sources of uncertainty, including the effects on benefits estimates of market-distorting factors such as the Federal farm programs. 

The inclusion of these possible improvements in future assessments is not 

likely, however, with the possible exception of market-distorting factors, to 

alter greatly the range of agricultural benefits provided in the Kopp et al. 

(1984) and Adams et al. (1984b) studies, for several reasons. First, the 

. 
current studies cover about 75 to 80 percent of U.S. agricultural crops (by 

value). For inclusion of the other 20 percent to change the estimates significantly would require that their sensitivities to 0 3 be much greater than for 

the crops included to date. Second, model sensitivity analyses from existing 

studies indicate that changes in key plant science parameters must be substantial to translate into major changes in economic estimates. From experience 

to date it seems unlikely that use of different dose measures or interaction 

effects would result in changes of the magnitude already addressed in some of 

the sensitivity analyses. Third, even if there are such changes, there are 

likely to be countervailing responses; e.g., longer exposure periods may 

predict greater yield losses but 0 3-water stress tends to dampen or reduce the 

yield estimates. Finally, it should be noted that potential improvements in 

economic estimates are policy-relevant only to the extent that they alter the 

relationship between total benefits and total costs of that policy. Uncertainties in other effects categories are probably greater. 

In conclusion, the recent economic estimates of benefits to agriculture 

of 03 control, particularly those estimates by Kopp et al. (1984) and Adams et 

al. (1984b), meet the general criteria discussed in Section 6.5 and hence 

provide the most defensible evidence given in the iiterature to date of the 

general magnitude of such effects. Relative to estimates given in the 1978 

criteria document (U.S. Environmental Protection Agency, 1978) and economic 

information on most other 0 3 effects categories (non-agricultural), these two 

studies, in combination with the underlying NCLAN data on yield effects, 

provide the most comprehensive economic information to date on which to base 

judgments regarding the economic efficiency of alternative SNAAQS. As noted 

above, there are still gaps in plant science and aerometric data and a strong 

need for meteorological modeling of 0 3 formation and transport processes for 

use in formulating rural 0 3 scenarios. With regard to the economic data and 

models used, the impact of factors that upset free-market equilibria needs 

further analysis. Additionally, it must be emphasized that none of the studies 

has accounted for the compliance costs of effecting changes in 0 3 concentrations in ambient air. For a cost-benefit analysis to be complete, the annualized estimated benefits to agriculture that would result from 0 3 control would 

have to be combined with benefits accruing to other sectors and then compared 

with the overall annualized compliance costs. 

:• 
1.5.10 Effects of Peroxyacetyl Nitrate on Vegetation 

Peroxyacetyl nitrate (PAN) is a highly phytotoxic air pollutant that is 

produced by photochemical reactions similar to those that produce 0 3 . Both 03 

and PAN can coexist in the photochemical oxidant complex in ambient air. The 

effects of PAN were a concern in southern California for almost 20 years 

before the phytotoxicity of 0 3 under ambient conditions was identified. The 

symptoms of photochemical oxidant injury that were originally described (prior 

to 1960) were subsequently shown to be identical with the symptoms produced by 

PAN. Following the identification of PAN as a phytotoxic air pollutant, PAN 

injury (foliar symptoms) has been observed throughout California and in several 

other states and foreign countries. 

1.5.10.1 Factors Affectinq Plant Response to PAN. Herbaceous plants are 

sensitive to PAN and cultivar differences in sensitivity have been observed in 

field and controlled studies. Trees and other woody species,. however, are 

apparently resistant to visible foliar injury from PAN (Taylor, 1969; Davis, 

1975, 1977). 

Taylor et al. (1961) demonstrated that there is an absolute requirement 

for light before, during, and after exposure or visible injury from PAN will 

not develop. Field observations showed that crops growing under moisture 

stress developed little or no injury during photochemical oxidant episodes 

while, adjacent to them, recently irrigated crops were severly injured (Taylor, 

1974). 

Only a few studies have investigated the effects of PAN and 03 mixtures 

on plants. When plants were exposed to both gases at their respective injury 

thresholds, no interaction between the gases was found (Tonneijck, 1984). At 

higher concentrations, the effects were less than additive. Studies with 

petunia confirmed that 0 3 tended to reduce PAN injury (Nouchi et al., 1984). 

1.5.10.2 Limiting Values of Plant Response. The limiting-value method has 

been used to estimate the lowest PAN concentration and exposure duration 

reported to cause visible injury on various plant species (Jacobson, 1977). 

The analysis yielded the following range of concentrations and exposure durations likely to induce foliar injury: (1) 200 ppb for 0.5 hr; (2) 100 ppb for 

1.0 hr; and (3) 35 ppb for 4.0 hr. 

Other studies, however, suggest that these values need to be lowered by 

30 to 40 percent to reduce the likelihood of foliar injury (Tonneijck,,1984). 

For example, foliar injury developed on petunia plants exposed at 5 ppb PAN 

1-90 
for 7 hr (Fukuda and Terakado, 1974). Under field conditions, injury symptoms 

may develop on sensitive species when PAN concentrations reach approximately 

15 ppb for 4 hr (Taylor, 1969). 

1.5.10.3 Effects of PAN on Plant Yield. Only a few limited studies have been 

conducted to determine the effects of PAN on plant growth and yield. In 

greenhouse studies, radish, oat, tomato, pinto bean, beet, and barley were 

exposed to PAN concentrations of up to 40 ppb for 4 hr/day, twice/wk, from 

germination to crop maturity (Taylor et al., 1983). No significant effects on 

yield were detected. This is supportive of field observations, in which 

foliar injury from ambient PAN exposures was found but no evidence was seen of 

reduced yield in these crops. In contrast, lettuce and Swiss chard exposed to 

PAN concentrations of up to 40 ppb for 4 hr/day,.twice/wk, from germination to 

crop maturity showed yield losses up to 13 percent (lettuce) and 23 percent 

(Swiss chard) without visible foliar injury symptoms (Taylor et al., 1983). 

The results indicate that PAN at concentrations below the foliar-injury 

threshold can cause significant yield losses in sensitive cultivars of leafy 

vegetable crops. In addition, photochemical oxidant events have caused foliar 

injury on leafy vegetables (Middleton et a1., 1950) for which the foliage is 

the marketable portion. After severe PAN damage, entire crops may be unmarketable or.else extensive hand work may be required to remove the injured leaves 

before the crop may be marketed. 

A comparison of PAN concentrations likely to cause either visible injury 

or reduced yield with measured ambient concentrations (see Chapter 5) indicates 

that it is unlikely that ambient PAN will impair the intended use of plants in 

the United States except in some areas of California and possibly in a few 

other localized areas. 

1.6 EFFECTS OF OZONE ON NATURAL ECOSYSTEMS AND TNEIR COMPONENTS 

1.6.1 Responses of Ecosystems to Ozone Stress 

The responses to ozone of individual species and subspecies of herbaceous 

and woody vegetation are well documented. They include (1) injury to foliage, 

(2) reductions in growth, (3) losses in yield, (4) alterations in reproductive 

capacity, and (5) alterations in susceptibility to pests and pathogens, especially "stress pathogens" (National Research Council, 1977; U.S. Environmental 

Protection Agency, 1978; this document, Chapter 6). The responses elicited by 

1-91 
ozone in individual species and subspecies of primary producers (green plants) 

have potential consequences for natural ecosystems because effects that alter 

the interdependence and interrelationships among individual components of 

populations can, if the changes are severe enough, perturb ecosystems. Because, 

however, of the numerous biotic and abiotic factors known to influence the 

response of ecosystem components such as trees (see, e.g., Cowling, 1985; 

Manion, 1985), it is difficult to relate natural ecosystem changes to ozone 

specifically, and especially to ozone alone. Ozone can only be considered a 

contributing factor. 

Evidence indicates that any impact of ozone on ecosystems will depend on 

the responses to ozone of the producer community. Producer species (trees and 

other green plants) are of particular importance in maintaining the integrity 

of an ecosystem, since producers are the source, via photosynthesis, of all 

new organic matter (energy/food) added to an ecosystem. Any significant 

alterations in producers, whether induced by ozone or other stresses, can 

potentially affect the consumer and decomposer populations of the ecosystem, 

and can set the stage for changes in community structure by influencing the 

nature and direction of successional changes (Woodwell, 1970; Bormann, 1985), 

with possibly irreversible consequences (see, e.g., Odum, 1985; Bormann, 

1985). 

1.6.2 Effects of Ozone on Producers 

In forest ecosystems, tree populations are the producers. As such, they 

determine the species composition, trophic relationships, and energy flow and 

nutrient cycling of forest ecosystems (Ehrlich and Mooney, 1983). Ozoneinduced effects on the growth of trees has been clearly demonstrated in 

controlled studies (see Chapter 6). For example, Kress and Skelly (1982) 

showed the following reductions in growth in height in seedlings exposed to 

ozone for 6 hr/day for 28 days: American sycamore, 9 percent (0.05 ppm 0 3 ); 

sweetgum, 29 percent (0.10 ppm 0 3 ); green ash, 24 percent•(0.10 ppm); willow 

oak, 19 percent (0.15 ppm 0 3 ); and sugar maple, 25 percent (0.15 ppm). Similar 

results have been obtained for other tree species by other investigators 

(e.g., Dochinger and Townsend, 1979; Mooi, 1980; Patton, 1981; Kr.ess et al., 

1982). Some species, however, have been shown to exhibit increased growth in 

short-term ozone exposures (e.g., yellow poplar and white ash; Kress and 

Skelly, 1982). Hogsett et al. (1985) found reductions in growth in height, in 

1- 92 
radial growth, and in root growth in slash pine seedlings exposed for up to 

112 days to 7-hr seasonal mean concentrations of 0.104 ppm 0 3 (with a 1-hr 

daily maximum of 0.126 ppm 0 3 ) and 0.076 ppm 0 3 (with a 1-hr daily maximum of 

0.094 ppm 0 3 ). 

Field studies on the Cumberland Plateau (near Oak Ridge, TN) have shown 

reductions in growth in eastern white pine exposed to ambient air 0 3 concentrations >0.08 ppm (1-hr) (Mann et al., 1980), with 1-hr concentrations ranging 

over the multi-year study from 0.12 ppm to 0.2 ppm (McLaughlin et al., 1982). 

It should be noted, however, that in the McLaughlin et al. (1982) study trees 

classified as ozone-tolerant sustained greater percentage reductions in radial 

growth in the last 4 years (1976 to 1979) of the 1962 to 1979 period for which 

growth was examined than the reductions observed in trees classified as ozonesensitive. In the Blue Ridge Mountains of Virginia, Benoit et al. (1982) 

found reductions in radial growth of sensitive eastern white pine in a multiF 

year study in which 1-hr 0 3 concentrations were generaliy 0.05 to 0.07 ppm but 

peaked at >0.12 ppm on as many as 5 consecutive days at a time. 

The concentrations of ozone reported for sites on the Cumberland Plateau 

and in the Blue Ridge Mountains may not fully represent the actual exposures 

at those sites, however, since measurements were made in the daytime only. 

For speci es i n whi ch stomates remai n open at ni ght, such as eastern whi te 

pine, the possible occurrence of peak ozone concentrations at night, from 

transported urban plumes, is an important consideration for accurately 

assessing concentration-response relationships. 

Exposures of trees and other producers to ozone have been shown to reduce 

photosynthesis (e.g., Miller et al., 1969; Botkin et al., 1972; Barnes, 1972; 

Carlson, 1979;,Coyne and Bingham, 1981; Yang et al., 1983; Reich and Amundson, 

1985) and to alter carbohydrate allocation, especially the partitioning of 

photosynthate between roots and tops '(e.g., Price and Treshow, 1972; Tingey 

et al., 1976; McLaughlin et al., 1982). Krause et al. (1984) have associated 

growth reductions in ozone-exposed seedlings with foliar leaching. A11 three 

of these effects have been postulated as mechanisms of the reduced growth seen 

in ozone-exposed vegetation. 

Responses to ozone are not uniform among plants of the same species and 

the same approximate age. Differential responses have been attributed in part 

to differences in genetic potential (e.g., Mann et al., 1980; Coyne and Bingham, 

1-93 
1981; Benoit et al., 1982). In addition, the age of the plant and its developmental stage at time of exposure influence its response to ozone (see Chapter 6). 

Other factors, as well, influence the types and magnitude of plant responses 

to ozone, including such macro- and microenvironmental factors as temperature, 

relative humidity, soil moisture, light intensity, and soil fertility (see 

Chapter 6). 

Trees may respond rapidly to 0 3 stress. Needles of sensitive eastern 

white pine usually exhibit injury symptoms within a few days after exposure to 

high 03 concentrations. In other instances, responses are more subtle and may 

not be observable for years because trees are perennials and must therefore 

cope over time with the cumulative effects of multiple short- and long-term 

stresses. Reductions in the growth of annual rings observed in ponderosa, 

Jeffrey, and eastern white pine have been attributed to the exposure of the 

trees to 03 over a period of 10 to 20 years (Miller and Elderman, 1977; Miller 

et al ., 1982; McLaughl i n et al ., 1982; Benoi t et al ., 1982). Decl i ne and 

dieback of red spruce in the northeastern United States and reduced growth 

rates of red spruce, balsam fir, and Fraser fir in central West Virginia and 

western Virginia also have been attributed to stresses, to which air pollution 

is a possible contributor, that began at least 20 years ago (Johnson and 

Siccama, 1983; Adams et al., 1985). 

1.6.3 Effects of Ozone on Other Ecosystem Components and on Ecosystem 

Interactions 

Evidence for the effects of ozone on other ecosystem components indicates 

that most are indirect, occurring chiefly as a result of the direct effects of 

ozone on trees and other producers. Significant alterations in producer 

species can change the ability of a species to compete and thus can influence 

the nature and direction of successiona1 changes in the ecosystem. Likewise, 

significant alterations in producers can result in changes in the consumer and 

decomposer populations that depend on producers as their food source. Studies 

in the San Bernardino Mountain ecosystems in the 1970s have provided some 

evidence of successional shifts and of predisposition to infestation by pests 

and pathogens as the result of oxidant-induced changes in ponderosa and Jeffrey 

pines (see Section 1.6.4 below). 

Marked morphological deterioration of the common lichen species, Hypogymnia 

enteromorpha, was documented in areas of the San Bernardino Mountains having 

high oxidant concentrations. A comparison of the species of lichens found 

1- 94 
growing on ponderosa and Jeffrey pine with collections from the early 1900's 

indicated the presence of 50 fewer species (Sigal and Nash, 1983). 

McCool et al. (1979) and Parmeter et al: (1962) reported decreases in 

mycorrhizal infections and rootlets in ozone-stressed citrange (a citrus 

hybrid) and ponderosa pine, respectively. Mahoney (1982), on the other hand, 

found no evidence of impairment in the development of mycorrhizal associations 

in loblolly pine seedlings exposed to ozone plus sulfur dioxide; however, 

shoot dry weight was decreased by 12 percent. 

The effects of ozone on mycorrhizae are of particular note here, since 

mycorrhizae are essential for the optimal development of most plants because 

of the functions they perform. Mycorrhizal fungi increase the solubility of 

minerals, improve the uptake of nutrients for host plants, protect roots 

against pathogens, produce plant growth hormones, and move carbohydrates from 

one plant to another (Hacskaylo, 1972). Ozone may disrupt the association 

between mycorrhizal fungi and plants, possibly by inhibiting photosynthesis 

and reducing the amounts of sugars and carbohydrates available for transfer 

from leaves of producers to the roots. Mycorrhizae are known to be sensitive 

to alterations in carbon allocation to the roots in host.plants (Hacskaylo, 

1973). 

Because of the complex interactions among plants, pests, pathogens, and 

other biotic and abiotic factors, Laurence and Weinstein (1981) have emphasized 

the critica7 importance of examining pollutant-pathogen and pollant-insect 

interactions in determining the growth impact of a pollutant. Manion (1985) 

has emphasized the necessity of taking non-pollutant stresses, both biotic and 

abiotic, into account when attempting to attribute changes in forest ecosystems 

to air pollutants. 

1.6.4Effects of Ozone on Specific Ecosystems 

One of the most thoroughly studied ecosystems in the United States is the 

mixed-conifer forest ecosystem in the San Bernardino Mountains of southern 

California. Sensitive plant species there began showing injury in the early 

1950's (Miller and Elderman, 1977) and the source of the injury was identified 

as oxidants (ozone) in 1962 (Miller et al., 1963). in an inventory begun in 

1968, Miller found that sensitive ponderosa and Jeffrey pines were being 

selectively removed by oxidant air pollution. Mortality of 8 and 10 percent 

was found in two respective populations of ponderosa pine studied between 1968 

1-95 
and 1972. Monitoring in that period showed ozone concentrations >0.08 ppm for 

>1300 hours, with concentrations rarely decreasing below 0.05 ppm at night 

near the crest of the mountain slope (Miller, 1973). 

In a subsequent interdisciplinary study (1973 through 1978), biotic and 

abiotic components and ecosystem processes were examined. The ecosystem 

components most directly affected were various tree species, the fungal microflora of needles, and the foliose lichens on the bark of trees. In May through 

September, 1973 through 1978, 24-hr-average ozone concentrations ranged from 

about 0.03 to 0.04 ppm to about 0.10 to 0.12 ppm. (Monitoring was done by the 

Mast meter through 1974 and by the UV method from 1975 through 1978). Foliar 

injury on sensitive ponderosa and Jeffrey pine was observed when the 24-hraverage ozone concentrations were 0.05 to 0.06 ppm (Miller et al., 1982). 

Injury, decline, and death of these species were associated with the major 

ecosystem changes observed (Miller et al., 1982). ' 

Growth reductions attributable to oxidant air pollution were calculated 

by McBride et al. (1975) for ponderosa pine saplings. Assuming 1910 to 1940 

to be a period of low oxidant pollution and 1944 to 1974 a period of high 

oxidant pollution, they used radial growth increments (dbh) to calculate an 

oxidant-induced decrease in diameter of 40 percent. On the basis of the 

3-year growth of saplings in.filtered and nonfiltered air in portable greenhouses, they calculated oxidant-induced reductions of 26 percent in height 

growth (McBride et al., 1975). No standardized methods.for determining tree 

ring widths were available at the time of this study. 

Carbon flow and mineral nutrient cycling were influenced by the accumulation of litter under stands with the most severe needle injury and by defoliation, as well as by a reduction in the number of species and the population 

density of the fungi that normally colonize living needles and later participate 

in decomposition. The most likely result of heavy litter accumulation is a 

reduction in pine seedling establishment and greater establishment and growth 

of oxidant-tolerant understory species on some sites and oxidant-tolerant 

trees on other sites (Miller et al., 1982). 

Changes in the energy available to trees influenced the biotic interactions, so that weakened ponderosa pines were more susceptible to attack by 

predators such as bark beetles and to pathogens such as root rot fungi (Stark 

and Cobb, 1969). Fewer western pine beetles were required to kill weakened 

trees (Dahlsten and Rowney, 1980); and stressed pines became more susceptible 

1- 96 
to root rot fungi (James et al., 1980) and showed a decrease in mycorrhizal 

rootlets and their replacement by saprophytic fungi (Parmeter et al., 1962). 

Accelerated rates of mortality of ponderosa and Jeffrey pine in the 

forest overstory, resulting from 0 3 injury, root rot, and pine beetle attack, 

and in some cases, removal by fire, changed the basic structure of the forest 

ecosystem (Phase IV; Bormann, 1985) by causing replacement.of the dominant 

conifers with self-perpetuating, fire-adapted, 0 3-tolerant shrub and oak 

species, which are considered less beneficial than the former pine forest and 

which inhibit reestablishment of conifers (Miller et al., 1982). 

Injury to vegetation in other ecosystems has also been reported. Duchelie 

et ai. (1983) found reductions in the growth and productivity of graminoid and 

forb vegetation in the Shenandoah National Park, where 1-hr ozone concentrati ons ranged from 0.08 to 0.10 ppm i n the 3-year study peri od, wi th 1-hr 

concentrations >0.06 ppm occurring for 1218, 790, and 390 hours in 1979, 1980, 

and 1981, respectively. Treshow and Stewart (1973) fumigated species that 

grow in the Salt Lake Valley and the Wasatch Mountains in Utah and found key, 

dominant species to be ozone-sensitive. The National Park Service (1985) has 

recently reported ozone-induced injury to vegetation in the Santa Monica 

Mountains National Recreational Area, the Sequoia and Kings Canyon National 

Parks, Indiana Dunes National Lakeshore, Great Smoky Mountains National Park, 

and the Congaree Swamp National Monument. The impact of injury to vegetation 

in these ecosystems has not been appraised. 

It should be emphasized that the relative importance of a given species 

in a given ecosystem must be considered in any assessment of the impact of 

ozone (or other stresses) on an ecosystem. Ozone has not had the impact on 

other ecosystems that it has had on the San Bernardino mixed-conifer forest 

because the plant species injured do not have a role equal in importance to 

the role of ponderosa and Jeffrey pines in the San Bernardino ecosystem. 

1.6.5Economic Vaivation of Ecosystems 

. At the present time, economists and ecologists remain unable to devise a 

mutually acceptable framework for estimating the economic value of ecosystems. 

In addition, the credibility of any attempt to estimate at present the economic 

value of ecosystems would be diminished by a lack of scientific data (1) on 

the time-course of the manifestation of stress-induced effects on ecosystems, 

(2) on the point at which ecosystems lose the capacity for self-repair, and 

1-97 
(3) on the points at which they begin to lose their ability to provide, 

respectively, priced and unpriced benefits to society. In addition, estimation 

of the economic losses that might be associated with the specific effects of 

ozone on ecosystems requires other data that are presently in short supply, 

i.e., better and more aerometric data and better and more data on additional 

variables, so that significant contributions from abiotic -Factors other than 

ozone, as well as from biotic factors, can be credibly estimated. 

1.7 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON NONBIOLOGICAL MATERIALS 

Over two decades of research show that ozone damages certain nonbiological 

materials; the amount of damage to actual in-use materials, however, is poorly 

characterized. Knowledge of indoor/outdoor ozone gradients, for example, has 

expanded considerably in recent years, and this type of exposure information 

has not been incorporated in materials damage studies. Moreover, virtually 

all materials research on photochemical oxidants has focused on ozone. Theoretically, a number of the less abundant oxidants may equal or surpass ozone 

in reactivity with certain materials, but this possibility has not been tested 

empirically. In the absence of photochemical pollution, oxidative damage to 

certain materials still occurs from atmospheric oxygen, but at a much reduced 

rate and through different chemical mechanisms. Generally, ozone damages 

elastomers by cracking along the line of physical stress, whereas oxygen 

causes internal damage to the material. 

The materials most studied in ozone research are elastomers and textile 

fibers and dyes. Natural rubber and synthetic polymers of butadiene, isoprene, 

and styrene, used in products like automobile tires and protective outdoor 

electrical coverings, account for most of the elastomer production in the 

United States. The action of ozone on these compounds is well known, and 

dose-response relationships have been established and corroborated by several 

studies. These relationships, however, must be correlated with adequate exposure information based on product use. For these and other economically 

important materials, protective measures have been formulated to reduce the 

rate of oxidative damage. When antioxidants and other protective measures are 

incorporated in elastomer production, the dose-cracking rate is reduced 

considerably, although the extent of reduction differs widely according to the 

material and the type and amount of protective measures used. 

.; 
The formation of cracks and the depth of cracking in elastomers are related to ozone dose and are influenced greatly by humidity and mechanical 

stress. Dose is defined as the product of concentration and time of exposure. 

The importance of ozone dose was demonstrated by Bradley and Haagen-Smit 

(1951), who used a specially formulated ozone-sensitive natural rubber. 

Samples exposed to ozone at a concentration of 20,000 ppm cracked almost 

instantaneously, and those exposed to lower concentrations took a proportionately longer time to crack. At concentrations of 0.02 to 0.46 ppm, and 

under 100-percent strain, the cracking rate was directly proportional to the 

time of exposure, from 3 to 65 min. 

Similar findings were reported by Edwards and Storey (1959), who exposed 

two SBR elastomers to ozone at a concentration of 0.25 ppm for 19 to 51 hr 

under 100-percent strain. With ozone doses of 4.75 ppm-hr to 12.75 ppm-hr, a 

proportional rate in cracking depth was.observed, averaging 2.34 pm/hr for 

cold SBR and 4.01 pm/hr for hot SBR. When antiozonants were added to the compounds, the reduction in cracking depth rate was proportional to the amount 

added. Haynie et al. (1976) exposed samples of a tire sidewall to ozone at 

concentrations of 0.08 and 0.5 ppm for 250 to 1000 hr under 10 and 20 percent-strain. Under 20-percent strain, the mean cracking rate for 0.08 ppm was 

1.94 pm/hr. From these and other data, they estimated that at the ozone standard of the time (0.08 ppm, 1-hr average), and at the annual NO xstandard of 

0.05 ppm, it would take 2.5 years for a crack to penetrate cord depth. 

In addition to stress, factors affecting the cracking rate include atmospheric pressure,. humidity, sunlight., and other atmospheric pollutants. Veith 

and Evans (1980) found a 16-percent difference in cracking rates reported from 

iaboratories located at various geographic elevations. 

Ozone has been found to affect the adhesion of plies (rubber-layered 

strips) in tire manufacturing. Exposure to ozone concentrations of 0.05 to 

0.15 ppm for a few hours significantly decreased adhesion in an NR/SBR blend, 

causing a. 30-percent decrease at the highest ozone level. This adhesion problem worsened at higher relative humidities. When fast-blooming waxes and 

antiozonants or other antioxidants were added, only the combination of protective measures allowed good adhesion and afforded protection from ozone and 

sunlight attack. Wenghoefer (1974) showed that ozone (up to 0.15 ppm), especially in combination with high relative humidity (up to 90 percent), caused 

greater adhesion losses than did heat and NO 2with or without high relative 

humidity. 

1-99 
The effects of ozone on dyes have been known for nearly three decades. 

In 1955, Salvin and Walker exposed certain red and blue anthraquinone dyes to 

a 0.1 ppm concentration of ozone and noted fading, which until that time was 

thought to be caused by NO 2 . Subsequent work by Schmitt (1960, 1962) confirmed 

the fading action of ozone and the importance of relative humidity in the 

absorption and reaction of ozone in vulnerable dyes. The acceleration in, 

fading of certain dyes by high relative humidity was noted later by Beloin 

(1972, 1973) at an ozone concentration of 0.05 ppm and relative humidity of 90 

percent. Kamath et al. (1982) also found that a slight rise in relative humidity 

(85 to 90 percent) caused a 20-percent dye loss in nylon fibers. 

Both the type of dye and the material in which it is incorporated are 

important factors in a fabric's resistance to ozone. Haynie et al. (1976) and 

Upham et al. (1976) found no effects from ozone concentrations of 0.1 to 0.5 

ppm for 250 to 1000 hr under high and low relative humidity (90 vs. 50 percent) 

on royal blue rayon-acetate, red rayon-acetate, or plum cotton. On the other 

hand, Haylock and Rush (1976, 1978) showed that anthraquinone dyes on nylon 

fibers were sensitive to fading from ozone at a concentration of 0.2 ppm at 70 

percent relative humidity and 40°C for 16 hr. Moreover, the same degree of 

fading occurred in only 4 hr at 90 percent relative humidity. At higher 

concentrations, there was a parallel increase in fading. Along with Heuvel et 

al. (1978) and Salvin (1969), Haylock and Rush (1976, 1978) noted the importance 

of surface area in relation to the degree of fading. In explaining this 

relationship, Kamath et al. (1982) found that ozone penetrated into the fiber 

itself and caused most of the fading through subsequent diffusion to the 

surface. 

Field studies by Nipe (1981) and laboratory work by Kamath et al. (1982) 

showed a positive association between ozone levels and dye fading of nylon 

materials at an ozone concentration of 0.2 ppm and various relative humidities. 

In summary, dye fading is a complex function of ozone concentration, relative 

humidity, and the presence of other gaseous pollutants. At present, the 

available research is insufficient to quantify the amount of damaged material 

attributable to ozone alone. Anthraquinone dyes incorporated into cotton and 

nylon fibers appear to be the most sensitive to ozone damage. 

The degradation of fibers from exposure to ozone is poorly characterized. 

In general, most synthetic fibers like modacrylic and polyester are relatively 

resistant, whereas cotton, nylon, and acrylic fibers have greater but varying 

1-100 
sensitivities to the gas. Ozone reduces the breaking strength of these fibers, 

and the degree of reduction depends on the amount of moisture present. Under 

laboratory conditions, Bogaty et al. (1952) found a 20 percent loss in breaking 

strength in cotton textiles under high-moisture conditions after exposure to a 

0.06 ppm concentration of ozone for 50 days; they equated these conditions to 

a 500- to 600-day exposure under natural conditions. Kerr et al. (1969) found 

a net loss of 9.percent in breaking strength of moist cotton fibers exposed to 

ozone at a concentration of 1.0 ppm for 60 days. The limited research i.n this 

area indicates that ozone in ambient air may have a minimal effect on textile 

fibers, but additional research is needed to verify this conclusion. 

The effects of ozone on paint are small in comparison with those.of other 

factors. Past studies have shown that, of various paints, only vinyl and 

acrylic coil coatings are affected,. and that this impact has a negligible 

effect on the useful life of the material coated. Preliminary results of 

current studies have indicated a statistically significant effect of ozone and 

relative humidity on latex house paint, but the final results of those studies 

are needed before conclusions can be drawn. 

For a number of important reasons, the estimates.of economic damage to 

materials are far from reliable. Most of the available studies ar.e now outdated in terms of the ozone concentrations, technologies, and supply-demand 

relationships that prevailed when the studies were.conducted. Additionally, 

little was (and is) known about the physical damage functions, and cost estimates were simplified to the point of not properly recognizing many of the 

scientific complexities of the impact of ozone. Assumptions about exposure to 

ozone generally ignored the difference between outdoor and indoor concentrations. 

Also, analysts have had difficulty separating ozone damage from other factors 

affecting materials maintenance and replacement schedules. For the most part, 

the studies of economic cost have not marshalled factual observations on how 

materials manufacturers have altered their technologies, materials, and methods 

in response to ozone. Rather, the analysts have mereiy made bold assumptions 

in this regard, most of which remain unverified through the present 4 time; 

Even more seriously, the studies followed engineering approaches,that,do 

not conform with acceptable methodologies for measuring economic welfare. 

Almost without exception, the studies reported one or more types of estimated 

or assumed cost increases.borne by materials producers, consumers, or both. 

The recognition of cost increase is only a preliminary step, however, towards 

1-101 
evaluating economic gains and losses. The analysis should then use these cost 

data to proceed with supply and demand estimation that will show how materials 

prices and production levels are shifted. Because the available studies fail 

to do this, there is a serious question as to what they indeed measure. 

Increased ozone levels increase sales for some industries even as they 

decrease welfare for others. For example, manufacturers of antiozonants for 

automobile tires conceivably stand to increase sales as ozone increases, while 

purchasers of tires stand to pay higher prices. This is only one illustration 

of a fundamental analytical deficiency in the various studies of materials 

damage: the absence of a framework for identifying gainers and losers, and the 

respective amounts they gain and lose. 

Among the various materials studies, research has narrowed the type of 

materials most likely to affect the economy from increased ozone exposure. 

These include elastomers and textile fibers and dyes. Among these, natural 

rubber used for tires is probably the most important economically for the 

following reasons: (1) significant ambient air exposure and long use life; 

(2) significant unit cost; and (3) large quantities and widespread distribution. 

The study by McCarthy et al. (1983) calculated the cost of antiozonants 

in tires for protection against ozone along with the economic loss to the 

retread industry. While limitations in this study preclude the reliable 

estimation of damage costs, the figures indicate the magnitude of potential 

damage from exposure to ozone in ambient air. 

Research has shown that certain textile fibers and dyes and house paint 

are also damaged by ozone, but the absence of reliable damage functions make 

accurate economic assessments impossible. Thus, while damage to these materials 

is undoubtedly occurring, the actual damage costs cannot be estimated confidently. 

It is apparent from the review presented in this chapter that a great 

deal of work remains to be done in developing quantitative estimates of materials damage from photochemical oxidant exposures. This is not meant to 

deprecate the years of research reported in this document, for much has been 

gained in refining the initial methodologies used for assessing damage. Yocom 

et al. (1985) have summarized the current state of knowledge: 

1-102 
We have learned that some costs may be difficult to quantify either 

because they are minimal or because they are overshadowed by other factors, 

such as wear or obsolescence. We have learned that damage functions are 

complex and are influenced by the presence of other pollutants and by weather. 

We have learned that more accurate estimates of materials in place may be 

obtained using selective sampiing and extrapolation. And we have learned that 

a mere cost-accounting of damage does not present a true estimate of economic 

cost if it does not account for the welfare effects induced by shifts.in the 

supply-demand relationship. 

1.8 TOXICOLOGICAL EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS 

1.8.1 Introduction 

The biological effects of 0 3 have been studied extensively in animals and 

a wide array of toxic effects have been ascribed to 0 3 inhalation. Although 

much has been accomplished to improve the existing data base, refine the concentration-response relationships and interpret better the mechanisms of 0 3 

effects, many of the present data were not accumulated with the idea that 

quantitative comparisons to man would be drawn. In many cases, only qualitative comparisons can be made. To maximize the extent that animal toxicological 

data can be used to estimate the human health risk of' exposure to 0 3 , the 

qualitative as well as quantitative similarities between the toxicity of 03 to 

animais and man must be considered more carefu7ly in the future. Significant 

advances have been made in understanding the toxicity of 0 3 through appropriate 

animal models. This summary highlights the significant results of selected 

studies that will provide useful data for better predicting and assessing, in 

a scientifically sound manner, the possible human responses to 0 3 . 

Summary figures and tables are presented in the following sections. The 

practical purpose of this presentation of the data is to help the reader focus 

on what types of effects or responses have been reported, what concentrations 

have been tested (1.0 ppm and lower), and as a convenient list of references 

with each of the biological parameters measured. Studies were selected for 

inclusion in these figures and tables on the basis of specific criteria presented below: 

, 

1. Studies have been cited when the reported effects are clearly due to 0 3 

exposure. Effects due to mixtures of 0 3 with other pollutants have been 

summarized in a separate figure and table. Studies involving exercise, 

diet deficiencies, or other possible modifiers of response to 0 3 have not 

been included. 

1-103 
2. Cited studies report the effects of 0 3 exposure over a broad range of 

animal species and strains and for varying lengths of time. Specific 

details on animal species, exposure duration, and observed biological 

effects can be obtained from the tables in Chapter 9. 

3. Each closed symbol on the figures represents one or more studies conducted 

at that particular concentration that caused effects. Specific references 

can be found in the accompanying tables. 

4. Each open circle represents one or more studies that used the given 

concentration, but reported no significant effects. No-effect levels are 

also indicated by brackets in the accompanying tables. 

5. Only pulmonary function effects were divided by short-term (<14 days) and 

long-term exposures to follow the discussion in the text. 

In order to keep this section brief and concise, it was necessary to be somewhat 

selective in determining what and how this information would be presented. A 

number of important factors, such as the specific length of exposure, were not 

included. Also, the parameter selected to illustrate a specific response was 

usually broad and very general. For example, the category "decreases in 

macrophage function" includes such diverse endpoints as measurements of lysosomal and phagocytic activity, macrophage mobility, or chemotactic response. 

These responses may or may not be related to one another. Thus, care must be 

taken in how these data are used and interpreted. The only appropriate use is 

to gain an overview of the broad array of the effects of ozone and the concentrations which did and did not cause these effects. 

1.8.2 Regional Dosimetry in the Respiratory Tract 

The amount of 0 3 acting at a given site in the lung is related to the 

airway luminal concentration at that level. As a result, 0 3 does not immediately 

interact with cellular components of the respiratory tract. Instead, it first 

comes into contact with the mucous or surfactant layer lining the airway. It 

should be noted that 0 3 is quite reactive chemically. Reactions with components 

of this layer cause an increase in total absorption of 0 3 in the upper airways 

and in a reduction of the amount of 0 3 reaching sensitive tissues. The site 

1-104 
at which uptake and subsequent interaction occur and the local dose (quantity 

of 0 3 absorbed per unit area per time), along with cellular sensitivity, will 

determine the type and extent of the injury. Also, the capacity for responding 

to a specific dose may vary between animals and-humans because of dissimilarities in detoxification systems, pharmacokinetics, metabolic rates, genetic 

makeup, or other factors. Thus, along with the above, a knowledge of the 

complex process of gas transport and absorption is crucial to understanding 

the effects of 0 3 and other oxidants in humans. 

The animal studies that have been conducted on ozone absorption are 

beginning to indicate the quantity and site of 0 3 uptake in the respiratory 

tract. Experiments on the nasopharyngeal removal of 0 3 in animals suggest 

that the fraction of 0 3 uptake depends inversely on flow rate, that uptake is 

greater for nose than for mouth breathing, and that tracheal and chamber 

concentrations are positively correlated. Only one experiment measured 0 3 

uptake in the lower respiratory tract, finding 80 to 87 percent uptake by the 

lower respiratory tract of dogs (Yokoyama and Frank, 1972). At present, 

however, there are no reported results for human nasopharyngeal• or lower 

respiratory tract absorption. Caution must be used in estimating nasopharyngeal 

uptake for normal respiration based upon experiments employing unidirectional 

flows. 

To further an understanding of 0 3 absorption, mathematical models have 

been developed to simulate the processes involved and to predict 0 3 uptake by 

various regions and sites within the respiratory tract. The model of Aharonson 

et al. (1974) has been used to analyze nasopharyngeal uptake data. Applied to 

0 3 data, the model indicates that the average mass transfer coefficient in the 

nasopharyngeal region increases with increasing air flow, but the actual 

percent uptake decreases. 

Three modeis have been developed to simulate lower respiratory uptake 

(McJilton et al., 1972; Miller et al., 1978b, 1985). These models are very 

simiiar in their treatment of 0 3 in the airways (taking into account convection, 

diffusion, wall losses, and ventilatory patterns) and in their use of morphological data to define the dimensions of the airways and liquid lining. The 

modeis differ in their treatment of the mechanism of absorption. Both of the 

models of Miller and co-workers take into account chemical reactions of 0 3 

with constituents of the liquid lining, whereas the model of McJilton et al. 

does not. The models of Miller et al. differ in their treatment of chemical 

1-105 
reactions, as well as in the fact that the newer model includes chemical reactions of 03 in additional compartments, such as tissue and blood. 

Tissue dose is predicted by the models of Miller et al. to be relatively 

low in the trachea, to increase to a maximum between the junction of the 

conducting airways and the gas-exchange region, and then to decrease distally. 

This is not only true for animal simulations (guinea pig and rabbit) but it 

is also characteristic of the human simulations (Miller et al., 1978b; 

1985). 

A comparison of the results of Miller and co-workers with morphological 

data (that shows the centriacinar region to be most affected by 0 3 ) indicates 

qualitative agreement between predicted tissue doses and observed effects in 

the pulmonary region. However, comparisons in the tracheobronchial region 

indicate that dose-effect correlations may be improved by considering other 

expressions of dose such as total absorption by an airway and by further 

partitioning of the mucous layer compartment in mathematical models. Further 

research is needed to define toxic mechanisms, as well as to refine our knowledge of important chemical, physical, and morphological parameters. 

At present, there are few experimental results that are useful in judging 

the validity of the modeling efforts. Such results are needed, not only to 

understand better the absorption of 0 3 and its role in toxicity, but also to 

support and to lend confidence to the modeling efforts. With experimental 

confirmation, models which further our understanding of the role of 0 3 in the 

respiratory tract will become practical tools. 

The consistency and similarity of the human and animal lower respiratory 

tract dose curves obtained thus far lend strong support to the feasibility of 

extrapolating to man the results obtained on animals exposed to 0 3 . In the 

past, extrapolations have usually been qualitative in nature. With additional 

research in areas which are basic to the formulation of dosimetry models, 

quantitative dosimetric differences among species can be determined. If in 

addition, more information is obtained on species sensitivity to a given dose, 

significant advances can be made in quantitative extrapolations and in making 

inferences about the likelihood of effects of 03 in man. Since animal studies 

are the only available approach for investigating the full array of potential 

disease states induced by exposure to 0 3 , quantitative use of animal data is 

in the interest of better establishing 0 3 levels to which man can safely be 

exposed. 

1-106 
1.8.3 Effects of Ozone on the Respiratory Tract 

1.8.3.1 Morphological Effects. The morphological changes which follow exposure 

to less than 1960 pg/m3 (1.0 ppm) 0 3 are very similar in all species of laboratory mammals studied. Of the many specific celi types found in the respiratory 

system, two types, ciliated cells and type 1 alveolar epitheiial cells, are 

the cells most damaged morphologically following 0 3 inhalation. Ciiiated cells 

are found in the conducting airways, e.g., trachea, bronchi, and nonrespiratory 

bronchioles. Ciliated cells function in the normal clearance of the airways 

and the removal of inhaled foreign material. Following 0 3 exposure of experimental animals, damaged ciliated cells have been reported in all of these 

conducting airways (Schwartz et al., 1976; Castleman et al., 1977). In rats, 

damage to ciliated cells appears most severe at the junction of the conducting 

airways with the gas exchange area (Stephens et al., 1974a; Schwartz et al., 

1976). Damage to type 1 alveolar epithelial cells is limited to those cells 

located near this junction, i.e., the centriacinar or proximal alveolar region 

of the pulmonary acinus (Stephens et al., 1974b; Schwartz et al., 1976; 

Castleman et al., 1980; Barry et al., 1983; Crapo et al., 1984). Type 1 

alveolar cells form most of the blood-air barrier where gas exchange occurs. 

Severely damaged ciliated and type 1 alveolar epithelial cells are shed (sloughed) 

from the tissue surface and are replaced by multiplication of other cell types 

less damaged by 0 3 (Evans et al., 1985). This process has been most extensively 

studied in the centriacinar region where nonciliated bronchiolar cells and 

type 2 alveolar epithelial cells become more numerous (Evans et al., 1976a,b,c; 

Lum et al., 1978). Some of these nonciliated bronchiolar and type 2 cells 

differentiate into ciliated and type 1 cells, respectively. Cell multiplication 

in bronchioles may be more than that required for replacement of damaged 

ciliated cells, and nonciliated bronchiolar cells may become hyperpiastic 

(Castleman et al., 1977; Ibrahim et al., 1980; Eustis et al., 1981) and sometimes 

appear as nodules (Zitnik et al., 1978; Moore and Schwartz, 1981; Fujinaka et 

al., 1985). Inflammatory changes characterized by a variety of leukocytes 

with alveolar macrophages predominating, intramural edema, and fibrin are also 

seen in the centriacinar region (Stephens et al., 1974a; Schwartz et al., 

1976; Castleman et a1.,.1977; Fujinaka et al., 1985). 

The damage to ciliated and centriacinar type 1 alveolar epithelial cells 

and the inflammatory changes tend to occur soon after exposure to concentrations 

of 03 as 1 ow as 392 pg/m (0.2 ppm). Damage to centriacinar type 1 alveolar 3 

1-107 
epithelium in rats has been well documented as early as 2 hours after exposure 

to 03 concentrations of 980 pg/m3 (0.5 ppm) (Stephens et al., 1974a). In the 

same publication the authors report damage to centriacinar type 1 alveolar 

epithelial cells after 2 hours exposure to 392 pg/m 3 (0.2 ppm) 0 3 , but this 

portion of their report is not documented by published micrographs (Stephens 

et al., 1974a). Loss of cilia from cells in the rat terminal bronchiole 

occurs following exposure to 980 pg/m 3 (0.5 ppm) 0 3 for 2 hours (Stephens et 

al., 1974a). Damage to ciliated cells has been seen following exposure of 

both rats and monkeys to 392 pg/m3 (0.2 ppm) 0 3 , 8 hr/day for 7 days (Schwartz 

et al., 1976; Castleman et al., 1977). Centriacinar inflammation has been 

reported as early as 6 hours after exposure to 980 pg/m 3 (0.5 ppm) 0 3 (Stephens 

et al., 1974b) and 4 hours after exposure to 1568 pg/m 3 (0.8 ppm) 0 3 (Castleman 

et al. , 1980). 

During long-term exposures, the damage to•ciliated cells and to centriacinar 

type 1 cells and centriacinar inflammation continue, though at a reduced rate. 

Damage to cilia has been reported in monkeys following 90-day exposure to 980 

pg/m3 (0.5 ppm) 03 , 8 hr/day (Eustis et al., 1981) and in rats exposed to 980 

pg/m3 (0.5 ppm) 0 3 , 24 hr/day for 180 days (Moore and Schwartz, 1981). Damage 

to centriacinar type 1 cells was reported following exposure of yo.ung rats to 

490 pg/m3 (0.25 ppm) 0 3 , 12 hrs/day for 42 days (Barry et al., 1983; Crapo et 

al., 1984). Changes in type 1 cells were not detectable after 392 pg/m3 (0.2 

ppm) 0 3 , 8 hr/day for 90 days but were seen in rats exposed to 980 pg/m3 (0.5 

ppm) for the same period (Boorman et al., 1980). Centriacinar inflammatory 

changes persist during 180-day exposures of rats to 980 lag/m 3 (0.5 ppm) 0 3 , 24 

hr/day (Moore and Schwartz, 1981) and one-year exposures of monkeys to 1254 

pg/m3 (0.64 ppm) 0 3 , 8 hr/day (Fujinaka et al., 1985). 

Remodeling of distal airways and centriacinar regions occurs following 

long-term exposures to 0 3 . Rats develop respiratory bronchioles between the 

terminal bronchiole to alveolar duct junction seen in control rats (Boorman et 

al., 1980; Moore and Schwartz, 1981)._ In monkeys, distal airway remodeling 

results in increased volumes of respi.ratory bronchioles which have.thicker 

walls and a smaller internal diameter (Fujinaka et al., 1985). The walls of 

centriacinar alveoli are also thickened (Schwartz et al., 1976; Boorman et 

al. , 1980; Barry et al ., 1983; Crapo et al ., 1984; Last et al ., 1984a). 

Studies of the nature of these thickened interalveolar septa and bronchiolar 

walls revealed increases in inflammatory cells, fibroblasts, and amorphous 

1-108 
extracellular matrix (Last et al., 1984a; Fujinaka et al., 1985). Three 

studies provide morphological evidence of mild fibrosis (i.e., local increase 

of collagen) in centriacinar interalveolar septa foliowing exposure to < 1960 

pg/m3 (< 1 ppm) of 0 3 (Last et al ., 1979; Boorman et al ., 1980; Moore and 

Schwartz, 1981). Changes in collagen location or amounts, or both, which 

occur with the remodeling of the distal airways, were reported in two of those 

studies (Boorman et al., 1980; Moore and Schwartz, 1981). 

While morphometry of small pulmonary arteries is not commonly studied in 

03 -exposed animals, pulmonary artery walls thickened by muscular hyperplasia 

and edema were reported in rabbits exposed to 784 pg/m 3 (0.4 ppm) 03 , 6 hr/day, 

5 days/week for 10 months (P'an et al., 1972). Thickened intima and media in 

pulmonary arterioles were reported in monkeys exposed to 1254 pg/m 3 (0.64 ppm) 

03 , 8 hr/day for 1 year (Fujinaka et al., 1985). 

Several of the effects of 03 inhalation persisted after the 0 3 inhalation 

ended and the animals breathed only filtered air several days or weeks. Lungs 

from rats exposed to 1568 pg/m 3 (0.8 ppm) 0 3 for 72 hours appeared normal 6 

days after the end of the exposure (Plopper et al., 1978). However, incomplete 

resolution of the nonciliated bronchiolar epithelial hyperplasia was reported 

in monkeys 7 days after 50 hours exposure to 1568 pg/m 3 (0.8 ppm) O B (Castleman 

et a1., 1980) and in mice 10 days after a 20-day exposure to 1568 pg/m 3 (0.8 

ppm)` 03 , 24 hr/day (Ibrahim et al., 1980). Centriacinar inflammation and 

distal airway remodeling were still apparent 62 days after a 180-day exposure 

to 980 pg/m3 (0.5 ppm) 0 3 , 24 hr/day (Moore and Schwartz, 1981). 

While not all species of laboratory mammals have been studied following a 

single 0:3 exposure regimen or using the same morphological techniques because 

investigators have asked different biological questions, there is a striking 

similarity of morphological effects in the respiratory system of all species 

studied. The ceil types most damaged are the same. One of these cells, the 

type 1 alveolar epithelial cell, has a wide distribution in the pulmonary 

acinus and.yet is damaged only in one specific location in all species studied. 

The other,'the ciliated cell, appears damaged wherever it is located in the 

conducting airways. Damage to these cells is seen within hours after exposure 

to concentrations of 0 3 much lower than 1 ppm and continues during exposures 

of weeks or months. Hyperplasia of other cell types is reported to start 

early in the exposure period, to continue throughout a long-term exposure, and 

when studied, to persist following postexposure periods of days or weeks. 

1-109 
Centriacinar inflammation is also seen early and is reported throughout long 

exposure periods. Duratio-n of centriacinar inflammation dur.ing postexposure 

periods has been studied less often and appears dependent upon length of the 

exposure period. 

Other effects which have been reported in fewer studies or in a more 

limited number of species include distal airway remodeling and thickened pulmonary arteriolar walls. Remodeling of distal airways has only been reported 

in rats and monkeys after long-term exposures. In rats, remodeling of distal 

airways has been reported to persist for several weeks after the 0 3 exposure 

has ended. Thickened pulmonary arteriolar walls have been reported only 

twice, once after long-term exposure of rabbits and once after long-term 

exposure of monkeys. 

Studies on the morphologic effects of 0 3 exposures of experimental animals 

are summarized in Figure 1-7 and Table 1-11 (see Section 1.8.1 for criteria 

used to summarize the studies). 

1.8.3.2Pulmonary Function . One of the limitations of animal studies is that 

many pulmonary function tests comparable to those conducted after acute exposure 

of human subjects are difficult to interpret. Methods exist, however, for 

obtaining similar measurements of many variables pertinent to understanding 

the effects of ozone on the respiratory tract, particularly after longer 

exposure periods. A number of newer studies reported here reflect recent 

advances in studying the effects of 0 3 on pulmonary function in small animals. 

Changes in lung function following ozone exposure have been studied in 

mice, rats, guinea pigs, rabbits, cats, dogs, sheep, and monkeys. Short-term 

exposure for 2 hr to concentrations of 431 to 980 pg/m 3 (0.22 to 0.5 ppm) 

produces rapid, shallow breathing and increased pulmonary resistance during 

exposure (Murphy et al., 1964; Yokoyama, 1969; Watanabe et al., 1973; Amdur 

et al., 1978). The onset of these effects is rapid and the abnormal breathing 

pattern usually disappears within 30 min after cessation o -P exposure. Other 

changes in lung function measured following short-term ozone exposures lasting 

3 hr to 14 days are usually greatest 1 day following exposure and disappear by 

7 to 14 days following exposure. These effects are associated with premature 

closure of the small, peripheral airways and include increased residual volume, 

closing volume, and closing capacity (Inoue et al., 1979). 

1-110 
v 

coGO A 

7~ 

~ ~Op py 

6'G Gd y,t 

~p 

r 

TQ 

Gp~ 

./ 

G O 

,rA C-% VA 

uGp 

G 

Qe- o "A 

Gp~pi 

Aip9 

~ r 

! 

AtG? 

~ 

~ 

O r' N M tL9 tp i0 

O 0O O ® ® O '® 

~ 

R 

E 

~ y 

~ A 

E ~ 

.~ O 

x m 

~ V 

'~ G9 

~ V 

C~ r 

C? ~ 

® ,rgv- 

® ~ E 'c 

ca 

®~ 

E~~i 

N ® s ~ 

~ 4-9 N 

E 

E 

Li ~ tq 

00 ®9 ® 

cudd 'uoileJ;uaouoo auoz® 

1-111 
TABLE 1-11. SUMMARY TABLE: MORPHOLOGICAL EFFECTS OF OZONE 

IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

Damaged ciliated [0.21, 0.5, 0.8 Boorman et al. (1980) 

and type 1 cells 0.2, 0.5, 0.8 Schwartz et al. (1976) 

0.2, 0.35 Castleman et al. (1977) 

0.25 Barry et al. (1983) 

0.25 Crapo et al. (1984) 

0.26, 0.50, 1.0 Boatman et al. (1974) 

0.5 Stephens et al. (1974b) 

0.5 Moore and Schwartz (1981) 

0.5 Evans et al. (1985) 

0.5, 0.8 Eustis et al. (1981) 

0.5, 0.8 Mellick et al. (1975, 1977) 

0.54, 0.88 Stephens et al. (1974a) 

0.8 Castleman et al. (1980) 

0.8 Plopper et al. (1978) 

0.85 Stephens et al. (1978) 

Proliferation of non- 0.2, 0.35 Castleman et al. (1977) 

ciliated bronchiolar 0.35, 0.50, 0.70, Evans et al. (1976b) 

and type 2 cells 0.75, 1.0 

0.5 Evans et al. (1985) 

0.5 Zitnik et al. (1978) 

0.5 Moore,and Schwartz (1981) 

0.5, 0.8 Eustis et al. (1981) 

0.54, 0.88 Freeman et al. (1974) 

0.64 Fujinaka et al. (1985) 

0.7 Evans et al. (1976a) 

0.8 Castleman et al. (1980) 

0.8 Lum et al. (1978) 

0.8 Ibrahim et al. (1980) 

1.0 Cavender et al. (1977) 

Centriacinar [0.2], 0.5, 0.8 Boorman et al. (1980) 

inflammation 0.2 Plopper et al. (1979) 

0.2, 0.5, 0.8 Schwartz et al. (1976) 

0.25 Barry et al. (1983) 

0.25 Crapo et al. (1984) 

0.35 Castleman et al. (1977) 

0.5 Stephens et al. (1974b) 

0.5 Moore and Schwartz (1981) 

0.5, 0.8 Mellick et al. (1975, 1977) 

0.5, 0.8 Brummer et al. (1977) 

0.5, 0.8 Last et al. (1979) 

0.54, 0.88 Stephens et al. (1974a) 

0.54, 0.88 Freeman et al. (1974) 

0.64 Fujinaka et al. (1985) 

0.8 Castleman et al. (1980) 

1.0 Freeman et al. (1973) 

1-112 
TABLE 1-11 (continued). SUMMARY TABLE: MORPHOLOGICAL EFFECTS OF OZONE 

IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

Distal airway 

remodeling 

[0.21, 0.5, 0.8 

0.2, 0.5, 0.8 

0.5 

0.64, 0.96 

0.64 

1.0 

Boorman et al. (1980) 

Schwartz et al. (1976) 

Moore and Schwartz (1981) 

Last et al. (1984a) 

Fujinaka et al. (1985) 

Freeman et al. (1973) 

Thickened pulmonary 0.4 P'an et al. (1972) 

arteriolar walls 0.64 Fujinaka et al. (1985) 

Studies of airway reactivity following short-term ozone exposure of 1 to 

2 hr duration in experimental animals show that 0 3 increases the reactivity of 

the lungs to a number of stimuli. Mild exercise, histamine aerosol inhalation, 

and breathing air with reduced oxygen or elevated carbon dioxide concentrations 

caused rapid, shallow breathing in conscious dogs immediately following 2-hr 

exposures to 1100 to 1666 pg/m 3 (0.56 to 0.85 ppm) of.0 3 (Lee et al., 1979, 

1980). Aerosolized ovalbumin caused an increased incidence of anaphylaxis in 

mice preexposed to 980 or 1568 pg/m 3 (0.5 or 0.8 ppm) of 03 continuously for 3 

to 5 days (Osebold et al., 1980). In addition, increased airway sensitivity 

to histamine or cholinomimetic drugs administered by aerosol or injection has 

been noted in several species after exposure to 980 to 5880 pg/m 3 (0.5 to 3.0 

ppm) of 03 (Easton and Murphy, 1967; Lee et al., 1977; Abraham et al., 1980, 

1984a,b; Gordon and Amdur, 1980; Gordon et ai., 1981, 1984; Roum and Murlas, 

1984). The mechanism responsible for 0 3-induced bronchial reactivity is still 

uncertain but may involve more than one specific factor. Ozone has been shown 

to cause increased sensitivity of vagal sensory endings in the dog airway (Lee 

et al., 1977, 1979, 1980). Ozone exposure may also enhance the airway responsiveness to bronchoconstrictors by altering sensitivity of the airway smooth 

muscle directly or through released cellular mediators (Gordon et ai., 1981, 

1984; Abraham et al., 1984a,b). In some species, increased airway hyperreactivity may be explained by increased transepithelial permeability or decreased 

thickness of the airway mucosa (Osebold et al., 1980; Abraham et al., 1984b). 

Ozone exposure may also decrease airway hyperreactivity by causing mucous 

1-113 
hypersectetion, thereby limiting the airway penetration of inhaled bronchoconstrictors (Abraham et al., 1984a). 

The time course of airway hyperreactivity after exposure to 980 to 5880 

pg/m (0.5 to 3.0 ppm) of 0 3 suggests a possible association with inflammatory 

cells and pulmonary inflammation (Holtzman et al., 1983a,b; Sielczak et al., 

1983; Fabbri et al., 1984; 0'Byrne et al., 1984a,b; Murlas and Roum, 1985). 

However, the time course of responsiveness is variable in different species 

and the relationships between airway inflammation and reactivity at different 

concentrations of 03 are not well understood. Additional studies that demonstrate increased collateral resistance following 30 min local exposure of 0 3 

or histamine in sublobar bronchi of dogs (Gertner et al., 1983a,b,c,1984) 

suggest that other mechanisms, along with amplification of reflex pathways, 

may contribute to changes in airway reactivity depending not only on the 

concentration of 03 in the airways but also on the extent of penetration of 

ozone into the lung periphery. 

The effects of short-term exposures to 03 on pulmonary function and 

airway reactivity in experimental animals are summarized in Figure 1-8 and 

Table 1-12 (see Section 1.8.1 for criteria used in developing this summary). 

Exposures of 4 to 6 weeks to ozone concentrations of 392 to 490 pg/m 3 

(0.2 to 0.25 ppm) increased lung distensibility at high lung volumes in young 

rats (Bartlett et al., 1974; Raub et al., 1983). Similar increases in lung 

distensibility were found in older rats exposed to 784 to 1568 pg/m 3 (0.4 to 

0.8 ppm) for up to 180 days (Moore and Schwartz, 1981; Costa et al., 1983; 

Martin et al., 1983). Exposure to 0 3 concentrations of 980 to 1568 pg/m3 (0.5 

to 0.8 ppm) increased pulmonary resistance.and caused impaired stability of 

the small peripheral airways in both rats and monkeys ( Wegner, 1982; Costa 

et al., 1983; Yokoyama et al., 1984; Kotlikoff et al., 1984). The effects in 

monkeys were not completely reversed by 3 months following exposure; lung 

distensibility had also decreased in the postexposure period, suggesting the 

development of lung fibrosis which has also been suggested morphologically and 

biochemically. 

The effects of long-term exposures to ozone on pulmonary function and 

airway reactivity in experimental animals are summarized in Figure 1-9 and 

Table 1-13 (see Section 1.8.1 for criteria used in developing this summary). 

1-114 
0 - - - - - - - - - - - - - - 

go 

m 

T 

O G 

t. 

J 

R co 

J~ ;niJ 

0 N 

~it~ V ~ 

.~ 

~00 

~ 7J A✓ 

J 

Jv O 

~JG 7d 

0 

JS~ "J~ 

7 

o~ 

~ 

! Od 

y 

J % J0 

76v ~O~ 

io 

~ O 

v 

4 

Olip AO 

I 

C 

O 

~ `OF 

L O~N 

H ~ O~ 

Q 

~~ 

c~ 

O 

N ~ 

O~ ~ 

E s 

~ ~ w 

cO~ E 

N O 7 

~ EW 

O i ~ O 

i' 4— 

x_ h 

es C y 

E ° c 

E~ o 

O 

~ V 

~ 

 ~

V 

C 

7E ~, 

LL Q L 

o ~ N M Re Ln co n ao c~ o 

wdd •suoileizuaouoo auozp 

1-115 
TABLE 1-12. SUMMARY TABLE: EFFECTS ON PULMONARY FUNCTION 

OF SHORT-TERM EXPOSURES TO OZONE IN EXPERIMENTAL ANIMALS 

Effect/response 0 3 concentration, ppm References 

Increased breathing 0.22, 0.41, 0.8 Amdur et al. (1978) 

frequency 0.34, 0.68, 1.0 Murphy et al. (1964) 

0.5 Yokoyama (1969) 

Decreased tidal volume 0.34, 0.68, 1.0 Murphy et al. (1964) 

Decreased lung [0.22], 0.41, 0.8 Amdur et al. (1978) 

compliance 0.26, 0.5, 1.0 Watanabe et al. (1973) 

1.0 Yokoyama (1974) 

Increased residual 0.24 - 1.0 Inoue et al. (1979) 

volume (RV), 

closing capacity 

(CC), and closing 

volume (CV) 

Decreased diffusion 0.26, 0.5, 1.0 Watanabe et al. (1973) 

capacity 

Increased pulmonary [0.22] Amdur et al. (1978) 

resistance 0.26, 0.5, 1.0 Watanabe et al. (1973) 

0.5 Yokoyama (1969) 

1.0 Yokoyama (1974) 

Increased airway [0.1]-0.8 Gordon and Amdur (1980) 

reactivity [0.1]-0.8, 1.0 Gordon et al. (1981, 1984) 

0.5, 1.0 Abraham et al. (1980, 1984a,b) 

0.7 Lee et al. (1977) 

1.0 Holtzman et al. (1983a,b) 

1.8.3.3Biochemical Effects . The lung is metabolically active, and several 

key steps in metabolism have been studied after 03 exposure. Since the procedures for such studies are invasive, this research has been conducted only in 

animals. Effects, to be summarized below, have been observed on antioxidant 

metabolism, oxygen consumption, proteins, lipids, and xenobiotic metabolism. 

The lung contains several compounds (e.g., vitamin E, sulfhydryls, glutathione) and enzymes (e.g., glutathione peroxidase, glutathione reductase, 

glucose-6-phosphate dehydrogenase, and superoxide dismutase) that function as 

antioxidants, thereby defending the lung against oxidant toxicity from the 

1-116 
~ 

7~ 

y 

o~ d 

A "o i d 

G 

`~G p 

A~~t d~AO 

d`~G VJQ' vodO 

G 

ip 

T

~5. 

vA ~J 

GO om 

? O 

N ~ 

~ ~d0

. 

I 

~00 

~A 

v 

i 

0-0 0 

O - O — — o— 0 • 

c ~ 

0 0 

ai ~ 

LM 

N~ 

O.~ 

d ~ 

4)~ C 

o V1 i 

~ 

E cli S 

*'E ~ 

~•~ •N 

~ cci 

R 

O 4ra- E 

N ~ ~ 

~ EN 

LD ~ •i tR 

O x ~ N 

eC C y 

~ O ~ 

E 5 . 0 

3 C +' 

~ ca `r = Oi A v L ~ 

(D O ~ 

~ E ~, 

CO 75 ~ IL C. L 

O a— N M tA Il 00 O~ O 

wdd •suoi;eiluaouoa auozp 

1-117 
TABLE 1-13. SUMMARY TABLE: EFFECTS ON PULMONARY FUNCTION 

OF LONG-TERM EXPOSURES TO OZONE IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

Increased lung volume [0.081, [0.12], 0.25 

0.2 

[0.21, 0.8 

0.4 

Raub et al. (1983) 

Bartlett et al. (1974) 

Costa et al. (1983) 

Martin et al. (1983) 

Increased pulmonary 0.2, 0.8 Costa et al. (1983) 

resistance 0.5, 1.0 Yokoyama et al., 1984 

0.64 Wegner (1982) 

0.64 Kotlikoff et al., 1984 

Decreased lung 0.5, 0.8 Eustis et al. (1981) 

compliance 0.64 Wegner (1982) 

Decreased inspiratory [0.081, 0.12, 0.25 Raub et al. (1983) 

f 1 ow 

Decreased forced 

expiratory volume 

(FEV ) and flow 

(FEFI 

0.2, 0.8 

0.64 

Costa et al. (1983) 

Wegner (1982) 

oxygen in air, from oxidants produced during metabolic processes, and from 

oxidizing air pollutants such as ozone. Obviously, this protection is only 

partial for 03 since exposure to ozone causes numerous effects on lung structure, function, and biochemistry. Acute exposure to high ozone levels 

(2920 pg/m3 , 2 ppm) typically decreases antioxidant metabolism, whereas repeated 

exposures to lower levels (between 272 and 1568 pg/m 3 , 0.2 and 0.8 ppm) increases this metabolism (DeLucia et al., 1975b). In rats maintained on normal 

diets, this response has been observed after a week of continuous or intermittent exposure to 392 pg/m3 (0.2 ppm) 0 3 (Mustafa, 1975; Mustafa and Lee, 1976; 

Plopper et al., 1979). Similar responses are seen in monkeys and mice, but at 

higher concentrations (980 pg/m3 , 0.5 ppm) (Fukase et al., 1978; Mustafa and 

Lee, 1976). 

The effects of 0 3 on oxygen consumption have been studied since oxygen 

consumption is a fundamental parameter of cellular metabolism, reflecting 

energy production by cells. As with antioxidant metabolism, acute exposure to 

1-118 
high ozone levels (> 3920 pg/m3 ; > 2 ppm) decreases metabolism (and thus, 

oxygen consumption); repeated exposure to lower levels (> 1568 pg/m 3 , 0.8 ppm) 

increases oxygen consumption (Mustafa et al., 1973; Schwartz et al., 1976; 

Mustafa and Lee, 1976). Effects in rats on normal diets have been observed 

after a short-term exposure to ozone 1 evel s as 1 ow as 392 pg/m 3 (0.2 ppm) 

(Schwartz et al., 1976; Mustafa et ai., 1973; Mustafa and Lee, 1976). Monkeys 

are affected at a higher level of ozone (980 pg/m 3 , 0.5 ppm). 

Similar patterns of response for both antioxidant metabolism and oxygen 

consumption are observed after exposure to ozone. A 7-day exposure to ozone 

produces linear concentration-related increases in activities of glutathione 

peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and 

succinate oxidase (Mustafa and Lee, 1976; Chow et al., 1974; Schwartz et al., 

1976; Mustafa et al., 1973). Rats on a vitamin E-deficient diet experience an 

increase in enzyme activities at 196 pg/m 3 (0.1 ppm) ozone as compared to 

392 pg/m3 (0.2 ppm) in animals on normal diets (Chow et al., 1981; Mustafa and 

Lee, 1976; Mustafa, 1975). Research on these enzymes has shown that there is 

no significant difference in efifects from continuous versus intermittent 

exposure; this, along with concentration-response data, suggests that the concentration of ozone is more important than duration of exposure in causing 

these effects (Chow et al., 1974; Schwartz et al., 1976; Mustafa and Lee, 

1976). 

Duration of exposure still plays a role, however. During exposures up to 

1 or 4 weeks, antioxidant metabolism and 0 2 consumption generally do not 

change on the first day of exposure; by about day 2, increases are observed 

and by about day 4 a plateau is reached (Mustafa and Lee, 1976; DeLucia et al., 

1975a). Recovery from these effects occurs by 6 days post-exposure (Chow 

et al., 1976). This plateauing of effects in the presence of exposure does 

not result in long-term tolerance. If rats are re-exposed after recovery is 

observed, the increase in enzyme activities is equivalent to that observed in 

animals exposed for the first time (Chow et al., 1976). 

The influence of age on responsiveness is also similar for antioxidant 

metabolism and oxygen consumption (Elsayed et al., 1982a; Tyson et al., 1982; 

Lunan et al., 1977). Suckling neonates (5 to 20 days old) generally exhibited 

a decrease in enzyme activities; as the animals grew older (up to about 180 days 

old), enzyme activities generally increased with age. Species differences may 

exist in this response (Mustafa and Lee, 1976; Mustafa et al., 1982; Chow 

1-119 
et al., 1975; DeLucia et al., 1975a). Studies in which monkeys have been 

compared to rats did not include a description of appropriate statistical 

considerations applied (if any); thus, no definitive conclusions about responsiveness of monkeys versus rats can be made. 

The mechanism responsible for the increase in antioxidant metabolism and 

oxygen consumption is not known. The response is typically attributed, however, 

to concurrent morphological changes, principally the loss of type 1 cells and 

an increase in type 2 cells that are richer in the enzymes measured. 

Monooxygenases constitute another class of enzymes investigated after 

ozone exposure. These enzymes function in the metabolism of both endogenous 

(e.g., biogenic amines, hormones) and exogenous (xenobiotic) substances. The 

substrates acted upon are either activated or detoxified, depending on the 

substrate and the enzyme. Acute exposure to 1470 to 1960 pg/m 3 (0.75 to 

1 ppm) ozone decreased cytochrome P-450 levels and enzyme activities related 

to both cytochrome P-450 and P-448. The health impact of these changes is 

uncertain since only a few elements of a complex metabolic system were measured. 

The activity of lactate dehydrogenase is increased in lungs of vitamin Edeficient rats receiving a short-term exposure to 196 pg/m 3 (0.1 ppm) ozone 

(Chow et al., 1981). Higher levels caused a similar response in rats, but not 

in monkeys, on normal diets (Chow et al., 1974, 1977). This enzyme is frequently used as a marker of cellular damage because it is released upon cytotoxicity. 

It is not known, however, whether the increase in this enzyme is a direct 

reflection of cytotoxicity or whether it is an indicator of an increased 

number of type 2 cells and macrophages in the lungs. 

An increase in a few of the measured activities of lysosomal enzymes has 

been shown in the lungs of rats exposed to > 1372 pg/m 3 (0.7 ppm) ozone (Dillard 

et al., 1972; Castleman et al., 1973a; Chow et al., 1974). This response is 

most likely the result of an increase in inflammatory cells in the lungs 

rather than an induction of enzymes, since lysosomal enzymes in alveolar 

macrophages decrease after in vivo or in vitro exposure to ozone (Hurst et al., 

1970; Hurst and Coffin, 1971). 

As discussed previously, long-term exposure to high 0 3 concentrations 

causes mild lung fibrosis (i.e., local increase of collagen in centriacinar 

interalveolar septa). This morphological change has been correlated with 

biochemical changes in the activity of prolyl hydroxylase (an enzyme that 

catalyzes the production of hydroxyproline) and in hydroxyproline content (a 

1-120 
component of collagen that is present in excess in fibrosis) (Last et al., 

1979; Bhatnagar et al., 1983). An increase in collagen synthesis has been 

observed, with 980 pg/m3 (0.5 ppm) 03 being the minimally effective concentration tested (Hussain et al., 1976a,b; Last et al., 1979). During a prolonged 

exposure, prolyl hydroxylase activity increases by day 7 and returns to control 

levels by 60 days of exposure. When a short-term exposure ceases, prolyl 

hydroxylase activity returns to normal by about 10 days post-exposure, but 

hydroxyproline levels remain elevated 28 days post-exposure. Thus, the product 

of the increased synthesis, collagen, remains relatively stable. One study 

(Costa et al., 1983) observed a small decrease in collagen levels of rats at 

392 and 1568 pg/m3 (0.2 and 0.8 ppm) 03 after an intermittent exposure for 62 

days. 

The effects of 03 on increasing collagen content may be progressive; 

i. e. , after a 6-week i ntermi ttent exposure of rats to 0.64 or 0.96 ppm 0 3 

ceased, collagen levels 6 week post-exposure were elevated over the levels 

immediately after exposure (Last et al., 1984b). Also, there appears to be 

little difference between continuous and intermittent exposure in increasing 

collagen levels in rat lungs (Last et al, 1984b). Thus, the intermittent 

clean air periods were not sufficient to permit recovery. 

Although the ability of 0 3 to initiate peroxidation of unsaturated fatty 

acids in vitro is well established, few in vivo studies of lung lipids have 

been conducted. Generally, ozone decreases unsaturated fatty acid content of 

the lungs (Roehm et al., 1972) and decreases incorporation of fatty acids into 

lecithin (a saturated fatty acid) (Kyei-Aboagye et al., 1973). These alterations, however, apparently do not alter the surface-tension-lowering properties 

of lung lipids that are important to breathing (Gardner et al., 1971; Huber 

et al., 1971). 

One of the earliest demonstrated effects of ozone was that very high 

concentrations caused mortality as a result of pulmonary edema. As more 

sensitive techniques were developed, lower levels (510 pg/m 3 , 0.26 ppm) were 

observed to increase the protein content of the lung (Hu et al., 1982). Since 

some of the excess protein could be attributed to serum proteins, the interpretation was that edema had occurred. This effect was more pronounced several 

hours after exposure ceased. At higher concentrations, a loss of carriermediated transport from the air side of the lung to the blood side was observed 

(Williams et al., 1980). These changes imply an effect on the barrier function 

1-121 
of the lung, which regulates fluxes of various substances with potential 

physiological activities across the alveolar walls. 

The biochemical effects observed in experimental animals exposed to 0 3 

are summarized in Figure 1-10 and Table 1-14 (see Section 1.8.1 for criteria 

used in developing this summary). 

1.8.3.4 Host Defense Mechanisms. Reports over the years have presented 

substantial evidence that exposure to ozone impairs the'antibacterial activity 

of the lung, resulting in an impairment of the lung's ability to kill inhaled 

microorganisms. Suppression of this biocidal defense of the lung can lead to 

microbial proliferation within the lung, resulting in mortality. The mortality 

response is concentration-related and is significant at concentrations as low 

as 157 to 196 pg/m3 (0.08 to 0.1 ppm) (Coffin et al., 1967; Ehrlich et al., 

=1977; Miller et al., 1978a; Aranyi et al., 1983). The biological basis for 

this response appears to be that ozone or one of its reactive products can 

impair or suppress the normal bactericidal functions of the pulmonary defenses, 

which results in prolonging the life of the infectious agent, permitting its 

multiplication and ultimately, in this animal model, resulting in death. Such 

infections can occur because of 0 3 effects on a complex host defense system 

involving alveolar macrophage functioning, lung fluids, and other immune 

factors. 

The data obtained in various experimental animal studies indicate that 

short-term ozone exposure can reduce the effectiveness of several vital defense 

systems including (1) the ability of the lung to inactivate bacteria and 

viruses (Coffin et al., 1968; Coffin and Gardner, 1972b; Goldstein et al., 

1974, 1977; Warshauer et al., 1974; Bergers et al; 1983. Schwartz and Christman, 

1979; Ehrlich et al., 1979); (2) the mucociliary transport system (Phalen 

et al., 1980; Frager et al., 1979; Kenoyer et al., 1981; (3) the immunological 

system (Campbell and Hilsenroth, 1976; Fujimaki et al., 1984; Thomas et al., 

1981b; Aranyi et al., 1983; and (4) the pulmonary macrophage (Dowell et al., 

1970; Goldstein et al., 1971a,b, and 1977; Hadley et al., 1977; McAllen et al., 

1981; Witz et al., 1983; Hurst et al., 1970; Hurst and Coffin, 1971; Amoruso 

et al., 1981). Studies have also indicated that the activity level of the 

test subject and the presence of other airborne chemicals are important variables that can influence the determination of the lowest effective concentration of the pollutant (Gardner et al., 1977; Aranyi et al., 1983; Ehrlich, 

1980, 1983; Grose et al., 1980, 1982; Phalen et al., 1980; Goldstein et al., 

1974; Illing et al., 1980). 

1-122 
N 

~ E_ y 

R ~ 

++ N 

C~ 

d C E y 

U. C 

x ~ 

,c c~ 

y ~ 

~ V IM C 

C ~ 

V ` 

•v ,O 

E d 

s~ 

o~ 

o f.. 

~ 

. E 

y 

(D' 

~ N .0 0 

O +C+ N i 

E 

a_,

°c.E 

LL 0N 

• 

0 ------- -------0----------• 

0-------0--- 

O•-------- 

0----------0------- C * 

r.~ 

Gs 

s 

co 

J 0 

vyJ 

~ 

O~Jti,1~~p0J% 

l

d d 

~G d~0 yJ 

O~ ,p0 ~ 

~~ 

N ~ O 9N v d 

~ o~ C~ J T G~O 9,ko ee, y i~. 

'r0 -00 

G~O J ~ ••O ,sAO, ,OG 

• v0, s0 JT vJGN 

d O ~O - ,p 

~ 

~ 

~ 

~ 

Go~ol~ 0s0~/~~ JGO 

GOJ O 

C4 d+Av 

O J~ 

OJ 

~A 

v JG 

~ 

O r- N c+) et U) cC t~ Oo (3) O 

O O O O O O O O O ® ~ 

wdd 'uoiieiluaouoo auozp 

1-123 
TABLE 1-14. SUMMARY TABLE: BIOCHEMICAL CHANGES 

IN EXPERIMENTAL ANIMALS EXPOSED TO OZONE 

Effect/response 0 3 concentration, ppm References 

Increased 02 

consumption 

Increased lysosomal 

enzyme activities 

[0.1], 0.2 Mustafa (1975) 

[0.1], 0.2, 0.35, 0.5, 0.8 Mustafa and Lee (1976) 

0.2, 0.5, 0.8 Mustafa et al. (1973) 

0.2, 0.5, 0.8 Schwartz et al. (1976) 

0.45 Mustafa et al. (1982) 

0.8 Chow et al. (1976) 

0.8 Elsayed et al. (1982a) 

[0.2], [0.5], 0.8 Chow et al. (1974) 

0.7, 0.8 Dillard et al. (1972) 

0.7, 0.8 Castleman et al. (1973a,b) 

Increased lung 

hydroxyproline 

and prolyl 

hydroxylase 

activity 

Altered mucus 

glycoprotein 

secretions 

Increased alveolar 

protein and 

permeability 

changes 

Increased LDH 

activity 

Increased NADPH - 

cytochrome c 

reductase 

activity 

[0.2], 0.5, 0.8 

0. 2, 0.8 

0.45, 0.8 

0.5, 0.64, 0.96 

0.5 

0.8 

[0.2], [0.4], 0.5, 0.6, 0.8 

0.5, 0.6, 0.8 

0.6, 0.8 

0.2, 0.35, 0.8 

0.2, 0.5, 0.8 

0.2, 0.5, 0.8 

Hussain et al. (1976a,b) 

Costa et al. (1983) 

Bhatnagar et al. (1983) 

Last et al. (1979, 1984b) 

Last and Greenberg (1980) 

Hesterberg and Last (1981) 

Last and Kaizu (1980) 

Last and Cross (1978) 

Last et al. (1977) 

Mustafa and Lee (1976) 

Schwartz et al. (1976) 

DeLucia et al. (1972, 1975a,b) 

[0.1], 0.26, 0.51, 1.0 Hu et al. (1982) 

[0.25], 0.5, 1.0 Alpert et al. (1971a) 

0.6, 1.0 Williams et al. (1980) 

1.0 Reasor et al. (1979) 

[0.1] Chow et al. (1981) 

[0.5], 0.8 Chow et al. (1977) 

0.8 Chow and Tappel (1973) 

Increased GSH [0.1] Chow et al. (1981) 

metabolism 0.1, 0.2 Plopper et al. (1979) 

0.2, 0.35, 0.5, 0.8 Mustafa and Lee (1976) 

0.2, 0.5 ; 0.8 Chow et al. (1974) 

0.2, 0.5, 0.8 DeLucia et al. (1972, 1975a,b) 

0.2, 0.5, 0.8 Schwartz et al. (1976) 

0.2, 0.5, 1.0 Fukase et al. (1975) 

0.32 Moore et al. (1980) 

0.45 Mustafa et al. (1982) 

0.5 Chow et al. (1975) 

1-124 
TABLE 1-14 (continued). SUMMARY TABLE: BIOCHEMICAL CHANGES 

IN EXPERIMENTAL ANIMALS EXPOSED TO OZONE 

Effect/response 03 concentration, ppm References 

0.5, 1.0 Fukase et al. (1978) 

0.7, 0.75, 0.8 Chow and Tappel (1972, 1973) 

0.8 Elsayed et al. (1982a,b; 

1983) 

0.8 Chow et al. (1976) 

0.9 Tyson et al. (1982) 

0.9 Lunan et al. (1977) 

Increased NPSH 0.1, 0.2 Plopper et al. (1979) 

0.2, 0.5, 0.8 DeLucia et al. (1975b) 

0.45 Mustafa et al. (1982) 

0.8 Chow et al. (1976) 

Decreased 0.5 Roehm et al., 1972 

unsaturated 

fatty acids 

Ciliated cells are damaged by 0 3 inhalation, as demonstrated by major 

morphological changes in these cells including necrosis and sloughing or by 

the shortening of the cilia in cells attached to the bronchi. Sufficient 

ciliated cell damage should result in decreased transport of viable and nonviable particies from the lung. Rats exposed to 784, 1568, 1960, or 2352 

pg/m3 (0.4, 0.8, 1.0, or 1.2 ppm) for times as short as 4 hr have decreased 

short-term clearance of particles from the lung (Phalen et al., 1980; Frager 

et al., 1979; Kenoyer et al., 1981). Short-term clearance is mostly due to 

mucus transport of particies, and the decreased short-term clearahce is an 

anticipated functional result predicted from morphological observations. The 

mucous glycoprotein production of the trachea is also altered by 0 3 exposure. 

Mucous glycoprotein biosynthesis, as measured ex vivo in cultured tracheal 

explants from exposed rats, was inhibited by short-term continuous exposure to 

1568 pg/m3 (0.8 ppm) of 0 3 for 3 to 5 days (Last and Cross, 1978; Last and 

Kaizu, 1980; Last'et al., 1977). Glycoprotein synthesis and secretion recovered 

to control values after 5 to 10 days of exposure and.increased to greater than 

control values after 10 days of exposure. with this increase in production of 

mucus, investigators have found that the velocity of the tracheal mucus was 

1-125 
significantly reduced following a 2 hr exposure to 1960 pg/m 3 (1.0 ppm) (Abraham 

et a1., 1980). 

A problem remains in assessing the relevance of these animal data to 

humans. Green (1984) reviewed the literature and compared the host antibacterial 

defense systems of the rodent and man and found that these two species had 

defenses that are very similar and thus provide a good basis for a qualitative 

extrapolation. Both defenses consist of an aerodynamic filtration system, a 

fluid layer lining the respiratory membranes, a transport mechanism for removing 

foreign particles, microorganisms, and pulmonary cells, and immune secretions 

of lymphocytes and plasma cells. In both rodents and humans, these components 

act in concert to maintain the lung free of bacteria. 

If the animal models are to be used to reflect the toxicological response 

occurring in humans, then the endpoint for comparison of such studies should 

be morbidity rather than mortality. A better index of 03 effect in humans 

might be the increased prevalence of infectious respiratory illness in the 

community. Such a comparison may be proper since both mortality from respiratory infections (animals) and morbidity from respiratory infections (humans) 

can result from a loss in pulmonary defenses (Gardner, 1984). Whether the 

microorganisms used in the various animal studies are comparable to the organisms responsible for the respiratory infections in a community still requires 

further investigation. 

Ideally, studies of pulmonary host defenses should be performed in man, 

using epidemiological or volunteer methods of study. Unfortunately, such 

studies have not been reported yet. Attention must therefore be paid to the 

results of host-defense experiments conducted with animals. 

In the area of host defense of the lung against infection, present knowledge of the physiology, metabolism, and function have come primarily from the 

study of various animal systems, but it is generally accepted that the basic 

mechanisms of action of these defense cells and systems function. similarly in 

both animals and man. There are also human data to support this statement, 

especially in such areas as immunosuppression, ciliostasis, and alveolar 

macrophages. The effects seen in animals represent alterations in basic 

biological systems. One can assume that similar alterations in basic defense 

mechanisms could occur in humans since they possess equivalent pulmonary 

defense systems. It is understood, however, that different exposure levels 

may be required to produce similar responses in humans. The concentration of 

1-126 
0 3 at which effects become evident can be influenced by a number of factors, 

such as preexisting disease, virulence of the infectious agent, dietary factors, 

concurrent exposure to other pollutants, exercise, or the presence of other 

environmental stresses, or a combination of these. Thus, one could hypothesize 

that humans exposed to 0 3 could experience effects on host defense mechanisms. 

At the present time, however, one cannot predict the exact concentration at 

which effects may occur in man nor the severity of the effects. 

The effects of 0 3 on host defense mechanisms in experimental animals are 

summarized in Figure 1-11 and Table 1-15 (see Section 1.8.1 for criteria used 

in developing this summary). 

1.8.3.5 Tolerance. Examination of responses to short-term, repeated exposures 

to 0 3 clearly indicates that with some of the parameters measured, animals 

have an increased capacity to resist the effects of subsequent exposure. This 

tolerance persists for varying times, depending on the degree of development 

of the tolerance. Previous exposure to low concentrations of 0 3 will protect 

against the effects of subsequent exposure to lethal doses and the development 

of lung edema (Stokinger et al., 1956; Fairchild, 1967; Coffin and Gardner, 

1972a; Chow, 1984): The prolongation of mucociliary clearance reported for 0 3 

can also be eliminated by pre-exposure to a lower concentration (Frager et 

al., 1979). This effect is demonstrated for a short period of time and is 

lost as soon as the mucus secretion rate returns to normal. However, not all 

of the toxic effects of 0 3 , such'as reduced functioning activity of the pulmonary 

defense system (Gardner et al., 1972); hyperplasia of the type 2 cells (Evans 

et al., 1971, 1976a,b); increased susceptibility to respiratory disease (Gardner 

and Graham, 1977); loss of pulmonary enzymatic activity (Chow, 1976, Chow 

et al., 1976); and inflammatory response (Gardner et al., 1972) can be totally 

prevented by'prior treatment with low levels of 0 3 . Dungworth et al. (1975) 

and Castleman et al. (1980) have attempted to explain tolerance by careful 

examination of the morphological changes that occur with repeated 0 3 exposures. 

These investigators suggest that during continuous exposure to 0 3 the injured 

cells attempt to initiate early repair of the specific lesion. The repair 

phase results in a reduction of the effect first observed but lasts only for a 

short time since the recovered cells are as sensitive to re-exposure to 0 3 as 

the pre-exposed counterpart (Plopper et al., 1978). This information is an 

important observation because it implies that the decrease in susceptibility 

to 03 persists only as long as the exposure to 0 3 continues. The biochemical 

studies of Chow et al. (1976) support this conclusion. 

1-127 
JA 

o~ 

O'r 

GD 

9~0J J+~O _y 

d .r ~ C 

.0 O 

Gp O`~G ' adAyJ,r ~ C 

~ JG -'O 

~ 

= = 

y~ o 

d 

~ ~4y9~ yJA v~6 S ~ 

Jy0 y~ N ~ 

. 7~J yJ0 O ~ ~ e— 

O O d 

~ 

Jtt0' 0yAp~ GJi~ AO O_y i 

~Joa+ yG E~ -°ai 

y ~ ;oo E M .N 

T 

j JJ 

0 ----------0 0 

N 0 

i C. d 

7 X :C 

~

ID _ ~ 

IL .E f~q 

O ~ N M et 1n c0 00 0) O 

O 0 O O p O O O O O ewdd 'uoileiluaouoo auozo 

1-128 
TABLE 1-15. SUMMARY TABLE: EFFECTS OF OZONE ON HOST DEFENSE 

MECHANISMS IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

Delayed mucociliary [0.1] Grose et al. (1980) 

clearance; accelerated 0.4, 0.8, 1.0 Kenoyer et al. (1981) 

alveolar clearance, [0.5] Friberg et al. (1972) 

ciliary beating [0.5], 1.0 Abraham et al. (1980) 

frequency 0.8 Phalen et al. (1980) 

1.2 Frager et al. (1979) 

Inhibited bactericidal 0.4 Coffin and Gardner (1972b) 

activity -0.4 Goldstein et al. (1972) 

0.5 Friberg et al. (1972) 

0.62 Goldstein et al. (1971b) 

0.7 Bergers et al. (1983) 

0.7 Warshauer et al. (1974) 

0.99 Goldstein et al. (1971a) 

Altered macrophage 0.1, 1.0 Gardner et al. (1971) 

membrane 0.5 Dowell et al. (1970) 

0.5 Hadley et al. (1977) 

0.5, 1.0 Goldstein et al. (1977) 

Decreased macrophage 0.25, 0.5 Hurst et al. (1970) 

function Hurst and Coffin (1971) 

0.5 Alpert et al. (1971b) 

0.5, 0.67 Coffin et al. (1968) 

0.5, 0.67 Coffin and Gardner (1972b) 

0.8 Schwartz and Christman (1979) 

1.0 Shingu et al. (1980) 

1.0 McAllen et al. (1981) 

Altered no. of defense 0.2 Plopper et ai. (1979) 

cells 0.2, 0.35, 0.5, 0.8 Dungworth et al. (1975) 

0.2, 0.35 Castleman et al. (1977) 

0.2, 0.5, 0.8 Boorman et al. (1977, 1980) 

0.25 Barry et al. (1983) 

0.5 Zitnik et al. (1978) 

0.5, 0.88 Stephens et al. (1974a) 

0.5 Last et al. (1979) 

0.5, 0.88 Brummer et al. (1977) 

0.5, 0.8 Eustis et al. (1981) 

0.54, 0.88 Freeman et al. (1974) 

0.8 Castleman et al. (1980) 

1.0 Freeman et al'. (1973) 

1.0 Cavender et al. (1977) 

1-129 
TABLE 1-15 (continued). SUMMARY TABLE: EFFECTS OF OZONE ON HOST DEFENSE 

MECHANISMS IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

Increased susceptibility to infection 

Altered immune 

activity 

0.08 

0.08, 0.1 

0.1 

0.1 

0.1, 0.3 

[0.2], 0.4, 0.7 

0.3 

0.5 

[0.64] 

0.7, 0.9 

1.0 

Coffin et al. (1967) 

Miller et al. (1978a) 

Ehrlich et al. (1977) 

Aranyi et al. (1983) 

Illing et al. (1980) 

Bergers et al. (1983) 

Abraham et al. (1982) 

Wolcott et al. (1982) 

[Sherwood et al. (1984)] 

Coffin and Blommer (1970) 

Thomas et al. (1981b) 

0.1 Aranyi et al. (1983) 

0.5, 0.8 Osebold et al. (1979, 1980) 

0.5, 0.8 Gershwin et al. (1981) 

0.59 Campbell and Hilsenroth 

(1976) 

0.8 Fujimaki et al. (1984) 

At this time, there are a number of hypotheses proposed to explain the 

mechanism of this phenomenon (Mustafa and Tierney, 1978; Schwartz et al., 

1976; Mustafa et al., 1977; Berliner et al., 1978; Gertner et al., 1983b; 

Bhatnagar et al., 1983). Evidence by Nambu and Yokoyama (1983) indicates that 

although the pulmonary antioxidant system (glutathione peroxidase, glutathione 

reductase, and glucose-6-phosphate dehydrogenase) may play an active role in 

defending the lung against ozone, it does not explain the mechanism of tolerance in that the development of tolerance does not coincide with the described 

biochemical enhancement of the antioxidant system in the lungs of rats. 

From this literature, it would appear that tolerance, as seen in animals, 

may not be the result of any one single biological process, but instead may 

result from a number of different events, depending on the specific response 

measured. Tolerance does not imply complete or absolute protection, because 

continuing injury does still occur, which could potentially lead to nonreversible pulmonary changes. 

Tolerance may not be long-lasting. During 0 3 exposure, the increase in 

antioxidant metabolism reaches a plateau and recovery occurs a few days after 

1-130 
exposure ceases. Upon re- exposure, effects observed are similar to those that 

occurred during the primary exposure (Chow et al., 1976). 

1.8.4Extrapulmonary Effects of Ozone 

It is still believed that 0 3 , on contact with respiratory system tissue, 

immediately reacts and thus is not absorbed or transported to extrapulmonary 

sites to any significant degree. However, several studies suggest that possibly 

products formed by the interaction of 0 3 and respiratory system fluids or 

tissue can produce effects in lymphocytes, erythrocytes, and serum, as well as 

in the parathyroid gland, the heart, the liver, and the CNS. Ozone exposure 

also produces effects on animal behavior that may be caused by pulmonary 

consequences of 0 3 , or by nonpulmonary (CNS) mechanisms. The mechanism by 

which 03 causes extrapulmonary changes is unknown. Mathematical models of 0 3 

dosimetry predict that very little 0 3 penetrates to the blood of the alveolar 

capillaries. Whether these effects result from 0 3 or a reaction product of 03 

which penetrates to the blood and is transported is the subject of speculation. 

1.8.4.1Central Nervous System and Behavioral Effects . Ozone significantly 

affects the behavior of rats during exposure to concentrations 'as low as 

235 pg/m3 (0.12 ppm) for 6 hr. With increasing concentrations of 0 3 , further 

decreases in unspecified motor activity and in operant learned behaviors have 

been observed (Konigsberg and Bachman, 1970; Tepper et al., 1982; Murphy 

et al., 1964; and Weiss et al., 1981). Tolerance to the observed decrease in 

motor activity may occur on repeated exposure. At low 03 exposure concentrations (490 pg/m3 , 0.25 ppm), an increase in activity is observed after exposure 

ends. tHigher 0 3 concentrations (980 pg/m 3 , 0.5 ppm) produce a decrease in 

rodent activity that persists for several hours after the end of exposure 

(Tepper et al., 1982, 1983). 

The mechanism by which behavioral performance is reduced is unknown. 

Physically active responses appear to enhance the effects of 0 3 , although this 

may be the result of an enhanced minute volume that increases the effective 

concentration delivered to the lung. Several reports indicate that it is 

unlikely that animals have reduced physiological capacity to respond, prompting Weiss et al. (1981) to suggest that 0 3 impairs the inclination to respond. 

Two studies indicate that mice will respond to remove themselves from an 

atmosphere containing greater than 980 pg/m 3 (0.5 ppm) (Peterson and Andrews, 

1963, Tepper et al., 1983). These studies suggest that the aversive effects 

1-131 
of 03 may be due to lung irritation. It is unknown whether lung irritation, 

odor, or a direct effect on the CNS causes change in rodent behavior at lower 

03 concentrations. 

1.8.4.2 Cardiovascular Effects. Studies on the effects of 0 3 on the cardiovascular system are few, and to date there are no reports of attempts to confirm these studies. The exposure of rats to 03 alone or in combination with 

cadmium (1176 pg/m3 , 0.6 ppm 0 3 ) resulted in measurable increases in systolic 

pressure and heart rate (Revis et al., 1981). No additive or antagonistic 

response was observed with the combined exposure. Pulmonary capillary blood 

flow and Pa0 2 decreased 30 min following exposure of dogs to 588 pg/m 3 (0.3 

ppm) of 03 (Friedman et al., 1983). The decrease in pulmonary capillary blood 

flow persisted for as long as 24 hr following exposure. 

1.8.4.3 Hematological and Serum Chemistry Effects. The data base.for the 

effects of 03 on the hemato1ogical system is extensive and indicates that 03 

or one of its reactive products can cross the blood-gas barrier, causing 

changes in the circulating erythrocytes (RBC) as well as significant differences in various components of the serum. 

Effects of 03 on the circulating RBCs can be readily identified by examining either morphological and/or biochemical endpoints. These cel1s are 

structually and metabolically well understood and are available through relative1y non-invasive methods, which makes them ideal candidates for both.human 

and animal studies. A wide range of structural effects have been reported in 

a variety of species of animals, including an increase in the fragility of 

RBCs isolated from monkeys exposed to 1470 pg/m3 (0.75 ppm) of 03 4 hr/day for 

4 days (Clark et al., 1978). A single 4-hr exposure to 392 pg/m 3 (0.2 ppm) 

also caused increased fragility as well as sphering of RBCs of rabbits (Brinkman 

et al., 1964). An increase in the number of RBCs with Heinz bodies was detected 

following a 4-hr exposure to 1666 pg/m 3 (0.85 ppm). The presence of such 

inclusion bodies in RBCs is an indication of oxidant stress (Menzel et al., 

1975a). 

These morphological changes are frequently accompanied by a wide range of 

biochemical effects. RBCs of monkeys exposed to 1470 pg/m 3 (0.75 ppm) of 03 

for 4 days also had a decreased level of glutathione (GSH) and decreased 

acetylcholinesterase (AChE) activity, an enzyme bound to the RBC membranes. 

The RBC GSH activity remained significantly lower 4 days postexposure (Clark 

et al., 1978). 

1-132 
Animals deficient in vitamin E are more sensitive to 0 3 . The RBCs from 

these animals, after being exposed to 0 3 , had a significant increase in the 

activity of GSH peroxidase, pyruvate kinase, and lactic dehydrogenase, but had 

a decrease in RBC GSH after exposure to 1568 pg/m 3 (0.8 ppm) for 7 days (Chow 

and Kaneko, 1979). Animals with a vitamin E-supplemented diet did not have 

any changes in glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase, 

or cataiase activities. At a lower level (980 pg/m 3 , 0.5 ppm), there were no 

changes in GSH level or in the activities of GSH peroxidase or GSH reductase 

(Chow et al., 1975): Menzel et al. (1972) also reported a significant increase 

in lysis of RBCs from vitamin E-deficient animals after 23 days of exposure to 

980 pg/m3 (0.5 ppm). These effects were not observed in vitamin E-suppleM'ented 

rats. Mice on a vitamin E-supplemented diet and those on a deficient diet 

showed an increase in G-6-PD activity after an exposure of 627 pg/m 3 (0.32 ppm) 

of 03 for 6 hr. Decreases observed in AChE activity occurred in both groups 

(Moore et al., 1980). 

Other blood changes are attributed to 0 3 . Rabbits exposed for 1 hr to 

392 pg/m3 (0.2 ppm) of 0 3 showed a significant drop in total blood serotonin 

(Veninga, 1967). Six- and 10-month exposures of rabbits'to 784 pg/m3 (0.4 ppm) 

of 03 produced an i ncrease i n serum protei n esterase and i n serum trypsi n 

inhibitor. This latter effect may be a result of thickening of the small 

puimonary arteries. The same exposure caused a significant decrease in albumin 

levels and an increase in alpha and gamma globulins (P'an and Jegier, 1971, 

1976; P'an et al., 1972; Jegier, 1973). Chow et al. (1974) reported that the 

serum lysozyme level of rats increased significantly after 3 days of continuous 

exposure to 03 but was not affected when the exposure was intermittent (8'hr/day, 

7 days). The 0 3 concentration in both studies was 1568 pg/m 3 '(0.8 ppm) of 03 . 

Short-term exposure to low concentrations of 0 3 induced a'n immediate 

change in the serum creatine phosphokinase level in mice. In this study, the 

03 doses were expressed as the product of concentration and time. The C x T 

value for this effect ranged from 0.4 to 4.0 (Veninga et al., 1981). 

A few of the hematological effects observed'in animals (i.e., decrease in 

GSH and AChE activity and the formation of Heinz bodies) following exposure to 

03 have also been seen following i_nvitroexposure of RBCs from humans (Freeman 

and Mudd, 1981; Menzel et al., 1975b; Verweij and Van Steveninck, 1981). A 

common effect observed by a number of investigators is that 0 3 inhibits the 

membrane ATPase activity of RBCs (Koontz and Heath, 1979; Kesner et ai., 1979; 

1-133 
Kindya and Chan, 1976; Freeman et al., 1979; Verweij and Van Steveninck, 

1980). It has been postulated that this inhibition of ATPase could be related 

to the spherocytosis and increased fragility of RBCs seen in animal and human 

cells. 

Although these in vitro data are useful in studying mechanisms of action, 

it is difficult to extrapolate these data to any effects observed in man. Not 

only is the method of exposure not physiological, but the actual concentration 

of 03 reaching the RBC cannot be determined with any accuracy. 

1.8.4.4 Cytogenetic and Teratogenic Effects. Uncertainty still exists regarding possible reproductive, teratogenic, and mutational effects of exposure to 

ozone. Based on various in vitro data, a number of chromosomal effects of 

ozone have been described for isolated cultured cell lines, human lymphocytes, 

and microorganisms (Fetner, 1962; Hamelin et al., 1977a,b, Hamelin and Chung, 

1975a,b, 1978; Scott and Lesher, 1963; Erdman and Hernandez, 1982; Guerrero 

et al., 1979; Dubeau and Chung, 1979, 1982). The interpretation, relevance, 

and predictive values of such studies to human health are questionable since 

(1) the concentrations used were many-fold greater than what is found in the 

ambient air (see Chapter 10); (2) extrapolation of in vitro exposure concentrations to human exposure dose is not yet possible; and (3) direct exposure of 

isolated cells to ozone is highly artifactual since it bypasses all the defenses 

of the host that would normally be functioning in protecting the individual 

from the inhaled gas. Furthermore, the direct exposure of isolated cells in 

vitro to ozone may result in chemical reactions between ozone and culture 

media that might not occur in vivo. 

Important questions still exist regarding in vivo cytogenetic effects of 

ozone in rodents and humans. Zelac et al. (1971a,b) reported chromosomal 

abnormalities in peripheral leukocytes of hamsters exposed to 0 3 (0.2 ppm). 

Combined exposures to ozone and radiation (227-233 rads) produced an additive 

effect on the number of chromosome breaks in peripheral leukocytes. These 

specific findings were not confirmed by Gooch et al. (1976) or by Tice et al. 

(1978), but sufficient differences in the various experimental protocols make 

a direct comparison difficult. The latter group did report significant increases 

in the number of chromatid deletions and achromatic lesions resulting from 

exposure to 0.43 ppm ozone. 

Because the volume of air inspired during pregnancy is significantly 

enhanced, the pregnant animal may be at greater risk to low levels of ozone 

1-134 
exposure. Early studies on the possible teratogenic effects of ozone have 

suggested that exposures as low as 0.2 ppm can reduce infant survival rate and 

cause uniimited incisor growth (Brinkman et al., 1964; Veninga, 1967). Kavlock 

et al. (1979, 1980) found that pregnant rats exposed to 1.0 and 1.49 ppm ozone 

showed a significant increase in embryo resorption rate, slower growth, slower 

development of righting reflexes, and delayed grooming and rearing behavior, 

but no increase in neonatal-mortality was observed. 

1.8.4.5Other Extrapulmonary Effects . A series of studies was conducted to 

show that 0 3 increases drug-induced sleeping time in a number of species of 

animals (Gardner et al., 1974; Graham, 1979; Graham et al., 1981, 1982a,b, 

1983, 1985). At 1960 pg/m3 (1.0 ppm), effects were observed after l, 2, and 3 

days of exposure. As the concentration of 0 3 was reduced, increasing numbers 

of daily 3-hr exposures were required to produce a significant effect. At the 

lowest concentration studied (196 pg/m3 , 0.1 ppm), the increase was observed 

at days 15 and 16 of exposure. It appears that this effect is not specific to 

the strain of mouse or to the three species of animals tested, but it is 

sex-specific, with females being more susceptible. Recovery was complete 

within 24 hr after exposure. Although a number of inechanistic studies have 

been conducted, the reason for this effect on pentobarbital-induced sleeping 

time is not known. It has been hypothesized that some common aspect related 

to liver drug metabolism is quantitatively reduced (Graham et al., 1983). 

Several investigators have attempted to elucidate the involvement of the 

endocrine system in 0 3 toxicity. Most of these studios were designed to 

investigate the hypothesis that the survival rate of mice and rats exposed to 

lethal concentrations of 0 3 could be increased by use of various thyroid 

blocking agents or by thyroidectomy. To follow up these findings, Clemons and 

Garcia (1980a,b) and Clemons and Wei (1984) investigated the effects of a 

24-hr exposure to 1960 pg/m 3 (1.0 ppm) of 0 3 on the hypothalamo-pituitary-thyroid 

system of rats. These three organs regulate the function of each other through 

various hormonal feedback mechanisms. Ozone caused decreases in serum concentration of thyroid stimulating hormone (TSH), in circulating thyroid hormones 

(T3 and T4 ) and in protein-bound iodine. No alterations were observed in many 

other hormone levels measured. Thyroidectomy prevented the effect of 0 3 on 

TSH and T4 and hypophysectomy prevented effects on T 4 , unless the animals were 

suppiemented with T 4 in their drinking water. The thyroid gland itself was 

altered (e.g., edema) by 0 3 . The authors hypothesyzed that 0 3 alters serum 

binding of these hormones. 

1-135 
The extrapulmonary effects of ozone in experimental animals are summarized 

in Figure 1-12 and Table 1-16. Criteria used in developing the summary were 

presented in Section 1.8.1. 

1.8.5 Interaction of Ozone With Other Pollutants 

Combined exposure studies in laboratory animals have produced varied 

results, depending upon the pollutant combination evaluated and the measured 

variables. Additive and/or possibly synergistic effects of 0 3 exposure in 

combination with NO 2 have been described for increased susceptibility to 

bacterial infection (Ehrlich et al., 1977, 1979; Ehrlich, 1980, 1983), morphological lesions (Freeman et al., 1974), and increased antioxidant metabolism 

(Mustafa et al., 1984). Additive or possibly synergistic effects from exposure 

to 03 and H2SO4 have also been reported for host defense mechanisms (Gardner 

et al., 1977; Last and Cross, 1978; Grose et al., 1982), pulmonary sensitivity 

(Osebold et al. 1980), and collagen synthesis (Last et al., 1983), but not for 

morphology (Cavender et al., 1977; Moore and Schwartz, 1981). Mixtures of 0 3 

and (NH4) 2 SO4 had synergistic effects on collagen synthesis and morphometry, 

including percentage of fibroblasts (Last et al., 1983, 1984a). 

Combining 03 with other particulate pollutants produces a variety of 

responses, depending on the endpoint measured. Mixtures of 03, Fe2(SO4)3' 

H2SO4 , and (NH4) 2SO4 produced the same effect on clearance rate as exposure to 

03 alone. However, when measuring changes in host defenses, the combination 

of 03 with NO2 and ZnSO4 or 03 with'S02 and (NH4 ) 2SO4 produced enhanced effects 

that can not be attributed to 03 only. 

However, since these issues are complex, they must be addressed experimentally using exposure regimens for combined pollutants that are more representative of ambient ratios of peak concentrations, frequency, duration, and time 

intervals between events. 

The interactive effects of 0 3 with other pollutants are summarized in 

Figure 1-13 and Table 1-17. 

1.8.6 Effects of Other Photochemical Oxidants 

There have been far too few controlled toxicological studies with the 

other oxidants to permit any sound scientific evaluation of their contribution 

to the toxic action of photochemical oxidant mixtures. When the effects seen 

after exposure to 0 3 and PAN are examined and compared, it is obvious that the 

1-136 
Jp 

.~.~ N 

~T 

~ 

o~G 

. ~JO 

~ 

J ~ 

~O 

d~d po~ 

~ 

O 

~ 

pip

p/paI A 

N 

~ 

i~ 

J~ 

O 

~O 

tiy 

Jp 

`

p

2 

t~ 

N 

~ 

~ 

7 

H 

~rO ,= N 

OOO O 

O *'' 

N ~ O v 

O V 

N = 

d ~ O 

Oi 

m 0 

O ~ 

E `' 

~ 

Q G~ 

X~ 

c ~ 

z N 

E y E~ ai 

7 r ~ 

~ ~ t 

~ ~ N 

r i 

i 

~ Q G 

LL O N 

uudd 'uoi;ej;uaouoo auozp 

1-137 
TABLE 1-16. SUMMARY TABLE: EXTRAPULMONARY EFFECTS OF OZONE 

IN EXPERIMENTAL ANIMALS 

Effect/response 03 concentration, ppm References 

CNS effects 0.05, 0.5 Konigsberg and Bachman (1970) 

0.1 - 1.0 Weiss et al. (1981) 

0.12 - 1.0 Tepper et al. (1982) 

0.2, 0.3, 0.5, 0.7 Murphy et al. (1964) 

0.5 • Tepper et al. (1983) 

0.5 Reynolds and Chaffee (1970) 

0.5 Xintaras et al. (1966) 

0.6 Peterson and Andrews (1963) 

1.0 Fletcher and Tappel (1973) 

1.0 Trams et al. (1972) 

Hematological effects 0.06, 0.12, 0.48 Calabrese et al. (1983) 

0.2 Brinkman et al. (1964) 

0.2, 1.0 Veninga (1967, 1970) 

Veninga et al. (1981) 

0.25, 0.32, 0.5 Moore et al. (1980; 1981a,b) 

0.4 Jegier (1973) 

0.4 P'an and Jegier (1972, 1976) 

0.5 Menzel et al. (1972) 

0.64 Larkin et al. (1983) 

0.75 Clark et al. (1978) , 

0.8 Chow and Kaneko (1979) 

0.8 Chow et al. (1974) 

0.85 Menzel et al. (1975a) 

0.86 Schlipkoter and Bruch (1973) 

1.0 Dorsey et al. (1983) 

1.0 Mizoguchi et al. (1973) 

1.0 Christiansen and Giese (1954) 

Chromosomal, reproduc- 0.1 Brinkman et al. (1964) 

tive, teratological 0.2 Veninga (1967) 

effects 0.24, 0.3 Zelac et al. (1971a) 

0.43 Tice et al. (1978) 

0.44 Kavlock et al. (1979) 

1.0 Kavlock et al. (1980) 

Liver effects 0.1, 0.25, 0.5, 1.0 Graham (1979) 

Graham et al. (1981, 1982a,b) 

0.82 Veninga et al. (1981) 

1.0 Gardner et al. (1974) 

Endocrine system 0.75 Atwal and Wilson (1974) 

effects 0.75 Atwal et al. (1975) 

0.75 Atwal and Pemsingh (1981, 1984) 

0.75 Pemsingh and Atwal (1983) 

1.0 Clemons and Garcia (1980a,b) 

1.0 Clemons and Wei (1984) 

1-138 
v0 v~i 

d d 

sGO~ 

i'r`~y ~?JGio 

. ~s0 ''r~•y d ~J 

y J O Q 

Go~~ dsAy o y~0~ 

~d •pd 

, J s ~0 

s 

s'~9A~ sG~ yi 

O, ,C T GA +rp, ct 

' ~• O~ •,~. 'sGp~9sG~d 

~s G~0 oJ ~ 

ia 000 

GD~s ~ d ~ ~ ~GO dip0°: 

. od sA 

~ JG 

o----------o-s----------o 

~ 

+~+ V 

~ C 

aD 

a~ 

K L 

4) L 

y O 

~ 

c~p r 

c ~ a> E.. 

'E ~ 

a 

d 4- y 

.s ~ 0 

N ~ s 

y O 0~ 

~ _ E 

c E 

E~~ 

~ ~ ~a 

~ E o 

r V c 

.0 

~ O ~ 

L1. O '0 

O r N c+0 tA CO m O 

O O O O O O O O O O eUl(jd 'UOItEJlUaoUOo 2UO2o 

1-139 
TABLE 1-17. SUMMARY TABLE: INTERACTION OF OZONE WITH OTHER POLLUTANTS 

IN EXPERIMENTAL ANIMALS 

Effect/response Pollutant concentrations References 

Increased [0.25 ppm 03 Freeman et al. (1974) 

pulmonary + 2.5 ppm NO21 

lesions [0.5 ppm 0 3 Moore and Schwartz (1981) 

+ 1 mg/m3 H2 SO4 1 

[0.5 ppm 0 3 Cavender et al. (1978) 

+ 10 mg/m3 H2 SO4 

0.64, 0.96 ppm 03 Last et al. (1984a) 

+ 5 mg/m3 (NH4)2 SO4 

0.9 ppm 03 Freeman et al. (1974) 

+ 0.9 ppm NO2 

1.2 ppm 03 Last et al. (1983) 

+ 5 mg/m3 (NH4)2SO4 

Increased 0.5 ppm 03 Osebold et al. (1980) 

pulmonary + 1 mg/m3 H2 SO4 

sensitivity 

Increased anti- 0.45 ppm 0 3 Mustafa et al. (1984) 

oxidant metabolism + 4.8 ppm NO2 

and 02 consumption 

Altered mucus 0.5 ppm 03 Last and Cross (1978); 

secretion + 1.1 mg/m3 H2 SO4 Last and Kaizu (1980) 

Increased collagen [0.5], [0.8], 1.5 ppm 0 3 Last et al. (1983) 

synthesis + 5 mg/m3 (NH4 ) 2 SO4 

0.5 ppm 03 Last et al. (1983) 

+ 1 mg/m3 H2 SO4 

0.64, 0.96 ppm 03 Last et al. (1984a) 

+ 5 mg/m3 (NH4)2SO4 

Increased 0.05 ppm 0 3 Ehrlich et al. (1977, 1979); 

susceptibility to + 3760 pg/m3 (NH4 ) 2 SO4 Ehrlich (1980) 

respiratory 0.05 ppm 0 3 Ehrlich (1983) 

infections + 100-400 pg/m 3 NO2 

+ 1.5 mg/m3 ZnSO4 

0.1 ppm 03 Gardner et al. (1977). 

+ 0.9 mg/m3 H2 SO4 

(sequential exposure) 

0.1 ppm 0 3 Grose et al. (1982) 

+ 4.8 mg/m3 H2 SO4 

0.1 ppm 03 Ehrlich (1980) 

+ 940 pg/m3 NO2 

0.1 ppm 03 Aranyi et al. (1983) 

+ 13.2 mg/m3 S02 

+ 1.0 mg/m3 (NH4)2SO4 

1-140 
TABLE 1-17 (continued). SUMMARY TABLE: INTERACTION OF OZONE 

WITH OTHER POLLUTANTS 

Effect/response Pollutant concentrations Referencesd 

Altered upper [0.1 ppm 03 Grose et al. (1980) 

respiratory + 1.1 mg/m3 H2 SO4 1 

clearance (sequential exposure) 

mechanisms 0.4 ppm 03 Goldstein et al. (1974) 

+ 7.0 ppm NO 2 

0.5 ppm 03 Last and Cross (1978) 

+ 3 mg/m3 H2 SO4 

[0.8 ppm 03 Phalen et al. (1980) 

+ 3.5 mg/m3 

{Fe2(SO4)s 

• H2 SO4 

• (NH4)2SO411 

test animals must be exposed to concentrations of PAN much greater than those 

needed with 0 3to produce a similar effect on lethality, behavior modification, 

morphology, or significant alterations in host pulmonary defense system (Campbell 

et al., 1967; Dungworth et al., 1969; Thomas et al., 1979, 1981a). The concentrations of PAN required to produce these effects are many times greater than 

what has been measured in the atmosphere (0.047 ppm). 

Similarly, most of the investigations reporting H 2O2toxicity have involved 

concentrations much higher than those found in the ambient air, or the investigations were conducted by using various in vitro techniques for exposure. 

Very limited information is available'on the health significance of inhalation 

exposure to gaseous H 2O2 . Because H2O2is highly soluble, it is generally 

assumed that it does not penetrate into the alveolar regions of the lung but 

is instead deposited on the surface of the upper airways (Last et al., 1982). 

Unfortunately, there have not been studies designed to look for possible 

effects in this region of the.respiratory tract. 

A`few in-vitro studies have reported cytotoxic, genotoxic, and biochemical 

effects ofH2O2 when.using isolated celis or organs (Stewart et al., 1981; 

Bradley et al., 1979; Bradley and Erickson, 1981; Speit et al., 1982; MacRae 

and Stich, 1979). Although these studies can provide useful data for studying 

possible mechanisms of action, it is not yet possible to extrapolate these 

responses to those that might occur in the mammalian system. 

1-141 
Field and epidemiological studies have shown that human health effects 

from exposure to ambient mixtures of oxidants and other airborne pollutants 

can produce human health effects (Chapter 12). Few such studies have been 

conducted with laboratory animals, because testing and measuring of such 

mixtures is not only complicated, but extremely costly. In these studies, the 

investigators attempted to simulate the photochemical reaction products produced under natural conditions and to define the cause-effect relationship. 

Exposure to complex mixtures of oxidants plus the various components 

found in UV-irradiated auto exhaust indicates that certain effects, such as 

histopathological changes, increase in susceptibility to infection, a variety 

of altered pulmonary functional activities were observed in this oxidant 

atmosphere which was not reported in the nonirradiated exhaust (Murphy et al., 

1963; Murphy, 1964; Nakajima et al., 1972; Hueter et al., 1966). Certain 

other biological responses were observed in both treatment groups, including a 

decrease in spontaneous activity, a decrease in infant survival rate, fertility, and certain pulmonary functional abnormalities (Hueter et al., 1966; 

Boche and Quilligan, 1960; Lewis et al., 1967). 

Dogs exposed to UV-irradiated auto exhaust containing oxidants either 

with or without SOxshowed significant pulmonary functional abnormalities that 

had relatively good correlation with structural changes (I-lyde et al., 1978; 

Gillespie, 1980; Lewis et al., 1974). There were no significant differences 

in the magnitude of the response in these two treatment groups, indicating 

that oxidant gases and SO xdid not interact in any synergistic or additive 

manner. 

1.9 CONTROLLED HUMAN STUDIES OF THE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL 

OXIDANTS 

A number of important controlled studies discussed in this chapter have 

reported significant decrements in pulmonary function associated with 0 3 

exposure (Table 1-18). In most of the studies reported, greatest attention 

has been accorded decrements in FEV 1 0 , as this variable:represents a summation 

of changes in both volume and resistance. While this is true, it must be 

pointed out that for exposure concentrations critical to the standard-setting 

process (i.e., <0.3 ppm 0 3 ), the observed decrements in FEV1 0primarily 

reflect FVC decrements of similar magnitude, with little or no contribution 

from changes in resistance. 

1-142 
W 

O 

UJ

O fC_. 

I

O 

X W 

z 

¢ 

f 

~ 

x 

w 

J 

O 

F ~ - 

Z 

O V 

W 'I 

m 

H 

r 

z 

¢ 

f 

~ 

~ 

N 

W 

r•7 

~ I 

W ' 

.J 

m 

¢ 

H 

0 d 

0.7 ^ ^ e,• • pl . 

IT rl - 

co O) d 

10 N 

U 

c 

^ 

+/ io ++ ^ +1 

L 

u 

d 

L io 

d 

+> 

d d n 

d 

4- +1 

d 

d 

d O p 

c 

tr N +> 

O C

r0o 

IO 

>G1 

C 

oM 

C t[7 

0 40 

N 

E M 

•C .- 1, {LI~ C1 M O C) Ol 1000 

Y uO.r~-1 Sr~i f ~ -

(n

•1 G g

1-i 

Q ~ -

(n

1 

• L 

7 X N 

d i-+ 4- N 

X n 

In In d 

A U a a C 

'O •r~ 

C L 

+1 O 

C i 

+1 O d 7 

L. 

ro? 

N 

r m r pl r N 

N 41 d 

O~ 

d 

d r• 

'G d 

d 

d d V d 

d f.- 

d•r N 

N r- +1 •r d 

U 

d C 

z o r ro 

lo E 

r~ 7 

ro•r N 

d N 

E 

ro•O 7 

E•r N 

r- ro d•- 

m E a u - la 

r• Itl 

m+a 

E d 

qE> 

r a E V- In •r a '1-• o U 

E E N 

M 

rl rl 

O"O X 

c{ v d W I, 

M'D X 

ri v d 

N U•r 

V' QO v,p 

N 

M 

O V 

ri v 

E N 

L+01 

d-~ a 

3 E E 

T a 

C 

m 

C 

m 

G d 

N u+~ 

L c m 

y N 

G E 

d o 

C 

d 

A o T> 

C N 

10 E T V'•" o ro c 3 

N a 

'O 

d 

E 

d 

E 

d d Tro '~ 

E C7 i+.+ ~ .- O 

TE+~ 

L d a 

ri+~ •r 

L r N 

d+> E d 

E a o a 

d d O 

1!) > 

7 7 

r~ 

7 L O N d.- ^ 4-1 •r I!7 10 N O L. E i-~ u A O7 N.- C 

• ro • r O 

7 E'O O' d 

>1 C d N 

ro•r r-1 

d+> 

O 

>, 

O 

> 

O tO N N N 

> L d d+~ d 

N d N 

L'O 

L L a 

O ro N 

O N ro L 17 

> V- d 

1A 

v 

L U+~ 

u dc6 

c'n 

>T L 

A 

L 

L•r i i ro C 

a 41 a u N 

L•r N T d'O i 

A 6 L L 

X d O 

d C•r d 

L O L L. 

d ~ ro 

d C L 

A> o A U 

L•r •r L d 

N 

i• 

r.p er 

7 ri 

o 

+~ 

0 

4~ 

0 3 d ro V d o 

Y fi 'Y +1 L 

d O+~ 

G- N 

3 > U 

In r 

04441 o'O 

+J U 41 aJ 

u 

d 

d N\ 

u N 

10 

L 

10 

t 

ro E L d L N 

L a•^•r E O 

'Q ro L 

d•- •r 

M ro+1 •N 

O U G 

td d L ro d 

L•+-~ 4..~ L E 

V4- 

d 

C. 

ro 41 'O 

+> Cf C 

•Q 

X 

•n 

X 

r a E 16 o a ~ 

•a a d c 

X N O. u O S. ro 

u a 

L L N 

O i-~ d E 

In d•r 

o'O •n L 

i~ O a+~ 

r,p C•r 7 

•a 7 d a'~ X N u N O 

a 

In c ro 

r d 

d d d rl r> 

~ 7- 07 G E 

W•r L ~. 

3 1 a 

r 7 c 

IA i N•r 

d C d> 

'^ o L 

d 

> 

L 

N r- E 

d ~ O. 

L tp O. 

'O 

d 

u 

-O 

d 

u 

"O O ri •r, •- c•r a 

d . U 10 •r R{ a 

U iJO dLL a 

C L 

r E d t0 

aEri 

d d L 

N 0.4) O 

c +~ i•> 

'O w u 

d C1 ^ N 

u t+1G1 V 

d 

N 

L 

T u N 

i 

o 

i. 

O 

f- ro a•r O) ~ 

O A ~ N+> > ^ N 

N C.I. O O f.. C 

a O• r d 

L. V C u'r 

O C C i•~ 

L 

0 

(0 M 

3 d • 

9- V- 4- ~ O N 

d+~ ~ 'o U c o 

C t0 A ~ d r-I N 4- 3 

d d a 

~ IO L ro 

.N != U 

L C O 

t0 ~ i-f 

C 

r 

C 

r 

C.F+ ro C C O 

r N R{ ro • nll 

d N E ~ 

E • E d-/ 

d O a ro 

L. d m 

L d 

C LLLJ 'r L C 

r 1..~ 

q0- ro 

O 10 

U L 

+> 

C 

•1•~ 

C 

+•~ Of a-1 T~ a ro+~ 

C O) C U d a ti t0 

U+~ 'O 

d 16 cr d 

ro•r r- C 

7 u O 

.i..l L'O i V 

G i~ d d d 

d G N a~ 

E d ~O c!' C L 

'O N uf 

d - •O 

_'a 7 .•• a -'O u) N d•r in a N 

E 3 N R7 

•U i-~ M L ~ 

d d. d N d iL 3 L. 3 L O' L. u t0 

•- E O d 

O/~ I L 

>. o L d M 

• - fL Y LL O d d N d 

L 3 L -- i 

d d u a u o u o u d u o C 0/ f0 r- u 

v

E

i > m'rCO a c H 

u o u 6 u 

tJ ~ 

a

i ro c0. c V- c w- -do'~ ~ nlcai d sd. e•~ +0+ Od v=•'C-~ C U 

N 

N 

N 1 d 

> 

L 

ro > L > 

(0 •r 

> .V 

r G d 

a w .. 

r d 

.y.> > 

c u7 E•- In 

U d In E 

1 

I~ 

1O 

u~ •r 

~O E 

1~ U> 1~ 

ri Cp v tn ~ v 1 v d d v 

1' 1' 1' 

w ~ 

H C~J 

w 

U 

W•~-i 

~-•~ @J 

w.p cw 

~ --1 ro•r U 

L O 

7 •r 1 

O R) d 

X7 

W II 

L L L tn L lA L O d 

E •r 

N N N N ri N rl v a 

U 

L 

~ 

N 

C K Y_ Y Y 

Eai t ¢ 

z z 

co 

z ~ O a ~ 9 

L. +~ 

Cro) E W U ~ 

~ m 

~ U ¢ ~ U 

~ 

2 

J 

C W 

O 

F 

J N OLn 2 N 00xI•00 l0 V'N 00iY00 OuO 

r E 

~••~ a 

2 

O 

M O 

. . 

N 

. U 1l . . U 

rl rl N M ~ 

. . . . . 

ri N M 

. . . 

rl N M c¢ 

. . . . 

N M 

. . 

ro N a 

C 4.L.1 

¢ O r-1 O 00 Z 00000 000 0000 00 

> N 

O U E J 

N d 

(-O O 00 6S uiMON ~}• ~PO1- M 00 a} NtD 

C 

O O) 

U S 

¢ 

W 

S 

N tD 

lD 01 

rl 

00 

01 

0.7 f, 

Q1 ~ 

rl 

W 

X 

W 

M t27 1, N 00 

N M V• tfl Iri I, N M ct ID 

LLO 7, Oo a0 

M ~~ 1- 

Ql W 

M t0 

1-143 
~ ° ~ ^ - ~ ~ 

u 7 a.+ c a1Do + ++ ^ sf m 

++ v 

C L O L~ A w ~ a NE L-~ 

C o 

• •

C•• c!' 

• r

C- > • E 00 > lD OCl o 

.r ^ N L 1~ 

tN r

~

l 

i 

40. t0-i ti S ti r~-t O • La_ m 

o N 

r N y N 

•1•~ 

L 

7 

6 

~ O L 

L 

6 O 

~ N CL • 

'on T +o~'o ~ d +°~ o C a m 7 u ^ L O 

v L 7 N 

^ i 07 

N t11 y U o 'O d Cl O N V N Gl 

O V- m Cl C Ol m Of 0! L Gl 6 iox C1 y L d 

zo ar€ a! in dmm E++ € N a! v~ iE •r N io E al rtl E••~rv~i ro E 

471- •.N•• E 4- E> oR 

4 

E~ ^ E N> O 

4 •r 6 

E al 

W Corl N ~Oriv r

p

l ^ cD 

~ v N NCO N rN-1 ^v N ~ d' 

Z 

O 

O 

p " C T- S

1011 r+~ L 

W 

O C 1 

G 6/ L T c Y m 

~ 

C 1 

L 

L t 

'O C 

C O 

L 

+t 'O 

C 

~ 

U Of 

'C C a+ L 

O m L 

R- •r 

m L Gl 

O L 

w o N C m +t t m O 

; op 

Vf 

O 

• o C O7 

~ u•r • 

N 6/ O. 

N L. N 

Gl O. 

E 

W tN 

G! N 7 u 

E m •^ 'O C 

C'O 

Gl a7 'O y p, E X L 

6. 

X 

.0 

€ m 01 r' 

L tli 

01 L 

~ i-~ 

• 

~ N c 

ul .Fj •r 

O 3 T r o O 

Wi I~ •N Z 4-~ 

u u 

C L o L R N y O Gl +~ ~ 

W 6 L. Cf m CI c N O E m U t O Gl•> O Io N O o m 3 N O tl'1 

6 7 L O L 

N m'D Cl 

•r C V 

O c 

>•r 

•- 

- 61 a•t 

•n•r 

> Cf +-t L T 

c~ m ^ • L 

U'F 

~/ ~ 

C1 

N N O ~ •r 3 T 6 m T L ~`'tL 3 

O O 

T m C L O L/'~ m 

i L m•r tt) o I- C 

c 

G1 •r 

L 

U y O 

C O ~ 

T O L4..t 

v L 

N 

6 > 

O X•^ N 

Y~ N 

•r Gl C 

T 

o m N+~ o u 6~/ tD O N r C O O .O 

= ya tV —~ G] •-• L. o i-t E o N +.~ c N Gl v E o+~ m +- C d 

C) 

u 

m 

O E C N 

i.~ L. 6•r C 

• 1 d C}.1 

m 

L N 

•1•> Gl O 

E ~ 

m CI O C W U 

L L•r •r 1-1 G lLl 7 

'O C; 

Gl O 41 L N 

u V C 

m N 

L Ol 

W 

J 

YYC7 6 o 

Cl L •1-1 O. ` 

m O C1 E 

R O 

N O 

N N^ 

d••~ i•t R7 rr 6 E 

•6 m'O L iJ R 

c E_- 

N C1 9•- 

C O 

m O•r 

y N 

6L C 

J 6/ L 00 7 N •L 

• C 

i-1 7 X i~ G7 X 9- L G 1~ N+.~ C 6 41 L N C+1 X+t O 

p 

C 'D 

7•r tn L 0f 

N L L 

m m w 

> L.. 

71 R 

E 

G G•- 

Gl •r m 

G/ o+•t m•r .r N•r 

C 3 N O) rl 

3 u v 

N N C 

N m 

•N 

.^ L 

al 6 

C N 

!•Z^ 6i O O T Y>t 

a~ C L 

V T 

47 N 

> L 

r}i 

'O Ol Cl T Gl L N 

41 'O U+> 'O L OI Ol O 

Cl 'O m 

L 

O! +~ 

d pt C 

'O O O! 

> 

L 

6 i~ a-t C 

X m L•r O U O7 m U •N 

G1 

N C V 7 C•r y • tT 'O Cl L C Gl L. 

Cl 

U Y 

pf••1 y 6/ ~ O r ~ 

C O •N 07 ~ ro ro A L 7 d U L N V 

a N N a U 

n O 

.O o E 

O> 

4-• •r C. L 

O U m m 

w c 6 G! ;+~ L 

O m 

• +•+ o 

~ ^ 0 40- .H a0.+ o 

^ cvmG . ~ u 

~ 

a+ NatN taMm Li roua 

LL6 

;~ u mm 

{i! 

-! 

o ~ GI 

'm 60 ~~+-• ~ 

N 

L4•~ 6 

c u 

•r y 

Gl 6•r 

L. 

C m o u u•r d 

•r E 71 m C+> > 

O O'O 01 C L 

ro 

•> 

G! T 

U.t.,t 

m 

•r L G N 

~ 

'O N v m d 

y > T' 

Cl C 

+~ m L . 

•n 

i~ L . 

T+~ 

'O ro 7 N Gl 41 C C> t0 Gl L XL m 

y 

tT y L 

y> y O 

O N C 7 Ol Cl E d G L 7 T•r G1 U N L. o u G ~ C N+1 N 

G! C i1 m 7 

a~ 1-1 O U C'O 

r• Y- € 

V- O 

•Cl 

GJ N U 

€ G 

N 

m ^ 

Gl •I•~ ~ r 1..~ • .L] 

E GI G1 C1 'F- o 

O C 1~ 

u O m 4- •E > E; m d 

m U•r y o o •r N+~ N m L 3 E Cl L. L 

L L L 

Cl +1 •- V CI E•r L 3 m m ro c O c at • L v i~ •r 

• 

u y y L ~ y ~ 4t at ++ •ra E L 

6w m d r O. 

ta c 6 6 

L tT•r € u o L U U O•- I-~ 6 m ~ 01 L O m 6 N 

0! 61 m•r L>f d ~ O C ~ 00 G/ •- 01 o m L O•r G) O L X 6 ~ D y V• ~~ 

p t1' m+~ N 6 L -1 N N N O ~ F 4- ~-• N ~ Ci 4- L{-u u> N; C.~ i•+ N ~/7 L O O tn V O 

N 

~ N N N N N 

m ^ m 

V 

o > rn > `d . L v L L 

•'• u ~ W i0Of Gl GI 

6 

m y 

~ 

~ N 

E ~ ^ 

v •> at w vm-. w •c E c 

~^ ~•r 

a73 c X 

Co 

ai > 

u C/ 

a~ •r 

O L U E 

t 

CU 'O' ~ 

~ t~I t -€ 

' 

E 

~ • 

X E 

u~ 

~ 

r^I 

t 

Q r- cn O N t 

V V_ •rf lJ7 

v r•1 CO 

v 

t0 

v 

O t0 I

v t37 

rt I 

vL7 

N 

v tyy v 

r1 

W H rOi u~f @l W v U U 1' t~ Ql . C C~j w 

J 

co 

Q 

FL O 7 •.-• 

N i1 

O m 

x7 L L L L L L L L 

lL V L 

N N rl rq N N N , M 

u 

oa 

-o 

c 

E o 2 Z X 2 2 to 

O W N ^ W V1 

~ 

C 

~ € N VN CD MtOL7 n 'LL7 Nf

Ln

V N N t+9tn at a• 

+-~ R 

m m 6 000 00 O O 00 000 O p C1 L 

C a.1 OC N v 

O ua NCn O NO N O G00 ~ u7 00 sh ~ 

C 01 N OO 

co m 

Q1 Ol 

~n v 

rl 

v' 

01 

v 

oo oo 

tn rn 

N Oo t~ 

r~ o+ ~ 

W 

r~ 

cp 

r~ 

1-144 

~ 
W 

Z ' O ' N ' C 

O F-' 

W 

N ' 

d 

zQ 

F 

QI 

J 

J 

C 

H 

Z I O 

U 

J 

m 

Y 

Q: 

~ m! 

7 

i•~ 

C 

O ; 

v 1 

~ I 

1 

r1 

W 

J 

m 

F•- 

14 

00 

.. CND ~-~-1 LO N U'1 . Cl ap dp n 

.- • r~-1 r- .U -~-1 ri ~ ro . 

C 

Gl 

t0 

m 

m •• •• •• 

y l 

~p 

L 41 4J 

ro ro ie y 41 a 

w .+ d ai 

c 

a 

O Y117 > 

N N 

N U C L 

7 t9m 67 Ol 

L. 

O 

~ 

N . 

C 

y 

Y OO ri S [O -J Y cn = rj = ~ rj

OT. O _ 

G! +•~ ~ 

ui U 

N 

d 

V ~ 

'O •~ •> 4- 

Ca 

20 

~ ~ v C L. ~ O ,r ~ v i 

~ C/ Ol O/ d 61 O O~ 

z o 

Gl m O/ L 

E 7 

•r

~ N N 

N i0 N i0 

61 r- 

.--• m 

GI r • +~ OJ 

cau> rs r= oE ~ m 

E ~ > d E E Ew Ew Ew E ~ L E 

m.-q o x v rn r-1 rl v OJ OJ N rl +A 00 M ri rl rl ~

21 

rNi 

~ 

++ m ai -c T 3 4- m a) -o a; o 

C 

~ n U ~ - 

07 rtt >~ 

E 7 L'O +~ 

OJ O L. c U L. 

O'~ O 

4- 

G! L. N • 

E O L v1 

TU 

L C 

•r 'O u1 

r 

a'O a L d O G! J O 

o GI •- 'O 

7 M i •r 

 O 7 th •--- 

i 

 N L 

7~n L>> 

 O 7 m 

O m 

 +•~ •1.~ 

y~ V 

 0 d y p 

>LV~ ~n -om 

 5 x ~ > 1••• 

 m a •• 

 o d U r-~ •~ 

 >XC~ .0 

 m 

 3ao 

 o d C.i ~ 

 >Xu 

 ~O V m d •ri 

u1 

v 

>> uf i O~1.+ m L M 

L O i+

j 

 •.- V i•r 

d o1 pJ d 

•~•~ O W m•r L U'1 G7 i L O C i ~ y L 

•d C E 

= y C ul O d 7 3 O N c m+1 r-~ O v1 O m d o V1 O 

X O 

G/ U m r 

L 

4••~ 

U 

y X U sf f~7 U L. 

m Gl U T U Cl 

d L GI O U m 

> i~ L C> rY~ ~ C 4- > 

m O O 

O> 

+•~ •r 

Y 4- C ~Fm O O 'C >> 

N~ 

yl •r d 

}'p 

L. CJ 61 O L a••~ a.~ O d 4/ •r U W r L d~ +~ Ql L d~ G7 m V L O U E 

' - 

O•r uf 

•d 6i w> L GI 'C 

L. N'O •Fi 

d "O •r C C 

~ VE C7 U 

~ d c C7 +~ G/ 

uf 

~ n G/ 

'O tn G! 

•d C G1 

U 3 

L. L C F1 

m L m 

• 7 

L.- OJ X'~ ~ • • ~ n C 

Gl O C'O +J w- C m 

'O 'O •r y 

+~ GJ 7/ > . 

X N L tn •r~ 

Gl r a 

61 ~ •M 7 

GJ Of 

C C 

X N L ~ n 

O/ r 

Cl W • ~n 

O•r 

~ m 

.~a ya 

1A •r Q1 

~a O 

y> 

~ O 61 U O C> L Y V1 M d d GI r 3 E a7 

> 

'O 'O O.•F~ m Ol d T 

y C VI N G7 L H m 

4

7 L aj 7 y y E 

E O! a ~ /1 N O 

"O t O L 

O/ +~ d i r 7 

•M 

'O L O i 

p! } ~ G7 

C U 

• 

~ yi 

y ~ •r . L m'O L. U N N•r L a ~ 6! 'O a-1 N ~ m•r b.1 

fp ~ d 61 U d 

V C d GI 

L C O +

, 

m N 

C L O 

U C d 

L C O 

r ~ F 

Uf •'- L+.~ (,~ -p 

7 N 

~ d•p y 

N O d LL C L 6/ OY 3 L. L. E O O•r'C C O U d O O•rV U ro•~

~ m ~ •N 

O 

~ F• L 4- G! V O'~- +a 

+~ O d C O ~ . 

L. 

U O U Cl >> 

•r> 3C .- Gl x u1 

w +~ C•r 

+•~ t0 m 

d X 

u7 07 CJ 

w •F~ C 

+~ f0 m 

C d 

N d Gl G1 

GJ L C O 67 ~ 

•r C c ~ L C C'O T 

61 ~F ~ V O/ 

L d.' a >t 

C vi 7 G1 

•r y c>>r 

d O 

L 

c u~ 7 

•r y C T 

E V> 

C1 

> y.r L U 

, C O O C a•r• O C m 

a.1 ..- m r• •r m ~ 

d >T'O C L 

'O T i 6J •r o 

+> y m a 

+~ m~ V m 

'O m 

'O c•r 

+J CJ m 

~-1 ro a•~ ~ 

L•O 

U C 

~m 

1A E 

. `p 

~ 

V•- 

y~ .... 

ya ~ 

C ~••~ Y ~ O,••~ G/ 61 .- O V a•~ C d+1 L 

G/ 

G! N+~ 

Yf 

m m ~c 

C d i.~ 

O! L t0 .0 

Cl Rf 

"O V•.-- O N 

. dL •.- 

CbQ >~ 

d a.t) +~ E 61 p ~ V U V OY 

6! ~ C~ C m C ~' /~ 

CO'O 61 L 

• d 67 •~ L C OYr 

E 01 +» 

• 

L 3 ~n~ •V1 

•r 

LL 

~ rn .-~ ^~ v:.~ ~r ~~n•U 

i N 6! mt O/ O L+1•r•rC d L 3 ~ A •'-' 7 •U ~ 4LL iaQ m U O1 +~ L L ~..~ 1•~ 61 L 

w 

i U id 1 ~ O ul 

L 

U O>> G7 C U•1•> GJ 

H •3 

U O T d m rN> y c 11 +•! U O d 

ro C Cf m t.f) W E m•1• ~ Q•.- d O/ O V C w•'O Y U +~ Ci 4-'O' ~1•~ cN C E •3 0 v V. 

o c e ~a 

L i 3 0 L i ~ W 

~v 

71 

C 

Cl 

C 

Y -0 

0 

6! d 

L Y 

4~ 

> ~ 

z> 

~ •r 

t XE C C ~ 

4- O! 

d ~ C 

t37 r 1 •E O 1~ • 

s~ 

~ ^ 

C•r 

.N.i O v v E v ~i•~ vti•f 

v i vrt N 1 W~ 

r~ ri 

M W 

CJ oU 

L O d 

~ •r 

~ n Y C• U 

X~7 L Y] L .0 t L L C L 

m N N N N tD N v N 

U 

a 

E L 

en 

c0 

y¢ ' ~ 

C 

+~ O. 

~ ` L O , O O O O O G O 

O C 

NN 

c, C 1E1 9 9 N N 

~ 

N n . O 

Ocm 

V 1 

I- f- co Ol 

14 

~ 

rf 

1-145 
Ln N M 

O ~ N M QO a0 

~Op 

r7 CC) ~ ~ ~ ~ 

Of ~O ~ rl~ 

C .• .. . . . 

L ~ ^ Y ro o 

~o ro ro ro 

N z d c a U ~ y ~ a' o~ Y a+ N ~ u

. aYi - ~ 

C 1t) C d C C C r L p~p C! ^ 

0(71 ~ C C 

• O 01 ~ ~ . S C J , 

y Y J J N Y Y . 

N 

4 U 

a 

N 

x a 

a! Y 

Ln 

7 .Ln a O .,.~ ^ ~ c 

rtci 5 ar 

+J 

T 

~ T 

ai d ro 

c 

o v- al u ~O a) E aJ N o0 b€ 2 O i0 i0 ~,,,1 ip € Ol e rl io N €V- ~O E E €r1 E VN- E 4- Ey0-•ri Ew 

~ N ri CO ln CfJ r-I ri M 

1~ rl r1 M i w 

N 4J V ~ N N tn r-4 '~!' 

~D v r'1 (~ 

W 

Z 

^ 

N 

O 

C 

p ~ N . 

_ 

d 

~S• i 

C 

O , 

O N 

~ L ~ 

.~ ~ U 

d O 

~..• i.i i.> +~ t1 U ~ N Y X 

W C ~ C ~ L L L f00 7 G! E O O 

f3' O Y 

~ 

n ~ 

w 'e d 

40- w t0 

~n 4- m c 

~n O N TL L ~ L X v 3 x m.n T X pd, L O 

> ai 

t0 Y 

~ L U O 

C tV 

x L Z 

C ~ 6d1 C C ~ t~0 N 'O E 9Ol r• 

W 

•0. 

O d S.. 

O€ ~ V~~U U 7 Ql € ro O 3 7 

•L 

1n 

v X 

€~ T L U i i O Y L O W v 

N 

~ 

N L. 7 O U > > 

4O•-~ x W C7 

~ 0 dy Y lL II Y 

Y L 0.0 C d 0. L 

c.n ~ c c 

c .ol c.o cro o ro = 

N r r 

il 

p ~ ~ •" •~

•'-yF 

Cd 

• ~ •y •y 

•N J d ~ ~ €O~i O ul C) VOf O U O 

~ •W•i 

C C O)Y 7 cdv 

O)Y Rl 

cn3 C 01 

XOl LL . Gl YL O ~ ~ ~ 

~ 

f„ 

^ ~ 

a 

C Gl e ~ orno 

~o L T C 

me L T C 

roL ~ 

L U 

U a • y C , r, 

L C Y L U L U 

U~ n O U ul O U C • tn ~ O O 

V y~ .I.a Y 

c'^ • 

U L € 

Y C 

~ o ro c o ro 

C] 

c o 

voi 

C Y O 

~ •~ II 

G d•r ~ ~ r, ~ ~ t0 i ro L ro ••II t0 

~ 

Nio U 

U N 

. E VVyOj Vu ~ 

', EC L ^ Y ~ 

-~ U G n. 

i.t0 ~ 

w- E w v- O 4- C fo R- c ro 4- o o U E a) 

~ N C d 

•C € N y 

•C E N Y •O L O C 

1••` ~ O N 

•C 

O ~ p~ pf 07 L C> OI L C 7 O) H 1p U •; O 

. 

• 

•y 

~ 

• oari • oavi • Ti 

Q[ 7 Ol 1n C L 

O U 

YI c 

O Yf ~ L~ N X ~ i T C. N N ~ ftl 

O L ,o 

€ ~ ~Olf L 

YfO 

~p r• > 

E O•r O•r c O•r O i O N L O Ol X X 

z a. o Gl z o 

y~ tI~ 

~ ro.«~ • 

tn > Y z Y -~ z Y z o z n O o n O 4J 

y w II d 

o >, 

~ N V tm 

~ v ~ m ro b OI u ^ 

~ 

c •• 

 in s _L _s> w a w i d ai al 

C U t. =.) b L C L 

o c ro.r 

~ •r o ro c 4- N L ~ •r 

 °4- ^ ^ = X r= 

•r 

O 

v V> ~ C X•E 

•ro ~ 

•b E jO u•l N N 

~ 6 ~ m•E N ~ v 1 > ~ v E cf rl y u1 O. 

~ 1 

v~-~-1 u•1 ~ y 

u! 

fw-a 1~ L H 

40-. Y 

f~j 

W ~ --' °U C C H@J W Nj Y Y Vl O O W N d E 

J W v V 0 Ln 

~ y c 

U 

ao 

Q w U L N • ai ro 

L O a N ~y ~ 4- 

L O y ~ p 

O b .0 

i~ V i 1- 5- L G/ L L E.O 

X O C ~ ~ L t L O Z L L ~ 

W'O N N N r/v .-J rl rl N' M p L\ 

W Y U Y J 

~ y H Gl C 

V ~ V- Y C •r 

U 

4- 

m 

= o: Y .-~ ~ 

• aCi v w ~ _ [C N Y . - C Z 

> ym Cc Q 

~ Z O CL 

. . y 

, N 

yL . W W N , 

to 

t~ U 

GS.7 U 

UM O F r ~ O O O O 

C Y L L • 

= N ~ = N v N 

YO E r' 

O ~ ~ Q N H N~ CO Y'1 N r'1 N M d• 

r- Y C Y 

€ 

~ 

N fV ~ O 

OC! 

Yp p0.- • Z O 

=I--• O O 

L2 O N O O O. O O 

Ip 

Cr.L1 N Q N V N 7 d Y 

O t0.1 E C tl'f J N O J lf] 

"~ CO 

LL7 M . 

M O LL9 Ol 

N ~ 01 OO IE Ol Rl ' 

C W M = Q1 Q1 O C7 t0.7=. W N Q M st . Od N N N M at M ~ f[1 a 

U•

O= 

1-146 

~ 
Results from studies of at-rest exposures to 0 3 have demonstrated decrements in forced expiratory volumes and flows occurring at and above 980 }ag/m 3 

(0.5 ppm) of 03 (Folinsbee et al., 1978; Horvath et al., 1979). Airway resistance is not clearly affected at these 0 3 concentrations. At or below 588 

pg/m 3

(0.3 ppm) of 03 , changes in pulmonary function do not occur during at 

rest exposure (Folinsbee et al., 1978), but the occurrence of some 0 3-induced 

pulmonary symptoms has been suggested (Konig et al., 1980). 

With moderate intermittent exercise at a VE of 30 to 50 L/min, decrements 

in forced expiratory volumes and flows have been observed at and above 588 

pg/m3 (0.30 ppm) of 03 (Folinsbee et al., 1978). With heavy intermittent 

exercise (VE = 65 L/min), pulmonary symptoms are present and decrements in 

forced expiratory volumes and .flows are suggested to occur following 2-hr 

exposures to 235 pg/m 3 (0.12 ppm) of 0 3 (McDonnell et al., 1983). Symptoms 

are present and decrements in forced expiratory volumes and flows definitely 

occur at 314 to 470 }ag/m 3 (0.16 to 0.24 ppm) of 0 3 following 1 hr of continuous 

heavy exercise at a VE of 57 L/min (Avol et al., 1984) or very heavy exercise 

at a V E of 80 to 90 L/min (Adams and Schelegle, 1983; Folinsbee et al., 1984) 

and following 2 hr of intermittent heavy exercise at a VE of 65 to 68 L/min 

(McDonnell et al., 1983; Kulle et al., 1985). Airway resistance is only 

modestly affected with moderate exercise (Kerr et al., 1975; Farrell et al., 

1979) or even with heavy exercise while exposed at levels as high as 980 pg/m 3 

(0.50 ppm) 0 3 (Folinsbee et al., 1978; McDonnell et al., 1983). Increased f R 

and decreased VT , while maintaining the same VE , occur with prolonged heavy 

exercise when exposed at 392 to 470 pg/m 3 (0.20 to 0.24 ppm) of 0 3 (McDonnell 

et al., 1983; Adams and Schelegle, 1983). While an increase in RV has been 

reported to result from exposure to 1470 pg/m 3 (0.75 ppm) of 0 3 (Hazucha et 

al., 1973), changes in RV have not been observed following exposures to 980 pg/ 

m3 (0. 50 ppm) of 0 3 or l ess, even wi th heavy exerci se (Fol i nsbee et al ., 

1978). Decreases in TLC and IC have been observed to resuit from exposures to 

980 pg/m3 (0.50 ppm) of 0 3 or less, with moderate and heavy exercise (Folinsbee 

et al., 1978). 

Recovery of the lung from the effects of 0 3 exposure consists of return 

of pulmonary function (FVC, FEV 1 , and SRaw) to preexposure levels. The time 

course of this recovery is related to the magnitude of the 0 3-induced functional 

decrement (i.e., recovery from small decrements is rapid). Despite apparent 

functional recovery of most subjects within 24 hr, an enhanced responsiveness 

1-147 
to a second 0 3 challenge may persist in some subjects for up to 48 hr (Bedi et 

al., 1985; Folinsbee and Horvath, 1986). 

Group mean decrements in pulmonary function can be predicted with some 

degree of accuracy when expressed as a function of effective dose of 0 3 , the 

simple product of 0 3 concentration, V E , and exposure duration (Silverman et 

al., 1976). The relative contribution of these variables to pulmonary decrements is greater for 03 concentration than for V E . A greater degree of 

predictive accuracy is obtained if the contribution of these variables is 

appropriately weighted (Folinsbee et al., 1978). However, several additional 

factors make the interpretation of prediction equations more difficult. There 

is considerable intersubject variability in the magnitude of individual pulmonary 

function responses to 0 3 (Horvath et al., 1981; Gliner et al, 1983; McDonnell 

et al., 1983; Kulle et al., 1985). Individual responses to a given 0 3 concentration have been shown to be quite reproducible (Gliner et al., 1983; McDonnell 

et al., 1985a), indicating that some individuals are consistently more responsive to 03 than are others. No information is available to account for these 

differences. Considering the great variability in individual pulmonary responses to 0 3 exposure, prediction equations that only use some form of effective dose are not adequate for predicting individual responses to 0 3 . 

In addition to overt changes in pulmonary function, enhanced nonspecific 

bronchial reactivity has been observed following exposures to 0 3 concentrations 

>588 pg/m3 (0.3 ppm) (Holtzman et al., 1979; Konig et al., 1980; Dimeo et al., 

1981). Exposure to 392 pg/m 3 (0.2 ppm) of 0 3 with intermittent light exercise 

does not affect nonspecific bronchial reactivity (Dimeo et a1., 1981). 

Changes in forced expiratory volumes and flows resulting from 0 3 exposure 

reflect reduced maximal inspiratory position (inspiratory capacity) (Folinsbee 

et al., 1978). These changes, as well as altered ventilatory control and the 

occurrence of respiratory symptoms, most likely result from sensitization or 

stimulation of airway irritant receptors (Folinsbee et al., 1978; Holtzman et 

al., 1979; McDonnell et al., 1983). The increased airways resistance observed 

following 0 3 exposure is probably initiated by a similar mechanism. Different 

efferent pathways have been proposed (Beckett et al., 1985) to account for the 

lack of correlation between individual changes in SR aw and FVC (McDonnell 

et al., 1983). The increased responsiveness of airways to histamine and 

methacholine following 0 3 exposure most likely results from an 0 3-induced 

increase in airways permeability or from an alteration of smooth muscle characteristics. 

1-148 
Decrements in pulmonary function were not observed for adult asthmatics 

exposed for 2 hours at rest.(Silverman, 1979) or with intermittent light 

exercise (Linn et al., 1978) to 0 3 concentrations of 490 pg%m3 (0.25 ppm) and 

less. Likewise, no significant changes in pulmonary function or symptoms were 

found i n adol escent asthmati cs exposed for 1 hr at rest to 235 pg/m 3 (0.12 

ppm) of 03 (Koenig et al., 1985). Although these results indicate that asthmatics are not more responsive to 0 3 than are healthy subjects, experimental-design 

considerations in reported studies suggest that this issue is still unresolved. 

For patients with COLD performing light to moderate intermittent exercise, no 

decrements in pulmonary function are observed for 1- and 2-hr exposures to 0 3 

concentrations of 588 pg/m3 (0.30 ppm) and less (Linn et al., 1982a, 1983; 

Solic et al., 1982; Kehrl et al., 1983, 1985) and only small decreases in 

forced expiratory volume are observed for 3-hr exposures of chronic bronchitics 

to 804 pg/m3 (0.41 ppm) (Kulle et al., 1984). Small decreases in Sa0 2 have 

al so been observed i n some of these studi es but not i n others; therefore, . 

interpretation of these decreases and their clinical significance is uncertain. 

Many variables have not been adequately addressed in the available clinical data. Information derived from 0 3 exposure of smokers and nonsmokers is 

sparse and somewhat inconsistent, perhaps partly because o -P undocumented 

variability in smoking histories. Although some degree of attenuation appears 

to occur in smokers, all tcurrent resuits should be interpreted with caution. 

Further and more precise studies are required to answer the complex problems 

associated with personal and ambient pollutant exposures. Possible age differences in response to 0 3 have not been explored systematically. Young adults 

usually provide the subject population, and where subjects of differing age 

are combined, the groups studied are often too small in number to make adequate 

statistical comparisons. Children (boys, aged 8 to 11 yr) have been the 

subjects in only one study (McDonnell et al., 1985b) and nonstatistical comparison with adult males exposed under identical conditions has indicated that the 

effects of 0 3 on lung spirometry were very similar (McDonnell et al., 1985c). 

While a few studies have investigated sex differences, they have not conclusively demonstrated that men and women respond differently to 03 , and consideration of differences in pulmonary capacities have not been adequately taken 

into account. Environmental conditions such as heat and relative humidity may 

enhance subjective symptoms and physiological impairment folTowing 0 3 exposure, 

but the results so far indicate that the effects are no more than additive. 

1-149 
In addition, there may be considerable interaction between these variables 

that may result in modification of interpretations made based on available 

information. 

During repeated daily exposures to 0 3 , decrements in pulmonary function 

are greatest on the second exposure day (Farrell et al., 1979; Horvath et al., 

1981; Kulle et al., 1982; Linn et al., 1982b); thereafter, pulmonary responsiveness to 03 is attenuated with smaller decrements on each successive day 

than on the day before until the fourth or fifth exposure day when small 

decrements or no changes are observed. Following a sequence of repeated daily 

exposures, this attenuated pulmonary responsiveness persists for 3(Kulle 

et al., 1982; Linn et al., 1982b) to 7(Horvath et al., 1981) days. Repeated 

daily exposures to a given low effective dose of 0 3 does not affect the magnitude of decrements in pulmonary function resulting from exposure at a higher 

effective dose of 0 3 (Gliner et al., 1983). 

There is some evidence suggesting that exercise performance may be limited 

by exposure to 03 . Decrements in forced expiratory flow occurring with 0 3 

exposure during prolonged heavy exercise (VE = 65 to 81 L/min) along with 

increased fR and decreased VT might be expected to produce ventilatory limitations at near maximal exercise. Results from exposure to ozone during high 

exercise levels (68 to 75 percent of max V02 ) indicate that discomfort associated with maximal ventilation may be an important factor in limiting performance (Adams and Schelegle, 1983; Folinsbee et al., 1984). However, there is 

not enough data available to adequately address this issue. 

No consistent cytogenetic or functional changes have been demonstrated in 

circulating cells from human subjects exposed to 0 3 concentrations as high as 

784 to 1176 pg/m 3 (0.4 to 0.6 ppm). Chromosome or chromatid aberrations would, 

therefore be unlikely at lower 03 levels. Limited data have indicated that 0 3 

can interfere with biochemical mechanisms in blood erythrocytes and sera but 

the physiological significance of these studies is questionable. 

No significant enhancement of respiratory effects has been consistently 

demonstrated for combined exposures of 03 with S02 , NO2 , and sulfuric acid or 

particulate aerosols or with multiple combinations of these pollutants. Most 

of the available studies with other photochemical oxidants have been limited 

to studies on the effects of peroxyacetyl nitrate (PAN) on healthy young and 

middle-aged males during intermittent moderate exercise. No significant 

effects were observed at PAN concentrations of 0.25 to 0.30 ppm, which are 

1-150 
higher than the daily maximum concentrations of PAN reported for relatively 

high oxidant areas (0.047 ppm). One study (Drechsler- Parks et al., 1984) 

suggested a possible simuitaneous effect of PAN and 0 3 ; however, there are not 

enough data to evaluate the significance of this effect. Further studies are 

also required to evaluate the relationships between 0 3 and the more complex 

mix of pollutants found in the natural environment. 

1.10 FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF OZONE AND OTHER 

PHOTOCHEMICAL OXIDANTS 

Field and epidemiological studies offer a unique view of health effects 

research because they involve the real world, i.e., the study of human popuiations in their natural setting. These studies have attendant limitations, 

however, that must be considered in a critical evaluation of their results. 

One major problem in singling out the effects of one air pollutant in field 

studies of morbidity in populations has been the interference of other environmental variables that are critical. Limitations of epidemiological research 

on the health effects of oxidants include: interference by other air pollutants 

or interactions between oxidants and other pollutants; meteorological factors 

such as temperature and relative humidity; proper exposure assessments, including determination of individual activity patterns and adequacy of number and 

location of poilutant monitors; difficulty in identifying oxidant species 

responsibie for observed effects; and characteristics of the popuiations such 

as smoking habits and socioeconomic status. 

The most quantitatively useful information of the effects of acute exposure 

to photochemical oxidants presented in this chapter comes from the field 

studies of symptoms and pulmonary function. These studies offer the advantage 

of studying the effects of naturally-occurring, ambient air on a local subject 

population using the methods and better experimental control typical of controlled-exposure studies. In addition, the measured responses in ambient air 

can be compared to clean, fiitered air without pollutants or to filtered air 

containing artificially-generated concentrations of 0 3 that are comparable to 

those found in the ambient environment. As shown in Table 1-19, studies by 

Linn et al. (1980, 1983) and Avol et al. (1983, 1984, 1985a,b,c) have demonstrated that respiratory effects in Los Angeles area residents are related to 

0 3 concentration and level of exercise. Such effects include: pulmonary 

1-151 
O ~ 

r•mi rl 

m ro 

+J +- m al 

c r 

c o •r> 

J Q 

U 

.c ro 

'1~ ~ 

ro Ni~ N 

Lr 1~Or 

~ 7 

UO Z7 O O 

sr ro uo ro 

L 

O 

W 

J 

BF••• 

~ 

~ tn 

r1 

~ 

W J 

~ H 

V 

C 

d 

L 

G1 w 

a~ 

~ 

t a7 

O a 

2 ~ 

N 

~ FO 

N 

~ 

y 

u 

V

4-

•• 

v 

L 

N 

~ 

G 

~ 

-~ v 

r 

i

~

.+ > 

G ~ 

61 C 

L O 

7 •r 

O 1y0 

W ~ 

u 

~ 

ca 

Cf O 

7 

N 

ro 

S 

c 

ro o~ 

c 4J o. 

L 

o 

N n 

 ~ 

C 

c d f0 U ♦~ 

O/ C 

U 7. 

a 

ro 

~ 

rl 

ro 

4J d 

0 

> 6 

N ~ +~ V T 

f0 N {n 

O N 

Q1 O rl 

t[9 r0 v 

N 

n > 

O•r 

LWL r 4J 

•• L G 

N ~ rl N 

v~ tpto 

v(1) 

~ W ~ c 

W L•r C 6. 7 

r~v ~ 

a1 fo i" U 

N Gl •r 

N~ O•r i 7!Q U C ~ 

•O a• N 

y.1 v C O 

C C 

t0 O.c 

~ 

4~ 

•1•) 

F ~ ; N 

c lWL r L 

tm L •• 61 N 

•N/~.1-1 L E 

c ~ o 

ou o n irov o_€ 

v~i v 4.Ol 01 VTi 

U 

m 

m Ol 

r-1 

d• 

m 

cn rl 

i0 

a~ al 

0 

> 

6 

v 

O.1 

~ T 

L u ~ 

++..a 

~ 

ro N Ol N 0) +> > i~ tr•r N 7i.1•r 

O O•rr Ln ro ••~ u 

N r- C 

O7 i ~ • L N 10 

t0.7 +j C 

Nz7f0o 

c •F,U r f0 N 

+O+r.sJ•rL• ~ ro 

T . •a N In Gt 

1 L •r 

C7 

>,v 

+~L >L 7 

L LWL 't0 Q 

n.c~ ~ 

N •r C 

~I i N •••O••

w 

L vi 0 O€ 3 ro airo ++ 

O L c F 

r U•r O 

^ ~ N V•• 

+• 07+~ M 

tN C C c0 

VOi UL cu 

r 

ro•rUa)n. 

L •r C V n 

U C IC •r

- 

 tD 

G Qf ~ Orl 

~ •N ^O 

r~ Ur C7 

C? roC 

~ IOLL U•r 

N i 

U O +- 

o .NOaci 

+•~ fo 3 a@ 

S 

rL 

 E r- ft1 0

67 N 

fO •r=- •r- CV~•. 

~ u N L 

c LL 

O @ "M 4-

OW/~ • 

NV- LL a@ N G1 L M u 

C dLv ~ 1 

% >s> L ~ 

U O 3 L

+J 

+~ +1 O N c rot i 10 

^•r .-w c 

C

y.r d 07 

+~ N L 

ENVOi 

1-4-U C OO N 61 X 

24- roZ7 N 

m 

M 

W 

U 

L 

ri 

I i 

F-~ 

Y 

I ~ Z 

i•'I M 

Qm lO mi 

rl r-i 

~ O id 

4~ 4J dd 

cr 

c o 

«- > 

J Q 

a _ t 

f0 N dJ (L) N L. ro 

L +~ 6! E 

7 +~ 

0a1- N tp iO v ro 

fC0 7 ~ 

~ OL 

~

,

rn 

M +~ N 

N 

LLL ~ 

Cr-I C 

r ro •r 

N O) zN 

01 7 •O L'0 c 

0 L • fl ai ai 

U N L 

L U w ai o v • C C 

~L J 

N 11 H 

r 3 a•+ 

NLL L 

'••~ ^Y 

= Z 

M 

m C1 

r-i 

CD 

m 

r-~ 

ro 

4j ai 

c 

c 

~ 

- U 

s ~ 

~ 

ISE 

N N •1-~ N 

7 7 

d•Z7O O M m M 10 

c~..~ ai

iT fpJ > 

U H O1 ro

}~ 

w- -0 o - 

CL O 

• C ~ C C rn N ro 

•tn C U U 

1.~ N •r 

rw•~ a 

Vt~it ro 

N~ •c 3 

U 1 C UO 

N v Ip y 

ra O 

I O > ••U- = i-~ 

~ 4J o.u_ Wro N> 

ra Tc.~c.L+~ 

N•'• t41A ;2 IUd v N m ro a GJ G1 G7 L 

N N.CL 

aroiaroiovT 

L L a M r U U\ r 

C Gl c/n ro 

a-1 •O •r N U 

ai 

N 

C! 

Xai 

i-Y 

C 

G! 

41 

E L 

N C 

II 

W 

ai 

N 

U Ol i 

:~

3 X v ai 

O N 

7 

> > 

•y

' . c 

INO C 

+1 O 

oau 

aO! W 

L. 

d ~ 

4- 

V. 

~ c 

a o 

b ro 

4J 

7 •1•~ 

c aci 

> 

~ h- C 

]G•r 

m 4•i 

L Z N 

• ~p ... L 

4- 

a ~ro O 

c G7 

a to r 

A 4~ n 

41 

+J +1 E 

O E E ro 

O O 

O O O ro 

~ O. G L 

o 

> a a c 

r °~ o o ` •E 

u m m w 

4- 

Gl 7 7 •O 

> ? ?_ O 

S. 

C7 N L 

a 

o v •o c 

4~ 

L = o 

N N i~ +~ 

03 6 E % 0 c ++ 

T d ~ d 

> 

G7 7 .0 1J 

~L N • 7 C ro r c ro. ai ~u • C S V S i0 a U 'C 

~ 

M Ln 

v v 

U U 

i L 

L t 

r1 1 rr 

> > > > 

v ~ 

r-1 r-1 

O O 

N O 

cD C 

N M 

C cIT 

X •E > 

r+ 

G! .. 4 + 

W W C 

U 1--1 @J •r 

.0 L 

rl N 

::^Nd 

 Z 

~ ~ ~ 

r 1 ri r-/ 

O O O 

uO M r ~ O 

M 

N 

M 

a• 

M 

1-152 
function decrements seen at 0 3 concentrations of 282 pg/m3 (0.144 ppm) in 

exercising healthy adolescents; and increased respiratory symptoms and pulmonary 

function decrements seen at 0 3 concentrations of 300 pg/m 3 (0.153 ppm) in 

heavily exercising athletes and at 0 3 concentrations of 341 pg/m3 (0.174 ppm) 

in lightly exercising normal and asthmatic subjects. The light exercise level 

is probably the type most likely to occur in the exposed population of Los 

Angeles. The observed effects are typically mild, and generally no substantial 

differences were seen in asthmatics versus persons with norinal, respiratory 

health, although symptoms lasted for a few hours longer in asthmatics. Many 

of the normal subjects, however, had a history of allergy and appeared to be 

more sensitive to 03 than "non-allergic" normal subjects. Concerns raised 

about the relative contribution to untoward effects in these field studies by 

pollutants other than 0 3 have been diminished by direct comparative finding.s 

in exercising athletes (Avol et al., 1984, 1985c) showing no differences in 

response between chamber exposures to oxidant-polluted ambient air with a mean 

03 concentration of 294 pg/m3 (0.15 ppm) and purified air containing a controlled concentration of generated 0 3 at 314 pg/m3 (0.16, ppm). The relative 

importance of exercise level, duration of exposure, and individual variations 

in sensitivity in producing the observed effects remains to be more fully 

investigated, although the results from field studies relative to those factors 

are consistent with results from controlled human exposure studies (Chapter 10). 

Studies of the effects of both acute and chronic exposures have been 

reported in the epidemiological literature on photochemical oxidants. Investigative approaches comparing communities with high 0 3 concentrations and 

communities with low 0 3 concentrations have usually been unsuccessful, often 

because actual pollutant levels have not differed enough during the study, or 

other important variables have not been adequately controlled. The terms 

"oxidant" and "ozone" and their respective association with health effects are 

often unclear. Moreover, information about the measurement and calibration 

methods used is often lacking. Also, as epidemiological methods improve, the 

incorporation of new key variables into the analyses is desirable, such as 

the use of individual exposure data (e.g., from the home and workplace). 

Analyses employing these variables are lacking for most of the community 

studies evaluated. 

1-153 
Studies of effects associated with acute exposure that are considered to 

be qualitatively useful for standard-setting purposes include those on irritative symptoms, pulmonary function, and aggravation of existing respiratory 

disease. Reported effects on the incidence of acute respiratory illness and 

on physician, emergency room, and hospital visits are not clearly related with 

acute exposure to ambient 0 3 or oxidants and, therefore, are not useful for 

deriving health effects criteria for standard-setting purposes. Likewise, no 

convincing association has been demonstrated between daily mortality and daily 

oxidant concentrations; rather, the effect correlates most closely with elevated 

temperature. 

Studies on the irritative effects of 0 3 have been complicated by the 

presence of other photochemical pollutants and their precursors in the ambient 

environment and by the lack of adequate control for other pollutants, meteorological variables, and non-environmental factors in the analysis. Although 0 3 

does not cause the eye irritation normally associated with smog, several 

studies in the Los Angeles basin have indicated that eye irritation is likely 

to occur in ambient air when oxidant levels are about 0.10 ppm. Qualitative 

associations between oxidant levels in the ambient air and symptoms such as 

eye and throat irritation, chest discomfort, cough, and headache have been 

reported at >0.10 ppm in both children and young adults (Hammer et al., 1974; 

Makino and Mizoguchi, 1975). Discomfort caused by irritative symptoms may be 

responsible for the impairment of athletic performance reported in high school 

students during cross-country track meets in Los Angeles (Wayne et al., 1957; 

Herman, 1972) and is consistent with the evidence from field studies (Section 

11.2.1) and from controlled human exposure studies (Section 10.4) indicating 

that exercise performance may be limited by exposure to 0 3 . Although several 

additional studies have shown respiratory irritation apparently related to 

exposure to ambient 0 3 or oxidants in community populations, none of these 

epidemiological studies provide satisfactory quantitative data.on acute 

respiratory illnesses. 

Epidemiological studies in children and young adults suggest an association 

of decreased peak flow and increased airway resistance with acute ambient air 

exposures to daily maximum 1-hr 0 3 concentrations ranging from 20 to 274 pg/m3 

(0.01 to 0.14 ppm) over the entire study period ( Lippmann et al., 1983; 

Lebowitz et al., 1982, 1983, 1985; Lebowitz, 1984; Bock et al., 1985; Lioy et 

al., 1985). None of these studies by themselves can provide satisfactory 

1-154 
quantitative data on acute effects of 0 3 because of inethodological problems 

along with the confounding influence of other pollutants and environmental 

conditions in the ambient air. The aggregation of individual studies, however, 

provides reasonably good evidence for an association between ambient 0 3 

exposure and acute pulmonary function effects. This association is strengthened 

by the consistency between the findings from the epidemiological studies and 

the results from the field studies in exercising adolescents (Avol et al., 

1985a,b) which have shown small decreases in forced expiratory volume and flow 

at 282 pg/m3 (0.144 ppm) of 0 3 in the ambient air; and with the results from 

the controlled human exposure studies in exercising children which have shown 

small decrements in forced expiratory volume at 235 pg/m 3 (0.12 ppm) of 0 3 

(Section 10.2.9.2). 

In studies of exacerbation of asthma and chronic lung diseases, the major 

problems have been the lack of information on the possible effects of inedications, the absence of records for all days on which symptoms could have occurred, and the possibie concurrence of symptomatic attacks resulting from the 

presence of other environmental conditions in ambient air. For example, 

Whittemore and Korn (1980) and Holguin et al. (1985) found small increases in 

the probability of asthma attacks associated with previous attacks, decreased 

temperature, and with incremental increases in oxidant and 0 3 concentrations, 

respectively. Lebowitz et al. (1982, 1983, 1985) and Lebowitz (1984) showed 

effects in asthmatics, such as decreased peak expiratory flow and increased 

respiratory symptoms, that were related to the interaction of 0 3 and temperature. A11 of these studies have questionable effects from other pollutants, 

particularly inhalable particles: There have been no consistent findings of 

symptom aggravation 'or changes in lung function in patients with chronic lung 

diseases other than asthma. 

Only a few prospective studies have been reported on morbidity, mortality, 

and chromosomal effects from chronic exposure to 0 3 or other photochemical 

oxidants. The lack of quantitative measures of oxidant exposures seriously 

limits the usefulness of many population studies of morbidity and mortality 

for standards-setting purposes. Most of these long-term studies have employed 

average annual levels of photochemicai oxidants or have involved broad ranges 

of pollutants; others have used a simple high-oxidant/low-oxidant dichotomy. 

In addition, these population studies are also limited by their inability to 

control for the effects of other factors that can potentially contribute to 

1-155 
the development and progression of respiratory disease over long periods of 

time. Thus, insufficient information is available in the epidemiological 

literature on possible exposure-response relationships between ambient 0 3 or 

other photochemical oxidants and the prevalence of chronic lung disease or the 

rates of chronic disease mortality. None - of the epidemiological studies 

investigating chromosomal changes have found any evidence that ambient 0 3 or 

oxidants affect the peripheral lymphocytes of the exposed population. 

1.11 EVALUATION OF HEALTH EFFECTS DATA FOR OZONE AND OTHER PHOTOCHEMICAL 

OXIDANTS 

1.11.1 Health Effects in the General Human Population 

Controlled human studies of at-rest exposures to 0 3 lasting 2 to 4 hr 

have demonstrated decrements in forced expiratory volume and flow occurring at 

and above 0.5 ppm of 0 3 (Chapter 10). Airway resistance was not significantly 

changed at these 0 3 concentrations. 8reathing 03 at rest at concentrations 

< 0.5 ppm did not significantly impair pulmonary function although the occurrence of some 0 3-related pulmonary symptoms`has been suggested in a number of 

studies. 

One of the principal modifiers of the magnitude of response to 0 3 is 

minute ventilation (VE ), which increases proportionately with increases in 

exercise work load. Adjustment by the respiratory system to an increased work 

load is characterized by increased frequency and depth of breathing. Consequent 

increases in VE not only increase the overall volume of inhaled pollutant, but 

the increased tidal volume may lead to a higher concentration of ozone in the 

lung regions most sensitive to ozone. These processes are further enhanced at 

high work loads (VE > 35 L/min), since the mode of breathing changes at that 

VE from nasal to oronasal. 

Statistically significant decrements in forced expiratory volume and flow 

are generally observed in healthy adult subjects (18 to 45 yr old) after 1 to 

3 hr of exposure as a function of the level of exercise performed and the 

ozone concentration inhaled during the exposure. Group mean data pooled from 

numerous controlled human exposure (Chapter 10) and field (Chapter 11) studies 

indicate that, on average, pulmonary function decrements occur: 

1. At >0.37 ppm 0 3 with light exercise (VE < 23 L/min); 

2. At >0.30 ppm 0 3 with moderate exercise (VE = 24-43 L/min); 

1-156 
3. At >0.24 ppm 0 3 with heavy,exercise (VE = 44-63 L/min); and 

4. At >0.18 ppm 0 3 with very heavy exercise (VE > 64 L/min). 

Note, however, that data from specific individual studies indicate that pulmonary function decrements occur with very heavy exercise in healthy adults at 

0.15 to 0.16 ppm 0 3 (Avol et al ., 1984) and suggest that such effects may 

occur i n heal thy adul ts at 1 evel s as 1 ow as 0.12 ppm 0 3 (Mc®onnel 1 et al ., 

1983). Also, pulmonary function decrements have been observed in children and 

adolescents at concentrations of 0.12 and 0.14 ppm 0 3 with heavy exercise 

(McDonnell et al., 1985b; Avol et al., 1985a). At the lower concentrations 

(0.12 to 0.15 ppm), the average changes in lung function are generally small 

(<5 percent) and are a matter of controversy in regard to their medical significance. 

In the majority of the studies reported, 15-min intermittent exercise 

alternated with 15-min rest was employed for the duration of the exposure. 

Figure 1-14 uses the pulmonary function measurement FEV1 to illustrate the 

effects of intermittent exercise and 03 concentration during 2-hr exposures. 

As noted above, larger decrements in lung function occur at higher exercise 

levels and at higher 03 concentrations. The maximum reponse to 0 3 exposure 

can be observed within 5 to 10 min following the end of each exercise period. 

Other measures of spirometric pulmonary function (e.g., FVC and FEF25-75%) are 

consistent with FEV1 and, therefore, are not depicted here. It is important 

to note, however, that any predictions of average pulmonary function responses 

to 0 3 only appiy under the specific set of exposure conditions at which these 

data were derived. 

Continuous exercise equivalent in duration to the sum of intermittent 

exercise periods at comparable ozone concentrations (0.2 to 0.4 ppm) and 

minute ventilation (60 to 80 L/min) seems to elicit greater changes in pulmonary 

function (Folinsbee et al., 1984; Avol et al., 1984, 1985c) but the differences 

between intermittent and continuous exercise are not clearly established. 

More experimental data are needed to make any quantitative evaluation o,f the 

differences in effects induced by these two modes of exercise. 

Functional recovery, at least from a single exposure with exercise, 

appears to progress in two phases: during the initial rapid phase, lasting 

between 1 and 3 hr, pulmonary function improves more than, 50 percent; this is 

followed by a much slower recovery that is usually completed in most subjects 

1-157 
00 

o 4) , 

O p ++ N 

p L L 

.`c ° ~ O a 

NE ~_s 

. . 

 . E v .0 •C 

3 LO 

p J W N 

co ~ 

~ Nnls 

~ ; VI•

~ W> — O 

~ ++ ~ N 

L .0 , a •k C~ ~ N 

rZ O p p p ~ •a y > .• 

~ V L C O_) 

~ p K 

d Z c~ °rcE 

C W U G~ C - O N a) E ,~ 

Z `- .- J C 

V = p • ~ M ,C 

fn p tD p 

Z pc ~ (D 

N ~ 

O 

p a) 

L N W G> 

~ N•>T v 

> p 

o E (D•~ O 

p .'-: C• 

3 .`~- •~ ~ 

O 'C E ~- 

C7 ~

s

"' ~ O 

~ •3M ~ I- r H 

~ +~+, 

e- ~ d• C p 

~ 

~ O N C E 

~ a Wp o 

'u. X•>U> 

0 

W 

U 

~ 

w X W Q W 

y 

W 

F- U 

= W W 

-i 0 W 

~ 

4if N 

40P > CC 

W X 

g W 

/ 4f 

> 

I 

LLi 

2 U 

js 

w X > W 

• ~ ' 

•~~ 

aoo 1 n c°c 

r- rluaoaed '3 Wfl"IOA JlaOlbaldX3 (330liO:l 03S - 6 

1-158 
within 24 hr. In some individuals, an enhanced responsiveness to a second 0 3 

challenge may persist for'up to 48 hr (Bedi et al., 1985; Folinsbee and Horvath, 

1986). In addition, despite apparent functional recovery, other regulatory 

systems may still exhibit abnormal responses when stimulated; e.g., airway 

hyperreactivity may persist for days. 

Group mean changes may be useful for making statistical inferences about 

homogeneous populations, but they are not adequate for describing difference 

in responsiveness to 0 3 among individuals. Even in well-controlled experiments 

on an apparently homogeneous group of healthy subjects, physiological responses 

to the same work and pollutant loads will vary widely among individuals (Horvath 

et a1., 1981; Gliner et al., 1983; McDonnell et al., 1983; Kulle et al., 1985). 

Despite large intersubject variability, individual responsiveness to a given 

0 3 concentration is quite reproducible (Gliner et al., 1983; McDonnell et al., 

1985a). Some individuals, therefore, are consistently more responsive to 0 3 

than are others. The term "responders" has been used to describe the 5 to 20 

percent of the studied population that is most responsive to 0 3 exposure. 

There are no clearly established criteria to define this group of subjects. 

Likewise, there are no known specific factors responsible for increased or 

decreased responsiveness to 03

. Characterization of individual responses to 

0 3 , however, is pertinent since it permits the assessment of a segment of the 

general population that is potentially at-risk to 03 exposure (see Section 

12.7.3) although statistical treatment of these data is still rudimentary and 

their validity is open to question. 

A close association has been observed between the occurrence of respiratory 

symptoms and changes in pulmonary function in adults acutely exposed in environmental chambers to 0 3 (Chapter 10) or to ambient air containing 03 as the 

predominant pollutant (Chapter 11). This association holds for both the 

time-course and magnitude of effects. Studies on children and adolescents 

exposed to 0 3 or ambient air containing 0 3 under similar conditions have found 

no significant increases in symptoms despite significant changes in pulmonary 

function (Avol et al., 1985a,b; McDonnell et al., 1985b,c). Epidemiological 

studies of exposure to ambient photochemical pollution are of limited use for 

quantifying exposure-response relationships for 0 3 because they have not 

adequately controlled for other pollutants, meteorological variables, and 

non-environmental factors in the data analysis. Eye irritation, for example, 

one of the most common complaints associated with photochemical pollution, is 

1-159 
not characteristic of clinical exposures to 0 3 , even at concentrations several 

times higher than any likely to be encountered in ambient air. There is 

limited qualitative evidence to suggest that at low concentrations of 0 3 , 

other respiratory and nonrespiratory symptoms, as well, are more likely to 

occur in populations exposed to ambient air pollution than in subjects exposed 

in chamber studies (Chapter 11). 

Discomfort caused by irritative symptoms may be responsible for the 

impairment of athletic performance reported in high school students during 

cross-country track meets in Los Angeles (Chapter 11). Only a few controlledexposure studies, however, have been designed to examine the effects of 0 3 on 

exercise performance (Chapter 10). In one study, light intermittent exercise 

(VE = 20-25 L/min) at a high 0 3 concentration (0.75 ppm) reduced postexposure 

maximal exercise capacity by limiting maximal oxygen consumption; submaximal 

oxygen consumption changes were not significant. The extent of ventilatory 

and respiratory metabolic changes observed during or following the exposure 

appears to have been related to the magnitude of pulmonary function impairment. 

Whether such changes are consequent to respiratory discomfort (i.e., symptomatic 

effects) or are the resul t of changes i n 1 ung mechani cs or both i s sti 11 

unclear and needs to be elucidated. 

Environmental conditions such as heat and relative humidity may alter 

subjective symptoms and physiological impairment associated with 0 3 exposure. 

Modification of the effects of 0 3 by these factors may be attributed to increased ventilation associated with elevated body temperature but there may 

also be an independent effect of elevated body temperature on pulmonary function 

(e. g. , VC). 

Numerous additional factors have the potential for altering responsiveness 

to ozone. For example, children and older individuals may be more responsive 

than young adults. Other factors such as gender differences (at any age), 

personal habits such as smoking, nutritional deficiencies, or differences in 

immunologic status may predispose individuals to susceptibility to ozone. In 

addition, social, cultural, or economic factors may be involved. Those actually 

known to alter sensitivity, however, are few, largely because they have not 

been examined adequately to determine definitively their effects on sensitivity 

to 03 . The following briefly summarizes what is actually known from the data 

regarding the importance of these factors (see Section 12.3.3 for details): 

1-160 
1. Age. Aithough changes in growth and development of the lung with 

age have been postulated as one of many factors capable of modifying responsiveness to 03 , sufficient numbers of studies have not been performed to provide 

any sound conclusions for effects of different age groups on responsiveness to 

0 3 . 

2. Sex. Sex differences in responsiveness to ozone,have not been 

adequately studied. Lung function of women, as assessed by changes in FEV1.0' 

might be affected more than that of inen under similar exercise and exposure 

conditions, but the possible differences have not been tested systematically. 

3. Smoking Status . Differences between smokers and nonsmokers have 

been studied often, but the smoking histories of subjects are not documented 

well. There is some evidence, however, to suggest that smokers may be less 

responsive to 03 than nonsmokers. 

4. Nutritional Status . Antioxidant properties of vitamin E in preventing 

ozone-initiated peroxidation invitro are well demonstrated and their protective 

effects invivo are clearly demonstrated in rats and mice. No evidence indicates, however, that man would benefit from increased vitamin E intake relative 

to ambient ozone exposures. 

5. Red Blood Cell Enzyme Deficiencies . There have been too few studies 

performed to document reliably that individuals with a hereditary deficiency 

of giucose-6-phosphate dehydrogenase may be at-risk to significant hematological effects from 0 3 exposure. Even if 0 3 or a reactive product of 0 3-tissue 

interaction were to penetrate the red blood cell after in vivoexposure, it is 

unlikely that any depletion of glutathione or other reducing compounds would 

be of functional significance for the affected individual. 

Successive daily brief exposures of healthy human subjects to 0 3 (<0.7 ppm 

for approximately 2 hr) induce a typical temporal pattern of response (Chapter 10, Section 10.3). Maximum functional changes that occur after the first 

or second exposure day become progressively attenuated on each of the subsequent 

days. By the fourth day of exposure, the average effects are not different 

from those observed foliowing control (air) exposure. Individuals need between 

3 and 7 days of exposure to develop full attenuation, with more sensitive 

subjects requiring more time. The magnitude of a peak response to 0 3 appears 

to be directly related to 03 concentration. It is not known how variations in 

the length or frequency of exposure will modify the time course of this altered 

1-161 
responsiveness. In addition, concentrations of 03 that have no detectable 

effect appear not to invoke changes in response to subsequent exposures at 

higher 03 concentrations. Full attenuation, even in ozone-sensitive subjects, 

does not persist for more than 3 to 7 days after exposure in most individuals, 

while partial attenuation might persist for up to 2 weeks. Although the 

severity of symptoms is generally related to the magnitude of the functional 

response, partial attenuation of symptoms appears to persist longer, for up to 

4 weeks after exposure. 

Whether populations exposed to photochemical air pollu-tion develop at 

least partial attenuation is unknown. No epidemiological studies have been 

designed to test this hypothesis and additional information is required from 

controlled laboratory studies before any sound conclusions can be made. 

Ozone toxicity, in both humans and laboratory animals, may be mitigated 

through altered responses at the cellular and/or subcellular level. At present, 

the mechanisms underlying altered responses are unclear and the effectiveness 

of such mitigating factors in protecting the long-term health of the individual 

against ozone is still uncertain. A growing body of experimental evidence 

suggests the involvement of vagal sensory receptors in modulating the acute 

responsiveness to ozone. It is highly probable that most of the decrements in 

lung volume reported to result from exposures of greatest relevance to standardsetting (<0.3 ppm 03 ) are caused by the inhibition of maximal inspiration 

rather than by changes in airway diameter. None of the experimental evidence, 

however, is definitive and additional research is needed to elucidate the 

precise mechanism(s) associated with ozone exposure. 

1.11.2 Health Effects in Individuals with Preexisting Disease 

Currently available evidence indicates that individuals with preexisting 

disease respond to 0 3 exposure to a similar degree as normal, healthy subjects. 

Patients with chronic obstructive lung disease and/or asthma have not shown 

increased responsiveness to 0 3 in controlled human exposure studies, but there 

is some indication from epidemiological studies that asthmatics may be sympto - 

matically and possibly functionally more responsive than healthy individuals 

to ambient air exposures. Appropriate inclusion and exclusion criteria for 

selection of these subjects, however, especially better clinical diagnoses 

validated by pulmonary function, must be considered before their responsiveness 

to 03 can be adequately determined. None of these factors has been sufficiently 

studied in relation to 0 3 exposures to give definitive answers. 

1-162 
1.11.3 Extrapolation of Effects Observed in Animals to Human Populations 

Animal experiments on a variety of species have demonstrated increased 

susceptibility to bacterial respiratory infections following 0 3 exposure. 

Thus, it could be hypothesized that humans exposed to 0 3 could experience 

decrements in their host defenses against infection. At the present time, 

however, these effects have not been studied in humans exposed to 0 3 . 

Animal studies have also reported a number of extrapulmonary responses to 

0 3 , including cardiovascular, reproductive, and teratological effects, aiong 

with changes in endocrine and metabolic function. The implications of these 

findings for human health are difficult to judge at the present time. In 

addition, central nervous system effects, alterations in red blood cell 

morphology and enzymatic activity, as well as cytogenetic effects on circulating 

lymphocytes, have been observed in laboratory .animals following exposure to 

03 . While similar effects have been described in circulating cells from human 

subjects exposed to high concentrations of 0 3 , the results were either inconsistent or of questionable physiological significance (Section 12.3.8). It is 

not known, therefore, if extrapulmonary responses would be likely to occur in 

humans when exposure schedules are used that are representative of exposures 

that the population at large might actually experience. 

Despite wide variations in study techniques and experimental designs, 

acute and subchronic exposures of animals to levels of ozone < 0.5 ppm produce 

remarkably similar types of responses in all species examined. A characteristic 

ozone lesion occurs at the junction of the conducting airways and the gasexchange regions of the lung after acute 0 3 exposure. Dosimetry model simulations predict that the maximal tissue dose of 0 3 occurs in this region of the 

lung. Continuation of the inflammatory process during longer 0 3 exposures is 

especially important since it appears to be correlated with increased airway 

resistance, increased lung collagen content, and remodeling of the centriacinar 

airways, suggesting the development of distal airway narrowing. No convincing 

evidence of emphysema in animals chronically exposed to 0 3 has yet been published, but centriacinar inflammation has been shown to'occur. 

Since substantial animal data exist for 0 3-induced changes in lung structure and function, biochemistry, and host defenses, it is conceivable that man 

may experience more types of effects from exposure to ozone than have been 

established in human clinical studies. It is important to note, however, that 

the risks to man from breathing ambient levels of ozone cannot fully be 

determined until quantitative extrapolations of animal results can be made. 

1-163 
1.11.4 Health Effects of Other Photochemical Oxidants and Pollutant Mixtures 

Controlled human studies have not consistently demonstrated any modification of respiratory effects for combined exposures of 0 3 with S0 2 , NO 2 , CO 3 or 

H2SO4 and other particulate aerosols. Ozone alone is considered to be responsible for the observed effects of those combinations or of multiple mixtures 

of these pollutants. Combined exposure studies in laboratory animals have 

produced varied results, depending upon the pollutant combination evaluated, 

the exposure design, and the measured variables (Section 12.6.3). Thus, no 

definitive conclusions can be drawn from animal studies of pollutant interactions. There have been far too few controlled toxicological studies with 

other oxidants, such as peroxyacetyl nitrate or hydrogen peroxide, to permit a 

sound scientific evaluation of their contribution to the toxic action of 

photochemical oxidant mixtures. There i.s still some concern, however, that 

combinations of oxidant pollutants with other pollutants may contribute to the 

symptom aggravation and decreased lung function described in epidemiological 

studies on individuals with asthma and in children and young adults. For this 

reason, the effects of interaction between inhaled oxidant gases and other 

environmental pollutants on the lung need to be systematically studied using 

exposure regimens that are more closely representative of ambient air ratios 

of peak concentrations, frequency, duration, and time intervals between events. 

1.11.5 Identification of Potentially At-Risk Group's 

Despite uncertainties that may exist in the data, it is possible to 

identify the groups that may be at potential risk from exposure to ozone, 

based on known health effects, activity patterns, personal habits, and actual 

or potential exposures to ozone. 

The first group that appears to be at potential risk from exposure to 

ozone is that group of the general population characterized as having preexisting respiratory disease. Available data on actual differences in 

responsiveness between these and healthy members of the general population 

indicate that under the exposure conditions studied to date, individuals with 

preexisting disease are as responsive to ozone as healthy individuals. Nevertheless, two primary considerations place individuals with preexisting respiratory 

disease among groups at potential risk from exposure to ozone. First, it must 

be noted that concern with triggering untoward reactions has necessitated the 

use of low concentrations and low exercise levels in most studies on'subjects 

1-164 
with mild, but not severe, preexisting disease. Therefore, few or no data on 

responses at higher concentrations, at higher exercise levels, and in subjects 

with more severe disease states are available for comparison with responses in 

healthy subjects. Thus, definitive data on the modification by preexisting 

disease of responses to ozone are not available. Second, however, it must be 

emphasized that in individuals with already compromised pulmonary function, 

the decrements in function produced by exposure to ozone, while similar.to or 

even the same as those experienced by normal subjects, represent a further 

decline in volumes and flows that are already diminished. It is possible that 

such declines may impair further the ability to perform normal activities. In 

individuals with preexisting diseases such as asthma or allergies, increases 

in symptoms upon exposure to ozone, above and beyond symptoms seen in the 

generai population, may also impair or further curtaii the ability to function 

normally. 

The second group at potential special risk from exposure to ozone.consists 

of the general population of normal, healthy individuals. Two specific factors 

place members of the general population at pote.ntial risk from exposure to 

ozone. First unusual responsiveness to ozone has been observed in some individuais ("responders"), not yet characterized medically except by their response 

to ozone, who experience greater decrements in lung function from exposure to 

ozone than the average response of the groups studied. It is not known if 

"responders" are a specific population subgroup or simply represent the upper 

5 to 20 percent of the ozone response distribution. As yet no means of determining in advance those members of the general population who are "responders" 

has been devised. Second, data presented in this chapter underscore the 

importance of exercise in the potentiation of effects from exposure to ozone. 

Thus, the general population potentially at risk from exposure to ozone includes 

those individuals whose activities out of doors, whether vocational or 

avocational, result in increases in minute ventilation, which is the most 

prominent modifier of response to ozone. 

Other biological and nonbiological factors have the potential for influencing responses to ozone. Data remain inconciusive at the present, however, 

regardi,ng the importance of age, gender, and other, factors in influencing 

response to ozone. Thus, at the present time, no other groups are thought to 

be biologically predisposed to increased sensitivity to ozone. It must be 

emphasized, however, that the final identification of those effects that are 

considered "adverse" and the final identification of "at-risk" groups are both 

the domain of the Administrator of the U.S. Environmental Protection Agency. 

1-165 
1.12 REFERENCES 

1.12.1 References for Introduction 

U.S. Environmental Protection Agency (1982a) Air quality criteria for oxides 

of nitrogen. Research Triangle Park, NC: U.S. Environmental Protection 

Agency; EPA report no. EPA-600/8-82-026. 

U.S. Environmental Protection Agency (1982b) Air quality criteria for particulate matter and sulfur oxides. Research Triangle Park, NC: U.S. Environmental Protection Agency; EPA report no. EPA-600/8-82-029a,b,c,d. 

U.S. Code (1982) Clean Air Act, §108, air quality criteria and control techni ques. U. S. C. 42: §7408. 

1.12.2 References for Properties, Chemistry, and Transport of Ozone and 

Other Photochemical Oxidants and Their Precursors 

Aikin, A. C. ; Herman, J. R. ; Maier, E. J. R. ; McQuillan, C. J. (1983) Influence of peroxyacetyl nitrate (PAN) on odd nitrogen in the troposphere 

and lower stratosphere. Planet. Space Sci. 31: 1075-1082. 

Altshuller, A. P. (1975) Evaluation of oxidant results at CAMP sites in the 

United States. J. Air Pollut. Control Assoc. 25: 19-24. 

Altshuller, A. P. (1983) Review: natural volatile organic substances and their 

effect on air quality in the United States. Atmos. Environ. 17: 2131-2165. 

Altshuller, A. P. (1986) Review paper: the role of nitrogen oxides in nonurban 

ozone formation in the planetary boundary layer over N America, W Europe 

and adjacent areas of ocean. Atmos. Environment. 20: 245-268. 

Altshuller, A. P.; Bufalini, J. J. (1971) Photochemical aspects of air pollution: a review. Environ. Sci. Technol. 5: 39-64. 

Atkinson, R. (1985) Kinetics and mechanisms of the gas phase reactions of 

the hydroxyl radical with organic compounds under atmospheric conditions. 

Chem. Rev. : i n press. 

Atkinson, R.; Aschmann, S. M. (1984) Rate constants for the reactions of 0 3 

and OH radicals with a series of alkynes. Int. J. Chem. Kinet. 16: 259-268. 

Atkinson, R.; Carter, W. P. L. (1984) Kinetics and mechanisms of the reactions 

of ozone with organic compounds in the gas phase. Chem. Rev. 84: 437-470. 

Atkinson, R.; Darnall, K. R.; Lloyd, A. C. ; Winer, A. M.; Pitts, J. N., Jr. 

(1979) Kinetics and mechanisms of the reactions of the hydroxyl radical 

with organic compounds in the gas phase. In: Pitts, J. N., Jr.; Hammond, 

G. S.; Gollnick, K.; Grosjean, D., eds. Advances in photochemistry, v. 

11. New York, NY: John Wiley and Sons. pp. 375-488. 

1-166 
References for Properties, Chemistry, Transport (cont'd.) 

Atkinson, R.; Plum, C. N.; Carter, W. P. L.; Winer, A. M.; Pitts, J. N., Jr. 

(1984a) Rate constants for the gas-phase reactions of NO 3 radicals with a 

series of organics in air at 298 ± 1 K. J. Phys. Chem. 88: 1210-1215. 

Atkinson, R.; Pitts, J. N., Jr.; Aschmann, S. M. (1984b) Tropospheric reactions of dimethyl sulfide with NO 3 and OH radicals. J. Phys. Chem. 88: 

1584-1587. 

Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N., Jr. (1984c) 

Kinetics of the gas-phase reactions o.f NO 3 radicals with .a series of 

dialkenes, cycloalkenes, and monoterpenes at 295 ± 1 K. Environ. Sci. 

Technol. 18: 370-375. 

Atkinson, R.; Carter, W. P. L.; Plum, C. N.; Winer, A. M.; Pitts, J. N., Jr. 

(1984d) Kinetics of the gas-phase reactions of NO aradicals with a series 

of aromatics at 296 ± 2 K. Int. J. Chem. Kinet. 16: 887-898. 

Atki nson, R. ; Pl um, C. N. ; Carter, W. P. L. ; Wi ner, A. M. ; Pi tts , J. N. , Jr. 

(1984e) Kinetics of the gas phase reactions of NO 3 radicals with a series 

of alkanes at 296 ± 2 K. J. Phys. Chem. 88: 2361-2364. 

Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N., Jr. (1985) Kinetics 

and atmospheric implications of the gas-phase reactions of NO 3 radicals 

with a series of monoterpenes and related organics at 294 ± 2 K. Environ. 

Sci. Technol. 19: 159-163. 

Bach, W. D., Jr. (1975) Investigation of ozone and ozone precursor concentrations in nonurban locations in the eastern United States; phase II. meteorological analyses. Research Triangle Park, NC: U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards; EPA report no. 

EPA-450/3-74-034a. Available from NTIS, Springfield, VA; PB.-246899. 

Bell, G. B. (1960) Meteorological conditions during oxidant episodes in 

coastal San Diego County in October and November, 1959. Sacramento, CA: 

Department of Public Health. 

Bollinger, M. J.; Parrish, D. D.; Hahn, C.; Albritton, D. L.; Fehsenfeld, F. 

C. (1982) NO measurements in clean continental air. In: Proceedings of 

2nd symposium on composition of the nonurban troposphere; May; Williamsburg, VA. 

Calvert, J. G.; Stockwell, W. R. (1983) Acid generation in the troposphere by 

gas-phase chemistry. Environ. Sci. Technol. 17: 428A-443A. 

Calvert, J. G.; Stockweil, W. R. (1984) The mechanism and rates of the gas-phase 

oxidation of suifur dioxide and nitrogen oxides in the atmosphere. In: 

Calvert, J. G., ed., Acid precipitation: S0 2 , NO and NO2 oxidation mechanisms: atmospheric considerations. Boston, MA: Butterworth Publishers. 

(Teasley, J. I., ed., Acid precipitation series v. 3) 

Carter, W. P. L.; Winer, A. M.; Darnall, K. R.; Pitts, J. N., Jr. (1979) Smog 

chamber studies of temperature effects in photochemical smog. Environ. 

Sci. Technol. 13: 1094-1100. 

1-167 
References for Properties, Chemistry, Transport (cont'd.) 

Carter, W. P. L.; Winer, A. M.; Pitts, J. N., Jr. (1981a) Major atmospheric 

sink for phenol and the cresols: reaction with the nitrate radical. 

Environ. Sci. Technol. 15: 829-831. 

Carter, W. P. L.; Winer, A. M.; Pitts, J. N., Jr. (1981b) Effect of peroxyacetyl 

nitrate on the initiation of photochemical smog. Environ. Sci. Technol. 

15: 831-834. 

Chameides, W. L.; Davis, D. D. (1982) The free radical chemistry of cloud droplets and its impact upon the composition of rain. JGR J. Geophys. Res. 

87: 4863-4877. 

Chock, D. P.; Dunker, A. M.; Kumar, S.; Sloane, C. S. (1981) Effect of NO 

emission rates on smog formation in the California South Coast Air Basln. 

Environ. Sci. Technol. 15: 933-939. 

Clark, T. L.; Clarke, J. F. (1982) Boundary layer transport of NO and 0 3 from 

Baltimore, Maryland--a case study. Presented at: 75th annuaf meeting of 

the Air Pollution Control Association; June; New Orleans, LA. Pittsburgh, 

PA: Air Pollution Control Association; paper no. 82-24.3. 

Clarke, J. F.; Ching, J. K. S.; Brown, R. M.; Westberg, J.; White, J. H. (1982) 

Regional transport of ozone. Presented at: Third conference on air pollution meteorology; January. Boston, MA: American Meteorological Society; 

paper no. 1.1. 

Cleveland, W. S.; Guarino, R.; Kleiner, B.; McRae, J. E.; Warner, J. L. (1976a) 

The analysis of the ozone problem in the northeast United States. In: 

Specialty conference on ozone/oxidants--interactions with the total environment. Pittsburgh, PA: Air Pollution Control Association; pp. 109-120. 

Cleveland, W. S.; Kleiner, B.; McRae, J. E.; Warner, J. L. (1976b) Photochemical 

air pollution: transport from New York City area into Connecticut and 

Massachusetts. Science (Washington, DC) 191: 179-181. 

Coffey, P. E.; Stasiuk, W. N. (1975) Evidence of atmospheric transport of ozone 

into urban areas. Environ. Sci. Technol. 9: 59-62. 

Countess, R. J.; Wolff, G. T.; Whitbeck, M. R. (1981) The effect of temperature 

on ozone formation in the propene/nitrogen dioxide/air system. J. Environ. 

Sci . Heal th. A16: 1-8. 

Cox, R. A.; Burrows, J. P. (1979) Kinetics and mechanism of the disproportionation of H02 in the gas phase. J. Phys. Chem. 83: 2560-2568. 

Cox, R. A.; Roffey, M. J. (1977) Thermal decomposition of peroxyacetyl nitrate 

in the presence of nitric oxide. Environ. Sci. Technol. 11: 900-906. 

Cronn, D. R. (1982) Monitoring of ambient halocarbons and natural hydrocarbons 

in the Smoky Mountains. In: Proceedings from 2nd symposium on composition of the nonurban troposphere; May; Williamsburg, VA. 

1-168 
References for Properties, Chemistry, Transport (cont'd.) 

Crutzen, P. J.; Fishman, J. (1977) Average concentrations of OH in the troposphere, and the budgets of CH 4s CO 3 H2 , and CH3 CC13 . Geophys. Res. Lett. 

4: 321-324. 

Danielsen, E. F. (1968) Stratospheric-tropospheric exchange based on radioactivity, ozone and potential vorticity. J. Atmos. Sci. 25: 502-518. 

Danielsen, E. F. (1980) Stratospheric source for unexpectedly large values of 

ozone measured over the Pacific Ocean during Gametag, August 1977. JGR 

J. Geophys. Res. 85: 401-412. 

Danielsen, E. F.; Mohnen, V. A. (1977) Project duststorm report: ozone transport, in situ measurements, and meteorological analyses of tropopause 

folding. JGR J. Geophys. Res. 82: 5867-5877. 

Darnal l, K. R. ; Lloyd, A. C. ; Winer, A. M. ; Pitts, J. N. , Jr. (1976) Reactivity scale for atmospheric hydrocarbons based on reaction with hydroxyl 

radical. Environ. Sci. Technol. 10: 692-696. 

Demerjian, K. L.; Schere, K. L. (1979) Applications of a photochemical box 

model for 03 air quality in Houston, Texas. Proceedings of Air Pollution 

Control Association Specialty Conference on Ozone/Oxidants: Interactions 

with the Total Environment. pp. 329-352. 

Demerjian, K. L.; Kerr, J. A.; Calvert, J. G. (1974) The mechanism of photochemical smog formation. In: Pitts, J. N., Jr.; Metcalf, R. L., eds. 

Advances in environmental science and technology: v. 4. New York, NY: 

John Wiley and Sons, Inc.; pp. 1-262. 

Demerjian, K. L.; Schere, K. L.; Peterson, J. T. (1980) Theoretical estimates 

of actinic (spherically integrated) fiux and photolytic rate constants of 

atmospheric species in the lower troposphere. In: Pitts, J. N., Jr.; 

Metcalf, R. L.; Grosjean, D., eds. Advances in environmental science and 

technology: volume 10. New York, NY: John Wiley and Sons; pp. 369-459. 

Derwent, R. G.; Hov, 0. (1980) Computer modeling studies of the impact of 

vehicle exhaust emission controls on photochemical air pollution formation in the United Kingdom. Environ. Sci. Technol. 14: 1360-1366. 

Dignon, J.; Hameed, S. (1985) A model investigation of the impact of increases 

in anthropogenic NO emissions between 1967 and 1980 on tropospheric ozone. 

J. Atmos. Chem. 3: ~91-506. 

Dimitriades, B. (1970) On the function of hydrocarbon and nitrogen oxides in 

photochemical smog formation..Washington, DC: U.S. Department of Commerce, 

Bureau of Mines. Report of Investigations, RI 7433. 

Dimitriades, B. (1972) Effects of hydrocarbon and nitrogen oxides on photochemical smog formation. Environ. Sci. Tech. 6: 253-260. 

1-169 
References for Properties, Chemistry, Transport (cont'd.) 

Dimitriades, B. (1977a) An alternative to the Appendix-J method for calculating 

oxidant- and NO2 -related control requirements. In: International Conference 

on Photochemical Oxidant Pollution and Its Control. Proceedings, Vol. II. 

Research Triangle Park, NC: U.S. Environmental Protection Agency, 

EPA-600/3-77-00Ib. 

Dimitriades, B. (1977b) Oxidant control strategies. Part I. Urban oxidantcontrol strategy derived from existing smog chamber data. Environ. Sci. 

Technol. 11: 80-88. 

Dodge, M. C. (1977a) Combined use of modeling techniques and smog chamber data 

to derive ozone-precursor relationships. In: International Conference on 

Photochemical Oxidant Pollution and Its Control. Proceedings, Vol. II. 

Research Triangle Park, NC: U.S. Environmental Protection Agency. 

EPA-600/3-77-001b. 

Dodge, M. C. (1977b) Effect of selected parameters on predictions of a photochemical model. Research Triangle Park, NC: U.S. Environmental Protection 

Agency. EPA-600/3-77-048. 

Dodge, M. C.; Arnts, R. R. (1979) A new mechanism for the reaction of ozone 

with olefins. Int. J. Chem. Kinet. 11: 399-410. 

Eaton, W. C.; Decker, C. E.; Tommerdahl, J. B.; Dimmock, F. E. (1979) Study of 

the nature of ozone, oxides of nitrogen, and nonmethane hydrocarbons in 

Tulsa, Oklahoma; v. 1: project description and data summaries. Research 

Triangle Park, NC: U.S. Environmental Protection Agency, Office of Air 

Quality Planning and Standards; EPA report no. EPA-450/4-79-008a. Available from: NTIS, Springfield, VA; PB-300481. 

F.R. (1979, November 14) 44: 65667-65670. 

Ferman, M. Z. A. (1981) Rural nonmethane hydrocarbon concentrations and composition. In: Bufalini, J. J.; Arnts, R. R., eds. Atmospheric biogenic hydrocarbons. Ann Arbor, MI: Ann Arbor Science Publishers, Inc. 

Ferman, M. Z. A.; Monson, P. R. (1978) Comparison of rural and urban air quality. 

Paper presented at 71st annual meeting of the Air Pollution Control Association; Houston, June. 

Fishman, J.; Carney, T. A. (1984) A one-dimensional photochemical model of the 

troposphere with planetary boundary-layer parameterization. J. Atmos. Chem. 

1: 351-376. 

Fishman, J.; Seiler, W. (1983) Correlative nature of ozone and carbon monoxide 

in the troposphere: Implications for the tropospheric ozone budget. J. 

Geophys. Res. 88: 3662-3670. 

Fishman, J.; Vukovich, F. M.; Browell, E. V. (1985) The photochemistry of 

synoptic-scale ozone synthesis: Implications for the global tropospheric 

ozone budget. J. Atmos. Chem. 3: 299-320. 

1-170 
References for Properties, Chemistry, Transport (cont'd.) 

Gelinas, R. J.; Vajk, J. P. (1979) Systematic sensitivity analysis of air 

quality simulation models. Research Triangle Park, NC: U.S. Environmental 

Protection Agency. EPA-600/4-49-035. 

Gertier, A. W.; Miller, D. F.; Lamb, D.; Katz, U. (1984) Studies of sulfur dioxide 

and nitrogen dioxide reactions in haze and cloud. In: Durham, J. L., ed. 

Chemistry of particies, fogs and rain. Boston, MA: Butterworth Publishers; 

pp. 131-160. (Teasley, J. I., ed. Acid precipitation series, v. 2). 

Glasson, W. A.; Tuesday, C. S. (1970) Inhibition of atmospheric photooxidation 

of hydrocarbons by nitric oxide. Environ. Sci. Technol. 4: 37-44. 

Hanna, S. R. (1973) A simple dispersion model for the analysis of chemically 

reactive pollutants. Atmos. Environ. 7: 803-817. 

Herron, J. T.; Huie, R. E. (1977) Stopped-flow studies of the mechanism of 

ozone-alkene reactions in the gas phase. Ethylene. J. Am. Chem. Soc. 99: 

5430-5435. 

Herron, J. T.; Huie, R. E. (1978) Stopped flow studies of inechanisms of 

ozone-alkene reactions in gas phase propene + isobutene. Int. J. Chem. 

Kinet. 10: 1019-1040. 

Hoffman, M. R.; Edwards, J. 0. (1975) Kinetics of the oxidation of sulfite by 

hydrogen peroxide in acidic solution. J. Phys. Chem. 79: 2096-2098. 

Holdren, M. W.; Westberg, H. H.; Zimmerman, P. R. (1979) Analysis of monoterpene hydrocarbons in rural atmospheres. JGR J. Geophys. Res. 84: 

5083-5088. 

Holdren, M. W.; Spicer, C. W.; Hales, J. M. (1984) Peroxyacetyl nitrate solubility and decomposition rate in acidic water. Atmos. Environ. 18: 

1171-1173. 

Holzworth, G. C. (1964) Estimates of inean maximum mixing depths in the contiguous United States. Mon. Weather Rev. 92: 235-242. 

Holzworth, G. C. (1972) Mixing heights, wind speeds, and potential for urban 

air pollution throughout the contiguous United States. Research Triangle 

Park, NC: U.S. Environmental Protection Agency; publication no. AP-101. 

Available from: NTIS, Springfield, VA;.PB-207103. 

Holzworth, G. C.; Fisher, R: W. (1979) Climatological summaries of the lower 

few kilometers of rawinsonde observations. Research Triangle Park, NC: 

U.S. Environmental Protection Agency, Environmental Sciences Research 

Laboratory; EPA report no. EPA-600/4-79-026. 

Hosler, C. R. (1961) Low-l'evel inversion frequency in the contiguous United 

States. Mon. Weather Rev. 89: 319-339. 

Husain, L.; Coffey, P. E.; Meyers, R. E.; Cederwall, R. T. (1977) Ozone 

transport from stratosphere to troposphere. Geophys. Res. Lett. 4: 

363-365. 

1-171 
References for Properties, Chemistry, Transport (cont'd.) 

Jaffee, R. J.; Smith, F. C., Jr.; West, K. W. (1974) Study of factors affecting 

reactions in environmental chambers: final report on phase III. Research 

Triangle Park, NC: U.S. Environmental Protection Agency, Office of Research 

and Development; EPA report no. EPA-650/3-74-004b. Available from: NTIS, 

Springfield, VA PB-256252. 

Japar, S. M.; Niki, H. (1975) Gas-phase reactions of the nitrate radical with 

olefins. J. Phys. Chem. 79: 1629-1632. 

Jeffries, H.; Fox, D.; Kamens, R. (1975) Outdoor smog chamber studies. Effect 

of hydrocarbon reduction on nitrogen dioxide. Research Triangle Park, 

NC: U.S. Environmental Protection Agency; EPA report no. EPA-650/3-75-011. 

Available from: NTIS, Springfield, VA; PB-245829. 

Jeffries, H.; Fox, D.; Kamens, R. (1976) Outdoor smog chamber studies: light 

effects relative to indoor chambers. Environ. Sci. Technol. 10: 1006-1011. 

Johnson, W. B.; Viezee, W. (1981) Stratospheric ozone in the lower troposphere-- 

I. Presentation and interpretation of aircraft measurements. Atmos. Environ. 

15: 1309-1323. 

Junge, C. E. (1963) Air chemistry and radioactivity. New York, NY: Academic 

Press. (van Mieghen, J.; Hales, A. L., eds. International geophysics series 

v. 4). 

Kamens, R. M.; Gery, M. W.; Jeffries, H. E.; Jackson, M.; Cole, E. I. (1982) 

Ozone-isoprene reactions: product formation and aerosol potential. Int. 

J. Chem. Kinet. 14: 955-975. 

Kelly, N. A. (1985) Ozone/precursor relationships in the Detroit metropolitan 

area derived from captive-air irradiations and an empirical photochemical 

model. J. Air Pollut. Control Assoc. 35: 27-34. 

Kelly, N. A.; Wolff, G. T.; Ferman, M. Z. A. (1982) Background pollutant measurements in air masses affecting the eastern half of the United States--I. Air 

masses arriving from the northwest. Atmos. Environ. 16: 1077-1088. 

Kelly, N. A.; Wolff, G. T.; Ferman, M. A. (1984) Sources and sinks of ozone in 

rural areas. Atmos. Environ. 18: 1251-1266. 

Kelly, N. A.; Ferman, M. A.; Wolff, G. T. (1986) The chemical and meteorological 

conditions associated with high and low ozone concentrations in southeastern 

Michigan and nearby areas of Ontario. J. Air Pollut. Control.Assoc. 

36: 150-158. 

Killus, J. P.; Whitten, G. Z. (1984) Isoprene: a photochemical kinetic 

mechanism. Environ. Sci. Technol. 18: 142-148. 

Korshover, J. (1967) Climatology of stagnating anticyclones east of the Rocky 

Mountains, 1936-1965. Cincinnati, Ohio: U.S. Department of Health, 

Education and Welfare, National Center for Air Pollution Control; Public 

Health Service publication no. 999-AP-34. Available from: NTIS, Springfield, 

VA; PB-174709. 

1-172 
References for Properties, Chemistry, Transport (cont'd.) 

Korshover, J. (1975) Climatology of stagnating anticyclones east of the Rocky 

Mountains, 1936-1975. Washington, DC: U.S. Department of Commerce, 

National Oceanic and Atmospheric Administration; NOAA technical memorandum ERL AR-55. Available from: NTIS, Springfield, VA; PB-257368. 

Lee, Y.-N.; Senum, G. I.; Gaffney, J. S. (1983) Peroxyacetyl nitrate (PAN) 

stability, soiubility, and reactivity--implications for tropospheric 

nitrogen cycles and precipitation chemistry. Presented at CACGP 

Symposium, Oxford, England; September. 

Levy, H. II; Mahlman, J. D.; Moxim, W. J. (1985) Tropospheric ozone: The roie 

of transport. J. Geophys. Res. 90: 3753-3772. 

Liu, C. S.; Grisinger, J. E. (1981) Review of SAI Airshed Model Sensitivity 

Study Conducted for the South Coast Air Basin by California Air Resources 

Board. .AQMP Technical Paper No. 5. South Coast Air Quality Management 

District; E1 Monte, CA. 

Liu, M.-K.; Morris, R. E.; Kiilus, J. P. (1984) Development of a regional oxidant 

model and application to the northeastern United States. Atmos. Environ. 

18: 1145-1161. 

Lloyd, A. C.; Atkinson, R.; Lurmann, F. W.; Nitta, B. (1983) Modeling 

potentia1 ozone impacts from natural hydrocarbons. I. Development and 

testing of a chemical mechanism for the NO -air photooxidations of isoprene 

and a-pinene under ambient conditions. A&os. Environ. 17: 1931-1950. 

Logan, J. A. (1983) Nitrogen oxides in the troposphere: globa1 and regional 

budgets. JGR J. Geophys. Res. 88: 10785-10807. 

Lynn, D. A:; Steigerwald, B. J.; Ludwig, J. H. (1964) The November-December 

1962 air pollution episode in the eastern United States. Cincinnati, OH: 

U.S. Department of Health, Education and Welfare, Division of Air Pollution; Public Health Service publication no. 999-AP-77. Available from: 

NTIS, Springfield, VA; PB-168878. 

Lyons, W. A.; Olsson, L. E. (1972) Mesoscale air pollution transport in the 

Chicago lake breeze. J. Air Pollut. Control Assoc. 22: 876-881. 

Martin, L. R.; Damschen, D. E'. (1981) Aqueous oxidation of sulfur dioxide by 

" hydrogen peroxide.at low pH. Atmos. Environ. 15: 1615-1621. 

Martinez, J. R.; Singh, H. B. (1979) Survey of the role of NO in nonurban 

ozone formation. SRI International, Menlo Park, CA. Finaxl report to 

U.S. Environmental Protection Agency, SRI Project 6780-8. Research 

Triangle Park, NC: U.S. Environmentai Protection Agency. 

Mohnen, V. A. (1977) Review and analysis. In: International conference on 

oxidants, 1976 -- Analysis of evidence and viewpoints. Part III. The issue 

of stratospheric ozone intrusion. Research Triangle Park, NC: U.S. 

Environmental Protection Agency. Report no. EPA-600/3-77-115. 

1-173 
References for Properties, Chemistry, Transport (cont'd.) 

Mueller, P. K.; Hidy, G. M. (1983) The sulfate regional experiment (SURE): 

report of findings. Palo Alto, CA: Electric Power Research Institute; 

report no. EA-1901. 

National Research Council (1977) Ozone and other photochemical oxidants. 

Washington, DC: National Academy of Sciences. 

Neiburger, M.; Johnson, D. S.; Chen, C. -W. (1961) Studies of the structure of 

the atmosphere over the eastern Pacific Ocean in the summer: I. the 

inversion over the eastern north Pacific Ocean. Berkeley, CA: University 

of California Press; publications in meteorology, v. 1, no. 1. 

Nicksic, S. W.; Harkins, J.; Mueller, P. K. (1967) Some analyses for PAN and 

studies of its structure. Atmos. Environ. 1: 11-18. 

Niki, H.; Maker, P. D.; Savage, C. M.; Breitenbach, L. P. (1981) An FT-IR 

stuc~y of a transitory product in the gas-phase ozone-ethylene reaction. 

J. Phys. Chem. 85: 1024-1027. 

Niki, H. ; Maker, P. D. ; Savage, C. M. ; Breitenbach, L. P. (1983) An FT-IR 

study of the mechanism for the reaction HO+ CH 3 SCH3 . Int. J. Chem. Kinet. 

15: 647-654. 

Peterson, J. T. (1976) Calculated actinic fluxes (290-700 nm) for air pollution 

photochemistry applications. Research Triangle Park, NC: U.S. Environmental Protection Agency, Environmental Sciences Research Laboratory; EPA 

report no. EPA-600/4-76-025. Available from: NTIS, Springfield, VA; 

PB-240125. 

Pitts, J. N., Jr.; Winer, A. M.; Darnall, K. R.; Lloyd, A. C.; Doyle, G. J. 

(1977) Hydrocarbon reactivity and the role of hydrocarbons, oxides of 

nitrogen, and aged smog in the production of photochemical oxidants. In: 

Dimitriades, B., ed. International conference on photochemical oxidant 

pol1ution and its control; September 1976; Raleigh, NC. Proceedings: v. 

II. Research Triangle Park, NC: U.S. Environmental Protection Agency; 

EPA-600/3-77-001b. 

Reiter, E. R. (1963) A case study of radioactive fallout. J. Appl. Meteorol. 

2: 691-705. 

Reiter, E. R. (1975) Stratospheric-tropospheric exchange processes. Rev. 

Geophys. Space Phys. 13: 459-473. 

Reiter, E. R.; Mahlman, J. D. (1965) Heavy radioactive fallout over the southern 

United States, November 1962. JGR J. Geophys. Res. 70: 4501-4519. 

Richards, L. W.; Anderson, J. A.; Blumenthal, D. L.; McDonald, J. A.; Kok, G. 

L.; Lazrus, A. L. (1983) Hydrogen peroxide and sulfur (IV) in Los Angeles 

cloud water. Atmos. Environ. 17: 911-914. 

1-174 
References for Properties, Chemistry, Transport (cont'd.) 

Richter, H. G. (1983) Analysis of organic compound data gathered during 1980 

in northeast corridor cities. Research Triangle Park, NC: U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards; 

EPA report no. EPA-450/4-83-017. Available from: NTIS, Springfield, VA; 

PB84-116052. 

Robinson, E. (1952) Some air pollution aspects of the Los Angeles temperature 

inversion. Buil. Am. Meteorol. Soc. 33: 247-250. 

Scheutzle, D.; Rasmussen, R. A. (1978) The molecuiar composition of secondary 

aerosol particles formed from terpenes. J. Air Pollut. Control Assoc. 

28: 236-240. 

Schwartz, S. E. (1984) Gas-aqueous reactions of sulfur and nitrogen oxides in 

liquid-water clouds. In: Calvert, J. G., ed., S0 2 , NO and NO2 Oxidation 

Mechamisms: Atmospheric Considerations, Chapter 4. Ann Arbor Science 

Publishers, Acid Precipitation Series, v. 3. Boston, MA: Butterworth 

Publishers, pp. 173-208. 

Seila, R. L. (1981) Nonurban hydrocarbon concentrations in ambient air north 

of Houston, TX. In: Bufalini, J. J.; Arnts, R. R., eds. Atmospheric 

biogenic hydrocarbons. Ann Arbor, MI: Ann Arbor Science Publishers, 

Inc. 

Sexton, K. (1982) Evidence of an additive effect for small city plumes. Presented at: the 75th annual meeting of the Air Pollution Control Association; June; New Orleans, LA. Pittsburgh, PA: Air Pollution Control Association; paper no. 82-31.4. 

Sexton, K.; Westberg, H. (1980) Elevated ozone concentrations measured downwind 

of the Chicago-Gary urban complex. J. Air Pollut. Control Assoc. 30: 

911-914. 

Sexton, K.; Westberg, H. (1984) Nonmethane hydrocarbon composition of urban 

and rural atmospheres. Atmos. Environ.: in press. 

Shreffler, J. H.; Evans, R. B. (1982) The surface ozone record from the 

regionai air poilution study, 1975-1976. Atmos. Environ. 16: 1311-1321. 

Si ngh, H. B. ; Ludwi g, F. L. ; Johnson, W. B. (1977) Ozone i n cl ean remote 

atmospheres: Concentrations and variabilities. SRI Project 5661. Menlo 

Park, CA: Stanford Research Institute (SRI). 

Singh, H. B.; Viezee, W.; Johnson, W. B.; Ludwig, F. L. (1980) The impact of 

stratospheric ozone on tropospheric air quality. J. Air Pollut. Control 

Assoc. 30: 1009-1017. 

Slade, D., H., ed. (1968) Meteorology and atomic energy 1968. Washington, DC: 

U.S. Atomic Energy Commission. Available from: NTIS, Springfield, VA; 

TID-24190. 

1-175 
References for Properties, Chemistry, Transport (cont'd.) 

Stephens, E. R. (1967) The formation of molecular oxygen by alkaline hydrolysis 

of peroxyacetyl nitrate. Atmos. Environ. 1: 19-20. 

Tiao, G. C. ; Box, G. E. P. ; Hamming, W. J. (1975) Analysis of Los Angeles 

photochemical smog data: a statistical overview. J. Air Pollut. Control 

Assoc. 25: 260-268. 

Tuazon, E. C.; Winer, A. M.; Pitts, J. N., Jr. (1981) Trace pollutant concentrations in a multiday smog episode in the California South Coast Air 

Basin by long-pathlength Fourier-transform infrared spectroscopy. Environ. 

Sci. Technol. 15: 1232-1237. 

U.S. Environmental Protection Agency (1977) Uses, limitations and technical 

basis of procedures for quantifying relationships between photochemical 

oxidants and precursors. Research Triangle Park, NC: Office of Air Quality 

Planning and Standards. Report no. EPA-450/2-77-021a. 

U.S. Environmental Protection Agency (1978) Air quality criteria for ozone 

and other photochemical oxidants. Research Triangle Park, NC: U.S. 

Environmental Protection Agency, Environmental Criteria and Assessment 

Office; pp. 116-135; EPA report no. EPA-600/8-78-004. Available from: 

NTIS, Springfield, VA; PB80-124753. 

U.S. Environmental Protection Agency (1980a) Procedures for the preparation 

of emission inventories for volatile organic compounds: v. 1. 2nd ed. 

Research Triangle Park, NC: U.S. Environmental Protection Agency; EPA 

report no. EPA-450/2-77-028. Available from: NTIS, Springfield, VA; 

PB-275292. 

U.S. Environmental Protection Agency (1980b) Final emission inventory requirements for 1982 ozone state implementation plans. Research Triangle 

Park, NC: U.S. Environmental Protection Agency; EPA report no. EPA-450/ 

4-80-016. Available from: NTIS, Springfield, VA; PB81-060434. 

U.S. Environmental Protection Agency (1982) Air quality criteria for oxides 

of nitrogen. Research Triangle Park, NC: U.S. Environmental Protection 

Agency; EPA-600/8-82-026. Available from: NTIS, Springfield, VA; 

PB83-131011. 

U.S. Environmental Protection Agency (1984) National air pollutant emission 

estimates, 1940-1983. Research Triangle Park, NC: U.S. Environmental 

Protection Agency. EPA-450/4-84-028. 

U.S. Environmental Protection Agency (1986) National air pollutant emission 

estimates, 1940-1984. Research Triangle Park, NC: U.S. Environmental 

Protection Agency. Report no. EPA-450/4-85-014. 

Vaughan, W. M.; Chan, M.; Cantrell, B.; Pooler, F. (1982) A study of persistent 

elevated pollution episodes in the Northeastern United States. Bull. Am. 

Meteorol. Soc. 63: 258-266. 

1-176 
References for Properties, Chemistry, Transport (cont'd.) 

Viezee, W.; Singh, H. B. (1982) Contribution of stratospheric ozone to ground 

level ozone concentrations -- a scientific review of existing evidence. 

Final report (revised draft). EPA grant CR 809330010. Menlo Park, CA: 

SRI International. 

Viezee, W.; Johnson, W. B.; Singh, H. B. (1979) Airborne measurements of 

stratospheric ozone intrusions into the troposphere over the United States: 

final report. Atlanta, GA: Coordinating Research Council; SRI project 6690. 

Viezee, W.; Johnson, W. B.; Singh, H. B. (1983) Stratospheric ozone in the lower 

troposphere-II. Assessment of downward flux and ground-level impact. Atmos. 

Environ. 17: 1979-1993. 

Wallington, T. J.; Atkinson, R.; Winer, A. M. (1984) Rate constants for the 

gas phase reaction of OH radicals with peroxyacetyl nitrate (PAN) at 273 

and 296 K. Geophys. Res. Lett. 11: 861-864. 

Weast, R. C., ed. (1977) CRC handbook of.chemistry and physics. 57th ed. Boca 

Raton, FL: CRC Press; p. D-194. 

Westberg, H.; Lamb, B. (1983) Ozone production and transport in the Atlanta, 

GA, region. Final report; EPA•grant no. CR 809221. Research Triangle 

Park, NC: U.S. Environmental Protection Agency, Atmospheric Sciences 

Research Laboratory. 

Westberg, H.; Sexton, K.; Roberts, E. (1981) Transport of pollutants along the 

western shore of Lake Michigan. J. Air Pollut. Control Assoc. 31: 385-388. 

Whitten, G. Z. (1983) The chemistry of smog formation: a review of current 

knowledge. Environ. Int. 9: 447-463. 

Whitten, G. Z.; Hogo, H. (1977) Mathematical modeling of simulated photochemical 

smog. Research Triangie Park, NC: U.S. Environmental Protection Agency. 

Report no. EPA-600/3-77-011. 

Whitten, G. Z.; Hogo, H. (1978) User's manual for kinetics model and ozone 

isopleth plotting package. Research Triangle Park, NC: U.S. Environmental 

Protection Agency; EPA report no. EPA-600/8-78-014a. 

Winer, A. M.; Breuer, G. M.; Carter, W. P. L.; Darnall, K. R.; Pitts, J. N., 

Jr. (1979) Effects of ultraviolet spectral distribution on the photochemistry of simulated polluted atmospheres. Atmos. Environ. 13: 989-998. 

Winer, A. M.; Atkinson, R.; Pitts, J. N., Jr. (1984) Gaseous nitrate radical: 

possible nighttime atmospheric sink for biogenic organic compounds. 

Science (Washington, DC) 224: 156-159. 

Wolff, G. T.; Lioy, P. J. (1978) An empirical model for forecasting maximum 

daily ozone levels in the northeastern U.S. J. Air Pollut. Control Assoc. 

28: 1034-1038. 

1-177 
References for Properties, Chemistry, Transport (cont'd.) 

Wolff, G. T.; Lioy, P. J. (1980) Development of an ozone river associated with 

synoptic-scale episodes in the eastern United States. Environ. Sci. 

Technol. 14: 1257-1260. 

Wol ff, G. T. ; Li oy, P. J. ; Meyers , R. E. ; Cederwal l, R. T. ; Wi ght, G. D. ; 

Pasceri, R. E.; Taylor, R. S. (1977a) Anatomy of two ozone transport 

episodes in the Washington, D.C., to Boston, Mass., corridor. Environ. 

Sci. Technol. 11: 506-510. 

Wolff, G. T.; Lioy, P. J.; Wight, G. D.; Pasceri, R. E. (1977b) Aerial i nvestigation of the ozone plume phenomenon. J. Air Pollut. Control Assoc. 

27: 460-463. 

Wolff, G. T.; Ferman, M. A.; Monson, P. R. (1979) The distribution of beryllium-7 within high-pressure systems in the eastern United States. Geophys. 

Res. Lett. 6: 637-639. (See also "Correction," Geophys. Res. Lett. 6: 816, 

1979.) 

Wolff, G. T.; Kelly, N. A.; Ferman, M. A. (1982) Source regions of summertime 

ozone and haze episodes in the eastern United States. Water, Air, Soil 

Pollut. 18: 65-81. 

1.12.3 References for Sampling and Measurement of Ozone and Other Photochemical 

Oxidants and Their Precursors 

A11en, A. 0.; Hochanadel, C. J.; Ghormley, J. A.; Davis, T. W. (1952) Decomposition of water and aqueous solutions under mixed fast neutron and 

gamma-radiation. J. Phys. Chem. 56: 575-586. 

Altshuller, A. P.; McPherson, S. P. (1963) Spectrophotometric ana1ysis of 

aldehydes in the Los Angeles atmosphere. J. Air Pollut. Control Assoc. 

13: 109-111. 

Andreae, W. A. (1955) A sensitive method for the estimation of hydrogen peroxide 

in biological materials. Nature (London) 175: 859-860. 

Armstrong, W. A.; Humphreys, W. G. (1965) A L.E.T. independent dosimeter based 

on the chemiluminescent determination of H 2 O 2 . Can. J. Chem. 43: 2576-2584. 

Bass, A. M.; Ledford, A. E., Jr.; Whittaker, J. K. (1977) Ultraviolet photometer 

for ozone calibration. In: Dimitriades, B., ed. International conference 

on photochemical oxidant pollution and its control; September 1976; 

Raleigh, NC. Proceedings: v. I. Research Triangle Park, NC: U.S. Environmental Protection Agency; pp. 13-17; EPA report no. EPA-600/3-77-001a. 

Available from: NTIS, Springfield, VA; PB-264232. 

Bowman, L. D.; Horak, R. F. (1972) A continuous ultraviolet absorption ozone 

photometer. Anal. Instrum. 10: 103-108. 

1-178 
References for Sampling and Measurement (cont'd.) 

Brewer, A. W.; Milford, J. R. (1960) The Oxford-Kew ozone sonde. Proc. R. Soc. 

London Ser. A 256: 470-495. 

Bruckmann, P. W.; Willner, H. (1983) Infrared spectroscopic study of peroxyacetyl nitrate (PAN) and its decomposition products. Environ. Sci. Technol. 

17: 352-357. 

Bufalini, J. J.; Brubaker, K. L. (1969) Symposium on chemical reactions in 

urban atmospheres; October. Warren, MI: General Motors Research Laboratories. 

Bufalini, J. J.; Gay, B. W., Jr.; Brubaker, K. L. (1972) Hydrogen peroxide 

formation from formaldehyde photooxidation and its presence in urban 

atmospheres. Environ. Sci. Technol. 6: 816-821. 

Burton, C. S.; Bekowies, P. J.; Poilack, R. I.; Connell, P. (1976) Oxidant/ 

ozone ambient measurement methods: an assessment and evaluation. San 

Rafael, CA: Systems Applications, Inc.; EF76-111R. 

Caiifornia Air Resources Board. (1976) A study of the effect of atmospheric 

humidity on analytical oxidant measurement methods. Presented at: 15th 

conference [on] methods in air pollution studies; January; Long Beach, 

CA. Berkeley, CA: California Air Resources Board, Air and Industrial 

Hygiene Laboratory. 

California Air Resources Board. (1978) California air quality data: JulyAugust-September. 10(13): 2-3. Available from: Technical Service Div., 

California Air Resources Board, Sacramento, CA. 

Chameides, W.L.; Tan, A. (1981). The two-demensionai diagnostic model for 

tropospheric OH: An uncertainty analysis. J. Geophys. Res. 86: 5209- 

5223. 

Chock, D. P.; Kumar, S.; Herrmann, R. W. (1982) An analysis of trends in 

oxidant air quality in the South Coast Air Basin of California. Atmos. 

Environ. 16: 2615-2624. 

Cohen, I. R.; Purcell, T. C.; Altshuller, A. P. (1967) Analysis of the oxidant 

in photooxidation reactions. Environ. Sci. Technol. 1: 247-252. 

Darley, E. F.; Kettner, K. A.; Stephens, E. R. (1963) Analysis of peroxyacyl 

nitrates by gas chromatography with electron capture detection. Anal. 

Chem. 35: 589-591. 

Das, T.N.; Moorthy, P.N.; Rao, K.N. (1982). Chemiluminescent method for the 

determination of low concentrations of hydrogen peroxide. J. Indian 

Chem. Soc. 59: 85-89. 

Das, T.N.; Moorthy, P.N.; Rao, K.N. (1983). Chemiluminescent measurement of 

hydrogen peroxide in the Bombay area. Atmos. Environ. 17: 79-82. 

1-179 
References for Sampling and Measurement (cont'd.) 

Dasgupta, P. K. (1980a) Discussion on "The importance of atmospheric ozone and 

hydrogen peroxide in oxidizing sulphur dioxide in cloud and rainwater [on 

Penkett et al., 1979]." Atmos. Environ. 14: 272-275. 

Dasgupta, P. K. (1980b) The importance of atmospheric ozone and hydrogen 

peroxide in oxidizing sulfur dioxide in cloud and rainwater--further 

discussion [on Penkett et al., 1979]. Atmos. Environ. 14: 620-621. 

Dasgupta, P. K.; Hwang, H. (1985) Application of a nested loop system for 

the flow injection analysis of trace aqueous peroxide. Anal. Chem. In 

press. 

Demerjian, K. L.; Kerr, J. A.; Calvert, J. G. (1974) The mechanism of photochemical smog formation. In: Pitts, J. N. , Jr. ; Metcalf, R. L. , eds. 

Advances in environmental science and technology: v. 4. New York, NY: 

John Wiley and Sons, Inc.; pp. 1-262. 

DeMore, W. B.; Patapoff, M. (1976) Comparison of ozo.ne determinations by 

ultraviolet photometry and gas-phase titration. ~ nviron. Sci. Technol. 

10: 897-899. 1 

DeMore, W. B.; Romanovsky, J. C.; Feldstein, M.; Hamming, W. J.; Mueller, P. 

K. (1976) Interagency comparison of iodometric methods for ozone determination. In: Calibration in air monitoring: a symposium; August 1975; 

Boulder, C0. Philadelphia, PA: American Society for Testing and Materials; 

pp. 131-143; ASTM special technical publication 598. 

Dietz, W. A. (1967) Response factors for gas chromatographic analyses. J. Gas 

Chromatogr. 5: 68-71. 

F. R. (1971, April 30) 36: 8186-8201. National primary and secondary air 

quality standards. 

F.R. (1975, February 18) 40: 7042-7070. Ambient air monitoring reference and 

equivalent methods. 

F.R. (1976, December 1) 41: 52686-52692. National primary and secondary ambient 

air quality standards: nitrogen dioxide measurement principle and calibration procedure. 

F.R. (1979, February 8) 44: 8221-8233. Calibration of ozone reference methods. 

Flamm, D. L. (1977) Analysis of ozone at low concentrations with boric acid 

buffered KI. Environ. Sci. Technol. 11: 978-983. 

Fontijn, A.; Sabadell, A. J.; Ronco, R. J. (1970) Homogeneous chemiluminescent 

measurement of nitric oxide with ozone: implications for continuous 

selective monitoring of gaseous air pollutants. Anal. Chem. 42: 575-579. 

Fried, A.; Hodgeson, J. (1982) Laser photoacoustic detection of nitrogen 

dioxide in the gas-phase titration of nitric oxide with ozone. Anal. 

Chem. 54: 278-282. 

1-180 
References for Sampling and Measurement (cont'd.) 

Gay, B. W., Jr.; Bufalini, J. J. (1972a) Hydrogen*peroxide in the urban atmosphere. I.n: Gould, R. F., ed., Photochemical smog and ozone reactions. 

Washington, DC: American Chemical Society; pp. 225-263. (Advances in 

chemistry series: 113.) 

0 

Gay, B. W., Jr.; Bufalini, J. J. (1972b) Hydrogen peroxide in the urban atmosphere. Environ. Lett. 3: 21-24. 

Gay, B. W.; Noonan, R. C.; Bufalini, J. J.; Hanst, P. L. (1976) Photochemical 

synthesis of peroxyacyl nitrates in gas phase via chlorine-aldehyde 

reaction. Environ. Sci. Technol. 10: 82-85. 

Grosjean, D. (1983) Distribution of atmospheric nitrogenous pollutants at a 

Los Angeles area smog receptor site. Environ. Sci. Technol. 17: 13-19. 

Grosjean, D.; Fung, K.; Collins, J.; Harrison, J.; Breitung, E. (1984) Portable 

generator for on-site calibration of peroxyacetyl nitrate analyzers. 

Anal. Chem. 56: 569-573. 

Hanst, P. L.; Wong, N. W.; Bragin, J. (1982) A long-path infrared study of Los 

Angeles smog. Atmos. Environ. 16: 969-981. 

Hauser, T. R.; Cummins, R. L. (1964) Increasing sensitivity of 3-methyl-2- 

benzothiazolone,hydrazone test for anaiysis of aliphatic aldehydes in air. 

Anal. Chem. 36: 679-681. 

Heikes, B.G. (1984) Aqueous H 2 O 2 production from 0 3 in glass impingers. 

Atmos. Environ. 18: 1433-1445. 

Heikes, B. G.; Lazrus, A. L.; Kok, G. L.; Kunen, S. M.; Gandrud, B. W.; Gitlin, 

' S. N.; Sperry, P. D. (1982) Evidence for aqueous phase hydrogen peroxide 

synthesis in the troposphere. JGR J. Geophys. Res. 87: 3045-3051. 

Hendry, D. G.; Kenley, R. A. (1977) Generation of peroxy radicals from peroxy 

nitrates (R0 2 NO2 ). Decomposition of peroxyacyl nitrates. Atmos. Environ. 

99: 3198-3199. 

Hodgeson, J. A.; Krost, K. J.; 0'Keeffe, A. E.; Stevens, R. K. (1970) Chemiluminescent measurement of atmospheric ozone: response characteristics 

and operating variables. Anal. Chem. 42: 1795-1802. 

Hodgeson, J. A.; Stevens, R. K.; Martin, B. E..(1972) A stable ozone source 

applicable as a secondary standard for calibration of atmospheric monitors. 

ISA Trans. 11: 161-167. 

Hodgeson, J. A.; Hughes, E. E.; Schmidt, W. P.; Bass, A. M. (1977) Methodology 

for standardization of atmospheric ozone measurements. In: Dimitriades, 

B., ed. International conference on photochemical oxidant pollution and 

its control; September 1976; Raleigh, NC. Proceedings: v. I. Research 

Triangle Park, NC: U.S. Environmental Protection Agency; pp. 3-12; EPA 

report no. EPA-600I3-77-001a. Available from: NTIS, Springfield, VA; 

PB-264232. 

1-181 
References for Sampling and Measurement (cont'd.) 

Holdren, M. W.; Spicer, C. W. (1984) Field compatible calibration procedure 

for peroxyacetyl nitrate. Environ. Sci. Technol. 18: 113-116. 

Hughes, E. E. (1975) Development of standard reference materials for air 

quality measurement. ISA Trans. 14: 281-291. 

Jayanty, R. K. M.; Blackard, A.; McElroy, F. F.; McClenny, W. A. (1982) 

Laboratory evaluation of nonmethane organic carbon determination in 

ambient air by cryogenic preconcentration and flame ionization detection. 

Research Triangle Park, NC: U.S. Environmental Protection Agency; EPA 

report no. EPA-600/4-82-019. Available from: NTIS, Springfield, VA; 

PB82-224965. 

Johnson, D. F.; Kok, G. L.; Sonner, R. J. (1981) Improved chromatographic acid 

technique for the determination of formaldehyde. In: Grosjean, D.; Kok, 

G. L., eds. Interlaboratory comparison study of inethods for measuring 

formaldehyde and other aldehydes in ambient air: final report. Atlanta, 

GA: Coordinating Research Council. 

Joshi, S. B.; Bufalini, J. J. (1978) Halocarbon interferences in chemiluminescent measurements of NO x . Environ: Sci. Technol. 12: 597-599. 

Katz, M. (1976) Nitrogen compounds and oxidants. In: Stern, A. C., ed. Air 

pollution; v. III. measurement, monitoring and surveillance of air pollution. 3rd ed. New York, NY: Academic Press; pp. 259-305. 

Kok, G. L.; Darnall, K. R.; Winer, A. M.; Pitts, J. N., Jr.; Gay, B. W., Jr. 

(1978a) Ambient air measurements of hydrogen peroxide in the California 

South Coast Air Basin. Environ. Sci. Technol. 12: 1077-1080. 

Kok, G. L.; Holler, T. P.; Lopez, M. B.; Nachtrieb, H. A.; Yuan, M. (1978b) 

Chemiluminescent method for determination of hydrogen peroxide in the 

ambient atmosphere. Environ. Sci. Tech.nol. 12: 1072-1076. 

Kravetz, T. M.; Martin, S. W.; Mendenhall, G. D. (1980) Synthesis of peroxyacetyl and peroxyaroyl nitrates: complexion of peroxyaeetyl nitrate with 

benzene. Environ. Sci. Technol. 14: 1262-1264. 

Kunen, S. M.; Lazrus, A. L.; Kok, G. L.; Heikes, B. G. (1983) Aqueous oxidation of S02 by hydrogen peroxides. JGR J. Geophys. Res. 88: 3671-3674. 

Kuntz, R.; Lonneman, W.; Namie, G:; Hull, L. A. (1980) Rapid determi nati on of 

aldehydes in air analyses. Anal. Lett. 13: 1409-1415. 

Lipari, F.; Swarin, S. (1982) Determination of formaldehyde and other aldehydes 

in automobile exhaust with an improved 2,4-dinitrophenylhydrazine method. 

J. Chromatogr. 247: 297-306. 

Littman, F. E.; Benoliel, R. W. (1953) Continuous oxidant recorder. Anal. 

Chem. 25: 1480-1483. 

1-182 
References for Samplinq and Measurement (cont'd.) 

Logan, J.A.; Prather, M.J.; Wofsy, S.C.; McElroy, M.B. (1981) Tropospheric 

chemistry: A global perspective. J. Geophys. Res. 86: 7210-7254. 

Lonneman, W. A.; Bufalini, J. J.; Namie, G. R. (1982) Calibration procedure 

for PAN based on its thermal decomposition in the presence of nitric 

oxide. Environ. Sci. Technol. 16: 655-660. 

Maeda, Y.; Aoki, K.; Munemori, M. (1980) Chemiluminescence method for the 

determination of nitrogen dioxide. Anal. Chem. 52: 307-311. 

Martin, L. R.; Damschen, D. E. (1981) Aqueous oxidation of sulfur dioxide by 

hydrogen peroxide at low pH. Atmos. Environ. 15: 1615-1621. 

Mast, G. M.; Saunders, H. E. (1962) Research and development of the instrumentation of ozone sensing. ISA Trans. 1: 325-328. 

McClenny, W. A.; Pleil, J. D.; Holdren, M. W.; Smith, R. N. (1984) Automated 

cryogenic preconcentration and gas chromatographic determination of 

volatile organic compounds in air. Anal. Chem. 56: 2947-2951. 

McElroy, F. F. (1979) Transfer standards for the calibration of ambient air 

monitoring analyzers for ozone: technicai assistance document. Research 

Triangle Park, NC: U.S. Environmental Protection Agency, Environmental 

Monitoring and Support Laboratory; EPA report no. EPA-600/4-79-056. 

Available from: NTIS, Springfield, VA; PB-146871. 

McElroy, F. F.; Thompson, V. L. (1975) Hydrocarbon measurement discrepancies 

among various analyzers. using flame-ionization detectors. Research 

Triangle Park, NC: U.S. Environmental Protection Agency, Environmental 

Monitoring and Support Laboratory; EPA report no. EPA-600/4-75-010. 

Mottola, H. A.; Simpson, B. E.; Gorin, G. (1970) Absorptiometric determination 

of hydrogen peroxide in s.ubmicrogram amounts with leuco crystal violet 

and peroxidase as catalyst. Anal. Chem. 42: 410-411. 

National Research Council (1977) Ozone and other photochemical oxidants. 

Washington, DC: National Academy of Sciences; pp. 45-125 and chapters 

4 and 6. 

Nederbragt, G. W.; van der Horst, A.; van Duijn, J. (1965) Rapid ozone determination near an accelerator. Nature (London) 206: 87. 

Nicksic, S. W.; Harkins, J.; Mueller, P. K. (1967) Some analyses for PAN and 

studies of its structure. Atmos. Environ. 1: 11-18. 

Nielsen, T.; Hansen, A. M.; Thomsen, E. L. (1982) A convenient method for preparation of pure standards of peroxyacetyl nitrate for atmospheric analyses. 

Atmos. Environ. 16: 2447-2450. 

1-183 
References for Sampling and Measurement (cont'd.) 

Ogle, L. D.; Hall, R. C.; Crow, W. L.; Jones, A. E.; Gise, J. P. (1982) Development of preconcentration and chromatographic procedures for the continuous and unattended monitoring of hydrocarbons in ambient air. Presented 

at: 184th national meeting of the American Chemical Society; September; 

Kansas City, M0. Austin, TX: Radian Corporation. 

0'Keeffe, A. E.; Ortman, G. C. (1966) Primary standards for trace gas analysis. 

Anal. Chem. 38: 760-763. 

Osman, M.; Hill, H. H.; Holdren, M. W.; Westberg, H. H. (1979) Vapor-phase 

silylation of alcohols for air analysis. In: Zlatkis, A., ed. Advances 

in chromatography, chromatography symposium; Houston, TX. 

Overton, J. H., Jr.; Durham, J. L. (1982) Acidification of rain in the presence 

of SOZ , H2 O2i 03 , and HNO3 . In: Keith, L. H., ed. Energy and environmental 

chemistry, v. 2: acid rain. Ann Arbor, MI: Ann Arbor Science; pp.=245-262. 

Paur, R. J.; McElroy, F. F. (1979) Technical assistance document for the 

calibration of ambient ozone monitors. Research Triangle Park, NC: U.S. 

Environmental Protection Agency, Environmental Monitoring and Support 

Laboratory; EPA final report no. EPA-600/4-79-057. Available from: NTIS, 

Springfield, VA; PB80-149552. 

Penkett, S. A.; Jones, B. M. R.; Brice, K. A.; Eggleton, A. E. J. (1979) The 

importance of atmospheric ozone and hydrogen peroxide in oxidising sulphur 

dioxide in cloud and rainwater. Atmos. Environ. 13: 123-137. 

Perschke, H.; Broda, E. (1961) Determination of very small amounts of hydrogen 

peroxide. Nature (London) 190: 257-258. 

Reckner, L. R. (1974) Survey of users of EPA Reference Method for measurement 

of non-methane hydrocarbon in ambient air. Research Triangle Park, NC: 

U.S. Environmental Protection Agency, Of.fice of Research and Development; 

EPA report no. EPA-650/4-75-008. Available from: NTIS, Springfield, VA; 

PB-247515. 

Regener, V. H. (1960) On a sensitive method for the recording of atmospheric 

ozone. JGR J. Geophys. Res. 65: 3975-3977. 

Regener, V. H. (1964) Measurement of atmospheric ozone with the chemiluminescent method. JGR J. Geophys. Res. 69: 3795-3800. 

Rehme, K.A.; Martin, B.E.; Hodgeson, J.A. (1974) Tentative method for the 

calibration of nitric oxide, nitrogen dioxide, and ozone analyzers by gas 

phase titration. U.S. Environmental Protection Agency, Research Triangle 

Park, N.C. EPA-R2-73-246. 

Rehme, K. A. ; Puzak, J. C. ; Beard, M. E. ; Smi th, C. F. ; Paur, R. J. (1981) 

Evaluation of ozone calibration procedures. Research Triangle Park, NC: 

U.S. Environmental Protection Agency, Environmental Monitoring Systems 

Laboratory; EPA final report no. EPA-600/4-80-050. Available from: NTIS, 

Springfield, VA; PB81-118911. 

1-184 
References for Sampling and Measurement (cont'd.) 

Richter, H. G. (1983) Analysis of organic compound data gathered during 1980 

in northeast corridor cities. Research Triangle Park, NC: U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards; 

EPA report no. EPA-450/4-83-017. Available from: NTIS, Springfield, VA; 

PB84-116052. 

Sawicki, E.; Hauser, T. R.; Stanley, T. W.; Elbert, W. (1961) The 3-methyl-2- 

benzothiazolone hydrazone test: sensitive new methods for the detection, 

rapid estimation, and determination of aliphatic aldehydes. Anal. Chem. 

33: 93-96. 

Scaringelli, F. P.; Rosenberg, P. E.; Rehme, K. A. (1970) Comparison of permeation devices and nitrite ion as standards for the colorimetric determination of nitrogen dioxide. Environ. Sci. Technol. 4: 924-929. 

Schiff, H. (1985) York University, Toronto, Canada. Personal communication: 

work in progress. 

Sevcik, J. (1975) Detectors in gas chromatography. Prague, Czechosiovakia: 

Elsevier Scientific Publishing Company. 

Sexton, F. W. ; McEI roy, F. F. ; Mi chi e, R. M. , Jr. ; Thompson, V. L. (1982) A 

comparative evaluation of seven automated ambient non-methane organic 

compound analyzers. Research Triangle Park, NC: U.S. Environmental 

Protection Agency; EPA report no. EPA-600/4-82-046. Available from: NTIS, 

Springfield, VA; PB82-230798. 

Singh, H. B.; Salas, L. J. (1983a) Peroxyacetyl nitrate in the free troposphere. 

Nature (London) 302: 326-328. 

~ 

Singh, H. B.; Salas, L. J. (1983b) Methodology for the analysis of peroxyacetyl 

nitrate (PAN) in the unpolluted atmosphere. Atmos. Environ. 17: 1507-1516. 

Stephens, E. R. (1964) Absorptivities for infrared determination of peroxyacyl 

nitrates. Anal. Chem. 36: 928-929. 

Stephens, E. R. (1969) The formation, reactions, and properties of peroxyacyl 

nitrates (PANs) in photochemical air pollution. In: Pitts, J. N., Jr.; 

Metcalf, R. L., eds. Advances in environmental sciences v. 1. New York, 

NY: Wiley-Interscience; pp. 119-146. 

Stephens, E. R.; Burleson, F. R.; Cardiff, E. A. (1965) The production of pure 

peroxyacyl nitrates. J. Air Pollut. Control Assoc. 15: 87-89. 

Stevens, R. K.; Hodgeson, J. A. (1973) Applications of chemiluminescent reactions to the measurement of air pollutants. Anal. Chem. 45: 443A-446A, 

449A. 

Stevens, R. K.; Clark, T. A.; Decker, C. E.; Ballard, L. F. (1972a) Field performance of advanced monitors for oxides of nitrogen, ozone, sulfur 

dioxide, carbon monoxide, methane and nonmethane hydrocarbons. Presented 

at: 65th annual meeting of the Air Pollution Control Association; June; 

Miami, FL. Pittsburgh, PA: Air Pollution Control Association. 

1-185 
References for Sampling and Measurement (cont'd.) 

Stevens, R. K.; Hodgeson, J. A.; Ballard,1. F.; Decker, C. E. (1972b) Ratio 

of sulfur dioxide to total gaseous sulfur compounds and ozone to total 

oxidants in the Los Angeles atmosphere - an instrument evaluation study. 

In: Mamantov, G.; Shults, W. D., eds. Determination of air quality: 

proceedings of the ACS symposium on determination of air quality; April 

1971; Los Angeles, CA. New York, NY: Plenum Press; pp. 83-108. 

Tokiwa, Y.; Twiss, S.; de Vera, E. R.; Mueller, P. K. (1972) Atmospheric ozone 

determination by amperometry and colorimetry. In: Mamantov, G.; Shults, 

W. D., eds. Determination of air quality: proceedings of the ACS symposium 

on determination of air quality; April 1971; Los Ange1es, CA. New York, 

NY: Plenum Press; pp. 109-130. 

Tuazon, E. C.; Graham, R. A.; Winer, A. M.; Easton, R. R.; Pitts, J. N., Jr. 

Hanst, P. L. (1978) A kilometer pathlength Fourier-transform infrared 

system for the study of trace pollutants in ambient and synthetic atmospheres. Atmos. Environ. 12: 865-875. 

Tuazon, E. C.; Winer, A. M.; Graham, R. A.; Pitts, J. N., Jr. (1980) Atmospheric measurements of trace pollutants by kilometer-pathlength FTIR 

spectroscopy. Adv. Environ. Sci. Technol. 10: 259-300. 

Tuazon, E. C.; Winer, A. M.; Graham, R. A.; Pitts, J. N., Jr. (1981a) Atmospheric measurements of trace pollutants: long path Fourier-transform 

infrared spectroscopy. Research Triangle Park, NC: U.S. Environmental 

Protection Agency; EPA report no. EPA-600/3-81-026. Available from: NTIS, 

Springfield, VA; PB81-179848. 

Tuazon, E. C.; Winer, A. M.; Pitts, J. N., Jr. (1981b) Trace pollutant concentrations in a multiday smog episode in the California South Coast Air 

Basin by long path length Fourier transform infrared spectroscopy. 

Environ. Sci. Technol. 15: 1232-1237. 

U.S. Environmental Protection Agency. (1975) Technical assistance document for 

the chemiluminescence measurement of nitrogen dioxide. Research Triangle 

Park, NC: U.S. Environmental Protection Agency; EPA report no. EPA-600/ 

4-75-003. Available from: NTIS, Springfield, VA. 

U.S. Environmental Protection Agency. (1977a) Air monitoring strategy for 

state implementation plans. Research Triangle Park, NC: Office of Air 

Quality Planning and Standards, Standing Air Monitoring Group; EPA report 

no. EPA-450/2-77-010. Available from: NTIS, Springfield, VA; PB-274014. 

U.S. Environmental Protection Agency. (1977b) Quality assurance,handbook for 

air pollution measurement systems, volume II: ambient air specific methods. 

Research Triangle Park, NC: U.S. Environmental Protection Agency; EPA 

report no. EPA-600/4-77-027. Available from: NTIS, Springfield, VA; 

PB-273518. 

1-186 
References for Sampling and Measurement (cont'd.) 

U.S. Environmental Protection Agency. (1978) Air quality criteria for ozone 

and other photochemical oxidants. Research Triangle Park, NC: U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office; 

pp. 116-135; EPA report no. EPA-600/8-78-004. Available from: NTIS, 

Springfield, VA; PB80-124753. 

U.S. Environmental Protection Agency. (1981) Technical assistance document 

for the calibration and operation of automated ambient non-methane organic 

compound analyzers. Research Triangle Park, NC: U.S. Environmental 

Protection Agency; EPA report no. EPA-600/4-81-015. Available from: NTIS, 

Springfield, VA; PB82-147406. 

U.S. Environmental Protection Agency. (1982) Air quality criteria for oxides 

of nitrogen. ResearchTriangle Park, NC: Environmental Criteria and 

Assessment Office; EPA report no. EPA-600/8-82-026. Available from: NTIS, 

Springfield, VA; PB83-131011. 

Wendel, G. J.; Stedman, D. H.; Cantreil, C. A. (1983) Luminol-based nitrogen 

dioxide detector. Anal. Chem. 55: 937-940. 

Westberg, H. H.; Holdren, M. W.; Hill, H. H. (1980) Analytical methodology for 

the identification and quantification of vapor phase organic pollutants. 

New York, NY: Coordinating Research Council; CRC-APRAC project no. CAPA11-71. 

Winer, A. M.; Peters, J. M.; Smith, J. P.; Pitts, J. N.,.Jr. (1974) Response 

of commercial chemiluminescent NO-NO 2 analyzers to other.nitrogen-containing 

compounds. Environ. Sci. Technol. 8: 1118-1121. 

Yoshizumi, K.; Aoki, K.; Nouchi, I. Okita, T.; Kobayashi, T. Kamakura, S. 

Tajima, M. (1984) Measurement of the concentration in rainwater and of 

the Henry's Law constant of hydrogen peroxide. Atmos. Environ. 18:395-401. 

Zaitsu, K.; Okhura, Y. (1980) New fluorogenic substrates for horseradish peroxidase: rapid and sensitive assays for hydrogen peroxide and peroxidase. 

Anal. Biochem. 109: 109-113. 

Zika, R. G.; Saltzman, E. S. (1982) Interaction of ozone and hydrogen peroxide 

in water: implications for .anaiysis of H 2 O 2 in air. Geophys. Res. Lett. 

9: 231-234. 

1.12.4 References for Coracentrations of Ozone and Other Photochemical Oxidants 

in Ambient Air 

Altshuller, A. P. (1983) Measurements of the products of atmospheric photochemical reactions in iaboratory studies and in ambient air--relationships between ozone and other products. Atmos. Environ. 17: 2383-2427. 

1-187 
References for Ambient Air Concentrations (cont'd. 

Berk, J. V.; Young, R. A.; Brown, S. R.; Hollowell, C. D. (1981) Impact of 

energy-conserving retrofits on indoor air quality in residential housing. 

Presented at: 74th annual meeting of the Air Pollution Control Assocciation; June; Philadelphia, PA. Pittsburgh, PA: Air Pollution Control 

Association; paper no. 81-22.1 

Cleveland, W. S.; Graedel, T. E.; Kleiner, B. (1976a) Photoch,emical air pollution: transport from the New York City area into Connecticut and Massachusetts. Science (Washington, DC) 191: 179-181. 

Cleveland, W. S.; Guarino, R.; Kleiner, B.; McRae, J. E.; Warner, J. L. (1976b) 

The analysis of the ozone problem in the northeast United States. In: 

Specialty Conference on: Ozone/oxidants--interactions with the total 

environment. Pittsburgh, PA: Air Pollution Control Association; pp. 

109-120. 

Coffey, P. E. ; Stasi uk, W. N. ; Mohnen, V. (1977) Ozone i n rural and urban 

areas of New York State. In: Dimitriades, B., ed. International conference 

on photochemical oxidant pollution and its control. Proceedings: v. I. 

Research Triangle Park, NC: U.S. Environmental Protection Agency, Office 

of Research and Development; pp. 89-96; EPA report no. EPA-600/3-77-001a. 

Available from: NTIS, Springfield, VA; PB-624232. 

Contant, C. F.; Gehan, B. M.; Stock, T. H.; Holguin, A. H.; Buffler, P. A. 

(1985) Estimation of individual ozone exposures using microenvironment 

measurements. In: APCA Specialty Conference: Scientific Basis for the 

Ozone Standard, Houston, TX, November 28-December 1, 1984. Pittsburgh; 

APCA. In Press. 

Darley, E. F.; Kettner, K. A.; Stephens, E. R. (1963) Analysis of peroxyacyl 

nitrates by gas chromatography with electron capture detection. Anal. 

Chem. 35: 589-591. 

Davies, T. D.; Ramer, B.; Kaspyzok, G.; Delany, A. C. (1984) Indoor/outdoor 

ozone concentrations at a contemporary art gallery. J. Air Pollut. Control 

Assoc. 31: 135-137. 

Evans, G. F. (1985) The National Air Pollution Background Network: final project 

report. Research Triangle Park, NC: U.S. Environmental Protection Agency, 

Office of Research and Development; EPA report no. EPA-600/4-85-038. 

Available from: NTIS, Springfield, VA; PB85-212413. 

Evans, G.; Finkelstein, P.; Martin, B.; Possiel, N.; Graves, M. (1983). Ozone 

measurements from a network of remote sites. J. Air Pollut. Control 

Assoc. 33: 291-296. 

Galbally, I. E.; Roy, C. R. (1980) Destruction of ozone at the earth's surface. 

Quart. J. R. Met. Soc. 106: 599-620. 

.. 
References for Ambient Air Concentrations (cont'd.') 

Grosjean, D. (1981) Critical evaluation and comparison of ineasurement methods 

for nitrogenous compounds in the atmosphere. Final report, A 706-05, for 

Coordinating Research Council. Environmental Research and Technology. 

Westiake Viliage, CA. 

Grosjean, D. (1983) Distribution of atmospheric nitrogenous pollutants at a 

Los Angeles area smog receptor site. Environ. Sci. Technol. 17: 13-19. 

Hanst, P. L.; Wong, N. W.; Bragin, J. (1982) A long path infrared study of Los 

Angeles smog. Atmos. Environ, 16: 969-981. 

Heikes, B. G.; Lazrus, A. L.; Kok, G. L.; Kunen, S. M.; Gandrud, B. W.; Gitlin, 

S. N.; Sperry, P. D. (1982) Evidence of aqueous phase hydrogen peroxide 

synthesis in the troposphere. JGR J. Geophys. Res. 87: 3045-3051. 

Jorgen, R. T.; Meyer, R. A.; Hughes; R. A. (1978) Routine peroxyacetyl nitrate 

(PAN) monitoring applied to the Houston Area Oxidant Study. Presented at: 

71st annual meeting of the Air Pollution Control Association; June; 

Houston, TX. Pittsburgh, PA: Air Pollution Control Association; paper no. 

78-50.1. 

Kelly, N. A.; Ferman, M. A.; Wolff, G. T. (1986) The chemical and meteorological 

conditions associated with high and low ozone concentrations in southeastern Michigan and nearby areas of Ontario. J. Air Pollut. Control Assoc. 

36: 150-158. 

Lefohn, A. S. (1984) A comparison of ambient ozone exposures for selected 

nonurban sites. Proceedings of 77th Annual Meeting of the Air Pollution 

Control Association. Vol. 6. Paper no. 84-104.1. Pittsburgh, PA: Air 

Pollution Control Assoc. 

Lefohn, A. S.; Benedict, H. M. (1985) Exposure considerations associated with 

characterizing ozone ambient air quality monitoring data. In: Proceedings 

of the APCA Specialty Conference: Evaluation of the Scientific Basis for 

Ozone/Oxidants Standards, Houston, TX, November 28-30, 1984. Pittsburgh, 

PA: Air Pollution Control Assoc. 

Lewis, T. E.; Brennan, E.; Lonneman, W. A. (1983) PAN concentrations in ambient 

air in New Jersey. J. Air Pollut. Control Assoc. 33: 885-887. 

Logan, J. A.; Prather, M. J.; Wofsy, S. C.; McElroy, M. B. (1981) Tropospheric 

chemistry: a global perspective. JGR J. Geophys. Res. 86: 7210-7254. 

Lonneman, W. A.; Bufalini, J. J.; Seila, R. L. (1976) PAN and. oxidant measurement in ambient atmospheres. Environ. Sci. Technol. 10: 374-380. 

Martinez, J. R.; Singh, H. B. (1979) Survey of the role of NOx in nonurban 

ozone formation. Research Triangle Park, NC: prepared by SRI International 

for U.S. Environmental Protection Agency. EPA report no. EPA-450/4-79-035. 

Available from: NTIS, Springfield, VA; PB80-122815. 

1-189 
References for Ambient Air Concentrations (cont'd. 

Mayrsohn, H.; Brooks, C. (1965) The analysis of PAN by electron capture gas 

chromatography. Presented at: Western regional meeting of the American 

Chemical Society; November; Los Angeles, CA. Los Angeles, CA: California 

State Department of Public Health. 

Miller, P. R.; McCutchan, M. H.; Ryan, B. C. (1972) Influence of climate and 

topography on oxidant air pollution concentrations that damage conifer 

forests in southern California. Mitt. Forst. Bundesversuchsanst. Wien 

97: 585-607. 

Mohnen, V. A. (1977) Review and analysis. In: International Conference on 

Oxidants, 1976 -- Analysis of evidence and viewpoints. Part III. The issue 

of stratospheric ozone intrusion. U.S. Environmental Protection Agency, 

Research Triangle Park, NC; Report no. EPA-600/3-77-115. 

Oltmans, S. J. (1981) Surface ozone measurements in clean air. J. Geophys. Res. 

86: 1174-1180. Cited in: Logan et al., 1981. 

Peterson, G. A.; Sabersky, R. H. (1975) Measurements of pollutants inside an 

automobile. J. Air Pollut. Control Assoc. 25: 1028-1032. 

Pratt, G. C.; Hendrickson, R. C.; Chevone, B. I.; Christopherson, D. A.; 

0'Brien, M. V.; Krupa, S. V. (1983) Ozone and oxides of nitrogen in the 

rural upper-midwestern U.S.A. Atmos. Environ. 17: 2013-2023. 

Reiter, E. R. (1977) Review and analysis. In: International Conference on 

Oxidants 1976 -- Analysis of evidence and viewpoints. Part III. The issue 

of stratospheric ozone intrusion. U.S. Environmental Protection Agency, 

Research Triangle Park, NC; Report no. EPA-600/3-77-115. 

Renzetti, N. A.; Bryan, R. J. (1961) Atmospheric sampling for aldehydes and 

eye irritation in Los Angeles smog - 1960. J. Air Pollut. Control Assoc. 

11: 421-424. 

Sabersl4Y, R. H. ; Sinema, D. A. ; Shair, F. H. (1973) Concentrations, decay 

rates, and removal of ozone and their relation to establishing clean 

indoor air. Environ. Sci. Technol. 1: 347-353. 

SAROAD, Storage and Retrieval of Aerometric Data [data base]. (1985a) Data 

file for 1976. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

SAROAD, Storage and Retrieval of Aerometric Data [data base]. (1985b) Data 

file for 1979. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

SAROAD, Storage and Retrieval of.Aerometric Data [data base]. (1985c) Data 

file for 1980. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

1-190 
References for Ambient Air Concentrations (cont'd.) 

SAROAD, Storage and Retrieval of Aerometric Data [data base]. (1985d) Data 

file for 1981. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

SAROAD, Storage and Retrieval of Aerometric Data [data base]. (1985e) Data 

file for 1982. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

SAROAD, Storage and Retrievai of Aerometric Data [data base]. (1985f) Data 

file for 1983. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards. Disc; ASCII. 

Seiler, W.; Fishman, J. (1981) The distribution of carbon monoxide and ozone 

in the free troposphere. JGR J. Geophys. Res. 86: 7255-7265. 

Singh, H. B.; Salas, L. J.; Smith, A. J.; Sh4geishi, H. (1981) Measurements of 

some potentially hazardous organic chemicals in urban environments. 

Atmos. Environ. 15: 601-612. 

Singh, H. B., Salas, L. J.; Stiles, R.; Shigeishi, H. (1982) Measurements of 

hazardous organic chemicals in the ambient atmosphere. Research Triangle 

Park, NC: U.S. Environmental Protection Agency, Environmental Sciences 

Research Laboratory. EPA report no. EPA-600/3-83-002. Available from: 

NTIS, Springfield, VA; PB83-156935. 

Smith, W. J. (1981) New York State air monitoring data report for the Northeast 

Corridor Regional Modeling Project (NECRMP). Aibany, NY:. New York State 

Department of Environment and Conservation. 

Spicer, C. W.; Gemma, J. L; Joseph, D. W.; Sticksel, P. R.; Ward, G. F. (1976) 

The transport of oxidant beyond urban areas. Columbus, OH: Battelle 

Columbus Laboratories; EPA report no. EPA-600/3-76-018a. Available from: 

NTIS, Springfield, VA; PB-253736. 

Stock, T. H. ; Hol gui n, A. H. ; Selwyn, B. J. ; Hsi , B. P. ; Contant, C. F. ; 

Buffler, P. A.; Kotchmar, D. J. (1983). Exposure estimates for the Houston 

area asthma and runners studies. In: Lee, S. D.; Mustafa, M: G.; Mehlman, 

M. A. eds. Adv. Modern Environ. Toxicol. Vol. V. International Symposium 

on the Biomedical Effects of Ozone and Related Photochemical Oxidants. 

Pinehurst, NC; March 14=18, 1982. Princeton, NJ: Princeton Scientific 

Publishers, Inc. 

Temple, P. J.; Taylor, 0. C. (1983) World-wide ambient measurements of peroxyacetyl nitrate (PAN) and implications for plant injury. Atmos. Environ. 

17: 1583-1587. 

Thompson, C. R.; Hensel, E. G.; Kats, G. (1973) Outdoor-indoor levels of six 

air pollutants. J. Air Pollut. Control Assoc. 23: 881-886. 

1-191 
References for Ambient Air Concentrations (cont'd.) 

Tuazon, E. C.; Winer, A. M.; Graham, R. A.; Pitts, J. N., Jr. (1981a) Atmospheric measurements of trace pollutants: long path Fourier transform 

infrared spectroscopy. Research Triangle Park, NC: U.S. Environmental 

Protection Agency, Environmental Sciences Research Laboratory. Available 

from: NTIS, Springfield, VA; PB81-179848. 

Tuazon, E. C.; Winer, A. M.; Pitts, J. N., Jr. (1981b) Trace pollutant concentrations in a multiday smog episode in the California South Coast Air 

Basin by long path length Fourier transform infrared.spectrometry. Environ. 

Sci. Technol. 15: 1232-1237. 

U.S. Department of Commerce, Bureau of the Census (1982) Statistical Abstract 

of the United States, 1982-1983. 103rd Ed. Washington, DC. 

U.S. Environmental Protection Agency (1978) Air quality criteria for ozone 

and other photochemical oxidants. Research Triangle Park, NC: U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office; 

EPA report no. EPA-600/8-78-004. Available from: NTIS, Springfield, VA; 

PB80-124 753. 

U.S. Environmental Protection Agency (1980) Air quality data--1979 annual 

statistics. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards; EPA report no. 

EPA-450/4-80-014. 

U.S. Environmental Protection Agency (1981) Air quality data--1980 annual 

statistics. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards;- EPA report no. 

EPA-450/4-81-027. 

U.S. Environmental Protection Agency (1982) Air quality data--1981 annual 

statistics. Research Triangle Park, NC: U.S. Environmental Protection 

Agency, Office of Air Quality Planning and Standards; EPA report no. 

EPA-450/4-82-007. 

U.S. Environmental Protection Agency (1984) National air quality and emission 

trends report, 1983. Research Triangle Park, NC: U.S. Environmental 

Protection Agency, Office of Air Quality Planning and Standards. EPA 

report no. EPA-450/4-84-029. 

U.S. Environmental Protection Agency (1986) National air quality and emissions 

trends report, 1984. Research Triangle Park, NC: U.S. Environmental 

Protection Agency, Office of Air Quality Planning and Standards. EPA 

report no. EPA-450/4-86-001. 

Viezee, W.; Johnson, W. B.; Singh, H. B. (1979) Airborne measurements of 

stratospheric ozone intrusions into the troposphere over the United 

States. Final report. SRI Proj. 6690, CRC-APRAC Proj. no. CAPA-15-76 

(1-77), Coordinating Research Council, Atlanta, GA. 

1-192 
Westberg, H.; Allwine, K.; Robinson, E. (1978) Measurement of light hydrocarbons and oxidant transport: Houston area 1976. Research Triangle Park, 

NC: U.S. Environmental Protection Agency, Office of Research and Development; EPA report no. EPA-600/3-78-662. Available from: NTIS, Springfield, 

VA; PB-285891. 

Wolff, G. T. ; Stasiuk, W. N. ; Coffey, P. E. ; Pasceri , R. E. (1975) Aerial 

ozone measurements over New Jersey, New York, and Connecticut. Presented 

at the 68th Annual Meeting of the Air Pollution Contro,l Association, 

Boston, MA: June. Pittsburgh, PA: Air Pollution Control Association. 

Paper no. 75-58.6. 

Wolff, G. T.; Lioy, P. J.; Tayior, R. S. (1986) The diurnal variations of ozone 

at different altitudes on a rural mountain in the eastern United States. 

J. Air Pollut. Control Assoc. 36: (In Press) 

1.12.5 References for Effects of Ozone and Other Photochemical Oxidants on 

Vegetation 

Adams, R. M.; Crocker, T. D. (1984) Economically relevant response estimation 

and the value of information: acid deposition. In: Crocker, T. D., ed. 

Economic perspectives on acid deposition control. Boston, MA: Butterworth 

Publishers; pp. 35-64. (Teasley, J. I., ed. Acid precipitation series -v. 

8.) 

Adams, R. M.; McCarl, B. A. (1985) Assessing the benefits of alternative 

oxidant standards on agriculture: the role of response infor.mation. J. 

Environ. Econ. Manage.: in press. 

Adams, R. M.; Crocker, R. M.; Katz, R. W. (1984a) The adequacy of natural 

science information in economic assessments of pollution control.: a 

Bayesian methodology. Rev. Econ. Stat. 66: 568-575. 

Adams, R. M.; Hamilton, S. A.; McCarl, B. A. (1984b) The economic effects of 

ozone on agriculture. Corvallis., OR: U.S. Environmental Protection Agency; 

EPA report no. EPA-600/3-84-090. Available from: NTIS, Springfield, VA; 

PB85-168441/XAB. 

Adams, R. M.; Crocker, T. D.; Thanavibulchai, N. (1982) An economic assessment 

of air pollution damages to selected annual crops in southern California.. 

J. Environ. Econ. Manage. 9: 42-58. 

Adedipe, N. 0.; Ormrod, D. P. (1974)' 0zone induced growth suppression in 

radish plants in relation to pre- and post-fumigation'temperatures. Z. 

Pflanzenphysiol. 71: 281-287. 

Adedipe, N. 0.; Barrett, R. E_; Ormrod, D. P. (1972) Phytotoxicity and growth 

responses of ornamental bedding plants to ozone and sulfur dioxide. J. 

Am. Soc. Hortic. Sci. 97: 341-345. 

Amiro, B. D.; Gillespie, T. J.; Thurtell, G. W. (1984) Injury response of 

Phaseolus vulgaris to ozone flux density. Atmos. Environ. 18: 1207-1215. 

1-193 
References for Vegetation Effects (cont'd.) 

Ashmore, M. R. (1984) Effects of ozone on vegetation in the United Kingdom. 

Proceedings of the OECD workshop on ozone; Gothenburg, Sweden. 

Benedict, H. M.; Miller, C. J.; Olson, R. E. (1971) Economic impact of air 

pollutants on plants in the United States. Research Triangle Park, NC: 

U.S. Environmental Protection Agency; report no. APTD-0953. Available 

from: NTIS, Springfield, VA; PB-209265. 

Bennett, J. H. (1979) Foliar exchange of gases. In: Heck, W. W.; Krupa, S. V.; 

Linzon, S. N., eds. Methodology for the assessment of air pollution 

effects on vegetation: a handbook from a specialty conference; April 

1978; Minneapolis, MN. Pittsburgh, PA: Air Pollution Control Association; 

ch. 10. 

Bennett, J. H.; Hill, A. C. (1974) Acute inhibition of apparent photosynthesis. 

In: Dugger, J., ed. Air pollution effects on plant growth. Washington, 

DC: American Chemical Society. (ACS symposium series 3.) 

Bennett, J. P. ; Oshima, R. J. ; Lippert, L. F. (1979) Effects of ozone on 

injury and dry matter partitioning in pepper plants. Environ. Exp. Bot. 

19: 33-39. 

Benson, E. J.; Krupa, S.; Teng, P. S.; Welsch, P. E. (1982) Economic assessment of air pollution damages to agricultural and silvicultural crops. 

In: Minnesota final report to Minnesota Pollution Control Agency. St. Paul, 

MN: University of Minnesota. 

Bisessar, S. (1982) Effect of ozone, antioxidant protection, and early blight 

on potato in the field. J. Am. Soc. Hortic. Sci. 107: 597-599. 

Bisessar, S.; Palmer, K. T. (1984) Ozone, antioxidant spray and Meloidogyne 

hapla effects on tobacco. Atmos. Environ. 18: 1025-1027. 

Black, V. J.; Ormrod, D. P.; Unsworth, M. H. (1982) Effects of low concentration of ozone, singly, and in combination with sulphur dioxide on net 

photosynthesis rates of Vicia faba L. J. Exp. Bot. 33: 1302-1311. 

Blum, U. T.; Smith, G. R.; Fites, R. C. (1982) Effects of multiple 0 3 exposures on carbohydrate and mineral contents of Ladino clover. Environ. 

Exp. Bot. 22: 143-154. 

Clarke, B. B.; Henninger, M. R.; Brennan, E. (1983) An assessment of potato 

losses caused by oxidant air pollution in New Jersey. Phytopathology 

73: 104-108. 

Coyne, P. E.; Bingham, G. E. (1978) Photosynthesis and stomatal light responses 

in snap beans exposed to hydrogen sulfide in ozone. J. Air Pollut. Control 

Assoc. 28: 1119-1123. 

Davis, D. D. (1975) Resistance of young ponderosa pine seedlings to acute 

doses of PAN. Plant Dis. Rep. 59: 183-184. 

1-194 
References for Vegetation Effects (cont'd.) 

Davis, D. D. (1977) Response of ponderosa pine primary needles to separate and 

simultaneous ozone and PAN exposures. Plant Dis. Rep. 61: 640-644. 

Dochinger, L. S.; Townsend, A. M. (1979) Effects of roadside deicer salts and 

ozone on red maple progenies. Environ. Pollut. 19: 229-237. 

Duchelle, S. F.; Skelly, J. M.; Sharick, T. L.; Chevone, B. I.; Yang, Y.-S.; 

Nellessen, J. E. (1983) Effects of ozone on the productivity of natural 

vegetation in a high meadow of the Shenandoah National Park of Virginia. 

J. Environ. Manage. 17: 299-308. 

Elkiey, T.; Ormrod, D. P. (1981) Absorption of ozone, sulphur dioxide, and 

nitrogen dioxide by petunia plants. Environ. Exp. Bot. 21: 63-70. 

Ensing, J.; Hofstra, G. (1982) Impact of the tair pollutant ozone on acetylene 

reduction and shoot growth of red clover. Can. J. Plant Pathol. 4: 237-242. 

Feder, W. A. (1968) Reduction in tobacco pollen germination and tube elongation, 

induced by low levels of ozone. Science (Washington, DC) 160: 1122. 

Feder, W. A. ; Campbel l, F. J. (1968) Infl uence of 1 ow 1 evels of ozone on 

flowering of carnations. Phytopathology 58: 1038-1039. 

Flagler, R. B.; Youngner, V. B. (1982) Ozone and sulfur dioxide effects on 

tall fescue: I. Growth and yield responses. J. Environ. Qual. 11: 386-389. 

Foster, K. W.; Timm, H.; Labanauskas, C. K.; Oshima, R. J. (1983) Effects of 

ozone and sulfur dioxide on tuber yield and quality of potatoes. J. 

Environ. Qual. 12: 75-80. 

Fukuda, H.; Terakado, K. (1974) On the damage of plants due to peroxyacyl 

nitrates (PAN). Tokyo Nogyo Shikenjo Sokuho: 35-36 [English abstract]. 

Guderian, R. (1977) Discussion of the suitability of plant responses as a 

basis for air pollution control measures. In: Air pollution: phytotoxicity of acidic gases and its significance in air pollution control. Berlin, 

West Germany: Springer Verlag; pp. 75-97. (Ecological studies: analysis 

and synthesis v. 22). 

Heagle, A. S. (1982) Interactions between air pollutants and parasitic plant 

diseases. In: Unsworth, M. H.; Ormrod, D. P., eds. Effects of gaseous air 

pollution in agriculture and horticulture. London,_United Kingdom: 

Butterworth Scientific; pp. 333-348. 

Heagle, A. S.; Heck, W. W. (1974) Predisposition of tobacco to oxidant air 

pollution injury by a previous exposure to oxidants. Environ. Pollut. 

7: 247-251. 

Heagle, A. S.; Heck, W. W. (1980) Field methods to assess crop losses due to 

oxidant air pollutants. In: Teng, P. S.; Krupa, S. V., 7 eds. Crop loss 

assessment: proceedings of E. C. Stakman commemorative symposium. University of Minnesota, Agricultural Experimental Station; miscellaneous 

publication no. 7; pp. 296-305. 

1-195 
References for Vegetation Effects (cont'd.) 

Heagle, A. S.; Johnston, J. W. (1979) Variable responses of soybean to mixtures 

of ozone and sulfur dioxide. J. Air Pollut. Control Assoc. 29: 729-732. 

Heagle, A. S.; Body, D. E.; Pounds, E. K. (1972) Effect of ozone on yield of 

sweet corn. Phytopathology 62: 683-687. 

Heagle, A. S., Body, D. E.; Neely, G. E. (1974) Injury and yield responses of 

soybean to chronic doses of ozone and sulfur dioxide in the field. Phytopathology 64: 132-136. 

Heagle, A. S.; Philbeck, R. B.; Knott, W. M. (1979a) Thresholds for injury 

growth, and yield loss caused by ozone on field corn hybrids. Phytopathology 69: 21-26. 

Heagle, A. S.; Philbeck, R. B.; Letchworth, M. B. (1979b) Injury and yield 

response of spinach cultivars to chronic doses of ozone in open-top field 

chambers. J. Environ. Qual. 8: 368-273. 

Heagle, A. S.; Letchworth, M. B.; Mitchell, C. A. (1983a) Effects of growth 

medium and fertilizer rate on the yield response of soybeans exposed to 

chronic doses of ozone. Phytopathology 73: 134-139. 

Heagle, A. S.; Heck, W. W.; Rawlings, J. 0.; Philbeck, R. B. (1983b) Effects 

of chronic doses of ozone and sulfur dioxide on injury and yield of 

soybeans in open-top field chambers. Crop Sci. 23: 1184-1191. 

Heagle, A. S.; Cure, W. W.; Rawlings, J. 0. (1985) Response of turnips to 

chronic doses of ozone in open-top field chambers. Environ. Poll. 

(Series A) 38: 305-320. 

Heck, W. W.; Tingey, D. T. (1971) Ozone time-concentration model to predict 

acute foliar injury. In: Englund, H. M.; Beery, W. T., eds. Proceedings 

of the second international clean air congress; December 1970; Washington, 

DC. New York, NY: Academic Press; pp. 249-255. 

Heck, W. W.; Dunning, J. A.; Hindawi, I. J. (1966) Ozone: nonlinear relation 

of dose and injury to plants. Science (Washington, DC) 151: 511-515. 

Heck, W. W.; Taylor, 0. C.; Adams, R.; Bingham, G.; Miller, J.; Preston, E.; 

Weinstein, L. (1982) Assessment of crop loss from ozone. J. Air Pollut. 

Control Assoc. 32: 353-361. 

Heck, W. W. ; Adams, R. M. ; Cure, W. W. ; Heagle, A. S. ; Heggestad, H. E. ; 

Kohut, R. J. ; Kress, L. W. ; Rawlings, I. 0. ; Taylor, 0. C. (1983a) A 

reassessment of crop loss from ozone. Environ. Sci. Technol. 

17: 573A-581A. 

Heck, W. W.; Taylor, 0. C.; Adams, R. M.; Miller, J. E.; Weinstein, L. (1983b) 

National Crop Loss Assessment Network (NCLAN) 1982 Annual Report. Report 

to U.S. Environmental Protection Agency, Corvallis Environmental Research 

Laboratory, Corvallis, OR. 

1-196 
References for Vegetation Effects (cont'd.) 

Heck, W. W. ; Cure, W. W. ; Rawlings, J. 0. ; Zaragoza, L. J. ; Heagle, A. S. ; 

Heggestad, H. E.; Kohut, R. J.; Kress, L. W.; Temple, P. J.; (1984) 

Assessing impacts of ozone on agricultural crops: II. Crop yield functions 

and alternative exposure statistics. J. Air Pollut. Control Assoc. 34: 

810-817. 

Heggestad, H. E. (1973) Photochemical air pollution injury to potatoes in the 

Atlantic coastal states. Am. Potato J. 50: 315-328. 

Heggestad, H. E.; Bennett, J. H. (1981) Photochemical oxidants potentiate 

yield losses in snap beans attributable to sulfur dioxide. Science 

(Washington, DC) 213: 1008-1010. 

Henderson, W. R.; Reinert, R. A. (1979) Yield response of four fresh market 

tomato cul ti vars after acute ozone exposure i n the seedl i ng stage. J. 

Am. Soc. Hortic. Sci. 104: 754-759. 

Hoffman, G. J.; Maas, E. V.; Rawlins, S. L. (1975) Sal i ni ty-ozone interactive 

effects on alfalfa yield and water relations. J. Environ. Qual. 

4: 326-331. 

Hofstra, G.; Littlejohns, D. A.; Wukasch, R. T. (1978) The efficacy of the 

antioxidant ethylene-diurea (EDU) compared to carboxin and benomyl in 

reducing yield losses from ozone in navy, bean. Plant. Dis. Rep. 

62: 350-352. 

Hogsett, W. E.; Tingey, D. T.; Holman, S. R. (1985) A programmable exposure 

control system for determination of the effects of pollutant exposure 

regimes on plant growth. Atmos. Environ. 19: 1135-1145. 

Horsman, D. C.; Nicholls, A. 0.; Calder, D. M. (1980) Growth responses of 

Dactylis glomerata, Loliumep renne and Phalaris aquatica to chronic ozone 

exposure. Aust. J. Plant Physiol. 7: 511-517. 

Howell, R. K.; Rose, L. P., Jr. (1980) Residual air pollution effects on soybean seed quality. Plant Dis. 64: 385-386. 

Howell, R. K.; Koch, E. J.; Rose, L. P., Jr. (1979) Field assessment of air 

pollution-induced soybean yield losses. Agron. J. 71: 285-288. 

Howitt, R. E.; Grossard, T. E.; Adams, R. M. (1984a) Effects of alternative 

ozone levels and response data on economic assessments: The case of 

California corps. J. Air Pollut. Control Assoc. 34: 1122-1127. 

Howitt, R. E.; Gossard, T. E.; Adams, R. M. (1984b) Applied'Welfare Economics 

and Public Policy. New York: Prentice-Hall. 

Jacobson, J. S. (1977) The effects of photochemical oxidants on vegetation. 

In: Ozon und Begleitsubstanzen im photochemischen Smog. [Ozone and other 

substances in photochemical smog]: VDI colloquium; 1976; Dusseldorf, 

West Germany. Dusseldorf, West Germany: Verein deutscher Ingenieure 

(VDI) GmbH; pp. 163-173. (VDI-Berichte no. 270). 

I a Ujl 
References for Vegetation Effects (cont'd.) 

Jacobson, J. S. (1982) Ozone and the growth and productivity of agricultural 

crops. In: Unsworth, M. H.; Ormrod, D. P., eds. Effects of gaseous air 

pollution in agriculture and horticulture. London, United Kingdom: 

Butterworth Scientific; pp. 293-304. 

Jacobson, J. S.; Colavito, L. J. (1976) The combined effect of sulfur dioxide 

and ozone on bean and tobacco plants. Environ. Exp. Bot. 16: 277-285. 

James, R. L. ; Cobb, F. W. , Jr. ; Mi l ler, P. R. ; Parmeter, J. R. , Jr. (1980) 

Effects of oxidant air pollution on susceptibility of pine roots to 

Fomes annosus. Phytopathology 70: 560-563. 

Johnston, J. W., Jr.; Heagle, A. S. (1982) Response of chronically ozonated 

soybean plants to an acute ozone exposure. Phytopathology 72: 387-389. 

Kopp, R. J.; Vaughan, W. J.; Hazilla, M. (1984) Agricultural sector benefits 

analysis for ozone: methods evaluation and demonstration. Research 

Triangle Park, NC: U.S. Enviornmental Protection Agency, Office of Air 

Quality Planning and Standards; EPA report no. EPA-450/5-84-003. 

Available from: NTIS, Springfield, VA; PB85-119477/XAB. 

Kress, L. W.; Miller, J. E. (1983) Impact of ozone on soybean yield. J. Environ. 

Qual. 12: 276-281. 

Kress, L. W.; Skelly, J. M. (1982) Response of several eastern forest tree 

species to chronic doses of ozone and nitrogen dioxide. Plant Dis. 

66: 1149-1152. 

Kress, L. W. , Mi 11 er, J. E. ; Smith, H. J. (1985) Impact of ozone on wi nter 

wheat yield. Environ. Exp. Bot. 25: 211-228. 

Larsen, R. I.; Heck, W. W. (1976) An air quality data analysis system for 

interrelating effects, standards, and needed source reductions: Part 3. 

Vegetation injury. J. Air Pollut. Control Assoc. 26: 325-333. 

Larsen, R. I. ; Heck, W. W. (1984) An ai r qual i ty data analysi s system for 

interrelating effects, standards, and needed source reductions: Part 8. 

An effective mean 0 3 crop reduction mathematical model. J. Air Pollut. 

Control Assoc. 34: 1023-1034. 

Larsen, R. I.; Heagle, A. S.; Heck, W. W. (1983) An air quality data analysis 

system for interrelating effects, standards, and needed source reductions: 

Part 7. An 03-S02 leaf injury mathematical model. J. Air Pollut. Control 

Assoc. 33: 198-207. 

Laurence, J. A. (1981) Effects of air pollutants on plant-pathogen interactions. 

Z. Pflanzenkr. Pflanzenschutz 87: 156-172. 

Lefohn, A. S.; Benedict, H. M. (1982) Development of a mathematical index that 

describes ozone concentration, frequency, and duration. Atmos. Environ. 

16: 2529-2532. 

1-198 
I ~ i • References for Vegetation Effects (cont'd.) 

Lefohn, A. S.; Tingey, D. T. (1984) The co-occurrence of potentiaily phytotoxic 

concentrations of various gaseous air pollutants. Atmos. Environ: in 

press. 

Legassicke, B. C.; Ormrod, D. P. (1981) Suppression of ozone-injury on tomatoes 

by ethylene diurea in controlled environments and in the field. HortScience 

16: 183-184. 

Leung, S. K.; Reed, W.; Geng, S. (1982) Estimations of ozone damage to selected 

crops grown in southern California. J. Air Pollut. Control Assoc. 32: 

160-164. 

Loucks, 0. L.; Armentano, T. V. (1982) Estimating crop yieid effects from 

ambient air pollutants in the Ohio River Valley. J. Air Pollut. Controi 

Assoc. 32: 146-150. 

MacLean, D. C.; Schneider, P. E. (1976) Photochemical oxidants in Yonkers, New 

York: effects on yieid of bean and tomato. J. Environ. Qual. 5: 75-78. 

Male, L.; Preston, E.; Neely, G. (1983) Yield response curves of crops exposed 

to SOZtime series. Atmos. Environ. 17: 1589-1593. 

Mann, L. K.; McLaughlin, S. B.; Shriner, D. S. (1980) Seasonal physiological 

responses of white pine under chronic air pollution stress. Environ. Exp. 

Bot. 20: 99-105. 

Manning, W. J.; Feder, W. A.; Perkins, ~ T. (1970a) Ozone and •infection of 

geranium flowers byBotrytis cinerea . Phytopathology 60: 1302. 

Manning, W. J.; Feder, W. A.; Perkins, I. (1970b) Ozone injury increases 

infection of geranium leaves byBotrytis cinerea . Phytopathology 60: 669- 

670. 

Manning, W. J.; Feder, W. A.; Vardaro, P. M. (1974) Suppression of oxidant 

injury by benomyl: effects on yields of bean cultivars in field. J. 

Environ. Qual. 2: 1 - 3. 

McLaughlin, S. B.; Taylor, G. E. (1981) Relative humidity: important modifier 

of pollutant uptake by plants. Science (Washington, DC) 22: 167-169. 

McLaughl i n, S. B. ; Shri ner, D. S. ; McConathy, R. K. ; Mann, L. K. (1979) The 

effects of S0 2 dosage kinetics and exposure frequency on photosynthesis 

and transpiration of kidney beans ( Phaseolus vulgaris L.). Environ. Exp. 

Bot. 19: 179-191. 

Menser, H. A.; Heggestad, H. E. (1966) Ozone and sulfur dioxide synergism: 

injury to tobacco plants. Science (Washington, DC) 153: 424-425. 

Menser, H. A.; Street, 0. E. (1962) Effects of air pollution, nitrogen levels, 

supplemental irrigation, and plant spacing on weather fleck and leaf 

losses of Maryland tobacco. Tobacco 155: 192-196. 

1-199 
References for Vegetation Effects (cont'd.) 

Middleton, J. T.; Kendrick, J. B., Jr.; Schwalm, H. W. (1950) Injury to herbaceous plants by smog or air pollution. Plant Dis. Rep. 34: 245-252. 

Miller, P. R.; Taylor, 0. C.; Wilhour, R. G. (1982) Oxidant air pollution 

effects on a western coniferous forest ecosystem. Corvallis, OR: Corvallis 

Environmental Research Laboratory; EPA report no. EPA-600/D-82-276. 

Available from: NTIS, Springfield, VA; PB83-189308. 

Mjelde, J. W.; Adams, R. M.; Dixon, B. L.; Garcia, P. (1984) Using farmers' 

actions to measure crop loss due to air pollution. J. Air Pollut. Control 

Assoc. 31: 360-364. 

Mukammal, E. I. (1965) Ozone as a cause of tobacco injury. Agricultural 

Meteorology 2: 145-165. 

Mumford, R. A.; Lipke, H.; Laufer, D. A.; Feder, W. A. (1972) Ozone-induced 

changes in corn pollen. Environ. Sci. Technol. 6: 427-430. 

Musselman, R. C.; Oshima, R. J.; Gallavan, R. E. (1983) Significance of pollutant concentration distribution in the response of 'red kidney' beans to 

ozone. J. Am. Soc. Hortic. Sci. 108: 347-351. 

Neely, G. E.; Tingey, D. T.; Wilhour, R. G. (1977) Effects of ozone and sulfur 

dioxide singly and in combination on yield, quality and N-fixation of 

alfalfa. In: Dimitriades, B., ed. International conference on photochemical oxidant pollution and its control: proceedings, vo1ume II; September 

1976; Raleigh, NC. Research Triang1e Park, NC: U.S. Environmental Protection Agency, Office of Research and Development; pp. 663-673; EPA report 

no. EPA-600/3-77-0016b. Available from: NTIS, Springfield, VA; PB-264233. 

Nouchi , I. ; Mayumi , H.°; Yamazoe, F. (1984) Fo1 i ar i n j ury response of petuni a 

and kidney bean to simultaneous and alternate exposure to ozone and PAN. 

Atmos. Environ. 18: 453-460. 

Ogata, G.; Maas, E. V. (1973) Interactive effects of salinity and ozone on 

growth and yield of garden beet. J. Environ. Qual. 2: 518-520. 

Olszyk, D. M.; Tibbitts, T. W. (1981) Stomatal response and leaf injury of 

Pisum sativum L. with S0 2 and 03 exposures. Plant Physiol. 67: 539-544. 

Ormrod, D. P. (1982) Air pollutant interactions in mixtures. In: Unsworth, 

M. H.; Ormrod, D. P., eds. Effects of gaseous air pollution in agriculture 

and horticulture. London, United Kingdom: Butterworth Scientific; 

pp. 307-331. 

Oshima, R. J. (1973) Effect of ozone on a'commercial sweet corn variety. Plant 

Dis. Rep. 57: 719-723. 

Oshima, R. J. (1978) The impact of sulfur dioxide on vegetation: a sulfur 

dioxide-ozone response model. Sacramento, CA: California Air Resources 

Board; final report; agreement no. A6-162-30. 

1-200 
References for Vegetation Effects (cont'd.) 

Oshima, R. J.; Taylor, 0. C.; Braegelmann, P. K.; Baldwin, D. W. (1975) Effect 

of ozone on the yield and plant biomass of a commercial variety of tomato. 

J. Environ. Qual. 4: 463-464. 

Oshima, R. J.; Braegelmann, P. K.; Baldwin, D. W.; Van Way, V.; Taylor, 0. C. 

(1977a) Reduction of tomato fruit size and yield by ozone. J. Am. Soc. 

Hortic. Sci. 102: 289-293. 

Oshima, R. J.; Braegelmann, P. K.; Baldwin, D. W.; Van Way, V.; Taylor, 0. C. 

(1977b) Responses of five cultivars of fresh market tomato to ozone: a 

contrast of cultivar screening with foliar injury and yield. J. Am. Soc. 

Hortic. Sci. 102: 286-289. 

Oshima, R. J.; Bennett, J. P.; Braegelmann, P. K. (1978) Effect of ozone on 

growth and assimilate partitioning in parsley. J. Am. Soc. Hortic. Sci. 

103: 348-350. 

Oshima, R. J. ; Braegelmann, P. K. ; Flagler, R. B. ; Teso, R. R. (1979) The 

effects of ozone on the growth, yield, and partitioning of dry matter in 

cotton. J. Environ. Qual. 8: 474-479. 

Page, W. P.; Arbogast, G.; Fabian, R. G.; Ciecka, J. (1982) Estimation of 

economic losses to the agricultural sector from airborne residuals in the 

Ohio River Basin region. J. Air Pollut. Control Assoc. 32: 151-154. 

Patton, R. L. (1981) Effects of ozone and sulfur dioxide on height and stem 

specifi.c gravity of Po ulus hybrids. Broomall, PA: Northeastern Forest 

Experiment Station; FSRP-NE-471. Available from: NTIS, Springfield, VA; 

PB81-171274. 

Pell, E. J.; Pearson, N. S. (1983) Ozone-induced reduction in quantity of 

ribulose-1,5-biphosphate carboxylase in alfaifa foliage. Plant Physiol. 

73: 185-187. 

Pell, E. J.; Weissberger, W. C.; Speroni, J. J. (1980) Impact of ozone on 

quantity and quality of greenhouse-grown potato plants. Environ. Sci. 

Technol. 14: 568-571. 

Rawlings, J. 0.; Cure, W. W. (1985) The Weibull function as a dose-response 

model to describe ozone effects on crop yields. Crop Science (in press). 

Reich, P. B.; Amundson, R. G. (1984) Low level 0 andlor S0 2 exposure causes 

a linear decline in soybean yield. Environ. Oollut. (Series A) 34: 345-355. 

Reinert, R. A.; Nelson, P. V. (1979) Sensitivity and growth of twelve elatior 

begonia cultivars to ozone. HortScience 14: 747-748. 

Reinert, R. A.; Heagle, A. S.; Heck, W. W. (1975) Plant responses to pollutant 

combinations. Mudd, B.; Kozlowski, T. T., eds. Responses of plants to air 

pollution. New York, NY: Academic Press, Inc.; pp. 159-177. 

1-201 
References for Vegetation Effects (cont'd.) 

Rowe, R. P.; Chestnut, L. G.; Miller, C.; Adams, R. M.; Thresher, M.; 

Mason, H. 0.; Howitt, R. E.; Trijonis, J. (1984) Economic assessment of 

the effect of air pollution in the San Joaquin Valley: draft report to 

the Research' Division, California Air Resources Board. Boulder, C0: 

Energy and Resource Consultants, Inc. 

Runeckles, V. C.; Rosen, P. M. (1977) Effects of ambient ozone pretreatment on 

transpiration and susceptibility to ozone injury. Can. J. Bot. 55: 193-197. 

Ryan, J. W.; Loehman, E.; Lee, W.; Trondsen, E.; Bland, M.; Goen, R.; Ludwig, 

F.; Eger, T.; Eigsti, S.; Conley, D.; Cummings, R. (1981) An estimate of 

the nonhealth benefits of ineeting the secondary national ambient air 

quality standards: final report. Menlo Park, CA: SRI International; project no. 2094. 

Shannon, J. G.; Mulchi, C. L. (1974) Ozone damage to wheat varieties at 

anthesis. Crop Sci. 14: 335-337. 

Shriner, D. S.; Cure, W. W.; Heagle, A. S.; Heck, W. W.; Johnson, D. W.; 

Olson, R. J.; Skelly, J. M. (1982) An analysis of potential agriculture 

and forestry impacts of long-range transport air pollutants. Oak Ridge, 

TN: Oak Ridge National Laboratory; ORNL report no. 5910. 

Stan, H-J.; Schicker, S. (1982) Effect of repetitive ozone treatment on bean 

plants-stress ethylene production and leaf necrosis. Atmos. Environ. 

16: 2267-2270. 

Taylor, 0. C. (1969) Importance of peroxyacetyl nitrate (PAN) as a phytotoxic 

air pollutant. J. Air Pollut. Control Assoc. 19: 347-351. 

Taylor, 0. C. (1974) Air pollutant effects influenced by plant-environmental 

interaction. In: Dugger, W. M., ed. Air pollution effects on plant growth. 

ACS Symp. Ser. 3: 1-7. 

Taylor, 0. C.; Dugger, W. M.; Cardiff, E. A.; Darley, E. F. (1961) Interaction 

of light and atmospheric photochemical products ("smog") within plants. 

Nature (London) 192: 814-816. 

Taylor, 0. C.; Temple, P. J.; Thill, A. J. (1983) Growth and yield responses 

of selected crops to k,'peroxyacetyl nitrate. HortScience 18: 861-863. 

Temple, P. J.; Bisessar, S. (1979) Response of white bean to bacterial blight, 

ozone, and antioxidant protection in the field. Phytopathology 

69: 101-103. 

Thomas, M. D.; Hendricks, R. H.; Hill, G. R. (1950) Sulfur metabolism of plants: 

effects of sulfur dioxide on vegetation. Indust. Eng. Chem. 42: 2231-2235. 

Thompson, C. R.; Kats, G.; Cameron, J. W. (1976a) Effects of photochemical air 

pollutants on growth, yield, and ear characteristics of two sweet corn 

hybrids. J. Environ. Qual. 5: 410-412. 

1-202 
References for Vegetation Effects (cont'd.) 

Thompson, C. R.; Kats, G.; Pippen, E. L.; Isom, W. H. (1976b) Effect of photochemical air pollution on two varieties of alfalfa. Environ. Sci. Technol. 

10: 1237-1241. 

Tingey, D. T. (1977) Ozone-induced alterations in plant growth and metabolism. 

In: Dimitriades, B., ed. International conference on photochemical 

oxidant pollution and its control: proceedings, v. II; Research Triangle 

Park, NC: U.S. Environmental Protection Agency; pp. 601-609; Report no. 

EPA-600/3-77-00Ib. 

Tingey, D. T.; Reinert, R. A. (1975) The effect of ozone and sulfur dioxide 

singly and in combination on plant growth. Environ. Pollut. 9: 117-125. 

Tingey, D. T.; Taylor, G. E., Jr. (1982) Variation in plant response to 

ozone: a conceptual model of physiological events. In: Unsworth, M. H. 

Ormrod, D. P., eds. Effects of gaseous air pollution in agriculture and 

horticulture. London, United Kingdom: Butterworth Scientific; pp. 113-138. 

Tingey, D. T.; Heck, W. W.; Reinert, R. A. (1971a) Effect of low concentrations 

of ozone and sulfur dioxide on foliage, growth and yield of radish. J. Am. 

Soc. Hortic. Sci. 96: 369-371. 

Tingey, D. T. ; Thutt, G. L. ; Gumpertz, M. L. ; Hogsett, W. E. (1982) Plant 

water status influences ozone sensitivity of bean plants. Agric. Environ. 

7: 243-254. 

Tonneijck, A. E. G. (1984) Effects of peroxyacetyl nitrate (PAN) and ozone on 

some plant species. In: Proceedings of the OECD workshop on ozone; 

Gothenburg, Sweden. 

U.S. Environmental Protection Agency. (1978) Air quality criteria for ozone 

and other photochemical oxidants. Research Triangle Park, NC: U.S. 

Environmental Protection Agency, Environmental Criteria and Assessment 

Office; EPA report no. EPA-600/8-78-004. Avaiiable from: NTIS, Springfield, VA; PB80-124753. 

Walmsley, L.; Ashmore, M. L.; Bell, J. N. B. (1980) Adaptation of radish Raphanus 

sativus L. in response to continuous exposure to ozone. Environ. Pollut. 

23: 165-177. 

Wilhour, R. G.; Neely, G. E. (1977) Growth response of conifer seedlings to 

low ozone concentrations. In: Dimitriades, B., ed. International 

conference on photochemical oxidant pollution and its controi: proceedings, 

vol. II; January; Research Triangle Park, NC. Research Triangle Park, NC: 

U.S. Environmental Protection Agency; pp. 635-645; EPA report no. 

EPA-600/3-77-001b. Available from: NTIS, Springfield, VA; PB-264233. 

Wukasch, R. T.; Hofstra, G. (1977a) Ozone and Botrytis interactions in onionleaf dieback: open-top chamber studies. Phytopathoiogy 67: 1080-1084. 

1-203 
References for Vegetation Effects (cont'd.) 

Wukasch, R. T.; Hofstra, G. (1977b) Ozone and Botrytis spp. interaction in 

onion-leaf dieback: field studies. J. Am. Soc. Hortic. Sci. 102: 543-546. 

Yang, Y.-S.; Skelly, J. M.; Chevone, B. I.; Birch, J. B. (1983) Effects of 

long-term ozone exposure on photosynthesis and dark respiration of eastern 

white pine. Environ. Sci. Technol. 17: 371-373. 

1.12.6 References for Effects of Ozone on Natural Ecosystems and Their Components 

Adams, H. S.; Stephenson, S. L.; Blasing, T. J.; Duvick, D. N. (1985) Growthtrend declines of jspruce and fir in mid-Appalachian subalpine forests. 

Environ. and Exptl. Bot. 25: 315-325. 

Barnes, R. L. (1972) Effects of chronic exposure to ozone on photosynthesis 

and respiration of pines. Environ. Pollut. 3: 133-138. 

Benoit, L. F. ; Skelly, J. M. ; Moore, L. D. ; Dochinger, L. S. (1982) Radial 

growth reductions of Pinus strobus L. correlated with foliar ozone sensitivity as an indicator of ozone-induced losses in eastern forests. C.an. 

J. For. Res. 12: 673-678. 

Bormann, F. H. (1985) Air pollution and forests: an ecosystem perspective. 

BioScience 35: 434-441. 

Botkin, D. B.; Smith, W. H.; Carlson, R. W.; Smith, T. L. (1972) Effects of 

ozone on white pine saplings: variation in inhibition and recovery of net 

photosynthesis. Environ. Pollut. 3: 273-289. © 

Carlson, R. W. (1979) Reduction in the photosynthetic rate of Acer, Quercus, 

and Fraxinus species caused by sulfur dioxide and ozone. Environ. Pollut. 

18: 159-170. 

Cowling, E. B. (1985) Effects of air pollution on forests: Critical review 

discussion papers. J. Air Pollut. Control Assoc. 35: 916-919. 

Coyne, P. E.; Bingham, G. E. (1981) Comparative ozone dose response of gas 

exchange in a ponderosa pine stand exposed to long-term fumigations. J. 

Air Pollut. Control Assoc. 31: 38-41. 

Dahlsten, D. L.; Rowney, D. L. (1980) Influence of air pollution on population 

dynamics of forest insects and on tree mortality. In: Miller, P. R., ed. 

Proceedings of the symposium on effects of air pollutants on Mediterranean 

and temperate forest ecosystems; June; Riverside, CA. Berkeley, CA: U.S. 

Department of Agriculture; Forest Service general technical report no. 

PSW-43; pp. 125-130. Available.from: NTIS, Springfield, VA; PB81-133720. 

Dochinger, L. S.; Townsend, A. M. (1979) Effects of roadside deicer salts and 

ozone on red maple progenies. Environ. Pollut. 19: 229-237. 

1-204 
References for Ecosystem Effects (cont'd.) 

Duchelle, S. F.; Skelly, J. M.; Sharick, T. L.; Chevone, B. I.; Yang, Y.-S.; 

Nellessen, J. E. (1983) Effects of ozone on the productivity of natural 

vegetation in a high meadow of the Shenandoah National Park of Virginia. 

J. Environ. Manage. 17: 299-308. 

Ehrlich, P. R.; Mooney, H. A. (1983) Extinction, substitution, and ecosystem 

services. BioScience 33: 248-254. 

Hacskayio, E. (1972) Mycorrhizae: the ultimate in reciprocal parasitism? 

BioScience 22: 577-583. 

Hacskaylo, E. (1973) The Torrey symposium on current aspects of fungal development; IV. Dependence of mycorrhizal fungi on hosts. Bull. Torrey Bot. 

Club 100: 217-223. 

Hogsett, W. E.; Plocher, M.; Wildman, V.; Tingey, D. T.; Bennett, I. P. (1985) 

Growth response of two varieties of slash pine seedlings to chronic ozone 

exposures. Can. J. Bot. 63: 2369-2376. 

James, RA.; Cobb, F. W., Jr.; Wilcox, W. W.; Rowney, D. L. (1980) Effects of 

photochemical oxidant injury of ponderosa and Jeffrey pines on susceptibility of sapwood and freshly cut stumps to Fomes annosus. Phytopathology 

70: 704-708. 

Johnson, A. H.; Siccama, T. G. (1983) Acid deposition and forest decline. 

Environ. Sci'. Technol. 17: 294A-305A. 

Krause, G. H. M.; Prinz, B.; Jung, K. D. (1984) Forest effects in West Germany. 

In: Davis, D. D.; Millen, A. A.; Dochinger, L., eds. Air pollution and 

the productivity of the forest: proceedings of the symposium; October 

1983; Washington, DC. Arlington, VA: Izaak Walton League of America; pp. 

297-332. 

Kress, L. W.; Skelly, J. M. (1982) Response of several eastern forest tree 

species to chronic doses of ozone and nitrogen dioxide. Plant Dis. 66: 

1149-1152. 

Kress, L. W.; Skelly, J. M.; Hinkelmann, K.H. (1982) Growth impact of 0 3 , NO 2 , 

..and/or S0 2 on Platanus occidentalis. Agric. Environ. 7: 265-274. 

Laurence, J. A.; Weinstein, L. H. (1981) Effects of air pollutants on plant 

productivity. Annu. Rev. Phytopathol. 19: 257-271. 

Mahoney, M. J. (1982) An analysis of the potential effects of air pollutants 

emitted during coal combustion on yellow poplar and loblolly pine and 

influences on mycorrhizal associations of loblolly pine. Unpublished. 

Blacksburg, VA: Virginia Polytechnical Institute and State University; 

Ph.D. Thesis. 

Manion, P. D. (1985) Effects of air pollution on forests: Critical review discussion papers. J. Air Pollut. Control Assoc. 35: 919-922. 

1-205 
References for Ecosystem Effects (cont'd.) 

Mann, L. K.; McLaughlin, S. B.; Shriner, D. S. (1980) Seasonal physiological 

responses of white pine under chronic air pollution stress. Environ. Exp. 

Bot. 20: 99-105. 

McBride, J. R.; Semion, V.; Miller, P. R. (1975) Impact of air pollution on 

the growth of ponderosa pine. Calif. Agric. 29: 8-10. 

McCool, P. M.; Menge, J. A.; Taylor, 0. C. (1979) Effects of ozone and HC1 gas on 

the development of the mycorrhizal fungus Glomus fasciculatus and growth of 

'Troyer' citrange. J. Amer. Soc. Hort. Sci. 104: 151-154. 

McLaughlin, S. B.; McConathy, R. K.; Duvick, D.; Mann, L. K. (1982) Effects of 

chronic air pollution stress on photosynthesis, carbon allocation, and 

growth of white pine trees. For. Sci. 28: 60-70. 

Miller, P. L. (1973) Oxidant-induced community change in a mixed conifer 

forest. In: Naegele, J. A., ed. Air pollution damage to vegetation. 

Washington, DC: American Chemical Society; pp. 101-117. (Advances in 

chemistry series: no. 122.) 

Miller, P. R.; Elderman, M. J., eds. (1977) Photochemical oxidant air pollutant effects on a mixed conifer forest ecosystem: a progress report, 

1976. Corvallis, OR: U.S. Environmental Protection Agency; EPA report no. 

EPA-600/3-77-104. Available from: NTIS, Springfield, VA; PB-274531. 

Miller, P. R.; Parmeter, J. R., Jr.; Taylor, 0. C.; Cardiff, E. A. (1963) 

Ozone injury to the foliage of Pinus ponderosa. Phytopathology 53: 1072- 

1076. 

Mi 11 er, P. R. ; Parmeter, J. R. , Jr. ; F1 i ck, B. H. ; Marti nez, C. W. (1969) 

Ozone dosage response of ponderosa pine seedlings. J. Air Pollut. Control 

Assoc. 19: 435-438. 

Mi 11 er, P. R. ; Tayl or, 0. C. ; Wi 1 hour, R. G. (1982) Oxi dant ai r pol l uti on 

effects on a western coniferous forest ecosystem. Corvallis, OR: Corvallis 

Environmental Research Laboratory; EPA report no. EPA-600/D-82-276. 

Available from: NTIS, Springfield, VA; PB83-189308. 

Mooi, J. (1980) Influence of ozone on the growth of two poplar cultivars. 

Plant Dis. 64: 772-773. 

National Park Service. (1985) Testimony of the National Park Service before 

the Subcommittee on Parks and Recreation. Washington, D.C.: U.S. House 

of Representatives, Committee on Interior and Insular Affairs; 99th 

Congress, lst session. _ 

National Research Council. (1977) Ozone and other photochemical oxidants. 

Washington, D.C.: National Academy of Sciences; pp. 437-585. 

Odum, E. P. (1985) Trends expected in stressed ecosystems. BioScience. 

35: 419-422. 

1-206 
References for Ecosystem Effects (cont'd.) 

Parmeter, J. R. , Jr. ; Bega, R. V. ; Neff, T. (1962) A chlorotic decl ine of 

ponderosa pine in southern California. Plant Dis. Rep. 46: 269-273. 

Patton, R. L. (1981) Effects of ozone and sulfur dioxide on height and stem 

I specific gravity of Po ulus hybrids. For. Sci. Res. Pop. NE-471. 

Price, H.; Treshow, M. (1972) Effects of ozone on the growth and reproduction 

of grasses. In: Proceedings of the international air pollution conference; 

Melbourne, Australia. pp. 275-280. 

Reich, P. B.; Amundson, R. G. (1985) Ambient levels of ozone reduce net photosynthesis in tree and crop species. Science. 230: 566-570. 

Sigal, L. L.; Nash, T. H. (1983) Lichen communities on conifers in southern 

California mountains: an ecological survey relative to oxidant air pollu= 

tion. Ecology 64: 1343-1354. 

Stark, R. W. ; Cobb, F. W. , Jr. (1969) Smog injury, root diseases and bark 

beetle damage in ponderosa pine. Calif. Agric. 23: 13-15. 

Tingey, D. T.; Wilhour, R. G.; Standley, E. (1976) The effect of chronic ozone 

exposures on the metabolite content of ponderosa pine seedlings. For. 

Sci. 22: 234-241. 

Treshow, M.; Stewart, D. (1973) Ozone sensitivity of plants in natural communities. Biol. Conserv. 5: 205-214. 

U.S. Environmental Protection Agency (1978) Air quality criteria for ozone 

and other photochemical oxidants. Research Triangle Park, NC: U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office; 

Report no. EPA-600/8-78-004. Available from: NTIS, Springfield, VA; 

PB83-163337. 

Woodwell, G. M. (1970) Effects of pollution on the structure and physiology of 

ecosystems. Science (Washington, DC) 168: 429-433. 

Yang, Y.-S.; Skelly, J. M.; Chevone, B. I.; Birch, J. B. (1983) Effects of 

long-term ozone exposure on photosynthesis and dark respiration of eastern 

white pine. Environ. Sci. Technol. 17: 371-373. 

1.12.7References for Effects of Ozone and Other Photochemical Oxidants on 

Nonbiological Materials 

Beloin, N. J. (1972) Fading of dyed fabrics by air pollution: a field study. 

Text. Chem. Color. 4: 77-78. 

Beloin, N. J. (1973) Fading of dyed fabrics exposed to air pollutants: a 

chamber study. Text. Chem. Color. 5: 128-133. 

1-207 
References for Nonbiological Materials (cont'd.) 

Bogaty, H.; Campbell, K. S.; Appel, W. D. (1952) The oxidation of cellulose by 

ozone in small concentrations. Text. Res. J. 22: 81-83. 

Bradley, C. E.; Haagen-Smit, A. J. (1951) The application of rubber in the 

quantitative determination of ozone. Rubber Chem. Technol. 24: 750-775. 

Edwards, D. C.; Storey, E. B. (1959) A quantitative ozone test for small 

specimens. Chem. Can. 11: 34-38. 

Haylock, J. C.; Rush, J. L. (1976) Studies on the ozone fading of anthraquinone 

dyes on nylon fibers. Text. Res. J. 46: 1-8, 

Haylock, J. C.; Rush, J. L. (1978) Studies on the ozone fading of anthraquinone 

dyes on nylon fibers; part II: in-service performance. Text. Res. J. 48: 

143-149. 

Haynie, F. H.; Spence, J. W.; Upham, J. B. (1976) Effects of gaseous pollutants 

on materials--a chamber study. Research Triangle Park, NC: U.S. Environmental Protection Agency, Environmental Sciences Research Laboratory; EPA 

report no. EPA-600/3-76-015. Available from: NTIS, Springfield, VA; 

PB-251580. 

Heuvel, H. M.; Huisman, R.; Schmidt, H. M. (1978) Ozone fading of disperse 

blue 3 on nylon 6 fibers. The influence of physical fiber properties. 

Text. Res. J. 48: 376-384. 

Kamath, Y. K.; Ruetsch, S. B.; Weigmann, H.-D. (1982) Microspectrophotometric 

study of ozone fading of disperse dyes in nylon. Text. Res. J.: 

53: 391-402. 

Kerr, N.; Morris, M. A.; Zeronian, S. H. (1969) The effect of ozone and laundering on a vat-dyed cotton fabric. Am. Dyest. Rep. 58: 34-36. 

McCarthy, E. F.; Stankunas, A. R.; Yocom, J. E.; Rae, D. (1983) Damage cost 

models for pollution effects on material. Research Triangle Park, NC: 

U.S. Environmental Protection Agency, Environmental Sciences Research 

Laboratory; EPA report no. EPA-600/3-84-012. Available from: NTIS, 

Springfield, VA; PB-140342. 

Nipe, M. R. (1981) Atmospheric contaminant fading. Text. Chem. Color. 

13: 18-28. 

Salvin, V. S. (1969) Ozone fading of dyes. Text. Chem. Color. 1: 245-251. 

Salvin, V. S.; Walker, R. A. (1955) Service fading of disperse dyestuffs by 

chemical agents other than the oxides of nitrogen. Text. Res. J. 25: 

571-585. 

Schmitt, C. H. A. (1960) Lightfastness of dyestuffs on textiles. Am. Dyest. 

Rep. 49: 974-980. 

1-208 

11 
References for Nonbiological Materiais (cont'd.) 

Schmitt, C. H. A. (1962) Daylight fastness testing by the Langley system. Am. 

Dyest. Rep. 51: 664-675. 

Upham, J. B.; Haynie, F. H.; Spence, J. W. (1976) Fading of selected drapery 

fabrics by air pollutants. J. Air Pollut. Control Assoc. 26: 790-792. 

Veith, A. G.; Evans, R. L. (1980) Effect of atmospheric pressure on ozone 

cracking of rubber. Polym. Testing 1: 27-38. 

Wenghoefer, H. M. (1974) Environmental effects on RFL adhesion. Rubber Chem. 

Technol. 47: 1066-1073. 

Yocom, J. E.; Kawicki, J. M.; Hoffnagle, G. F. (1985) Estimating materials 

damage from oxidant pollutants. In: Proceedings of the APCA Specialty 

Conference: evaivation of the scientific Basis for Ozone/Oxidants Standards, Houston, TX, November 28-30, 1984. Pittsburgh, PA: Air Pollution 

Control Association. 

1.12.8 References for Toxicoiogical Effects of Ozone and Other Photochemical 

Oxidants 

Abraham, W. M.; Januszkiewicz, A. J.; Mingle, M.; Welker, M.; Wanner, A.; 

Sackner, M. A. (1980) Sensitivity of bronchoprovocation and tracheal 

mucous velocity in detecting airway responses to 0 3 . J. Appl. Physiol.: 

Respir. Environ. Exercise Physiol. 48: 789 - 793. 

Abraham, W. M.; Lauredo ; I.; Sielczak, M.; Yerger, L.; King, M. M.; Ratzan, K. 

(1982) Enhancement of bacterial pneumonia in sheep by ozone exposure. Am. 

Rev. Respir. Dis. Suppl. 125(4 pt. 2): 148. 

Abraham, W.; Chapman, G. A.; Marchette, B. (1984a) Differences between inhaled 

and intravenous carbachol in detecting 0 3-induced airway effects. Environ. 

Res. 35: 430-438. 

Abraham, W. M.; Delehunt, J. C.; Yerger, L.; Marchette, B.; Oliver, W., Jr. 

(1984b) Changes in airway permeability and responsiveness after exposure 

to ozone. Environ. Res. 34: 110-119. 

Aharonson, E. F.; Menkes, H.; Gurtner, G.; Swift, D. - L.; Proctor, D. F. (1974) 

Effect of respiratory airflow rate on removal of soluble vapors by the 

nose. J. Appl. Physiol. 37: 654-657. 

Alpert, S. M.; Schwartz, B. B.; Lee, S. D.; Lewis, T. R. (1971a) Alveolar 

protein accumulation: a sensitive indicator of low level oxidant toxicity. Arch. Intern. Med. 128: 69-73. 

Alpert, S. M. ; Gardner, D. E. ; Hurst, D. J. ; Lewis, T. R. ; Coffin, D. L. 

(1971b) Effects of exposure to ozone on defensive mechanisms of the lung. 

J. Appl. Physioi. 31: 247-252. 

1-209 
References for Toxicoloqical Effects (cont'd.) 

Amdur, M. 0.; Ugro, V.; Underhill, D. W. (1978) Respiratory response of guinea 

pigs to ozone alone and with sulfur dioxide. Am. Ind. Hyg. Assoc. J. 39: 

958-961. 

Amoruso, M. A.; Witz, G.; Goldstein, B. D. (1981) Decreased superoxide anion 

radical production by rat alveolar macrophages following inhalation of 

ozone or nitrogen dioxide. Life Sci. 28: 2215-2221. 

Aranyi, C.; Vana, S. C.; Thomas, P. T.; Bradof, J. N.; Fenters, J. D.; Graham, 

J. A.; Miller, F. J. (1983) Effects of subchronic exposure to a mixture 

of 03 , S02 , and (NH4 )2SO4 on host defenses of mice. J. Toxicol. Environ. 

Health 12: 55-71. 

Atwal, 0. S.; Pemsingh, R. S. (1981) Morphology of microvascular changes and 

endothelial regeneration in experimental ozone-induced parathyroiditis. 

III. Some pathologic considerations. Am. J. Pathol. 102: 297-307. 

Atwal, 0. S.; Pemsingh, R. S. (1984) Occurrence of mallory body-like inclusions 

in parathyroid chief cells of ozone-treated dogs. J. Pathol. 142: 169-174. 

Atwal, 0. S.; Wilson, T. (1974) Parathyroid gland changes following ozone 

inhalation: a morphologic study. Arch. Environ. Health 28: 91-100. 

Atwal, 0. S.; Samagh, B. S.;,Bhatnagar, M. K. (1975) A possible autoimmune 

parathyroiditis following ozone inhalation. II. A histopathologic, ultrastructural, and immunofluorescent study. Am. J. Pathol. 80: 53-68. 

Barry, B. E.; Miller, F. J.; Crapo, J. D. (1983) Alveolar epithelial injury 

caused by inhalation of 0.25 ppm of ozone. In: Lee, S. D.; Mustafa, 

M. G.; Mehlman, M. A., eds. International symposium on the biomedical 

effects of ozone and related photochemical oxidants; March 1982; Pinehurst, 

NC. Princeton, NJ: Princeton Scientific Publishers, Inc; pp. 299-309. 

(Advances in modern environmental toxicology: v. 5). 

Bartlett, D., Jr.; Faulkner, C. S. II; Cook, K. (1974) Effect of chronic ozone 

exposure on lung elasticity in young rats. J. Appl. Physiol. 37: 92-96. 

Bergers, W. W. A.; Gerbrandy, J. L. F.; Stap, J. G. M. M.; Dura, E. A. (1983) 

Influence of air polluting components viz ozone and the open air factor 

on host-resistance towards respiratory infection. In: Lee, S. D.; Mustafa, 

M. G.; Mehlman, M. A., eds. International symposium on the biomedical effects of ozone and related photochemical oxidants; March 1982; Pinehurst, 

NC. Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 459-467. 

(Advances in modern environmen.tal toxicology: v. 5). 

Berliner, J. A.; Kuda, A.; Mustafa, M. G.; Tierney, T. F. (1978) Pulmonary 

morphologic studies of ozone tolerance in the rat.(a possible mechanism 

for tolerance). Scanning Electron Microsc. 2: 879-884. 

1-210 
References for Toxicological Effects (cont'd.) 

Bhatnagar, R. S.; Hussain, M. Z.; Sorensen, K. R.; Mustafa, M. G.; von Dohlen, 

F. M.; Lee, S. D. (1983) Effect of ozone on lung collagen biosynthesis. 

In: Lee, S. D.; Mustafa, M. G.; Mehlman, M. A., eds. International 

symposium on the biomedical effects of ozone and related photochemical 

oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton 

Scientific Publishers, Inc.; pp. 311-321. (Advances in modern environmental toxicology: v. 5). 

Boatman, E. S. ; Sato, S. ; Frank, R. (1974) Acute effects of ozone on cat 

lungs. II. Structural. Am. Rev. Respir. Dis. 110: 157-169. 

Boche, R. D.; Quilligan, J. J., Jr. (1960) Effects of synthetic smog on spontaneous activity of mice. Science (Washington, DC) 131: 1733-1734. 

Boorman, G. A. ; Schwartz, L. W. ; McQui l len, N. K. ; Brummer, M. E. G. (1977) 

Pulmonary response following long-term intermittent exposure to ozone: 

structural and morphometric changes. Am. Rev. Respir. Dis. 115: 201. 

Boorman, G. A.; Schwartz, L. W.; Dungworth, D. L. (1980) Pulmonary effects of 

prolonged ozone insult in rats: morphometric evaluation of the central 

acinus. Lab. Invest. 43: 108-115. 

Bradley, M. 0.; Erickson, L. C. (1981) Comparison of the effects of hydrogen 

peroxide and X-ray irradiation on toxicity, mutation, and DNA damage/ 

repair in mammalian cells (V-79). Biochim. Biophys. Acta 654: 135-141. 

Bradley, M. 0.; Hsu, I. C.; Harris, C. C. (1979) Relationships between sister 

chromatid exchange and mutagenicity, toxicity, and DNA damage. Nature 

(London) 282: 318-320. 

Brinkman, R.; Lamberts, H. B.; Veninga, T. S. (1964) Radiomimetic toxicity of 

ozonised air. Lancet (7325): 133-136. 

Brummer, M. E. G.; Schwartz, L. W.; McQuillen, N. K. (1977) A quantitative 

study of lung damage by scanning electron microscopy: inflammatory cell 

response to high-ambient levels of ozone. Scanning Electron Microsc. 2: 

513-518. 

Caiabrese, E. J.; Moore, G. S.; Grunwald, E. L. (1983) Ozone-induced decrease 

of erythrocyte survival in adult rabbits. In: Lee, S. D.; Mustafa, M. G.; 

Mehlman, M. A., eds. International symposium on the biomedical effects of 

ozone and related photochemical oxidants; March 1982; Pinehurst, NC. 

Princeton, N:.1: Princeton Scientific Publishers, Inc.; pp. 103-117. (Advances in modern environmental toxicology: v. 5). 

Campbell, K. I.; Hilsenroth, R. H. (1976) Impaired resistance to toxin in 

toxoid-immunized mice exposed to ozone or nitrogen dioxide. Clin. Toxicol. 

9: 943-954. 

Campbell, K. I.; Clarke, G. L.; Emik, L. 0.; Plata, R. L. (1967) The atmospheric contaminant peroxyacetyl nitrate. Arch. Environ. Health 15: 739-744. 

1-211 
References for Toxicoloqical Effects (cont'd.) 

Castleman, W. L.; Dungworth, D. L.; Tyler, W. S. (1973a) Cytochemical1y detected alterations of lung acid phosphatase reactivity following ozone 

exposure. Lab. Invest. 29: 310-319. 

Castleman, W. L.; Dungworth, D. L.; Tyler, W. S. (1973b) Flistochemically 

detected enzymatic alterations in rat lung exposed to ozone. Exp. Mol. 

Pathol. 19: 402-421. 

Castleman, W. L.; Tyler, W. S.; Dungworth, D. L. (1977) Lesions in respiratory 

bronchioles and conducting airways of monkeys exposed to ambient levels 

of ozone. Exp. Mol. Pathol. 26: 384-400. 

Castleman, W. L.; Dungworth, D. L.; Schwartz, L. W.; Tyler, W. S. (1980) Acute 

respiratory bronchiolitis: an ultrastructural and autoradiographic study 

of epithelial cell injury and renewal in rhesus monkeys exposed to ozone. 

Am. J. Pathol. 98: 811-840. 

Cavender, F. L.; Steinhagen, W. H.; Ulrich, C. E.; Busey, W. M.; Cockrell, B. 

Y.; Haseman, J. K.; Hogan, M. D.; Drew, R. T. (1977) Effects in rats and 

guinea pigs of short-term exposures to sulfuric acid mist, ozone, and 

their combination. J. Toxicol. Environ. Health 3: 521-533. 

Cavender, F. L.; Singh, B.; Cockrell, B. Y. (1978) Effects in rats and guinea 

pigs of six-month exposures to sulfuric acid mist, ozone, and their 

combination. J. Toxicol. Environ. Health 4: 845-852. 

Chow, C. K. (1976) Biochemical responses in lungs of ozone-tolerant rats. 

Nature (London) 260: 721-722. 

Chow,- C. K. (1984) Glutathione peroxidase system in the lungs of ozone-tolerant 

and non-tolerant rats. In: Bors, W.; Saran, M.; Tait, D., eds. Oxygen 

radicals in chemistry and biology; proceedings of the third international 

conference; July 1983; Neuherberg, West Germany. Berlin, West Germany: 

Walter de Gruyter & Co.; pp. 707-712. 

Chow, C. K.; Kaneko, J. J. (1979) Influence of dietary vitamin E on the red 

cells of ozone-exposed rats. Environ. Res. 19: 49-55. 

Chow, C. K.; Tappel, A. L. (1972) An enzymatic protective mechanism against 

lipid peroxidation damage to lungs of ozone-exposed rats. Lipids 7: 

518-524. 

Chow, C. K.; Tappel, A. L. (1973) Activities of pentose shunt and glycolytic 

enzymes in lungs of ozone-exposed rats. Arch. Environ. Health 26: 205-208. 

Chow, C. K.; Dillard, C. J.; Tappel, A. L. (1974) Glutathione peroxidase 

system and lysozyme in rats exposed to ozone or nitrogen dioxide. Environ. 

Res. 7: 311-319. 

Chow, C. K.; Mustafa, M. G.; Cross, C. E.; Tarkington, B. K. (1975) Effects of 

ozone exposure on the lungs and the erythrocytes of rats and monkeys: 

relative biochemical changes. Environ. Physiol. Biochem. 5: 142-146. 

1-212 
References for Toxicological Effects (cont'd.) 

Chow, C. K.; Hussain, M. Z.; Cross, C. E.; Dungworth, D. L.; Mustafa, M. G. 

(1976) Effect of low levels of ozone on rat lungs. I. Biochemical responses during recovery and reexposure. Exp. Mol. Pathol. 25: 182-188. 

Chow, C. K.; Cross, C. E.; Kaneko, J. J. (1977) Lactate dehydrogenase activity 

and isoenzyme pattern in lungs, erythrocytes, and plasma of ozone-exposed 

rats and monkeys. J. Toxicol. Environ. Health 3: 877-884. 

Chow, C. K.; Plopper, C. G.; Chiu, M.; Dungworth, D. L. (1981)'Dietary vitamin E 

and pulmonary biochemical and morphological alterations of rats exposed 

to 0.1 ppm ozone. Environ. Res. 24: 315-324. 

Christensen, E.; Giese, A. C. (1954) Changes in absorption spectra of nucleic 

acids and their derivatives following exposure to ozone and ultravioiet 

radiation. Arch. Biochem. Biophys. 51: 208-216. 

Clark, K. W.; Posin, C. I.; Buckley, R. D. (1978) Biochemical response of 

squirrel monkeys to ozone. J. Toxicol. Environ. Health 4: 741-753. 

Clemons, G. K.; Garcia, J. F. (1980a) Endocrine aspects of ozone exposure in 

rats. Arch. Toxicol. Suppl. (4): 301-304. 

Clemons, G. K.; Garcia, J. F. (1980b) Changes in thyroid function after shortterm ozone exposure in rats. J. Environ. Pathol. Toxicol. 4: 359-369. 

Clemons, G. K.; Wei, D. (1984) Effect of short-term ozone exposure on exogenous 

thyroxine levels in thyroidectomized and hypophysectomized rats. Toxicol. 

Appl. Pharmacol. 74: 86-90. 

Coffin, D. L.; Blommer, E. J. (1970) Alteration of the pathogenic role of 

streptococci group C in mice conferred by previous exposure to ozone. In: 

Silver, I. H., ed. Aerobiology: proceedings of the third international 

symposium; September 1969; Sussex, United Kingdom. New York, NY: Academic 

Press, Inc.; pp. 54-61. 

Coffin, D. L.; Gardner, D. E. (1972a) The role of tolerance in protection of 

the lung against secondary insults. In: MEDICHEM: first international 

symposium of occupational physicians of the chemical industry; April; 

Ludwigshafen, West Germany. Ludwigshafen, West Germany: Badische 

Anilin-und Soda-Fabrik (BASF); pp. 344-364. 

Coffin, D. L.; Gardner, D. E. (1972b) Interaction of biological agents and 

chemical air pollutants..Ann. Occup. Hyg..15: 219-235. 

Coffin, D. L.; Blommer, E. J.; Gardner, D. E.; Holzman, R. (1967) Effect of 

air pollution on alteration of susceptibility to pulmonary infection. In: 

Proceedings of the third annual conference on atmospheri,c contamination 

in confined spaces; May; Dayton, OH. Wright-Patterson Air Force Base, OH: 

Aerospace Medical Research Laboratories; pp. 71-80; report no. 

AMRL-TR-67-200. Available from: NTIS, Springfield, VA; AD-835008. 

1-213 
References for Toxicological Effects (cont'd.) 

Coffin, D. L.; Gardner, D. E.; Holzman, R. S.; Wolock, F. J. (1968) Influence 

of ozone on pulmonary cells. Arch. Environ. Health 16: 633-636. 

Costa, D. L. ; Kutzman, R. S. ; Lehmann, J. R. ; Popenoe, E. A. ; Drew, R. T. 

(1983) A subchronic multi-dose ozone study in rats. In: Lee, S. D.; 

Mustafa, M. G.; Mehlman, M. A., eds. International symposium on the 

biomedical effects of ozone and related photochemical oxidants; March 

1982; Pinehurst, NC. Princeton,. NJ: Princeton Scientific Publishers, 

Inc.; pp.• 369-393. (Advances in modern environmental toxicology: v. 5). 

Crapo, J. D.; Barry, B. E.; Chang, L.-Y.; Mercer, R. R. (1984) Alterations in 

lung structure caused by inhalation of oxidants. J. Toxicol. Environ. 

Health 13: 301-321. 

DeLucia, A. J.; Hoque, P. M.; Mustafa, M. G.; Cross, C. E. (1972) Ozone interaction with rodent lung: effect on sulfhydryls and sulfhydryl-containing 

enzyme activities. J. Lab. Clin. Med. 80: 559-566. 

DeLucia, A. J.; Mustafa, M. G.; Cross, C. E.; Plopper, C. G.; Dungworth, 

D. L.; Tyler, W. S. (1975a) Biochemical and morphological alterations in 

the lung following ozone exposure. In: Rai, C.; Spielman, L. A., eds. 

Air: I. pollution control and clean energy; 1973; New Orleans, LA; 

Detroit, MI; Philadelphia, PA; Vancouver, British Columbia. New York, 

NY: American Institute of Chemical Engineers; pp. 93-100. (AIChE symposium series: v. 71, no. 147). 

DeLucia, A. J. ; Mustafa, M. G. ; Hussain, M. Z. ; Cross, C. E. (1975b) 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. 

Dillard, C. J.; Urribarri, N.; Reddy, K.; Fletcher, B.; Taylor, S.; de Lumen, 

B.; Langberg, S.; Tappel, A. L. (1972) Increased lysosomal enzymes in 

lungs of ozone-exposed rats. Arch. Environ. Health 25: 426-431. 

Dorsey, A. P.; Morgan, D. L.; Menzel, D. B. (1983) F'ilterability of erythrocytes from ozone-exposed mice. In: Abstracts of the third international 

congress on toxicology; September; San Diego, CA. Toxicol. Lett. 

18(suppl. 1): 146. 

Dowell, A. R.; Lohrbauer, L. A.; Hurst ~ D.; Lee, S. D. (1970) Rabbit alveolar 

macrophage damage caused by in vivo ozone inha.lation. Arch. Environ. 

Health 21: 121-127. 

Dubeau, H.; Chung, Y. S. (1979) Ozone response in wild type and radiationsensitive mutants of Saccharomyces_ cerevisiae. Mol. Gen. Genet. 176: 

393-398. 

Dubeau, H.; Chung, Y. S. (1982) Genetic effects of ozone: induction of point 

mutation and genetic recombination in Saccharomyces cerevisiae. Mutat. 

Res. 102: 249-259. 

1-214 
References for Toxicological Effects (cont'd.) 

Dungworth, D. L.; Clarke, G. L.; Plata, R. L. (1969) Pulmonary lesions produced 

in A-strain mice by long-term exposure to peroxyacetyl nitrate. Am. Rev. 

Respir. Dis. 99: 565-574. 

Dungworth, D. L.; Castleman, W. L.; Chow, C. K.; Mellick, P. W.; Mustafa, M. 

G.; Tarkington, B.; Tyler, W. S. (1975) Effect of ambient levels of 

ozone on monkeys. Fed. Proc. Fed. Am. Soc. Exp. Biol. 34: 1670-1674. 

Easton, R. E.; Murphy, S. D. (1967) Experimental ozone preexposure and histamine. Arch. Environ. Health 15: 160-166. 

Ehrlich, R. (1980) Interaction between environmental pollutants and respiratory 

infections. EHP Environ. Health Perspect. 35: 89-100. 

Ehrlich, R. (1983) Changes in susceptibility to respiratory infection caused 

by exposures to photochemical oxidant pollutants. In: Lee, S. D.; Mustafa, 

M. G.; Mehiman, M. A., eds. International symposium on the biomedical 

effects of azone and related photochemical oxidants; March 1982; Pinehurst, 

NC. Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 273-285. 

(Advances in modern environmental toxicology: v. 5). 

Ehrlich, R.; Findlay, J. C.; Fenters, J. D.; Gardner, D. E. (1977) Health 

effects of short-term inhalation of nitrogen dioxide and ozone mixtures. 

Environ. Res. 14: 223-231. 

Ehrlich, R.; Findlay, J. C.; Gardner, D. E. (1979) Effects of repeated exposures 

to peak concentrations of nitrogen dioxide and ozone on resistance to 

streptococcal pneumonia. J. Toxicol. Environ. Health 5: 631-642. 

Elsayed, N. M.; Mustafa, M. G.; Postlethwait, E. M. (1982a) Age-dependent 

pulmonary response of rats to ozone exposure. J. Toxicol. Environ. Health 

9: 835-848. 

Elsayed, N. M.; Hacker, A.; Mustafa, M.; Kuehn, K.; Schrauzer, G. (1982b) 

Effects of decreased glutathione peroxidase activity on the pentose 

phosphate cycle in mouse lung. Biochem. Biophys. Res. Commun. 104: 

564-569. 

Eisayed, N. M.; Hacker, A. D.; Kuehn, K.; Mustafa, M. G.; Schrauzer, G. N. 

(1983) Dietary antioxidants and the biochemical response to oxidant 

inhalation. II. Influence of dietary selenium on the biochemical effects 

of ozone exposure in mouse lung. Toxicol. Appl. Pharmacol. 71:. 398-406. 

Erdman, H. E.; Hernandez, T. (1982) Adult toxicity and dominant lethals induced 

by ozone at specific s_tages in spermatogenesis in Droso p ila virilis h . 

Environ. Mutagen. 4: 657-666. 

Eustis, S. L.; Schwartz, L. W.; Kosch, P. C.; Dungworth, D. L. (1981) Chronic 

bronchiolitis in nonhuman primates after prolonged ozone exposure. Am. J. 

Pathol. 105: 121-137. 

1-215 
References for Toxicological Effects (cont'd.) 

Evans, M. J.; Mayr, W.; Bils, R. F.; Loosli, C. G. (1971) Effects of ozone on 

cell renewal in pulmonary alveoli of aging mice. Arch. Environ. Health 

22: 450-453. 

Evans, M. J.; Johnson, L. V.; Stephens, R. J.; Freeman, G. (1976a) Renewal of 

the terminal bronchiolar epithelium in the rat following exposure to NO 2 

or 0 3 . Lab. Invest. 35: 246-257. 

Evans, M. J.; Johnson, L. V.; Stephens, R. J.; Freeman, G. (1976b) Cell renewal 

in the lungs of rats exposed to low levels of ozone. Exp. Mol. Pathol. 

24: 70-83. 

Evans, M. J.; Stephens, R. J.; Freeman, G. (1976c). Renewal of pulmonary 

epithelium following oxidant injury. In: Bouhuys, A., ed. Lung cells in 

disease: proceedings of a Brook Lodge conference; April; Augusta, MI. New 

York, NY: Elsevier/North-Holland Biomedical Press; pp. 165-178. 

Evans, M. J.; Dekker, N. P.; Cabral-Anderson, L. J.; Shami, S. G. (1985) 

Morphological basis of tolerance to ozone. Exp. Mol. Pathol. 42: 366-376. 

Fabbri, L. M. ; Aizawa, H. ; Alpert, S. E. ; Walters, E. H. ; 0' Byrne, P. M. ; 

Gold, B. D.; Nadel, J. A.; Holtzman, M. J. (1984) Airway hyperresponsiveness and changes in cell counts in bronchoalveolar lavage after ozone 

exposure in dogs. Am. Rev. Respir. Dis. 129: 288-291. 

Fairchild, E. J., II. (1967) Tolerance mechanisms: determinants of lung responses 

to injurious agents. Arch. Environ. Health 14: 111-126. 

Fetner, R. H. (1962) Ozone-induced chromosome breakage in human cell cultures. 

Nature (London) 194: 793-794. 

Fletcher, B. L.; Tappel, A. L. (1973) Protective effects of dietary a-Tocopherol in rats exposed to toxic levels of ozone and nitrogen dioxide. 

Envi ron. Res. 6: 165-175. 

Frager, N. B.; Phalen, R. F.; Kenoyer, J. L. (1979) Adaptations to ozone in 

reference to mucociliary clearance. Arch. Environ. Health 34: 51-57. 

Freeman, B. A.; Mudd, J. B. (1981) Reaction of ozone with sulfhydryls of human 

erythrocytes. Arch. Biochem. Biophys. 208: 212-220. 

Freeman, B. A.; Sharman, M. C.; Mudd, J. B. (1979) Reaction of ozone with 

phospholipid vesicles and human erythrocyte ghosts. Arch. Biochem: 

Biophys. 197: 264-272. 

Freeman, G.; Stephens, R. J.; Coffin, D. L.; Stara, J. F. (1973) Changes in 

dogs' lungs after long-term exposure'to ozone: light and electron microscopy. Arch. Environ. Health 26: 209-216. 

Freeman; G. ; Juhos, L. T. ; Furiosi , N. J. ; Mussenden, R. ; Stephens, R. J. ; 

Evans, M. J. (1974) Pathology of pulmonary disease from exposure to 

interdependent ambient gases (nitrogen dioxide and ozone). Arch. Environ. 

Health 29: 203-210. 

1-216 
References for Toxicological Effects (cont'd.) 

Friberg, L.; Holma, B.; Ryiander, R. (1972) Animal lung reactions after 

inhalation of lead and ozone. Environ. Physiol. Biochem. 2: 170-178. 

Friedman, M.; Gallo, J. M.; Nichols, H. P.; Bromberg, P. A. (1983) Changes in 

inert gas rebreathing parameters after ozone exposure in dogs. Am. Rev. 

Respir. Dis. 128: 851-856. 

Fujimaki, H.; Ozawa, M.; Imai, T.; Shimizu, F. (1984) Effect of short-term 

exposure to 0 3 on antibody response in mice. Environ. Res. 35: 490-496. 

Fujinaka, L. E.; Hyde, D. M.; Plopper, C. G.; Tyier, W. S.; Dungworth, D. L. 

Lollini, L. 0. (1985) Respiratory bronchiolitis following long-term 

ozone exposure in Bonnet monkeys: a morphometric study. Exp. Lung Res. 

8: 167-190. 

Fukase, 0.; Isomura, K.; Watanabe, H. (1975) Effect of ozone on glutathione 

invivo . Taiki Osen Kenkyu 10: 58-62. 

Fukase, 0.; Watanabe, H.; Isomura, K. (1978) Effects of exercise on mice 

exposed to ozone. Arch. Environ. Health 33: 198-200. 

Gardner, D. E. (1984) Oxidant-induced enhanced sensitivity to infection in 

animal models and their extrapoiation to man. In: Miller, F. J.; Menzel, 

D. B., ed. Fundamentals of extrapolation modeling of inhaled toxicants. 

Washington, DC: Hemisphere Publ. Co.; pp. 423-439. 

Gardner, D. E.; Graham, J. A.-(1977) Increased pulmonary disease mediated 

through altered bacterial defenses. In: Sanders, C. L.; Schneider, R. P.; 

Dagle, G. E.; Ragen, H. A., eds. Pulmonary macrophage and epithelial 

ceils: proceedings of the sixteenth annual Hanford biology symposium; 

September 1976; Richland, WA. Washington, DC: Energy Research and Development Administration; pp. 1-21. (ERDA symposium series: 43). Available 

from: NTIS, Springfield, VA; CONF-760927. 

Gardner, D. E.; Pfitzer, E. A.; Christian; R. T.; Coffin, D. L. (1971) Loss of 

protective factor for alveolar macrophages when exposed to ozone. Arch. 

Intern. Med. 127: 1078-1084. 

Gardner, D. E.; Lewis, T. R.; Alpert, S. M.; Hurst, D. J.; Coffin, D. L. 

(1972) The role of tolerance in pulmonary defense mechanisms. Arch. 

Environ. Heaith 25: 432-438. 

Gardner, D. E.; Illing, J. W.; Miller, F. J. Coffin, D. L. (1974) The effect 

of ozone on pentobarbital sleeping time in mice. Res. Commun. Chem. 

Pathol. Pharmacol. 9: 689-700. 

Gardner, D. E.; Miller, F. J.; Illing, J. W.; Kirtz, J. M. (1977) Increased 

infectivity with exposure to ozone and sulfuric acid. Toxicol. Lett. 1: 

59-64. 

1-217 
References for Toxicological Effects (cont'd.) 

Gershwin, L. J.; Osebold, J. W.; Zee, Y. C. (1981) Immunoglobulin E-containing 

cells in mouse lung following allergen inhalation and ozone exposure. 

Int. Arch. Allergy Appl. Immunol. 65: 266-277. 

Gertner, A.; Bromberger-Barnea, B.; Dannenberg, A. M., Jr.; Traystman, R.; 

Menkes, H. (1983a) Responses of the lung periphery to 1.0 ppm ozone. J. 

Appl. Physiol. Respir. Environ. Exercise Physiol. 55: 770-776. 

Gertner, A.; Bromberger-Barnea, B.; Traystman, R.; Berzon, D.; Menkes, H. 

(1983b) Responses of the lung periphery to ozone and histamine. J. Appl. 

Physiol.: Respir. Environ. Exercise Physiol. 54: 640-646. 

Gertner, A.; Bromberger-Barnea, B.; Traystman, R.; Menkes, H. (1983c) Effects 

of ozone in peripheral lung reactivity. J. Appl. Physiol.: Respir. Environ. 

Exercise Physiol. 55: 777-784. 

Gertner, A.; Bromberger-Barnea, B.; Kelly, L.; Traystman, R.; Menkes, H. (1984) 

Local vagal responses in the lung periphery. J. Appl. Physiol:: Respir. 

Environ. Exercise Physiol. 57: 1079-1088. 

Gillespie, J. R. (1980) Review of the cardiovascular and pulmonary function 

studies on beagles exposed for 68 months to auto exhaust and other air 

pollutants In: Stara, J. F.; Dungworth, D. L.; Orthoefer, J. C.; 

Tyler, W. S., eds. Long-term effects of air pollutants in canine species. 

Cincinnati, OH: U.S. Environmental Protection Agency, Environmental Criteria 

and Assessment Office; pp. 115-154; EPA report no. EPA 600/8-80-014. Available from: NTIS, Springfield, VA; PB81-144875. 

Goldstein, E.; Tyler, W. S.; Hoeprich, P. D.; Eagle, C. (1971a) Ozone and the 

antibacterial defense mechanisms of the murine lung. Arch. Intern. Med. 

127: 1099-1102. 

Goldstein, E.; Tyler, W. S.; Hoeprich, P. D.; Eagle, C. (1971b) Adverse influence of ozone on pulmonary bactericidal activity of murine lungs. Nature 

(London) 229: 262-263. 

Goldstein, E.; Eagle, M. C.; Hoeprich, P. D. (1972) Influence of ozone on pulmonary defense mechanisms of silicotic mice. Arch. Environ. Health 24: 444-448. 

Goldstein, B. D.; Lai, L. Y.; Cuzzi-Spada, R. (1974) Potentiation of complement-dependent membrane damage by ozone. Arch. Environ. Health 28: 

40-42. 

Goldstein, B. D.; Hamburger, S. J.; Falk, G. W.; Amoruso, M. A. (1977) Effect 

of ozone and nitrogen dioxide on the agglutination of rat alveolar macrophages by concanavalin A. Life Sci. 21: 1637-1644. 

Gooch, P. C.; Creasia, D. A.; Brewen, J. G. (1976) The cytogenetic effect of 

ozone: inhalation and in vitro exposures. Environ. Res. 12: 188-195. 

Gordon, T.; Amdur, M. 0. (1980) Effect of ozone on respiratory response of 

guinea pigs to histamine. J. Toxicol. Environ. Health 6: 185-195. 

1-218 
References for Toxicolo ical Effects (cont'd.) 

Gor'don, T. ; Tayl or, B. F. ; Amdur, M. 0. (1981) Ozone i nhi bi -ti on of ti ssue 

cholinesterase in guinea pigs. Arch. Environ. Health 36: 284-288. 

Gordon, T.; Venugopalan, C. S.; Amdur, M. 0.; Drazen, J. M. (1984) Ozone-induced 

airway hyperreactivity in the guinea pig. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 57: 1034-1038. 

Graham, J. A. (1979) Alteration of hepatic xenobiotic metabolism by ozone [dissertation]. Durham, NC: Duke University. Available from: University 

Microfilms, Ann Arbor, MI: pubiication no. 80-09646. 

Graham, J. A. ; Menzel , D. B. ; Mi 11 er, F. J. ; I11 i ng, J. W. ; Gardner, D. E. 

(1981) Influence of ozone on pentobarbital-induced sleeping time in mice, 

rats, and hamsters. Toxicol. Appl. Pharmacol. 61: 64-73. 

Graham, J. A.; Menzei, D. B.; Miller, F. J.; Illing, J. W.; Gardner, D. E. 

(1982a) Effect of ozone on drug-induced sleeping time in mice pretreated 

with mixe.d-function oxidase inducers and inhibitors. Toxicol. Appl. 

Pharmacol. 62: 489-497. 

Graham, J. A.; Miller, F. J.; Gardner, D. E.; Ward, R.; Menzel, D. B. (1982b) 

Influence of ozone and nitrogen dioxide on hepatic microsomal enzymes in 

mice. J. Toxicol. Environ. Health 9: 849-856. 

Graham, J. A.; Menzel, D. B.; Miller, F. J.; Illing, J. W.; Ward, R.; Gardner, 

D. E. (1983) Influence of ozone on xenobiotic metabolism. In: Lee, 

S. D. Mustafa, M. G.; Mehlman, M. A., eds. International symposium on 

the biomedical effects of ozone and related photochemical oxidants; March 

1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers ; 

Inc.; pp. 95-117. (Advances in modern environmental toxicology: v. 5). 

Graham, J. A. ; Menzel , D. B. ; Mol e, M. L. ; Mi l ler, F. J. ; Gardner, D. E. 

(1985) Influence of ozone on pentobarbital pharmacokinetics in mice. 

Toxicol. Lett. 24: 163-170. 

Green, G. M. (1984) Similarities of host defense mechanisms against pulmonary 

disease in animals and man. J. Toxicol. Environ. Health 13:-471-478. 

Grose, E. C. Gardner, D. E.; Miiler, F. J. (1980) Response of ciliated epithelium to ozone and sulfuric.acid. Envi, ron. Res. 22: 377-385. 

Grose, E. C. Richards, J. H.; Illing, J. W.; Mi11er, F. J.; Davies, D. W.; 

Graham, J. A.; Gardner, D. E. (1982) Pulmonary host defense responses to 

inhalation of sulfuric acid and ozone. J. Toxicol. Environ. Health 10: 

351-362.. : 

Guerrero, R. R.; Rounds, D. E.; Olson, R. S.; Hackney, J. D. (1979) Mutagenic 

effects of ozone on human cells exposed in vivo and in vitro based on 

sister chromatid exchange analysis. Environ. Res. 18: 336-346. 

1-219 
References for Toxicological Effects (cont'd.) 

, 

Hadley, J. G.; Gardner, D. E.; Coffin D. L.; Menzel, D. B. (1977) Enhanced 

binding of autologous cells to the macrophage plasma membrane as a sensitive indicator of pollutant damage. In: Sanders, C. L.; Schneider, R. 

P.; Dagle G. E.; Ragan, H. A., eds. Pulmonary macrophage and epithelial 

cells: proceedings of the sixteenth annual Hanford biology symposium; 

September 1976; Richland, WA. Washington, DC: Energy Research and 

Development Administration; pp. 1-21. (ERDA symposium series: v. 43). 

Available from: NTIS, Springfield, VA; CONF-760927. 

Hamelin, C.; Chung, Y. S. (1975a) The effect of low concentrations of ozone on 

Escherichia coli chromosome. Mutat. Res. 28: 131-132. 

Hamelin, C.; Chung, Y. S. (1975b) Characterization of mucoid mutants of 

Escherichia coli K-12 isolated after exposure to ozone. J. Bacteriol. 

122: 19-24. 

Hamelin, C.; Chung, Y. S. (1978) Role of the pol, rec, and DNA gene products 

in the repair of lesions produced in Escherichia coli DNA by ozone. Stud. 

Biophys. 68: 229-335. 

Mamelin, C.; Sarhan, F.; Chung, Y. S. (1977a) Ozone-induced DNA degradation 

in different DNA polymerase I mutants of Escherichia coli K12. Biochem. 

Biophys. Res. Commun. 77: 220-224. 

Mamelin, C.; Sarhan, F.; Chung, Y. S. (1977b) DNA degradation caused by ozone 

in mucoid mutants of Escherichia coli K12. FEMS Microbiol. Lett. 2: 

149-151. 

Hesterberg, T. W.; Last, J. A. (1981) Ozone-induced acute pulmonary fibrosis 

in rats: prevention of increased rates of collagen synthesis by methylprednisolone. Am. Rev. Respir. Dis. 123: 47-52. 

Holtzman, M. J.; Fabbri, L. M.; Skoogh, B.-E.; 0'Byrne, P. M.; Walters, E. H.; 

Aizawa, H.; Nadel, J. A. (1983a) Time course of airway hyperresponsiveness 

induced by ozone in dogs. J. Appl. Physiol.: Respir. Environ. Exercise 

Physiol. 55: 1232-1236. 

Holtzman, M. J.; Fabbri, L. M.; 0'Byrne, P. M.; Gold, B. D.; Aizawa, H.; 

Walters, E. H.; Alpert, S. E.; Nadel, J. A. (1983b) Importance of airway 

inflammation for hyperresponsiveness induced by ozone. Am. Rev. Respir. 

Dis. 127: 686-690. 

Hu, P. C.; Miller, F. J.; Daniels, M. J.; Hatch, G. E.; Graham, J. A.; Gardner, 

D. E.; Selgrade, M. K. (1982) Protein accumulation in lung lavage fluid 

following ozone exposure. Environ. Res. 29: 377-388. 

Huber, G. L. ; Mason, R. J. ; LaForce, M. ; Spencer, N. J. ; Gardner, D. E. ; 

Coffin, D. L. (1971) Alterations in the lung following the administration 

of ozone. Arch. Intern. Med. 128: 81-87. 

Hueter, F. G.; Contner, G. L.; Busch, K. A.; Hinners, R. G. (1966) Biological 

effects of atmospheres contaminated by auto exhaust. Arch. Environ. 

Health 12: 553-560. 

1-220 
References for Toxicological Effects (cont'd.) 

Hurst, D. J.; Coffin, D. L. (1971) Ozone effect on lysosomal hydrolases of 

alveolar macrophages in vitro . Arch. Intern. Med. 127: 1059-1063. 

Hurst, D. J. ; Gardner, D. E. ; Coffin, D. L. (1970) Effect of ozone on acid 

hydrolases of the pulmonary alveolar macrophage. J. Reticuloendothel. 

Soc. 8: 288-300. 

Hussain, M. Z.; Mustafa, M. G.; Chow, C. K.; Cross, C. E. (1976a) Ozone-induced 

increase of lung proline hydroxylase activity and hydroxyproline content. 

Chest 69 (suppl. 2): 273-275. 

Hussain, M. Z.; Cross, C. E.; Mustafa, M. G.; Bhatnagar, R. S. (1976b) Hydroxyproline contents and prolyl hydroxylase activities in lungs of rats 

exposed to low levels of ozone. Life Sci. 18: 897-904. 

Hyde, D.; Orthoefer, J. G.; Dungworth, D.; Tyler, W.; Carter, R.; Lum, H. (1978) 

Morphometric and morphologic evaluation of pulmonary lesions in beagle 

dogs chronicaily exposed to high ambient levels of air pollutants. Lab. 

Invest. 38: 455-469. 

Ibrahim, A. L.; Zee, Y. C.; Osebold, J. W. (1980) The effects of ozone on the 

respiratory epithelium of mice. II. Ultrastructural alterations. J. 

Environ. Pathol. Toxicol. 3: 251-258. 

Illing, J. W.; Mi11er, F. J.; Gardner, D. E. (1980) Decreased resistance to 

infection in exercised mice exposed to NO 2 and 0 3 . J. Toxicol. Environ. 

Health 6: 843-851. 

Inoue, H. ; Sato, S. ; Hi rose, T. ; Ki kuchi , Y. ; Ubukata, T. ; Nagashima, S. ; 

Sasaki, T.; Takishima, T. (1979) A comparative study between functional 

and pathologic alterations in lungs of rabbits exposed to an ambient 

levei of ozone: functional aspects. Nikkyo Shikkai-Shi 17: 288-296. 

Jegier, Z. (1973) L'ozone en tant que polluant atmosph4rique [Ozone as an air 

. pollutant]. Can. J. Public Health 64: 161-166. 

Kavlock, R.; Daston, G.; Grabowski, C. T. (1979) Studies on the developmental 

toxicity of ozone. I. Prenatal effects. Toxicol. Appl. Pharmacol. 48: 

19-28. 

Kavlock, R. J.; Meyer, E.; Grabowski, C. T. (1980) Studies on the devel.opmental 

toxicity of ozone: postnatal effects. Toxicol. Lett. 5: 3-9. 

Kenoyer, J. L.; Phalen, R. F.; Davis, J. R. (1981) Particle clearance from the 

respiratory tract as a test of toxicity: effect of ozone ori short and 

iong term clearance. Exp. Lung Respir. 2: 111-120. 

Kesner, ~ .; +indya, R. J.; Chan, P. C. (1979) Inhibition of erythrocyte membrane 

(Na + K)-activated ATPase by ozone-treated phospholipids. J. Bioi. Chem. 

254: 2705-2709. ' 

1-221 
References for Toxicological Effects (cont'd.) 

Kindya, R. J.; Chan, P. C. (1976) Effect of ozone on erythrocyte membrane 

adenosine triphosphatase. Biochim. Biophys. Acta 429: 608-615. 

Konigsberg, A. S.; Bachman, C. H. (1970) Ozonized atmosphere and gross motor 

activity of rats. Int. J. Biometeorol. 14: 261-266. 

Koontz, A. E.; ~eath, R. L. (1979) Ozone alteration of transport of cations 

and the Na /K -ATPase in human erythrocytes. Arch. Biochem. Biophys. 

198: 493-500. 

Kotlikoff, M. I.; Jackson, A. C.; Watson, J. W. (1984) Osc -illatory mechanics 

of the respiratory system in ozo,ne-exposed rats. J. Appl. Physiol.: 

Respir. Environ. Exercise Physiol. 56: 182-186. 

Kyei-Aboagye, K.; Hazucha, M.; Wyszogrodski, I.; Rubinstein, D.; Avery, M. E. 

(1973) The effect of ozone exposure in vivo on the appearance of lung 

tissue lipids in the endobronchial lavage of rabbits. Biochem. Biophys. 

Res. Commun. 54: 907-913. 

Larkin, E. C.; Goheen, S. C.; Rao, G. A. (1983) Morphology and fatty acid 

composition of erythrocytes from monkeys exposed to ozone for one year. 

Environ. Res. 32: 445-454. 

Last, J. A.; Cross, C. E. (1978) A new model for health effects of air pollutants: evidence for synergistic effects of mixtures of ozone and sulfuric 

acid aerosols on rat lungs. J. Lab. Clin. Med. 91: 328-339. 

Last, J. A.; Greenberg, D. B. (1980) Ozone- induced alterations in collagen 

metabolism of rat lungs. II. Long-term exposure. Toxicol. Appl. Pharmacol. 

55: 108-114. 

Last, J. A.; Kaizu, T. (1980) Mucus glycoprotein secretion by tracheal explants: 

effects of pollutants. EHP Environ. Health Perspec't. 35: 131-138. 

Last, J. A.; Jennings, M. D.; Schwartz, L. W.; Cross, C. E. (1977) Glycoprotein 

secretion by tracheal explants cultured from rats exposed to ozone. Am. 

Rev. Respir. Dis. 116: 695-703. 

Last, J. A.; Greenberg, D. B.; Castleman, W. L. (1979) Ozone-induced alterations in collagen metabolism of rat lungs. Toxicol. Appl. Pharmacol. 51: 

247-258. 

Last, J. A.; Dasgupta, P. K.; DeCesare, K.; Tarkington, B. K. (1982) Inhalation 

toxicology of ammonium persulfate, an oxidant aerosol, in rats. Toxicol. 

Appl. Pharmacol. 63: 257-263. 

Last, J. A.; Gerriets, J. E.; Hyde, D. M. (1983) Synergistic effects on rat 

lungs of mixtures of oxidant air pollutants (ozone or nitrogen dioxide) 

and respirable aerosols. Am. Rev. Respir. Dis. 128: 539-544. 

Last, J. A.; Hyde, D. M.; Chang, D. P. Y. (1984a) A mechanism of synergistic 

lung damage by ozone and a respirable aerosol. Exp. Lung Res. 7: 223-235. 

1-222 
References for Toxicoloqicai Effects (cont'd.) 

Last, J. A.; Reiser, K. M.; Tyler, W. S.; Rucker, R. B. (1984b) Long-term 

consequences of exposure to ozone. I. Lung collagen content. Toxicol. 

Appl. Pharmacol. 72: 111-118. 

Lee, L.-Y.; Bleecker, E. R.; Nadel, J. A. (1977) Effect of ozone on bronchomotor 

response to inhaled histamine aerosol in dogs. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 43: 626-631. 

Lee, L. -Y. ; Dumont, C. ; Djokic, T. D. ; Menzel , T. E. ; Nadel , J. A. (1979) 

Mechanism of rapid, shallow breathing after ozone exposure in conscious 

dogs. J. Appl. Physiol.: Respir. Environ. Exercise Physioi. 46: 1108-1114. 

Lee, L.-Y.; Djokic, T. D.; Dumont, C.; Graf, P. D.; Nadel, J. A. (1980) Mechanism 

of ozone-induced tachypneic response to hypoxia and hypercapnia in conscious 

dogs. J. Appl. Physiol.: Respir. Environ. Exercise Physiol. 48: 163-168. 

Lewis, T. R.; Hueter, F. G.; Busch, K. A. (1967) Irradiated automobile exhaust: 

its effects on the reproduction of mice. Arch. Environ. Health 15: 26-35. 

Lewis, T. R.; Moorman, W. J.; Yang, Y.; Stara, J. F. (1974) Long-term exposure 

to auto exhaust and other pollutant mixtures: effects on pulmonary function 

in the beagie. Arch. Environ. Health 29: 102-106. 

Lum, H.; Schwartz, L. W.; Dungworth, D. L.; Tyler, W. S. (1978) A comparative 

study of cell renewal after exposure to ozone or oxygen: response of 

terminal bronchiolar epithelium in the rat. Am. Rev. Respir. Dis. 118: 

335-345. 

Lunan, K. D.; Short, P.; Negi, D.; Stephens, R. J. (1977) Glucose-6-phosphate 

dehydrogenase response of postnatal lungs to NO 2 and 03 . In: Sanders, 

C. L.; Schneider, R. P.; Dagle, G. E.; Ragan, H. A., eds. Pulmonary 

macrophage and epithelial cells: proceedings of the sixteenth annual 

Hanford biology symposium; September 1976; ftichland, WA. Washington, DC: 

Energy Research and Development Administration; pp. 236-247. (ERDA 

symposium series: 43). Available from: NTIS, Springfield, VA; CONF-760927. 

MacRae, W. D.; Stich, H. F. (1979) Induction of sister chromatid exchanges in 

Chinese hamster ovary cells by thiol and hydrazene compounds. Mutat. 

Res. 68: 351-365. 

Martin, C. J.; Boatman, E. S.; Ward, G. (1983) Mechanical properties of alveolar wall after pneumonectomy and ozone exposure. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 54: 785-788. 

McAllen, S. J.; Chiu, S. P.; Phalen, R. F.; Rasmussen, R. E. (1981) Effect of 

in vivo ozone exposure on in vitro pulmonary alveolar macrophage mobility. 

J. Toxicol. Environ. Health 7: 373-381. 

McJilton, C..; Thielke, J.; Frank, R. (1972) Ozone uptake model for the respiratory system. In: Abstracts of technical papers: American industrial 

hygiene conference; May; San Francisco, CA. Am. Ind. Hyg. Assoc. J. 

33: paper no. 45. 

1-223 
References for Toxicological Effects (cont'd.) 

Mellick, P. W.; Mustafa, M. G.; Tyler, W. S.; Dungworth, D. L. (1975) Morphologic and biochemical changes in primate lung due to low-level ozone 

exposure. In: Proceedings of the 23rd international tuberculosis conference; 

September; Mexico. Bull. Int. Union Tubercul. 51: 565-567. 

Mellick, P. W.; Dungworth, D. L.; Schwartz, L. W.; Tyler, W. S. (1977) Short 

term morphologic effects of high ambient levels of ozone on lungs of 

rhesus monkeys. Lab. Invest. 36: 82-90. 

Menzel, D. B.; Roehm, J. N.; Lee, S. D. (1972) Vitamin E: the biological and 

environmental antioxidant. J. Agric. Food Chem. 20: 481-486. 

Menzel, D. B.; Slaughter, R. J.; Bryant, A. M.; Jauregui, H. 0. (1975a) Heinz 

bodies formed in erythrocytes by fatty acid ozonides and ozone. Arch. 

Environ. Health 30: 296-301. 

Menzel, D. B.; Slaughter, R. J.; Bryant, A.M.; Jauregui, H. 0. (1975b) Prevention of ozonide-induced Heinz bodies in human erythrocytes by vitamin E. 

Arch. Environ. Health 30: 234-236. 

Miller, F. J.; Illing, J. W.; Gardner, D. E. (1978a) Effect of urban ozone 

7evels on laboratory-induced respiratory infections. Toxicol. Lett. 

2: 163-169. 

Miller, F. J.; Menzel, D. B.; Coffin, D. L. (1978b) Similarity between man and 

laboratory animals in regional deposition of ozone. Environ. Res. 17: 

84-101. 

Mi 11 er, F. J. ; Overton, J. H. , Jr. ; Jas kot, R. H. ; Menzel , D. B. ;(1985) 

A model of the regional uptake of gaseous pollutants in the lung. I. The 

sensitivity of the uptake of ozone in the human lung to lower respiratory 

tract secretions and to exercise. Toxicol. Appl. Pharmacol. 79: 11-27. 

Mizoguchi, I.; Osawa, M.; Sato, Y.; Makino, K.; Yagyu, H. (1973) Studies on 

erythrocyte and photochemical smog. I. Effects of air pollutants on 

erythrocyte resistance. Taiki Osen Kenkyu 8: 414. 

Moore, P. F.; Schwartz, L. W. (1981) Morphological effects of prolonged exposure 

to ozone and sulfuric acid aerosol on the rat lung. Exp. Mol. Pathol. 

35: 108-123. 

Moore, G. S.; Calabrese, E. J.; Grinberg-Funes, R. A. (1980) The C57L/J mouse 

strain as a model for extrapulmonary effects of ozone exposure. Bull. 

Environ. Contam. Toxicol. 25: 578-585. 

Moore, G. S.; Calabrese, E. J.; Labato, F. J. (1981a) Erythrocyte survival in 

sheep exposed to ozone. Bull. Environ. Contam. Toxicol. 27: 126-138. 

Moore, G. S.; Calabrese, E. J.; Schulz, E. (1981b) Effect of in vivo ozone 

exposure to Dorset sheep, an animal model with low levels of erythrocyte 

glucose-6-phosphate dehydrogenase activity. Bull. Environ. Contam. Toxicol. 

26: 273-280. 

1-224 
References for Toxicological Effects (cont'd.) 

Murlas, C. G.; Roum, J. H. (1985) Sequence of pathologic changes in the airway 

mucosa of guinea pigs during ozone-induced bronchial hyperractivity. Am. 

Rev. Respir. Dis. 131: 314-320. 

Murphy, S. D. (1964) A review of effects on animals of exposure to auto exhaust 

and some of its components. J. Air Pollut. Control Assoc. 14: 303-308. 

Murphy, S. D.; Leng, J. K.; Ulrich, C. E.; Davis, H. V. (1963) Effects on 

animals of exposure to auto exhaust. Arch. Environ. Health 7: 60-70. 

Murphy, S. D.; Ulrich, C. E.; Frankowitz, S. H.; Xintaras, C. (1964) Altered 

function in animals inhaling low concentrations of ozone and nitrogen 

dioxide. Am. Ind. Hyg. Assoc. J. 25: 246-253. 

Mustafa, M. G. (1975) Influence of dietary vitamin E on lung cellular sensitivity to ozone in rats. Nutr. Rep. Int. 11: 473-476. 

Mustafa, M. G.; Lee, S. D. (1976) Pulmonary biochemical alterations resulting 

from ozone exposure. Ann. Occup. Hyg. 19: 17-26. 

Mustafa, M. G.; Tierney, D. F. (1978) Biochemical and metabolic changes in the 

lung with oxygen, ozone, and nitrogen dioxide toxicity. Am. Rev. Respir. 

Dis. 118: 1061-1090. 

Mustafa, M. G. ; DeLucia, A. J. ; York, G. K. ; Arth, C. ; Cross, C. E. (1973) 

Ozone interaction with rodent lung. II. Effects on oxygen consumption of 

mitochondria. J. Lab. Clin. Med. 82: 357-365. 

Mustafa, M. G. ; Hacker, A. D. ; Ospital, J. J. ; Hussain, M. Z. ; Lee, S. D. 

(1977) Biochemicai effects of environmental oxidants pollutants in animal 

lungs. In: Lee, S. D.., ed. Biochemical effects of environmental pollutants. Ann Arbor, MI: Ann Arbor Science Publi.shers, Inc.; pp. 59-96. 

Mustafa, M. G.; Elsayed, N. M.; Quinn, C. L.; Postlethwait, E. M.; Gardner, D. 

E.; Graham, J. A. (1982) Comparison of pulmonary biochemical effects of 

low level ozone exposure on mice and rats. J. Toxicol. Environ. Health 

9: 857-865. 

Mustafa, M. G.; Elsayed, N. M.; von Doh7en, F. M.; Hassett, C. M.; Postlethwait, 

E. M.; Quinn, C. L.; Graham, J. A.; Gardner, D. E. (1984) A comparison of 

biochemicai effects of nitrogen dioxide, ozone, and their combination in 

mouse lung. I. Intermittent exposures. Toxicol. Appl. Pharmacol. 72: 82-90. 

Nakajima, T.; Kusumoto, S.; Tsubota, Y.;;Yonekawa, E.; Yoshida, R.; Motomiya, 

K.; Ito, K.; Ide, G.; Otsu, H. (1972). Histopathological studies on the 

respiratory organs of mice exposed;to photochemi"calsoxidants and automobile exhaust. Osaka-furitsu Koshu Eisei Kenkyusho Kenkyu Hokoku Rodo 

Eisei Hen 10: 35-42. 

Nambu, Z.; Yokoyama, E. (1983) Antitoxidant system and,ozone tolerance. Environ. 

Res. 32: 111-117. 

1-225 
References for Toxicoloqical Effects (cont'd.) 

0'Byrne, P. M.; Walters, E. H.; Gold, B. D.; Aizawa, H. A.; Fabbri, L. M.; 

Alpert, S. E.; Nadel, J. A.; Hbltzman, M. J. (1984a) Neutrophil depletion 

inhibits airway hyperresponsiveness induced by ozone exposure. Am. Rev. 

Respir. Dis. 130: 214-219. 

0'Byrne, P. M.; Walters, E. H.; Aizawa, H.; Fabbri, L. M.; Holtzman, M. J.; 

Nadel, J. A. (1984b) Indomethacin inhibits the airway hypperresponsiveness 

but not the neutrophil influx induced by ozone in dogs. Am. Rev. Respir. 

Dis. 130: 220-224. 

Osebold, J. W.; Owens, S. L.; Zee, Y. C.; Dotson, W. M.; LaBarre, D. D. (1979) 

Immunological alterations in the lungs of mice following ozone exposure: 

changes in immunoglobulin levels and antibody- containing cells. Arch. 

Environ. Health 34: 258-265. 

Osebold, J. W.; Gershwin, L. J.; Zee, Y. C. (1980) Studies on the enhancement 

of allergic lung sensitization by inhalation of ozone and sulfuric acid 

aerosol. J. Environ. Pathol. Toxicol. 3: 221-234. 

P'an, A. Y. S.; Jegier, Z. (1971) The serum trypsin inhibitor capacity during 

ozone exposure. Arch. Environ. Health 23: 215-219. 

P'an, A. Y. S.; Jegier, Z. (1972) Trypsin protein esterase in relation to 

ozone-induced vascular damage. Arch. Environ. Health 24: 233-236. 

P'an, A. Y. S.; Jegier, Z. (1976) Serum protein changes during exposure to ozone. 

Am. Ind. Hyg. Assoc. J. 37: 329-334. 

P'an, A. Y. S.; Beland, J.; Jegier, Z. (1972) Ozone-induced arterial lesions. 

Arch. Environ. Health 24: 229-232. 

Pemsingh, R. S.; Atwal, 0. S. (1983) Occurrence of APUD-type cells in the 

ciliated cyst of the parathyroid gland of ozone-exposed dogs. Acta Anat. 

116: 97-105. 

Peterson, D. C.; Andrews, H. L. (1963) The role of ozone in radiation avoidance 

in the mouse. Radiat. Res. 19: 331-336. 

Phalen, R. F. ; Kenoyer, J. L. ; Crocker, T. T. ; McClure, T. R. (1980) Effects 

of sulfate aerosols in combination with ozone on elimination of tracer 

particles inhaled by rats. J. Toxicol. Environ. Health 6: 797-810. 

Plopper, C. G.; Chow, C. K.; Dungworth, D. L.; Brummer, M.; Nemeth, T. J. 

(1978) Effect of low level of ozone on rat lungs. II. Morphological 

responses during recovery and re-exposure. Exp. Mol. Pathol. 29: 400-411. 

Plopper, C. G.; Chow, C. K.; Dungworth, D. L.; Tyler, W. S. (1979) Pulmonary 

alterations in rats exposed to 0.2 and 0.1 ppm ozone: a correlated morphological and biochemical study. Arch. Environ. Health 34: 390-395. 

1-226 
References for Toxicoloqical Effects (cont'd.) 

Raub, J. A.; Miller, F. J.; Graham, J. A. (1983) Effects of low-level ozone 

exposure on pulmonary function in adult and neonatal rats. In: Lee, 

S. D.; Mustafa, M. G.; Mehlman, M. A., eds. International symposium on 

the biomedical effects of ozone and related photochemical oxidants; March 

1982; Pinehurst, NC Princeton, NJ: Princeton Scientific Publishers, 

Inc.; pp. 363-367. (Advances in modern environmental toxicology: v. 5). 

Reasor, M. J.; Adams, G. K., III; Brooks, J. K.; Rubin, R. J. (1979) Enrichment 

of albumin and IgG in the airway secretions of dogs breathing ozone. J. 

Environ. Sci. Health C13: 335-346. 

Revis, N. W. Major, T.; Dalbey, W. E. (1981) Cardiovascular effects of ozone 

and cadmium inhalation in the rat. In: Northrop Services, Inc., ed. 

Proceedings of the research planning workshop on health effects of oxidants; 

January 1980; Raieigh, NC. Research Triangle Park, NC: U.S. Environmental 

Protection Agency, Health Effects Research Laboratory; EPA-600I9-81-001; 

pp. 171-179. Available from: NTIS, Springfield, VA; PB81-178832. 

Reynolds, R. W.; Chaffee, R. R. J. (1970) Studies on the combined effects of 

ozone and a hot environment on reaction time in subhuman primates. In: 

Project clean air: v. 2. Santa Barbara, CA: University of California; 

research project S-6. 

Roehm, J. N.; Hadley, J. G.; Menzel, D. B. (1972) The influence of vitamin E 

on the lung fatty acids of rats exposed to ozone. Arch. Environ. Health 

24: 237-242. 

Roum, J. H.; Murlas, C. (1984) Ozone-induced changes in muscarinic bronchial 

reactivity by different testing methods. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 57: 1783-1789. 

Schlipkoter, H.-W.; Bruch, J. (1973) Funktionelle und morphologische Veranderung 

bei Ozonexposition [Functional and morphological alterations caused by 

exposure to ozone]. Zentralbl. Bakteriol. Parasitenkd. Infektionskr. Hyg. 

Abt. 1: Orig. Reihe B 156: 486-499. 

Schwartz, L. W.; Christman, C. A. (1979) Alveolar macrophage migration: influence of lung lining material and acute lung insult. Am. Rev. Respir. 

Dis. 120: 429-439. 

Schwartz, L. W.; Dungworth, D. L.; Mustafa, M. G.; Tarkington, B. K.; Tyler, 

W. S. (1976) Pulmonary responses of rats to ambient levels of ozone: 

effects of 7-day intermittent or continuous exposure. Lab. Invest. 34: 

565-578. 

Scott, D. B. M. Lesher, E. C. (1963) Effect of ozone on survival and permeability of Escherichia coii. J. Bacteriol. 85: 567-576. 

Sherwood, R. L.; Kimura, A.; Donovan, R.; Goldstein, E. (1984) Effect of 0.64 

ppm ozone on rats with chronic pulmonary bacterial infection. J. Toxicol. 

Environ. Health 13: 893- ~ 04. 

1-227 
References for Toxicological Effects (cont'd.) 

Shingu, H.; Sugiyama, M.; Watanabe, M.; Nakajima, T. (1980) Effects of ozone 

and photochemical oxidants on interferon production by rabbit alveolar 

macrophages. Bull. Environ. Contam. Toxicol. 24: 433-438. 

Sielczak, M. W.; Denas, S. M.; Abraham, W. M. (1983) Airway cell changes in 

tracheal lavage of sheep after ozone exposure. J. Toxicol. Environ. Health 

11: 545-553. 

Speit, G.; Vogel, W.; Wolf, M. (1982) Characterization of sister chromatid 

exchange induction by hydrogen peroxide. Environ. Mutagen. 4: 135-142. 

Stephens, R. J.; Sloan, M. F.; Evans, M. J.; Freeman, G. (1974a) Early response 

of lung to low levels of ozone. Am. J. Pathol. 74: 31-58. 

Stephens, R. J.; Sloan, M. F.; Evans, M. J.; Freeman, G. (1974b) Alveolar type 

1 cell response to exposure to 0.5 ppm 03 for short periods. Exp. Mol. 

Pathol. 20: 11-23. 

Stephens, R. J.; Sloan, M. F.; Groth, D. G.; Negi, D. S.; Lunan, K. D. (1978) 

Cytologic response of postnatal rat lungs to 0 3 or NO2 exposure. Am. J. 

Pathol. 93: 183-200. 

Stewart, R. M.; Weir, E. K.; Montgomery, M. R.; Niewoehner, D. E. (1981) Hydrogen peroxide contracts airway smooth muscle: a possible endogenous mechanism. Respir. Physiol. 45: 333-342. 

Stokinger, H. E.; Wagner, W. D.; Wright, P. G. (1956) Studies on ozone toxicity. 

I. Potentiating effects of exercise and tolerance.development. AMA Arch. 

Ind. Health 14: 158-162. 

Tepper, J. L.; Weiss, B.; Cox, C. (1982) Microanalysis of ozone depression of 

motor activity. Toxicol. Appl. Pharmacol. 64: 317-326. 

Tepper, J. L.; Weiss, B.; Wood, R. W. (1983) Behavioral indices of ozone 

exposure. In: Lee, S. D.; Mustafa, M. G.; Mehlman, M. A., eds. International symposium on the biomedical effects of ozone and related photochemical oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton 

Scientific Publishers, Inc.; pp. 515-526. (Advances in modern environmental toxicology: v. 5). 

Thomas, G.; Fenters, J. D.; Ehrlich, R. (1979) Effect of exposure to PAN and 

ozone on susceptibility to chronic bacterial infection. Research Triangle 

Park, NC: U.S. Environmental Protection Agency, Health Effects Research 

Laboratory; EPA `report no. EPA-600/1-79-001. Available from: NTIS, 

Springfield, VA; PB-292267. 

Thomas, G. B.; Fenters, J. D.; Ehrlich, R.; Gardner, D. E. (1981a) Effects of 

exposure to peroxyacetyl nitrate on susceptibility to acute and chronic 

bacterial infection. J. Toxicol. Environ. Health 8: 559-574. 

Thomas, G. B.; Fenters, J. D.; Ehrlich, R.; Gardner, D. E. (1981b) Effects of 

exposure to ozone on susceptibility to experimental tuberculosis. Toxicol. 

Lett. 9: 11-17. 

1-228 
References for Toxicoiogical Effects (cont'd.) 

Ti ce, R. R. ; Bender, M. A. ; Ivett, J. L. ; Drew, R. T. (1978) Cytogeneti c 

effects of inhaled ozone. Mutat. Res. 58: 293-304. 

Trams, E. G.; Lauter, C. J.; Brown, E. A. B.; Young, 0. (1972) Cerebral cortical metabolism after chronic exposure to ozone. Arch. Environ. Health 24: 

153-159. 

Tyson, C. A.; Lunan, K. D.; Stephens, R. J. (1982) Age-related differences in 

GSH-shuttle enzymes in NO2 - or 0 3 -exposed rat lungs. Arch. Environ. 

Health 37: 167-176. 

Veninga, T. S. (1967) Toxicity of ozone in comparison with ionizing radiation. 

Strahlentherapie 134: 469-477. 

Veninga, T. S. (1970) Ozone-induced alterations in murine blood and liver. 

Presented at: Second international clean air congress; December; 

Washington, DC. Washington, DC: International Union of Air Pollution 

Prevention Associations; paper no. MB-15E. 

Veninga, T. S.; Wagenaar, J.; Lemstra, W. (1981) Distinct enzymatic responses 

in mice exposed to a range of low doses of ozone. EHP Environ. Health 

Perspect. 39: 153-157. 

Verweij, H.; Van Steveninck, J. (1980) Effects of semicarbazide on oxidative 

processes in human red blood cell membranes. Biochim. Biophys. Acta 602: 

591-599. 

Verweij, H.; Van Steveninck, J. (1981) Protective.effects of semicarbazide and 

p-aminobenzoic acid against ozone toxicity. Biochem. Pharmacol. 30: 1033- 

1037. 

Warshauer, D.; Goldstein, E.; Hoeprich, P. D.; Lippert, W. (1974) Effect of 

vitamin E and ozone on the .pulmonary antibacterial defense mechanisms. 

J. Clin. Med. 83: 228-240. 

Watanabe, S.; Frank, R.; Yokoyama, E. (1973) Acute effects of ozone on lungs 

of cats. I. Functional. Am. Rev. Respir. Dis. 108: 1141-1151. 

Wegner, C. D. (1982) Characterization of dynamic respiratory mechanics by measuring pulmonary and respiratory system impedances in adult bonnet 

monkeys (Macaca radiata): including the effects of long-term exposure to 

low-level ozone [dissertation]. Davis, CA: University of California. 

Available from: University Microfilms, Ann Arbor, MI; publication 

no. 82-27900. 

Weiss, B.; Ferin, J.; Merigan, W.; Stern, S.; Cox, C. (1981) Modification of 

rat operant behavior by ozone exposure. Toxicol. Appl. Pharmacol. 

58: 244-251. 

Williams, S. J.; Charles, J. M.; Menzel, D. B. (1980) Ozone induced al terations in phenol red absorption from the rat lung. Toxicol. Lett. 6: 

213-219. 

1-229 
References for Toxicological Effects (cont'd.) 

Witz, G.; Amoruso, M. A.; Goldstein, B. D. (1983) Effect of ozone on alveolar 

macrophage function: membrane dynamic properties. In: Lee, S. D.; Mustafa, 

M. G.; Mehlman, M. A., eds. International symposium on the biomedical 

effects of ozone and related photochemical oxidants; March 1982; Pinehurst, 

NC. Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 263-272. 

(Advances in modern environmental toxicology: v. 5). 

Wolcott, J. A.; Zee, Y. C.; Osebold, J. W. (1982) Exposure to ozone reduces 

influenza disease severity and alters distribution of influenza viral 

antigens in murine lungs. Appl. Environ. Microbiol. 44: 723-731. 

Xintaras, C.; Johnson, B. L.; Ulrich, C. E.; Terrill, R. E.; Sobecki, M. F. 

(1966) Application of the evoked response technique in air pollution 

toxicology. Toxicol. Appl. Pharmacol. 8: 77-87. 

Yokoyama, E. (1969) A comparison of the effects of S0 2 , NO2 and 03 on the 

pulmonary ventilation: guinea pig exposure experiments. Sangyo Igaku 11: 

563-568. 

Yokoyama, E. (1974) On the maximal expiratory flow volume curve of rabbits 

exposed to ozone. Nipon Kyobu Shikkan Gakkai Zasshi 12: 556-561. 

Yokoyama, E.; Frank, R. (1972) Respiratory uptake of ozone in dogs. Arch. 

Environ. Health 25: 132-138. 

Yokoyama, E.; Ichikawa, I.; Nambu, Z.; Kawai, K.; Kyono, Y. J. (1984) Respiratory 

effects of intermittent exposure to ozone of rats. Environ. Res. 33: 

271-283. 

Zelac, R. E.; Cromroy, H. L.; Bolch, W. E., Jr.; Dunavant, B. G.; Bevis, H. A. 

(1971a) Inhaled ozone as a mutagen. I. Chromosome aberrations induced in 

Chinese hamster lymphocytes. Environ. Res. 4: 262-282. 

Zelac, R. E.; Cromroy, H. L.; Bolch, W. E., Jr.; Dunavant, B. G.; Bevis, H. A. 

(1971b) Inhaled ozone as a mutagen. II. Effect on the frequency of chromosome aberrations observed in irradiated Chinese hamsters. Environ. Res. 

4: 325-342. 

Zitni k, L. A. ; Schwartz, L. W. ; McQui 11 en, N. K. ; Zee, Y. C. ; Osebol d, J. W. 

(1978) Pulmonary changes induced by low-level ozone: morphological observations. J. Environ. Pathol. Toxicol. 1: 365-376. 

1.12.9 References for Controlled Human Studies of the Effects of Ozone and 

Other Photochemical Oxidants 

Adams, W. C.; Schelegle, E. S. (1983) Ozone and high ventilation effects on 

pulmonary function and endurance performance. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 55: 805-812. 

1-230 
References for Controlled Human Studies (cont'd. 

Avol, E. L.; Linn, W. S.; Venet, T. G.; Shamoo, D. A.; Hackney, J. D. (1984) 

Comparative respiratory effects of ozone and ambient oxidant pollution 

exposure during heavy exercise. J. Air Pollut. Control Assoc. 34: 804-809. 

Beckett, W. S.; McDonnell, W. F.; Horstman, D. H.; House, D. E. (1985) Role 

of the parasympathetic nervous system in the acute lung response to ozone. 

J. Appl. Physiol. 59: 1879-1885. 

Bedi, J. F.; Drechsler-Parks, D. M.; Horvath, S. M. (1985) Duration of increased pulmonary function sensitivity to an initial ozone exposure. 

Am. Ind. Hyg. Assoc. J. 46: 731-734. 

Dimeo, M. J. ; Glenn, M. G. ; Ho'ltzman, M. J. ; Sheiler, J. R. ; Nadel , J. A. ; 

Boushey, H. A. (1981) Threshold concentration of ozone causing an increase 

in bronchial reactivity in humans and adaptation with repeated exposures. 

Am. Rev. Respir. Dis. 124: 245-248. 

Drechsler-Parks, D. M.; Bedi, J. F.; Horvath, S. M. (1984) Interaction of 

peroxyacetyl nitrate and ozone on pulmonary functions. Am. Rev. Respir. 

Dis. 130: 1033 - 1037. 

Farrell, B. P.; Kerr, H. D.; Kulle, T. J.; Sauder, L. R.; Young, J. L. (1979) 

Adaptation in human subjects to the effects of inhaled ozone after 

repeated exposure. Am. Rev. Respir. Dis. 119: 725-730. 

Folinsbee, L. J.; Drinkwater, B. L.; Bedi, J. F.; Horvath, S. M. (1978) The 

influence of exercise on the pulmonary changes due to exposure to low 

concentrations of ozone. In: Folinsbee, L. J.; Wagner, J. A.; Borgia, J. 

F. ; Dri nkwater, B. L. ; Gl i ner, J. A. ; Bedi , J. F. , eds. Envi ronmental 

stress: individual human adaptations. fVew York, NY: Academic Press; 

pp. 125-145. 

Folinsbee, L. J.; Bedi, J. F.; Horvath, S. M. (1984) Pulmonary function changes 

after 1-hour continuous heavy exercise in 0.21 ppm ozone. J. Appl. 

Physiol.: Respir. Environ. Exercise Physiol. 57: 984-988. 

Folinsbee, L. J.; Horvath, S. M. (1986) Persistence of the acute effects of 

ozone exposure. Aviat. Space Environ. Med. (in press). 

Gliner, J. A.; Horvath, S. M.; Folinsbee, L. J. (1983) Pre-exposure to low 

ozone concentrations does not diminish the pulmonary function response on 

exposure to higher ozone concentration. Am. Rev. Respir. Dis. 127: 51-55. 

Hazucha, M.; Silverman, F.; Parent, C.; Field, S.; Bates, D. V. (1973) Pulmonary 

function in man after short-term exposure to ozone: Arch. Environ. Health_ 

27: 183-188. 

Holtzman, M. I.; Cunningham, J. H.; Sheller, J. R.; Irsigler, G. B.; Nadel, J. 

A.; Boushey, H. A. (1979) Effect of ozone on bronchial reactivity in 

atopic and nonatopic subjects. Am. Rev. Respir. Dis. 120: 1059-1067. 

1-231 
References for Controlled Human Studies (cont'd.) 

Horvath, S. M.; Gliner, J. A.; Matsen-Twisdale, J. A. (1979) Pulmonary function 

and maximum exercise responses following acute ozone exposure. Aviat. 

Space Environ. Med. 50: 901-905. 

Horvath, S. M.; Gliner, J. A.; Folinsbee, L. J. (1981) Adaptation to ozone: 

duration of effect. Am. Rev. Respir. Dis. 123: 496-499. 

Kehrl, H. R.; Hazucha, M. J.; Solic, J.; Bromberg, P. A. (1983) The acute 

effects of 0.2 and 0.3 ppm ozone in persons with chronic obstructive lung 

disease (COLD). In: Mehlman, M. A. ; Lee, S. D. ; Mustafa, M. G. , eds. 

International symposium on the biomedical effects of ozone and related 

photochemical oxidants; March 1982; Pinehurst, NC. Princeton, NJ: 

Princeton Scientific Publishers, Inc.; pp. 213-225. (Advances in modern 

environmental toxicology: v. 5). 

Kehrl, H. R.; Hazucha, M. J.; Solic, J. J.; Bromberg, P. A. (1985) Responses 

of subjects with chronic pulmonary disease after exposures to 0.3 ppm 

ozone. Am.,Rev. Respir. Dis. 131: 719-724. 

Kerr, H. D.; Kulle, T. J.; McIlhany, M. L.; Swidersky, P. (1975) Effects of 

ozone on pulmonary function in normal subjects: Am. Rev. Respir. Dis. 

111: 763-773. 

Koenig, J. Q.; Covert, D. S.; Morgan, M. S.; Horike, M.; Horike, N.; Marshall, 

S. G.; Pierson, W. E. (1985) Acute effects of 0.12 ppm ozone or 0.12 ppm 

nitrogen dioxide on pulmonary function in healthy and asthmatic adolescents. Am. Rev. Respir. Dis. 132: 648-651. 

Konig, G.; Rommelt, H.; Kienele, H.; Dirnagl, K.; Polke, H.; Fruhmann, G. 

(1980) Changes in the bronchial reactivity of humans caused by the influence of ozone. Arbeitsmed. Sozialmed. Praeventivmed. 151: 261-263. 

Kul le, T. J. ; Sauder, L. R. ; Kerr, H. D. ; Farrel l, B. P. ; Bermel , M. S. ; 

Smith, D. M. (1982) Duration of pulmonary function adaptation to ozone 

in humans. Am. Ind. Hyg. Assoc. J. 43: 832-837. 

Kul le, T. J. ; Mi lman, J. H. ; Sauder, L. R. ; Kerr, H. D. ; Farrel 1, B. P. ; 

Miller, W. R. (1984) Pulmonary function adaptation to ozone in subjects 

with chronic bronchitis. Environ. Res. 34: 55-63. 

Kulle, T. J.; Sauder, L. R.; Hebel, J. R.; Chatham, M. D. (1985) Ozone 

response relationships in healthy nonsmokers. Am. Rev. Respir. Dis. 

132: 36-41. 

Linn, W. S. ; Buckley, R. D. ; Spier, C. E. ; Blessey, R. L. ; Jones, M. P. ; 

Fischer, D. A.; Hackney, J. D. (1978) Health effects of ozone exposure in 

asthmatics. Am. Rev. Respir. Dis. 117: 835-843. 

Li nn, W. S. ; Fi scher, D. A. ; Medway, D. A. ; Anzar, U. T. ; Spi er, C. E. ; 

Valencia, L. M.; Venct, T. G.; Hackney, J. D. (1982a) Short-term respiratory effects of 0.12 ppm ozone exposure in volunteers with chronic obstructive lung disease. Am. Rev. Respir. Dis. 125: 658-663. 

1-232 
References for Controlled Human Studies (cont'd.) 

Linn, W. S.; Medway, D. A.; Anzar, U. T.; Valencia, L. M.; Spier, C. E.; Tsao, 

F. S-0.; Fischer, D. A.; Hackney, J. D. (1982b) Persistence of adaptation 

to ozone in volunteers exposed repeatedly over six weeks. Am. Rev. Respir. 

Dis. 125: 491-495. 

Li nn, W. S. ; Shamoo, D. A. ; Venet, T. G. ; Spi er, C. E. ; Val enci a, L. M. ; 

Anzar, U. T.; Hackney, J. D. (1983) Response to ozone in volunteers with 

chronic obstructive pulmonary disease. Arch. Environ. Health 38: 278-283. 

McDonnell, W. F.; Horstmann, D. H.; Hazucha, M. J.; Seal, E., Jr.; Haak, E. 

D.; Salaam, S.; House, D. E. (1983) Pulmonary effects of ozone exposure 

during exercise: dose-response characteristics. J. Appl. Physioi.: Respir. 

Environ. Exercise Physiol. 54: 1345-1352. 

McDonnell, W. F., III; Hortsman, D. H.; Abdul-Salaam, S.; House, D. E. (1985a) 

Reproducibility of individual responses to ozone exposure. Am. Rev. 

Respir. Dis. 131: 36-40. 

McDonnell, W. F., III; Chapman, R. S.; Leigh, M. W.; Strope, G. L.; Collier, 

A. M. (1985b) Respiratory responses of vigorously exercising children to 

0.12 ppm ozone exposure. Am. Rev. Respir. Dis. 132: 875-879. 

McDonnell, W. F.; Chapman, R. S.; Horstman, D. H.; Leigh, M. W.; Abdul-Salaam, 

S. (1985c) A comparison of the responses of children and adults to acute 

ozone exposure. In: Lee, S. D., ed. Evaluation of the scientific basis for 

ozone/oxidants standards; November 1984; Houston, TX. Pittsburgh, PA: Air 

Pollution Control Association; pp. 317-328 (APCA international specialty 

conference transactions: TR-4). 

Silverman, F. (1979) Asthma and respiratory irritants (ozone). EHP Environ. 

Health Perspect. 29: 131-136. 

Silverman, F.; Folinsbee, L. J.; Barnard, J.; Shephard, R. J. (1976) Pulmonary 

function changes in ozone - interaction of concentration and ventilation. 

J. Appl. Physiol. 41: 859-864. 

Solic, J. J.; Hazucha, M. J.; Bromberg, P. A. (1982) The acute effects of 0.2 

ppm ozone in patients with chronic obstructive pulmonary disease. Am. 

Rev. Respir. Dis. 125: 664-669. 

1.12.10 References for Field and Epidemiological Studies of the Effects of 

Ozone and Other Photochemical Oxidants 

Avol, E. L.; Linn, W. S.; Shamoo, D. A.; Venet, T. G.; Hackney, J. D. (1983) 

Acute respiratory effects of Los Angeles smog incontinuously exercising 

adults. J. Air Pollut. Control Assoc. 33: 1055-1060. 

Avol, E. L.; Linn, W. S.; Venet, T. G.; Shamoo, D. A.; Hackney, J. D. (1984) 

Comparative respiratory effects of ,ozone and ambient oxidant pollution 

exposure during heavy exercise. J. Air Pollut. Control Assoc. 34: 804-809. 

1-233 
References for Field and Epidemioloqical Studies (cont'd.) 

Avol, E. L.; Linn, W. S.; Shamoo, D. A.; Valencia, L. M.; Anzar, U. T.; Hackney, 

J. D. (1985a) Respiratory effects of photochemical oxidant air pollution 

in exercising adolescents. Am. Rev. Respir. Dis. 132: 619-622. 

Avol , E. L. ; Li nn, W. S. ; Shamoo, D. A. ; Val enci a, L. M. , Anzar, U. T. ; 

Hackney, J. D. (1985b) Short-term health effects of ambient air pollution 

in adolescents. In: Lee, S. D., ed. Evaluation of the scientific basis 

for ozone/oxidants standards; November 1984; Houston, TX. Pittsburgh, PA: 

Air Pollution Control Association; pp. 329-336. (APCA international 

specialty conference transactions: TR-4). 

Avol , E. L. ; Li nn, W. S. ; Venet, T. G. ; Shamoo, D. A. ; Spi er, C. E. ; 

Hackney, J. D. (1985c) Comparative effects of laboratory generated ozone 

and ambient oxidant exposure in continuously exercising subjects. In: 

Lee, S. D., ed. Evaluation of the scientific basis for ozone/oxidants 

standards; November 1984; Houston, TX. Pittsburgh, PA: Air Pollution 

Control Association; pp. 216-225. (APCA international specialty 

conference transactions: TR-4). 

Bock, N.; Lippmann, M.; Lioy, P.; Munoz, A.; Speizer, F. (1985) The effects of 

ozone on the pulmonary function of children. In: Lee, S. D., ed. 

Evaluation of the scientific basis for ozone/oxidants standards; November 

1984; Houston, TX. Pittsburgh, PA: Air Pollution Control Association; 

pp. 297-308. (APCA international specialty conference transactions: TR-4). 

Hammer, D. I.; Hasselblad, V.; Portnoy, B.; Wehrle, P. F. (1974) Los Angeles 

student nurse study: daily symptom reporting and photochemical oxidants. 

Arch. Environ. Health 28: 255-260. 

Herman, D. R. (1972) The effect of oxidant air pollution on athletic performance [master's thesis]. Chapel Hill, NC: Unive.rsity of North Carolina. 

Holguin, A. H.; Buffler, P. A.; Contant, C. F., Jr.; Stock, T. H.; Kotchmar, 

D.; Hsi, B. P.; Jenkins, D. E.; Gehan, B. M.; Noel, L. M.; Mei, M. (1985) 

The effects of ozone on asthmatics in the Houston area. In: Lee, S. D., ed. 

Evaluation of the scientific basis for ozone/oxidants standards; November 

1984; Houston, TX. Pittsburgh, PA: Air Pollution Control Association; pp. 

262-280. (APCA international specialty conference transactions: TR-4). 

Lebowitz, M. D. (1984) The effects of environmental tobacco smoke exposure and 

gas stoves on daily peak flow rates in asthmatic and non-asthmatic families. 

Eur. J. Respir. Dis. 65 (suppl. 133): 90-97. 

Lebowitz, M. D.; 0'Rourke, M. K. Dodge, R.; Holberg, C. J.; Corman, G. 

Hoshaw, R. W. ; Pinnas, J. L. ; Barbee, R. A. ; Snel ler, M. R. (1982) The 

adverse health effects of biological aerosols, other aerosols, and indoor 

microclimate on asthmatics and nonasthmatics. Environ. Int. 8: 375-380. 

Lebowitz, M. D.; Holberg, C. J.; Dodge, R. R. (1983) Respiratory effects on 

populations from low level exposures to ozone. Presented at: 76th annual 

meeting of the Air Pollution Control Association; June; Atlanta, GA. 

Pittsburgh, PA: Air Pollution Control Association; paper no. 83-12.5. 

1-234 
References for Field and Epidemiolo ical Studies (cont'd.) 

Lebowitz, M. D.; Holberg, C. J.; Boyer, B.; Hayes, C. (1985) Respiratory 

symptoms and peak flow associated with indoor and outdoor air pollutants 

in the southwest. J. Air Pollut. Control Assoc. 35: 1154-1158. 

Linn, W. S.; Jones, M. P.; Bachmayer, E. A.; Spier, C. E.; Mazur, S. F.; Avol, 

E. L.; Hackney, J. D. (1980) Short-term respiratory effects of polluted 

ambient air: a laboratory study of volunteers in a high-oxidant community. 

Am. Rev. Respir. Dis. 121: 243-252. 

Linn, W. S.; Avol, E. L.; Hackney, J. D. (1983) Effects of ambient oxidant 

pollutants on humans: a movable environmental chamber study. In: Lee, S. 

D.; Mustafa, M. G.; Mehlman, M. A., eds. International symposium on the 

biomedical effects of ozone and related photochemical oxidants; March 

1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers, 

Inc.; pp. 125-137. (Advances in modern toxicology: v. 5). 

Lioy, P. J.; Vollmuth, T. A.; Lippman, M. (1985) Persistance of peak flow 

decrement in children following ozone exposures exceeding the National 

Ambient Air Quality Standard. J. Air Pollut. Control Assoc.: 35: 1068-1071. 

Lippmann, M.; Lioy, P. J.; Leikauf, G.; Green, K. B.; Baxter, D.; Morandi, M.; 

Pasternack, B. S. (1983) Effects of ozone on the pulmonary function of 

children. In: Lee, S. D.; Mustafa, M. G.; Mehlman, M. A., eds. International symposium on the biomedical effects of ozone and related photochemical oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton 

Scientific Publishers, Inc.; pp. 423-446. (Advances in modern toxicology: 

v. 5). 

Makino, K.; Mizoguchi, I. (1975) Symptoms caused by photochemical smog. Nippon 

Koshu Eisei Zasshi 22: 421-430. 

Wayne, W. S.; Wehrle, P. F.; Carroll, R. E. (1967) Oxidant air pollution and 

athletic performance. J. Am. Med. Assoc. 199: 901-904. 

Whittemore, A. S.; Korn, E. L. (1980) Asthma and air pollution in the Los 

Angeles area. Am. J. Public Health 70: 687-696. 

1.12.11 References for Evaivation of Health Effects Data for Data for Ozone and 

Other Photochemical Oxidants 

Avol, E. L.; Linn, W. S.; Venet, T. G.; Shamoo, D. A.; Hackney, J. D. (1984) 

Comparative respiratory effects of ozone and ambient oxidant pollution 

exposure during heavy exercise. J. Air Pollut: Control Assoc. 34: 804-809. 

Avol , E. L. ; Li nn, W. S. ; Shamoo, D. A. ; Val enci a, L. M. ; Anzar., U. T. ; 

Hackney, J. D. (1985a) Respiratory effects of photochemical oxidant air 

pollution in exercising adolescents. Am. Rev. Respir. Dis. 132: 619-622. 

1-235 
References for Evaluation of Health Effects Data (cont'd.) 

Avol , E. L. ; Li nn, W. S. ; Shamoo, D. A. ; Val enci a, L. M. ; Anzar, U. T. ; 

Hackney, J. D. (1985b) Short-term health effects of ambient air pollution 

in adolescents. In: Lee, S. D., ed. Evaluation of the scientific basis 

for ozone/oxidants standards; November 1984; Houston, TX. Pittsburgh, PA: 

Air Pollution Control Association; pp. 329-336 (APCA international 

specialty conference transactions: TR-4). 

Avol, E. L.; Linn, W. S.; Venet, T. G.; Shamoo, D. A.; Spier, C. E.; Hackney, 

J. D. (1985c) Comparative effects of laboratory generated ozone and ambient 

oxidant exposure in continously exercising subjects. In: Lee, S. D., ed. 

Evaluation of the scientific basis for ozone/oxidants standards; November 

1984; Houston, TX. Pittsburgh, PA: Air Pollution Control Association;= 

pp. 216-225. (APCA international specialty conference transactions: TR-4). 

Bedi, J. F.; Dreschsler-Parks, D. M.; Horvath, S. M. (1985) Duration of increased 

pulmonary function sensitivity to an initial ozone exposure. Am. Ind. Hyg. 

Assoc. J. 46: 731-734. 

Folinsbee, L. J.; Horvath, S. M. (1986) Persistence of the acute effects of ozone 

exposure. Aviat. Space Environ.,Med. (in press). 

Folinsbee, L. J.; Bedi, J. F.; Horvath, S. M. (1984) Pulmonary function changes 

after 1-hour continuous heavy exercise in 0.21 ppm ozone. J. Appl. Physiol.: 

Respir. Environ. Exercise Physiol. 57: 984-988. 

Gliner, J. A.; Horvath, S. M.; Folinsbee, L. J. (1983) Pre-exposure to low 

ozone concentrations does not diminish the pulmonary function response on 

exposure to higher ozone concentration. Am. Rev. Respir. Dis. 127: 51-55. 

Horvath, S. M.; Gliner, J. A.; Folinsbee, L. J. (1981) Adaptation to ozone: 

duration of effect. Am. Rev. Respir. Dis. 123: 496-499. 

Kulle, T. J.; Sauder, L. R.; Hebel, J. R.; Chatham, M. D. (1985) Ozone 

response relationships in healthy nonsmokers. Am. Rev. Respir. Dis. 

132: 36-41. 

McDonnell, W. F.; Horstmann, D. H.; Hazucha, M. J.; Seal, E., Jr.; Haak, E. D.; 

Salaam, S.; House, D. E. (1983) Pulmonary effects of ozone exposure during 

exercise: dose-response characteristics. J. Appl. Physiol.: Respir. 

Environ. Exercise Physiol. 54: 1345-1352. 

McDonnell, W. F., III; Horstman, D. H.; Abdul-Salaam, S.; House, D. E. (1985a) 

Reproducibility of individual responses of ozone exposure. Am. Rev. Respir. 

Dis. 131: 36-40. 

McDonnell, W. F., III; Chapman, R. S.; Leigh, M. W.; Strope, G. L. 

Collier, A. M. (1985b) Respiratory responses of vigorously exercising 

chi 1 dren to 0.12 ppm ozone exposure. Am. Rev. Respi r. Di s. 132: 875-879. 

1-236 
References for Evaluation of Health Effects Data (cont'd.) 

McDonnell ; W. F.; Chapman, R. S.; Horstman, D. H.; Leigh, M. W.; Abdul-Salaam, 

S. (1985c) A comparison of the responses of chiidren and adults to 

acute ozone exposure. In: Lee, S. D., ed. Evaluation of the scientific 

basis for ozone/oxidants standards; November 1984; Houston, TX. 

Pittsburgh, PA: Air Pollution Control Association; pp. 317-328. 

(APCA international specialty conference transactions: TR-4). 

.~ 

1-237 

U. S. GOVERZalENT PRINTING OFFICB:1986- 6 4 6- 1 1 6/ 4 0 6 5 7 




~ O DmC 

ci (a :3 m ~ 5. r: 

. ~o Q 

o t" 3 cn 

uci m o: ~ 

~

(D 

<' CD — 

CD p 

C: ~ 

(n n 

(D 

' O 

N ~ 

W 

O 

O 

(D 

o o =3 

53 c~~D 

p~ ~• o -• O 1 

O m _ < c~n o 

N :3 

~ 

0D cp 

7 

.. 

0~ 

~ 

m m 

'0 ~i, 

c a, 

•c :e ,

~. ~ a~ » w w 

N cD 

~ ^ 

? c a m ~ m 

c~i O a~ ~ o ~ 7 O 3 S °^ w ° o m , 

Oo t =v° f a < N 7,°< m w ~ 

a~ 

~ w ~ w 

C:~ 

0) 7 w 

O

(I ~ 

~ a fSD d a m S 7 w 

7D 

» O 

tG 

CD 

Q- M 

a O 

w = ~ Gi 

nn ~ o ;K 

w ~ 

w < 

c w 

m 9d 

~. m 1° ~  ~ 

w 

=r O w .. 

t .